tag:blogger.com,1999:blog-83243796935639031832024-03-13T06:47:35.448-07:00Biology ResourcesGudang Informasi BiologiAry Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.comBlogger16125tag:blogger.com,1999:blog-8324379693563903183.post-74181519870063074762010-01-07T17:33:00.000-08:002010-01-07T17:45:34.691-08:00<center><h2>Amino Acid Metabolism</h2></center> <div style="text-align: justify;">This page describes the amino acids that are important in human nutrition. It covers the digestion and absorbtion of proteins in the gut, some of the amino acid degradation pathways in the tissues, and the urea cycle. There are separate pages dealing with nucleotide and 'one carbon' metabolism and with porphyrin metabolism. Other aspects of amino acid biochemistry are covered in the section on the integration of metabolism. Click here to skip over the detailed contents section.<br /><br /></div> <a name="start"><h3>Protein turnover</h3></a> <div style="text-align: justify;"><img src="http://www.bmb.leeds.ac.uk/illingworth/metabol/turnover.gif" align="right" width="200" height="240" />The recommended minimal protein intake required to achieve nitrogen balance in healthy adults is about 50g per day, although in developed countries many people may eat double this amount. This compares with an average daily protein turnover of about 250g per day. Human proteins have very different lifetimes. Total body protein is about 11kg, but about 25% of this is collagen, which is metabolically inert. A typical muscle protein might survive for three weeks, but many liver enzymes turn over in a couple of days. Some regulatory enzymes have half-lives measured in hours or minutes. The majority of the amino acids released during protein degradation are promptly re-incorporated into fresh proteins. Net protein synthesis accounts for less than one third of the dietary amino acid intake, even in rapidly growing children consuming a minimal diet. Most of the ingested protein is ultimately oxidised to provide energy, and the surplus nitrogen is excreted, a little as ammonia but mostly as urea.<br /></div><p style="text-align: justify;">Soluble intracellular proteins are tagged for destruction by attaching ubiquitin, a low molecular weight protein marker. They are then degraded in proteasomes to short peptides. A very few of these are displayed on the cell surface by the MHC [major histocompatibility] complex as part of the immune system, but most of them are further metabolised to free amino acids. Some proteins are degraded by an alternative system within the lysosomes.<br /></p><p style="text-align: justify;">Dietary proteins are initially denatured by the stomach acid, in conjunction with limited proteolysis by pepsin. In young mammals gastric rennin [do not confuse with renin!] partially hydrolyses and precipitates milk casein and increases gastric residence time. Gastric acid also kills most ingested bacteria, rendering the upper part of the gut almost sterile.<br /></p><p style="text-align: justify;">Protein digestion is largely completed in the small intestine at a slighlty alkaline pH. The pancreatic proteases trypsin, chymotrypsin and elastase divide the proteins into short peptides. These are attacked from both ends by aminopeptidase and carboxypeptidase, and the fragments are finished off by dipeptidases secreted from the gut wall.<br /></p><div style="text-align: justify;">Amino acid uptake from the gut lumen into enterocytes is driven by the sodium gradient. There is a relatively high sodium concentration in the gut (regardless of dietary intake, as a result of the pancreatic secretion of sodium bicarbonate) and a low concentration in the enterocytes, as a result of the sodium pump in the basolateral membrane. A multiplicity of sodium-linked amino acid carriers operate within the intestinal brush border, balanced by sodium-independent export carriers on the serosal surface (i.e. the opposite side) of the cells.<br /></div><p><a name="gluta"><h3>Central role of glutamate</h3></a></p><div style="text-align: justify;"> Four of the amino acids: glutamate, aspartate, alanine and glutamine are present in cells at much higher concentrations than the other 16. All four have major metabolic functions in addition to their roles in proteins, but glutamate occupies the prime position.<br /></div><p> <img style="width: 366px; height: 183px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/amacids.gif" align="middle" /> </p><p style="text-align: justify;">Glutamate and aspartate function as excitatory neurotransmitters in the central nervous system, and glutamate is partly responsible for the flavour of food. (It is the mono sodium glutamate listed on processed food labels.) However, glutamate also occupies a special position in amino acid breakdown, and most of the nitrogen from dietary protein is ultimately excreted from the body via the glutamate pool.<br /></p><div style="text-align: justify;">Glutamate is special because it is chemically related to 2-oxoglutarate (= alpha keto glutatarate) which is a key intermediate in the citric acid (Krebs) cycle. Glutamate can be reversibly converted into oxoglutarate by transaminases or by glutamate dehydrogenase. In addition, glutamate can be reversibly converted into glutamine, an important nitrogen carrier, and the most common free amino acid in human blood plasma.<br /></div><p><a name="trans"><h3>Transamination reactions</h3></a></p><div style="text-align: justify;"> Most common amino acids can be converted into the corresponding keto acid by transamination. This reaction swops the amino group from one amino acid to a different keto acid, thereby generating a new pairing of amino acid and keto acid. There is no overall loss or gain of nitrogen from the system - it is simply a question of "robbing Peter to pay Paul".<br /></div><p> <img style="width: 312px; height: 104px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/aminoket.gif" align="middle" /> </p><p style="text-align: justify;">Transamination reactions are readily reversible, and the equilibrium constant is close to 1. One of the two pairs is almost invariably glutamate and its corresponding keto acid oxoglutarate, although there are a few exceptions to this rule. All transaminases require pyridoxal phosphate (derived from vitamin b6) as a cofactor.<br /></p><div style="text-align: justify;">The substrates bind to the active centre one at a time, and the function of the pyridoxal phosphate is to act as a temporary store of amino groups until the next substrate comes along. In the process the pyridoxal phosphate is converted into pyridoxamine phosphate, and then back again. Enzymologists call this a "ping pong" mechanism, and it leads to a characteristic pattern in the reaction kinetics.<br /></div><p> <img style="width: 353px; height: 353px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/pingpong.gif" align="middle" /> </p><div style="text-align: justify;">The condensation between the alpha amino group and the aromatic aldehyde to form a "Schiff base" makes the alpha carbon atom chemically reactive, so the isomerisation of the Schiff base takes place very easily. In practice the pyridoxal form of the coenzyme condenses with the epsilon amino group of a lysine residue in the enzyme protein when no amino acid is bound, and the free aldehyde form of the coenzyme has only a transitory existence. Many of the enyzmes that metabolise amino acids require pyridoxal phosphate as a cofactor. Unexpectedly, this compound also serves in a different manner in the active centre of glycogen phosphorylase.<br /></div><p><a name="got"><h3>Glutamate:oxaloacetate transaminase [GOT]</h3></a></p><div style="text-align: justify;"> This enzyme is also known as aspartate aminotransferase and is one of the most active enzymes in the cell. It exists in mitochondrial and cytosolic variants, and the detailed iso-enzyme pattern is tissue-specific. It escapes in large amounts from dead or dying tissues and enters the bloodstream, so GOT is often measured in blood samples for medical diagnostic purposes.<br /></div><p> <img style="width: 301px; height: 145px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/gotdiag.gif" align="middle" /> </p><p style="text-align: justify;">The metabolic importance of this enzyme is that it brings about a free exchange of amino groups between glutamate (which is the most common amino acid) and aspartate which is a second major amino acid pool. Glutamate and aspartate are each required for separate but essential steps in the urea cycle, which is responsible for ammonia detoxication and nitrogen excretion. The free movement of nitrogen between the glutamate and aspartate pools is an important balancing process that is vital for normal cellular metabolism.<br /></p><div style="text-align: justify;">This reaction is close to equilibrium in both the cytosol and the mitochondrial compartments. It forms an integral part of the malate - asparate shuttle which is effectively responsible for the "transport" of NADH across the inner mitochondrial membrane. </div><p><a name="gptcy"><h3>Glutamate:pyruvate transaminase [GPT]</h3></a></p><div style="text-align: justify;">This very active enzyme is also known as alanine aminotransferase and exists in mitochondrial and cytosolic variants. The detailed iso-enzyme pattern is tissue-specific. It escapes in large amounts from dead or dying tissues and GPT may be measured in blood samples for medical diagnostic purposes.<br /></div><p> <img style="width: 336px; height: 162px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/gptdiag.gif" align="middle" /> </p><div style="text-align: justify;">Alanine is the principal amino acid released from muscle tissue during starvation. It is an important substrate for hepatic gluconeogenesis, and alanine transamination is required for the proper maintenance of fasting blood glucose concentrations.<br /><a name="gludh"><h3>Glutamate dehydrogenase [GluDH]</h3></a></div><p style="text-align: justify;"> This enzyme is the first committed step on the final common pathway for mammalian nitrogen excretion, leading eventually to urea. A few of the amino acids have specific deamination pathways, but about 75% of ingested protein nitrogen follows the glutamate route.<br /></p><div style="text-align: justify;">Glutamate dehydrogenase in mammals is almost entirely confined to the liver mitochondrial matrix space, where it accounts for a significant proportion of the total protein. In contrast to the transamination reactions which merely swop amino groups from one compound to another, GluDH catalyses a net loss of nitrogen from the amino acid pool. The process is therefore termed "oxidative deamination". It is the only common dehydrogenase which is non-specific for NAD or NADP, and this may be important for its overall regulation.<br /></div><p> <img style="width: 289px; height: 162px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/gludh.gif" align="middle" /> </p><p style="text-align: justify;">NADH / NAD and NADPH / NADP have the same standard redox potential of -420mV when the oxidised and reduced forms are present in equal concentrations. In practice these coenzymes have different effective redox potentials and perform specialised functions within cells. The NADPH / NADP pool operates almost entirely in the reduced form, but the NADH / NAD pool is rarely more than 30% reduced. In general NADPH is used to drive reductive biosynthetic reactions, whereas NAD is the coenzyme for the oxidative energy-yielding pathways.<br /></p><p style="text-align: justify;">The dual coenzyme specificity is a potential source of difficulty for the cell, since in theory this readily reversible enzyme could catalyse a futile cycle, proceeding first in the oxidative direction with NAD, followed by a reductive step using NADPH. The effect would be to "short circuit" the two coenzyme pools, which normally require considerable investment in substrates and cellular equipment to keep them separate. If this futile cycle happens to any significant extent then it must be an <i>advantage</i> for the cell, because it has persisted unchanged for 2,000,000,000 years of evolutionary development.<br /></p><p style="text-align: justify;">The most likely explanation at present is that this futile cycle takes place, but for various reasons it does not place an excessive burden on its owner. The Km of GluDH for ammonia is quite high, and the free ammonia concentration is kept very low by the next enzyme in the pathway, carbamyl phosphate synthetase. This will severely reduce the rate of the synthetic reaction, and allow the enzyme to catalyse a net glutamate oxidation at a slow controlled rate that provides the maximum opportunity for regulatory interference.<br /></p><p style="text-align: justify;">Regulation is plainly critical at this point, since GluDH and carbamyl phosphate synthetase jointly control the overall rate of nitrogen excretion and determine whether a particular individual will be in positive, neutral or negative nitrogen balance. Control of unwanted nitrogen losses remains an important unsolved problem after major surgery, burns or other serious traumatic injuries.<br /></p><p style="text-align: justify;">The enzyme is indeed modulated by adenine and guanine nucleotides, although it is difficult to make much sense of the observed effects. GluDH has all the hallmarks of a large multimeric allosteric enzyme, although the true nature of the regulation</p><div style="text-align: justify;"> Remains to be identified. The situation is in some ways similar to the parallel NAD and NADP linked oxidation pathways for malate and isocitrate, although the competing reactions for these substrates are separately regulated and catalysed by different proteins.<br />The liver GluDH gene is located on chromosome 10. OMIM link Surp<br /></div><br /><div style="text-align: justify;">risingly few genetic defects have been reported, possibly reflecting the catastrophic nature of the resulting fault. There are reports of an additional GluDH gene located on the X chromosome <a href="http://www3.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?300144"></a>OMIM link which is expressed in testis and neural tissues. This seems to be a processed pseudogene that is still functional.<br /></div><p><a name="trand"><h3>Trans-deamination</h3></a></p><div style="text-align: justify;"> Most transaminases share a common substrate and product (glutamate and oxoglutarate) with glutamate dehydrogenase, and this permits a combined nitrogen excretion pathway for individual amino acids that is commonly described as "trans-deamination".<br /></div><p> <img style="width: 366px; height: 133px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/trandeam.gif" align="middle" /> </p><div style="text-align: justify;">This process underlines the central role of glutamate in the overall control of nitrogen metabolism.<br /></div><p><a name="ureac"><h3>Urea cycle</h3></a></p><div style="text-align: justify;"> Ammonium ions are in equilibrium with about 1% free ammonia at physiological pH. Ammonium salts are toxic compounds, causing vomiting, convulsions and ultimately coma and death when the blood concentration exceeds approximately 0.25mM. It is not entirely clear why this should be so: it may be that ammonium ions mimic potassium ions, but gain access as uncharged ammonia to areas from which they should be excluded. Alternatively, they may favour the synthesis of excessive amounts of glutamate and glutamine which have excitatory effects on neural tissues.<br /></div><p style="text-align: justify;">It is therefore necessary to have an efficient means to remove ammonia from the body. Water-living species commonly excrete free ammonia through their gills [ammonotelism], but this easy option is not available to land dwellers which produce a variety of less toxic nitrogenous end products. Urea synthesis and excretion [ureotelism] first evolved in lungfish and primitive amphibia about 400 million years ago. The process is replicated today when ammonotelic tadpoles leave the water and metamorphose into ureotelic frogs. Urea is also used in humans, and in all placental mammals, which start to express the urea cycle genes around the time of birth. Urea is very soluble, but still requires appreciable quantities of water for its removal via the kidneys. This imposes a minimum daily water requirement and limits the range of environments that these species can exploit.<br /></p><p style="text-align: justify;">Urea is not the only possible solution to the problem: spiders excrete guanine, which packs no less than 5 surplus nitrogen atoms into a single small molecule, while reptiles and birds excrete mainly uric acid [uricotelism]. Uric acid is an extremely insoluble purine compound that readily forms supersaturated solutions. This has been turned to advantage in uricotelic species, which can survive in extremely arid environments. They regurgitate concentrated urine, supersaturated with uric acid, from the cloaca into the hindgut where the uric acid crystalises and the residual water is resorbed. The uric acid forms the fine pasty mass of white crystals that is familiar to us in bird droppings.<br /></p><p style="text-align: justify;">Uricotelism is also an advantage to animals that lay shelled eggs, which of necessity have a zero water intake. The uric acid crystalises within the allantois, part of which eventually becomes incorporated into the lower gut as the embryo develops. In humans the insolubility of uric acid is a considerable nuisance, since it gives rise to the extremely painful deposits of small crystals [called "tophi"] within the joints of patients suffering from gout.<br /></p><p style="text-align: justify;">Urea is synthesised via the urea cycle, which is confined to mammalian liver. Individual enzymes from the urea cycle are present in other tissues, and may be important for arginine biosynthesis, but the complete cycle does not occur. Extra-hepatic tissues export their surplus nitrogen to the liver by other routes, principally as the amino acids alanine and glutamine. In addition, the cleavage of arginine by nitric oxide synthetase generates citrulline, which is a urea cycle intermediate. Citrulline is recycled to arginine, and in tissues which use the nitric oxide signalling system the relevant urea cycle enzymes have sufficient activity to maintain cellular arginine supplies.<br /></p><div style="text-align: justify;">The urea cycle takes place partly in the cytosol and partly in the mitochondria, and the individual reactions are as follows.<br /></div><p><a name="cps1"><h4>carbamyl phosphate synthetase 1 [CPS1]</h4></a></p><div style="text-align: justify;"> This mitochondrial enzyme converts the ammonia produced by glutamate dehydrogenase into carbamyl phosphate (=carbamoyl phosphate) which is an unstable high energy compound. It is the mixed acid anhydride of carbamic acid and phosphoric acid, and requires two molecules of ATP to drive its synthesis.<br /></div><p> <img style="width: 342px; height: 159px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/cpsynth.gif" align="middle" /> </p><p style="text-align: justify;">CPS1 is strongly activated by N-acetyl glutamate, which controls the overall rate of urea production. This bizarre method of regulation is not fully understood: N-acetyl glutamate is an intermediate in the bacterial synthesis of ornithine, but this feature has been lost from mammals and only the regulatory system has survived. There is a futile cycle catalysed by the enzymes N-acetylglutamate synthetase and N-acetylglutamate hydrolase. This is plainly important for the control of nitrogen metabolism, but we do not yet know how it works.<br /></p><div style="text-align: justify;">CPS1 deficiency results in hyperammonemia. <a href="http://www3.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?237300"></a>OMIM link The neonatal cases are usually lethal, but there is also a less severe, delayed-onset form. Ammonia-dependent CPS1 is present only in the liver mitochondrial matrix space. It should be distinguished from a second <i>cytosolic</i> glutamine-dependent carbamyl phosphate synthetase [CPS2] which is found in all tissues and is involved in pyrimidine biosynthesis. Carbamyl phosphate synthesis is a major burden for liver mitochondria. This enzyme accounts for about 20% of the total protein in the matrix space. Glutamate dehydrogenase is also present in very large amounts.<br /></div><p><a name="otcase"><h4>ornithine transcarbamylase [OTCase]</h4></a></p><div style="text-align: justify;"> The next reaction also takes place in the liver mitochondrial matrix space, where ornithine is converted into citrulline.<br /></div><p> <img style="width: 318px; height: 158px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/otcase.gif" align="middle" /> </p><p style="text-align: justify;">This enzyme has no regulatory significance. However, the OTCase gene is on the X chromosome and an inherited deficiency is observed in males, with an incidence of about 1 in 80,000 people. <a href="http://www3.ncbi.nlm.nih.gov/htbin-post/Omim/dispmim?311250"></a>OMIM link This is the most common of the inherited urea cycle defects. Patients show all the symptoms of hyperammonemia, and in addition may excrete abnormal amounts of orotate, since the unused carbamyl phosphate escapes into the cytosol and enters the pyrimidine biosynthetic pathway.<br /></p><h4><a name="oport">ornithine</a> and <a name="cport">citrulline</a> porters</h4><div style="text-align: justify;"> The remainder of the urea cycle takes place in the cytosol. This requires the continuous export of citrulline and the uptake of ornithine across the inner mitochondrial membrane. These processes are catalysed by specific amino acid porters, which are present only in liver mitochondria. A very rare deficiency state has been described.<br /></div><h4 style="text-align: justify;"><a name="glutp">Glutamate</a> and <a name="glasp">glutamate:aspartate porters</a></h4><div style="text-align: justify;"> Urea production requires continuous mitochondrial glutamate uptake, to replenish the substrate for the glutamate dehydrogenase reaction. This process is catalysed by a specific electroneutral glutamate / hydroxyl antiporter, which is largely confined to liver mitochondria.<br /></div><div style="text-align: justify;">In addition, depending on the diet, mitochondria may also need to export aspartate in exchange for glutamate in order to balance the supplies of nitrogen to the mitochondrial and cytosolic segments of the urea cycle. This electrical process is driven by the mitochondrial membrane potential and is discussed more fully in connection with the malate - aspartate cycle.<br /></div><p><a name="argss"><h4>arginino-succinate synthetase</h4></a></p><div style="text-align: justify;"> Once in the cytosol, citrulline condenses with aspartate and the reaction is driven by ATP. In this way aspartate contributes the second nitrogen atom to urea, the first having come from glutamate.<br /></div><p> <img style="width: 354px; height: 177px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/asucsyn.gif" align="middle" /> </p><div style="text-align: justify;">Production of arginino-succinate is an energetically expensive process, since the ATP is split to AMP and pyrophosphate. The pyrophosphate is then cleaved to inorganic phosphate using pyrophosphatase, so the overall reaction costs two equivalents of high energy phosphate per mole.<br /></div><p><a name="aslya"><h4>arginino-succinate lyase</h4></a></p><div style="text-align: justify;"> Elimination of fumarate from arginino-succinate then yields arginine.<br /></div><p> <img style="width: 335px; height: 189px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/asucase.gif" align="middle" /> </p><p style="text-align: justify;">This reaction sequence is very similar to the conversion of IMP to AMP in the purine biosynthetic pathway. In each case fumarate is formed as a by-product. Fumarate is not transported by mitochondria, so this requires the presence of cytosolic <a name="fumac"><b>fumarase</b></a> to form malate.<br /></p><center> fumarate + H<sub>2</sub>O = malate </center><br /><p style="text-align: justify;">The reaction is readily reversible, and the equilibrium slightly favours malate. The cytosolic and mitochondrial fumarase isoenzymes are extremely similar and derived from the same gene through alternative mRNA splicing reactions. OMIM link<br /></p><div style="text-align: justify;">Cleavage of arginine by <a name="argin"><b>arginase</b></a> to produce urea regenerates ornithine, which is then available for another round of the cycle.<br /></div><p> <img style="width: 390px; height: 206px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/arginase.gif" align="middle" /> </p><div style="text-align: justify;">The transcriptional regulation of the urea cycle genes was reviewed by Takaguchi & Mori (1995) Biochem. J. 312, 649 - 659. Unfortunately this document is not available on line, but a more recent wide-ranging review on arginine metabolism (Wu & Morris (1998) Biochem. J. 336, 1 - 17) and an article by Kimura et al (1998) J. Biol. Chem. 273, 27505 - 27510 can both be downloaded in Adobe portable document format. In essence, the urea cycle enzymes appear around the time of birth, and thereafter reflect the rate of amino acid catabolism, either from dietary sources or from tissue breakdown. The principal inducing stimuli are glucagon and glucocorticoids, and the main repressor is insulin. The CCAAT/enhancer binding protein (C/EBP) seems to play a major role. Urea cycle regulation and control of blood ammonia levels are impaired in C/EBP knockout mice.<br /></div><p><a name="nitric"><h3>Nitric Oxide</h3></a></p><div style="text-align: justify;"> In addition to its metabolic functions in the urea cycle, arginine is also the immediate precursor for nitric oxide [NO], an important signalling molecule involved in the local regulation of blood flow. Nitric oxide synthase uses oxygen and NADPH, and the other products are citrulline and NADP.<br /></div><p> <img style="width: 334px; height: 176px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/nitrox.gif" align="middle" /> </p><p style="text-align: justify;">The citrulline is reconverted to arginine using two of the urea cycle enzymes, although the full urea cycle does not take place outside the liver. See also the review by Wu & Morris mentioned above.<br /><a name="essen"><h3>Essential and non-essential amino acids</h3></a> Humans can degrade all the amino acids that are commonly found in proteins, but we have very limited synthetic capacity. However, the initial transamination step in most of the amino acid breakdown pathways is freely reversible. If the corresponding keto acids are produced during normal metabolism, then it may be possible to use surplus nitrogen from other sources to make good a dietary deficiency in some of these "non-essential" amino acids, providing that the total nitrogen intake is sufficient.<br /></p><p style="text-align: justify;">In addition, a few amino acids are degraded to form other amino acids (for example, phenylalanine is metabolised initially to tyrosine) so that tyrosine is essential on a minimal diet, but becomes non-essential if sufficient phenylalanine is eaten. Tyrosine is therefore described as a "conditionally essential" amino acid.<br /></p><div style="text-align: justify;">Relatively few keto acids and amino acids can be produced from alternative sources, so about half of the amino acids are essential in the diet. [See table below.]<br /></div><p><a name="glyco"><h3>Glycogenic and ketogenic amino acids</h3></a></p><div style="text-align: justify;"> The carbon skeletons from the majority of amino acids are degraded to Krebs cycle intermediates after removal of the amino group by transamination. This means that they can give rise to blood glucose via the gluconeogenic pathway. They are termed 'glycogenic' amino acids, because it was observed many years ago that they made diabetic glycosuria worse. In contrast to this 'ketogenic' amino acids exacerbated diabetic ketoacidosis, and these amino acids are degraded to compounds such as acetoacetate and acetyl-CoA. 'Mixed' amino acids are degraded to both Krebs cycle acids and to acetyl-CoA.<br /></div><br /><center><br /></center> <a name="glunh2"><h3>Glutamine metabolism</h3></a><div style="text-align: justify;"> In view of the toxicity of free ammonia and ammonium salts, cells require a non-toxic source of nitrogen for use in nitrogen transport and biosynthetic reactions. This need is satisfied by glutamine, which is the most common free amino acid in human blood plasma.<br /></div><div style="text-align: justify;">Glutamine is readily synthesised from glutamate and ammonium ions by the enzyme glutamine synthetase. This enzyme is present in liver and in many other body tissues. It has a low Km for ammonium, and works efficiently at non-toxic ammonium concentrations. The required energy comes from ATP:<br /></div><p> <img style="width: 357px; height: 201px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/glusyn.gif" align="middle" /> </p><p style="text-align: justify;">Glutamine supplies most of the nitrogen required for purine and pyrimidine biosynthesis, and for the manufacture of amino sugars. When necessary it can be degraded back to glutamate by the enzyme glutaminase:<br /></p><center>glutamine + H<sub>2</sub>O = glutamate + NH<sub>4</sub><sup>+</sup></center><br /><p style="text-align: justify;">Glutaminase is activated by inorganic phosphate. It is obvious that glutamine synthetase and glutaminase constitute a potential futile cycle, and the arrangment must be delicately regulated to avoid wasteful hydrolysis of ATP. <i>The two enzymes are commonly present in different cells,</i> and this seems to be particularly important in the liver and in the central nervous system. In liver, the urea cycle enzymes, glutamate:pyruvate transaminase and glutaminase are concentrated in the periportal cells, whereas glutamine synthetase is concentrated in the perivenous cells near the hepatic veins. See, for example, Racine et al (1995) Biochem. J. <b>305,</b> 263-268; Dingemanse et al (1996) Hepatology <b>24,</b> 407-411 and also Lie-Venema et al (1997) Biochem. J. <b>323,</b> 611-619. Subscribers can download the last article <a href="http://www.biochemj.org/bj/323/0611/3230611.pdf"></a>here in Adobe pdf format.<br /></p><div style="text-align: justify;">In addition to the numerous biosynthetic uses for glutamine, kidney tubules can use ammonia derived from glutamine to control the urinary pH, and avoid large cation losses under acidotic conditions. In neural tissues, formation of glutamine is thought to terminate the action of glutamate, an excitatory neurotransmitter. Glutamine is a particularly important fuel for the cells lining the gut, and has been used experimentally in the treatment of gastrointestinal disease. Large amounts of glutamine and alanine are released from muscle cells during starvation, and these are important substrates for hepatic gluconeogenesis under fasting conditions.<br /></div><p><a name="pku"><h3>Phenylketonuria</h3></a></p><div style="text-align: justify;"> Phenylalanine is normally metabolised by conversion to tyrosine. The enzyme responsible for this conversion is phenylalanine hydroxylase, a mixed function oxygenase with a tetrahydrobiopterin cofactor:<br /></div><p> <img style="width: 325px; height: 219px;" src="http://www.bmb.leeds.ac.uk/illingworth/metabol/phetyr.gif" align="middle" /> </p><p style="text-align: justify;">Half of the oxygen molecule re-appears in the tyrosine -OH group and the other half is reduced to water. The "dihydrobiopterin" in the above reaction is an isomer of the folic acid compounds involved in one-carbon metabolism. It is recycled back to tetrahydrobiopterin using NADH:<br /></p><center> "dihydrobiopterin" + NADH = tetrahydrobiopterin + NAD</center><br /><p style="text-align: justify;">Approximately one person in 45 American whites is a carrier for a defective phenylalanine hydroxylase gene, or (less frequently) the dihydrobiopterin cofactor. These mutations are particularly common in people of Celtic origin, but are less frequent in Eastern Europe. OMIM link Blood phenylalanine levels are elevated, but otherwise these heterozygotes show no symptoms and may even enjoy a heterozygote advantage. Homozygotes occur about 1 in 8,000 live births (45 * 45 * 4) and are very severely affected. Unless treated they are seriously mentally defective and excrete large quantities of phenylpyruvate in the urine. This compound gives the disease its name, and is formed by the transamination of phenylalanine, a reaction that is normally insignificant. These patients are often tyrosine deficient, and have abnormally light skin pigmentation, because they have insufficient tyrosine to synthesise melanin in normal amounts.<br /></p><p style="text-align: justify;">When this condition was first recognised in the 1930's, a significant proportion of <u>all</u> long term patients in mental institutions proved to be undiagnosed phenylketonuriacs. Nowadays the condition can be readily diagnosed by a heel-prick blood test performed on all new-born babies.<br /></p><div style="text-align: justify;">Treatment consists of a very low phenylalanine diet, supplemented with extra tyrosine that the patients cannot synthesise from phenylalanine. This diet must be instituted at birth, but can be discontinued after a few years when brain maturation is completed. For obvious reasons it must be restarted during pregnancy. The artificial sweetner aspartame is a phenylalanine derivative, and this fact is declared on soft drinks cans to assist those following the special diet.<br /></div><a name="memau"><h3>Methyl malonic aciduria</h3></a><div style="text-align: justify;"> Four amino acids: isoleucine, methionine, threonine and valine are degraded to propionyl CoA. Some additional propionate is formed in the gut from bacterial fermentation, and a little from the oxidation rare odd-numbered fatty acids. Patients with a metabolic block in the vitamin B12 dependent conversion of propionyl CoA to succinyl CoA suffer from a severe metabolic acidosis, and excrete large quantities of methyl malonic acid in their urine.</div>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-16680318095872273632010-01-06T16:52:00.000-08:002010-01-06T16:55:02.816-08:00<p><span style="font-family:Arial, Helvetica, sans-serif;font-size:100%;"><b><span style="font-size:180%;">REPRODUCTIVE SYSTEM</span><br /></b></span></p><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;"><br /></span><p><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;"><b><a name="intro"></a><span style="font-size:130%;">Introduction</span></b></span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">Sexual reproduction is the process of producing offspring for the survival of the species, and passing on hereditary traits from one generation to the next. The male and female reproductive systems contribute to the events leading to fertilization. Then, the female organs assume responsibility for the developing human, birth, and nursing. The male and female gonads (testes and ovaries) produce sex cells (ova and sperm) and the hormones necessary for the proper development, maintenance, and functioning of the organs of reproduction and other organs and tissues.</span></p> <p><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/9885.jpg" width="400" height="320" /></p> <p><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;"><a href="http://www.besthealth.com/besthealth/bodyguide/reftext/html/repr_sys_fin.html#menu"><br /></a></span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The reproductive system comprises the reproductive organs. In the male, the organs include the testes, accessory ducts, accessory glands, and penis. In the female, the organs include the uterus, uterine tubes, ovaries, vagina, and vulva.</span></p> <p><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;"><b><a name="male"></a><span style="font-size:130%;">Male reproductive organs</span></b></span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The testes are paired reproductive organs in the scrotum, which hangs outside the human body. Normal sperm production requires the cooler outside temperature. Each testis contains coiled seminiferous tubules where sperm (male reproductive cells) production occurs. Between the seminiferous tubules are Leydig cells, clusters of endocrine (secretory) cells. Leydig cells produce androgens (sex hormones), mostly testosterone.</span></p> <p><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/sperm_parts.jpg" width="400" height="320" /></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">Each sperm cell has three parts: a head, middle piece, and tail. An acrosome at the head tip produces enzymes that help penetrate the female ovum (egg). During conception, chromosomes (genetic material) in the nucleus (cell control center) join with chromosomes in the ovum. The middle piece contains mitochondria, structures that provide energy for the sperm. The mitochondria are tightly spiraled around the axial filaments (contractile portion) of the flagellum (tail). Centrioles form the tail, which moves the sperm toward the ovum. An ejaculation (ejection of sperm from the penis) has 300 to 500 million sperm.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The accessory ducts store secretions from the testes and accessory glands and deliver secretions to the penis. The epididymis, a coiled tube next to each testis, receives sperm from the seminiferous tubules. The epididymis has three parts: a head, body, and tail. The epididymis stores sperm and propels it toward the penis. Smooth muscle contractions in the epididymis walls move sperm through the duct. As sperm pass through the epididymis, the sperm mature and receive nourishment.</span></p> <p><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/10016.jpg" width="400" height="320" /></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The vas deferens is the dilated continuation of the epididymis. The vas deferens travels out of the scrotum and into the abdomen (gut cavity) through the inguinal canal. Once in the abdomen, the vas deferens passes behind the urinary bladder and expands to form an ampulla (expanded end part). Each ampulla joins with a seminal vesicle (an accessory gland) to form an ejaculatory duct. The vas deferens is the main sperm carrier. Its walls contain three layers of smooth muscle innervated by sympathetic nerves. Stimulation of these nerves propels sperm into the ejaculatory ducts. Here, the ampulla of the vas deferens and seminal vesicles meet and secretions from the seminal vesicles and sperm are stored. From this junction, the ejaculatory ducts pass through the prostate gland, where they receive more secretions, then join with the single urethra (tube through which sperm and urine pass out of body).</span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The urethra is the final section of the duct system. It passes from the urinary bladder and the ends of the ejaculatory ducts through the prostate gland and into the penis. The urethra receives secretions from the ejaculatory ducts, the prostate gland, and the bulbourethral glands (accessory glands). The urethra carries sperm through the penis during intercourse; during urination, urine passes through it. The urethra cannot execute both functions simultaneously. During ejaculation, a muscular sphincter (ring of muscle) closes off the bladder.</span></p> <p><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/8677.jpg" width="400" height="320" /></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The accessory glands produce fluids that nourish and energize the sperm for the journey to the ovum. For example, during sexual excitement the seminal vesicles add secretions to the sperm in the ejaculatory duct. These secretions provide energy for the sperm and a neutralizing chemical that reduces vaginal acidity.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The prostate gland lies under the urinary bladder and surrounds the first part of the urethra. Its secretions also help neutralize vaginal acidity and make sperm motile (able to move).</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The bulbourethral glands secrete a clear fluid that neutralizes the acidity of remaining urine in the urethra. When secretions of these glands combine with sperm, the result is seminal fluid, or semen. Only 1 percent of semen is sperm. The remainder contains fructose to nourish the sperm, an alkaline component to neutralize vaginal and urethral acidity, and salts and phospholipids, substances that make sperm motile.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The penis (male sexual organ) deposits semen into the vagina during sexual intercourse and carries urine through the urethra during urination. It contains erectile tissue that becomes engorged with blood during sexual excitement, resulting in an erection. The penis includes the shaft (tubular portion), glans (penis tip and sexual sensation center), and the prepuce, or foreskin (loose skin fold over glans). In a circumcision procedure, the prepuce is removed.</span></p> <span style="text-decoration: underline;"><br /></span> <p><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;"><b><a name="female"></a><span style="font-size:130%;">Female reproductive organs</span></b></span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The female reproductive system is more complex than that of the male. It produces ova (egg cells); nourishes, carries, and protects the developing embryo; and nurses the newborn after birth. The system structures are the ovary, uterine tubes, uterus, vagina, vulva, and mammary glands.</span></p> <p style="text-align: justify;"><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/9110.jpg" width="400" height="320" /></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">Ovaries, a pair of female gonads (sex organs), reside in the pelvic part of the abdomen on either side of the uterus. Ovaries produce ova and estrogen (female sex hormone).</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">At puberty onset, the menstrual (uterine) cycle, a series of cyclic changes to the endometrium (uterine lining) begins. The ovarian cycle, fluctuating levels of ovarian hormones in the blood, causes the menstrual cycle.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The ovarian and menstrual cycles begin each month when a follicle (developing ovum surrounded by a cluster of cells) develops in the ovary. The hypothalamus in the brain produces hormones that cause these cycles. The hypothalamus releases gonadotropin-releasing hormone (GnRH), which acts on the anterior pituitary gland. GnRH causes the pituitary to release two more hormones: follicle-stimulating hormone (FSH) and luteinizing hormone (LH). FSH causes the primary oocyte within the follicle to develop into a secondary oocyte. Development occurs through meiosis (cell division that reduces the chromosome number in the cell from 46 to 23). Each secondary oocyte completes this division only when sperm fertilizes it.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The developing follicle produces estrogen, which causes the endometrium to prepare to nourish a fertilized egg. Estrogen also inhibits pituitary gland production of FSH. The elevated estrogen level causes the anterior pituitary to release LH. This action causes ovulation, a process in which the follicle rapidly enlarges and releases the secondary oocyte. LH also causes the collapsed follicle to become the corpus luteum, an endocrine (secretory) body. The corpus luteum secretes estrogen and progesterone (hormone that stimulates endometrium thickening). These hormones complete the endometrium development and maintain the endometrium for 10 to 14 days.</span></p> <p style="text-align: justify;"><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/8652.jpg" width="400" height="320" /></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">Unless sperm fertilize the secondary oocyte, the corpus luteum begins to degenerate, dropping blood progesterone levels. Without progesterone to maintain the endometrial lining, the lining is shed with the degenerated oocyte approximately 14 days after ovulation.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">After ovulation, estrogen and progesterone act in the bloodstream to inhibit anterior pituitary production of LH and FSH. This negative feedback control ensures that only one follicle develops each cycle. Each cycle lasts approximately 28 days.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The uterine tubes (oviducts or fallopian tubes) are paired tubes that receive the developing ovum from the ovary. The infundibulum end is beside the ovary; its fimbria (feathery structures) "sweep" the developing ovum into the tube. The ampulla, the middle part of the uterine tube, contains smooth muscle to move the egg. Cilia (inner wall little projections) also sweep the egg along the tube. The unfertilized ovum degenerates in the ampulla; the fertilized ovum resumes its journey to the uterus. The isthmus end of the uterine tube opens into the uterus.</span></p> <p><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The uterus is a hollow muscular organ in front of the rectum and behind the urinary bladder. The fundus is the wide upper portion. The body is the tapered middle part that ends at the cervix (junction between the vagina and uterus). The isthmus is the constricted region between the body and cervix. The round ligaments hold the uterus anteverted (inclined forward) over the urinary bladder.</span></p> <p><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/uterus_parts.jpg" width="400" height="320" /></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The uterus has three layers. The outer serous layer forms ligaments that hold it to the pelvic walls. The middle muscular layer has three muscle layers used in labor to deliver a baby. The endometrium inner mucosal lining has two layers, the stratum functionalis and stratum basalis.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">Every month the stratum functionalis is built up in response to estrogen secretion. It contains blood vessels and glands to nourish the fertilized ovum. Unless sperm fertilizes the secondary oocyte, the corpus luteum disintegrates into corpus albicans, and estrogen and progesterone secretion cease. Without these hormones, the endometrium breaks down and menstruation (expulsion of endometrial lining from the uterus through the vagina) occurs. After menstruation, progesterone and LH levels decrease. The inhibition of LH causes the anterior pituitary to secrete FSH, which stimulates development of another ovum. The monthly cycle begins again.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The vagina is a muscular tube from the uterus to outside the body. In some women, the hymen (thin tissue) partially covers the vaginal orifice. Initial sexual intercourse or other form of penetration ruptures the hymen. The vagina receives sperm from sexual intercourse, channels menstrual flow out of the body, and is a birth canal for the baby during childbirth. Normally collapsed, it can enlarge to accommodate an erect penis or a birth.</span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The vulva, external genitalia, includes the mons pubis, labia majora, labia minora, and clitoris. The mons pubis is a mound of fatty tissue at the junction of the thighs and torso. During puberty, pubic hair covers it. The labia majora are skin folds that form the vulva outer border. During puberty, pubic hair covers the labia majora, too. The labia minora are inner, smaller skin folds that surround the urethral and vaginal openings. The labia minora merge anteriorly to form the prepuce (foreskin) of the clitoris. This small erectile structure, comparable to the male penis, becomes engorged with blood during sexual excitement and is the female center of sexual sensation.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The mammary glands have 15 to 20 lobes of glandular tissue. The lobes contain lactiferous ducts that converge toward the nipple. These ducts dilate just before they reach the lactiferous sinus, then constrict again before passing out of the nipple through 15 to 20 openings.</span></p> <p style="text-align: justify;"><img src="http://www.besthealth.com/besthealth/bodyguide/reftext/images/Breast.jpg" width="400" height="320" /></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The mammary glands are in the breasts. These glands overlie the pectoral muscles and are attached to them via fascia (connective tissue). The glands are connected to the skin by the suspensory ligaments of the breast. These glands are modified sweat glands that produce and secrete milk during the lactation process to feed the newborn. During pregnancy, high blood estrogen and progesterone levels stimulate lactation. The corpus luteum produces these hormones during early pregnancy; the placenta takes over later. The hormones stimulate the ducts and glands in the breasts, enlarging the breasts.</span></p> <p><span style="font-family:Arial, Helvetica, sans-serif;font-size:130%;"><a href="http://www.besthealth.com/besthealth/bodyguide/reftext/html/repr_sys_fin.html#menu"><br /></a></span></p> <p><span style="font-family:Arial, Helvetica, sans-serif;font-size:130%;"><b><a name="development"></a>Development of sex cells</b></span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">The formation of sex cells begins before birth; spermatozoa form in males and oocytes in females. Spermatogenesis (sperm cell production) occurs in the seminiferous tubules. Spermatogonia (stem cells) line these tubules at birth and contain 46 chromosomes (genetic material). After birth, spermatogonia continue to divide during mitosis. This cell division process produces two daughter cells with the same chromosome number (46) as the parent.</span></p><div style="text-align: justify;"> </div><p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">At puberty onset, some spermatozoa grow to become primary spermatocytes. These cells undergo meiosis, the cell division process that cuts back the number of chromosomes from 46 to 23. Each primary spermatocyte undergoes the first meiotic division to produce two secondary spermatocytes. Each secondary spermatocyte undergoes the second meiotic division to produce two spermatids. Each spermatid develops into a mature spermatozoon (sperm cell). In this way, meiosis produces millions of sperm every day.</span></p> <p style="text-align: justify;"><span style="font-family:Arial, Helvetica, sans-serif;font-size:85%;">Oogenesis is the formation of the ovum (female sex cells), which begin as hundreds of thousands of oogonia (stem cells) in the fetal ovaries. During prenatal development, the oogonia grow to become primary oocytes that contain 46 chromosomes. Each oocyte undergoes meiosis; at birth, oocytes are in prophase. During this first meiotic division, oocytes enter a resting phase that lasts until the oocyte resumes development during the ovarian cycle (puberty). The female is born with all the oocytes she will ever have.</span></p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-87719785548753644732010-01-05T16:30:00.000-08:002010-01-05T16:32:29.309-08:00<div class="title"><h1>Konsep Pembelahan sel</h1></div> <div class="info-single"> <div class="gravatar"><br /></div> <strong></strong></div> <p style="font-weight: bold;" align="justify"><span style="font-size:180%;"><span style="font-size: small;">Tujuan Pembelahan Sel</span></span></p> <p align="justify">Sel merupakan struktur terkecil dari makhluk hidup, oleh karena itu sel sangat menentukan fungsi dan bentuk dari organ atau jaringan yang disusunnya. Kumpulan dari banyak sel dengan struktur dan fungsi yang sama disebut jaringan dan kumpulan jaringan dengan tujuan fungsi tertentu disebut organ.</p> <p align="justify">Untuk bisa mencapai jumlah banyak, sel melakukan pembelahan. Pembelahan sel mempunyai tujuan sebagai berikut :</p> <ul><li> <div>Regenerasi sel-sel yang rusak/mati</div> </li><li> <div>Pertumbuhan dan perkembangan</div> </li><li> <div>Berkembang biak (reproduksi)</div> </li><li> <div>Variasi individu baru</div> </li></ul> <p align="justify"><span style="font-size: small;">Macam-macam Pembelahan Sel</span></p> <p align="justify">Terdapat 3 macam pembelahan sel dengan tujuan dan fungsi yang berbeda, yaitu :</p> <p align="justify"><span style="font-weight: bold;">1</span>. <strong>Pembelahan Mitosis</strong></p> <p align="justify">Pembelahan mitosis adalah pembelahan sel dimana sel anak identik dengan sel induk. Tahapan pembelahan mitosis sebagai berikut :</p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1pQfJLveQWvPCINeL8Ypppa7pCYn1IzEj0up6iaLtjNMO6FZeHUojkWcObBNJlsk1JyaCcQeIRUExo100_5X_OQg?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pLVB6brcwsPFjJFd1MrzPZXPsJQQm2DFvFo3FViA4SqQgG5-oVTLckJPmj11T5QbLA3KGmE55KiI?PARTNER=WRITER" alt="Mitosis" border="0" width="420" height="271" /></a></p> <p align="justify"><span style="text-decoration: underline;">gambar 1.1 : tahapan pembelahan mitosis</span></p> <p align="justify">Dari gambar diatas diketahui bahwa sel anak dan sel induk identik dan mempunyai jumlah kromosom yang sama.</p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1prZDz9ItHxkoROWkJf6KZPrs7unfLWxCcqIN_C76-j0pT0FG8FsaQjWCjv1HvroBZ2HtXsaQCWJKXLzPuyd1Qcw?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pKLiTC3xlMafG-Duwa_8sB4fKoZgXNcA3ArJ7TAFlrSjv3xs8NPy5mHYlR6_9VSzVzfyOLh5GaPk?PARTNER=WRITER" alt="mitosis fase" border="0" width="410" height="264" /></a></p> <p align="justify"><span style="text-decoration: underline;">gambar 1.2 : tahapan pembelahan mitosis dan check point</span></p><br /><p><span id="more-16"></span><span style="font-weight: bold;">2. </span><strong>Pembelahan Meiosis</strong></p> <p align="justify">Meiosis atau pembelahan reduksi adalah pembelahan dengan proses yang hampir sama dengan pembelahan mitosis namun pada meiosis terjadi pngurangan (reduksi) jumlah kromosom. Meiosis terbagi menjadi 2 tahapan besar yaitu meiosis I dan meiosis II, masa istirahat antara keduanya disebut interfase.</p> <p align="justify">Sel somatik manusia terdiri dari 46 kromosom (23 pasang kromosom), setengah berasal dari tiap orang tua. Masing-masing dari 22 autosom maternal memiliki kromosom paternal yang homolog. Pasangan kromosom ke 23 adalah kromosom seks yang menentukan jenis kelamin seseorang,</p> <p align="justify">Sel ovum dan sperma hanya mempunyai setengah kromosom (haploid / n), apabila ovum dan sperma bersatu (fertilisasi) akan terbentuk zigot diploid (2n) yang akan tumbuh menjadi individu baru dengan gen hasil kombinasi dari ovum dan sperma. Tahapan pembelahan meiosis sebagai berikut :</p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1pLqAV9BRK3IB99N3k0l1CRVN5s9d0m9Mv4RVTJk9-BJ_eM7kX5jCtMTM_dDi7s668DPKTTXh77uYpVWiSgb0C6A?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pzU1IWRUyXfvNWMnpy-AlftB2UmmdZ1Wt-CS4bnD6ro1iMr8fWPAY9OMyEFbCPxqtXAdXWhWP1Qs?PARTNER=WRITER" alt="meiosis" border="0" width="408" height="250" /></a></p> <p align="justify"><span style="text-decoration: underline;">gambar 2.1 : tahapan pembelahan meiosis</span></p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1pX0LQQthLm1zQ7Dfv2AjxSUcTu1EW6ZChDXecOkNlz0ARJlN4zQLeGtNEulvACJZW2exhJnXv06yl8BH2wK5o8g?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1p0DknxNrPdNAC1x1gzEIaXCJppjz8RCeQJ6z3GKt1w4NAT5U56OCkvp-AYcmZBSn7g7CzaBD2m6A?PARTNER=WRITER" alt="meiosis1" border="0" width="419" height="314" /></a></p> <p align="justify"><span style="text-decoration: underline;">gambar 2.2 : tahapan pembelahan meiosis I dan II</span></p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1p339Mnfo2gHNboMs3KbRyNS8gt3r5Bj3etYdnxZjkPQbdeN65WwqjASlyOcMJEOAUuxYYnH9MlTkQ1qsSwHyD1w?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pCM8NuBBs3oQkRGiOYMnmPChMAFigWojk5tbopov3Pl-Ka7ssKuHaeNW4bSAxIfxaJXu-8LlYytg?PARTNER=WRITER" alt="mitosis vs meiosis" border="0" width="423" height="322" /></a></p> <p align="justify"><span style="text-decoration: underline;">gambar 2.3 : perbedaan tahapan meiosis dan mitosis</span></p> <p align="justify"><strong>Gangguan Pembelahan Meiosis</strong></p> <p align="justify">Kesalahan selama pembelahan meiosis dapat merubah :</p> <ol><li> <div>Jumlah kromosom per sel</div> </li><li> <div>struktur tiap kromosom</div> </li></ol> <p align="justify">Kedua kesalahan diatas bisa berakibat pada fenotip (sifat yang muncul pada individu).</p> <p align="justify"> </p><p align="justify"><strong>2.1. Kesalahan Jumlah kromosom</strong></p> <p align="justify">Nondisjunction meiosis dapat terjadi jika homolog gagal berpisah selama anafase M-1 dan kromatid gagal berpisah selama M-2 yang pada akhirnya gamet memiliki jumlah kromosom yang abnornal.</p> <p align="justify">Terdapat 2 gangguan jumlah kromosom :</p> <p align="justify">1. Aneuploid</p> <ul><li> <div>Trisomik (2n+1)</div> </li><li> <div>Monosomik (2n-1)</div> </li></ul> <p align="justify">2. Poliploid</p> <ul><li> <div>Triploid (3n)</div> </li><li> <div>Tetraploid (4n)</div> </li></ul> <p align="justify"><strong>2.2 Kesalahan Struktur Kromosom</strong></p> <p align="justify">Perubahan struktur kromosom dapat menyebabkan terjadinya empat macam struktur, yaitu :</p> <ul><li> <div>Delesi</div> </li><li> <div>Duplikasi</div> </li><li> <div>Inversi</div> </li><li> <div>Translokasi</div> </li></ul> <p align="justify">a. Delesi</p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1p_wNz-vci-_-jZGVDtPcyQ0VP0JpdqBJcgFYw1vTRaUaTxa2IaNzjox0Kn1jRW0P4mZds-8OmjJvO3SZfVmD7mA?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pKul5AFD7D3kk94pKhNiYCAtf6FgGmPbxIzUHDTkUvu5TyuIz_yWFJ64bx5_VwMhqnhW_-jMIeCE?PARTNER=WRITER" alt="duplikasi" border="0" width="419" height="242" /></a></p> <p align="justify">b. Duplikasi</p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1pGhb694kQkIaa2ANYFw3SaNennTKzygcGKK3TyfF_o0Iwo5-bdeeAfhnPcmEhQJSkr6cFys5V6UPpVjTCZMYN5g?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pIb0chKBrLcSoeNY8vtU6WgOElKSmGbObGyhk6uyJevez726-SqYvO5_R4Pxml6LA2yVCnZTmjy0?PARTNER=WRITER" alt="duplication" border="0" width="427" height="318" /></a></p> <p align="justify">c. Inversi</p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1pZrjEBc0pj1cZq2B4-vCgs-oZO9_YBp9-mREakgSaHoKpTa3NF6YEBoGHFXpIkFBLTEseCbsy_cseALiXjgq03Q?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pXbmbhF7w2lTA_1xWuTi9GDqMfoU2_FW1alhQVens7A9GM3sKkcvhHLeqlqXePF3nZ0yMCxSaCaw?PARTNER=WRITER" alt="inversi" border="0" width="426" height="274" /></a></p> <p align="justify">d. Translokasi</p> <p align="justify"><a href="http://eiyegw.bay.livefilestore.com/y1pp2qSLctDlktH98p-WOM_EqfTCyxDsfwYNMGviVnyTA21BqhhROtKQiuz0FgPKx97mrjrbE0QkhRWOjfxR6c5ag?PARTNER=WRITER" rel="nofollow"><img style="border-width: 0px;" src="http://byfiles.storage.msn.com/y1pEsp3oIndGreRraPWEQy0_BDHbWId5MIDuq3W1ukvr6W6AI9d31vo49I59zWbANTj6_o75M3QU-Q?PARTNER=WRITER" alt="translokasi" border="0" width="425" height="270" /></a></p> <p align="justify"><strong>3. Pembelahan Amitosis</strong></p> <p>Amitosis adalah reproduksi sel di mana sel membelah diri secara langsung tanpa melalui tahap-tahap pembelahan sel. Pembelahan cara ini banyak dijumpai pada sel-sel yang bersifat prokariotik, misalnya pada bakteri, ganggang biru.</p> <p>Pembelahan amitosis sengaja tidak dibahas disini karena tidak terjadi pada manusia.</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-20552596677447894192010-01-04T19:17:00.001-08:002010-01-04T19:17:17.381-08:00<h1 id="firstHeading" class="firstHeading">Virus</h1><br /><table class="infobox biota" style="text-align: left; width: 200px;"> <tbody><tr> <th colspan="2" style="text-align: center; background-color: rgb(238, 130, 238);">Viruses</th> </tr> <tr> <td colspan="2" style="text-align: center;"><a href="http://en.wikipedia.org/wiki/File:Rotavirus_Reconstruction.jpg" class="image"><img alt="" src="http://upload.wikimedia.org/wikipedia/en/thumb/f/fa/Rotavirus_Reconstruction.jpg/180px-Rotavirus_Reconstruction.jpg" height="158" width="180" /></a></td> </tr> <tr> <td colspan="2" style="text-align: center; font-size: 88%;"><a href="http://en.wikipedia.org/wiki/Rotavirus" title="Rotavirus">Rotavirus</a></td> </tr> <tr> <th colspan="2" style="text-align: center; background-color: rgb(238, 130, 238);"><a href="http://en.wikipedia.org/wiki/Virus_classification" title="Virus classification">Virus classification</a></th> </tr> <tr> <td>Group:</td> <td>I–VII</td> </tr> <tr> <th colspan="2" style="text-align: center; background-color: rgb(238, 130, 238);">Groups</th> </tr> <tr> <td colspan="2" style="text-align: left;"> <p>I: dsDNA viruses<br />II: ssDNA viruses<br />III: dsRNA viruses<br />IV: (+)ssRNA viruses<br />V: (−)ssRNA viruses<br />VI: ssRNA-RT viruses<br />VII: dsDNA-RT viruses</p> </td> </tr> </tbody></table> <div style="text-align: justify;">A virus (from the Latin virus meaning toxin or poison) is a small infectious agent that can only replicate inside the cells of another organism. Viruses are too small to be seen directly with a light microscope. Viruses infect all types of organisms, from animals and plants to bacteria and archaea. Since the initial discovery of tobacco mosaic virus by Martinus Beijerinck in 1898,[about 5,000 viruses have been described in detail, although there are millions of different types. Viruses are found in almost every ecosystem on Earth and these minute structures are the most abundant type of biological entity. The study of viruses is known as virology, a sub-specialty of microbiology. Unlike prions and viroids, viruses consist of two or three parts: all viruses have genes made from either DNA or RNA, long molecules that carry genetic information; all have a protein coat that protects these genes; and some have an envelope of fat that surrounds them when they are outside a cell. Viroids do not have a protein coat and prions contain no RNA or DNA. Viruses vary from simple helical and icosahedral shapes, to more complex structures. Most viruses are about one hundred times smaller than an average bacterium. The origins of viruses in the evolutionary history of life are unclear: some may have evolved from plasmids—pieces of DNA that can move between cells—while others may have evolved from bacteria. In evolution, viruses are an important means of horizontal gene transfer, which increases genetic diversity.Viruses spread in many ways; plant viruses are often transmitted from plant to plant by insects that feed on sap, such as aphids, while animal viruses can be carried by blood-sucking insects. These disease-bearing organisms are known as vectors. Influenza viruses are spread by coughing and sneezing. The norovirus and rotaviruses, common causes of viral gastroenteritis, are transmitted by the faecal-oral route and are passed from person to person by contact, entering the body in food or water. HIV is one of several viruses transmitted through sexual contact or by exposure to infected blood. Viral infections in animals provoke an immune response that usually eliminates the infecting virus. These immune responses can also be produced by vaccines, which give immunity to specific viral infections. However, some viruses including HIV and those causing viral hepatitis evade these immune responses and cause chronic infections. Microorganisms also have defences against viral infection, such as restriction modification systems.<br />Antibiotics have no effect on viruses, but a few antiviral drugs have been developed. However, there are relatively few antivirals because there are few targets for these drugs to interfere with. This is because a virus reprograms its host's cells to make new viruses and almost all the proteins used in this process are normal parts of the body, with only a few viral proteins.</div><p><br /></p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-82412454837341032622010-01-04T19:14:00.000-08:002010-01-04T19:15:02.819-08:00<h2><span class="mw-headline" id="History">History of Virus<br /></span></h2> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Mwb_in_lab.JPG" class="image"><img alt="An old, bespectacled man wearing a suit and sitting at a bench by a large window. The bench is covered with small bottles and test tubes. On the wall behind him is a large old-fashioned clock below which are four small enclosed shelves on which sit many neatly labelled bottles." src="http://upload.wikimedia.org/wikipedia/commons/thumb/d/d2/Mwb_in_lab.JPG/180px-Mwb_in_lab.JPG" class="thumbimage" height="251" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Mwb_in_lab.JPG" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> </div></div></div> <div style="text-align: justify;">Martinus Beijerinck in his laboratory in 1921 In 1884, the French microbiologist Charles Chamberland invented a filter (known today as the Chamberland filter or Chamberland-Pasteur filter) with pores smaller than bacteria. Thus, he could pass a solution containing bacteria through the filter and completely remove them from the solution. In 1892 the Russian biologist Dmitry Ivanovsky used this filter to study what is now known as tobacco mosaic virus. His experiments showed that the crushed leaf extracts from infected tobacco plants are still infectious after filtration. Ivanovsky suggested the infection might be caused by a toxin produced by bacteria, but did not pursue the idea. At the time it was thought that all infectious agents could be retained by filters and grown on a nutrient medium—this was part of the germ theory of disease. In 1898 the Dutch microbiologist Martinus Beijerinck repeated the experiments and became convinced that this was a new form of infectious agent. He went on to observe that the agent multiplied only in dividing cells, but as his experiments did not show that it was made of particles, he called it a contagium vivum fluidum (soluble living germ) and re-introduced the word virus. Beijerinck maintained that viruses were liquid in nature, a theory later discredited by Wendell Stanley, who proved they were particulate. In the same year, 1899, Friedrich Loeffler and Frosch passed the agent of foot-and-mouth disease (aphthovirus) through a similar filter and ruled out the possibility of a toxin because of the high dilution; they concluded that the agent could replicate. In the early 20th century, the English bacteriologist Frederick Twort discovered the viruses that infect bacteria, which are now called bacteriophages, and the French-Canadian microbiologist Félix d'Herelle described viruses that, when added to bacteria on agar, would produce areas of dead bacteria. He accurately diluted a suspension of these viruses and discovered that the highest dilutions, rather than killing all the bacteria, formed discrete areas of dead organisms. Counting these areas and multiplying by the dilution factor allowed him to calculate the number of viruses in the suspension. By the end of the nineteenth century, viruses were defined in terms of their infectivity, filterability, and their requirement for living hosts. Viruses had been grown only in plants and animals. In 1906, Harrison invented a method for growing tissue in lymph, and, in 1913, E. Steinhardt, C. Israeli, and R. A. Lambert used this method to grow vaccinia virus in fragments of guinea pig corneal tissue. In 1928, H. B. Maitland and M. C. Maitland grew vaccinia virus in suspensions of minced hens' kidneys. Their method was not widely adopted until the 1950s, when poliovirus was grown on a large scale for vaccine production.Another breakthrough came in 1931, when the American pathologist Ernest William Goodpasture grew influenza and several other viruses in fertilised chickens' eggs.[18] In 1949 John F. Enders, Thomas Weller, and Frederick Robbins grew polio virus in cultured human embryo cells, the first virus to be grown without using solid animal tissue or eggs. This work enabled Jonas Salk to make an effective polio vaccine. With the invention of electron microscopy in 1931 by the German engineers Ernst Ruska and Max Knoll came the first images of viruses. In 1935 American biochemist and virologist Wendell Stanley examined the tobacco mosaic virus and found it to be mostly made from protein. A short time later, this virus was separated into protein and RNA parts.Tobacco mosaic virus was the first one to be crystallised and whose structure could therefore be elucidated in detail. The first X-ray diffraction pictures of the crystallised virus were obtained by Bernal and Fankuchen in 1941. On the basis of her pictures, Rosalind Franklin discovered the full structure of the virus in 1955. In the same year, Heinz Fraenkel-Conrat and Robley Williams showed that purified tobacco mosaic virus RNA and its coat protein can assemble by themselves to form functional viruses, suggesting that this simple mechanism was probably how viruses assembled within their host cells.The second half of the twentieth century was the golden age of virus discovery and most of the 2,000 recognised species of animal, plant, and bacterial viruses were discovered during these years.In 1957, equine arterivirus and the cause of Bovine virus diarrhea (a pestivirus) were discovered. In 1963, the hepatitis B virus was discovered by Baruch Blumberg, and in 1965, Howard Temin described the first retrovirus. Reverse transcriptase, the key enzyme that retroviruses use to translate their RNA into DNA, was first described in 1970, independently by Howard Temin and David Baltimore. In 1983 Luc Montagnier's team at the Pasteur Institute in France, first isolated the retrovirus now called HIV.</div> <p><br /></p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-20690293512501158492010-01-04T19:12:00.001-08:002010-01-04T19:12:55.192-08:00<h2><span class="mw-headline" id="Origins">Origins of Virus<br /></span></h2> Viruses are found wherever there is life and have probably existed since living cells first evolved. The origin of viruses is unclear because they do not form fossils, so molecular techniques have been the most useful means of investigating how they arose. These techniques rely on the availability of ancient viral DNA or RNA, but, unfortunately, most of the viruses that have been preserved and stored in laboratories are less than 90 years old. There are three main hypotheses that try to explain the origins of viruses: Regressive hypothesis Viruses may have once been small cells that parasitised larger cells. Over time, genes not required by their parasitism were lost. The bacteria rickettsia and chlamydia are living cells that, like viruses, can reproduce only inside host cells. They lend support to this hypothesis, as their dependence on parasitism is likely to have caused the loss of genes that enabled them to survive outside a cell. This is also called the degeneracy hypothesis. Cellular origin hypothesis Some viruses may have evolved from bits of DNA or RNA that "escaped" from the genes of a larger organism. The escaped DNA could have come from plasmids (pieces of naked DNA that can move between cells) or transposons (molecules of DNA that replicate and move around to different positions within the genes of the cell). Once called "jumping genes", transposons are examples of mobile genetic elements and could be the origin of some viruses. They were discovered in maize by Barbara McClintock in 1950. This is sometimes called the vagrancy hypothesis. Coevolution hypothesis Viruses may have evolved from complex molecules of protein and nucleic acid at the same time as cells first appeared on earth and would have been dependent on cellular life for many millions of years. Viroids are molecules of RNA that are not classified as viruses because they lack a protein coat. However, they have characteristics that are common to several viruses and are often called subviral agents. Viroids are important pathogens of plants. They do not code for proteins but interact with the host cell and use the host machinery for their replication. The hepatitis delta virus of humans has an RNA genome similar to viroids but has protein coat derived from hepatitis B virus and cannot produce one of its own. It is therefore a defective virus and cannot replicate without the help of hepatitis B virus. Similarly, the virophage 'sputnik' is dependent on mimivirus, which infects the protozoan Acanthamoeba castellanii. These viruses that are dependent on the presence of other virus species in the host cell are called satellites and may represent evolutionary intermediates of viroids and viruses. Prions are infectious protein molecules that do not contain DNA or RNA. They cause an infection in sheep called scrapie and cattle bovine spongiform encephalopathy ("mad cow" disease). In humans they cause kuru and Creutzfeldt-Jakob disease. They are able to replicate because some proteins can exist in two different shapes and the prion changes the normal shape of a host protein into the prion shape. This starts a chain reaction where each prion protein converts many host proteins into more prions, and these new prions then go on to convert even more protein into prions. Although they are fundamentally different from viruses and viroids, their discovery gives credence to the idea that viruses could have evolved from self-replicating molecules. Computer analysis of viral and host DNA sequences is giving a better understanding of the evolutionary relationships between different viruses and may help identify the ancestors of modern viruses. To date, such analyses have not helped to decide on which of these hypotheses are correct. However, it seems unlikely that all currently known viruses have a common ancestor and viruses have probably arisen numerous times in the past by one or more mechanisms.<p><br /></p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-67527238489929772632010-01-04T19:11:00.001-08:002010-01-04T19:11:59.304-08:00<h2><span class="mw-headline" id="Microbiology">Microbiology of Virus<br /></span></h2> <h3><span class="mw-headline" id="Life_properties">Life properties</span></h3><p style="text-align: justify;">Opinions differ on whether viruses are a form of life, or organic structures that interact with living organisms. They have been described as "organisms at the edge of life", since they resemble organisms in that they possess genes and evolve by natural selection, and reproduce by creating multiple copies of themselves through self-assembly. Although they have genes, they do not have a cellular structure, which is often seen as the basic unit of life. Viruses do not have their own metabolism, and require a host cell to make new products. They therefore cannot reproduce outside a host cell (although bacterial species such as rickettsia and chlamydia are considered living organisms despite the same limitation). Accepted forms of life use cell division to reproduce, whereas viruses spontaneously assemble within cells. They differ from autonomous growth of crystals as they inherit genetic mutations while being subject to natural selection. Virus self-assembly within host cells has implications for the study of the origin of life, as it lends further credence to the hypothesis that life could have started as self-assembling organic molecules.</p> <div class="thumb tright"> <div class="thumbinner" style="width: 257px;"><a href="http://en.wikipedia.org/wiki/File:Hexon.svg" class="image"><img alt="A cartoon showing several identical molecules of protein forming a hexigon" src="http://upload.wikimedia.org/wikipedia/en/thumb/e/ee/Hexon.svg/255px-Hexon.svg.png" class="thumbimage" height="175" width="255" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Hexon.svg" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> Diagram of how a virus capsid can be constructed using multiple copies of just two <a href="http://en.wikipedia.org/wiki/Protein_molecule" title="Protein molecule" class="mw-redirect">protein molecules</a></div> </div> </div> <div style="text-align: justify;"><span style="font-size:130%;"><span style="font-weight: bold;">Structure</span></span><br /><br />Viruses display a wide diversity of shapes and sizes, called morphologies. Generally viruses are much smaller than bacteria. Most viruses that have been studied have a diameter between 10 and 300 nanometres. Some filoviruses have a total length of up to 1400 nm; their diameters are only about 80 nm. Most viruses cannot be seen with a light microscope so scanning and transmission electron microscopes are used to visualise virions. To increase the contrast between viruses and the background, electron-dense "stains" are used. These are solutions of salts of heavy metals, such as tungsten, that scatter the electrons from regions covered with the stain. When virions are coated with stain (positive staining), fine detail is obscured. Negative staining overcomes this problem by staining the background only. A complete virus particle, known as a virion, consists of nucleic acid surrounded by a protective coat of protein called a capsid. These are formed from identical protein subunits called capsomers. Viruses can have a lipid "envelope" derived from the host cell membrane. The capsid is made from proteins encoded by the viral genome and its shape serves as the basis for morphological distinction.Virally coded protein subunits will self-assemble to form a capsid, generally requiring the presence of the virus genome. Complex viruses code for proteins that assist in the construction of their capsid. Proteins associated with nucleic acid are known as nucleoproteins, and the association of viral capsid proteins with viral nucleic acid is called a nucleocapsid. The capsid and entire virus structure can be mechanically (physically) probed through atomic force microscopy.In general, there are four main morphological virus types:</div> <div class="thumb tright" style="width: 192px;"> <div class="thumbinner"> <div style="margin: 1px; width: 182px;"> <div class="thumbimage"><a href="http://en.wikipedia.org/wiki/File:TMV_Structure.png" class="image" title="RNA coiled in a helix of repeating protein sub-units"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/3/3f/TMV_Structure.png/180px-TMV_Structure.png" height="166" width="180" /></a></div> <div class="thumbcaption" style="clear: left;"><a href="http://en.wikipedia.org/wiki/RNA" title="RNA">RNA</a> coiled in a helix of repeating protein sub-units</div> </div> <div style="margin: 1px; width: 182px;"> <div class="thumbimage"><a href="http://en.wikipedia.org/wiki/File:Icosahedral_Adenoviruses.jpg" class="image" title="Electron micrograph of icosahedral adenovirus"><img alt="" src="http://upload.wikimedia.org/wikipedia/en/thumb/f/f2/Icosahedral_Adenoviruses.jpg/180px-Icosahedral_Adenoviruses.jpg" height="72" width="180" /></a></div> <div class="thumbcaption" style="clear: left;">Electron micrograph of icosahedral <a href="http://en.wikipedia.org/wiki/Adenovirus" title="Adenovirus" class="mw-redirect">adenovirus</a></div> </div> <div style="margin: 1px; width: 182px;"> <div class="thumbimage"><a href="http://en.wikipedia.org/wiki/File:Varicella_%28Chickenpox%29_Virus_PHIL_1878_lores.jpg" class="image" title="Herpes viruses have a lipid envelope"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/1/16/Varicella_%28Chickenpox%29_Virus_PHIL_1878_lores.jpg/180px-Varicella_%28Chickenpox%29_Virus_PHIL_1878_lores.jpg" height="180" width="180" /></a></div> <div class="thumbcaption" style="clear: left;"><a href="http://en.wikipedia.org/wiki/Herpesviridae" title="Herpesviridae">Herpes viruses</a> have a lipid envelope</div> </div> </div> </div> <dl><dt>Helical </dt><dd style="text-align: justify;">These viruses are composed of a single type of capsomer stacked around a central axis to form a helical structure, which may have a central cavity, or hollow tube. This arrangement results in rod-shaped or filamentous virions: these can be short and highly rigid, or long and very flexible. The genetic material, generally single-stranded RNA, but ssDNA in some cases, is bound into the protein helix by interactions between the negatively charged nucleic acid and positive charges on the protein. Overall, the length of a helical capsid is related to the length of the nucleic acid contained within it and the diameter is dependent on the size and arrangement of capsomers. The well-studied Tobacco mosaic virus is an example of a helical virus.</dd></dl> <dl><dt>Icosahedral </dt><dd style="text-align: justify;">Most animal viruses are icosahedral or near-spherical with icosahedral symmetry. A regular icosahedron is the optimum way of forming a closed shell from identical sub-units. The minimum number of identical capsomers required is twelve, each composed of five identical sub-units. Many viruses, such as rotavirus, have more than twelve capsomers and appear spherical but they retain this symmetry. Capsomers at the apices are surrounded by five other capsomers and are called pentons. Capsomers on the triangular faces are surround by six others and are call hexons.</dd></dl> <dl><dt>Envelope </dt><dd style="text-align: justify;">Some species of virus envelope themselves in a modified form of one of the cell membranes, either the outer membrane surrounding an infected host cell, or internal membranes such as nuclear membrane or endoplasmic reticulum, thus gaining an outer lipid bilayer known as a viral envelope. This membrane is studded with proteins coded for by the viral genome and host genome; the lipid membrane itself and any carbohydrates present originate entirely from the host. The influenza virus and HIV use this strategy. Most enveloped viruses are dependent on the envelope for their infectivity.</dd></dl> <dl><dt>Complex </dt><dd style="text-align: justify;">These viruses possess a capsid that is neither purely helical, nor purely icosahedral, and that may possess extra structures such as protein tails or a complex outer wall. Some bacteriophages, such as Enterobacteria phage T4 have a complex structure consisting of an icosahedral head bound to a helical tail, which may have a hexagonal base plate with protruding protein tail fibres. This tail structure acts like a molecular syringe, attaching to the bacterial host and then injecting the viral genome into the cell.</dd></dl> <p style="text-align: justify;">The poxviruses are large, complex viruses that have an unusual morphology. The viral genome is associated with proteins within a central disk structure known as a nucleoid. The nucleoid is surrounded by a membrane and two lateral bodies of unknown function. The virus has an outer envelope with a thick layer of protein studded over its surface. The whole virion is slightly pleiomorphic, ranging from ovoid to brick shape. Mimivirus is the largest known virus, with a capsid diameter of 400 nm. Protein filaments measuring 100 nm project from the surface. The capsid appears hexagonal under an electron microscope, therefore the capsid is probably icosahedral.</p> <p style="text-align: justify;">Some viruses that infect Archaea have complex structures that are unrelated to any other form of virus, with a wide variety of unusual shapes, ranging from spindle-shaped structures, to viruses that resemble hooked rods, teardrops or even bottles. Other archaeal viruses resemble the tailed bacteriophages, and can have multiple tail structures.</p> <h3> <span class="mw-headline" id="Genome">Genome</span></h3><div style="text-align: justify;">An enormous variety of genomic structures can be seen among viral species; as a group they contain more structural genomic diversity than plants, animals, archaea, or bacteria. There are millions of different types of viruses; though only about 5,000 of them have been described in detail. A virus has either DNA or RNA genes and is called a DNA virus or a RNA virus respectively. By far most viruses have RNA. Plant viruses tend to have single-stranded RNA and bacteriophages tend to have double-stranded DNA. Viral genomes are circular, such as polyomaviruses, or linear, such as adenoviruses. The type of nucleic acid is irrelevant to the shape of the genome. Among RNA viruses, the genome is often divided up into separate parts within the virion and is called segmented. Each segment often codes for one protein and they are usually found together in one capsid. Every segment is not required to be in the same virion for the overall virus to be infectious, as demonstrated by the brome mosaic virus. A viral genome, irrespective of nucleic acid type, is either single-stranded or double-stranded. Single-stranded genomes consist of an unpaired nucleic acid, analogous to one-half of a ladder split down the middle. Double-stranded genomes consist of two complementary paired nucleic acids, analogous to a ladder. Some viruses, such as those belonging to the Hepadnaviridae, contain a genome that is partially double-stranded and partially single-stranded. For viruses with RNA or single-stranded DNA, the strands are said to be either positive-sense (called the plus-strand) or negative-sense (called the minus-strand), depending on whether it is complementary to the viral messenger RNA (mRNA). Positive-sense viral RNA is identical to viral mRNA and thus can be immediately translated by the host cell. Negative-sense viral RNA is complementary to mRNA and thus must be converted to positive-sense RNA by an RNA polymerase before translation. DNA nomenclature is similar to RNA nomenclature, in that the coding strand for the viral mRNA is complementary to it (−), and the non-coding strand is a copy of it (+).Genome size varies greatly between species. The smallest viral genomes code for only four proteins and have a mass of about 106 Daltons; the largest have a mass of about 108 Daltons and code for over one hundred proteins. RNA viruses generally have smaller genome sizes than DNA viruses because of a higher error-rate when replicating, and have a maximum upper size limit. Beyond this limit, errors in the genome when replicating render the virus useless or uncompetitive. To compensate for this, RNA viruses often have segmented genomes where the genome is split into smaller molecules, thus reducing the chance of error. In contrast, DNA viruses generally have larger genomes because of the high fidelity of their replication enzymes.</div> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Influenza_geneticshift.jpg" class="image"><img alt="A cartoon showing how viral genes can be shuffled to form new viruses" src="http://upload.wikimedia.org/wikipedia/en/thumb/b/b6/Influenza_geneticshift.jpg/180px-Influenza_geneticshift.jpg" class="thumbimage" height="234" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Influenza_geneticshift.jpg" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> How antigenic shift, or reassortment, can result in novel and highly pathogenic strains of <a href="http://en.wikipedia.org/wiki/Human_influenza" title="Human influenza" class="mw-redirect">human influenza</a></div> </div> </div> <div style="text-align: justify;">Viruses undergo genetic change by several mechanisms. These include a process called genetic drift where individual bases in the DNA or RNA mutate to other bases. Most of these point mutations are "silent"—they do not change the protein that the gene encodes—but others can confer evolutionary advantages such as resistance to antiviral drugs.Antigenic shift occurs when there is a major change in the genome of the virus. This can be a result of recombination or reassortment. When this happens with influenza viruses, pandemics might result. RNA viruses often exist as quasispecies or swarms of viruses of the same species but with slightly different genome nucleoside sequences. Such quasispecies are a prime target for natural selection.Segmented genomes confer evolutionary advantages; different strains of a virus with a segmented genome can shuffle and combine genes and produce progeny viruses or (offspring) that have unique characteristics. This is called reassortment or viral sex Genetic recombination is the process by which a strand of DNA is broken and then joined to the end of a different DNA molecule. This can occur when viruses infect cells simultaneously and studies of viral evolution have shown that recombination has been rampant in the species studied. Recombination is common to both RNA and DNA viruses.</div> <h3><span class="mw-headline" id="Replication_cycle">Replication cycle</span></h3> <p>Viral populations do not grow through cell division, because they are acellular; instead, they use the machinery and metabolism of a host cell to produce multiple copies of themselves, and they <i>assemble</i> in the cell.</p> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"> <div class="thumbimage"><a href="http://en.wikipedia.org/wiki/File:HepC_replication.png" class="image" title="A typical virus replication cycle"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/d/da/HepC_replication.png/180px-HepC_replication.png" height="135" width="180" /></a></div> <div class="thumbcaption">A typical virus replication cycle</div> <span style="display: block; height: 2px;font-size:78%;" > </span> <div class="thumbimage"><a href="http://en.wikipedia.org/wiki/File:Phage_injecting_its_genome_into_bacterial_cell.png" class="image" title="Some bacteriophages inject their genomes into bacterial cells"><img alt="" src="http://upload.wikimedia.org/wikipedia/en/thumb/0/03/Phage_injecting_its_genome_into_bacterial_cell.png/180px-Phage_injecting_its_genome_into_bacterial_cell.png" height="135" width="180" /></a></div> <div class="thumbcaption">Some bacteriophages inject their <a href="http://en.wikipedia.org/wiki/Genome" title="Genome">genomes</a> into bacterial cells</div> </div> </div> <p>The life cycle of viruses differs greatly between species but there are six basic stages in the life cycle of viruses:</p> <ul><li style="text-align: justify;"><i>A</i>ttachment is a specific binding between viral capsid proteins and specific receptors on the host cellular surface. This specificity determines the host range of a virus. For example, HIV infects only human T cells, because its surface protein, gp120, can interact with CD4 and receptors on the T cell's surface. This mechanism has evolved to favour those viruses that only infect cells in which they are capable of replication. Attachment to the receptor can induce the viral-envelope protein to undergo changes that results in the fusion of viral and cellular membranes.</li><li style="text-align: justify;">Penetration follows attachment; viruses enter the host cell through receptor mediated endocytosis or membrane fusion. This is often called viral entry. The infection of plant cells is different from that of animal cells. Plants have a rigid cell wall made of cellulose and viruses can only get inside the cells after trauma to the cell wall. Viruses such as tobacco mosaic virus can also move directly in plants, from cell to cell, through pores called plasmodesmata. Bacteria, like plants, have strong cell walls that a virus must breach to infect the cell. Some viruses have evolved mechanisms that inject their genome into the bacterial cell while the viral capsid remains outside.</li><li style="text-align: justify;">Uncoating is a process in which the viral capsid is degraded by viral enzymes or host enzymes thus releasing the viral genomic nucleic acid.</li><li style="text-align: justify;">Replication involves synthesis of viral messenger RNA (mRNA) for viruses except positive sense RNA viruses (see above), viral protein synthesis and assembly of viral proteins and viral genome replication.</li><li style="text-align: justify;">Following the assembly of the virus particles, post-translational modification of the viral proteins often occurs. In viruses such as HIV, this modification (sometimes called maturation) occurs after the virus has been released from the host cell.</li><li style="text-align: justify;">Viruses are released from the host cell by lysis—a process that kills the cell by bursting its membrane. Enveloped viruses (e.g., HIV) typically are released from the host cell by budding. During this process the virus acquires its envelope, which is a modified piece of the host's plasma membrane.</li></ul> <p>The genetic material within viruses, and the method by which the material is replicated, vary between different types of viruses.</p> <dl><dt><a href="http://en.wikipedia.org/wiki/DNA_viruses" title="DNA viruses" class="mw-redirect">DNA viruses</a> </dt><dd style="text-align: justify;">The genome replication of most DNA viruses takes place in the cell's nucleus. If the cell has the appropriate receptor on its surface, these viruses enter the cell by fusion with the cell membrane or by endocytosis. Most DNA viruses are entirely dependent on the host cell's DNA and RNA synthesising machinery, and RNA processing machinery. The viral genome must cross the cell's nuclear membrane to access this machinery.</dd><dt><a href="http://en.wikipedia.org/wiki/RNA_viruses" title="RNA viruses" class="mw-redirect">RNA viruses</a> </dt><dd style="text-align: justify;">These viruses are unique because their genetic information is encoded in RNA. Replication usually takes place in the cytoplasm. RNA viruses can be placed into about four different groups depending on their modes of replication. The polarity (whether or not it can be used directly to make proteins) of the RNA largely determines the replicative mechanism, and whether the genetic material is single-stranded or double-stranded. RNA viruses use their own RNA replicase enzymes to create copies of their genomes.</dd><dt><a href="http://en.wikipedia.org/wiki/Reverse_transcribing_viruses" title="Reverse transcribing viruses" class="mw-redirect">Reverse transcribing viruses</a> </dt><dd style="text-align: justify;">These replicate using reverse transcription, which is the formation of DNA from an RNA template. Reverse transcribing viruses containing RNA genomes use a DNA intermediate to replicate, whereas those containing DNA genomes use an RNA intermediate during genome replication. Both types use the reverse transcriptase enzyme to carry out the nucleic acid conversion. Retroviruses often integrate the DNA produced by reverse transcription into the host genome. They are susceptible to antiviral drugs that inhibit the reverse transcriptase enzyme, e.g. zidovudine and lamivudine. An example of the first type is HIV, which is a retrovirus. Examples of the second type are the Hepadnaviridae, which includes Hepatitis B virus.</dd></dl> <h3><span class="mw-headline" id="Effects_on_the_host_cell">Effects on the host cell</span></h3> <p style="text-align: justify;">The range of structural and biochemical effects that viruses have on the host cell is extensive. These are called cytopathic effects. Most virus infections eventually result in the death of the host cell. The causes of death include cell lysis, alterations to the cell's surface membrane and apoptosis. Often cell death is caused by cessation of its normal activities because of suppression by virus-specific proteins, not all of which are components of the virus particle.</p> <p style="text-align: justify;">Some viruses cause no apparent changes to the infected cell. Cells in which the virus is latent and inactive show few signs of infection and often function normally. This causes persistent infections and the virus is often dormant for many months or years. This is often the case with herpes viruses. Some viruses, such as Epstein-Barr virus, can cause cells to proliferate without causing malignancy, while others, such as papillomaviruses, are established causes of cancer.</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-72623660705818505032010-01-04T19:10:00.001-08:002010-01-04T19:10:33.220-08:00<h2><span class="mw-headline" id="Classification">Classification of Virus<br /></span></h2> <p style="text-align: justify;">Classification seeks to describe the diversity of viruses by naming and grouping them on the basis of similarities. In 1962, André Lwoff, Robert Horne, and Paul Tournier were the first to develop a means of virus classification, based on the Linnaean hierarchical system. This system bases classification on phylum, class, order, family, genus, and species. Viruses were grouped according to their shared properties (not those of their hosts) and the type of nucleic acid forming their genomes. Later the International Committee on Taxonomy of Viruses was formed.</p> <h3><span class="mw-headline" id="ICTV_classification">ICTV classification</span></h3> <p style="text-align: justify;">The International Committee on Taxonomy of Viruses (ICTV) developed the current classification system and wrote guidelines that put a greater weight on certain virus properties to maintain family uniformity. A unified taxonomy (a universal system for classifying viruses) has been established. The 7th lCTV Report formalised for the first time the concept of the virus species as the lowest taxon (group) in a branching hierarchy of viral taxa. However, at present only a small part of the total diversity of viruses has been studied, with analyses of samples from humans finding that about 20% of the virus sequences recovered have not been seen before, and samples from the environment, such as from seawater and ocean sediments, finding that the large majority of sequences are completely novel.</p> <p>The general taxonomic structure is as follows:</p> <dl><dd><a href="http://en.wikipedia.org/wiki/Order_%28biology%29" title="Order (biology)">Order</a> (-virales) <dl><dd><a href="http://en.wikipedia.org/wiki/Family_%28biology%29" title="Family (biology)">Family</a> (-viridae) <dl><dd><a href="http://en.wikipedia.org/wiki/Subfamily" title="Subfamily" class="mw-redirect">Subfamily</a> (-virinae) <dl><dd><a href="http://en.wikipedia.org/wiki/Genus" title="Genus">Genus</a> (<i>-virus</i>) <dl><dd><a href="http://en.wikipedia.org/wiki/Species" title="Species">Species</a> (<i>-virus</i>)</dd></dl> </dd></dl> </dd></dl> </dd></dl> </dd></dl> <p style="text-align: justify;">In the current (2008) ICTV taxonomy, five orders have been established, the Caudovirales, Herpesvirales, Mononegavirales, Nidovirales, and Picornavirales. The committee does not formally distinguish between subspecies, strains, and isolates. In total there are 5 orders, 82 families, 11 subfamilies, 307 genera, 2,083 species and about 3,000 types yet unclassified.</p> <h3><span class="mw-headline" id="Baltimore_classification">Baltimore classification</span></h3> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Virus_Baltimore_Classification.svg" class="image"><img alt="A diagram showing how the Baltimore Classification is based on a virus's DNA or RNA and method of mRNA synthesis" src="http://upload.wikimedia.org/wikipedia/commons/thumb/1/18/Virus_Baltimore_Classification.svg/180px-Virus_Baltimore_Classification.svg.png" class="thumbimage" height="164" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Virus_Baltimore_Classification.svg" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> The Baltimore Classification of viruses is based on the method of viral <a href="http://en.wikipedia.org/wiki/MRNA" title="MRNA" class="mw-redirect">mRNA</a> synthesis.</div> </div> </div> <p style="text-align: justify;">The Nobel Prize-winning biologist David Baltimore devised the Baltimore classification system. The ICTV classification system is used in conjunction with the Baltimore classification system in modern virus classification.</p> <p style="text-align: justify;">The Baltimore classification of viruses is based on the mechanism of mRNA production. Viruses must generate mRNAs from their genomes to produce proteins and replicate themselves, but different mechanisms are used to achieve this in each virus family. Viral genomes may be single-stranded (ss) or double-stranded (ds), RNA or DNA, and may or may not use reverse transcriptase (RT). Additionally, ssRNA viruses may be either sense (+) or antisense (−). This classification places viruses into seven groups:</p> <ul><li>I: <b><a href="http://en.wikipedia.org/wiki/DsDNA_virus" title="DsDNA virus" class="mw-redirect">dsDNA viruses</a></b> (e.g. <a href="http://en.wikipedia.org/wiki/Adenovirus" title="Adenovirus" class="mw-redirect">Adenoviruses</a>, <a href="http://en.wikipedia.org/wiki/Herpesvirus" title="Herpesvirus" class="mw-redirect">Herpesviruses</a>, <a href="http://en.wikipedia.org/wiki/Poxvirus" title="Poxvirus" class="mw-redirect">Poxviruses</a>)</li><li>II: <b><a href="http://en.wikipedia.org/wiki/SsDNA_virus" title="SsDNA virus" class="mw-redirect">ssDNA viruses</a></b> (+)sense DNA (e.g. <a href="http://en.wikipedia.org/wiki/Parvovirus" title="Parvovirus">Parvoviruses</a>)</li><li>III: <b><a href="http://en.wikipedia.org/wiki/DsRNA_virus" title="DsRNA virus" class="mw-redirect">dsRNA viruses</a></b> (e.g. <a href="http://en.wikipedia.org/wiki/Reovirus" title="Reovirus" class="mw-redirect">Reoviruses</a>)</li><li>IV: <b><a href="http://en.wikipedia.org/wiki/Positive-sense_ssRNA_virus" title="Positive-sense ssRNA virus" class="mw-redirect">(+)ssRNA viruses</a></b> (+)sense RNA (e.g. <a href="http://en.wikipedia.org/wiki/Picornavirus" title="Picornavirus">Picornaviruses</a>, <a href="http://en.wikipedia.org/wiki/Togavirus" title="Togavirus" class="mw-redirect">Togaviruses</a>)</li><li>V: <b><a href="http://en.wikipedia.org/wiki/Negative-sense_ssRNA_virus" title="Negative-sense ssRNA virus" class="mw-redirect">(−)ssRNA viruses</a></b> (−)sense RNA (e.g. <a href="http://en.wikipedia.org/wiki/Orthomyxovirus" title="Orthomyxovirus" class="mw-redirect">Orthomyxoviruses</a>, <a href="http://en.wikipedia.org/wiki/Rhabdovirus" title="Rhabdovirus" class="mw-redirect">Rhabdoviruses</a>)</li><li>VI: <b><a href="http://en.wikipedia.org/wiki/SsRNA-RT_virus" title="SsRNA-RT virus" class="mw-redirect">ssRNA-RT viruses</a></b> (+)sense RNA with DNA intermediate in life-cycle (e.g. <a href="http://en.wikipedia.org/wiki/Retrovirus" title="Retrovirus">Retroviruses</a>)</li><li>VII: <b><a href="http://en.wikipedia.org/wiki/DsDNA-RT_virus" title="DsDNA-RT virus" class="mw-redirect">dsDNA-RT viruses</a></b> (e.g. <a href="http://en.wikipedia.org/wiki/Hepadnavirus" title="Hepadnavirus" class="mw-redirect">Hepadnaviruses</a>)</li></ul> <p style="text-align: justify;">As an example of viral classification, the chicken pox virus, varicella zoster (VZV), belongs to the order Herpesvirales, family Herpesviridae, subfamily Alphaherpesvirinae, and genus Varicellovirus. VZV is in Group I of the Baltimore Classification because it is a dsDNA virus that does not use reverse transcriptase.</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com1tag:blogger.com,1999:blog-8324379693563903183.post-68336538589642448692010-01-04T19:07:00.002-08:002010-01-04T19:08:48.287-08:00<h2><span class="mw-headline" id="Viruses_and_human_disease">Viruses and human disease</span></h2> <div class="rellink boilerplate seealso"><a href="http://en.wikipedia.org/wiki/Table_of_clinically_important_viruses" title="Table of clinically important viruses" class="mw-redirect"><br /></a></div> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Viral_infections_and_involved_species.png" class="image"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/1/16/Viral_infections_and_involved_species.png/180px-Viral_infections_and_involved_species.png" class="thumbimage" height="172" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Viral_infections_and_involved_species.png" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> Overview of the main types of viral infection and the most notable species involved.</div> </div> </div> <p style="text-align: justify;">Examples of common human diseases caused by viruses include the common cold, influenza, chickenpox and cold sores. Many serious diseases such as ebola, AIDS, avian influenza and SARS are caused by viruses. The relative ability of viruses to cause disease is described in terms of virulence. Other diseases are under investigation as to whether they too have a virus as the causative agent, such as the possible connection between human herpes virus six (HHV6) and neurological diseases such as multiple sclerosis and chronic fatigue syndrome. There is controversy over whether the borna virus, previously thought to cause neurological diseases in horses, could be responsible for psychiatric illnesses in humans.</p> <p style="text-align: justify;">Viruses have different mechanisms by which they produce disease in an organism, which largely depends on the viral species. Mechanisms at the cellular level primarily include cell lysis, the breaking open and subsequent death of the cell. In multicellular organisms, if enough cells die the whole organism will start to suffer the effects. Although viruses cause disruption of healthy homeostasis, resulting in disease, they may exist relatively harmlessly within an organism. An example would include the ability of the herpes simplex virus, which causes cold sores, to remain in a dormant state within the human body. This is called latency and is a characteristic of the all herpes viruses including the Epstein-Barr virus, which causes glandular fever, and the varicella zoster virus, which causes chickenpox. Most people have been infected with at least one of these types of herpes virus. However, these latent viruses might sometimes be beneficial, as the presence of the virus can increase immunity against bacterial pathogens, such as Yersinia pestis. On the other hand, latent chickenpox infections return in later life as the disease called shingles.</p> <p style="text-align: justify;">Some viruses can cause life-long or chronic infections, where the viruses continue to replicate in the body despite the host's defence mechanisms. This is common in hepatitis B virus and hepatitis C virus infections. People chronically infected are known as carriers, as they serve as reservoirs of infectious virus. In populations with a high proportion of carriers, the disease is said to be endemic. In contrast to acute lytic viral infections this persistence implies compatible interactions with the host organism. Persistent viruses may even broaden the evolutionary potential of host species.</p> <h3><span class="mw-headline" id="Epidemiology">Epidemiology</span></h3> <p style="text-align: justify;">Viral epidemiology is the branch of medical science that deals with the transmission and control of virus infections in humans. Transmission of viruses can be vertical, that is from mother to child, or horizontal, which means from person to person. Examples of vertical transmission include hepatitis B virus and HIV where the baby is born already infected with the virus.[116] Another, more rare, example is the varicella zoster virus, which although causing relatively mild infections in humans, can be fatal to the foetus and newly born baby. Horizontal transmission is the most common mechanism of spread of viruses in populations. Transmission can be exchange of blood by sexual activity, e.g. HIV, hepatitis B and hepatitis C; by mouth by exchange of saliva, e.g. Epstein-Barr virus, or from contaminated food or water, e.g. norovirus; by breathing in viruses in the form of aerosols, e.g. influenza virus; and by insect vectors such as mosquitoes, e.g. dengue. The rate or speed of transmission of viral infections depends on factors that include population density, the number of susceptible individuals, (i.e. those who are not immune), the quality of health care and the weather.</p> <p style="text-align: justify;">Epidemiology is used to break the chain of infection in populations during outbreaks of viral diseases. Control measures are used that are based on knowledge of how the virus is transmitted. It is important to find the source, or sources, of the outbreak and to identify the virus. Once the virus has been identified, the chain of transmission can sometimes be broken by vaccines. When vaccines are not available sanitation and disinfection can be effective. Often infected people are isolated from the rest of the community and those that have been exposed to the virus placed in quarantine. To control the outbreak of foot and mouth disease in cattle in Britain in 2001, thousands of cattle were slaughtered. Most viral infections of humans and other animals have incubation periods during which the infection causes no signs or symptoms. Incubation periods for viral diseases range from a few days to weeks but are known for most infections. Somewhat overlapping, but mainly following the incubation period, there is a period of communicability; a time when an infected individual or animal is contagious and can infect another person or animal. This too is known for many viral infections and knowledge the length of both periods is important in the control of outbreaks. When outbreaks cause an unusually high proportion of cases in a population, community or region they are called epidemics. If outbreaks spread worldwide they are called pandemics.</p> <h3><span class="mw-headline" id="Epidemics_and_pandemics">Epidemics and pandemics</span></h3><br /><div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Reconstructed_Spanish_Flu_Virus.jpg" class="image"><img alt="An electron micrograph of the virus that caused Spanish influenza" src="http://upload.wikimedia.org/wikipedia/commons/thumb/e/ee/Reconstructed_Spanish_Flu_Virus.jpg/180px-Reconstructed_Spanish_Flu_Virus.jpg" class="thumbimage" height="111" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Reconstructed_Spanish_Flu_Virus.jpg" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> <a href="http://en.wikipedia.org/wiki/Transmission_electron_microscopy" title="Transmission electron microscopy">Transmission electron microscope</a> image of a recreated <a href="http://en.wikipedia.org/wiki/1918_influenza" title="1918 influenza" class="mw-redirect">1918 influenza</a> virus</div> </div> </div> <p style="text-align: justify;">Native American populations were devastated by contagious diseases, particularly smallpox, brought to the Americas by European colonists. It is unclear how many Native Americans were killed by foreign diseases after the arrival of Columbus in the Americas, but the numbers have been estimated to be close to 70% of the indigenous population. The damage done by this disease significantly aided European attempts to displace and conquer the native population.</p> <p style="text-align: justify;">A pandemic is a worldwide epidemic. The 1918 flu pandemic, commonly referred to as the Spanish flu, was a category 5 influenza pandemic caused by an unusually severe and deadly influenza A virus. The victims were often healthy young adults, in contrast to most influenza outbreaks, which predominantly affect juvenile, elderly, or otherwise weakened patients.</p> <p style="text-align: justify;">The Spanish flu pandemic lasted from 1918 to 1919. Older estimates say it killed 40–50 million people, while more recent research suggests that it may have killed as many as 100 million people, or 5% of the world's population in 1918. Most researchers believe that HIV originated in sub-Saharan Africa during the twentieth century; it is now a pandemic, with an estimated 38.6 million people now living with the disease worldwide.[133] The Joint United Nations Programme on HIV/AIDS (UNAIDS) and the World Health Organization (WHO) estimate that AIDS has killed more than 25 million people since it was first recognised on June 5, 1981, making it one of the most destructive epidemics in recorded history. In 2007 there were 2.7 million new HIV infections and 2 million HIV-related deaths.</p> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Marburg_virus.jpg" class="image"><img alt="An electron micrograph of the filamentous Marburg virus" src="http://upload.wikimedia.org/wikipedia/commons/thumb/9/99/Marburg_virus.jpg/180px-Marburg_virus.jpg" class="thumbimage" height="122" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Marburg_virus.jpg" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> <a href="http://en.wikipedia.org/wiki/Marburg_virus" title="Marburg virus">Marburg virus</a></div> </div> </div> <p style="text-align: justify;">Several highly lethal viral pathogens are members of the Filoviridae. Filoviruses are filament-like viruses that cause viral hemorrhagic fever, and include the ebola and marburg viruses. The Marburg virus attracted widespread press attention in April 2005 for an outbreak in Angola. Beginning in October 2004 and continuing into 2005, the outbreak was the world's worst epidemic of any kind of viral hemorrhagic fever.[136]</p> <h3><span class="mw-headline" id="Cancer">Cancer</span></h3> <p style="text-align: justify;">Viruses are an established cause of cancer in humans and other species. Viral cancers only occur in a minority of infected persons (or animals). Cancer viruses come from a range of virus families, including both RNA and DNA viruses, and so there is no single type of "oncovirus" (an obsolete term originally used for acutely transforming retroviruses). The development of cancer is determined by a variety of factors such as host immunity and mutations in the host. Viruses accepted to cause human cancers include some genotypes of human papillomavirus, hepatitis B virus, hepatitis C virus, Epstein-Barr virus, Kaposi's sarcoma-associated herpesvirus and human T-lymphotropic virus. The most recently discovered human cancer virus is a polyomavirus (Merkel cell polyomavirus) that causes most cases of a rare form of skin cancer called Merkel cell carcinoma. Hepatitis viruses can develop into a chronic viral infection that leads to liver cancer. Infection by human T-lymphotropic virus can lead to tropical spastic paraparesis and adult T-cell leukemia. Human papillomaviruses are an established cause of cancers of cervix, skin, anus, and penis. Within the Herpesviridae, Kaposi's sarcoma-associated herpesvirus causes Kaposi's sarcoma and body cavity lymphoma, and Epstein–Barr virus causes Burkitt's lymphoma, Hodgkin’s lymphoma, B lymphoproliferative disorder and nasopharyngeal carcinoma. Merkel cell polyomavirus closely related to SV40 and mouse polyomaviruses that have been used as animal models for cancer viruses for over 50 years.</p> <h3><span class="mw-headline" id="Host_defence_mechanisms">Host defence mechanisms</span></h3> <p style="text-align: justify;">The body's first line of defence against viruses is the innate immune system. This comprises cells and other mechanisms that defend the host from infection in a non-specific manner. This means that the cells of the innate system recognise, and respond to, pathogens in a generic way, but unlike the adaptive immune system, it does not confer long-lasting or protective immunity to the host.</p> <p style="text-align: justify;">RNA interference is an important innate defence against viruses. Many viruses have a replication strategy that involves double-stranded RNA (dsRNA). When such a virus infects a cell, it releases its RNA molecule or molecules, which immediately bind to a protein complex called dicer that cuts the RNA into smaller pieces. A biochemical pathway called the RISC complex is activated, which degrades the viral mRNA and the cell survives the infection. Rotaviruses avoid this mechanism by not uncoating fully inside the cell and by releasing newly produced mRNA through pores in the particle's inner capsid. The genomic dsRNA remains protected inside the core of the virion.</p> <p style="text-align: justify;">When the adaptive immune system of a vertebrate encounters a virus, it produces specific antibodies that bind to the virus and render it non-infectious. This is called humoral immunity. Two types of antibodies are important. The first called IgM is highly effective at neutralizing viruses but is only produced by the cells of the immune system for a few weeks. The second, called, IgG is produced indefinitely. The presence of IgM in the blood of the host is used to test for acute infection, whereas IgG indicates an infection sometime in the past. IgG antibody is measured when tests for immunity are carried out.</p> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Rotavirus_with_antibody.jpg" class="image"><img alt="Two spherical rotavirus particles, one is coated with antibody which looks like many small birds, regularly spaced on the surface of the virus" src="http://upload.wikimedia.org/wikipedia/commons/thumb/9/98/Rotavirus_with_antibody.jpg/180px-Rotavirus_with_antibody.jpg" class="thumbimage" height="97" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Rotavirus_with_antibody.jpg" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> Two <a href="http://en.wikipedia.org/wiki/Rotavirus" title="Rotavirus">rotaviruses</a>: the one on the right is coated with antibodies that stop its attaching to cells and infecting them</div> </div> </div> <p style="text-align: justify;">A second defence of vertebrates against viruses is called cell-mediated immunity and involves immune cells known as T cells. The body's cells constantly display short fragments of their proteins on the cell's surface, and if a T cell recognises a suspicious viral fragment there, the host cell is destroyed by killer T cells and the virus-specific T-cells proliferate. Cells such as the macrophage are specialists at this antigen presentation. The production of interferon is an important host defence mechanism. This is a hormone produced by the body when viruses are present. Its role in immunity is complex, but it eventually stops the viruses from reproducing by killing the infected cell and its close neighbours.</p> <p style="text-align: justify;">Not all virus infections produce a protective immune response in this way. HIV evades the immune system by constantly changing the amino acid sequence of the proteins on the surface of the virion. These persistent viruses evade immune control by sequestration, blockade of antigen presentation, cytokine resistance, evasion of natural killer cell activities, escape from apoptosis, and antigenic shift. Other viruses, called neurotropic viruses, are disseminated by neural spread where the immune system may be unable to reach them.</p> <h3><span class="mw-headline" id="Prevention_and_treatment">Prevention and treatment</span></h3> <p style="text-align: justify;">Because viruses use vital metabolic pathways within host cells to replicate, they are difficult to eliminate without using drugs that cause toxic effects to host cells in general. The most effective medical approaches to viral diseases are vaccinations to provide preventative immunity to infection, and antiviral drugs that selectively interfere with viral replication.</p> <h4><span class="mw-headline" id="Vaccines">Vaccines</span></h4> <p style="text-align: justify;">Vaccination is a cheap and effective way of preventing infections by viruses. Vaccines were used to prevent viral infections long before the discovery of the actual viruses. Their use has resulted in a dramatic decline in morbidity (illness) and mortality (death) associated with viral infections such as polio, measles, mumps and rubella. Smallpox infections have been eradicated. Vaccines are available to prevent over thirteen viral infections of humans, and more are used to prevent viral infections of animals. Vaccines can consist of live-attenuated or killed viruses, or viral proteins (antigens). Live vaccines contain weakened forms of the virus that causes the disease. Such viruses are called attenuated. Live vaccines can be dangerous when given to people with a weak immunity, (who are described as immunocompromised), because in these people, the weakened virus can cause the original disease. Biotechnology and genetic engineering techniques are used to produce subunit vaccines. These vaccines use only the capsid proteins of the virus. Hepatitis B vaccine is an example of this type of vaccine. Subunit vaccines are safe for immunocompromised patients because they cannot cause the disease. The yellow fever virus vaccine, a live-attenuated strain called 17D, is probably the safest and most effective vaccine ever generated.</p> <h4> <span class="mw-headline" id="Antiviral_drugs">Antiviral drugs</span></h4> <div class="rellink boilerplate seealso"><br /></div> <div class="thumb tright" style="width: 229px;"> <div class="thumbinner"> <div style="margin: 1px; float: left; width: 115px;"> <div class="thumbimage"><a href="http://en.wikipedia.org/wiki/File:Guanosin.svg" class="image" title="Guanosine"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/1/16/Guanosin.svg/113px-Guanosin.svg.png" height="85" width="113" /></a></div> <div class="thumbcaption" style="clear: left;"><a href="http://en.wikipedia.org/wiki/Guanosine" title="Guanosine">Guanosine</a></div> </div> <div style="margin: 1px; float: left; width: 102px;"> <div class="thumbimage"><a href="http://en.wikipedia.org/wiki/File:Aciclovir.svg" class="image" title="The guanosine analogue Aciclovir"><img alt="" src="http://upload.wikimedia.org/wikipedia/commons/thumb/f/f3/Aciclovir.svg/100px-Aciclovir.svg.png" height="95" width="100" /></a></div> <div class="thumbcaption" style="clear: left;">The guanosine analogue <a href="http://en.wikipedia.org/wiki/Aciclovir" title="Aciclovir">Aciclovir</a></div> </div> </div> </div> <p style="text-align: justify;">Over the past twenty years, the development of antiviral drugs has increased rapidly. This has been driven by the AIDS pandemic. Antiviral drugs are often nucleoside analogues, (fake DNA building blocks), which viruses incorporate into their genomes during replication. The life-cycle of the virus is then halted because the newly synthesised DNA is inactive. This is because these analogues lack the hydroxyl groups, which, along with phosphorus atoms, link together to form the strong "backbone" of the DNA molecule. This is called DNA chain termination. Examples of nucleoside analogues are aciclovir for Herpes simplex virus infections and lamivudine for HIV and Hepatitis B virus infections. Aciclovir is one of the oldest and most frequently prescribed antiviral drugs. Other antiviral drugs in use target different stages of the viral life cycle. HIV is dependent on a proteolytic enzyme called the HIV-1 protease for it to become fully infectious. There is a large class of drugs called protease inhibitors that inactivate this enzyme.</p> <p style="text-align: justify;">Hepatitis C is caused by an RNA virus. In 80% of people infected, the disease is chronic, and without treatment, they are infected for the remainder of their lives. However, there is now an effective treatment that uses the nucleoside analogue drug ribavirin combined with interferon. The treatment of chronic carriers of the hepatitis B virus by using a similar strategy using lamivudine has been developed.</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-69391622936954998002010-01-04T19:07:00.001-08:002010-01-04T19:07:12.109-08:00<h2><span class="mw-headline" id="Infection_in_other_species">Infection in other species of Virus<br /></span></h2> <p style="text-align: justify;">Viruses infect all cellular life and, although viruses occur universally, each cellular species has its own specific range that often infect only that species. A few viruses called satellites are parasites of other viruses, since they can only replicate within cells that have already been infected by another virus. Viruses are important pathogens of livestock. Diseases such as Foot and Mouth Disease and bluetongue are caused by viruses. Companion animals such as cats, dogs, and horses, if not vaccinated, are susceptible to serious viral infections. Canine parvovirus is caused by a small DNA virus and infections are often fatal in pups. Like all invertebrates, the honey bee is susceptible to many viral infections. Fortunately, most viruses co-exist harmlessly in their host and cause no signs or symptoms of disease.</p> <h3><span class="mw-headline" id="Plants">Plants</span></h3> <div class="rellink relarticle mainarticle"><a href="http://en.wikipedia.org/wiki/Plant_pathology" title="Plant pathology"><br /></a></div> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Pepper_mild_mottle_virus.png" class="image"><img alt="A red pepper (Capsicum) with a brown bruise caused by viruses" src="http://upload.wikimedia.org/wikipedia/commons/thumb/c/cf/Pepper_mild_mottle_virus.png/180px-Pepper_mild_mottle_virus.png" class="thumbimage" height="156" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Pepper_mild_mottle_virus.png" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> <a href="http://en.wikipedia.org/wiki/Capsicum" title="Capsicum">Peppers</a> infected by mild mottle virus</div> </div> </div> <p style="text-align: justify;">There are many types of plant virus, but often they cause only a loss of yield, and it is not economically viable to try to control them. Plant viruses are often spread from plant to plant by organisms, known as vectors. These are normally insects, but some fungi, nematode worms and single-celled organisms have been shown to be vectors. When control of plant virus infections is considered economical, for perennial fruits for example, efforts are concentrated on killing the vectors and removing alternate hosts such as weeds. Plant viruses are harmless to humans and other animals because they can reproduce only in living plant cells.</p> <p style="text-align: justify;">Plants have elaborate and effective defence mechanisms against viruses. One of the most effective is the presence of so-called resistance (R) genes. Each R gene confers resistance to a particular virus by triggering localised areas of cell death around the infected cell, which can often be seen with the unaided eye as large spots. This stops the infection from spreading. RNA interference is also an effective defence in plants When they are infected, plants often produce natural disinfectants that kill viruses, such as salicylic acid, nitric oxide, and reactive oxygen molecules.</p> <h3><span class="mw-headline" id="Bacteria">Bacteria</span></h3> <div class="rellink relarticle mainarticle"><a href="http://en.wikipedia.org/wiki/Bacteriophage" title="Bacteriophage"><br /></a></div> <div class="thumb tright"> <div class="thumbinner" style="width: 182px;"><a href="http://en.wikipedia.org/wiki/File:Phage.jpg" class="image"><img alt="An electron micrograph showing a portion of a bacterium covered with viruses" src="http://upload.wikimedia.org/wikipedia/commons/thumb/5/52/Phage.jpg/180px-Phage.jpg" class="thumbimage" height="211" width="180" /></a> <div class="thumbcaption"> <div class="magnify"><a href="http://en.wikipedia.org/wiki/File:Phage.jpg" class="internal" title="Enlarge"><img src="http://en.wikipedia.org/skins-1.5/common/images/magnify-clip.png" alt="" height="11" width="15" /></a></div> Transmission electron micrograph of multiple bacteriophages attached to a bacterial cell wall</div> </div> </div> <p style="text-align: justify;">Bacteriophages are a common and diverse group of viruses and are the most abundant form of biological entity in aquatic environments—there are up to ten times more of these viruses in the oceans than there are bacteria, reaching levels of 250,000,000 bacteriophages per millilitre of seawater. These viruses infect specific bacteria by binding to surface receptor molecules and then entering the cell. Within a short amount of time, in some cases just minutes, bacterial polymerase starts translating viral mRNA into protein. These proteins go on to become either new virions within the cell, helper proteins, which help assembly of new virions, or proteins involved in cell lysis. Viral enzymes aid in the breakdown of the cell membrane, and, in the case of the T4 phage, in just over twenty minutes after injection over three hundred phages could be released.</p> <p style="text-align: justify;">The major way bacteria defend themselves from bacteriophages is by producing enzymes that destroy foreign DNA. These enzymes, called restriction endonucleases, cut up the viral DNA that bacteriophages inject into bacterial cells. Bacteria also contain a system that uses CRISPR sequences to retain fragments of the genomes of viruses that the bacteria have come into contact with in the past, which allows them to block the virus's replication through a form of RNA interference. This genetic system provides bacteria with acquired immunity to infection.</p> <h3><span class="mw-headline" id="Archaea">Archaea</span></h3> <p style="text-align: justify;">Some viruses replicate within archaea: these are double-stranded DNA viruses with unusual and sometimes unique shapes. These viruses have been studied in most detail in the thermophilic archaea, particularly the orders Sulfolobales and Thermoproteales.[184] Defences against these viruses may involve RNA interference from repetitive DNA sequences within archaean genomes that are related to the genes of the viruses.</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-22271473476593771322010-01-04T19:01:00.000-08:002010-01-04T19:03:29.337-08:00<h2><span class="mw-headline" id="Applications">Applications of Virus<br /></span></h2> <h3><span class="editsection"></span><span class="mw-headline" id="Life_sciences_and_medicine">Life sciences and medicine</span></h3> <p style="text-align: justify;">Viruses are important to the study of molecular and cellular biology as they provide simple systems that can be used to manipulate and investigate the functions of cells. The study and use of viruses have provided valuable information about aspects of cell biology. For example, viruses have been useful in the study of genetics and helped our understanding of the basic mechanisms of molecular genetics, such as DNA replication, transcription, RNA processing, translation, protein transport, and immunology.</p> <p style="text-align: justify;"><a href="http://en.wikipedia.org/wiki/Genetics" title="Genetics"></a>Geneticists often use viruses as vectors to introduce genes into cells that they are studying. This is useful for making the cell produce a foreign substance, or to study the effect of introducing a new gene into the genome. In similar fashion, virotherapy uses viruses as vectors to treat various diseases, as they can specifically target cells and DNA. It shows promising use in the treatment of cancer and in gene therapy. Eastern European scientists have used phage therapy as an alternative to antibiotics for some time, and interest in this approach is increasing, because of the high level of antibiotic resistance now found in some pathogenic bacteria.<sup id="cite_ref-pmid16258815_188-0" class="reference"><a href="http://en.wikipedia.org/wiki/Virus#cite_note-pmid16258815-188"><span></span></a></sup></p> <h3><span class="editsection"></span><span class="mw-headline" id="Materials_science_and_nanotechnology">Materials science and nanotechnology</span></h3> <p style="text-align: justify;">Current trends in nanotechnology promise to make much more versatile use of viruses. From the viewpoint of a materials scientist, viruses can be regarded as organic nanoparticles. Their surface carries specific tools designed to cross the barriers of their host cells. The size and shape of viruses, and the number and nature of the functional groups on their surface, is precisely defined. As such, viruses are commonly used in materials science as scaffolds for covalently linked surface modifications. A particular quality of viruses is that they can be tailored by directed evolution. The powerful techniques developed by life sciences are becoming the basis of engineering approaches towards nanomaterials, opening a wide range of applications far beyond biology and medicine.<sup id="cite_ref-fischlechner_189-0" class="reference"><a href="http://en.wikipedia.org/wiki/Virus#cite_note-fischlechner-189"><span></span></a></sup></p> <p style="text-align: justify;">Because of their size, shape, and well-defined chemical structures, viruses have been used as templates for organizing materials on the nanoscale. Recent examples include work at the Naval Research Laboratory in Washington, DC, using Cowpea Mosaic Virus (CPMV) particles to amplify signals in DNA microarray based sensors. In this application, the virus particles separate the fluorescent dyes used for signalling to prevent the formation of non-fluorescent dimers that act as quenchers. Another example is the use of CPMV as a nanoscale breadboard for molecular electronics.<sup id="cite_ref-191" class="reference"><a href="http://en.wikipedia.org/wiki/Virus#cite_note-191"><span></span></a></sup></p> <h3><span class="editsection"></span><span class="mw-headline" id="Weapons">Weapons</span></h3> <p style="text-align: justify;">The ability of viruses to cause devastating epidemics in human societies has led to the concern that viruses could be weaponised for biological warfare. Further concern was raised by the successful recreation of the infamous 1918 influenza virus in a laboratory. The smallpox virus devastated numerous societies throughout history before its eradication. There are officially only two centers in the world which keep stocks of smallpox virus—the Russian Vector laboratory, and the United States Centers for Disease Control. But fears that it may be used as a weapon are not totally unfounded; the vaccine for smallpox is not safe—during the years before the eradication of smallpox disease more people became seriously ill as a result of vaccination than did people from smallpox — and smallpox vaccination is no longer universally practiced.Thus, much of the modern human population has almost no established resistance to smallpox.<sup id="cite_ref-pmid18844596_193-2" class="reference"><a href="http://en.wikipedia.org/wiki/Virus#cite_note-pmid18844596-193"><span></span><span></span></a></sup></p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-80974386240822514822009-12-07T20:29:00.000-08:002009-12-07T20:32:42.457-08:00<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/_JiaaHMAFpyg/Sx3W1sgLEKI/AAAAAAAAACU/nMrxNpL9I9M/s1600-h/800px-CellRespiration.svg.png"><img style="margin: 0pt 10px 10px 0pt; float: left; cursor: pointer; width: 320px; height: 226px;" src="http://1.bp.blogspot.com/_JiaaHMAFpyg/Sx3W1sgLEKI/AAAAAAAAACU/nMrxNpL9I9M/s320/800px-CellRespiration.svg.png" alt="" id="BLOGGER_PHOTO_ID_5412718545136717986" border="0" /></a><br /><p><span style="font-size:180%;"><b>Cellular respiration</b></span></p><p><b>Cellular respiration</b>, also known as 'oxidative metabolism<a href="http://en.wikipedia.org/wiki/Metabolism" title="Metabolism"></a>', is one of the key ways a cell gains useful energy. It is the set of the metabolic reactions and processes that take place in organisms' cells to convert biochemical energy from nutrients into adenosine triphosphate (ATP), and then release waste products. The reactions involved in respiration are catabolic reactions that involve the oxidation of one molecule and the reduction of another.</p> <p>Nutrients commonly used by animal and plant cells in respiration include glucose, amino acids and fatty acids, and a common oxidizing agent (electron acceptor) is molecular oxygen (O<sub>2</sub>). Bacteria and archaea can also be lithotrophs and these organisms may respire using a broad range of inorganic molecules as electron donors and acceptors, such as sulfur, metal ions, methane or hydrogen. Organisms that use oxygen as a final electron acceptor in respiration are described as aerobic, while those that do not are referred to as anaerobic<sup id="cite_ref-0" class="reference"><a href="http://en.wikipedia.org/wiki/Cellular_respiration#cite_note-0"><span></span><span></span></a></sup>.</p> <p>The energy released in respiration is used to synthesize ATP to store this energy. The energy stored in ATP can then be used to drive processes requiring energy, including biosynthesis, locomotion or transportation of molecules across cell membranes.</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-87451563430521331222009-12-07T20:15:00.000-08:002009-12-07T20:20:21.188-08:00<h3 style="font-family: georgia;"><span style="font-size:130%;">Aerobic Respiration</span></h3> <p>The pyruvate produced in glycolysis undergoes further breakdown through a process called <i>aerobic respiration</i> in most organisms. This process requires oxygen and yields much more energy than glycolysis. Aerobic respiration is divided into two processes: the Krebs cycle, and the Electron Transport Chain, which produces ATP through chemiosmotic phosphorylation. The energy conversion is as follows:</p> <p align="center">C<sub>6</sub>H<sub>12</sub>O<sub>6</sub> + 6O<sub><2</sub> -> 6CO<sub>2</sub> + 6H<sub>2</sub>O + energy (ATP)</p> <p><b>Krebs Cycle</b></p> <p>The pyruvate molecules produced during <a href="http://library.thinkquest.org/C004535/glycolysis.html"></a>glycolysis contain a lot of energy in the bonds between their molecules. In order to use that energy, the cell must convert it into the form of ATP. To do so, pyruvate molecules are processed through the Kreb Cycle, also known as the citric acid cycle.</p> <p align="center"><img style="width: 439px; height: 413px;" src="http://library.thinkquest.org/C004535/media/kreb_cycle.gif" border="0" /></p> <p>1. Prior to entering the Krebs Cycle, pyruvate must be converted into acetyl CoA (pronounced: acetyl coenzyme A). This is achieved by removing a CO<sub>2</sub> molecule from pyruvate and then removing an electron to reduce an NAD<sup>+</sup> into NADH. An enzyme called coenzyme A is combined with the remaining acetyl to make acetyl CoA which is then fed into the Krebs Cycle. The steps in the Krebs Cycle are summarized below:</p> <p>2. Citrate is formed when the acetyl group from acetyl CoA combines with oxaloacetate from the previous Krebs cycle..</p> <p>3. Citrate is converted into its isomer isocitrate..</p> <p>4. Isocitrate is oxidized to form the 5-carbon α-ketoglutarate. This step releases one molecule of CO<sub>2</sub> and reduces NAD<sup>+</sup> to NADH<sub>2</sub><sup>+</sup>.</p> <p>5. The α-ketoglutarate is oxidized to succinyl CoA, yielding CO<sub>2</sub> and NADH<sub>2</sub><sup>+</sup>.</p> <p>6. Succinyl CoA releases coenzyme A and phosphorylates ADP into ATP.</p> <p>7. Succinate is oxidized to fumarate, converting FAD to FADH<sub>2</sub>.</p> <p>8. Fumarate is hydrolized to form malate.</p> <p>9. Malate is oxidized to oxaloacetate, reducing NAD<sup>+</sup> to NADH<sub>2</sub><sup>+</sup>.</p> <p>We are now back at the beginning of the Krebs Cycle. Because glycolysis produces two pyruvate molecules from one glucose, each glucose is processes through the kreb cycle twice. For each molecule of glucose, six NADH<sub>2</sub><sup>+</sup>, two FADH<sub>2</sub>, and two ATP.</p> <p><b>Electron Transport Chain</b></p> <p>What happens to the NADH<sub>2</sub><sup>+</sup> and FADH<sub>2</sub> produced during the Krebs cycle? The molecules have been reduced, receiving high energy electrons from the pyruvic acid molecules that were dismantled in the Krebs Cycle. Therefore, they represent energy available to do work. These carrier molecules transport the high energy electrons and their accompanying hydrogen protons from the Krebs Cycle to the electron transport chain in the inner mitochondrial membrane.</p> <p>In a number of steps utilizing enzymes on the membrane, NADH<sub>2</sub><sup>+</sup> is oxidized to NAD<sup>+</sup>, and FADH<sub>2</sub> to FAD. The high energy electrons are transferred to ubiquinone (Q) and cytochrome c molecules, the electron carriers within the membrane. The electrons are then passed from molecule to molecule in the inner membrane of the mitochondron, losing some of their energy at each step. The final transfer involves the combining of electrons and H<sub>2</sub> atoms with oxygen to form water. The molecules that take part in the transport of these electrons are referred to as the electron transport chain.</p> <p>The process can be summarized as follows: the electrons that are delivered to the electron transport system provide energy to "pump" hydrogen protons across the inner mitochondrial membrane to the outer compartment. This high concentration of hydrogen protons produces a free energy potential that can do work. That is, the hydrogen protons tend to move down the concentration gradient from the outer compartment to the inner compartment.</p> <p>However, the only path that the protons have is through enzyme complexes within the inner membrane. The protons therefore pass through the channel lined with enzymes. The free energy of the hydrogen protons is used to form ATP by phosphorylation, bonding phosphate to ADP in an enzymatically-mediated reaction. Since an electrochemical osmotic gradient supplies the energy, the entire process is referred to as chemiosmotic phosphorylation.</p> <p>Once the electrons (originally from the Krebs Cycle) have yielded their energy, they combine with oxygen to form water. If the oxygen supply is cut off, the electrons and hydrogen protons cease to flow through the electron transport system. If this happens, the proton concentration gradient will not be sufficient to power the synthesis of ATP. This is why we, and other species, are not able to survive for long without oxygen!</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-79483012448492131362009-12-07T20:03:00.000-08:002009-12-07T20:07:43.956-08:00<h3>Anaerobic Respiration</h3> <p><br /></p> <p>The last few sections have talked extensively about aerobic respiration. What defines it as aerobic is its use of oxygen as the terminal electron accepter. Since this is very similar to the type of respiration that humans use, our bias is obvious. Now let me fill you in on a little secret. Microbes are capable of using all sorts of other terminal electron accepters besides oxygen. Below we talk about a few examples of anaerobic respiration. The one thing that they all have in common is the use of an electron transport system in a membrane and the synthesis of ATP via ATP synthase. In both nitrate reduction and sulfate reduction there are two types of pathways, assimilatory and dissimilatory. Assimilatory pathways are methods for taking a nutrient in the soil, moving it into the cell and using it for biosynthesis of macromolecules. Dissimilatory pathways use the substrate as a place to dump electrons and generate energy. Here we examine dissimilatory pathways. <a href="http://lecturer.ukdw.ac.id/dhira/Metabolism/Anabolism.html"></a>Assimilatory pathways will be explained in the context of cell biosynthesis.</p><h3>Nitrate reduction</h3><p>Some microbes are capable of using nitrate as their terminal electron accepter. The ETS used is somewhat similar to aerobic respiration, but the terminal electron transport protein donates its electrons to nitrate instead of oxygen. Nitrate reduction in some species (the best studied being <i>E. coli</i>) is a two electron transfer where nitrate is reduced to nitrite. Electrons flow through the quinone pool and the cytochrome b/c<sub>1</sub> complex and then nitrate reductase resulting in the transport of protons across the membrane as discussed earlier for aerobic respiration.</p><blockquote>N0<sub>3</sub><sup>-</sup> + 2e<sup>-</sup> + 2H<sup>+</sup><img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" />N0<sub>2</sub><sup>-</sup>+ H<sub>2</sub>0</blockquote><p>Figure 1 - The reaction for nitrate reduction. N0<sub>3</sub><sup>-</sup>, nitrate; N0<sub>2</sub><sup>-</sup>, nitrite</p><p>This reaction is not particularly efficient. Nitrate does not as willingly accept electrons when compared to oxygen and the potential energy gain from reducing nitrate is less. If microbes have a choice, they will use oxygen instead of nitrate, but in environments where oxygen is limiting and nitrate is plentiful, nitrate reduction takes place. </p><h3>Denitrification</h3><p>Nitrite, the product of nitrate reduction, is still a highly oxidized molecule and can accept up to six more electrons before being fully reduced to nitrogen gas. Microbes exist (<i>Paracoccus species, Pseudomonas stutzeri, Pseudomonas aeruginosa</i>, and <i>Rhodobacter sphaeroides</i> are a few examples) that are able to reduce nitrate all the way to nitrogen gas. The process is carefully regulated by the microbe since some of the products of the reduction of nitrate to nitrogen gas are toxic to metabolism. This may explain the large number of genes involved in the process and the limited number of bacteria that are capable of denitrification. Below is the chemical equation for the reduction of nitrate to N<sub>2</sub>.</p><p>N0<sub>3</sub><sup>-</sup><img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" />N0<sub>2</sub><sup>-</sup><img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" /> NO <img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" /> N<sub>2</sub>O<img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" /> N<sub>2</sub></p><p>Figure 2 - The reduction of nitrate to nitrogen gas. NO, nitric oxide; N<sub>2</sub>O, nitrous oxide; N<sub>2</sub>, nitrogen gas.</p><p>The advantage for the cell of carrying out a complete reduction of nitrate is two fold. The nitrate ETS serves as a place to oxidize NADH and free it to be used in catabolism of more substrate. Denitrification take eight electrons from metabolism and adds them to nitrate to form N<sub>2</sub> versus just two for nitrate reduction alone. Also, donation of electrons from NADH through the cytochrome b/c<sub>1</sub> complex and eventually to nitrous oxide (N<sub>2</sub>O) reductase provides another opportunity to pump protons across the membrane. The figure below presents a schematic of the spacial arrangement of the denitrification enzymes in the membrane</p><p><img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/nitrateETS.gif" alt="nitrateETS picture" border="0" width="404" height="242" /></p><p>Figure 3 - Denitrification in the membrane. NADH dehydrogenase complex (DH), nitrate reductase (NAR), nitrite reductase (NIR), NO reductase (NOR), and N<sub>2</sub>O reductase (N<sub>2</sub>OR)</p><p>Nitrate reduction has been extensively studied in bacteria due to its significance in the global nitrogen cycle. Denitrification removes nitrate, an accessible nitrogen source for plants, from the soil and converts it to N<sub>2</sub> a much less tractable source of nitrogen that most plants cannot use. This decreases soil fertility making farming more expensive. Intermediates of denitrification, nitrous oxide and nitric oxide, are gases and will sometimes escape the cell before being completely reduced. These compounds, when in the atmosphere, contribute to the greenhouse effect and exacerbate global warming. The use of high nitrate fertilizers in modern agriculture makes matters worse. For more information, there is an <strong>extensive</strong> <a href="http://mmbr.asm.org/cgi/content/abstract/61/4/533"></a>review of denitrification available on line.</p><h3>Sulfate reduction</h3><p>The disimilatory reduction of sulfate seems to be a strictly anaerobic process as all the microbes capable of carrying it out only grow in environments devoid of oxygen. Sulfate (SO<sub>4</sub><sup>-2</sup> is reduced to sulfide (S<sup>-2</sup>), typically in the form of hydrogen sulfide (H<sub>2</sub>S). Eight electrons are add to sulfate to make sulfide </p><blockquote>acetate + SO<sub>4</sub><sup>-2</sup> + 3H<sup>+</sup> + <img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" /> 2CO<sub>2</sub> + H<sub>2</sub>S + 2H<sub>2</sub>O </blockquote><p>Figure 4 - The reduction of sulfate to sulfide during growth on acetate.</p><p>The electron potential and energy yield for sulfate reduction is much lower than for nitrate or oxygen. However, there is still enough energy to allow the synthesis of ATP when the catabolic substrate used results in the formation of NADH or FADH. Substrates for sulfate reducers range from hydrogen gas to aromatic compounds such as benzoate. The most commonly utilized are acetate, lactate and other small organic acids (lactate, malate, pyruvate and ethanol are some examples). These compounds are prevalent in anaerobic environments where anaerobic catabolism of complex organic polymers such as cellulose and starch is taking place.</p><h4>Biochemistry of sulfate reducers</h4><p>Sulfate reducers take these growth substrates and metabolize them to acetate. The reducing power generated travels down an electron transport chain eventually reducing sulfate to hydrogen sulfide and generating energy using ATP synthase.</p><p><img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/SulfateRed.gif" alt="SulfateRed picture" border="0" width="378" height="499" /></p><p>Figure 5 - Pathway of sulfate reduction when grown on lactate. Lactate (in blue) is oxidized to acetate (in red) and the electrons remove eventually end up reducing sulfate (in blue) to sulfide (in red). Note that the energy gained in the process by SLP - converting acetyl phosphate to acetate - is used up to activate sulfate in the first step of sulfate reduction. Energy for metabolism is only generated via an electron transport chain.</p><p>Recent work in bioremediation of anaerobic sediments has resulted in the isolation of many novel sulfate reducing species capable of metabolizing environmentally intractable compounds including TNT, PCP and benzoate. It is becoming apparent that this group of bacteria are very important in recycling carbon to CO<sub>2</sub> as part of the global carbon cycle in anaerobic environments. For a look at some recent research on sulfate reducing bacteria, check out the "Journal of Bacteriology"</p><h3>Carbonate reduction</h3><p>Several groups of microbes are capable of using carbonate (CO<sub>2</sub>) as a terminal electron accepter. Carbonate is a poor choice to leave your electrons with due to its low reduction potential and energy yields from CO<sub>2</sub> reduction are low. However, carbonate is one of the most common anions in nature and its ready availability makes it a tempting target.</p><p>Several groups of microbes have evolved mechanisms to take advantage of carbonate. The most important group among these is the methanogens. Methanogens are <i>Archaea</i> and comprise one phylogenetic group that is very closely related. Methanogenesis seems to be highly conserved and have deeps roots in the phylogenetic tree of life. It must have evolve early on and practitioners of methanogenesis cannot mess with the genes too much, lest they die.</p><blockquote>HC0<sub>3</sub><sup>-</sup> + 4H<sub>2</sub> + H<sup>+</sup> <img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" /> CH<sub>4</sub> + 3H<sub>2</sub>O</blockquote><p>Methanogens use compounds that contain very high energy electrons as their electron donors and in the process convert CO<sub>2</sub> to methane (CH<sub>4</sub>). Above is shown the use of hydrogen as the source of electrons. They are the only group of microbes that produce a hydrocarbon as major end product of their metabolism. </p><p>Another group of carbonate reducing microbes are the homoacetogens. They utilize hydrogen as the electron source and use it to reduce CO<sub>2</sub> to acetic acid.</p><blockquote>HC0<sub>3</sub><sup>-</sup> + 4H<sub>2</sub> + H<sup>+</sup> <img src="http://lecturer.ukdw.ac.id/dhira/Metabolism/images/arrow.gif" alt="arrow picture" border="0" width="100" height="16" /> CH<sub>3</sub>-COO<sup>-</sup> + 4H<sub>2</sub>O</blockquote>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-53136187204944135182009-12-07T17:49:00.001-08:002009-12-07T18:22:53.433-08:00<a onblur="try {parent.deselectBloggerImageGracefully();} catch(e) {}" href="http://1.bp.blogspot.com/_JiaaHMAFpyg/Sx2yETzkD5I/AAAAAAAAABU/ZkHxrtrhR2k/s1600-h/katak.jpg"><img style="margin: 0pt 0pt 10px 10px; float: right; cursor: pointer; width: 298px; height: 224px;" src="http://1.bp.blogspot.com/_JiaaHMAFpyg/Sx2yETzkD5I/AAAAAAAAABU/ZkHxrtrhR2k/s320/katak.jpg" alt="" id="BLOGGER_PHOTO_ID_5412678114274971538" border="0" /></a><br /><span style="color: rgb(51, 255, 51);font-size:180%;" ><a style="font-weight: bold;" href="http://gemster.wordpress.com/2009/07/17/bagi-katak-bulan-purnama-saatnya-pesta-seks/" rel="bookmark" title="Permanent Link to Bagi Katak, Bulan Purnama Saatnya Pesta Seks">Bagi Katak, Bulan Purnama Saatnya Pesta Seks</a></span><p style="color: rgb(0, 0, 0);"><br /></p><p style="color: rgb(0, 0, 0);"><br /></p><p style="color: rgb(0, 0, 0);">Selama ini bulan purnama identik dengan romantisme dan saat yang asyik untuk bermesraan dengan kekasih. Ternyata hal tersebut juga benar dan berlaku di dunia hean khususnya amfibi.</p> <p style="color: rgb(0, 0, 0);">Para peneliti menemukan bahwa amfibi di seluruh muka bumi melakukan pesta kawin pada saat bulan purnama. Walaupun belum banyak diketahui, tetapi fenomena ini terjadi secara global. Semua spesies amfibi seperti katak, kodok, dan salamander melakukan aktivitas perkawinannya selama periode itu.<span id="more-106"></span></p> <p style="color: rgb(0, 0, 0);">Pergerakan bulan yang tengah berada pada fase penuh umum dimanfaatkan hewan. Amfibi pun menggunakan siklus ini untuk mengumpulkan spesies katak jantan dan betina dalam waktu yang sama. Dengan demikian, potensi kesuksesan pembuahan telur dapat dimaksimalkan.</p> <p style="color: rgb(0, 0, 0);">Pada 2005, ahli biologi Rachel Grant yang sedang meneliti mengenai salamander dekat sebuah telaga di wilayah Italia Tengah, tanpa sengaja melihat begitu banyak katak memenuhi jalan di bawah bulan purnama.</p> <p style="color: rgb(0, 0, 0);">“Meski masih ada kemungkinan ini hanya suatu kebetulan, tapi di bulan berikut saya melewati jalan yang sama di hari senja, dan kembali menemukan sejumlah katak. Jumlahnya meningkat seiring bulan bertambah besar, mencapai puncaknya pada bulan purnama, lantas berangsur-angsur berkurang,” ujarnya.</p> <p style="color: rgb(0, 0, 0);">Oleh sebab itu, Grant kembali ke lokasi tersebut pada 2006 dan 2007. Ia kemudian membandingkan data perolehannya dengan data penelitian perilaku kawin katak-katak di sebuah kolam dekat Oxford, Inggris yang dikumpulkan oleh Tim Halliday; serta data Elizabeth Chadwick dari Universitas Cardiff mengenai katak-katak dan kadal-kadal di Wales.</p> <p style="color: rgb(0, 0, 0);">Hasilnya, disimpulkan terdapat 3 fase hidup pada amfibi yang dipengaruhi perputaran bulan, yakni fase pembiakan (<em>breeding site</em>), fase perkawinan (<em>mating site</em>), dan fase bertelur (<em>spawning site</em>). Spesies katak biasa <em>Bufo bufo</em> melakukan ketiga fase ini selama masa bulan purnama. Begitu pula dengan spesies katak Jawa <em>Bufo melanostictus</em>, yang melakukan fase perkawinannya dalam periode bulan purnama, di mana katak betina melakukan ovulasi pada saat berdekatan atau di waktu yang sama.</p> <p style="color: rgb(0, 0, 0);">Sementara spesies katak <em>Rana temporaria</em> melakukan fase bertelur pada bulan purnama. Perkawinan kadal juga dipengaruhi siklus bulan walaupun hasil yang ditunjukkannya tidak sejelas pada katak.</p> <p style="color: rgb(0, 0, 0);">“Kami kira gejala ini tersebar di seluruh dunia. Bagaimanapun, perbedaan ekologi dan cara reproduksi juga akan mempengaruhi hal ini, dan itu perlu diselidiki lebih lanjut,” ujar Grant.</p>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0tag:blogger.com,1999:blog-8324379693563903183.post-37555201431383766292009-12-07T16:40:00.000-08:002009-12-07T18:22:53.435-08:00<a style="color: rgb(0, 0, 0);" name="3118798736698952195"></a><span style="color: rgb(51, 255, 51);font-size:180%;" ><a style="font-weight: bold;" href="http://leoriset.blogspot.com/2008/10/sumber-gula-baru.html">Sumber Gula Baru</a></span><h3 style="color: rgb(0, 0, 0);" class="post-title entry-title"> </h3> <div style="color: rgb(0, 0, 0);" align="justify"><blockquote></blockquote>Secara umum, kondisi pergulaan nasional, paling tidak, memiliki tiga persoalan utama. Pertama, rendahnya harga beli gula bagi produksi petani karena rendahnya harga gula dipasaran dunia. Kedua, rendahnya produktivitas pabrik gula dan banyak yang tidak efisien. Ketiga, perkembangan industri gula nasional terus merosot. Produksi gula di Indonesia mengalami penurunan pertahunnya sebesar 2,14% atau 44.328,695 ton. Sedangkan perkembangan konsumsi gula di Indonesia meningkat dari tahun 1991/1992 sampai tahun 2000/2001 sebesar 2,03% atau 61.186 ton. Kedua faktor tersebut memicu kenaikkan trend impor gula di Indonesia per tahunnya sebesar 11,94% atau 116.535,839 ton.<br /><br /></div><div style="color: rgb(0, 0, 0);" align="justify">Sumber utama gula di Indonesia saat ini adalah tebu (Saccharum officinale) yang sekarang produktivitasnya menurun disebabkan oleh perubahan iklim di Indonesia yang tidak menentu. Jika hanya mengandalkan produksi gula dari tebu, penurunan produksi gula akan terus turun dan impor gula akan terus meningkat. Maka dari itu, diperlukan sumber produksi gula selain tebu yang dapat menjawab tantangan masalah perikliman dan situasi produksi industri yang ada di Indonesia saat ini.<br /><br /></div><div style="color: rgb(0, 0, 0);" align="justify">Caryota mitis Lour. (fish-tail palm) memiliki kandungan sukrosa yang sangat tinggi pada air bunganya, yaitu sebesar 83,5 %. Karena hanya memanfaatkan bunganya saja, Caryota mitis dapat dikelola sebagai tanaman perkebunan, seperti halnya kelapa sawit, yang dapat dipanen terus-menerus selama waktu reproduktif pohon tersebut. Hipotesis kami adalah air bunga (nira) pada Caryota mitis Lour. dapat digunakan sebagai sumber gula alternatif pengganti tebu. </div><div style="color: rgb(0, 0, 0);" align="justify">Proses untuk mendapatkan sukrosa murni dari air bunga pohon tersebut dapat dilakukan melalui proses ekstraksi air bunga, pengendapan kotoran, pemurnian air gula & pemisahan dari kandungan senyawa lainnya, kristalisasi dan dilakukan penyimpanan untuk selanjutnya diproses menjadi kristal gula murni.<br /><br /></div><div style="color: rgb(0, 0, 0);" align="justify">Keberhasilan introduksi sumber gula yang satu ini akan menjadi wacana baru dalam perkembangan bio-industri skala nasional sekaligus menjawab tantangan kebutuhan salah satu komoditas pangan terpenting baik di Indonesia maupun dunia.<br /><br /></div><div style="color: rgb(0, 0, 0);" align="justify">Sumber: <a href="http://www.forumsains.com/">www.forumsains.com</a></div>Ary Bloghttp://www.blogger.com/profile/01964427892066078835noreply@blogger.com0