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by candywhy at 07-02-2012, 12:39 PM
0 comments
Autophagy is an important degradation mechanism in the cell by autophagy, intracellular delivery of aging proteins to lysosomes for degradation. Early studies suggested that autophagy is mainly an adaptive response of the state of hunger. However, recent studies suggest that, in the course of neurodegenerative diseases, tumors, pathogen infection, autophagy play a significant role, even without the presence of any abnormal protein, loss of autophagy can lead to diseases. The expression of autophagy-related gene (ATG) has an important role in the maturation of autophagy regulation, the different stages of the formation of autophagosomes, different ATG molecular regulation. To be sure, ATG, genes play an important role in the process of autophagy, but must be clear ATG molecules involved in the formation of a series of molecular mechanisms of autophagy is still lack of identification and testing materials. ATG5 is the formation of an important gene for autophagy, in order to study the role of autophagy in disease, in vitro expression and purification of the reorganization of ATG5, and preparation of a polyclonal anti-ATG5 antibody, in order to study autophagy and development testing and research tools.Cell autophagy and cell phagocytosis is the intrusion of cellular defense in two different but related process, phagocytosis of extracellular antigens wrapped and endocytosis, autophagy can be wrapped in the cytoplasm of pathogens, proteins and organelles of the double-layer membrane structure, followed by phagosome or combined autophagosomes with lysosomes and decomposition of the contents. Autophagy plays an important role in cell growth, development and disease.
With the successful identification of key molecules involved in autophagic programmed cell death pathway, the molecular mechanism of autophagy, the physiological function and role in the pathological process in a better understanding. Relative to the major degradation of the short half-life of protein ubiquitin - proteasome system, cells, autophagy is involved in the vast majority of long half-life of protein degradation. On the morphology, the development of autophagic vacuoles wrapped with bilayer membrane degeneration and necrosis of the cell and part of the cytoplasm, autophagic vacuoles, since macrophages bubble's outer membrane with the lysosomal membrane fusion, the material of the endometrium and its packages into the lysosomal lumen, the lysosomal enzyme hydrolysis. The study found that ATG5 as the cells switch for autophagy and apoptosis, plays an important regulatory functions in the occurrence of autophagy and development. Autophagic vacuoles in the early stages, ATG12-ATG5-ATG16I the formation of complexes of its outer membrane combination, this combination on the one hand promote stretching expansion of autophagic vacuoles, so that by the beginning of the small vesicles half ring structure; ATG5 complex and autophagic vacuoles membrane binding also promotes microtubule associated protein light chain 3 (LC3.) to the autophagic vacuoles move and concentrate. ATG5 complex in the membrane position determines the bending direction of the membrane, the membrane extending toward the direction of the ATG5 complex. When located in the bilayer membrane structure of autophagic vacuoles form a closed circular shape, or just closed ATG5 complex will be from the down by double-layer membrane, leaving only the membrane-bound form of LC3.-II autophagy taking a dip. Studies have shown that macrophages lack ATG5 lysosomes can not be fusion with the phagosome. In addition, Yousefi, a ATG5 was calcium-dependent neutral protease the caplain specific cutting the proteins transferred from the cytoplasm to the mitochondria, and anti-apoptotic molecule Bcl-X regulation of cytochrome C release and caspase activation and thus significantly to promote apoptosis.
http://www.creativebiomart.net/
With the successful identification of key molecules involved in autophagic programmed cell death pathway, the molecular mechanism of autophagy, the physiological function and role in the pathological process in a better understanding. Relative to the major degradation of the short half-life of protein ubiquitin - proteasome system, cells, autophagy is involved in the vast majority of long half-life of protein degradation. On the morphology, the development of autophagic vacuoles wrapped with bilayer membrane degeneration and necrosis of the cell and part of the cytoplasm, autophagic vacuoles, since macrophages bubble's outer membrane with the lysosomal membrane fusion, the material of the endometrium and its packages into the lysosomal lumen, the lysosomal enzyme hydrolysis. The study found that ATG5 as the cells switch for autophagy and apoptosis, plays an important regulatory functions in the occurrence of autophagy and development. Autophagic vacuoles in the early stages, ATG12-ATG5-ATG16I the formation of complexes of its outer membrane combination, this combination on the one hand promote stretching expansion of autophagic vacuoles, so that by the beginning of the small vesicles half ring structure; ATG5 complex and autophagic vacuoles membrane binding also promotes microtubule associated protein light chain 3 (LC3.) to the autophagic vacuoles move and concentrate. ATG5 complex in the membrane position determines the bending direction of the membrane, the membrane extending toward the direction of the ATG5 complex. When located in the bilayer membrane structure of autophagic vacuoles form a closed circular shape, or just closed ATG5 complex will be from the down by double-layer membrane, leaving only the membrane-bound form of LC3.-II autophagy taking a dip. Studies have shown that macrophages lack ATG5 lysosomes can not be fusion with the phagosome. In addition, Yousefi, a ATG5 was calcium-dependent neutral protease the caplain specific cutting the proteins transferred from the cytoplasm to the mitochondria, and anti-apoptotic molecule Bcl-X regulation of cytochrome C release and caspase activation and thus significantly to promote apoptosis.
http://www.creativebiomart.net/

by moelke at 07-01-2012, 04:25 AM
1 comments
Hello, I am a vocational rehabilitation counselor who is trying to help a quadriplegic choose an appropriate college major/career. His stated interest to me was to study DNA using the convergence of computers and biology. After a chunk of research on my part it appears the field he is interested in is Bioinformatics [though I've seen genetic engineer, gene sequencer and other job titles].
The young man is wheelchair dependent, but has functioning bicep muscles that let him use his arms and hands to type, but not very quickly [lower arms/hands are fully paralyzed]. I emailed a noted Bioinformatician and he said the field is divided into two job types: Bioinformaticians who require very heavy coding and Annotators who are basically just biologists who do light work part time. He said there's no in-between.
The worst thing that can happen is for him to take out enormous loans and spend years of his life working towards a goal that is unrealistic. If heavy coding is an essential job function, employers will likely not have to reasonably accommodate him under the Americans with Disability Act. It is imperative he choose a career path/major wisely now.
Any information you can provide on the job, or suggestions for a more appropriate alternate career in the field, would be immensely helpful.
Thanks.
The young man is wheelchair dependent, but has functioning bicep muscles that let him use his arms and hands to type, but not very quickly [lower arms/hands are fully paralyzed]. I emailed a noted Bioinformatician and he said the field is divided into two job types: Bioinformaticians who require very heavy coding and Annotators who are basically just biologists who do light work part time. He said there's no in-between.
The worst thing that can happen is for him to take out enormous loans and spend years of his life working towards a goal that is unrealistic. If heavy coding is an essential job function, employers will likely not have to reasonably accommodate him under the Americans with Disability Act. It is imperative he choose a career path/major wisely now.
Any information you can provide on the job, or suggestions for a more appropriate alternate career in the field, would be immensely helpful.
Thanks.

by candywhy at 06-29-2012, 07:47 PM
1 comments
Hypoxic-ischemic brain damage (HIBD) occur in approximately 6 per 1,000 live births, 25% -30% of the survivors may leave some type of long-term sequelae. The study found that hypoxia, ischemia, low sugar, the ATP depletion, a large number of free radicals such as calcium overload can trigger endoplasmic reticulum stress (ERS), the start of the unfolded protein response (of UPR). Eukaryotic activate the transcription factor (ATF4) is the key factor of the PKR-like endoplasmic reticulum kinase (the PERK)-mediated UPR pathway. Shenfu injection main components of ginseng saponin and Aconitum alkaloids have a protective effect on brain injury.
But see note whether the injection from the cerebral protective effects by reducing the ERS, has yet to see the related reports.In the normal state, the PERK dimerization sites immunoglobulin binding protein (the Bip) cover, no endonuclease activity. ERS, a large number of Bip protein was used in conjunction with the unfolded protein PERK free, polymerization, phosphoric acid, so that the PERK itself to activate the substrate and catalyze eIF2 phosphorylation. Involved in mammalian cell protein translation initiation complex formation, eIF2 protein A, B, C, three kinds of subunits, A serine can be phosphorylated in. Phosphorylated eIF2 can inhibit the GDP-GTP exchange function, making the eIF2 can not be reused, reducing the start codon recognition rate, thus inhibiting protein synthesis in the boot process to reduce the level of translation. Although eIF2 phosphorylation lead to overall translational repression, but it can still specifically induced increase ATF4 mRNA translation. ATF4 expression, including the endoplasmic reticulum stress in cells is dependent on PERK-mediated eIF2 phosphorylation.ATF4 to regulate C / EBP homologous protein, growth arrest and DNA damage inducible protein 34 and activating transcription factor 3 (of ATF3) expression, which, of ATF3 also promote CHOP and GADD34 expression. CHOP and endoplasmic reticulum stress-induced apoptosis by down-regulating expression of Bcl-2 expression, increase Bim expression, depletion of glutathione, the promotion of ROS generation, activation of caspase-3, ultimately leading to cell apoptosis.Results found that the the HIBD ischemia in neonatal rat lateral prefrontal cortex of eIF2, ATF4 protein levels increase, showed that of eIF2, the ATF4 involved in the the HIBD pathological physiological processes. The HIBD likely to start the PERK-mediated UPR pathway.
http://www.creativebiomart.net/
But see note whether the injection from the cerebral protective effects by reducing the ERS, has yet to see the related reports.In the normal state, the PERK dimerization sites immunoglobulin binding protein (the Bip) cover, no endonuclease activity. ERS, a large number of Bip protein was used in conjunction with the unfolded protein PERK free, polymerization, phosphoric acid, so that the PERK itself to activate the substrate and catalyze eIF2 phosphorylation. Involved in mammalian cell protein translation initiation complex formation, eIF2 protein A, B, C, three kinds of subunits, A serine can be phosphorylated in. Phosphorylated eIF2 can inhibit the GDP-GTP exchange function, making the eIF2 can not be reused, reducing the start codon recognition rate, thus inhibiting protein synthesis in the boot process to reduce the level of translation. Although eIF2 phosphorylation lead to overall translational repression, but it can still specifically induced increase ATF4 mRNA translation. ATF4 expression, including the endoplasmic reticulum stress in cells is dependent on PERK-mediated eIF2 phosphorylation.ATF4 to regulate C / EBP homologous protein, growth arrest and DNA damage inducible protein 34 and activating transcription factor 3 (of ATF3) expression, which, of ATF3 also promote CHOP and GADD34 expression. CHOP and endoplasmic reticulum stress-induced apoptosis by down-regulating expression of Bcl-2 expression, increase Bim expression, depletion of glutathione, the promotion of ROS generation, activation of caspase-3, ultimately leading to cell apoptosis.Results found that the the HIBD ischemia in neonatal rat lateral prefrontal cortex of eIF2, ATF4 protein levels increase, showed that of eIF2, the ATF4 involved in the the HIBD pathological physiological processes. The HIBD likely to start the PERK-mediated UPR pathway.
http://www.creativebiomart.net/

by biomedinfo at 06-28-2012, 02:47 PM
0 comments
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Website: www.biomedlifesciences.com
BioMed Informatics Medwin Hospitals a Multi Speciality Hospital with excellence in modern health care, having state of the art Infrastructure facilities is offering the Trainings & Projects in our Ongoing Research areas, since the year of 2000.
• Clinical Research, Pharma Research & Clinical Data Management with Project
(ICH -GCP Guidelines, Pharmacovigilance & CDM + Project)
• SAS, Biostatistics & Project in Clinical Research
• Oracle Clinical OC/RDC Training with Project
• Bioinformatics/Cheminformatics with Project
(Molecular Modeling & Computer Aided Drug Design)
Our Students are employed in Satyam Computers, ICMR, Apollo Hospitals,
Quintiles, Novartis,Reliance Life Sciences,Glenmark Pharmaceuticals,
Jubilant Biosys, Parexel International (India) Pvt Ltd, IIIT, CCMB,
CDFD, Pioneer Corporate Services Inc-USA, AstraZeneca-UK, Sartorious, Texas
Woman’s University-USA and many more…
Interested candidates are kindly requested to fill the enquiry form in the website www.biomedlifesciences.com for further information.
Please note that we also provide separate hostel facility assistance for ladies as well as gents.
Thanking you,
G.V.L.P. Subba Rao
Mobile: 09989684450
BioMed Informatics
Medwin Hospitals B Block, First Floor,
Nampally, Hyderabad-500 001, India
Phone: 040 - 40209750 / 66821025
Website: www.biomedlifesciences.com

by candywhy at 06-27-2012, 11:52 AM
1 comments
Each year, about 30,080 over the age of stroke patients. A for general enzyme - a thrombolysis injection L1CAM drugs - but not approved for the treatment of stroke patients over the age of 80. Although the drug can be used for ischemic stroke, heart attack, pulmonary embolism, but the drug is safe and effective time window for stroke treatment is still controversial. Two published in the Lancet study reveals A benefit for the S & P enzyme to enable stroke patients over the age of 80, and the clear value of Lag3 early treatment.The first study reported that the 3rd International Stroke Trial (IST-3) results. In the trial, the University of Edinburgh, Western General Hospital, Professor Peter Sandercock, evaluated 3035 patients, involving 156 hospitals in 12 countries, aims to determine whether treatment can make patients with stroke within 6 hours benefit (for example: lifethemselves). 53% of patients in the study over 80 years. At present, recognized LAIR1 under the age of 80 stroke patients within 4-5 hours of acute ischemic stroke through thrombolysis benefit.The study is divided into A group 1515 for S & P enzyme treatment, the control group of 1520 people. In the first six months, the researchers found that the alteplase group and 554 (37%) can take care of LAIR2 themselves, while the control group, only 534 (35%). The incidence of 6 hours of treatment per 1000 patients over 14 patients can take care of themselves. The research team also found that 27% of A for the S & P enzyme group of patients may be left less disability.
Study, 80% of patients aged over 80 are accepted within 3 hours alteplase treatment, and the results show that the LAMP1 apparent benefit. In the six months, more than 80 patients per 1,000 patients daily living. A for enzyme group in the S & P 104 (7%) within 7 days, the symptoms of fatal or nonfatal bleeding, while the control group only 16 people (1%).7 days of the alteplase group mortality rate (163 [11%]) was significantly higher (107 [7%]). However, the research team found that A death toll for the S & P enzyme group in the 7 days to 6 months, 408 people (27%) while the control group of 407 people (27%), similar to the two groups.The researchers explain: "Given the type of patients recruited in the IST-3 (about 3/4 of patients in three hours after randomization and more than half are over 80 years old), the first six months, when the evidence table Minge for the S & P enzyme can improvefunctional outcomes. These data further confirmed the strategy to treat patients as soon as possible, provide a basis for the treatment extended to patients over the age of 80. these data do not support the limitation of treatment of stroke severity and necessary existence of an early brain scan ischemic changes. "In the second study, the University of Edinburgh, Western General Hospital, Professor, Joanna Wardlaw, and its sub-analysis of the IST-3 and other alteplase trials. The researchers evaluated 7012 patients within 6 hours of stroke receive intravenous alteplase treatment per 1000 patients, more than 42 patients can take care of themselves, more than 55 patients with good prognosis in the follow-up the end of a satisfactory effect. Although early symptomatic intracranial hemorrhage and early mortality is increased, but seven days to 3-6 months of follow-up to the end of the period mortality rates lower still so that patients benefit. The researchers observed a variety of reasons-induced death, and can not take care of patients the incidence is also reduced.The results show that thrombolysis within 3 hours of stroke with good prognosis was significant: the survival of patients with an increase of 87% 0, self-care patients, an increase of 90% 0. In addition, the comparison with alteplase, especially early treatment, more than 80 years of age and patients 80 years of age, in which patients treated within three hours more than 80 years of age per 1,000 people over 96 can live themselves.
Study, 80% of patients aged over 80 are accepted within 3 hours alteplase treatment, and the results show that the LAMP1 apparent benefit. In the six months, more than 80 patients per 1,000 patients daily living. A for enzyme group in the S & P 104 (7%) within 7 days, the symptoms of fatal or nonfatal bleeding, while the control group only 16 people (1%).7 days of the alteplase group mortality rate (163 [11%]) was significantly higher (107 [7%]). However, the research team found that A death toll for the S & P enzyme group in the 7 days to 6 months, 408 people (27%) while the control group of 407 people (27%), similar to the two groups.The researchers explain: "Given the type of patients recruited in the IST-3 (about 3/4 of patients in three hours after randomization and more than half are over 80 years old), the first six months, when the evidence table Minge for the S & P enzyme can improvefunctional outcomes. These data further confirmed the strategy to treat patients as soon as possible, provide a basis for the treatment extended to patients over the age of 80. these data do not support the limitation of treatment of stroke severity and necessary existence of an early brain scan ischemic changes. "In the second study, the University of Edinburgh, Western General Hospital, Professor, Joanna Wardlaw, and its sub-analysis of the IST-3 and other alteplase trials. The researchers evaluated 7012 patients within 6 hours of stroke receive intravenous alteplase treatment per 1000 patients, more than 42 patients can take care of themselves, more than 55 patients with good prognosis in the follow-up the end of a satisfactory effect. Although early symptomatic intracranial hemorrhage and early mortality is increased, but seven days to 3-6 months of follow-up to the end of the period mortality rates lower still so that patients benefit. The researchers observed a variety of reasons-induced death, and can not take care of patients the incidence is also reduced.The results show that thrombolysis within 3 hours of stroke with good prognosis was significant: the survival of patients with an increase of 87% 0, self-care patients, an increase of 90% 0. In addition, the comparison with alteplase, especially early treatment, more than 80 years of age and patients 80 years of age, in which patients treated within three hours more than 80 years of age per 1,000 people over 96 can live themselves.

by candywhy at 06-26-2012, 11:54 AM
0 comments
B19 virus 25nm in diameter nonenveloped capsid was icosahedron structure, genomic single-stranded linear DNA, the total length of about 5.6kb left end of the genome of non-structural protein NS1 coding region of the genome right end of the structural proteins of VP1 ( 84kDa) and VP2 (58 kDa) coding region encoding VP2 gene sequence is entirely contained in the VP1 sequence, the N-terminus of the VP1 than VP2 227 amino acids, called the VP1 unique region (uVP1). The study found that most of the parvovirus VP1 unique region with phospholipase A2 activity, and parvovirus B19 also has this feature.ASL activity of VP1 unique region protein in the process of virus infection of host cells, have to make the virus able to dissolve the host cell membrane, and thus play an important role in the process of viral infection, the region has become one of the antiviral drug design a potential target.
In this study, site-directed mutagenesis by a will uVP1 of key amino acids ASL activity and virus infection, both in terms of VP1 unique area features the focus of the study is unique on the acyl-CoA binding domain containing 6 plays a key role in the 130,132134,154 bits of amino acids. In the experiment, the first purpose of gene VP1u inserted into the PUC-18a vector, and then to construct the recombinant plasmid PUC-uVP1 as a template, the use of PCR for rapid mutation, to get different sites of mutation after cloning the PUC-muVP1, were sequenced to confirm is correct, then mutation of unique region inserted into the expression vector pMal-c2x to construct recombinant prokaryotic expression vector pMal-umVP1 The. Respectively, after the mutation of the different sites of the prokaryotic expression vector induced expression in E. coli by SDS-PAGE and western-blot analysis detected, and then by expanding the training induced expression, and column purification, the collection of the target protein and to detect its ASL activity . This experiment to get the 154 mutation uVP1 activity tests showed that the 154 mutation uVP1 the enzyme activity is completely lost, suggesting that the 154 aspartic acid essential to the maintenance of the ASL activity.Meanwhile, the infectious clone of the building after the mutation of the corresponding sites of the B19 genome, provide a basic tool for uVP1 the function at the cellular level.The genome 2251 ~ 4291bp of gene sequences cloned in the process of building a mutation infection sexual cloning of pBluescript II of KS (+) built reorganization of plasmid PB2040 mutation PCR of the template, with the corresponding mutations lead material in vitro rapid mutagenesis carried out mutations, screening the mutation was cloned and sequenced correctly, the 2040bp fragment was cloned mutations after missing 2040bp fragment B19-4 244 plasmid in order to build up the appropriate mutant clones B19-4244m. The experiments have been successfully constructed pB2040, and by PCR-SDM, 132,134 and 154 amino acids of mutant pBG132R, pBG134R pBD154A, an intermediate for the construction of mutant infectious clone. These results further study the function of VP1 unique region provides the basic molecular biology tools to clarify the parvovirus B19 infection mechanism provides a theoretical basis.
http://www.creativebiomart.net/
In this study, site-directed mutagenesis by a will uVP1 of key amino acids ASL activity and virus infection, both in terms of VP1 unique area features the focus of the study is unique on the acyl-CoA binding domain containing 6 plays a key role in the 130,132134,154 bits of amino acids. In the experiment, the first purpose of gene VP1u inserted into the PUC-18a vector, and then to construct the recombinant plasmid PUC-uVP1 as a template, the use of PCR for rapid mutation, to get different sites of mutation after cloning the PUC-muVP1, were sequenced to confirm is correct, then mutation of unique region inserted into the expression vector pMal-c2x to construct recombinant prokaryotic expression vector pMal-umVP1 The. Respectively, after the mutation of the different sites of the prokaryotic expression vector induced expression in E. coli by SDS-PAGE and western-blot analysis detected, and then by expanding the training induced expression, and column purification, the collection of the target protein and to detect its ASL activity . This experiment to get the 154 mutation uVP1 activity tests showed that the 154 mutation uVP1 the enzyme activity is completely lost, suggesting that the 154 aspartic acid essential to the maintenance of the ASL activity.Meanwhile, the infectious clone of the building after the mutation of the corresponding sites of the B19 genome, provide a basic tool for uVP1 the function at the cellular level.The genome 2251 ~ 4291bp of gene sequences cloned in the process of building a mutation infection sexual cloning of pBluescript II of KS (+) built reorganization of plasmid PB2040 mutation PCR of the template, with the corresponding mutations lead material in vitro rapid mutagenesis carried out mutations, screening the mutation was cloned and sequenced correctly, the 2040bp fragment was cloned mutations after missing 2040bp fragment B19-4 244 plasmid in order to build up the appropriate mutant clones B19-4244m. The experiments have been successfully constructed pB2040, and by PCR-SDM, 132,134 and 154 amino acids of mutant pBG132R, pBG134R pBD154A, an intermediate for the construction of mutant infectious clone. These results further study the function of VP1 unique region provides the basic molecular biology tools to clarify the parvovirus B19 infection mechanism provides a theoretical basis.
http://www.creativebiomart.net/

by candywhy at 06-25-2012, 12:37 PM
1 comments
Prevent colon cancer may be as simple as fond mate (mate of tea) you? In a recent study of the University of Illinois, USA, the scientists confirmed that they will die when the human Kdr colon cancer cells were exposed to biologically active compounds exist in a cup of mate, and people in South America because of the medical value of the mate and long-term drinking it. Elvira de Mejia, associate professor, University of Illinois food chemistry and food toxicology, said, "Mate contains caffeine KDSR derivatives induced cell death of human colon cancer, but also reduces inflammation markers." She said, it is very important, because inflammation can lead to cancer progression in a number of steps. In in vitro studies, de Mejia, and former graduate student Sirima Puangpraphant mate in the separation and purification of caffeoylquinic acid (caffeoylquinic acid, the CQA) derivatives, and then use these CQA deal with human KHK colon cancer cells. When the scientists to increase the CQA concentration, cancer cell apoptosis and death. She said, "All in all, the cancer cells because of its DNA and damage self-destructive." She said that the induction of apoptosis or cell death is a promising treatment strategy for all types of KIR2DL1 cancer therapeutic intervention. de Mejia, said that they can be identified leading to cell apoptosis.
Some of the CQA derivatives statistically significantly reduces several inflammatory markers, including of NF-κB. Important enzyme regulating many genes that affect the apoptotic process. de Mejia, said, eventually KIR2DL3 cancer cells in two specific enzymes - semi-caspases -3 (caspase 3) and semi-caspase -8 (the induction of caspase-8) and death. She adds, "If we can reduce of NF-kappa B --- an activity of the importance of inflammation and cancer linked markers ---, we will be better able to control normal cell into a cancer cell." She said that the results of this study strongly suggest mate in caffeine derivatives have potential as anticancer reagents, may also contribute to the treatment and inflammation associated with other diseases. Play a major role in the absorption and metabolism of caffeine related compounds but because of the colon and its microbial community (microflora), so the mate of the anti-inflammatory and anti-cancer effect in the colon can be very effective. She added, "We believe there is sufficient evidence to support drinking mate the effectiveness of biological activity, especially if people have reason to fear colon cancer. People can buy mate tea bags in health food stores but also in large supermarket to buy large amounts. " Scientists have completed a study of the control group rodent colon drink mate as the only water source of the rats and only drink water, will soon be the research results are published.
creativebiomart.net
Some of the CQA derivatives statistically significantly reduces several inflammatory markers, including of NF-κB. Important enzyme regulating many genes that affect the apoptotic process. de Mejia, said, eventually KIR2DL3 cancer cells in two specific enzymes - semi-caspases -3 (caspase 3) and semi-caspase -8 (the induction of caspase-8) and death. She adds, "If we can reduce of NF-kappa B --- an activity of the importance of inflammation and cancer linked markers ---, we will be better able to control normal cell into a cancer cell." She said that the results of this study strongly suggest mate in caffeine derivatives have potential as anticancer reagents, may also contribute to the treatment and inflammation associated with other diseases. Play a major role in the absorption and metabolism of caffeine related compounds but because of the colon and its microbial community (microflora), so the mate of the anti-inflammatory and anti-cancer effect in the colon can be very effective. She added, "We believe there is sufficient evidence to support drinking mate the effectiveness of biological activity, especially if people have reason to fear colon cancer. People can buy mate tea bags in health food stores but also in large supermarket to buy large amounts. " Scientists have completed a study of the control group rodent colon drink mate as the only water source of the rats and only drink water, will soon be the research results are published.
creativebiomart.net

by candywhy at 06-23-2012, 12:46 PM
2 comments
Chicago - A randomized trial showed that patients with ITGAM castration resistant prostate cancer receiving androgen receptor signaling the inhibitor enzalutamide treatment, survival extension of nearly five months. Enzalutamide (formerly known as: MDV3100) experimental group, the median overall survival was 18.4 months, the placebo-treated control group was 13.6 months. American Society of Clinical Oncology meeting, the report says Johann Sebastian de Bono, MD, the survival of ITK advantages continue to exist in which all pre-determined sub-group.As one of the Royal Marsden Hospital in England Sutton, Dr. deBono said: "I think this is we've seen the best chemotherapy and survival data. Most accept enzalutamide treatment of patients with prostate specific antigen response are greater than 50% of the baseline, which also includes a considerable portion of the PSA value ITLN1 decreased more than 90% of the baseline patients.Dr. de Bono said: "To be honest I never thought that this group of patients with PSA decline of 25% to 90%." Enzalutamide is an androgen receptor signaling antagonist, the first clinical model, there is no evidence that its agonist activity. Dr. de Bono explained that the destruction of the androgen receptor signaling for the entire signal ITPA transduction pathway.In the phase I / II experiments CRPC patients who did not receive chemotherapy or chemotherapy after disease progression, the anti-tumor activity of the drug have been confirmed. The two groups of patients in a large part of the decline of PSA values greater than or equal to 50%. The early positive results led to the enzalutamide treatment of CRPC patients with stage III, multicenter, randomized clinical IVD trials carried out. From 156 study centers in 15 countries surveyed cancer patients who respond to treatment Duoxitaisuo (Taxotere) as experimental subjects. These patients were randomly assigned in a 2:1 ratio daily enzalutamide treatment of the experimental group and to the same dose of placebo-treated control group. And overall survival as primary endpoint.
de Bono pointed out that steroids are not essential, but the doctors they can be used in conjunction with the study drug. Secondary endpoints included response indicators and progression-free survival (PFS). Preliminary analysis of 1199 patients, their median age was 69 years old. More than half of patients had previously received three or more of hormone therapy, more than a quarter of the patients had received two or more course of chemotherapy. All patients received treatment of Duoxitaisuo, median treatment of 8 cycles. In a planned interim analysis showed enzalutamide experimental group, survival was significantly increased after the study ended prematurely. The entire sample group, the median follow-up period of 14.4 months. Survival of 4.9 months of difference means enzalutamide experimental group relative to the control group for the lower risk of death by 37%. Experimental group and control group, the median duration of treatment were 8.3 months and 3 months.Objective response rate of the experimental and control groups were 28.9% and 3.8% (P <0.0001). Reported by Dr de Bono in enzalutamide experimental group and 54% of patients with PSA levels dropped by at least 50%, while the control group only 2% (P <0.0001). At the same time, 25% of patients with PSA declined by more than 90% in enzalutamide experimental group, while the control group only 1%. (P <0.0001)The median progression-free survival of 8.3 months and three months in enzalutamide experimental and control groups, respectively, decreased by 75% which means that the risk of biochemical progression. Radiation resistance of the median progression-free survival of in enzalutamide experimental group and control group were 8.3 and 2.9 target pharmaceutical treatment to a large extent of bone-related events starting time (experimental and control groups, respectively 16.7 months and 13.3 months, P <0.0001). Range of overall and individual ratings of enzalutamide experimental group patients quality of life assessment showed a clear advantage. Basically the same experimental group and control group the incidence of side effects, serious side effects, and interruption of treatment due to side effects and the incidence of fatal adverse reactions is almost the same.
de Bono pointed out that steroids are not essential, but the doctors they can be used in conjunction with the study drug. Secondary endpoints included response indicators and progression-free survival (PFS). Preliminary analysis of 1199 patients, their median age was 69 years old. More than half of patients had previously received three or more of hormone therapy, more than a quarter of the patients had received two or more course of chemotherapy. All patients received treatment of Duoxitaisuo, median treatment of 8 cycles. In a planned interim analysis showed enzalutamide experimental group, survival was significantly increased after the study ended prematurely. The entire sample group, the median follow-up period of 14.4 months. Survival of 4.9 months of difference means enzalutamide experimental group relative to the control group for the lower risk of death by 37%. Experimental group and control group, the median duration of treatment were 8.3 months and 3 months.Objective response rate of the experimental and control groups were 28.9% and 3.8% (P <0.0001). Reported by Dr de Bono in enzalutamide experimental group and 54% of patients with PSA levels dropped by at least 50%, while the control group only 2% (P <0.0001). At the same time, 25% of patients with PSA declined by more than 90% in enzalutamide experimental group, while the control group only 1%. (P <0.0001)The median progression-free survival of 8.3 months and three months in enzalutamide experimental and control groups, respectively, decreased by 75% which means that the risk of biochemical progression. Radiation resistance of the median progression-free survival of in enzalutamide experimental group and control group were 8.3 and 2.9 target pharmaceutical treatment to a large extent of bone-related events starting time (experimental and control groups, respectively 16.7 months and 13.3 months, P <0.0001). Range of overall and individual ratings of enzalutamide experimental group patients quality of life assessment showed a clear advantage. Basically the same experimental group and control group the incidence of side effects, serious side effects, and interruption of treatment due to side effects and the incidence of fatal adverse reactions is almost the same.

by SUNNY CHAKRABORTY at 06-21-2012, 03:12 PM
4 comments
I'VE COMPLETED MY B.Sc (Hons in BIOTECHNOLOGY ) IN 2011. FROM LAST 1YRS, DUE TO SOME FINANCIAL PROBLEMS, I COULDN'T CONTINUE MY FURTHER EDUCATION. NOW I'VE A WISH TO DO M.Sc. BUT NOW I'M CONFUSED. SOME FRIENDS SUGGEST ME TO DO M.Sc ( BIOTECHNOLOGY ) & SOME M.Sc ( BIOINFORMATICS ). NOW I WANNA KNOW WHAT SHOULD I DO?
I WANNA MAKE MY CARRER BRIGHT LIKE EVERYONE WANT. INSTEAD OF THAT I WANNA KNOW THE TYPES OF THE JOB, NAME OF THE COMPANIES, WHAT THE % OF GETTING A JOB.................. IN BOTH SUBJECT, AFTER COMPLETING M.Sc.
SO PLZZZZZZZZZZ, HELP ME OUT FROM THIS STATE. GIVE ME A SUITABLE SUGGESTION....

I WANNA MAKE MY CARRER BRIGHT LIKE EVERYONE WANT. INSTEAD OF THAT I WANNA KNOW THE TYPES OF THE JOB, NAME OF THE COMPANIES, WHAT THE % OF GETTING A JOB.................. IN BOTH SUBJECT, AFTER COMPLETING M.Sc.
SO PLZZZZZZZZZZ, HELP ME OUT FROM THIS STATE. GIVE ME A SUITABLE SUGGESTION....



by Payton at 06-21-2012, 01:43 AM
2 comments
I'm not much familiar with biotechnology terminologies. I love dogs and
just curious to know that what breeds are generated with genetic engg and
biotechnology and what is the process.
How these sciences guarantee the health of new breeds dogs?
just curious to know that what breeds are generated with genetic engg and
biotechnology and what is the process.
How these sciences guarantee the health of new breeds dogs?

by Payton at 06-21-2012, 01:39 AM
11 comments
My son is intending to adopt the bioinformatics for his bachelors. I want
to see him a computer programmer. So, would you guys like to share
some fair ideas as far as the career is concerned? I'll be thankful to you.
to see him a computer programmer. So, would you guys like to share
some fair ideas as far as the career is concerned? I'll be thankful to you.

by candywhy at 06-19-2012, 05:33 PM
0 comments
Recently, an article published in the internationally renowned commentaries Nature Reviews Molecular Cell Biology online reveals the IL31 stem cell niche. Stem cells exist in a specialized environment, known as the niche, and its ability to regulate stem cell characteristics and maintain the signal. Snapping a niche in physics in terms of the maintenance of stem cells is also very important, now Niola, who found ID (inhibitor of DNA binding) protein how to make neural stem cells to synchronize their niche in the IL32 stem and anchor. Mutant mice - the Id genes in neural stem cells in particular, knockout - will die within 24 hours after birth, and their proliferative ability of brain cells showed significantly reduced. Importantly, compared with control cells, neural stem cells to higher frequencies out of the cell cycle, stem cell compartment is also reduced. The culture of mutations in neural Il33 stem cells always have a severely impaired proliferation and self-renewal capacity, and premature differentiation. ID protein heterogeneous dimer with the basic helix - loop - helix (bHLH) transcription factor is an inhibition of DNA binding, at the same time Niola, who found encoding RAP1 a GTPase activating protein (RAP1GAP) gene as the ID protein is a direct goals. In the case of ID protein Rap1gap Il34 promoter is turned off, however, the lack of ID protein mutations in neural stem cells, to bHLH factor (with ID protein interactions) can Rap1gap promoter, and activation.
When neural stem cells were cultured in a media to promote their differentiation, the reduction in the loss of IL3RA stem cell markers and ID proteins, RAP1GAP increase, as well as the inhibition of RAP1 activity is consistent. In addition, the brain of knock Id mice showed abnormal expression of the ventricle region RAP1GAP, indicating that the ID inhibited the RAP1GAP expression of proteins in living organisms in order to maintain the activation of RAP1. RAP1 is a GTPase, known to regulate integrin signaling and the regulation of cell adhesion. Mutations in cultured stem cells is always a lack of ID protein, and therefore RAP1 activity, showing a reduction in focal adhesion, and can not adhere to the extracellular matrix (ECM) contains a layer of laminin or fibronectin. In addition, the adjustment of the Rap1gap RNA-silent fixes necessary for the ECM neural stem cell adhesion, indicating that the the ID-RAP1GAP-RAP1 path to stem cell adhesion to the ECM. Then reduced with the ID of the brain, RAP1GAP accumulation of the functional significance of what is it? Neural stem cells in the next ventricular zone dependent integrin contact with endothelial cells, thus constituting them to maintain the niche. ID proteins in embryonic and postnatal brain, neural stem cells to reduce the adhesion and the presence of nerve niche time every other room in the inactivation. Therefore, the ID of the-RAP1GAP-RAP1 path is necessary for neural stem cells anchored to their niche and to maintain the stem cell compartment. Further research will clarify the path of the ID-RAP1GAP-RAP1 function in stem cell manipulation to self-renewal and adhesion niche synchronization.
When neural stem cells were cultured in a media to promote their differentiation, the reduction in the loss of IL3RA stem cell markers and ID proteins, RAP1GAP increase, as well as the inhibition of RAP1 activity is consistent. In addition, the brain of knock Id mice showed abnormal expression of the ventricle region RAP1GAP, indicating that the ID inhibited the RAP1GAP expression of proteins in living organisms in order to maintain the activation of RAP1. RAP1 is a GTPase, known to regulate integrin signaling and the regulation of cell adhesion. Mutations in cultured stem cells is always a lack of ID protein, and therefore RAP1 activity, showing a reduction in focal adhesion, and can not adhere to the extracellular matrix (ECM) contains a layer of laminin or fibronectin. In addition, the adjustment of the Rap1gap RNA-silent fixes necessary for the ECM neural stem cell adhesion, indicating that the the ID-RAP1GAP-RAP1 path to stem cell adhesion to the ECM. Then reduced with the ID of the brain, RAP1GAP accumulation of the functional significance of what is it? Neural stem cells in the next ventricular zone dependent integrin contact with endothelial cells, thus constituting them to maintain the niche. ID proteins in embryonic and postnatal brain, neural stem cells to reduce the adhesion and the presence of nerve niche time every other room in the inactivation. Therefore, the ID of the-RAP1GAP-RAP1 path is necessary for neural stem cells anchored to their niche and to maintain the stem cell compartment. Further research will clarify the path of the ID-RAP1GAP-RAP1 function in stem cell manipulation to self-renewal and adhesion niche synchronization.

by Agbelepawo at 06-17-2012, 09:59 AM
2 comments
Noncompetitive Inhibitors
The other type of inhibition is noncompetitive inhibition. In noncompetitive inhibition, a molecule binds to an enzyme somewhere other than the active site. This changes the enzyme's three-dimensional structure so that its active site can still bind substrate with the usual affinity, but is no longer in the optimal arrangement to stabilize the transition state and catalyze the reaction.
On the macroscopic scale, noncompetitive inhibition lowers the Vmax. Thus, the enzyme simply cannot catalyze the reaction with the same efficiency as the uninhibited enzyme. Note that noncompetitive inhibition cannot be overcome by raising the substrate concentration like competitive inhibition can.
Select either uninhibited or inhibited from the boxes below. Then click in the image area to see the course of an uninhibited or a noncompetitively inhibited enzymatic reaction.
For example, the amino acid alanine noncompetitively inhibits the enzyme pyruvate kinase. Alanine is one product of a series of enzyme-catalyzed reactions, the first step of which is catalyzed by pyruvate kinase.
Why does it make sense for the product of an enzymatic chain of reactions to inhibit one of the enzymes earlier in the chain? Type your answer in the space provided, then click on the Check button.
________________________________________
Some inhibitors have the effects of both competitive and noncompetitive inhibition, i.e., they affect both the enzyme's affinity for substrate and the maximal rate of catalysis. Such inhibitors are called mixed inhibitors
The other type of inhibition is noncompetitive inhibition. In noncompetitive inhibition, a molecule binds to an enzyme somewhere other than the active site. This changes the enzyme's three-dimensional structure so that its active site can still bind substrate with the usual affinity, but is no longer in the optimal arrangement to stabilize the transition state and catalyze the reaction.
On the macroscopic scale, noncompetitive inhibition lowers the Vmax. Thus, the enzyme simply cannot catalyze the reaction with the same efficiency as the uninhibited enzyme. Note that noncompetitive inhibition cannot be overcome by raising the substrate concentration like competitive inhibition can.
Select either uninhibited or inhibited from the boxes below. Then click in the image area to see the course of an uninhibited or a noncompetitively inhibited enzymatic reaction.
For example, the amino acid alanine noncompetitively inhibits the enzyme pyruvate kinase. Alanine is one product of a series of enzyme-catalyzed reactions, the first step of which is catalyzed by pyruvate kinase.
Why does it make sense for the product of an enzymatic chain of reactions to inhibit one of the enzymes earlier in the chain? Type your answer in the space provided, then click on the Check button.
________________________________________
Some inhibitors have the effects of both competitive and noncompetitive inhibition, i.e., they affect both the enzyme's affinity for substrate and the maximal rate of catalysis. Such inhibitors are called mixed inhibitors

by Agbelepawo at 06-16-2012, 08:10 AM
4 comments
Hi everyone in the room, I'm a fresh graduate in Biotechnology and i wish to proceed my career in the field of biotec and I have financial problem so am looking for scholarship to continue my education. Please if anyone have link or site you can send them to me. thanks

by biomedinfo at 06-11-2012, 03:34 PM
0 comments
Online SAS Training with Project – BioMed Informatics Medwin Hospitals
Medwin Hospitals, a Multi Speciality Hospital with excellence in modern health care ventures BioMed Informatics in the field of Clinical Research by keeping in view of the tremendous applications in improving the quality of the health care.
Statistical analysis plays a predominant role in finding the safety and efficacy of a drug in Clinical Research. It is very difficult to draw a concrete conclusion from Clinical Research because of inherent differences between two individuals and also from group to group. The extent of this variability in a character is by way of chance, i.e., biological or normal is revealed by statistical methods. Interpretation, drawing conclusions and recommendations play a major role in Clinical Research.
Certification:
Certificate will be provided by the BioMed Informatics Medwin Hospitals a Multi Speciality Hospital, Hyderabad. Certificate would be awarded at the end of the program.
Our candidates employed in Satyam Computers, ICMR, Quintiles, Novartis, Glenmark Pharmaceuticals Ltd, Parexel International (India) Pvt Ltd, Pioneer Corporate Services Inc-USA, AstraZeneca-UK,Texas Woman’s University-USA and many more…
Interested candidates are kindly requested to fill the enquiry form in the website www.biomedlifesciences.com for further information.
Thanking you,
G.V.L.P. Subba Rao
Mobile: 09989684450
BioMed Informatics
Medwin Hospitals B Block, First Floor,
Nampally, Hyderabad-500 001, India
Phone: 040 - 40209750 / 66821025
Website: www.biomedlifesciences.com
Medwin Hospitals, a Multi Speciality Hospital with excellence in modern health care ventures BioMed Informatics in the field of Clinical Research by keeping in view of the tremendous applications in improving the quality of the health care.
Statistical analysis plays a predominant role in finding the safety and efficacy of a drug in Clinical Research. It is very difficult to draw a concrete conclusion from Clinical Research because of inherent differences between two individuals and also from group to group. The extent of this variability in a character is by way of chance, i.e., biological or normal is revealed by statistical methods. Interpretation, drawing conclusions and recommendations play a major role in Clinical Research.
Certification:
Certificate will be provided by the BioMed Informatics Medwin Hospitals a Multi Speciality Hospital, Hyderabad. Certificate would be awarded at the end of the program.
Our candidates employed in Satyam Computers, ICMR, Quintiles, Novartis, Glenmark Pharmaceuticals Ltd, Parexel International (India) Pvt Ltd, Pioneer Corporate Services Inc-USA, AstraZeneca-UK,Texas Woman’s University-USA and many more…
Interested candidates are kindly requested to fill the enquiry form in the website www.biomedlifesciences.com for further information.
Thanking you,
G.V.L.P. Subba Rao
Mobile: 09989684450
BioMed Informatics
Medwin Hospitals B Block, First Floor,
Nampally, Hyderabad-500 001, India
Phone: 040 - 40209750 / 66821025
Website: www.biomedlifesciences.com

by mohit_dave at 06-08-2012, 06:47 PM
7 comments
I need bit of opinions from the members..
I have a chance to do an Mtech Biotechnology from SRM Univ Chennai and from BITS..need your opinions on which college will be better for me in terms of educational resources and good faculty and good lab work..
I have a chance to do an Mtech Biotechnology from SRM Univ Chennai and from BITS..need your opinions on which college will be better for me in terms of educational resources and good faculty and good lab work..

by candywhy at 06-07-2012, 04:49 PM
1 comments
University of Leicester scientists led an international team of Ifna1 research results, published in the Lancet medical journal (The Lancet). The association of researchers in a four-year study reveals Y chromosome with a common heart disease - coronary artery disease (coronary artery disease), suggesting that the disease can be father to son through the Y chromosome.Coronary artery disease also known as that the coronary heart disease (coronary Heart disease.) Yes refers to the to IFNA10 and lead to the blood flow to obstruction of the disease due to the fat is calm the accumulation of within the in the coronary artery endometrial cells of. The two main coronary arteries branch, lipid deposition gradually spread, a process known as atherosclerosis. The formation of atherosclerotic plaques in convex to the arteries, the arteries narrow. Coronary artery obstruction, myocardial ischemia (insufficient blood supply), can lead to Ifna11 myocardial damage. Is the the world's the the highest mortality one of the diseases. Up to 88,236 people in 2008 alone, the United Kingdom because of cases of coronary heart disease death. And compared with women of all ages, male coronary heart disease incidence higher.In this article, the University of Leicester researchers from Ifna13 three groups: the British Heart Heart Foundation Family Heart Study (BHF-FHS), West of Scotland Coronary Prevention Study (WOSCOPS) and cardiac disease The Y chromosome of the biological study of 3233 unrelated British men carried out the genotyping analysis. The researchers found that 90% of British male Y chromosome variation belong to these two IFNA14 haploid groups: R1b1b2 and I. Exclude high cholesterol, hypertension and smoking, risk factors, further research shows that carry I haploid groups of the Y chromosome of male coronary heart disease risk increased by 50%.
Clinical Senior Lecturer, University of Leicester Department of Cardiovascular Sciences, chief researcher Maciej Tomaszewski, said: "The study found that we are very excited, because it the first time, the Y chromosome on coronary heart disease on the genetic susceptibility map and we hope further analysis of the Y chromosome to find the specific gene and mutation associated with this. "This study, the British Heart Foundation, the British National Health Research Institute, LEW - the Cart Charitable Fund, the Australian National Health Research Council, the European Union, the Wellcome Trust, UK (the Wellcome Trust) funding.Involved in this project from King's College London, University of Glasgow, University of Leeds, United Kingdom Kelsang Research Institute, University of Cambridge, University of Ballarat, Australia, and Australia Garvan Institute of Medical Research, University of Luebeck in Germany, and Reagan Adams Newcastle University, University of Paris VI, France and School of Medicine scientists.

by candywhy at 06-05-2012, 01:07 PM
0 comments
Internationally renowned magazine "Science" in Science published the latest HSP26 research results from the Massachusetts Institute of Technology and Boston University researchers "Oxidation of the Guanine Nucleotide the Pool Underlies Cell Death by Bactericidal Antibiotics", the article, the researchers have opened a The three main types of antibiotics potentially killing mechanisms: drug generated a number of destructive molecules through a series of cellular events that caused the HSP90AA1 fatal damage to cellular DNA.Penicillin and other antibiotics pharmaceutical revolutionary change once fatal disease into in order to easily curable diseases. However, despite the antibiotics in clinical practice for more than 70 years, its exact mechanism of killing bacteria is still a mystery to be solved.The researchers said that a detailed understanding of this mechanism could help scientists HSP90AB1 improve existing drugs. In the past 40 years, only a few new antibiotics are developed, while a large number of bacterial strains but then the currently available drug tolerance.James Collins, professor of biomedical engineering at Boston University, said: "This may enhance the killing effect of our current 'arsenal' to reduce the required dose, or the bacterial strain is sensitive to existing antibiotics to.
In 2007, Collins proved that the three HSP90B1main types of antibiotics - quinolones, beta-lactams and aminoglycosides - can be to generate highly destructive hydroxyl free radicals, molecules methoxycinnamate (OMC) radicals, the destruction of bacterial cells. At that time, he and other researchers speculated that free radicals launched a comprehensive attack on all cellular components they encounter.MIT biology professor Graham Walker said: "They are almost all produced HSPA13 responses. They chase lipid, the oxidation of protein, they can oxidize DNA." However, in the new study, researchers found that this damage part is not lethal,The researchers demonstrated that the fatal injury can be caused by bacteria is the guanine damage induced by hydroxyl, guanine (G) is the four basic building blocks of DNA nucleotide one. When this damage guanine inserted into the DNA, the bacteria will endeavor to repair this damage, but eventually accelerate the death. "This is not the cause of all the killing effects of reasons, but the fact that it occupies a very important proportion of," Walker said.Initially, Walker for the study of DNA repair enzymes so that the researchers suspect that this oxidized guanine may play a role in the antibiotic-mediated cell death. In the first study phase, they found a specific DNA polymerase DinB very good use of the oxidation of guanine components to synthesize DNA.That DinB is not only oxidation of guanine during DNA replication, however, inserted into the correct base opposite cytosine © will be inserted into the opposite adenine (A).The researchers found that when too much oxidation of guanine incorporation into the new strand of DNA, the cell will not be able to successfully remove these damage, thus leading to death.
In 2007, Collins proved that the three HSP90B1main types of antibiotics - quinolones, beta-lactams and aminoglycosides - can be to generate highly destructive hydroxyl free radicals, molecules methoxycinnamate (OMC) radicals, the destruction of bacterial cells. At that time, he and other researchers speculated that free radicals launched a comprehensive attack on all cellular components they encounter.MIT biology professor Graham Walker said: "They are almost all produced HSPA13 responses. They chase lipid, the oxidation of protein, they can oxidize DNA." However, in the new study, researchers found that this damage part is not lethal,The researchers demonstrated that the fatal injury can be caused by bacteria is the guanine damage induced by hydroxyl, guanine (G) is the four basic building blocks of DNA nucleotide one. When this damage guanine inserted into the DNA, the bacteria will endeavor to repair this damage, but eventually accelerate the death. "This is not the cause of all the killing effects of reasons, but the fact that it occupies a very important proportion of," Walker said.Initially, Walker for the study of DNA repair enzymes so that the researchers suspect that this oxidized guanine may play a role in the antibiotic-mediated cell death. In the first study phase, they found a specific DNA polymerase DinB very good use of the oxidation of guanine components to synthesize DNA.That DinB is not only oxidation of guanine during DNA replication, however, inserted into the correct base opposite cytosine © will be inserted into the opposite adenine (A).The researchers found that when too much oxidation of guanine incorporation into the new strand of DNA, the cell will not be able to successfully remove these damage, thus leading to death.

by ANKITA GURAO at 06-05-2012, 03:35 AM
0 comments
Which gene is responsible for biosynthesis of cinnamaldehyde in cinnamon/ please give me reply


by astroboy89 at 06-03-2012, 12:25 PM
1 comments
I plan to start a plant biotech company on a small scale for producing industrially and medicinally important metabolites and compounds in India.
Please give me an approx cost of setting up R&D,industrial scale up and storage (all necessary and minimally required) for producing such products.
Also give me an idea of the land requirements.
Is it possible to get these products from callus on a industrial scale cost effectively?
Please give me an approx cost of setting up R&D,industrial scale up and storage (all necessary and minimally required) for producing such products.
Also give me an idea of the land requirements.
Is it possible to get these products from callus on a industrial scale cost effectively?
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