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- 07/08/14--07:03: Question on Telomeres
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- 07/21/14--23:39: Genetic basis of schizophrenia: new insights
- 07/22/14--00:51: High fat diet can damage your sense of smell
- 07/22/14--01:21: R&D staff cuts likely as Allergan fights Valeant hostile takeover
I am about to graduate with a Bachelor's degree in Bioengineering and I am debating whether or not to continue my education and enroll in a Master's program or to jump straight into finding a job in the industry. How important would you say it is to get a Master's degree in Bioengineering?
Of course, I have been told that a Master's degree makes it easier to find a job in the field; however, is it really extremely difficult to find a job in Bioengineering with only a Bachelor's degree? Furthermore, is it worth the cost (about $30,000 - $40,000 in most colleges) of enrolling in a graduate degree program?
Thanks for your help!
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i need every information about the released of "The sequence of the human genome" Thanks a lot!
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I understand the general concept of Telomeres buffering the genetic sequence, and that they degrade over time with each division of the cell. My question is: What creates and/or repairs the Telomeres in sex cells and related cells, to ensure a full amount of cell divisions for the resultant zygote? Is it Telomerase, and if so, why is the process specific to only the sexual reproduction process? If this didn't happen, wouldn't the genetic code of even sex cells degrade with every iteration meiosis? I know sex cells only divide once, however after many generations? wouldn't their DNA degrade without the protection provided by Telomeres?
I apologize for the bulk of questions, I am only trying to clarify my exact question, so as to avoid general answers that may be found online with a quick web query.
Thank you for your time and effort!
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i know that glyoxalate cycle is a shunt pathway of krebs cycle..and important enzymes malate synthase and isocitrate dehydrogase which play vital role in the glyoxalate pathway.
can any one help me in knowing micro organisms which has this two enzymes?
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what are the enzymes that can be produced by ecoli ?
i mean genes present in ecoli genome which produces enzymes or enzyme producing genes present in ecoli DH5 alpha strain?
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A new study supports the idea that good oral hygiene can help protect against cardiovascular disease risk. The oral anaerobic bacteria Porphyromonas gingivalis can evade host immune recognition and increase systemic inflammation and increased atherosclerosis risk by altering a surface molecule called lipid A so that it blocks activation of a key host immune receptor called toll-like receptor 4 (TLR-4). This results in an attenuated production of anti-bacterial inflammatory cytokines by the host and allows the bacteria to survive in macrophages, host cells that normally ingest and kill bacteria. These are the main findings of a new paper in the journal PLoS Pathogens from researchers in Boston University School of Medicine and the University of Washington.
P. gingivalis is an oral gram negative bacteria that causes local inflammation, resulting in destruction of tissues that support the teeth and resorption of bone. However, it is also associated with increased systemic inflammation with increased risk of diseases including diabetes and cardiovascular disease. It has been detected in atherosclerotic lesions in humans and has been shown to increase atherosclerosis in animal models. In the current study, the researchers sought to determine the mechanism behind this increased systemic inflammation and atherosclerosis. The results indicated that the mechanism behind systemic inflammation differed from that underlying local inflammation.
In common with other gram-negative bacteria, P. gingivalis expresses a protein called lipid A, which is the part of the lipopolysaccharide in the bacterial cell wall recognised by the key host TLR-4 immune receptor. Recognition of lipid A by TLR-4 initiates an immediate immune response characterised by release of pro-inflammatory cytokines and bacterial ingestion and killing by host macrophages. However, many bacteria have evolved strategies to modify lipid A and evade host recognition via TLR-4. P. gingivalis produces a number of modified lipid A structures, some of which are antagonistic to TLR-4 or induce no response from the receptor. The current study shows that the increased systemic inflammation and atherosclerosis induced by P. gingivalis involves the modified lipid A structures.
The research team used modified strains of P. gingivalis incorporating distinct lipid A versions, one of which activated TLR-4 (agonist) and one of which inhibited TLR-4 activation (antagonist). They used these P. gingivalis strains to infect a mouse model which was prone to atherosclerosis. The results indicated that use of the antagonist P. gingivalis strain resulted in reduced production of pro-inflammatory mediators and bacterial survival in macrophages with chronic vascular inflammation. By contrast, infection with the agonist P. gingivalis strain increased the production of proinflammatory mediators and macrophage killing of bacteria. The results also indicated that lipid A variations had no impact on the local response leading to oral tissue and bone damage, indicating that this is mediated by a separate mechanism.
The researchers conclude, “P gingivalis modifies its lipid A structure in order to evade host defenses and establish chronic infection leading to persistent systemic low-grade inflammation…uniquely among gram-negative pathogens, P. gingivalis evasion of TLR4-mediated host immunity results in progression of inflammation at a site that is distant from local infection by gaining access to the vasculature.”
Slocum C, Coats SR, Hua N, Kramer C, Papadopoulos G, et al. (2014) Distinct Lipid A Moieties Contribute to Pathogen-Induced Site-Specific Vascular Inflammation. PLoS Pathog 10(7): e1004215. doi:10.1371/journal.ppat.1004215; http://dx.plos.org/10.1371/journal.ppat.1004215
A new study suggests that the Xpert MTB/RIF, a recently implemented tuberculosis (TB) test, would be effective in helping control the TB epidemic in India. However, the mathematical model described in the study of tuberculosis transmission, care-seeking behaviour, and diagnostic/treatment practices shows that such improvements would depend on a major overhaul of the implementation strategy currently in place for TB diagnosis and treatment, involving both the public and private sectors. The study is published today in the journal PLoS Medicine, from researchers in the USA, India and Canada, led by Dr David Dowdy of Johns Hopkins University.
Tuberculosis (TB) remains a significant health problem internationally, causing 1.4 million deaths per year. Over one quarter of these occur in India, prompting the country to announce a goal of universal access to quality TB diagnosis and treatment. This goal is complicated by the complex health care system in India, with many people depending on private providers with no formal medical training or with some training in allopathic or non-allopathic training. While a Revised National Tuberculosis Control Programme (RNTCP) has made progress over the last 15 years in improving TB control in the public sector, many people turn to the public sector only as a last resort. There is a need to extend the current narrow implementation strategy to include the private sector and improve referral networks between the private and public sectors. In this context, combined with improved funding, the Xpert MTB/RIF, a recently implemented tuberculosis (TB) test, has the potential to control the TB epidemic in India.
Xpert MTB/RIF is a new TB diagnostic test with improved sensitivity compared to other currently used diagnostic tests, including the sputum smear microscopy test commonly used in the public sector in India and the even lower-performing tests used in the private sector, such as antibody or interferon-gamma release assays. It is a molecular test that uses semi-automated PCR to detect mycobacterial DNA. It has the added advantage of being able to detect resistance to the most effective TB antibiotic rifampicin, due to inclusion of specific primers. However, the cost of Xpert MTB/RIF is substantial and resource constraints currently dictate that the RNTCP is implementing this test chiefly as a rapid drug susceptibility testing method in vulnerable adults and children with HIV or at high risk of multi-drug resistant TB, rather than as a rapid and sensitive diagnostic test for TB.
In the current study, the research team constructed a mathematical model of tuberculosis transmission, care-seeking behaviour and diagnostic/treatment practices in India to predict the impact on TB incidence if six different rollout strategies were to be implemented. The most effective predicted scenario envisaged adding Xpert MTB/RIF access for 20% of all individuals with TB symptoms seeking diagnosis in the public sector and 20% of individuals seeking care from qualified private practitioners. Compared to the current implementation strategy, this scenario would be predicted to reduce TB incidence by 14.1%. However, it would entail substantial cost as it would require more than 2,200 Xpert machines and reliable treatment referral. It is worth noting that a scenario envisaging encouragement of informal private providers to refer suspected TB cases to the public sector for diagnosis using currently available tests predicted a greater impact on TB incidence than if the Xpert system were scaled up only within the public sector.
While the authors acknowledge that their findings must be interpreted in the light of uncertainties in the assumptions made in the model, they are confident that: “Xpert [MTB/RIF] ... could substantially reduce the burden of TB disease due to poor diagnosis in India; however, this impact depends not only on the accuracy of the test, but also on the behavior of both patients and providers, their level of access to new tools, and quality TB treatment following diagnosis.”
The authors conclude: “any Xpert [MTB/RIF] rollout strategy must also consider the complex health-care infrastructure into which the test is being rolled out. To achieve maximum impact of novel diagnostics, India should engage the private sector, improve quality of care across all sectors, and dramatically increase resources.”
Salje H, Andrews JR, Deo S, Satyanarayana S, Sun AY, et al. (2014) The Importance of Implementation Strategy in Scaling Up Xpert MTB/RIF for Diagnosis of Tuberculosis in the Indian Health-Care System: A Transmission Model. PLoS Med 11(7): e1001674. doi:10.1371/journal.pmed.1001674;
News source: PLoS Medicine
What are my chances of getting admission into NUS in Department of Chemical and Biomolecular Engg? Ive got first class with distinction in my B.tech with a GATE percentile of 93 and my GRE score is 313. I have done my final year project in Molecular Biology. Do I have to take TOEFL?
Can any one tell me about the qualifications for medical coding and billing courses in India
A new study sheds new light on the genetic underpinnings of schizophrenia. The study, from the international, multi-institution Schizophrenia Working Group of the Psychiatric Genomics Consortium (PGC) is published today in the journal Nature. It involved a genome-wide association study (GWAS) on 36,989 schizophrenia cases and 113,075 controls. This represents the largest GWAS to date in any psychiatric illness. 128 independent associations were identified over 108 specific locations of the human genome associated with schizophrenia risk; 83 of these had not been previously reported in schizophrenia risk.
Schizophrenia is a heritable disorder present in about 1:100 of the population. It features hallucinations, delusions, and disordered thinking and exacts an enormous human and financial cost. Current therapies mainly tackle the psychosis element; there are no effective treatments for the cognitive elements of the disease. Recent research suggests that the genetic basis of schizophrenia is highly complex, involving interaction of many genes. The current study, using a total of 55 datasets from more than 40 different contributors, confirmed and built on this knowledge as a result of years of work from the Schizophrenia Working Group of the Psychiatric Genomics Consortium. One of the contributors, Dr Jo Knight of Canada's Centre for Addiction and Mental Health (CAMH) explains: "Large collaborative efforts such as this one are needed to identify genes that influence complex disorders…The result is a major advance in understanding the genetic basis of brain functioning in schizophrenia."
The study identified the importance of genes expressed in brain tissue, particularly those related to neuron functioning and of signalling via synapses. They included genes implicated in control of synaptic plasticity, which is crucial in learning and memory, and pathways in the cells receiving the signal. A smaller number of immune system genes were also identified, supporting hypotheses concerning links between schizophrenia and immunity. While many of these findings point to new insights into the aetiology of schizophrenia, associations at the dopamine receptor DRD2 and many genes associated with glutamatergic neurotransmission point to molecules already known to have potential therapeutic relevance to schizophrenia.
Senior author Dr Michael O’Donovan of the MRC Centre for Neuropsychiatric Genetics and Genomics at Cardiff University School of Medicine concludes: "The fact that we were able to detect genetic risk factors on this massive scale shows that schizophrenia can be tackled by the same approaches that have already transformed our understanding of other diseases…The wealth of new findings has the potential to kick-start the development of new treatments in schizophrenia, a process which has stalled for the last 60 years."
Schizophrenia Working Group of the Psychiatric Genomics Consortium. Biological insights from 108 schizophrenia-associated genetic loci. Nature (2014)doi:10.1038/nature13595
Press release: CAMH; available at http://www.eurekalert.org/pub_releases/2...072114.php [Accessed 22 July 2014]
The International Bioprinting Congress taking place between July 24-25 at the Biopolis Research and Development Center in Singapore will feature leading international scientists who will share insights into the latest developments and techniques in 3D bioprinting. Advances that will be featured will include additive manufacturing of tissues and biofabrication, scaffolds and biomaterials for tissue engineering, biological laser printing, biological inkjet printing, and research into achieving synergy by fusion of bio-additive and micro manufacturing.
Among the invited speakers will be Dr. Mark DeCoster, the James E. Wyche III Endowed Professor in Biomedical Engineering at Louisiana Tech University. Dr DeCoster is an eminent scientist who has published 60 peer-reviewed papers, generating over 1,750 citations. He will present a lecture titled, “Bioprinting interfaces for 2D and 3D cell and tissue models.” This will highlight the work of Dr DeCoster’s lab in developing a novel, matrix-free method for generating 3D cell spheroids. This combines knowledge from bioprinting methods on 2D surfaces to link 3D cellular structures.
Dr DeCoster explains the potential for 3D bioprinting techniques in biology and medicine: “The cells of our bodies exist in both a three dimensional (3D) environment, which is rounder, as well as places that are more two dimensional (2D) or flattened…What is so new and exciting about 3D printers in the biomedical sciences and engineering is that we can now enable our imagination to convert a good idea into something that is printable and testable in 3D, and could have significant impacts on human health…3D printers are now replicating materials that are compatible with biology and medicine such as delivery of drugs to fight off cancer or growth-promoting materials that can be used for tissue engineering to heal a wound or repair a damaged part of the body.”
Dr DeCoster’s lab uses 3D printers to generate cell-compatible building blocks which they then use to study cell groups in both 3D and 2D. Dr DeCoster clarifies the relevance of this: “We feel this is important because we need to understand how to put cells together to grow better tissues or repair them, and also to understand how damaged or diseased cells behave…We need to understand both the 2D and 3D environments since different parts of the body use different materials to function, and this complexity of materials will most likely also be needed in bioprinting…In my presentation at the International Bioprinting Congress, I look forward to sharing the research we’re doing at Louisiana Tech on how normal cells of the brain as well as cancer cells (such as in brain tumors), can be studied using materials from 3D printers and how we combine those materials with cells.”
Press release: Louisiana Tech University; available at http://news.latech.edu/2014/07/21/biomed...singapore/ [Accessed 22 July 2014]
A high-fat diet can impact on the sense of smell, which during obesity could perpetuate poor dietary decision making. This is suggested by a recent study on a mouse model in the Journal of Neuroscience led by researchers in Florida State University.
Obesity has reached epidemic proportions in western nations, with for example 65% of Americans considered to be overweight or obese and perhaps even more disturbingly, about one third of children and adolescents. Obesity has serious health implications, for example in terms of increased risk of cancer, cardiovascular disease, diabetes and cognitive decline. However, there is little understanding of how obesity impacts on sensory systems such as the olfactory system or sense of smell. Olfaction is important in that it has an input into food choice, which directly links to development of obesity if poor choices are consistently made.
In the current study, the researchers used a mouse model in order to induce long-term, diet-induced obesity by feeding both obesity-prone (C57BL/6J) and obesity-resistant (Kv1.3−/−) mice with high-fat diets. They compared these mice models to another type of mouse, MC4R−/−, which features late-onset, genetic-induced obesity. Over a six-month study period, the mice were taught to associate between a particular odour and a reward (water).
The results indicated that the mice fed on a fatty diet were comparatively slower to learn reward-reinforced behaviours and also could not rapidly adapt when a new odour was introduced to monitor their adjustment. Furthermore, the changes were long-lasting as when the obese mice were taken off the high-fat diet and changed to a chow diet on which they regained normal weight and resting glucose, the olfactory dysfunction remained. The changes in olfactory perception and reduced reward association responses corresponded to loss of olfactory sensory neurons and their axonal projections with a high fat diet.
First author Dr Nicolas Thiebaud says: "This opens up a lot of possibilities for obesity research." Current plans include examining whether exercise can impact on the effects of the high-fat diet on smell and whether a high-sugar diet has similar effects to a high-fat diet. For now, the research contributes another layer of understanding on the negative effects of poor dietary choices over time.
Thiebaud N. et al. (2014) Hyperlipidemic Diet Causes Loss of Olfactory Sensory Neurons, Reduces Olfactory Discrimination, and Disrupts Odor-Reversal Learning. Journal of Neuroscience 34(20): 6970-6984; doi: 10.1523/JNEUROSCI.3366-13.2014
Press release: Florida State University; available at http://www.eurekalert.org/pub_releases/2...072114.php [Accessed 22 July 2014]
As Allergan attempts to evade a hostile takeover attempt value at $53 billion from Canadian company Valeant, Fierce Biotech reports that its R&D division is likely to be hard hit. This is despite optimism at the beginning of the year from CEO David Pyott that the R&D wing would be further enhanced in the company. The newly announced Allergan plans include letting 1500 workers go and removing 250 vacant positions. In this way Allergan claims it can reduce its 2015 budget by $475 million. While all elements of the company would be affected by such major cost-cutting, including commercial, general, administrative and manufacturing staff, R&D is likely to be particularly impacted. Emphasis would be in maintenance of ‘customer-facing’ staff and protection of current key development programmes rather than in new discoveries.
Valeant has a reputation for taking over drug companies, as with Medicis in 2012, and then laying off R&D staff and severely cutting ongoing development projects. While Valeant attempts to raise the resources for a 25% stake in Allergan, David Pyott has been emphasising that Allergan are themselves looking to make new acquisitions, indicating that they would be most interested in companies with a profile that is “specialist in nature" and a with new therapeutic "pillar" that could be used in new product development. However, Allergan has suffered the loss of one of its major investors, Capital Research & Management, and has also faced the blow of a third time rejection of its migraine drug Semprana by the US Food and Drug Administration (FDA).
The announced proposed cutbacks from Allergan may make the acquisition more difficult for Valeant to effect. Sterne Agee analyst Shibani Malhotra noted: “Today's announcement by Allergan makes it more difficult for Valeant to demonstrate how a merger can add incremental value and AGN shareholders may now require Valeant to pay a greater premium for Allergan, we believe."
Fierce Biotech: http://www.fiercebiotech.com/story/aller...2014-07-21 [Accessed 22 July 2014]
Fierce Biotech: http://www.fiercebiotech.com/story/hosti...2014-06-11 [Accessed 22 July 2014]