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by mtwalsh01 at 06-11-2014, 10:58 PM
0 comments
The prevalence of type 2 diabetes among Latin Americans is approximately twice as high as among Europeans and White Americans. A new study in the journal JAMA from an international team of researchers known as the SIGMA Diabetes Consortium has uncovered a genetic variant that confers a substantially increased risk of type 2 diabetes and is primarily observed in Latin American patients but not others. The variant is in a gene called hepatocyte nuclear factor 1-a (HNF1A); this is the gene responsible for a rare type of diabetes called maturity onset diabetes of the young type 3 (MODY3). The finding sheds light on the population genetics of type 2 diabetes among Latin Americans and may have implications for screening programmes and tailored therapies.
In this study, the research team performed a technique called exome sequencing, which analyses the parts of the genome that encode proteins, on samples from 3756 Mexican and US Latino individuals with or without type 2 diabetes. The results indicated that a rare variant in HNF1A was associated with prevalence of type 2 diabetes. When this p.E508K variant was explored further in a multi-ethnic set of 14276 patients, it was observed that it occurred only in Latino patients and was associated with type 2 diabetes. Corresponding author Jose Florez explained: "We've identified a genetic risk factor that is present in roughly 2 percent of Mexicans with type 2 diabetes, and its effects are substantial — raising a person's risk of developing the disease fivefold." Functional studies on the variant revealed that it had reduced activity compared to wild type.
The role of the p.E508K variant is new but its effects appear to be less severe than the situation in MODY, in which the HNF1A function is fully disabled. MODY usually emerges earlier in life than type 2 diabetes whereas the new variant did not appear to be associated with earlier age of onset. It appears that the newly identified variant spares some HNF1A functionality. MODY is often responsive to an inexpensive class of drugs called sulfonylurea, being much more sensitive to these drugs than to the first-line type 2 diabetes drug metformin. Therefore, this study raises the question whether type 2 diabetes associated with p.E508K may also be effective. For now, the research team are cautious about therapeutic implications, stressing the necessity for more studies. Study co-author Teresa Tusie-Luna concludes: "This is an outstanding discovery — one that helps explain the epidemic rates of type 2 diabetes in Latin American populations…But we must be mindful that, while the finding is associated with high levels of risk for the disease, we still do not know how the mutation behaves and if there is a specific therapeutic method can be safely applied in the clinic for individuals that carry the mutation. There is much more we need to learn."
Sources
The SIGMA Type 2 Diabetes Consortium (2014). Association of a Low-Frequency Variant in HNF1A with Type 2 Diabetes in a Latino Population. JAMA. 2014; 311(22):2305-2314. doi:10.1001/jama.2014.6511
Press release: JAMA, available from http://www.eurekalert.org/bysubject/biology.php
In this study, the research team performed a technique called exome sequencing, which analyses the parts of the genome that encode proteins, on samples from 3756 Mexican and US Latino individuals with or without type 2 diabetes. The results indicated that a rare variant in HNF1A was associated with prevalence of type 2 diabetes. When this p.E508K variant was explored further in a multi-ethnic set of 14276 patients, it was observed that it occurred only in Latino patients and was associated with type 2 diabetes. Corresponding author Jose Florez explained: "We've identified a genetic risk factor that is present in roughly 2 percent of Mexicans with type 2 diabetes, and its effects are substantial — raising a person's risk of developing the disease fivefold." Functional studies on the variant revealed that it had reduced activity compared to wild type.
The role of the p.E508K variant is new but its effects appear to be less severe than the situation in MODY, in which the HNF1A function is fully disabled. MODY usually emerges earlier in life than type 2 diabetes whereas the new variant did not appear to be associated with earlier age of onset. It appears that the newly identified variant spares some HNF1A functionality. MODY is often responsive to an inexpensive class of drugs called sulfonylurea, being much more sensitive to these drugs than to the first-line type 2 diabetes drug metformin. Therefore, this study raises the question whether type 2 diabetes associated with p.E508K may also be effective. For now, the research team are cautious about therapeutic implications, stressing the necessity for more studies. Study co-author Teresa Tusie-Luna concludes: "This is an outstanding discovery — one that helps explain the epidemic rates of type 2 diabetes in Latin American populations…But we must be mindful that, while the finding is associated with high levels of risk for the disease, we still do not know how the mutation behaves and if there is a specific therapeutic method can be safely applied in the clinic for individuals that carry the mutation. There is much more we need to learn."
Sources
The SIGMA Type 2 Diabetes Consortium (2014). Association of a Low-Frequency Variant in HNF1A with Type 2 Diabetes in a Latino Population. JAMA. 2014; 311(22):2305-2314. doi:10.1001/jama.2014.6511
Press release: JAMA, available from http://www.eurekalert.org/bysubject/biology.php

by Arti Kumari at 06-11-2014, 06:23 PM
0 comments
hi all
i am arti kumari in biotechnology in 2005. after that due to family reason i was not able to join any of the research institute or industry. in april 2008 i joined as research assistant at rajendra memorial research institute of medical sciences, at patna bihar. i worked till april 2010. after that i am not able to join any where for my further career . how can i overcome this gap in my career. please anyone suggest me. i want to do phd in biotechnology.
please anyone suggest me.
i am arti kumari in biotechnology in 2005. after that due to family reason i was not able to join any of the research institute or industry. in april 2008 i joined as research assistant at rajendra memorial research institute of medical sciences, at patna bihar. i worked till april 2010. after that i am not able to join any where for my further career . how can i overcome this gap in my career. please anyone suggest me. i want to do phd in biotechnology.
please anyone suggest me.

by SunilNagpal at 06-11-2014, 02:45 PM
2 comments
Hi all,
Recently got a query from one of the members who couldn't score much in M.Tech from a foreign univeristy but had a brilliant percentage in B.Tech. PhD indeed becomes difficult to grab for such cases. There are two possible options for such students:
1. Apply for GATE (forgetting that you have pursued M.Tech) and prepare well to grab a PhD position based upon your B.Tech percentage.
2. Apply at KPOs like Evalueserve, Genpact to get some consultant position. Kinapse is also a possible consultancy firm one can apply at under such a scenario.
3. There are some Pharmaceutical companies in Himachal you can apply at, but the pay package wont be very high.
This is all I can recommend right now. I'll discuss with some contacts to find out some possible job opportunity in such cases.
Till then you may try out the above options,
Best Regards
Sunil
P.S: There's a road for every traveller, so don't get disappointed.
Recently got a query from one of the members who couldn't score much in M.Tech from a foreign univeristy but had a brilliant percentage in B.Tech. PhD indeed becomes difficult to grab for such cases. There are two possible options for such students:
1. Apply for GATE (forgetting that you have pursued M.Tech) and prepare well to grab a PhD position based upon your B.Tech percentage.
2. Apply at KPOs like Evalueserve, Genpact to get some consultant position. Kinapse is also a possible consultancy firm one can apply at under such a scenario.
3. There are some Pharmaceutical companies in Himachal you can apply at, but the pay package wont be very high.
This is all I can recommend right now. I'll discuss with some contacts to find out some possible job opportunity in such cases.
Till then you may try out the above options,
Best Regards
Sunil
P.S: There's a road for every traveller, so don't get disappointed.

by mtwalsh01 at 06-11-2014, 04:46 AM
0 comments
While it has been known for some time that the gastrointestinal microbiota- microbial population of the gut- influences host weight gain and adiposity, the mechanisms behind this have not been fully understood. A recent study in the journal Proceedings of the National Academy of Sciences USA implicates a bacterial enzyme called bile salt hydrolase in communication between host and microbe that profoundly influences host weight gain, lipid metabolism and cholesterol levels in mice. The research team behind the study are based in University College Cork in Ireland and are currently considering the relevance of these findings in humans and for rational design of probiotics for control of obesity and metabolic syndrome.
The researchers developed a mouse model system that allowed them to study microbial alleles in the gut. The results of the study showed that bacterial bile salt hydrolase, which is commonly made by gut bacteria, can alter bile acids, which have been previously implicated in gut signalling pathways. Dr Cormac Gahan, senior author on the paper, further explained the significance of bile acid modification: “Recent work by other groups has shown that bile acids act as signalling molecules in the host, almost like a hormonal network, with an ability to influence host metabolism. What we have done is to show that a specific mechanism exists by which bacteria in the gut can influence this process with significant consequences for the host.”
The research team showed that if cloned bile salt hydrolase enzymes were expressed in the gastrointestinal tract of mice, they changed bile acid expression profiles and regulated expression of genes involved in lipid metabolism, cholesterol metabolism, gastrointestinal homeostasis and circadian rhythm. Furthermore, high level expression of these enzymes in conventionally raised mice resulted in reduced weight gain and plasma cholesterol. The results imply that gut microbe interactions with bile acid metabolism is a potential pathway to target in intervention in obesity and metabolic syndrome. Lead author Dr Susan Joyce concluded: “the findings may be used as a basis for the future selection of probiotics or dietary interventions which target this mechanism to regulate weight gain or high cholesterol. We now have the potential for matching probiotic strains with specific end-user needs. Work is underway to determine how this system operates in humans.”
Sources
Joyce, S.A., McSharry, J., Casey, P.G., Kinsella, M., Murphy, E.F., Shanahan, F., Hill, C. and Gahan, C.G.M. (2014). Regulation of host weight gain and lipid metabolism by bacterial bile acid modification in the gut. PNAS 111(20): 7421-7426. www.pnas.org/cgi/doi/10.1073/pnas.1323599111
Press release: Science Foundation of Ireland
The researchers developed a mouse model system that allowed them to study microbial alleles in the gut. The results of the study showed that bacterial bile salt hydrolase, which is commonly made by gut bacteria, can alter bile acids, which have been previously implicated in gut signalling pathways. Dr Cormac Gahan, senior author on the paper, further explained the significance of bile acid modification: “Recent work by other groups has shown that bile acids act as signalling molecules in the host, almost like a hormonal network, with an ability to influence host metabolism. What we have done is to show that a specific mechanism exists by which bacteria in the gut can influence this process with significant consequences for the host.”
The research team showed that if cloned bile salt hydrolase enzymes were expressed in the gastrointestinal tract of mice, they changed bile acid expression profiles and regulated expression of genes involved in lipid metabolism, cholesterol metabolism, gastrointestinal homeostasis and circadian rhythm. Furthermore, high level expression of these enzymes in conventionally raised mice resulted in reduced weight gain and plasma cholesterol. The results imply that gut microbe interactions with bile acid metabolism is a potential pathway to target in intervention in obesity and metabolic syndrome. Lead author Dr Susan Joyce concluded: “the findings may be used as a basis for the future selection of probiotics or dietary interventions which target this mechanism to regulate weight gain or high cholesterol. We now have the potential for matching probiotic strains with specific end-user needs. Work is underway to determine how this system operates in humans.”
Sources
Joyce, S.A., McSharry, J., Casey, P.G., Kinsella, M., Murphy, E.F., Shanahan, F., Hill, C. and Gahan, C.G.M. (2014). Regulation of host weight gain and lipid metabolism by bacterial bile acid modification in the gut. PNAS 111(20): 7421-7426. www.pnas.org/cgi/doi/10.1073/pnas.1323599111
Press release: Science Foundation of Ireland

by mtwalsh01 at 06-10-2014, 11:18 PM
0 comments
Dispersal of bacterial biofilms from atherosclerotic carotid arteries may be the trigger for heart attacks in response to stress, fear or over-exertion. This is the major finding of a new study in the American Society for Microbiology online, open access journal mBio®, led by researchers from Binghamton University in New York. The dispersal may be in response to release of stress hormones such as norepinephrine and result in release of arterial plaques to which the biofilms are bound.
In this study, the research team isolated and cultured bacteria from carotid arteries that had been obtained from atherosclerotic patients. The results showed that multiple bacterial species were present in the form of biofilms on plaque-covered arteries from patients with atherosclerosis. This is the first direct observation of bacterial biofilms from carotid artery plaques. Studies on biofilms cultured on silicon tubing showed that norepinephrine at levels compatible with those observed in response to stress or exertion could induce biofilm dispersal. Dr David Davies, an author on the study, explained further: "At least one species of bacteria - Pseudomonas aeruginosa - commonly associated with carotid arteries in our studies, was able to undergo a biofilm dispersion response when exposed to norepinephrine, a hormone responsible for the fight-or-flight response in humans."
Biofilms are normally adherent and are resistant to attack from the immune system or from antibiotics. However, a molecular trigger can cause them to disperse and release enzymes which can destroy the scaffold keeping the bacteria adherent. These enzymes would also be capable of breaking down tissues that would stop arterial plaques from being released into the bloodstream. The study suggests that management of bacteria within arterial plaques should form part of the panoply of protective measures against heart attack, along with measures such as cholesterol management.
Sources
Lanter, B.B., Sauer, K. and Davies, D.G. (2014). Bacteria Present in Carotid Arterial Plaques Are Found as Biofilm Deposits Which May Contribute to Enhanced Risk of Plaque Rupture. mBio 5 (3) e01206-14; doi: 10.1128/mBio.01206-14
Press release: American Society for Microbiology; Available from http://www.eurekalert.org/pub_releases/2...060514.php [Accessed 10 June 2014]
In this study, the research team isolated and cultured bacteria from carotid arteries that had been obtained from atherosclerotic patients. The results showed that multiple bacterial species were present in the form of biofilms on plaque-covered arteries from patients with atherosclerosis. This is the first direct observation of bacterial biofilms from carotid artery plaques. Studies on biofilms cultured on silicon tubing showed that norepinephrine at levels compatible with those observed in response to stress or exertion could induce biofilm dispersal. Dr David Davies, an author on the study, explained further: "At least one species of bacteria - Pseudomonas aeruginosa - commonly associated with carotid arteries in our studies, was able to undergo a biofilm dispersion response when exposed to norepinephrine, a hormone responsible for the fight-or-flight response in humans."
Biofilms are normally adherent and are resistant to attack from the immune system or from antibiotics. However, a molecular trigger can cause them to disperse and release enzymes which can destroy the scaffold keeping the bacteria adherent. These enzymes would also be capable of breaking down tissues that would stop arterial plaques from being released into the bloodstream. The study suggests that management of bacteria within arterial plaques should form part of the panoply of protective measures against heart attack, along with measures such as cholesterol management.
Sources
Lanter, B.B., Sauer, K. and Davies, D.G. (2014). Bacteria Present in Carotid Arterial Plaques Are Found as Biofilm Deposits Which May Contribute to Enhanced Risk of Plaque Rupture. mBio 5 (3) e01206-14; doi: 10.1128/mBio.01206-14
Press release: American Society for Microbiology; Available from http://www.eurekalert.org/pub_releases/2...060514.php [Accessed 10 June 2014]

by mtwalsh01 at 06-10-2014, 11:11 PM
0 comments
The mystery of how viruses use certain RNAs as ‘Trojan horses’ to allow the virus to hijack infected cells may have been solved. A new study published in the journal Nature suggest that the viral RNAs exploit their ‘two-faced’ architecture, with one face acting to mimic host RNA structures and the other face being less similar, enabling the viral RNA to switch between structures and carry out multiple tasks during infection. The study was led by researchers in the University of Colorado School of Medicine.
Viruses are a threat to both health and agriculture worldwide. They establish themselves and multiply by infecting a host cell and then taking over the machinery of that cell for their own ends. Different viruses have different mechanisms for achieving this. One such mechanism is use of molecular mimics, whereby viral molecules mimic the structure and function of host cell molecules, thereby evading elimination by the immune system. These viral ‘Trojan horses’ help the virus to establish themselves in the host and multiply.
While the existence of viral RNA molecular mimics had been recognised for some time, the ways in which it acts as a mimic and also how it could switch between structures enabling multiple tasks to be carried out during infection was a mystery. In the current study, the research team used a technique called X-ray crystallography in order to visualise the three-dimensional structure of the turnip yellow mosaic virus RNA to high resolution. This led to the observation of the ‘two-faced’ nature of the RNA architecture. One face acts as the mimic of the host cell RNA while the other face confers the multi-tasking ability of the virus during infection. Molecular mimicry of this type is common among viruses, so this research could be relevant to many different viruses, with applications in development of therapies and vaccines.
Sources
Colussi, T.M., Costantino, D.A., Hammond, J.A., Ruehle, G.M., Nix, J.C. and Kieft, J.S. (2014). The structural basis of transfer RNA mimicry and conformational plasticity by a viral RNA. Nature
doi:10.1038/nature13378
Press release: University of Colorado; available from http://www.eurekalert.org/pub_releases/2...060914.php [Accessed 10 June 2014]
Viruses are a threat to both health and agriculture worldwide. They establish themselves and multiply by infecting a host cell and then taking over the machinery of that cell for their own ends. Different viruses have different mechanisms for achieving this. One such mechanism is use of molecular mimics, whereby viral molecules mimic the structure and function of host cell molecules, thereby evading elimination by the immune system. These viral ‘Trojan horses’ help the virus to establish themselves in the host and multiply.
While the existence of viral RNA molecular mimics had been recognised for some time, the ways in which it acts as a mimic and also how it could switch between structures enabling multiple tasks to be carried out during infection was a mystery. In the current study, the research team used a technique called X-ray crystallography in order to visualise the three-dimensional structure of the turnip yellow mosaic virus RNA to high resolution. This led to the observation of the ‘two-faced’ nature of the RNA architecture. One face acts as the mimic of the host cell RNA while the other face confers the multi-tasking ability of the virus during infection. Molecular mimicry of this type is common among viruses, so this research could be relevant to many different viruses, with applications in development of therapies and vaccines.
Sources
Colussi, T.M., Costantino, D.A., Hammond, J.A., Ruehle, G.M., Nix, J.C. and Kieft, J.S. (2014). The structural basis of transfer RNA mimicry and conformational plasticity by a viral RNA. Nature
doi:10.1038/nature13378
Press release: University of Colorado; available from http://www.eurekalert.org/pub_releases/2...060914.php [Accessed 10 June 2014]

by mtwalsh01 at 06-10-2014, 10:39 PM
0 comments
In a similar way to the use of human DNA forensic evidence in criminal trials, the new discipline of microbial forensics involves use of microbial genetic information to answer questions about disease outbreaks. Microbial forensics shares challenges with other disciplines including medicine and public health. A new report from the National Research Council in the USA establishes a set of research priorities that are needed to optimise the capabilities of microbial forensic methods and tools for identification of biothreats and attribution of sources and causes. The challenges exist in basic science, technologies, analytic methods, data sharing, and training and education and stretch across international boundaries, necessitating adoption of a harmonised approach between nations.
Microbial outbreaks can occur for a range of reasons from natural outbreaks and accidental releases from laboratories to criminal acts including biocrimes directed against individuals or small groups and full-scale bioterrorism or biowarfare. There is a need to test and validate methods for identifying the source of an outbreak and distinguishing between more common events like natural outbreaks, usually first identified via the public health infrastructure, and rare events like bioterrorism where the full range of microbial forensics techniques are likely to be needed. The report identifies three key sets of needs, in which biotechnological research would play an important role.
One set of needs relates to those that are very technologically challenging or require long lead times. For example, there is a lack of basic information about a lot of microbes that would be essential in order to have confidence in methods for distinguishing between causes of any outbreaks. A coordinated international effort would be needed for identification, monitoring and characterisation of microbial species, beginning with the known ones and expanding to encompass close relatives and emerging pathogens. This would include sharing of data via establishment of more systematic and comprehensive reference collections and databases.
A second set of needs relates to capitalising on ongoing efforts common to both microbial forensics and public health, for example research on pathogenicity and immune responses; improvements in global monitoring and surveillance of diseases in humans, plants, and animals; improved international access to molecular diagnostic techniques; and refinement of evidence evaluation via bioinformatics and statistical methods.
A final set of needs relates to those with either relatively short lead times to make substantial progress or that can capitalise on existing markets to incentivise industry to produce what is required. Examples would be developing faster, cheaper, and more reliable sequencing technologies, compilation of all protocols with information on whether and how they were validated, and expanded technical training.
The report findings recommend development of international agreements and standards in microbial forensics, with an international framework that rewards data sharing while respecting security and law enforcement concerns.
Study sponsors: U.S. Navy, U.S. Department of State, and National Academy of Sciences. The National Academy of Sciences, National Academy of Engineering, Institute of Medicine, and National Research Council make up the National Academies.
Source:
Press release: National Academy of Sciences; available from http://www8.nationalacademies.org/onpine...rdID=18737 [Accessed 10 June 2014].
Microbial outbreaks can occur for a range of reasons from natural outbreaks and accidental releases from laboratories to criminal acts including biocrimes directed against individuals or small groups and full-scale bioterrorism or biowarfare. There is a need to test and validate methods for identifying the source of an outbreak and distinguishing between more common events like natural outbreaks, usually first identified via the public health infrastructure, and rare events like bioterrorism where the full range of microbial forensics techniques are likely to be needed. The report identifies three key sets of needs, in which biotechnological research would play an important role.
One set of needs relates to those that are very technologically challenging or require long lead times. For example, there is a lack of basic information about a lot of microbes that would be essential in order to have confidence in methods for distinguishing between causes of any outbreaks. A coordinated international effort would be needed for identification, monitoring and characterisation of microbial species, beginning with the known ones and expanding to encompass close relatives and emerging pathogens. This would include sharing of data via establishment of more systematic and comprehensive reference collections and databases.
A second set of needs relates to capitalising on ongoing efforts common to both microbial forensics and public health, for example research on pathogenicity and immune responses; improvements in global monitoring and surveillance of diseases in humans, plants, and animals; improved international access to molecular diagnostic techniques; and refinement of evidence evaluation via bioinformatics and statistical methods.
A final set of needs relates to those with either relatively short lead times to make substantial progress or that can capitalise on existing markets to incentivise industry to produce what is required. Examples would be developing faster, cheaper, and more reliable sequencing technologies, compilation of all protocols with information on whether and how they were validated, and expanded technical training.
The report findings recommend development of international agreements and standards in microbial forensics, with an international framework that rewards data sharing while respecting security and law enforcement concerns.
Study sponsors: U.S. Navy, U.S. Department of State, and National Academy of Sciences. The National Academy of Sciences, National Academy of Engineering, Institute of Medicine, and National Research Council make up the National Academies.
Source:
Press release: National Academy of Sciences; available from http://www8.nationalacademies.org/onpine...rdID=18737 [Accessed 10 June 2014].

by kanchan at 06-10-2014, 02:22 PM
0 comments
i had done my graduation in biotechnology but now i m confused what i m done now. i want to doing M.SC but in which field please suggest me. WHICH FIELD IS GOOD FOR MY CARRIER NOW?

by mtwalsh01 at 06-09-2014, 10:56 PM
0 comments
Analysis of copy number variations, which are deletions or insertions in DNA, has revealed that several defective gene family interaction networks (GFINs) are potentially involved in autism spectrum disorders. The genome-wide association study’s results were published on 6th June in the journal Nature Communications. The study was led by researchers in the Center for Applied Genomics at The Children's Hospital of Philadelphia and has implications for development of new drugs for autism-spectrum disorders or re-purposing of existing drugs that target these networks.
Autism-spectrum disorders, of which autism is the best known, are heritable, childhood, neurological conditions that feature impairment in social interaction and communication as well as restricted behaviours. In the current study, the research team compared copy number variants from the DNA of over 6700 autism-spectrum disorder patients to that of over 12,500 healthy control subjects. The results indicated defects in several gene family interaction networks, including three in which the gene variant affects gene-protein interactions.
Of particular interest was the metabotropic glutamate receptor (mGluR), a member of the GRM family which helps mediate signalling by the neurotransmitter glutamate. This neurotransmitter is involved in memory, learning, cognition, attention and behaviour. The research team had previously shown that CNVs in GRM genes are prevalent in attention deficit disorder patients while others had shown GRM defects in schizophrenia. Thus despite the heterogeneous nature of these neurological disorders, all of them may be amenable to drugs targeting the GRM family. Senior author Dr Hakon Hakonarson explains: "Neurodevelopmental disorders are extremely heterogeneous, both clinically and genetically…However, the common biological patterns we are finding across disease categories strongly imply that focusing on underlying molecular defects may bring us closer to devising therapies."
Defects were also observed in other important gene families. These included the CALM1 network which includes calmodulin proteins, responsible for cell signalling regulation and neurotransmitter function. They also included the MXD-MYC-MAX gene network which is linked to cancer and may contribute to the observed association between some cancer types and autism.
The GRM findings from this and the group’s previous study has prompted Dr Hakonarson to begin a clinical trial in selected ADHD patients of a GRM pathway-activating drug. Dr Hakonarson says: "If drugs affecting this pathway prove successful in this subset of patients with ADHD, we may then test these drugs in autism patients with similar gene variants." In autism-spectrum disorders and other neurological conditions, the genetic picture is complex, with common gene variants often exerting only small individual effects while rare variants exert stronger influence, which may offer targets for new or re-purposed drugs. Dr Hakonarson cautions that even larger studies are needed to continue to unravel the genetics behind these condtions. He concludes: "Even though our own study was large, it captures only about 20 percent of genes causing…However, strong animal data support an important role for the glutamate receptor pathway in socially impaired behaviours modelling ASDs. Because the GRM pathway seems to be a major driver in three diseases-- autism, ADHD and schizophrenia--there is a compelling rationale for investigating treatment strategies focused on this pathway."
Sources:
Press release: Children's Hospital of Philadelphia; available from: http://www.eurekalert.org/pub_releases/2...060414.php [Accessed 6 June 2014]
Hakonarson, H. et al. The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism. Nature Communications, June 2014 DOI: 10.1038/ncomms5074
Autism-spectrum disorders, of which autism is the best known, are heritable, childhood, neurological conditions that feature impairment in social interaction and communication as well as restricted behaviours. In the current study, the research team compared copy number variants from the DNA of over 6700 autism-spectrum disorder patients to that of over 12,500 healthy control subjects. The results indicated defects in several gene family interaction networks, including three in which the gene variant affects gene-protein interactions.
Of particular interest was the metabotropic glutamate receptor (mGluR), a member of the GRM family which helps mediate signalling by the neurotransmitter glutamate. This neurotransmitter is involved in memory, learning, cognition, attention and behaviour. The research team had previously shown that CNVs in GRM genes are prevalent in attention deficit disorder patients while others had shown GRM defects in schizophrenia. Thus despite the heterogeneous nature of these neurological disorders, all of them may be amenable to drugs targeting the GRM family. Senior author Dr Hakon Hakonarson explains: "Neurodevelopmental disorders are extremely heterogeneous, both clinically and genetically…However, the common biological patterns we are finding across disease categories strongly imply that focusing on underlying molecular defects may bring us closer to devising therapies."
Defects were also observed in other important gene families. These included the CALM1 network which includes calmodulin proteins, responsible for cell signalling regulation and neurotransmitter function. They also included the MXD-MYC-MAX gene network which is linked to cancer and may contribute to the observed association between some cancer types and autism.
The GRM findings from this and the group’s previous study has prompted Dr Hakonarson to begin a clinical trial in selected ADHD patients of a GRM pathway-activating drug. Dr Hakonarson says: "If drugs affecting this pathway prove successful in this subset of patients with ADHD, we may then test these drugs in autism patients with similar gene variants." In autism-spectrum disorders and other neurological conditions, the genetic picture is complex, with common gene variants often exerting only small individual effects while rare variants exert stronger influence, which may offer targets for new or re-purposed drugs. Dr Hakonarson cautions that even larger studies are needed to continue to unravel the genetics behind these condtions. He concludes: "Even though our own study was large, it captures only about 20 percent of genes causing…However, strong animal data support an important role for the glutamate receptor pathway in socially impaired behaviours modelling ASDs. Because the GRM pathway seems to be a major driver in three diseases-- autism, ADHD and schizophrenia--there is a compelling rationale for investigating treatment strategies focused on this pathway."
Sources:
Press release: Children's Hospital of Philadelphia; available from: http://www.eurekalert.org/pub_releases/2...060414.php [Accessed 6 June 2014]
Hakonarson, H. et al. The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism. Nature Communications, June 2014 DOI: 10.1038/ncomms5074

by mtwalsh01 at 06-09-2014, 05:20 PM
0 comments
A lot of research in recent years has focused on the issue of targeting therapies to tumours and sparing surrounding healthy cells and tissues. Nanoparticles have emerged as a potential vehicle for this kind of targeted delivery. In a new study in the journal Nature Materials a nanoparticle with certain unique properties is described which allows targeting of tumour cells, ready visualisation of internalised nanoparticles and breakdown of non-internalised and potentially toxic nanoparticles for elimination. These silver nanoparticles were developed in the laboratory of Prof Erkki Ruoslahti of the University of California in Santa Barbara.
The research team exploited a phenomenon called plasmonics when developing the nanoparticles in which nanostructured materials including gold and silver resonate in light such that their electromagnetic fields are concentrated near the surface. This allows enhancement of the fluorescence of dyes used to label the nanoprobes, making them much more readily detectable. In the current study, the researchers designed an etching technique in which biocompatible materials were used to break down and remove non-internalised silver nanoparticles with minimum toxicity. This left only the internalised pool for imaging and quantification. Lead author Dr Gary Braun explains: "The disassembly is an interesting concept for creating drugs that respond to a certain stimulus…It also minimizes the off-target toxicity by breaking down the excess nanoparticles so they can then be cleared through the kidneys."
The particles were spherical in shape and were coated with a peptide that enabled it to be targeted to tumour cells. While some drugs can penetrate the cell membrane, others cannot, for example RNA and DNA genetic drugs. This is where nanoparticle carriers that can be internalised in the tumour cell come in. Dr Braun explains: "This typically requires a nanoparticle carrier to protect the drug and carry it into the cell…And that's what we measured: the internalization of a carrier via endocytosis." The intense fluorescence of the plasmonic nanoparticles made internalisation readily detectable while the etching technology meant that excess nanoparticles could be broken down and expelled by the kidneys.
The peptide coating of the core nanoparticles has the potential to be varied to allow different types of tumours or bacterial organisms to be targeted. Senior author Prof Ruoshlati concludes: "These new nanoparticles have some remarkable properties that have already proven useful as a tool in our work that relates to targeted drug delivery into tumours…They also have potential applications in combating infections. Dangerous infections caused by bacteria that are resistant to all antibiotics are getting more common, and new approaches to deal with this problem are desperately needed. Silver is a locally used antibacterial agent and our targeting technology may make it possible to use silver nanoparticles in treating infections anywhere in the body."
Figure: Prostate cancer cells were targeted by two separate silver nanoparticles (red and green), while the cell nucleus was labeled in blueusing Hoescht dye. (UCSB)
Sources
Etchable plasmonic nanoparticle probes to image and quantify cellular internalization. Braun, G. B., Friman, T., Pang, H.-B., Pallaoro, A., de Mendoza, T. H., Willmore, A.-M. A., Kotamraju, V. R., Mann, A. P., She, Z.-G., Sugahara, K. N., Reich, N. O., Teesalu, T., and Ruoslahti, E. (2014). (8 June 2014), doi:10.1038/nmat3982
Press release: UC Santa Barbara, available from: http://www.eurekalert.org/pub_releases/2...060614.php
The research team exploited a phenomenon called plasmonics when developing the nanoparticles in which nanostructured materials including gold and silver resonate in light such that their electromagnetic fields are concentrated near the surface. This allows enhancement of the fluorescence of dyes used to label the nanoprobes, making them much more readily detectable. In the current study, the researchers designed an etching technique in which biocompatible materials were used to break down and remove non-internalised silver nanoparticles with minimum toxicity. This left only the internalised pool for imaging and quantification. Lead author Dr Gary Braun explains: "The disassembly is an interesting concept for creating drugs that respond to a certain stimulus…It also minimizes the off-target toxicity by breaking down the excess nanoparticles so they can then be cleared through the kidneys."
The particles were spherical in shape and were coated with a peptide that enabled it to be targeted to tumour cells. While some drugs can penetrate the cell membrane, others cannot, for example RNA and DNA genetic drugs. This is where nanoparticle carriers that can be internalised in the tumour cell come in. Dr Braun explains: "This typically requires a nanoparticle carrier to protect the drug and carry it into the cell…And that's what we measured: the internalization of a carrier via endocytosis." The intense fluorescence of the plasmonic nanoparticles made internalisation readily detectable while the etching technology meant that excess nanoparticles could be broken down and expelled by the kidneys.
The peptide coating of the core nanoparticles has the potential to be varied to allow different types of tumours or bacterial organisms to be targeted. Senior author Prof Ruoshlati concludes: "These new nanoparticles have some remarkable properties that have already proven useful as a tool in our work that relates to targeted drug delivery into tumours…They also have potential applications in combating infections. Dangerous infections caused by bacteria that are resistant to all antibiotics are getting more common, and new approaches to deal with this problem are desperately needed. Silver is a locally used antibacterial agent and our targeting technology may make it possible to use silver nanoparticles in treating infections anywhere in the body."
Figure: Prostate cancer cells were targeted by two separate silver nanoparticles (red and green), while the cell nucleus was labeled in blueusing Hoescht dye. (UCSB)
Sources
Etchable plasmonic nanoparticle probes to image and quantify cellular internalization. Braun, G. B., Friman, T., Pang, H.-B., Pallaoro, A., de Mendoza, T. H., Willmore, A.-M. A., Kotamraju, V. R., Mann, A. P., She, Z.-G., Sugahara, K. N., Reich, N. O., Teesalu, T., and Ruoslahti, E. (2014). (8 June 2014), doi:10.1038/nmat3982
Press release: UC Santa Barbara, available from: http://www.eurekalert.org/pub_releases/2...060614.php

by Vyshnavie R.Sarma at 06-08-2014, 04:28 PM
1 comments
Hello
I have questions related to Genome mapping.
1.what is genome mapping
2.what is genome mapping used for?
3.what are the techniques used
4.case study related to genome mapping
Thank you
I have questions related to Genome mapping.
1.what is genome mapping
2.what is genome mapping used for?
3.what are the techniques used
4.case study related to genome mapping
Thank you

by mtwalsh01 at 06-06-2014, 09:25 PM
0 comments
A phase 3 clinical trial of a new drug called MM-398, given in combination with 5-fluorouracil and leucovorin, has demonstrated an increased survival rate for pancreatic cancer patients. The trial was sponsored by Merrimack Pharmaceuticals and conducted by scientists in Virginia G. Piper Cancer Center Clinical Trials, which is a partnership between Scottsdale Healthcare and the Translational Genomics Research Institute (TGen). The trial results are due to be presented at the European Society for Medical Oncology World Conference on Gastrointestinal Cancer being held June 25-28 in Barcelona, Spain.
Pancreatic cancer is usually diagnosed late as symptoms are not often noticed early on. This complicates treatment and contributes to the dismal prognosis with this form of cancer, with only a quarter of patients surviving beyond one year and 6% beyond 5 years. Once the cancer has spread, surgery is not usually a treatment option and the patient is given chemotherapy.
Phase 3 trials are carried out for final confirmation of a drug’s safety and efficacy. This trial, called the NAPOLI-1 (NAnoliPOsomaL Irinotecan) Phase 3 study, was conducted on 417 patients at over 100 sites in North America, South America, Europe, Asia and Australia. Combining MM-398 with 5-fluorouracil and leucovorin resulted in an overall survival of 6.1 months, which represents a 1.9 month improvement over 5-fluorouracil and leucovorin alone. Merrimack will be submitting a New Drug Application to the US Food and Drug Administration for the combined MM-398 treatment in pancreatic cancer.
Dr. Daniel D. Von Hoff, who is the global Principal Investigator for the NAPOLI-1 study concludes: "This demonstration of a survival benefit from the MM-398 plus 5-FU and leucovorin combination is particularly important given that we have very few treatment options for patients in this tough clinical setting."
Source:
Press release: TGen-Scottsdale Healthcare; available from: https://www.tgen.org/news/2014-media-rel...5Gf0mlOPIV [Accessed 6 June 2014].
Pancreatic cancer is usually diagnosed late as symptoms are not often noticed early on. This complicates treatment and contributes to the dismal prognosis with this form of cancer, with only a quarter of patients surviving beyond one year and 6% beyond 5 years. Once the cancer has spread, surgery is not usually a treatment option and the patient is given chemotherapy.
Phase 3 trials are carried out for final confirmation of a drug’s safety and efficacy. This trial, called the NAPOLI-1 (NAnoliPOsomaL Irinotecan) Phase 3 study, was conducted on 417 patients at over 100 sites in North America, South America, Europe, Asia and Australia. Combining MM-398 with 5-fluorouracil and leucovorin resulted in an overall survival of 6.1 months, which represents a 1.9 month improvement over 5-fluorouracil and leucovorin alone. Merrimack will be submitting a New Drug Application to the US Food and Drug Administration for the combined MM-398 treatment in pancreatic cancer.
Dr. Daniel D. Von Hoff, who is the global Principal Investigator for the NAPOLI-1 study concludes: "This demonstration of a survival benefit from the MM-398 plus 5-FU and leucovorin combination is particularly important given that we have very few treatment options for patients in this tough clinical setting."
Source:
Press release: TGen-Scottsdale Healthcare; available from: https://www.tgen.org/news/2014-media-rel...5Gf0mlOPIV [Accessed 6 June 2014].

by Jittler at 06-05-2014, 08:30 AM
4 comments
(The text below may sound like a soap opera.sorry!)
Hello,all of you!
I am an individual who wishes to learn a subject that enables him to help in the fields of anti aging process and improving human body capacities in general(on a molecular level).I have come to the conclusion that the best way to do this would be studying Biotechnology or Biomedical Science.Actually,first I thought Biotechnology is the way to go,because I didn't know anything about Biomedical Science.So,according to my delusional goals,which one should I choose?For my bachelor deggree,that is.
My second question is this:In bachelor deggree level courses,do the professors all teach the same stuff?Or relatively similar stuff?If so,would you be so kind as to redirect me to some links with which I could prepare myself for Uni?
Aaaand.Third.I never was good at math.I blame that on my teachers though.Having said that,could you pretty please tell me just what math skills I should have mastered prior to entering Uni?!
Thanks in advance!
Hello,all of you!
I am an individual who wishes to learn a subject that enables him to help in the fields of anti aging process and improving human body capacities in general(on a molecular level).I have come to the conclusion that the best way to do this would be studying Biotechnology or Biomedical Science.Actually,first I thought Biotechnology is the way to go,because I didn't know anything about Biomedical Science.So,according to my delusional goals,which one should I choose?For my bachelor deggree,that is.
My second question is this:In bachelor deggree level courses,do the professors all teach the same stuff?Or relatively similar stuff?If so,would you be so kind as to redirect me to some links with which I could prepare myself for Uni?
Aaaand.Third.I never was good at math.I blame that on my teachers though.Having said that,could you pretty please tell me just what math skills I should have mastered prior to entering Uni?!
Thanks in advance!

by SunilNagpal at 06-05-2014, 01:36 AM
0 comments
Dear all,
I've been getting some frequent mails regarding the chances of getting a call from NUS pertaining to different academic cut-offs. One of the recent ones was from animesh.jain88:
=======================================================
hello sir,
i am animesh jain and i have done my graduation in EEE from MANIPAL INSTITUTE
OF TECHNOLOGY,KARNATAKA,INDIA with a CGPA of 7.48.
I appeard for GATE '14 AND SECURED A PERCENTILE OF 97.85. what are my chances
of admission at NUS singapore.
please guide me further.
Thanks,
yours faithfully,
animesh jain
=======================================================
Thought to share a generalized response that could cater to the queries of all of you.
Minimum academic eligibility criterion for PG/PhD admission at NUS is an "Honours Degree". Different universities/insitutes have different criteria to award graduate degrees with Honours. Mostly it's awarded to Top 10 students of a course or above a particular percentage threshold (often 80% and above). Another way to look at it is in terms of "Division"-- if you pass your degree exam in FIRST DIVISION, then you are eligible for getting shortlisted (if you have proper GATE score).
What if your percentage is Just Average?:
You shouldn't loose hope. If you have really good GATE score (97-100 percentile), accompanied by a good Major Project and internship experiences, along-with nice recommendations, even then you have a strong case to be considered for interview.
I hope this post clears the doubts of many.
About Animesh's case:
Your CGPA is indeed a hiccup, but your GATE percentile is really good. If you apply at department of Biomedical Engineering or Biotechnology, you might have a strong case considering the interdisciplinary factor in your profile. I hope that you've some good internship experience and have opted for a standard Major project in B.Tech. Gather some nice recommendations and draft a nice letter of motivation, you can crack the call for interview.
Best Regards
Sunil
I've been getting some frequent mails regarding the chances of getting a call from NUS pertaining to different academic cut-offs. One of the recent ones was from animesh.jain88:
=======================================================
hello sir,
i am animesh jain and i have done my graduation in EEE from MANIPAL INSTITUTE
OF TECHNOLOGY,KARNATAKA,INDIA with a CGPA of 7.48.
I appeard for GATE '14 AND SECURED A PERCENTILE OF 97.85. what are my chances
of admission at NUS singapore.
please guide me further.
Thanks,
yours faithfully,
animesh jain
=======================================================
Thought to share a generalized response that could cater to the queries of all of you.
Minimum academic eligibility criterion for PG/PhD admission at NUS is an "Honours Degree". Different universities/insitutes have different criteria to award graduate degrees with Honours. Mostly it's awarded to Top 10 students of a course or above a particular percentage threshold (often 80% and above). Another way to look at it is in terms of "Division"-- if you pass your degree exam in FIRST DIVISION, then you are eligible for getting shortlisted (if you have proper GATE score).
What if your percentage is Just Average?:
You shouldn't loose hope. If you have really good GATE score (97-100 percentile), accompanied by a good Major Project and internship experiences, along-with nice recommendations, even then you have a strong case to be considered for interview.
I hope this post clears the doubts of many.
About Animesh's case:
Your CGPA is indeed a hiccup, but your GATE percentile is really good. If you apply at department of Biomedical Engineering or Biotechnology, you might have a strong case considering the interdisciplinary factor in your profile. I hope that you've some good internship experience and have opted for a standard Major project in B.Tech. Gather some nice recommendations and draft a nice letter of motivation, you can crack the call for interview.
Best Regards
Sunil

by SunilNagpal at 05-30-2014, 04:33 AM
1 comments
Recently I got a query from one of the biotechnologyforums user: shirly21. Thought to share the response with all of you. And I would encourage all queries to be made here in the forum itself (rather than personal message), as it can help others too.
=============================================================
Message from shery21:
"Sir,
Dear Shirly21,
I'm glad that the tips helped ease your nerves. Well, to start with I would recommend going through Immunology (Kuby's book is best for it). As I said to one of the forum members here (link here), as you are new to the subject, read the book thoroughly like a story (start with introduction chapter, it has plethora of MCQ material). Later on switch to Antibodies chapter (only after finishing introduction, chapter1 and chapter 2). Try to finish this thing in 1 month and let me know once you are done).
Simultaneously, do browse through previous year GATE papers and dig deep into the details of each question (and it's options) asked in previous year exams. Google the options of every question and learn as much as you can about the reasons of an option being right/wrong. If there's a doubt in any question of previous year papers, let me know, I'll try to address your problem to the best of my ability.
There's a long way to go, and there's ample time too. Don't worry! All gona be well.
All the best!
Cheers
Sunil
=============================================================
Message from shery21:
"Sir,
Your tips have really simplified the idea of the gate exam as otherwise it seems to be really difficult. I am a 3rd year bioinformatics student, how do I prepare for gate exam as the syllabus is totally different and I have just 1 year to go?. It would be really helpful if you replied."
=============================================================Dear Shirly21,
I'm glad that the tips helped ease your nerves. Well, to start with I would recommend going through Immunology (Kuby's book is best for it). As I said to one of the forum members here (link here), as you are new to the subject, read the book thoroughly like a story (start with introduction chapter, it has plethora of MCQ material). Later on switch to Antibodies chapter (only after finishing introduction, chapter1 and chapter 2). Try to finish this thing in 1 month and let me know once you are done).
Simultaneously, do browse through previous year GATE papers and dig deep into the details of each question (and it's options) asked in previous year exams. Google the options of every question and learn as much as you can about the reasons of an option being right/wrong. If there's a doubt in any question of previous year papers, let me know, I'll try to address your problem to the best of my ability.
There's a long way to go, and there's ample time too. Don't worry! All gona be well.
All the best!
Cheers
Sunil

by mtwalsh01 at 05-29-2014, 10:43 PM
0 comments
Following a programme of Tai Chi is as beneficial as a brisk walking exercise programme in promoting haematopoietic CD34+ stem cells, which are blood cell precursors. As the life of CD34+ stem cells are limited by factors including aging, they are considered to be an indicator of aging. Both Tai Chi and brisk walking promoted CD34+ stem cell numbers when compared to people who did not follow any specific exercise programme. These are the main findings of a study published in the journal Cell Transplantation from researchers in different institutions in Taiwan.
Tai Chi is a Chinese martial art. Its practice has been associated with moderation of Parkinson’s disease and fibromyalgia. It is also suggested to be beneficial in a range of ways including pain reduction, sleep quality, stress reduction and quality of life. These suggested benefits led the research team in the current study to consider if Tai Chi might have anti-aging benefits.
The researchers used flow cytometry to measure levels of CD34+ stem cells from blood samples of study participants as an aging indicator. In a retrospective cross-sectional study, they recruited a cohort of young subjects to avoid confounding factors such as underlying diseases or long-term medication use. Out of sixty possible participants, they finally assigned 32 eligible participants to the Tai Chi group (TCC) (n=10), brisk walking group (BW) (n=10) and a group with no fixed exercise habit (NEH) (n=12). The Tai Chi group had been practicing for at least one year for 2.5 hours or more per week and the brisk walking group had also been practicing for a minimum of one year for 2.5 hours or more per week. Brisk walking was chosen as a comparison as it requires about the same level of physical effort as Tai Chi, with both being considered moderate intensity exercise.
The results of the study indicated that the TCC group had significantly higher levels of CD34+ progenitor stem cells compared to the NEH group. There was no significant difference between the TCC and BW groups in terms of CD34+ stem cells. However, there was also no significant difference when the BW group was compared to the NEH group. Results of a shorter pilot study over two months did not show any improvement in CD34+ levels with Tai Chi suggesting that the duration of practice is important.
Overall, the results indicate that Tai Chi is at least as efficacious as brisk walking in promoting anti-aging effects. The study corresponding author Dr. Shinn-Zong Lin said: "It is possible that Tai Chi may prompt vasodilation and increase blood flow…Considering that BW may require a larger space or more equipment, Tai Chi seems to be an easier and more convenient choice of anti-aging exercise." It is a small study based on young people around the age of 20. Larger studies on people with different age profiles will be needed for full assessment of the effects of Tai Chi but according to Dr. Paul R. Sanberg, of the Center of Excellence for Aging and Brain Repair in the University of South Florida, this preliminary study provides "the first step into providing scientific evidence for the possible health benefits of Tai Chi."
Sources:
Ho, T.-J., Ho, L.-I., Hsueh, K.-W., Chan, T.-M., Huang, S.-L., Lin, J.-G., Liang, W.-M., Hsu, W.-H., Harn, H.-J., and Lin, S.-Z. (2014). Tai Chi Intervention Increases Progenitor CD34+ Cells in Young Adults. Cell Transplantation, 23: 613-620.http://dx.doi.org/10.3727/096368914x678355
Press release: Cell Transplantation Center of Excellence for Aging and Brain Repair, available at http://www.eurekalert.org/pub_releases/2...052814.php
Tai Chi is a Chinese martial art. Its practice has been associated with moderation of Parkinson’s disease and fibromyalgia. It is also suggested to be beneficial in a range of ways including pain reduction, sleep quality, stress reduction and quality of life. These suggested benefits led the research team in the current study to consider if Tai Chi might have anti-aging benefits.
The researchers used flow cytometry to measure levels of CD34+ stem cells from blood samples of study participants as an aging indicator. In a retrospective cross-sectional study, they recruited a cohort of young subjects to avoid confounding factors such as underlying diseases or long-term medication use. Out of sixty possible participants, they finally assigned 32 eligible participants to the Tai Chi group (TCC) (n=10), brisk walking group (BW) (n=10) and a group with no fixed exercise habit (NEH) (n=12). The Tai Chi group had been practicing for at least one year for 2.5 hours or more per week and the brisk walking group had also been practicing for a minimum of one year for 2.5 hours or more per week. Brisk walking was chosen as a comparison as it requires about the same level of physical effort as Tai Chi, with both being considered moderate intensity exercise.
The results of the study indicated that the TCC group had significantly higher levels of CD34+ progenitor stem cells compared to the NEH group. There was no significant difference between the TCC and BW groups in terms of CD34+ stem cells. However, there was also no significant difference when the BW group was compared to the NEH group. Results of a shorter pilot study over two months did not show any improvement in CD34+ levels with Tai Chi suggesting that the duration of practice is important.
Overall, the results indicate that Tai Chi is at least as efficacious as brisk walking in promoting anti-aging effects. The study corresponding author Dr. Shinn-Zong Lin said: "It is possible that Tai Chi may prompt vasodilation and increase blood flow…Considering that BW may require a larger space or more equipment, Tai Chi seems to be an easier and more convenient choice of anti-aging exercise." It is a small study based on young people around the age of 20. Larger studies on people with different age profiles will be needed for full assessment of the effects of Tai Chi but according to Dr. Paul R. Sanberg, of the Center of Excellence for Aging and Brain Repair in the University of South Florida, this preliminary study provides "the first step into providing scientific evidence for the possible health benefits of Tai Chi."
Sources:
Ho, T.-J., Ho, L.-I., Hsueh, K.-W., Chan, T.-M., Huang, S.-L., Lin, J.-G., Liang, W.-M., Hsu, W.-H., Harn, H.-J., and Lin, S.-Z. (2014). Tai Chi Intervention Increases Progenitor CD34+ Cells in Young Adults. Cell Transplantation, 23: 613-620.http://dx.doi.org/10.3727/096368914x678355
Press release: Cell Transplantation Center of Excellence for Aging and Brain Repair, available at http://www.eurekalert.org/pub_releases/2...052814.php

by mtwalsh01 at 05-29-2014, 04:50 PM
0 comments
Use of high-throughput DNA sequencing techniques has revealed that the underlying genetic cause of schizophrenia appears to lie in damage to several genes rather than being pinpointed to a single gene. The number and types of mutations also influences severity of this devastating psychiatric disorder. These are the main findings of a study published in the journal Neuron from researchers in Columbia University Medical Centre and Pretoria University.
Schizophrenia is a psychiatric disorder characterised by hallucinations, delusions and cognitive issues. With an incidence of 1 in 100, it is relatively common and the risk of schizophrenia is increased in people with a family history of the disease. Previous studies have attempted to identify single genes that could lie behind schizophrenia. However, the rise of high-throughput sequencing techniques means that a more far-reaching approach can be taken, as in the current study.
The research team recruited 231 schizophrenia patients and their non-schizophrenic parents and applied the high-throughput DNA sequencing techniques to the ‘exome’ of these individuals. This means the part of the genome that actually encodes proteins rather than any intervening regions. The results indicated that the schizophrenia patients had DNA damage extending over several genes. The types of mutations were also examined and the research team observed that there was a higher than expected incidence of so-called ‘loss-of-function’ mutations which were not inherited from the patients’ parents. These types of mutations are rare but, as their name implies, have a more severe effect on gene function than other types of mutation.
The team turned their attention to the identities of some of the genes that were mutated and found that there was a preponderance of mutations in genes encoding proteins involved in a process called chromatin regulation. This process dictates how DNA is packaged and how genes are regulated. Alterations in chromatin regulation genes have recently been observed in other psychiatric disorders. In particular, the researchers noted two loss-of-function mutations in a gene called SETD1A, which encodes a subunit of the protein histone methyltransferase, a key enzyme in chromatin regulation.
Study author Dr Joseph Gogos explained the clinical significance of these findings: “A clinical implication of this finding is the possibility of using the number and severity of mutations involved in chromatin regulation as a way to identify children at risk of developing schizophrenia and other neurodevelopmental disorders…Exploring ways to reverse alterations in chromatic modification and restore gene expression may be an effective path toward treatment." The research team is now seeking to identify further genes associated with schizophrenia and identify common functions of these genes.
Sources
Takata, A. et al. (2014). Loss-of-Function Variants in Schizophrenia Risk and SETD1A as a Candidate Susceptibility Gene. Neuron 82(4): 773-780. http://dx.doi.org/10.1016/j.neuron.2014.04.043
Press release: Columbia University Medical Centre
Schizophrenia is a psychiatric disorder characterised by hallucinations, delusions and cognitive issues. With an incidence of 1 in 100, it is relatively common and the risk of schizophrenia is increased in people with a family history of the disease. Previous studies have attempted to identify single genes that could lie behind schizophrenia. However, the rise of high-throughput sequencing techniques means that a more far-reaching approach can be taken, as in the current study.
The research team recruited 231 schizophrenia patients and their non-schizophrenic parents and applied the high-throughput DNA sequencing techniques to the ‘exome’ of these individuals. This means the part of the genome that actually encodes proteins rather than any intervening regions. The results indicated that the schizophrenia patients had DNA damage extending over several genes. The types of mutations were also examined and the research team observed that there was a higher than expected incidence of so-called ‘loss-of-function’ mutations which were not inherited from the patients’ parents. These types of mutations are rare but, as their name implies, have a more severe effect on gene function than other types of mutation.
The team turned their attention to the identities of some of the genes that were mutated and found that there was a preponderance of mutations in genes encoding proteins involved in a process called chromatin regulation. This process dictates how DNA is packaged and how genes are regulated. Alterations in chromatin regulation genes have recently been observed in other psychiatric disorders. In particular, the researchers noted two loss-of-function mutations in a gene called SETD1A, which encodes a subunit of the protein histone methyltransferase, a key enzyme in chromatin regulation.
Study author Dr Joseph Gogos explained the clinical significance of these findings: “A clinical implication of this finding is the possibility of using the number and severity of mutations involved in chromatin regulation as a way to identify children at risk of developing schizophrenia and other neurodevelopmental disorders…Exploring ways to reverse alterations in chromatic modification and restore gene expression may be an effective path toward treatment." The research team is now seeking to identify further genes associated with schizophrenia and identify common functions of these genes.
Sources
Takata, A. et al. (2014). Loss-of-Function Variants in Schizophrenia Risk and SETD1A as a Candidate Susceptibility Gene. Neuron 82(4): 773-780. http://dx.doi.org/10.1016/j.neuron.2014.04.043
Press release: Columbia University Medical Centre

by jiml at 05-28-2014, 10:23 PM
0 comments
I'm hoping someone can direct me to someone who may know whether EMF (electromagnetic radiation) has been used in any commercial fermentation processes as a way to promote growth.
The reason for my question actually has to do with the effect of pulsed EMF (PEMF), which is a low-frequency EMF therapy used to promote tissue healing, on microbiota.
Online I've found only a few relevant studies and articles, such as:
http://www.researchgate.net/profile/Andr...ion_detail
http://www.ncbi.nlm.nih.gov/pubmed/23046211
Thanks very much for your help.
The reason for my question actually has to do with the effect of pulsed EMF (PEMF), which is a low-frequency EMF therapy used to promote tissue healing, on microbiota.
Online I've found only a few relevant studies and articles, such as:
http://www.researchgate.net/profile/Andr...ion_detail
http://www.ncbi.nlm.nih.gov/pubmed/23046211
Thanks very much for your help.

by ierek at 05-28-2014, 05:50 PM
0 comments
International Conference on: Urban Planning and Architectural Design for Sustainable Development (www.ierek.com)
We have the honor to invite you to attend our international conference on: “Urban Planning and Architectural Design for Sustainable Development”
This conference is planned to be held on The Kore University of Enna, Italy.
IEREK organizes this conference to exchange the better understanding of the sustainable development between social and economic development with the environmental resources, exploring the problems between the resources of the environment and sustainable development in the academia, engineering technology, management and policy.
The conference deals with all aspects of development and planning and brings together scientists and other stakeholders from across the globe to discuss the latest advances in the field, as well as to seek and highlight developments in managerial strategies and assessment tools for policy and decision makers.
For registering and more details about the conference:
http://www.ierek.com/Conferences/Confere...4BPu_mSyAU
Follow us at:
https://twitter.com/IEREKcom
http://www.linkedin.com/groups/IEREK-743...dx%3A1-1-1
Contact us at:
diana@ierek.com
omnia@ierek.com
Call us at:
(+2) 01027233310
(+2) 01000028021
We have the honor to invite you to attend our international conference on: “Urban Planning and Architectural Design for Sustainable Development”
This conference is planned to be held on The Kore University of Enna, Italy.
IEREK organizes this conference to exchange the better understanding of the sustainable development between social and economic development with the environmental resources, exploring the problems between the resources of the environment and sustainable development in the academia, engineering technology, management and policy.
The conference deals with all aspects of development and planning and brings together scientists and other stakeholders from across the globe to discuss the latest advances in the field, as well as to seek and highlight developments in managerial strategies and assessment tools for policy and decision makers.
For registering and more details about the conference:
http://www.ierek.com/Conferences/Confere...4BPu_mSyAU
Follow us at:
https://twitter.com/IEREKcom
http://www.linkedin.com/groups/IEREK-743...dx%3A1-1-1
Contact us at:
diana@ierek.com
omnia@ierek.com
Call us at:
(+2) 01027233310
(+2) 01000028021

by mtwalsh01 at 05-27-2014, 07:40 PM
0 comments
Calorific restriction reduces metastasis (spreading to secondary sites) of tumours in a mouse model of triple-negative breast cancer. This effect is augmented by ionising radiation. While the effect is mediated partially by reduction in expression of microRNAs, calorific restriction is likely to have many molecular targets and could form part of the therapeutic arsenal aimed at reducing triple negative breast cancer metastasis. These are the findings of a new study from researchers in Thomas Jefferson University in Philadelphia and the National Cancer Institute, NIH, Bethesda. The study is published in the journal Breast Cancer Research and Treatment.
Triple-negative breast cancer lacks oestrogen receptor, progesterone receptor and the HER2 protein. These are therapeutic targets in other forms of breast cancer and their absence makes it all the more difficult to develop effective therapies to triple-negative breast cancer. New strategies are desperately needed as this form of breast cancer features high incidence of recurrence and metastasis to sites such as the brain and lung. Calorific restriction is a form of dieting in which food intake is carefully reduced by a specified percentage and has been previously shown to induce tumour regression in mouse models of triple-negative breast cancer. The treatments given to breast cancer patients, such as hormonal therapy to reduce tumour growth and steroids to counteract chemotherapy side-effects, themselves contribute to the weight gain often experienced by women being treated for breast cancer. Too much weight has been shown to reduce the effectiveness of standard breast cancer therapies, inspiring the research team to look at metabolism and calorific restriction in women with breast cancer.
In the current study the researchers examined whether this regression was mediated by a type of small, regulatory RNA called microRNA (miR). These miRs exert their cellular effects by altering expression of other genes. The researchers examined miRarrays from mice which had been subjected to calorific restriction compared to mice which were given free access to food. The results showed that calorific restriction reduced the expression of miR-17/miR-20a. These have been previously shown to be up-regulated in patients with metastasising triple-negative breast cancer. The research team further investigated how these miRs might be regulating the response to calorific restriction. They discovered that the gene targets were related to the extracellular matrix, which would be highly relevant to tumour metastasis. Senior author Dr Nicole Simon explains the significance of this finding: “Calorie restriction promotes epigenetic changes in the breast tissue that keep the extracellular matrix strong…A strong matrix creates a sort of cage around the tumour, making it more difficult for cancer cells to escape and spread to new sites in the body."
Identification of the link to miR-17/miR-20a should be helpful in identifying triple-negative breast cancer patients whose cancer is more likely to metastasise and may suggest a potential new drug target. However, Dr Simon stresses that the effects of calorific restriction, especially when used to augment ionising radiation treatment, are likely to be more widespread than simply a targeted effect on miR-17/miR-20a. Triple negative breast cancers differ genetically between patients. Calorific restriction has the potential to ‘hit’ a large group of genes simultaneously, thus offering non-toxic benefits to patients whose cancers have different genetic bases.
To test this, Dr Simon is currently enrolling triple-negative breast cancer patients in a trial called CaReFOR (Calorie Restriction for Oncology Research). In this trial, women receiving radiation therapy for their breast cancer will also receive nutritional counselling and guidance in weight loss as they progress through their treatment.
Sources
L. Jin, et al., "The metastatic potential of triple-negative breast cancer is decreased via caloric restriction-mediated reduction of the miR-17~92 cluster," Breast Cancer Research and Treatment[/u][/i]. DOI 10.1007/s10549-014-2978-7, 2014.
Press release: Thomas Jefferson University. Available at http://www.eurekalert.org/pub_releases/2...052114.php
Triple-negative breast cancer lacks oestrogen receptor, progesterone receptor and the HER2 protein. These are therapeutic targets in other forms of breast cancer and their absence makes it all the more difficult to develop effective therapies to triple-negative breast cancer. New strategies are desperately needed as this form of breast cancer features high incidence of recurrence and metastasis to sites such as the brain and lung. Calorific restriction is a form of dieting in which food intake is carefully reduced by a specified percentage and has been previously shown to induce tumour regression in mouse models of triple-negative breast cancer. The treatments given to breast cancer patients, such as hormonal therapy to reduce tumour growth and steroids to counteract chemotherapy side-effects, themselves contribute to the weight gain often experienced by women being treated for breast cancer. Too much weight has been shown to reduce the effectiveness of standard breast cancer therapies, inspiring the research team to look at metabolism and calorific restriction in women with breast cancer.
In the current study the researchers examined whether this regression was mediated by a type of small, regulatory RNA called microRNA (miR). These miRs exert their cellular effects by altering expression of other genes. The researchers examined miRarrays from mice which had been subjected to calorific restriction compared to mice which were given free access to food. The results showed that calorific restriction reduced the expression of miR-17/miR-20a. These have been previously shown to be up-regulated in patients with metastasising triple-negative breast cancer. The research team further investigated how these miRs might be regulating the response to calorific restriction. They discovered that the gene targets were related to the extracellular matrix, which would be highly relevant to tumour metastasis. Senior author Dr Nicole Simon explains the significance of this finding: “Calorie restriction promotes epigenetic changes in the breast tissue that keep the extracellular matrix strong…A strong matrix creates a sort of cage around the tumour, making it more difficult for cancer cells to escape and spread to new sites in the body."
Identification of the link to miR-17/miR-20a should be helpful in identifying triple-negative breast cancer patients whose cancer is more likely to metastasise and may suggest a potential new drug target. However, Dr Simon stresses that the effects of calorific restriction, especially when used to augment ionising radiation treatment, are likely to be more widespread than simply a targeted effect on miR-17/miR-20a. Triple negative breast cancers differ genetically between patients. Calorific restriction has the potential to ‘hit’ a large group of genes simultaneously, thus offering non-toxic benefits to patients whose cancers have different genetic bases.
To test this, Dr Simon is currently enrolling triple-negative breast cancer patients in a trial called CaReFOR (Calorie Restriction for Oncology Research). In this trial, women receiving radiation therapy for their breast cancer will also receive nutritional counselling and guidance in weight loss as they progress through their treatment.
Sources
L. Jin, et al., "The metastatic potential of triple-negative breast cancer is decreased via caloric restriction-mediated reduction of the miR-17~92 cluster," Breast Cancer Research and Treatment[/u][/i]. DOI 10.1007/s10549-014-2978-7, 2014.
Press release: Thomas Jefferson University. Available at http://www.eurekalert.org/pub_releases/2...052114.php
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