Biotechnology winners in the 2013 Presidential Green Chemistry Challenge Awards

December 18, 2013, 5:53 am

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A bio-based oil for use as an insulating fluid for high-voltage electrical transformers and a less wasteful method for producing the chemicals used in polymerase chain reaction (PCR) were among the winners of the 2013 Presidential Green Chemistry Challenge Awards announced last week and awarded by the U.S. Environmental Protection Agency.

One award went to Cargill Inc. who developed a vegetable-oil-based transformer fluid called EnvirotempTM FR3TM dielectric fluid. As the fluid is based on vegetable, it is much less flammable than petroleum-based mineral oil commonly used in transformers, which may also be toxic to aquatic species. EnvirotempTM FR3TM dielectric fluid is also less hard on the insulating material used in transformers, often cellulose. Testing of a transformer called BEES® 4.0, a transformer using FR3TM fluid, across its lifecycle revealed that the carbon footprint is significantly reduced to about 55-times lower than a mineral oil based transformer, for example in terms of raw materials, manufacturing, and transportation phases. The EnvirotempTM FR3TM dielectric fluid is also more biodegradable, less toxic and based on a renewable source material. There has yet to be a known fire or explosion caused by any of the hundreds of thousands of transformers using the Cargill fluid.

In terms of the less wasteful process for making PCR chemicals, researchers at the company Life Technologies devised a three-step process using only one pot to synthesise deoxyribonucleotide triphosphates (dNTPs), which are the DNA building blocks essential in PCR. Conventional processes for synthesising dNTPs entail complex multiple-step processes using various hazardous reagents and chemicals. The Life Technologies process eliminates much of these reagents and improves the process E-factor (the ratio of amount of waste to amount of product) by about a factor of 10. The company implemented this technology in their manufacturing plant in Austin, Texas in 2011 and since then have reduced organic solvent consumption by up to 95% and other hazardous waste products by up to 65%. This has also led to substantial financial savings.

Sources

http://www.scientificamerican.com/articl...me-plating [Accessed 18 December 2013].

http://www2.epa.gov/green-chemistry/2013...cals-award [Accessed 18 December 2013].

http://www2.epa.gov/green-chemistry/2013...ways-award [Accessed 18 December 2013].

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Flow Chemistry India 2014 | January 23-24 2014 | Hyderabad, India

December 18, 2013, 6:14 am

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Flow Chemistry India 2014

Organisers: Flow Chemistry Society

Dates: January 23rd- 24th, 2014

Location: CSIR-Indian Institute of Chemical Technology, Hyderabad, India.

Website: http://selectbiosciences.com/conferences...conf=FCI14

The website gives all the necessary information on registration, abstract submission, fees, conference agenda, hotel, exhibitions and other important facts.

Purpose of the conference
Following a one-day workshop in Mumbai in 2012, this will be the first full conference to be held in India under the auspices of the Flow Chemistry Society. The society aims to unite and represent those who are actively working on this rapidly developing field. This meeting is dedicated to the integration of flow chemistry into everyday practice throughout the world by delivering the latest knowledge and making it available for the entire chemistry community. Training courses in Micro and Continuous Flow Reactors for Industrial Scale Organic Synthesis will be available.

Topics:
Aspects of the following topics will feature:
• Catalysis
• Flow Chemistry - From Lab to Industrial Scale
• Flow Nanotechnology
• Meso Flow Chemistry
• Microfluidic Flow Chemistry
• Microwave Assisted Flow Synthesis
• Novel Applications of Flow Chemistry
• Process Analysis and Control

Speakers

Keynote speakers
• Ferenc Darvas, President, Flow Chemistry Society
• Oliver Kappe, Professor/Director, Karl Franzens University of Graz
• Vivek Ranade, Deputy Director and Chair, National Chemical Laboratory
• Paul Watts, Professor & Research Chair in Microfluidic Bio/Chemical Processing, Nelson Mandela Metropolitan University

Other speakers
• Robert Ashe, Managing Director, AM Technology
• Kirti Sahu, Assistant Professor, Indian Institute of Technology Hyderabad
• P Sai Prasad, Chief Scientist, Indian Institute of Chemical Technology
• Amol Kulkarni, Scientist, National Chemical Laboratory
• Anil Kumar, Professor, Indian Institute of Technology Bombay
• Akhilesh Verma, Associate Professor, University of Delhi
• Aiichiro Nagaki, Senior Lecturer, Kyoto University
• Vijay Kirpalani, Director, Sharon Bio-Medicine Ltd & CEO-Pi
• Ravi Arun, Scientist, CSIR-CMERI
• Kumar Oza, Chief Chemistry Officer, Pi- Process Intensification Experts LLP.
• Aria Farjam, Vice President, Microfluidic Chipshop GmbH
• V Kumaran, Professor, Indian Institute of Science
• Usha Virendra, Sr Principal Scientist, Indian Institute of Chemical Technology
• Dipankar Bandyopadhyay, Assistant Professor, Indian Institute of Technology Guwahati
• P Selvam, Professor, Indian Institute of Technology Madras
• Mahender Siripragada, Vice President, Panacea Biotec Ltd
• Amin Ismaili, Sr. General Manager, Cadila Pharmaceutical Ltd.

Important dates:
Poster Submission Deadline: 31 December 2013

Who are the organisers?

The Flow Chemistry Society was formed by internationally recognized flow chemistry experts in 2010 to unite and represent those who are actively working on this rapidly developing field. The Society is dedicated to enhance the public appreciation of flow chemistry and its integration into everyday practice throughout the world by delivering the latest knowledge and making it available for the entire chemistry community. Their website address is: http://www.flowchemistrysociety.com/

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How to print an eye cell: potential for bioprinting in a future cure for blindness

December 18, 2013, 1:18 pm

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A research group based in Cambridge University in the UK have published a study in today’s issue of the journal Biofabrication in which they demonstrate successful use of inkjet printing technology to print eye cells for the very first time. The group used a piezoelectric printhead to print two types of rat central nervous system (CNS) cells, namely retinal ganglion cell (RGC) neurons and retinal glia. Although this is a preliminary study and there is a long way to go before possible human trials, this is potentially significant for blindness as many blinding eye diseases feature loss of retinal nerve cells. The paper’s co-authors, Professor Keith Martin and Dr Barbara Lorber, from the John van Geest Centre for Brain Repair, University of Cambridge have stated that “the aim is to develop this technology for use in retinal repair in the future”.

The researchers performed different tests on the printed cells to check their cell number and viability and their survival and RGC neural outgrowth in culture. They found that the cells were not appreciably deformed upon exiting the printhead, despite being subjected to significant shear pressure. However, final cell counts were lower than for non-printed control cells, probably due to sedimentation. Importantly, cell viability was unaffected. In addition, there were no significant differences in cell survival or neurite outgrowth in culture after 5 days between control and printed RGCs or in survival of control or printed retinal glia. Finally, RGCs grew longer neurites when plated on a glial substrate and this occurred to a similar extent whether the RGCs and glia were printed or not prior to plating.

The authors plan to extend their studies to other cells of the retina and determine if light-sensitive photoreceptors can be printed using this technology. This would be the key to possible cures for some forms of blindness. They also would like to translate their work from their current printer system to a commercial, multi-nozzle printhead such as MicroFab.

Sources

LORBER, B., HSIAO, W.-K. , HUTCHINGS, I.M. and MARTIN, K.R., 2014. Adult rat retinal ganglion cells and glia can be printed by piezoelectric inkjet printing. Biofabrication, 6(1), pp. 015001.

http://www.bbc.co.uk/news/health-25405542

http://www.cam.ac.uk/research/news/cells...first-time

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Are antibacterial handwashes safe? Why soap and water may be the best option.

December 18, 2013, 1:53 pm

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The US Food and Drug Administration (FDA) have raised concerns over health risks of substances in antibacterial soaps and handwashes. As a result, the organisation has called for a safety review of such products. This has come about due to recent studies which have suggested that ingredients such as triclosan in liquid soaps and triclocarban in bar soaps may be contributing to the huge public health issue of bacterial resistance to antibiotics, according to a statement released on Monday by Dr Colleen Rogers, a lead FDA microbiologist. The statement also raises concerns that these ingredients may also have "unanticipated hormonal effects that are of concern" according to in vivo animal studies. Dr Rogers’s statement points out that "New data suggest that the risks associated with long-term, daily use of antibacterial soaps may outweigh the benefits." Furthermore, according to Dr Rogers, there is no current evidence to suggest that over-the-counter antibacterial soap products are any more effective at preventing illness than plain soap and water. The FDA took up the matter following a federal appeals court decision in March to approve a lawsuit by the non-profit Natural Resources Defense Council, which aimed to force the FDA to review the health impacts of triclosan.

In the light of these questions and concerns, the FDA has proposed a rule that will require manufacturers to prove that these antibacterial products are safe and more effective against infection than plain soap and water. Hitherto, laboratory tests to evaluate the effectiveness of these products have not included any test of the product on infection rates; the proposed new FDA rule would change that. It would not, however apply to the types of alcohol-based hand-sanitizers that are typically used in healthcare settings. The FDA has given manufacturers until the end of 2014 to submit the results of clinical trials on their products and they aim to have new regulations finalised in 2016. The FDA is collaborating with the Environmental Protection Agency (EPA), which is responsible for regulation of triclosan in its other role as a pesticide, to ensure consistency across government agencies.

Meanwhile, the FDA is encouraging consumers, clinicians, environmental groups, scientists, industry representatives and others to submit their views on the proposed new rule; this comment period is available for 180 days. The FDA continues to emphasise that appropriate hand washing remains one of the most important ways to avoid becoming sick or passing on infections to others. They recommend consulting the Centers for Disease Control and Prevention (CDC) website for advice on hand washing at http://www.cdc.gov/handwashing.

Sources

http://www.fda.gov/ForConsumers/Consumer...378393.htm

http://www.bbc.co.uk/news/world-us-canada-25405037

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EU concerns on potential neonicotinoid pesticide effects on brain development

December 19, 2013, 12:39 am

≫ Next: ENOVEO: Biotech Internship- Placement programme- 2014‏‏‏‏‏

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The European Food Safety Authority (EFSA) has proposed that guidance levels for exposure to two members of the neonicotinoid class of pesticide, namely imidacloprid (IMI) and acetamiprid (ACE), be reduced. They have based this proposal on studies that indicate these pesticides may have greater than previously thought effects on developing mammalian brains and nervous systems. These pesticides are used worldwide to protect crops from pest insects and domestic animals from fleas and have become the most prominent class of insecticides in the world. Their popularity has grown as they are perceived as being less harmful to human health and to the environment than older pesticides. However, the European Union (EU) had already introduced a two year moratorium on the use of these pesticides on crops attractive to bees amid growing evidence that their increasingly widespread use was harmful to bees.

The concerns on possible detrimental effects on the developing human nervous systems have arisen from the results of studies on, for example, neonatal rat cerebellar neurons. The neonicotinoids are agonists of nicotinic acetylcholine receptors (nAChRs). They were considered to be have selective binding affinity for insect nAChRs, hence their toxicity to insects. However, a growing body of evidence suggested that they could also have greater than previously thought stimulatory effects on mammalian nAChRs. Studies on neonatal rat cerebellar neurons showed that both ACE and IMI induced significant excitatory Ca2+ influxes at concentrations greater than 1 µM in small neurons in cerebellar cultures expressing mRNA of the α3, α4, and α7 nAChR subunits. These effects were significantly inhibited by nAChR inhibitors. In other studies, young rodents exposed to IMI experienced effects including brain shrinkage, weight loss and reduced movement. Exposure in utero to IMI resulted in decreased sensorimotor performance in neonatal rats while IMI has also been shown to stimulate human α4β2 nAChR subtypes.

The EFSA has acknowledged that the available evidence is limited but maintains that the concerns raised are sufficient to suggest that the current guidelines "may not be protective enough to protect against developmental neurotoxicity and should be reduced". The chemical companies concerned are now being invited to comment on the research findings prior to a possible amendment of the reference values by March 2014. Other experts suggest that the EFSA is precautionary. For example Prof Alan Boobis of Imperial College London has pointed out that “the conclusions of EFSA do not suggest that exposure of humans to these compounds at the levels that occur normally in food or in the environment is a cause for concern."

Sources

Kimura-Kuroda, J., Komuta, Y., Hayashi, M. and Kawano, H., 2012. Nicotine-Like Effects of the Neonicotinoid Insecticides Acetamiprid and Imidacloprid on Cerebellar Neurons from Neonatal Rats. PLoS ONE 7(2): e32432. doi:10.1371/journal.pone.0032432.

http://www.bbc.co.uk/news/science-environment-25421199

http://www.efsa.europa.eu/en/press/news/130116.htm

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ENOVEO: Biotech Internship- Placement programme- 2014‏‏‏‏‏

December 19, 2013, 1:27 am

≫ Next: Smoking induces differential epigenetic changes in DNA

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ENOVEO is a biotechnology based organisation operating in environmental research and product development, located in Patia, Bhubaneswar, Odisha. It has its office in US, Brazil and France. We have a series of research projects and biotech product development projects.

We are currently looking for students pursuing Masters, B.tech, M.tech into life science, Biotechnology and Environment, to be a part of our Internship programme, by which the students can pursue their dissertation work.

Placement assistance: We are seeking internship applicant to create skilled life science professionals, after which they shall be accommodated with our partnering companies nation wide.
Accommodation: We can arrange for accommodation for students in Bhubaneswar, with paying Guest or working hostel facilities.

Dissertation Areas:
Infection biology
Enzymatic screening and characterization
Environmental biotech: Metagenome DNA isolation and analysis, Biocontrol
Insitu pond water treatment: Bio engineering process
New product development: Eco product development
Contaminated soil assessment and treatment
Microbial Fuel cells

Fees: Depends on the project topic. The relative fees structure are
3 months: Rs 12,000 : Jan to March 2014
6 months: Rs 20,000: Jan to June 2014
Please feel free to contact us for any further communication:
Er. Ashutosh Padhi: +91 876 333 39 54
Dr. Regalin Rout: +91 943 731 31 12

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Smoking induces differential epigenetic changes in DNA

December 19, 2013, 6:22 am

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It is now well-accepted that cigarette smoking is associated with risk of developing different cancers as well as other diseases including diabetes. Reduced fertility has also been linked to smoking. Greater understanding of one of the possible mechanisms behind this association has been revealed in a study published this month in the journal Human Molecular Genetics. The study from Uppsala University in Sweden involved a genome-wide DNA methylation study in order to compare the epigenetic changes in DNA caused by smoking compared to consumption of snuff (smokeless tobacco). The study interestingly found that smoking induced methylation changes that were not observed as a result of smokeless tobacco, suggesting that the changes are due to products related to burning of tobacco rather than the basic components of the tobacco itself.

Specifically, the study found that there were 95 sites that were differentially methylated in smokers and that a subset of differentially methylated loci was additionally differentially expressed. By contrast, in the smokeless tobacco group, no sites encoding biological functions or molecular processes were differentially methylated. Among the loci that were differentially methylated in the smokers were CPOX, CDKN1A, and PTK2, which are involved in response to arsenic-containing substances. This is consistent with cigarette smoke containing arsenic. In addition, there were loci associated with disease conditions that were observed to be differentially methylated in smokers. These included the diabetes-associated “insulin receptor binding”, and “negative regulation of glucose import”, the immune response-associated interleukin-6-mediated signaling pathway”, “regulation of T-helper 2 cell differentiation”, and “positive regulation of interleukin-13 production” and the male fertility-associated “sertoli cell fate commitment”. Since repressed immune response, reduced fertility and diabetes have all been associated with cigarette smoking, this study suggests that epigenetic changes mediated by chemicals in burnt tobacco may contribute to these problems. This kind of information may help inform development of more targeted drug therapies.

Sources

BESINGI, W. and JOHANSSON, Å., 2013. Smoke related DNA methylation changes in the etiology of human disease. Human Molecular Genetics, 2013

Uppsala Universitet. "Smoking changes our genes." ScienceDaily, 17 Dec. 2013. Web. 19 Dec. 2013.

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query regarding h1b visa sponsor in usa

December 19, 2013, 7:41 am

≫ Next: Serotonin receptor polymorphism links stress reactions to cardivascular disease risk

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Hai all!..hope all is well....I had a question regarding H1 B visa sponsorers for international biotechnologists. I did my masters in biotechnology at Andhra University, AP, INDIA and now I am on H4 residing in Maryland, US. I am willing to file my H1 B in April 2014. Do University of Maryland sponsors H1B for international biotechnologists? Or there anyone or any other companies who sponsors H1 visa for international biotech people?

Please reply if u know any information regarding H1 B sponsoring so that it will be great help to me...

Thank You!!!

Pranavi Chennupati[/size]

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Serotonin receptor polymorphism links stress reactions to cardivascular disease risk

December 20, 2013, 12:46 am

≫ Next: International Regulations on Human Genetic Engineering and Designer Babies

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Researchers in Duke University have uncovered a genetic polymorphism in a serotonin receptor gene that helps explain the link between risk and outcomes of cardiovascular disease (CVD) and reaction to mental stress. There is substantial evidence to suggest that there is a link between emotional stress responses, elevation of the stress hormone cortisol and morbidity and mortality for CVD. Illnesses such as depression are linked to incidence of heart disease.

The current study, published this week in PLoS ONE established that a polymorphism in the 5HTR2C gene for a serotonin receptor is significantly associated with the study end-point of all-cause mortality or myocardial infarction (MI) among Caucasian participants. Serotonin (5-HT) is a neurotransmitter which is intimately involved in regulation of mood, sleep and appetite. There are multiple serotonin receptors. The 5HTR2C, which is the subject of this study, mediates serotonin-induced activation of the hypothalamic-pituitary-adrenal (HPA) axis and hence release of cortisol. Illnesses such as depression, especially when associated with anxiety, tend to feature hyperactivity of the HPA axis.

The study focused on the rs6318 Ser23 C allele of the 5HTR2C gene. This allele had been previously associated in men with larger increases in plasma cortisol and higher subjective rating of negative emotions when remembering occasions that had made them happy or sad compared to carriers of the Cys23G allele. The allele was also linked to stronger adrenocorticotropic hormone (ACTH) responses, a measure of HPA activity, to an agonist of 5HTR2C. This allele has also been associated with, for example, higher central obesity, poorer glucose metabolism and higher levels of serum lipids, all of which can contribute to increased risk levels of CVD. The study population was 6126 Caucasian participants consecutively recruited through the cardiac catheterization laboratory at Duke University Hospital (Durham, NC) as part of the CATHGEN biorepository. The study showed that the rs6318 Ser23 C allele is associated with increased risk for CVD mortality and morbidity. The allele was not however, associated with traditional cardiac risk factors such as body mass index, diabetes, hypertension, dyslipidemia, smoking history, number of diseased coronary arteries, or left ventricular ejection.

The researchers are working on a hypothesis that the link between 5HTR2C via cortisol to increased CVD mortality and morbidity may lie with a recently demonstrated connection between cortisol to unstable atherosclerotic plaque in the coronary arteries. Cortisol has been associated with increased matrix metalloproteinase (MMP-9) which degrades collagen contributes to development of vulnerable plaques. Redford B. Williams Jr., M.D., the lead author of the study, is satisfied that their findings lead the way to helping to “ begin to develop and test early interventions for those heart patients who are at high risk of dying or having a heart attack."

Sources

Brummett BH, Babyak MA, Jiang R, Shah SH, Becker RC, et al. (2013) A Functional Polymorphism in the5HTR2C Gene Associated with Stress Responses Also Predicts Incident Cardiovascular Events. PLoS ONE 8(12): e82781. doi:10.1371/journal.pone.0082781

Duke Medicine. "Stress reaction gene linked to death, heart attacks." ScienceDaily, 19 Dec. 2013. [Accessed 20 Dec. 2013]

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International Regulations on Human Genetic Engineering and Designer Babies

December 26, 2013, 2:53 am

≫ Next: Stem Cell and Gene therapy

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I was wondering which country has the most lax laws on human genetic intervention, or where so called designer babies are legal, that would actually have the technology to accomplish said task. (Obviously third world countries without any modern scientific technology would be unlikely to have any regulations regarding said technology but would be useless unless you've got the millions to setup your own genetics corporation).

Essentially I'm wanting to have a kid in a few years and my family has some very positive and some very negative genetic factors, and I realized people like myself who want their own biological children without the risk of genetic defects would pay a lot of money to do so. Also same sex couples being able to have their own genetic offspring would be a huge market as well.

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Stem Cell and Gene therapy

December 26, 2013, 11:34 pm

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Gene Therapy is advisable for genetic diseases which cannot be cured. Here stem cells are very important and most potent cells which can be used for gene therapy and after that they can be transplanted in to human. For gene therapy, DNA can be efficiently introduced with homologous recombination as for gene therapy we need to correct the specific gene defect without addition of harmful extraneous DNA sequences. Such correction is possible with homologous recombination between input DNA sequences and identical homologous sequences in the genome for target gene. To select the target cells, there are techniques for developing virtually pure populations of hematopoietic stem cells from heterogeneous population and it should permit the use of the highly efficient nuclear microinjection methods for transfer of DNA. It is important that the therapeutic DNA introduced into target cells must remain functional and the cells containing the therapeutic DNA must be long-lived and stable. Problems with integrating therapeutic DNA into the genome and the rapidly dividing nature of many cells prevent gene therapy from achieving any long-term benefits. Techniques combined with new highly sensitive methods for detecting cells with the specified genetic modification of non-expressed genes would make homologous recombination-mediated gene therapy feasible for hematopoietic stem cells. Now stem cell based gene therapy has been introduced for many genetic diseases like Leukemia and recently for skin diseases.

Sometime obtaining the stem cells from same individual is difficult and to come up with this problem in future it was suggested to derive the stem cells from placental cord at the time of baby birth. In recent development, obtaining stem cells from placental cord and cryo-preservation of them for future use has been introduced. This can be used once someone will be identified with genetic disorder. It is expected that the development in recent studied of stem cell based gene therapy will be revolutionary in future of health science.

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Gene cloning for expression

December 27, 2013, 3:17 am

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Cloning of a gene for expression purpose (in bacterial, yeast, mammalian or other systems) involves many steps. Depending up on the information available on the gene of interest, various methods can be used to isolate and amplify it.
Steps for the cloning of a gene

1. Getting the Gene of interest:
Firstly you must get the DNA and that you quantity in sufficient quantities to clone, you need to use following method depending upon the availability of starting materials.

a) DNA as starting material: (From genomic DNA or piece of DNA),
If you had a very small quantity of the DNA and knew enough of the sequence to make primers you can use PCR to amplify it.

b) RNA as starting material: (eg mRNA)
You would need to use reverse transcriptase to 'reverse transcribe' it into DNA fallowed by PCR amplification to get the product.

c) Protein as starting material:
If you know the sequence of protein then you need software to reverse translate it to get the gene sequence. You can bias it depending upon the expression system.

2. Vector selection for expression of gene:
Most of the time gene is cloned for expression purposes and depending of the requirement/application you can select vector. A vector is circular DNA (Modified Plasmid) that replicates in a bacterium or yeast system so it has origin of replication for that system.
So, you can see, a gene inserted into a plasmid will be replicated many of times in single bacteria. And it is possible to grow millions of bacteria in a 1 litre flask. So this is a good way to make lots of copies of a gene of interest.
These vectors are now a day’s commercially available which will have restriction sites for cloning and upstream regulatory sequence which will help for better expression of gene.

3. Cloning of DNA:
Next you will use restriction enzymes to cut out the DNA/gene you want from the amplified product. You use the same restriction enzymes to cut the vector also, so that the ends will be compatible. This means that if you will use a "sticky ends" restriction enzymes (Available in market), then the DNA sequences of the trailing bits will be compatible and will want to stick to each other. This makes it much easier to do the cloning.
Once restriction digestion is done you can purify the specific DNA from Agarose gel using Gel electrophoresis. These fragment (Vector + Gene/DNA) can be ligated using a Ligase enzyme (Available commercially)
Once the ligation is done, it can be transformed to Bacteria strains (E coli) where is will be amplified while growing on Agar plate. Here you will get many colonies of E coli which will contain clones of DNA in vector. These clones can be further grown in culture media and DNA can be isolated from here.

Sometime you will get false clone which can be further eliminated by screening using PCR or restriction digestion. Once you get the positive clone they can be used for expression in bacterial or homologous systems.

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Top Biotech companies

December 27, 2013, 6:08 am

≫ Next: Beauty product or biological weapon? An inhibitory peptide developed for botulinum

≪ Previous: Gene cloning for expression

Hello everyone ..! This is pooja ..am a biotech student and have completed my btech biotech ..and i have started a blog related to biotechnology ...here is the link for the top biotech companies --> http://www.bmccorner.com/2013/12/biotech...rabad.html

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Beauty product or biological weapon? An inhibitory peptide developed for botulinum

December 15, 2013, 11:48 pm

≫ Next: Genetic disorder and its diagnosis

≪ Previous: Top Biotech companies

Researchers in the University of Utrecht in the Netherlands and the Paul Scherrer Institute in Switzerland have identified a substance that can protect nerve cells from the effect of the deadly toxin, botulinum (BoNT/A). (BoNT/A) is best known for its use in tiny amounts in the beauty product Botox. However, in amounts of just 15 ng, it is lethal, causing paralysis of nerves, and is used in biological weapons. It is also used in small amounts in antidotes to conditions such as migraine. In nature, it mainly kills waterfowl and fish.

In a study published recently in Nature, the researchers examined one of the receptors for BoNT/A, namely the synaptic vesicle glycoprotein 2 (SV2) family. In this study, they developed high resolution crystal structures of the BoNT/A receptor binding domain (BoNT/A-RBD) complexed to the SVC2 luminal domain (SVC2-LD). They determined the backbone-backbone interactions that occurred between toxin and receptor, which resembled those of inter-strand interactions in amyloid structures. They then introduced peptides to determine if they could inhibit formation of the complex between toxin and receptor. This enabled the researchers to identify an inhibitory peptide that prevented absorption of the toxin into nerve cells. This peptide could, the researchers maintain, be the basis to an antidote to BoNT/A poisoning and could be protective against the effects of biological weapons based on this lethal toxin.

Sources
Roger M. Benoit, R.M. et al (2013) Structural basis for recognition of synaptic vesicle protein 2C by botulinum neurotoxin A Nature (2013) doi:10.1038/nature12732

http://www.uu.nl/university/research/EN/...toxin.aspx

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Genetic disorder and its diagnosis

December 28, 2013, 10:54 am

≫ Next: Designer babies

≪ Previous: Beauty product or biological weapon? An inhibitory peptide developed for botulinum

Disease caused genetic disorder are abnormality in an individual's DNA. These abnormalities can range from a small mutation in a single gene to the addition or deletion of an entire chromosome or set of chromosomes.

Determination of genetic disorder at embryonic level

Diagnosis can be done by prenatal testing of cells from an embryo, means that genetic disorders can now be detected before birth. At embryonic level genetic disorder can be detected with the help of amniotic fluid. Analysis of amniotic fluid, drawn out of the mother's abdomen is an amniocentesis procedure, which can reveal many aspects of the baby's genetic health. This is because the fluid also contains fetal cells, which can be examined for genetic defects.

In case of designer babies it is very important to diagnose the genetic status and in these process techniques of in vitro fertilization followed by Pre-implantation Genetic Diagnosis (PGD) are performed. One it is found normal then decision can be taken whether to implant the embryo or not.

Diagnosis can be done on the basis of person’s physical characteristics and family history, or on the results of a screening test.

Genetic testing is one of several tools that doctors use to diagnose genetic conditions. The approaches to making a genetic diagnosis include:

1- Physical examination: Distinctive facial features by organ measurements and imaging studies including x-rays, computerized tomography scans, or magnetic resonance imaging to see structures inside the body.

2- Personal and family medical history: Information about an individual’s health can provide clues to a genetic diagnosis. A personal medical history includes past health issues, hospitalizations and surgeries, allergies, medications, and the results of any medical or genetic testing that has already been done. As genetic conditions often run in families, information about the health of family members can be a critical tool for diagnosis of genetic disorders.

3- Laboratory tests, including genetic testing: chromosomal, molecular and biochemical testing are used to diagnose genetic disorders. There are laboratory tests that measure the levels of certain substances in blood and urine can also be done for diagnosis.

Testing of genetic imbalance is available for many genetic diseases. However, some diseases do not have a genetic test and in that condition either the genetic cause of the disorder is unknown or a test has not yet been discovered.

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Designer babies

December 28, 2013, 11:28 am

≫ Next: Familial Alzheimer’s Disease

≪ Previous: Genetic disorder and its diagnosis

It is new era where babies can be designed with the help of In vitro fertilization. It has helped for many difficulties with having children. However, it raises a number of ethical issues, one of which is the ability to select for particular traits or diseases using a technique called pre-implantation genetic diagnosis (PGD).

pre-implantation genetic diagnosis was firstly done in 1989 to test embryos fertilized in vitro for inherited diseases such as cystic fibrosis, Huntingdon’s disease, and Fragile-X syndrome or for diseases causes by abnormal chromosome structure, such as Down’s Syndrome. After testing the unaffected embryos are implanted into the mother’s uterus. Earlier, the testing option for couples at risk of passing an inherited condition to their children was by sampling foetal cells from the placenta or amniotic fluid. If a foetus was observed to be affected, parents would then have to choose whether to continue with the pregnancy, or have an abortion.

Pre-implantation genetic diagnosis (PGD)

At the time of in vitro fertilization, eggs are removed from ovaries and fertilized with sperm in a Petri-plate. The fertilized eggs undergo normal cell division (Mitotic) until they have eight cells. At this phase, one or two of these cells are removed. DNA from the cells is extracted and tested for the presence of genetic disorders. The removal of cells for testing does not affect the development of the embryo, as these cells are restored as the embryo’s cells continue to divide and grow.

The genetics of the cells can be tested by using polymerase chain reaction (PCR) or fluorescence in situ hybridization (FISH). PCR is used to look for single gene abnormalities, whereas fluorescence in situ hybridization is used to look for abnormal chromosomes.

Embryos that are not at risk of disease are then transferred into the woman’s uterus where they can be implanted and developed.

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Familial Alzheimer’s Disease

December 28, 2013, 11:59 am

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Alzheimer's disease is a disorder caused by neurological problems in which the death of brain cells causes memory loss and cognitive decline. A neurodegenerative type of dementia, the disease starts mild and gets progressively worse.

Alzheimer’s disease where there is a family link, called familial Alzheimer’s disease (FAD), is more common amongst younger people.

All the Familial Alzheimer’s disease known so far has an early commencement, and as many as 50 percent of the cases are now known to be caused by defects in three different genes located at three different chromosomes of human, the structures inside cells that house the genetic code. Some families have mutations in a gene called amyloid precursor protein (APP), which causes an abnormal form of the amyloid protein to be produced. The other families have mutations in a gene called presenilin-1, which causes an abnormal Presenilin-1 protein to be produced. Still others have mutations in a very similar gene called presenilin-2, which causes an abnormal Presenilin 2 protein to be produced.

Even if one of these mutations is present in only one of the two copies of a gene inherited from a person's parents, the person will inevitably develop that form of early-onset Alzheimer's (this is called autosomal dominant inheritance). However, the total known number of these cases is small (between 100 and 200 worldwide), and there is as yet no evidence that any of these mutations play a major role in the more common, sporadic or non-familial form of late-onset Alzheimer's. Scientists are working to reveal the normal function of APP and presenilins and to determine how mutations of these genes cause the onset of familial Alzheimer’s disease.

Treatment:

Till date there is no preventative or curative treatment for this disease. Many of drugs exist, which can help to ease certain symptoms such as depression, anxiety, confusion, agitation, hallucinations, and insomnia. Regrettably, these drugs have a propensity to be effective for a limited number of patients, only for a small period of time and may cause adverse side effects.

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Modified Microorganisms - Advice Needed!

January 2, 2014, 10:42 am

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Hello,

I am working on a (currently) theoretical project whose goal is to get rid of water pollution and infection through modifying microorganisms to "eat"/"absorb" the type of pollution detected, for example, sulfur.I am working on a (currently) theoretical project whose goal is to get rid of water pollution and infection through modifying microorganisms to "eat"/"absorb" the type of pollution detected, for example, sulfur.

My question is, can i genetically modify a microorganism in order to make it resilient and resistant to a certain matter and also to consume this same matter, for example a sulfur-consuming bacteria.

If such thing can be done (now or in the not-too-far future), can it be done automatically or does it have to be manual?
e.g. a scanner detects that a lake has a "patch" infected by X, it then modifies a bacteria to be X resistant and X consuming, without the need of a human being telling it what genes need to be inserted.

Thanks for your time and have a happy new year! Smile

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Durham College Biotech Courses - Oshawa, Ontario Canada

January 4, 2014, 5:00 pm

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Durham is one of the oldest colleges of Canada where natural and social sciences are efficiently taught. It has a different department that deals with biotechnology and research.

Here goes the admission requirements :
1. Official transcript demonstrating proof of successful completion of a post-secondary degree program
2. Course-by-course evaluation to demonstrate the required pre-admission courses indicated (for international students)
3. BSc from any famous university with a grade of 60 or a C in two chemistry courses and one biochemistry course where at least one of these courses has a lab component
4. Additional information may be requested such as demonstration of lab practical experience
5. English skills assessment (could be required)

Career Growth

As a graduate, you can get employment in any of the following organizations:
a) Government institute
b) Quality control laboratory
c) Manufacturing
d) Research laboratory
e) Administration in a pharmaceutical, agricultural, food or environmental company

The following Positions can be offered :
1) Production technologist
2) Instrumentation technologist
3) Pharmaceutical sales manager
4) Quality assurance technologist
5) University laboratory research assistant
6) Clinical study technologist
7) Microbiology technologist
8) Food technologist
9) Immunologist technologist
10) Pharmaceutical technologist

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Intergrin inhibition in cancer therapy may depend on timing and cellular targeting

January 5, 2014, 11:35 pm

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The failure of drugs directed against the αvβ3-integrin in phase III clinical trials against aggressive brain cancer may be a result of not targeting the timing or cell type specificity of application of the antagonists precisely enough. That is the conclusion from new research published in Circulation Research and led by the laboratory of Prof. Stephen Robinson in the University of East Anglia (UEA). The group used knockout mice in which endothelial αvβ3-integrin was specifically targeted.

In order to grow and metastasise, solid tumours rely on angiogenesis, which means recruitment of their own blood supply from the existing vasculature that surrounds them. They achieve this by release of growth factors such as vascular endothelial growth factor (VEGF). A series of steps in the angiogenic process culminates in degradation of the endothelial cell basement membrane and the extracellular matrix (ECM), with proliferation of endothelial cells and their migration towards the tumour. These last parts of the process depend on integrins such as αvβ3-integrin, which is expressed in endothelial cells that have been stimulated by angiogenic growth factors and synergises with VEGF to promote angiogenesis. As such, αvβ3-integrin has been an attractive target for anti-angiogenic therapeutic drug strategies. However, the effectiveness of this integrin as a cancer drug target has been called into question by the failure of the αvβ3-integrin peptide antagonist Cilengitide to increase overall survival when administered along with standard chemotherapy in patients with aggressive brain cancer.

The study from UEA focused on knockout specifically of endothelial αvβ3-integrin, unlike previous studies which have adopted a global knockout approach. In these mice, the researchers found that the depletion of the endothelial αvβ3-integrin inhibited tumour growth and angiogenesis in a preventative manner but not in tumours that were already established. Similarly to the results obtained in the disappointing clinical trials, the protective effects were transient. The researchers hypothesised that other molecular changes that occurred from long-term αvβ3-integrin depletion, such as reduction in focal adhesion kinase (FAK) expression may provide an escape route from the inhibition of angiogenesis achieved initially by αvβ3-integrin-inhibition.

The researchers conclude that our current understanding of the best way to target anti- αvβ3-integrin reagents is too limited to allow this integrin to be abandoned as a potential tumour therapeutic target. This is especially in view of the fact that, unlike many other FDA-approved anti-angiogenic drugs, αvβ3-integrin antagonists are well-tolerated. Further studies are needed to establish better ways of using these antagonists in terms of timing of delivery to achieve prevention rather than using in an interventional regime and in terms of exploiting nanotechnology to allow endothelial targeting. The future may not be so bleak for anti- αvβ3-integrin reagents as possible cancer drugs.

Sources

Steri, V. Ellison, T.S., Gontarczyk, A.M., Weilbaecher, K., Schneider, J.G., Edwards, D., Fruttiger, M., Hodivala-Dilke, K.M. and Robinson, S.D. Acute Depletion of Endothelial beta3-Integrin Transiently Inhibits Tumour Growth and Angiogenesis in Mice. Circulation Research, January 2014. Epub Oct. 2013, PMID: 24103390

University of East Anglia. "Scientists make advance in cancer research." ScienceDaily, 3 Jan. 2014. [Accessed 6 Jan. 2014].

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