What is the difficulty of identifying or diagnosing diseases caused by E.Coli using the 16S rRNA sequencing technique??
molecular diagnosis of bacteria
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New mutations discovered in the MC4R "obesity gene"
A recent study on the genetics of obesity found novel variants in the MC4R gene promoter region in a population of obese children. To characterize the functional roles of these naturally-occurring DNA mutations, the researchers used GenScript's mutagenesis service to produce variant constructs for reporter gene assays. They found the mutant promoters have decreased basal transcriptional activity, suggesting that MC4R may be a valuable diagnostic or therapeutic target in future efforts to combat the raging epidemic of obesity-related disease.
With advances in genome sequencing and personalized medicine, it’s more critical than ever to understand how genetic variants actually influence physiology and disease etiology. GenScript is the leading provider of custom molecular biology services to accelerate your findings by delivering the DNA constructs you need, without the limitations and headaches of traditional PCR-based manipulation of pre-existing templates.
my orignal
With advances in genome sequencing and personalized medicine, it’s more critical than ever to understand how genetic variants actually influence physiology and disease etiology. GenScript is the leading provider of custom molecular biology services to accelerate your findings by delivering the DNA constructs you need, without the limitations and headaches of traditional PCR-based manipulation of pre-existing templates.
my orignal
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Salary for QA/QC positions
Hi,
I'm trying to find entry-level salaries for QA/QC positions and I am having difficulty.
Does anyone know the typical starting salaries?
Specifically, I am looking in MD and have a M.S.
Thanks!
I'm trying to find entry-level salaries for QA/QC positions and I am having difficulty.
Does anyone know the typical starting salaries?
Specifically, I am looking in MD and have a M.S.
Thanks!
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Carriers of a loss-of-function mutation for ZnT8, a zinc transporter,
A new study in Nature Genetics* shows, for the first time, that a loss-of-function mutation may be beneficial in preventing type 2 diabetes (T2D). This study included analyzing the genotype of ~150,000 individuals from diverse ancestry groups and found that carriers with rare protein-truncating variants in SLC30A8, which encodes islet zinc transporter (ZnT8), have a 65% reduction in type 2 diabetes risk.
The implication from this study uncovers a target and a pathway of treating T2D: selective inhibitors of ZnT8 may alleviate glucose intolerance with potentially minimal or no side effects. There are a number of ways to pursue antagonists for ZnT8, and GenScript can provide relevant services to explore them!
? Single domain antibodies (sdAb)
? Peptide library screening followed by peptibody construction to extend half-life in serum
? Cell therapy via genome editing technology such as CRISPR
? Assay development for small-molecule library screening
Common mouse models are unsuitable for in-vivo evaluation of therapeutic leads or candidates, because of the difference in physiology between mouse and human pancreatic tissue. Via collaboration, GenScript is open to collaborations of investigating humanized mouse carrying human pancreas tissue as a potentially efficacy model.
aritcle source :* Flannick J. et al. Loss-of-function mutations in SLC30A8 protect against type 2 diabetes. Nat. Gen. 2014.
![.jpg]()
peptide_libraries_02.jpg (Size: 95.1 KB / Downloads: 6)
The implication from this study uncovers a target and a pathway of treating T2D: selective inhibitors of ZnT8 may alleviate glucose intolerance with potentially minimal or no side effects. There are a number of ways to pursue antagonists for ZnT8, and GenScript can provide relevant services to explore them!
? Single domain antibodies (sdAb)
? Peptide library screening followed by peptibody construction to extend half-life in serum
? Cell therapy via genome editing technology such as CRISPR
? Assay development for small-molecule library screening
Common mouse models are unsuitable for in-vivo evaluation of therapeutic leads or candidates, because of the difference in physiology between mouse and human pancreatic tissue. Via collaboration, GenScript is open to collaborations of investigating humanized mouse carrying human pancreas tissue as a potentially efficacy model.
aritcle source :* Flannick J. et al. Loss-of-function mutations in SLC30A8 protect against type 2 diabetes. Nat. Gen. 2014.
peptide_libraries_02.jpg (Size: 95.1 KB / Downloads: 6)
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Colorectal cancer: the two faces of p38 could MAP the way to new therapies
Colorectal cancer now ranks second in causing cancer deaths globally. New research from researchers in the Institute for Research in Biomedicine (IRB) in Barcelona suggests that an enzyme called p38, part of the MAP kinase family of proteins, has a dual role in colorectal cancer that could be exploited in future combination therapies. On the one hand, p38 contributes to intestinal barrier integrity, helping to keep out toxins and pathogens that could contribute to inflammation and tumour formation. On the other hand, once tumours have developed, p38 contributes to their growth and proliferation. The study is published online this week in the journal Cancer Cell.
MAP kinases are involved in relaying messages from outside the cell to the inside, thereby instructing the cell to make key decisions by controlling the activation or switching off of other proteins. P38 is a member of this family expressed in all cells of the body but with diverse functions depending on location or disease state. One of the roles of p38 is in inflammatory responses. It is well accepted that gastrointestinal inflammatory conditions such as Crohn’s disease is associated with increased risk of colorectal cancer. This link between inflammation and colorectal cancer prompted interest in dissecting the role of p38.
In the study, the researchers created mouse models of colorectal cancer and gastrointestinal inflammation. In one set of experiments, p38 gene expression was knocked down in epithelial cells forming the intestinal barrier and then the mice were subjected to tumour-inducing treatments. The mice that lacked p38 developed double the number of tumours than the p38-expressing mice. This indicates a crucial role for p38 in maintenance of the integrity of the gastrointestinal barrier which is protective against agents such as toxins and pathogens. This would be protective against tumour development.
However, in another arm of the study, the researchers studied mice that already had tumours and found another face of p38. They administered a p38 inhibitor to some mice and compared them to untreated mice. In the mice treated with p38 inhibitor, the tumours became substantially smaller. This suggests that in a scenario where cancer has developed, p38 contributes to tumour growth and proliferation.
The tumour-reducing capacity of p38 could be exploited in therapies for colorectal cancer but the use would have to be balanced by mindfulness of the protective role of p38 on intestinal barriers. Dr Angel R. Nebreda, senior author on the paper said: "p38 inhibitors may have clinical applications, but probably—and this forms part of the medicine of the future—these will be in combination with other drugs. We are trying to find out what p38 inhibitors should be combined with to make the tumour, which is now smaller, finally disappear." Meanwhile first author Dr Jalaj Gupta cautions: "Our study highlights the complexity of p38 functions, both in cancer and in the normal maintenance of tissues, and shows why an inhibitor of this molecule could effectively have undesirable side effects. This is why it is necessary to study in depth the patients and contexts in which treatment with such inhibitors would be suitable."
The two faces of p38 need to be considered in application to therapies in the future but the molecule shows promise as an effective target for reducing tumour size in preparation for surgical removal of tumours.
Sources
Dual function of p38alpha MAPK in colon cancer: suppression of colitis-associated tumor initiation but requirement for cancer cell survival. Jalaj Gupta, Ivan del Barco Barrantes, Ana Igea, Stratigoula Sakellariou, Ioannis S. Pateras, Vassilis G. Gorgoulis and Angel R. Nebreda. Cancer Cell (2014) http://dx.doi.org/10.1016/j.ccr.2014.02.019
Press release: Institute for Research in Biomedicine (IRB Barcelona), available at: http://www.eurekalert.org/pub_releases/2...032714.php
MAP kinases are involved in relaying messages from outside the cell to the inside, thereby instructing the cell to make key decisions by controlling the activation or switching off of other proteins. P38 is a member of this family expressed in all cells of the body but with diverse functions depending on location or disease state. One of the roles of p38 is in inflammatory responses. It is well accepted that gastrointestinal inflammatory conditions such as Crohn’s disease is associated with increased risk of colorectal cancer. This link between inflammation and colorectal cancer prompted interest in dissecting the role of p38.
In the study, the researchers created mouse models of colorectal cancer and gastrointestinal inflammation. In one set of experiments, p38 gene expression was knocked down in epithelial cells forming the intestinal barrier and then the mice were subjected to tumour-inducing treatments. The mice that lacked p38 developed double the number of tumours than the p38-expressing mice. This indicates a crucial role for p38 in maintenance of the integrity of the gastrointestinal barrier which is protective against agents such as toxins and pathogens. This would be protective against tumour development.
However, in another arm of the study, the researchers studied mice that already had tumours and found another face of p38. They administered a p38 inhibitor to some mice and compared them to untreated mice. In the mice treated with p38 inhibitor, the tumours became substantially smaller. This suggests that in a scenario where cancer has developed, p38 contributes to tumour growth and proliferation.
The tumour-reducing capacity of p38 could be exploited in therapies for colorectal cancer but the use would have to be balanced by mindfulness of the protective role of p38 on intestinal barriers. Dr Angel R. Nebreda, senior author on the paper said: "p38 inhibitors may have clinical applications, but probably—and this forms part of the medicine of the future—these will be in combination with other drugs. We are trying to find out what p38 inhibitors should be combined with to make the tumour, which is now smaller, finally disappear." Meanwhile first author Dr Jalaj Gupta cautions: "Our study highlights the complexity of p38 functions, both in cancer and in the normal maintenance of tissues, and shows why an inhibitor of this molecule could effectively have undesirable side effects. This is why it is necessary to study in depth the patients and contexts in which treatment with such inhibitors would be suitable."
The two faces of p38 need to be considered in application to therapies in the future but the molecule shows promise as an effective target for reducing tumour size in preparation for surgical removal of tumours.
Sources
Dual function of p38alpha MAPK in colon cancer: suppression of colitis-associated tumor initiation but requirement for cancer cell survival. Jalaj Gupta, Ivan del Barco Barrantes, Ana Igea, Stratigoula Sakellariou, Ioannis S. Pateras, Vassilis G. Gorgoulis and Angel R. Nebreda. Cancer Cell (2014) http://dx.doi.org/10.1016/j.ccr.2014.02.019
Press release: Institute for Research in Biomedicine (IRB Barcelona), available at: http://www.eurekalert.org/pub_releases/2...032714.php
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GATE Advice to Low Scorers
Hi all,
Lately, I have been receiving mails from many of the members of biotechnologyforums (India) to shed some tips on procuring a seat in IITs. Well, I'm sorry for the delay, (was over occupied with my new job), but here I'm!
As, I said in my Previous Post it's very easy to crack GATE and it's really easy to get a seat too, only if you do it the right way.
Just keep a note of following things if you have cracked GATE:
1. If your GATE score/marks are just touching the cut-off (i.e marginally above the cut-off), apply at:
CTARA (Center for Technology Alternatives for Rural Areas) at IIT Bombay and CRDT IIT Delhi (You'll definitely get a call).
2. If you are at 90 percentile (or around 93 percentile): 1st of all apply at NUS! It's much better than IITs! Then, consider applying at :
Department of Pulp and Paper Technology IIT Roorkee
Environmental Engineering IIT Roorkee
Goes without saying for CTARA and CRDT
3. If you are above 95 percentile apply at:
IIT Guwahati (all departments you are eligible for)
IIT Delhi Chemical Engineering
IIT Madras Biochemical/Biotech (though it varies between 95-97 percentile as cut-off)
IIT Delhi Atmospheric Sc.
IIT Kanpur Environmental
IIT Kharagpur (apply all departments you are eligible for)
Goes without saying for NUS, IIT Roorkee, CTARA and CRDT
4. Above 98 percentile but below 99 percentile you WILL NOT GET CALL from only the following:
IIT Kanpur Biomedical
IIT Bombay Biomedical
IIT Delhi Biochemical
Once you get a call, it's all about being crystal clear of your concepts and confidence during interview (your GATE score matters least there). You can make it or you may mar it, it's all upto "the way you act (during applying for IITs and during interview equally".
Hope it solves some confusions.
Let me know if I can help in some other way(s).
Cheers!
Sunil
Lately, I have been receiving mails from many of the members of biotechnologyforums (India) to shed some tips on procuring a seat in IITs. Well, I'm sorry for the delay, (was over occupied with my new job), but here I'm!
As, I said in my Previous Post it's very easy to crack GATE and it's really easy to get a seat too, only if you do it the right way.
Just keep a note of following things if you have cracked GATE:
1. If your GATE score/marks are just touching the cut-off (i.e marginally above the cut-off), apply at:
CTARA (Center for Technology Alternatives for Rural Areas) at IIT Bombay and CRDT IIT Delhi (You'll definitely get a call).
2. If you are at 90 percentile (or around 93 percentile): 1st of all apply at NUS! It's much better than IITs! Then, consider applying at :
Department of Pulp and Paper Technology IIT Roorkee
Environmental Engineering IIT Roorkee
Goes without saying for CTARA and CRDT
3. If you are above 95 percentile apply at:
IIT Guwahati (all departments you are eligible for)
IIT Delhi Chemical Engineering
IIT Madras Biochemical/Biotech (though it varies between 95-97 percentile as cut-off)
IIT Delhi Atmospheric Sc.
IIT Kanpur Environmental
IIT Kharagpur (apply all departments you are eligible for)
Goes without saying for NUS, IIT Roorkee, CTARA and CRDT
4. Above 98 percentile but below 99 percentile you WILL NOT GET CALL from only the following:
IIT Kanpur Biomedical
IIT Bombay Biomedical
IIT Delhi Biochemical
Once you get a call, it's all about being crystal clear of your concepts and confidence during interview (your GATE score matters least there). You can make it or you may mar it, it's all upto "the way you act (during applying for IITs and during interview equally".
Hope it solves some confusions.
Let me know if I can help in some other way(s).
Cheers!
Sunil
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Difference between Adaptor and Scaffold protein
What is the difference between and scaffold protein??
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AAPS National Biotechnology Conference | May 19-21 | San Diego
Organisers: American Association of Pharmaceutical Scientists
Dates: May 19th- 21st 2014
Location: Sheraton San Diego Hotel and Marina, San Diego
Website: http://www.aaps.org/nationalbiotech/
The website gives all the necessary information on conference agenda, hotel, exhibitions and other important facts. The conference brochure including preliminary programme is attached.
Conference Theme
One Conference: Four Themes
• Biomanufacturing
• Biomarker and PK/PD
• Research and Discovery
• Immunogenicity and Administration Routes
Both theory and application will be considered from different perspectives including discovery, development, engineering, and regulatory aspects. Short courses, open forums and hot topics will be featured in the programme. A link to the programme is available here: http://www.aaps.org/NBCProgram/
Short courses:
• Short Course 1—Manufacturing Facilities of the Future
• Short Course 2—Design of FIH Studies for Biotherapeutics
• Short Course 3—Process Validation for Biologic Drug Products: What Is Different than Before?
Open forums:
• Biotec Open Forum—Challenges to Develop and Validate Clinical ADA and/or NAB Assays to Not Your Typical Biologics
• Biotec Open Forum—The Science of Particulate Material in Biopharmaceuticals
• Biotec Open Forum—Open Debate—PK and ADA Bioanalysis of Biosimilar Compounds
• FDD Open Forum—New Developments in Container-Closures and Delivery Devices for Biopharmaceuticals
Important dates:
Early bird registration deadline: 4th April 2014
Presenting author registration deadline: 4th April 2014
Notification of presentation schedule/poster number: 9th April 2014
Plenary Speakers:
Kári Stefánsson, Ph.D, president, chairman, CEO, and co-founder of deCODE Genetics, Iceland
Victoria Hale, Ph.D., founder of Medicines360, USA
Peter G. Schultz, Ph.D, Scripps Institute
Dates: May 19th- 21st 2014
Location: Sheraton San Diego Hotel and Marina, San Diego
Website: http://www.aaps.org/nationalbiotech/
The website gives all the necessary information on conference agenda, hotel, exhibitions and other important facts. The conference brochure including preliminary programme is attached.
Conference Theme
One Conference: Four Themes
• Biomanufacturing
• Biomarker and PK/PD
• Research and Discovery
• Immunogenicity and Administration Routes
Both theory and application will be considered from different perspectives including discovery, development, engineering, and regulatory aspects. Short courses, open forums and hot topics will be featured in the programme. A link to the programme is available here: http://www.aaps.org/NBCProgram/
Short courses:
• Short Course 1—Manufacturing Facilities of the Future
• Short Course 2—Design of FIH Studies for Biotherapeutics
• Short Course 3—Process Validation for Biologic Drug Products: What Is Different than Before?
Open forums:
• Biotec Open Forum—Challenges to Develop and Validate Clinical ADA and/or NAB Assays to Not Your Typical Biologics
• Biotec Open Forum—The Science of Particulate Material in Biopharmaceuticals
• Biotec Open Forum—Open Debate—PK and ADA Bioanalysis of Biosimilar Compounds
• FDD Open Forum—New Developments in Container-Closures and Delivery Devices for Biopharmaceuticals
Important dates:
Early bird registration deadline: 4th April 2014
Presenting author registration deadline: 4th April 2014
Notification of presentation schedule/poster number: 9th April 2014
Plenary Speakers:
Kári Stefánsson, Ph.D, president, chairman, CEO, and co-founder of deCODE Genetics, Iceland
Victoria Hale, Ph.D., founder of Medicines360, USA
Peter G. Schultz, Ph.D, Scripps Institute
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Request for career advice.
Hey,
I am zeeshan, an engineer with biotech specialiazation. I qualified the GATE 2014 exam with AIR 277, gate score 563 and 98 percentile. I wanted career advice from people in our field.
I am very interested in bioprocess engineering, taking things from lab scale to industrial scale![Smile]( "Smile")
.. I have read the sticky posts and have already applied to IITD(MS biochem),IITM(MS Biotech), IIT kgp(Biotech).. I am facing a problem with IITB as they have Biotechnology & BioSystems Engineering in chemical department and I am unable to apply for it as my BE was in Biotech..
My questions are
1.Which other colleges are good at Bioprocess Engineering that i can apply to?
2.Should i apply for phd's?.. Its a common advise from elders..
3.Also how is the market for Bioprocess engineers and can i look for enterpreneurship options after my MS/M.tech/PhD?
Thank you for your time
Regards
Zeeshan.
I am zeeshan, an engineer with biotech specialiazation. I qualified the GATE 2014 exam with AIR 277, gate score 563 and 98 percentile. I wanted career advice from people in our field.
I am very interested in bioprocess engineering, taking things from lab scale to industrial scale
.. I have read the sticky posts and have already applied to IITD(MS biochem),IITM(MS Biotech), IIT kgp(Biotech).. I am facing a problem with IITB as they have Biotechnology & BioSystems Engineering in chemical department and I am unable to apply for it as my BE was in Biotech.. My questions are
1.Which other colleges are good at Bioprocess Engineering that i can apply to?
2.Should i apply for phd's?.. Its a common advise from elders..
3.Also how is the market for Bioprocess engineers and can i look for enterpreneurship options after my MS/M.tech/PhD?
Thank you for your time
Regards
Zeeshan.
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Stem cell self-renewal and differentiation: hydrogelling together
One of the main barriers to stem cell therapy and regenerative medicine is the lack of a system which allows both self-renewal of stem cells and differentiation of the cells into specific cell types with specialised roles, in the same material environment. The culturing conditions required for self-renewal versus differentiation differ and up until now there has not been a system available that allows both processes to be carried out. In a new study published in PNAS, researchers from the University of Nottingham describe a hydrogel-based system with a simple chemical switch mechanism that overcomes these difficulties.
Regenerative medicine is a rapidly developing field underpinned by advances in biotechnology aimed at, for example, enhancing long-term survival of stem cells and their differentiation in vivo. In previous threads in this forum we have described new research in this field, for example the use of nanoparticles to deliver trophic factor mimetics to transplanted embryonic stem cells in animal models (http://www.biotechnologyforums.com/thread-2558.html). The current study addresses the issue of developing a practical, single system supporting both stem cell renewal and differentiation to specific cell types as a step towards mass production of fully differentiated tissues. The potential for this is of major importance in advancing regenerative medicine use in repair of human tissue and in maintenance of organ function win people with chronic or age-related diseases.
The researchers built on previous work in which they had used an alginate hydrogel system to promote self-renewal of stem cells. They introduced collagen into the alginate gel; collagen is used to make an extracellular matrix hydrogel which allows adhesion of stem cells and differentiation into specific cell types.
The innovation in this system was the introduction of a simple chemical switch, based on chelation of calcium ions, which resulted in conversion of the environment from alginate-dominated to collagen-dominated. On checking the cells after the switch by methods including confocal microscopy and PCR for biomarkers of stem cells or of differentiation, the researchers were able to confirm that the switch resulted in significant differentiation of the stem cells from the self-renewing profile observed in alginate-dominated hydrogel. The switch could be timed to generate cells of different stages in cell lineage and the efficiency of differentiation could be further improved by changes to the culture medium. The efficacy of the system was further confirmed by its use to generate terminally differentiated cardiomyocytes (heart cells).
Senior author on the paper, Prof. Kevin Shakesheff, said: “Our new combination of hydrogels is a first. It allows dense tissue structures to be produced from human pluripotent stem cells (HPSC) in a single step process never achieved before. The discovery has important implications for the future of manufacturing in regenerative medicine. This field of healthcare is a major priority for the UK and we are seeing increasing investment in future manufacturing processes to ensure we are ready to deliver real treatments to patients when HPSC products and treatments go to trial and become standard.”
Sources:
Dixon, J.E., Shah, D.A., Rogers, C., Hall, S., Weston, N., Parmenter, C.D.J., McNally, D., Denning, C. and Shakesheff, K.M. (2014). Combined hydrogels that switch human pluripotent stem cells from self-renewal to differentiation. PNAS 2014 : 1319685111v1-201319685. Published online before print March 27, 2014, doi: 10.1073/pnas.1319685111; PNAS March 27, 2014
Press release: University of Nottingham; available at http://www.nottingham.ac.uk/news/pressre...ology.aspx
Regenerative medicine is a rapidly developing field underpinned by advances in biotechnology aimed at, for example, enhancing long-term survival of stem cells and their differentiation in vivo. In previous threads in this forum we have described new research in this field, for example the use of nanoparticles to deliver trophic factor mimetics to transplanted embryonic stem cells in animal models (http://www.biotechnologyforums.com/thread-2558.html). The current study addresses the issue of developing a practical, single system supporting both stem cell renewal and differentiation to specific cell types as a step towards mass production of fully differentiated tissues. The potential for this is of major importance in advancing regenerative medicine use in repair of human tissue and in maintenance of organ function win people with chronic or age-related diseases.
The researchers built on previous work in which they had used an alginate hydrogel system to promote self-renewal of stem cells. They introduced collagen into the alginate gel; collagen is used to make an extracellular matrix hydrogel which allows adhesion of stem cells and differentiation into specific cell types.
The innovation in this system was the introduction of a simple chemical switch, based on chelation of calcium ions, which resulted in conversion of the environment from alginate-dominated to collagen-dominated. On checking the cells after the switch by methods including confocal microscopy and PCR for biomarkers of stem cells or of differentiation, the researchers were able to confirm that the switch resulted in significant differentiation of the stem cells from the self-renewing profile observed in alginate-dominated hydrogel. The switch could be timed to generate cells of different stages in cell lineage and the efficiency of differentiation could be further improved by changes to the culture medium. The efficacy of the system was further confirmed by its use to generate terminally differentiated cardiomyocytes (heart cells).
Senior author on the paper, Prof. Kevin Shakesheff, said: “Our new combination of hydrogels is a first. It allows dense tissue structures to be produced from human pluripotent stem cells (HPSC) in a single step process never achieved before. The discovery has important implications for the future of manufacturing in regenerative medicine. This field of healthcare is a major priority for the UK and we are seeing increasing investment in future manufacturing processes to ensure we are ready to deliver real treatments to patients when HPSC products and treatments go to trial and become standard.”
Sources:
Dixon, J.E., Shah, D.A., Rogers, C., Hall, S., Weston, N., Parmenter, C.D.J., McNally, D., Denning, C. and Shakesheff, K.M. (2014). Combined hydrogels that switch human pluripotent stem cells from self-renewal to differentiation. PNAS 2014 : 1319685111v1-201319685. Published online before print March 27, 2014, doi: 10.1073/pnas.1319685111; PNAS March 27, 2014
Press release: University of Nottingham; available at http://www.nottingham.ac.uk/news/pressre...ology.aspx
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Entire skull replaced by 3D printed copy
The continuing development of 3-D printing technology in biomedicine has been further demonstrated by doctors in the University Medical Center in Utrecht in the Netherlands who have recently carried out the first skull transplant using parts that were generated from a 3-D printer. The procedure was carried out on a young woman who had been suffering from a condition whereby extra bone grew on the inside of her skull, exerting severe pressure on her brain. Before the procedure, the woman had been experiencing severe headaches and was suffering negative effects on her eyesight and coordination.
The doctors worked with an Australian 3D printing firm called Anatomics. The first step was to take CT scans of the woman’s skull and then print out an acrylic copy, which was modified to remove the excess growth. Surgeons then removed most of the woman’s cranium and replaced it with the printed copy. While surgical procedures to remove parts of the skull in cases of severe cranial swelling are not unusual, removal and implantation of an entire skull had not been attempted before.
The chief surgeons in this procedure, were Dr Bon Verweij and Dr Marvick Muradin. Dr Verweij explained that previously implants have been created in the operating theatre using a type of cement, but these types of implants have issues with, for example, poor fit. He went on to say: "Now, these parts can be precisely created using 3D printing. This not only offers large cosmetic benefits, but patients often have better brain function compared to the old method."
The efficacy of the procedure in this case is attested to by the fact that three months later the young woman is now back at work and suffering no ill effects or any visible scarring. Her eyesight has been fully restored.
Sources:
http://www.ibtimes.co.uk/3d-printed-skul...nt-1441924
http://www.theregister.co.uk/2014/03/29/...stic_copy/
The doctors worked with an Australian 3D printing firm called Anatomics. The first step was to take CT scans of the woman’s skull and then print out an acrylic copy, which was modified to remove the excess growth. Surgeons then removed most of the woman’s cranium and replaced it with the printed copy. While surgical procedures to remove parts of the skull in cases of severe cranial swelling are not unusual, removal and implantation of an entire skull had not been attempted before.
The chief surgeons in this procedure, were Dr Bon Verweij and Dr Marvick Muradin. Dr Verweij explained that previously implants have been created in the operating theatre using a type of cement, but these types of implants have issues with, for example, poor fit. He went on to say: "Now, these parts can be precisely created using 3D printing. This not only offers large cosmetic benefits, but patients often have better brain function compared to the old method."
The efficacy of the procedure in this case is attested to by the fact that three months later the young woman is now back at work and suffering no ill effects or any visible scarring. Her eyesight has been fully restored.
Sources:
http://www.ibtimes.co.uk/3d-printed-skul...nt-1441924
http://www.theregister.co.uk/2014/03/29/...stic_copy/
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Nerve regeneration after central nervous system injury: Hope for the future
A spinal cord injury or brain trauma often spells disaster for victims due to failure of central nervous system (CNS) nerve cells to regenerate axons, the nerve fibres that project from nerve cells and are essential for relaying information to other nerve cells. However, a new study from researchers in Imperial College London in the UK and the Hertie Institute in the University of Tuebingen in Germany may hold out hope for the future. In the study, published today in the journal Nature Communications, the researchers contrasted the inability of CNS nerves to regenerate to the situation in the peripheral nervous system (PNS). Injury to the PNS results in initiation of a programme of coordinated gene expression resulting in substantial nerve fibre regeneration. In the study, a protein called histone acetyltransferase p300/CBP-associated factor (PCAF) was identified as key to the PNS regeneration programme. When administered to mice with CNS injury, PCAF promoted significant nerve fibre regeneration.
The researchers used both in vivo mouse models and in vitro cell culture models to study the responses of a type of neuron known as a dorsal root ganglion to both CNS and PNS damage. Epigenetic changes in genes were focused on, i.e. alterations to gene activity caused by mechanisms that do not change the sequence of DNA. These are often chemical modifications such as acetylation or methylation. The researchers were interested in how in the PNS, damaged nerves are able to send ‘retrograde’ signals back to the cell body to instruct the cell to initiate epigenetic changes responsible for nerve regeneration.
The results showed that PCAF is central to this process as it promotes acetylation modifications at the promoters of established key regeneration-associated genes. However, this occurs only following a peripheral axonal injury, not a central nervous system injury. Importantly, injection of PCAF into mice with central nervous system damage resulted in a significant increase in nerve fibre re-growth.
Lead author on the study, Professor Simone Di Giovanni of Imperial College London explained the potential significance of this study for victims of central nervous system injuries when he said: "The results suggest that we may be able to target specific chemical changes to enhance the growth of nerves after injury to the central nervous system….The ultimate goal could be to develop a pharmaceutical method to trigger the nerves to grow and repair and to see some level of recovery in patients. We are excited about the potential of this work but the findings are preliminary.
Professor Di Giovanni added: "The next step is to see whether we can bring about some form of recovery of movement and function in mice after we have stimulated nerve growth through the mechanism we have identified. If this is successful, then there could be a move towards developing a drug and running clinical trials with people. We hope that our new work could one day help people to recover feeling and movement, but there are many hurdles to overcome first."
Sources:
R. Puttagunta et al. 'PCAF-dependent epigenetic changes promote axonal regeneration in the central nervous system', Nature Communications (2014), doi: 10.1038/n-comms4527
Press release: Imperial College London; available at http://www.eurekalert.org/pub_releases/2...033114.php
The researchers used both in vivo mouse models and in vitro cell culture models to study the responses of a type of neuron known as a dorsal root ganglion to both CNS and PNS damage. Epigenetic changes in genes were focused on, i.e. alterations to gene activity caused by mechanisms that do not change the sequence of DNA. These are often chemical modifications such as acetylation or methylation. The researchers were interested in how in the PNS, damaged nerves are able to send ‘retrograde’ signals back to the cell body to instruct the cell to initiate epigenetic changes responsible for nerve regeneration.
The results showed that PCAF is central to this process as it promotes acetylation modifications at the promoters of established key regeneration-associated genes. However, this occurs only following a peripheral axonal injury, not a central nervous system injury. Importantly, injection of PCAF into mice with central nervous system damage resulted in a significant increase in nerve fibre re-growth.
Lead author on the study, Professor Simone Di Giovanni of Imperial College London explained the potential significance of this study for victims of central nervous system injuries when he said: "The results suggest that we may be able to target specific chemical changes to enhance the growth of nerves after injury to the central nervous system….The ultimate goal could be to develop a pharmaceutical method to trigger the nerves to grow and repair and to see some level of recovery in patients. We are excited about the potential of this work but the findings are preliminary.
Professor Di Giovanni added: "The next step is to see whether we can bring about some form of recovery of movement and function in mice after we have stimulated nerve growth through the mechanism we have identified. If this is successful, then there could be a move towards developing a drug and running clinical trials with people. We hope that our new work could one day help people to recover feeling and movement, but there are many hurdles to overcome first."
Sources:
R. Puttagunta et al. 'PCAF-dependent epigenetic changes promote axonal regeneration in the central nervous system', Nature Communications (2014), doi: 10.1038/n-comms4527
Press release: Imperial College London; available at http://www.eurekalert.org/pub_releases/2...033114.php
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3rd Max Planck Freiburg Epigenetics Meeting | December 3-5 2014 | Freiburg, Germany
3rd Max Planck Freiburg Epigenetics Meeting
Organisers: Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
Dates: December 3rd – 5th 2014
Location: Max Planck Institute of Immunobiology and Epigenetics
Website: http://events.ie-freiburg.mpg.de/
The website gives all the necessary information on conference agenda, hotel, exhibitions and other important facts.
About the conference:
Registration opens today for the 3rd Max Planck Freiburg Epigenetics Meeting to be held in the Max Planck Institute of Immunobiology and Epigenetics in December. A broad range of topics in the field of chromatin and epigenetics will be explored in the international conference. The programme includes both invited and selected talks along with poster presentations.
Important dates:
Registration: 1st April 2014 to 31st August 2014.
Notification of acceptance for the meeting: 30th September 2014.
Deadline for payment: 15th October 2014
Confirmed speakers:
An international line-up of eminent speakers have been confirmed:
KAREN ADELMAN; NIEHS/NIH North Carolina
Title: “Interplay between promoter-associated Pol II and chromatin structure”
DEBORAH BOURC'HIS; Institut Curie, Paris
Title: "A new model of dynamic genomic imprinting in mammals"
BRADLEY CAIRNS; Huntsman Cancer Institute, University of Utah
Title:"Epigenetic states and reprogramming of zebrafisch gametes and early embryos"
CHRISTINE DISTECHE; UW Medicine Pathology, Seattle
Title: TBA
PETER FRASER; The Babraham Institute, Cambridge
Title: TBA
EILEEN FURLONG; EMBL, Heidelberg
Title: “Temporal regulation of development enhancers: It’s all in the timing”
SUSAN GASSER; Friedrich Miescher Institute, Basel
Title: "Sequestering heterochromatin during development: how and why"
JOOST GRIBNAU; Erasmus MC, Rotterdam
Title: TBA
KONRAD HOCHEDLINGER; HMS Massachusetts General Hospital
Title: TBA
SAADI KHOCHBIN; Institut Albert Bonniot, Grenoble
Title: "Molecular basis of post-melotic male genome programming"
ROBERT KINGSTON; Massachusetts General Hospital
Title: "Nucleosomes and lncRNas as components of epigenetic regulation"
TONY KOUZARIDES; The Gurdon Institute, Cambridge
Title: TBA
MATTHIAS MERKENSCHLAGER; MRC London
Title: TBA
ERIC MISKA; The Gurdon Institute, Cambridge
Title: "Social RNA making an (epigenetic) mark"
VINCENZO PIRROTTA; Rutgers University, New Jersey
Title: "Global mechanisms regulating access to genomic DNA and their implications"
ANJANA RAO; La Jolla Institute, California
Title: "TET proteins and methylcytosine oxidation"
DANNY REINBERG; NYU Langone MC, New York
Title: TBA
BING REN; University of California School of Medicine, San Diego
Title: TBA
HIROYUKI SASAKI; Kyushu University
Title: "Mouse germ cell methylomes and small RNAs"
DIRK SCHÜBELER; Friedrich Miescher Institute, Basel
Title: TBA
RAMIN SHIEKHATTAR; Wistar Institute, Philadelphia
Title: "Epigenetics and noncoding RNAs in health and disease"
MARIA ELENA TORRES PADILLA; IGBMC, Strasbourg
Title: "Epigenetic mechanisms in early mammalian development"
BAS VAN STEENSEL; The Netherlands Cancer Institute, Amsterdam
Title: "Genomics technologies to study chromatin organization"
JERRY WORKMAN; Stowers Institute, Kansas City
Title: TBA
Organisers: Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany
Dates: December 3rd – 5th 2014
Location: Max Planck Institute of Immunobiology and Epigenetics
Website: http://events.ie-freiburg.mpg.de/
The website gives all the necessary information on conference agenda, hotel, exhibitions and other important facts.
About the conference:
Registration opens today for the 3rd Max Planck Freiburg Epigenetics Meeting to be held in the Max Planck Institute of Immunobiology and Epigenetics in December. A broad range of topics in the field of chromatin and epigenetics will be explored in the international conference. The programme includes both invited and selected talks along with poster presentations.
Important dates:
Registration: 1st April 2014 to 31st August 2014.
Notification of acceptance for the meeting: 30th September 2014.
Deadline for payment: 15th October 2014
Confirmed speakers:
An international line-up of eminent speakers have been confirmed:
KAREN ADELMAN; NIEHS/NIH North Carolina
Title: “Interplay between promoter-associated Pol II and chromatin structure”
DEBORAH BOURC'HIS; Institut Curie, Paris
Title: "A new model of dynamic genomic imprinting in mammals"
BRADLEY CAIRNS; Huntsman Cancer Institute, University of Utah
Title:"Epigenetic states and reprogramming of zebrafisch gametes and early embryos"
CHRISTINE DISTECHE; UW Medicine Pathology, Seattle
Title: TBA
PETER FRASER; The Babraham Institute, Cambridge
Title: TBA
EILEEN FURLONG; EMBL, Heidelberg
Title: “Temporal regulation of development enhancers: It’s all in the timing”
SUSAN GASSER; Friedrich Miescher Institute, Basel
Title: "Sequestering heterochromatin during development: how and why"
JOOST GRIBNAU; Erasmus MC, Rotterdam
Title: TBA
KONRAD HOCHEDLINGER; HMS Massachusetts General Hospital
Title: TBA
SAADI KHOCHBIN; Institut Albert Bonniot, Grenoble
Title: "Molecular basis of post-melotic male genome programming"
ROBERT KINGSTON; Massachusetts General Hospital
Title: "Nucleosomes and lncRNas as components of epigenetic regulation"
TONY KOUZARIDES; The Gurdon Institute, Cambridge
Title: TBA
MATTHIAS MERKENSCHLAGER; MRC London
Title: TBA
ERIC MISKA; The Gurdon Institute, Cambridge
Title: "Social RNA making an (epigenetic) mark"
VINCENZO PIRROTTA; Rutgers University, New Jersey
Title: "Global mechanisms regulating access to genomic DNA and their implications"
ANJANA RAO; La Jolla Institute, California
Title: "TET proteins and methylcytosine oxidation"
DANNY REINBERG; NYU Langone MC, New York
Title: TBA
BING REN; University of California School of Medicine, San Diego
Title: TBA
HIROYUKI SASAKI; Kyushu University
Title: "Mouse germ cell methylomes and small RNAs"
DIRK SCHÜBELER; Friedrich Miescher Institute, Basel
Title: TBA
RAMIN SHIEKHATTAR; Wistar Institute, Philadelphia
Title: "Epigenetics and noncoding RNAs in health and disease"
MARIA ELENA TORRES PADILLA; IGBMC, Strasbourg
Title: "Epigenetic mechanisms in early mammalian development"
BAS VAN STEENSEL; The Netherlands Cancer Institute, Amsterdam
Title: "Genomics technologies to study chromatin organization"
JERRY WORKMAN; Stowers Institute, Kansas City
Title: TBA
↧
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Primer designing - What are universal primers?
Can anyone tell me about primer designing? Like how does one decide which part of the genome to consider for designing primer. And what if one doesn't know the genome like in case of designing primers for 16s rRNA of new organisms, how does one decide which part of the genome is 16s rRNA and how does he design primer? What are universal primers?
↧
Obesity transmits epigenetic signals for colorectal cancer
Obesity has become so widespread in westernised countries that it has reached epidemic levels. It is associated with higher risk of multiple life-threatening diseases including cancer. Now a new study led by researchers from the National Institute of Environmental Health Sciences (NIEHS), part of NIH, suggests that obesity rather than diet is the major driver of genetic changes in the colon which can lead to colorectal cancer. The study is published online today in the journal Cell Metabolism.
Colorectal cancer is globally the third most common cancer and ranks second in causing cancer deaths. Obesity is the target of major public health campaigns worldwide but incidence keeps increasing. For example, the majority of Americans are now considered overweight or obese. Obesity is a risk factor for diseases ranging from cardiovascular disease and diabetes to cancer. The association of obesity with colorectal cancer is stronger in men than in women. In the present study, the researchers assumed that the contributing factors linking obesity and colorectal cancer would be complex and that relative effects of diet, weight gain and obesity need to be considered carefully.
The study employed a transgenic mouse model containing a human version of a gene called NAG-1 (non-steroidal anti-inflammatory drug (NSAID)-activated gene-1) and made comparisons to mice who lacked this gene. NAG-1 protects against colon cancer in other rodent studies. The researchers fed some mice in both groups a high-fat diet in which 60% of calories came from fat and some mice a low-fat diet in which 10% of calories came from diet. The NAG-1 positive mice did not gain weight on the high-fat diet while the wild type mice lacking NAG-1 became obese. This provided a method for observing relative effects of diet and obesity.
The researchers observed changes in enhancer regions of genes in colonic epithelial cells. Enhancer regions are involved in regulation of gene expression. Enhancers are influenced by a group of proteins called histones, whose activity is dependent on patterns of acetylation. Study results showed that high-fat diet could cause alterations in the histone acetylation patterns and enhancer landscape of colonic epithelial cells that resembled changes that occur in colorectal cancer. However, these changes only occurred in the wild type, obese mice not in the NAG-1, thin mice. This suggests that obesity rather than diet per se is the relevant driver of the epigenetic changes associated with development of colorectal cancer.
The next step for the research team is to find out how and why obesity drives development of colorectal cancer. They have identified fat cells as likely candidates for triggering colonic tumour growth but there are other possibilities. Dr Paul Wade, senior author on the paper, said: "Once we identify the signalling pathways and understand how the signal is transduced, we may be able to design ways to treat colorectal cancer in obese patients."
Sources:
Li R, Grimm SA, Chrysovergis K, Kosak J, Wang X, Du Y, Burkholder A, Janardhan K, Mav D, Shah R, Eling TE, Wade, PA. 2014. Obesity, rather than diet, drives epigenomic alterations in colonic epithelium resembling cancer progression. Cell Metab; doi:10.1016/j.cmet.2014.03.012 [Online 1 April 2014].
Press release: NIH/National Institute of Environmental Health Sciences; available from http://www.eurekalert.org/pub_releases/2...033114.php
Colorectal cancer is globally the third most common cancer and ranks second in causing cancer deaths. Obesity is the target of major public health campaigns worldwide but incidence keeps increasing. For example, the majority of Americans are now considered overweight or obese. Obesity is a risk factor for diseases ranging from cardiovascular disease and diabetes to cancer. The association of obesity with colorectal cancer is stronger in men than in women. In the present study, the researchers assumed that the contributing factors linking obesity and colorectal cancer would be complex and that relative effects of diet, weight gain and obesity need to be considered carefully.
The study employed a transgenic mouse model containing a human version of a gene called NAG-1 (non-steroidal anti-inflammatory drug (NSAID)-activated gene-1) and made comparisons to mice who lacked this gene. NAG-1 protects against colon cancer in other rodent studies. The researchers fed some mice in both groups a high-fat diet in which 60% of calories came from fat and some mice a low-fat diet in which 10% of calories came from diet. The NAG-1 positive mice did not gain weight on the high-fat diet while the wild type mice lacking NAG-1 became obese. This provided a method for observing relative effects of diet and obesity.
The researchers observed changes in enhancer regions of genes in colonic epithelial cells. Enhancer regions are involved in regulation of gene expression. Enhancers are influenced by a group of proteins called histones, whose activity is dependent on patterns of acetylation. Study results showed that high-fat diet could cause alterations in the histone acetylation patterns and enhancer landscape of colonic epithelial cells that resembled changes that occur in colorectal cancer. However, these changes only occurred in the wild type, obese mice not in the NAG-1, thin mice. This suggests that obesity rather than diet per se is the relevant driver of the epigenetic changes associated with development of colorectal cancer.
The next step for the research team is to find out how and why obesity drives development of colorectal cancer. They have identified fat cells as likely candidates for triggering colonic tumour growth but there are other possibilities. Dr Paul Wade, senior author on the paper, said: "Once we identify the signalling pathways and understand how the signal is transduced, we may be able to design ways to treat colorectal cancer in obese patients."
Sources:
Li R, Grimm SA, Chrysovergis K, Kosak J, Wang X, Du Y, Burkholder A, Janardhan K, Mav D, Shah R, Eling TE, Wade, PA. 2014. Obesity, rather than diet, drives epigenomic alterations in colonic epithelium resembling cancer progression. Cell Metab; doi:10.1016/j.cmet.2014.03.012 [Online 1 April 2014].
Press release: NIH/National Institute of Environmental Health Sciences; available from http://www.eurekalert.org/pub_releases/2...033114.php
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How do viruses and nanoparticle delivery vehicles get into cells?
New "viral video" captures approach and attachment of viral-like particles to live cells
The study of how viruses or nanoparticles designed to deliver therapuetics function requires knowledge of how a particle approaches and attaches to a cell membrane, enters the cell, and is subsequently trafficked within the cell. Although delivery of viral payloads to cellular machinery have been visualized, the visualization of the approach and attachment of a particle to a cell membrane has remained more elusive.
The study of how viruses or nanoparticles designed to deliver therapuetics function requires knowledge of how a particle approaches and attaches to a cell membrane, enters the cell, and is subsequently trafficked within the cell. Although delivery of viral payloads to cellular machinery have been visualized, the visualization of the approach and attachment of a particle to a cell membrane has remained more elusive.
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Age-related sleep decline is not inevitable: Clues from fruit flies
Just like many elderly humans, elderly flies experience age-related decline in sleep quality. The fruit fly Drosophila melanogaster (see accompanying figure, MPI f. Biology of Ageing/ W. Weiss) is used as a model organism in sleep studies as it also shares other features of sleep patterns with humans such as waking during the day and sleeping at night. A new study from researchers in the Max Planck Institute for Biology of Ageing in Cologne have therefore used fruit flies in a new study in which they show that dampening of nutrient sensing pathways can correct or reverse problems in sleep quality associated with ageing. The study was published on 1st April in the journal PLoS Biology.
Studies in humans have hinted at an association between diet and nutrition and sleep and a link between poor sleep quality and risk of obesity and diabetes. However, studies have tended to be small and the biological basis of the association is not clear. The current study implicates the nutrient sensing insulin/IGF (IIS) and TOR (Target of Rapamycin) signalling networks. Reduction in activity of these pathways has been previously associated with lifespan extension in both flies and mammals. Significantly the functions of these pathways are conserved among flies and humans.
The study results indicated that different elements of these pathways are involved in daytime activity versus night sleep. Author on the study Luke Tain explains: "Daytime activity and night-time sleep are thereby controlled by two different components: during the day, the neurotransmitter octopamine and the adipokinetic hormone AKH increase activity in flies. At night, on the other hand, the neurotransmitter dopamine and the kinase TOR reduce the sleep periods."
The researchers administered the TOR inhibitor rapamycin to elderly flies and found that the flies’ sleep quality improved, with longer periods of night sleep. Dr Tain says: “As a result, we were able to reverse the deterioration in sleep quality as a consequence of ageing." The next step is to examine the effects in higher organisms such as mice. The ultimate aim is to develop therapeutic agents based on these signalling networks to help reverse the problem of age-related decline in sleep quality with all its associated problems with physical and mental ill-health.
Sources:
Metaxakis A, Tain LS, Grönke S, Hendrich O, Hinze Y, Birras, U. and Partridge, L. (2014). Lowered Insulin Signalling Ameliorates Age-Related Sleep Fragmentation in Drosophila. PLoS Biol 12(4): e1001824. doi:10.1371/journal.pbio.; available at http://www.plosbiology.org/article/info:...io.1001824
Press release: Max-Planck-Gesellschaft; available at http://www.eurekalert.org/pub_releases/2...040114.php
![.jpg]()
71086_web.jpg (Size: 14.87 KB / Downloads: 3)
Studies in humans have hinted at an association between diet and nutrition and sleep and a link between poor sleep quality and risk of obesity and diabetes. However, studies have tended to be small and the biological basis of the association is not clear. The current study implicates the nutrient sensing insulin/IGF (IIS) and TOR (Target of Rapamycin) signalling networks. Reduction in activity of these pathways has been previously associated with lifespan extension in both flies and mammals. Significantly the functions of these pathways are conserved among flies and humans.
The study results indicated that different elements of these pathways are involved in daytime activity versus night sleep. Author on the study Luke Tain explains: "Daytime activity and night-time sleep are thereby controlled by two different components: during the day, the neurotransmitter octopamine and the adipokinetic hormone AKH increase activity in flies. At night, on the other hand, the neurotransmitter dopamine and the kinase TOR reduce the sleep periods."
The researchers administered the TOR inhibitor rapamycin to elderly flies and found that the flies’ sleep quality improved, with longer periods of night sleep. Dr Tain says: “As a result, we were able to reverse the deterioration in sleep quality as a consequence of ageing." The next step is to examine the effects in higher organisms such as mice. The ultimate aim is to develop therapeutic agents based on these signalling networks to help reverse the problem of age-related decline in sleep quality with all its associated problems with physical and mental ill-health.
Sources:
Metaxakis A, Tain LS, Grönke S, Hendrich O, Hinze Y, Birras, U. and Partridge, L. (2014). Lowered Insulin Signalling Ameliorates Age-Related Sleep Fragmentation in Drosophila. PLoS Biol 12(4): e1001824. doi:10.1371/journal.pbio.; available at http://www.plosbiology.org/article/info:...io.1001824
Press release: Max-Planck-Gesellschaft; available at http://www.eurekalert.org/pub_releases/2...040114.php
71086_web.jpg (Size: 14.87 KB / Downloads: 3)
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Motor neuron generation from stem cells: improving efficiency
Efficient and quick generation of human motor neurons from stem cells is a matter of careful timing of addition of critical signalling molecules to the stem cells. Bringing forward the addition of signalling molecules from six days to three days increases the rapidity of recovery of motor neurons to 20 days compared to 40 to 50 days and the proportion of motor neurons to 70% from 20-30%. These are the findings of a new study from researchers in the University of Illinois in the USA and the Chinese Academy of Sciences and Chinese Academy of Medical Sciences and Peking Union Medical College. The study is published in the journal Nature Communications.
Defects in motor neurons cause the devastating group of motor neuron diseases. These include the most common human form, amyotrophic lateral sclerosis (ALS), as well as primary lateral sclerosis, progressive muscular atrophy and progressive bulbar palsy. Essential voluntary muscle activity such as speaking, walking, breathing, and swallowing is adversely affected. Therefore, research on how stem cells develop into motor neurons is essential to gain insight into motor neuron disease processes. Methods for improving speed and efficiency of motor neuron generation are vital to improve tools for prospective drug screening and ultimately generate cells for therapeutic use.
Previous studies on generation of motor neurons from stem cells featured addition of two important signalling molecules at Day 6, i.e. 6 days after exposure to cells to a previously discovered molecule called compound C which converts stem cells into “neural progenitor cells. The simple but critical innovation in this study was to push back the addition of these signalling molecules to Day 3 after compound C addition. This resulted in the much more rapid and efficient differentiation of neural progenitor cells to motor neurons. The authors explain that Day 3 therefore represents a previously unrecognised neural progenitor cell stage. As a result of the study, the researchers identified a protein called Islet-1 as crucial for formation of mature and functional human motor neurons.
Senior author Dr Fei Wang of the University of Illinois concluded: “To have a rapid, efficient way to generate motor neurons will undoubtedly be crucial to studying – and potentially also treating – spinal cord injuries and diseases like ALS.”
Sources:
Qu, Q., Li, D., Louis, K. R., Li, X., Yang, H., Sun, Q., Crandall, S. R., Tsang, S., Zhou, J., Cox, C. L., Cheng, J., and Wang, F. (2014). High-efficiency motor neuron differentiation from human pluripotent stem cells and the function of islet-1. Nature Communications, 5; doi:10.1038/ncomms4449
Press release: University of Illinois; available from: http://news.illinois.edu/news/14/0331ste...iWang.html [Accessed 2 April 2014].
http://www.ninds.nih.gov/disorders/motor...seases.htm [Accessed 2 April 2014].
Defects in motor neurons cause the devastating group of motor neuron diseases. These include the most common human form, amyotrophic lateral sclerosis (ALS), as well as primary lateral sclerosis, progressive muscular atrophy and progressive bulbar palsy. Essential voluntary muscle activity such as speaking, walking, breathing, and swallowing is adversely affected. Therefore, research on how stem cells develop into motor neurons is essential to gain insight into motor neuron disease processes. Methods for improving speed and efficiency of motor neuron generation are vital to improve tools for prospective drug screening and ultimately generate cells for therapeutic use.
Previous studies on generation of motor neurons from stem cells featured addition of two important signalling molecules at Day 6, i.e. 6 days after exposure to cells to a previously discovered molecule called compound C which converts stem cells into “neural progenitor cells. The simple but critical innovation in this study was to push back the addition of these signalling molecules to Day 3 after compound C addition. This resulted in the much more rapid and efficient differentiation of neural progenitor cells to motor neurons. The authors explain that Day 3 therefore represents a previously unrecognised neural progenitor cell stage. As a result of the study, the researchers identified a protein called Islet-1 as crucial for formation of mature and functional human motor neurons.
Senior author Dr Fei Wang of the University of Illinois concluded: “To have a rapid, efficient way to generate motor neurons will undoubtedly be crucial to studying – and potentially also treating – spinal cord injuries and diseases like ALS.”
Sources:
Qu, Q., Li, D., Louis, K. R., Li, X., Yang, H., Sun, Q., Crandall, S. R., Tsang, S., Zhou, J., Cox, C. L., Cheng, J., and Wang, F. (2014). High-efficiency motor neuron differentiation from human pluripotent stem cells and the function of islet-1. Nature Communications, 5; doi:10.1038/ncomms4449
Press release: University of Illinois; available from: http://news.illinois.edu/news/14/0331ste...iWang.html [Accessed 2 April 2014].
http://www.ninds.nih.gov/disorders/motor...seases.htm [Accessed 2 April 2014].
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A brain region that helps us limit alcohol consumption
A brain region called the lateral habenula (LHb) may be vital in directing control of ethanol consumption by mediation of learning driven by the aversive effects of the drug. These are the findings of a study on laboratory rats from researchers in the University of Utah which has relevance for understanding of alcohol addiction in humans. The study was published in the journal PLoS One on April 2nd 2014.
The lateral habenula is well established as having an important role in learning driven by negative outcomes. Previous studies had indicated that the lateral habenula is implicated in negative regulation of motivation to take drugs of abuse such as cocaine and nicotine, suggesting that it drives learning from the aversive effects of these drugs. Similarly, ethanol consumption is associated with initially positive effects but ultimately aversive effects such as delayed hangover. Animal studies had previously demonstrated a link between conditioned taste aversion (CTA) and decreased ethanol consumption, suggesting a role for learning driven by aversive outcomes in reduction of ethanol consumption. This has likely clinical relevance as it is established that in humans, decreased sensitivity to the aversive effects of alcohol is more likely to result in problem drinking such as binge drinking and alcoholism.
These existing studies inspired the University of Utah scientists to examine the role of the lateral habenula in regulation of ethanol intake. They studied two groups of rats. In one group the lateral habendula was inactivated while in the other a sham procedure was performed leaving the brain region intact. The researchers studied patterns of consumption of ethanol in the two groups of rats, both in terms of voluntary consumption of ethanol provided in the rats’ cages and in a system whereby the rats could self-administer the ethanol.
The results showed that in the lesioned rats who lacked the lateral habendula, voluntary ethanol intake escalated significantly more rapidly over the course of eight weeks of observation and levelled off at a significantly higher level than in the control rats. Levels of self-administration of ethanol were also significantly higher in the lesioned rats. In an effort to determine if the removal of the lateral habendula function affected conditioned taste aversion associated with alcohol, the researchers made a desirable supersaccharin solution available to the rats for thirty minutes before immediate injection with either ethanol or saline. Conditioned taste aversion to the supersaccharin arose in both groups associated with ethanol administration, but it was lower in the lesioned rats and they also tended to recover more quickly from this conditioned taste aversion.
First co-author on the study, Andrew Haack explained the potential clinical significance of these findings: "The way I look at it is the rewarding effects of drinking alcohol compete with the aversive effects….When you take the aversive effects away, which is what we did when we inactivated the lateral habenula, the rewarding effects gain more purchase, and so it drives up drinking behavior."
This can help explain some of the physiological reasons why some people become problem drinkers as they are less sensitive to the negative effects of alcohol. The researchers think that the lateral habendula may either regulate how bad an individual feels after over-indulgence in alcohol or else regulates how effectively they learn from the adverse experience. Future studies will address these theories.
Sources
Haack AK, Sheth C, Schwager AL, Sinclair MS, Tandon S, et al. (2014) Lesions of the Lateral Habenula Increase Voluntary Ethanol Consumption and Operant Self-Administration, Block Yohimbine-Induced Reinstatement of Ethanol Seeking, and Attenuate Ethanol-Induced Conditioned Taste Aversion. PLoS ONE 9(4): e92701. doi:10.1371/journal.pone.0092701
Press release: University of Utah Health Sciences; available at http://www.eurekalert.org/pub_releases/2...040214.php [Accessed 3 April 2014].
The lateral habenula is well established as having an important role in learning driven by negative outcomes. Previous studies had indicated that the lateral habenula is implicated in negative regulation of motivation to take drugs of abuse such as cocaine and nicotine, suggesting that it drives learning from the aversive effects of these drugs. Similarly, ethanol consumption is associated with initially positive effects but ultimately aversive effects such as delayed hangover. Animal studies had previously demonstrated a link between conditioned taste aversion (CTA) and decreased ethanol consumption, suggesting a role for learning driven by aversive outcomes in reduction of ethanol consumption. This has likely clinical relevance as it is established that in humans, decreased sensitivity to the aversive effects of alcohol is more likely to result in problem drinking such as binge drinking and alcoholism.
These existing studies inspired the University of Utah scientists to examine the role of the lateral habenula in regulation of ethanol intake. They studied two groups of rats. In one group the lateral habendula was inactivated while in the other a sham procedure was performed leaving the brain region intact. The researchers studied patterns of consumption of ethanol in the two groups of rats, both in terms of voluntary consumption of ethanol provided in the rats’ cages and in a system whereby the rats could self-administer the ethanol.
The results showed that in the lesioned rats who lacked the lateral habendula, voluntary ethanol intake escalated significantly more rapidly over the course of eight weeks of observation and levelled off at a significantly higher level than in the control rats. Levels of self-administration of ethanol were also significantly higher in the lesioned rats. In an effort to determine if the removal of the lateral habendula function affected conditioned taste aversion associated with alcohol, the researchers made a desirable supersaccharin solution available to the rats for thirty minutes before immediate injection with either ethanol or saline. Conditioned taste aversion to the supersaccharin arose in both groups associated with ethanol administration, but it was lower in the lesioned rats and they also tended to recover more quickly from this conditioned taste aversion.
First co-author on the study, Andrew Haack explained the potential clinical significance of these findings: "The way I look at it is the rewarding effects of drinking alcohol compete with the aversive effects….When you take the aversive effects away, which is what we did when we inactivated the lateral habenula, the rewarding effects gain more purchase, and so it drives up drinking behavior."
This can help explain some of the physiological reasons why some people become problem drinkers as they are less sensitive to the negative effects of alcohol. The researchers think that the lateral habendula may either regulate how bad an individual feels after over-indulgence in alcohol or else regulates how effectively they learn from the adverse experience. Future studies will address these theories.
Sources
Haack AK, Sheth C, Schwager AL, Sinclair MS, Tandon S, et al. (2014) Lesions of the Lateral Habenula Increase Voluntary Ethanol Consumption and Operant Self-Administration, Block Yohimbine-Induced Reinstatement of Ethanol Seeking, and Attenuate Ethanol-Induced Conditioned Taste Aversion. PLoS ONE 9(4): e92701. doi:10.1371/journal.pone.0092701
Press release: University of Utah Health Sciences; available at http://www.eurekalert.org/pub_releases/2...040214.php [Accessed 3 April 2014].
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Launch of multi-national response to threat of antibiotic misuse
Antibiotics have long been a mainstay of treatment for potentially deadly bacterial infections. However, long-term over-prescription and misuse of antibiotics and other anti-microbial drugs has resulted in the rise of drug-resistant bacteria. Multi-drug resistant bacteria, such as extended-spectrum β-lactamase (ESBL)–producing Enterobacteriaceae, third-generation cephalosporin-resistant (G3CR) Enterobacteriaceae and methicillin resistant Staphylococcus aureus are now a serious international public health threat. These bacteria used to arise almost exclusively in healthcare settings but since the 1990s they have been increasingly emerging in community settings. They are spreading globally at ever-increasing rates as mobility of people increases.
In response to the international nature of this threat, a joint programme initiative, namely the Joint Programme on Antimicrobial Resistance (JPIAMR), aims to gather research funders from different countries concerned with antimicrobial resistance under one umbrella. This programme includes several countries, including nineteen European countries, Canada and Israel, as well as having support from other countries ranging from Australia to South Africa. The JPIAMR launched its strategic research agenda today, 3rd April, in Brussels.
The Strategic Research Agenda (SRA) covers six priority topics that aim to introduce a multi-dimensional approach to the issue of antibiotic resistance. The topics come under the headings of therapeutics, diagnostics, surveillance, transmission, environment and interventions. The ultimate goal is to translate these topics into new unified prevention and intervention strategies that cross borders to improve public health of populations and deliver economic and societal benefits throughout Europe and beyond. The idea is to reduce the fragmentation of effort that arises when individual national initiatives are not unified.
The programme emphasises the necessity of unifying the efforts of all concerned groups, from the scientific community to research funders and from policy makers and societal stakeholders to industry and SMEs. This should provide a firm foundation for a coherent approach to reduction in inappropriate antibiotic use and increasing sustainability of antibiotics. The next stage for the programme is to use funding from the European Commission, the International Medicines Initiative (IMI), national funding contributions and public-private partnerships, to fund research within these six priority areas.
Dr Mats Ulfendahl of the Swedish Research Council explained: "As this is an active research field and AMR (anti-microbial resistance) is a very real and present societal challenge, the strategic research agenda will need to stay a living document that is continuously updated to keep pace with developments within research and society.” Further information is available on the programme website at http://www.jpiamr.eu and the SRA can be viewed at http://www.jpiamr.eu/wp-content/uploads/...RA-v1.pdf.
Source
Press release: Swedish Research Council; available at http://www.eurekalert.org/pub_releases/2...040214.php [Accessed 3 April 2014].
In response to the international nature of this threat, a joint programme initiative, namely the Joint Programme on Antimicrobial Resistance (JPIAMR), aims to gather research funders from different countries concerned with antimicrobial resistance under one umbrella. This programme includes several countries, including nineteen European countries, Canada and Israel, as well as having support from other countries ranging from Australia to South Africa. The JPIAMR launched its strategic research agenda today, 3rd April, in Brussels.
The Strategic Research Agenda (SRA) covers six priority topics that aim to introduce a multi-dimensional approach to the issue of antibiotic resistance. The topics come under the headings of therapeutics, diagnostics, surveillance, transmission, environment and interventions. The ultimate goal is to translate these topics into new unified prevention and intervention strategies that cross borders to improve public health of populations and deliver economic and societal benefits throughout Europe and beyond. The idea is to reduce the fragmentation of effort that arises when individual national initiatives are not unified.
The programme emphasises the necessity of unifying the efforts of all concerned groups, from the scientific community to research funders and from policy makers and societal stakeholders to industry and SMEs. This should provide a firm foundation for a coherent approach to reduction in inappropriate antibiotic use and increasing sustainability of antibiotics. The next stage for the programme is to use funding from the European Commission, the International Medicines Initiative (IMI), national funding contributions and public-private partnerships, to fund research within these six priority areas.
Dr Mats Ulfendahl of the Swedish Research Council explained: "As this is an active research field and AMR (anti-microbial resistance) is a very real and present societal challenge, the strategic research agenda will need to stay a living document that is continuously updated to keep pace with developments within research and society.” Further information is available on the programme website at http://www.jpiamr.eu and the SRA can be viewed at http://www.jpiamr.eu/wp-content/uploads/...RA-v1.pdf.
Source
Press release: Swedish Research Council; available at http://www.eurekalert.org/pub_releases/2...040214.php [Accessed 3 April 2014].
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