GARVAN INSTITUTE |
Australian scientists have identified one way of making a frustratingly tricky transplant – of insulin-producing ‘islets of Langerhans’ into patients with Type 1 diabetes – more successful.
The islets of Langerhans are the part of the pancreas that produce insulin. A Sydney team, part of the Commonwealth-funded Australian Islet Transplant Consortium formed in 2006, has found that islets are severely handicapped from the outset. They are full of inflammatory molecules before they ever reach their mark, much like stressed or damaged tissue. Associate Professor Shane Grey and Drs Mark Cowley and Anita Weinberg, from Sydney’s Garvan Institute of Medical Research, detailed the ‘molecular signatures’ of islets that were transplanted into 15 recipients as part of a 5-year clinical trial spanning Sydney, Melbourne and Adelaide. Their findings, published online in Cell Transplantation, used the latest sequencing technologies to identify inflammatory signatures. A very large initiative overall, the Sydney arm of the Consortium alone has operated with 5 teams: one team isolated islets; a second undertook transplants; a third monitored the patient’s quality of life afterwards; a fourth monitored the liver; and the Garvan group compared gene signatures of grafts with patient outcomes, seeing what constituted a ‘good’ or a ‘poor’ graft. “The importance of our finding in the context of the whole process of transplantation – which is very complex – is that it tells us the grafts we are using are not at ground zero,” said Associate Professor Grey. “They’re like little smoking guns we’re sending into patients, either doomed to fail, or have only partial success.” “Islets are easier to manipulate than patients' immune systems, and this finding will help us establish targets for therapy. In other words, we have the potential to treat islets with anti-inflammatory compounds prior to transplantation.” “This should have a marked effect on the success of transplants – currently at 80% survival after a year and 10-15 % survival after 5 years – not nearly the same success rates as other organ transplants.” Since the 1960s, when pioneering anatomist Dr Paul Lacy first implanted islets into rodents, islet transplantation has offered a compelling yet elusive, treatment for diabetes. Decades of work led to very limited success, until a great leap forward a Canadian team brought to transplantation practices in 2000 – known as the ‘Edmonton Protocol’. The work of the Edmonton team showed that recipients need many islets for the procedure to be effective – normally the islets from up to 3 whole human pancreases. This compounds the difficulty as donors are in limited supply, the pancreas has to be removed quickly after death, islets must be isolated within a matter of hours after that, and they happen to be intrinsically fragile. “Until now, the state of islets used in transplantation has not been well understood, and this gives us better insight into what has been happening,” said Grey. “And while progress has been a little slow, at least those patients who are prone to lethal glycaemic unawareness – in other words, likely to lapse into hypoglycaemic comas and die – have been helped by transplants. Even when the grafts fail, in that they stop producing insulin, for some unknown reason the patients appear to remain protected against these lethal comas.” To show the importance of their findings, the group compared the difference between transplanting ‘pristine’ islets into mice and transplanting islets with an ‘inflammatory signature’. As expected, the mice fared much better with the ‘good’ grafts.
Editor's Note: Original news release can be found here.
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Wednesday, March 14, 2012
Insulin-maker transplant improved
Rare disease origins revealed
THE UNIVERSITY OF SYDNEY |
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Knowledge of a disease prevalent among Northern Territory Indigenous communities has been overhauled thanks to research contributed by the University of Sydney's Garth Nicholson.
"This advance in our understanding of the origins of Machado-Joseph Disease in Australia will hopefully contribute to the development of a cure of this debilitating condition which affects people from as young as 10 years old," said Associate Professor Nicholson from the ANZAC Institute at the University. Machado-Joseph Disease is a neurodegenerative disorder which causes a progressive deterioration of muscle control and coordination. The world's highest known incidence of the disease occurs in Indigenous people of Groote Eylandt and Yirrkala in the Northern Territory. "Elsewhere the disease has only been seen rarely and nearly always in populations from East Asia or the Azores, a Portuguese autonomous zone in the North Atlantic," Associate Professor Nicholson said. Until now the prevailing theory has been that the disease was passed to Indigenous populations in Australia by Macassan traders who were in contact with Portuguese colonies and travelled to Australia in the 16th century and 17th century. By comparing blood samples from sufferers worldwide, recent international research, published in the Archives of Neurology, contradicts this theory. Instead of being associated with versions of the disease originating from Portugal, the Australian version of the disease is related to those from Japan, India and Taiwan. "We believe the Australian variant of the disease has a common ancestor, dating back 7000 years, with those seen in the Asian region," said Professor Nicholson who conducted the research on the Groote Eylandt community. Machado-Joseph Disease currently affects an estimated 50 people in the Northern Territory with another 500 family members at risk.
Editor's Note: Original news release can be found here.
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Opening the brain to new treatments
A researchers uses an MRI machine to guide the focus ultrasound used to disrupt specific areas of the blood-brain barrier. Credit: © The Journal of Visualized Experiments
One of the trickiest parts of treating brain conditions is the blood brain barrier, a blockade of cells that prevent both harmful toxins and helpful pharmaceuticals from getting to the body's control center. But, a technique published in JoVE, uses an MRI machine to guide the use of microbubbles and focused ultrasound to help drugs enter the brain, which may open new treatment avenues for devastating conditions like Alzheimer's and brain cancers.
"It's getting close to the point where this could be done safely in humans," said paper-author Meaghan O'Reilly, "there is a push towards applications."
The current method of disrupting the blood-brain barrier (BBB) is by using osmotic agents such as mannitol, which suck the water out of the cells that form the barrier, causing the gaps between them to get bigger. Unfortunately, this method opens large areas of the barrier, leaving the brain exposed to toxins.
The benefit of the microbubble technique is that it can be used on a very small area of the BBB. The microbubbles, made of lipids (fats) and gas, are injected into the blood stream. When focused ultrasound is applied, the bubbles expand and contract. It is thought that the force of the movement in the bubbles causes the cells that form the BBB to temporarily separate, which allows drugs to reach the brain.
"Microbubble technology has been around for years, though its applications have mostly been as contrast agents for diagnostic ultrasound," said JoVE Editorial Director, Dr. Beth Hovey. "This newer approach, using ultrasound to help the bubbles permeablize the blood brain barrier, will hopefully allow for better treatment of diseases within the brain."
In this method, O'Reilly and her colleagues use the MRI machine to ensure that the barrier opens, and they can also time how long it takes for it to close, which will be important for when the technique is used on patients.
O'Reilly chose to publish the technique in JoVE, the Journal of Visualized Experiments, to help other scientists learn the method.
JoVE is the first and only peer-reviewed, PubMed-indexed science journal to publish all of its content in both text and video format.
"The ability of focused ultrasound combined with microbubbles to disrupt the blood brain barrier has been known for over a decade. However, because the actual technique can be challenging— there are critical steps involved— the video article fills a gap in the literature that is a major hindrance to people getting into the field," she said.
More information: The article will be published on March 13 and can be viewed here: http://www.jove.co … -a-rat-model
Provided by The Journal of Visualized Experiments
"Opening the brain to new treatments." March 13th, 2012. http://medicalxpress.com/news/2012-03-brain-treatments.html
Posted by
Robert Karl Stonjek
Robert Karl Stonjek
Just 60 seconds of combat impairs memory
Just 60 seconds of all-out physical exertion in a threatening situation can seriously damage the memories of those involved for many details of the incident, according to a new study of police officers.
Police officers, witnesses and victims of crime suffer loss of memory, recognition and awareness of their environment if they have had to use bursts of physical energy in a combative encounter, according to scientists.
Researchers, led by Dr Lorraine Hope of the University of Portsmouth, found that less than 60 seconds of all-out exertion, as might happen when an officer is forced to chase-down a fleeing suspect or engage in a physical battle with a resistant criminal, can seriously impair their ability to remember details of the incident – or even identify the person who was involved. Even officers in top condition are not immune to the rapid drain of physical prowess and cognitive faculties resulting from sustained hand-to-hand combat.
The findings, published in Psychological Science, a journal of the Association for Psychological Science, are a stark warning to police officers, police chiefs and the courts, according to Dr Hope, a Reader in applied cognitive psychology of the university's Department of Psychology.
She said: "Police officers are often expected to remember in detail who said what and how many blows were received or given in the midst of physical struggle or shortly afterwards. The results of our tests indicate it may be very difficult for them to do this.
"As exhaustion takes over, cognitive resources tend to diminish. The ability to fully shift attention is inhibited, so even potentially relevant information might not be attended to. Ultimately, memory is determined by what we can process and attend to.
"The legal system puts a great deal of emphasis on witness accounts, particularly those of professional witnesses like police officers. Investigators and courts need to understand that an officer who cannot provide details about an encounter where physical exertion has played a role is not necessarily being deceptive or uncooperative. An officer's memory errors or omissions after an intense physical struggle should not unjustly affect his or her credibility."
The research, conducted on police officers in Winnipeg, Canada was coordinated and funded by the Force Science Institute. The research team in Canada included Dr Lorraine Hope (University of Portsmouth), Dr Bill Lewinski (Force Science Institute) and specialists from the Metropolitan Police in the UK.
Researchers recruited 52 officer volunteers (42 males, 10 females), with an average of eight years on the job. All officers were fit and healthy and engaged in regular exercise.
During an initial briefing, the officers were given background information about a recent spate of armed robberies in the city. The briefing included details of how the robberies were conducted and witness descriptions of the perpetrators. Half of the officers then engaged in a full-force physical attack on a 300lb hanging water bag and the others (a control group) were assigned as observers. Officers selected their own "assault movements" on the bag attack — punches, kicks, and/or palm, elbow, and knee strikes—and were verbally encouraged by a trainer during the task. They continued the assault on the bag until they no longer had strength to keep going or until they were breathless and struggling to continue.
The next part of the test required the officers to approach a trailer that a "known criminal" was suspected of occupying. On entering the trailer, the officer found themselves in a realistic living area where a number of weapons, including an M16 carbine, a revolver, a sawn-off shotgun and a large kitchen knife were visible. After a short delay, the "target individual" emerged from another room and shouted aggressively at the officer to get out of his property. The individual was not armed, but several of the weapons were within easy reach.
Dr Hope found those who had been asked to exert themselves physically remembered less about the target individual and made more recall errors compared to the control group of observers. The officers who had been exerted also recalled less about the initial briefing information and what they did report was less accurate. Officers who had been exerted also reported less about an individual they encountered incidentally while en route to the trailer. While more than 90 per cent of non-exerted observers were able to recall at least one descriptive item about him, barely one-third of exerted officers remembered seeing him at all.
Everyone remembered seeing the angry suspect in the trailer, but non-exerted observers provided a significantly more detailed description of him and made half as many errors in recall as those who were exhausted. These observers were also twice as likely to correctly identify the suspect from a line-up.
However, another striking aspect of the findings showed that exerted officers were able to register threat cues in the environment to the same degree at non-exerted officers.
These new findings reveal that although exerted officers were able to pay attention to the threatening aspects of the scene, their ability to then process other aspects of the interaction was affected. As a result of this, some information may only have been processed weakly or not at all – resulting in an impaired memory for many details of the encounter.
Provided by Association for Psychological Science
"Just 60 seconds of combat impairs memory." March 13th, 2012. http://medicalxpress.com/news/2012-03-seconds-combat-impairs-memory.html
Posted by
Robert Karl Stonjek
Robert Karl Stonjek
Tuesday, March 13, 2012
சுஜாதாவின் பத்துக் கட்டளைகள்… (கண்டிப்பாக படிக்கவும் !!!)
1. ஒன்றின் மேல் நம்பிக்கை வேண்டும், ஏதாவது ஒன்று. உதாரணம் கடவுள், இயற்கை, உழைப்பு, வெற்றி இப்படி எதாவது… நம்பிக்கை நங்கூரம் போல. கேள்வி கேட்காத நம்பிக்கை. கேள்வி கேட்பது சிலவேளை இம்சை. நவீன விஞ்ஞானம் அதிகப்படியாகக் கேள்வி கேட்டு இப்போது தவித்துக் கொண்டிருக்கிறது.
2. அப்பா, அம்மா இரண்டு பேரும் வேலை சொல்வது பல சமயங்களில் கடுப்பாக இருக்கும். ஒருமாறுதலுக்கு அவர்கள் சொல்வதைச் செய்து பாருங்கள். அவர்கள் கேட்பது உங்களால் செய்யக் கூடியதாகவே இருக்கும். பொடிநடையாகப் போய் நூறு கிராம் காப்பி பவுடர் (அ) ரேஷன் கார்டு புதுப்பித்தல் இப்படிதான் இருக்கும்.
3. மூன்று மணிக்குத் துவங்கும் மாட்டனி போகாதீர்கள். க்ளாஸ் கட்பண்ண வேண்டி வரும். தலைவலி வரும். காசு விரயம். வீட்டுக்குப் போனதும் பொய் சொல்வதற்கு ரொம்ப ஞாபக சக்தி வேண்டும். இந்த உபத்திரத்துக்கு உண்மையைச் சொல்லிவிடுவது சுலபம். இளமைக்காலம், ஒளிக் கீற்றைப் போல் மிகவும் குறைந்த காலம், அதை க்யூ வரிசைகளிலும் குறைபட்ட தலைவர்களுக்காகவும் விரயம் செய்யாதீர்கள்.
4. நான்கு பக்கமாவது ஒரு நாளைக்குப் பொது விஷயங்களைப் படியுங்கள். பொது விஷயங்கள் என்றால் கதை, சினிமா, காதல் இல்லாதவை. உதாரணம் – யோக்கியமான செய்தித்தாள், மற்ற பேரைப் பற்றிக் கவலைப்படும் பத்திரிகைகள் அல்லது லைப்ரரியிருந்து ஒரு புத்தகம்.
5. ஐந்து ரூபாய் சம்பாதித்துப் பாருங்கள். சொந்தமாக உங்கள் உழைப்பில், முயற்சியில், யோக்கியமாக, மனச்சாட்சி உறுத்தாமல். அடுத்த முறை அப்பாவிடம் ஆயிரம் ரூபாய்க்கு ஷர்ட், சுடிதார் கேட்கும் முன்.
6. இந்தச் தகவல்களை படிக்கும் நிலைமை பெற்ற நீங்கள் இந்திய சனத்தொகையின் மேல்தட்டு ஆறு சதவிகித மக்களில் ஒருவர். அன்றாடம் சோற்றுக்காக அலையும், வசதியில்லாத கோடிக்கணக்கான மக்களைத் தினம் ஒரு முறை எண்ணிப் பாருங்கள்.
7. வாரத்தின் ஏழாவது தினமான ஞாயிறன்று என்ன செய்தாலும் காதல் பிஸினஸ் வேண்டாம். காதலுக்கு ரொம்பச் செலவாகும். மனம், வாக்கு, காயம்(உடல்), எல்லாவற்றையும் ஆக்கிரமிக்கும் தீ அது. பொய் நிறையச் சொல்ல வேண்டும். வினோதமான இடங்களில் காத்திருக்க வேண்டும். இந்த வயதில் நாசமாய்ப்போன படிப்புத்தான் உங்களுக்கு முக்கியம்.குறிப்பு: பெண்களை சைட் அடிப்பதும், கலாட்டா பண்ணுவதும், அவர்களுக்கு கர்சீப் முதலியன ரோடிலிருந்து பொறுக்கிக் கொடுப்பதும், உபத்திரமில்லாத கவிதைகள் எழுதுவதும், காதலோடு சேர்த்தியில்லை.
8.எட்டு முறை மைதானத்தை சுற்றி ஓடினால் எந்தச் சீதோஷ்ணமாக இருந்தாலும் நெற்றி வியர்வை அரும்பும். எதாவது தேகப் பயிற்சி செய்யவும். கடிகாரத்துக்குச் சாவி கொடுப்பதோ சீட்டாடுவதோ தேகப் பயிற்சி ஆகாது. எதையாவது தூக்குங்கள், எதையாவது வீசி எறியுங்கள். உங்கள் உடலில் ஊறும் உற்சாகத்துக்கு ஓர் ஆரோக்கியமான வடிகால் தேவை. ராத்திரி சரியாக தூக்கம் வரும். கன்னா பின்னா எண்ணங்கள் தவிர்க்கப்படும். ஒழுங்காக சாப்பிடத்தோன்றும். பொதுவாகவே சந்தோஷமாக இருக்கும்.
9. ஒன்பது மணிக்குள் வீட்டுக்கு வரவும். மிஞ்சிப் போனால் ஒன்பது மணி இரண்டு நிமிடம். ஒரு மணி நேரம் பாடம் அல்லது புத்தகம் படிக்கலாம்.
10. படுக்கப் போகும் முன் பத்து நிமிஷமாவது அம்மா, அப்பா, அண்ணன், தங்கை யாருடனாவது பேசவும் (பேசுவது என்று சொன்னவுடன் காதலியுடன் என்று நினைக்க வேண்டாம், நான் சொன்னது குடும்பத்தினருடன் மட்டும்). எதாவது ஒரு அறுவை ஜோக் அல்லது காலேஜில் நடந்த நிகழ்வுகள். சப்ஜெக்ட் முக்கியமில்லை. பேசுவது தான்.
இந்த பத்தில் தினம் ஒன்று என்று முயற்சி செய்து தான் பாருங்களேன்...
Correcting human mitochondrial mutations
by Biomechanism
Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.
Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.
Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson’s disease, heart disease, stroke, Alzheimer’s disease and cancer.
“I think this is a finding that could change the field,” Teitell said. “We’ve been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans.”
The study appears March 12, 2012 in the peer-reviewed journal Proceedings of the National Academy of Sciences.
The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad Stem Cell Research Center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing “power plant” of a cell.
Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.
The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.
The study in Cell outlined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited and energy production was compromised, leading to stalled cell growth.
The findings from the current study provide a form of gene therapy for mitochondria by compensating for mutations that cause a wide range of diseases, said study co-senior author Koehler.
“This opens up new avenues to understand and develop therapies for mitochondrial diseases,” Koehler said. “This has the potential to have a really big impact. We just have to get it to the next step.”
Gene therapy is often used to express proteins that can treat the cause of a variety of diseases. In this case, post-doctoral fellow Geng Wang developed a strategy to target and import specific RNA molecules encoded in the nucleus into the mitochondria and, once there, to express proteins needed to repair mitochondrial gene mutations.
First, the research team had to figure out a way to stabilize the reparative RNA so that it was transported out of the nucleus and then localized to the mitochondrial outer membrane. This was accomplished by engineering an export sequence to direct the RNA to the mitochondrion. Once the RNA was in the vicinity of the transport machinery on the mitochondrial surface, then a second transport sequence was required to direct the RNA into the targeted organelle. With these two modifications, a broad spectrum of RNAs were targeted to and imported into the mitochondria, where they functioned to repair defects in mitochondrial respiration and energy production in two different cell line models of human mitochondrial disease.
“This study indicates that a wide range of RNAs can be targeted to mitochondria by appending a targeting sequence that interacts with PNPASE, with or without a mitochondrial localization sequence, to provide an exciting, general approach for overcoming mitochondrial genetic disorders,” the study states.
Going forward, Teitell and Koehler will test their new method in small animal models to determine whether they can fix a mitochondrial defect as it occurs in a whole organism. One potential use for the new method would also be to repair mitochondrial defects in reprogrammed, embryonic or adult-type stem cells for use in regenerative medicine therapies.
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The one-year study was supported by the California Institute of Regenerative Medicine, the National Institutes of Health, the American Heart Association and the Broad Stem Cell Research Center at UCLA.
Courtesy University of California – Los Angeles Health Sciences
Eurostar Group Jobs
Dear Sir / Madame ,
Eurostar Group is a multimillion group with varied business interests. The Group with its head quarters in Dubai comprises business interests in Satellite Equipments, Consumer Electronics, Commodities Trading, IPTV, Tendering, Properties and Facilities Management and has its operations in across Middle East, Africa, India and China. As a part of our Group’s business expansions, we are looking for qualified and experienced professionals at different levels in the following areas of business.
Eurostar Group is a multimillion group with varied business interests. The Group with its head quarters in Dubai comprises business interests in Satellite Equipments, Consumer Electronics, Commodities Trading, IPTV, Tendering, Properties and Facilities Management and has its operations in across Middle East, Africa, India and China. As a part of our Group’s business expansions, we are looking for qualified and experienced professionals at different levels in the following areas of business.
Business Unit | Brief Details |
Satellite Equipments | HD Set Top Boxes, Digital Satellite Antenna & Cables, LNB. |
Consumer Electronics & Home Appliances | LCD & Plasma , Home Theatre, DVD Player, Air Conditioners, Refrigerators, Water Dispenser, Washing Machine, Microwave Ovens, Cooking range, Blender, Vacuum cleaners, Steam press & iron, room heaters, Emergency Lamp & torch. |
Trading | Trading FMCG, Commodities , Perfumery |
IPTV & Tendering | Tendering for Telecom companies in MEA & CIS countries for IPTV (Internet protocol Television) projects, FTTH (Fiber To The Home) solutions and Power & Telecom Cables |
Properties & Facilities Management | Property sourcing & acquisition, Leasing, planning & selling, Facilities management |
Multimedia | MultimediaPay TV Channels , Technical Maintenance of Hotels & Commercial premises |
Corporate Sales | Hotel LCD & LED TV, LED Lighting bulb, Kitchen Appliances, Mini Bars, safes, Media Hub, Door lock items and Systems, CCTV and others. |
We request you to kindly forward this email to your friends, business associates or relatives who would be looking for a job in any of the above mentioned business fields.
Relevant candidates should send their resume to eurostarjobs@eurostargroup.com. Please mention the Business Unit & Position in the subject line. For eg., Satellite Equipments – Sales for the candidate applying for Sales position in Satellite
Regards,
Recruitment Manager,
Eurostar Group
Read more: http://www.livingextra.com/2012/03/blog-post.html#ixzz1p0dHn513
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