(I didn't know this myself) A woman suddenly died unexpectedly with signs of bleeding from her ears,nose, mouth & eyes. After a preliminary autopsy it was diagnosed that deathwas due to arsenic poisoning. Where did the arsenic come from? The police launched an in-depth and extensive investigation. A medical school professor was invited to come to solve the case. The professor carefully looked at the contents from the deceased's stomach. In less than half an hour, the mystery was solved. The professor said: 'The deceased did not commit suicide and neither was she murdered, she died of accidental death due to ignorance!' Everyone was puzzled, why accidental death? The professor said: 'The arsenic is produced in the stomach of thedeceased.' The deceased used to take 'Vitamin C' everyday, which in itself is not a problem. The problem was that she ate a large portion of shrimp/prawn during dinner. Eating shrimp/prawn is not the problem that's why nothing happened to her family even though they took the same shrimp/prawn. However at the same time the deceased also took 'vitamin C', that is where the problem is Researchers at the University of Chicago in the United States , found through experiments, food such as soft-shellshrimp/prawn contains a much higher concentration of five potassium arsenic compounds. Such fresh food by itself has no toxic effects on the human body. However,in taking 'vitamin C', chemical reaction occur and the original non-toxic elements change to toxic elements. Arsenic poisoning has magma role and can cause paralysis to the small bloodvessels. Therefore, a person who dies of arsenic poisoning will show signs of bleeding from the ears, nose, mouth & eyes. Thus as a precautionary measure,DO NOT eat shrimp/prawn when taking 'vitamin C'. After reading this; please do not be stingy. Forward to your friends Dr NEWTON JAYAWARDANE MBBS MS FRCS(Eng) Consultant Surgeon Teaching Hospital RAGAMA 11010. Sri LANKA .
Potential clues to how autism miswires the brain are emerging from a study of a rare, purely genetic form of the disorders that affects fewer than 20 people worldwide. Using cutting-edge “disease-in a-dish” technology, researchers funded by the National Institutes of Health have grown patients’ skin cells into neurons to discover what goes wrong in the brain in Timothy Syndrome. Affected children often show symptoms of autism spectrum disorders along with a constellation of physical problems.
Abnormalities included changes in the composition of cells in the cortex, the largest brain structure in humans, and of neurons that secrete two key chemical messengers. Neurons that make long-distance connections between the brain’s hemispheres tended to be in short supply.
Most patients with Timothy Syndrome meet diagnostic criteria for an autism spectrum disorder. Yet, unlike most cases of autism, Timothy syndrome is known to be caused by a single genetic mutation.
“Studying the consequences of a single mutation, compared to multiple genes with small effects, vastly simplifies the task of pinpointing causal mechanisms,” explained Ricardo Dolmetsch, Ph.D., of Stanford University, a National Institute of Mental Health (NIMH) grantee who led the study. His work was partially funded by a NIH Director’s Pioneer Award.
Dolmetsch, and colleagues, report on their findings Nov. 27, 2011 in the journal Nature Medicine.
“Unlike animal research, the cutting-edge technology employed in this study makes it possible to pinpoint molecular defects in a patient’s own brain cells,” said NIMH Director Thomas R. Insel, M.D. “It also offers a way to screen more rapidly for medications that act on the disordered process.”
Prior to the current study, researchers knew that Timothy syndrome is caused by a tiny glitch in the gene that codes for a calcium channel protein in cell membranes. The mutation results in too much calcium entering cells, causing a tell-tale set of abnormalities throughout the body. Proper functioning of the calcium channel is known to be particularly critical for proper heart rhythm – many patients die in childhood of arrhythmias – but its role in brain cells was less well understood.
To learn more, Dolmetsch and colleagues used a new technology called induced pluripotent stem cells (iPSCs). They first converted skin cells from Timothy Syndrome patients into stem cells and then coaxed these to differentiate into neurons.
“Remarkable reproducibility” observed across multiple iPSC lines and individuals confirmed that the technique can reveal defects in neuronal differentiation – such as whether cells assume the correct identity as the brain gets wired-up in early development, said the researchers. Compared to those from controls, fewer neurons from Timothy Syndrome patients became neurons of the lower layers of the cortex and more became upper layer neurons. The lower layer cells that remained were more likely to be the kind that project to areas below the cortex. In contrast, there were fewer-than-normal neurons equipped to form a structure, called the corpus callosum, which makes possible communications between the left and right hemispheres.
Caption: Forebrain of a mouse genetically engineered to express the mutated gene that causes Timothy syndrome (TS) shows fewer neurons contributing to a brain structure responsible for long-distance communications between the left and right hemispheres, called the corpus callosum, compared to the same structure in a control animal (Ctrl). Human iPSCs from TS patients showed a similar reduction. Credit: Ricardo Dolmetsch, Ph.D., Stanford University
Many of these defects were also seen in parallel studies of mice with the same genetic mutation found in Timothy syndrome patients. This supports the link between the mutation and the developmental abnormalities.
Several genes previously implicated in autism were among hundreds found to be expressed abnormally in Timothy Syndrome neurons. Excess cellular calcium levels also caused an overproduction of neurons that make key chemical messengers. Timothy Syndrome neurons secreted 3.5 times more norepinephrine and 2.3 times more dopamine than control neurons. Addition of a drug that blocks the calcium channel reversed the abnormalities in cultured neurons, reducing the proportion of catecholamine-secreting cells by 68 percent.
The findings in Timothy Syndrome patient iPSCs follow those in Rett Syndrome, another single gene disorder that often includes autism-like symptoms. About a year ago, Alysson Muotri, Ph.D., and colleagues at University of California, San Diego, reported deficits in the protrusions of neurons, called spines, that help form connections, or synapses. The Dolmetsch team’s discovery of earlier (neuronal fate) and later (altered connectivity) defects suggest that disorders on the autism spectrum affect multiple stages in early brain development.
“Most of these abnormalities are consistent with other emerging evidence that ASDs arise from defects in connectivity between cortex areas and show decreased size of the corpus callosum,” said Dolmetsch. “Our study reveals how these might be traceable to specific mechanisms set in motion by poor regulation of cellular calcium. It also demonstrates that neurons derived from iPSCs can be used to identify the cellular basis of a neurodevelopmental disorder.”
The mechanisms identified in this study may become potential targets for developing new therapies for Timothy Syndrome and may also provide insights into the neural basis of deficits in other forms of autism, said Dolmetsch.
________
Reference:
Using iPS cell-derived neurons to uncover cellular phenotypes associated with Timothy Syndrome. Pasca SP, Portmann T, Voineagu I, Yazawa M, Shcheglovitov O, Pasca AM, Cord B, Palmer TD, Chikahisa S, Seiji N, Bernstein JA, Hallmayer J, Geschwind DH, Dolmetsch RE. November 27, 2011.Nature Medicine.
The newfound defence cell generates antibody responses against viral and bacterial invasions.
Image: DNY59/iStockphoto
Researchers from The Australian National University have discovered a new type of cell which boosts the human body’s ability to fight off infections and life-threatening diseases.
Professor Carola Vinuesa from The John Curtin School of Medical Research has found a type of cell which recognises lipid antigens, or foreign molecules, which sit on infectious bacteria which invade the body. Once recognising the lipids, the cell, called Natural killer T follicular helper (NKTfh), generates antibody responses in B cells – which are the body’s natural defence against invasion by viruses and bacteria.
Professor Vinuesa said that the cell represents a non-chemical based and natural way for the human body to fight-off bacteria and infection.
“Natural killer T cells, unlike other T cells, recognise molecules known as lipids instead of just recognising proteins expressed by infectious bacteria. These types of bacteria can cause life-threatening infections, including meningitis and pneumonia. NKT cells don’t just recognise lipids – they can be naturally activated by them,” she said.
“Not surprisingly, NKT cells have been shown to play important roles in combating infection and in other immune processes including allergy, cancer and autoimmunity.
“What we have found is a subset of NKT cells, the NKTfh, which are specialised in generating antibody responses in B cells that recognise lipid-containing antigens. NKTfh cells also induce specialised structures called germinal centres, similar to those which have previously been shown to generate high affinity antibody responses to protein antigens. Both these qualities provide a natural boost to B cells, subsequently strengthening the human immune system and its ability to stave off infection.”
Professor Vinuesa also discovered that the NKTfh cells provide this boost over a very short and sharp period of time without generating long-lived antibody-producing cells.
“The discovery of the NKTfh will help us understand how to elicit immune protection against lipid-containing microbes and which natural antibody responses can best fight each type of infection,” she said.
“For example, the ability of NKTfh cells to promote faster antibody responses than conventional helper T cells may be important for protection against life-threatening infections, whereas their inability to induce long-lived antibody producing cells may be key to the prevention of autoimmune diseases.”
Professor Vinuesa’s recent discoveries have been published in two separate papers in the journals Nature Immunology and Immunity. Copies of the articles are available from the ANU Media Office.
Editor's Note: Original news release can be found here.
The study finds that the loss of a loved one can really break our hearts.
Image: BrianAJackson/iStockphoto
A study involving University of Sydney cardiac researchers has shown the loss of a loved one can really break your heart.
Dr Anastasia Susie Mihailidou, from the Sydney Medical School says when we lose someone we love it may feel as if our heart is breaking.
Dr Milhailidou, a clinical senior lecturer at Royal North Shore Hospital (RNSH), is part of a multi-disciplinary team led by Professor Geoff Tofler, Professor of Medicine and Dr Tom Buckley, Sydney Nursing School, based on the RNSH campus. The team is involved in a study providing insight into why people grieving the loss of a loved one, such as a spouse or a parent, experience a heightened blood pressure variability. Increased blood pressure variability has been shown to be predictive for stroke and other cardiovascular complications.
The team - made up of doctors, nurses, scientists and social workers from RNSH, the University of Sydney, University of Technology, Sydney and the Kolling Institute - examined the heart rate and blood pressure of 63 people who had a spouse or parent die in hospital.
Their blood pressure and heart rate were recorded two weeks after the death and then again at six months.
Dr Anastasia Mihailidou said all of the participants recorded at the two-week mark showed heightened blood pressure variability.
She said the most telling sign was at the six-month mark. Heart rates had returned to normal but blood pressure was still fluctuating.
These results were compared to a group of 78 participants who saw their sick loved ones return home from hospital. Their heart rates and blood pressure records remained unchanged.
"The results indicate that someone who is grieving and who is already experiencing blood pressure issues would find these problems amplified during or because of bereavement," Dr Mihailidou said.
"These changes aren't large, but if heightened blood pressure variability goes unnoticed they can cause problems," she said.
The team is now embarking on a second phase of the study. This will involve treating those who are grieving.
Dr Mihailidou hopes this research will encourage people who are busy caring for those who are sick or dying to be aware of their own physical health, as well as their emotional and psychological wellbeing.
Editor's Note: Original news release can be found here.
The finding overrules the belief that temperature is the key variable in banana development.
Image: narvikk/iStockphoto
NEW research has found bananas are photoperiod responsive, overruling the widely accepted belief that temperature is the key variable in banana development.
Seasonal variation in banana production is an issue for growers worldwide, and has driven research focused on what influences the plant’s rate of development and flowering.
The UWA – Chiquita Brands study has found that longer photoperiods—the time from sunrise to sunset—during the reproductive phase, are correlated with an increased rate of bunch appearance at the top of the pseudostem 8-10 weeks later.
Long photoperiods during the mid-vegetative stage hasten flowering, and the 2–3 months before formation of the bunch are most important for photoperiod.
This information is expected to help growers develop better planting timetables to ensure consistent fruit production.
Recently published in CSIRO’s Functional Plant Biology, the study, ‘Evidence that banana (Musa spp.), a tropical monocotyledon, has a facultative long-day response to photoperiod,’ collated data from four major research projects from around the world.
Data from Puerto Rico, Ivory Coast, New South Wales and South Africa were analysed and the sensitivity of the plants to photoperiod in each location were calculated.
The juvenile phase, the mid-vegetative phase, and the flowering phase were studied closely in relation to photoperiod, temperature, soil conditions and overall growth pattern to find what minimised the variation in flowering.
Co-Author and UWA Honorary Research Fellow David Turner says the effects of photoperiod on bananas had not been fully explored before now.
“Originally we thought the development of bananas wouldn’t be responsive to photoperiod but there’s some literature that says temperature isn’t the only thing that explains it,” Prof Turner says.
“Once we got into the numbers we were surprised that the message seemed to be so clear across all locations.
“We had several data sets—we were able to calculate what happened in one and then use those numbers to predict what was happening somewhere else.”
Prof Turner says this information gives plant breeders potential to breed banana crops that are either more or less sensitive to photoperiod.
There is debate whether it is the length of day or the amount of sunshine that is important in photoperiod.
The rate of change of sunrise and sunset and the photoperiod’s effect on plants in the fruit- bearing stage will be studied further.
An experiment initiated in the Canary Islands using artificial light to prolong the photoperiod will test its affects on banana crops in the next year.
Editor's Note: Original news release can be found here.
To feed nine billion people by 2050, global food production needs to increase by 70 percent. Farmers in Africa, and across the world, are using Climate-Smart Agriculture practices to combat the impacts of Climate Change on crop production
Only about 24 percent of Mali's people have electricity. A series of programs is now working to provide more energy, while safeguarding the environment by using renewable sources.
Sometimes the best way to build wealth is to take tips from people just like you. These ordinary people have done incredibly well doing things that anyone can do. Find out the successful ways they have built up wealth here!
Profiles and Strategies Of Some Typical Wealth Builders
#1 The Real Estate Investor
This guy took the “Kiyosaki’s Rich Dad, Poor Dad” series to heart and embarked on a real estate investing rampage starting in 2003. It was prompted by a family crisis involving his disabled child, during which he realized the worries of a parent who wondered how his child would be taken care of once he and his wife could no longer do so. Being in California, it was easy for him to build up equity, take it out and apply it to real estate ventures nationwide. He now owns around 15 houses in various states and somehow manages this “empire” on his off days from his engineering job. Kudos to him. By the way, there’s also a way to fail at this.Main Asset: Hard Work
#2 Stock Market Investor
Everyone's doing this simply by investing in their retirement plans. With the many plans available these days: 401Ks, 403Bs, IRAs, pension plans and such, there’s no way you’ve escaped building wealth in the last 20 years. What I find a little frustrating is that while people invest well in their retirement plans, they don’t do so well with their disposable income. Some acquaintances view their retirement accounts as “serious money” while their disposable income is treated as “play money”. From a casual poll I conducted among colleagues, I found that most weren’t sure what to do with their non-retirement funds, which could be either stuck in cash and CDs or used to do wild, aggressive trades. Reading these books could help The Random Walk Down Wall Street or Asset Allocation: Balancing Financial Risk. Main Asset: Persistence
#3 Stock Market Trader
This other guy does part-time stock trading and seems quite successful at it. Sure, there was a time (circa late 1990′s) when many people tried their luck at day trading and eventually fizzled miserably. But this guy is good. But that’s because he’s some kind of software genius and a mathematical whiz. If I were a betting woman, I’d back this guy on any trade he makes. He says that 99% of wannabe traders will lose out because people like him are there to scalp the noobs. Is it arrogance? Perhaps. But he’s hard-working (he sleeps 3 hours a night to trade after work), is skilled and talented at technical analysis, and has done his homework on that Forex stuff. He’s also very low key, but I can sense that “Millionaire Next Door” aura. Main Asset: Genius
#4 Serial Startup Hopper (or Juggler)
Now here’s the typical way people try to get rich around Silicon Valley, and it was the norm in the 1990′s. It actually worked for a few former colleagues. I admit I joined a startup, but that didn’t pan out. Instead, I lost out on $13,000, the money I spent to own my stock options on the penny to maximize potential return in case the startup I joined actually succeeded. It didn’t work for me, but it did for others, who amazingly went from one successful startup to another, raking in stock options that made them millions with every stint. This regular engineer managed to build a massive fortune by just being at the right places at the right time. He eventually bankrolled his money into a company he founded that netted him at least double his net worth in 8 months. Life flies around here, I guess, and some were born with a clover leaf tattooed on their bum. Of course, that is the exception, but you can’t help but find inspiration in that. Main Asset: Luck
#5 Consultant (or Contractor)
This has worked well for those who ride any kind of job boom, such as the tech wave in Silicon Valley in the previous decade. Depending on the job market, this can be a lucrative strategy. During a tougher job market, your skills and knowledge will be responsible for getting you those higher consulting fees. If you want a big income as a consultant, it’s all a matter of being an expert in a competitive field. Or is the only one offering such a service. Main Asset: Skill
Holiday parties mean much more than free food and fun. They also can bring entrepreneurs many new opportunities to network and build relationships.
Most people think of networking only through traditional venues, whether chamber of commerce events, business contact referral groups, or online sites such as LinkedIn. But holiday parties, including professional and industry social events where you can network with people outside your business, can be an even better time to introduce yourself to a new contact or share a friendly conversation with someone you already know.
To make the most of holiday party networking, here are a few things to keep in mind:
Be prepared. Try to learn in advance the names of people you will likely chat with, their jobs and their recent accomplishments. You will need to do a little homework, a Google search and a look at their LinkedIn or Facebook pages. Use the information you glean to break the ice.
Ask good questions. From the CEO to the intern level, people love to talk about themselves. Here are some suggested conversation starters: How did you get started? What were some of the challenges with. . . ? Have you read any good books lately? My favourite is: How can I help you?
Have a “teaser” topic ready. Approaching the end of the year, every business executive is thinking about how to increase profits and performance in the new year. Have an idea that describes the steps you’d take to improve your networking contact’s business. Make this research part of the homework you do ahead of time. But don’t give away the goose; save the details for a later conversation.
Don’t have more than a couple of drinks. It’s a party, but you don’t want to smell of liquor or be too relaxed when you approach people you want to connect with. Impressions count. Make the right one.
Be confident of your value. Introducing yourself to an executive can be an intimidating experience, so give yourself a pep talk before the party. List your accomplishments over the past year and figure out how you might weave them into conversations. Once you’ve got that down, you should feel good about yourself.
வளைகுடா நாடுகளில் வெளிநாட்டு பணியாளர்களைக் கவரும் பிரதேசங்களுள் ஐக்கிய அரபு அமீரகத்திலுள்ள துபாய் மிக முக்கிய இடத்தைப் பிடித்துள்ளது. வேலைவாய்ப்புக்காக இங்கு வருபவர்கள் பல்வேறு சிரமங்களைச் சந்திக்க வேண்டியுள்ளது. சுற்றுலா விசாவில் வந்தவர்கள் வேலை கிடைத்ததும் சட்டவிரோதமாக பணிசெய்வதால் அந்நாட்டு அரசு பல்வேறு சிரமங்களை எதிர்கொள்ள வேண்டியுள்ளது.
சுற்றுலா விசாவில் வந்துள்ளவர்களைப் பணியில் அமர்த்தும் நிறுவனங்களுக்கு 50,000 திர்ஹம்வரை அபராதம் விதிக்கப்படுவதோடு, அவ்வாறு பணியாற்றும் ஊழியர்களைத் திரும்ப நாடு கடத்தவும் செய்கின்றது. எனினும், துபாய் மோகத்தால் இத்தகைய சட்டவிரோத வேலைவாய்ப்புகள் வெவ்வேறு வகைகளில் நடந்து வருவதை அந்நாட்டு அரசினால் கட்டுப்படுத்த முடியவில்லை.
இந்நிலையில் கடந்த 3 வருடங்களுக்கு முன்பு குடிபுகல் நடைமுறைகளை மாற்றியமைத்து பல கட்டுப்பாடுகளை விதித்தது. அவ்வகையில் சுற்றுலாப் பயணியாக வந்தவர்கள் சம்பளத்திற்கோ அல்லது பயிற்சி பெறும்நோக்கிலோ வேலைசெய்வதைக் கட்டுப்படுத்தியது. எனினும், அங்குள்ள சில நிறுவனங்கள் உடனடியாக நிரந்தர ஊழியர்களை நியமிப்பதைவிட சுற்றுலா விசா காலம் முடிவதற்குள் வேலைவாங்கிக்கொண்டு, அவகாசம் முடியும் தருவாயில் குறைந்த ஊதியத்திற்கு பணியாற்ற ஒப்புக்கொள்ளச் செய்து பிறகு வேலைக்கான விசாவுக்கான நடைமுறையை பின்பற்றுகின்றன.
இதைத் தவிர்க்கும் வகையில் ஐக்கிய அரபு அமீரகத்திலுள்ள துபாய், மூன்று மாதங்கள் செல்லுபடியாகும் குறுகியகால வேலைவாய்ப்பு விசாவை அறிமுகப்படுத்தியுள்ளதாக அந்நாட்டு பணியாளர் நலத்துறை அமைச்சக உயரதிகாரி குமைத் பின் டீமாஸ் தெரிவித்துள்ளதாக செய்தி வெளியாகியுள்ளது. அதன்படி, குறுகிய காலத்திற்கு விசா தேவைப்படும் நிறுவனங்கள் 3 மாதங்கள் செல்லுபடியாகத்தக்க குறுகிய கால "குறிக்கோள் விசா" (Mission Visa) கோரி விண்ணப்பிக்கலாம்.
இது, ஏற்கனவே அந்நாட்டிலுள்ள தற்காலிகப் பணியாளர்களுக்கும் ,புதிதாக விசா வேண்டுபவர்களுக்கும் பொருந்தும் என்றும் தெரிவிக்கப்பட்டுள்ளது. இந்தக் குறுகிய கால விசா வழங்கப்பட்ட 60 நாட்களுக்குள் அந்நாட்டிற்குள் வந்து செல்லவேண்டும். அதிகபட்சம் 90 நாட்கள் இந்த விசா அனுமதியுடன் வேலை செய்யலாம். புதுப்பிக்க வேண்டும் எனில் நாட்டைவிட்டு வெளியேறிய 90 நாட்கள் கழித்தே மீண்டும் புதுப்பிக்க முடியும் என்றும் தெரிவிக்கப்பட்டு உள்ளது.
இந்தக் குறுகியகால விசா மூலம் வருகை தந்தவர்களுக்கு நிரந்தர வேலைகிடைக்கும் பட்சத்தில் புதிய விசாவுக்கு விண்ணப்பிக்க முடியும் என்பது குறிப்பிடத்தக்கது.
Collaborations between Johns Hopkins and National Taiwan University researchers have successfully manipulated the life span of common, single-celled yeast organisms by figuring out how to remove and restore protein functions related to yeast aging.
A chemical variation of a “fuel-gauge” enzyme that senses energy in yeast acts like a life spanclock: It is present in young organisms and progressively diminished as yeast cells age.
In a report in the September 16 edition of Cell, the scientists describe their identification of a new level of regulation of this age-related protein variant, showing that when they remove it, the organism’s life span is cut short and when they restore it, life span is dramatically extended.
In the case of yeast, the discovery reveals molecular components of an aging pathway that appears related to one that regulates longevity and lifespan in humans, according to Jef Boeke, Ph.D.,professor of molecular biology, genetics and oncology, and director of the HiT Center and Technology Center for Networks and Pathways, Johns Hopkins University School of Medicine.
“This control of longevity is independent of the type described previously in yeast which had to do with calorie restriction,” Boeke says. “We believe that for the first time, we have a biochemical route to youth and aging that has nothing to do with diet.” The chemical variation, known as acetylation because it adds an acetyl group to an existing molecule, is a kind of “decoration” that goes on and off a protein — in this case, the protein Sip2 — much like an ornament can be put on and taken off a Christmas tree, Boeke says. Acetylation can profoundly change protein function in order to help an organism or system adapt quickly to its environment. Until now, acetylation had not been directly implicated in the aging pathway, so this is an all-new role and potential target for prevention or treatment strategies, the researchers say.
The team showed that acetylation of the protein Sip2 affected longevity defined in terms of how many times a yeast cell can divide, or “replicative life span.” The normal replicative lifespan in natural yeast is 25. In the yeast genetically modified by researchers to restore the chemical modification, life span extended to 38, an increase of about 50 percent.
The researchers were able to manipulate the yeast life span by mutating certain chemical residues to mimic the acetylated and deacetylated forms of the protein Sip2. They worked with live yeast in a dish, measuring and comparing the life spans of natural and genetically altered types by removing buds from the yeast every 90 minutes. The average lifespan in normal yeast is about 25 generations, which meant the researchers removed 25 newly budded cells from the mother yeast cell. As yeast cells age, each new generation takes longer to develop, so each round of the experiment lasted two to four weeks.
“We performed anti-aging therapy on yeast,” says the study’s first author, Jin-Ying Lu, M.D., Ph.D., of National Taiwan University. “When we give back this protein acetylation, we rescued the life span shortening in old cells. Our next task is to prove that this phenomenon also happens in mammalian cells.”
-Scientific Research
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The research was supported by the National Science Council, National Taiwan University Hospital, National Taiwan University, Liver Disease Prevention & Treatment Research Foundation of Taiwan, and the NIH Common Fund.
Authors on the paper, in addition to Boeke and Lu, are Yu-Yi Lin, Jin-Chuan Sheu, June-Tai Wu, Fang-Jen Lee, Min-I Lin, Fu-Tien Chian, Tong-Yuan Tai, Keh-Sung Tsai, and Lee-Ming Chuang, all of National Taiwan University; Yue Chen and Yinming Zhao, both of the University of Chicago; and Shelley L. Berger, Wistar Institute.
The newfound scientific power to quickly “fingerprint” species via DNA is being deployed to unmask quack herbal medicines, reveal types of ancient Arctic life frozen in permafrost, expose what eats what in nature, and halt agricultural and forestry pests at borders, among other applications across a wide array of public interests.
This is the cover of the report: "Barcoding Life Highlights 2011." Credit: International Barcode of Life initiative
The explosion of creative new uses of DNA “barcoding” — identifying species based on a snippet of DNA — will occupy centre stage as 450 world experts convene at Australia’s the University of Adelaide Nov. 28 to Dec. 3.
DNA barcode technology has already sparked US Congressional hearings by exposing widespread “fish fraud” — mislabelling cheap fish as more desirable and expensive species like tuna or snapper. Other studies this year revealed unlisted ingredients in herbal tea bags.
Hot new applications include:
Substitute ingredients in herbal medicines
Barcoding experts have discovered that high demand is causing regular “adulteration or substitution of herbal drugs,” barcoding experts have found.
Indeed, Malaysian researcher Muhammad Sharir Abdul Rahman, one fraudster in his country, treated rubber tree wood with quinine to give it a bitter taste similar to Eurycoma longifolia — a traditional medicine for malaria, diabetes and other ailments.
A library of DNA barcodes for Malaysia’s 1,200 plant species with potential medicinal value is in development, eventually offering “a quick one-step detection kit” to reduce fraud in the lucrative herbal medicine industry, says Mr Sharir.
His concerns resonate in other countries around the true contents of certain ginseng brands and other products.
DNA barcode libraries are under construction for the medicinal plants of several other nations, including South Africa, India and Nigeria.
Barcoding permafrost
From the woolly rhino to plants and mushrooms, scientists using DNA decipher what lived in the ancient Arctic environment, creating new insights into climate change.
“DNA barcoding” analyses of cylinders of sediment cored from Arctic permafrost ranging in age from 10,000 to several hundred thousand years have shed light on past animal and fungal distributions and allowed researchers to infer which plant species likely co-existed.
DNA analyses of permafrost sediment 15,000 to 30,000 years old from northeastern Siberia revealed a grassland steppe plain during the glacial period supporting a diverse mammal community, including bison, moose and the DNA of the rare woolly rhino, the first ever found in permafrost sediments.
Researchers recently completed a library that characterizes 1,264 of the 1,338 species (94 percent) of butterflies and large moths of Germany. Local agricultural pests and invasive species can now be identified by DNA and distinguished from non-harmful relatives. Credit: A HAUSMANN
Says University of Oslo-based researcher Eva Bellemain, who will present project BarFrost (Barcoding of Permafrost): “In the Arctic, fossils are scarce and time-consuming to find and analyze. However, DNA is one tough molecule. It had to be to serve its purpose the last billion years and more. It can linger in the soil for thousands of years and stay relatively intact.”
What eats what
The technology can even distinguish species contained in the gut or dung of animals, revealing what eats what. University of Adelaide researcher Hugh Cross, for example, will detail his investigation into the diet of Australia’s fast-growing, 1 million-strong population of wild camels, which severely impact the country’s ecology.
Introduced in the 1800s as pack animals, Australia’s wild camels eat 80% of available plant species.
Says conference organizer David Schindel, Executive Secretary of the CBOL, based at the Smithsonian Institution, Washington, D.C.: “Biologists used to sit and wait and watch to learn how food webs work in Nature and what happens when they collapse. Now they can process stomach contents and dung samples to get the complete picture in a few hours.”
Invasive pests
Until now, border inspection to keep agricultural pests, disease-carrying insects and invasive species from entering a country has been a hit-and-miss effort. Barcoding offers a tool to get same-day answers for accepting or rejecting imports, an issue of acute economic importance to Australia and New Zealand.
With European Union funding, a consortium of 20 universities, research institutes, and other organizations are partners in Project QBoL (Quarantine Barcode of Life, www.qbol.org), developing a library of DNA barcodes to help quickly identify common invasive organisms that authorities want to stop at national borders.
With the new DNA barcode tool, inspectors can more easily and surely identify and thus prevent the entry of invading pests, including bacteria, fungi, fruit flies, other insects, nematodes, viruses, plants and other organisms. Trade of timber cut from endangered species may also be slowed with barcodes to identify wood and lumber products.
Hundreds of topics in Adelaide
“From tea to tuna, DNA identification is entering everyday life,” remarked Jesse Ausubel, chair of the International Barcode of Life (iBOL) initiative, a 6-year program now in midstream of a group of the most active labs building the barcode library.
Adds Dr. Schindel: “Like Google and Wikipedia, DNA barcoding scarcely existed a decade ago, and now we are a vibrant community built on 21st-century scientific tools.”
“DNA barcoding is the express lane to solving many of Nature’s mysteries relevant to a spectrum of national interests.”
He notes that scores of additional topics will be explored in Adelaide, spanning health, cultural and environmental protection, such as:
Identifying the prey of disease-carrying insects based on analysis of their meals of blood
“Barcoding Nemo” and other species of the ornamental fish trade
Identifying mushrooms and molds
Assessment of the global status of pollinators such as bees, and
Assessing water quality
The blood meals of biting insects
Resembling a common housefly, the African tsetse fly transmits Human African trypanosomiasis, AKA sleeping sickness, to people and animals. One of the world’s most dangerous disease vectors, it spread the 2008 epidemic in which 48,000 Ugandans died. And the annual economic impact is estimated at US$4.5 billion, with around 3 million cattle killed yearly.
In East Africa, researchers analyzed blood meals of tsetse flies (Glossina swynnertoni), the vector of trypanosomiasis, documenting geographic differences in animal hosts, helping inform local control strategies. Credit: Philip Nguruma
Scientists use DNA barcodes to identify tsetse fly species and their prey based on analysis of the insect’s blood meals, unravelling the relationship between hosts and vectors.
By developing the barcode library, tools and ability to readily distinguish species of tsetse flies, mosquitos, ticks and other vectors of diseases such as malaria, leishmaniasis, schistosomiasis, Japanese encephalitis, and Lyme disease, scientists can map risk areas more efficiently and alert authorities to the spread of health threats.
Barcoders have taken up an ambitious five-year goal a comprehensive library of 10,000 insect species that damage or destroy so many human lives: 3,000 mosquitoes, 1,000 sandflies, 2,000 blackflies, 2,000 fleas and 1,000 tick species.
Nemo and friends
According to scientists, over 1 billion ornamental fish — comprising more than 4,000 freshwater and 1,400 marine species — are traded each year internationally, a US $5 billion industry growing annually at 8 per cent.
Researchers at work on this issue include Gulab Khedkar of India, who says: “To facilitate ornamental fish trading, and in compliance of (India’s) Biodiversity Act, a universal method must validate the ornamental fish with their species names. This can help assure a sustainable ornamental fish trade.”
Fungi
Fungi are a taxonomic group of many prominent, distinct evolutionary lineages, ranging from mushrooms to moulds. Although two species of fungi can be more distantly related than a fish is associated with an insect, all fungi are classified in the same group.
Researchers at the conference are expected to announce the selection of the barcode region for fungi. The standard barcode regions used for animals and plants is not practical for fungi, and an international working group has been conducting comparative analyses of candidate regions for two years. The decision is expected to open the floodgates to fungal barcoding research.
A project on indoor fungi that cause human health problems will also be unveiled in Adelaide, showing the enormous potential for fungal studies.
Australian scientist Wieland Meyer argues that, given steadily increasing invasive fungal infections, inadequate identification, limited therapies and the emergence of resistant strains, “there is an urgent need to improve fungal identification” to improve the successful treatment.
Fungi also provide humanity with food and antibiotics and the services of fermentation and decay. DNA-based taxonomy promises to revolutionize the understanding of fungal diversity and connect their life stages.
Barcoders aim to create a library of at least 10,000 fungal species by 2015, especially for indoor fungi, for basidiomycetes (the “higher fungi”) and for pathogens of agriculture and forestry.
Insect pollinators
The ecosystem service of plant pollination by insects has a global value estimated at more than $400 billion annually.
Facilitated by the International Barcode of Life (iBOL), barcoders are surveying long-term population trends by assembling barcode libraries for all bees and other important pollinators — flies and beetles. Combined with campaigns to barcode moths, butterflies and birds, they will provide the database needed to assess the state of pollinator communities worldwide.
Assessing water quality
Scientists in Southern California and elsewhere are pioneering barcodes to assess freshwater marine water quality and its impact on marine life in, sand, sediment, and rocks or in mud in rivers and offshore.
Traditionally after collecting a bulk water sample, taxonomists must identify by sight several thousand invertebrates, a process requiring months and thousands of dollars. DNA barcodes enable them to analyze bulk samples in a fraction of the time at a fraction of the cost.
Similar projects underway in Korea, Iraq, Belgium and the Baltic region will be presented in Adelaide.
DNA barcoding is emerging as the tool of choice for monitoring water quality, DNA barcode libraries of aquatic insects under construction. New technologies are being developed and tested to allow faster and more complete analyses of entire biological communities in streamwater on ‘DNA microchips’ and through next-generation sequencing.
Says Dr. Schindel: “It used to take weeks or months to analyze the organisms in streams to determine water quality. Now it takes hours at a fraction the cost.”
A global barcode blitz
Scientists in Adelaide will also advance progress towards an international library of barcodes for 500,000 plant, animal and fungi species within five years – “a barcode blitz” that could transform biology science. The Barcode of Life Database includes more than 167,000 reliably named and provisional species today. Butterflies and moths are the largest well-analyzed group, with over 60,000 named and provisional species — much of the world’s estimated total of 170,000.
Gold mines for barcoding are the world’s museums and herbaria, where countless species specimens are concentrated and organized thanks to great investments of time and dollars.
Five Biodiversity Institute of Ontario researchers conducted a barcode blitz in the Australian National Insect Collection a year ago. Focusing on moths and butterflies for 10 weeks, they processed over 28,000 specimens representing over 8,000 species and 65 per cent of the country’s 10,000 known insect species. Meanwhile, at the Smithsonian Institution’s National Museum of Natural History, another team recently barcoded over 3,000 frozen bird tissues from over 1,400 species, adding more than 500 new species to the world avian DNA library, now covering about 40% of known birds.
New DNA extraction techniques bring older and older specimens in natural history museums into the age range where DNA barcoding can be effective. These breakthroughs will open up new research questions about changes in species over the past centuries of human impact on natural populations.
The Munich Botanical Garden is the latest institution with an essential collection of authoritative reference specimens opening its collection to a DNA barcode blitz.
-Latest Research
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The ability to identify and distinguish known and unknown species ever more quickly, cheaply, easily and accurately based on snippets of DNA code grew from a research paper in 2003 to a burgeoning global enterprise today, led by the Consortium for the Barcode of Life (CBOL) at the Smithsonian Institution.
The International Barcode of Life Conference in Adelaide is the 4th series that began at the Natural History Museum, London, in February, 2005.
Potential clues to how autism miswires the brain are emerging from a study of a rare, purely genetic form of the disorders that affects fewer than 20 people worldwide. Using cutting-edge “disease-in a-dish” technology, researchers funded by the National Institutes of Health have grown patients’ skin cells into neurons to discover what goes wrong in the brain in Timothy Syndrome. Affected children often show symptoms of autism spectrum disorders along with a constellation of physical problems.
