Zebrafish Provide New Hope for Cancer Treatment

ScienceDaily (Dec. 20, 2010) — The imaging of tumour growth in zebrafish has revealed for the first time how newly formed cancer cells have the capacity to co-opt the immune system into spreading the disease, leading the way for investigations into potential therapies for eliminating early-stage cancer in humans. Using different coloured fluorescent tags, scientists at the University of Bristol labelled immune cells and tumour-forming cells in the translucent zebrafish in order to track their behaviour and interactions by live cell imaging.
These dramatic findings, which are the result of a collaboration between academic colleagues in the UK (University of Bristol and University of Manchester) and Italy (Institute of Molecular Oncology, Milan) are published in the online, open access journal PLoS Biology.
Tests showed that cancer cells are less likely to proliferate if white blood cells can be prevented from contacting the precursor cancer cells, suggesting that white blood cells -- the immune cells -- have the ability to promote disease by providing some kind of growth signal. Interestingly, the chemical compound that acts as a draw between the two sets of cells was shown here to be hydrogen peroxide -- commonly used as a disinfectant or antiseptic, but also a natural by-product produced by the body's metabolic process.
Describing the work, Paul Martin, Professor of Cell Biology at the University of Bristol's Schools of Biochemistry and Physiology & Pharmacology, who supervised post-doctoral fellow Yi Feng in the research project, said: "By visualizing the earliest interactions between cancer cells and their host environment, we have shown that even from their earliest stages tumours don't just avoid being destroyed by the immune system. Rather, they appear to court an immune response, co-opting the body's innate immune system to aid and abet their growth."
The team used a method to switch on the human oncogene, HRAS, in specific pigment cells (melanocytes) in the skin of early stage zebrafish embryos. Studies were carried out using zebrafish because they conserve many of the molecular and cellular components of tumour formation seen in mammals and are almost translucent, making it easy to see the cells as they move around and grow. Researchers monitored the first hours and days of development and as the embryo grew, some of the cells were transformed, ie, made cancerous by HRAS. Those transformed cells were found to actively attract the innate immune cells. The researchers got the same results, after inserting HRAS into different, mucous-secreting cells, and again when experimenting with a different oncogene, SRC. They discovered that the tumour cells produced hydrogen peroxide and that immune cells were drawn up the hydrogen peroxide gradient towards the cancer.
The researchers' movies show that the immune cells appear to engulf cancerous cells in a bid to destroy them. However, other cells formed cytoplasmic tethers linking them to cancerous cells and in some cases the cancerous cells appeared to drag the immune cells back when they started to leave the region. In order to see whether the tumour was avoiding destruction or actually co-opting the immune cells, the researchers blocked the immune response in three different ways: they prevented the development of immune cells for the first three days of the zebrafish embryos' life, and separately, they used two different strategies to limit hydrogen peroxide production. In each case, immune cells failed to migrate to the cancer site. And each time, when the immune response was blocked, fewer cancer cells formed.
Professor Martin added: "Yi's movies in Zebrafish larvae give us the first insight into how immune cells sense and then attempt to deal with the earliest stages of cancer. Now we can look closer to discover why it is that immune cells seem to aid growth of these young cancer cells and figure out ways for guiding immune cells how better to search and destroy."

UCSB researchers discover new biotechnology to identify and engineer substrates for proteases



This technology should help solve the puzzles of cancer, Alzheimer’s, atherosclerosis and infectious diseases.

Santa Barbara, California – May 1 , 2006 – Researchers at UC Santa Barbara have developed a new biotechnology that enables scientists to identify and engineer protease substrates, giving them the means of crafting pharmaceuticals to outsmart disease. Their work, authored by Patrick Daugherty, an assistant professor of Chemical Engineering, and Kevin Boulware, a PhD candidate, are published online today in the Proceedings of the National Academy of Sciences.
Proteases (or peptidases) are encoded by about two percent of genes in the human genome and play key roles in nearly all diseases. They act as "molecular scissors" by attaching to specific sequences contained within other proteins, called substrates, and cutting them in specific locations. For example, proteases are responsible for digesting food, for determining the proper time for cells to die, and for removing damaged proteins from the body.

But the substrates for most proteases are unknown, and this has limited researchers' ability to facilitate or thwart protease action. By identifying substrates, scientists gain the ability to regulate protein function, creating the capacity to speed up, slow down or eliminate particular protease actions. Daugherty's approach also makes it easier to measure protease action and thus develop pharmaceuticals that control protease activity.

Daugherty and Boulware developed a general combinatorial approach to identify optimal substrates of proteases, using quantitative kinetic screening of cellular libraries of peptide substrates (CLiPS). The results suggest that CLiPS will be broadly useful for characterizing proteases and developing optimal substrates for therapeutic applications.

Of the roughly 1,000 proteases in the human genome, only about ten percent of the targets have been identified, but Daugherty believes that scientists will identify nearly all of them in the next five to ten years. "This technology will give us a scalable tool that will allow us to effectively tackle this challenge," he says.

Mice missing protein burn more fat



PHILADELPHIA — Scientists are learning how they might stoke the body’s fat-burning furnace by turning up a molecular thermostat.

Mice lacking a protein that responds to the hunger-promoting hormone ghrelin burn more energy in their brown fat than other mice, Yuxiang Sun of Baylor College of Medicine in Houston reported December 13 at the American Society for Cell Biology’s annual meeting. This revved-up brown fat helps keep mice lean and energetic into middle age. The finding could eventually lead to a way to help people fight obesity.

Brown fat burns energy instead of just storing it the way white fat does. This metabolically active fat is important in helping rodents and other animals maintain their body temperature. Recently researchers learned that adult humans have brown fat, and that the amount of energy burned by brown fat decreases with age and weight. The discovery has spurred interest in learning how to turn brown fat on.

Sun and her colleagues didn’t start out trying to rev up brown fat. Because the hormone ghrelin has been shown to make animals eat more, the researchers reasoned that blocking the molecule’s activity might reduce appetite and help animals and people lose weight. Sun and her colleagues genetically engineered mice to completely lack either ghrelin or the ghrelin receptor, a protein that interacts with ghrelin and sets off a series of biological reactions in cells that leads to the hormone’s effect.

Disappointingly, mice lacking either molecule ate and exercised just as much as normal mice. But mice lacking the ghrelin receptor burned more energy and stayed lean even as they aged, while normal mice and mice lacking ghrelin tended to gain weight as they got older.

Mice missing ghrelin had a hard time maintaining their body temperature when placed in the cold. But mice without the ghrelin receptor stayed warm. Those pieces of evidence led Sun and her colleagues to examine brown fat in the mutant mice.

Sun’s team found that removing the ghrelin receptor causes brown fat cells to make more of a protein called UCP1. That protein makes the cell’s power plants less efficient and as a result, they release more heat. These inefficient brown fat cells may burn their own supply of fat and then gobble up fat that otherwise would be stored in white fat cells, leading to leaner rodents, Sun speculated.

If researchers can discover why removing the ghrelin receptor turns up brown fat’s furnace, it may be possible to design a drug that will do the same thing. “There may be more than just exercise and willpower that can keep us in shape,” Sun said.

There is no question that increasing the activity of brown fat can have a big effect on weight, said Lewis Landsberg, an endocrinologist at Northwestern University in Evanston, Ill. About 10 percent of a rodent’s total energy expenditure comes from brown fat. Extrapolating to humans, turning up brown fat to burn a similar amount of a person’s calories would be about equal to the energy burned while walking 2.5 miles each day, he said.

Landsberg said that it is not clear whether removing the ghrelin receptor directly affects the energy expenditure of brown fat or if the mutation somehow spurs the sympathetic nervous system to turn up the furnace.

Sun hopes to answer that question by removing the ghrelin receptor in just brown fat cells.

Cells reprogrammed to treat diabetes



PHILADELPHIA — Sperm-forming stem cells in the testes can be converted to insulin-producing cells that could replace diseased ones in the pancreas, researchers from Georgetown University Medical Center in Washington, D.C., reported December 12 at the annual meeting of the American Society for Cell Biology. The new technique is edging closer to producing the amount of insulin needed to cure diabetes in humans.

Ian Gallicano, a developmental biologist at Georgetown, and his colleagues isolated sperm-producing stem cells from the testes of organ donors. These cells could easily revert to an embryonic state, capable of making nearly any cell in the body. The Georgetown researchers treated the cells with chemicals to coax them into mimicking beta-islet cells from the pancreas, the same kind of cells that are compromised in diabetes.

Reprogrammed sperm-producing cells cured diabetes in mice for about a week before their insulin levels dropped again. “If you’re a mouse and you have diabetes, you’re in good shape these days,” Gallicano says.

But cells need to make much more insulin in order to cure diabetes in humans. In islet cells in the human pancreas, insulin accounts for about 10 percent of the proteins secreted by the cell. No stem cell from the testes or anywhere else has come close to making that amount of insulin, Gallicano says. He and his colleagues have developed a new way of programming insulin-producing cells and are getting closer to the goal of creating islet-like cells in which insulin accounts for 1 to 10 percent of the proteins in the cells.
Although testes-derived stem cells would be useful only for men, Gallicano thinks the tricks he’s developing could be adapted to other stem cells that could help women with diabetes too.

Apartments share tobacco smoke


Children in nonsmoking families have higher levels of secondhand exposure if they live in multifamily dwellings.
By Janet Raloff

Children who grow up in apartment buildings are more likely to inhale secondhand tobacco smoke than are kids living in detached homes, a new study finds — even if no one in their household ever lights a cigarette.

“This is the first study to show significant evidence of increased tobacco-smoke exposure among children who live in multi-unit housing,” reports pediatrician Jonathan Winickoff of the Massachusetts General Hospital for Children in Boston, who directed the study. Compared to children who grew up in detached houses, his team finds that those living in apartments excreted 45 percent more cotinine, which is a marker of nicotine exposure. The findings were released online December 13 in Pediatrics.

“Our new study is really the last link in the chain of evidence demonstrating the need for smoke-free buildings,” Winickoff says, “because it proves that children are absorbing that smoke.”

Overall, depending on the type of dwelling in which they lived, cotinine concentrations were quite low, averaging 0.053 to 0.075 nanograms per milliliter of urine among all 5,002 kids, aged 6 to 18. But a host of studies have linked even low-level exposures to behavioral changes and increased risk of allergy and asthma.

“The 2006 surgeon general’s report is clear: There’s really no safe level of secondhand smoke,” notes Gary Adamkiewicz of the Harvard School of Public Health, an environmental health scientist unaffiliated with the new research.

In the new study, Winickoff’s team examined data collected as part of the National Health and Nutrition Examination Survey conducted between 2001 and 2006 by the U.S. Centers for Disease Control and Prevention. Almost three-quarters of children excreted cotinine, including 84.5 percent living in apartments and 70 percent of those from detached homes. There was less than a 1 percent probability that the difference was due to chance. The prevalence of cotinine residues in children from attached homes fell in between.

The common occurrence of the smoke marker among children living in detached houses points to the importance of community exposures, Winickoff says. Kids may have been exposed by being near a parent's smoky clothing, by walking though doorways where smokers are clustered, riding in cars with a smoker or hanging out indoors where smokers previously have lit up.

While dramatic, the new findings hardly come as a surprise, since another recent study measured nicotine from tobacco smoke tainting the air in roughly 90 percent of 49 low-income apartments inhabited by nonsmokers.

“Our study confirmed on-the-ground evidence that folks who live in multi-family housing were reporting,” explains Adamkiewicz, an author of that study. People in nonsmoking residences often could smell smoke, which likely seeped in through ventilation systems, cracks around plumbing or under doors.

Concentrations that his team measured were low — “but not trivial,” he says. They were highest in those households where the residents had reported smelling smoke most frequently. By analyzing air movement in and out of an apartment, “we could calculate how many cigarettes someone would have had to have smoked to yield this level of nicotine in the air,” he says. “And in the apartments of nonsmokers, it started to approach a cigarette a day.” His team reported its findings in the December 2009 Tobacco Control.

The new study takes those results a step further, Winickoff says. “Although we now protect bartenders and people in restaurants in many places from secondhand smoke, we’ve forgotten to protect one critical segment: where children live.” But owing to the strong data that his team has just turned up, he says, “Landlords are soon going to be deciding not whether to go smokefree but how soon to go smokefree.”

And if they don’t, the Department of Housing and Urban Development may force the issue, says toxicologist Bruce Lanphear of Simon Fraser University in Vancouver, British Columbia. “You can’t ban smoking in private housing,” he acknowledges, “but HUD can ban smoking in public housing if there’s sufficient evidence to suggest that it’s in the best interest of kids’ health.”

Another reason the new study is important: It points to housing-related issues, Lanphear says, that at least on a population level may explain why kids in certain ethnic and low-income communities “have higher rates of wheezing or learning problems.”

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Legionnaires' caught from compost

A hidden danger in the garden has been highlighted by the case of a man who contracted Legionnaires' disease from handling compost.


Doctors discovered that the 67-year-old man was infected through a cut in his hand.

Reporting the "rare" incident in The Lancet medical journal, they said compost was known to harbour Legionnaires' bugs.

The man, described as previously fit and healthy and a "keen gardener", was inexplicably struck down by a serious fever in March.

Doctors saw him in hospital after eight days of trembling, confusion, lethargy and shortness of breath. He had a high temperature and an X-ray revealed signs of pneumonia in his left lung.

Dr Simon Patten and colleagues from the Royal Alexandra Hospital, Paisley, Scotland, wrote: "We treated our patient with oxygen, intravenous fluids and antibiotics, but his respiratory function deteriorated, necessitating transfer to the intensive care unit for intubation."

"When we questioned the patient to find out the source of this infection, we discovered that he was a keen gardener and had lacerated his left index finger two days before the onset of his symptoms, while planting with compost," they wrote. "We presumed that this cut was the site of entry of the organism."

The patient's condition improved, and seven days later he was moved to a respiratory ward before being discharged.

Legionnaires' disease is normally caused by the bug Legionella pneumophili, which lives naturally in rivers, lakes, and reservoirs, and can also be found in man-made structures containing water such as air conditioning systems. Legionella longbeachae is a less common species first isolated from a patient in Long Beach, California. Unlike its cousin, it is mostly found in soil and potting compost. Infection by this type of Legionnaires' bug is sometimes called Pontiac Fever.

In the UK, just nine cases have been reported since 1984. L. longbeachae infections are much more common in Australia, New Zealand and Japan, where it accounts for about 30% of all cases of Legionnaires' disease. They added: "The UK Royal Horticultural Society has issued warnings about the risk of contracting Legionnaires' disease from handling compost and has announced that bags of potting compost will carry cautionary statements."

Self-Irrigating Desert Plant Discovered



A desert plant has apparently figured out how to water itself.

Ecologists had been puzzling over the desert rhubarb for years: Instead of the tiny, spiky leaves found on most desert plants, this rare rhubarb boasts lush green leaves up to a meter wide.

Now scientists from the University of Haifa-Oranim in Israel have discovered that ridges in the plant’s giant leaves actually collect water and channel it down to the plant’s root system, harvesting up to 16 times more water than any other plant in the region.

“It is the first example of a self-irrigating plant,” said plant biologist Gidi Ne’eman, a co-author on the paper published in March in Naturwissenschaften, a German journal of ecology. “This is the only case we know, but in other places in the world there might be additional plants that use the same adaptions.”

The desert rhubarb grows in the mountainous deserts of Israel and Jordan, where there’s only about 75mm of rainfall each year. Even during the rainy season, the region’s light rainfalls often don’t penetrate the rocky soil of the desert. Plants with large leaves and a deep root system, like the desert rhubarb, typically can’t survive in such an arid climate.

But when the researchers measured the plant’s water absorption during a light rain, they discovered that water infiltrated the soil 10 times deeper around the desert rhubarb than in surrounding areas. Upon closer examination, scientists discovered deep grooves around the plant’s veins, which are coated in a waxy cuticle that helps channel water down to the root.

“Even in the slightest rains,” the researchers wrote, “the typical plant harvests more than 4,300 cubic centimeters of water per year and enjoys a water regime of about 427 millimeters per year, equivalent to the water supply in a Mediterranean climate.”

Some scientists say the desert rhubarb isn’t all that, however. “Many plants channel water to their base to be absorbed by the root,” Lindy Brigham, a plant ecologist from the University of Arizona, wrote in an email. “Just look at the way plant leaves are shaped and how they branch from the base in many cases.” The architecture of the desert rhubarb’s leaves is unusual, she said, but not necessarily the only example of this adaptation.

Square Watermelons! It's true.



It's not a fad. The technique actually has practical applications. "The reason they're doing this in Japan is because of lack of space," said Samantha Winters of the National Watermelon Promotion Board in Orlando, Florida.

A fat, round watermelon can take up a lot of room in a refrigerator, and the usually round fruit often sits awkwardly on refrigerator shelves. But clever Japanese farmers have solved this dilemma by forcing their watermelons to grow into a square shape.

Farmers insert the melons into square, tempered glass cases while the fruit is still growing on the vine.

The square boxes are the exact dimensions of Japanese refrigerators, allowing full-grown watermelons to fit conveniently and precisely onto refrigerator shelves.

But cubic fruit comes with a price: Each square watermelon costs 10,000 yen, the equivalent of about $82. Regular watermelons in Japan cost from $15 to $25 each.

Japanese farmers have perfected the art of growing square watermelons, but they aren’t about to reveal their secret process. When a square watermelon sells for $82 who can blame them.

Buddha shaped Pears

Gao Xianzhang has managed to create what some would call the holiest fruits ever, pears shaped like


Gao has been working on his pear-growing technique for six years and this season he managed to grow 10,000 Buddha-shaped baby pears. Each fruit is grown in an intricate Buddha mould and ends up looking like a juicy figurine. The ingenious farmer says the locals in his home village of Hexia, norther China, have been buying his Buddha pears as soon as he picks them from the trees. Most of them think they are cute and that they bring good luck.

Gao Xianzhang pears aren’t cheap, roughly $1.8 each, but their success in China convinced him to start exporting them into Europe.

Lifeline Hospitals & Loyola College joint PG Diplomo course on "Stem Cell Therapeutics"

Loyola College (LIVE), Chennai & Lifeline Institute of Regenerative Medicine (LIRM), Perungudi, Chennai jointly invites applications for the following course.


Course:
P.G. Diploma in “Stem cell therapeutics”.


Duration:
01 year program
03 hours of class per day on weekdays.


Eligibility:
BTech / Msc Life Sciences/ MBBS/ BDS/ BVSc and final year candidates also may apply.


Course Commencement:
17 August 2009


Application deadline:
10 August 2009


To apply:
Contact: 09884407195/ 09840940283

Email: stemcell.lirm@gmail.com / lirm@lifelinehospitals.com

Lifeline Institute of Regenerative Medicine also offers:

1. Special trainings and projects in stem cell research to all branches of life science students through out the year.
2. Special training on the advanced flowcytometric techniques (FACS Aria).

Loyola College (LIVE) also offers:
1) Summer training / project works on Bioinformatics and Medical Transcriptions to all branches of life science students through out the year.

TURTLES MAKE SENSE AFTER AL

Evolutionary development study describes a critical fold that sends the reptile off on its own By Susan Milius
Turtles may be weird, but according to new research, they’re not that weird. Their funny arrangement of shell and shoulder is just the same old land-dweller vertebrate stuff — with a little fold.

At first a turtle embryo grows much like a chicken or mouse. But then the developing body wall makes a critical fold, and the usual body plan starts to become an unusual turtle, Hiroshi Nagashima of Kobe University and his colleagues report in the July 10 Science.

Nothing else has a body plan like a turtle. Its ribs don’t grow inside its chest as a cage but instead fuse in the developing skin layer on its back to create one bony armored covering.

“It is not just that turtles 'grew a shell,'” says paleontologist Ben Kear of La Trobe University in Melbourne, Australia. In the evolution of that shell, bones and muscles had to shift around relative to other reptiles, birds and mammals, and turtle shoulders ended up inside the rib cage. “In essence this means that the turtle skeleton is inside-out,” he says.

Odd as they are, turtles clearly belong to the lineage of amniotes, which includes mammals, birds and reptiles. Turtles, which are at least 200 million years old, “have survived all kinds of stuff — we’re talking extinction of the dinosaurs and myriad climate changes,” Kear says. Yet there’s scant fossil evidence of turtles in the making to explain how their forms arose as they split off from birds and crocodiles.

Knowing how a basic amniote embryo ends up developing into something so radically different could shed light on turtle history, says paleontologist Michael Lee of the South Australian Museum in Adelaide. “Some intermediate stages in this process might resemble real intermediate — fossil — stages in evolution,” he says.

To sort out how turtles develop, Nagashima and his colleagues worked with eggs of Chinese soft-shelled turtles (Pelodiscus sinensis) bought from a farm. The researchers used tissue-specific stains as well as substances that detect activity of particular genes to figure out which bits of the tiny embryos were on their way to becoming the bones and muscles of the adult. At each stage in development, the researchers compared their embryos with developing chickens and mice at comparable stages.

Any features shared by all three embryos probably came from distant common ancestors of all amniotes, including people, the researchers note.

In turtles, chickens and mice, the earliest stages of development looked much the same, the researchers reported. Then the turtle embryos veered off on their own path. The developing muscle tissue that would lie along adult ribs in a standard amniote began to fold underneath itself in the turtle. This tissue tucked inward, bending up to lie below the developing ribs. On this kinked-under section, the shoulder blades, or scapulas, formed.

If this fold could be straightened out, the scapulas would lie outside the rib cage, as they do in chickens, mice and people. For turtles then, “the position of the scapula is not a novelty,” Nagashima says. Essentially, “turtles have the same body plan as other amniotes.”

That critical fold in the tissue maps out the line that becomes an important embryological feature of turtle embryos called the carapacial ridge. Earlier research has shown that this ridge drives the development of the bony back of the animal. The fold also allows developing muscles to form connections in ways that they don’t in the mouse and the chicken.

The researchers also noted that the turtle ribs stop short in comparison with mice and chickens. Turtle ribs grow out only along the sides of what will become the backbone instead of curving into the body wall to form the whole rib cage. Those short turtle ribs mingle with the skin tissue creating the fused bony shell on the turtle’s back.

“Very, very sophisticated work,” says reptile paleontologist Olivier Rieppel of the Field Museum in Chicago in describing the extensive detective work required to trace all the tissues and muscles.

He has studied the oldest known fossil of an ancestral turtle, and he says the new interpretation of turtle embryology may fit well with the fossil record. Last year he and colleagues described Odontochelys semitestacea from a fossil collected in 220-million-year-old marine sediments in southwestern China. The turtle had a standard armored underside but not a full shell on its back. Its ribs widened, but its shoulder blades still lay forward of instead of inside the ribs.

Nagashima speculates that the embryonic fold was evolving a bit at a time and maybe hadn’t reached as far around the body in this ancestral turtle as it does today. Clever suggestion, Rieppel says.

To understand turtle history, paleontologists really need more fossils, says Robert Reisz of the University of Toronto’s Mississauga campus in Canada. In the meantime, the new Japanese paper “clarifies a unique evolutionary event, one that gave rise to a really neat group of animals, our beloved turtles.”

Calorie-Counting Monkeys Live Longer


Rodents, yeast, and roundworms all have something in common: They live longer when they consume less. Now a primate has joined the calorie-restriction club. After 20 long years of waiting, scientists have concluded that rhesus monkeys that eat nearly a third less food than normal monkeys age more slowly. The results come as close as any can to proving that calorie restriction could significantly slow aging in humans--even if such a lean diet would not appeal to most of us.
Researchers first discovered the connection between lean diets and extended life spans in a 1935 study of calorie-restricted rats. In the past decade, studies in yeast and worms have pinpointed some genes that may be responsible. Scientists believe the genes somehow ramp up systems to protect an organism from environmental stress and may have evolved to help organisms survive in environments where food was scarce. In rodent studies, calorie restriction can extend life span by 20% to 80%. Whether calorie restriction also slows aging in primates wasn't known, however.

Two decades ago, three different research groups in the United States decided to fill this gap. The groups have previously published updates on their monkeys' health, but in tomorrow's issue of Science, one of them reports survival data from their colony of 76 rhesus monkeys. The team, led by gerontologist Richard Weindruch of the University of Wisconsin, Madison, began monitoring the animals when they hit 7 to 14 years old--monkey adulthood. Researchers allowed half of the monkeys to eat as much as they wanted during the day, while restricting the other half to a diet with 30% fewer calories. The scientists gave the restricted monkeys vitamin and mineral supplements to ensure they did not suffer malnutrition and treated any animals that fell sick, says Weindruch.

Studying aging in monkeys takes patience. Mice and rats only live for a couple of years, while these monkeys can live to 40, and the average life span is 27 years. Now that the surviving monkeys have reached their mid- to late 20s, the Wisconsin group could glean how calorie restriction was affecting their life span. Sixty-three percent of the calorie-restricted animals are still alive compared to only 45% of their free-feeding counterparts. For age-related deaths caused by illnesses such as cardiovascular disease and cancer, the voracious eaters died at three times the rate of restricted monkeys: 14 versus five monkeys, respectively. Another seven control and nine lean monkeys died from causes not related to aging such as complications from anesthesia or injuries. Leaner diets also reduced muscle and brain gray matter deterioration, two conditions associated with aging. (The team has not yet studied cognitive differences between the two groups.)

Researchers who study aging are split on how much stock to put in the study. Leonard Guarente, a molecular biologist at the Massachusetts Institute of Technology in Cambridge who has studied aging in yeast, believes that not enough monkeys have died yet to make definitive comparisons between the two groups. As of March, when Weindruch's group submitted the paper, about half of the colony was still alive. "The gap [in survival rates] may separate more, but it's still too early to tell," Guarente says. On the other hand, molecular biologist Matthew Kaeberlein of the University of Washington, Seattle, thinks the gap as it stands now is still compelling. He points to the difference in age-related deaths between the two groups as the more relevant statistic. "The fact that they see a significant effect at this point suggests there will be a robust effect when they finish the study," he says.

Weindruch and his collaborators plan to continue monitoring the remaining monkeys, which could stretch the study's length past 3 decades. "If we reach the 40-year-old life span, the study could continue for another 15 years," Weindruch said. "That would probably round out my career."

IISc to extract oil from Diatoms, algae


Driving will soon be a pollution-friendly activity if a small team of scientists from India and Canada have their way. Scientists at the Indian Institute of Science (IISc) have collaborated with their counterparts in Canada to ensure that global warming becomes a thing of the past.

According to the scientists, the answer to a clean and sustainable energy production lies in the microscopic algae — diatoms.

Some geologists believe that a majority of the world’s crude oil originated from diatoms. “Diatoms are the lowest in the order of the food chain, but are known to have oil glands that can yield an effective amount of oil. They also act as carbon sequesters trapping in carbon and releasing oxygen. We hope that this could work as a replacement for conventional energy or gasoline paving the way for a clean fuel that can effectively work as a solution to tackle global warming,” said Dr T.V. Ramachandra at IISc.

The research, that will soon be published in an international journal, indicates that a solution to the impending crude oil scarcity exists. It offers solutions for a cost-effective renewable source of alternative energy and also helps stop the emission of carbon dioxide into the atmosphere to an extent. Diatoms can trap and store carbon, sending out emissions free of any pollutants.

The team that comprises IISc professors Durga Madhab Mahapatra, Karthick B. and Dr Ramachandra and Richard Gordon from the University of Manitoba in Canada have also proposed a new approach to sustainable energy that uses solar panels by incorporating altered diatoms that secrete oil products.

IBAB- Job assured Biotechnology / Bioinformatics PG diplomo courses admissions- 2009

Institute of Bioinformatics and Applied Biotechnology (IBAB) (Government of Karnataka), Bangalore,invites applications for the following job oriented courses which almost has 100% placement record.


Courses:
Postgraduate Diploma in Bioinformatics
Postgraduate Diploma in Biotechniques
Postgraduate Diploma in Cheminformatics


Eligibility:
B.Sc /B.Tech /M.Sc /M.Tech and final year students awaiting final results.


Selection method:
Written test and Interview


Application deadline:
12 July 2009
Date of entrance test:
19 July 2009

Need Hydrogen Storage? Think Poultry

By Phil Berardelli
ScienceNOW Daily News
23 June 2009

Here's a case for which solving an energy problem could ease a challenging environmental problem as well. Researchers have discovered that carbonized chicken feathers could provide an inexpensive, environmentally friendly way to store hydrogen fuel for future motor vehicles. If the concept is proven--and perhaps a bigger if, accepted by the automobile industry--it could go a long way toward helping to dispose of the 2.7 billion kilograms of chicken feathers generated each year by commercial poultry operations.
Hydrogen is a leading alternative fuel for vehicles. The byproducts of its combustion are nonpolluting, and its source--water--is superabundant. One hitch is the amount of energy required to manufacture it, and another is storing enough of it onboard to give vehicles a cruising range that approaches that of gasoline or diesel fuel. Hydrogen has proven notoriously difficult to store in sufficient quantities without placing it under enormous pressure, something that greatly adds to the weight of a vehicle and adds a serious explosion hazard. The best idea so far has been carbon nanotubes--microscopic structures that can pack away large quantities of hydrogen at normal pressure within a relatively small space. But a storage tank made of the nanotubes would cost millions of dollars.

Now a team at the University of Delaware, Newark, says it has an unlikely candidate: chicken feathers. It turns out that the feathers, which are made of keratin--the same protein in fingernails and beaks--comprise strong, hollow tubes. The team, led by chemical engineer Richard Wool, had been investigating the feathers' potential for improving the performance of electronic microcircuits. The air inside the tubes helps to speed electrons along the printed wiring, but the feathers weren't stiff enough to hold the circuit boards together very well. So the team tried a heating technique to strengthen the bonds between the carbon atoms in the keratin.

As the team reported today at the 13th Annual Green Chemistry and Engineering Conference in College Park, Maryland, carbonizing the feathers gave them a strength approaching that of the nanotubes. They could also store up to 1.7% of their weight as hydrogen, about as much as carbon nanotubes could store. Moreover, the feathers cost virtually nothing to produce. "They're a nuisance commodity," says Wool.

The researchers estimate that a hydrogen-storage tank using the carbonized feathers would cost only about $200 when mass-produced. It's a major step forward, but the U.S. Department of Energy has set a target capacity for hydrogen-storage techniques of 6% of weight, so the carbonized feathers need improvement. Still, Wool is confident that the goal can be achieved. "There are all kinds of next steps," he says.

Even if hydrogen doesn't become the next primary transportation fuel, finding a safer and economical way to store the gas would still be of great value, says chemical engineer John Dorgan of the Colorado School of Mines in Golden. Hydrogen has several important nontransportation uses, he explains, such as a cooling medium in electricity generation. So the innovative storage technique developed by Wool and his team could be much less hazardous than pressurized tanks. In addition, he says, "it simply makes sense to use renewable materials to build the renewable energy infrastructure."

Soybeans Grow Where Nuclear Waste Glows


Soy crops are so tough they can flourish in the contaminated soil around Chernobyl and produce healthy offspring.

If scientists can understand how plants survive in ultra-hostile environments, it will help them engineer super hearty plants to withstand drought conditions or grow on marginal cropland.

“The fact that plants were able to adapt to the area of the world’s largest nuclear accident, is very encouraging,” says Martin Hajduch, a plant biotechnology expert at the Slovak Academy of Sciences and coauthor of the study in the Journal of Proteome Research. “So we were interested to know how plants can do such a job.”

Hajduch’s team built and harvested seeds from a garden near the village of Chistogalovka, which is roughly five kilometers from the ruined nuclear power plant. They analyzed the seeds with all sorts of modern proteomics tricks, going a step beyond the narrowly-focused studies that other scientists have done.

Biologists have been studying the effects of radiation on plants for decades, and they have identified a handful of proteins that seem to protect crops from genetic damage, but this is the first time that anyone has taken a snapshot of everything that’s going on inside of Chernobyl-grown vegetables.

The Slovak scientists started by freezing each seed with liquid nitrogen and crushing it to extract a mix of proteins. Then they sorted those molecules in an electrified block of gel, and identified each one with a mass spectrometer. As a reference, they did the same thing to seeds from a garden 100 kilometers from the disaster area.

Hajduch learned that the contaminated plants make a lot of changes to defend themselves, adjusting the levels of dozens of proteins that also guard against disease, heavy metals, and salt. All of that makes sense, but the biggest difference between plants from the wasteland and the controls was somewhat surprising. The levels of hundreds of proteins that are known for their ability to shuttle other proteins around — or lock them up in storage — had been lowered.

As a result of those adjustments, the levels of Cesium-137 in the beans was remarkably low. The plants are healthy and fertile, but definitely not safe to eat.

TEST MIGHT ASCERTAIN WHO NEEDS APPENDECTOMY

Biomarker in urine could minimize unnecessary surgery By Nathan Seppa

A compound identifiable in urine might help doctors distinguish appendicitis from other abdominal problems and avoid needless surgery, researchers report online June 23 in the Annals of Emergency Medicine.

Because signs of appendicitis are particularly difficult to assess in young children and elderly adults, surgeons unnecessarily remove a healthy appendix in 10 to 20 percent of appendectomies performed in the United States, says pediatrician Alex Kentsis of Harvard Medical School and Children’s Hospital Boston.

True appendicitis, on the other hand, often goes untreated because it may cause few symptoms until the appendix ruptures. At that point, a patient risks intestinal infection and severe complications, Kentsis says.

In an effort to find biomarkers that tip off appendicitis better, Kentsis teamed with biochemist Hanno Steen and physician Richard Bachur, both also at Children’s Hospital, to test for 57 compounds in the urine of 67 children being treated for suspected appendicitis. The children had an average age of 11.

Overall, 25 of these patients were found to have appendicitis and underwent surgery. The diagnoses resulted from physical examination, symptom assessment and tests such as CT scans, ultrasounds or other measures. Tissue analysis after surgery confirmed the original diagnoses.

In conducting the urine sample analysis, the researchers didn’t know which children were ultimately diagnosed with appendicitis and which had other diagnoses. These included ovarian cysts, constipation, abdominal pain or other problems that were ascertained by follow-up phone calls six to eight weeks later.

The compound that stood out among the children with appendicitis was leucine-rich alpha-2-glycoprotein, or LRG. Immune cells called neutrophils make LRG. “Release of LRG from neutrophils is a kind of specific feature of appendicitis,” Kentsis says.

LRG is not the only compound overproduced during an attack of appendicitis. But in this analysis, it was the most reliable biomarker to show up in the urine. High levels of LRG in the urine correctly identified a child who had appendicitis and low LRG levels suggested no appendicitis 97 percent of the time, the researchers found.

“They may have found a biomarker that’s really sensitive,” says Robert C. Barber, a geneticist at the University of Texas Southwestern Medical Center at Dallas. “This is a very interesting finding.” Nevertheless, he cautions, “appendicitis is unlikely to have a magic bullet biomarker.” More likely, researchers will eventually need more than one.

Kentsis agrees, noting that other teams have already found some promising biomarkers. “You could imagine using them in combination, if one isn’t sufficient,” he says.

The team will now concentrate on validating the new findings and creating a simpler, clinic-ready kit for testing urine, Kentsis says. Meanwhile, the researchers plan to look at whether the LRG test might also work in adults.

The use of CT scans and ultrasound has improved appendicitis diagnosis in recent years, but these tests still fail to catch some inflamed appendices and wrongly pinpoint healthy ones, the authors note. Also, in some regions of the world, Kentsis says, such high-tech diagnostics just aren’t readily available.

Gene Protects Alcoholism


In an interesting finding, a study revealed that a gene variant detected among a tribe in Orissa has been protecting them from harmful effects of alcohol.

The study conducted by the department of anthropology at Utkal University here has showed that the Bondas — one the most primitive tribes of Orissa- are immune to the side effects of alcoholism.

Alcohol is an agent of cirrhosis of liver, toxic psychosis, gastritis, pancreatitis, cardiac myopathy and so on. But surprisingly none of these diseases are seen among the Bonda highlanders, who are addicted to different kinds alcoholic beverages.

The reason: presence of a gene variant ALDH2.

Jayant Kumar Nayak, a research scholar of Anthropological Survey of India, in association of with the Utkal University has conducted a study on Bondas to know whether they are genetically protected from alcoholism. On a proportionate random sampling, out of 25 villages, he selected nine for the study covering 714 households of 2,700 population. Genomic DNA was extracted from 110 unrelated adult Bondas by the ASI following ethical guidelines after taking their consents. Both ADH and ADLH2 genes, considered protecting variants for alcohol, were detected.

Curry leaves Fights Tooth Decay


The curry leaf tree (Murraya Koenigii spreng – a green leafy vegetable) is grown all over India and other countries for its aromatic leaves which are used daily as an ingredient in Indian cuisine.

The fresh curry leaves contain 2.6% volatile essential oils (containing sesquiterpenes and monoterpenes) and the essential oils in the curry leaves are sufficiently soluble in water.

They contain 21000mug total carotene, 7100mug beta carotene, 93.9mug total folic acid, 0.21mg riboflavin, 0.93mg iron, 830mg calcium, 57mg phosphorus and 0.20mg zinc per 100g.

The cold extract of curry leaves (10g of cut fresh curry leaves in 200ml of distilled water) has a pH of 6.3 to 6.4. (unpublished personal observations). Chlorophyll has been proposed as an anticariogenic agent and it also helps to reduce halitosis8.

We have observed that holding curry leaves in the mouth for 5 to 7 minutes is helpful in reducing halitosis and that the terpenes have been found to reduce airborne chemicals and bacteria.

In addition to the presence of EO, the curry leaves contain chlorophyll, beta carotene and folic acid, riboflavin, calcium and zinc and all these can act on the oral tissues and help in keeping up good oral health. Chewing 2 to 4 fresh curry leaves with 10 to 15mls water in the mouth, swishing for 5 to 7 minutes and rinsing the mouth out with water can be of help in keeping good oral hygiene and as the curry leaf is a green leafy vegetable it will be safe and cheap to use as mouthwash. as an ingredient in Indian cuisine.

The fresh curry leaves contain 2.6% volatile essential oils (containing sesquiterpenes and monoterpenes) and the essential oils in the curry leaves are sufficiently soluble in water.

They contain 21000mug total carotene, 7100mug beta carotene, 93.9mug total folic acid, 0.21mg riboflavin, 0.93mg iron, 830mg calcium, 57mg phosphorus and 0.20mg zinc per 100g.

The cold extract of curry leaves (10g of cut fresh curry leaves in 200ml of distilled water) has a pH of 6.3 to 6.4. (unpublished personal observations). Chlorophyll has been proposed as an anticariogenic agent and it also helps to reduce halitosis8.

We have observed that holding curry leaves in the mouth for 5 to 7 minutes is helpful in reducing halitosis and that the terpenes have been found to reduce airborne chemicals and bacteria.

In addition to the presence of EO, the curry leaves contain chlorophyll, beta carotene and folic acid, riboflavin, calcium and zinc and all these can act on the oral tissues and help in keeping up good oral health. Chewing 2 to 4 fresh curry leaves with 10 to 15mls water in the mouth, swishing for 5 to 7 minutes and rinsing the mouth out with water can be of help in keeping good oral hygiene and as the curry leaf is a green leafy vegetable it will be safe and cheap to use as mouthwash.