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How does nutrition affect healthy aging, longevity? The correct combination of proteins is decisive for healthy aging, not reducing the calories in our diet

from a press release from the Max Planck Institute for Biology of Ageing......

"A new study from the Max Planck Institute for Biology of Ageing could help us understand the positive effect of dietary restriction on healthy ageing. Previous evidence from different organisms (fruit flies and mice) have shown that dietary restriction increases longevity, but with a potential negative side effect of diminished fertility. So the female fruit fly reproduces less frequently with a reduced litter size on a low calorie diet, but its reproductive span lasts longer. This is the result of an evolutionary trait, as scientists believe: essential nutrients are diverted towards survival instead of reproduction. (Nature, December 3, 2009)

Researchers from the newly created Max Planck Institute for Biology of Ageing in Cologne have studied whether health benefits stem from a reduction in specific nutrients or calorie intake in general, by manipulating the diet of female fruit flies. The fruit flies were fed a diet of yeast, sugar and water, but with differing amounts of key nutrients, such as vitamins, lipids and amino acids. The scientists were able to show that longevity and fertility are affected by a combination of the type and amount of amino acids; whilst varying the amount of the other nutrients had little or no effect.

Furthermore, the researchers found out in previous studies that levels of a particular amino acid - methionine - were crucial to increasing lifespan without decreasing fertility. By carefully manipulating the balance of amino acids, both lifespan and fertility were maximised. For the first time, this indicates that it is possible to extend lifespan without wholesale dietary restriction and without lowering reproductive capacity.

As the effects of dietary restriction on lifespan is evolutionary conserved - observed in different organisms - researchers believe that the essential mechanisms apply to it as well. Even though the human genome has about four times the number of genes as the fruit fly genome, there are many similarities on a genetic level, allowing these results to be of significance for humans as well.

 

Walter Derzko

Fighting white fat with brown fat to combat obesity

From  a German press release:

Brown fat cells make 'spare tires' shrink; Bonn scientists discover a promising new approach to combat obesity

Brown adipose tissue is different from white fat pads. It contains loads of mitochondria, miniature power stations which among other things can 'burn' fat. In doing this, they normally generate a voltage similar to that of a battery, which then provides energy for cellular processes. However, the mitochondria of brown fat cells have a short circuit. They go full steam ahead all the time. The energy released when the fat is broken down is released as heat.

'This is actually what is intended,' Professor Alexander Pfeifer from the Bonn PharmaCentre explains. 'Brown fat acts like a natural heating system.' For example, babies would get cold very quickly without this mechanism. Up to now, it was thought that brown fat only occurred in newborn babies and was lost with age. However, this year different groups were able to show that this is not true: even adults have a deposit of brown fat in the neck area. But with very overweight people this deposit is only moderately active or is completely absent.

PKG turns on the heating

The scientists from Bonn, Heidelberg, Cologne, Martinsried and the Bundesinstitut für Arzneimittel und Medizinprodukte, BfArM, were now able to show which signals prompt the body to produce brown fat cells. A signalling pathway which is controlled by the PKG enzyme takes on a key role in this process. This signalling pathway results in the stem cells of the fatty tissue becoming brown fat cells. For this it switches on the mass production of mitochondria and ensures that UCP is formed, the substance that creates the short circuit. 'Furthermore, we were able to show that PKG makes brown fat cells susceptible to insulin,' Alexander Pfeifer explains. 'Therefore PKG also controls how much fat is burnt in general.'

Mice without PKG have a lower body temperature, as the researchers were able to show with a thermographic camera. Above all, animals in the thermal image lack an 'energy spot' between the shoulder blades, i.e. the place where normally the brown fat is active.

Fighting fat with fat

The researchers suspect that a disorder of the brown fatty tissue can lead to obesity in adults. If it were possible to turn on the 'natural heating system' on again, the problem of unwanted fat would be quickly solved: according to estimates, 50 grams of active brown fatty tissue is sufficient for increasing the basal metabolic rate by 20 per cent. '

With the same nutrition and activity the fat reserves would melt at a rate of five kilos per year,' Professor Pfeifer explains. This makes our results interesting from a therapeutic perspective. By blocking the PKG signalling path in the brown fat we basically want to fight fat with fat.'

Designer Oncolytic (tumor -attacking) virus called RAMBO kills brain tumor cells & blocks tumor blood vessel growth

From OSU press release:

"Ohio State University cancer researchers in the USA have developed a tumor-attacking virus that both kills brain-tumor cells and blocks the growth of new tumor blood vessels.

Their research shows that viruses designed to kill cancer cells – oncolytic viruses – might be more effective against aggressive brain tumors if they also carry a gene for a protein that inhibits blood-vessel growth.

The protein, called vasculostatin, is normally produced in the brain. In this study, an oncolytic virus containing the gene for this protein in some cases eliminated human glioblastoma tumors growing in animals and significantly slowed tumor recurrence in others. Glioblastomas, which characteristically have a high number of blood vessels, are the most common and devastating form of human brain cancer. People diagnosed with these tumors survive less than 15 months on average after diagnosis.

"This is the first study to report the effects of vasculostatin delivery into established tumors, and it supports further development of this novel virus as a possible cancer treatment," says study leader Balveen Kaur, associate professor of neurological surgery and a researcher with the Ohio State University Comprehensive Cancer Center-Arthur G. James Cancer Hospital and Richard J. Solove Research Institute. "Our findings suggest that this oncolytic virus is a safe and promising strategy to pursue for the treatment of human brain tumors.

"This study shows the potential of combining an oncolytic virus with a natural blood-vessel growth inhibitor such as vasculostatin. Future studies will reveal the potential for safety and efficacy when used in combination with chemotherapy and radiation therapy," she says.

The findings were recently published online in the journal Molecular Therapy.

Jayson Hardcastle, a graduate student in Dr. Kaur's laboratory, injected the cancer-killing virus, called RAMBO (for Rapid Antiangiogenesis Mediated By Oncolytic virus), directly into human glioblastoma tumors growing either under the skin or in the brains of mice.

Of six animals with tumors under the skin, those treated with RAMBO survived an average of 54 days. In addition, three of the RAMBO mice were tumor-free at the end of the experiment. Control animals treated with a similar virus that lacked the vasculostatin gene, on the other hand, survived an average of 26 days and none were tumor-free.

Of the animals with a human glioblastoma in the brain, five were treated with RAMBO and lived an average of 54 days. One animal remained tumor-free for more than 120 days. Control animals, by comparison, lived an average of 26 days with no long-term survivors."

In another experiment, the investigators followed the course of tumor changes in animals with tumors in the brain. After an initial period of tumor shrinkage, the remaining cancer cells began regrowing around day 13 in animals given the virus that lacked the blood-vessel inhibitor. In animals treated with RAMBO, tumor regrowth didn't begin until about day 39.

"With additional research, this virus could lead to a new therapeutic strategy for combating cancer," Kaur says.

ETA: 5-10 years away

Walter Derzko

When are errors and mistakes good ? Cells defend themselves from viruses, bacteria with an army of protein errors

Our education system teaches us to avoid errors and mistakes, we are taught to aim to get the right answer…however in nature it’s not as clear cut as that...in some cases errors are helpfull.

 

A good rule of thumb in  science is "look under your nose."  and "challenge assumptions." The following story is a good example of how complex our body is and what we don't know about how our body works.

When cells are confronted with an invading virus or bacteria or exposed to an irritating chemical, they protect themselves by going off their DNA recipe and inserting the wrong amino acid into new proteins to defend them against damage, scientists have discovered.

 

These "regulated errors" comprise a novel non-genetic mechanism by which cells can rapidly make important proteins more resistant to attack when stressed, said Tao Pan, Professor of Biochemistry and Molecular Biology at the University of Chicago. A team of 18 scientists from the University of Chicago and the National Institute of Allergy and Infectious Disease led by Pan and Jonathan Yewdell will publish the findings tomorrow, Thursday in the journal Nature.

 

"This mechanism allows every protein to get some protection," Pan said. "The genetic code is considered untouchable, but this is a non-genetic strategy used in cells to create a bodyguard for proteins."

Proteins are constructed through a process called translation where cellular elements use the genetic code to guide the assembly of building blocks called amino acids into the correct sequence. First, a copy of the DNA, called messenger RNA, is made and transferred to a cellular structure called a ribosome. Transfer RNAs (tRNA), one for each of the 20 amino acids used in building proteins, read the messenger RNA code and bring the proper amino acids to the ribosome, where they are bonded together to form a complete protein.

Each tRNA can be attached to only one of 20 amino acids, a specificity that prevents errors during the construction of proteins. In artificial laboratory preparations, scientists have observed that only one out of every 10,000 amino acids is placed into a protein incorrectly, and thus protein errors were thought to be exceptionally rare.

But Jeffrey Goodenbour, University of Chicago graduate student and co-lead author along with Nir Netzer of the NIAID, decided to look at how often tRNA errors, called misacylations, occurred in live cells.

 

After developing a novel technique for measuring these errors, published for the first time in this paper, the authors were surprised to find a much higher error rate in those cells for the amino acid methionine. As high as one out of every 100 methionines was incorrectly placed in proteins, they found.

 

When the cells were stressed by exposure to a virus, bacteria or a toxic chemical such as hydrogen peroxide, that error rate went even higher, as up to 10 percent of methionines placed into new proteins were different from what the gene specified.

"That was 1,000 times more than the textbook says should be there," Pan said.

 

Further experiments revealed that it was always the same amino acid, methionine, placed incorrectly into new proteins. Methionine is one of only two amino acids to carry sulfur atoms on its side chains, a feature that allows it to neutralize dangerous molecules called reactive oxygen species (ROS) that form inside an infected or stressed cell. ROS can damage proteins through a chemical process called oxidation, but methionine can be oxidized (and restored through a process called reduction) without being permanently damaged.

"The idea is that methionine can protect you from having oxidation of the active site of protein, which would ultimately completely block function of the protein," Goodenbour said. "You end up reducing the total reactive oxygen species load in the cell. It's a very interesting mechanism."

Cells normally put methionines near important parts of a protein to protect those segments from being damaged by reactive oxygen species. When the cell is under stress, and the amount of ROS increases, the number of methionine "errors" is ramped up tenfold, allowing new proteins to be even more resistant to attack.

"Think of a boxing match," Pan said. "If you put methionine close to active site, the reactive oxygen species has to get past it to get to the active site residues for oxidization. You've put something right in front of it so a protein can take a hit. If you have a lot of methionines, to knock this protein out will take many, many hits. So this is a strategy used in cells to create a bodyguard for a protein."

A remaining puzzle is to determine why extra protective methionines are not encoded as part of the DNA in the first place, instead of being left to the post-genetic random placement described in this paper. Pan suggests that random placement of the amino acids makes proteins even more resistant to attack, since no two are created alike. (Pay attention computer platform and anti-virus software designers !!)

 

"This sounds chaotic and doesn't make a lot of sense according to the textbook," Pan said. "But this way the cells can always ensure that a subset of these proteins is somewhat less sensitive to the extra hits. I think that's the most important part of this - to make every protein molecule different - and you cannot do this genetically."

Walter Derzko

 

Scientists use novel imaging mass spectrometry to visualize how bacteria communicate with one another

Great scientific discoveries are often preceded by spectacular advances in instrumentation. Just think back to the telescope, the x-ray or the electron microscope

 

Now, using imaging mass spectrometry, researchers at the University of California, San Diego have developed tools that will enable scientists to visualize how different populations of cells communicate. Their study shows how bacteria talk to one another - an understanding that may lead to new therapeutic discoveries for diseases ranging from cancer to diabetes and allergies.

 

In the paper published in the November 8 issue of Nature Chemical Biology, Pieter C. Dorrestein, PhD, assistant professor at UC San Diego's Skaggs School of Pharmacy and Pharmaceutical Sciences, and colleagues describe an approach they developed to describe how bacteria interface with other bacteria in a laboratory setting. Dorrestein and post-doctoral students Yu-Liang Yang and Yuquan Xu, along with Paul Straight from Texas A&M University, utilized technology called natural product MALDI-TOF (Matrix Assisted Laser Desorption Ionization-Time of Flight) imaging mass spectrometry to uniquely translate the language of bacteria.

 

Microbial interactions, such as signaling, have generally been considered by scientists in terms of an individual, predominant chemical activity. However, a single bacterial species is capable of producing many bioactive compounds that can alter neighboring organisms. The approach developed by the UCSD research team enabled them to observe the effects of multiple microbial signals in an interspecies interaction, revealing that chemical "conversations" between bacteria involve many signals that function simultaneously.

 

"Scientists tend to study the metabolic exchange of bacteria, for example penicillin, one molecule at a time," said Dorrestein. "Actually, such exchanges by microbes are much more complex, involving 10, 20 or even 50 molecules at one time. Now scientists can capture that complexity."

 

The researchers anticipate that this tool will enable development of a bacterial dictionary that translates the output signals. "Our ability to translate the metabolic output of microbes is becoming more important, as they outnumber other cells in our body by a 10 to one margin," Dorrestein explain. "We want to begin to understand how those bacteria interact with our cells. This is a powerful tool that may ultimately aid in understanding these interactions."

In order to communicate, bacteria secrete molecules that tell other microbes, in effect, "I am irritated, stop growing," "I need more nutrients" or "come closer, I can supply you with nutrients." Other molecules are secreted that may turn off the body's defense mechanisms. The team is currently mapping hundreds of such bacterial interactions. Their hope is that this approach will also enable them to translate these bacterial-mediated mechanisms in the future.

Understanding the means by which microorganism cells talk to one another will facilitate therapeutic discovery, according to Dorrestein. For instance, knowing how microbes interact with human immune cells could lead to discovery of novel immune system modulators, and how these molecules control bacterial growth may lead to new anti-invectives. Both are active areas of investigation in his laboratory.

 

 

Source: University of California - San Diego

 

Walter Derzko

Nanostructured Integrated Circuit Detects Type and Severity of Cancer

A team of investigators from the University of Toronto have used nanomaterials to develop an inexpensive microchip sensitive enough to quickly determine the type and severity of a patient's cancer so that the disease can be detected earlier for more effective treatment. Their work, reported in two papers published in the journals ACS Nano and Nature Nanotechnology, could herald an era when inexpensive yet sophisticated molecular diagnostics will become commonplace.

The researchers' new device can readily detect the signature biomarkers that indicate the presence of cancer at the cellular level, even though these biomolecules - genes that indicate aggressive or benign forms of the disease and differentiate subtypes of the cancer - are generally present only at low levels in biological samples. Analysis can be completed in 90 minutes, a significant improvement over the existing diagnostic procedures that generally take days.

"Today, it takes a room filled with computers to evaluate a clinically relevant sample of cancer biomarkers and the results aren't quickly available," said team co-leader Shana Kelley. "Our team was able to measure biomolecules on an electronic chip the size of your fingertip and analyse the sample within half an hour. The instrumentation required for this analysis can be contained within a unit the size of a BlackBerry."

The nanoelectrode device that Kelley, collaborator Edward Sargent, and their students created is able to detect disease-related genes without the use of PCR to amplify low-level DNA. The electrodes, which are the key component of the device, have a novel highly-branched nanostructured shape that can detect attomolar concentrations of DNA. Using arrays of electrodes, each differing in the degree of nanostructured branching, the investigators were able to construct a device capable of sensing DNA molecules over six orders of magnitude, overcoming the dynamic range issue - the ability to detect both common and rare molecules - that has plagued other devices

Using their device, the investigators analyzed messenger RNA samples from prostate cancer biopsies. Their analysis showed that the device can detect gene fusions characteristic of prostate cancer. More importantly, the device was able to distinguish between gene fusions associated with either fast- or slow-growing forms of prostate cancer.

The paper describing the construction of this nanobiosensor is titled, "Programming the detection limits of biosensors through controlled nanostructuring." An abstract of this paper is available at the journal's Web site.

The paper detailing the use of the nanobiosensor to detect and characterize cancers is titled, "Direct Profiling of Cancer Biomarkers in Tumor Tissue Using a Multiplexed Nanostructured Microelectrode Integrated Circuit." An abstract of this paper is available at the journal's Web site

 

Walter Derzko

 

Why vaccines, antibiotics and antivirals are now obsolete- surpassed by hydrated fullerenes (C60 HYFN)

When Buckyballs or Fullerenes (Carbon 60, which is a form of carbon, just like coal, activated charcoal, soot, diamonds or the lead in your pencil,) were first discovered several decades ago, they were lauded as a “silver bullet” in medicine. The hype quickly subsided when most researchers realized that both natural and synthetic fullerenes were not very water soluble, hence they only saw weak medical effects. But a team of Ukrainian researchers persisted and a decade ago, they discovered a way to make fullerenes water soluble without making them more toxic. Now, after undergoing clinical trials, they are launching a fullerene-based  water solution (FWS) drink shortly on the Ukrainian market as a natural food supplement, Fullerenes are found naturally in lightening discharges, in nano-quantities in molasses or in some natural spring. spa waters and in shungite rocks.

Governments around the world should fast-track the approval of hydrated fullerenes (C60 HyFNs) or Fullerene Water Solution (FWS) drinks, which are anti-microbial (both anti viral and anti bacterial) and can protect people from all colds and flu. WFS is about to be launched by Ukrainian scientists on the Ukrainian market as a natural food supplement

So why the Ukrainians and not another country-you might ask yourself? Well they all tried (UK, Americans, Germans, China, Japan, South Korea, etc)  to make safe nontoxic watersoluble fullernes but failed except for Ukrainian researchers.

So here are the benefits of FWS over conventional approaches

1) FWS are not viral specific like vaccines -they don't need several months lead time to be manufactured  for each new viral season. The turnaround for FWS is 2-3 days. FWS work on all viruses and bacteria year round, by suppressing the viral or bacterial spread from cell to cell. FWS don't kill microbes but block mobility from cell to cell, due to water clusters formed around the fullerene molecule. Your  immune system then decides which  microbes are invaders and which microbes  are beneficial for the body.

2) People and especially teenagers who have died due to swine flu (due to cytokine cascades or secondary bacterial infections) could have been saved if FWS was on the market today.

3) High risk groups -like Canadian aboriginal Indians, could be saved from flu death by taking a combination of Vitamin D (to tune up the immune system in the winter) and FWS

4) With FWS you don't need annual immunization campaigns and 6 hour long lineups, like we have seen in Toronto this past week. Public health money could be used for other priorities.

5) With FWS, you don't need to distinguish between high and low risk groups like you do in rollouts for vaccines. If  FWS were available from Walmart to corner health food stores as a health drink , you'd have equal access

6) FWS are cheaper to produce then antibiotics and vaccines

7) FWS are safer then vaccines and antibiotics (see http://toxnet.nlm.nih.gov/and type in "fullerene" under Hazardous Substance Data Bank). FWS don' t build up resistance in bacteria the way antibiotics do.

8)FWS would reduce the work load on hospital ICU's and protect front line staff

9) Feeding fullerne laced water to animals would eliminate the need for conventional antibiotics

10) Dipping plant seeds in fullerene water solutions increases growth, health  and resilience of growing plants

For more information contact me from your corporate email

Walter Derzko

Other medical/biological effects of HyFN's see http://www.fullwater.com.ua/page6.html )

Water-soluble fullerenes (also known as buckyballs) or hydrated fullerenes (HyFN's) appear to possess an impressive list of in vivo and in vitro effects which have been researched by Ukrainian scientists and are summarized below:

The following table was reproduced with the permission of the authors:

Basic biological properties of aqueous solutions of the hydrated C60 fullerene (HyFn) detected to the present time (May 2005)

In vitro experiments revealed that HyFn with C60 concentrations up to 100mM/l:

1. Are non-toxic for cells including hepatocytes;

2. Do not suppress, but promote the growth of isolated micro-organisms (microbes, fungi, etc.) and improve the survival rate and viability of cells (e.g., spermatozoa) and of frozen-thawed cells;

3. Do not inhibit cell respiration;

4. Do not suppress membrane-bonded ATP-ase activity;

5. Possess greater anti-oxidant properties then vitamin E, b-carotene and BHT (2,6-di-tert-butyl-4-kresol);

6. Stabilize cellular membranes and enhance their resistance under adverse conditions;

7. Do not affect blood coagulation;

8. Increase by 5-10 degrees C the temperature of biomolecules denaturation (DNA, albumin, collagen and etc.);

9. Increase catalytic activity of isolated enzymes (e.g., serine proteases).

In vivo experiments revealed that HyFn with C60 total doses up to 25mg/kg of b.w.:

1. Are non-toxic, not immunogenic, none allergenic;

2. Increase resistance of plasma membranes to damaging factors;

3. Positively influence anti-oxidant and energetic systems of organisms;

4. Possess radioprotective properties due to suppression of excess level of free radicals;

5. Possess antihistaminic and allergy-suppressing abilities, i.e., act as anti-inflammatory agents,

6. Positively influence activity of adrenergic, GABA-, hystaminic- and, especially, serotoninergic systems and, as a consequence, enhance adaptogenic functions of organisms; adaptive homeostasis

7. Show positive neuroprotecting effects (e.g., in Alzheimer's disease) and non-specific analgesic effects;

8. Do not kill tumor cells, inhibition of development of cancer pathologies, cancer metastasis,

9. Possess anti-atherosclerotic (anti-atherogenic) properties;

10. Are able to protect against viral infection (e.g., influenza, etc.): (HyFn do not kill viruses and microbes, but do not allow them to incorporate into cells)....(HYFNs plus Vitamin D supplements  could make antibiotics and vaccines obsolete in the future)

Source: Fullerenes, Nanotubes, and Carbon Nanostructures, 13: 363-376, 2005;Is the C60 Fullerene Molecule Toxic?!

Gene discovered –p16 that 'cancer-proofs' rodent's cells

Scientists have discovered that the naked mole rat, the only known cancerless animal, has two-tier defense against cancer. Despite a 30-year lifespan that gives ample time for cells to grow cancerous, a small rodent species called a naked mole rat has never been found with tumors of any kind—and now biologists at the University of Rochester think they know why.

 

 

The findings, presented in today's issue of the Proceedings of the National Academy of Sciences, show that the mole rat's cells express a gene called p16 that makes the cells "claustrophobic," stopping the cells' proliferation when too many of them crowd together, cutting off runaway growth before it can start. The effect of p16 is so pronounced that when researchers mutated the cells to induce a tumor, the cells' growth barely changed, whereas regular mouse cells became fully cancerous.

"We think we've found the reason these mole rats don't get cancer, and it's a bit of a surprise," say Vera Gorbunova and Andrei Seluanov, professors of biology at the University of Rochester and lead investigators on the discovery. "It's very early to speculate about the implications, but if the effect of p16 can be simulated in humans we might have a way to halt cancer before it starts."

Like many animals, including humans, the mole rats have a gene called p27 that prevents cellular overcrowding, but the mole rats use another, earlier defense in gene p16. Cancer cells tend to find ways around p27, but mole rats have a double barrier that a cell must overcome before it can grow uncontrollably.

"We believe the additional layer of protection conferred by this two-tiered contact inhibition contributes to the remarkable tumor resistance of the naked mole rat," says Gorbunova in PNAS . Gorbunova and Seluanov are now planning to delve deeper into the mole rat's genetics to see if their cancer resistance might be applicable to humans.

Full Story here

Walter Derzko

Carbon nanotubes affect lining of the lungs

Study shows how carbon nanotubes (CNT)  can affect lining of the lungs (the CNT dose makes the posion)

Carbon nanotubes are being considered for use in everything from sports equipment to medical applications, but a great deal remains unknown about whether these materials cause respiratory or other health problems. Now a collaborative study from North Carolina State University, The Hamner Institutes for Health Sciences, and the National Institute of Environmental Health Sciences shows that inhaling these nanotubes can affect the outer lining of the lung, though the effects of long-term exposure remain unclear.

Using mice in an animal model study, the researchers set out to determine what happens when multi-walled carbon nanotubes are inhaled. Specifically, researchers wanted to determine whether the nanotubes would be able to reach the pleura, which is the tissue that lines the outside of the lungs and is affected by exposure to certain types of asbestos fibers which cause the cancer mesothelioma. The researchers used inhalation exposure and found that inhaled nanotubes do reach the pleura and cause health effects.

Short-term studies described in the paper do not allow conclusions about long-term responses such as cancer. However, the inhaled nanotubes "clearly reach the target tissue for mesothelioma and cause a unique pathologic reaction on the surface of the pleura, and caused fibrosis," says Dr. James Bonner, associate professor of environmental and molecular toxicology at NC State and senior author of the study. The "unique reaction" began within one day of inhalation of the nanotubes, when clusters of immune cells (lymphocytes and monocytes) began collecting on the surface of the pleura. Localized fibrosis, or scarring on parts of the pleural surface that is also found with asbestos exposure, began two weeks after inhalation.

The study showed the immune response and fibrosis disappeared within three months of exposure. However, this study used only a single exposure to the nanotubes. "It remains unclear whether the pleura could recover from chronic, or repeated, exposures," Bonner says. "More work needs to be done in that area and it is completely unknown at this point whether inhaled carbon nanotubes will prove to be carcinogenic in the lungs or in the pleural lining."

The mice received a single inhalation exposure of six hours as part of the study, and the effects on the pleura were only evident at the highest dose used by the researchers – 30 milligrams per cubic meter (mg/m3). The researchers found no health effects in the mice exposed to the lower dose of one mg/m3.

Source: The study, "Inhaled Carbon Nanotubes Reach the Sub-Pleural Tissue in Mice,"   is published in the Oct. 25 issue of Nature Nanotechnology

Walter Derzko

Genes Determine Susceptibility to H5N1 Avian Influenza A Virus Infection

A new study found genetic variations in mice affect their susceptibility to and severity of H5N1 avian influenza A virus infection suggesting that humans who contract the virus may be genetically predisposed. The researchers from St. Jude Children's Research Hospital, VA Medical Center and MidSouth Center for Biodefense and Security, and the University of Tennessee Health Science Center, Memphis, Tennessee report their findings in the October 2009 issue of the Journal of Virology. Over the last 10 years, highly pathogenic H5N1 avian influenza A has spread from Southeast Asia into Europe and Africa killing millions of chickens and ducks along the way. It has also infected tigers, cats, dogs and humans often resulting in death.

Despite the countless cases reported in birds, the number of human cases remains few and of those few more than 90% occurred in genetically related family members indicating a possible genetic correlation. In the study researchers conducted genome-wide linkage analysis to identify chromosomes that contribute to varying susceptibility to H5N1 in two inbred strains of mice challenged with a lethal dose of a highly pathogenic H5N1 virus. Results revealed five quantitative trait loci for influenza virus resistance located on multiple chromosomes also associated with H5N1 resistance.

Additionally, a number of candidate susceptibility genes were identified, one of which affected virus titers 7 days following infection. "An important and novel finding of this study is that H5N1-induced pathology is greatly affected by genetic polymorphisms in the genome of the infected host," say the researchers. "We have also found that, at least in mice, H5N1 pathogenesis is a complex genetic trait with multiple genes affecting disease outcome."

Source: A.C.M. Boon, J. deBeauchamp, A. Hollmann, J. Luke, M. Kotb, S. Rowe, D. Finkelstein, G. Neale, L. Lu, R.W. Williams, R.J. Webby. 2009. Host genetic variation affects resistance to infection with a highly pathogenic H5N1 influenza A virus in mice. Journal of Virology, 83. 20: 10417-10426.

Walter Derzko