Tuesday, July 31, 2007

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Wednesday, July 18, 2007

Microbes Convert Wastewater into Useable Electricity

Millions of tiny microbes infest the water that carries the detritus of human life and society. Some of them steadily break down the organic material in waste streams and produce electrons in the process. By harvesting these electrons, scientists have created microbial fuel cells. New research shows how such biological power plants can be stacked to create usable current.
Willy Verstraete and his colleagues at Ghent University in Belgium tested the fuel cells in an array of configurations: in a series, in parallel and individually. Over the course of more than 200 days, the researchers fed the microbes a diet of anaerobic and aerobic sludge, as well as hospital and potato processing factory wastewater. By the end of the experimental time frame, the short-term power densities--a measure of power produced per unit of mass--of the fuel cells had tripled. The team also found that the parallel stack was most efficient at producing an electric charge, consistently creating stronger current.
The scientists main discovery, however, had to do with the co-evolution of the electrochemical properties of the fuel cell and the actual microbial community. At the start of the experiment, the tiny power plants relied on a diverse community of proteobacteria, including several species of Geobacter and Shewanella, and produced power somewhat inefficiently. But by the end of the experiment--when performance was at its peak--one species, Brevibacillus agri, made up the majority of the electron-producing microbes.
This microbial evolution calls for further research into the electron-producing properties of various species and their interaction, the authors write. A paper presenting the findings will be published in the May 15 issue of Environmental Science & Technology.

Tuesday, July 17, 2007

Scientists Discover How Cells Decide What Type Of Tissue To Become

As a fertilized egg develops into a full-grown adult, mammalian cells adopt careers as different cell types, from liver cells to neurons. One of the most fundamental mysteries in biomedicine is how cells make such different career decisions despite having exactly the same DNA.
Now a team led by scientists at the Broad Institute of MIT and Harvard and Massachusetts General Hospital has unveiled a special code--not within DNA, but rather within the so-called "chromatin" proteins surrounding it--that could unlock these mysterious choices underlying cell identity.
One of the most surprising findings of the study, published in the July 1 advance online edition of Nature, is that this chromatin-based code may reveal the developmental choices cells have already made as well as those decisions that lie ahead.
"If true, this would have enormous implications for our understanding of developmental biology and for guiding regenerative medicine," said Broad Institute Director Eric Lander, a co-senior author of the study, MIT professor of biology and member of the Whitehead Institute for Biomedical Research.
"Unraveling the mysteries of chromatin holds great promise for understanding how cells in the body...assume such different forms and functions," said co-senior author Bradley Bernstein, an associate member of the Broad Institute and an assistant professor at Massachusetts General Hospital and Harvard Medical School. "By applying a new technology for sequencing DNA, we have been able to look across the genome at chromatin, with greater resolution and efficiency than ever before."
The team has already created genome-wide chromatin maps for embryonic stem (ES) cells and two cell types derived from them.
Chromatin proteins are more than just packing material for the genome. By virtue of different chemical groups fastened to them, these proteins influence which parts of the DNA double helix are open--or not--to the cellular machinery, thus controlling which genes get turned on or off.
To decipher this code requires ways of determining precisely which chromatin proteins sit at which locations along a cell's DNA. In principle, scientists could infer the locations using specialized DNA chips. In practice, though, the technique has proven to be slow and expensive.
Empowered by a new method of massively parallel DNA sequencing, the researchers set out to study chromatin in cells with drastically different behaviors: mouse ES cells--known for their unusual ability to form nearly any tissue--as well as two other types of descendant cells that are more limited in the developmental paths they can choose.
One of the most remarkable findings involves a way of using chromatin to look into a cell's past to determine the developmental decisions it has already made, and to peer into the future to read its potential choices. The fortuneteller lies in a unique form of modified chromatin known as a "bivalent domain," which marks the control regions of important genes. Such domains merge both activating and repressive chemical tags, keeping genes quiet yet poised for later activity.
Bivalent domains had been noted for their role in ES cells, helping keep these cells' developmental options wide open. But with the new genome-wide chromatin data, the scientists discovered that these domains also function in more specialized kinds of stem cells. In neural stem cells, for example, bivalent domains sit near genes important to various types of brain cells but are notably absent from genes that would be active only in, say, skin cells or blood cells.
"Looking at a cell through a microscope often cannot tell you what kind of cell it is, or more importantly, what it has the potential to become," said first author Tarjei Mikkelsen, a Broad Institute researcher and a graduate student in the Harvard-MIT Division of Health Sciences and Technology. "But by decoding its chromatin on a genomic scale, we can now begin to systematically address such questions."
This research was supported by the National Human Genome Research Institute, the National Cancer Institute, the Burroughs Wellcome Fund, Massachusetts General Hospital and the Broad Institute of MIT and Harvard.

Wednesday, July 11, 2007

Cell type

A specific subset of cells within the body, defined by their appearance, location and function.
i) adipocyte: the functional cell type of fat, or adipose tissue, that is found throughout the body, particularly under the skin. Adipocytes store and synthesize fat for energy, thermal regulation and cushioning against mechanical shock
ii) cardiomyocytes: the functional muscle cell type of the heart that allows it to beat continuously and rhythmically
iii) chondrocyte: the functional cell type that makes cartilage for joints, ear canals, trachea, epiglottis, larynx, the discs between vertebrae and the ends of ribs
iv) fibroblast: a connective or support cell found within most tissues of the body. Fibroblasts provide an instructive support scaffold to help the functional cell types of a specific organ perform correctly.
v) hepatocyte: the functional cell type of the liver that makes enzymes for detoxifying metabolic waste, destroying red blood cells and reclaiming their constituents, and the synthesis of proteins for the blood plasma
vi) hematopoietic cell: the functional cell type that makes blood. Hematopoietic cells are found within the bone marrow of adults. In the fetus, hematopoietic cells are found within the liver, spleen, bone marrow and support tissues surrounding the fe tus in the womb.
vii) myocyte: the functional cell type of muscles
viii) neuron: the functional cell type of the brain that is specialized in conducting impulses
ix) osteoblast: the functional cell type responsible for making bone
x) islet cell: the functional cell of the pancreas that is responsible for secreting insulin, glucogon, gastrin and somatostatin. Together, these molecules regulate a number of processes including carbohydrate and fat metabolism, blood glucose levels and acid secretions into the stomach

How We Can Stop Stress From Making Us Obese

In what they call a "stunning research advance," investigators at Georgetown University Medical Center have been able to use simple, non-toxic chemical injections to add and remove fat in targeted areas on the bodies of laboratory animals. They say the discovery, published online in Nature Medicine on July 1, could revolutionize human cosmetic and reconstructive plastic surgery and treatment of diseases associated with human obesity.
Investigators say these findings may also, over the long-term, lead to better control of metabolic syndrome, which is a collection of risk factors that increase a patient's chances of developing heart disease, stroke, and diabetes. Sixty million Americans were estimated to be affected by metabolic syndrome in 2000, according to a study funded by the Centers for Disease Control in 2004.
In the paper, the Georgetown researchers describe a mechanism they found by which stress activates weight gain in mice, and they say this pathway -- which they were able to manipulate -- may explain why people who are chronically stressed gain more weight than they should based on the calories they consume.
This pathway involves two players -- a neurotransmitter (neuropeptide Y, or NPY) and the receptor (neuropeptide Y2 receptor, or Y2R) it activates in two types of cells in the fat tissue: endothelial cells lining blood vessels and fat cells themselves. In order to add fat selectively to the mice they tested, researchers injected NPY into a specific area. The researchers found that both NPY and Y2R are activated during stress, leading to apple-shape obesity and metabolic syndrome. Both the weight gain and metabolic syndrome, however, were prevented by administration of Y2R blocker into the abdominal fat.
"We couldn't believe such fat remodeling was possible, but the numerous different experiments conducted over four years demonstrated that it is, at least in mice; recent pilot data also suggest that a similar mechanism exist in monkeys as well," said the study's senior author, Zofia Zukowska, M.D., Ph.D., professor and chair of the Department of Physiology & Biophysics at Georgetown University Medical Center.
"We are hopeful that these findings might eventually lead to control of metabolic syndrome, which is a huge health issue for many Americans," she said. "Decreasing fat in the abdomen of the mice we studied reduced the fat in their liver and skeletal muscles, and also helped to control insulin resistance, glucose intolerance, blood pressure and inflammation. Blocking Y2R might work the same way in humans, but much study will be needed to prove that."
More immediately, the findings could provide some comfort to stressed individuals who blame themselves for a weight gain that seems outsized given the food they eat, said Lydia Kuo, a medical student who earned her Ph.D. in physiology due to work on the study.
"This is the first study to show that stress has a direct effect on fat accumulation, body weight and metabolism," she said. "In humans, this kind of stress-mediated fat gain may have nothing to do with the brain, and is actually just a physiological response of their fat tissue."
And perhaps the most rapid clinical application of these results will be in both cosmetic and reconstructive plastic surgery, said co-author Stephen Baker, M.D., D.D.S, associate professor of plastic surgery at Georgetown University Hospital. The ability to add fat as a graft would be useful for facial rejuvenation, breast surgery, buttock and lip enhancement, and facial reconstruction, he said, and using injections like those tested in this study could make fat grafts predictable, inexpensive, biocompatible and permanent.
Equally important, blocking Y2R resulted in local elimination of adipose, or fat, tissue, said Baker. "This is the first well-described mechanism found that can effectively eliminate fat without using surgery," he said. "A safe, effective, non-surgical means to eliminate undesirable body fat would be of great benefit to our patients."
Roxanne Guy, MD, president of the American Society of Plastic Surgeons, of which Baker is a member, is also excited by the findings, although she agrees that more research is needed to find out how the animal findings translate in humans. "Providing a long lasting, natural wrinkle filler and a scientifically studied, non-surgical method for melting fat could revolutionize 'growing old gracefully,'" she said. "This discovery could also have positive implications for reconstructive plastic surgery procedures performed on the face and breasts."

Stress + "comfort" foods = excess weight gain
As part of the study, Zukowska and her team examined the effect of several forms of chronic stress that mice in the wilderness can encounter, such as exposure for an hour a day over a two-week period to standing in a puddle of cold water or to an aggressive alpha mouse, and they conducted the experiments in combination with a regular diet or with a high-fat, high-sugar diet. Stressed animals fed a normal diet did not gain weight, but stressed mice given a high-fat diet did. In fact, the researchers found these mice put on more weight than expected given the calories they were consuming.
"They gained twice as much fat as would be expected, and it was all in their belly area," Kuo said. Stressed versus non-stressed animals ate the same amount of food, but the stressed animals processed it differently, she said, explaining, "the novel finding here is that NPY works on fat tissue, not in the brain."
This finding makes sense if evolutionary advantage is considered, Zukowska said. "If you can store fat for times of hardship, you have a fat reserve that can be turned into energy for the next fight.
"The same mechanism may be happening in humans," she said. "An accumulation of chronic stressors, like disagreements with your boss, taking care of a chronically ill child, or repeated traffic road rages, could be acting as an amplifier to a hypercaloric diet when protracted over time. Depression may also be acting as a stressor."
Not only were the stressed mice much fatter, they began to exhibit the metabolic and cardiovascular consequences of obesity, Kuo said. "They had the glucose intolerance seen in diabetes, elevated blood pressure, inflammation in the blood vessels, and fat in their livers and muscles."
"Although we don't expect that, in the future, a person will be able to eat everything he or she wants, chase it down with a Y2R blocking agent, and end up looking like a movie star," said Zukowska, "we are encouraged that these findings could improve human health."
"The concepts described in this study might give us the tools to design one method to remodel fat and another to tackle obesity and metabolic syndrome," Baker said. "It is very exciting."

Saturday, July 7, 2007

Do mosquitoes spread AIDS

It has been categorically proved in many ways that mosquitoes or any other insect vector cannot transmit human immuno deficiency (HIV) which is responsible for causing the acquired immuno deficiency syndrome (AIDS). In case of malaria or filarial, the mosquito acts as an intermediary host in which the parasite undergoes one life cycle. The malarial parasite multiplies in the body of a mosquito and gets collected in the mouth, ready for deposition on a host. Thus, it acts as a vector. In the case of HIV,mosquito is not a vector. The HIV cannot live in mosquito’s blood and survive in human blood only. that is why it is called Human immuno deficiency virus. The moment the virus enters the body of a mosquito it is killed. Mosquito uses its proboscis only to suck blood and not to inject blood into our body whereas a needle is used for both . this also supports the argument that HIV will not be transmitted by mosquitoes.

Wednesday, July 4, 2007

Researchers Find 'Missing Link' Stem Cells

A team of scientists at Oxford University has discovered a new type of embryonic stem cell in mice and rats that is the closest counterpart yet to human embryonic stem cells.
The cells are expected to serve as an improved model for human stem cells in studies of regeneration, disease pathology and basic stem cell biology, bringing scientists closer to realising the potential of stem cells in treatments for disease.
The findings, reported in Nature, are the result of a collaborative effort between scientists at the University of Oxford and the National Institutes of Health (NIH) in the USA – a collaboration brought about by the paper's lead author, Paul Tesar, who is a student on NIH and Oxford's joint doctoral programme. Stem cell expert Professor Sir Richard Gardner in Oxford's Department of Zoology is the senior author from Oxford.
Up until now, embryonic stem cells derived in humans and mice had looked different and behaved differently. They had in common their 'pluripotency', or ability to turn into any type of cells, but researchers had found that mouse and human stem cells maintained this state in quite different ways, which required distinct techniques for their growth in culture.
In the new research, the team found that when mouse stem cells were derived from slightly older mouse embryos, they looked very similar to human embryonic stem cells under the microscope and had many of the same properties. Importantly, these new mouse stem cells could be maintained using the same growth factors as those used in the culture of human embryonic stem cells.

Tuesday, July 3, 2007

Lets see our forefathers

Fathers of Biology-Lamarck, Traviranus.
Fathers of Botany-Thepratus
Fathers of Biology and Zoology-Aristotle
Fathers of Phaecology-P.A.Micheli
Fathers of Bacteriology-Robert Koch
Fathers of Microbiology- Anton Von Leeuwenhoek
Fathers of Fermentation-louis pasteur
Fathers of Immunology-Edward Jenner
Fathers of Polio vaccine-Salk
Fathers of Modern taxonomy-Carolus Linnaeus
Fathers of Paleontology-Leonardo Da Vinci
Fathers of Cytology-Robert Hook
Fathers of Modern Cytology-Swanson
Fathers of Genetics-Gregor John Mendel
Fathers of Modern Genetics-Bateson
Fathers of Experimental Genetics-T.H.Morgan
Fathers of Eugenics-Galton
Fathers of Mutation Theory Of Evolution-Hugo De Vries
Fathers of ATP Cycle-Lipmann
Fathers of Antibiotics-Alexander Fleming
Fathers of Medicine-Hippocrates

Sunday, July 1, 2007

A brief history of microbiology

Bacteria were first observed by Anton van Leeuwenhoek in 1676 using a single-lens microscope of his own design. The name "bacterium" was introduced much later, by Ehrenberg in 1828, derived from the Greek word βακτηριον meaning "small stick". While Antony van Leeuwenhoek is often cited as the first microbiologist, the first recorded microbiological observation, that of the fruiting bodies of molds, was made earlier in 1665 by Robert Hooke.
The field of bacteriology (later a subdiscipline of microbiology) is generally considered to have been founded by Ferdinand Cohn (1828–1898), a botanist whose studies on algae and photosynthetic bacteria led him to describe several bacteria including Bacillus and Beggiatoa. Ferdinand Cohn was also the first to formulate a scheme for the taxonomic classification of bacteria.
Louis Pasteur (1822–1895) and Robert Koch (1843–1910) were contemporaries of Cohn’s and are often considered to be the founders of medical microbiology. Pasteur is most famous for his series of experiments designed to disprove the then widely held theory of spontaneous generation, thereby solidifying microbiology’s identity as a biological science. Pasteur also designed methods for food preservation (pasteurization) and vaccines against several diseases such as anthrax, fowl cholera and rabies. Robert Koch is best known for his contributions to the germ theory of disease, proving that specific diseases were caused by specific pathogenic microorganisms. He developed a series of criteria that have become known as the Koch's postulates. Koch was one of the first scientists to focus on the isolation of bacteria in pure culture resulting in his description of several novel bacteria including Mycobacterium tuberculosis, the causative agent of tuberculosis.
While Louis Pasteur and Robert Koch are often considered the founders of microbiology, their work did not accurately reflect the true diversity of the microbial world because of their exclusive focus on microorganisms having medical relevance. It was not until the work of Martinus Beijerinck (1851–1931) and Sergei Winogradsky (1856–1953), the founders of general microbiology (an older term encompassing aspects of microbial physiology, diversity and ecology), that the true breadth of microbiology was revealed. Martinus Beijerinck made two major contributions to microbiology: the discovery of viruses and the development of enrichment culture techniques. While his work on the Tobacco Mosaic Virus established the basic principles of virology, it was his development of enrichment culturing that had the most immediate impact on microbiology by allowing for the cultivation of a wide range of microbes with wildly different physiologies. Sergei Winogradsky was the first to develop the concept of chemolithotrophy and to thereby reveal the essential role played by microorganisms in geochemical processes. He was responsible for the first isolation and description of both nitrifying and nitrogen-fixing bacteria.

Methicillin-resistant Staphylococcus aureus (MRSA)

MRSA stands for methicillin-resistant Staphylococcus aureus. It is a type of bacterium commonly found on the skin and/or in the noses of healthy people. Although it is usually harmless at these sites, it may occasionally get into the body (e.g. through breaks in the skin such as abrasions, cuts, wounds, surgical incisions or indwelling catheters) and cause infections. These infections may be mild (e.g. pimples or boils) or serious (e.g. infection of the bloodstream, bones or joints).

The treatment of infections due to Staphylococcus aureus was revolutionized in the 1940s by the introduction of the antibiotic penicillin. Unfortunately, most strains of Staphylococcus aureus are now resistant to penicillin. This is because Staphylococcus aureus has 'learnt' to make a substance called β-lactamase (pronounced beta-lactamase), that degrades penicillin, destroying its antibacterial activity.

Some related antibiotics, such as methicillin and flu cloxacillin, are not affected by β -lactamase and can still be used to treat many infections due to β -lactamase-producing strains of Staphylococcus aureus. Unfortunately, however, certain strains of Staphylococcus aureus, known as MRSA, have now also become resistant to treatment with methicillin and flu cloxacillin.

Although other types of antibiotics can still be used to treat infections caused by MRSA, these alternative drugs are usually not available in tablet form and must be administered through a drip inserted into a vein.

MRSA infections most often occur in patients in hospitals and are rarely seen among the general public. As with ordinary strains of Staphylococcus aureus, some patients harbors MRSA on their skin or nose without harm (such patients are said to be 'colonised'), whereas other patients may develop infections.

Some patients are at increased risk of developing infection. They include those with breaks in their skin due to wounds (including those caused by surgery), indwelling catheters or burns, and those with certain types of deficiency in their immune system, such as low numbers of white cells in their blood.

When MRSA spread from an initial site of colonisation to a site where they cause infection in the same patient (eg spread from the colonised nose to a wound), the resulting infection is described as 'endogenous'.

In addition to causing endogenous infections, MRSA can spread between patients, usually by direct or indirect physical contact. For example, hospital staff attending to a colonised or infected patient may become contaminated or colonised with MRSA themselves (perhaps only briefly). They may then spread the bacteria to other patients with whom they subsequently have contact. These patients may in turn become colonised and/or infected. The spread of MRSA (or for that matter other bacteria) between patients is called cross-infection.

Some strains of MRSA that are particularly successful at spreading between patients may also spread between hospitals, presumably when colonised patients or staff moves from one hospital to another. These strains are known as epidemic MRSA (or EMRSA for short)

Facts About Microbes


Microbes first appeared on earth about 3.8 billion years ago. They are critically important in sustaining life on our planet.

Microbes outnumber all other species and make up most living matter.


Less than .5% of the estimated 2 to 3 billion microbial species have been identified.


Microbes comprise ~60% of the earths biomass.


Microbes drive the chemistry of life and affect the global climate.


Microbial cycling of such critical chemical elements as carbon and nitrogen helps keep the world inhabitable for all life forms.


Microbes generate at least half the oxygen we breathe.


Microbes thrive in an amazing diversity of habitatsin extremes of heat, cold, radiation, pressure, salinity, acidity, and darkness, and often where no other life forms could exist and where nutrients come only from inorganic matter.


Microbes offer unusual capabilities reflecting the diversity of their environmental niches. These may prove useful as a source of new genes and organisms of value in addressing bioremediation, global change, biotechnology, and energy production.


Microbial studies will help us define the entire repertoire of organisms in specialized niches and, ultimately, the mechanisms by which they interact in the biosphere.


Diversity patterns of microorganisms can be used for monitoring and predicting environmental change.


Microbes are roots of life's family tree. An understanding of their genomes will help us understand how more complex genomes developed.


Microbial genomes are modest in size and relatively easy to study (usually no more than 10 million DNA bases, compared with some 3 billion in the human and mouse genomes).


Microbial communities are excellent models for understanding biological interactions and evolution.


Most microbes do not cause disease.