Beneficial & Negative Effects of Microbes Microbioz India,February 2015 Issue

MICROBIOZ INDIA

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MICROBIOZ ISSUE. FEBRUARY 2015. VOLUME .12

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Microbes Beneficial & Negative Effects of

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DIABETIC FOOT DISORDERS.FEATURED ARTICLE. AN INTERVIEW WITH DR.JAI SHREE PAUL, JNU, NEW DELHI, INDIA. CURRENT NEWS AND RESERACHES. RECENT OPEN SCHOLARSHIPS POSITION. MICROBIOZ INDIA, CROSS WORD GAME. LIST OF WINNERS

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Contents

“The planet earth is full of bacteria and they play an important role in the different functions whether they are related to humans, animals or plants.”

Microbioz India, Cover Story Beneficial and Negative effects of Microbes on humanity.

A featured article of this month’s: Diabetic foot Ulcer: A genetic disorders.

A brief info on current research and news information on Microbiology.

Microbioz India,Cross Word Games of February Issue and list of winners of January Edition.

An Interview with Dr.Jai Shree Paul, School of Life Science, JNU, New Delhi, Under Scientist Speak.

Current Research Scholarships openings from around the world.

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ear readers Microbioz India, going to launch 12th Issue of Microbioz India magazines. I would

Like to thanks you all for great support and day by day progress in our audiences and memberships around the world. The cover story of this issue is very common entitled “Beneficial and Negative Effects of Microbes” but discuss various interested topic about how bacteria influences our in different positive and negative responses. According to article published in live sciences, The human gut is teeming with bacteria, most of which helps us digest food and fend off the bad guys in the belly. But how does the body tell the good from the bad? New research is pointing to gut-specific white blood cells (called Treg cells), which "learn" to identify and then protect the good gut bacteria, telling our bodies "Don't mess with them.""Since we've had these microbes living with us for the millennia, we've developed a tolerance to them," said Josef Neu, a researcher from the University of Florida who wasn't involved in the study. "That same tolerance with those Treg cells helps prevent us from getting certain types of diseases, like colitis." The study, led by Chyi-Song Hsieh, of Washington University School of Medicine, in St. Louis, looked at the white blood cells present in the guts of lab mice. They saw that the gut naturally has its own population of the Treg cells which protect friendly gut bacteria. These protecting cells must rely on some common factor shared by foreign (yet friendly) gut bacteria as well as our own gut cells. If that's the case, Neu speculated what would happen if the protector cells weren't around when our immune system was developing, saying if those bacteria aren't there, the body could react badly to our normal cells. Bacteria are all around us and most people only consider these prokaryotic organisms to be disease causing parasites. While it is true that bacteria are responsible for a large number of human diseases, they also make it possible for certain elements such as carbon, nitrogen, and oxygen to be returned to the atmosphere. Life as we know it would not exist without bacteria to decompose waste and dead organisms. These bacteria ensure that the cycle of chemical exchange between organisms and their environment is continuous. The decision as to whether bacteria are friend or foe becomes more difficult when both the positive and negative aspects of the relationship between humans and bacteria are considered. Let's discuss three types of symbiotic relationships: commensalism, mutualism, and parasitism. Commensalism is a relationship that is beneficial to the bacteria which live off of the host, but does not help or harm the host. Most of the bacteria that reside within the bodies of humans are commensalistic. In a mutualistic relationship, both the bacteria and the host benefit. For example, there are several kinds of bacteria which live inside the mouth, nose, throat, and intestines of humans and animals. These bacteria receive a place to live and feed while keeping other harmful microbes from taking up residence. A parasitic relationship is one in which the bacteria benefit while the host is harmed. Pathogenic parasites, which cause disease, do so by resisting the host's defenses and growing at the expense of the host. Apart from cover story magazine also has an interesting articles entitled: Diabetic Foot Disorders: The Inherent Risk in Diabetic patients, Published by Dr.Muslim Dhaher Musa, Nasiriya, Iraq. Article briefly discuss diabetic foot ulcer. Microbioz India this issue of magazines also discusses number of current news and researches collected from different world wide sources.

As we did in our earlier issues each month our team introduces with Scientist/Academic Staff/Professors this month we perform an interview with one of reputed Microbiologist and Professors, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India. For better support to our dearest readers who would like to pursue higher education in different reputed university of world, Magazines has different list of openings given in side. And in last phase of magazine an interesting Microbiology Cross Word is given.

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Editor-in-Chief, Microbioz International Journals


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Cover Story…

Microbes Beneficial & Negative Effects of

BBeenneeffiittss ooff MMiiccrroobbeess ttoo SSoocciieettyy aanndd IIttss NNeeggaattiivvee EEffffeeccttss oonn HHuummaanniittyy

BBacteria are the part of the environment and ecosystem.

Almost all types of bacteria are helpful to mankind except few species which cause diseases in the human body. Life as we know it would not exist without bacteria to decompose waste and dead organisms. These bacteria ensure that the cycle of chemical exchange between organisms and their environment is continuous. The decision as to whether bacteria are friend or foe becomes more difficult when both the positive and negative aspects of the relationship between humans and bacteria are considered. Let's discuss three types of symbiotic relationships: commensalism, mutualism, and parasitism. Commensalism is a relationship that is beneficial to the bacteria which live off of the host, but does not help or harm the host. Most of the bacteria that reside within the bodies of humans are commensalistic. In a mutualistic relationship, both the bacteria and the host benefit.

TT “One of the major areas we find bacteria is of course in the gut. These bacteria generally congregate where there is slower transition through the system – the end of the small intestine and throughout the large intestine.”

he planet earth is full of bacteria and they play an important role in the different functions whether they are related to humans, animals or plants. All the bacteria are unicellular that is single celled. They do not have proper cell structure and cell organelles are scattered in the cytoplasm including the genetic material because they also lack nucleus. A thick cell wall, called capsule encloses all the organelles and gives the proper shape to the bacteria. They reproduce by

binary fission, a process involving division of the organism into two (half).

Bacteria are the part of the environment and ecosystem. Almost all types of bacteria are helpful to mankind except few species which cause diseases in the human body. Life as we know it would not exist without bacteria to decompose waste and dead organisms. These bacteria ensure that the cycle of chemical exchange between organisms and their environment is continuous. The decision as to whether bacteria are friend or foe becomes more difficult when both the positive and negative aspects of the relationship between humans and bacteria are considered. Let's discuss three types of symbiotic relationships: commensalism, mutualism, and parasitism. Commensalism is a relationship that is beneficial to the bacteria which live off of the host, but does not help or harm the host. Most of the bacteria that reside within the bodies of humans are commensalistic. In a mutualistic relationship, both the bacteria and the host benefit. For example, there are several kinds of bacteria which live inside the mouth, nose, throat, and intestines of humans and animals. These bacteria receive a place to live and feed while keeping other harmful microbes from taking up residence. A parasitic relationship is one in which the bacteria benefit while the host is harmed. Pathogenic parasites, which cause disease, do so by resisting the host's defenses and growing at the expense of the host. These bacteria produce poisonous substances called endotoxins and exotoxins which are responsible for the symptoms that occur with an illness. When all of the facts are considered, bacteria are more helpful than harmful. Humans have exploited bacteria for a wide variety of uses, such as: making cheese and butter, decomposing waste in sewage plants, and developing antibiotics. Bacteria have been able to survive without us, but we could never live without them.

According to Blog report publish at Dr.Harold Eddleman, Ph.D,

We look upon bacteria which kill humans as being harmful. That same bacterium may have made our present civilization possible by killing off over populations of the past which would otherwise destroyed our forests and other resources so that we could not destroy the resources now to build our homes and universities. The bacterium that lives in the gut of the termite enabling him to eat the wood frame of our house, enables the same termite to eat (on a different day) the wood of a tree stump in the yard to promote its decay and enrichment of a flower bed. While true, the first example above is not very pleasant to think about. Therefore, we have various foundations to collect money to fight bacteria diseases cheaply and quickly so we save money which we can use to buy the trees and resources of other countries so the animals and humans of those countries perish from lack of food and resources. In these examples, economics has enabled additional types of competition between species for available resources. Without microbes, there would be no fertile soil to grow vegetables and flowers, no bread or cheese, and no beer or wine! Long ago, before people were able to see microbes under microscopes or even knew that they existed, human societies began learning how to put them to use. Commercial use of microorganisms, called biotechnology, has been revolutionized through the advent of genetic engineering, which has shown great potential for medical use.

Cover Story…

Bacteria Humanity

& Effect on

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For example, many people cannot digest the sugar present in raw milk (lactose). When animals were domesticated about 10,000 years ago, people learned how to use bacteria to digest raw milk from domesticated animals and turn it into yogurt and cheese, which are more palatable. An entire dairy industry was born from bacteria.

Beneficial Bacteria (Friendly Behaviour)

Some species of bacteria live in the human intestines where they help in digestion of food by releasing certain components. For instance, E. coliresides in the digestive tract of humans where it helps in breaking down lactose. They also produce some vitamins (such as Vitamin A and K) which are helpful for the human body large intestine. In specific, enteric bacteria secrete vitamin K and vitamin B12 in the large intestine. The main function of bacteria residing in the stomach is to maintain the ph and acidity level in the stomach. New born babies have fewer chances of suffering from diarrhea if they are administered with the bacteria Lactobacillusreuteri or Bifidobacterium.

The process of fermentation takes place with the help of bacteria. Fermented milk contains live bacteria Lactobacillus casei, which removes the harmful bacteria Helicobacter pylori from children's body. Similarly, Saccharomyces boulardii also helps to reduce the risk of antibiotic associated diarrhea from the children. Some bacterial species live on our skin and protect it from getting fungal infections. Humans also learned how to use yeast, another kind of microbe, to digest the sugars in fruit such as grapes, into alcohol to make wine. Yeast also digests sugars in grains like barley malt to make alcohol in beers. Some experts think that the ancient Egyptians developed grain and yeast to make beer even before they used it to make bread. The tablet, from Nippur in Iraq, contains prescriptions for salves and internal remedies. Most of the medicines are to be taken with beer.

Inside all of us, and on our skin we are hosts to millions of bacteria. From the moment we are being born (and passing out the birth canal), our little friends are getting ready to create their habitats and ‘shape’ our future health.

Scientists have even recently been looking at making ‘artificial’ gut models to study the ways we process food, and how the different types of bacteria in the gut affect our health.

One of the major areas we find bacteria is of course in the gut. These bacteria generally congregate where there is slower transition through the system – the end of the small intestine and throughout the large intestine. Many factors can interact to decide how these colonies will develop: our surroundings, our parents, our genetics, our age, as well as what we chose to ‘put into’ our bodies. The ‘microbiome’ is the term used to describe these communities of bacteria which are classed as being commensal (living on or in an organism and gaining benefits from them without harming them), symbiotic (having an interdependent relationship) and pathogenic (capable of producing disease).Many different areas of the microbiome are being studied to discover more about how these colonies interact with us. Some of these include the genetic make-up of these colonies (Metagenomics), and others the chemical fingerprints that are left behind after specific cellular processes occur (Metabolomics). What is fascinating about the microbiome is that their presence can not only affect the way we process food, but also affect how our immune system works, how susceptible we may be to suffering from different diseases or even how susceptible we may be to putting on or losing weight, to name but a few. It is also now believed that our microbiomes are almost unique to each of us. We can have familial similarities but the actual make up of each microbiome is totally specific, personal and functionally relevant. This microbiome can become unbalanced by a number of factors for example antibiotic use or disease process and this makes the studying of this area not only complex but also diverse and exciting.

Few of friendly behavior of Bacteria proves by following different valuable aspects.

Decay and decomposition

Soil bacteria are important to us because they cause decomposition of the organic matter. By this, harmful wastes are removed and when disintegrated, the organic matters serve as the nutrient of the plants.

The dead bodies and organic wastes liberated by the organisms (both of plants and animals) are decomposed by saprophytic bacteria. The decomposition of carbohydrates is caused by bacteria even in the absence of oxygen.

The process is called fermentation. Also, decomposition of proteinaceous materials is done by bacteria by the process of putrefaction. The amino acids thus, liberated, are utilized by the plant world as nutrient.

MICROBIOZ INDIA www.microbiozindia.com February 2015

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“A healthy population of gut flora features roughly 1,000 trillion microorganisms! There’s a number that’s tough to imagine, isn’t it! While it’s true that some bacteria are not friendly toward humans and, in fact, can be dangerous to our health and well-being, the vast majority of bacteria are harmless or beneficial to us.”

Enhancing Soil Fertility

Some bacteria maintain the soil fertility and others enhance it. The fertility of the soil is proportional to the nitrogen content. Nitrogen is an important ingredient in the structure and function of the living beings.

Yet excepting certain bacteria, no living organism can fix nitrogen although nearly four fifths (80%) of the atmosphere contain nitrogen. This work is done by ammonifying, nitrifying and nitrogen fixing bacteria.

Ammonifying bacteria break amino acids that constitute proteins. Nitrifying bacteria bring it to nitrate form which can be assimilated by the plants from the soil.

Nitrogen fixing bacteria like Azotobacter, Clostridium live free in the soil and fix atmospheric nitrogen. Rhizobium like bacteria lives symbiotically with root systems of leguminous plants and fix from the atmosphere nitrogen.

Bacteria in industry Man has utilized the services of bacteria for various industrial purposes. The diary industry solely depends on bacteria. Souring

and curdling of milk is done by lactic acid bacteria (Lactobacillus).Through the process of lactic acid fermentation, the disaccharide of lactose sugar that constitutes the carbohydrate component of milk is converted to lactic acid and carbon dioxide. The acid causes the souring and thereby, the milk protein coagulates.

Oxidation of alcohol to vinegar (acetic acid) is done by certain bacteria. The curing of tea, tobacco and indigo are other economically beneficial effect of bacteria. The processes of tanning hides in leather industry, manufacture of sponges also involve use of bacteria.

The production of jute and linen is done by bacterial activity. The retting bacteria loosen the fibers when the plants are submerged in water and thereby help extraction of fibers which are used for making clothes, ropes etc.

The cocoa beans are white colored and quite bitter in taste. The bacteria digest the bitter coverings of the seeds and give it the characteristic color, flavor and aroma. Saprophytic bacteria. The decomposition of carbohydrates is caused by bacteria even in the absence of oxygen. The process is called fermentation. Also, decomposition of proteinaceous materials is done by bacteria by the process of putrefaction. The amino acids thus, liberated, are utilized by the plant world as nutrient.

The bacteria digest the bitter coverings of the seeds and give it the characteristic color, flavor and aroma.

Flavor to the beverages, sweets and food materials. Vitamins produced from bacteria have nutritive value.

Bacteria in medicine

(a) As antibiotics

Antibiotics arc prepared from secretions of microorganisms which are selectively toxic. First antibiotic extracted from a bacterium was streptomycin by Walksman in 1941 (Penicillin was however, the first antibiotic to be discovered from a fungus, Penicillium notatum by Fleming in 1929). It was obtained from Streptomycin. Now- a-days, a number of bacterial antibiotics are available.

(b) Serums and Vaccines

These are substances obtained from bacteria to develop immunity to various diseases. Serums are used against the diseases like diphtheria, pneumonia etc and vaccines are used against cholera, typhoid etc.

Cover Story…


“Bacteria are an important tool of God. We could not live without them, and they have been well controlled in the past by the hygienic rules that God has given. The ancient Israelites had washings and practiced quarantine that reduced the problems of spreading diseases and infections. By contrast, King Henry IV of England caused controversy by requiring his knights to bathe at least once in their lifetime.”

Enhancing Soil Fertility

Some bacteria maintain the soil fertility and others enhance it. The fertility of the soil is proportional to the nitrogen content. Nitrogen is an important ingredient in the structure and function of the living beings.

Yet excepting certain bacteria, no living organism can fix nitrogen although nearly four fifths (8o %) of the atmosphere contain nitrogen. This work is done by ammonifying, nitrifying and nitrogen fixing bacteria. Ammonifying bacteria break amino acids that constitute proteins. Nitrifying bacteria bring it to nitrate form which can be assimilated by the plants from the soil.

Nitrogen fixing bacteria like Azotobacter, Clostridium live free in the soil and fix atmospheric nitrogen. Rhizobium like bacteria lives symbiotically with root systems of leguminous plants and fix from the atmosphere nitrogen.

Bacteria in genetic engineering and biotechnology Plasmids that occur in bacteria are important tools in the modern field of biological science called biotechnology. Genes obtained

from the bacteria are transferred and incorporated in other living organisms to develop their disease resistance, productivity, quality etc. A number of genetically modified crops have been developed using bacteria. Ex-Bt-cotton developed from Bacillus thuringensis.

According to Blog Living Intentionally

As I’ve gotten older, I’ve noticed a trend in society that I find both unnecessary and disturbing: The fear of germs. People have become so afraid of bacteria; it’s evident that they don’t have a thorough understanding of the vital role bacteria play in ecology. Bacteria are vital to life itself. To illustrate this concept, it’s worth noting that our intestinal tract is home to trillions of bacteria. These bacteria are largely responsible for the digestion and, therefore, bio-availability of the foods and nutrients we ingest. Humans tend to think that digestion happens in our stomach by way of bile, but that’s mostly a precursor to the real work. We are only able to absorb nutrients, vitamins, proteins, etc. thanks to the work our gut flora do for us. What we eat, they eat. And what we can’t use in its raw form, they prepare for us. Our gut flora are the chefs of our intestinal tract. Another way bacteria help us is in training our immune system to recognize threats. The vast majority of germs are of no risk to humans whatsoever, as long as the immune system is functioning correctly and the body is in good health. One of the ways we train our immune systems is by getting dirty. It might be tempting to say that “cleanliness is next to godliness”, but it’s more realistic to say, “Dirtiness leads to healthiness”.

Children, especially babies, train their immune systems by way of experiencing dirt. Lots and lots and lots of dirt. Soil is, by definition, decomposed organic matter mixed with broken-down rock and sand. Soil, therefore, is replete with a vast population of living bacteria. Babies begin training their immune systems to recognize non-harmful, “friendly” bacteria by way of their tendency to put nearly everything they can get their hands on into their mouths. This exposure to a plethora of non-harmful microorganisms teaches the immune system to recognize the non-harmful relationship between the body and the organisms. In recognizing the organisms to be of no risk whatsoever, the immune system learns to tailor its responses and act appropriately to risk. A well-tuned immune system only responds to real threats. Kids playing in the sandbox, rolling on the ground, falling down and getting a mouthful of dirt, and babies putting all manner of stuff in their mouths all contribute to training the immune response to act only on threats. It also serves to help populate the gut with an abundance of “good” bacteria. A healthy population of gut flora features roughly 1,000 trillion microorganisms! There’s a number that’s tough to imagine, isn’t it! While it’s true that some bacteria are not friendly toward humans and, in fact, can be dangerous to our health and well-being, the vast majority of bacteria are harmless or beneficial to us. It’s by far in our best interest to relax and not worry about germs. For the most part, germs only make us sick when our overall health is much less than optimal and our immune systems are lacking the “practice” of recognizing good versus bad bacteria.

Cover Story…


“In some parts of the world, the disease accounts for 7-8% of total mortality. “That’s a lot for one disease and one microbe,” says Blaser. He thought that perhaps our microbes, involved in most everything we do, might also be involved in our biological clocks.”

The best practice, therefore, is to enjoy a lifestyle that doesn’t worry about a little dirt. If your kids are outside rolling around in the dirt, be happy in the knowledge that they’re doing what kids instinctively know to do: They’re making sure their immune systems are exposed to the largest array of healthful and harmless bacteria possible, and in so doing, these kids are helping to ensure their immune systems respond appropriately.It’s common to see antibacterial soaps, sprays and lotions available in public places. My personal thoughts are that while well-intentioned, they actually do more harm than good. Antimicrobial soaps potentially cause antibiotic-resistant bacterial strains. This happens because hand-washing is typically ineffective in killing germs in the first place (despite common “knowledge” to the contrary). As germs are exposed to non-lethal antimicrobials, they develop resistance.As a secondary issue; excessive hand-washing carries a very real risk of developing dermatitis. Soap dries out the skin, causing cracking and fissures that actually expose us more to the risk of infection from unfriendly bacteria. Our skin is our first defence against environmental pollutants and exposure to unfriendly bacteria. As such, it’s in our best interest to take the best care of it as we possibly can. While we generally do most of our immune-system training in our childhood years, it’s never too late to help whip our system into shape. The first step is to relax and trust your immune system to always do the right thing and respond appropriately to threats. The second step is to let you get dirty and not freak out about it.

Bacteria as foe: (As Negative Behavior)

The microbes that threaten us come in a vast variety of shapes, sizes, and lifestyles. They stand ready to invade the body, feed off our bodies' cells, grow and reproduce, causing an infection. Microbes are constantly changing, adapting to new environments, finding new places to live and survive. They are found in soil, water, and animals as well as inside our bodies. They can cause minor illness, such as a cold or stomach flu, or deadly diseases such as AIDS/HIV, tuberculosis or Ebola fever.

At the close of the 19th century, in the story The War of the Worlds, author HG Wells wrote about Martians that invaded the earth yet succumbed to our planet’s bacteria and viruses. The Martians had long since eradicated micro-organisms from their own planet, only to die due to their lack of immunity to those on ours. Even today some say bacteria will inherit the earth. It’s a nod to their resilience, and also a wry observation about their ability to outwit scientists’ ongoing attempts to wipe them out. But what if instead of trying to see off the bugs, we harnessed them, or redirected the role they play and made them work for us, instead of against us?Bacteria are an important tool of God. We could not live without them, and they have been well controlled in the past by the hygienic rules that God has given. The ancient Israelites had washings and practiced quarantine that reduced the problems of spreading diseases and infections. By contrast, King Henry IV of England caused controversy by requiring his knights to bathe at least once in their lifetime. The lifestyle of the Israelites involved living in the open in isolated open air conditions. We have built huge cities and placed ourselves in very dense populations so that the problems of infection and the spreading of disease have become more critical. A seventh grader in Florida recently made the news by proving that there were more bacteria in the ice machines in fast food restaurants than in toilet bowl water. We have also complicated our situation by misinformation and the injudicious use of chemicals and radiation. A simple example is that antibacterial soap is no more effective at preventing infection than regular soap, and the active ingredient (triclosan) has a negative effect on hormones.

These bacteria cause great losses to animal and plant life by causing various diseases in them. Cholera, typhoid, pneumonia, dysentery, tuberculosis, tetanus, etc., are more common human diseases. ‘Ring disease of potato’, ‘yellowing rot of wheat,’ ‘Citrus canker,’ ‘wilt of cucumber’ and ‘crown gall’ are the common bacterial diseases of plants. Some saprophytic bacteria grow on unprotected foodstuffs like fruits, pickles, jams, jellies, bread, etc., and spoil them by causing decay. The use of salt, sugar and oil, etc., in preservation of pickles and jams, checks the growth of such bacteria. Clostridium botulinum produces a very virulent poison in canned food and many deaths occur due to it.


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According to article publish in mBio Sphere, a new online open access journal from American Society of Microbiology,

Commensal bacteria are friends, then Foes to keep population in check…

Published: 12/16/2014

Martin Blaser, 66, and Glenn Webb, 72, often discuss aging on their long summer hikes up to the Continental Divide near Fraser, Colorado. Not their own, but rather that of the human population. No other species has such a long, extended period of aging past the age of reproduction, or senescence. The two long-time collaborators often wondered and debated while they walked, why would evolution have selected such an age structure for the human population? After all, when resources are limited, the more mouths to feed past the age of reproduction, the greater the burden on the young’s survival. Blaser, a microbiologist at New York University Langone Medical Center who has spent 30 years studying the commensal gut microbe Helicobacter pylori, decided to view the question from the symbiont’s point of view. Although a peaceful co-existor for much of our lives, H. pylori is a major cause of stomach cancer and that risk increases with age. In some parts of the world, the disease accounts for 7-8% of total mortality. “That’s a lot for one disease and one microbe,” says Blaser. He thought that perhaps our microbes, involved in most everything we do, might also be involved in our biological clocks. “I began to think that a real symbiont is an organism that keeps you alive when young and kills you when you are old. That’s not particularly good for you, but it’s good for the species.” It’s also beneficial to the microbe community to keep the human population healthy, because if the human population crashes completely, then no more microbial homes. Webb, a mathematician at Vanderbilt University, could devise a mathematical model to test this hypothesis. Webb’s forte is coming up with nonlinear differential equations to describe dynamic biological processes.“Differential equations are all about change,” says Webb. “There’s a kind of magic in them that relates different rates of change to each other. And that relationship between them, the combination of those rates acting together, can reveal something unintuitive or unappreciated about the entire biological process.”


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Webb and Blaser incorporated three types of mortality into their model of an early human, hunter-gatherer population: all-cause mortality, the mortality created by the burden of a large senescent population on the juvenile population, and finally the mortality associated with particular microbes. Running a baseline version of the model, with the microbial mortality component set to zero, the team showed in a study published this week that the population stabilizes at around 200 years with about 7,000 individuals and a mean age of 18.Using this baseline model, they next tweaked the starting parameters, such as doubling the fertility rate. Intuition says that boosting fertility should help more juveniles survive and the population thrives. But surprisingly, it causes wild oscillations in the population over time.“You get into a boom or bust cycle and the oscillation is so great that the population can easily reach extinction,” if a low point coincides with a crisis such as a food shortage, says Blaser. “This might help explain why modern hunter-gatherers don’t have 20 kids, but rather six on average.”If a higher birth rate was not the answer, perhaps another solution would be to increase the mortality affecting only senescent individuals. Enter the microbes.

Blaser and Webb ran the model, adding in mortality risks based on particular microbial profiles. In one version they added a Shigella-like risk, which increases mortality only for children, and the population crashed to zero. Next, they ran a version incorporating risk from a microbe like H. pylori, which affects older adults and increases with age. At the same time, they held juvenile mortality to a constant, low level. In this scenario, the human population reaches a stable equilibrium. “If you have an organism that preferentially kills old people, then you get a robust population,” says Blaser. “This is what Nature is doing,” he argues. Webb says the modeling also revealed an underlying truth about human population growth—that we have the right fertility and mortality rates to maintain our species, even with our very unusual age structure of prolonged juvenile and senescent phases. “That’s what mathematics does for you. It verifies that our age structure is very stable and has been for a very long time.


“One of the most important groups of commensal bacteria is the genus Streptococcus, which can cause numerous infections including pneumonia. Streptococcus pyogenes is perhaps the most infamous and is sometimes known as the ‘flesh-eating’ bacterium.”

”Blaser envisions a phase shift in our relationship with our symbiotic microbes over our lifetimes. Early on, natural selection has favored organisms that aid digestion or other metabolic functions and those that help protect against pathogenic invaders. But as we age, selection favors organisms that begin contributing to inflammation and degenerative processes. He points to species like Bacteroides that make vitamins for us, but if they escape the gut, can kill us. In modern times of increased longevity, the cancer, inflammation, and degeneration these microbes cause place a major burden on the aging population. “Living with diseases caused by various microbes is inherent in our species,” notes Webb. “But the question is, can we improve longevity or manage it better?”Blaser cautions that simply getting rid of microbes that cause mischief late in life may not be the best solution—especially if their beneficial effects on immunity and metabolism in early life aren’t fully understood.“Our relationship with microbes is a fact of life in all directions.”

For much of the last 100 years or so, bacteria have been thought of as the enemy, to be eliminated at all costs. But many of the bacteria we come contact with play a vital role in our health, and our relationship with these “friendly” bacteria starts in the womb and lasts throughout our lives. Swedish microbiologist, Bengt Bjorksten, found that Estonian children had more lactobacilli (a friendly form of bacteria) than Swedish children. He found that 1-3 Swedish children had allergies, while only 1-10 Estonian children did. He also discovered that the digestive tracts of Swedish children housed the nasty bacteria Clostridium difficile, or C. diff, at much higher rates than the Estonian children. C. diff occurs in people who have very little in the way of healthy gut flora. A common way adults end up with C. diff is after a round of antibiotics destroys their healthy gut flora. In children C. diff often occurs when no healthy gut flora was established in the first place. Estonian children were far more likely to be exposed to less sanitary environments than Swedish children. And perhaps most importantly, Estonian children were more likely to be, not only breastfed, but breastfed for longer periods of time than Swedish children. Not having enough good bacteria in our colon, called gut dysbiosis, often leads to chronic low-level inflammation. Chronic low-level inflammation can cause insulin resistance, obesity, type 1 diabetes and other metabolic issues. It can also lead to an increased risk for heart disease, stroke, and some cancers.

Dr. Paresh Dandona, of the University at Buffalo, saw this first hand during a study he conducted some years back. First, he gave his patients a blood test. He then fed his patients a high carbohydrate McDonalds breakfast, followed by blood tests periodically in the hours after the breakfast. What he found was groundbreaking. After the patients consumed the high carbohydrate McDonalds breakfast, the bacteria in their guts released endotoxins into the bloodstream. When those endotoxins hit the blood stream, an immune response was triggered, leading to high levels of inflammation throughout the body. The effects lasted for about five hours.

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“This is because the bacterial communication pathways are a possible therapeutic target for new medicines. If the relevant communication options are prevented, the bacteria cannot develop their pathogenic properties.”

Each healthy strain of bacteria will confer its own health benefits. For instance, Lactobacillus rhamnosus is highly effective in treating antibiotic associated diarrhea. The strain also keeps E. coli and Salmonella from sticking to the intestinal wall. It may also result in less stress signals via the gut-brain connection. In other words, Lactobacillus rhamnosus may limit the stress signals sent from the gut to the brain, leading to lower levels of stress hormones. For those who don’t respond to probiotics, a fecal transplant may be necessary.

A fecal transplant is where healthy “poo” is taken, processed down to where the healthy bacteria are isolated, and then transplanted inside the rectum. Fecal transplants have a high rate of success in those who suffer from certain debilitating gut problems. The tricky part is finding a good match. There are many different fecal types, so before a fecal transplant can be had, one must first find a match. Surprisingly, many bacteria that cause disease are ones that are naturally present in or on our bodies. Bacteria that co-exist with the human body are known as commensal bacteria. It is a change in the normal situation, caused for example by a wound, which gives them a chance to grow and become a menace rather than remain a harmless natural inhabitant. Commensal also maintain a natural microbial balance in the body and help prevent pathogens from becoming abundant.

One of the most important groups of commensal bacteria is the genus Streptococcus, which can cause numerous infections including pneumonia. Streptococcus pyogenes is perhaps the most infamous and is sometimes known as the ‘flesh-eating’ bacterium. In fact, the condition known as necrotizing fasciitis, an infection of the deeper layers of the skin, causing large-scale deterioration of flesh, is very rare. More commonly Streptococcus pyogenes strains are involved in causing skin infections, meningitis and pharyngitis (‘strep throat’); each one of these may be caused by different strains. About one-tenth of the population carry the Strep. pyogenes bacterium around in their throats and noses and usually it does no harm at all. (Note that because the genera Streptococcus and Staphylococcus can be easily confused if referred to in their abbreviated form, simply by the first letter of their genus, their names are instead often shortened to Strep. and Staph.) Strep. pyogenes is not destroyed by the immune system because it carries proteins on its cell surface that resemble human proteins, thus fooling the system into thinking it is part of the human body and preventing it being destroyed. About one-fifth of the population has Strep. Pneumoniae in their body and it too can produce a surface layer that allows it to evade the immune system. A commensal species can cause an infection if its growth becomes out of balance with the rest of the natural microbial population in the human body. The population size and activity of each commensal species are normally kept in check by competition from other commensal, but if the balance is disrupted then some commensal or even foreign microbes may get a chance to multiply and become more active. Surprisingly, many bacteria that cause disease are ones that are naturally present in or on our bodies. Bacteria that co-exist with the human body are known as commensal bacteria. It is a change in the normal situation, caused for example by a wound, which gives them a chance to grow and become a menace rather than remain a harmless natural inhabitant. Commensal also maintain a natural microbial balance in the body and help prevent pathogens from becoming abundant. One of the most important groups of commensal bacteria is the genus Streptococcus, which can cause numerous infections including pneumonia. Streptococcus pyogenes is perhaps the most infamous and is sometimes known as the ‘flesh-eating’ bacterium. In fact, the condition known as necrotizing fasciitis, an infection of the deeper layers of the skin, causing large-scale deterioration of flesh, is very rare. More commonly Streptococcus pyogenes strains are involved in causing skin infections, meningitis and pharyngitis (‘strep throat’); each one of these may be caused by different strains. About one-tenth of the populations carry the Strep. Pyogenes bacterium around in their throats and noses and usually it does no harm at all. (Note that because the genera Streptococcus and Staphylococcus can be easily confused if referred to in their abbreviated form, simply by the first letter of their genus, their names are instead often shortened to Strep. and Staph.) Strep. pyogenes is not destroyed by the immune system because it carries proteins on its cell surface that resemble human proteins, thus fooling the system into thinking it is part of the human body and preventing it being destroyed. About one-fifth of the population has Strep. Pneumoniae in their body and it too can produce a surface layer that allows it to evade the immune system. A commensal species can cause an infection if its growth becomes out of balance with the rest of the natural microbial population in the human body. The population size and activity of each commensal species are normally kept in check by competition from other commensal, but if the balance is disrupted then some commensal or even foreign microbes may get a chance to multiply and become more active. According to report publish in open learn (The home of open learn University)

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According to article published in Science Daily News, 21st January 2015

New bacterial 'language' discovered: Previously unknown communication pathway

Bacteria communicate by means of chemical signals and can develop common characteristics through this "agreement" and also develop their potential pathogenic effects in this way. Scientists working with Dr. Helge B. Bode, an Merck-endowed professor for molecular biotechnology at the Goethe University in Frankfurt, and Dr. Ralf Heermann from the department of microbiology at the Ludwig Maximilian University in Munich, have now described a hitherto unknown communication pathway that appears to be widely distributed. The investigation of bacterial communication is also of medical interest.

This is because the bacterial communication pathways are a possible therapeutic target for new medicines. If the relevant communication options are prevented, the bacteria cannot develop their pathogenic properties. "When pathogens are no longer destroyed by antibiotics as we have seen to date, but rather be impaired beforehand the formation of the pathogenic properties, the danger of resistance development would be substantially reduced," says Bode. Different types of bacteria also have different methods of communication. The team leads by Heerman and Bode had already discovered a new bacterial communication pathway in 2013. Now they have succeeded in decoding a further new and widely distributed chemical type of bacterial communication.

To date, the best known communication between bacteria occurs via the N-acyl homoserine lactone (AHL): The enzyme Luxl produces signals that are recognized by the LuxR receptor, at which point the bacteria develop certain properties and modulate their behavior towards one another. Since a certain number of bacteria must be available for this to occur, this process is known as "quorum sensing."

However, Heermann's and Bode's working groups investigate bacteria that possess a LuxR receptor, but not the enzyme Luxl. In the current study, the microbiologists have investigated the bacteria Photorhabdus asymbiotica, which is a deadly pathogen in insects, which also infects humans and can cause skin infections. These bacteria communicate via the signal molecule dialkylresorcinol, which recognized the associated LuxR receptor. "The influence on the pathogenic properties of the bacteria is at its strongest in this 'quorum sensing' system. P. asymbiotica requires dialkylresorcinol and in this way coordinates the communication with the conspecifics for the successful infection of the larvae," says Helge Bode, whose group in 2013 also described the biosynthesis of this new signal molecule.

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The researchers have not only investigated P. asymbiotica, but also a series of other bacterial genomes. The newly discovered signal pathway appears to be widely distributed. "We were able to identify several other bacteria that are pathogenic to humans that also do not express Luxl and also possess this ability for forming these signals," says Heerman.

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DD “Ulcerations are prone to colonization by nearly every microorganism that can come in contact with their surface. Usually ulcerations contain mixed flora, consisting of several strains of bacteria. Most often these are aerobic bacteria, such as S. aureus, Streptococcus pyogenes, Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, and anaerobic bacteria, for example, Bacteroides fragilis, Clostridium perfringens, Peptostreptococcus spp., and Prevotella oralis”.

-Dr. Moslim Dhaher Musa, Nasiriya, Iraq

iabetic foot disorder (abnormalities) is clearly one of the most important complications of diabetes mellitus (DM) and is the leading cause of hospitalization with substantial morbidity, impairment of quality of life and engenders high treatment costs [1].

The term diabetic foot disorders DFDs refers to a group of disorders which clinically present with one or more of the following clinical manifestations: foot ulceration, infection, neuropathy, deformity, gangrene and/or ischemia [2]. Due to the impaired metabolic mechanisms in DM, there is an increased risk of infection and

poor wound healing due to a series of mechanisms which include decreased cell and growth factor response, diminished peripheral blood flow and decreased local angiogenesis. Thus, the feet are predisposed to peripheral vascular disease, damage of peripheral nerves, deformities, ulcerations and gangrene [3].

Many factors contribute to the pathogenesis of foot ulceration, including loss of protective sensation due to peripheral neuropathy where the feet become numb and the injury goes unnoticed. Also, arterial insufficiency complicates the neuropathic ulcer which leads to poor wound healing [4]. Approximately 45%-60% of all diabetic foot ulcerations are purely neuropathic, whereas 45% have both neuropathic and ischemic components [5]. In this review we are trying to explain the important points in pathogenesis of diabetic foot disorders that may lead dramatically to foot amputation. In 2005 the International Diabetes Federation (IDF) published a position statement about common diabetes complications, data from epidemiological studies have indicated that between 40 – 70% of all lower extremity amputations are related to diabetes. Eighty five percent of all amputations related to diabetes are preceded by foot ulcers. Researchers established that between 49-85% of all amputations can be prevented [16].

The mechanism of neuropathy development include that the increased level of glucose in blood leads to increased enzyme production such as aldose reductase and sorbitol dehydrogenase. These enzymes convert glucose into sorbitol and fructose. As these sugar products accumulate, the synthesis of nerve cell myoinositol is decreased, affecting nerve conduction. Moreover , hyperglycaemia induced microangiopathy leads to reversible metabolic, immunologic and ischemic injury of autonomic, motor and sensory nerves [6,7].

Sensory neuropathy is a major component leading to the development of diabetic foot ulceration. Motor neuropathy leads to atrophy of the small muscles of the foot and this will lead to foot deformities. Development of foot deformities with lack of foot care awareness and lack of proper foot wear in Arabian patients significantly contributes to the increasing problems of foot complications in our diabetic patients [8]. High levels of glucose in the blood provide an excellent breeding ground for bacteria and fungi, and can reduce the body's ability to heal itself [9]

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DDiiaabbeettiicc FFoooott ““TThhee IInnhheerreenntt RRiisskk iinn DDiiaabbeettiicc ppaattiieennttss”

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A recent report estimated that the risk of hospitalization and lower-extremity amputation was nearly 56 and 155 times greater in diabetic people who had a foot infection than for healthy individual, respectively [10]. The underlying causes of risk factors leading to the onset of diabetic foot ulcers have recently been identified. The afore-mentioned conditions, together with peripheral neuropathy, contribute to a lack of sensation in poorly vascularized lower extremities that are prone to the development of chronic wounds. Lack of sensation leads to exacerbation of the injury. Dry, stiff skin cracks easily and causes splits or fissures.

A fissure in the protective epidermal covering (stratum corneum), can become infected, resulting in localized cellulitis or even small longitudinal ulcerations that can potentially become infected and frequently lead to the spread of infection and the ultimate loss of the lower limb, either partial or full. Poor circulation occurs in conducting vessels, consequently affecting microcirculation, which in turn affects the basement membrane, thickening and diminishing vascular reparative capacity diabetic foot infection (DFI) may be caused by pathogenic bacteria originating from the external environment as well as by bacteria forming physiological microflora of the skin e.g. Staphylococcus epidermidis, Staphylococcus aureus, and Propionibacterium acnes [11].

Ulcerations are prone to colonization by nearly every microorganism that can come in contact with their surface. Usually ulcerations contain mixed flora, consisting of several strains of bacteria. Most often these are aerobic bacteria, such as S. aureus, Streptococcus pyogenes, Escherichia coli, Proteus mirabilis, Pseudomonas aeruginosa, and anaerobic bacteria, for example, Bacteroides fragilis, Clostridium perfringens, Peptostreptococcus spp., and Prevotella oralis. It is suggested that the main role is played by the pathogenic virulence factors of bacteria, such as:

Bacterial adhesions, proteins present on the surface of bacterial cells are responsible for their adhesion to host cells, allowing colonization of the ulceration.

Exoenzymes decomposing cell materials such as collagen and fibrinogen, allowing deeper penetration to tissues and modifying bacterial resistance.

Toxins, protein substances released from bacterial cells responsible for clinical signs of infection [12]. Identification and

management of foot infection in diabetic Patients are often problematic due to difficulty in :

Differentiating infection from colonization. all chronic wounds are colonized by microorganisms, the diagnosis of DFI should not be based on the microbiological analysis of a wound culture but on clinical finding[13]. DFI is defined by the presence at least two inflammatory manifestations (purulence or erythema, pain, tenderness, warmth or induration) mentioned of these, clinical signs or symptoms of foot wound infection may be much reduced in diabetic patients. This means that reliance on these signs for diagnosis may result in some infections being undetected when they first present. The resultant delay in starting treatment may lead to progression of infection from limited to severe and limb threatening. This progression is often rapid because of associated ischemia, diabetic immunopathy and the particular anatomic characteristics of the foot[14].

Understanding the actual extent of the infectious process when suspected Treating infection because of the increasing frequency of multidrug-resistant bacteria and altered pharmacokinetic

properties of antibiotic agents due to poor quality of arterial supply to the foot.

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Determining duration of therapy as the optimal duration of antibiotic treatment is not clearly defined and criteria for cure are poor, especially for osteomyelitis [13]. The better explanation of why patient with diabetes mellitus frequently suffering of chronic wound is established by (Liu and Velazquez 2008) , as they found that the ,diabetes mellitus affects signaling intermediates responsible for coordinating/regulating wound healing angiogenesis and vasculogenesis. Due to the deficiencies in either endothelial progenitor cell or peripheral tissue homing and engraftment of bone marrow, diabetic patients are prone to the development of chronic wounds [14] . This short review has been accomplished to simplify the order sequential events in the pathogenesis of diabetic foot disorder, as many of diabetic patient do not realize the dramatic complication of their disease.

References New JP, McDowell D, Burns E, Young RJ. Problem of amputations in patients with newly diagnosed diabetes mellitus. Diabetes Med 1998;

15:760–4. F. A. Qari and D. Akbar, “Diabetic Foot: Presentation and Treatment,” Saudi Medical Journal, Vol. 21, No. 5, 2000, pp. 443-446

Brem H, Tomic-Canic M (2007) Cellular and molecular basis of wound healing in diabetes. J Clin Invest 117: 1219-1222.

Farahani RM, Kloth LC. The hypothesis of ‘biophysical matrix contraction’: wound contraction revisited. Int Wound J 2008; 5: 477-482

Reiber GE, Vileikyte L, Boyko EJ, del Aguila M, Smith DG, Lavery LA, Boulton AJ. Causal pathways for incident lower extremity ulcers in

patients with diabetes from two settings. Diabetes Care 1999; 22: 157-162

Clayton W, Elcasy TA (2009) A Review of the Pathophysiology, Classification, and Treatment of Foot Ulcers in Diabetic Patients. Clin Diabetes 27: 52-58.

Younger DS, Rosoklija G, Hays AP (1998) Diabetic peripheral neuropathy. Semin Neurol 18: 95-104.

Dr.Almoutaz Alkhier Ahmed1,Emad Elsharief, Ali Alsharief, The Diabetic Foot in the Arab World, The Journal of Diabetic Foot Complications, 2011; Volume 3, Issue 3, No. 3, Pages 55-61

Ceriello A. Postprandial hyperglycemia and diabetes complications: is it time to treat? Diabetes 2005;54:1-7.

Lavery LA, Armstrong DG, Wunderlich RP, Mohler MJ, Wendel CS, Lipsky BA. Risk factors for foot infections in individuals with diabetes.

Diabetes Care 2006; 29: 1288-1293

Citron DM, Goldstein EJC, Merriam CV, Lipsky BA, Abramson MA. Bacteriology of moderate-to-severe diabetic foot infections and in vitro activity of antimicrobial agents. J Clin Microbiol 2007; 45:2819–2828.

Gadepalli R, Dhawan B, Sreenivas V, Kapil A, Ammini AC, Chaudhry A clinico-microbiological study of diabetic foot ulcers in an Indian tertiary care hospital. Diabetes Care 2006; 29:1727–1732.

Jeffcoate WJ, Lipsky BA, Berendt AR, Cavanagh PR, Bus SA, Peters EJ, van Houtum WH, Valk GD, Bakker K. Unresolved issues in the

management of ulcers of the foot in diabetes. Diabet Med 2008; 25: 1380-1389

Lipsky BA. Infectious problems of the foot in diabetic patients. In: Levin and O’Neal’s The diabetic Foot (7th ed). In: Bowker JH, Pfeifer MA, editors. Philadelphia: Mosby Elsevier, 2008: 305-318

Liu ZJ, Velazquez OC. Hyperoxia, endothelial progenitor cell mobilization, and diabetic wound healing. Antioxid Redox Signal 2008; 10: 1869-1882

http://www.idf.org/position-statement-diabetic-foot

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CC

anine distemper, a viral disease that's been infecting the famed lions of Tanzania's Serengeti National Park, appears to be spread by multiple animal species, according to a study published by a transcontinental team of scientists. Writing in the journal Proceedings of the National Academy of Sciences, they say domestic dogs are no longer the primary source of the disease's transmission to lions and that wild carnivores may contribute as well. Their findings demonstrate that in natural ecosystems, a deadly virus can jump between species and thrive, thereby threatening

vulnerable animal populations."Our study shows that the dynamics of canine distemper virus are extremely complex, and a broadened approach -- focusing not only on domestic dogs--is required if we are to control the disease among lions and other wild animal species," said veterinary researcher Felix Lankester of Washington State University's Paul G. Allen School for Global Animal Health, a co-author based in Tanzania. In 1994, a mysterious neurological ailment wiped out 30-percent of the lion population in the Serengeti, one of the largest wildlife regions in the world. Scientists determined it was canine distemper, a disease previously thought to infect only dogs, coyotes and a small number of other mammals. Evidence suggested the lions had contracted the virus from dogs living in villages and settlements nearby. A domestic dog vaccination campaign was launched to curb the infection's spread. It worked--among dogs, at least. After analyzing three decades of blood serum data collected from lions and domestic dogs, the study's researchers discovered that the virus continues to circulate in the lion population while significantly declining among dogs. The dog's role in spreading the disease appears to be shrinking, conclude the paper's authors, an international team of veterinarians, disease ecologists, epidemiologists and mathematical biologists."Domestic dog populations immediately surrounding the Serengeti National Park are not the sole driver of canine distemper infections in lions, and its persistence is likely to involve a larger multi-host community," they write. Other species, including hyenas and jackals, are probably transmitting the disease and keeping it looming in the wild, they say. Consequently, outbreaks among lions and other already-threatened animals could occur at any time. Researchers say more work is necessary to identify which species spread distemper and what triggers the spillovers. For example, it's believed that an infected hyena or other carnivore feeding on a carcass can disperse the virus through mucus secretions to other predators at the same site.A better understanding of canine distemper virus and its dynamics in the wild is necessary to effectively monitor and better control the disease among lions and other threatened animals, the scientists report.

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Dog disease in lions spread by multiple species

News Credit: Science Daily News


The origin of life: Labyrinths as crucibles of life -News Credit: Science Daily

Recent Research News…

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HHow and in what habitats did the first life-forms arise on the young Earth? One crucial precondition

for the origin of life is that comparatively simple bimolecular must have had opportunities to form more complex structures, which were capable of reproducing themselves and could store genetic information in a chemically stable form. But this scenario requires some means of accumulating the precursor molecules in highly concentrated form in solution. In the early oceans, such compounds would have been present in vanishingly low concentrations. But LMU physicists led by Professor Dieter Braun now describe a setting which provides the necessary conditions. They show experimentally that pore systems on the seafloor that were heated by volcanic activity could have served as reaction chambers for the synthesis of RNA molecules, which serve as carriers of hereditary information in the biosphere today.

"The key requirement is that the heat source be localized on one side of the elongated pore, so that the water on that side is significantly warmer than that on the other," says Braun. Preformed bimolecular that are washed into the pore can then be trapped, and concentrated, by the action of the temperature gradient -- thus fulfilling a major prerequisite for the formation and replication of more complex molecular structures. The molecular trapping effect is a consequence of thermophoresis: Charged molecules in a temperature gradient preferentially move from the warmer to the cooler region, allowing longer polymers in particular to be securely trapped. This is an important factor in the evolution of nucleic acids such as RNA and DNA, simply because longer molecules can store more genetic information.

Recreating rock pores in the laboratory

Braun and his colleagues have shown that this mechanism works in the laboratory: "We used tiny glass capillary tubes to construct an analog of the natural pores found in rock, heated the pore from one side and allowed water containing dissolved fragments of linear DNA of varying lengths to percolate through it. Under such conditions, the long strands are indeed trapped within the pore," Braun explains. "Pores that were exposed to heat are frequently found in igneous rock formations, and they were certainly common in rocks of volcanic origin on the early Earth. So this scenario is quite realistic. And the temperature effect is enhanced by the presence of metal inclusions within the rock, which conduct heat at rates 100 times higher than water."

Temperature gradients and replication

Not only are nucleic acids retained in the pore, they are also capable of replication under these conditions. In the hotter zone, double-stranded strands are separated into its component strands within minutes. The single strands can then be transported by convection -- cyclical flow along the pore perpendicular to the orientation of temperature gradient -- back to the colder region of the pore. Here they encounter the chemical precursors from which each DNA strand is built, which are fed into the pore by a continuous inflow. The preformed strands then act as templates for the polymerization of complementary strands. This cycle makes it possible not only to replicate the strands but also to elongate them by stitching fragments together. When the nucleic acids accumulate to levels beyond the storage capacity of the pore, newly replicated molecules can escape and colonize neighboring pore systems. Thus, the LMU group has succeeded in constructing a system which permits autonomous and continuous Darwinian evolution of ever more complex bimolecular -- thus defining realistic conditions under which life could in principle have evolved. "Life is fundamentally a thermodynamic non-equilibrium phenomenon. That is why the emergence of the first life-forms requires a local imbalance driven by an external energy source -- for example, by a temperature difference imposed from outside the system," Dieter Braun explains. "That this can be achieved in such a simple and elegant way was surprising even to us. The success of the project is a tribute to the close cooperation between all members of the team."

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uccessfully treating rabies can be a race against the clock. Those who suffer a bite from a rabid animal have a brief window of time to seek medical help before the virus takes root in the central nervous system, at which point the disease is almost invariably fatal. Now, researchers at the University of Georgia have successfully tested a new treatment on mice that cures the disease even after the virus has spread to the brain. They published their findings

recently in the Journal of Virology."Basically, the best way to deal with rabies right now is simple: Don't get rabies," said study co-author Biao He, a professor of infectious diseases in the UGA College of Veterinary Medicine. "We have vaccines that can prevent the disease, and we use the same vaccine as a kind of treatment after a bite, but it only works if the virus hasn't progressed too far."Our team has developed a new vaccine that rescues mice much longer after infection than what was traditionally thought possible."In their mouse experiments, the animals were exposed to a strain of the rabies virus that generally reaches the brain of infected mice within three days. By day six, mice begin to exhibit the telltale physical symptoms that indicate the infection has become fatal. However, 50 percent of mice treated with the new vaccine were saved, even after the onset of physical symptoms on day six."This is the most effective treatment we have seen reported in the scientific literature," He said. "If we can improve these results and translate them to humans, we may have found one of the first useful treatments for advanced rabies infection."He and his colleagues developed their vaccine by inserting a protein from the rabies virus into another virus known as parainfluenza virus 5, or PIV5, which is thought to contribute to upper respiratory infections in dogs but is completely harmless to humans.PIV5 acts as a delivery vehicle that carries the rabies protein to the immune system so it may create the antibodies necessary to fight off the virus.


Beating the clock: researchers develop new treatment for rabies

-News Credit: Science Daily

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"This is only the beginning of our work," He said. "While these preliminary results are very exciting, we are confident that we can combine this new vaccine with other therapies to boost survival rates even higher and rescue animals even when symptoms are severe."Apart from being very effective in saving the infected mice, the researchers emphasized that their vaccine is much safer when compared to the best current treatment in mice, which uses a weakened version of the rabies virus."It doesn't matter how we weaken the current vaccine, the virus inside it is still rabies," said study co-author Zhen Fu, a professor of pathology in the college. "That is not a concern with our PIV5 vaccine."The researchers will continue to perfect their vaccine's design and hope to move into more advanced animal trials soon."There is an urgent need in many parts of the world for a better rabies treatment, and we think this technology may serve as an excellent platform," He said. "Ultimately, we just want to try to save more lives."

Researcher’s image, measure tubulin transport in cilia -News Credit: Science Daily

DDefective cilia can lead to a host of diseases and conditions in the human body--from rare,

inherited bone malformations to blindness, male infertility, kidney disease and obesity. Scientists knew that somehow these tiny cell organelles become deformed and cause these diseases because of a problem related to their assembly, which requires the translocation of vast quantities of the vital cell protein tubulin. What they didn't know was how tubulin and another cell organelle known as flagella fit into the process. Now, a new study from University of Georgia cellular biologists shows the mechanism behind tubulin transport and its assembly into cilia, including the first video imagery of the process. The study was published in the Journal of Cell Biology.

"Cilia are found throughout the body, so defects in cilia formation affect cells that line airways, brain ventricles or the reproductive track," said the study's lead author Julie Craft, a sixth-year doctoral student at UGA. "One of the main causes of male infertility is the cilia won't function properly."

An interdisciplinary team from the UGA Franklin College of Arts and Sciences and the College of Engineering collaborated on the research, which used total internal reflection fluorescence microscopy to analyze moving protein particles inside the cilia of Chlamydomonas reinhardtii, a green alga widely used as a model for cilia analysis.

The team exploited the natural behavior of the organism--which is to attach by its cilia to a smooth surface, such as a microscope glass cover. This positions the cilia within the 200-nanometer reach of the total internal reflection fluorescence microscope allowing for the imaging of individual proteins as they move inside the cilia. "Tubulin is transported by this process, which we call intraflagellar transport, or IFT," said study co-author Karl Lechtreck, an assistant professor in the department of cellular biology and a member of the Integrated Life Sciences Program. "Though it has long been suspected in the field and there was indirect evidence to support the theory, this is the first time it has been shown directly, through live imaging, that IFT does function as a tubulin pump.



HHuman activities are disrupting the migration patterns of many species, including monarch butterflies. Some monarchs

have stopped migrating to their traditional overwintering sites in Mexico, remaining in the southern U.S. to breed during the winter. A new study by University of Georgia ecologists, just published in the journal Proceedings of the Royal Society B, has found that these sedentary winter-breeding butterflies are at increased risk of disease, a finding that could apply to other migratory species as well. But, for the monarchs at least, there may be a relatively simple solution.

Every year, millions of monarch butterflies travel from breeding grounds in the eastern U.S. and Canada to spend the winter in central Mexico. In recent years, however, their numbers have declined sharply as changing agricultural practices and land use patterns have reduced the availability of milkweed, the plant on which monarchs lay their eggs.

In response, concerned gardeners have started planting milkweed to help replace some of the butterflies' lost breeding habitat. The most readily available commercially grown milkweed sold by garden centers is the exotic species Asclepias curassavica, or tropical milkweed. Monarchs love it, but, according to the study's lead author Dara Satterfield, a doctoral student in the UGA Odum School of Ecology, tropical milkweed does not naturally die back in fall like perennial milkweeds native to North America. In fact, in parts of the southern U.S. from the Gulf Coast to the Atlantic, tropical milkweed can produce foliage and flowers year-round. This allows monarchs in those areas to stay put and keep breeding all winter. And that's how problems with disease arise.

Satterfield and her colleagues processed more than 5,000 samples taken from monarchs at over 100 sites across the U.S., Canada and Mexico, testing them for infection by a debilitating protozoan parasite. The non-destructive samples, about half of which were collected by citizen scientists through Project Monarch Health, were taken by gently pressing clear tape against the butterfly's abdomen; the samples were then viewed under a microscope. The researchers found that the non-migratory, winter-breeding monarchs in the southern U.S. were five times more likely to be infected with parasites than migratory monarchs sampled in their summer breeding range or at overwintering sites in Mexico.

Satterfield said that previous studies by co-author Sonia Altizer, Odum School associate dean and UGA Athletic Association Professor in Ecology, showed that for some wildlife species, including monarchs, long distance migration helps to reduce infectious disease transmission. "Long distance migration can reduce disease in animal populations when it weeds out infected individuals during the strenuous journey, or when the migrating animals get to take a break and move away from contaminated habitats where parasites accumulate," she said. "Our non-migratory monarchs don't have those benefits of migration, so we see that in many cases the majority of monarchs at winter breeding sites are infected."

News Credit: Science Daily


Cancelled flights: For monarch butterflies, loss of migration means more

Credit: Dara Satterfield/University of Georgia

How malaria-spreading mosquitoes can tell you are home -News Credit: Phys.org


FFemales of the malaria-spreading mosquito tend to obtain their blood meals within human dwellings.

Indeed, this mosquito, Anopheles gambiae, spends much of its adult life indoors where it is constantly exposed to human odor - from used clothing, bedding, etc. - even when people are absent. But is human odor enough as a reliable cue for the mosquitoes in finding humans to bite?

Not quite, reports a team of entomologists at the University of California, Riverside in a research paper published online earlier this month in the Journal of Chemical Ecology. The researchers' experiments with female Anopheles gambiae show that the mosquitoes respond very weakly to human skin odor alone. The researchers found that the mosquitoes' landing on a source of skin odor was dramatically increased when carbon dioxide was also present, even at levels that barely exceed its background level. The researchers suggest, too, was that the mosquitoes use a "sit-and-wait" ambush strategy during which they ignore persistent human odor until a living human is present.

"Responding strongly to human skin odor alone once inside a dwelling where human odor is ubiquitous is a highly inefficient means for the mosquito of locating a feeding site," said Ring Cardé, a distinguished professor of entomology, whose lab conducted the research. "We already know that mosquitoes will readily fly upwind towards human skin odor but landing, the final stage of host location, which typically takes place indoors, does not occur unless a fluctuating concentration of carbon dioxide indicates that a human host is present. It may be that upwind flight towards human odor has more to do with locating a human dwelling, which emits human odor even when its occupants are absent, than locating a feeding site per se."Cardé explained that mosquitoes, once indoors, conserve their energy by ignoring omnipresent human odor in an unoccupied room. Small increases in carbon dioxide indicate to the mosquitoes the probable presence of a human. This then triggers the mosquitoes to land on human skin.

The findings could help in the design on new types of mosquito control. One take-home message from this work is that studies defining which human odors mediate host finding and which compounds are good repellents need to precisely control exposure to above ambient carbon dioxide - an experimenter entering an assay room quickly elevates the level of carbon dioxide and thereby alters the mosquitoes' behavior.

The research shows that when it comes to feeding on humans indoors, malaria mosquitoes have developed a striking adaptation to how carbon dioxide affects their landing on human targets in response to skin odor."It also would be useful next to see if mosquitoes' response to skin odor is similarly affected by carbon dioxide in outdoor situations and how these interactions play out in human dwellings," Cardé said. Larvae of Anopheles gambiae can breed in diverse habitats. This mosquito has evolved to search in human dwellings for blood meals to carry out egg production. The mosquito enters houses throughout the night, peaking around midnight and continuing at a high rate until the early morning hours. Following a blood meal, the mosquito often remains in dwellings until it is ready to lay eggs. Mosquitoes also seek refuge inside human dwellings during the day, taking shelter from high daytime temperatures outside.


Scientists identify important mechanism Involved in production of mosquito eggs

–News Credit: Phys.Org


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DDiseases transmitted by mosquitoes have contributed to the death and suffering of

millions throughout human history, earning the mosquito the title as the world's most dangerous animal. Even today, several devastating mosquito-borne diseases (such as malaria, dengue fever and West Nile virus) continue to rage. The urgent need to better control mosquito numbers and interfere with disease transmission has guided much mosquito research in laboratories worldwide. Female mosquitoes rely on a blood-meal as a source of nutrients required for reproduction. The thinking is that if the mechanisms that govern mosquitoes' egg production are better understood, novel approaches to controlling the reproduction and population of mosquitoes can be devised. Now a team of scientists at the University of California, Riverside has made a research breakthrough in understanding, at the molecular level, one such mechanism related to the mosquito reproductive process. This mechanism includes small regulatory RNA molecules known as microRNAs or miRNAs.

The researchers report in this week's issue of the Proceedings of the National Academy of Sciences that they have identified microRNA-8 (miR-8) as an essential regulator of mosquito reproductive events. They note that its depletion in the female mosquito results in severe defects related to egg development and deposition.

Using newly established genetic tools in mosquito biology and doing analysis that identifies microRNA targets, they were able to show that miR-8 plays an essential role in the female mosquito "fat body" (fatty tissue analogous to the mammalian liver) by regulating a molecule, called "swim," that miR-8 directly targets. High levels of this molecule are detrimental to egg development.

"To our knowledge, this is the first time a mosquito miRNA has been investigated in this specific manner," said Alexander Raikhel, a distinguished professor of entomology, who has received wide acclaim for his research in the areas of insect reproductive biology. "In the lab, female transgenic mosquitoes with deficiency in miR-8 displayed severely compromised ovary development and reduced egg-laying."

While the researchers focused in this study on only Aedes aegypti, the mosquito that spreads dengue and yellow fever, their research results can be applied also to other disease-spreading mosquitoes.


MICROBIOZ INDIA

Scientist Talk FEBRUARY 2015

Dr. Jai Shree Paul

UGC Research Scientist "C" (Professor) School of Life Sciences, Jawaharlal Nehru University New Delhi -110067, India.

An

Interview Microbioz: Why you opt MICROBIOLOGY as a career?

Dr.Paul: The Microbiology helps to explore the relationship of microorganisms with other organisms and how they influence life of human beings. Microbiologists play a significant role in the society, as their expertise help to conduct research on the positive as well as negative effects of microorganisms on human life and our environment.

Microbioz: Tell us a little more about your professional experiences; particularly those not mention your resume/application?

Dr.Paul : I am engaged in both teaching and research activities in the School of Life Sciences, Jawaharlal Nehru University past 27 years in the field of Microbiology. It is a great pleasure in teaching the basic and advanced microbiology course to M.Sc students through different semesters. I also get an opportunity to discuss current research themes and peer reviewed research papers while teaching Applied Microbiology to Pre-PhD students. Currently my research themes involve questions related to Medical Microbiology. We want to unravel the interplay between Microbes during 1. Inflammatory Bowel disease (an autoimmune disease) and 2. Amoebiasis, an endemic disease of our country.

Microbioz: What is your favorite part of your current job and why is it your favorite part?

Dr.Paul : Research work involving patients and clinical samples are quite fascinating and challenging since we can connect our research findings with the disease pattern directly..

Microbioz: How would your background and experiences strengthen this academic department?

Dr.Paul: Teaching and research going hand-in-hand has helped me to enrich my knowledge on the subject. It has also helped me to keep myself updated with the recent literature and improvise our teaching materials accordingly.

Microbioz: What is one or two of your proudest professional accomplishments?

Dr.Paul: Designing a low cost and fast technique to screen large number of clinical samples using molecular probes for a target parasite

Developing a high through put screening technique to detect single nucleotide polymorphism in susceptible genes of Inflammatory Bowel disease

Microbioz: Mention few of your words in favour of Microbioz India. Dr.Paul: I am quite confident that this would be an ideal opportunity to bring our fellow microbiologists on a common platform who is working passionately but silently.

“Microbioz India, perform an interview with Dr.Jaishree Paul from one of the reputed University of India named Jawahar Lal University, New Delhi, Here are few of interesting points of interview with her are given, Microbioz India team prays a great future a head for Dr.Paul.”


AA

Estrogen-producing neurons influence aggression in both sexes –News Credit: Phys.Org

miniscule cluster of estrogen-producing nerve cells in the mouse brain exerts highly specific effects on aggressive behavior in both males and females, according to new research by UC San Francisco scientists. The cells in question, known as aromatase-expressing (aromatase+) cells, represent less than five one-hundredths of a percent of the neurons in the mouse brain, but they play crucial roles in sexual differentiation during early development and in

regulating sexual and social behavior in adulthood. Though estrogen is generally thought of as a female sex hormone, during the 1970s it was discovered that the male sex hormone testosterone can be converted to estrogen in the brain by aromatase, an enzyme also found in many other mouse and human tissues. In the male mouse, estrogen, presumably synthesized by aromatase+ neurons in the brain, is known to be involved in diverse social behaviors, including the ultrasonic "singing" that males produce when courting females, and in mating, aggression, and the marking of territory. Aromatase+ neurons are also present, in smaller numbers, in females. But because females produce high levels of circulating estrogen and very little testosterone, it has been unclear whether aromatase+ cells in the female brain are purely vestigial or serve some other function.To more precisely investigate the workings of aromatase+ cells, a team in the UCSF laboratory of senior author Nirao Shah, MD, PhD, used genetic methods to selectively deplete these neurons in a single brain region known as the posterodorsal medial amygdala, or MeApd, in adult mice. This structure, in which aromatase+ cells make up 40 percent of the neurons, forms part of a circuit that is vital to normal social and reproductive behavior."The part of the olfactory bulb that receives pheromonal information—which is what mice use to identify other mice and to respond appropriately—projects directly to the amygdala, so we know that it's important for social behavior," said first author Elizabeth K. Unger, a graduate student in the Shah lab who led the research. After the research group eliminated aromatase+ neurons from the MeApd in male mice, the mice exhibited mostly normal social behaviors: they continued to mark their territory, and they recognized, courted, and successfully mated with females. If presented with an unfamiliar male, however, the mice acted quite differently from their normal counterparts. When male mice encounter a strange male in their territory they typically rattle their tail threateningly and attack the intruder shortly thereafter. But male mice lacking aromatase+ neurons were slower and less aggressive in their response to other males: their tail-rattling was significantly diminished, and it took much longer for them to mount an attack. This lag in mounting attacks on intruders was correlated with the number of aromatase+ cells that had been eliminated by the researchers' genetic manipulation. Once these mice did launch an attack, however, the aggressiveness of their fighting behavior resembled that of normal males. In females, the consequences of depleting aromatase+ cells were also sharply restricted. These females exhibited normal responses to males, including in their mating behaviors. But if they had given birth, females lacking aromatase+ cells did not display normal levels of maternal aggression. Female mice with nursing pups will generally attack unfamiliar male mice, because males sometimes kill rival males' pups. In a strikingly similar pattern to that seen in males lacking aromatase+ cells, however, nursing females in which these cells were depleted were much slower than normal mice to mount an attack. Again, once attacks were initiated they were indistinguishable from those launched by normal female mice with nursing pups. "In theory, these estrogen-producing neurons could have controlled any part of social behavior, or all social behaviors, but we found they control only a very small component of aggression," said Unger. "And considering females do not need these cells to produce estrogen, it was quite surprising to find that these cells play a similar role in both males and females."

For Shah, professor of anatomy, the results are a compelling example of "modularity" in the neural control of complex social behavior. "Though social behaviors—marking of territory, recognizing potential mates, successfully mating, fighting—seem quite 'seamless' when we observe them, this study shows that different neural systems control quite distinct, specific components of these behaviors."



II

n a study published in Cell, researchers lead by Zanvil A. Cohn and Ralph M. Steinman Professor Michel C. Nussenzweig at Rockefeller University and their collaborators describe new insights on which cells likely do, and do not, harbor this lurking threat."It has recently been shown that infected white blood cells can proliferate over time, producing many clones, all containing HIV's genetic code. However, we found that these clones do not appear to harbor the latent reservoir of virus," says study author Lillian Cohn a graduate student in Nussenzweig's Laboratory of Molecular

Immunology. "Instead our analysis points to cells that have never divided as the source of the latent reservoir."HIV belongs to a family of viruses that insert themselves directly into the host cell's genome where they can hide out quietly after the initial infection. HIV mostly targets CD4 T lymphocytes, a type of T cell involved in initiating an immune response.

When HIV integrates itself into the genetic code of a CD4 T cell, it may produce an active infection, hijacking the cell to produce more copies of itself in order infect other cells, and killing it in the process. Antiretroviral drugs that suppress HIV infection work by disrupting this hijacking. But the virus may also fail to produce an active infection, remaining a quiet, tiny fragment of DNA tucked within the host cell's genome. If so, the drugs have nothing to disrupt, and the infection remains latent. Most often, however, what happens is actually something in between. While the virus does manage to get at least some of itself into the T cell's genome, problems with the process leave it incapable of hijacking the cell to replicate itself. But those few successful integrations still do damage, and the resulting depletion in the victim's immune system leaves him or her vulnerable to potentially fatal opportunistic infections years, or even decades, after the initial infection."If a patient stops taking antiretrovirals, the infection rebounds. It is truly amazing that the virus can give rise to AIDS 20 years after the initial infection," Cohn says.Researchers think the reservoir of latent virus may be hiding out in a type of CD4 T cell: long-lived memory cells that help the immune system remember particular pathogens. When these cells encounter a pathogen they have previously seen, they spur the proliferation of T cells tuned to recognize it, in a process called clonal expansion. Prior research has suggested clonal expansion is crucial to maintaining HIV's latent reservoir. Following up on work initiated by Mila Jankovic, a senior research associate in the lab, Cohn and her colleagues examined cloned and unique CD4 T cells in blood samples from 13 people infected with HIV. An analytical computational technique developed by Israel Tojal da Silva, a research associate in the lab, made it possible to identify integration sites into which HIV had inserted itself within individual cells."Given the size of the human genome, it is highly unlikely the virus would insert itself in exactly the same place more than once. So, if multiple cells contained virus with identical integration sites, we classified them as clones. Meanwhile if a cell had a unique integration site, one not shared with any other cell, then we assumed that cell was unique" Cohn says. The researchers tested 75 viral sequences taken from the expanded clones of cells to see if they had the potential to produce more of the virus. None could."While we cannot rule out the possibility that a rare clone of cells may contain an active virus, it appears most likely that latent reservoir -- and the potential target for therapies meant to cure HIV -- resides in the more rare single cells containing unique integrations," Cohn says.


Latent HIV may lurk in 'quiet' immune cells, research suggests

-News Credit: Science Daily

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Water purification: Running fuel cells on bacteria

-News Credit: Science Daily News

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Nature’s own generator

The biological fuel cell is powered by entirely natural processes -- with the help of living microorganisms.

"In simple terms, this type of fuel cell works because the bacteria consume the waste materials found in the water," explains SINTEF researcher Luis Cesar Colmenares, who is running the project together with his colleague Roman Netzer. "As they eat, the bacteria produce electrons and protons. The voltage that arises between these particles generates energy that we can exploit. Since the waste in the wastewater (organic material) is consumed and thus removed, the water itself becomes purified," he says.

Searching for the best bacteria

"Our challenge has been to find the mechanisms and bacteria that are best suited for use in this water purification method," says Netzer. "To start with, we had to find a bacterium which was not only able to consume the waste products in the water, but which could also transfer electrons to a metal electrode," he says.

The idea behind this water purification approach was born many years ago when the two scientists first met and began discussing how bacteria could be used to generate energy. Since then, they have both been working to put the idea into practice -- each from their own respective fields of expertise. While Netzer is an expert in bacteria, Colmenares is an electrochemist with a knowledge of, and interest in, water purification.

Today, they have a small demonstration plant bubbling away in the lab -- efficiently exploiting the bacterias' ability to purify dirty water and generate electricity. The wastewater comes from the local Tine dairy and is rich in organic acids, which are ideal for this process. But this is not essential -- other types of wastewater work just as well.

"At the moment, we're not talking about producing large volumes of energy," says Netzer. "But the process is very interesting because water purification processes are very energy-demanding using current technology. We're particularly pleased at being able to produce just as much energy using low-cost materials as others are achieving using much more expensive approaches," he says.

““TThis is an environmentally-friendly process for the purification of water derived from industrial processes and suchlike. It also generates small amounts of electricity -- in practice enough to drive a small fan, a sensor or a light-emitting diode.”



Gut bacteria from high-fat animal products may cause kidney failure, study finds

By : Melinda Carstensen

Source: Fox news

AA digestion byproduct derived from high-fat animal products and previously found to increase the risk of heart

disease has now also been linked to chronic kidney disease (CKD), according to a study published Thursday in the journal Circulation. Researchers at the Cleveland Clinic observed that elevated levels of Trim ethylamine N-oxide (TMAO) in a person’s blood helped predict whether he or she would develop CKD. In a separate part of the study, using animals, researchers found that a TMAO-rich diet debilitated mice’s kidneys and, as the compound accumulated, expedited the development of CKD and heart disease.“What this suggests to us is that this pathway that makes TMAO is both a mediator of cardiovascular disease and now appears to be a mediator in the development of CKD,” lead study author Stanley Hazen, chair of the department of molecular medicine at the Lerner Research Institute at the Cleveland Clinic, told FoxNews.com. “But it’s also linked to the heightened cardiovascular disease risk if they have kidney disease. It’s a spiraling kind of thing: The worse the kidney function gets, the higher the TMAO gets.”TMAO is formed when the digestive system metabolizes foods like red meat, veal and egg yolk. Previous research has linked TMAO to atherosclerosis, a disease in which cholesterol-rich material accumulates in the arteries. These pockets form plaque, and when plaque breaks apart, heart attack or stroke can occur. TMAO is formed when the digestive system metabolizes foods like red meat, veal and egg yolk. Previous research has linked TMAO to atherosclerosis, a disease in which cholesterol-rich material accumulates in the arteries. These pockets form plaque, and when plaque breaks apart, heart attack or stroke can occur. The Centers for Disease Control and Prevention (CDC) estimates that over 20 million Americans have CKD, many of whom are undiagnosed. CKD is caused by a gradual loss in kidney function over time. Kidneys are involved in excretion— the process of getting rid of metabolites— and previous research has suggested that people with CKD are at a higher risk of heart disease. But traditional risk factors don’t adequately account for the excess cardiovascular risk that is observed in subjects with CKD, Hazen said.“We thought this may explain the excess risk,” Hazen said. Study authors examined TMAO levels in the blood of nearly 4,000 adults and followed them for five years to observe mortality rate. Over the first three years of follow-up, they monitored whether the patients experienced a heart attack or stroke. Researchers also recorded the patients’ kidney function at the beginning and end of the study. When the study began, about 520 study participants were diagnosed with CKD and 3,166 patients were not. People with a history of congenital heart disease or known acute coronary syndromes, and those who had revascularization procedures within 30 days of enrollment were excluded from the study. The analysis also adjusted for traditional risk factors such as age, sex, blood pressure, abnormal cholesterol, smoking and diabetes. Researchers observed that TMAO levels were highest in patients with CKD. But regardless of whether a patient had been diagnosed with the condition, elevated levels of the compound were still associated with a greater all-cause mortality risk over a five-year period. Stroke and heart attack incidence also correlated with elevated TMAO levels, Hazen noted. To verify whether dietary habits played a role in CKD risk, study authors studied three groups of mice: one that they fed a control diet, and two other diets that were each enriched with a different compound known to predict CKD. One of those groups ate a diet rich in TMAO, and the other group ate a diet rich in the metabolite choline. “We were very surprised but also gratified to see that both of those diets led to progressive renal dysfunction,” Hazen said. After analyzing TMAO levels in the mice’s blood, researchers also noted that the degree of renal dysfunction and renal fibrosis had a linear relationship with TMAO accumulation. Researchers studied multiple strains of mice and noted that TMAO affected all of the animals’ kidneys— even those among a strain of mice known to be resistant to loss of renal function, Hazen said.Hazen noted that while a link between dietary-derived TMAO and CKD in animals has been identified, researchers still don’t know whether such an association exists in humans. Further study is needed to determine if a diet intervention program in humans is effective in halting TMAO buildup and preventing CKD.Hazen added that his team’s findings are notable because they offer insight into why one person may be more susceptible to chronic diseases than another person.“These studies help us to understand why there are interindividual differences for risks for developing kidney disease and heart disease,” he said.


MICROBIOZ INDIA

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Find your

Scholarships….


Academic Excellence International Masters Scholarship in UK, 2015-2016

About

University of Essex is inviting applications for Academic Excellence International Masters Scholarship which supports overseas students from specified countries who are funding their own studies at the University of Essex. Awards will be made on the basis of grades obtained by the applicants in their first degree, so all applications for relevant courses will automatically be considered.

Eligibility

These scholarships are restricted to applicants who are overseas fee payers and are entirely self-funded. They are not available to students who are fully or partly sponsored.

-These scholarships may be awarded to students who have completed relevant school or university studies in the specified countries and whose declared country of residence is that country.

-Students must have been awarded a first degree with the grade specified or above. -Eligible courses are those which are full-time taught Masters courses leading to MA, MSc, LLM, MFA and MRes degrees.

How to Apply

Applicants who have firmly accepted an offer of a place by 30 September 2015, and met the academic conditions of entry, will be considered for these scholarships. Applications submitted after that date may be considered depending on availability of funds. The University will use official transcripts and certificates, submitted as part of the original application, as evidence of grades achieved and no alternative supporting evidence will be accepted.

Deadline

Applicants who have firmly accepted an offer of a place by 30 September 2015, and met the academic conditions of entry, will be considered for these scholarships.

Details http://www.essex.ac.uk

Current Open Positions….


British Council IELTS Scholarship Prize for Applicants of East Asia Region, 2015 About

British Council announces IELTS Prize for students of Malaysia, Hong Kong/Macau, Indonesia, Japan, Korea, Malaysia, Myanmar, the Philippines, Singapore, Taiwan, Thailand and Vietnam. The prize enables students to study any chosen course in an undergraduate or postgraduate programme of a higher institution that accepts IELTS as part of its admission requirements. Five scholars with the top scores from the whole of the East Asia region will each receive a scholarship to the value of NTD 600,000.The application deadline is 31 May, 2015.

Eligibility Be a permanent resident of Hong Kong/Macau, Indonesia, Japan, Korea, Malaysia, Myanmar, the Philippines,

Singapore, Taiwan, Thailand and Vietnam. Begin undergraduate or postgraduate study in 2015 (academic year). Attend a higher educational institution that accepts IELTS as part of its admission requirements. Have a valid IELTS score obtained from the British Council on or after 1 June 2014. Have a minimum band score of 6 in each of the four component parts of the test. Be able to provide an acceptance letter from the attending institution by 30 June 2015.

How to Apply: The applications are currently open for: Malaysia, Taiwan, Indonesia, Hong Kong/Macau and Japan

-Take an IELTS test at a British Council authorized centre and receive your scores. -Download and complete the application form. An original hard copy of your application should be sent by post.

Deadline

Application must be received before 31 May, 2015.

Details http://www.britishcouncil.org/

“Chinese Government Scholarship – Chinese University Program” of Zhejiang University 2015



About

Chinese Government Scholarship –Chinese University Program is established by the Ministry of Education of China (hereinafter referred to as MOE), aiming to develop outstanding international talent and improve the perception of China’s higher education. Under the mandate of the MOE, Zhejiang University is opening application for full-time postgraduate studies under the 2015 Chinese Government Scholarship –Chinese University Program.

Eligibility

Applicants must be non-Chinese citizens and in good health. Applicants must NOT be registered students in Chinese universities at the time of application or graduates from

Chinese universities whose graduation is less than one year ago. Education background and age limit: a) Applicants for master's degree studies must have bachelor's degree and be under the age of 35; b) Applicants for doctoral degree studies must have master's degree and be under the age of 40.

Applicants should have a competitive academic record. Applicants should have strong scientific research ability. Applicants should not be beneficiaries of any other scholarships. Language proficiency requirements: Applicants for Chinese-taught programs of literature, history, philosophy, education and law should have an HSK test score

of level 5(or above) or new HSK test level 4-score 210(or above); applicants for other Chinese-taught programs should have an HSK test score of level 4(or above) or new HSK test level 4-score 190(or above).

There are no Chinese language proficiency requirements for the applicants of English-taught programs, but they (except for English native speakers) must have an internet-based TOEFL test score 90 or IELTS test score 6.5 (or above).

How to Apply

Applicants can submit the application materials (refer to section V below) to the Admissions Office (postgraduate program) of the International College of Zhejiang University, by post or in person. The application materials submitted by email will not be accepted.

Deadline Application deadline: April 20, 2015.

Details

http://iczu.zju.edu.cn

SINGA PhD Awards for International Students in Singapore, 2016 About

Applications are invited for SINGA Awards for August 2016 intake. Up to 240 SINGA Awards are given every year to top students from all over the world. SINGA only supports PhD studies in the field of science and engineering. PhD training will be carried out in English at applicant’s chosen lab at A*STAR Research Institutes, NTU, NUS or SUTD. The award provides financial support for up to 4 years. The application deadline is 1 June 2015 for January 2016 intake.



Eligibility

Open to all international students Graduates with a passion for research and excellent academic results Good skills in written and spoken English Good reports from academic referees

Deadline

The application deadline is 1 June 2015 for January 2016 intake.

How to Apply Application for August 2015 intake has closed. (https://sms.a-star.edu.sg/applicant/Login.aspx) to apply for January 2016 intake.Please note that the application deadline for January 2016 intake is 1 June 2015. Only applications with complete supporting documents submitted before or on 1 June 2015 (2359hrs GMT+8 SINGAPORE Time) will be processed.

Details

http://www.a-star.edu.sg/singa-award/The-Awards.aspx

School of Biological Sciences Taught Postgraduate Bursaries in UK, 2015-2016 About

University of Edinburgh is inviting applications for postgraduate bursaries of £5,000 within the School of Biological Sciences. Applicants must have been offered a place on an eligible MSc at the University of Edinburgh and should have firmly accepted that offer or be intending to do so. The award is intended to assist with tuition fees and is only tenable for the current session. The application deadline is 2nd May 2015.

Eligibility

Applicants must have been offered a place on an eligible MSc at the University of Edinburgh and should have firmly accepted that offer, or be intending to do so.

How to Apply

Applicants should send an email to pgtbiol-at-ed.ac.uk registering their interest in applying for the bursary to the email address noted below. Applicants should only email their interest once they have been offered a place on a relevant MSc programme. When emailing, applicants must include both their UUN/application ID and the name of the programme(s) that they are applying for

Deadline

The application deadline is 2nd May 2015.



Details http://www.ed.ac.uk/schools-departments/student-funding/postgraduate/international/science-engineering/biological-bursaries

2015 University of Oslo PhD Research Fellowship in Structural Biology, Norway About University of Oslo is inviting applications for a PhD research fellowship to work on protein purification and structural biology experiments at the Department of Biosciences. The fellowship is available for a period of up to 4 years with 25 % compulsory work. The ideal starting date is 1 April 2015 and no later than 1 July 2015. The purpose of the fellowship is research training leading to the successful completion of a PhD degree. The fellowship requires admission to the PhD programme at the Faculty of Mathematics and Natural Sciences. The application deadline is 28 February, 2015.

Eligibility

Applicants must hold a Master’s degree or equivalent in Biochemistry, Structural Biology, or related fields. In addition, the candidate should have gained insights into modern molecular biology, biochemistry, and structural biology techniques during his/her studies. Ideal candidates have previously worked experimentally with proteins, using either x-ray crystallography or NMR during their MSc thesis.

The purpose of the fellowship is research training leading to the successful completion of a PhD degree. The fellowship requires admission to the PhD programme at the Faculty of Mathematics and Natural Sciences. The

application to the PhD programme must be submitted to the department no later than two months after taking up the position.

A good command of English is required.

How to Apply The mode of applying is online.

The application must include:

Application letter CV (summarizing education, positions and academic work – scientific publications) Copies of educational certificates, transcript of records and letters of recommendation Documentation of English proficiency List of publications and academic work that the applicant wishes to be considered by the evaluation committee Names and contact details of 2-3 references (name, relation to candidate, e-mail and telephone number)

Foreign applicants are advised to attach an explanation of their University’s grading system. Please remember that all documents should be in English or a Scandinavian language.

Deadline

The application deadline is 28 February, 2015.



Details http://uio.easycruit.com/vacancy/1329301/96323?iso=no

Science without Borders Program for Young Talent Researchers in Brazil, 2015 About

Applications are invited for Science without Borders Program available for Young Talent researchers to perform a two to three year-long research project in Brazil. Up to 100 scholarships will be awarded to cover the period of 12 to 36 months. Scholarships are awarded to researchers who have a highlighted scientific and technology production within the areas of interest to the Science Without Borders.

Eligibility

The scholarship program for “Young Talent Attraction” aims to attract young researchers living abroad, especially Brazilians, who have a highlighted scientific and technology production within the areas of interest to the Science Without Borders.

How to Apply Only host researcher in Brazil can submit the proposal, exclusively by the Internet. When the research contributor submits the proposal, it’s necessary to attach to the form, a file with the research project and the candidate’s Curriculum resume into platform lattes application or the summary of the candidate’s resume. New Public Call has been released in March, 5th, 2015. For the institutional proposals related to postgraduate programs in Brazil, recommended by CAPES, and corresponding to Line 1 on the previous calls.

Deadline

The proposal to receive a Special Visiting Researcher must only be submitted by the host researcher in Brazil, exclusively by internet, through the Online Application Form available in the website. It is necessary to attach a file with the research project and the candidate's Curriculum resume into Lattes Platform or the summary of the candidate's resume. New Public Call has been released in March, 5th 2015.

Details http://www.cienciasemfronteiras.gov.br/web/csf-eng/opportunities-for-individuals-from-abroad



List of winners of January 2015

Edition

Following candidates are successfully solved Microbioz India Cross -

Word game of January 2015 Edition.

Cross WW MICROBIOZ INDIA

Ord 2 015 February

February

2015

Issue

Sumit Tripathi Bhopal,M.P. India

Shikha Moni Ghaziabad, India

Rahul Negi Bhopal, M.P., India

Soni Meena Pune Maharashtra

Mansoor Ahmd Kohat,Pakistan

Vaishnavi Ramesh Guntur, A.P, India

Asma Beg Faisalabad, Pakistan

S.Cuks Singapore,(NUS)

Pavol Court Mc Gil University, Canada

Marry D.Pamela Medical Technology. Peru

Taylor Francis Ireland

S.Sherr Peru

Hints Key

Spiral-shaped bacteria An organism that obtains its nut rients From dead organic matter An organism that lives in, on, or at the

Expense of another organism without contributing to the

Host’s survival A microorganism that lives and grows in

The presence of free oxygen A potent toxin that is secreted or excreted

By living organisms Bacteria that are permanent and generally

Beneficial resident s in the human body An organism in which another, usually

Parasitic organism is nourished and Harbored. A carrier of pathogenic organisms, Especially one that can transmit a di sea Se.

Solve this cross word and forward us scanned Copy of answers by 15th of February 2015

Solve

Today

Dear readers here we are not mentioning names of few winners because of Late submission of answers, Winners will be communicated later via e-mail for Microbioz India, Certificate.

MICROBIOZ INDIA February 015 2

Beneficial & Negative Effects of Microbes Microbioz India,February 2015 Issue

Documents

Transcript of Beneficial & Negative Effects of Microbes Microbioz India,February 2015 Issue