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If you have never tried protein powders before then you don’t know what you are missing. I tried one a couple of weeks ago with chocolate flavor and I couldn’t believe I haven’t tried any before. It was surprisingly delicious and nutritious. I skipped an entire meal after taking a full glass of this tasty drink.

I searched a lot and found out that Wonderlife offer similar protein powder supplements to the one I used. Judging from their supplement facts they also taste great.

Whey Protein Powder

It offers you two different flavors – chocolate and vanilla. There is no way not to like one of them. Mine is chocolate

Whey protein is one of the best and most valuable proteins for human body. It is isolated from whey and is very easily digested and absorbed. Whey protein powders contain all of the essential amino acids in biologically significant amounts, which make them one of the best and most complete sources of proteins and amino acids you can find.

Whey proteins have three main forms: concentrate, isolate and hydrolysate. Wonderlife Whey Protein Powder contains all of them. Here are its ingredients in short: whey protein concentrate, partially predigested (hydrolyzed) whey protein concentrate, micro-filtered and ion-exchanged whey protein isolate.

Egg Protein Powder

If you love vanilla flavor then this egg protein powder is just for you.

Egg white protein is very high valued and very important for our bodies. It scores 1.0 at PDCAAS (Protein Digestibility Corrected Amino Acid Score), which is the most relevant measure of the quality of proteins for humans and by the way that is the official rating system used by the World Health Organization.

This egg white protein powder contains 23 g of proteins and 113 calories per serving. No sugar, no cholesterol and completely fat free.

With antibiotic resistance on the rise, tuberculosis is emerging as a bigger global health threat than ever before.

But now, innovative research at Weill Cornell Medical College suggests that Mycobacterium tuberculosis has an as yet unsuspected weakness -- one that could be a prime target for drug development.

"Using novel techniques, we have identified a key membrane protein that's essential to the defense that M. tuberculosis mounts against the acidic environment of immune cells called macrophages. Without this protein, called Rv3671c, the bacterium becomes vulnerable to acidification and is killed," explains lead author Omar H. Vandal, a postdoctoral fellow in the lab of study co-senior author Dr. Sabine Ehrt, associate professor of microbiology and immunology at Weill Cornell Medical College.

"M. tuberculosis does not depend on Rv3671c under standard growth conditions in the test tube, so it has been overlooked as a candidate drug target," says Dr. Carl F. Nathan, also a senior author of the study and the R.A. Pritchett Professor of Microbiology. He is also chairman of the Department of Microbiology and Immunology at Weill Cornell.

Drs. Ehrt and Nathan co-supervised Dr. Vandal in this work while Dr. Vandal was a student at the Weill Cornell Graduate School of Medical Sciences. "However, when M. tuberculosis infects the host, then the Rv3671c protein becomes essential," added Dr. Ehrt. "This is an example of a new class of potential targets for anti-infective agents," continues Dr. Nathan, "those that the pathogen only needs in order to survive in the host environment."

The research was just published in Nature Medicine.

In numerous papers published in leading journals, Dr. Nathan has long pushed for an innovative approach to the development of anti-infective agents that goes beyond the traditional antibiotic paradigm. "That's exactly what we sought to do in this research," he says.

One of the study's innovations involved the examination of M. tuberculosis as it interacted with bone marrow-derived macrophages during the infective process.

"That's a huge change from standard anti-infective research, which typically deals with the pathogen simply replicating in culture," explains Dr. Vandal. "In our experiments, we wanted to see if biochemical actors would emerge in the infective process that might be inoperative in the usual in vitro setting."

The team specifically focused on changes in the pH (acidity) of the phagosome -- a structure that macrophages use to consume and destroy pathogens, including bacteria.

"As part of this process, the phagosome becomes acidic, which is thought to contribute to its ability to break down and destroy the pathogen," Dr. Ehrt explains. "However, M. tuberculosis appears to survive the acidification process, keeping its own internal pH stable."

How does the bacteria do this, despite being surrounded by the more highly acidic phagosome? To find out, the team used a kind of genetic tweaking that effectively disabled M.tuberculosis' ability to produce a key protein lying at its membrane -- a protease (enzyme) called Rv3671c.

They then watched how the organism fared without it.

"What we observed was pretty amazing -- without functioning Rv3671c, the mutant bacterium was easily destroyed in a low-pH environment, both in culture and inside the more acidic environment of the macrophage," says Dr. Vandal. "This revealed a new point of vulnerability for the bacterium."

The experiment also broke new ground because the researchers were able to accurately gauge the bacterium's internal pH with the organism lying inside a host cell.

"The ability to make those kinds of measurements will expand research into this type of host-pathogen interaction," Dr. Nathan believes.

The next step is to find out why Rv3671c is so crucial to M. tuberculosis' defense.

"Right now, we have very little idea of the mechanism at work here. Perhaps as an enzyme Rv3671c cleaves a transcription regulator that then turns on some kind of defensive program within the bacterium. Only further study will reveal those secrets," says Dr. Ehrt.

"What is clear is that by targeting an element involved directly in the infective process, we may develop a line of drugs that work in collaboration with, rather than in difference to, the host environment, including host immune responses," Dr. Nathan says. "Hopefully, this kind of approach can help solve the ongoing problem of bacterial drug resistance."

The new study is also another example of an interdisciplinary approach -- this time among biochemists, microbiologists, immunologists and cell biologists.

"In the ideal collaboration, each participant brings key insights from their particular discipline to the table," Dr. Nathan says. "The results are discoveries like these."

http://www.med.cornell.edu/

People with schizophrenia have an increased number of unusual chromosomal changes, particularly structural changes that have the potential to alter the function of the genes. These results were published today in the scientific journal Nature.

Research scientists found changes in the structure of the genes in patients with schizophrenia when they studied what are known as copy number variants. Genetic diseases are caused by a large number of different possible changes in human DNA. The type of mutation or change referred to as CNV means that large pieces of DNA may exist in several copies, have disappeared or have been transposed. In some diseases such changes in the genome may be protective, for example in HIV infection and malaria.

"The results strongly support the notion that schizophrenia may be partly caused by the effects of such structural changes in genes, both across the whole genome and in specific chromosomes," says Christina Hultman, associate professor at Karolinska Institutet.

A breakthrough in genetic research on diabetes and prostate cancer, among other diseases, has been achieved in 2007 and 2008 by mapping the whole genome in what are known as genomwide association studies. There is now much to suggest that a breakthrough may also be made in schizophrenia in 2008, when up to seven studies relating to a total of 20,000 cases have been carried out. An important step will then be to understand the biological mechanisms underlying a complex pattern of genes that can be linked to schizophrenia and also what is known as epigenetics, that is to say how genes are switched on and off during the lifespan.

"We anticipate a breakthrough in the near future in research into psychiatric diseases such as schizophrenia, bipolar disease and autism. At the same I wish to stress that in such a complex disease as schizophrenia there is a need for research on both genetic and environmental causes and on treatment and management," says Christina Hultman.

Schizophrenia is a common psychiatric disease. There are around 35,000 people in Sweden today who have at some time been in institutional care with the diagnosis of schizophrenia, and just as many who have been treated for other psychotic diseases.

It has long been known through family studies, adoption studies and twin studies that there appear to be hereditary causes of schizophrenia. The risk among both first-degree relatives (a person's children) and second-degree relatives of people with schizophrenia is raised. The search for specific genetic causes in the last ten years has been intensive, but schizophrenia has a complex pattern of heredity, and the results of previous studies have been unclear. Various research teams have presented several different suggestions for genes that may be involved, including genes that control the development of brain cells.

Publication: "Rare chromosomal deletions and duplications increase risk of schizophrenia", International Schizophrenia Consortium, which includes Christina Hultman from the Department of Medical Epidemiology and Biostatistics of Karolinska Institutet. Nature on line, www.nature.com, Digital Object Identifier (DOI): 10.1038/nature07239.

http://ki.se/

Low levels of naturally occurring antibodies may represent an increased risk of developing cardiovascular disease, particularly stroke in men. This discovery, published in the academic journal Atherosclerosis, has now led to attempts to develop an immunization against cardiovascular disease.

Atherosclerosis (hardening of the arteries) is an inflammatory disease in which the walls of the blood vessels are thickened and become less elastic. It can cause blood clots and other cardiovascular diseases. It is not known precisely what causes atherosclerosis, but the immune system probably plays an important role. Research scientists suspect that various oxidised forms of what is known as bad cholesterol, LDL (low-density lipoprotein), contribute to the development of the disease. A research team from Karolinska Institutet, in cooperation with Lund University, has now shown that a particular type of naturally occurring antibodies, anti-PC, which are targeted against the lipid portion of the LDL molecule, play an important role in the development of cardiovascular disease. The findings show that individuals who have low levels of anti-PC are at increased risk of cardiovascular disease. The risk is particularly high in men who develop stroke, with an almost fourfold increase.

This newly discovered risk factor, low levels of anti-PC, is independent of previously known risk factors such as high blood pressure, high blood lipids, diabetes and smoking.

"Our findings suggest that anti-PC can be used as a complement to the traditional risk factors to improve diagnosis and treatment. In addition we are currently developing anti-PC as a vaccine for atherosclerosis and cardiovascular disease," says Professor Johan Frosteg?, who directed the study.

The study is based on data from 349 people who at some time over a 12-year period have suffered a heart attack or stroke and 693 individuals without symptoms of cardiovascular disease. The research has been carried out under the EU consortium CVDIMMUNE, http://www.cvdimmune.com/, which is led by Johan Frosteg? at Karolinska Institutet.

Publication:

"Low levels of IgM antibodies against phosphorylcholine - a potential risk marker for ischemic stroke in men." Beatrice Sjöberg, Jun Su, Ingrid Dahlbom, Hans Grönlund, Max Wikström, Bo Hedblad, Göran Berglund, Ulf de Faire and Johan Frosteg?. Atherosclerosis 2008, in press, accepted manuscript, available online.

http://ki.se/

A University of Central Florida researcher may have found a defense against the Black Plague, a disease that wiped out a third of Europe's population in the Middle Ages and which government agencies perceive as a terrorist threat today.

UCF Professor Henry Daniell and his team have developed a vaccine that early research shows is highly effective against the plague. Findings of his National Institutes of Health and USDA funded research appear in the August edition of Infection and Immunity. The vaccine, which is taken orally or by injection, was given to rats at UCF and the efficacy was evaluated by measuring immunity (antibody) developed in their blood.

All untreated rats died within three days while all orally immunized animals survived this challenge with no traces of the plague in their bodies. The rats were exposed to a heavy dose of Yersinia Pestis bacteria, which causes the plague, at the U.S. Army Medical Research Institute of Infectious Diseases in Maryland. It is one of a few labs in the world authorized to store and work with the highly dangerous agent.

"We are very excited because it appears the oral vaccine is even more effective than traditional injectable vaccine," Daniell said. "This could really make a difference."

In the event of a bioterror attack, the oral form makes the vaccine practical, as the distribution of pills would be much quicker and likely more effective because no special skills or sterile needles are needed to administer them.

"It worked beautifully," Daniell said. "It's expensive to create an injectible vaccine. But with oral vaccines, it is quite cheap. You grow your plants and then you convert them into capsules."

The plague had a deadly impact on early Europe, it continues to make appearances today in places like Africa and Asia. The World Health Organization reports at least 2,000 cases of the plague annually. The most recent outbreak in 2005 killed 56 people in the Congo and another 124 were infected before the epidemic was stopped. In the mid 1990s more than 400 people were infected in India.

Although human trials are still needed, Daniell is confident the vaccine will work for the bubonic and pneumonic plague based on animal studies. Pneumonic plague is spread through the air. Without treatment a person can die within days. Bubonic plague is the more common form and is transmitted through fleabites and kills about 70 percent of those infected within 4-7 days if not treated. It was the version that ravaged Europe. If the early findings hold true, this vaccine could mean an extra layer of protection against natural epidemics and man-made threats.

The Centers for Disease Control lists the pneumonic plague as a potential bioterrorism agent because of the speed of which it can be spread and its 60 percent fatality rate if not treated early enough with an aggressive array of antibiotics.

Daniell was inspired to investigate an oral vaccine for the plague because of his pioneering work in diabetes. He and his team genetically engineered tobacco and lettuce plants with the insulin gene and then administered freeze-dried plant cells to five-week-old diabetic mice for eight weeks. By the end of this study, the diabetic mice had normal blood and urine sugar levels, and their cells were producing normal levels of insulin.

Daniell figured the same approach might work with a vaccine. He genetically engineered plant cells with a protein found on the outside of Yersinia pestis. The vaccine was inside the plant cells, which were given to the rats. The vaccine was protected from digestion in the stomach and was then absorbed in the gut. It kick started the immune system into producing antibodies, which protects against the deadly disease. Three to five doses seem to do the trick.

Daniell, who was born and raised in India, has dedicated his life to finding treatments and cures to diseases that ravage poor countries. He is conducting research into seven of the top 10 diseases ranked by the World Health Organization and the Centers for Disease Control, which remain real issues developing nations.

"I've seen the need. There may be some very expensive treatments available," Daniell said. "But they are so expensive that developing countries can't access them. I want to help change that."

http://www.ucf.edu/