HEMAGGLUTININ

I've just been infected with one of these...YES...the FLU VIRUS!

Such simple structures yet they are indeed formidable in making one feel so sick!

In general, viruses are composed of 2 main components - a protein envelope and a core composed of genetic material (which can either be DNA or RNA). It cannot survive on its own but is dependent on a host cell to replicate and propagate! Sigh...in my case...that's my cells!

Viruses are host specific. Meaning a plant virus cannot infect a bacterial cell. Neither can a bacterial virus infect a human cell. However, at times, mutation in the viral genome can occur which allows the virus to "cross" their host boundaries. That's when pandemics can arise. An example of this is the recent "Bird Flu virus"!

Well, I suppose I should be thankful that mine is just a case of the common influenza virus. So, back to bed for now and hopefully I'll be back on my feet in a couple of days!

Spotlight on Disease: Type 2 Diabetes

Diabetes results from a lack of a hormone that stimulates cells to take up (a type of sugar) from the bloodstream. Cells need glucose as fuel to produce energy.  lack insulin because their immune systems destroy the pancreatic cells that produce it. Type 2 diabetics progress through two stages of the disease. In the first stage, called “insulin resistance”, cells no longer respond to insulin.  The pancreas compensates for this resistance by producing more insulin. As insulin resistance persists, the pancreas cannot make enough insulin to keep up with the increased demand. The pancreas eventually shuts down insulin production altogether, resulting in type 2 diabetes.

Without sugar that can be converted to energy, cells starve and glucose levels build up in the blood, which can lead to life-threatening complications such as cardiovascular disease. Since fat interferes with the body’s ability to process insulin and overweight people are at increased risk for the disease, type 2 diabetes is sometimes called “obesity-related” diabetes. Type 2 diabetics are encouraged to carefully monitor their diet and exercise in order to prevent dangerous fluctuations in blood sugar levels.

New Insights into Scar Prevention

Dr. Erkki Ruoslahti

Bike accidents, C-sections and battlefield wounds can all leave scars. But those are only the scars you can see. Any tissue can scar (not just skin), making scar tissue more than a cosmetic problem. Heart muscle, for example, can scar after a heart attack, and the lungs, kidneys, the liver, and many other tissues can be damaged by inflammation. Current options for reducing scar formation require local intervention at the scarring site – plastic surgery, for example. But what if there was a pill you could take after an injury to prevent scar tissue from forming in the first place?
At Sanford-Burnham’s  at  and his team have developed a new prototype therapy that inhibits scarring in mice. The compound contains two elements discovered by the Ruoslahti laboratory. One is a peptide that homes in on new blood vessels that form during wound healing. The other is a naturally occurring protein called  which they prevents the buildup of fibrous connective tissue that causes scarring. The combination of the peptide and protein turns out to be particularly powerful.

Protecting Beta Cells from the Immune System

A pancreatic beta cell. Image by Itkin-Ansari lab

 is caused by an overactive immune response that kills off insulin-producing beta cells. While beta cells can be transplanted to replace the ones that have been lost, the immune system will eventually kill those off as well.
For transplantation to be a viable treatment, the immune system must be controlled. Current transplant recipients take immunosuppressive drugs to prevent their  from attacking replacement presenting patients with a stark choice between diabetes and a suppressed immune system.
Sanford-Burnham adjunct assistant professor  is taking a different approach. Her laboratory has placed human pancreatic precursor cells in an immuno-protective device and transplanted them into mice. She was testing whether precursor cells will mature into productive beta cells in the body and whether the encapsulation device, made from a material akin to Gore-Tex, could prevent the immune system from attacking transplanted cells.

Spotlight on Disease: Type 1 Diabetes

A model of an insulin molecule. Though insulin is an effective treatment for diabetes, it is not a cure. Image courtesy of Wikimedia Commons.

Type 1 diabetes is an  – a person’s own immune system attacks found in the pancreas. Beta cells normally respond to high levels of sugar in the blood by releasing  a protein hormone that acts like a key binding to a lock (or receptor) that is present on every cell in the body. When insulin binds to its receptor, it unlocks a door in cells that allows this sugar—known as to enter and be used for energy.
Since type 1 diabetics lack insulin-producing beta cells, glucose remains in the blood and cells starve. Even with insulin therapy, the level of blood glucose in type 1 diabetics is not normal. Glucose is a highly reactive molecule that damages the cells and tissues that it contacts, particularly the cells that line blood vessels. As a result, diabetes is a leading cause of blindness, kidney disease, limb amputation and heart disease. Because type 1 diabetes commonly manifests in childhood, it has traditionally been called “juvenile” diabetes. Type 1 diabetes treatment is life-long; diabetics must carefully monitor their blood sugar and receive daily insulin injections or wear an insulin-delivering pump.

The Truth About AMPK

Researchers at Salk and Sanford-Burnham used tiny C. elegans to study AMPK and autophagy.

You may not be familiar with the protein  but if you exercise regularly, like to drink red wine, take certain diabetes medications or practice caloric restriction in hopes of extending your life, AMPK is very important to you. AMPK is a master switch that controls a number of key cellular mechanisms, and all the activities listed above stimulate AMPK signals.
Recently,  at the with assistance from at Sanford-Burnham, published a showing how AMPK triggers a process called  which recycles damaged parts when cells are low on energy. Problems with AMPK and autophagy are associated with type 2 diabetes, cancer, Alzheimer’s and other age-related diseases.

Crowdsourcing Science with TOPSAN

New advances in technology are allowing scientists to sequence genomes and determine the structures of the proteins they encode at a faster rate and lower cost than ever before. The  centers, such as the (JCSG), have been instrumental in establishing the structures of hundreds of proteins each year. While this flood of new data is a boon to science, the time and resources needed to analyze it all has become a major bottleneck.
“We have become victims of our own success,” explains  director of the Bioinformatics and Systems Biology program at Sanford-Burnham. “New protein structures are being determined all the time. And while it’s important to know what a protein looks like, we need to better leverage that information to improve our understanding of how a protein works and what biological functions it performs in a cell.” Moreover, knowledge of a protein’s structure and function is necessary for identifying its role in human health and disease, as well as unveiling its potential as a therapeutic target.
Several years ago, Dr. Godzik and his research team came up with an idea to protein structure annotation. In 2006, along with their JCSG colleagues, they launched (TOPSAN), a central portal for scientists to collect, share and distribute information about three-dimensional protein structures. TOPSAN embodies the idea that many can succeed where the individual cannot. No matter how much any one person knows about a particular protein, there are others in the scientific community who know more about other aspects of the same protein. Thus, the collective analyses from multiple experts around the world are far more informative than the localized information that any one individual – or even single research group – could contribute.