Body

When a cell is seriously stressed, say by a heart attack, stroke or cancer, a protein called Bak just may set it up for suicide, researchers have found.

In a deadly double whammy, Bak helps chop the finger-like filament shape of the cell’s powerhouse, or mitochondrion, into vulnerable little spheres. Another protein Bax then pokes countless holes in those spheres, spilling their pro-death contents into the cell.

By bypassing a well-known gene implicated in almost one-third of all cancers and instead focusing on the protein activated by the gene, Dr. Christopher Counter and colleagues at the Duke University Medical Center have identified IL6 as a new target in the battle against Ras-induced cancers.

A chemically-modified version of a mitochondrial toxin long used to control species of invasive fish in lakes has been found to selectively inhibit two "survival proteins” in cancer cells. The research is a first step toward developing a molecularly-targeted drug that could eliminate cellular-level resistance to multiple types of chemotherapy and radiation therapy found in many types of cancers.

Researchers from Boston University School of Medicine (BUSM) and Boston University School of Public Health (BUSPH) have developed a method to estimate sickle cell disease severity and predict the risk of death in people with this disease. The study appears online in the June issue of the journal Blood.

A research team at the Swedish medical university Karolinska Institutet has shown for the time that microRNA, small RNA molecules, may play an important role in the development of inflammatory skin diseases such as psoriasis and atopic eczema. The research team is led by Professor Mona Ståhle, one of Sweden’s most prominent scientists in the field.

To protect us from disease our immune system employs macrophages, cells that roam our body in search of disease-causing bacteria. With the help of long tentacle-like protrusions, macrophages can catch suspicious particles, pull them towards their cell bodies, internalise and destroy them.

Contrary to textbook models, many genes that should be 'off' in embryonic stem cells and specialized adult cells remain primed to produce master regulatory proteins, leaving those cells vulnerable to identity changes

Biologists have long thought that a simple on/off switch controls most genes in human cells. Flip the switch and a cell starts or stops producing a particular protein. But new evidence suggests that this model is too simple and that our genes are more ready for action than previously thought.

When a strand of DNA breaks in the body's cells, it normally does not take long until it has been repaired. Now researchers at the Swedish medical university Karolinska Institutet have discovered a new mechanism that helps to explain how the cell performs these repairs.

Chitin and Chitosan have been extracted from lobster waste and used in medicine and biomedicine by a team from the University of Havana. These researchers’ work has led to the development of a procedure to obtain surgical materials with great healing and antiseptic properties.

Chitin is a polymer very common in nature as part of animals’ and plants’ physical structures. Only cellulose is more abundant than chitin, which makes this compound a highly important renewable resource that can easily be found in arthropods, insects, arachnids, molluscs, fungus and algae.

For the first time, it can now be shown what enzyme copies the genetic make-up of cells. The discovery is being published in the journal Science by researchers at Umeå University in Sweden in collaboration with a team in the U.S. led by Thomas A. Kunkel.

The human genome has already been mapped, as have the genomes of several other organisms. On the other hand, little has been known how genes are copied and repaired so efficiently and precisely.