February 8, 2012
Reviving a theory first proposed in the late 1800s that the development of organs in the normal embryo and the development of cancers are related, scientists at the Salk Institute for Biological Studies have studied organ development in mice to unravel how breast cancers, and perhaps other cancers, develop in people. Their findings provide new ways to predict and personalize the diagnosis and treatment of cancer.
In a paper published February 3 in Cell Stem Cell, the scientists report striking similarities between genetic signatures found in certain types of human breast cancer and those of stem cells in breast tissue in mouse embryos. These findings suggest that cancer cells subvert key genetic programs that guide immature cells to build organs during normal growth.
February 8, 2012
University of Utah biologists found new evidence why mice, people and other vertebrate animals carry thousands of varieties of genes to make immune-system proteins named MHCs – even though some of those genes make us susceptible to infections and to autoimmune diseases.
“Major histocompatibility complex” (MHC) proteins are found on the surface of most cells in vertebrate animals. They distinguish self from foreign, and trigger an immune response against foreign invaders. MHCs recognize invading germs, reject or accept transplanted organs and play a role in helping us smell compatible mates.
“This study explains why there are so many versions of the MHC genes, and why the ones that cause susceptibility to diseases are being maintained and not eliminated,” says biology Professor Wayne Potts. “They are involved in a never-ending arms race that causes them, at any point in time, to be good against some infections but bad against other infections and autoimmune diseases.”
February 1, 2012
Using a liquid laser, University of Michigan researchers have developed a better way to detect the slight genetic mutations that might predispose a person to a particular type of cancer or other diseases.
Their results are published in the current edition of the German journal Angewandte Chemie.
This work could advance understanding of the genetic basis of diseases. It also has applications in personalized medicine, which aims to target drugs and other therapies to individual patients based on a thorough knowledge of their genetic information.
November 21, 2011
Many infections, even those caused by antibiotic-sensitive bacteria, resist treatment. This paradox has vexedphysicians for decades, and makes some infections impossible to cure.
A key cause of this resistance is that bacteria become starved for nutrients during infection. Starved bacteria resist killing by nearly every type of antibiotic, even ones they have never been exposed to before.
What produces starvation-induced antibiotic resistance, and how can it be overcome? In a paper appearing this week in Science, researchers report some surprising answers.
“Bacteria become starved when they exhaust nutrient supplies in the body, or if they live clustered together in groups known as biofilms,” said the lead author of the paper, Dr. Dao Nguyen, an assistant professor of medicine at McGill University.
November 19, 2011
For people who initially survive a heart attack, a significant cause of death in the next few days is cardiac rupture — literally, bursting of the heart wall.
A new study by University of Iowa researchers pinpoints a single protein as the key player in the biochemical cascade that leads to cardiac rupture. The findings, published Nov. 13 as an Advance Online Publication (AOP) of the journal Nature Medicine, suggest that blocking the action of this protein, known as CaM kinase, may help prevent cardiac rupture and reduce the risk of death.
After a heart attack, the body produces a range of chemicals that trigger biological processes involved in healing and repair. Unfortunately, many of these chemical signals can become “too much of a good thing” and end up causing further damage often leading to heart failure and sudden death.
November 19, 2011
Scientists are reporting development and successful initial testing of the first practical “smart” material that may supply the missing link in efforts to use in medicine a form of light that can penetrate four inches into the human body. Their report on the new polymer or plastic-like material, which has potential for use in diagnosing diseases and engineer new human tissues in the lab, appears in ACS’ journal Macromolecules.
Adah Almutairi and colleagues explain that near-infrared (NIR) light (which is just beyond what human can see) penetrates through the skin and almost four inches into the body, with great potential for diagnosing and treating diseases. Low-power NIR does not damage body tissues as it passes. Missing, however, are materials that respond effectively to low-power NIR. Plastics that disintegrate when hit with NIR, for instance, could be filled with anti-cancer medicine, injected into tumors, and release the medicine when hit with NIR. Current NIR-responsive smart materials require high-power NIR light, which could damage cells and tissues. That’s why Almutairi’s team began research on development of a new smart polymer that responds to low-power NIR light.
December 22, 2009
Scientists at Queen Mary, University of London have uncovered fundamental differences between the bone which makes up the skull and the bones in our limbs, which they believe could hold the key to tackling bone weakness and fractures.
It is well know that bones in the arms and legs become weak and vulnerable to breaks when they are not maintained by weight bearing exercise. However skull bone, which bears almost no weight remains particularly resistant to breaking.
The new research published in PLoS ONE* offers an explanation for this phenomenon for the first time. The researchers say that their new understanding of the differences between the two types of bone could lead to new ways to treat or prevent osteoporosis.