P22phox is emerging as a critical subunit of a family of enzymes that produce reactive oxygen species (ROS).   ROS were simply thought of as destructive molecules that can kill infecting bacteria but also damage human cells. More recently, however, ROS have been shown to play a key role in many normal cell processes, including development and blood pressure regulation. The group of enzymes that produce ROS are called NADPH oxidases (Nox).   Disruption of these enzymes has been implicated in a range of diseases, including cardiovascular and neurodegenerative diseases as well as immune deficiencies like CGD.

In this study, although inner ear cells looked normal in the mutant mice, the researchers discovered that otoconia — tiny calcium carbonate crystals that are essential for sensing gravity — do not form in the inner ears of these mice.   It is speculated that the superoxide radicals under the right pH and calcium concentrations promote such crystal formation.  Restoring the normal gene to the mutant mice rescued otoconial production and prevented the balance disorder. However, although the treatment did improve the mice’s immune response, the partial restoration of gene expression was not sufficient to cure the immune deficiency completely.

In this study the scientists performed a genome-wide association study of LDL cholesterol concentrations. Their analysis used genetic data from 11,685 participants across five studies. They found evidence for a statistically significant link between LDL cholesterol and the chromosome region 1p13.3. The magnitude of the association was consistent across the studies examined and showed independent evidence for statistical association in each study, according to Cambridge team.  These results potentially offer insight into the biological mechanisms that lie behind the regulation of LDL cholesterol and might help in the discovery of novel therapeutic targets for cardiovascular disease.

CDC and international authorities expect Brisbane/10, a version of the H3N2 flu, to still be lingering aroud next year. They predict a second new Type A strain, known as H1N1/Brisbane/59, also will hit, along with a newer Type B/Florida strain.  The recipe must be set about eight months before manufacturers start shipping doses because flu vaccine production is so complex. Health authorities come up with seed stocks of the virus strains that manufacturers then must grow in chicken eggs.  As for the rest of this winter, the CDC says the current vaccine should provide some protection, perhaps resulting in a milder case of flu than if someone hadn’t been inoculated. Every year, the flu infects up to 20 percent of the population, hospitalizes 200,000 people and kills 36,000.

The advent of bioinformatics has allowed researchers to more readily search the entire mouse genome for imprinted genes, but the real power of this approach has been recently demonstrated in its application to the human genome. While 2.5 percent of the mouse genome contains potentially imprinted genes, only 0.75 percent of the human genome is predicted to be imprinted. This means that the mouse genome may not be a suitable model for assessing human disease risk due to epigenetic mutations in imprinted genes.  It is necessary to develop bioinformatic models that can identify metastable epialleles in order to characterize all of the genes susceptible to environmental influences.

With the identification of epigenetically unstable locations in the human genome, it will be possible to screen individuals at an early age for epigenetically susceptible diseases, allowing for closer monitoring and more frequent follow-up. In addition, unlike genetic mutation, epigenetic profiles are potentially reversible. Therefore, epigenetic approaches for prevention and treatment, such as nutritional supplementation and/or pharmaceutical therapies may be developed to counteract negative epigenomic profiles.  The future of epigenomics therapy holds tremendous potential for not only individualized health care but also for population-wide disease diagnostic, screening, and prevention strategies.

Frédéric Dardel and colleagues crystallized both the narrow and broad-spectrum resistance forms of the antibiotic-modifying acetyltransferase enzyme. Their new study reveals that this particular enzyme has a flexible active site that can evolve to accommodate new antibiotics, allowing the bacteria to break them down and render them useless in killing off an infection. This type of enzyme is now carried by millions of bacteria struggling for survival in the antibiotic age.

More importantly, the research provides new insight for the design of new antibiotics that could evade this form of resistance, and new inhibitors that would extend the effectiveness of current antibiotics, both of which could help in the fight against the deadly infections becoming more frequent in hospitals.

      Serum albumin has a long half-life of approximately 15 to 20 days, with an average of 4% degraded per day.  Due to slow turnover, the serum albumin is not considered to be a good indicator of acute or mild liver dysfunction. Therefore only minimal changes in the serum albumin are seen in acute liver conditions such as viral hepatitis, drug-related hepatoxicity, and obstructive jaundice. Albumin levels <3 g/dL should raise the possibility of chronic liver disease in patients with hepatitis.

      Hypoalbuminemia, is therefore more common in chronic liver disorders such as cirrhosis and usually reflects severe liver damage and decreased albumin synthesis. One exception is the patient with ascites in whom synthesis may be normal or even increased, but laboratory levels of albumin are low because of the increased volume of distribution.  However, hypoalbuminemia is not specific for liver disease and may occur in protein malnutrition of any cause, as well as protein-losing enteropathies, nephrotic syndrome, and chronic infections that are associated with prolonged increases in levels of serum interleukin 1 (IL-1) and/or tumor necrosis factor (TNF), and cytokines that inhibit albumin synthesis. Serum albumin is therefore not measured for screening in patients in whom there is no suspicion of liver disease.

      Thus the varied roles and functions of albumin in day-to-day living make it a vital entity to be studied for tapping its potential in diagnosing, healing or even curing.