Archive for May, 2009

Chewing Gum Appears to Reduce Troublesome Belching

By Ed Susman

CHICAGO, IL – Chewing gum might be one way to prevent belching episodes, especially in individuals for whom belching appears to have a psychological cause.

Reseachers led by George Karamanolis, MD, of the hepatogastroenterology unit at Athens Medical School, Greece, studied five men and seven women who were diagnosed with aerophagia – troublesome belching. Tests determined the subjects belched an average of nearly 50 times an hour, but the studies were unable to find a correlation with acid reflux as the cause.img_2388

“Belching is considered as a subconscious abnormal learned behavior,” he said.

However, the belching virtually vanished when the indivudals were sleeping, Dr. Karamanolis reported at the 2009 Digestive disease Week here. “The belching mainly occurred in the daily upright position underlying the importance of psychological factors,” he said in his poster presentation.

When the patients were asked to chew gum, the supragastric belching dropped dramatically from a rate of 46 and hour to 11 an hour, a statistically significant results (P<.001).

“The use of chewing gum, as a putative distracting mechanism, decreased the incidence of supragastric belches and seems to be effective in these patients,” Dr. Karamanolis reported.

Digestive Disease Week 2009 is co-sponsored by the American Association for the Study of Liver Diseases, the AGA Institute, the American Society for Gastrointestinal Endoscopy and the society for Surgery of the Alimentary Tract.

–05-31-2009

  • Share/Bookmark

No Comments

MicroRNA Regulation of Tumor-Killing Viruses Avoids Unwanted Viral Pathology

SAN FRANCISCO, CA – Scientists have determined how to produce replication-competent viruses with key toxicities removed, providing a new platform for development of improved cancer treatments and better vaccines for a broad range of viral diseases.

Cellular microRNA molecules regulate the stability of mRNA in different cell types, and this newly-understood mechanism provides the possibility to engineer viruses for cell-specific inactivation. Cancer Research UK scientists at the University of Oxford, United Kingdom, with support from colleagues at Vrije Universiteit, Amsterdam, report that this approach can be used to regulate proliferation of adenovirus in a study published recently in the open-access journal Public Library of Science Pathogens.

Adenovirus is a DNA virus widely used in cancer therapy but which causes hepatic disease in mice. Professor Len Seymour and colleagues found that introducing sites into the virus genome that are recognized by microRNA 122 leads to hepatic degradation of important viral mRNA, thereby diminishing the virus’ ability to adversely affect the liver, while maintaining its ability to replicate in and kill tumor cells.

Tumor-killing replicating viruses are a hot topic in the biotherapeutics arena, with many clinical trials ongoing worldwide. That Professor Seymour’s group set out to and has now defined a mechanism whereby wild type virus potency could be maintained in tumor cells but the virus could be ‘turned off’ in tissues vulnerable to pathology adds important information to the current base of knowledge.

“This approach is surprisingly effective and quite versatile. It could find a range of applications in controlling the activity of therapeutic viruses, both for cancer research and also to engineer a new generation of conditionally-replicating vaccines, where the vaccine pathogen is disabled in its primary sites of toxicity,” Professor Seymour says.

The present study was intended mainly to explore and demonstrate the potential of this new mechanism to regulate virus activity. Although the current tumor-killing virus is useful in mice, transfer of the technology into the clinical setting will require re-engineering of the virus to overcome virus pathologies seen in humans, and it will be at least two years before this can be tested in the clinics.

- MFP Wire Services
- 5-30-2009

  • Share/Bookmark

No Comments

Development of DNA Drugs Gives Hope to Lupus Patients

LONDON, UK – A generation of DNA-like compounds, class R inhibitory oligonucleotides, have been shown to effectively inhibit cells responsible for the chronic autoimmune condition lupus. Researchers writing in BioMed Central’s open access journal Arthritis Research & Therapy have demonstrated the anti-inflammatory effects of the inhibitory oligonucleotides in both in vitro and mouse experiments.

Petar Lenert, from the University of Iowa, worked with a team of researchers to develop and test the compounds. He said, “The increased potency of class R inhibitory oligonucleotides for certain cells involved in lupus flare-ups will help patients by providing specific inhibition, yet allowing them to generate a protective immune response when needed”.

Lenert and his colleagues found that their inhibitory oligonucleotide drugs, composed of double-stranded DNA-like analogues carrying autoimmune-inhibitory sequences, were able to selectively reduce the activity of autoreactive B cells and dendritic cells. When given to mice with lupus, the compounds delayed death and reduced kidney damage.

Systemic lupus erythematosus, more commonly known simply as lupus, is thought to affect around a million people in the USA, but prevalence varies by country and ethnicity. It is much more common in women than men and there is currently no known cure. During periodic ‘flares’, the immune system of people with the condition mounts an attack on cells and tissues throughout the body, resulting in a range of symptoms including the characteristic ‘butterfly rash’ across the cheeks. With further testing, Lenert and his colleagues hope that class R inhibitory oligonucleotides may become another weapon in the fight against the disease.

- MFP Wire Services
- 5-30-2009

  • Share/Bookmark

No Comments