Biomedical subjects

Chintan Patel

Publications and source records attributed to Chintan Patel.

3 recordsLinked to original sources

PubMed2006

Towards a reference model for representing nursing information needs.

Information needs studies in clinical settings often face the problem of integrating and analyzing data collected using different study tools. Generally, a coding taxonomy or a model is developed to capture and code the study data. Significant efforts are required to develop a model that not only captures the study data but is also closer to the clinical domain to draw meaningful real world inferences. Further, a study-specific model limits comparative evaluation of studies across different institutions. In this paper, we propose a reference model for representing nursing information needs. We use an iterative and collaborative approach in representing the concepts in the model. The model consists of 33 information (need) concepts, 29 information sources and 7 categories of nursing tasks which were used to code 228 identified information need instances.

Hospitals, Urban↗

PubMed2005

Short-term and long-term in vivo exposure to an ephedra- and caffeine-containing metabolic nutrition system does not induce cardiotoxicity in B6C3F1 mice.

Although conventional biomedical research has largely focused on mechanisms of weight loss and genetic aspects of obesity, most medical solutions are plagued by side-effects and fraught with complex questions. As a consequence, consumers are seriously considering herbal products, nutraceuticals and functional foods as alternatives to conventional medications. This is evidently driven by a growing consumer understanding of diet/disease links, aging-related consequences, rising health care costs, and advances in food technology and nutrition. This study investigated the effects of up to 12 months exposure to a multinutrient and botanical extract supplement (Metabolic Nutrition System Orange (MNSO) - sold by AdvoCare, Carrollton, TX, USA) at five dietary concentrations on serum biochemistry and target organ histopathology of the hearts of B6C3F1 mice. The MNSO is a unique combination of vitamins, minerals, omega-3 fatty acids and herbal extracts designed to provide a strong foundation of nutritional support, and to enhance thermogenesis and perception of energy. The MNSO contain extracts of citrus, ephedra, guarana, gingko, green tea and Ocimum. In this study, female B6C3F1 mice were fed control (-MNSO) or MNSO (one time to ten times, one time = daily human dose) diets. Animals were sacrificed after 4, 8 and 12 months', at which time blood was collected for serum chemistry analysis, and hearts were prepared for histopathology and tissue biochemistry. Food consumption and body weight changes were also monitored throughout the study. The MNSO exposure did not significantly affect any of the cardiosensitive enzymes [including creatine kinase (CK), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST)] and normal histopathological architecture of the heart was observed. Although animals given the MNSO diet consumed more food, they were relatively leaner and more active compared to controls. The results indicate that ingestion of ephedra and caffeine for one year in the doses used as part of a comprehensive metabolic nutrition system does not significantly alter normal serum chemistry or induce any irreversible histological changes in the mouse heart, since this study employed up to ten times the normal human consumption dose of ephedra and the metabolic nutrition system.

Animals↗

PubMed2002

Antagonist-induced micro-opioid receptor up-regulation decreases G-protein receptor kinase-2 and dynamin-2 abundance in mouse spinal cord.

Chronic treatment with opioid receptor antagonists has been shown to increase the density of micro-, delta- and kappa-opioid receptors in cell culture and in the intact animal. Although opioid receptor antagonist-induced up-regulation is a robust phenomenon, the mechanisms responsible for the increase in receptor density remain unclear. In the present study, changes in a kinase and a GTPase that have been implicated in G-protein-coupled receptor regulation were examined following opioid receptor antagonist treatment. Mice were implanted s.c. with a naltrexone pellet or placebo pellet. On the eighth day following implantation, spinal cord was removed and G-protein receptor kinase-2 (GRK-2) and dynamin-2 abundance were determined using a quantitative immunoblot approach. Changes in micro-opioid receptor density were also determined. Naltrexone treatment produced a significant (145%) increase in micro-opioid receptor density. Naltrexone treatment was associated with a significant 36% decrease in GRK-2 and 30% decrease in dynamin-2 abundance in spinal cord. These data raise the possibility that opioid receptor antagonist-induced micro-opioid receptor up-regulation in the intact animal may be due to a reduction in constitutive internalization of opioid receptors.

Animals↗