Early Detection Of Mild Cognitive Impairment In Older Adults Through The Use Of Annual Screening In The Primary Care Setting

The purpose of this study was to determine primary care providers’ adherence to USPSTF (2015), and the Alzheimer’s Association’s (2013) recommendations and guidelines advocating annual cognitive impairment screening on patients ages 65 years and older. The Alzheimer’s Association issued an algorithm for detecting cognitive impairment in older adults; this cognitive assessment algorithm was accepted and mandated by U.S. Centers for Medicare and Medicaid Services during annual wellness visits of patients 65 years and older. In addition to the Alzheimer’s Association, USPSTF acknowledges the increasing prevalence of cognitive impairment and the benefits of early detection. However, USPSTF argues a lack o f research and information on the subject; to which, the current study attempted to aid the increasing data on cognitive screening in older adults (USPSTF, 2014). This study examined the amount of primary providers’ compliance in completing cognitive impairment screenings of older adults, probable barriers decreasing provider adherence of implementing annual cognitive testing of older adults, and the preferred methods and tools utilized for cognitive impairment screening o f those adults ages 65 years and older

Ghrelin and its potential in the treatment of eating/wasting disorders and cachexia

The gastrointestinal “hunger” hormone ghrelin is the only known circulating peripheral molecule with the ability to decrease body fat utilization and to increase body weight gain. Accordingly, due to ghrelin’s effects to promote food intake while decreasing energy expenditure ghrelin may offer potential as a drug for treatment of eating/wasting disorders and cachexia. Therapeutic potential of ghrelin and ghrelin analogues to promote food intake and body weight gain was recently indicated in several clinical studies. The recent discovery of the ghrelin O-acyltransferase as the key enzyme responsible for ghrelin acylation has further deepened our understanding of ghrelin activation, thereby paving the way for more efficient targeting of the ghrelin pathway. Here, we summarize the current knowledge pertaining to the potential of the endogenous ghrelin system as a drug target for the treatment of eating/wasting disorders and cachexia

In vitro and in vivoefficacy of fluorodeoxycytidine analogs against highly pathogenic avian influenza H5N1,seasonal, and pandemic H1N1 virus infections

Various fluorodeoxyribonucleosides were evaluated for their antiviral activities against influenza virus infections in vitro and in vivo. Among the most potent inhibitors was 2′-deoxy-2′-fluorocytidine (2′-FdC). It inhibited various strains of low and highly pathogenic avian influenza H5N1 viruses, pandemic H1N1 viruses, an oseltamivir-resistant pandemic H1N1 virus, and seasonal influenza viruses (H3N2, H1N1, influenza B) in MDCK cells, with the 90% inhibitory concentrations ranging from 0.13 to 4.6 μM, as determined by a virus yield reduction assay. 2′-FdC was then tested for efficacy in BALB/c mice infected with a lethal dose of highly pathogenic influenza A/Vietnam/1203/2004 H5N1 virus. 2′FdC (60 mg/kg/d) administered intraperitoneally (i.p.) twice a day beginning 24 h after virus exposure significantly promoted survival (80% survival) of infected mice (p = 0.0001). Equally efficacious were the treatment regimens in which mice were treated with 2′-FdC at 30 or 60 mg/kg/day (bid X 8) beginning 24 h before virus exposure. At these doses, 70–80% of the mice were protected from death due to virus infection (p = 0.0005, p = 0.0001; respectively). The lungs harvested from treated mice at day four of the infection displayed little surface pathology or histopathology, lung weights were lower, and the 60 mg/kg dose reduced lung virus titers, although not significantly compared to the placebo controls. All doses were well tolerated in uninfected mice. 2′-FdC could also be administered as late as 72 h post virus exposure and still significantly protect 60% mice from the lethal effects of the H5N1 virus infection (p = 0.019). Other fluorodeoxyribonucleosides tested in the H5N1 mouse model, 2′-deoxy-5-fluorocytidine and 2′-deoxy-2′,2′-difluorocytidine, were very toxic at higher doses and not inhibitory at lower doses. Finally, 2′-FdC, which was active in the H5N1 mouse model, was also active in a pandemic H1N1 influenza A infection model in mice. When given at 30 mg/kg/d (bid X 5) beginning 24 h before virus exposure), 2′-FdC also significantly enhanced survival of H1N1-infected mice (50%, p = 0.038) similar to the results obtained in the H5N1 infection model using a similar dosing regimen (50%, p \u3c 0.05). Given the demonstrated in vitro and in vivoinhibition of avian influenza virus replication, 2′FdC may qualify as a lead compound for the development of agents treating influenza virus infections