Medical Staffing Organization and Quality of Care Outcomes in Post-acute Care Settings.

BACKGROUND AND OBJECTIVES: Medical providers are significant drivers of care in post-acute long-term care (PALTC) settings, yet little research has examined the medical provider workforce and its role in ensuring quality of care. RESEARCH DESIGN AND METHODS: This study examined the impact of nursing home medical staffing organization (NHMSO) dimensions on the quality of care in U.S. nursing homes. The principal data source was a survey specifically designed to study medical staff organization for post-acute care. Respondents were medical directors and attending physicians providing PALTC. We linked a number of medical provider and nursing home characteristics to the Centers for Medicaid and Medicare Services Nursing Home Compare quality measures hypothesized to be sensitive to input by medical providers. RESULTS: From the sample of nursing home medical providers surveyed (n = 1,511), 560 responses were received, yielding a 37% response rate; 425 medical provider responses contained sufficient data for analysis. The results of the impact of NHMSO dimensions were mixed, with many domains not having any significance or having negative relationships between provider characteristics and quality measures. Respondents who reported having a formal process for granting privileges and nursing homes with direct employment of physicians reported significantly fewer emergency visits. DISCUSSION AND IMPLICATIONS: Further research is needed regarding what quality measures are sensitive to both medical provider characteristics and NHMSO characteristics.

Enantiospecific synthesis of pseudoacarviosin as a potential antidiabetic agent.

A pseudo-1,4'- N-linked disaccharide, pseudoacarviosin 5, was constructed via a key palladium-catalyzed coupling reaction of pseudoglycosyl chloride 8 (prepared from d-glucose via a novel direct intramolecular aldol addition in 12 steps) and pseudo-4-amino-4,6-dideoxy-alpha- d-glucose 9 (prepared from l-arabinose via an unusual trans-fused isoxazolidine-selective intramolecular nitrone-alkene cycloaddition in 11 steps). Pseudoacarviosin 5 has been shown to be a potent inhibitor of alpha-glucosidases, particularly the intestinal mucosal enzymes sucrase and glucoamylase of relevance to blood glucose control.

Resistance training enhances components of the insulin signaling cascade in normal and high-fat-fed rodent skeletal muscle.

Our laboratory recently reported that chronic resistance training (RT) improved insulin-stimulated glucose transport in normal rodent skeletal muscle, owing, in part, to increased GLUT-4 protein concentration (Yaspelkis BB III, Singh MK, Trevino B, Krisan AD, and Collins DE. Acta Physiol Scand 175: 315-323, 2002). However, it remained to be determined whether these improvements resulted from alterations in the insulin signaling cascade as well. In addition, the possibility existed that RT might improve skeletal muscle insulin resistance. Thirty-two male Sprague-Dawley rats were assigned to four groups: control diet (Con)-sedentary (Sed); Con-RT; high-fat diet (HF)-Sed; and HF-RT. Animals consumed their respective diets for 9 wk; then RT animals performed 12 wk of training (3 sets, 10 repetitions at 75% one-repetition maximum, 3x/wk). Animals remained on their dietary treatments over the 12-wk period. After the training period, animals were subjected to hindlimb perfusions. Insulin-stimulated insulin receptor substrate-1-associated phosphatidylinositol-3 kinase activity was enhanced in the red gastrocnemius and quadriceps of Con-RT and HF-RT animals. Atypical PKC-zeta/lambda and Akt activities were reduced in HF-Sed and normalized in HF-RT animals. Resistance training increased GLUT-4 protein concentration in red gastrocnemius and quadriceps of Con-RT and HF-RT animals. No differences were observed in total protein concentrations of insulin receptor substrate-1, Akt, atypical PKC-zeta/lambda, or phosphorylation of Akt. Collectively, these findings suggest that resistance training increases insulin-stimulated carbohydrate metabolism in normal skeletal muscle and reverses high-fat diet-induced skeletal muscle insulin resistance by altering components of both the insulin signaling cascade and glucose transporter effector system.

Chronic leptin treatment enhances insulin-stimulated glucose disposal in skeletal muscle of high-fat fed rodents.

The aim of this investigation was to evaluate if chronic leptin administration corrects high fat diet-induced skeletal muscle insulin resistance, in part, by enhancing rates of glucose disposal and if the improvements are accounted for by alterations in components of the insulin-signaling cascade. Sprague-Dawley rats consumed normal (CON) or high fat diets for three months. After the dietary lead in, the high fat diet group was further subdivided into high fat (HF) and high fat, leptin treated (HF-LEP) animals. HF-LEP animals were injected twice daily with leptin (5 mg/100 g body weight) for 10 days, while the CON and HF animals were injected with vehicle. Following the treatment periods, all animals were prepared for and subjected to hind limb perfusion. The high fat diet decreased rates of insulin-stimulated skeletal muscle glucose uptake and glycogen synthesis in the red gastrocnemius (RG), but did not affect glycogen synthase activity, rates of glucose oxidation or nonoxidative disposal of glucose. Of interest, IRS-1-associated PI3-K activity and total GLUT4 protein concentration were reduced in the RG of the high fat-fed animals. Leptin treatment increased rates of insulin-stimulated glucose uptake and glucose oxidation, and normalized rates of glycogen synthesis. Leptin appeared to mediate these effects by normalizing insulin-stimulated PI3-K activation and GLUT4 protein concentration in the RG. Collectively, these data suggest that chronic leptin treatment reverses the effects of a high fat diet thereby allowing the insulin signaling cascade and glucose transport effector system to be fully activated which in turn affects the amount of glucose that is transported across the plasma membrane and made available for glycogen synthesis.

Facile, efficient, and enantiospecific syntheses of 1,1'-N-linked pseudodisaccharides as a new class of glycosidase inhibitors.

This article describes an efficient synthesis of a potent trehalase inhibitor, 1,1'-N-linked pseudodisaccharide 1 (consisting of two valienamines), in 14 steps with an overall yield of 12% and a first synthesis of 2 (consisting of two 2-epi-valienamines) in 15 steps with an overall yield of 24% from (-)-quinic acid. The synthesis involves a stereospecific palladium-catalyzed coupling reaction between an allylic amine and an allylic chloride as the crucial step. The acetonide blocking groups were shown to be the best hydroxyl protecting groups, compatible with the palladium-catalyzed allylic amination reaction that afforded high yields of the 1,1'-N-linked pseudodisaccharides with a minimum amount of an elimination diene side product.