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Predicting rehospitalization and outpatient services from administration and clinical databases.

The study tests whether psychiatric services utilization may be predicted from administrative databases without clinical variables equally as well as from databases with clinical variables. Persons with a psychiatric hospitalization at an urban medical center were followed for 1 year postdischarge (N = 1384.) Dependent variables included statewide rehospitalization and the number of hours of outpatient services received. Three linear and logistic regression models were developed and cross-validated: a basic model with limited administrative independent variables, an intermediate model with diagnostic and limited clinical indicators, and a full model containing additional clinical predictors. For rehospitalization, the clinical cross-validated model accounted for twice the variance accounted by the basic model (adjusted R2 = .13 and .06, respectively). For outpatient hours, the basic cross-validated model performed as well as the clinical model (adjusted R2 = .36 and .34, respectively). Clinical indicators such as assessment of functioning and co-occurring substance use disorder should be considered for inclusion in predicting rehospitalization.

Adult↗

Progress in demographic methodology.

"This paper examines developments in demographic methodology during the past decade or so. It focuses on methodological advances in the analysis of mortality of infants and young children, of adults, and on problems of mortality estimation in small populations. The other major areas reviewed here are related to the study of birth intervals, parity progression, proximate determinants of fertility, and the demography of the family. Concluding remarks relate the methodological issues to the information explosion in demography."

Adult↗

Evaluation of a sorbitol dehydrogenase inhibitor on diabetic peripheral nerve metabolism: a prevention study.

AIMS/HYPOTHESIS: Studies of the role of sorbitol dehydrogenase in nerve functional deficits induced by diabetes reported contradictory results. We evaluated whether sorbitol dehydrogenase inhibition reduces metabolic abnormalities and enhances oxidative stress characteristic of experimental diabetic neuropathy. METHODS: Control and streptozotocin-diabetic rats were treated with or without sorbitol dehydrogenase inhibitor (SDI)-157 (100 mg x kg(-1) x day(-1), in the drinking water, for 3 weeks). Sciatic nerve free mitochondrial (cristae and matrix) and cytosolic NAD(+): NADH ratios were calculated from the beta-hydroxybutyrate, glutamate and lactate dehydrogenase systems. Concentrations of metabolites, e. g. sorbitol pathway intermediates and variables of energy state were measured in individual nerves spectrofluorometrically by enzymatic procedures. RESULTS: The flux through sorbitol dehydrogenase (manifested by nerve fructose concentrations) was inhibited by 53 % and 74 % in control and diabetic rats treated with SDI compared with untreated control and diabetic groups. Free NAD(+):NADH ratios in mitochondrial cristae, matrix and cytosol were decreased in diabetic rats compared with controls and reduction in either of the three variables was not prevented by sorbitol dehydrogenase inhibitor. Phosphocreatine concentrations and phosphocreatine:creatine ratios were decreased in diabetic rats compared with controls and were further reduced by the inhibitor. Malondialdehyde plus 4-hydroxyalkenals concentration was increased and reduced gluthathione concentration was reduced in diabetic rats compared with the control group, and changes in both variables were further exacerbated by sorbitol dehydrogenase inhibitor. Neither NAD-redox and energy states nor lipid aldehyde and reduced gluthathione concentrations were affected by treatment with the inhibitor in control rats. CONCLUSION/INTERPRETATION: Inhibition of sorbitol dehydrogenase does not offer an effective approach for prevention of oxidation and metabolic imbalances in the peripheral nerve that is induced by diabetes and is adverse rather than beneficial. [Diabetologia (1999) 42: 1187-1194]

Animals↗

Metabolic risk factors for atherosclerosis in heart transplant recipients.

Development of coronary artery disease (CAD) in the cardiac allograft limits long-term survival after heart transplantation. Previous studies, focusing on lipoprotein metabolism, have paid little attention to changes in glucose and insulin metabolism that increase the risk of CAD in these patients. To address this issue, plasma glucose and insulin responses to an oral glucose load and lipid and lipoprotein concentrations were measured in male normal volunteers (n = 40) and cardiac transplant recipients with pretransplant diagnoses of either idiopathic cardiomyopathy (n = 24) or ischemic heart disease (n = 28), matched for age and body mass index. Patients with a pretransplant diagnosis of ischemic heart disease had higher plasma glucose and insulin concentrations in response to oral glucose as well as higher fasting plasma triglyceride, cholesterol, and low-density lipoprotein cholesterol concentrations than did the control group (p < 0.005 to p < 0.001). In addition, high-density lipoprotein cholesterol concentrations were lower and the ratio of cholesterol to high-density lipoprotein cholesterol higher than control values in those with a pretransplant diagnosis of ischemic heart disease (p < 0.001). Values for almost all variables were intermediate in patients with a pretransplant diagnosis of idiopathic cardiomyopathy and in most instances were significantly different from both. Thus, male cardiac transplant recipients are dyslipidemic, relatively glucose intolerant, and hyperinsulinemic compared to normal volunteers. These changes, observed in patients with a pretransplant diagnosis of either ischemic heart disease or idiopathic cardiomyopathy, emphasize the important role of immunosuppression in the development of metabolic risk factors for CAD in these individuals.

Blood Glucose↗

A new analysis of United Nations mortality statistics.

Demographic data published by the United Nations in 1987 are analysed in terms of the Gompertz function. Projections for maximum life spans are obtained, with the data broadly divisible into three clusters. These are attributable not only to the influence of high infant mortality, but suggest also constitutional and/or environmental variations among members of the clusters. The difference between life span and life expectancy is estimated analytically. A comparison with an earlier analysis supports the view that there are important differences between the life expectancies of the sexes.

Adult↗

Epigenetic selection as a possible component of transdifferentiation. Further study of the commitment of hypertrophic chondrocytes to become osteocytes.

Transdifferentiation of hypertrophic chondrocytes into osteogenic cells was induced in 14 day chick embryo femurs by cutting through the region of hypertrophic cartilage. The process was studied in organ culture, using electron microscopy, staining for alkaline phosphatase, immunocytochemistry of collagen type I and proliferative cell nuclear antigen, and in situ localization of DNA strand-breaks. In addition, DNA and RNA synthesis were studied by 3[H]-T and 3[H]-U radioautography. Loss of ECM components from the cut edge occurred in culture. During the 12 day period necessary for transdifferentiation we observed phenotypic instability and bi-potentiality, the death of some cells and the gradual promotion of the osteoblastic phenotype in the survivors. Transition from chondrocytic to osteoblastic phenotype progressed stepwise, through variable mosaic intermediates, and involved a few cell cycles including asymmetric (differential) divisions. Proliferating and apoptotic cells were found in close proximity. As judged by the relative proportion of apoptotic cells and composition of the surrounding intralacunar matrix, negative selection of intermediate cell types displaying chondrocytic and altered mosaic phenotypes occurred. When the osteoblastic lineage was finally established, apoptotic cells were no longer present. Our hypothesis is that after disruption of cell-cell or cell-matrix interactions and lack of growth factors certain cells are selected and channelled through proliferation into the new stable phenotype. This process is targeted by the environment through a set of pre-determined steps.

Animals↗

Choroidal neovascular membranes: reproducibility of angiographic interpretation.

PURPOSE: To determine interobserver agreement for classifying choroidal neovascular membranes in age-related macular degeneration. METHODS: Six fluorescein angiograms of choroidal neovascular membranes were interpreted by 21 retina specialists. Reliability was measured by percent agreement and kappa coefficient. RESULTS: Interobserver agreement of membrane types ranged from perfect concordance for a small, classic membrane to near-random classification for a complex pattern. Mean kappa coefficient was.64. Interobserver agreement of membrane size was most variable for intermediate size lesions (mean kappa coefficient =.40). CONCLUSION: Fluorescein angiographic interpretation of choroidal neovascular membrane type and size can vary considerably. Interobserver agreement is better for membrane type than for membrane size.

Choroidal Neovascularization↗

Bacterial vaginosis, vaginal fluid neutrophil defensins, and preterm birth.

OBJECTIVE: To examine the association between bacterial vaginosis, vaginal fluid neutrophil defensins, and preterm birth. METHODS: Vaginal fluid specimens were obtained at 24-29 weeks' gestation from 242 cases with preterm birth and 507 noncases sampled using a case-cohort study design. We tested for bacterial vaginosis by Gram staining and Nugent scores and assayed for neutrophil defensins by enzyme-linked immunosorbent assay. Bacterial vaginosis was studied as a categoric variable (negative, intermediate, and positive), whereas defensins were studied as a continuous, categoric (based on percentiles), and dichotomous measure (presence versus absence). Three gestational age cut points were used to define preterm birth. Modified Cox proportional hazard models were used to evaluate the associations between bacterial vaginosis, defensins, and degree (less than 32, less than 34, and less than 37 weeks) and type (premature rupture of membranes, preterm labor) of preterm birth. RESULTS: Elevated vaginal fluid neutrophil defensins were not associated with birth before 37 weeks. Compared with women who did not have measurable vaginal fluid defensins, women with higher defensin levels (0-2.8 micro g/mL, 2.8-8.2 micro g/mL, and greater than 8.2 micro g/mL) had a greater risk of delivering before 32 weeks. Hazard ratios adjusted for maternal race and vaginal bleeding during pregnancy and 95% confidence intervals for these defensin levels were 1.7 (0.4, 6.9), 2.4 (0.7, 7.9), and 3.1 (1.0, 9.8), respectively. Bacterial vaginosis status did not influence the association between defensins and preterm birth. CONCLUSION: Elevated concentrations of vaginal fluid neutrophil defensins at 24-29 weeks' gestation might predict preterm birth before 32 weeks.

Adult↗

[Hormone replacement therapy in ischemic heart disease prevention in women. Arguments in favor].

Numerous evidence have suggested a physiologic action of sexual steroids upon the cardiovascular system and the coherence of epidemiological studies have raised the possibility of a positive action of estradiol in preventing cardiovascular disease, specially through atheroma inhibition and other vascular wall-related mechanisms. From an experimental point of view, some clinical trials have demonstrated an improvement in some intermediate clinical variables, such as hypercholesterolemia and hypertension, after the administration of estradiol. Nonetheless, the HERS study, the first secondary prevention trial of estrogen and cardiovascular disease, failed to demonstrate these positive actions suggested by epidemiological studies and the efficacy of estradiol in the treatment of postmenopausal women with cardiovascular disease has been questioned. In spite of this, the HERS study has also been questioned because of different pitfalls in its development and, for some authors, it is inconclusive. Therefore, at present, it is not possible to make an evidence based clinical decision regarding the key question about the real actions of estradiol in the prevention of cardiovascular disease in postmenopausal women.

Adult↗