Absence of contour linking in peripheral vision

Human foveal vision is subserved initially by groups of spatial, temporal and orientational 'filters', the outputs of which are combined to define perceptual objects. Although a great deal is known about the filtering properties of individual cortical cells, relatively little is known about the nature of this 'linking' process. One recent approach has shown that the process can be thought of in terms of an association field whose strength is determined conjointly by the orientation and distance of the object. Here we describe a fundamental difference in this feature-linking process in central and peripheral parts of the visual field, which provides insight into the ways that foveal and peripheral visual perception differ. In the fovea, performance can be explained only by intercellular linking operations whereas in the periphery intracellular filtering will suffice. This difference represents a substantial economy in cortical neuronal processing of peripheral visual information and may allow a recent theory of intercellular binding to be tested.     

Localization of neutral endopeptidase in the ovine uterus and conceptus during the oestrous cycle and early pregnancy

Allylamine (AA) is an electrophilic amine with a long history of experimental usage because of its extremely potent and relatively specific cardiovascular toxicity; it has been utilized in a variety of experimental models attempting to mimic human atherosclerotic lesions, myocardial infarction, and vascular injury. Even though the exact mechanisms by which AA causes vascular lesions remain unresolved, recent studies on the acute effects of AA exposure in rats strongly suggest that deamination to the aldehyde acrolein, oxidative stress, and the resultant increase in lipid peroxidation, generation of .OH radicals, and acute depletion of glutathione (GSH) may be some of the causative factors in AA-induced vascular lesions. Since glutathione S-transferase 8-8 (GST8-8) of rat belongs to a distinct subgroup of GST isozymes involved in the detoxification of products of lipid peroxidation, we designed studies to examine the effects of AA exposure on this GST isoform in rat aorta using Western blotting and immunohistochemical techniques. The results of these studies demonstrate that GST8-8 is expressed in rat aorta and is dramatically induced upon AA exposure. By immunohistochemistry, GST8-8 was localized in the smooth muscle cells of the vascular media which is believed to be the site of metabolism of AA. A significant increase in gamma-glutamylcysteine synthetase activity and GST activity toward 4-hydroxynonenal and acrolein, which are preferred substrates of GST8-8, was seen as early as 3 days following AA treatment. Alterations in GSH and other GSH-related enzymes at 3 and 10 days support the concept that--upon AA exposure--aortic defense mechanisms respond early and induction of GSH biosynthesis and rat GST8-8 occur to alleviate the toxic effects of acrolein, a major, genotoxic product of AA metabolism. The presence of GST8-8 in the vasculature, which is constantly exposed to products of lipid peroxidation, and its induction by AA, suggest that GST8-8 plays a key role in protecting blood vessels against oxidative stress and hence, may be involved in the atherogenic process.     

Functional NMDA receptors are transiently active and support the survival of Purkinje cells in culture

Conflicting evidence exists concerning the activity of NMDA receptors (NMDARs) in cerebellar Purkinje cells and their possible functions. To investigate the activity of NMDARS, we used whole-cell recording on immunocytochemically identified Purkinje cells in primary culture. In addition, we used mice with a disrupted NMDAR1 gene that lack functional NMDARs (NR1-/-) to assess the physiological role of NMDARs. In cultures from normal mice, NMDA-medicated currents were detected in all identified Purkinje cells at 4 d in vitro (div). After 14 d, however, NMDA responses were reduced in amplitude, whereas the responses to kainate and glutamate increased steadily in amplitude. In addition, the NMDA-induced current displayed a pronounced desensitization at these later stages; peak current declined to zero during steady application of NMDA. At 7 div, the number of surviving Purkinje cells was less in cultures treated with NMDA antagonists, and their survival was dose-dependent. Purkinje cell survival was correspondingly poorer in cultures from the NR1-/- mice than in wild-type controls, suggesting that NMDAR activity enhances the survival of Purkinje cells in vitro. The addition of moderate doses of NMDA promoted the survival of wild-type Purkinje cells in the presence of tetrodotoxin. Feeder layers of cerebellar granule cells derived from wild-type or NR1-/- mice promoted survival of Purkinje cells to a similar degree, suggesting that the NMDAR in Purkinje cells, but not in other cells, is directly involved in Purkinje cell viability. The results demonstrate that NMDARs transiently produce membrane current in Purkinje cells and may serve as one of the epigenetic factors that support the survival of Purkinje cells in vitro.     

Clinical features of tuberculosis associated with HIV infection in Taiwan

To understand the clinical characteristics and outcome of tuberculosis (TB) in patients with acquired immunodeficiency syndrome (AIDS) in Taiwan, we reviewed the medical records of 118 adult AIDS patients who were hospitalized at National Taiwan University Hospital between January 1988 and September 1995. Among them, 29 (24.6%) had TB. The mean age of the AIDS patients with TB was 37 years (range, 25-66 yr). Most patients were in the advanced stages of AIDS when human immunodeficiency virus (HIV) infection and/or TB were first diagnosed. The mean CD4+ lymphocyte count was 0.037 x 10(9)/L (range, 0-0.152 x 10(9)/L) at the time TB was diagnosed. There was no statistically significant difference in the mean CD4+ lymphocyte count between patients with isolated pulmonary TB and those with extrapulmonary involvement. Twenty-two patients (75.8%) had extrapulmonary TB with the most common site being the lymph nodes (72.7%). Clinical symptoms were nonspecific, and the chest physical examination was not helpful in the diagnosis. Acid-fast bacilli were detected in sputum smears from eight patients (36.4%). A primary tuberculosis pattern (hilar adenopathy, pleural effusion, middle or lower lobe infiltrates) in the chest radiographs was the most common radiologic finding (36.4%) in patients with pulmonary TB. The reactivation pattern (predominant upper-lobe infiltrates with or without cavitation) could only be found in cases of pulmonary TB without extrapulmonary involvement. Atypical patterns (diffuse interstitial infiltrates mimicking Pneumocystis carinii pneumonia or other patterns) and normal chest radiographs were noted in nearly one-third of the patients with pulmonary TB. A good response to antituberculosis drugs and a favorable outcome were demonstrated in the patients, except for two with drug-resistant Mycobacterium tuberculosis infection. Early identification of TB in HIV-infected patients requires clinical awareness of the unusual clinical presentations, especially among patients in the advanced stages of AIDS.     

Comparison of regularly scheduled with as-needed use of albuterol in mild asthma. Asthma Clinical Research Network

This in vitro study investigated the temperature changes experienced during electric welding of titanium to determine if the welding heat presented a potential danger to pulpal vitality. Welds were applied to cast titanium simulations of a three-unit fixed partial denture containing two thermocouples measuring temperature changes. Mean maximal temperature changes were 127.4 degrees F near the weld and 68.6 F degrees at the axial wall. The mean times for the temperature to drop to within 10.0 degrees F of the starting temperature ranged from 84.1 to 133.7 seconds. The relatively low temperatures recorded in this study suggest that further investigation is warranted into the use of the welder intraorally.     

Nonmedical bed-days for stroke patients admitted to acute-care hospitals in Montreal, Canada

BACKGROUND AND PURPOSE: Reducing the amount of nonoptimal time stroke patients spend in the hospital should be a priority because prolonged hospitalization is not only costly but may be detrimental for persons with stroke through deconditioning, social isolation, and the fostering of dependent relationships. The purpose of this study was to determine the amount of time spent by stroke patients in acute-care hospitals that was not justified for medical reasons and to identify mechanisms contributing to nonmedical bed-days. METHODS: A retrospective cohort study was performed with 2232 persons admitted for acute stroke to one of 13 hospitals in Montreal, Canada, during 1991. Information was collected on the patient, the stroke, functional status, course in hospital, services, and discharge. Nonmedical bed-days were calculated as the difference between the time to meet specified criteria and time of discharge. Associations with nonmedical bed-days were estimated with adjustment for patient mix. RESULTS: Acute-care stay averaged 27 days, yielding 60,279 bed-days. Almost 50% of the cohort remained in the hospital after meeting criteria for medical discharge, resulting in 43% of total bed-days not accounted for medically. Fifty percent of persons with delayed discharge did not go home but were discharged to another acute-care hospital or to rehabilitation or long-term care, accounting for 66% of the nonmedical bed-days. Hospital and discharge destination remained strongly associated with nonmedical days, even after adjustment for patient mix. CONCLUSIONS: The single greatest contributor to excessive nonmedical stay appeared to be the need in Quebec for increased access to alternate levels of care, including skilled nursing facilities and rehabilitation centers.     

Effect of non-random missing data mechanisms in clinical trials

A simple form of non-ignorable missing data mechanisms based on two parameters is used to characterize the amount of missing data and the severity of non-randomness in clinical trials. Based on the formulation, the effect of non-randomly missing data on simple analyses which ignore the missing data is studied for binary and normally distributed response variables. In general, the effect of the non-randomly missing data on the bias and the power increases with the severity of non-randomness. The bias can be positive or negative and the power can be less than or greater than when the data are missing at random. The results of the analysis, ignoring the missing data, can be seriously flawed if the non-randomness is severe, even when only a small proportion of the sample is missing. The problem is more pronounced in the case of normally distributed response variables with unequal variances.     

Evidence for a major gene elevating serum bilirubin concentration in Utah pedigrees

In case-control studies, lower serum bilirubin levels have been associated with increased risk of developing coronary heart disease (CHD). We have also previously shown that serum bilirubin has a significant polygenic component. The purpose of the present investigation was to determine whether there was statistical evidence for a major gene explaining a significant portion of individual variation in serum total bilirubin levels and whether this gene might alter the risk of CHD. Serum bilirubin measurements were obtained from 1240 adults in 84 Utah pedigrees screened twice: from 1980 to 1983 and again from 1983 to 1986. Bivariate maximum-likelihood segregation analysis of serum bilirubin levels obtained from the two clinic visits indicated that a major gene was responsible for elevated levels in 11.5% of the persons in these pedigrees. Phenotypic variations in visit 1 bilirubin arising from polygenes were highly correlated with the phenotypic variation due to polygenes in visit 2 bilirubin, indicating a stable genetic contribution to bilirubin over 2.5 years of follow-up. The major gene explained 27% and 28% of the variance in bilirubin levels at visit 1 and visit 2, respectively. There were no correlations of unmeasured environmental factors influencing bilirubin between the two clinic visits. At both visits, persons with early CHD had lower levels of bilirubin than unaffected persons (P < .01). The odds ratio for the risk of CHD in the high-homozygote group was 0.31, P = .09. We conclude that there is a major gene modestly raising serum bilirubin levels. Since cross-sectional data indicate that low serum bilirubin levels increase the risk of CHD, this major gene may be protective against CHD for about 12% of the persons in this study.