Psychophysical evidence for a functional hierarchy of motion processing mechanisms

Current models of motion perception typically describe mechanisms that operate locally to extract direction and speed information. To deal with the movement of self or objects with respect to the environment, higher-level receptive fields are presumably assembled from the outputs of such local analyzers. We find that the apparent speed of gratings viewed through four spatial apertures depends on the interaction of motion directions among the apertures, even when the motion within each aperture is identical except for direction. Specifically, local motion consistent with a global pattern of radial motion appears 32% faster than that consistent with translational or rotational motion. The enhancement of speed is not reflected in detection thresholds and persists in spite of instructions to fixate a single local aperture and ignore the global configuration. We also find that a two-dimensional pattern of motion is necessary to elicit the effect and that motion contrast alone does not produce the enhancement. These results implicate at least two serial stages of motion-information processing: a mechanism to code the local direction and speed of motion, followed by a global mechanism that integrates such signals to represent meaningful patterns of movement, depending on the configuration of the local motions.     

Invasive group A streptococcal disease in Taiwan is not associated with the presence of streptococcal pyrogenic exotoxin genes

We reviewed the clinical features of 44 patients with invasive group A streptococcal (GAS) disease who were treated at two teaching hospitals in southern Taiwan from 1991 to 1994. Genes encoding streptococcal pyrogenic exotoxin types A (speA), B (speB), C (speC), and F (speF) and serotypes of M1, M6, and M12 were determined by polymerase chain reaction to target specific sequences in the 44 isolates recovered from these patients and in 28 isolates recovered from upper respiratory sites in 28 additional patients during the study period. The protease activity of these isolates was tested by using the casein plate method. Of the 44 patients with invasive diseases, 25 (57%) had no obvious underlying diseases, and 14 (32%) had preexisting neoplastic diseases or had previously used steroids. Twenty-five patients (57%) presented with cellulitis or necrotizing fasciitis, 24 (55%) had bacteremia, and eight (18%) had streptococcal toxic shock syndrome (STSS). Eight patients (18%) died of invasive GAS disease; seven had STSS, and seven had underlying diseases. All eight patients died within 48 hours after hospitalization. The presence of speA, speC, or speF was not implicated in any particular clinical syndrome in patients with invasive GAS disease. High-level protease activity and the M1 serotype of the isolates were significantly associated with the clinical signs of STSS and with mortality. M1 serotype and protease activity, as well as host immune status, might play significant roles in the pathogenesis of invasive GAS disease in Taiwan.     

A comparison of gene organization in the zwf region of the genomes of the cyanobacteria Synechococcus sp. PCC 7942 and Anabaena sp. PCC 7120

The region of the genome encoding the glucose-6-phosphate dehydrogenase gene zwf was analysed in a unicellular cyanobacterium, Synechococcus sp. PCC 7942, and a filamentous, heterocystous cyanobacterium, Anabaena sp. PCC 7120. Comparison of cyanobacterial zwf sequences revealed the presence of two absolutely conserved cysteine residues which may be implicated in the light/dark control of enzyme activity. The presence in both strains of a gene fbp, encoding fructose-1,6-bisphosphatase, upstream from zwf strongly suggests that the oxidative pentose phosphate pathway in these organisms may function to completely oxidize glucose 6-phosphate to CO2. The amino acid sequence of fructose-1,6-bisphosphatase does not support the idea of its light activation by a thiol/disulfide exchange mechanism. In the case of Anabaena sp. PCC 7120, the tal gene, encoding transaldolase, lies between zwf and fbp.     

Veterinary practice and occupational health. An epidemiological study of several professional groups of Dutch veterinarians. I. General physical examination and prevalence of allergy, lung function disorders, and bronchial hyperreactivity

The prevalence of allergy, lung function disorders, and bronchial hyperreactivity was studied in 102 Dutch veterinarians, subdivided into five professional groups (predominantly working with either swine, cattle, poultry, companion animals, or as a non-practitioner). The mean age of the participants was 43 years; 6 participants were females. Twenty-two per cent of the participants were overweight, and relatively more non-practitioners than practitioners were overweight. Approximately 23% of the vets reported complaints of prolonged fatigue. The data suggest a relationship between complaints of prolonged fatigue and a more than average number of daily working hours. Only a small proportion of vets were sensitized against several allergens. There were no significant differences in prevalence of distinct lung function disorders or bronchial hyperreactivity between professional groups. It is hypothesized that the respiratory complaints (chronic coughing, chronic phlegm production, stuffed nose, sneezing) reported by the vets predominantly working in swine and/or poultry practice could be caused by irritation and/or inflammation of the first part of the trachea-bronchial tree that has no measurable and permanent consequences for changes in lung function or increased bronchial hyperreactivity. The results of a skin test against allergens and determination of allergen-specific IgE in blood indicated that the respiratory complaints were probably not related to allergy against the panel of allergens tested.     

Quality of care problems among Medicare and Medicaid patients

The purpose of this study was to characterize quality of care problems among Medicare and Medicaid inpatients in New York State. The patients selected for this study comprised 1991 and 1992 Medicare and all 1992 Medicaid inpatients in whom quality of care problems with actual or potential adverse effects were found. The patients in this study were drawn from public, proprietary, voluntary and teaching hospitals. A total of 1000 quality of care problems with either actual or potential adverse effects were found in 706 Medicare patients. Two hundred and seventy-five (275) quality of care problems with actual or potential adverse effects were found in 154 Medicaid patients. Premature death occurred in 53 (7.4%) of the 706 Medicare and in 42 (27.2%) of the 154 Medicaid patients. Treatment problems and monitoring failures accounted for the majority of quality of care problems with actual or potential adverse effects for both Medicare (63.0%) and Medicaid (75.7%) patients. Among Medicare patients, the treatment of infections and antibiotic use, fluid and electrolyte management, and inappropriate drug use were among the leading causes of quality of care problems. Attending physicians were associated with the majority of Medicare quality of care problems while house staff and attending physicians were associated with the majority of those among Medicaid patients. The results of this study indicate that there are several leading causes of quality of care problems among Medicare and Medicaid patients. Treatment problems and monitoring failures together comprise the majority of such problems. Among Medicare patients, it was found that most quality of care problems were associated with the treatment of infections and antibiotic use, fluid and electrolyte management, and inappropriate drug use. Most quality of care problems among Medicaid patients were associated with these categories as well as with labor and delivery problems, and poor discharge planning. The results of this study reflect the peer-review process in which providers are given an opportunity to respond to physician-reviewer decisions about the presence of actual or potential adverse effects. Such a process, which permits the presentation of additional data and information by providers, produces fewer final adverse outcome determinations than a process uniquely based on chart review. The quality of care problems observed in this study are amenable to focused educational interventions. Such remedial interventions could yield significant improvements in the quality of care for all patients.     

VH gene family utilization of anti-acetylcholine receptor antibodies in experimental autoimmune myasthenia gravis

The immunoglobulin heavy chain (VH) gene family usage in experimental autoimmune myasthenia gravis (EAMG) model was investigated by RNA slot blot hybridization using VH gene family specific probes. Anti-acetylcholine receptor (AChR) monoclonal antibodies (mAbs) isolated from susceptible C57BL/6 and resistant BALB/c mice were found to be encoded by VH genes from at least six different families. The Vgam3.8 family was overrepresented in alpha-bungarotoxin blocking mAbs. Expression of cross-reactive idiotypes by anti-AChR mAbs was irrespective of the VH gene family usage. Strain dependent differences in susceptibility for EAMG were not reflected in an aberrant VH gene family usage of anti-AChR mAbs.     

Distribution of alpha 1A, alpha 1B and alpha 1E voltage-dependent calcium channel subunits in the human hippocampus and parahippocampal gyrus

The distribution of voltage-dependent calcium channel subunits in the central nervous system may provide information about the function of these channels. The present study examined the distribution of three alpha-1 subunits, alpha 1A, alpha 1B and alpha 1E, in the normal human hippocampal formation and parahippocampal gyrus using the techniques of in situ hybridization and immunocytochemistry. All three subunit mRNAs appeared to be similarly localized, with high levels of expression in the dentate granule and CA pyramidal layer. At the protein level, alpha 1A, alpha 1B and alpha 1E subunits were differentially localized. In general, alpha 1A-immunoreactivity was most intense in cell bodies and dendritic processes, including dentate granule cells, CA3 pyramidal cells and entorhinal cortex pre-alpha and pri-alpha cells. The alpha 1B antibody exhibited relatively weak staining of cell bodies but stronger staining of neuropil, especially in certain regions of high synaptic density such as the polymorphic layer of the dentate gyrus and the stratum lucidum and radiatum of the CA regions. The alpha 1E staining pattern shared features in common with both alpha 1A and alpha 1B, with strong immunoreactivity in dentate granule, CA3 pyramidal and entorhinal cortex pri-alpha cells, as well as staining of the CA3 stratum lucidum. These findings suggest regions in which particular subunits may be involved in synaptic communication. For example, comparison of alpha 1B and alpha 1E staining in the CA3 stratum lucidum with calbindin-immuno-reactivity suggested that these two calcium channels subunits may be localized presynaptically in mossy fibre terminals and therefore may be involved in neurotransmitter release from these terminals.