Experimental amyloidosis: deposition in the general and oral tissues of mice.
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Biomedical subjects
Publications and source records attributed to A S Miller.
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BACKGROUND: How Type A personality is related to the stress process has been investigated. However, in the occupational health field, stressful aspects of the work environment for Type A or B workers have not been fully revealed. METHODS: In the present study, using signal detection analysis, we analyzed data concerning work stressors and social support (SS) at work among Japanese white-collar workers (n = 560) and identified the respective aspects of work that are stressful for Type A and B workers. We also evaluated the interactions of SS at work and stressor variables among Type A and B workers, individually. RESULTS: Except for one significant predictor, i.e., being unable to learn new things at work, the significant predictors of mental stress were generally quite different for Type A and B workers. Specifically, SS from management was a cause of mental stress for certain groups of Type A workers. CONCLUSIONS: It was revealed that the stressful aspects of work environment varied markedly in accord with the Type A vs Type B personality status of the subjects. The results also implied that even support from management can be stressful for Type A workers who had heavy workloads. The present study used specific measures sensitive to individual stressors and identified specific subgroups with the same work stressors. The findings provide information that is useful for stress reduction intervention.
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To determine the relationship between brain energy metabolites and neurologic status after ischemia-hypoxia, we measured cortical tissue levels of adenosine triphosphate (ATP), phosphocreatine, and lactate. Rats with permanent unilateral carotid occlusion were exposed to 5, 10, and 15 min of hypoxic atmosphere (FIO2 0.048) and, to examine metabolic restitution, 60 min after recovery in rats exposed to the same hypoxic mixture for 15 min. At 5 and 10 min of hypoxia, there were significant reductions in phosphocreatinine and elevations in tissue lactate, but only after 15 min of hypoxia, did ATP levels significantly decrease. By 60 min after recovery, phosphocreatinine values returned to the normal range, ATP values to 15% less than normal, and tissue lactate toward normal. In parallel survival studies, neurological status was examined following hypoxic exposure (PaO2 18 to 19 torr) for 5 an 10 min. Evidence for neurological injury in the form of posthypoxic seizures occurred at a point in time preceding significant changes in brain tissue ATP level. Since injury occurs prior to ATP reduction, changes in brain tissue ATP level may not be an appropirate endpoint for determining brain tissue injury in hypoxia.
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A patient initially diagnosed by clinical findings and pulmonary biopsy as suffering from idiopathic hemosiderosis was subsequently proven by renal biopsy and serologic assay to have Goodpasture's syndrome with minimal renal alterations. The authors speculate on the relationship of these two complex disorders.
The pathogenesis of adult polycystic kidney disease (PCKD) remains an enigma. In an attempt to find a defect that might explain the cyst formation, an ultrastructural study was performed on seven fresh bilateral nephrectomies of seven patients suffering from adult PCKD. Marked electron microscopic changes of the tubular basement membranes were detected, including thickening, splitting, fraying, and multilayering of the basement membranes. By contrast, glomerular basement membranes lacked these alterations. The kidneys from two control groups (five donor kidneys harvested for transplantation; 10 patients who suffered from end stage renal disease) showed none of the lesions detected in the polycystic kidneys. The lesions of the tubular basement membrane, the principal support of tubular wall, may be the primary phenotypic expression and cause of the inherited defect.
A case is presented of immune complex proliferative glomerulonephritis associated with peripheral eosinophilia, renal deposits of IgE, and eosinophils in glomeruli and interstitial tissue. Two sequential renal specimens are described. This study also reviews prior reports of IgE in glomerulonephritis and discusses possible explanations for the presence of IgE.
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