Hematuria and Legionella pneumonia.
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Biomedical subjects
Publications and source records attributed to S H Feinsilver.
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Tyrosine hydroxylase and tryptophan hydroxylase are widely held to be rate-limiting for the synthesis of the catecholamines and serotonin, respectively. Both enzymes are oxygen-requiring and kinetic properties suggest that oxygen availability may limit synthesis of these neurotransmitters in the brain. Using pheochromocytoma cells as a cell culture model for catecholamine synthesis, and neuroblastoma cells as a model for serotonin synthesis, enzyme activity was measured under control and hypoxic conditions. Both tyrosine hydroxylase and tryptophan hydroxylase activity increased substantially with chronic exposure but not with acute exposure. In the case of tyrosine hydroxylase, increased enzyme content with hypoxia accounts for increased activity. This suggests a mechanism for the maintenance of neurotransmitter synthesis with chronic hypoxia. Measurement of intracellular metabolites revealed no change in dopamine or norepinephrine in hypoxic pheochromocytoma cells, consistent with a simple adaptive mechanism. However, in neuroblastoma cells, hypoxia was associated with an increase in serotonin concentration. The reasons for this are still unclear.
Nonresolving pneumonia is a common and frequently misunderstood problem faced by the practicing pulmonologist. While radiographic resolution of most infections is relatively long and lags behind clinical signs of recovery, data suggest that a variety of host defense problems are a consequence of systemic illness and are often involved. When such factors are not implicated, other specific etiologies should be sought, including unusual organisms like mycobacteria, higher order bacteria, and fungi. Noninfectious causes for delayed resolution include neoplastic disease, immunologic disease, thromboemboli, and inhalation injuries. This article discusses the natural history of common pneumonias to establish the usual clinical limits of resolution and outlines a diagnostic strategy to use when these limits are exceeded.
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We reviewed our experience with fiberoptic bronchoscopy (FOB) in patients with pleural effusion of unknown origin. Seventy patients underwent FOB for the investigation of pleural effusion between 1978 and 1983. Those with a second reason for FOB, a mass on chest roentgenogram, or lobar atelectasis were excluded. Forty five patients remained: 28 patients with unexplained pleural effusion after pleural fluid analysis and pleural biopsy (UPE), and 17 patients with malignant pleural fluid cytology and/or pleural biopsy but no known primary tumor (MPE). In the UPE group, only one FOB demonstrated malignancy, despite a final diagnosis of tumor in seven. No other specific diagnoses were made by FOB in this group. In the MPE group, FOB demonstrated bronchogenic carcinoma in two; ultimately, five patients were found to have a bronchogenic neoplasm. Although pleural effusion of unknown origin is frequently caused by bronchogenic carcinoma, FOB in the absence of other indications for this procedure is rarely diagnostic and should not be routinely employed.
A well-documented case of acquired immunodeficiency syndrome (AIDS) with diffuse lymphadenopathy and disseminated mycobacteriosis in whom serial Ga-67 studies were performed is presented.