Gastric ulcer: effect of healing on gastric acid secretion and fasting serum gastrin levels

In 15 patients with uncomplicated gastric ulcers, basal and peak gastric acid outputs and fasting serum gastrin levels were studied before and after healing. The mean basal acid output [4.0 +/- 1.3 (SEM) mEq H+/hr], the mean peak acid output (29.5 +/- 5.1 mEq H+/hr), and the mean fasting serum gastrin level (80.3 +/- 16.7 pg/ml) in these patients did not change significantly with healing. Failure of gastric secretory function to change with healing suggests that mucosal resistance factors are more important than gastric acid secretion in the pathogenesis of a gastric ulcer.     

Pulmonary tuberculosis in a sulfur-crested cockatoo

An adult, female sulfur-crested cockatoo (Kakatoe sp) was examined because of dyspnea associated with hemoptysis. On radiographic examination there was a large cystic pulmonary mass that, on aspiration, was found to contain thick sanguineous fluid. Ziehl-Neelsen staining of aspirate smears revealed numerous acid-fast organisms. Gross necropsy and microscopic findings suggested a diagnosis of tuberculosis, with primary focus of infection in the pulmonary tissues. Bacteriologic isolation and typing confirmed a diagnosis of tuberculosis and established Mycobacterium avium as the etiologic agent.     

Inheritance of acridine orange R variants in human acrocentric chromosomes

A case is reviewed of bilateral temporal bone metastases from a carcinoma of the uterine cervix. The pertinent literature is reviewed and the temporal bone histology is described.     

Immunochemical detection of human enzymes in hybrid cells

Maximal expiratory flow rate (Vmax) was measured at 20, 35, 50, 65, and 80% vital capacity in 4 young healthy subjects breathing air, SF6/O2, and He/O2 mixtures. The flows of SF6/O2 and He/O2 were corrected to normal alveolar gasflow by means of only the density of the gases. The values for normal alveolar gasflow and corrected SF6/O2 flow were identical at 35% VC and larger volumes while the values for normal alveolar gasflow and corrected He/O2 flow were not. The results indicate that in young healthy subjects it is possible to correct Vmax at lung volumes above 35% VC for the changes induced by an increase in density of the gas breathed, provided viscosity is not much changed. Without correction, Vmax after O2-breathing will be underestimated by about 6%, compared with Vmax for normal alveolar gas, whereas a change in alveolar CO2 concentrations between 3 and 9% only causes a 1% decrease of Vmax.