[The studies on the serum Ig levels in patients with pulmonary tuberculosis (author's transl)].
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Biomedical subjects
Publications and source records attributed to Y Fukuda.
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This is a case report of a 35-year-old female who showed a relatively short clinical course of severe liver cirrhosis and proteinuria. On light microscopical studies of autopsy material, besides active postnecrotic type liver cirrhosis, typical membranous glomerulonephritis was found. Immunofluorescent study disclosed not only clustered HBsAg (hepatitis type B surface antigen) in occasional hepatic cells but also beaded granular type deposition of HBsAg, IgG, IgM, IgA and complement C3 along renal glomerular basement membrane (GBM). Electron microscopical study disclosed multiple particulated material in occasional inclusion bodies of hepatic cells and in subepithelial and subendothelial dense deposits along the GBM. Enzymatic immunoelectron microscopical study confirmed these particles especially along the GBM being HBsAg themselves. It was concluded that HBsAg-Ab (antibody) complex was the pathogenetic factor responsible for the glomerular change of this particular case. Although HBsAg and Ab were examined to be negative in serum throughout the patient's clinical course, the possibility of the presence of circulating HBsAg-Ab complex in serum was discussed.
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The effects of diazepam, clomipramine, and chlorpromazine upon cerebral metabolism and blood flow were examined separately in 18 dogs. After the administration of diazepam or clomipramine, cerebral cortical oxygen consumption (CMRO2) decreased significantly by a maximum of 17% and 13% of control within 10 minutes and 15 minutes, and returned to control at 120 minutes and 90 minutes, respectively. Chlorpromazine, however, decreased by a maximum of 10% of control, a level which continued throughout the period of observation. It was observed that reduction in CMRglucose was followed by the reduction in CMRO2 at an interval during the early stages of CMRO2 depression. Diazepam produced a significant decrease in CBF accompanied by reduction in CMRO2, but neither clomipramine nor chlorpromazine had any effect on CBF in spite of reduction in CMRO2. Reduction in CMRO2 both with diazepam and clomipramine was accompanied by slow wave activities of EEG, but with chlorpromazine reduction in CMRO2 was accompanied with less pronounced slow wave activities. It was concluded that the three drugs examined were cerebral metabolic depressants.
In the lateral geniculate body (LGB) of urethane-anesthetized and Flaxedil-immobilized rats, unit responses of principal cells (P-cells) were recorded by using flash stimulation of the eyes. By measuring response latencies to electrical stimulation of the optic tract, all P-cells were classified into the fastor slow group according to the criterion established by Fukuda. Flash-evoked unit responses consisted of the two kinds of discharges, i.e. the early discharge (ED) with latencies less than 100 msec and the late discharges of spike burst (LDs) often recurring twice or more (LD1, LD2 and so on). Cells' firings were suppressed during the interval between ED and LD1 and those between successive LDs. The ED- and LD1-latencies, measured in dark with strong flashes, were shorter in the fast cells than in the slow one. The interval between ED and LD1 was shorter in the fast cells than in the slow ones. It was common to the both types of P-cells that as flash intensity was reduced, the ED-latency increased and the LD1-latency decreased. However, the ED-LD1 interval remained shorter in the fast cells than in the slow ones. Upon shifting from dark to light, the LD1-latency markedly increased or decreased in the slow cells, whereas such was not seen in the fast cells. These findings seem to provide a further support for the classification of P-cells into the fast and slow types.
The calcium content and inulin space of the atrial and ventricular muscle were determined in isolated perfused heart of the toad, bullfrog, guinea pig, rat, and cat. In all species studied, the total and "cellular" calcium content of the atrium were higher than those of the ventricle. A high calcium content of the atrial muscle was also observed in fresh unperfused hearts. The total calcium content of atrial and ventricular muscles increased when extracellular phosphate concentration was increased. When severe ventricular arrhythmia such as fibrillation occurred during perfusion, the total calcium content of the ventricle increased. The decay of tissue calcium content with calcium washout was examined in the toad, guinea pig, and rat heart. It was revealed that about 80 percent of total calcium existed as "exchangeable" calcium in both atrial and ventricular muscles. When the extracellular calcium concentration ([Ca]o) was altered in the toad, guinea pig, and rat heart preparation, the cellular calcium content of atrial muscle varied in proportion to [Ca]o, whereas that of ventricular muscle remained fairly constant at a higher [Ca]o value. The development of contractile tension in the atrial and ventricular muscles at various [Ca]o values corresponded well to these changes in the cellular calcium content except for the rat ventricle in which the contractile tension was almost proportional to [Ca]o. The relationship between the development of contractile tension and the level of cellular calcium content or [Ca]o was discussed.
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