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Biomedical subjects

S Kuroda

Publications and source records attributed to S Kuroda.

At least 451 records · Page 25Linked to original sources
PubMed1975

Studies on complement-fixation reaction in equine infectious anemia. II. Identification of complement-fixing inhibitors.

The substances responsible for inhibiting complement-fixation (CF) reaction of the late-stage serum of an equine infectious anemia (EIA)-infected horse were investigated. It was found that the IgG and IgG(T) classes in the late-stage serum were responsible for the CF inhibition. IgA could not be detected in partially purified IgG(T) by an immunodiffusion test using rabbit anti-human IgA serum. Other serum components could not be demonstrated in purified IgG by immunoelectrophoresis using rabbit anti-horse serum. The IgG class simultaneously showed CF and CF-inhibiting (CFI) activities, whereas the IgG(T) class showed only CFI activity. The IgG(T) class could exert CFI activity only when it had been reacted with the EIA antigen before addition of the reference CF serum and complement. In contrast, the IgG class converted the CF-active reference serum into a non-CF-reactive one irrespective of whether it was simultaneously reacted with the EIA antigen and the reference CF serum, whether it was added to the reaction mixture of the EIA antigen and the reference CF serum, or whether it was sensitized with the EIA antigen before addition of the reference CF serum. Inhibitory activities of the IgG and IgG(T) classes seemed to be different from each other in their reaction pattern as far as tested under our experimental conditions. Their CFI activities seemed to be specific for EIA, being negative in CFI activity in reaction with other antigens.

Animals↗
PubMed1975

Neurotoxicity with chloramphenicol--an electron microscopic study.

The peripheral nerve and spinal ganglion of chloramphenicol-administered and normal animals were examined mainly with the electron microscopy. The experimental animals consisted of three dogs and one rabbit. They were highly injected or given orally high doses of chloramphenicol with a duration from 70 to 130 days. Pathological finginds were briefly summarized as follows. In the sural nerve the changes in myelin sheaths and Schwann cells were more prominent than those in axons. The myelin sheaths were swollen and had a tendency to be curled and compress the azon in some fibers. Other fibers showed the degeneration of myelin sheaths, revealing fragmentation, thinning, and honeycomb structure. The changes in axons were mild, showing an increase of neurofilaments and local accumulation of mitochondria. Schwann cells were often hypertrophied and abundant endoplasmic reticula, vacuoles and ribosomes were observed in the cytoplasm. The processes of Schwan cells were not active, but the picture that a myelinated fiber was surrounded by some processes of Schwann cells was seen in some occasions. In the posterior root ganglion at the lumbar cord, some of nerve cells showed changes, such as breakdown of Nissl substance, swollen mitochondria and indentation of nuclear membrane. The satellite cells showed no significant change.

Animals↗
PubMed1975

Neurotoxity of iodoxyquinoline: a further study on beagle dogs.

Eight beagle dogs were treated orally with iodoxyquinoline (chinoform, clioquinol) again, and all of them manifested similar neurologic symptoms to those observed in our previous experiments on mongrel dogs, beagle dogs, cats and a monkey. The neurologic symptoms were identical both clinically and pathologically with those of subacute myelo-optico-neuropathy (abbreviated to SMON) in man. In the present study, the neurologic manifestations evolved with less total chinoform doses (5.1-13.8 g/kg) in shorter periods (19-47 days) and there was no difference between each group on the increasing dosage and on fixed dosage. It is discussed in the present paper that onset of the neurologic symptoms is associated with unconjugated chinoform levels in the blood.

Administration, Oral↗
PubMed1974

Morphologic evidence to support the role of tubular leakage as a cause of anuria induced by meercury poisoning.

The qualitative Hanssen technic was used to study the mechanism of anuria produced in rabbits by mercury poisoning. Twenty-four to 30 hours after intravenous injection of a low dose of HgCl(2), the animals were almost completely anuric. Sodium ferrocyanide injected intravenously was visualized as Prussian blue in essentially all glomeruli in anuric kidneys, and the amount of the dye in the glomerular tufts was almost the same as in control kidneys. Thus there was no evidence for a severe reduction in glomerular capillary blood flow. Besides, the distribution of Prussian blue in tubular lumina indicated that the anuria occurred in the presence of a significant glomerular filtration. Tubular walls of the anuric kidneys showed an abnormally increased permeability to sodium ferrocyanide. These findings suggested that the anuria during this stage was caused more by tubular leakage than by intrarenal vasoconstriction and subsequent cessation of glomerular filtration.

Animals↗