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Biomedical subjects

R Wada

Publications and source records attributed to R Wada.

At least 163 records · Page 9Linked to original sources
PubMed1980

Equine Getah virus infection: isolation of the virus from racehorses during an enzootic in Japan.

A primary enzootic of equine Getah virus infection involving 722 of 1,903 racehorses occurred at a training center in Japan between September and November of 1978. Sixty-two viral agents were isolated from the plasma of 209 sick horses which exhibited pyrexia with rectal temperatures ranging from 38.5--40 degrees C, urticarial rash on various portions of the body, and edema of the hind legs. The viruses were antigenically related to the AMM 2021, Haruna, and Sagiyama strains of Getah virus. Infection and disease were produced experimentally in horses when inoculated by the intramuscular or intranasal routes.

Alphavirus↗
PubMed1980

Clinicopathologic consideration of protein-losing enteropathy due to lymphangiectasia of the intestine.

The pathogenesis of intestinal lymphangiectasia and mechanism of enteric loss of serum protein has been discussed from the pathologic and roentgenologic viewpoints of the two patients with this disease. Enteric loss of serum protein was attributed to exudation of lymph from ruptured lymphatic vessels, resulting from non-specific multiple ulcers of the small intestine in one patient and malrotation of the gut in another.

Adult↗
PubMedDate not supplied

Effects of long-term treatment with alpha-glucosidase inhibitor on the peripheral nerve function and structure in Goto-Kakizaki rats: a genetic model for type 2 diabetes.

BACKGROUND: Continuous hyperglycemia is implicated in the pathogenesis of chronic diabetic complications. It is not well known, however, how and to what extent the development of neuropathy is inhibited by blood glucose control in subjects with Type 2 diabetes. We investigated therefore the effects of an alpha-glucosidase inhibitor (voglibose; Vg) on neuropathic changes in diabetic Goto-Kakizaki (GK) rats, a genetic model for Type 2 diabetes. METHODS: Twelve week-old male GK rats were given a diet containing Vg (50 ppm) for 24 weeks and monitored for blood glucose, glycated hemoglobin, motor nerve conduction velocity (MNCV). At the end of the administration period (Na(+), K(+))-ATPase activity and the structure of the peripheral nerves were examined. Age- and sex-matched normal Wistar rats were treated similarly and served as controls. RESULTS: GK rats showed fasting hyperglycemia after 8 weeks of age, and Vg treatment significantly lowered levels of blood glucose and glycated hemoglobin. Slowing of MNCV to 80% of normal control levels was detected in GK rats. Vg treatment inhibited this delay by 24% at 24 weeks and 57% at 36 weeks of age. Nerve (Na(+), K(+))-ATPase activity was reduced to 80% of normal control levels in GK rats and was restored by Vg treatment. Teased fiber studies revealed a higher incidence of fibers with paranodal, segmental demyelination and axonal degeneration in GK rats. Vg treatment significantly inhibited the development of these nerve-fiber abnormalities. CONCLUSIONS: Lowering of high blood glucose levels achieved by the use of Vg in GK rats improved MNCV and demyelinative nerve changes with restoration of (Na(+), K(+))-ATPase activity.

Animals↗