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Biomedical subjects

V Kumar

Publications and source records attributed to V Kumar.

At least 847 records · Page 47Linked to original sources
PubMed1978

Prevalence and severity of tooth attrition in Nigerians in rural areas.

A study of the prevalence and severity of attrition in both anterior and posterior teeth has been conducted in two rural communities in Nigeria. 5984 teeth in 190 subjects were examined. Age range of the subjects was from 15-55 years and 58.9% of them were male, while 41.1% were female. The number of subjects with little or no attrition increased with increasing age while varying degrees of severity of attrition increased with increase in age. Attrition was more marked in the mandibular teeth (56.52%) than in the Maxilla (46.71%). The first molar was the most consistently attrited and since tooth attrition can be a cause of neuralgia in the oral region, dentine exposure due to severe attrition should be considered in the differential diagnosis of pain in and around the mouth.

Adolescent↗
PubMed1978

Chemotherapy of helminthiasis among wild mammals. IV. Efficacy of flubendazole 5% (R17889) against Trichuris trichiura infection of baboons, Papio hamadryas L.

Flubendazole 5%, a parafluor analog of benzimidazole derivative, mebendazole, was found efficient in eliminating Trichuris trichiura infection of baboons when administered orally at a dose rate of 27 to 50 mg of the active ingredient per kg body weight twice daily for five days. The drug was found safe, without toxic effects and its palatability was excellent.

Animal Diseases↗
PubMed1977

Periodontosis.

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Humans↗
PubMed1977

Host response to Treponema pallidum infection. I. Quantitative changes of lipids in rabbit organs.

Levels of phospholipids, glycolipids and cardiolipin were determined in various organs of Treponema pallidum-infected rabbits. The phospholipid levels on the second week of infection decreased significantly in the spleen but remained unchanged in other organs. During the same time, glycolipids decreased significantly in both kidney and heart. 3 days after infection, a brief but significant increase of cardiolipin in the spleen was observed. Heat-killed T. pallidum but not Treponema reiteri caused a similar effect. The possible implication of these changes in the immunopathology of syphilis is discussed.

Animals↗
PubMed1976

Mechanisms of genetic resistance to Friend virus leukemia in mice. II. Resistance of mitogen-responsive lymphocytes mediated by marrow-dependent cells.

Friend leukemia virus suppresses the proliferative responses of normal thymus-dependent (T) and bursa equivalent-dependent (B) lymphocytes from spleen, thymus, lymph node, and bone marrow to mitogens. The suppressive effect of Friend virus complex (FV) requires fully infectious virions. Friend erythroleukemic cells, washed to removed extracellular virus, fail to suppress concanavalin A (Con-A)-induced mitogenesis of normal spleen cells. This indicates that FV does not mediate its immunosuppressive effect via transformed erythropoietic cells. The in vitro suppressive effect of FV on lymphocyte mitogenesis is under host genetic control. Spleen, bone marrow, and thymus cells from strains of mice susceptible to FV-induced leukemogenesis in vivo were quite susceptible to the suppressive effects of FV in vitro. On the other hand, similar cells from strains of mice such as C57BL/6 resistant to Friend erythroleukemia, were quite resistant to in virto immunosuppression by FV. Mitogenesis of splenic T cells from resistant B6 mice, previously treated with 89Sr, became susceptible to suppression by FV. This indicated that the in vitro resistance of lymphocytes to FV-induced suppression is not an intrinsic property of T cells, but is controlled by marrow-dependent (M) cells which are selectively eliminated by treatment with 89Sr. M-cell function does not develop in mice less than 3-wk old. The Con A response by thymus cells from 2-wk-old B6 mice was susceptible to suppression by FV, further supporting the concept that M cells may regulate the genetic resistance to FV.

Age Factors↗