[Occurrence of oral trichomonads (Trichomonas tenax) in subgingival plaque materials].
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Biomedical subjects
Publications and source records attributed to M Shiraki.
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In order to clarify role of lpr gene of MRL/Mp-lpr/lpr (MRL/l) mice in the development of immunological abnormalities and lupus nephritis, F2 mice were obtained from crosses of (MRL/1 X AKR) F1 mice and examined with regard to lymph node enlargement, numbers of immunoglobulin (IgM and IgG) producing cells (PC) in the spleen, serum levels of anti-trinitrophenyl (TNP) and anti-DNA antibodies, amounts of circulating immune complexes (IC) and histopathological findings of the kidney. Out of total numbers of 234 F2 mice, 54 mice (F2[+]mice) (23.1%) were with lymphoproliferation and 180 mice (F2[-]mice) (76.9%) without it. As parental controls, 39 MRL/1, 27 AKR and 21 F1 mice were also checked. There were significant differences in the all of the parameters tested between F2 (+) and F2 (-) mice. Significant differences were also observed between F2 (+) and MRL/l mice in the weight of mesenteric lymph nodes, numbers of IgGPC, levels of IgG antibodies and amounts of IC, but not in the numbers of IgMPC and levels of IgM antibodies. All of F1 mice tested mimicked AKR mice in the values of various parameters described above. In MRL/l and F2 (+) mice, there were no significant correlations between the weight of mesenteric lymph nodes and other parameters. These data seem to show that the lpr gene behaves as a single recessive trait and there exists gene(s) which suppresses expression of the lpr gene.
The effects of a growth hormone releasing factor, human pancreatic growth hormone releasing factor-44 (hpGRF-44), on growth hormone (GH) secretion in calves, heifers and cows were studied. A single intravenous (iv) injection of 0.1, 0.25, 0.5 or 1.0 microgram of synthetic hpGRF-44 per kg of body weight (bw) in calves significantly elevated the circulating GH level within 2-5 min, while no increase in plasma GH was observed in saline injected control calves. The plasma GH level increased proportionally to the log dose of hpGRF-44, and reached a peak at 5-10 min (p less than 0.01). Subcutaneous injection of hpGRF-44 also elevated the plasma GH level, but the peak value at 15 min was 37% of that of iv injection (p less than 0.05). Intravenous injection of 0.25 microgram of hpGRF-44 per kg of bw to female calves, heifers, and cows significantly elevated mean the GH levels from 8.5, 2.3, and 1.6 ng/ml at 0 time to peak values of 97, 26, and 11.6 ng/ml, respectively (p less than 0.01). The plasma GH response and basal level in calves were significantly higher than those of heifers or cows (p less than 0.025). The plasma GH response to hpGRF-44 as well as the basal level decreased with advancing age. The plasma GH response to hpGRF-44 and basal GH in male calves were significantly greater than those in female calves (p less than 0.001). These results indicate that synthetic hpGRF-44 is a potent secretogogue for bovine GH, and suggest its usefulness in the assessment of GH secretion and reserve in cattle.
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Weekly injection of cyclophosphamide (Cy) into MRL/Mp-lpr/lpr (MRL/l) mice, at a dose of 10-20 mg/kg, from 1 month of age prevented the development of generalized lymph node enlargement, decreased serum levels of anti-DNA antibodies and immune complexes, and markedly prolonged their life span. Cy effectively suppressed enhanced differentiation of B cells, as evidenced by decreased number of immunoglobulin secreting cells in the spleen. Cy was also shown to suppress abnormal expansion of Thy-1 positive cells in lymphoid organs of MRL/1 mice. These results suggested that Cy prevented the development of murine lupus like syndrome in MRL/1 mice through suppression of spontaneous polyclonal B cell activation and also by reducing the number of T cells to exert excessive helper activity on B cells.
Weekly injections of cyclophosphamide (Cy) at a dose of 20 mg/kg body weight prevented IgM to IgG class switch of serum anti-DNA antibodies and also immunoglobulin secreting cells in the spleen of MRL/Mp-lpr/lpr (MRL/1) mice. Culture experiments revealed that splenic B cells of Cy treated mice gave rise to more IgM and less IgG secreting cells than those of untreated mice in response to lipopolysaccharide. These results suggested that Cy suppressed enhanced differentiation of B cells into IgG secreting cells in MRL/1 mice, which would result in reduction of IgG anti-single stranded DNA antibodies and improvement of murine lupus like syndrome.
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Thromboxane A2 has been implicated in thrombotic vascular diseases. The diabetic population has a high incidence of vascular complications. In the present study, activity of thromboxane synthetase in platelets of type 2 (non-insulin dependent) diabetic patients was studied. Thromboxane synthesizing activity in diabetic platelets was significantly higher than that in controls (p less than 0.05). An effect of dietary arachidonic acid on thromboxane synthesizing activity in platelets was also studied. Dietary arachidonic acid supplementation containing 1.7g of arachidonic acid per day for 1 week caused a significant increase of arachidonic acid content in plasma total lipids (p less than 0.05), but the increase of arachidonic acid in plasma total lipids did not correlate with the level of arachidonic acid in platelet phospholipids. Thromboxane synthesizing activity in platelets from the diabetics and the controls was augmented by a diet enriched in arachidonic acid from 2.20 +/- 0.15 to 2.56 +/- 0.20 and from 1.71 +/- 0.23 to 2.01 +/- 0.34, respectively. The increase in diabetic subjects was statistically significant (p less than 0.05). These results suggest that fatty acids of dietary origin are important factors in development of thrombotic vascular diseases.
Two-month old MRL/1 mice, which spontaneously develop lymphoproliferative syndrome and severe lupus nephritis at 4-5 months of age, were irradiated and reconstituted with bone marrow cells from a congenic strain MRL/n mice. In the chimeric (n----1) mice, the early onset of the lupus nephritis was prevented as evidenced by decrease in the degree of proteinuria, diminished intensity of immune deposits in glomeruli, and milder histopathologic changes in kidneys. Lymph node swelling as well as generation of a large number of splenic IgSC was also prevented. Anti-ss DNA antibody response in the chimeric mice, however, varied tremendously from one animal to another.
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Cryostat sections of the liver representing fulminant B-viral hepatitis were investigated with antisera against human immunoglobulin G(IgG), immunoglobulin M(IgM), C3, C4, C1q, hepatitis B surface antigen (HBsAg), and T-lymphocytes using the immunofluorescence and immunoperoxidase techniques. The liver showed positive staining for IgG, IgM, C3, C4, C1q, and HBsAg in the viable and necrotic hepatocytes and Kupffer cells in a granular fashion. Furthermore, the cell membrane of lymphocytes present in the liver were positively stained with anti T-lymphocyte sera. The numbers of T-lymphocytes recognized were predominant both in portal tracts and within hepatic lobules over those of non-T-lymphocytes. It suggests that perhaps some of the end results of fulminant hepatitis inflammatory reactions may be mediated in part by T-lymphocytes.
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