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Biomedical subjects

L Yin

Publications and source records attributed to L Yin.

At least 145 records · Page 8Linked to original sources
PubMed1989

Diet-induced DNA damage and altered nucleotide metabolism in lymphocytes from methyl-donor-deficient rats.

Tumor induction with chronic feeding of methyl-donor-deficient diets has been well established; however, the biochemical and molecular mechanisms which predipose to tumorigenesis in this model are still not well understood. The purpose of the present investigation was to assess DNA damage and altered nucleotide metabolism in lymphocytes from Fischer 344 rats fed one of four semi-purified diets: (i) deficient in methionine and choline; (ii) deficient in folic acid; (iii) deficient in methionine, choline and folic acid; or (iv) a supplemented control diet. The accumulation of DNA-strand breaks, as assessed by DNA unwinding in alkali, was increased in lymphocytes from both the methionine/choline-deficient and folate-deficient groups, but was most severe in the group deficient in all three methyl donors. Lymphocyte DNA damage was consistently associated with alterations in folate-dependent thymidylate synthesis, and a decrease in intracellular levels of the DNA-repair-associated pyridine nucleotide, nicotinamide adenine dinucleotide. In the liver, a synergistic lipotropic interaction between folate deficiency and methionine/choline deficiency was observed, confirming the metabolic inter-relationship between these nutrients. Taken together, the results suggest that folate deficiency interacts with methionine/choline deficiency to potentiate symptoms of methyl-donor deficiency and that alterations in folate-dependent thymidylate synthesis are related to DNA damage in lymphocytes. These metabolic aberrations may contribute to immune dysfunction with chronic feeding of methyl-donor-deficient diets.

Animals↗
PubMed1989

DNA strand break accumulation, thymidylate synthesis and NAD levels in lymphocytes from methyl donor-deficient rats.

Although tumor development with methyl donor-deficient diets has been well established, the biochemical and molecular mechanisms which predispose to tumor development are not yet understood. In the present study, DNA damage and nucleotide metabolism associated with DNA synthesis and repair were evaluated in splenic lymphocytes from rats fed a basal diet low in methionine and lacking in choline and folate or a supplemented control diet for a period of 3 wk. The accumulation of DNA strand breaks, as assessed by DNA unwinding in alkali, was found to be significantly elevated in lymphocytes from rats fed the methyl donor-deficient diet and was associated with an increase in mitogen-stimulated incorporation of [3H]-thymidine via the salvage pathway for thymidylate synthesis. In addition, a significant decrease in the DNA repair-associated pyridine nucleotide, NAD, was observed in lymphocytes from the deficient group and was associated with a decrease in total spleen cell numbers. These results suggest that alterations in nucleotide metabolism and DNA damage are induced when methyl donor pools are stressed by dietary deficiency.

Animals↗
PubMed1989

[The in vitro effect of silica fibers on macrophage-mediated cytotoxic activities in mice].

The in vitro effects of silica fibers on macrophage-mediated cytotoxic activities in mice were studied, including 1) macrophage-mediated tumor cytolysis (MTC), 2) macrophage-mediated tumor cytostasis (MTCS) and 3) antibody-dependent cell-mediated cytolysis (ADCC), we found that silica fibers markedly inhibited both MTC and ADCC but slightly promoted MTCS. Silica fibers were active during the activation phase mediated by macrophage-activating factor as well as in the effector phases of MTC and MTCS. In ADCC, increasing the antibody titer could not abrogate the inhibitory effect of silica fibers.

Animals↗
PubMed1987

Examination of the clonal deletion hypothesis following transfusions in rat cardiac transplants.

To test the clonal deletion hypothesis, different levels of immunization were carried out by 0, 1, 2, or 3 transfusions preoperatively, together with 10 methods of immunosuppression. In this way, it was hoped that we could determine the optimal way to immunize and the optimal immunosuppressant treatment to deactivate the responding cells. With the Buffalo-to-Lewis rat heart allograft model, the control mean survival rate was 7 days. Rats with 2 or 3 transfusions had 5- and 12-day survival rates, respectively. If azathioprine was given in addition before grafting, 19- and 18-day survival rates were seen, and if azathioprine was given after grafting, extended survivals of 33 and 34 days were achieved. The longest survival rate of greater than 52 days was obtained by a single transfusion and 25 mg/kg/day of cyclophosphamide given before transplantation. Splenectomy following 2 or 3 transfusions prolonged survival rates to 16-18 days, suggesting that mechanical removal of immunized cells is somewhat effective. Most of the antibody produced by one transfusion was IgM, as were antibodies that resulted from transfusions followed by azathioprine. It is possible that reduction of IgG-producing cells is important. These results are consistent with the clonal deletion theory, although they do not necessarily provide final proof. The experiments suggest that the optimal transfusion effect may be obtained with minimal immunization (1 transfusion) and proper immunosuppression before transplantation.

Animals↗
PubMed1986

Cochlear implants: overview of safety and effectiveness. The FDA evaluation.

Under authority of the Federal Food, Drug, and Cosmetic Act, as amended in 1976, the Food and Drug Administration requires manufactures of new medical devices, such as cochlear implants, to demonstrate the safety and effectiveness of their devices before marketing them. This article describes the FDA review process and the kinds of data the FDA is looking for in premarket approval applications for cochlear implants. It also discusses some of the issues surrounding the premarket approval applications which have already been approved.

Clinical Trials as Topic↗
PubMed1985

Mesenteric cysts and intra-abdominal cystic lymphangiomas.

Although mesenteric cysts and intra-abdominal cystic lymphangiomas are uncommon and clinically confusing lesions, histologic and ultrastructural evidence suggests that they are pathologically distinct. Differentiation of these lesions is important since lymphangiomas may follow a proliferative and invasive course. Of 28 cases documented at laparotomy, histologically eight patients (29%) had cystic lymphangiomas and 20 patients (71%) had mesenteric cysts. Lymphangioma was found to be exclusively a disease of childhood and young adulthood (mean age, 10 years); mesenteric cyst was found in all age groups (mean age, 44 years), and two thirds of these patients were over 40 years old. Patients with lymphangiomas more frequently were male (75% vs 30%), symptomatic (88% vs 35%), and had ascites (50% vs 0%) and larger lesions (mean, 8.8 vs 4.7 cm) when compared with patients with mesenteric cysts. Complete excision was possible in all but four patients, with no operative deaths and a postoperative complication rate of 7%. After a mean follow-up period of four years, there were no recurrences among 16 patients who had undergone complete excision.

Abdominal Neoplasms↗