Showing papers on "Meth- published in 1980"

Long-term effects of multiple doses of methamphetamine on tryptophan hydroxylase and tyrosine hydroxylase activity in rat brain

Abstract: Tryptophan hydroxylase (TPH) activity was measured in various rat brain regions after administering large doses of methamphetamine (METH). After four sequential doses of METH (15 mg/kg), given every 6 hr, TPH activity was decreased (to approximately 10% of control) in both the neostriatum and hippocampus. The depression of enzyme activity persisted for at least 30 days. When compared with the depression of neostriatal tyrosine hydroxylase activity, the depression of neostriatal and hippocampal TPH activity occurred sooner and was more pronounced. The depression of TPH activity was dependent on the number of doses and the amount of drug administered. Five days after one to two doses of METH, a transient recovery was observed but when four doses were given, the enzyme was depressed. No decrease in TPH activity was observed in brain areas containing serotonergic cell bodies. Agents which prevent the METH-induced decrease of neostriatal tyrosine hydroxylase activity, i.e., haloperidol, alpha-methyl-p-tyrosine and gamma-aminobutyric acid transaminase inhibitors also prevented the decrease in TPH activity caused by METH. In addition, fluoxetine, an inhibitor of 5-hydroxytryptamine re-uptake, prevented the METH-induced decrease in neostriatal and hippocampal TPH activity but did not alter the decrease in nenostriatal tyrosine hydroxylase activity.

T-cell-mediated suppression of anti-tumor immunity. An explanation for progressive growth of an immunogenic tumor.

Abstract: The results of this paper are consistent with the hypothesis that progressive growth of the Meth A fibrosarcoma evokes the generation of a T-cell-mediated mechanism of immunosuppression that prevents this highly immunogenic tumor from being rejected by its immunocompetent host. It was shown that it is possible to cause the regression of large, established Meth A tumors by intravenous infusion of tumor-sensitized T cells from immune donors, but only if the tumors are growing in T-cell-deficient recipients. It was also shown that the adoptive T-cell-mediated regression of tumors in such recipients can be prevented by prior infusion of splenic T cells from T-cell-intact, tumor-bearing donors. The results leave little doubt that the presence of suppressor T cells in T-cell-intact, tumor-bearing mice is responsible for the loss of an earlier generated state of concomitant immunity, and for the inability of intravenously infused, sensitized T cells to cause tumor regression. Because the presence of suppressor T cells generated in response to the Meth A did not suppress the capacity of Meth A-bearing mice to generate and express immunity against a tumor allograft, it is obvious that they were not in a state of generalized immunosuppression.

Immunogenic Properties of Soluble Cytosol Fractions of Meth A Sarcoma Cells

Abstract: Tumor-associated transplantation antigen (TATA) was found to be present in fractions derived from the cytosol of the Meth A cell. Meth A ascites cells were disrupted, nuclei and membranes were removed by low- and high-speed centrifugation, and the soluble protein was fractionated by ammonium sulfate precipitation and gel filtration chromatography. The TATA of the soluble cytosol fractions appears to be identical with the TATA solubilized from plasma membranes. The TATA of the cytosol fractions was found to be associated with proteins of an approximate apparent molecular weight of 60,000, specific for the Meth A tumor, and as immunogenic as the membranederived TATA. In addition, the most enriched TATA cytosol fraction shows inhibition of an antiserum capable of detecting a tumor-specific surface antigen of Meth A. These results suggest that Meth A TATA is not an integral membrane protein and may be related to the tumor-specific surface antigen detected serologically.

Refrigeranttresisting*lowwsmelling* solventtfree varnish composition

Abstract: PURPOSE:Title composition, excellent in refrigerant-resisting property, and giving cured insulation texture, composed of a (meth)acrylate-modified epoxy resin, a (meth)acrylate-modified polybutadiene, an aliphatic long-chain (meth)acrylate and a vinyl monomer. CONSTITUTION:(A) 25-50pts.wt. of a (meth)acrylate-modified epoxy resin obtained from the reaction of 1mol of bisphenol A glycidylether-type epoxy resin of expoxy equivalent 180-1,000, with 0.8-1.2mol of (meth)acrylic acid, (B) 5- 30pts.wt. of a (meth)acrylate-modified polybutadiene obtained from the reaction of 2-hydroxyethyl (meth)acrylate of acid value 20-120, with a maleinized polybutadiene, (C) 5-20pts.wt. of an aliphatic long-chain (8-20C)(meth)acrylate, (D) 20-55pts.wt. of a liquid copolymerizable vinyl monomer of high boiling point (>=90 deg.C/10mm.Hg) and (E) 0.1-3.0pts.wt. of a polymerization catalyst, such as benzoyl peroxide, are mixed.

Transparent high polymer with oxygen permeability

Abstract: PURPOSE:To obtain a (meth)acrylate ester polymer for use as contact lens, having improved oxygen permeability, cutting processing characteristics, and dimensional stability, by blending specific amounts of specified (meth)acrylate, which are afterwards polymerized. CONSTITUTION:A (meth)acrylate ester polymer comprising 20-100wt% of at least one selected from the group consisting of (meth)acrylates shown by the formulae I, II, and III (R1 is H or methyl; R2, R3, and R4 are H or 1-6C atomic group; R5, R6 and R7 are H or hydrocarbon ; R8, R9, and R10 are H or hydrocarbon)as a repeating unit. A) 20-100wt% of the (meth)acrylate ester, B) 0-80wt% of methyl (meth)acrylate, and if necessary, C) 0.5-20wt% of hydroxyl group-containing (meth)acrylate are polymerized, for example, in the presence of a peroxide under heating, to give the desired high polymer.

Characterization of the responding populations for the generation of proliferative response to syngeneic Meth A tumor in BALB/c mice: requirement of T and B cell collaboration.

Abstract: High levels of primary proliferative response to a chemically induced sarcoma Meth A can be induced in syngeneic BALB/c spleen cells. Testing at the peak of proliferative response (2 days after sensitization in the mixed lymphocyte tumor cell culture), we found the responders to be resistant to anti-Thy 1.2 antibody lysis but susceptible to anti-Ia antibody lysis. When responders were subjected to various treatments before sensitization, it was found that removal of macrophages had no effect on the generation of proliferative response; high levels of proliferative response could be induced in enriched B cell preparations and in spleen cells from nude mice, but there was only a negligible amount of response in enriched T cell preparations. These findings indicate that the responders are primarily B lymphocytes. However, it was also found that the enriched B cell preparations usually gave only 50 to 75% of the response of whole spleen cells, whereas these B cells gave a 2- to 3-fold increase in the response to a B cell mitogen, LPS; this result indicate that collaboration from other types of lymphocytes was required for the generation of an optimal proliferative response to Meth A. Addition of 10% of T cells indeed produced a helper effect on this B cell response, and the maximal helper effect was seen for a mixture containing equal parts of T cells and B cells or for a slight T cell excess. These results indicate that the proliferative response to a syngeneic Meth A tumor is a macrophage-independent T-dependent B cell response.