(1) A search for other mutations in N-RAS exon-1 in T-ALL revealed a codon 13 mutation substituting aspartic acid (GAT) for glycine (GGT) in one of 18 patients.
(2) Thus, these data physically verify the serological characteristics of GAT-TsF1 that were originally defined solely on the basis of biological activity.
(3) We found that the cell-associated form of a factor specific for L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT-TsF1) is a 66 kDa protein which exhibits a slightly acidic isoelectric point, but no carbohydrate as determined by enzymatic analysis and lectin-affinity chromatography.
(4) Thus, helper T cells can serve as the cellular target of antigen-specific, MHC-restricted GAT-TsF2, and cloned helper T cells can be used as a homogeneous target population for analysis of the molecular mechanisms of T cell suppression.
(5) The maternal defect was shown to be a frameshift mutation with the deletion of a single T in the aspartic acid codon at position 690 (GAT), 11 amino acids N-terminal to the beginning of the transmembrane domain.
(6) The small inequality tau re gat greater than tau off2 suggests that charges which have returned from immobilization are not immediately available for displacement.
(7) Simultaneous immunization in vivo with the various GAT-Mphi or GAT-MBSA plus soluble GAT modulated the response pattern of these F(1) spleen cells such that they developed secondary responses only to F(1) and parental responder GAT-Mphi regardless of the response pattern observed after immunization with the various GAT-Mphi or GAT-MBSA alone.
(8) Two clonal cell lines, Cl-3 and Cl-7, were cloned from the PC-1 cell line, and these cell lines also carried the GAT point mutation at codon 12.
(9) Body weight was affected by Ea-B, Ir-GAT, and the interaction between Ea-B and Ir-GAT, but not by interaction with RSV response.
(10) The Charity Commission, which has already opened a case against the GAT, has been told of footage obtained by ITV’s Exposure: Charities Behaving Badly documentary.
(11) These results showed that immunization of (responder X responder)F1 mice with parental GAT-M phi results in the development of antigen-specific helper and suppressor T cells.
(12) The Plowell allele was shown in one M3P heterozygous individual to be due to a GAT(Asp) to GTT(Val) change at codon 256, in agreement with a previous study based on hybridization with allele-specific oligonucleotides.
(13) T cell subsets from virgin and immunized mice, which are Ir gene controlled nonresponders to GAT, which regulate antibody responses to GAT have been characterized.
(14) When cultured in the presence of exogenous rIL-2 as a growth factor, GAT-specific Th cell lines secreted mainly IL-4, whereas bacillus Calmette Guérin-specific lines produced predominantly IL-2.
(15) Addition of GAT to cultures of spleen cells from nonresponder mice also prevents development of the GAT-specific PFC responses stimulated by GAT-MBSA.
(16) Anti-idiotypic antisera made against each of the 15 hybridoma anti-GAT antibodies preferentially bound homologous ligand and showed minimal binding activity to specifically purified serum anti-GAT antibodies.
(17) The inequality tau re gat greater than tau re Na was larger and statistically significant at -100 and -110 mV.
(18) Haplotypes with high antibody responses to GAT had significantly higher antibody titers to PM and MG vaccines than haplotypes with low antibody responses.
(19) In contrast, the Th cell line 52.3 used as control could be induced to express high levels of IL2R only after exposure to GAT; nevertheless, IL2 seems to play a critical role in the in vitro survival of the resting state of 52.3 T cells.
(20) These results suggest that posttranslational modification, including glycosylation, is not required for biological activity or for expression of the I-J epitope on the GAT-TsF2 molecule.
Git
Definition:
(n.) See Geat.
Example Sentences:
(1) Not because we are “chippy, moronic gits” (thank you, Twitter), but because we do not see the social benefit of a two-tier education system that provides a small minority with vastly more opportunities than the rest.
(2) The addition of EGF did not stimulate, but rather inhibited, the growth of HSC-1 cells in GIT medium as well as Dulbecco's modified essential medium with low concentrations of fetal calf serum (0.5-1%) in vitro.
(3) To date, 12 subjects completed two months of goal blood pressure with nifedipine GITS.
(4) Spouses of younger patients receiving atenolol reported deterioration in sexual satisfaction as compared to spouses of patients taking nifedipine GITS (P less than .02).
(5) Sixteen autistic children with WISC Performance IQs of 70 or above were analyzed to determine their conceptions of spatial relations, size comparisons, and gesture imitations through the use of the WISC, an originally devised Language Decoding Test (LDT), and a modified Gesture Imitation Test (GIT).
(6) Neurofilament immunoreactivity was not detected in normal GIT and pancreatic NE cells, whereas CR immunoreactivity was always present.
(7) In the diabetic group iv administration of idazoxan 20 min before the GIT did not alter the insulin response to the GIT.
(8) These results indicate nifedipine GITS is well-tolerated and effective as monotherapy in the treatment of severe hypertension.
(9) Disorders of postprandial reactions of the endocrine system which were specific for these nosological forms, were revealed in GIT diseases.
(10) Two methods to preserve gastrointestinal tract (GIT) organs and tissues, plastic coating (PC) and plastination (PN), were investigated and compared.
(11) This study was a randomized, complete crossover trial with 12 healthy male volunteers who were given single doses of the 24-h GITS under fed and fasted conditions.
(12) Necrotizing lesions, due to the parasite could be seen in brain, heart, lungs, pancreas, adrenal glands and testis, only intracellular trophozoites without tissue damage in GIT, liver, lymphnodes, spleen, prostate, kidney and gl.
(13) Two experiments were conducted to compare body composition, plasma concentrations of glucose, lipid and protein, gastrointestinal tract (GIT) morphology, and digestive enzyme activities among populations of chickens exhibiting wide differences in growth.
(14) Significance of this mechanism is emphasized not only for the GIT activity but as a "timer" for ultraradian rhythms as well.
(15) To evaluate differences in efficacy, safety, and quality of life, 394 male patients with mild-to-moderate hypertension were randomized to receive 20 weeks of either atenolol or nifedipine gastrointestinal therapeutic system (GITS) in a multicenter double-blind trial.
(16) The mean over-all survival time was 11.7 months (range of one to 60 months) after surgical treatment of a first metastasis to the GIT and 3.6 months (range of zero to 12 months) postoperatively for a second GIT metastasis.
(17) Forty-nine patients, with ages ranging from eighteen to seventy years and with mild to moderate primary hypertension (sitting diastolic blood pressure of greater than or equal to 95 mmgH and less than or equal to 115 mmHg) were randomized into a twenty-one-week, double-blind, prospective study to determine the effects of monotherapy of nifedipine GITS (gastrointestinal therapeutic system) versus atenolol on serum lipids, lipid subfractions, apolipoproteins, (apo), and blood pressure (BP).
(18) Thus, results from this open-label, crossover trial suggest that nifedipine GITS dosing is similar to multidose standard nifedipine with equivalent 24-hour efficacy for nifedipine GITS.
(19) Overall, nifedipine GITS significantly reduced the weekly number of anginal episodes from 5.7 to 1.8 (p = 0.0001) and the number of ischemic events from 7.3 to 4 (p = 0.0001) reported during the 48-h monitoring periods, with a significant increase in both during the placebo withdrawal period.
(20) The nifedipine-GITS (gastrointestinal therapeutic system) tablet formulation and the clonidine-TTS (transcutaneous delivery system) patch may also reduce side effects in patients while preserving the therapeutic efficacy of the origin drug formulations (nifedipie capsule, clonidine tablet).