Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.10.2 (
focal adhesion kinase
)
44,029
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Int J
STD
AIDS 1990
Sep
PMID:AIDS Literature Index. 209 59
2405 high risk subjects (1193 patients attending
STD
clinics, 1012 blood donors and 200 hospital personnel) and 500 apparently healthy individuals representing all the twelve districts of the State of Himachal Pradesh were screened for HBs Ag employing reverse passive haemagglutination (RPHA) technique. HBs Ag positivity was found to be 6.77 per cent in test groups and 3.6 per cent in the control group. Maximum positivity was found in
STD
patients (9.55 per cent) followed by hospital personnel (8 per cent) and blood donors (3.26 per cent). The highest incidence was noticed in district Kullu and no positive case was found in Lahaul and Spiti district of Himachal Pradesh. Remedial measures for prevention of Hepatitis-B virus infection have been emphasized.
J Commun Dis 1990
Sep
PMID:Incidence of australia antigen (HBs Ag) in Himachal Pradesh. 209 21
Of 3450 women tested for antibodies to human immunodeficiency virus HIV-1 and HIV-2 between September 1985 and July 1989, 61 were positive (1.8%). Twenty-seven of these (44%) were presumed to have acquired their HIV infection by heterosexual contact and 23 (38%) were intravenous drug addicts. In geographical origin, 23 (38%) of the patients were from the UK and 19 (31%) from Africa. Amongst these 61 women, 2 (3%) have since died, one committed suicide and one was suspected of committing suicide.
Int J
STD
AIDS 1990
Sep
PMID:Risk factors of female HIV-seropositive patients attending the clinic for sexually transmitted diseases at St Mary's Hospital, London. 204 8
The effect of the currently fielded therapeutic antidotal (DRUG) combination (a cholinolytic, 2 mg of atropine sulfate, and an oxime, 600 mg of pralidoxime chloride) in combination with chemical protective Mission Oriented Protective Posture clothing (MOPP IV) was studied. Eight healthy male subjects participated in intermittent light physical activity (1.4-2.1 kcal/minute) in two distinct environments: 35 degrees C, 60% rh (95 degrees F, HOT) and 13 degrees C, 44% rh (55 degrees F, COOL). Subjects were exposed once to HOT wearing MOPP (CON) and once wearing MOPP after DRUG. Similarly, each subject was exposed to COOL wearing MOPP and MOPP after DRUG. Rectal temperature (Tre) and mean weighted skin temperature (
Tsk
) were not different between DRUG and CON during COOL. Exposure time during COOL was 350 minutes. Tre averaged .5 degrees C higher in DRUG than CON in HOT. The rate of core temperature increase was 2 times faster in DRUG than CON in HOT.
Tsk
was 1.0 degrees C higher in DRUG experiments in HOT. Whole-body sweating rate was 40% lower (p less than .05) in DRUG than CON experiments in HOT. Heart rate was 27 beats/minute higher by 30 minutes post-injection in DRUG at 35 degrees C. Exposure time was 213 +/- 30 minutes in CON and 190 +/- 38 minutes in DRUG at 35 degrees C. These data indicate the currently fielded therapeutic antidotal drug combination increases thermal strain in subjects exposed to a hot environment when wearing protective clothing. The results are applicable to subjects performing light, intermittent work. At higher work intensities, these findings of increased thermal strain would be exacerbated.
Mil Med 1990
Sep
PMID:Heat exchange after cholinolytic and oxime therapy in protective clothing. 212 Jun 21
The effect of ionizing radiation on methotrexate (MTX) resistance and gene amplification in cultured mammalian cells was investigated. X-irradiation of mouse
EMT
-6 cells induced cell killing and MTX resistance due to amplification of dihydrofolate reductase (dhfr) gene in a dose-dependent manner. The highest yields of mutant cells were obtained at approximately D37 (the dose at which 37% of the cells survive), where the frequency of MTX-resistant cells was four- to eightfold over that of the unirradiated population. The proportion of MTX-resistant cells among the survivors increased logarithmically with dose, up to a 1000-fold increase over unirradiated cells at 1000 cGy, the highest dose tested. The induced frequency of MTX resistance after X-irradiation was greater than the induced frequency of 8-azaguanine resistance, which indicates deletion of the hypoxanthine phosphoribosyltransferase gene. Inhibition of poly(ADP-ribose) polymerase by the addition of 3-aminobenzamide before irradiation increased both cell killing and MTX resistance. Metaphase spreads of chromosomes from
EMT
-6 cells that had been irradiated and subjected to stepwise increases in MTX concentration showed numerous double minutes. Pulsed-field gel electrophoresis of the DNA from cells containing radiation-induced double minutes showed that many copies of the dhfr gene were present on circular DNA molecules of 10(6), 2 x 10(6), and 3 x 10(6) base pairs. These results suggest a relationship between the induction of chromosome aberrations and the induction of gene amplification.
Somat Cell Mol Genet 1990
Sep
PMID:X-ray induction of methotrexate resistance due to dhfr gene amplification. 212 27
Over a 4-year period a total of 8974 women were screened for Neisseria gonorrhoeae and Chlamydia trachomatis. There were 489 cases of cervical gonorrhoea, 261 serogroup WI and 228 serogroup WII/III. A total of 169 (34.6%) cases had a dual infection with C. trachomatis, 92 from the WI serogroup and 77 from the WII/III. Using Fisher's exact test, no statistically significant difference was observed in the rates of chlamydial carriage between the two serogroups (P = 0.39). These findings are at odds with previously reported data, which suggested a biological interaction resulting in a positive correlation between colonization with serogroup WI and C. trachomatis. Possible reasons for the difference between the findings are discussed.
Int J
STD
AIDS 1990
Sep
PMID:Is coexisting chlamydial infection more common in gonococcal infections with serogroup WI? 212 9
Int J
STD
AIDS 1990
Sep
PMID:Diabetic ketoacidosis precipitated by primary genital herpes. 212 10
Neisseria gonorrhoeae culture gave a positive result in 42 of 64 male adults with purulent urethral discharge. The majority of the infections were acquired outside Libya. Twenty-seven strains (64.3%) were non-penicillinase producing (NPPNG) and 15 (35.7%) were penicillinase producing (PPNG) by starch paper technique. Antimicrobial susceptibility of the strains to 5 antibiotics was carried out by agar-plate dilution technique. Twenty-three NPPNG strains (54.8%) were susceptible to penicillin with a minimum inhibitory concentration (MIC) of less than or equal to 0.5 micrograms/ml. In 4 strains (9.5%), a high resistance to penicillin (MIC greater than or equal to 16 micrograms/ml) appeared to be chromosomally-mediated (CMRNG). All PPNG strains were resistant to penicillin (MIC greater than or equal to 1 microgram/ml). While resistance to erythromycin (MIC greater than or equal to 1 microgram/ml) and tetracycline (MIC greater than or equal to 1 microgram/ml) was observed in 5 strains, resistance to kanamycin (MIC 32 micrograms/ml) and spectinomycin (MIC 64 micrograms/ml) was present in only one strain. Whereas no significant differences were recorded in MICs of erythromycin, tetracycline, kanamycin and spectinomycin between NPPNG and PPNG strains, one PPNG strain was found to be resistant in vitro to all 5 antibiotics.
Int J
STD
AIDS 1990
Sep
PMID:Antimicrobial susceptibility of non-penicillinase and penicillinase-producing Neisseria gonorrhoeae strains isolated in Tripoli, Libya. 215 9
The roles of secreted and membrane-associated TNFs were investigated in activated macrophage cytolysis of L929,
EMT
-6, and P815 targets. While all three targets were susceptible to cytolysis in coculture, an anti-TNF antiserum blocked lysis of L929 and
EMT
-6 but not of the P815 targets. Of the three targets, recombinant human or mouse TNF could only lyse the L929 target; despite the fact that a role for TNF was invoked in lysis of
EMT
-6 targets in coculture, the latter was strongly resistant to soluble rTNF, even at concentrations 30-40-fold higher than the Ka for its TNF-receptor. Cytolysis of the L929 target occurred when it was cocultured with BCG-activated macrophages even when these effector cells did not secrete TNF, either due to prior chemical crosslinking or to lack of exposure to a triggering level of lipopolysaccharide. Furthermore, by introduction of the anti-TNF antiserum over a dose-range, it was shown that macrophage cytolysis both of L929 and
EMT
-6 targets occurred in the absence of bioavailable, fluid-phase TNF. Thus, even for targets susceptible to fluid-phase TNF, TNF-dependent, direct macrophage-mediated cytolysis appears to be a function independent of secreted TNF and one that utilizes effector-target contact to express the action of a membrane form of the molecule.
J Leukoc Biol 1990
Sep
PMID:Tumoricidal effector mechanisms of murine BCG-activated macrophages: role of TNF in conjugation-dependent and conjugation-independent pathways. 216 18
Activation of the c-abl protooncogene occurs in Abelson murine leukemia virus, in Hardy-Zuckerman 2 feline sarcoma virus, and during the chromosomal translocations that generate BCR-
ABL
gene fusion products. To study the molecular mechanism involved in the c-abl activation, we have created a series of modifications in murine c-abl and assayed these constructs for oncogenic activity using the NIH 3T3 cell transformation assay. Our results show that amino-terminal deletions are sufficient for oncogenic activation of c-abl and high levels of oncogenic activities were generated by a deletion of 114 codons from the 5' end that deleted the SH3 region. A deletion of 53 codons from the 5' end (inclusive of deletions seen in Hardy-Zuckerman 2 feline sarcoma virus and BCR-
ABL
gene products) that retains the SH3 region of c-abl resulted in the generation of low levels of transforming activity. This transforming potential was substantially increased with the introduction of a G----A point mutation in codon 832 that is present in v-abl. The point mutation was found to affect the secondary structure and the tyrosine kinase activity of the mutant gene products.
Proc Natl Acad Sci U S A 1990
Sep
PMID:Activation of murine c-abl protooncogene: effect of a point mutation on oncogenic activation. 216 50
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