Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.10.2 (focal adhesion kinase)
 44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have investigated the role of L-arginine in macrophage tumor cytotoxicity in coculture. L929, EMT-6, MCA-26, and P815 targets were all susceptible to cytolysis by activated macrophages when cocultured in medium containing L-arginine. When cocultured in arginine-free medium, these targets displayed comparable or even higher levels of lysis. L1210 targets were lytically resistant under either condition. However, 59Fe release from this target did reflect strong dependence on the presence of arginine. The structural analogue, NG-monomethyl-L-arginine, was an effective inhibitor of iron-release from L1210 targets cocultured with activated macrophages, whereas it had minimal inhibitory effects on release of 51Cr from cocultured L929 cells. These results suggest that the L-arginine requiring cytotoxic pathway of activated macrophage is independent of major effector mechanisms involved in tumor cell lysis.
Biochem Biophys Res Commun 1989 Dec 29
PMID:L-arginine independent macrophage tumor cytotoxicity. 269 64

The cause of detrusor instability and mixed incontinence remains elusive. Although DI is most prevalent at the extremes of age, GSI becomes more common with aging and child bearing, and therefore mixed incontinence is common, especially after menopause. Cystometry is used to diagnosis detrusor instability, but urethral closure pressure profilometry is required for assessment of mixed incontinence. DI is managed initially by behavioral therapy, and if this is not satisfactory then FES should be used depending upon availability. Drug therapy should start with oxybutynin at 2.5 to 5 mg twice-daily and increased as necessary to control symptoms. If the effects of therapy are minimal or side effects are too great, other medications or medication combinations should be tried. When the patient does not respond to this level of therapy, transvesical phenol injections should be considered, or, alternatively, a sacral selective neurolysis or neurectomy should be considered. Finally, invasive procedures will have to be considered starting with bladder transection, especially for the patient showing response to medication but intolerant of side effects. Mixed incontinence should be approached with conservative measures for each component. FES or imipramine therapy may help both conditions. If conservative therapy is not beneficial, surgical correction for GSI should be undertaken, with the knowledge that 35 to 50 per cent of patients will also have cure of DI, while the remainder can be treated medically for the DI.
Obstet Gynecol Clin North Am 1989 Dec
PMID:Etiology and management of detrusor instability and mixed incontinence. 269 19

The effect of photodynamic therapy on the tumor microvasculature in the first few hours after treatment was studied at the light and electron microscopy levels. BALB/c mice with EMT-6 tumor received ip injections of hematoporphyrin derivative, chlorin, or phthalocyanine, and 24 hours later, the tumors were treated with light at 100 J/cm2 at the appropriate therapeutic wavelength for each photosensitizer. Animals were killed and their tumors removed at time 0, 30 minutes, 1 hour, and 2, 4, 6, 8, 12, 16, and 24 hours after treatment. The results indicate that for all three sensitizers the effects of photodynamic therapy leading to rapid necrosis of tumor tissue are not the result of direct tumor cell kill but are secondary to destruction of the tumor microvasculature. The first observable signs of destruction occur in the subendothelial zone of the tumor capillary wall. This zone, composed of dense collagen fibers and other connective tissue elements, is destroyed in the first few hours after phototherapy. However, the ultrastructural changes seen in this zone are different for the hematoporphyrin derivative, compared with chlorin and phthalocyanine. Binding of photosensitizers to the elements in this zone as well as altered permeability and transport through the endothelial cell layer because of the increased intraluminal pressure may be key features of tumor destruction.
J Natl Cancer Inst 1988 Dec 21
PMID:Mechanism of tumor destruction following photodynamic therapy with hematoporphyrin derivative, chlorin, and phthalocyanine. 297 28

Human papillomavirus is a sexually transmitted virus that has been associated with intraepithelial neoplasia. The incidence and prevalence of the disease has risen dramatically, to epidemic proportions, within the last two decades. Risk factors for HPV are similar to those for intraepithelial neoplasia: early onset of sexual activity, multiple sexual partners, high-risk sexual practices, and poor hygiene. Health care workers need to screen all patients for HPV through the use of a comprehensive history, including sexual history, a thorough physical examination, and appropriate laboratory methods. Pregnant women must be thoroughly screened because they are at increased risk for HPV, plus there has been an association between genital warts at the time of delivery and subsequent laryngeal papillomas in their infants. Treatment is aimed at the elimination of the lesions. Although in some cases lesions spontaneously resolve without treatment, in other cases there is a significant incidence of recurrence, even with treatment. Cell-mediated immunity seems to play a role in recurrence and regression as well as transformation to atypical cells. Transformation of HPV to neoplasia also seems to be related to co-factors that act synergistically in the oncogenic process. Public education, identification of high risk groups, and prevention are mandatory if the spread of HPV is to be contained. Equally essential is to remain cognizant of the fact that HPV is an STD with potentially carcinogenic properties; thus, screening and treatment of sexual partners are mandatory!
Nurs Clin North Am 1988 Dec
PMID:Human papillomavirus infection: a potentially carcinogenic sexually transmitted disease (condylomata acuminata, genital warts). 305 72

In summary, there are a number of STDs in our society that present a significant increased risk of morbidity and mortality when encountered by the pregnant woman and her fetus. It behooves us as practitioners to be alert to the possibility of STDs when any increased risk factors are present upon the initial sexual history. Also, we need to remain alert and vigilant throughout the woman's pregnancy to pick up and to elucidate any factors that might suggest the presence of an STD. In dealing with the pregnant woman during the intrapartal period, we need to be constantly aware of any factors that might contribute to an increased incidence of infection during delivery and postpartum. We cannot be too cautious in scrupulously ruling out any possible perinatal STDs that might adversely influence the neonate. Sexually transmitted diseases are not new to us; however, they present as an ever changing array of entities with ever changing protocols of treatment. The best we can do is to remain attentive and to question minute changes that might indicate a pathologic condition in the pregnant woman or her neonate.
Nurs Clin North Am 1988 Dec
PMID:Sexually transmitted diseases in pregnancy. 305 73

The presence of chronic STD is due to various factors such as lifestyle behaviors, psychological factors, stress, reinfection, deviations of the urogenital tract, failure of treatment, resistant strains, allergic response, alternate sites, no known treatment, and errors in diagnosis. The presence of a chronic STD may have varying effects on the individual. It is important to consider the factors that cause chronic infections. The most common cause of chronic infections is reinfection. The assessment of the client should include both a nursing history and through physical examination. The nursing history should include a sexual history to identify health risks for the development of STD. Sensitivity and caring are needed in approaching the client with chronic STD exposure.
Nurs Clin North Am 1988 Dec
PMID:Chronic exposure to sexually transmitted diseases. 305 74

The carAB operon, encoding carbamoylphosphate synthetase (CPSase; EC 6.3.5.5) is transcribed from two tandem promoters. The upstream promoter (P1) is controlled by pyrimidines and the downstream promoter (P2) is controlled by arginine. We have isolated a new type of constitutive mutation (carP) that specifically affects the control of the pyrimidine-sensitive promoter but does not appear to influence other genes of the pyrimidine pathway. The carP mutation acts in trans and is dominant, which suggests that the carP product is an activator of car transcription. The downstream promoter P2, which is repressed by arginine, overlaps two operator modules characteristic of the arginine regulon. We have isolated two operator-constitutive mutations that specifically affect P2; both map in the upstream ARG box at a strongly conserved position.
J Mol Biol 1988 Dec 20
PMID:carP, a novel gene regulating the transcription of the carbamoylphosphate synthetase operon of Escherichia coli. 306 18

The control region of the carAB operon, encoding carbamoylphosphate synthetase, comprises two tandem promoters (P1, upstream and P2, downstream) located 67 base-pairs apart and repressed respectively by pyrimidines and arginine. RNA polymerase and pure arginine repressor bind to the P2 region in mutually exclusive ways. Repressor protects the two adjacent palindromic ARG boxes overlapping P2 against DNase I. Binding of RNA polymerase to P1 is abnormal; the region protected against DNase I is shifted upstream by about 20 nucleotides with respect to the position expected from the transcription startpoint. This pattern is not due to interference with polymerase binding at P2, since it is observed also in the presence of repressor and on an isolated P1 region. Binding of RNA polymerase is relatively weak and heparin-sensitive suggesting that, in vivo, an ancillary factor is required to promote the formation of an open complex. S1 nuclease mapping experiments show that the simultaneous presence of pyrimidines and arginine represses the downstream arginine-specific promoter (P2) more efficiently than arginine alone. This effect is not due to a direct regulatory interaction between pyrimidines and P2, since it is not observed when P1 is inactivated by insertion mutations or partial deletion. It has been shown that transcription initiated at P1 can proceed even when arginine represses P2. We therefore suggest that P2 operator-arginine repressor complex is destabilized by RNA polymerase binding at P1 or transcription from P1. We describe a novel technique to select for expression-down mutants in a lac fusion context.
J Mol Biol 1988 Dec 20
PMID:Molecular interactions in the control region of the carAB operon encoding Escherichia coli carbamoylphosphate synthetase. 306 19

The number of gene assignments to human chromosome 20 has increased slowly until recently. Only seven genes and one fragile site were confirmed assignments to chromosome 20 at the Ninth Human Gene Mapping Workshop in September 1987 (HGM9). One fragile site, 13 additional genes, and 10 DNA sequences that identify restriction fragment length polymorphisms (RFLPs), however, were provisionally added to the map at HGM9. Five mutated genes on chromosome 20 have a relation to disease: a mutation in the adenosine deaminase gene results in a deficiency of the enzyme and severe combined immune deficiency; mutations in the gene for the growth hormone releasing factor result in some forms of dwarfism; mutations in the closely linked genes for the hormones arginine vasopressin and oxytocin and their neurophysins are probably responsible for some diabetes insipidus; and mutations in the gene that regulates both alpha-neuraminidase and beta-galactosidase activities determine galactosialidosis. The gene for the prion protein is on chromosome 20; it is related to the infectious agent of kuru, Creutzfeld-Jacob disease, and Gertsmann-Straussler syndrome, although the nature of the relationship is not completely understood. Two genes that code for tyrosine kinases are on the chromosome, SRC1 the proto-oncogene and a gene (HCK) coding for haemopoietic kinase (an src-like kinase), but no direct relation to cancer has been shown for either of these kinases. The significance of non-random loss of chromosome 20 in the malignant diseases non-lymphocytic leukaemia and polycythaemia vera is not understood. Twenty-four additional loci are assigned to the chromosome: five genes that code for binding proteins, one for a light chain of ferritin, genes for three enzymes (inosine triphosphatase, s-adenosylhomocysteine hydrolase, and sterol delta 24-reductase), one for each of a secretory protein and an opiate neuropeptide, a cell surface antigen, two fragile sites, and 10 DNA sequences (one satellite and nine unique) that detect RFLPs.
J Med Genet 1988 Dec
PMID:The map of chromosome 20. 307 44

A unique, recently described rat alveolar macrophage cell line (NR8383) was used to study the interaction of the pulmonary immune system with a mucoid cystic fibrosis isolate of Pseudomonas aeruginosa (SRM-3), its nonmucoid revertant (SRM-3R), and a non-cystic fibrosis isolate (PAO-1). Strain SRM-3 was cultivated in a chemostat system to allow maintenance of an entirely mucoid population. The alveolar macrophage response to the mucoid and nonmucoid strains of P. aeruginosa was determined by visually quantitating phagocytosis in acridine orange-stained monolayers and measuring the induction of an oxidative burst as indicated by chemiluminescence and H2O2 production. In all experiments, fewer than 2% of the NR8383 cells engulfed the mucoid SRM-3 isolate, while SRM-3R and PAO-1 were phagocytized by 15 and 41%, respectively. Opsonization by normal serum (complement) provided minimal phagocytic enhancement of these strains, whereas specific anti-P. aeruginosa antibody slightly elevated phagocytic responses to strains with nonmucoid phenotypes while providing a sevenfold increase in uptake of SRM-3. Chemiluminescent and H2O2 responses were comparable with the levels of phagocytosis observed, with very little or no response to the mucoid strain SRM-3. The data indicate that the strains with mucoid phenotypes are refractile to ingestion and that studies which describe ingestion of mucoid strains were likely measuring ingestion of revertants. Alginic acid (2 mg/ml) was found to inhibit stimulation of macrophage response to the opsonized and unopsonized nonmucoid strain PAO-1.
Infect Immun 1988 Dec
PMID:Resistance of mucoid Pseudomonas aeruginosa to nonopsonic phagocytosis by alveolar macrophages in vitro. 314 Dec 84


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