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

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Certain conjugated biliary acids (total pool - choliglycine - sulpholytic choliglycine) and the following haematochemical parameters: total bilirubin and its direct quota, alkaline phosphatase, albumin, prothrombin activity, gamma globulin, oxalacetic and pyruvic transaminase were radioimmunologically (RIA) studied in 115 subjects. Subjects were divided into the following subgroups: --20 normal controls; --20 cases of persistent chronic hepatitis; --20 cases of active chronic hepatitis; --15 cases of A.C.H. with cirrhosis; --20 cases of cirrhosis without direct hyperbilirubinaemia; --20 cases of cirrhosis with direct hyperbilirubinaemia. Each case was assigned to its particular group on the basis of the histological report on each patient. The following observations were drawn from the results obtained: --there is a progressive increase in above normal biliary acid rate in proportion to the gravity of the liver pathology; --choliglycine especially and to a lesser extent the total pool increased sufficiently to distinguish between normal and hepatopathic subjects (PCH and ACH) and also between PCH and ACH patients; --the combination of cirrhosis and ACH causes a significant increase in total pool and chliglycine over levels noted in ACH alone; --in contrast no difference is found between the levels of these acids in inactive (or minimally active) cirrhosis and ACH with cirrhosis; --gamma globulin, oxalacetic and pyruvic transaminase levels were found to have substantially the same diagnostic significance as choliglycine in the early stages of liver diseases. Significant correlations were also encountered between total conjugated biliary acid pool and choliglycine (not in the group with cirrhosis without direct hyperbilirubinaemia) and between total pool and choliglycine with haematochemical cholestasis test results (alkaline phosphatase and total and direct bilirubin) the latter only in the two cirrhotics groups. In conclusion, choliglycine was found to be the most sensitive of the biliary acids routinely measured by RIA and is valuable in clinical practice not as a substitute for the main liver tests but as an extremely useful and sensitive addition to them. In clinical practice, its use is recommended in the diagnosis and monitoring of healthy subjects at risk and those with chronic liver conditions (PCH, ACH, ACH + C).
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PMID:[Clinico-diagnostic significance of the determination of bile acids in chronic liver diseases]. 671 31

The effect of hypoxemia and acidemia on the fetal cardiac response to acetylcholine (ACh) was studied in 24 baboon fetuses in utero. A bolus injection of ACh was given intravenously to the fetus at a dose that ranged from 5 to 160 micrograms/kg of estimated fetal weight. The responses were divided into two groups according to fetal oxygenation and acid-base state. Fetuses in group I were well oxygenated (PaO2, 31 +/- 1.4 mm Hg; pHa, 7.32 +/- 0.154; only five atrioventricular (A-V) heart blocks were induced with 50 +/- 3.3 micrograms/kg of ACh. Fetuses in Group II were hypoxemic (PaO2, 18 +/- 1.2 mm Hg) and acidemic (pHa, 7.05 +/- 0.048); ten A-V heart blocks were induced with a comparable dose of ACH (45 +/- 6.8 micrograms/kg). Dose response relationship is noted in individual fetuses with multiple dosage injections. These findings suggest that the fetal cardiac response to ACh is both dose related and more profound when the fetus is hypoxemic and acidemic, and indicate that the hypoxic and acidotic fetus is at a greater risk from strong stimulation of the parasympathetic nervous system. Atropine prevented myocardial conduction defect induced by intravenous injection of ACh even in the severely hypoxemic baboon fetus. This observation suggests that judicious use of atropine could be a life-saving measure when a prolonged severe degree of cord occlusion is suspected.
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PMID:Effect of hypoxemia and acidemia on the fetal cardiac response to acetylcholine: experimental observations in fetal baboons. 719 81

Interaction of acetyl-choline in 10(-4) . 10(-12) M concentration with a water-soluble fraction of homogenates of different brain areas (medulla oblongata, pons varolii, sensomotor cortex, dorsal and ventral hippocamp, hypothalamus, amygdaloid nuclei region and septal region) was studied by the spectrofluorimetric method. Fluorescence complexes spectra at excitation wavelength of 280, 296 nm were investigated. It is shown that the ACH addition to the water-soluble fractions results in reduction of the spectrum intensity and in insignificant shift of the fluorescence maxima to a short-wave region. This effect is supposed to be due to ACH interaction with the cholinoreceptor (CHR). The number of CHR in all the brain regions studied is calculated. Good correlation is observed between the regional distribution of CHR and the acetylcholinesterase activity.
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PMID:[Spectrofluorimetric study of interaction between acetylcholine and brain proteins]. 725 47

Following a short review of the viruses underlying viral hepatitis and those which, as a secondary factory in the clinical picture, may cause fleeting liver damge, the subdivision of chronic hepatitis conditions on histopathological bases is described. Particular attention is paid to pathogenesis, with a study of the elimination of B virus, correlated to particular histopathological types. A series of 27 PCH and 49 ACH cases is reported. Of special significance was the observation of 14 ACH out of 17 biopsied drug addicts. The therapeutic problem of chronic hepatitis is then tackled.
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PMID:[Chronic hepatitis caused by B virus (HBV)]. 737 13

Inhalation of acetylcholine causes increased histamine concentration in the arterial plasma. This increase is smaller than that following allergen inhalation. The increase in Edyn following ACH inhalation may be related to the histamine released to only a very limited extent. Comparison of the effects of histamine inhalation and allergen inhalation on Edyn and plasma histamine concentration leads to the assumption that sensory receptors are located nearer to the surface of the mucosa than that of the mast cells. Hypoxemia is followed by a slight increase in the arterial plasma histamine concentration. The increase in Edyn corresponds to that caused by allergen inhalation although the increase in Edyn and that in the plasma histamine are much smaller.
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PMID:[Effects of acetylcholine- and histamine inhalations also of hypoxia on the arterial plasma-histamine concentration (experiments on dogs). III. Communication (author's transl)]. 744 75

Oltipraz (5-pyrazinyl-4-methyl-1,2-dithiole-3-thione), which is undergoing clinical evaluation as an anticarcinogen, also inhibits HIV-1 replication (IC50 approximately equal to 10 microM). The inactivation of RT appears to be a relevant antiviral mechanism since oltipraz blocks viral replication in acutely infected T-cell lines, but is ineffective in chronically infected ACH-2 cells (H. J. Prochaska, W. G. Bornmann, P. Baron, and B. Polsky (1995) Mol. Pharmacol. 48, 15-20). Since a nucleophilic amino acid is a likely target for oltipraz, we assessed whether the conserved cysteine residues of HIV-1 RT (38Cys or 280Cys) were the target(s) for oltipraz, and we synthesized [Me 14C]oltipraz to determine if oltipraz forms a stable adduct with RT. Thus, HIV-2 RT as well as wild-type, 38Cys-->Ser, 280Cys-->Ser, and the Cys-->Ser double mutant of HIV-1 RT were purified from the lysates of transformed Escherichia coli strain DH5 alpha (A. Hizi, M. Shaharabany, R. Tal, and S. H. Hughes (1992) J. Biol. Chem. 267, 1293-1297) via a purification procedure that included (NH4)2SO4 fractionation followed by gel filtration, dye-ligand, and ion-exchange chromatographies. Procion yellow H4R was chosen as the dye-ligand chromatography since it was the most potent and selective inhibitor of RT among seventy reactive dyes that were screened. Mono Q anion-exchange chromatography with diethanolamine (pH 9) resulted in the generation of heterodimeric RT from a predominantly homodimeric enzyme preparation. Because the instability of dilute RT preparations at room temperature rendered the kinetic evaluation of inactivation difficult, we sought to identify conditions that prevent denaturation of these enzymes. High concentrations (25 mM) of MgCl2 had a stabilizing effect. Oltipraz behaved kinetically as an irreversible inhibitor of all RTs purified, and the kinetic constants for the inactivation of these enzymes were not significantly different from wild-type HIV-1 RT (Ki = 17.0 +/- 4.1 microM; k3 = 0.214 +/- 0.051 h-1). In stark contrast, oltipraz neither inhibited nor inactivated the Klenow fragment of DNA polymerase I, whose subdomain structure is similar to the p66 subunit of RT. Wild-type RT was incubated with 60 microM [Me 14C]oltipraz for 4 h and was then subjected to gel filtration chromatography. The [14C] label comigrated with RT with a stoichiometry of binding of 0.88 +/- 0.05 oltipraz per inactivated RT subunit (N = 3 experiments), and the [14C] label remained bound after treatment with 4 M urea.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Inactivation of human immunodeficiency virus type 1 reverse transcriptase by oltipraz: evidence for the formation of a stable adduct. 750 49

To study the basis of cellular latency of human immunodeficiency virus (HIV), we have used a recombinant luciferase-encoding HIV (HXB-Luc) to superinfect nonproductively HIV-1-infected human leukemic cell lines. HXB-Luc contains the Photinus pyralis luciferase gene in place of the nef gene and provides a highly sensitive, simple assay for HIV infection and expression. To circumvent any superinfection block in latently infected cells, we also generated viruses pseudotyped with murine leukemia virus amphotropic envelope (HXB-Luc:ampho). The parental uninfected lines, U937 and A3.01, from which the latently infected cell lines U1 and ACH-2, respectively, were derived could be readily infected with pseudotyped or nonpseudotyped reporter viruses. However, superinfection of U1 cells with either HXB-Luc or HXB-Luc:ampho resulted in only low levels of luciferase activity. Like the endogenous provirus, HXB-Luc provirus could be efficiently activated by phorbol ester treatment of HXB-Luc:ampho-superinfected U1 cells. In contrast, superinfection of ACH-2 cells resulted in active expression of the secondarily introduced virus even in unstimulated cells and luciferase production higher than in the parental cell line A3.01. Thus, the proviral latency in U1 cells appears to result from a defect in the cellular environment (a trans effect), whereas the latency in ACH-2 is specific to the integrated provirus and is probably a cis effect due to the site of integration. These results demonstrate distinct modes of proviral latency in these two cell line models and may have implications in our understanding of the regulation and significance of cellular latency in HIV infection.
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PMID:Distinct modes of human immunodeficiency virus type 1 proviral latency revealed by superinfection of nonproductively infected cell lines with recombinant luciferase-encoding viruses. 750 83

Recent information has suggested that posttranscriptional mechanisms, whereby human immunodeficiency virus type 1 (HIV-1) RNA exists as multiply spliced transcripts without promoting an accumulation of the larger messages, are responsible for maintaining a stable state of nonproductive viral expression or viral latency. To test the universality of these observations, we compared the patterns of viral RNA splicing and the frequencies of cells actually harboring HIV-1 RNA in four chronically HIV-1-infected cell lines (U1 [promonocytic], ACH-2 [T lymphocytic], OM-10.1 [promyelocytic], and J1.1 [T lymphocytic]). In uninduced U1 and ACH-2 cultures, a high frequency of cells (approximately one in six) contained HIV-1 RNA but mainly as multiply spliced transcripts, again supporting a posttranscriptional mechanism maintaining viral latency. In sharp contrast, only 1 in 50 cells in uninduced OM-10.1 and J1.1 cultures contained HIV-1 RNA, indicating a primary transcriptional mechanism controlling viral expression in these cells. Furthermore, those OM-10.1 and J1.1 cells that did contain viral RNA were in a state of productive HIV-1 expression marked by the presence of both spliced and unspliced transcripts. Even though the total absence of viral RNA in the majority of OM-10.1 and J1.1 cells indicated a state of absolute latency, treatment with tumor necrosis factor alpha induced transcription of HIV-1 RNA in nearly 100% of the cells in all four of the chronically infected cultures. Tumor necrosis factor alpha induction of U1, ACH-2, and OM-10.1 cultures resulted in an initial accumulation of multiply spliced HIV-1 RNA followed by a transition to the larger unspliced viral RNA transcripts. This RNA splice transition was less apparent in the J1.1 cell line. These results demonstrate that host cell-specific transcriptional and posttranscriptional mechanisms are important factors in the control of HIV-1 latency.
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PMID:Human immunodeficiency virus type 1 RNA expression by four chronically infected cell lines indicates multiple mechanisms of latency. 751 Nov 77

Human chorionic gonadotropin (hCG)--a pregnancy-associated immunomodulating hormone--has been recently shown in vitro to suppress reverse transcriptase activity in chronically HIV-infected lymphocytes and monocytes and to block viral transmission resulting from cell-cell contact between virus-carrying lymphocytes and placental trophoblasts. In further pursuit of the query into the mechanism of action, purified alpha and beta subunits of hCG were tested for the inhibition of p24 gag protein synthesis in virus-producing ACH-2 lymphocytes and U1 monocytes. Unlike the alpha subunit, beta-hCG displayed a distinct U-shaped dose response, characteristic of the effect of dimer hCG. Maximum inhibition of viral expression has been achieved at 10-100 ng/ml, the concentration corresponding to blood levels of beta-hCG in pregnant women. The doses that were several logs higher of normal levels seemed to increase viral production in monocytes. The data presented supports our original observations regarding the effect of intact hCG on HIV replication. While the mechanism of action remains to be established, the results suggest that the virus-interfering activity of hCG is determined by hormone-specific beta chain but not by the alpha subunit--shared with the family of glycoprotein hormones from the pituitary--follicle-stimulating hormone, luteinizing hormone and thyrotropin.
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PMID:Anti-HIV effect of beta subunit of human chorionic gonadotropin (beta hCG) in vitro. 753 8

CD30, a member of the tumor necrosis factor (TNF) receptor family, is expressed constitutively on the surface of the human T cell line ACH-2, which is chronically infected with human immunodeficiency virus type-1 (HIV)-1. We demonstrate that cross-linking CD30 with an anti-CD30-specific monoclonal antibody, which mimics the described biological activities of the CD30 ligand (CD30L), results in HIV expression. CD30 cross-linking does not alter proliferation of ACH-2 cells and the induction of HIV expression is not mediated by endogenous TNF alpha/beta. Furthermore, cross-linking of CD30 leads to NF-kappa B activation and enhanced HIV transcription. Thus, CD30-CD30L interactions mediate the induction of HIV expression by a kappa B-dependent pathway that is independent of TNF. This mechanism may be important in the activation of HIV expression from latently infected CD4+ T cells, especially in lymphoid organs where cell to cell contact is conducive to receptor-ligand interactions.
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PMID:Cross-linking of CD30 induces HIV expression in chronically infected T cells. 754 Sep 42


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