Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A tumor-derived factor that inhibits cellular DNA synthesis was identified. The factor was extractable from a small-cell lung carcinoma cell line grown in either chemically defined medium or nu/nu mice and inhibited tritiated thymidine ([3H]dThd) incorporation by tumor cell lines of autologous, allogeneic, and xenogeneic origins. The viability of nonproliferating cells from normal tissue was not affected. Tumor extract inhibitory activity was trypsin labile but was resistant to other proteases, neuraminidase, lipase, DNase, RNase, glucosidase, extremes of pH-temperature, and reducing conditions. Inhibitory activity was reversibly bound to helix pomatia lectin but not to lentil, wheat germ, or concanavalin A lectins. Purification by size-exclusion high-performance liquid chromatography yielded a bioactive unimodal 12-kilodalton (kd) peak. The bioactive 12-kd moiety could be eluted from sodium dodecyl sulfate-polyacrylamide gels. Redosing of populations of the T-lymphoblastoid cell line CEM achieved an early (24 hr) sustained depression of pulse [3H]dThd incorporation and ultimately led to decreased population density of factor-treated populations. DNA histogram analysis demonstrated no change in cell cycle phase distribution after factor treatment. 5-Bromo-2'-deoxyuridine (BrdUrd) vs. propidium iodide with the two-parameter Fluorescence-Activated Cell Sorter analysis showed relative inhibition of non-S-phase BrdUrd uptake at 24 hours. A cell-free DNA polymerase assay demonstrated significant inhibition of non-alpha-polymerase-associated DNA synthesis in factor-treated cells. These studies suggest that this tumor-derived inhibitor of DNA synthesis represents a class of cellular products involved in the autoregulation of growth by regulation of DNA synthetic activity.
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PMID:Inhibition of DNA synthesis by a small-cell lung carcinoma-derived protein. 302 Mar 1

The uptake of 14C-glu by rat renal brushborder membrane vesicles was assayed in the presence of transmembrane ionic gradients for the purpose of characterizing surface properties which influence the transport process. Preincubation of membranes with the cationic protein lysozyme led to a significant decrease in transport activity. Similar results were obtained with polylysine and lysine. Polycations such as lysozyme and polylysine were capable of aggregating membrane vesicles whereas lysine was ineffective. Neither aggregation nor membrane injury provided an explanation for the depression of 14C-glu transport. The cationic drug harmaline at a concentration of 2.5 mM significantly reduced sodium dependent 14C-glu uptake provided drug and membranes were pre-equilibrated prior to the transport assay. Using an indirect spectrophotometric method to estimate harmaline concentrations, no evidence was obtained for strong harmaline binding to the membrane. The effect of harmaline could be eliminated by washing membranes in drug-free buffer or diluting membranes in larger volumes of sodium chloride. Membranes pretreated with the lectin Concanavalin A or the enzyme neuraminidase transported glu at control rates, but the proteolytic enzyme papain markedly impaired the transport function without altering mean vesicle volume. The optimal temperature for the assay was 30 degrees C. No temperature discontinuities in the Arrhenius plot of glu transport rates were found between 5 and 30 degrees C. These results with glutamic acid differ from data reported by other investigators on the transport characteristics of glucose and neutral amino acids by brushborder membrane vesicles. The results enhance the possibility that dicarboxylic acid binding proteins may be present on the luminal surface of proximal tubular epithelium.
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PMID:Surface properties of kidney brushborder membranes affecting the transport of glutamic acid. 612 41

Calcium binding to fragmented sarcolemma isolated from dog heart was measured by an ultracentrifugation technique. Two classes of binding sites with dissociation constants of 4.2 x 10(-5) M and 1.2 x 10(-3) M were identified. The maximum number of high and low affinity sites were 15 and 452 nmol/mg, respectively. The effects of various cations and drugs on calcium binding were studied in the presence of 0.1 mM total calcium. All cations tested inhibited calcium binding to a certain degree. La3+ (1 mM) and Mn2+ (1 mM) abolished calcium binding to the sarcolemma. The other divalent cation, Mg2+, used at a concentration of 1 mM, produced a partial inhibition Na+ and K+ also depressed calcium binding, with Na+ being the more potent inhibitor. Verapamil produced a depression at concentrations as low as 10(-7) M and abolished calcium binding at 10(-3) M. The effects of these cations and drugs on fragmented sarcolemma appear different from those reported for the isolated sarcoplasmic reticulum. Thus it is unlikely that the calcium binding observed was caused by a contamination of the sarcolemmal preparation by the fragmented sarcoplasmic reticulum. In addition, the calcium binding seems to be on the sarcolemma itself, rather than to the remaining fragments of the basement membrane, because the calcium binding was not significantly modified by pretreatment with purified neuraminidase (0.25 U/g of sarcolemma).
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PMID:Influence of cations and agents on sarcolemmal calcium binding. 624 41

In September 1980, an outbreak of febrile respiratory disease was observed in a herd of sows (1-2 years of age) in Ehime Prefecture, Japan. Most of the swine showed clinical signs of disease such as depression, anorexia, fever, nasal discharge, and cough. A hemagglutinating agent was isolated from a nasal swab from one of the diseased pigs. By cross-hemagglutination-inhibition and neuraminidase-inhibition tests with antisera to influenza viruses of swine origin, the isolate was identified as an influenza A virus of the H1N2 (former designation, Hsw1N2) subtype, and designated A/swine/Ehime/1/80 (H1N2). Significant antibody rises against the surface antigens of the isolate were found in convalescent swine sera. The distribution of antibody against H1N2 virus in swine sera in Ehime Prefecture was examined. Seven (8%) of 93 sera collected after the outbreak (in 1981) showed antibodies to only H1 and N2 antigens but none of the sera before the outbreak contained such antibodies, indicating that H1N2 virus had been restricted prevalent among swine but was not wide-spread until 1981.
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PMID:Further isolation of a recombinant virus (H1N2, formerly Hsw1N2) from a pig in Japan in 1980. 630 8

A method for monitoring ADP-induced thromboembolism in mice by means of the measurement of respiratory rate and depth was studied. The measurement were accurately carried out with a new method devised by us. In mice intravenously injected with 5-40 mg ADP/kg, it was found that the respiratory rate decreased transiently and dose-responsively, and that the platelet count also decreased transiently. On the other hand, no decrease in respiratory rate after administration of ADP was observed in neuraminidase-pretreated mice, in which the platelet count was significantly reduced. In the histological examination, platelet thrombi formed in the pulmonary vessels were observed 10 sec after administration of 10 and 40 mg/kg of ADP in mice which had not been treated with neuraminidase. The extent of thromboembolism at the dose of 40 mg/kg showed a tendency to be more marked than that at 10 mg/kg. Pretreatment with 300 mg dipyridamole/kg p.o. prevented the respiratory depression at 40 mg ADP/kg. However, with 10 mg dimorpholamine/kg i.v. or 30 mg warfarin/kg p.o., no preventive effect was observed. Therefore, it was concluded that it is possible to monitor ADP-induced thromboembolism in mice by means of the accurate measurement of the respiratory rate and depth.
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PMID:A method for monitoring ADP-induced thromboembolism in mice. 646 62

The percentage of peripheral blood lymphocytes (PBLs) which formed rosettes with sheep erythrocytes declined from 62 +/- 2% to 29 +/- 4% (p = 0.001) when PBLs were incubated 18 h at 37 degrees C. In the presence of alpha interferon (IFN-alpha), a dose-dependent increase occurred in the percentage of sheep erythrocyte-binding PBL at the end of incubation compared with PBL incubated without IFN-alpha. Change in the number of sheep erythrocyte "receptors" (SER) probably did not account for the observed modulation of rosetting capacity, since the frequency and density of an SER-associated determinant (T11, as defined by immunofluorescence flow cytometry using the monoclonal antibody OKT11A) was unaffected by incubation with or without IFN-alpha. Treatment of PBL, control or IFN-alpha-treated, with neuraminidase (0.4 u/ml), restored rosetting capacity to levels characteristic of freshly prepared PBL. Neuraminidase did not affect rosetting or T11 expression by freshly prepared PBL, nor did it affect T11 expression on PBL cultured with or without IFN-alpha. We thus postulated that steric interference with SER function by sialic acid residues might result from de novo protein synthesis and glycosylation at the cell surface. Inhibition of either protein glycosylation by tunicamycin or protein synthesis by cycloheximide prevented the incubation-induced depression of rosetting capacity. IFN-alpha may modulate functional expression of SER and other surface receptors by altering cell-surface glycoprotein composition and distribution.
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PMID:Effects of interferon alpha on the sheep erythrocyte "receptor" of human lymphocytes. 650 43

Cell-mediated immunity (CMI) was evaluated in 8 patients with focal glomerular sclerosis (FGS), 50 patients suffering from chronic mesangial proliferative glomerulonephritis without renal insufficiency and 24 healthy controls. The following parameters were measured: delayed skin reactivity to purified protein derivative, circulating lymphocytes, lymphocyte cell-surface markers (neuraminidase-treated sheep erythrocyte and erythrocyte-antibody-complement rosettes) and functional markers (mitogenic responses to concanavalin A and phytohemagglutinin). The FGS patients with nephrotic syndrome (NS) had a significant depression in CMI, characterized by decreased responses of the lymphocytes to both concanavalin A and phytohemagglutinin, impaired delayed hypersensitivity to purified protein derivative and a decreased proportion of T lymphocytes as compared with normal subjects. In contrast, the levels of all CMI parameters studied in FGS patients in remission and in patients with chronic glomerulonephritis with or without NS did not differ from normal subjects. Thus, the majority of FGS patients with NS demonstrated an impaired response in a CMI assay system. The possible significance of these phenomena in the pathophysiology of FGS is discussed.
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PMID:Impaired cell-mediated immunity in focal glomerular sclerosis. 660 85

In 4 adults with malignant lymphoma and in 3 cases of acute lymphoblastic leukemia the acid phosphatase activity in lymphocytes during the consecutive cycles of polychemotherapy was examined paralelly with the estimation of the receptors for sheep erythrocytes. Depression of the enzymatic reaction was observed immediately after the onset of the cytostatic treatment, its normalization between the cycles and after the full remission was reached. A remarkable and lasting decrease of the phosphatase positive lymphocytes and a change in the expression of the enzymatic reaction was noticed in the course of L-asparaginase administration. The presented investigations are the continuation of the authors' earlier studies on the positive correlation between the rosette test with neuraminidase treated sheep erythrocytes and the acid phosphatase activity in lymphoproliferative diseases.
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PMID:Acid phosphatase activity of the lymphocytes during polychemotherapy of lymphoproliferative diseases. 694 30

The effects of lanthanum on the resting membrane potential, action potential, membrane resistance, twitch tension, and potassium contracture were investigated and the localization of the drug was studied electron microscopically in isolated frog ventricular muscle. Lanthanum in concentration of 0.2 to 5 mM decreased the resting potential by about 5-8 mV, which was accompanied by an increase in the membrane resistance of about 43% for the depolarizing and 40% for the hyperpolarizing direction. Lanthanum caused a decrease in height and a prominent shortening of the action potential, and also, a depression of the plateau level. In addition, it increased the threshold for action potential generation depending on its concentration. The slow response action potential was inhibited by lanthanum in parallel with twitch inhibition. This finding suggests that the twitch inhibition resulted from the suppression of the slow inward calcium current. In contrast, potassium contracture was not inhibited by lanthanum. When the muscle preparation was treated with neuraminidase, the twitch inhibition caused by lanthanum was strongly depressed. Electron microscopic observation revealed that the precipitates of lanthanum were localized on the external lamina of myocytes as well as in the extracellular spaces but could never be found within the cytoplasm. No such precipitates could be detected in the neuraminidase-treated muscle. From these results it is suggested that lanthanum takes the place of calcium at the membrane surface: it modifies permeabilities to sodium, potassium and calcium ions and the excitation-contraction coupling of the ventricular muscle by replacing calcium bound to the membrane-surface.
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PMID:Effects of lanthanum on the electrical and mechanical activities of frog ventricular muscle. 698 17

Using a cytotoxicity assay, we have shown that all of 40 normal human sera tested contained antibodies cytotoxic for neuraminidase-treated red blood cells in the presence of complement. The antibodies were shown to be specific for the T disaccharide by studies using a synthetic T antigen (formula: see text). Certain patients with metastatic gastrointestinal cancer were found to have depressed serum levels of anti-T when compared to normal controls. There was a correlation between depression of circulating anti-T and disease burden in that 83% of patients with extensive disease had lower than normal levels of cytotoxic anti-T as compared to 45% of patients with moderate disease and none with minimal disease. There was no correlation between the concentration of cytotoxic anti-T and the age of the patients, time since surgery or the type of therapy the patient was receiving. Patients with low levels of cytotoxic anti-T had normal levels of cytotoxic anti-sheep red blood cell antibody. Measurement of circulating anti-T in the serum of certain cancer patients may prove valuable in the monitoring of disease progression.
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PMID:Decreased levels of circulating lytic anti-T in the serum of patients with metastatic gastrointestinal cancer: a correlation with disease burden. 709 22


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