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)

We report a case of methionine synthase deficiency associated with cellular immune deficiency discovered in a 14-year-old boy. Principal findings were: developmental delay, recurrent upper and lower respiratory tract infections, megaloblastic anemia, discovered at 3 months of age, unresponsive to cyanocobalamin and poorly responsive to folinic acid. Biochemical studies showed: an abnormal deoxyuridine suppression test despite normal serum folate, cobalamin and transcobalamin levels; a normal intracellular uptake of these two coenzymes; and an absolute requirement of methionine for fibroblast growth, suggestive of defective methionine synthesis. An absence of methionine synthase activity in the patient's bone marrow and a profound depression of this activity in lymphocytes and liver were found. Hypergammaglobulinemia with variable lymphopenia, depressed lymphocyte transformation after lectin or recall-antigen stimulation, defective delayed-type hypersensitivity and decreased natural killer activity were noted as well. The patient died at the age of 14.
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PMID:Megaloblastic anemia and immune abnormalities in a patient with methionine synthase deficiency. 342 20

Interleukin 2 used in vitro and in vivo induces effectively the recovery of cytotoxic activity of natural killers and lectin-dependent cellular cytotoxicity effectors in stress-immobilized CBA mice. This lymphokin can be used for correction of stressor depression in the cells of the natural anti-tumor resistance system.
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PMID:[Interleukin-2 restoration of the activity of natural killers during stress]. 348 54

The effect of thymopoietin penta- (TP-5), tetra-(TP-4), and tripeptides (TP-3) was studied on the depressed lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 target cells by peripheral blood mononuclear cells from patients with active systemic lupus erythematosus (SLE). LDCC activity was evaluated by detachment from the monolayer of 3H-thymidine-prelabelled HEp-2 cells in the presence of concanavalin A (Con A). While 10(-5)M TP-3 moderated the depression, 10(-5) M TP-5 strongly enhanced LDCC activity in SLE patients up to the normal level. On the other hand, LDCC activity by normal donors was not influenced by TP-3 and TP-5. TP-4 had no major effect either in control or in SLE patients. In parallel experiments none of the thymopoietin peptides affected the Con A-induced suppressor activity on the blastogenesis of lymphocytes. A selective immunostimulatory effect of TP-3 and TP-5 on the generation of LDCC effector cells in patients with SLE is suggested.
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PMID:Stimulation by thymopoietin oligopeptides of lectin-dependent cell-mediated cytotoxicity in patients with systemic lupus erythematosus. 391 Aug 38

The effects of cyclosporin A, prostaglandin E1 and indomethacin were studied on lectin-dependent cell-mediated cytotoxicity (LDCC) against adherent HEp-2 human epipharynx carcinoma target cells. LDCC activity by human peripheral blood lymphocytes was evaluated by detachment from the monolayer of [3H]thymidine-prelabelled HEp-2 cells in a 24-h assay at 50:1 effector:target cell ratio in the presence of 25 micrograms/ml concanavalin A. Under these conditions, but without concanavalin A, considerable natural cell-mediated cytotoxicity was not elicited although LDCC was significantly augmented in the presence of concanavalin A. Addition of both cyclosporin A (0.1, 1.0 or 10 micrograms/ml) and prostaglandin E1 (10(-8), 10(-7) or 10(-6) M) dose-dependently suppressed LDCC activity. Indomethacin (0.1, 1.0 or 10 micrograms/ml) did not in itself influence LDCC although suppression of LDCC by cyclosporin A, but not prostaglandin E1, was abrogated in the presence of indomethacin. Similar to indomethacin, acetyl salicylic acid also reversed the inhibition of LDCC by cyclosporin A. In parallel experiments, cyclosporin A elicited a more than two-fold increase of prostaglandin E production under LDCC assay conditions as measured by radioimmunoassay. Contrary to LDCC, depression of concanavalin A induced blastogenesis by cyclosporin A was not influenced by indomethacin, suggesting that the inhibition by cyclosporin A of LDCC and concanavalin A-induced blastogenesis proceed via different mechanisms.
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PMID:Indomethacin abrogates the suppression by cyclosporin A of lectin-dependent cell-mediated cytotoxicity to HEp-2 cells. 395 49

The effects of cyclic nucleotides on the proliferation of cultured T-lymphocytes (CTC) stimulated by either phytohemagglutinin (PHA) or lectin-free interleukin-2 (IL-2) were studied. The addition of either N6,O2-dibutyryl cyclic AMP (DB-cAMP), aminophylline or isoproterenol to CTC cultures significantly suppressed the proliferation of CTC stimulated by either PHA or IL-2. This inhibitory effect was maximal when added at initiation of the assay; however, significant depression was still observed when added 24 h later. When DB-cAMP and aminophylline were added together, the inhibitory effects were additive. When DB-cGMP was added to the CTC cultures, inhibition of both PHA- and IL-2-stimulated cultures was also found, but the degree of activity was considerably less than for DB-cAMP or aminophylline. In contrast, when carbachol was added, no inhibition or modulation in proliferation was seen. Lastly, DB-cGMP was not found to antagonize the inhibitory effect of DB-cAMP, but instead to further increase the level of inhibition. In summary, these studies illustrate that cyclic nucleotides modulate the proliferation of IL-2-stimulated CTC as well as PHA-treated cells. This model system should provide an approach to study, in more depth, the mechanism by which cyclic nucleotides or their inducers can modulate the latter stages of the lymphocyte proliferative response, which is mediated by the lymphokine, IL-2.
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PMID:The effects of cyclic nucleotides on the proliferation of cultured human T-lymphocytes. 609 9

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

Following removal of a skin patch from each hind limb of a series of adult newts, the limbs were explanted into small dishes of Holtfreter solution containing various combinations of test drugs. Later, the amount of wound epithelium that formed on each limb was determined using a planimeter on wound tracings obtained with the aid of a drawing tube-equipped microscope. Exposure of migrating cells to the plant lectin, concanavalin A (con A), lowered cyclic AMP (cAMP) levels and depressed migration. Exposure to cholera toxin and theophylline (CTX) significantly elevated cAMP levels and significantly depressed migration rate. Exposure of CTX-treated cells to con A tended to lower CTX-elevated cAMP levels while depressing the migration rate well beyond the depression caused by CTX alone. These results provide further evidence that cAMP can regulate the rate of newt epidermal cell migration. They also show that the inhibitory effect of con A on motility in these cells is independent of its effects on cAMP.
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PMID:Effects of concanavalin A and cholera toxin on epidermal cAMP and migration rate during wound closure in adult newts. 615 47

Butyric acid produces multiple effects on mammalian cells in culture, including alterations in morphology, depression of growth rate, increased histone acetylation, and modified production of various proteins and enzymes. The latter effect is exemplified by the induction in HeLa cells of the glycoprotein hormone alpha subunit by millimolar concentrations of the fatty acid. This report demonstrates that increased subunit accumulation in response to sodium butyrate is strikingly dependent on the presence of glucose (or mannose) in the growth medium. In contrast, basal levels of subunit synthesis are only marginally affected when the culture medium is supplemented with one of a variety of hexoses. An increase in the accumulation of HeLa alpha does not occur in medium containing pyruvate as the energy source, and sustained induction requires the simultaneous and continued presence of both glucose and butyrate. The effects of butyrate on HeLa cell morphology and subunit induction can be separated, since the latter is glucose-dependent while the former is not. Failure of butyrate to induce alpha in medium containing pyruvate does not result from restricted subunit secretion, since the levels of intracellular alpha are not increased disproportionately relative to those in the medium. The hexoses which support induction of HeLa alpha (glucose greater than or equal to mannose greater than galactose greater than fructose) are identical to those which have been shown previously to stimulate the glucosylation of lipid-linked oligosaccharides and enhance the synthesis of certain glycoproteins. Labeling of various glycosylation intermediates with [3H]mannose indicates that in glucose medium there is a decrease in the level of radioactivity associated with both dolicholpyrophosphoryl oligosaccharide and cellular glycoproteins and a concomitant increase in the fraction of label recovered in secreted glycoproteins. Butyrate also causes a decrease in [3H]mannose-labeled cellular glycoproteins and an increase in tritiated extracellular glycoproteins, particularly in glucose medium. Likewise, glucose stimulates the incorporation of [3H]glucosamine into immunoprecipitable alpha subunit relative to the bulk of HeLa-secreted glycoproteins, and this is further enhanced by butyrate. However, as demonstrated by lectin chromatography of conditioned media, a nonglycosylated subunit does not accumulate in pyruvate medium, either in the absence or presence of butyrate.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Glucose requirement for induction by sodium butyrate of the glycoprotein hormone alpha subunit in HeLa cells. 620 30

Various types of mouse peritoneal macrophages were studied for H(2)O(2) release in the presence of wheat germ lectin or phorbol myristate acetate. Macrophages elicited 3 days before harvest by a single injection of thioglycolate, zymosan A, or a streptococcal preparation (OK-432) were highly responsive to wheat germ lectin, resulting in a marked increase in H(2)O(2) release. However, immunologically activated macrophages induced by double injections of live and heat-killed BCG at 15 and 3 days before harvest or by double injections of zymosan A or OK-432 at 20 and 3 days before harvest did not show any significant response to wheat germ lectin. On the other hand, all macrophages tested responded well to phorbol myristate acetate by augmentation of H(2)O(2) release. Concanavalin A inhibited wheat germ lectin- and phorbol myristate acetate-triggered H(2)O(2) release from all types of macrophages, but inhibition was much more marked in the case of wheat germ lectin-stimulated H(2)O(2) release. Succinylated concanavalin A (divalent concanavalin A) showed only slight suppressive action against macrophage H(2)O(2) release, and prostaglandin E(1) and dibutyryl cyclic adenosine 3', 5'-monophosphate caused depression of H(2)O(2) release from OK-432-induced macrophages.
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PMID:Hydrogen peroxide-releasing function of chemically elicited and immunologically activated macrophages: differential response to wheat germ lectin and concanavalin A. 626 Jun 53

Immunoregulation of lymphocyte blastogenesis was studied in 13 patients with acute-phase cytomegalovirus (CMV) mononucleosis and 9 of these patients during the convalescent phase of the illness. Peripheral blood mononuclear leukocytes from acute-phase patients displayed depressed uptake of [3H-]thymidine in response to the lectin-mitogen concanavalin A (Con A) and immune-specific viral antigens (CMV, herpes simplex virus (HSV), mumps virus) compared with convalescent patients or normal donors. Removal of plastic-adherent cells from the patients' samples resulted in further depression of lymphocyte blastogenesis to Con A and CMV and HSV antigens, suggesting a helper function for the predominantly monocytic, adherent cell population in this response. Preliminary culture of mononuclear leukocytes from acute-phase patients for 18 hr at 37 degrees C resulted in significantly enhanced blastogenesis to Con A. In sharp contrast, lymphocyte blastogenesis to viral antigens was not significantly enhanced after preculture. These results suggest that different mechanisms are operative in immunoregulation of lymphocyte recognition responses to the polyclonal activator Con A and immune-specific viral antigens during human CMV infection.
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PMID:Alteration of immunoregulatory mechanisms during cytomegalovirus mononucleosis: effect of in vitro culture on lymphocyte blastogenesis to viral antigens. 630 73


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