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)

Ionizing radiation inhibited the development of specific haemolysin-producing cells (PFC) and depressed the incorporation of (3H) thymidine by rabbit spleen explants responding to SRC in the culture medium. In contrast to these effects, the rates of incorporation of precursors for protein and RNA synthesis were much less affected. The depression of (3H) thymidine incorporation was found to result from a quantitative reduction of new DNA synthesis, without any change in the proportion of labelled cells, at any time after irradiation. The DNA synthesis occurring in these cells preparing to develop antibody-producing capacity was thus radio-sensitive, but the exact nature of the defect resulting from exposure to radiation requires further study.
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PMID:The acute effects of ionizing radiation on DNA synthesis and the development of antibody-producing cells. 617 68

Mice infected with Nematospiroides dubius were incapable of responding normally to i.p. or i.v. challenge with SRBC. The HA and PFC response to SRBC in infected animals was characterized by a severe depression of antibody to SRBC on day 4 and a reduced HA peak titre during the following week. The greatest depression of the response to SRBC was associated with an interval of 14 days between infection and the administration of antigen, suggesting that a particular stage of the parasite contributed significantly to immunodepression during this critical period. It was proposed that a combination of parasite induced damage to the intestine, release of parasite secretory/excretory products and loss of appetite by the host produced trauma during which the host was incapable of responding normally. However, mice given low-level and long-standing infections also showed reduced responses to SRBC, although these animals were not severely depressed. It is possible that this generalized weakening of host immunocompetence is the inevitable consequence of a parasite mechanism which operates more specifically to suppress the expression of homologous immunity at the intestinal level.
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PMID:Nematospiroides dubius: factors affecting the primary response to SRBC in infected mice. 636 45

Sera from 60 gastric cancer patients and 20 patients with benign gastric diseases and 8 healthy controls were tested for inhibitory effects on the humoral response to sheep erythrocytes (SRBC) by the plaque forming cell assay (PFC R.I.) using mouse spleen cells and on the phytohemagglutinin (PHA)-induced blastogenesis of normal mouse spleen cells (PHA S.R.). Gastric cancer patient sera showed a significantly lower PFC R.I. than did sera from benign gastric disease patients and from the healthy controls. However, there was no appreciable interstage difference in the degree of depression. The PHA-induced blastogenesis of normal spleen cells was also decreased in the presence of sera from cancer patients, as compared to that in the presence of sera from benign disease patients and from the healthy controls. The depression progressed with advancing stage of cancer. The PHA S.R. showed significant negative correlations with serum levels of IAP, IS, alpha 1-acid glycoprotein and alpha 1-antitrypsin, but there were no such correlations between PFC R.I. and these glycoproteins in serum. There was also no correlation between the values of the PHA S.R. and the PFC R.I. These results suggest that these two assays may depict immunosuppressive activities operating through entirely different mechanisms.
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PMID:Immunosuppressive activity of sera from gastric cancer patients. 643 Nov 62

Measurement of C1q, C2, C4, C5, C6, factor B, properdin, beta1H, and C3bINA were made in acute sera from 31 patients with Reye syndrome. Abnormalities were found in 18 patients. The magnitude of the complement component depression correlated with disease severity. Sera from patients with stage IV illness had significantly lower complement levels than did sera from patients with state I (P less than 0.001), II (P less than 0.05), and III (P less than 0.05) disease. Circulating immune complex measurements were performed on all 31 acute sera and were present in six (19%). However, from the results of the present study, it would appear that in the majority of the patients circulating immune complexes are not the cause of the lowered levels of, at least, C3 and factor B. Rather, these low levels could be explained as secondary to reductions in the levels of the C3b amplification loop control proteins beta1H and C3bINA.
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PMID:Hypocomplementemia in Reye syndrome: relationship to disease stage, circulating immune complexes, and C3b amplification loop protein synthesis. 645 14

A long-term epidemiological genetic study was conducted in which all new patients were evaluated prospectively at the Foundation for Depression and Manic Depression and two Lithium/Affective Disorders clinics at the Columbia-Presbyterian Medical Center between the years of 1972 and 1978. All patients met Feighner, RDC and DSM III criteria for Major Depressive Disorder after initial clinical screening interviews and were further subtyped using the Fieve-Dunner 7-point criteria. All 604 probands and 90% of 2711 first-degree relatives were interviewed blindly by diagnosticians trained in the use of the SADS structured interview. Cumulative morbid risk in parents, siblings and children of 490 bipolar probands was 15.6 +/- 3% and 14.0 +/- 1.7% in the first-degree relatives of 114 unipolar probands. A number of biological and genetic marker studies were simultaneously performed on samples of the overall population. The enzymes catechol O-methyltransferase and dopamine beta-hydroxylase, and the dexamethasone suppression test (SDT) did not show any biological marker value for outpatients even though both enzymes were determined to have hereditability. The HLA system, monoamine oxidase and acetylcholinesterase segregated differently from normal controls in samples of the patient population. The positive association findings with monoamine oxidase and the HLA system conflicted with the positive findings of other investigators, leaving doubtful their biological marker value. Red cell acetylcholinesterase was found to be significantly lower in affective disorder patients than in controls. This positive association finding was recently replicated by Mathews et al. (1982) but needs further confirmation. Using 28 blood group markers, a prior association study between the trait defining susceptibility to affective disorder and the genetic marker was positive for haptoglobin GC, and properdinfactor B, confirming earlier findings. Using the sib-pair method on the remaining 25 blood groups revealed that none other than peptidase A showed significant linkage with affective disorder since one significant finding is expected by chance. We conclude from the overall morbid risk data and segregation analyses that bipolar manic-depressive illness is a spectrum disease inherited through a multifactorial mode of genetic transmission (which is not synonymous with polygenetic inheritance) with possible genetic heterogeneity and find no evidence for X-linkage. Additional studies with acetylcholinesterase, haptoglobin, GC, and properdin-factor B are needed to confirm their positive biological/genetic marker value suggested by our long-term epidemiological study.
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PMID:Search for biological/genetic markers in a long-term epidemiological and morbid risk study of affective disorders. 651 12

We studied complement and immunoglobulin profiles on the serum and ascitic fluid of a patient before and during gram-negative spontaneous bacterial peritonitis (SBP). During the infection, activation of the alternative complement pathway in ascitic fluid was manifested by a 35% reduction in functional activity and depression of both properdin and factor B concentrations to nondetectable levels. Activation of the complement cascade was also demonstrated by a 50% reduction in the C3 concentration and depression of total hemolytic complement. There was no evidence of complement activation of a functionally intact complement system in the ascitic fluid of cirrhotic patients. Complement consumption in ascitic fluid may predispose the cirrhotic to SBP.
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PMID:Activation of the alternative complement pathway in ascitic fluid during spontaneous bacterial peritonitis. 674 61

Mycelial- or spherule-phase derivatives of Coccidioides immitis caused a decrease in vitro of total hemolytic complement in serum from a nonsensitized person. Activation involved both classic and alternative pathways as shown by deprssion of hemolytic C4 and by generation of products of activation of components C3, C4, and factor B. In addition, functional complement activity or immunoreactive levels of complement components or both were measured in 23 patients with self-limited or disseminated coccidioidomycosis. Low total hemolytic complement was found in nine, usually during the early phase of primary illness, and was transient. Hemolytic C4 was low, and the effect of inulin to decrease complement levels was blunted, suggested both classic and alternative pathways may be deficient. However, associated depression of immunoreactive levels of components assayed (C3, C4, C5, factor B, and properdin) was not consistently found. This disparity raises the possibility of enhanced in vitro inactivation analogous to activation by immune complexes.
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PMID:Complement activation by Coccidioides immitis: in vitro and clinical studies. 690 3

Splenocytes of C57BL/6J mice injected with a Trichinella spiralis larval extract for 7 consecutive days were transferred in two doses into isogenic, immunocompetent mice. On the 3rd day, some recipients were immunized with 10(9) sheep red blood cells and others were killed to investigate blastogenic response of their splenocytes to concanavalin A (Con A), Escherichia coli lipopolysaccharide (LPS), and Mycobacterium's purified protein derivative (PPD). On the 8th day of immunization, the corresponding mice were killed to study rosette-forming cells (RFC) and direct and indirect plaque-forming cells (D- and I-PFC) in their spleens. Transfer of 10(6) cells depressed the Con A reactivity and the number of RFC and 1-PFC, but increased the PPD reactivity and the number of D-PFC in the recipients, as compared to control mice receiving splenocytes from donors injected with a saline solution. Ten million cells inhibited only the Con A reactivity, but enhanced the number of LPS- and PPD-responding cells and of D-PFC in the recipients over the controls. Inoculation of cells from mice injected with bovine serum albumin did not reproduce the same effects. Splenocytes of mice treated with T. spiralis extract simultaneously inhibit and enhance diverse functions of the immune system. Stimulation is exerted on IgG antibody production and appears to be mediated by suppressor T-cells. Stimulation is exerted mainly on IgM antibody formation. Depression seems to be antigen-specific; it is partially compensated by the concurrent suppression, and it is probably a result of macrophage activation.
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PMID:Responses of B-cells to mitogens and antigen in mice receiving isogenic splenocytes from animals treated with Trichinella extract. 697 Feb 60

Abnormalities of the immune response can be secondary to old age, to several pathologic conditions (i.e. diabetes mellitus, renal failure, solid and lymphohematologic neoplasias, leukopenia, malnutrition, autoimmune diseases, AIDS), to surgical stress or to burns, and to immunosuppressive therapies, both medical (corticosteroids, cytotoxic agents, antilymphocytic globulins) and surgical (splenectomy) as well as radiant (extensive radiotherapy). Old age can affect both humoral (reduced antibody synthesis) and cell-mediated (thymus involution, diminished ratio Th/Ts, depression of both delayed hypersensitivity reactions and cytotoxic activity of K cells) immune response. Hyponutrition, often observed in the elderly, adds a reduced production of secretory IgA, lysozyme and interferon, diminished complementary activity, phagocytosis defects, and vitamin deficits. Furthermore, in some chronic diseases we can observe reduced primary antibody response or depression of delayed hypersensitivity reactions (renal failure, neoplasias), changes in leukocyte functions (diabetes mellitus, leukemias and lymphomas) and, in particular in solid neoplasias, increased activity of Ts lymphocytes and the presence of circulating immunocomplexes. Changes in phagocytosis, opsonization and chemotaxis are typically seen in burns, whereas surgical stress can cause some inhibition of cell-mediated immunity. Finally, after splenectomy it is possible to observe an increased synthesis of IgA and IgG and, on the contrary, reduced production of IgM and properdin.
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PMID:[Pathogenetic mechanisms responsible for producing a secondary immunodeficiency state]. 786 Dec 9

Investigations have been carried out in experimental systems in vivo on noncastrated and ovariectomized female [correction of male] mice and in vitro. The secondary immune response to sheep erythrocytes has been estimated on the 5-th day after reimmunization by IgM and IgG levels in the antibody-forming cells (AFC). It has been established, that in a dose of 40, IU, chorionic gonadotropin (CG) does not influence the formation of a secondary immune response. All the effects of the hormone are associated with the dose of 200 IU, extrapolated from the maximum CG level during pregnancy. CG in this dose reduces spleen cellularity and suppresses the PFC formation processes. Ovarian sexual steroids do not mediate CG immunodepressive effects, but they are able to abolish the effect of G-AFC depression. An hour preincubation of CG (200 IU) with sensitized splenocytes in vitro suppresses M-AFC formation processes. So, if CG (200 IU) interacts with immunocompetent cells before their repeated contact with antigen, the M-AFC counts decreases; after reimmunization the G-AFC counts decreases.
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PMID:[The effect of chorionic gonadotropin on the formation of a secondary immune response]. 811 59


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