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)

Several experiments conducted by our group over a period of 6 years have shown that nutritional stress, especially protein and/or calorie deprivation, leads to many, often dramatic, changes in the immune responses of mice, rats, and guinea pigs. Chronic protein deprivation (CPD) has been shown to create an enhancing effect on the cell-mediated immune responses of these animals. Humoral responses under CPD conditions were most often found to be depressed, but sometimes were unaffected, depending on the nature of the antigen employed. Chronic protein deprivation, consistent with the pattern just mentioned, improved tumor immunity by depressing production of B-cell blocking factors, and, in at least one instance, resistance to development of mammary adenocarcinoma in C3H mice was associated with evidence of increased numbers of T suppressor cells. Profound nutritional deficits (less than 5% protein per total daily food intake) depressed both cellular and humoral immunity. Early, though temporary, protein deprivation caused a long-term depression of both cellular and humoral immunity also, with the humoral component being the first to recover. Manipulation of protein and calories was found to have a profound effect on certain autoimmune conditions. Diets high in fat and low in protein favored reproduction but shortened the life of NZB mice, whereas diets high in protein and low in fat inhibited development of autoimmunity and prolonged life. Chronic moderate protein restriction permitted NZB mice to maintain their normally waning immunologic functions much longer than mice fed a normal protein intake. Further, the low-protein diet was associated with a delay in development of manifestations of autoimmunity. Decreasing dietary calories by a reduction of fats, carbohydrates, and proteins more than doubled the average life span of (NZB X NZW)F1 mice, a strain prone to early death from autoimmune disease. Histopathologic studies using immunofluorescent microscopy revealed that the development of the renal lesions caused by the deposition of antigen-antibody complexes, which is so characteristic of these mice, was markedly delayed.
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PMID:Nutritional deficiency, immunologic function, and disease. 0 88

A five-year retrospective study of obstetric admissions to the Surgical Intensive Care Unit (SICU) in the National University Hospital, Singapore was carried out with the aim of determining the incidence, causes and outcome of these admissions. Most of the patients were admitted following emergency caesarean sections. Obstetric complications was the reason for admission in 56.8% with hypertensive disease of pregnancy being the major cause and haemorrhage accounting for the rest. Anaesthetic complications accounted for 21.6% of admissions and these included difficult intubation, aspiration pneumonitis, cardiac arrhythmias and respiratory depression. Medical complications due to cardiovascular disease, autoimmune disease and malignancy also accounted for 21.6% of admissions. Only 37 out of 16264 deliveries (0.22%) required intensive care support. The median of duration of stay was one day.
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PMID:Obstetric admissions to the intensive care unit--a retrospective review. 129 21

Systemic lupus erythematosus is a multisystem autoimmune disease that may affect skin, joints, mucous membranes, heart, lungs, kidneys, nervous system and all the blood cell lines. Although its cause is unknown, abnormal immune function results in the formation of antibodies directed against various components of the human body (autoantibodies). Treatment depends of the severity of the illness and may include nonsteroidal antiinflammatory agents for arthritis; antimalarial therapy for skin disease and other mild lupus manifestations; and corticosteroids and immunosuppressive agents including azathioprine, cyclophosphamide, and methotrexate for more severe lupus manifestations. Persons affected by lupus and their families need help in understanding the condition and require support as they deal with fear, depression, and possible disability. Implications for nursing are varied and include patient/family education about medication, joint protection principles, energy conservation, pain and stress management, and coping techniques.
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PMID:Systemic lupus erythematosus: medical and nursing treatments. 149 76

64 members of a large kindred with inherited deficiency of the seventh component of complement, C7, were studied for plasma levels of antigenetic and functional components of complement as well as for clinical manifestations of infections and autoimmune diseases. Thirty-six individuals showed a low level of C2, C7, C8, and/or C9, including null alleles for C4A and C4B. Two subjects had a complete C7 deficiency. One of them concomitantly presented a low C2 level and a C4BQ0 allele. HLA allotyping strongly suggested C2 depression associated with a C4BQ0 allele. The 2 individuals with total absence of C7 suffered from fulminant disseminated meningococcal infections. The partial depression of one or more complement components associated with apparent good health. These results may indicate that simultaneous partial depressions of up to four complement components do not lead to clinical manifestation of infectious and autoimmune disease.
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PMID:Clinical manifestations in humans of combined C7 and C4 deficiency associated with low levels of C2, C8, and C9. 205 10

In Brown-Norway (BN) rats mercuric chloride induces an autoimmune disease characterized by an increase in serum IgE concentration, and by the production of anti-glomerular basement membrane antibodies responsible for a glomerulonephritis with a heavy proteinuria. (i) This disease results from a B-cell polyclonal activation probably due to frequent anti-class II T cells. (ii) The self limitation observed in this model is associated with both a decrease in the frequency of anti-class II T cells and the emergence of CD8+ T cells able to suppress these autoreactive T cells. (iii) In Lewis (LEW) rats which do not develop autoimmunity, HgCl2 provokes the appearance of non-antigen-specific CD8+ T cells responsible for a depression of T-cell functions. The aim of this work was to test the effect of treatment with an anti-CD8 monoclonal antibody (MoAb) in both BN and LEW rats. Anti-CD8 MoAb-treated rats were effectively depleted in CD8+ T cells. However, neither the induction nor regulation phases of mercury-induced autoimmunity were modified in BN rats. Mercury-induced immunosuppression in LEW rats was abrogated; however, depletion in CD8+ T cells did not allow the disease to occur in that strain. Finally, CD8 depletion induced in normal BN rats the appearance of rare anti-class II T cells showing that these cells are normally present in that strain but negatively controlled by suppressor T cells.
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PMID:Role of CD8+ T cells in mercury-induced autoimmunity or immunosuppression in the rat. 213 55

Immunization with attenuated activated autoreactive T cell lines and clones induces a response in syngeneic animals which can induce protection or recovery from autoimmune disease. This process has been termed T cell vaccination. The aim of the present study was to investigate the effect of immunization with MHC-reactive T cells on the mixed lymphocyte reaction (MLR). By injecting attenuated activated T cells primed for an alloantigen, we markedly reduced the MLR in both rats and mice. This depression appeared to be mediated by active suppression; lymphoid cells from T cell-vaccinated animals suppressed the MLR responsiveness of T cells from naive animals. Suppression of the MLR was not restricted to the major histocompatibility complex (MHC) alleles used to prime the animals from which the T cell vaccines were prepared; the MLR to other MHC allelic stimulator cells was also suppressed. This MHC-unrestricted suppression could not be attributed to an anti-ergotypic response to non-MHC-linked activation markers on T cells; an anti-ergotypic response augmented rather than suppressed the MLR. We herein propose that T cell vaccination might influence the MLR by suppressing the responses of diverse T cells which bear shared T cell receptor idiotypes.
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PMID:Inhibition of the mixed lymphocyte reaction by T cell vaccination. 214 51

Myasthenia gravis is an autoimmune disease involving the acetylcholine receptors at neuromuscular junctions. Perioperative management of patients with myasthenia gravis is complicated by their enhanced sensitivity to nondepolarizing neuromuscular blocking agents and their resistance to depolarizing drugs (1). Prolonged respiratory depression commonly occurs when these agents are used. Atracurium dibesilate is one of a new series of nondepolarizing agents and is promising by virtue of its rapid degradation by 'Hoffmann elimination', leaving products with little or no muscle blocking activity. After encouraging results were obtained with atracurium (2-6), we investigated the neuromuscular blocking effect of different doses of the drug (0.2 mg/kg, 0.5 mg/kg) in sixteen myasthenic patients undergoing thymectomy, with continuous monitoring of neuromuscular function.
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PMID:Evaluation of atracurium in myasthenic patients undergoing thymectomy. 224 32

Chronic idiopathic thrombocytopenic purpura (ITP) is an autoimmune disorder in which the abnormality in cellular immunity has remained only vaguely defined. Previously we have shown that patients with ITP in its active phase have abnormal T cell subsets. We then examined the phenotypes of T and B lymphocytes in an additional 28 patients with ITP and 32 age- and sex-matched normal controls and compared the lymphocytes' capacity to respond to polyclonal T, T cell-dependent B, and B cell mitogens. Blastogenesis to optimal (5.0 micrograms/mL) and suboptimal (0.5 microgram/mL) concentrations of the polyclonal T cell mitogens were markedly depressed in patients compared with normal controls (P less than .0005). Similarly, a severe depression in response was noted with the polyclonal T cell-dependent B cell mitogen (P less than .000001). No difference was seen, however, with the polyclonal B cell mitogen. The proportions of pan-T and T helper/inducer lymphocytes were significantly depressed (P less than .005 and P less than .000005 respectively), and the T suppressor/cytotoxic lymphocytes increased (P less than .02) in patients relative to controls. But there was no difference in the proportion of B lymphocytes or in their functional response. The abnormal cellular immunity appears to be due to a defect in the T lymphocyte population without involvement of the B lymphocytes.
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PMID:Depressed functional and phenotypic properties of T but not B lymphocytes in idiopathic thrombocytopenic purpura. 325 71

B6-lpr/lpr mice develop massive T cell lymphoproliferation, as associated with autoimmune disease. We found a reduced NK activity in the spleen of B6-lpr/lpr mice. Neonatal thymectomy markedly retarded the development of lymphoproliferation and the development of autoantibodies in the B6-lpr/lpr mice. These animals had a higher level of NK activity in the spleen. When the neonatally thymectomized B6-lpr/lpr mice were given anti-asialo GM1 serum (30 microliter) four times at 6-day intervals, initiated at the 8th-10th postnatal week, these mice developed lymphoproliferative disorders and splenomegaly, concomitantly with depression of NK activity. It is therefore tempting to speculate that NK cells are involved in the regulation of the occurrence of lymphoproliferative disorders.
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PMID:Does depression of NK activity cause lymphadenopathy in lpr mice? 326 41

Brown-Norway (BN) rats injected with HgCl2 develop a systemic autoimmune disease associated with a polyclonal B cell activation, due to autoreactive T cells specific for self-class II molecules, while Lewis (LEW) rats injected with HgCl2 do not exhibit autoimmunity and develop a non-antigen-specific, CD8-mediated immunosuppression assessed by a depression of T cell functions, and a protection against experimental autoimmune encephalomyelitis (EAE). Resistance to HgCl2-induced autoimmunity is not due to these suppressor cells since treatment with an anti-CD8 monoclonal antibody (mAb) did not allow autoimmunity to appear. The absence of autoimmunity in this strain could result from the absence of autoreactive T cells, or from quantitative or qualitative differences of these cells between susceptible and resistant strains. In the present study, we show that CD4+ anti-class II T cells are present in HgCl2-injected LEW rats and are as frequent as in BN rats when assessed by limiting dilution analysis. LEW CD4+ autoreactive T cell lines were derived. They proliferated in the presence of normal class II-bearing cells, secreted interleukin 2, and did not induce B cells to produce immunoglobulins. Transfer of one of these lines, LEW Hg A, into normal LEW rats led to the appearance of CD8+ cells responsible for a non-antigen-specific immunosuppression that induced complete protection from EAE. Immunosuppression was abrogated after treatment with an anti-CD8 mAb. In vitro, CD8+ cells from rats injected with the LEW Hg A T cell line proliferated in the presence of activated T cells whatever their origin. We conclude that HgCl2 induces CD4+ autoreactive T cells that proliferate in the presence of class II+ cells in susceptible BN as well as in resistant LEW rats. But while these cells collaborate with B cells to produce autoantibodies in BN rats, they initiate in LEW rats a suppressor circuit involving antiergotypic CD8+ suppressor cells.
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PMID:Mercury-induced autoreactive anti-class II T cell line protects from experimental autoimmune encephalomyelitis by the bias of CD8+ antiergotypic cells in Lewis rats. 809 39


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