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)

Since the discovery that interferon inducers depress hepatic drug metabolism, the depressant action of cytochrome P450 (P450) has been demonstrated to be shared by cytokines such as interferon alpha/beta and interferon gamma as well as interleukin-1 and tumor necrosis factor. Because these cytokines are inflammatory mediators, it is not surprising that theophylline toxicity has been reported in patients with influenza B epidemic. Hence, to lay a foundation for studies of altered steroid and drug metabolism, the alteration of P450 isozymes was studied after polyriboinosinic acid:polyribocitidylic acid (poly I:poly C) administration. Twenty-four hours after poly I:poly C administration, hepatic P450 content decreased to 57% of control, whereas depression of other microsomal enzymes was less pronounced: P450 reductase (69%), cytochrome b5 (74%) and NADH-cytochrome b5 reductase (85%). The depression of mRNA for cytochrome P450 1A1, 1A2, 2C11 and 2E1 was more than 60% of the controls. Recovery of mRNA levels was not complete within 72 hr. The changes in mRNAs, in general, paralleled alterations of monooxygenase activities and P450 isozyme content suggesting that the effect of poly I:poly C is pretranslational for all P450 isozymes studied. No overt differential effect on P450 isozymes was found after an administration of poly I:poly C. This study complements the previous report which demonstrated down-regulation of mRNA for cytochrome P450 2C11 and 3A2.
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PMID:Suppression of hepatic drug metabolism by the interferon inducer, polyriboinosinic acid:polyribocitidylic acid. 140

Jurors on criminal trials carry a considerable burden of responsibility. They determine the defendant's fate. Additionally, during trials they can be exposed to stressful, frightening, and sordid aspects of life. The stressfulness varies depending upon the nature of the trial, its length, the nature of the testimony and evidence, the jurors' interpersonal relationships, the difficulty establishing guilt or innocence, the public's attitude, etc. These experiences can create psychological and/or physical discomfort that can be transient and mildly or moderately intense, or more serious and constitute illness. The authors have studied juries of four criminal trials--two murder cases, one child abuse case, and one obscenity case. Forty jurors were interviewed. Twenty-seven had one or more discomforting physical and/or physiological symptoms. These involved gastrointestinal distress (10 jurors); generalized nervousness (4 jurors); heart palpitation (6 jurors); headaches (4 jurors); sexual inhibitions (4 jurors); depression (4 jurors); anorexia (4 jurors); faintness (2 jurors); and numbness, lump in throat, chest pain, hives, and flu (1 juror each). Seven of the jurors became clearly ill. Illnesses included: peptic ulcer reactivation and hives, phobic reaction, anxiety state and increased alcohol use, hypertensive episode and visual scotomata, sexual inhibition, chills, fever, and depression, and post-traumatic stress disorder.
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PMID:The occupational hazards of jury duty. 142 62

The possible association between depression and type I allergies (i.e. immunoglobulin E-mediated hay fever, asthma, eczema, hives) was examined in a nonclinical sample of 379 college students. Measures included self-reports of depression, tiredness, fearfulness, allergic disorders, and environmental allergens and irritants. Seventy-one percent of the subjects who had ever received a professional diagnosis of depression also indicated a history of allergy: those with greater self-rated current depression overall reported a significantly higher prevalence of asthma (p less than 0.05). Type I allergic (43%) and nonallergic subjects did not differ in self-rated frequency of depression, fatigue, or anxiety. However, type I subjects reported significantly worse mood after the flu than did nonallergic subjects (p less than 0.001). The data support the hypothesis that individuals prone to clinical depression have more allergies than nondepressives. Allergics may experience more postflu mood worsening but not current depression in comparison with nonallergics.
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PMID:Depression and allergies: survey of a nonclinical population. 186 37

The effects of in vivo cocaine administrations on cellular cytotoxicity were studied. Cocaine induced a dose-related immunosuppression of natural killer cell activity, with maximal depression at 1-5 mg/kg. In addition, the degree of inhibition following a single intraperitoneal (i.p.) or intravenous cocaine dose (acute treatment, 1 mg/kg) was similar to that after repeated administration (subchronic treatment: 1 mg/kg/day i.p. for 7 consecutive days or subcutaneous administration by Alzet 2001 osmotic minipumps). T cells from cocaine-treated mice failed to generate cytotoxic T lymphocytes (CTL) in mixed lymphocyte cultures and acute or subchronic cocaine treatment also inhibited CTL generation in vivo. On the other hand, acute administration induced a very rapid (24-hour) inhibition of natural cytotoxicity, with a return to normal within 72 h after treatment. By contrast, repeated doses led to more protracted immunologic consequences and a delayed recovery (144 h). The effect of cocaine on susceptibility to influenza virus (PR8) infection was also investigated. Both acute and subchronic treatment significantly decreased resistance to PR8 infection. The results clearly indicate that cocaine has a potent suppressive effect on cellular immunity and that abuse can adversely affect the outcome of infectious diseases.
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PMID:Effect of acute or daily cocaine administration on cellular immune response and virus infection in mice. 196 12

The relationship between depression of early protection against influenza virus infection and the decrease in the number of peripheral polymorphonuclear leukocytes in cyclophosphamide-treated mice was investigated by means of a novel synthetic compound, Y-19995 [2,4'-bis(1-methyl-2-dimethyl-aminoethoxyl)-3-benzoylpyridine dimaleate], which had been shown to exert a potent restorative effect on leukocytopenia in immunocompromised hosts. Following intranasal inoculation with influenza virus (1.5 x 10(3) plaque-forming units) into untreated mice, the pulmonary virus titer progressively increased during 3 days and decreased gradually from day 7 after infection. The treatment with cyclophosphamide 2 days before infection markedly enhanced the pulmonary virus multiplication from the early phase of infection, and the higher virus titer was maintained thereafter. When mice were given Y-19995 after cyclophosphamide treatment, virus titers from the early to late phases of infection were lower than those in untreated mice. The number of peripheral polymorphonuclear leukocytes in cyclophosphamide-treated mice rapidly decreased and returned to normal levels only 9 days after the treatment, while such leukocytopenia was prevented to some extent and the leukocyte count was restored completely up to 7 days by postcyclophosphamide treatment with Y-19995. Furthermore, the treatment with Y-19995 augmented the inactivation of virus by the polymorphonuclear leukocytes. However, the virus inactivation by alveolar macrophages was modified only slightly by Y-19995 treatment. In addition, Y-19995 treatment could potentiate antibody-dependent cell-mediated cytotoxicity of polymorphonuclear leukocytes against the virus-infected target cells, and the production of serum neutralizing antibody to influenza virus in untreated and cyclophosphamide-treated mice. Y-19995 revealed neither antiviral nor interferon-inducing activities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Depression of early protection against influenza virus infection by cyclophosphamide and its restoration by Y-19995 [2,4'-bis(1-methyl-2-dimethyl-aminoethoxyl)-3-benzoylpyridine dimaleate]. 205 18

Natural killer (NK) cell activity was measured in the peripheral blood mononuclear cells (PBMC) from malnourished (MN) and well-nourished (WN) cancer patients and in healthy controls. A marked depression of NK activity was observed in MN cancer patients with moderate protein-calorie malnutrition (PCM), but not in WN cancer patients nor in the healthy controls. The depression of NK activity did not correlate with the localisation of the tumour, patient's age or body weight reduction. The defective NK activity of PBMC from MN cancer patients was restored to normal by rIL-2, but not by alfa-rIFN. Parenteral nutrition of MN patients with the proper amount of proteins and calories quickly corrected the depressed NK activity, indicating a central role of malnutrition in the genesis of their immune disfunction. PBMC from MN cancer patients produced lower amounts of IL-2, as compared with healthy controls, when stimulated in vitro; the most frequently affected were the responses to recall antigens such as influenza virus vaccine (FLU), while those to allogeneic PBMC (ALLO) and phytohaemagglutinin (PHA) were less affected. However, for each patient the ability to produce IL-2 in vitro did not correlate with NK activity, thus showing how the impairment of NK activity is not subsequent to a decreased production of endogenous IL-2. In summary, it can be concluded that malnutrition, rather than malignancy, plays a major role in the immune dysfunction of cancer patients.
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PMID:Reduced natural killer cell activity and IL-2 production in malnourished cancer patients. 206 35

Neonatal exposure to Gross murine leukemia virus results in a profound inhibition of the virus-specific T and B cell responses of adult animals. Animals exposed to virus as neonates exhibit a marked depression in virus-specific T cell function as measured by the virtual absence of in vivo delayed type hypersensitivity responses and in vitro proliferative responses to virally infected stimulator cells. Further, serum obtained from neonatally treated mice failed to either immunoprecipitate viral proteins or neutralize virus in an in vitro plaque assay, suggesting the concurrent induction of a state of B cell hyporesponsiveness. The specificity of this effect at the levels of both T and B cells was demonstrated by the ability of neonatally treated mice to respond normally after adult challenge with either irrelevant reovirus or influenza virus. The replication of Gross virus within both stromal and lymphocytic compartments of the neonatal thymus suggests that thymic education plays a key role in the induction of immunologic nonresponsiveness to viruses.
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PMID:Neonatal exposure to thymotropic gross murine leukemia virus induces virus-specific immunologic nonresponsiveness. 214 51

Polymyalgia rheumatica is a syndrome that occurs in the elderly and is characterized by pain and stiffness involving the neck, the shoulder girdle, and the hip girdle. The aching should be present for greater than one month. Polymyalgia rheumatica may be more common than reported. The etiology remains unknown. There is generally little found pathologically in this disease. The physical examination is often not impressive. Synovitis may be a main contributing factor to many of the symptoms seen in patients with polymyalgia rheumatica. Symptoms often do not correlate with physical findings. Polymyalgia rheumatica must be differentiated from many conditions since the diagnosis remains entirely clinical. Osteoarthritis, flu syndromes, inflammatory myopathies, fibromyalgia, and depression all have features that may mimic polymyalgia rheumatica. Malignancies and infections may also be difficult to separate from polymyalgia rheumatica. Polymyalgia rheumatica may also be extremely difficult to differentiate from seronegative rheumatoid arthritis in patients older than 50 years. Although some patients with polymyalgia rheumatica have underlying giant cell arteritis, the majority apparently do not. The distinction between polymyalgia rheumatica and giant cell arteritis cannot be made on the basis of laboratory studies and relies solely on clinical symptoms and physical findings. Although nonsteroidal antiinflammatory medications may control symptoms in patients with mild disease, most patients with polymyalgia rheumatica require low-dose corticosteroids. The tapering schedule for the corticosteroids is contingent upon the response of symptoms and laboratory parameters. Polymyalgia rheumatica usually follows a benign course with almost complete response to an adequate treatment program. Recently, there have been several studies suggesting that the course of polymyalgia rheumatica may not be as short and simple as once proposed. Nevertheless, many patients may be completely weaned from corticosteroids. Other agents have been used in this disease, but for the most part their use remains somewhat controversial. Patients must be monitored carefully. Most patients do well, and treatment is effective.
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PMID:Polymyalgia rheumatica. 218 54

Benzo[a]pyrene (B[a]P) in combination with coal, asbestos, or metal particles was studied for its inhibitory effects on interferon-alpha/beta induction by influenza virus in rhesus monkey kidney (LLC-MK2) cell monolayers. B[a]P per se had no adverse effect on the induction process. However, when cell cultures were pretreated with B[a]P that was bioactivated by rat liver S9 homogenate, from 52 to 65% inhibition of interferon induction occurred. Significantly greater (P less than 0.05) depression (coinhibition) of viral interferon induction (greater than 83%) resulted when bioactivated B[a]P was incorporated with coal particles representative of coal rank (anthracite, bituminous, lignite, peat). Coinhibition affected by bioactivated B[a]P was coal rank-independent but any interferon inhibitory activity affected by coal particles per se was coal rank-dependent. When metals (aluminum, aluminum oxide, ferric oxide, nickel, or chromium) or asbestos fibers (chrysotile, crocidolite, anthophyllite, or amosite) were individually mixed with bioactivated B[a]P, coinhibition of cellular interferon synthesis also resulted which was significantly greater (P less than 0.05) than that manifested by bioactivated B[a]P or particles per se. Coinhibition of interferon induction by silicates (Min-U-Sil, DQ-12, hypersthene, or wollastonite) and the bioactivated hydrocarbon was not in evidence although some silicates alone partially inhibited the induction process. Viral interferon induction was inhibited in a dose-response manner by B[a]P (+/- S9) in combination with selected particles. The adsorption of B[a]P to all types of particles was no more than 5.98 micrograms B[a]P/mg of particles and, moreover, less than 0.5% by weight. These findings provide further evidence that bioactivated B[a]P and occupation-related particles act together to coinhibit a biological defense mechanism, the interferon induction phase of the interferon system.
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PMID:Coinhibition of viral interferon induction by benzo[a]pyrene in association with occupation-related particles. 235 Nov 30

In a clinical phase II study nine patients (five men and four women; mean age 48 [42-58] years) in an early stage of chronic lymphatic leukaemia (CLL) of the B-cell type were treated with recombinant alpha-2b interferon (IFN alpha-2b), initially at a dosage of 5 mega units subcutaneously three times weekly, but in some cases reduced to 2.5 or raised to 10 mega units. Duration of treatment has been 15-36 months. Through-flow cytometry in seven patients demonstrated a definite fall in circulating B1-positive lymphocytes. Lasting partial remission (duration of 106-134 weeks) was achieved in four patients, in a further four the condition remained stable. A recurrence was noted in the patient with the initially highest lymphocyte count (52,000/microliters) after 28 weeks, control being achieved only after 64 weeks of chemotherapy. Side effects were flu'-like symptoms and (in two instances) depression. In three patients there was a clear rise in serum immunoglobulin concentrations as sign of IFN alpha-2b-induced increased immune response, while in four HLA-DR expression on monocytes was doubled. It is concluded that early treatment of CLL with IFN alpha-2b may delay the onset of necessary chemotherapy, any antibody-deficiency may be improved and survival time may ultimately be lengthened.
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PMID:[Interferon alfa-2B in chronic lymphatic leukemia of the B-cell type]. 237 39


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