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)

During phase-II studies monitored by Hoechst AG (Germany) and Daiichi (Japan) and phase-III/IV studies of Hoechst AG 577 adverse drug reactions were recorded among 13,717 patients treated with ofloxacin. Treatment was stopped in about 40% of the patients with adverse drug reactions. Most of the adverse reactions concerned the gastrointestinal tract. 124 adverse reactions concerned the central nervous system, mostly headache and sleep disturbances (n = 84). For the rare occurrences of other symptoms of the central nervous system, such as hallucinations (n = 1), nightmares (n = 1), confusion (n = 1), and depression (n = 2) the data are inadequate to appraise the relative importance of possible contributing factors.
Infection 1986
PMID:Safety of ofloxacin--adverse drug reactions reported during phase-II studies in Europe and in Japan. 295 61

1. Ten Friesian male calves of about 100 kg and 3 months old were reared similarly and were worm-free. From 13 weeks of age five calves received a dose of 640 infective larvae (L3) of lungworms (Dictyocaulus viviparus) twice weekly for 8 weeks to simulate continuous infection. Animals not infected were fed to the same level as the infected animals (about 1.2-1.3 kg concentrates and 1.4-1.5 kg good-quality hay/d). 2. Heat production was measured twice weekly during 48 h (days 2 and 3, and days 5 and 6) in each group of experimental animals. 3. Infection caused considerable damage to the lungs, increased respiration frequency and clearly produced antibody titres against D. viviparus. 4. Animals infected with lungworms had on average a lower rate of weight gain, reduced by 70 g/d per animal. Digestibility was not affected. Nitrogen retention was much lower in infected animals (12.0 v. 14.6 g/d per animal in controls). 5. Metabolizability of energy was slightly reduced in infected animals. Heat production as found in infected animals may be associated with an increased maintenance energy requirement of 30 kJ/kg live weight 0.75 per d or reduced partial efficiency of feed conversion above maintenance in animals infected with lungworms (58.5 v. 64.1% in the control animals). 6. It was concluded that the depression in rate of gain was related to reduced intake of feed and to decreased N retention.
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PMID:Effect of infection with lungworms (Dictyocaulus viviparus) on energy and nitrogen metabolism in growing calves. 296 Mar 73

Infections with gastrointestinal (GI) nematodes are among the most prevalent infections of man. Not only are they common and widespread in populations throughout the world, but they are frequently chronic and occur repeatedly throughout the lifetime of an individual. It is now well established that such parasites can be highly immunogenic and that their environment, the gastrointestinal tract, is well equipped to mount potent immune and inflammatory responses. The abundance and long-term survival of GI nematodes therefore present a paradox. This review takes the standpoint that man as a species has the capacity to produce effective and protective responses against GI infections, but that this capacity is subject to a number of powerful constraints, arising from parasite evasion, depression of response capacity and deficiency in response capacity. These constraints are discussed in the light of evidence drawn from experimental studies with animal models.
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PMID:Genetic and other constraints on resistance to infection with gastrointestinal nematodes. 311 Oct 21

Infection of mice with a temperature-sensitive mutant of Salmonella typhimurium C5TS allowed the survival of genetically susceptible mice. The ability to mount a delayed-type hypersensitivity (DTH) response to sheep erythrocytes during infection with C5TS was studied in various inbred mouse strains, recombinant inbred strains derived from C57BL/6 (susceptible) and A/J (resistant) mice, and C3H congenic mice. Suppression of the DTH response to sheep erythrocytes was found in mice that carried the Itys allele, the H-2b haplotype, or both. These genes are known to increase susceptibility to S. typhimurium infection. In contrast, no DTH response suppression was observed in mouse strains that carried other genes that increased susceptibility to S. typhimurium, e.g., DBA/2 and C3H/HeJ. Apart from a transient suppression in A/J mice, the DTH responses of resistant mice (A/J and CBA) were normal or increased. The DTH response to sheep erythrocytes could be restored in immunodepressed mice by increasing the immunizing dose, suggesting the possible role of activated macrophages in depression of the DTH response.
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PMID:Genetic control of Salmonella typhimurium-induced depression of delayed-type hypersensitivity to sheep erythrocytes in mice. 312 86

Infection of mice with Trypanosoma cruzi results in a severe immunosuppression, accompanied by the appearance of autoimmune symptoms. We have previously shown that proliferation and interleukin 2 production by concanavalin A-stimulated T cells from infected mice is severely depressed. In this study we show that at least two phenomena are responsible for this depression. First, mixing experiments showed the existence, in spleens of infected animals, of adherent, Thy-1-negative and radioresistant suppressor cells. Second, studies of enriched T cell populations and analysis of precursors by limiting dilution showed that the T cell compartment itself was impaired in infected animals: responses of enriched T cells, even when reconstituted with normal accessory cells, reached only 40% of those obtained with normal uninfected mice.
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PMID:T lymphocyte function during experimental Chagas' disease: production of and response to interleukin 2. 315 31

Studies of rabies virus in several animal models consistently showed hypothalamic infection, hypophyseal infection, dramatic growth impairment (in the form of failure to thrive), wasting syndrome, and immune depletion. Rabies virus infection was studied through routine monoclonal antinucleocapsid antibody immunofluorescence and through a peroxidase-antiperoxidase immunoperoxidase method. The latter was modified to detect the in situ production of growth hormone by uninfected and rabies virus-infected adeno-a-pituicytes (with confirmation of the results both in vivo and in vitro). Infection with rabies virus made the specialized pituicytes produce less growth hormone. Growth before rabies virus infection and its reduction due to infection were investigated in a linear regression model. The fit was statistically significant (P less than .05) in all species studied: mouse, rat, rabbit, cow, and cat. Immune depression was studied in terms of alterations in the immunotopography of the thymus and also the specific T- and B-cell homing areas of the spleen (although spleen data are not presented here). On the basis of these results and a thorough review of wasting syndromes encountered in other diseases, a primary failure to thrive and an ensuing wasting syndrome were described and characterized for rabies, and their origin was assigned to a dysfunction of the hypophyseal/hypothalamic/thymic axis associated with at least (but not necessarily only) one of the centrally controlled growth hormones.
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PMID:Failure to thrive, wasting syndrome, and immunodeficiency in rabies: a hypophyseal/hypothalamic/thymic axis effect of rabies virus. 320 86

Leprosy, a chronic infectious disease of man, is caused by the obligate intracellular bacterium M. leprae. Infection with M. leprae affects the peripheral nerves and the dermis, causing an accumulation of macrophages and other immune cells at the infected sites. Host resistance to the bacterium determines the extent of local inflammatory reactions and its resulting damage to the affected tissues. In lepromatous disease little if any cellular immunity develops. Bacterial multiplication is uncontrolled and M. leprae disseminate throughout most of the dermis. In tuberculoid disease, marked cellular immunity is observed and bacterial growth and dissemination are controlled. The depression of cellular immunity in lepromatous patients is not fully understood. Since M. leprae cannot be grown in vitro, and a suitable animal model has not yet been developed, the study of host immunity to the pathogen is limited primarily to investigations of the cutaneous lesions of patients and to in vitro responses of the peripheral blood leukocytes to M. leprae. While the blood monocytes of leprosy patients appear to be activated normally by lymphokines, T cell proliferation and production of lymphokines in response to M. leprae are impaired in lepromatous patients. Attempts to restore responsiveness in cells from these patients have been unsuccessful in our hands. The addition of exogenous IL-2 to leukocyte cultures does not appear to restore responsiveness to M. leprae in cells from nonresponsive patients. Rather, some enhancement, often not antigen specific, is observed in cells from patients with a preexisting response. Similarly, depletion of monocytes does not restore responsiveness to M. leprae in nonresponder patients, but a nonspecific enhancement of proliferation is observed in monocyte-free cultures from patients that do respond to M. leprae. Thus, the defect in lepromatous nonresponder patients does not result from a simple lack of IL-2 production or suppression by monocytes and/or their products. Possibly, there is a low level or lack of M. leprae-responsive T cells in the circulation of these patients. Attempts to overcome the defect in immunity of patients with lepromatous leprosy by immunoprophylaxis and immunotherapy are being investigated. This approach has become of major importance since the development of widespread drug resistance to Dapsone as well as to the other chemotherapeutic agents used to control leprosy.
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PMID:The immunobiology of leprosy. 351 11

Mechanisms which disturb mucociliary transport may act on the mucus, the ciliary action or both. Inflammation of the airways almost invariably induces reversible functional disturbances but can, in chronic diseases, also lead to irreversible morphological lesions. Infectious inflammation acts mainly through ciliostatic or cytotoxic effects on ciliated cells. Infections with rhinovirus, influenza virus A and M. pneumoniae may induce profound disturbances of the mucociliary system, with effects lasting up to 1 year. In non-infectious inflammation, the mucociliary system might be influenced by serum factors leaking through the bronchial wall, by inflammatory cells such as granulocytes and eosinophils, and by mediators released from mast cells. In a very early phase of the acute allergic reaction in bronchial asthma, these mediators are responsible for an acceleration of mucus transport, which is followed by a long-standing depression mainly due to the production of highly viscous mucus. Any positive therapeutic effects resulting from drug administration can only be achieved in early phases of the disease, before irreversible morphological lesions have occurred.
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PMID:Mucus transport and inflammation. 353 95

Mice exposed to primary infections with the parasite intestinal nematode Nematospiroides dubius failed to show the mucosal mast cell (MMC) response which is characteristic of infections with other species of intestinal nematode and which was readily induced in these mice by infections with Nippostrongylus brasiliensis or Trichinella spiralis. The failure to generate a mucosal mastocytosis was independent of host strain or sex. When infections with N. dubius were established before, or concurrently with, T. spiralis or N. brasiliensis, the MMC response elicited by these species was delayed and/or depressed as was expulsion of the worms themselves. Infection with N. dubius given when a MMC response was already established, by exposure to T. spiralis, had no effect on MMC numbers. The possibility that the effects of N. dubius upon MMC responses reflect a lack of mastocytopoietic potential, rather than an active interference, was excluded by showing that SJL mice, which expel primary infections with N. dubius and express strong immunity to reinfection, developed marked mastocytosis during secondary infections. The depression of MMC responses by N. dubius is discussed in relation to the known immunosuppressive properties of this parasite and in relation to the T cell mediated control of MMC development.
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PMID:Suppression of mucosal mastocytosis by infection with the intestinal nematode Nematospiroides dubius. 357 74

A prospective multicenter study concerning the incidence, onset time, risk factors and mortality of pneumonia was carried out by the Intensive Care Units Collaborative Group for Infection Control in Lombardy, Northern Italy. Out of 1304 patients admitted over 3 months in 16 intensive care units (ICUs), 441 met the criteria for the protocol (no previous pulmonary infection or irreversible terminal illness, ICU stay greater than 48 h). The incidence of acquired pneumonia was 21.3% (94/441), with 54.2% of cases diagnosed within 4 days of admission (early onset pneumonia). Impairment of airway reflexes on admission and more than 24 h respiratory assistance were shown as significant risk factors (RR) for early onset pneumonia (respectively RR = 12.4, with 95% confidence interval (CI) = 5.3-28.9 and RR = 3.3, with 95% CI = 1.8-5.9). A suggested pathogenetic mechanism is aspiration of oropharyngeal contents at the onset of acute illness, due to depression of protective reflexes with delayed clearance of bacterial contamination. No protection was offered by routinely applied prophylactic antibiotic therapy.
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PMID:Early onset pneumonia: a multicenter study in intensive care units. 365 99


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