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)

Acute causes and chronic risk factors for the development of acute renal failure were analyzed in prospective acquired data of 261 patients in a medical ICU. The population was divided into a group requiring dialysis treatment for established renal failure (n = 95) and a collective maintaining mild renal insufficiency (n = 166). Bivariate and linear discriminant analyses revealed that, above all, variables related to bacterial infections (sepsis and administration of antibiotic agents) and pancreatitis contributed to the discrimination, followed by bleeding, volume depletion, and chronic liver disease in the discriminant function. Bivariate analysis also yielded significant results for mechanical ventilation, CNS depression, and surgery. The importance of the nephrotoxic properties of aminoglycosides may be outweighed by their role as an indicator of severe infectious disease. The overall correct classification rate of the discriminant function was 78.5%, which reflects the importance of the predictor variables, but does not allow individual predictions.
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PMID:Impairment of renal function in medical intensive care: predictability of acute renal failure. 218 66

The concentrations of plasma ceruloplasmin, plasma fibrinogen, serum haptoglobin and the major cell types in blood together with liveweight changes were monitored during the acute phase response in sheep. Five control sheep, five sheep that underwent sham bronchial obstruction, and five sheep that developed pneumonia after bronchial obstruction were examined. Blood samples were taken and liveweights were recorded from four to six days before until 14 days after the surgical operations (sham and bronchial obstruction). The operations led to an acute phase response in the sheep and the development of pneumonia increased and sustained the response or led to a secondary response. Statistically significant changes observed in the blood of the sheep during the acute phase response included increased concentrations of plasma ceruloplasmin and plasma fibrinogen, depression of erythrocyte numbers and elevation of neutrophil numbers (means on day of maximum change as percentage of pretreatment values; 250 per cent, 400 per cent, 80 per cent and 200 per cent, respectively). Serum haptoglobin showed a pronounced and significant increase in concentration (over 6000 per cent of pretreatment values in some sheep). All three groups of sheep showed significant depression of liveweight after overnight confinement in the surgery but this was sustained for the period of the experiment only in the bronchial obstruction group. The results indicated that measurement of the concentrations of the three plasma proteins may be more useful in the diagnosis of tissue injury and infectious disease than the number of circulating neutrophils in sheep.
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PMID:Acute phase response of sheep: changes in the concentrations of ceruloplasmin, fibrinogen, haptoglobin and the major blood cell types associated with pulmonary damage. 246 10

The compromised host has recently increased because of the improvement of medical diagnosis and technology. Infection in the compromised host is somewhat different from that in common patients, since this infection is caused by impairment of the host defense mechanism. And the compromised host easily suffers from opportunistic infections. This situation prompted us to study the effect of biological response modifiers (BRMs), which activate the host defense mechanism against infections in the compromised host. We used streptozotocin (STZ)-induced diabetic mice, as experimental models of the compromised host. First, we investigated the bactericidal capacity of the perineal exudating neutrophils in diabetic mice, as one of the host defense mechanism. Second, we also studied the effect of Granulocyte-Colony Stimulating Factor (G-CSF) on diabetic mice with ascending pyelonephritis by P. aeruginosa. At 1 and 2 weeks after inducing the diabetic state, no difference was found in the bactericidal capacity of the perineal exudating neutrophils between normal mice and diabetic mice. At 3 weeks, however, this bactericidal capacity was markedly suppressed in these mice. This result suggested that a depression of host defense mechanisms in diabetics was caused by, in part, a suppression of bactericidal capacity of neutrophils. When G-CSF (2 micrograms/mouse) was injected subcutaneously once a day into diabetic mice, the suppression of the bactericidal capacity of neutrophils significantly recovered. We thus studied the effect of G-CSF on diabetic mice against infection. Diabetic mice increased their susceptibility to bacterial infection more than normal mice. In diabetic mice, administration of G-CSF (2 micrograms/mouse) yielded a lower incidence of infection and infection-induced mortality than those of controls. These data show that G-CSF may be of great value for prevention and treatment of opportunistic infections in the compromised host, especially in patients whose bactericidal capacity of neutrophils is depressed, as in diabetics.
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PMID:[Study of the prophylactic effect of human granulocyte-colony stimulating factor (G-CSF) on experimental pyelonephritis induced by Pseudomonas aeruginosa in diabetic mice]. 248 17

After peroral infection with cysts of Toxoplasma gondii, C57BL/6 mice died and A/J mice survived. To better understand the reasons for this difference in survival, host defenses during acute infection were studied: initial portal of entry of T. gondii contributed to susceptibility as more C57BL/6 mice survived after i.p. than peroral infection (p less than 0.001). Susceptible (C57BL/6) mice had more necrosis and inflammation in their brains, livers, and mesenteric lymph nodes than resistant (A/J) mice. Susceptible mice had less IgM antibody to T. gondii (p less than 0.0005) than resistant mice 7 days after infection, but amounts of IgG antibody to T. gondii were similar. Infection reduced percentages of spleen cells with the Lyt-2+ phenotype in susceptible (p less than 0.02) but not resistant mice; infection decreased percentages of spleen cells with the L3T4+ phenotype similarly in both strains of mice. Spleen cells from infected susceptible mice had greater depression in their blastogenic response to Con A (p less than 0.05) and produced significantly more IFN-gamma in culture with (p = 0.009) or without (p less than 0.05) Toxoplasma Ag than spleen cells from infected resistant mice. Infection increased serum levels of IFN-gamma substantially in susceptible but not resistant mice. Lymphocyte IL-2 production was similar in both groups of mice. Peritoneal macrophages from both strains of mice became activated to inhibit or kill T. gondii by 7 days after infection, but Kupffer cells became activated only in susceptible mice. These results indicate that increased resistance to peroral Toxoplasma infection is likely to be mediated by a number of immune responses acting together. They suggest that increased susceptibility may result from inadequately regulated inflammatory responses that increase tissue destruction.
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PMID:Immune responses associated with early survival after peroral infection with Toxoplasma gondii. 249 63

Encephlitozoonosis was induced in 35 of 38 vervet monkeys (Cercopithecus pygerythrus). They were either directly (orally) inoculated with Encephlitozoon cuniculi or indirectly exposed to this protozoan parasite. Cell-culture-grown spores of E. cuniculi, isolated from the kidneys of dogs with natural, fatal disease, were administered orally to 29 of these monkeys. Another 5 were exposed in utero by orally infecting pregnant females, and 3 were exposed to horizontal infection by nursing infected infants. Only one was given an intravenous inoculation of spores. The disease was induced in non-gravid and late-pregnant adults, immunocompetent infants, and in infants that were immunologically compromised by parenteral steroid administration, as well as in one infant that was immunologically immature because of its premature birth. The effects of age, dosage, post-inoculation (PI) interval, passage level of the parasite in cell culture and immunological status of the host were correlated with macroscopical and microscopical lesions. The experimentally induced infection was confirmed either by reisolation of the parasite in cell culture or by observation of spores in tissue sections. Both confirmatory methods were supported by serological examination. Reisolation of the organism in primary cell culture prepared from kidneys usually resulted in more frequent isolates and larger yields of spores from infants than from adult vervets. Infection with E. cuniculi invariably induced subclinical disease. Based on histology, lesions were minimal to moderately severe, depending on age, PI interval, and immunological status of the host. Alimentary tract infections were seen histologically as early as three days PI. Subsequently, infections resulted in detectable lesions most consistently in the liver, kidneys and brain. Lesions in these organs were generally granulomatous and were similar to those found in canine encephalitozoonosis. In addition, multifocal interstitial pneumonitis and myocarditis as well as vasculitis and perivasculitis were seen in other tissues and organs. Infants had more severe and more widespread lesions than adults. Although lesions and spores were still present in the brain of one immunocompetent infant 36 weeks after initial infection, the disease in immunocompetent infants and adults is thought to be self-limiting. However, infection may persist. Immunological depression favoured increased growth and multiplication of the organism, and resulted in detection of more spores within inflammatory lesions as well as more intracellular colonies of the organism that were free of inflammatory reaction.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies of encephalitozoonosis in vervet monkeys (Cercopithecus pygerythrus) orally inoculated with spores of Encephalitozoon cuniculi isolated from dogs (Canis familiaris). 249 97

The influence of Ly146032, a new acidic lipopeptide, on chemotaxis, luminol-dependent chemiluminescence of human polymorphonuclear leukocytes (PMN) and phythemagglutinin induced lymphocyte transformation of murine cells was investigated. At therapeutic range there was no remarkable effect on the parameters tested. Incubation with more than 20 mg/l Ly146032 was followed by depression of chemiluminescence, whilst transformation of maximally PHA stimulated lymphocytes was suppressed by more than 32 mg/l Ly146032.
Infection
PMID:Influence of Ly146032 on chemotaxis, chemiluminescence of PMN and lymphocyte transformation in vitro. 255 38

We have compared the in-vitro interaction of five macrolides (roxithromycin, erythromycin, spiramycin, oleandomycin and josamycin) with human neutrophils (PMN). Only roxithromycin strongly impaired the oxidative burst of PMN assessed by luminol amplified chemiluminescence, superoxide anion generation, and myeloperoxidase-mediated iodination of proteins. This effect was observed only for high concentrations of this drug (100 and 50 mg/l). Furthermore, the sensitivity of PMN to the depressive effect of roxithromycin permitted the definition of two kinds of PMN: in Highly Sensitive (HS)-PMN, the oxidative response was completely abolished while in Moderately Sensitive (MS)-PMN, a decreased, but yet measurable (20-50% of the control), response was obtained. The roxithromycin-induced depression of PMN was time-dependent and partly reversed by washing. Chemotaxis was also impaired by roxithromycin (100 mg/l) but phagocytosis of Klebsiella pneumoniae was unaltered even at high concentrations of the drug. Since roxithromycin displays the highest intracellular uptake, compared with the other macrolides assessed in this study, this could explain the results observed here. The relevance to the clinical situation needs further study. This effect of roxithromycin could be useful to control the inflammatory process associated in certain infectious diseases, in particular if high concentrations of the drug are obtained in tissues.
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PMID:Comparison of the in-vitro effect of several macrolides on the oxidative burst of human neutrophils. 255 72

Cachectin/tumor necrosis factor-alpha (TNF), a protein produced by macrophages upon stimulation, has been implicated as an important mediator of inflammatory processes and of clinical manifestations in chronic infectious diseases. In order to study further the potential role of TNF in infectious diseases, a homologous system was employed in which recombinant Escherichia coli (E. coli) derived bovine TNF (rBoTNF) was injected in cattle, either as a single bolus or in a repetitive treatment-regime. No clinical signs were observed, although changes occurred in hematologic and immunologic parameters when less than 0.5 mg of TNF/100 kg body weight was administered twice daily for 18 days. Prolonged treatment with 0.05-0.5 mg/100 kg induced histologic but no gross changes in the kidneys and liver. When doses were increased above 0.5 mg/100 kg, depression, anorexia, cachexia, and diarrhea appeared rapidly. Pathologic changes were apparent in various tissues including liver, kidneys, and lymphoid organs; body fat depots were depleted. Most of these changes appeared to be reversible; return to normal tissue-morphology occurred within 3 weeks of withdrawal of rBoTNF. The clinical and pathologic changes induced by prolonged rBoTNF administration resembled those observed in some chronic parasitic and viral infections of cattle in which macrophage-activation characteristically occur. Our finding may be relevant to the elucidation of the pathogenesis of these and other chronic infections.
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PMID:Effect of chronic administration of recombinant bovine tumor necrosis factor to cattle. 260 27

During an outbreak of a serious apparently infectious disease among harbour seals (Phoca vitulina), which started in the Kattegat area in April 1988 and rapidly spread to the North sea, the Wadden sea and the Baltic sea, greater than 17,000 animals died within a period of eight months. In August 1988 it was realized that the clinical symptoms and pathological lesions were similar to those found in canine distemper: apart from general depression and fever, the animals suffered from severe respiratory, gastrointestinal and central nervous disease and a variety of viral, bacterial and parasitic infections were frequently encountered, suggesting a severe malfunctioning of the immune system. At different expert meetings, held in several of the countries involved, possible explanations for the deaths were not only attributed to an infectious agent, but also to effects of overpopulation and environmental pollution. Seroepizootiological studies and the failure of vaccination experiments suggested that a herpesvirus and a picornavirus, which had been isolated from dead seals at the beginning of the outbreak, were opportunistic infections occurring in animals suffering from another infection rather than being the primary cause of the outbreaks. Serological studies were then extended to other viruses of carnivores, known to cause similar symptoms. Screening of a large panel of seal sera from the Netherlands, Denmark, FRG, Sweden and the UK, collected before and during the outbreak, in a virus neutralization test for the presence of canine distemper virus (CDV) neutralizing antibodies, indicated that CDV or a closely related morbillivirus was the primary cause of the disease outbreak.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A morbillivirus causing mass mortality in seals. 260 21

The effect of the infection with the mycelial form of a Candida albicans strain (Mycology Dept.) upon the immune system in mice was studied. BALB/c mice were infected intraperitoneally in a single dose of a 3 x 10(6), 6 x 10(6) and 12 x 10(6) cell suspension of the strain. Macrophages's activity was studied the days 7, 14, 21, 28, 35, and 42 after inoculation, by the following assays: phagocytosis in vitro, mononucleated phagocytic system by the colloidal carbon clearance technique, the lymphocyte's activity by the direct plaque forming cells technique (PFC) and delayed hypersensitivity (DTH). Infection with the mycelial form did not affect the peritoneal macrophage's phagocytic ability, neither modified the delayed hypersensitivity to sheep red blood cells (SRBC). However, a slight and transient depression of the lymphocyte stimulation was found. Suppression of PFC to SRBC was high when a 12 x 10(6) cell suspension was used in contrast to the infection with blastospores. These results suggest that systemic infection by Candida albicans in its mycelial form do not induce a non specific immunosuppression.
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PMID:Immune response in mice infected with Candida albicans in the mycelial form. 267 35


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