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)

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

As a result of decreases in maternal mortality and infectious diseases, women's life expectancy has increased rapidly in this century and is expected to reach 83 years by the year 2000. However, there are a large number of chronic conditions that negatively affect the quality of life of women today: urinary tract infection, menstrual cycle disorders, hypertension, diabetes, osteoporosis, arthritis, eating disorders, substance abuse, and mental depression. Although women's life expectancy is 7.5 years greater than that of men, the morbidity rates are significantly higher for women. As women continue to enter the labor force in large numbers, questions are being raised regarding the physical and psychological hazards of jobs traditionally considered to be women's work, the risks associated with jobs that are physically demanding or involve exposure to toxic substances, and the association between pregnancy outcome and employment. Further research is needed on the effects of multiple role stress on women's health. Another recent trend has been the feminization of poverty: 2/3 of all US adults classified as poor are women. The lack of financial resources has a detrimental effect on nutrition, access to health care, and other preventive behaviors. Yet another social change related to women's health is the increasing number of elderly in the population. Women comprise 72% of the elderly poor, and over 80% of all retiring female workers do not have pension benefits. Access to, availability of, and payment for health care are problems for elderly women. It is important that research address the physiologic, psychosocial, and economic factors that together affect women's health status.
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PMID:Changing factors and changing needs in women's health care. 351 29

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

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

The enormous socio-cultural arrangements of the last centenary led to transformations in the course of diseases. Child mortality and infectious diseases could be largely eliminated. On the other hand, there appeared new diseases because of prolongation of life, increase of population, stress and conflicts. They, therefore, are called 'specific human diseases'--as depressions, neurosis, psychosomatic disturbances and drug abuse. In the last years depression more and more appeared as somatically masked depression.
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PMID:Psychosomatics and depression. 357 18

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

Infection often complicates renal failure and frequently causes death, but the association between renal failure, impaired immunity and infection has not been proved. A recent study showed that patients on dialysis did not show an expected leucocytic response to infection, suggesting that the blunted response was evidence of the immunocompromised state of the uraemic patient. In this study, the relationship between leucocytic responses and infectious challenge was investigated in an animal model of chronic renal failure. Bacteraemia, peritonitis and a chronic lung infection were induced in normal and uraemic rats; the leucocytic response was then monitored. In all three infections, the total white blood cell response was significantly less in the uraemic animals. Neutrophil numbers actually increased, but this response was disguised by a pronounced depression in lymphocyte numbers. Our conclusion is that, although the leucocytic response of the uraemic host to infection may be depressed, the changes to individual leucocyte components in the peripheral blood are sufficiently characteristic to provide useful evidence of infection.
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PMID:Host immune status in uraemia. VI. Leucocytic response to bacterial infection in chronic renal failure. 388 87

Plagemann, Peter G. W. (Western Reserve University, Cleveland, Ohio), and H. Earle Swim. Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell. J. Bacteriol. 91:2317-2326. 1966.-The replication of mengovirus was studied in two strains of Novikoff (rat) hepatoma cells propagated in vitro. The replicative cycle in both strains required 6.5 to 7 hr. Infection resulted in a marked depression of ribonucleic acid (RNA) and protein synthesis by strain N1S1-63. Inhibition of RNA synthesis was reflected by a decrease in the deoxyribonucleic acid (DNA)-dependent RNA polymerase activity of isolated nuclei. Mengovirus had no effect on either protein or RNA synthesis or on the DNA-dependent RNA polymerase activity of a second strain, N1S1-67. The time course of viral-induced synthesis of RNA by cells was studied in cells treated with actinomycin D. It was first detectable between 2.5 and 3 hr after infection and continued until 6.5 to 7 hr. The formation of mature virus was estimated biochemically by measuring the amount of RNA synthesized as a result of viral infection which was resistant to degradation by ribonuclease in the presence of deoxycholate. Approximately 70% of the deoxycholate-ribonuclease-resistant RNA was located in mature virus, and the remainder was double-stranded. The formation of mature virus began about 45 min after viral-directed (actinomycin-resistant) synthesis of RNA was detectable in the cell, and only about 18 to 20% of the total RNA synthesized was incorporated into virus. Release of virus from cells began about 1 hr after maturation was first detectable. Release of virus from cells was accompanied by a loss of a large proportion of their cytoplasmic RNA and protein.
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PMID:Replication of mengovirus. I. Effect on synthesis of macromolecules by host cell. 428 85

Amyloid goitre is a rare manifestation of amyloidosis; about 50 cases have been recorded and this paper adds a further six cases, the first to be described from Uganda. The condition has to be distinguished from the more common types of goitre, and histological differentiation from medullary carcinoma may be difficult with small biopsies. Irrespective of an underlying cause, the distribution of amyloidosis in Uganda resembles the classical secondary type, and the findings in 81 cases confirm this. The age of onset of the primary type is earlier than seen elsewhere and it is possible that these variations result from immune depression following malnutrition or endemic infectious diseases.
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PMID:Amyloid goitre. 507 3

Infection of adult BALB/c mice with Friend disease virus results in a leukemia-like disease characterized by erythropoietic changes and splenomegaly. A marked depression of formation of cellular and serum antibody occurs in infected animals. Electron-microscopic examination of the ultrastructure of spleen sections from infected mice with depressed immunity revealed that virus particles can be detected only in immature blastlike lymphoid cells and not in plasmocytes characteristic of the immune response in spleens of noninfected mice immunized with sheep erythrocytes.
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PMID:Leukemia virus suppression of antibody-forming cells: ultrastructure of infected spleens. 563 63


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