Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a 14-year-old boy of North-African origin, presenting a phagocytic sinus histiocytosis is reported. The main features of this now classical disease are illustrated: its localization to the neck, its chronicity, the fact that it is well tolerated, the pseudotumoral appearance of the adenomegaly as well as the intensive phagocytic (essentially lymphocytophagic) activity of the sinus macrophages. The bringing to light in a picture of hyperimmunity of an elevated percentage of antibodies against the measles and EB viruses, associated with a temporary depression of the cellular immunity, suggest that this lymphophagocytosis could be controlled and facilitated by preferential opsonization of lymphoid cells carrying on their membrane the antigen of the virus or viruses initially responsible.
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PMID:[Adenomegalic cytophagic sinusal histiocytosis. Morphological and immunologic study of a case]. 20 85

Twenty 1-day-old specific-pathogen-free chickens each were given an intraabdominal inoculation of either a type-8 avian adenovirus, [AMG 5 (2a], or a type-5 avian adenovirus, inclusion body hepatitis virus (IBHV). The diseases produced were similar. High (60-100%) mortality and statistically significant depression of body weights occurred in both infections. There were necrotizing hepatitis and pancreatitis, lymphoid depletion in the spleen, bursa of Fabricius and thymus, hydropericardium, nephritis and enteritis. Intranuclear inclusions occurred in affected organs. Fluorescent-antibody staining, the Feulgen reaction for deoxyribonucleic acid and electron microscopic studies, as well as studies from the literature, indicated that basophilic inclusions consisted of assembled adenovirions.
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PMID:Comparative study of experimental inclusion body hepatitis of chickens caused by two serotypes of avian adenovirus. 20 21

An 8 to 10-week-old female New Zealand white rabbit, Oryctolagus cuniculus, which exhibited clinical signs of anorexia, depression, and torticollis was found to have lymphosarcoma with lymphoblastic leukemia. The multiple visceral involvement with neoplastic lymphoid cells observed in this animal was similar to previously reprted cases of lymphosarcoma in the rabbit. An unusual finding was the occurrence of lymphoblastic leukemia since lymphosarcoma in the rabbit has previously been reported as aleukemic.
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PMID:Lymphosarcoma with lymphoblastic leukemia in a New Zealand white rabbit. 27 19

An immunodepressive action of the anticellular sera was cause by the competition of the serum and viral antigens, as well as by the specific influence of the sera on the corresponding cells. The antimacrophagal serum decreased the monocyte content in the peripheral blood, peritoneal exudate, and retarded the antibody formation in the lymphoid organs. The antilymphocytic serum depressed the development of the plasma cell reaction in the lymph nodes and the spleen, this being expressed in a depression of the increase of the serum antihemagglutinin titre. The antithymocytic serum shortened the period of the active antibody formation.
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PMID:[Comparison of the immunodepressant effect of antimacrophage, antilymphocyte and antithymocyte sera following immunization with influenza virus A2]. 30 Feb 5

The induction of tolerance to the 2,4,6-trinitrophenyl (TNP) hapten has been studied in a system utilizing haptenated syngeneic lymphoid cells. Specific depression of the direct and indirect plaque-forming cell (PFC) responses to TNP-protein conjugates was regularly achieved by pretreatment of Lewis rats with 1 X 10(7) trinitrophenylated spleen cells or TNP lymph node cells. Very low numbers of haptenated lymphocytes were active since tolerance could be induced in vivo with as few as 10(5)-10(6) TNP spleen cells (SC). SC exposed to as little as 10-100 mug of the reactive hapten, trinitrobenzene sulfonic acid, were effective tolerogens in this system. Tolerance induced with 10(7) haptenated spleen cells persisted for at least 4 weeks. Viable intact cells did not seem to be required in this system since the cell-free supernatants from TNP-SC cultured for 24 h were also active. In addition, significant depression of an ongoing immune response could also be imposed by haptenated isologous lymphoid cells. Moderate suppression of the "hapten-specific" delayed hypersensitivity response (measured by the accumulation of 51Cr-labeled bone marrow cells) was also achieved with TNP-SC. These results suggest that haptenated isologous lymphoid cells are potent tolerogenic conjugates capable of inducing tolerance affecting antibody formation and delayed hypersensitivity. However, since we and others have shown that TNP-SC do not adversely affect the generation of hapten-specific cytotoxic T cells, it is postulated that there is a differential recognition of, or response to, hapten-modified self-carriers by functionally distinct lymphocyte subpopulations.
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PMID:Role of self-carriers in the immune response and tolerance. II. Parameters of tolerance induced by haptenated lymphoid cells. 30 Mar 26

When normal mice are exposed for short periods to ultraviolet light (UV), they support the progressive growth of transplanted syngeneic UV-induced tumors. Normal nonirradiated mice almost always reject these tumor implants. The UV-mediated suppression of the antitumor response can be adoptively transferred to normal syngeneic mice with lymphoid cells derived from short-term UV-irradiated donors. Transfer of the suppressive effect is dosage dependent and also appears to require the presence of viable T lymphocytes. Suppressive activity was observed in both the spleen and thymus of UV-irradiated donors. In the preceding paper we have established that UV irradiation does not cause a general depression of testable immune functions. Collectively these data suggest that short-term UV irradiation of mice leads to an increase in suppressor cell activity, thereby causing an inhibition in the host's ability to respond to an antigenic UV-induced tumor. The possible role of this phenomenon in the mechanism of UV carcinogenesis is discussed.
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PMID:Modification of immunological potential by ultraviolet radiation. II. Generation of suppressor cells in short-term UV-irradiated mice. 30 10

The effects of infection on various aspects of lymphoid function in gnotobiotic dogs with 2 virulent strains of canine distemper virus (CDV), Snyder-Hill CDV and R252-CDV, were compared. Both infections resulted in a viremia-related lymphopenia which was nonselective in that the percentages of B and T cells remained unchanged throughout the observation period. Nonfatal Snyder-Hill-CDV infection resulted in a transient depression of in vitro lymphocyte responses to phytohemagglutinin-P, whereas R252-CDV produced prolonged in vitro suppression of phytohemagglutinin-P stimulation. The differences observed are of minor significance and do not explain the differences in central nervous system demyelinating potential between these 1 strains of CVD.
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PMID:Comparison of canine distemper virus strains in gnotobiotic dogs: effects on lymphoid tissues. 30 24

The authors present the results from the study of the cellular immunoreactivity of immunocompetent lymphoid cells in 23 patients with gastric carcinoma and 30 patients with ulcer disease of the stomach, by applying the test for the confirmation of rosette-forming T-lymphocytes, according to the method of Bach and Lay. A significantly decreased number of T-lymphocytes was found both in case of ulcer disease of the stomach and gastric carcinoma. Best manifested is the depression of the cellular immunoreactivity in gastric carcinoma and it corresponds to the degree of the generalization of the process.
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PMID:[Spontaneous rosette test in peptic ulcer of the stomach and stomach cancer]. 31 Jun 2

Patients with acute myelogenous leukemia in remission have pronounced deficiency in antibody-dependent cellular cytotoxicity (ADCC) and mitogen-induced cellular cytotoxicity. The deficiency in ADCC was partly explained by reduction in the number of circulating effector cells (Fc receptor-bearing cells) demonstrable at a time when white blood cell and platelet counts were normal. These cytotoxic functions, as well as the circulating numbers of T-cells and Fc receptor-bearing cells were further decreased by the administration of monthly cycles of combination chemotherapy with 1-beta-D-arabinofuranosylcytosine and 6-thioguanine. Following each cycle of chemotherapy, progressive recovery of these functions occurs during the third and fourth weeks with occasional increases above base line in patients in whom chemotherapy is withheld for longer than five weeks. In selected patients recovery of one cytotoxic function preceded the other, indicating that these functions are mediated by different effector cells. Administration of a single dose of daunomycin i.v. had no effect in either of these cytotoxic functions or in the circulating numbers of lymphocytes. The decrease in ADCC effector cell function induced by phase cycle-specific agents correlated with the level of reactivity exhibited by patients after achieving bone marrow and clinical remission. Patients showing low levels of reactivity postremission experienced highest degree of depression. In two patients, complete abrogation of ADCC effector function was demonstrated with minimal recovery even six weeks after stopping chemotherapy. These findings indicate that effector cells in ADCC and mitogen-induced cellular cytotoxicity are highly susceptible to phase cycle-specific agents, and their recovery takes longer that of other lymphoid and nonlymphoid populations.
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PMID:Deficiency of antibody-dependent cellular cytotoxicity and mitogen-induced cellular cytotoxicity effector cell function in patients with acute myelogenous leukemia in remission. 31 32

This paper analyses impairment of the primary immune response of mice bearing the plasmacytoma TEPC-183. Healthy animals and mice bearing the reported non-immunosuppressive tumour MOPC-104E were used as controls. The defect was shown to affect both primary IgG and IgM responses to chicken cells (CRBC) and to be related to tumour size. However, the primary immune depression could be overcome either by increasing the antigen dose or by using Freund's complete adjuvant together with antigen. Secondary responses were also depressed. This depression was more pronounced if the animals was primed after, rather than before, tumour implantation. Further studies involved the measurement of primary immune responses of immunologically deprived syngeneic mice, after they had been reconstituted with cells from normal or tumour-bearing mice. Lymphocyte reconstitution experiments were carried out in mice which had been irradiated with 950R. Various lymphoid preparations from TEPC-183-bearing mice were unable to bring about such restoration. It is concluded that the impairment of the primary immune response of mice bearing the plasmacytoma TEPC-183 is due to a macrophage, rather than a lymphocyte, abnormality. However, none of these transfer studies suggested that positive suppression of primary immune responses was being mediated by cells from TEPC-183-bearing mice.
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PMID:Immune suppression in BALB/c mice bearing the plasmacytoma TEPC-183: evidence for normal lymphocyte but defective macrophage function. 37 67


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