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)

The effect of exogenous neuraminidase on spontaneous and evoked synaptic activity was investigated following injection of the enzyme into frog spinal cord and into cord and into the carp optic tectum. 1. Injection of enzyme into spinal cord segments caused a significant increase of motoneuron activity in the corresponding spinal nerve, which lasted for 7--31 min. 2. The amplitude of postsynaptic evoked potentials in the optic tectum was increased after neuraminidase injection up to 200% of control level for 20--40 min, whereas the amplitude of summed action potentials of retino-tectal afferents remained unchanged. 3. Similar effects were observed in single cell responses of the optic tectum with some differences in the degree of increase in activity, as well as latency and final depression of the stimulus response. 4. The extent of neuraminic acid liberation following neuraminidase treatment was determined biochemically. In both tissues investigated the amount of free neuraminic acid was increased significantly (4--5.5 fold) after enzyme treatment. Whereas after enzyme injection into spinal cord and optic tectum the percentage release of total glycoprotein- and glycolipidbound neuraminic acid was 12% and 15%, respectively, liberation from enzyme incubated tissue homogenates was somewhat higher (20.5% and 24%).
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PMID:Effects of exogenous neuraminidase on unit activity in frog spinal cord and fish optic tectum. 21 38

Infection of susceptible strains of mice with Friend leukemia virus (FLV) results in a profound depression of cell-mediated immunity as assessed by lymphocyte-mediated cytotoxicity. This depression occurs early in the disease, before the onset of splenomegaly, and is associated with a decline in the susceptibility of splenocytes from FLV-infected mice to lysis by anti-Thy-1. 2 serum and complement. Treatment of splenocytes from FLV-infected mice with neuraminidase restores, in large part, their susceptibility to anti-Thy-1.2 serum as well as their cytolytic capacity. These studies suggest that one early immunosuppressive consequence of infection with FLV involves alteration of the effector T-lymphocyte cell surface.
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PMID:Friend virus-induced immunodepression: effect of neuraminidase treatment on Thy-1.2 antigen expression and cytotoxic potential of splenocytes from virus-infected mice. 30 16

Using the agglutination of sheep red cells by human antibodies as an indicator of microbial antibody activity, a highly significant association was found between the response to the e antigen of the hepatitis B virus and the formation of strong antibody levels to microbial substances (chi 2(1) = 33). This kind of association was not found among chronic carriers of the hepatitis B virus who do not produce antibodies to the e antigen (chi 2(1) = 3,7). In the presence of e antigen activity, patients with acute virus B hepatitis almost always show significantly reduced levels of antibodies to microbial substances (chi 2(1) = 20). The findings indirectly reveal that e activity is associated with the inability of the liver to trap bacterial antigens. Circumstantial evidence further suggests that the e factor may bear antigens on its immunoglobulin-like structure very similar to microbial cell wall components. Accepting that human antibodies to the T (Thomsen-Friedenreich) antigen represent reactions to cryptantigenic membrane structure of autologous tissues, it was significant to record that increased anti-t activity is always demonstrated when virus B infections progress from the acute to the chronic carrier stage (chi 2(1) = 73). The most intense anti-T activity is commonly found in subjects who produce antibodies to the hepatitis B surface antigen (chi 2(1) = 138). In the presence of e antigen the amount of anti-T in circulation is always significantly depressed. Since this type of depression is not seen in patients with acute virus B hepatitis who lack the e antigen, we suspect that the reduced anti-T levels in e antigen-positive patients are linked with the in vivo exposure of T receptors by microbial neuraminidase.
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PMID:Hepatic infections. Part II. The effect of acute and chronic hepatitis B antigenaemia on the reaction to antibodies to sheep red cells (microbial antigens) and human T-activated cells (exposed autologous tissue antigens). 31 18

Two-tumour-cell-aggregation factors derived from rat ascites hepatoma cells had different antigenicity; one, with a strong potency, was not absorbed by immunoadsorbent chromatography with anti-rat serum antibody and the other, with a weak potency, was. The unabsorbed factor possessed mitogenic activity on lymphocytes from thymus, spleen and lymph node of rats; its effect was compared with that of lectins (including phytohaemagglutinin, concanavalin A, pokeweed mitogen, lipopolysaccharide and soybean agglutinin) in the form of increased DNA and protein synthesis, blast transformation and mitosis. In the use of anti-thymocyte serum-resistant spleen cells and hydrocortisone-resistant thymocytes, the cells stimulated were assumed to be T-lymphocytes. DNA synthesis by this factor seemed to be characterized by a 2-step increase, suggesting the presence of 2 subpopulations of the cells activated, especially thymocytes. At high concentration this factor induced no depression of DNA synthesis. Favourable cell density for the response to this factor was 2-8 X 10(6) cells. Its effect was not influenced by treatment of the cells with neuraminidase.
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PMID:Rat lymphocyte mitogenesis by aggregation factor from rat ascites hepatoma cell surface. 35 20

The effects of direct intratumoral inoculation with Vibrio cholerae neuraminidase and inoculation of tumor-bearing mice with tumor cells incubated with neuraminidase in vitro were studied in C57BL/6 X DBA/2 F1 mice bearing s.c.-transplanted, methylcholanthrene-induced pulmonary squamous cell or Lewis lung carcinomas. The growth of the squamous cell tumor was more greatly inhibited by both treatments than was the Lewis lung tumor. In the squamous cell tumor-bearing mice, both modes of neuraminidase treatment depressed tumor growth by approximately 80%. However, 20% of the mice in the group treated with the neuraminidase-incubated squamous cell vaccine and 10% of those treated intratumorally underwent total tumor regression and developed specific immunity to the squamous cell tumor. although the growth rate of the Lewis lung tumor was suppressed by both types of treatment, the direct intratumoral neuraminidase treatment group underwent a greater depression in tumor growth (73 versus 42%). A possible explanation of the different results of the two treatments in squamous cell and Lewis lung tumor systems may be based on tumor etiology and cellular composition.
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PMID:Effectiveness of neuraminidase in experimental immunotherapy of two murine pulmonary carcinomas. 83 Apr 25

The expression of selected lymphocyte surface-membrane markers was evaluated in 37 patients with acute viral hepatitis B, 10 of whom were studied serially through the resolving and convalescent phases of disease. Bone marrow-derived (B) lymphocytes were identified by reference to surface immunoglobulin, whereas normal thymus-derived (T) lymphocytes were assayed by their capacity to form spontaneous nonimmune rosettes with sheep erythrocytes (E rosettes, ER). During the acute and resolving phases of viral hepatitis B, the relative and absolute number of ER-positive lymphocytes was significantly reduced, whereas the number of surface immunoglobulin-positive lymphocytes and the absolute lymphocyte count remained normal. This resulted in the appearance of a third population of cells, deficient in respect to both surface immunoglobulin and ER markers. Such cells accounted for nearly 25% of peripheral blood lymphocytes, approximately 5 x 105ml blood. Depression of the number of ER-positive lymphocytes occurred at least once during the course of disease in every patient studied serially, and was observed in 55 of 67 individual assays of the 37 cases of acute viral hepatitis B. Lymphocytes from some patients reacquired ER function when cultured in fetal calf serum but not in the presence of autologous serum. Such autologous serum was capable of suppressing ER function of lymphocytes from normal donors. The extrinsic suppression of er function by a serum factor (designated as the Rosette Inhibitory Factor), was found to be time dependent, characterized by a 4-h latent period and requiring approximately 18 h for maximum attenuation of ER function. The Serum Rosette Inhibitory Factor was: (a) heat and freeze-thaw stable, (b) nondialyzable, (c) physically separable from hepatitis B surface antigen, (d) not a lymphocytotoxic antibody, and (e) had the buoyant density of a lipoprotein. This extrinsic mechanism was observed in 41.8% of patients with reduced numbers of ER-positive lymphocytes. The Rosette Inhibitory Factor was not detectable in the serum of the remaining 58.2% of the cases of acute and resolving viral hepatitis B despite the presence of reduced numbers of ER-positive lymphocytes. The lymphocytes from these cases did not reacquire ER function when cultured in the absence of autologous serum. The mechanisms responsible for the suppression of normal ER function in these cases appears to be intrinsic to the lymphocytes and not the result of a humoral factor. The T lymphocyte lineage of cells deficient in respect to ER function, whether of intrinsic or extrinsic type, was demonstrated by their capacity to form spontaneous rosettes with neuraminidase-treated sheep erythrocytes. Both intrinsic and extrinsic suppression of T lymphocyte ER function commonly occurred during the first 4 wk of acute viral hepatitis B.9 of the 10 patients followed serially continued to manifest defective ER function at 12 wk...
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PMID:Mechanisms responsible for defective human T-lymphocyte sheep erythrocyte rosette function associated with hepatitis B virus infections. 108 96

The three-dimensional structure of human rhinovirus 14 has a deep surface depression or "canyon" encircling each of the twelve fivefold vertices. The canyon's surface is inaccessible to the broad antigen binding region of antibodies, permitting conservation of residues that might be required for host cell receptor recognition without danger of attack by the host's immune system. In contrast, the exposed surface features, where neutralizing antibodies are known to bind, change rapidly under pressure from the host's immune system. It was, therefore, hypothesized that this depression was the site of receptor attachment. Similar, but smaller, depressions had been observed previously on both the hemagglutinin and neuraminidase spikes of influenza virus. These have also been shown to be the site of host cell interaction. Although support for the canyon hypothesis was only circumstantial in the first place, there are now extensive confirmatory data. These include site-specific mutations of residues in the canyon and conformational changes induced in the canyon by the binding of small organic molecules, all of which alter receptor attachment. The strategy used in human rhinovirus 14 to protect the viral receptor attachment site from immune surveillance may be utilized not only in other picornaviruses but also in many other types of viruses including human immunodeficiency virus.
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PMID:The canyon hypothesis. 256 Sep 13

The three-dimensional structure of human rhinovirus 14 has a deep surface depression or "canyon" encircling each of the twelve 5-fold vertices. The canyon's surface is inaccessible to the broad antigen binding region of antibodies, permitting conservation of residues that might be required for host cell receptor recognition without danger of attack by the host's immune system. In contrast, the exposed surface features, where neutralizing antibodies are known to bind, change rapidly under pressure from the host's immune system. It was, therefore, hypothesized that this depression was the site of receptor attachment. Similar, but smaller, depressions had been observed previously on both the hemagglutinin and neuraminidase spikes of influenza virus. These have also been shown to be the site of host cell interaction. Although support for the canyon hypothesis was only circumstantial in the first place, there are now extensive confirmatory data. These include site-specific mutations of residues in the canyon and conformational changes induced in the canyon by the binding of small organic molecules, all of which alter receptor attachment. The strategy used in human rhinovirus 14 to protect the viral receptor attachment site from immune surveillance may be utilized not only in other picornaviruses but also in many other types of viruses including human immunodeficiency virus.
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PMID:The canyon hypothesis. Hiding the host cell receptor attachment site on a viral surface from immune surveillance. 267 Sep 20

The effect of various strains of influenza virus on polymorphonuclear leucocyte (PMNL) function were studied by chemiluminescence (CL) and bacterial killing assays. All virus strains induced PMNL CL and peak CL correlated with haemagglutination (HA) but not neuraminidase (NA) activity of virus pools. Heat-treatment of virus pools generally had little effect on HA activity or ability to generate a PMN CL response but almost completely destroyed NA activity. Exposure of PMNL to each of the six virus strains resulted in loss of surface-associated sialic acid and a marked depression in both zymosan-induced PMNL CL and PMNL bactericidal capacity. However, there was no correlation between the degree of PMNL functional impairment and virus NA activity and, furthermore, heat treatment of virus pools removed NA activity but generally had little effect on their ability to reduce PMNL function. NA does not appear to play a primary role in impairment of PMNL function by influenza virus.
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PMID:Effect of influenza A on phagocytic cell function. 274 89

Influenza viruses have been shown to decrease the ability of polymorphonuclear leukocytes (PMN) to respond to a variety of stimuli. This study was done to determine if viral neuraminidase was responsible for decreased PMN function. Treatment of human PMN with purified neuraminidases from influenza virus, Vibrio cholerae, or Clostridium perfringens did not significantly affect the ability of human PMN to respond to stimulation. Occasional virus preparations that lacked the ability to depress PMN function did not differ in neuraminidase activity from viruses capable of causing depression. These results demonstrate that neuraminidase activity is not the cause of influenza virus-induced PMN dysfunction.
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PMID:Neuraminidase activity is not the cause of influenza virus-induced neutrophil dysfunction. 286 60


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