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 plasma concentration of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the site labeled by tritiated imipramine, was measured by a radial immunodiffusion assay in 36 normal human volunteers and 51 drug-free patients who fulfilled DSM-III criteria for major depression. The depressed patients exhibited a significant elevation in the plasma concentration (+/- SEM) of alpha 1-acid glycoprotein (79.6 +/- 4 mg/dL) when compared with the age- and sex-matched controls (61.7 +/- 3 mg/dL). Fourteen of the 51 patients with major depression had plasma alpha 1-acid glycoprotein concentrations that were higher than the highest values of the normal controls. There was no relationship between plasma alpha 1-acid glycoprotein concentrations and sex or affinity of platelet tritiated imipramine binding of either the normal volunteers or the depressed patients. In the depressed patients, there was a significant positive correlation between plasma concentrations of alpha 1-acid glycoprotein and postdexamethasone plasma cortisol concentrations, and two measures of depression severity, the Montgomery-Asberg Rating Scale for Depression and the Center for Epidemiologic Studies-Depression Scale, and a significant negative correlation with age. These data provide the first evidence of alterations of an endogenous inhibitor of the tritiated imipramine binding site/serotonin transporter in depressed patients.
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PMID:Elevated plasma concentrations of alpha 1-acid glycoprotein, a putative endogenous inhibitor of the tritiated imipramine binding site, in depressed patients. 215 80

The safety of an Aujeszky's disease virus vaccine based on strain 783, a deletion mutant which does not express glycoprotein I and thymidine kinase, was assessed in pigs, calves and sheep. Four-day-old piglets which were inoculated intranasally and intramuscularly with 10(7) plaque forming units (PFU) developed only slight depression and fever. The virus was transmitted to a sentinel piglet. Six weeks after inoculation, the pigs were injected with high doses of corticosteroids in an attempt to reactivate the vaccine virus. The pigs did not shed Aujeszky's disease virus, did not develop a rise in virus neutralising antibody titres and sentinel pigs remained seronegative to Aujeszky's disease virus. Strain 783 was passaged in two series of three- to five-day old piglets, but after the third and fourth passages virus could no longer be recovered. Pregnant sows were inoculated with 10(7) PFU of virus strain 783 around day 35 or on day 85 of pregnancy, and their fetuses and piglets were assayed for Aujeszky's disease virus and antibodies against Aujeszky's disease virus. No evidence was found for transplacental transmission of the virus. Calves and sheep were given 10(7) PFU of virus strain 783 intranasally or intramuscularly; they survived and did not develop clinical signs of Aujeszky's disease. All the sheep and the calves inoculated intramuscularly developed neutralising antibodies to Aujeszky's disease virus.
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PMID:Safety of an Aujeszky's disease vaccine based on deletion mutant strain 783 which does not express thymidine kinase and glycoprotein I. 217 88

Fibronectin is a large-molecular-weight glycoprotein present on most cell surfaces, in extracellular fluids, and in plasma. Both cell-associated and soluble fibronectin are thought to have important roles in the inflammatory response and host defense and may contribute to the maintenance of microvascular integrity during septic episodes. Newborn infants have levels of fibronectin in plasma that are one-third to one-half those found in the healthy adult. In addition, neonates with respiratory distress syndrome, perinatal asphyxia, bacterial sepsis, intrauterine growth retardation, or postnatal malnutrition have a further depression in their plasma levels of fibronectin. The low plasma concentration of fibronectin in newborn infants may contribute to the hypofunction of the neonatal reticuloendothelial system and predispose to the development of sepsis. Rates of synthesis of plasma fibronectin are diminished in the neonate, and an inverse correlation between fibronectin half-life and gestational age exists. The role of fibronectin in treatment or prophylaxis of neonatal sepsis remains to be determined.
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PMID:Role of fibronectin in diseases of newborn infants and children. 219 69

Surgical operations have been shown to cause a variety of immunological disturbances in man both in vivo and in vitro. With few exceptions the overall picture is one of a generalized state of immunodepression in the postoperative period. The implications of these observations are that host defences may be compromised by surgical procedures, thus providing a 'fertile soil' for bacterial invasion and tumour cell metastasis at the very time when risks from invading pathogens and viable tumour cells are maximal. We have studied the effects of surgical operations on the immune system in 35 patients with benign disease. Surgical procedures were classified as either minor (n = 15) or major (n = 20). A panel of monoclonal antibodies was used to identify peripheral blood lymphocyte subpopulations and analysis was performed using flow cytometry. Simultaneous estimations of plasma alpha-1 proteinase inhibitor (alpha-1-PI), alpha-2-macroglobulin (alpha-2-M), alpha-2-pregnancy-associated glycoprotein (alpha-2-PAG) and plasma suppressive activity (PSA) on stimulated allogeneic lymphocytes were performed before operation and on postoperative days 1, 3, 7, 17 and 21. Circulating numbers of all lymphocyte subpopulations fell significantly following surgery, except for B lymphocytes which did not change. The magnitude, and duration of the reduction in cell numbers and the subpopulation affected was significantly related to the degree of surgical trauma, and returned to pre-operative values by postoperative day 7. Changes in alpha-1-PI, alpha-2-M, alpha-2-PAG and PSA were also significantly related to the degree of surgical trauma, and these plasma changes persisted longer than the cellular disturbances. Surgical operations induce a reversible depression of cellular immunity which precedes plasma suppressive activity in its return to pre-operative levels. Immunostimulating agents such as interferon and the interleukins deserve evaluation as prophylactic agents pre-operatively.
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PMID:The influence of surgical operations on components of the human immune system. 241 26

Serum viscosity's increase in diabetes has been linked to the presence of microvascular sequelae and to changes in serum protein composition. The major change is a decline in albumin and an increase in the levels of acute-phase proteins. In this study, albumin and five acute phase proteins--alpha-1 acid glycoprotein, alpha-1 antitrypsin, haptoglobin, ceruloplasmin, and C-reactive protein--were measured. Levels in adult diabetes (principally type II) were compared with those in both subjects with glucose intolerance and control subjects (healthy subjects and nondiabetic ambulatory patients). Haptoglobin, alpha-1 acid glycoprotein, and C-reactive protein increased markedly in both diabetes and glucose intolerance; ceruloplasmin and alpha-1 antitrypsin increased more marginally. Serum albumin level decreased more strikingly as hyperglycemia advanced. Acute-phase proteins also increased in advanced glucose intolerance as in established diabetes. The acute-phase protein elevation did not differ with degree of control or duration of diabetes. When diabetics were divided into those with and without clinically detectable evidence of microvascular sequelae, elevation of haptoglobin, C-reactive protein and alpha-1 acid glycoprotein, and depression of albumin were found to progress with number of sequelae. The levels of these proteins, particularly haptoglobin, were also highly correlated with serum viscosity expressed as viscosity number. Mild serum albumin depression and a more striking acute-phase protein elevation are greater in diabetes with microangiopathy, develop in glucose intolerance, and contribute substantially to elevated plasma viscosity in diabetes.
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PMID:Increased levels of acute-phase serum proteins in diabetes. 247 61

Infection of polymorphonuclear leukocytes (PMNL) with influenza virus causes depression of PMNL metabolic and bactericidal activities. The studies reported here were undertaken to determine whether the hemagglutinin (HA) glycoprotein of influenza virus mediates this depression. PMNL were incubated with purified HA and the oxidative responses to exogenous stimuli were measured. The results indicate that HA, in either liposomes or protein aggregates referred to as rosettes, depressed PMNL oxidative responses. Depression was observed within 2 min of initial interaction of HA with PMNL and lasted more than 2 h. The membrane fusion activity of HA requires proteolytic cleavage of the HA, whereas the receptor binding activity does not. There was no difference in the ability of virions with cleaved or uncleaved HA to depress PMNL responses suggesting that the fusion event is not required for PMNL dysfunction. Inasmuch as the HA glycoprotein binds to sialic acid-containing receptors on the surface of the PMNL, we tested whether other sialic acid-specific binding proteins can mediate the reduction of PMNL responses. Sialic acid-specific lectins from Limulus polyphemus or Limax flavus were incubated with PMNL before measuring their responses to secondary stimulus. Depression was observed upon incubation with the lectins similar to that seen upon incubation with the HA or influenza virus. These results suggest that attachment of influenza virus to sialic acid-containing receptors is responsible at least in part, for suppressing PMNL oxidative responses.
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PMID:Depression of polymorphonuclear leukocyte functions by purified influenza virus hemagglutinin and sialic acid-binding lectins. 272 34

During early starvation-induced development, amoebae of Dictyostelium discoideum have been previously shown to increase sulfation and fucosylation of glycoprotein-linked oligosaccharides to levels above those observed in axenically growing cells. We report here that the axenic broth culture itself induces generation of high levels of fucosylated glycoprotein-linked oligosaccharides at all stages in the growth curve. However, when grown on bacteria, amoebae of both the axenic strain and the wild type show dramatic depression in fucose incorporation during early exponential growth. In mid- and late-exponential stages of growth, fucosylation rises to the levels found at all stages of axenic culture. Sulfation also increases during early development, but, in contrast to fucosylation, oligosaccharide sulfation is not altered by growth in axenic medium and does not increase during growth on bacteria. Starvation of bacterially grown cells results in increased sulfation and a further rise in fucosylation, as is also characteristic of broth-grown cells. The ability of axenic culture to uncouple control of these two classes of glycan-modification steps suggests that the synchronous increases during early development actually reflect responses to different regulatory signals, even though they participate in the same metabolic process. The increase in in vivo fucosyltransferase activity, which can act on many substrate glycoproteins, may alter many characteristics of the cells.
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PMID:Differential regulation of glycoprotein sulfation and fucosylation during growth of Dictyostelium discoideum. 274 70

Retroviruses cause cancer by several different mechanisms including addition of an oncogene, addition of a modified viral glycoprotein, activation of a proto-oncogene, transactivation of a proto-oncogene, immune depression, and stimulation of lymphoid cell proliferation. Both the evolution of oncogenes and tumor induction by most retroviruses is multi-step. Study of the evolution of a particular oncogene, v-rel, indicates that this evolution could not have been selection-driven, but that it resulted from the high rate of mutation in retroviruses replication, that is, it was mutation-driven. Argument is made that much other cancer is also mutation-driven.
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PMID:Retroviruses and the genetics of cancer. 284 85

Thrombospondin, a trimeric glycoprotein contained in the platelet alpha-granules, has been proposed as a marker of in vivo platelet activation. However, it is also synthesised by a range of other cells. The extraplatelet contribution to plasma levels of thrombospondin was therefore estimated by investigating the relationship between plasma thrombospondin levels and platelet count in samples from profoundly thrombocytopenic patients with marrow hypoplasia, using the platelet-specific alpha-granule protein beta-thromboglobulin as control. Serum concentrations of both proteins were highly correlated with platelet count, but while plasma beta-thromboglobulin levels and platelet count also correlated, there was no relationship between the number of platelets and thrombospondin concentrations in plasma. Serial sampling of patients recovering from bone marrow depression indicated that the plasma thrombospondin contributed by platelets is superimposed on a background concentration of at least 50 ng/ml probably derived from a non-platelet source, and plasma thrombospondin levels do not simply reflect platelet release.
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PMID:Do extra-platelet sources contribute to the plasma level of thrombospondin? 296 80

Mammalian cells in culture express membrane receptors for C3b when infected with HSV-1. C3b binding is mediated by glycoprotein C (gC), a virus-specified membrane glycoprotein. In view of the inhibitory functions of other C3b-binding proteins, we studied the capacity of gC to modulate complement activation. Glycoprotein C was purified from HSV-1-infected cells by immunoaffinity chromatography. Glycoprotein C, but not a control viral glycoprotein, demonstrated dose-dependent acceleration of decay of C3bBb sites. In addition, gC produced a dose-dependent, time-independent depression of the overall hemolytic efficiency of C3bBb sites. Inhibition of C5b6-initiated reactive lysis of cells bearing C3b, but not cells bearing antibody alone, by gC suggests that the second effect represents interference with the C3b-C5/5b interaction. This hypothesis is supported by the failure of gC to inhibit reactive lysis when added after C5b67 insertion into target cells. Glycoprotein C does not accelerate C14b2a decay, nor does it impair classical pathway hemolytic efficiency when excess C5 is present. By limiting available C5/5b, some gC inhibition of C3b-C5/5b interactions can be unmasked in the classical pathway system. Glycoprotein C is devoid of factor I co-factor activity. HSV-1 gC is a modulator of complement activation, especially via the alternative pathway, and may represent a novel viral mechanism for evading host defense processes.
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PMID:Glycoprotein C of herpes simplex virus 1 is an inhibitor of the complement cascade. 301 78


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