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)

Eastern equine encephalomyelitis (EEE) was the cause of heavy mortality in coturnix quail (Coturnix coturnix) reared commercially in South Carolina. The birds showed depression, tremor, and partial paralysis that advanced into complete paralysis, torticollis, and death within a few hours. The only consistent lesion on necropsy was a catarrhal enteritis in the duodenal area. The disease spread rapidly to all pens throughout the two houses on the farm in all birds over 2 weeks old, and mortality ranged from 40 to 90% in the various pens within the house. Total mortality exceeded 90,000 birds. Age groups on the farm ranged from 1 day to 8 weeks, at which time the birds went for slaughter. It appears that the initial infection was spread by cannibalism. EEE was diagnosed by isolating the virus in fertile eggs and suckling mice, with subsequent identification by complement-fixation. This is the first documented case of EEE in coturnix quail.
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PMID:Eastern equine encephalomyelitis outbreak in coturnix quail. 69 63

Experimental allergic encephalomyelitis (EAE) was induced in rats of the Lewis strain fed diets adequate or deficient in essential fatty acids (EFA). After induction of the disease, the diets were supplemented with aspirin (3.75 g/kg diet), and the effects of the drug on the course of EAE and on the synthesis of prostaglandin F (PGF) by brain slices from diseased animals and their Freund controls were examined. Aspirin supplementation delayed the onset of EAE in both dietary groups. EFA-deficient rats experienced an incidence and severity of the disease similar to that of aspirin-free, EFA-deficiet rats, while the EFA-adequate group showed a greater severity but not an increased incidence, compared to aspirin-free controls. Aspirin treatment led to an increased PGF production by brain slices from rats on either diet and not subjected to an immunochallenge. When the diet was deficient in EFA, challenge with antigen plus adjuvant or adjuvant alone tended to decrease PGF synthesis by brain slices, and when the diet was adequate in EFA, immunochallenge caused a marked depression on PGF synthesis. It was concluded that the PG synthetase inhibitor aspirin can alter the course of EAE in the rat, providing further evidence that PGs or related metabolites may be involved in the immune response in this disease.
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PMID:Incidence and severity of experimental allergic encephalomyelitis and cerebral prostaglandin synthesis in essential fatty acid deficient and aspirin-treated rats. 75 Aug 27

Less pronounced intensity of extrapyramidal hyperkineses and aggravation of motor disturbances in patients with diffuse sclerosis occurring under the effect of tegretol prompted the authors to study the action of this drug on the course of experimental allergic encephalomyelitis. Daily administration of tegretol in a dose of 375 mg/kg retarded the development of the affection and produced a marked adynamia in the animals. Slowing down of the dominant rhythm and depression of its amplitude were recorded on the EEG. Shifts in the potassium and sodium content and reduced brain cholesterase activity were noted. The authors ascribe these changes to a mediated action of tegretol upon deep-seated cerebral structures.
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PMID:[Study of the mechanism of action of tegretol in experimental allergic encephalomyelitis]. 122 93

Theiler murine encephalomyelitis virus strains are categorized into two groups, a neurovirulent group that rapidly kills the host, and a demyelinating group that causes a generally nonlethal infection of motor neurons followed by a persistent infection of the white matter with demyelinating lesions similar to those found in multiple sclerosis. The three-dimensional structure of the DA strain, a member of the demyelinating group, has been determined at 2.8 A resolution. As in other picornaviruses, the icosahedral capsid is formed by the packing of wedge-shaped eight-stranded antiparallel beta barrels. The surface of Theiler virus has large star-shaped plateaus at the fivefold axes and broad depressions spanning the twofold axes. Several unusual structural features are clustered near one edge of the depression. These include two finger-like loops projecting from the surface (one formed by residues 78-85 of VP1, and the other formed by residues 56-65 of VP3) and a third loop containing three cysteines (residues 87, 89, and 91 of VP3), which appear to be covalently modified. Most of the sequence differences between the demyelinating and neurovirulent groups that could play a role in determining pathogenesis map to the surface of the star-shaped plateau. The distribution of these sequence differences on the surface of the virion is consistent with models in which the differences in the pathogenesis of the two groups of Theiler viruses are the result of differences in immunological or receptor-mediated recognition processes.
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PMID:Three-dimensional structure of Theiler virus. 154 65

Myenteric ganglioneuritis and encephalomyelitis were diagnosed in an umbrella cockatoo. The cockatoo exhibited clinical signs that were milder than those associated with this syndrome, such as anorexia, muscle wasting, regurgitation, depression, and changes in fecal consistency. The gross lesions also differed from earlier reports in that only the duodenum and proximal jejunum were grossly dilated. Normally the proventriculus and ventriculus are dilated without visible intestinal changes. The histopathological lesions, however, such as perivascular cuffs in the brain stem and muscular mass of the ventriculus and proventriculus, were similar to earlier reports. A virus was suspected, although transmission and isolation of a virus has not occurred in other reports and was not attempted in this case.
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PMID:Encephalitis, proventricular and ventricular myositis, and myenteric ganglioneuritis in an umbrella cockatoo. 275 72

A 2-year-old Boston Terrier was referred because of depression and hindlimb and tail paresis. Clinical examination and serum biochemical analysis resulted in a diagnosis of encephalomyelitis and myositis. Results of testing for Dirofilaria immitis were positive. Gross and histologic examination revealed an aberrant adult heartworm infection resulting in thrombosis of the femoral artery and multiple muscular branches, with subsequent muscle necrosis and inflammation in one hindlimb. Additionally, an unusual larval-tissue interaction to microfilariae yielded a multifocal encephalomyelitis in the brain and spinal cord.
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PMID:Heartworm disease manifested by encephalomyelitis and myositis in a dog. 355 82

In multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) the cytokines tumour necrosis factor-alpha (TNF), lymphotoxin-alpha (LT), and interferon-gamma (IFN-gamma) are of central pathogenetic importance. A therapy capable of stopping neurological deterioration in MS patients is not yet available. Here, we report that rolipram, a selective type IV phosphodiesterase inhibitor, stereospecifically suppresses the production of TNF/LT and less strongly also IFN-gamma in human and rat auto-reactive T cells. Moreover, we show that rolipram is an effective treatment for EAE. Rolipram has extensively been studied in humans for the treatment of depression, but has not yet been marketed. The data presented here identify rolipram as potential therapy for multiple sclerosis and provoke the immediate initiation of clinical trials.
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PMID:The antidepressant rolipram suppresses cytokine production and prevents autoimmune encephalomyelitis. 758 35

In the LEW/N rat model, a decreased hypothalamic-pituitary-adrenal (HPA) axis response to inflammatory and immune mediators confers susceptibility to the development of a variety of inflammatory and immune diseases, including experimental allergic encephalomyelitis. In humans with optic neuritis, early intervention with steroids is associated with a decrease in the number of patients who go on to develop multiple sclerosis (MS). The current study was designed to determine whether patients with MS show evidence of a hypoactive HPA axis. Thirteen patients with MS were studied at baseline and with provocative tests of HPA axis function [ovine CRH, arginine vasopressin (AVP), and ACTH stimulation]. Compared to matched controls, patients with MS had significantly higher plasma cortisol levels at baseline. Despite this hypercortisolism and in contrast to patients with depression who had similar elevations in plasma cortisol levels, patients with MS showed normal, rather than blunted, plasma ACTH responses to ovine CRH, suggesting that the pathophysiology of hypercortisolism in MS is different from that in depression. Patients with MS also showed blunted ACTH responses to AVP stimulation and normal cortisol responses to high and low dose ACTH stimulation. Taken together, these findings are compatible with data from studies of experimental animals exposed to chronic inflammatory stress, which showed mild increased activation of the HPA axis with increased relative activity of AVP in the regulation of the pituitary-adrenal axis. These data do not support a role for hypocortisolism in MS once the disease is established.
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PMID:Multiple sclerosis is associated with alterations in hypothalamic-pituitary-adrenal axis function. 807 72

Brown-Norway (BN) rats injected with HgCl2 develop a systemic autoimmune disease associated with a polyclonal B cell activation, due to autoreactive T cells specific for self-class II molecules, while Lewis (LEW) rats injected with HgCl2 do not exhibit autoimmunity and develop a non-antigen-specific, CD8-mediated immunosuppression assessed by a depression of T cell functions, and a protection against experimental autoimmune encephalomyelitis (EAE). Resistance to HgCl2-induced autoimmunity is not due to these suppressor cells since treatment with an anti-CD8 monoclonal antibody (mAb) did not allow autoimmunity to appear. The absence of autoimmunity in this strain could result from the absence of autoreactive T cells, or from quantitative or qualitative differences of these cells between susceptible and resistant strains. In the present study, we show that CD4+ anti-class II T cells are present in HgCl2-injected LEW rats and are as frequent as in BN rats when assessed by limiting dilution analysis. LEW CD4+ autoreactive T cell lines were derived. They proliferated in the presence of normal class II-bearing cells, secreted interleukin 2, and did not induce B cells to produce immunoglobulins. Transfer of one of these lines, LEW Hg A, into normal LEW rats led to the appearance of CD8+ cells responsible for a non-antigen-specific immunosuppression that induced complete protection from EAE. Immunosuppression was abrogated after treatment with an anti-CD8 mAb. In vitro, CD8+ cells from rats injected with the LEW Hg A T cell line proliferated in the presence of activated T cells whatever their origin. We conclude that HgCl2 induces CD4+ autoreactive T cells that proliferate in the presence of class II+ cells in susceptible BN as well as in resistant LEW rats. But while these cells collaborate with B cells to produce autoantibodies in BN rats, they initiate in LEW rats a suppressor circuit involving antiergotypic CD8+ suppressor cells.
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PMID:Mercury-induced autoreactive anti-class II T cell line protects from experimental autoimmune encephalomyelitis by the bias of CD8+ antiergotypic cells in Lewis rats. 809 39

The clinical signs, enteritis, weight depression, and hypoglycemia of spiking mortality syndrome were experimentally reproduced in broiler breeders and broiler chicks. Inocula included 1) virus-like particles from intestines of chicks with spiking mortality syndrome that had been banded in a discontinuous Renograffin gradient, 2) homogenized darkling beetles collected from litter of farms where spiking mortality syndrome had occurred repeatedly, and 3) homogenized embryos which had been inoculated with the Renograffin-banded material. Arkansas variant infectious bronchitis virus and arenavirus-like particles were identified in the inocula. Serology on samples from surviving chicks suggested the presence of an avian encephalomyelitis virus in one of the inocula. One-day-old (n = 172) and 2.5-day-old (n = 30) chicks were inoculated orally, and some were also injected intraperitoneally or subcutaneously, with 0.5 ml of the inocula. Twelve to fourteen days postinoculation, chicks were fasted for 4-6 hours, then briefly stressed with a cool water spray. Within 1.5 hours, inoculated chicks began dying with severe hypoglycemia and clinical signs of spiking mortality syndrome. Body weights were significantly depressed. Uninoculated controls (n = 130) from the same hatches, also fasted and stressed, were unaffected clinically and were not hypoglycemic. One group (n = 52) of inoculated chicks exposed to a controlled lighting program was unaffected clinically, had significantly higher mean plasma glucose levels, and had significantly less body weight depression than chicks exposed to continuous lighting. We concluded that exposure to controlled amounts of light/darkness can ameliorate much of the hypoglycemia, mortality, and runting-stunting associated with spiking mortality syndrome of chickens. The significance of the viruses and virus-like particles detected in the inocula is currently under investigation.
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PMID:Experimental reproduction of severe hypoglycemia and spiking mortality syndrome using field-derived and embryo-passaged preparations. 871 30


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