Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental transmission of the Stetsonville, Wisconsin, U.S.A. source of transmissible mink encephalopathy (TME) to outbred Syrian golden hamsters resulted in two distinct syndromes, termed hyper (HY) and drowsy (DY), that diverge by the third hamster passage. The syndromes differed with respect to clinical signs, incubation period, brain titre, brain lesion profile and pathogenicity in mink. HY hamster TME had an incubation period of 65 +/- 1 days and was characterized by clinical signs of hyperaesthesia and cerebellar ataxia. Lethargy and the absence of hyperexcitability or cerebellar ataxia were representative of DY hamster TME which had an incubation period of 168 +/- 2 days. At endstage, HY and DY infected animals had brain titres of 10(9.5) LD50/g and 10(7.4) LD50/g of tissue, respectively, indicating that the replication kinetics of these two strains is different. Hamster TME passaged back into mink revealed that only DY retained mink pathogenicity. This suggests that the DY agent is the major mink pathogen in the Stetsonville TME source that is also pathogenic in hamsters after a long incubation period. The HY agent is likely to be a minor component of the original TME mink brain that replicates more rapidly than DY agent in hamsters, but alone is non-pathogenic in mink. The presence of the HY and DY strains of agent that retain their biological characteristics on repeated hamster passage in the Stetsonville TME source requires that the informational molecule encoding these transmissible agents has the capacity to account for this biological diversity.
J Gen Virol 1992 Feb
PMID:Identification of two biologically distinct strains of transmissible mink encephalopathy in hamsters. 153 75

Epidemiological investigation of a new incident of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin, U.S.A. in 1985 revealed that the mink rancher had never fed sheep products to his mink but did feed them large amounts of products from fallen or sick dairy cattle. To investigate the possibility that this occurrence of TME may have resulted from exposure to infected cattle, two Holstein bull calves were injected intracerebrally with mink brain from the Stetsonville ranch. Each bull developed a fatal spongiform encephalopathy 18 and 19 months after inoculation, respectively, and both bovine brains passaged back into mink were highly pathogenic by either intracerebral or oral inoculation. These results suggest the presence of a previously unrecognized scrapie-like infection in cattle in the United States.
J Gen Virol 1991 Mar
PMID:Epidemiological and experimental studies on a new incident of transmissible mink encephalopathy. 182 23

The antigenic relatedness of minute virus of mice (MVM), Kilham rat virus (KR), H-1 virus (H-1), haemorrhagic encephalopathy of rats virus (HER), porcine parvovirus (PPV), canine parvovirus (CPV), feline panleukopenia virus (FPV), goose parvovirus (GPV) and bovine parvovirus (BPV) was studied by immunofluorescence microscopy (FA) and by serum neutralization (SN). An antigenically related group comprising MVM, KR, HER, PPV, CPV and FPV was recognized by FA and most reactions within the group were reciprocal. Antigenic relatedness was less evident when the same viruses and antisera were tested by SN. Only CPV and FPV were closely and reciprocally related. Other cross-reactions by SN were quantitatively minor and included neutralization of CPV and FPV by pig anti-PPV serum and neutralization of H-1 and HER by rat anti-KR serum. Neither FA nor SN revealed any antigenic relationship of BPV and GPV either with each other or with any of the other viruses tested.
J Gen Virol 1986 Dec
PMID:Antigenic relationships among autonomous parvoviruses. 243 67

Immune-stimulating complexes (iscoms), which have recently been shown to be highly effective for the antigenic presentation of membrane proteins of viruses, were prepared with affinity-purified fusion (F) protein of measles virus (MV), using an adaptation of the standard method for iscom preparation. Immunization of monkeys with the F iscom preparation induced biologically active anti-F protein antibodies as was shown in haemolysis inhibition and cell-cell fusion inhibition tests. A whole MV iscom preparation, which also contained the haemagglutinin protein, induced not only also haemolysis-inhibiting antibodies, but, in contrast to the F iscom preparation, also haemagglutination-inhibiting and virus-neutralizing antibodies. In addition the F iscom preparation was shown to activate measles virus-specific T cells in mice. This was demonstrated by the generation of an MV-specific delayed type hypersensitivity response in F iscom-immunized animals and by the isolation of T cell clones specific for MV F protein with the T helper phenotype. Vaccination of mice with MV iscom or F iscom protected them from MV-induced fatal encephalopathy. The data concerning the immunogenicity of MV proteins presented in iscoms are discussed in relation to their potential for the development of an inactivated measles vaccine.
J Gen Virol 1988 Mar
PMID:Measles virus fusion protein presented in an immune-stimulating complex (iscom) induces haemolysis-inhibiting and fusion-inhibiting antibodies, virus-specific T cells and protection in mice. 325 55

Lewis and Brown Norway (BN) rats which are susceptible or resistant to autoimmune reactions against brain antigen, respectively, were inoculated intracerebrally with a neurotropic measles virus. Suckling rats died from a rapidly fatal acute encephalopathy (AE). With increasing age Lewis rats developed a subacute measles encephalomyelitis (SAME) whereas BN rats showed a clinically silent encephalitis (CSE). Infectious virus could occasionally be recovered from SAME animals using cocultivation techniques but not from BN rats with CSE. With monoclonal antibodies against measles virus, viral proteins were localized in brain tissue. Nucleocapsid and phosphoprotein were detected in infected brain cells of all animals with AE, SAME and CSE, whereas measles virus haemagglutinin, fusion and matrix proteins were either reduced or absent, suggesting a restricted synthesis of measles virus envelope proteins. These data suggest that the different diseases of the two rat strains are related to the immunogenetic background rather than to the replication of measles virus in the central nervous system. This animal model provides the opportunity to investigate further the events occurring during establishment of measles virus persistence in the brain, and the genetic control of associated immunological and immunopathological reactions.
J Gen Virol 1987 Jun
PMID:Virological aspects of measles virus-induced encephalomyelitis in Lewis and BN rats. 349 33

The treatment of portal hypertensive gastrointestinal hemorrhage has seen many new and innovative advances in the past 15 years, including pharmocotherapy, sclerotherapy, transjugular intrahepatic portacaval shunt, partial portacaval shunt, and hepatic transplantation. Such an array of therapeutic options provides great flexibility for the physicians managing this complex disorder. The less invasive procedures tend to be associated with higher rates of rebleeding from esophageal varices. However, these procedures serve as excellent bridges to hepatic transplantation in poor-risk patients. Surgical portasystemic shunts offer a permanent solution to portal hypertensive bleeding but also have several drawbacks. Standard (end-to-side or side-to-side) portacaval shunts are associated with unacceptably high rates of p4rtasystemic encephalopathy because of complete diversion of portal flow away from the liver. Selective shunts, such as the distal splenorenal shunt, result in maintenance of portal perfusion, but this is not lasting in alcoholic cirrhotics. Partial shunting (small-diameter portacaval H-graft with collateral ligation) is the most recent addition to the surgical armamentarium. This allows for hepatic portal perfusion, thus minimizing encephalopathy rates, but it violates the right upper quadrant if the patient is a candidate for hepatic transplantation. This large array of treatment options, each with its own advantages and disadvantages, permits for careful selection of the best modality based on several influencing factors. These include the underlying liver disease, the prognosis, the health team's experience, the resources available to the patient and the community, and the cost-effectiveness of each treatment.
Curr Opin Gen Surg 1993
PMID:Portal hypertension. 758 83

The possible involvement of human parvovirus B19 infection in encephalopathy has been reported. To determine the characteristics of B19 viruses involved in such cases, we molecularly cloned a part of the B19 DNAs derived from the sera of three patients with encephalopathy (B19 strains N80, N81 and N82), following amplification by PCR. The nucleotide (nt) sequences of the cloned DNAs (nt 3147-3405) were then determined. The nucleotide sequence of N80 was similar to that of the known genome type of group II. The nucleotide sequences of N81 and N82 were similar to each other, but distinctly different from those of other B19 strains reported previously. Almost the entire genome of strain N81 (nt 229-4812) was molecularly cloned following amplification by PCR. Analyses of the restriction site polymorphisms of the cloned N81 DNAs showed that N81 is distantly related to other B19 strains. Therefore, the two strains of N81 and N82 were defined as belonging to a new genome type, group V. Group V B19 virus has so far been isolated only from patients with encephalopathy.
J Gen Virol 1995 Nov
PMID:A new genome type of human parvovirus B19 present in sera of patients with encephalopathy. 759 71

Experimental infection of transmissible mink encephalopathy (TME) in two closely related mustelids, black ferret (Mustela putorius furo) and mink (Mustela visa), revealed differences in their susceptibility to the TME agent. When challenged with the Stetsonville TME agent, a longer incubation period was observed in ferrets (28 to 38 months) than mink (4 months). Western blot analysis of ferret and mink prion proteins (PrP) demonstrated no detectable differences between the proteins. Northern blot analysis of ferret brain RNA indicated that PrP mRNA abundance is similar in infected and uninfected individuals. We amplified the PrP coding region from ferret DNA using the polymerase chain reaction and compared the deduced amino acid sequence of the ferret PrP gene with the mink PrP gene. This comparison revealed six silent base changes and two amino acid changes between mink and ferret: Phe-->Lys at codon 179 and Arg-->Gln at codon 224, respectively. These changes may indicate the region of PrP that is responsible for the species barrier effect between mink and ferret.
J Gen Virol 1994 Nov
PMID:Transmissible mink encephalopathy species barrier effect between ferret and mink: PrP gene and protein analysis. 796 4

To determine whether the aetiological agent of bovine spongiform encephalopathy (BSE) is pathogenic for mink, standard dark mink were inoculated with coded homogenates of bovine brain from the U.K. Two homogenates were from cows affected with BSE. The third was from a cow that came from a farm with no history of having had BSE or having been fed ruminant-derived, rendered by-products, the proposed vehicle for introduction of the BSE agent. Each homogenate was inoculated intracerebrally into separate groups of mink and a pool of the three was fed to a fourth group. Signs of neurological disease appeared in mink an average of 12 months after intracerebral inoculation and 15 months after feeding. Decreased appetite, lethargy and mild to moderate pelvic limb ataxia were the predominant clinical signs, quite unlike the classic clinical picture of transmissible mink encephalopathy (TME). Microscopic changes in brain sections of most affected mink were those of a scrapie-like spongiform encephalopathy. Vacuolar change in grey matter neuropil was accompanied by prominent astrocytosis. Varying greatly in severity from one mink to another, the degenerative changes occurred in the cerebral cortex, dorsolateral gyri of the frontal lobe, corpus striatum, diencephalon and brainstem. Although resembling TME, the encephalopathy was distinguishable from it by less extensive changes in the cerebral cortex, by more severe changes in the caudal brainstem and by sparing of the hippocampus. The results of this study extend the experimental host range of the BSE agent and demonstrate for the first time the experimental oral infection of mink with a transmissible spongiform encephalopathy agent from a naturally infected ruminant species.
J Gen Virol 1994 Sep
PMID:Experimental infection of mink with bovine spongiform encephalopathy. 807 14

A virus causing a vacuolating encephalopathy and retinopathy in juvenile sea bass, Dicentrarchus labrax, was isolated from brain tissue in a fish cell line (SSN-1) derived from striped snakehead, Channa striatus. The isometric, non-enveloped, 30 nm diameter virus particles were resistant to pH 2-9 and heating at 56 degrees C for 30 min. Infectious particles had a buoyant density of approximately 1.31 g/cm3 in CsCl. Two structural polypeptides of molecular mass 40 and 42 kDa were identified and the ssRNA consisted of two fragments of molecular mass 1.10 and 0.51 x 10(6) Da. From these characteristics the virus was identified as a nodavirus. Due to the broad range of susceptible fish hosts and the consistent neuropathology of the disease condition, the generic term piscine neuropathy nodavirus (PNN) is proposed for this infectious agent.
J Gen Virol 1996 Sep
PMID:Cell culture isolation of piscine neuropathy nodavirus from juvenile sea bass, Dicentrarchus labrax. 881 Oct 4


1 2 3 4 Next >>