Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032463 (polycythemia vera)
 3,374 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Swine were used as an experimental animal model to evaluate immunomodulating effects of the opiate drug, morphine, on antigen-specific humoral and cell-mediated immune responses. Morphine free base in peanut oil was administered at 4-day intervals for up to 42 days to maintain drug levels at or above 100 ng/ml. The effect of morphine administration on humoral immune responses was evaluated by immunization on day 7 of morphine treatment with a battery of antigens, including swine herpes virus (also known as pseudorabies virus, PRV), Brucella abortus and the Escherichia coli pilus antigens K88, K99, 987P and F41. Fourteen days later, swine were reimmunized with B. abortus and E. coli pilus antigens. Antibody titers to these antigens were evaluated on a weekly basis. Cell-mediated immunity was evaluated by measuring skin immune responses to the antigen 2,4-dintroflurobenozene (DNFB). In one experiment, swine were sensitized with DNFB on day 7 of morphine treatment at the same time as immunization with the other antigens. In a second series of experiments, swine were sensitized either 7 days before or 7 days after initiation of morphine treatment. Pigs were challenged with DNFB administered 27 days after the initiation of morphine treatment and skin responses were evaluated 24 h later. The ability of swine to resist PRV infection was evaluated by exposure to virulent virus on day 28 of morphine treatment. Chronic morphine administration did not impair the induction of the humoral immune responses to bacterial or viral antigens. In addition, morphine treatment did not alter the resistance of immunized swine to PRV infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic morphine administration impairs cell-mediated immune responses in swine. 131 Jul 38

Several conventional and genetically recombinant modified-live viral (MLV) vaccines are used to control pseudorabies virus infections (Aujeszky's disease, PRV) in swine. Differentiating vaccinal PRV (V-PRV) from wild PRV (WT-PRV) is important for herd health, regulatory and forensic purposes, and for studies of PRV latency and epidemiology. All PRV vaccines used currently contain glycoprotein I (gI) and/or thymidine kinase (TK) gene deletions, whereas WT-PRV typically contain intact gI and TK genes. Utilizing these differences we developed an effective but simple differential polymerase chain reaction (PCR) approach based upon the amplification of gI and TK gene polymorphisms. The primary immunoreactive epitope-encoding region of the gI gene and nearly the entire TK gene were amplified and analyzed using nested PCR procedures. TK and gI PCR products were cleaved with Sal I and Sac I, and Nco I restriction enzymes respectively. PCR product and restriction fragment length polymorphisms enabled most V-PRV to be clearly distinguished from each other, and all of them, as a group, clearly differentiated from typical WT-PRV. Mixtures of V-PRV and WT-PRV could be identified as such. The uncommon but occasional occurrence of atypical WT-PRV containing altered gI and/or TK genes indicates the need for interpretive caution, particularly if aberrant gene segment polymorphisms are observed. This rapid and precise molecular approach will facilitate regulatory monitoring, epidemiological investigations, diagnostic differentiation, purity testing and latency/recrudescence studies with the class of biologicals and offers a model for similar analyses of other MLV biologicals as well.
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PMID:Molecular analysis of pseudorabies viral vaccines and their rapid differentiation from wild-type isolates using DNA-amplified glycoprotein I and thymidine kinase gene segment polymorphisms. 133 75

Stillbirths, mummies, abortions, and early embryonic death have a substantial impact on the profitability of a farm in both endemic and epidemic conditions. Fetal death is highly dependent on stage of gestation. Implantation occurs around day 14 postmating in sows, and fetal death of an entire litter at this time usually results in a regular return to service. If more than four embryos remain alive, the sow may go on to farrow normally. If fetal death occurs after implantation but before calcification (around 35 days gestation), the sow will either return to estrus at an irregular interval or will farrow a normal litter of reduced size. Although fetuses are normally resorbed prior to calcification, fetal death after that stage of development leads to mummification. Abortions are more directly related to maternal control of pregnancy than fetal failure. Stillbirths are those pigs that appear normal at birth but have lungs that do not float in water. Causes of fetal death can be divided into infectious and noninfectious categories. Infectious causes perhaps are overemphasized but are certainly important in epidemic situations. Some infectious causes of fetal death are primarily systemic maternal pathogens, whereas others may attack the fetus and/or placenta, directly such as PPV, PEV, PRV, SIRS virus, and Leptospira sp. Several other infectious agents have been associated with fetal death. Noninfectious causes of stillborns, mummies, abortions, and early embryonic death are most common in endemic situations. Most stillbirths are due to difficulty at or around parturition, primarily extended duration causing fetal anoxia. Environmental factors such as increased ambient temperature and seasonal infertility affect death rates, as do specific individual sow characteristics, nutritional factors, and toxicities. The causes of stillborns, mummies, abortions, and early embryonic death are often difficult to ascertain, but the potential rewards make investigation efforts worthwhile.
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PMID:Stillbirths, mummies, abortions, and early embryonic death. 144 74

Male Sprague-Dawley rats were placed in hypobaric hypoxia for 17-21 d (FIO2 10%) to establish pulmonary hypertension (PH) and control rats were kept in normobaric room air. Right mean atrial and ventricular pressures (PRA, PRV) were recorded, left ventricular (LV) blood was collected, and lungs were perfused with heparinized saline. Hearts were removed to evaluate right ventricular (RV) hypertrophy (RV/(LV+septum)%). Peptides were quantitated with radioimmunoassay in lung tissue extracts and plasma. Wet lung weight, PRA, PRV, and RV/(LV+S)% were higher and body weight was lower in hypoxia rats, and lung morphometry revealed increased arterial medial thickness (MT/OD%) and elastification of arterioles and capillaries. Lung tissue CGRP, PYY, gamma 2-MSH, and SOM were higher in PH rats and ANP was unchanged. Blood AVP, CGRP, PYY, VIP, and SOM were reduced in PH rats and ANP was unchanged. Lung levels of PYY and SOM correlated significantly with the time in hypoxia and with all parameters examined and CGRP and gamma 2-MSH correlated with all but medial thickness. PYY had the highest correlation of the peptides with body weight, PRV, and RV/(LV+S)%, and SOM the highest with time in hypoxia, wet lung weight, PRA, MT/OD%, and elastification of arterioles and capillaries. Blood peptides correlated inversely with these parameters. ANP had the overall weakest correlations and CGRP, PYY, and SOM had the highest. SOM correlated the highest with arterial medial hypertrophy, PRV, RV hypertrophy, and elastification of peripheral capillaries. VIP correlated the highest of the blood peptides with body weight and wet lung weight. Statistically significant correlations do not necessarily imply causal relationships. The putative roles of these peptides in pulmonary function are discussed.
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PMID:Dynamic aspects of regulatory lung peptides in chronic hypoxic pulmonary hypertension. 157 30

The aberrant overexpression of interleukin 6 (IL-6) is implicated as an autocrine mechanism in the enhanced proliferation of the neoplastic cell elements in various B- and T-cell malignancies and in some carcinomas and sarcomas; many of these neoplasms have been shown to be associated with a mutated p53 gene. The possibility that wild-type (wt) p53, a nuclear tumor-suppressor protein, but not its transforming mutants might serve to repress IL-6 gene expression was investigated in HeLa cells. We transiently cotransfected these cells with constitutive cytomegalovirus (CMV) enhancer/promoter expression plasmids overproducing wt or mutant human or murine p53 and with appropriate chloramphenicol acetyltransferase (CAT) reporter plasmids containing the promoter elements of human IL-6, c-fos, or beta-actin genes or of porcine major histocompatibility complex (MHC) class I gene in pN-38 to evaluate the effect of the various p53 species on these promoters. Murine and human wt p53 derived from pCMVNc9 and pC53-SN3, respectively, strongly repressed the IL-6 (promoter position -225 to +13), c-fos (-711 to +42), beta-actin (-3400 to +912), and MHC (-528 to -38) promoters in serum-induced HeLa cells; additionally, IL-6 promoter/CAT transcription unit constructs induced by IL-1, phorbol ester, or pseudorabies virus were also repressed by wt human and murine p53. The murine transforming mutant p53 (pCMVc5) was less active in repressing the IL-6, c-fos, beta-actin, and MHC promoter constructs. The human p53 mutant derived from pC53-SCX3 was also less active than the wt protein in repressing the IL-6, c-fos, beta-actin, and MHC promoters, except that serum-induced IL-6/CAT expression was equally repressed by both human wt and mutant p53. In similar transient transfection experiments in HeLa cells, overexpression of the wt human retinoblastoma susceptibility gene product, RB, was found to repress the serum-induced IL-6 (-225 to +13), c-fos (-711 to +42), and beta-actin (-3400 to +912) promoters but not the PRV-induced IL-6 (-110 to +13) or the serum-induced MHC (-528 to -38) promoters. These observations identify transcriptional repression as a property of p53 and suggest that p53 and RB may be involved as transcriptional repressors in modulating IL-6 gene expression during cellular differentiation and oncogenesis.
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PMID:Repression of the interleukin 6 gene promoter by p53 and the retinoblastoma susceptibility gene product. 165 55

To investigate various aspects of the latency of pseudorabies virus in swine (PRV, suid herpesvirus 1) we developed in vitro nucleic acid amplification methods based upon the polymerase chain reaction. Primers flanking a 156-bp region of the pseudorabies virus gp II gene were annealed to purified PRV DNA as well as DNA isolated from the trigeminal ganglia of swine latently infected with PRV and subjected to PCR amplification. Following amplification, 100 fg of PRV DNA was visualizable on stained gels and 1 fg (equivalent to 6 viral genome copies) was detectable when amplification was combined with blot hybridization. PRV-specific DNA sequences which remained undetectable by direct blot hybridization assays were amplified to levels visualizable on ethidium-bromide-stained gels in 5 of 5 experimental latently infected animals. In addition, oligonucleotide primers specific for a 223-bp region of the PRV immediate-early gene (IE 180) were capable of amplifying overlapping latency associated transcripts (LATs), via a cDNA intermediate, in 6 of 6 latently infected swine. These nucleic acid amplification methods should be applicable to the investigation of PRV latency, and gene expression during latency and reactivation, in which few cells harbor latent virus.
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PMID:Enzymatic amplification of latent pseudorabies virus nucleic acid sequences. 165 80

The gene encoding the complete glycoprotein of pseudorabies virus (PRV, Yamagata-S81 strain glycoprotein gIII) has been inserted into the baculovirus transfer vector pAcYM1S derived from the nuclear polyhedrosis virus of Autographa californica (AcNPV). A Spodoptera frugiperda cell line, SF21AE, was efficiently co-transfected with the transfer vector containing the gIII gene and AcNPV DNA by cationic liposomes (Lipofectin). The gene was placed under the control of the AcNPV polyhedrin promoter and expressed to high levels by the derived recombinant virus using SF21AE. Three polypeptides of different molecular weight were expressed. The principal products were glycosylated and transported to the cell surface. The smallest product was not glycosylated. Despite their lower molecular weight, it has been established that the antigenic properties of the peptides were conserved by comparison with those of the authentic glycoprotein gIII of PRV. Immunogenicity of the expressed products was also demonstrated. Intraperitoneal injection of expressed gIII induced neutralizing antibodies in mice. The results have raised the possibility that the protein expressed by baculovirus recombinant may be used to analyze biologically functional sites, develop a subunit vaccine and diagnostic antigens.
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PMID:Characterization of pseudorabies virus neutralization antigen glycoprotein gIII produced in insect cells by a baculovirus expression vector. 166 81

Overlapping fragments of the gene encoding glycoprotein gI of pseudorabies virus (PRV; herpesvirus suis 1) were expressed in bacteria. Using the fusion proteins and a panel of monoclonal antibodies (MAbs) against gI as well as swine sera we found that the N-terminal part of gI (residues 33 to approximately 100) contains a highly antigenic and immunogenic domain. Transfer of antibodies binding to this region as well as vaccination with fusion proteins containing the N terminus of gI are able to confer protection to mice against a lethal challenge of virus. The results show that gI, which is non-essential for virus replication in tissue culture, can induce neutralizing and protective antibodies. The potential suitability of fusion proteins encompassing N-terminal parts of gI as diagnostic tools is demonstrated.
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PMID:Pseudorabies virus glycoprotein gI: in vitro and in vivo analysis of immunorelevant epitopes. 169 64

Uptake and transneuronal passage of wild-type and attenuated strains of a swine alpha-herpesvirus (pseudorabies [PRV]) were examined in rat visual projections. Both strains of virus infected subpopulations of retinal ganglion cells and passed transneuronally to infect retino-recipient neurons in the forebrain. However, the location of infected forebrain neurons varied with the strain of virus. Intravitreal injection of wild-type virus produced two temporally separated waves of infection that eventually reached all known retino-recipient regions of the central neuraxis. By contrast, the attenuated strain of PRV selectively infected a functionally distinct subset of retinal ganglion cells with restricted central projections. The data indicate that projection-specific groups of ganglion cells are differentially susceptible to the two strains of virus and suggest that this sensitivity may be receptor mediated.
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PMID:Two alpha-herpesvirus strains are transported differentially in the rodent visual system. 171 50

Purified DNA from 45 isolates of suis herpes virus 1 (SHV1) collected between 1980 and 1987 from clinical outbreaks of Aujeszky's disease on French farms was compared by restriction fragment pattern (RFP) analysis. The BamHI generated RFPs were found to be distinguishable, confirming RFP analysis as a potential epidemiological tool. The RFP could be assigned to two established major electrophoretic types and different subtypes. The RFP analysis indicated that the majority of outbreaks were caused by ADV with a central European genome type. The heterogeneity of RFPs among PRV isolates recovered from the central nervous system, lung, and foetus was not restricted specifically to one clinical entity. Variations in the virulence of the 45 isolates studied in mice, chicks, or piglets were unrelated to the RFP subtypes. One unusual RFP has been described for one strain of low virulence.
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PMID:Restriction fragment pattern analysis of genomes from French isolates of suis herpes virus 1 (Aujeszky's disease virus). 197 30


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