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)

An infectious herpesvirus mutant has been constructed in which a major structural envelope glycoprotein gene was replaced by a hybrid gene encoding a novel fusion protein consisting of the N-terminus of the viral glycoprotein joined to Escherichia coli beta-galactosidase (beta Gal). Specifically, we fused DNA encoding the first 157 amino acids of the structural glycoprotein gIII from pseudorabies virus strain Becker to the E. coli lacZ gene in a bacterial expression vector. The resulting hybrid gene was then used to replace the wild-type gIII gene in the virus by cotransfection of plasmid and viral DNA. The desired viral recombinants were identified by their inability to react with specific monoclonal antibodies that recognized only wild-type gIII protein. One such mutant virus, PRV-Z1, was chosen for further analysis. PRV-Z1 expressed a glycosylated gIII-beta Gal fusion protein after infection of PK15 cells. The fusion protein has no demonstrable beta Gal activity and, although glycosylated, remains sensitive to the enzyme endo-beta-N-acetylglucosaminidase H, unlike the mature gIII gene product, indicating that the fusion protein was incompletely processed.
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PMID:Construction of an infectious pseudorabies virus recombinant expressing a glycoprotein gIII-beta-galactosidase fusion protein. 303 31

The possible role of herpesviral infections of the inner ear in suddenly appearing inner ear disturbances was investigated. Experimental pseudorabies virus (PRV, Herpes sui 1) infection of mice and swine was used as a model system. Infected mice represented the productive cycle of PRV infection (acute phase), whereas the latent phase of infection could be tested in swine. From the acutely infected mice the virus could be reisolated from perilymphatic fluid and various parts of the brain. Massive histopathologic alterations and signs of total cell damage to the organ of Corti and the vestibular organ were found. Accordingly, in all of the cells of the inner ear multiple copies of the PRV genome could be demonstrated. We therefore suggest that the disturbances of the inner ear were induced by the acute virus infection. In two latently infected swine (sixty weeks after infection), PRV could not be recovered either from the perilymphatic fluid or from a variety of different neural and extraneural tissues. However, histopathologic changes similar to those found in the acutely infected mice were observed. The presence of viral DNA could be demonstrated by in situ cytohybridization in both sensory and supportive cells of the inner ear and vestibular organ, but not in the corresponding nerve fibers, which is in contrast to the acutely infected mice. The distribution of the viral genome was further analyzed in adjacent areas of the central nervous system. An involvement of acute and latent herpes virus infection in inner ear dysfunction including sudden deafness and vestibular neuronitis in man, might be suggested from the results described. The presented animal model system, PRV-infected swine, should permit further studies on a possible role of herpetic recurrences, particularly with regard to inner ear disturbances.
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PMID:The role of acute and latent virus infections in the pathogenesis of inner ear disturbances. 303 32

In HPCD pigs inoculated with PRV, latent PRV could be reactivated in-vivo by the administration of large doses of prednisolone 3 months after the primary infection. In two pigs, virus shedding was without clinical signs of disease, whereas depression of circulating lymphocytes was prominent. Reactivation of PRV was also demonstrated by cultivation of the brain cortex on the 7th day and the mandibular lymph node on the 9th day after the prednisolone began treatment. Coincident with the virus isolation, characteristic lesions were observed in 2 pigs in the central nervous tissues and mandibular lymph nodes and these were composed of cell necrosis and eosinophilic intranuclear inclusion bodies. Cells containing the intranuclear inclusion bodies had immature and mature PRV particles. Results of the present study with HPCD pigs indicated that the lesions in the brain and lymph node accompanied by eosinophilic intranuclear inclusion bodies were pathogonomonic lesions induced by reactivation of PRV.
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PMID:Pathological changes in HPCD pigs with prednisolone induced recrudescence of pseudorabies virus. 303 71

The ratio of peak pressure in the right ventricle to that in the left ventricle (PRV/LV) in the operating room thirty minutes after repair of tetralogy of Fallot by an atrial approach, with or without a concomitant transatrial approach, was 0.58 +/- 0.217. It was 0.52 +/- 0.158 when repair was through a right ventricular approach (p for difference = 0.16). This ratio 18 to 24 hours postoperatively was 0.49 +/- 0.148 and 0.45 +/- 0.121 for the right atrial and right ventricular approaches, respectively. The reduction in PRV/LV between the two observations was -0.09 +/- 0.147 for the right atrial and -0.07 +/- 0.110 for the right ventricular approach (p for difference = 0.4). Therefore, the predictive rules for placing a transannular patch, rules derived from patients in whom the right ventricular approach was used and depending in part on the fall in PRV/LV during the first 24 hours after operation, are also applicable to patients in whom an atrial approach, with or without a transpulmonary approach, is used.
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PMID:The relief of pulmonary stenosis by a transatrial versus a transventricular approach to the repair of tetralogy of Fallot. 333 80

Experiments in dogs inoculated intracerebrally with biological variants of paralytic (PRV) and convulsive (CRV) rabies virus isolated from the Yak strain population of street rabies virus demonstrated distinct differences in the biological properties of the variants PRV induced in dogs paralytic rabies with a short incubation period (average 6.4 days) and CRV induced an atypical convulsive form characterized by attacks of tonic convulsions of the body, legs, and head twitching, and a longer incubation period (18.5 and 9.6 days, respectively). This explains a wide variability of the biological properties of street rabies virus strains.
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PMID:[Biological properties of variants of the rabies street virus]. 341 67

Based on our experience and the data presented here the following general approach may be used in the management of patients with tetralogy of Fallot: 1. Symptomatic infants under 6 months of age should be considered for an initial palliative shunt, preferably a Blalock-Taussig shunt or a Gore-tex modification of that procedure. 2. Symptomatic patients older than 6 months of age should be considered candidates for total correction, unless there are anatomic contraindications (anomalous left anterior descending artery, severe hypoplasia of the main pulmonary artery, multiple branch stenoses, multiple ventricular septal defects, or pulmonary atresia), or the predicted PRV/LV is greater than 0.7. 3. Total correction with closure of shunt should be undertaken in all patients prior to 5 years of age.
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PMID:Tetralogy of Fallot. 616 37

Between 1975 and 1982, valve xenograft conduits were used to establish continuity between the right ventricle and the pulmonary arteries in 28 patients between the ages of 3 to 39 years (mean 14.7 years) with 4 hospital deaths (14%). The indications for operation were pulmonary atresia types I and II in 7, extreme tetralogy of Fallot with hypoplastic pulmonary artery and valvular ring in 10, secondary obliteration of the infundibulum following Waterston shunt in 4, pulmonary valve insufficiency after transannular right ventricular outflow tract patch in 5 and tetralogy of Fallot with anomalous coronary artery in 2. Twenty-one patients (87%) between 9 and 41 years of age (mean 17.4 years) were available for follow-up 1/2 to 8 years after operation. The late death incidence during the follow-up period was 8% (2/24). Postoperative cardiac catheterization, which included right and left ventriculogram and measurements of gradients, was performed in 14 patients 4 months to 6 years after operation. Four patients were in New York Heart Association (NYHA) class 1, 6 in class II and 4 in class III. The other 7 non-catheterized patients were in class II. There were resting peak systolic gradients of 15 to 35 mmHg in 4, 36 to 55 mmHg and more than 55 mmHg across the xenograft valve and the proximal anastomosis in 4 other patients. The right and left ventricular end-diastolic pressures (RVEDP, LVEDP) averaged 18 and 17.5 mmHg, respectively, in 3 patients. The mean ratio of PRV/PLV quotient in NYHA class I group was 0.3, in class II 0.45 to 0.7 and in class III greater than 0.7 (including 2 with residual VSD and pulmonary hypertension). Late densitometric studies for assessing pulmonary valve competence revealed regurgitant fraction of up to 40% of the total stroke volume in the absence of a residual shunt 2 to 4 years after conduit implantation. Three children underwent uneventful surgical replacement of calcified xenograft conduit 1 1/2 to 4 1/2 years after surgery with antibiotic-sterilized valve allograft. Four other patients have residual ventricular septal defects (VSD), 2 of them underwent surgical reclosure while the other 2 patients with pulmonary hypertension still have their residual VSD open.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Late results of valve xenograft conduits between the right ventricle and the pulmonary arteries in patients with pulmonary atresia and extreme tetralogy of Fallot. 620 17

The hemodynamics, contractility and compliance of the right ventricle were examined during the early postoperative phase in 9 children operated for correction of tetralogy of Fallot. The same assessments were made in 5 patients after the transventricular closure of ventricular septal defects (control group). A further reduction of the PRV/LV quotient was observed in the Fallot group during the first 3 hours postoperatively. The contractility of the right ventricle (dp/dt max) was greatly reduced in all cases. The pressure/volume relationship of the right ventricle showed severe disturbance in compliance. The type of correction (with/without outflow tract patch or monocusp) did not appreciably affect the results. The hemodynamic changes observed in the control group (VSD) were considerably less pronounced. Apparently it is not the ventriculotomy but the infundibulectomy which is the traumatic factor of corrections in the area of the right ventricular outflow tract.
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PMID:The hemodynamics and contractility of the right ventricle in the early postoperative phase following correction of tetralogy of Fallot. 620 18

Pseudorabies is a rarely reported disease of raccoons. Laboratory and field evidence of PRV infection suggests the raccoon is a "dead end" host with little opportunity for raccoon-to-raccoon spread of virus. All reported field cases have been associated closely with infected swine and swine have been considered the source of the raccoon infection. The clinical signs of PRV in raccoons closely resembles those of canine distemper and rabies virus infections. Infection with the latter viruses are considered more prevalent and likely to be mistaken for PRV infection. Both CD and rabies virus may be maintained in raccoon populations with raccoon-to-raccoon transfer while PRV may not. Differentiation of PRV, CD and rabies infections is best achieved by histopathologic analysis of lung and brain tissue, together with virus isolation. It is of utmost public health importance that wildlife authorities recognize the similarities between these diseases, together with the different epidemiologic behavior of the viruses and the means to differentiate clinical cases.
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PMID:Pseudorabies virus infection in raccoons: a review. 628 8

Only 8% of the sequences of the genomes of pseudorabies (PRV) and herpes simplex (type 1) (HSV) viruses are homologous. These homologous sequences have been shown previously to be distributed throughout most of the genomes of the two viruses. By means of blot hybridization of restriction fragments of HSV-1 DNA to cloned, nick-translated restriction fragments of PRV DNA, it was possible to compare the location on the genomes of these viruses of the homologous regions. The results showed that the genome of PRV is, for the most part, colinear with the IL arrangement of the genome of HSV-1. An inversion or translocation of sequences mapping on the PRV genome between 0.07 and 0.39 map units was observed on the genome of one of these viruses. A comparison of the map positions of five genes with known functions confirmed these findings. The genes coding for the major immediate-early protein, the major capsid protein, and the thymidine kinase occupy similar positions on the genome of PRV and on the genome of HSV-1 in the IL arrangement. However, the genes for DNA polymerase and for the major DNA binding protein appear to be inverted relative to one another on the genomes of the two viruses.
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PMID:Localization of the regions of homology between the genomes of herpes simplex virus, type 1, and pseudorabies virus. 630 15


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