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)

The long-term results of 414 patients who underwent repair of tetralogy of Fallot between 1967 and 1977 were studied and correlated with the results of others. There were nine late deaths (8-year actuarial survival 95.8%). Six of the deaths wee directly related to the malformation or its treatment. Eight patients (2.4%) required reoperation. Ten patients (4.8%) had arrhythmic symptoms. Eight (3.1%) had congestive heart failure that required treatment. The risk factors associated with late events of all types, including death, were: older age at repair, a high mean ratio of peak systolic right-to-left ventricular pressures (PLV/RV) immediately after repair, and the presence of a Potts anastomosis. Neither a transannular patch nor a previous Blalock-Taussig or Waterson anastomosis was an incremental risk factor. Bacterial endocarditis was not observed. Three hundred seven patients underwent repair primarily or after a single Blalock-Taussig or Waterston shunt and had a PRV/LV of 0.85 or less after repair. Among these selected patients, the actuarial survival was 98.1%, which is still lower than that for the general population (p = 0.12), and freedom from events was 95.9%. Late after repair, PRV/LV was lower by 6 +/- 28% (+/- SD) than PRV/LV immediately after repair (p = 0.03) in the 33 restudied patients with such data. The higher the PRV/LV immediately after repair, the greater the percent reduction.
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PMID:Late survival and symptoms after repair of tetralogy of Fallot. 705

Ventilatory responses to changes in right ventricular (RV) load were studied in spontaneous breathing anesthetized dogs. Moving average RV pressure leads to (PRV) was used as an index of the RV strain. RV load was changed in two ways: 1) cardiac output (Q) was increased by infusion of isoproterenol (0.7-1.2 micrograms/min) and reduced by infusion of vasopressin (0.3-0.5 U/min); and 2) RV pressure was increased independently on Q by partial balloon obstruction of the RV outflow. When Q was changed by drug infusion there was a linear correlation between leads to PRV and Q (avg r = 0.04). Well-correlated linear relationships were found between expired minute ventilation (VE) and leads to PRV (avg r greater than 0.03), the slopes and intercepts of which were not significantly different whether leads to PRV was changed by altering Q, partial obstruction of RV outflow, or combining both procedures. Bilateral vagotomy did not alter the VE/leads to PRV slope resulting from RV balloon inflations. It is suggested that the RV strain may act as a controller of ventilation and provide a link between Q and VE.
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PMID:Cardiac output as a controller of ventilation through changes in right ventricular load. 711 35

Nine anaesthetized, splenectomized dogs, heparinized with 300 IU/kg bodyweight heparin i.v. had one tenth of their total blood volume returned to them by autotransfusion under maximum pressure with the Bentley-system. For the "Heparin"-autotransfusion (n = 49) 1:5 0,9% NaCl was added to the blood; whilst for the "Citrate"-autotransfusion 1:5 ACD-B(n = 28) or CPD (n = 30) stabilisor was added. Autotransfusion was performed as follows: Heparin-ACD-B- Heparin-DPD- Heparin-ACD-B etc. The pump function of the right ventricular myocardium was measured by the force of contraction (PRV, IP, SV, T1) as well as by criteria of contractility (dp/dtmax, VCEmax, KI1, KI2). Immediately after acute bleeding a reduction of the force of contraction to 50% was seen, but the contractility remained unchanged. During the maximum pressure autotransfusion of the blood the force of contraction consistently increased irrespective of the anticoagulant used. The contractility remained unchanged. In the following phase the force of contraction and the contractility normalised when heparin was employed, whilst when citrate was used there was a reduction of the force of contraction and of the contractility corresponding with the different dose of citrate of ACD-B and CPD. This short phase was followed by spontaneous stabilisation of the circulation. The force of contraction and the contractility returned to normal when heparin and ACD-B were employed, whilst a reduction of these criteria occurred when CPD was used. From these findings, the scheme of anticoagulation for citrate under clinical conditions should be modified by a prior injection of 2,000-3,000 IE of heparin i.v. and the addition of citrate in the ratio of 1:7 for ACD-B or 1:8 for CPD.
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PMID:[Changes in the pump function of the right ventricle during "pressure-autotransfusion" with citrate and heparin (author's transl)]. 730 5

Retrospective analysis was undertaken to determine the influence of residual pulmonary stenosis and surgically induced pulmonary insufficiency on the operative mortality rate in 104 patients with tetralogy of Fallot who underwent total correction between 1967 to 1970 at First Department of Surgery, Osaka University Hospital. This study revealed that, in order to improve the operative outcome in this anomaly, it is necessary to correct pulmonary stenosis to the point of the right-to-left ventricular peak pressure ratio (PRV/LV) less than 0.8 as well as preventing severe pulmonary insufficiency. Through this study, the criteria for enlargement of the right ventricular outflow tract (RVOT) for each given body size which will produce a PRV/LV of less than 0.8 were derived in 1971. If the size of the RVOT after infundibulectomy and valvotomy is smaller than that prescribed by the criteria, an outflow patch must be placed on the pulmonary outflow tract. Since 1971, these criteria have been used in total correction of this anomaly in our affiliated hospital without any problem and have been yielding good operative results. Postoperative hemodynamic studies have shown that our criteria are suitable.
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PMID:The criteria for reconstruction of right ventricular outflow tract in total correction of tetralogy of Fallot. 742 Dec 90

Equine herpesviruses type 1 (EHV-1) and type 4 (EHV-4) induce a complement receptor protein on the surface of infected cells capable of binding to the third component of complement (C3). The protein mediating the binding to the C3 component of complement was identified as glycoprotein 13 (gp13, EHV-gC), as expression of the cloned viral gene under the control of a CMV promoter induced C3 binding activity at the transfected cell surface. Comparable to glycoprotein C (gC) from herpes simplex virus type 1 (HSV-1-gC), glycoprotein III from pseudorabiesvirus (gIII, PRV-gC) and bovine herpesvirus-1 (gIII, BHV-1-gC), gp13 derived from EHV-infected cell lysates bound to C3 fixed to solid phase, showing preferential binding to the appropriate host complement component. Similar to wild-type isolates, a highly attenuated vaccine EHV-1 strain also displayed complement receptor activity despite apparent differences of the gp13 gene in restriction enzyme digest pattern and reactivity with monoclonal antibodies. In addition, other structural proteins were altered in the vaccine strain as compared to wild-type strains, which might contribute to its attenuated phenotype. In contrast to the situation observed with HSV-1-gC, the interaction of gp13 (EHV-gC) with horse complement was not inhibited by polyanionic substances like heparin or dextran sulfate. These results suggest structural differences in the particular binding mechanism of the respective viral envelope proteins.
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PMID:gp13 (EHV-gC): a complement receptor induced by equine herpesviruses. 748 25

Following the transection of one pelvic nerve and both hypogastric nerves, the urinary bladder of male Sprague-Dawley rats was injected with pseudorabies virus (PRV; Bartha strain). The central stump of the transected pelvic nerve was labelled with fast blue (FB), and rats were maintained for 2, 2.5, and 3 days following viral infection. Tissue was processed with antisera against PRV and choline acetyltransferase (CAT). In the L6-S1 spinal cord, neurons in the ipsilateral intermediolateral area (IML) were labelled after 2 days. After 2.5 days, labelled neurons were also found in the dorsal gray commissure (DGC), the ipsilateral superficial dorsal horn, and the contralateral IML area. After 3 days, many labelled neurons appeared in the superficial dorsal horns and, bilaterally, in the L6-S1 dorsal root ganglia. In both IMLs, two groups of PRV-labelled neurons were found: 1) CAT-positive preganglionic cells and 2) smaller, CAT-negative cells located slightly dorsal to the preganglionic neurons. No other doubly stained neurons were found in the spinal cord. Contralateral DRG neurons stained for either PRV or FB or both. Ipsilateral DRG neurons stained only for PRV. PRV-immunoreactive (IR) neurons appeared in the brainstem only after 3 days. These were located primarily in the pontine micturition centers (equal numbers), the ventral locus coeruleus, and the raphe and lateral reticular areas.
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PMID:Central nervous system neurons infected by pseudorabies virus injected into the rat urinary bladder following unilateral transection of the pelvic nerve. 749 40

Antifreeze glycopeptides (AFGP) have been isolated from the fully pelagic high-Antarctic silverfish Pleuragramma antarcticum of the suborder Notothenioidei (Perciformes). The fishes were caught during the PRV Polarstern expedition EPOS III (Jan-Mar, 1989) in the eastern and southeastern Weddell Sea. Glycoconjugate and amino acid analysis of antifreeze glycopeptides (AFGP) indicate that the glycopeptide structure is identical to the polymers of H2N[Ala-Ala(beta-galactosyl(1-->3)-alpha-N- acetylgalactosamine)Thr]nAla-Ala-COOH of previously studied Antarctic notothenioids. The content of AFGPs in P. antarcticum is lower than in other notothenioid fish from the same region. Antifreeze activity shows a maximal hysteresis of 1.19 degrees C at a concentration of 20 mg/ml AFGP. A linear increase in activity of the antifreeze glycopeptides could be demonstrated concomittant with a decreasing ice content. The freezing point of blood serum is -1.9 degrees C.
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PMID:Antifreeze glycopeptides of the high-Antarctic silverfish Pleuragramma antarcticum (Notothenioidei). 765 79

The retinal ganglion cells giving rise to retinohypothalamic projections in the rat were identified using retrograde transport of horseradish peroxidase (HRP) or FluoroGold injected into the suprachiasmatic nucleus (SCN), and using transneuronal transport of the Bartha strain of the swine herpesvirus (PRV-Bartha). When PRV-Bartha is injected into one eye, it is taken up by retinal ganglion cells, replicated, transported to axon terminals in the SCN, and released. There the virus may take one, or both, of two paths to retinal ganglion cells in the contralateral eye: 1) uptake by SCN neurons, replication, and release from the neurons with uptake and retrograde transport in retinal afferents originating in the contralateral retina; 2) transneuronal passage through axo-axonic appositions between retinal afferents in the SCN with subsequent retrograde transport of virus to the contralateral retina. The ganglion cells thus labeled are a homogeneous population of small neurons (mean diameter, 12.8 +/- 2.2 microns and mean area, 81.8 +/- 21.8 microns 2) with sparsely branching dendrites that are widely distributed over the retina. This population is best identified when virus labeling of retinal projections in areas beyond the hypothalamus is eliminated by lateral geniculate lesions that transect the optic tract at its entry into the geniculate complex. The same population is labeled with retrograde tracers but, with both HRP and FluoroGold, other ganglion cells are labeled, presumably from uptake by fibers of passage, indicating that the virus is a more reliable marker for ganglion cells giving rise to retinohypothalamic projections. The ganglion cells identified correspond to a subset of type III, or W, cells.
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PMID:The retinohypothalamic tract originates from a distinct subset of retinal ganglion cells. 770 57

Calcium antagonists inhibit hypoxic pulmonary vasoconstriction (HPV), which was recently shown to be biphasic in isolated vessels, but the sensitivity of the two phases to calcium antagonism is unknown. We studied HPV in rat isolated large pulmonary arteries (PA) and resistance pulmonary arteries (PRV), using a small vessel myograph. Two phases of acute hypoxic pulmonary vasoconstriction were confirmed to occur in both sizes of vessel. The first phase was short-lived and was followed by a more persistent phase of gradual onset. The magnitude of the first phase of contraction was greater than the second (p < 0.01). The first phase was reproducible, but the second was variable. Tension generated per square millimeter of vessel during both phases of hypoxic contraction was significantly greater in PRV than in PA (p < 0.05). Amlodipine caused dose-dependent inhibition of the first phase of HPV (p = 0.01), with a greater effect in PRV (p < 0.01). The second phase was not significantly inhibited. These results confirm that HPV is biphasic in isolated large and small PA, with a greater sensitivity of the first phase to calcium antagonism. Therefore, the first phase may represent HPV as observed in vivo.
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PMID:Effect of the calcium antagonist amlodipine on the two phases of hypoxic pulmonary vasoconstriction in rat large and small isolated pulmonary arteries. 775 59

Some data dealing with the establishment of a quantitative PCR assay are presented. The assay is based on the use of an internal standard (mimic) which differs from the target by a deletion of a few base pairs and which is co-amplified with the target DNA. The resulting PCR products are labelled with fluorescent primers and then separated and detected by an automated sequencer. A highly specific and sensitive PCR assay for the envelope glycoprotein gp50 gene has been developed. This assay is highly reproducible with a detection limit of one copy of PRV DNA. Several mimics were then constructed. As a result we can confirm that the strategy that we have chosen is adequate for the quantification of low amounts of virus DNA present in latently infected swine.
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PMID:Pseudorabies virus latency: a quantitative approach by polymerase chain reaction. 781 Apr 21


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