Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rat urinary esterase A, a plasminogen activator with kininogenase activity, was recently purified and characterized (J. Chao (1983) J. Biol. Chem. 258, 4434-4439). A sensitive radioimmunoassay for esterase A has been developed. This assay uses a rabbit antiserum in a final dilution of 1:160 000 and the purified enzyme was labelled with 125I using a lactoperoxidase method. It detects 80 pg of immunoreactive material per tube. This antiserum has some cross-reactivity with rat urinary kallikrein (approximately 5%) but a previously characterized tissue kallikrein antiserum has negligible cross-reactivity with the urinary esterase A in the assays. Therefore, kallikrein levels are measured simultaneously in all samples to obtain accurate levels of immunoreactive esterase A. Dilutions of urine or tissue homogenates showed complete parallelism with esterase A standard curves. No cross-reactivity with dog, human or monkey urine was seen. The recovery of esterase A from rat urine was 99.7 +/- 3.5%. Intra- and between-assay errors were 6.5 and 11.2%, respectively. Immunoreactive esterase A was measured and compared with kallikrein levels in rat urine, kidney, pancreas, submandibular gland, descending colon and ileum. The urinary esterase A excretion rate was reduced significantly in rats on a high sodium, compared with a low sodium diet, but not significantly increased above control by the latter. Nonetheless, a significant correlation between urinary kallikrein and esterase A excretion rate was present. This radioimmunoassay can now be used to measure esterase A levels in urine and tissue as questions have arisen about its regulation and functional significance.
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PMID:Measurement of the rat urinary plasminogen activator (esterase A) by direct radioimmunoassay in urine and tissue. 656 99

Peritoneal macrophages derived from CD-1 and C57BL/6 mice were separated into distinct groups based on their buoyant densities on discontinuous gradients of Percoll and assayed for antibacterial activity against Listeria monocytogenes. Subpopulations of peritoneal macrophages derived from Listeria-immune mice present a wide variation in their ability to control intracellular infection. Distinct subsets were found which exhibited bacteriostatic and listericidal activity. The fractionation procedure yielded a population of peroxidase-positive macrophages which were devoid of antilisterial action. Subpopulations of resident and elicited macrophages were also functionally heterogeneous in their ability to restrict intracellular growth of bacterial. In some experiments, subclasses were examined for secretion of plasminogen activator and phagocytosis of latex particles. These activities varied considerably with the status of activation of the macrophages, but failed to correlate with antimicrobial activity within given subpopulations.
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PMID:Fate of Listeria monocytogenes in murine peritoneal macrophage subpopulations. 679 45

Each of 11 tumors tested produced a factor that markedly suppressed the ability of macrophages to release H2O2 or O.2- in response to phorbol myristate acetate or zymosan. Four of seven normal cell types produced a similar activity, which was 3.5-7 times lower in titer than that in tumor cell-conditioned medium (TCM), and which was much more rapidly reversible in its effects. TCM caused 50% inhibition of H2O2 release when it was present in the medium for 48 h at a concentration of 13%, or when 100% TCM was present in the medium for 18 h. The H2O2-releasing capacity of macrophages incubated in TCM only returned to control levels by 6 d after its removal. TCM prevented augmentation of H2O2-releasing capacity by lymphokines. The titer of suppressive activity in TCM depended on both the concentration of tumor cells and the duration of their incubation. TCM did not augment the activity of catalase, myeloperoxidase, glutathione peroxidase, or glutathione reductase or the content of glutathione within macrophages, suggesting that decreased synthesis rather than increased catabolism was responsible for reduced secretion of H2O2. Suppression of the release of H2O2 or O.2- by TCM appeared to be a relatively specific effect, in that TCM increased macrophage spreading and adherence to glass while exerting little influence on rates of phagocytosis, synthesis of protein, or secretion of lysozyme, plasminogen activator, or arachidonic acid and its metabolites. Thus, tumor cells and some normal cells can secrete a factor that selectively deactivates macrophage oxidative metabolism.
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PMID:Suppression of macrophage oxidative metabolism by products of malignant and nonmalignant cells. 715 14

Neutrophil accumulation and free radical release are implicated in the genesis of reperfusion injury. However, little is known about the changes in myocardial lipid peroxidation and antioxidant activity in relation to coronary artery thrombosis and thrombolysis. To investigate this issue, 18 dogs with electrically induced occlusive thrombus in the left anterior descending (LAD) coronary artery were given tissue-type plasminogen activator (TPA). Sustained reflow (lasting > 120 min) occurred in 4 dogs, reocclusion after initial thrombolysis (transient reflow, duration of reflow 5 to 25 min) occurred in 7 dogs, and no reperfusion was evident in 7 dogs. Myocardial neutrophil infiltration was determined by measuring myeloperoxidase (MPO) activity, lipid peroxidation by malondialdehyde (MDA) levels and antioxidant activity by superoxide dismutase (SOD) activity in the myocardial regions supplied by the nonischemic left circumflex (Cx) and the ischemic LAD coronary arteries. In dogs with ischemia alone (no reperfusion), MPO activity and MDA levels in the LAD-supplied myocardium were modestly higher and SOD activity modestly lower than in the corresponding Cx-supplied myocardium. In dogs with sustained reperfusion there was a marked increase in MPO and MDA and a marked reduction in SOD activity in the reperfused myocardium. The MPO and MDA values in the myocardium of dogs with transient reperfusion, although much higher than the corresponding normal myocardial values, were less marked than in the myocardium of dogs with sustained reperfusion, and the SOD activity was preserved in the transiently reperfused regions. Myocardial shortening fraction in the LAD region was worse in dogs with sustained reperfusion than in those with sustained ischemia or transient reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial neutrophil infiltration, lipid peroxidation, and antioxidant activity after coronary artery thrombosis and thrombolysis. 783 91

E. coli O157:H7 produces a cytotoxin active against Vero cells that has been termed verotoxin. In this study, we demonstrated that local intraarterial injection of verotoxin induced a decrease in blood flow and an increase in hemorrhagic lesions in rat small intestine. Significant increases in the area of hemorrhagic lesions were observed at 120 min after verotoxin injection. These lesions were produced by either verotoxin 1 or 2, but verotoxin 2 produced more extensive lesions. The temporal alteration of vasoactive substances in microcirculatory beds was determined after the administration of culture filtrate of E. coli O157:H7. Tissue-type plasminogen activator activity in regional plasma was significantly elevated as early as 30 min, suggesting that local fibrinolytic activation mediated by microvascular endothelium occurred. There was also early elevation of platelet-activating factor content in the ileal mucosa and its level remained significantly elevated thereafter. Intestinal blood flow, as determined by a laser Doppler flowmeter, started to decrease at about 45 min. The platelet-activating factor antagonist CV6209 was shown to attenuate the decrease in blood flow as well as the development of hemorrhagic lesions, demonstrating that platelet-activating factor is an important mediator for the microcirculatory damage. Accumulation of neutrophils demonstrated by myeloperoxidase activity in the intestinal mucosa and overproduction of oxygen-radicals from neutrophils of the mesenteric veins determined by the luminol-dependent chemiluminescence assay were observed at 60 min, corresponding with the decreased blood flow. Platelet-activating factor may be closely involved in the process of leukocyte accumulation and increased oxygen radical generation, because CV6209 also significantly attenuated these changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Verotoxin induces hemorrhagic lesions in rat small intestine. Temporal alteration of vasoactive substances. 820 Feb 55

Antigenic variation among 13 Quebec isolates of bovine viral diarrhea virus (BVDV), 4 reference strains and 2 American isolates were studied by peroxidase-linked antibody assay (PLA assay) and neutralization test (NT). The Quebec strains consisted of 3 isolates before 1993 and 10 isolates from 1993. In the PLA assay, we compared 2 different fixatives, acetone and formalin. Acetone-fixation allowed us to identify 6 groups from amongst the viruses tested. All the Quebec isolates were different from the reference strains. In addition, antigenic variation was detected between Quebec isolates obtained before and during 1993. However, PLA assays performed after formalin fixation did not detect these antigenic variations. Neutralization tests were carried out with 2 polyclonal antibodies (PAb) and 6 monoclonal antibodies (MAb). They were used to classify BVDV strains and isolates into 4 groups and 7 subgroups respectively. In conclusion, we demonstrated that the BVDV isolates from the 1993 outbreak in Quebec are antigenically different from reference strains and from isolates existing in Quebec before 1993. In addition, we have shown that 2 internationally used fixation-methods in PLA assay give different results. The usefulness of each method is discussed.
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PMID:Antigenic variation among bovine viral diarrhea virus (BVDV) strains and the role of different cell fixation methods in immunoassays. 900 98

Following oral surgery, there are sometimes disturbances in wound healing. It was the aim of this investigation to look for relationships between the composition of saliva and disturbed wound healing. Resting as well as stimulated fasting whole saliva was collected from 96 patients (19 to 53 years of age) prior to oral surgery. Flow rate, pH, standard bicarbonate, total buffer bases, peroxidase, lysozyme, thiocyanate, secretory immunoglobulin A, lactoferrin, total protein, tissue type plasminogen activator, and plasminogen activator inhibitor were determined. The salivary data of eight patients who suffered from disturbed wound healing were compared to the data of 20 randomly selected patients with normal wound healing. Patients with disturbed wound healing revealed increased activities and secretion rates for peroxidase in resting saliva. In stimulated saliva, decreased secretion rates for thiocyanate and total protein were found. Not a single salivary factor was able to discriminate both groups of patients with sufficient accuracy, but with a combination of tissue type plasminogen activator, peroxidase, plus secretory immunoglobulin A measurements from resting whole saliva a clearly improved and acceptable discrimination of the two patient groups was possible. A discriminant function including six salivary factors could be used to completely separate both groups.
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PMID:[Components of antibacterial and fibrinolytic activity of human saliva in normal and disordered wound healing]. 1007 67

Although there is considerable interest in the role of neutrophils and platelets in acute cerebral ischemia-reperfusion, there are very little data related to the effect of systemic thrombolytic therapy on these blood elements. In the present study a rabbit model was used to examine the effects of cerebral ischemia, tissue-plasminogen activator therapy, or both on neutrophil and platelet peripheral counts and activity, the latter studied by stimulated neutrophil and platelet impedance aggregation and neutrophil oxygen-free radical chemiluminescence. New Zealand white rabbits (n = 25) were randomized to receive either tissue-plasminogen activator (6.3 mg/kg IV; 20% bolus, remainder as a 2-hour infusion) or vehicle (0.9% saline) 3 hours following either autologous clot embolization or sham carotid artery isolation. Thus, four groups were examined: sham (n = 4), tPA only (n = 4), stroke only (n = 8), and stroke plus tPA (n = 9). Two hours after completion of thrombolytic therapy or vehicle infusion, the experiments were terminated, that is, 7 hours following autologous clot embolization or sham instrumentation. Blood was sampled from the thoracic aorta, and neutrophil and platelet peripheral counts and activity were determined prior to embolization and 0.5, 2.0, 4.0, and 7.0 hours following autologous clot embolization. No significant difference in platelet counts, either over time or between groups, was noted. In contrast to the platelet counts, the neutruphil count significantly increased over time, rising approximately 2.5-fold from baseline in all four groups (p < 0.001). No significant increase in neutrophil accumulation (myeloperoxidase assay; 10 (7) PMNs/g tissue; mean +/- SEM) was noted within infarcted regions of either the stroke (1.26 +/- 0.07; n = 5) or stroke plus tissue-plasminogen activator (1.26 +/- 0.09; n = 5) groups when compared to either viable brain regions within the ischemic hemisphere (1.29 +/- 0.03; n = 4) or in sham controls (1.36 +/- 0.35; n = 4). Neutrophil activity (aggregation, oxygen-free radical release) in both groups undergoing autologous clot embolization demonstrated a trend toward higher values when compared to the two sham-operated groups. Tissue-plasrninogen activator administration did not significantly affect ex vivo neutrophil activity. In contrast, platelet aggregation was significantly reduced by the administration of tPA with (p = 0.001) or without (p < 0.01) autologous clot embolization. Thus, in the present rabbit model platelet but not neutrophil activity is modulated by the administration of tissue-plasminogen activator, while autologous clot embolization results in a trend toward acute neutrophil activation.
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PMID:Neutrophil and Platelet Activity and Quantification Following Delayed tPA Therapy in a Rabbit Model of Thromboembolic Stroke. 1060 28

To elucidate the possible inhibitory effect of a novel carboxamide derivative (IS-741) on biliary carcinogenesis, Syrian hamsters were subjected to cholecystoduodenostomy and ligation of the distal end of the common duct, and then given a regular diet (group I) or a diet containing 200 p.p.m. of IS-741 (group II). All hamsters were subcutaneously injected with N-nitrosobis(2-oxopropyl)amine until 10 weeks after surgery, and continued to feed on their respective dietary regimen until termination of the experiment at 16 weeks after surgery. Biliary adenocarcinomas were evaluated histologically. Non-cancerous and cancerous hepatobiliary tract tissues were analyzed for phospholipase A(2) (PLA(2)) activity, myeloperoxidase (MPO) activity, and the concentrations of prostaglandin (PG), i.e., prostaglandin E(2), 6-ketoprostaglandin F(1)alpha and thromboxane B(2). IS-741 significantly inhibited the development and multiplicity of hepatobiliary adenocarcinomas and reduced the proliferating cell nuclear antigen labeling indices in non-cancerous hepatobiliary tissues, compared with group I. The anti-cancerous effect of IS-741 was associated with a significant inhibition of PLA(2) and MPO levels in non-cancerous tissues of the extrahepatic biliary tract and the liver, and in cancerous tissue of the liver. Furthermore, IS-741 reduced the production of PGs in non-cancerous hepatobiliary tissues, compared with group I. Although the precise mechanism of action of IS-741 in preventing biliary tumorigenesis remains to be elucidated, it is likely to be related to modulation of arachidonic acid metabolism and/or suppression of neutrophil accumulation.
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PMID:Chemoprevention of biliary carcinogenesis in syrian hamsters by the novel carboxamide derivative IS-741 after initiation with N-nitrosobis(2-oxopropyl)amine (BOP). 1091 Sep 46

A new method for preparing protein-loaded biodegradable microspheres by a process involving solid-in-oil-in-water (S/O/W) emulsion was established using poly(ethylene glycol) (PEG). In the first step, a protein solution was lyophilized with PEG, which resulted in the formation of spherical protein microparticles, less than 5 microm in diameter, dispersed in a continuous PEG phase. This process was well explained by the aqueous phase separation phenomenon induced by freezing-condensation. Since this lyophilizate could be directly dispersed in an organic phase containing biodegradable polymer by dissolving PEG with methylene chloride, a conventional in-water drying method could be adopted in the second step. Through this S/O/W emulsion process, horseradish peroxidase was effectively entrapped into monolithic-type microspheres of poly(DL-lactic-co-glycolic acid) (PLGA), without significant loss of activity. Bovine superoxide dismutase (bSOD), as another model protein, could be encapsulated into reservoir-type microspheres by the 'polymer-alloys method' using both poly(DL-lactic acid) (PLA) and PLGA. The initial release of bSOD from this reservoir-type microsphere was efficiently reduced. Further, the bSOD release kinetics could be suitably modified by adjusting the loading amounts of PEG or polymer composition. In this study, the multi-functional nature of PEG was successfully utilized in the preparation and designing of protein-loaded microspheres.
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PMID:Protein encapsulation into biodegradable microspheres by a novel S/O/W emulsion method using poly(ethylene glycol) as a protein micronization adjuvant. 1110 83


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