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)

Carcinoma of the bile duct at the hepatic hilar region is not a rare condition but with a low resectability rate. The incidence of this disease seems to be on increasing. In a previous report, 60 cases were explored surgically from 1975 to 1985, but resection was only possible in 5 cases (9.1%); while in the recent years from June, 1986 to June 1989, 24 cases were explored in the Surgical Department of General Hospital of PLA, 16 cases were resected, with a resectability rate of 66%. The increase of resectability rate was due to earlier recognition of this condition and the extension of surgery, including major resection of liver as well as radical dissection of the hepato-duodenal ligament and reparative operations on the blood vessels. Among these 16 cases, major hepatic resection was performed in 10 cases, in which, 3 cases of resections of the middle lobe of the liver were done instead of right or extended right lobectomy. No operative mortality in the 30 days' postoperative period, but the postoperative morbidity rate was still high and most of the complications were related to biliary leakage and infect ion. Three patients died in the postoperative follow up period at 6.14 and 15 months respectively. All of them died from biliary infection. The remaining 13 patients were still living, the longest being 40 months and the average living time was 16.1 months. Probably, lowering of the operative mortality rate and morbidity rate are still the most important considerations in the surgical treatment of hilar carcinoma at the present time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical treatment of hilar bile duct carcinoma]. 208 22

Lung injury is a common and severe complication in acute pancreatitis. The pathogenesis of which has not been completely understood. To explore the mechanism of lung injury, ST and FFA and PLA in bronchoalveolar perfusate, FFA and PLA in blood were measured; clinical symptoms and chest film were analysed; blood gas analysis was performed. The results indicated that lung injury mostly occurs in ABNP and less in AEP. Pulmonary edema and atelectasis are essential changes of lung injury. It is believed that FFA is an important factor responsible for pulmonary edema. PLA, which plays the most important role in lung injury, not only results in atelectasis by degradating the SA in alveolar, but also induces pulmonary edema. The main reason for the increase of ST is the degradation of SA in alveolar. The levels of FFA and PLA in the blood may indicate the severity of acute pancreatitis. However, it remains unknown whether the synthesis of SA in patient with acute pancreatitis is inhibited.
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PMID:[Clinical study of lung injury in acute pancreatitis]. 209 52

Mechanical ventilation with high peak airway pressures (Paw) has been shown to induce pulmonary edema in animal experiments, but the relative contributions of transvascular filtration pressure and microvascular permeability are unclear. Therefore, we examined the effects of positive-pressure ventilation on two groups of open-chest dogs ventilated for 30 min with a peak Paw of 21.8 +/- 2.3 cm H2O (Low Paw) or 64.3 +/- 3.5 cm H2O (High Paw). No hemodynamic changes were observed in the Low Paw group during ventilation, but mean pulmonary artery pressure (Ppa) increased by 9.9 cm H2O, peak inspiratory Ppa by 24.6 cm H2O, and estimated mean microvascular pressure by 12.5 cm H2O during High Paw ventilation. During the same period, lung lymph flow increased by 435% in the High Paw and 35% in the Low Paw groups, and the terminal extravascular lung water/blood-free dry weight ratios were 5.65 +/- 0.27 and 4.43 +/- 0.13 g/g, respectively, for the two groups. Lung lymph protein clearances and minimal lymph/plasma ratios of total protein were significantly higher (p less than 0.05) after 2 h of increased left atrial pressure (PLA) in the High Paw group versus the Low Paw group, which indicates a significant increase in microvascular permeability. Lymph prostacyclin concentration in pulmonary lymph, measured as the stable metabolite 6-0-PGF1 alpha, was increased significantly by 70 to 150% from baseline (p less than 0.05) in both groups during the periods of increased Paw and increased PLA, but it was not significantly different between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lung edema caused by high peak inspiratory pressures in dogs. Role of increased microvascular filtration pressure and permeability. 211 48

Poly-L-lactic acid (MW 6000) microspheres (PLA-MS) containing 5-fluoro-2'-deoxyuridine (FUdR) or four ester prodrugs of FUdR were prepared and examined with regard to the in vitro release kinetics. The incorporation efficiency of the lipophilic prodrugs into the PLA-MS was higher than that of FUdR or the hydrophilic prodrugs. The release of the lipophilic FUdR prodrugs from PLA-MS was sustained as compared with that of FUdR from PLA-MS. The release kinetics of the FUdR prodrugs appears to fit the Higuchi, Baker, and Lonsdale model in the early stage of the release process. The slope of the Baker and Lonsdale plots of the release of divaleryl-FUdR from PLA-MS decreased as the initial drug loading was decreased. The order of the release rates of FUdR prodrugs from PLA-MS with the same prodrug content was similar to that of the water solubilities of the prodrugs. These results suggest that the ester prodrugs could be released from PLA-MS by diffusion through water-filled capillaries or a series of pores rather than by diffusion through the PLA matrix.
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PMID:Controlled release of 3',5'-diester prodrugs of 5-fluoro-2'-deoxyuridine from poly-L-lactic acid microspheres. 214 64

When a variety of ferric chelates are reacted with hydrogen peroxide in phosphate buffer deoxyribose is damaged and this damage is protected against by formate, thiourea and mannitol. Damage done by ferric complexes of citrate, EDTA, NTA, EGTA and HEDA is substantially inhibited by superoxide dismutase (SOD) whereas complexes of PLA, ADP and CDTA are moderately inhibited by SOD. The effects of SOD argue against hydrogen peroxide acting as a reductant in Fenton chemistry driven by ferric complexes and hydrogen peroxide. EDTA has proved to be a useful model for Fenton chemistry that is inhibited by SOD although, it is not unique in this respect.
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PMID:Superoxide-dependent formation of hydroxyl radicals from ferric-complexes and hydrogen peroxide: an evaluation of fourteen iron chelators. 216 86

Poly(lactic acid) [PLA] and its co-polymers with glycolic acid [PLCG] have been known to be biodegradable and histocompatible for the past 20 years. Their physico-chemical and biological properties have been found suitable, in many instances, for sustaining drug release in vivo for days or months. Several dosage forms for parenteral administration have been investigated using these polymers and a microencapsulation technique is chosen frequently for its unique properties. There are a limited number of published papers concerning preparation and characterization of PLA or PLCG microcapsules, possibly because of commercial unavailability and difficulties in the synthesis of reproducible batches of these polymers. However, microcapsules can be made using different traditional and non-traditional techniques containing core materials ranging from biological proteins to synthetic drugs. An attempt is made here to review problems associated with the different microencapsulation techniques using PLA or PLCG. In vivo and in vitro drug release from these microcapsules is also reviewed.
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PMID:Biodegradable poly(lactic acid) and poly(lactide-co-glycolide) microcapsules: problems associated with preparative techniques and release properties. 220 Aug 61

Eight harbour seals (Phoca vitulina), two of them seronegative, six seropositive against PDV and a seronegative grey seal (Halichoerus grypus) were exposed to a low doses of a cell culture-propagated phocine distemper virus isolate (PDV 2558/Han 88). An intranasal route of inoculation was chosen. Clinical signs, resembling those of 1988's seal disease and seroconversion were observed in both seronegative harbour seals. One of them succumbed to the infection. The virus was not transmitted to another susceptible harbour seal which served as in-contact animal. Virus could be recovered from leucocytes of the diseased seals. Viremia was also present in a seropositive harbour seal that developed mild clinical signs; other seropositive seals were protected from clinical disease. The grey seal showed seroconversion upon inoculation, but did not develop any signs of disease. The humoral immune response of the seals plainly discriminated between homologous (PDV) and heterologous (canine distemper virus, CDV) virus as shown by virus neutralization tests and an antibody-binding assay (PLA).
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PMID:Morbillivirus infections of seals during the 1988 epidemic in the Bay of Heligoland: III. Transmission studies of cell culture-propagated phocine distemper virus in harbour seals (Phoca vitulina) and a grey seal (Halichoerus grypus): clinical, virological and serological results. 226 88

Poly (L-lactic acid) [L-PLA] microcapsules containing phenobarbitone were prepared from a w/o emulsion system, using light liquid paraffin as the continuum and a solution of phenobarbitone and L-PLA in acetonitrile as the disperse phase. Increasing stirring rate and emulsifying agent concentration were found to reduce microcapsule size. Spans (sorbitan esters of fatty acids) and Brijs (polyoxy ethylene ethers of fatty acids) with different physicochemical properties have been found to produce microcapsules of differing size. An attempt has been made to correlate emulsifier properties and the corresponding microcapsule size. It was found that the emulsifiers had little or no effect on the interfacial tension between light liquid paraffin and acetonitrile and there was no correlation between HLB of the emulsifiers and the resulting microcapsule size. It was postulated that microcapsule size would be affected by the packing of the emulsifier at the interface which would depend on the structure of the emulsifier. Closer, more uniform packing by the straight chain saturated fatty acid containing emulsifiers produced smaller microcapsules than when lose packing, which existed when emulsifiers containing either three fatty acid chains or a 'V' shaped cis-double bond containing fatty acid chain, were used. Microcapsule size was found to increase rapidly with an increase in polymer concentration, if this polymer concentration was increased in conjunction with an increase in the total solid content of the dispersed phase. Increases in polymer concentration by reducing the quantity of solvent for the dispersed phase caused little increase in mean microcapsule size. The phenobarbitone content in the microcapsules was not affected significantly by variations in the preparative parameters.
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PMID:Microencapsulation using poly (L-lactic acid) II: Preparative variables affecting microcapsule properties. 230 52

Poly(DL-lactic acid) (DL-PLA, molecular weight 20,500) microcapsules containing phenobarbitone (PB) as a reference core were prepared using a water/oil (W/O) emulsion system. Surface morphology, particle size and 'encapsulation efficiency' of the microcapsules prepared using different preparative variables have been investigated. Buffer pH 9 was used as a dissolution medium to determine the affect of preparative variables on the release rate from these microcapsules. With an increase in temperature of evaporation the microcapsule surface became increasingly irregular and porous, due to deposition of phenobarbitone crystals near the vicinity of the microcapsule surface leading to rapid release of the core. The normalized release rate was found to increase exponentially with an increase in the temperature of evaporation. Microcapsule morphology was also severely affected due to differences in polymer concentration in the disperse phase solvent. With the increase in polymer concentration, the microcapsule surface was found to be increasingly irregular and non-continuous, due to rapid precipitation of the polymer. Increased polymer concentrations also increased mean microcapsule diameter. The release rate increased with the increase in polymer concentration due to surface defects and did not exhibit a straight line correlation. When core loading was very high (e.g. C:P, 2:1 and 1:1), crystals of phenobarbitone appeared at the surface and these caused a very rapid burst effect. However, microcapsules containing a lower phenobarbitone content were found to follow t1/2 dependent release. The encapsulation efficiency was not seriously affected due to variations in temperature of preparation and polymer concentration. However, with the decrease in initial core loading the encapsulation efficiency of microcapsules was found to be reduced.
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PMID:Microencapsulation using poly(DL-lactic acid). I: Effect of preparative variables on the microcapsule characteristics and release kinetics. 232 48

Crotoxin is a neurotoxic phospholipase A2 capable of blocking synaptic transmission by inhibiting the release of neurotransmitters. The photoaffinity labeling technique was used to identify the neural membrane molecules involved in the binding of crotoxin. A photoactivatable, radioactive derivative of crotoxin was synthesized by reacting crotoxin with N-hydroxysuccinimidyl-4-azidobenzoate and with Na[125I]. Photoirradiation of synaptosomes from guinea pig brains in the presence of the crotoxin derivative resulted in the formation of a major radioactive conjugate of 100,000 daltons as revealed by autoradiography of a sodium dodecyl sulfate-polyacrylamide gel electrophoretic pattern. Pretreatment of the synaptosomes with trypsin, Staphylococcus aureus protease, or papain prevented the formation of this conjugate. The conjugate was not detected when plasma membranes from several nonneural tissues replaced the brain synaptosomes. Unmodified crotoxin inhibited the formation of this adduct with an IC50 of about 10(-8)M. Mojave toxin, caudoxin, notexin, Naja naja PLA, and taipoxin also inhibited adduct formation with different potencies, while beta-bungarotoxin and pancreatic PLA were ineffective. We concluded that an 85,000-dalton protein is the major component responsible for the binding of crotoxin to synaptosomal membranes.
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PMID:Identification of a crotoxin-binding protein in membranes from guinea pig brain by photoaffinity labeling. 234 82


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