Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of the autoimmune or autoallergic process in Progressive Chronic Polyarthritis, has been the subject of a great deal of study in the last four decades. In this work, using the synovial fluid of 312 patients suffering Chronic Progressive Polyarthritis and other arthropaties, the immunopathologic aspects of these diseases are studies. The following techniques had been used: 1. Total protein determination 2. Animal immunization. 3. Gel diffusion. 4. Immunoelectrophoresis. 5. Cellogel electrophoresis. 6. Radial immunodiffusion. 7. Absorption. After a systematic discussion of each of the results obtained (comparing these findings with those of other authors) we have arrived to the following conclusions. 1. The great importance of the immunoglobulins' role in the immunization process and their relation with high total protein titres, especially in PCP. 2. The importance of the IgA role in Rheumatoid Arthritis and in Acute Lymphatic Leukemia, behaving in the former as a Rheumatoid Factor with autoantibody nature. 3. An antigenic community between plasma and synovial proteins, and protein fractions. 4. The existence o af synovial "self" protein could not be demonstrated "in vivo".
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PMID:A contribution to the synovial fluid immunopathology in rheumatoid arthritis and other arthropathies. 122 74

Activation of rat basophilic leukaemia cells (RBL-2H3) leads to the secretion of allergic and inflammatory mediators. These cells can be permeabilized, yet still retain their ability to secrete in response to antigen. Secretion can also be induced in permeabilized cells by the addition of the ATP analogue, ATP gamma S [adenosine-5'-O-(3-thiotriphosphate)], which is relatively resistant to phosphatase activity. ATP gamma S-induced secretion (35-50% of total amine) is temperature and concentration-dependent. Calcium enhances secretion, but unlike antigen-induced secretion, it does occur in the absence of calcium and without the requirement for inositol phospholipid hydrolysis. Other ATP analogues induced secretion in the rank order AMP-PNP > or = ATP gamma S >>> AMP-PCP > ATP alpha S = ATP [AMP-PNP, adenylyl-imidodiphosphate; AMP-PCP, adenylyl (beta,gamma-methylene)-diphosphonate; ATP alpha S, adenosine-5'-O-(1-thiotriphosphate)]. At equimolar concentrations, ATP inhibits ATP gamma S-induced secretion by 50%, but prolonged incubation in the presence of ATP gamma S surmounts the ATP inhibition. ADP is nearly as effective an inhibitor, but GTP and ITP are ineffective. It is likely that secretion occurs through attachment at an ATP-binding site, effectively blocking the action of a phosphatase, active later in the normal secretory pathway.
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PMID:Calcium-independent secretion by ATP gamma S from a permeabilized rat basophilic leukaemia cell line (RBL-2H3). 808 86

Drug discrimination procedures in mice are used to study the neuropharmacology of a wide variety of drugs. In C57 B1/6 mice, infection with the LP-BM5 murine leukemia virus leads to a syndrome (murine acquired immunodeficiency syndrome-MAIDS) characterized by immunocompromise, neurochemical alterations, and learning and memory deficits. Because the neurochemical and behavioral changes suggest that altered glutamatergic neurotransmission follows LP-BM5 infection, we studied the effects of infection on discriminative stimulus properties of phencyclidine (PCP), a Ca2+ channel blocker at NMDA receptors. We also tested D-amphetamine and dizocilpine to assess the specificity of the discrimination. As expected, dizocilpine produced PCP-like responding. After animals were trained to discriminate PCP from saline, they were inoculated with LP-BM5 and the PCP dose-response functions repeatedly determined. The potency of PCP in this procedure was unchanged 3 weeks after infection, but was increased approximately fivefold 6 and 9 weeks after infection. Amphetamine 9 weeks after inoculation did not produce PCP-like responding, showing that the results were not caused by a loss of specificity of the discrimination. The time course for changes in PCP potency is similar to those of other behavioral and neurochemical changes reported after LP-BM5 infection. The results are consistent with an action of LP-BM5 infection at glutamatergic synapses.
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PMID:Increased discriminative stimulus potency of phencyclidine in C57B1/6 mice infected with the LP-BM5 retrovirus. 1008 57

The ability of the carcinogenic environmental toxin pentachlorophenol (PCP, 1) to react with DNA bases has been assessed using MS and NMR. Treatment of PCP (100 microM) with horseradish peroxidase (HRP/H(2)O(2)) or myeloperoxidase (MPx/H(2)O(2), from human leukocytes) in the presence of excess deoxyguanosine (dG, 2 mM) led to the isolation and identification of the oxygen-bonded C8-dG nucleoside adduct 4. The reaction was absolutely specific for dG; no detectable adduct(s) was observed from HRP/H(2)O(2) and PCP in the presence of deoxyadenosine, deoxycytidine, or thymidine. Formation of 4 was also specific for peroxidase activation that is known to oxidize PCP into the phenoxyl radical. Treatment of PCP/dG with rat liver microsomes (RLM) failed to generate 4; instead, an adduct derived from the benzoquinone electrophile tetrachloro-1,4-benzoquinone (chloranil) was observed in the extracted ion chromatogram from the RLM/NADPH-treated PCP/dG sample. The adduct 4 is the first structurally characterized O-bonded phenolic DNA nucleoside adduct and highlights the ambident electrophilicity of phenoxyl radicals (O- vs C-) in reaction at C8 of dG, as we have previously demonstrated that the para-chlorophenolic toxin, ochratoxin A (2), reacts at C8 of dG to give the C-bonded adduct 3 via the intermediacy of the OTA phenoxyl radical. Given that PCP is known to induce DNA adduct formation in vivo and human exposure has been linked to incidences of leukemia, the adduct 4 could play a key role in PCP-mediated carcinogenesis.
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PMID:An oxygen-bonded c8-deoxyguanosine nucleoside adduct of pentachlorophenol by peroxidase activation: evidence for ambident c8 reactivity by phenoxyl radicals. 1287 Aug 83

Pneumocystis jiroveci (formerly carinii) pneumonia (PCP) is a serious opportunistic infection in children and adolescents with cancer. It was the most common cause of death among children receiving chemotherapy prior to the inclusion of PCP prophylaxis as part of standard care for children with leukemia. The incidence of PCP has decreased significantly since initiation of prophylaxis; however, breakthrough cases continue to occur. Hematologic malignancies, brain tumors necessitating prolonged corticosteroid therapy, hematopoietic stem cell transplantation, prolonged neutropenia, and lymphopenia are the most important risk factors for PCP in children not infected with HIV. Of children with leukemia, 15-20% may develop PCP in the absence of prophylaxis. Infection with P. jiroveci occurs early in life in most individuals. However, clinically apparent disease occurs almost exclusively in immunocompromised persons. Dyspnea, cough, hypoxia, and fever are the most common presenting symptoms of PCP. Chest radiography and high-resolution CT scans of the chest demonstrate a characteristic ground-glass pattern. Induced sputum analysis and bronchoalveolar lavage are the diagnostic procedures of choice. Gomori's methenamine-silver stain, Geimsa or Wright's stain, and monoclonal immunofluorescent antibody stains are most commonly used to make a diagnosis. However, identification of P. jiroveci DNA using polymerase chain reaction assays in bronchoalveolar lavage fluid is more sensitive. Trimethoprim-sulfamethoxazole (TMP-SMZ; cotrimoxazole) is the recommended drug for the treatment of PCP. Patients who are intolerant of TMP-SMZ or who have not responded to treatment after 5-7 days of therapy with TMP-SMZ should be treated with pentamidine. A short course of corticosteroids is recommended for moderate to severe cases of PCP within the first 72 hours after diagnosis. Mutations in the dihydropteroate synthetase gene may confer resistance to TMP-SMZ; however, the clinical relevance of these mutations is not well established. TMP-SMZ is the most commonly used agent for prophylaxis. Myelosuppression is the most important adverse effect of TMP-SMZ and the most frequent cause for choosing alternative prophylactic agents in children undergoing chemotherapy. Alternative agents for chemoprophylaxis include dapsone, aerosolized pentamidine, and atovaquone. Alternative prophylactic agents must be used in patients developing myelosuppression secondary to TMP-SMZ or dapsone.
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PMID:Management of Pneumocystis jiroveci pneumonia in children receiving chemotherapy. 1792 2