Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.16.2 (PCP)
3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pneumocystis carinii is the most common protozoan organism causing infection in immunosuppressed patients. This study, based on a review of 32 lung biopsies and 13 autopsies of patients with neoplastic diseases who developed P carinii pneumonia, emphasizes the morphologic variation of this disease. Excluded from this study are those patients with PCP secondary to bone marrow transplantation and AIDS. P carinii pneumonia occurred predominately in patients with malignant lymphoreticular neoplasms, 73% of those in our series, and the remaining 27% had solid tumors. There were 27 males and 18 females and their ages ranged from 1 to 73 years, with a median age of 30 years. Microscopically, the diagnostic intraalveolar foamy exudate of P carinii pneumonia was present in only 58% of the cases. Furthermore, diffuse alveolar damage alone was present in 26% of cases. This change was especially prominent when the characteristic foamy material was scanty. Other tissue reactions to P carinii included the presence of giant cells, epithelioid granulomas, desquamative interstitial-like pneumonitis, and interstitial lymphoid infiltrate. Extrapulmonary dissemination was not observed in this patient population. The pathologist should be aware of the marked variations that occur in the morphologic appearance of PCP, and the diagnosis of Pneumocystis infection should not be discarded until a careful search for the organisms using silver stains is rendered negative.
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PMID:Spectrum of pathologic manifestations of Pneumocystis carinii pneumonia in patients with neoplastic diseases. 279 14

We hypothesized that therapy with granulocyte-macrophage colony stimulating factor (GM-CSF) would decrease intensity of murine Pneumocystis carinii pneumonia by upregulating alveolar macrophage function. Mice were depleted of CD4+ T lymphocytes and then inoculated intratracheally with P. carinii. Four weeks later, they received recombinant murine GM-CSF (rmGM-CSF) 5 micrograms/d subcutaneously for 7 and 14 d. At the end of therapy lung tissue was scored for intensity of P. carinii infection by silver methenamine stain and for inflammation by hematoxylin-eosin stain. We found that rmGM-CSF therapy significant decreased the intensity scores of PCP infection in comparison to control mice (1.88 +/- 0.47 vs 3.06 +/- 0.12, p < 0.001). Inflammation scores were not significantly different in the rmGM-CSF group compared with the control group (1.83 +/- 0.47 vs 2.83 +/- 0.67). Alveolar macrophages from mice treated with rmGM-CSF released significantly more tumor necrosis factor-alpha (TNF-alpha) than cells from control mice after in vitro stimulation with lipopolysaccharide (LPS) alone (2.65 +/- 0.30 vs 1.45 +/- 0.26 ng/ml, p = 0.01) or with LPS plus murine recombinant interferon-gamma (4.16 +/- 0.51 vs 2.25 +/- 0.34 ng/ml, p = 0.01). We conclude that GM-CSF therapy reduces the intensity of PCP and this effect is associated with an enhanced alveolar macrophage TNF-alpha production.
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PMID:Granulocyte-macrophage colony stimulating factor and Pneumocystis carinii pneumonia in mice. 769 58

Infants generally acquire HIV form mother during gestation, or delivery by contact with maternal blood and body fluids or breast feeding. At Saraburi Hospital, from January 1989 to December 1992, there were 17,766 mothers who gave birth, 80 anti HIV positive mothers were included. Up to now, four cases of PCP have been reported in HIV infants born to anti HIV positive mothers at this hospital. All cases presented with symptoms of pneumonia and bilateral bronchopneumonia by chest X-ray. Diagnosis was confirm with positive organism identification by methenamine silver stain of lung tissues autopsy, lung fluid, tracheal secretion and by toluidine blue O stain of lung percussion fluid. Two infants died before specific treatment was administered. The other two recovered with the specific treatment of trimethoprim and sulfamethoxazole. Conventional treatment was given after the definitive diagnosis was confirmed. Pediatricians should be aware of PCP. Specific treatment should be considered in infants with HIV who fail to respond to antibiotics treatment for lower respiratory infection symptoms.
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PMID:Pneumocystis carinii pneumonia in infants born to anti HIV positive mothers. 796 41

The aim of this retrospective study is to evaluate the correlation between T-cell immunity and pulmonary disorders in a group of Italian subjects with HIV infection. HIV-infected patients seen at the Institute of Infectious Diseases, University of Verona, were included in this study if they had a specific acute pneumonia, a CD4+ cell count and a CD4+/CD8+ ratio during the 60 days immediately before the onset of pulmonary disease. Cases receiving any antimicrobial prophylaxis were excluded. Pneumonia was recognized by usual clinical and radiologic abnormalities. The diagnostic procedure included sputum examination, bronchoscopy with bronchoalveolar lavage and transbronchial biopsy. The specimens were processed for bacterial, mycobacterial and fungal stains and cultures. Ziehl-Neelsen, periodic acid-Schiff and silver methenamine stains were performed on the transbronchial biopsy specimens in addition to usual pathologic examinations mononuclear. Determination of percentage of peripheral blood mononuclear cells bearing CD4+ and CD8+ markers was done by conventional fluorescent antibody cell-sorter analysis of the mononuclear cell population. Absolute number of CD4+ lymphocytes was determined by multiplying the total lymphocyte count by the percent of mononuclear cells bearing CD4+ marker. From October 1987 to August 1991, 61 patients, 50 males and 11 females, had 65 episodes of specific pneumonia. The average age of patients was 31.4 years (range 29-59 years). The risk factors for HIV infection included intravenous drug abuse (47 patients), homosexuality (6 patients), bisexuality (3 patients) and heterosexual contact (5 patients). Before the onset of pulmonary disorders, patients were classified in the following clinical HIV-related stages: asymptomatic state (22 episodes), ARC (22 episodes) and AIDS (21 episodes). In decreasing order of frequency diagnosis of pneumonias were PCP (29 episodes), community-acquired bacterial pneumonia (16 episodes), pulmonary tuberculosis (8 episodes), nonspecific interstitial pneumonia (4 episodes), PCP and pulmonary tuberculosis (3 episodes), cytomegalovirus pneumonia (2 episodes), and one of each episode of PCP and pulmonary cryptococcosis, pulmonary candidiasis, pulmonary Kaposi's sarcoma. The mean and the standard deviation of immunologic values regarding the four primary diagnostic groups were: PCP CD4+/CD8+ 0.50 +/- 0.42, CD4+/mm3 196 +/- 190; bacterial pneumonia CD4+/CD8+ 0.53 +/- 0.44, CD4+/mm3 247 +/- 139; pulmonary tuberculosis CD4+/CD8+ 0.62 +/- 0.38, CD4+/mm3 260 +/- 170; nonspecific interstitial pneumonia CD4+/CD8 + 0.57 +/- 0.48, CD4+/mm3 240 +/- 189. No significant statistical differences with respect to CD4+/CD8 ratios and CD4+ cell counts among these diagnostic groups were found by standard analysis of variance.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Acute pneumonia and cell-mediated immunity in patients with HIV infection]. 849 71

Phencyclidine (PCP) has recently been shown to induce apoptosis of a subpopulation of striatopallidal neurons which lie in the dorsomedial caudate-putamen. The pharmacological mechanisms underlying this PCP-induced striatal death were investigated in a series of small experiments. Striatal silver-methenamine-stained sections from rats injected acutely with dizocilpine (MK-801; 1.5-5 mg/kg, i.p.) were analysed to determine whether other non-competitive N-methyl-D-aspartate (NMDA) receptor antagonists could induce apoptotic-like changes in striatal cells. The effects of amphetamine (3-12 mg/kg, i.p.) were similarly investigated as PCP can elevate extracellular dopamine levels and dopamine has the potential to be neurotoxic. The potential involvement of dopamine transmission in PCP-induced striatal apoptosis was also tested by determining the effect of co-administering SCH23390 (D1 dopamine receptor antagonist) and quinpirole (D2 dopamine receptor agonist) on PCP (80 mg/kg, s.c.)-induced striatal apoptotic-like cell death. Equivalent experiments were performed using scopolamine (cholinergic antagonist) as this drug blocks PCP-induced damage of the retrosplenial cortex and RU38486 (corticosteroid receptor antagonist) as a similar subpopulation of striatal neurons undergoes apoptosis following dexamethasone administration. Injection of neither MK-801 nor amphetamine induced elevations of apoptotic-like cells in the striatum nor did co-administration of SCH23390 or scopolamine affect the levels of PCP-induced striatal cell death. In contrast, quinpirole elevated the levels of PCP-induced apoptotic-like striatal cell death and RU38486 markedly reduced it. Within the retrosplenial cortex, scopolamine lowered PCP-induced apoptotic-like cell death whereas RU38486 was without effect. These results suggest that PCP-induced striatal apoptosis results from a corticosteroid-dependent mechanism. The results further demonstrate that different pathological mechanisms underlie PCP-induced neuronal damage in the striatum and the retrosplenial cortex.
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PMID:Pharmacological mechanisms mediating phencyclidine-induced apoptosis of striatopallidal neurons: the roles of glutamate, dopamine, acetylcholine and corticosteroids. 1065 Jan 24

The lipopolysaccharide of Salmonella and other Gram negative pathogenic species has been implicated as a major virulence determinant and in this study we report the role of LPS of S. Enteritidis in the colonisation and persistent gastrointestinal infection of young poultry. The gene encoding the unique O-antigen ligase, waaL, was mutated by insertional inactivation in a well characterised S. Enteritidis strain, S1400/94. The waaL mutant, designated PCP, produced rough colonies on agar medium, did not agglutinate O9 antiserum, did not produce an LPS ladder on silver stained gels and was serum sensitive. PCP and a nalidixic acid marked derivative of S1400/94 (S1400/94 Nalr) were used to orally challenge young chicks, separately and together in competitive index experiments. At post-mortem examination of 1-day-old chicks challenged S1400/94 Nalr and PCP separately there were no significant differences in the numbers of S1400/94 Nalr and PCP bacteria in tissues sampled on days 1, 2, and 5. By day 42 after challenge S1400/94 Nalr bacteria were recovered in significantly higher numbers than PCP from the caecal contents (P < 0.001). In competitive index studies in the 1-day-old chick PCP colonised, invaded and persisted in lower numbers than S1400/94 Nalr. In 4-week-old chicks challenged separately, PCP bacteria were recovered from all tissues examined in significantly lower numbers than S1400/94 Nalr. In competitive index experiments in 4-week-old chicks, PCP was not detected at any site and at any time point. Therefore, the O-antigen of S. Enteritidis plays an important role in poultry infections although this role is less important in the newly hatched chick.
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PMID:The O-antigen of Salmonella enterica serotype Enteritidis PT4: a significant factor in gastrointestinal colonisation of young but not newly hatched chicks. 1528 29

Three new multidimensional coordination polymers have been constructed from the reaction of AgX, where X = OTf-, BF4-, or tfa-, with the novel phosphonite PhP(3-OCH2C5H4N)2, PCP-32, 1. It is seen that regardless of the ratio of reactants mixed, polymeric growth of the compounds always reveals a ligand-to-metal ratio of 1:2 for PCP-32AgOTf, 2, 1:1 for PCP-32AgBF4, 3, and 1:2 for PCP-32Ag(tfa), 4. The coordination number, metal environment, ligand conformation, and polymer dimensionality are found to vary greatly from 2 to 4 and are dependent upon the anion present. Coordination numbers from 2 to 4, representing linear, trigonal, and distorted tetrahedral environments are displayed. PCP-32AgOTf polymerizes as a linear chain containing both two- and four-coordinate silvers, PCP-32AgBF4 repeats a single trigonal motif throughout its structure, and PCP-32Ag(tfa) shows two unique distorted tetrahedral silver centers. Ligand flexibility allows for cross-ligand Ag-Ag distances to range from 3.1918(8) to 14.015(2) A. The coordination polymers have been characterized by elemental analysis, variable-temperature multinuclear NMR spectroscopy, single-crystal X-ray diffraction, and fluorometric studies.
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PMID:Anion-dependent silver(I) coordination polymers of the tridentate pyridylphosphonite: PPh(3-OCH2C5H4N)2. 1585 79

Acute and subchronic administration of N-methyl-D-aspartate antagonists to rats in the early postnatal period has been reported to produce widespread and selectively cortical neurotoxicity, respectively. To resolve this apparent discrepancy, we sought to clarify these data by determining the dose and temporal and regional characteristics of acute and subchronic phencyclidine (PCP)-induced neurotoxicity. Measurement of degenerating neurons with the cupric silver technique following a single dose of PCP on postnatal day (PN) 7 revealed that neurodegeneration increased in all areas measured (frontal, parietal and cingulate cortices, striatum, hippocampus, subiculum, and thalamus) within 9 hr. Silver staining peaked at 9-16 hr and was then not detectable or was greatly reduced after 24 hr depending on the specific region. Dose-response analysis at 9 hr showed that the lowest effective dose was 1, 3, and 10 mg/kg for the frontal cortex, hippocampus, and striatum, respectively. However, repeated PCP administration (10 mg/kg) on PN 7, 9, and 11 elicited an increase in silver staining only in the frontal cortex. To determine whether the loss of effect in the striatum and hippocampus was due to a "tolerance" mechanism or to a developmental phenomenon, we compared the effects of PCP given on PN 7, 9, or 11 with those of two doses given on PN 7 and 9 or three doses administered on PN 7, 9, and 11. Analysis of these experiments shows that both developmental factors and unknown mechanisms of tolerance underlie the apparent selective cortical neurotoxicity observed following subchronic PCP administration in perinatal rat pups.
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PMID:Differential effects of acute and subchronic administration on phencyclidine-induced neurodegeneration in the perinatal rat. 1594 53

The goal of this study is to present the clinical and evolutive features of Pneumocystis infection (PCP) in infants admitted in our clinic. We summarise these aspects from 17 cases (10 male and 7 female infants), admitted between 1st January 2004 and 31st May 2005. PCP infection is rare. It represents 1,5/1000 children (17 cases of 11328 total patients) admitted in our hospital. The risk factors for PCP were age between 6 weeks and 6 months (average 3,38 months) low birth weight (average = 2428 grams), low weight for age, prolonged hospital admission (88,23% of the 17 infants were abandoned in nursery). Only one of them had HIV infection and none presented neoplastic disease. The most prominent clinical aspect was tachypnea (average 78 breath/minute, maximum 130). 16 (94,11%) had difficult breathing with chest in-drawing and flaring of ala nasi. 14 (82,35%) had generalised cyanosis. Only two (11,72%) infants had fever. Radiologic aspects were evocative, with diffuse pulmonary involvement in almost all cases (88,23%). 6 infants (35,29%) had pneumothorax and 2 (11,76%) presented pneumomediastinum. Positive diagnosis was made by microscopic examination of secretions from endotracheal tube aspiration (Grocott methenamine silver stain and Romanowsky stain). 14 infants were ventilated with a good outcome--12 surviving infants (85,7%). All infants had a full course of intravenous Co-trimoxazole. The deceased infants had more risk factors--congenital heart disease 1 case, severe cerebral palsy with organic epilepsy 2 cases. The apparent increase of PCP cases can be related to the number of abandoned children in Romanian pediatric hospitals and nurseries.
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PMID:[Pneumocystis pneumonia in infants]. 1653 25

This study determined the role of caspase-3 in phencyclidine (PCP)-induced neurodegeneration in postnatal rats. PCP administration to postnatal day 7 rats induced a dose-dependent increase in caspase-3 enzymatic activity in frontal cortex, striatum, and hippocampus. Enzymatic activation was present at 4 h, peaked between 6 and 12 h, and disappeared by 24 h. Further, cleaved caspase-3-immunoreactive neurons were detected as early as 2 h in the cortex, and were found throughout the brain, including, in addition, the thalamus and striatum. Within the cingulate, frontal, parietal, and retrosplenial cortices, immunoreactivity was specific for layers II-IV (especially layer II). Neurons positive for both silver staining and terminal deoxynucleotidyl transferase biotin-d-UTP nick-end labeling (TUNEL) were found in the same brain regions and subregions. Double labeling experiments confirmed that cleaved caspase-3 and TUNEL were coexpressed in many neurons in all brain regions and subregions studied. Temporal studies revealed that procaspase-3 cleavage preceded TUNEL staining by about 3 h, with many neurons being positive for both caspase-3 and TUNEL 9 h after PCP treatment. In organotypic corticostriatal slices, PCP caused a concentration- and time-dependent cleavage of procaspase-3 that was also colocalized with TUNEL staining in layers II-IV of the parietal cortex. Caspase-3 activation again preceded PCP-induced DNA damage assessed by TUNEL. PCP-induced neuronal death in vitro as measured by TUNEL staining was blocked 85% by Ac-AAVALLPAVLLALLAPDEVD-CHO, a cell-permeable selective caspase-3 inhibitor. These data demonstrate that caspase-3 activation plays a necessary role in the regionally selective neuronal death induced by PCP in the developing rat brain.
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PMID:The role of caspase-3 activation in phencyclidine-induced neuronal death in postnatal rats. 1698 4


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