69 research outputs found
Peroxisome Proliferator-Activated Receptor alpha (PPAR alpha) down-regulation in cystic fibrosis lymphocytes
Background: PPARs exhibit anti-inflammatory capacities and are potential modulators of the inflammatory response. We hypothesized that their expression and/or function may be altered in cystic fibrosis (CF), a disorder characterized by an excessive host inflammatory response.
Methods: PPARα, β and γ mRNA levels were measured in peripheral blood cells of CF patients and healthy subjects via RT-PCR. PPARα protein expression and subcellular localization was determined via western blot and immunofluorescence, respectively. The activity of PPARα was analyzed by gel shift assay.
Results: In lymphocytes, the expression of PPARα mRNA, but not of PPARβ, was reduced (-37%; p < 0.002) in CF patients compared with healthy persons and was therefore further analyzed. A similar reduction of PPARα was observed at protein level (-26%; p < 0.05). The transcription factor was mainly expressed in the cytosol of lymphocytes, with low expression in the nucleus. Moreover, DNA binding activity of the transcription factor was 36% less in lymphocytes of patients (p < 0.01). For PPARα and PPARβ mRNA expression in monocytes and neutrophils, no significant differences were observed between CF patients and healthy persons. In all cells, PPARγ mRNA levels were below the detection limit.
Conclusion: Lymphocytes are important regulators of the inflammatory response by releasing cytokines and antibodies. The diminished lymphocytic expression and activity of PPARα may therefore contribute to the inflammatory processes that are observed in CF
Suppression of back-to-back hadron pairs at forward rapidity in d+Au Collisions at sqrt(s_NN)=200 GeV
Back-to-back hadron pair yields in d+Au and p+p collisions at sqrt(s_NN)=200
GeV were measured with the PHENIX detector at the Relativistic Heavy Ion
Collider. Rapidity separated hadron pairs were detected with the trigger hadron
at pseudorapidity |eta|<0.35 and the associated hadron at forward rapidity
(deuteron direction, 3.0<eta<3.8). Pairs were also detected with both hadrons
measured at forward rapidity; in this case the yield of back-to-back hadron
pairs in d+Au collisions with small impact parameters is observed to be
suppressed by a factor of 10 relative to p+p collisions. The kinematics of
these pairs is expected to probe partons in the Au nucleus with low fraction x
of the nucleon momenta, where the gluon densities rise sharply. The observed
suppression as a function of nuclear thickness, p_T, and eta points to cold
nuclear matter effects arising at high parton densities.Comment: 381 authors, 6 pages, 4 figures. Published in Phys. Rev. Lett.
(http://link.aps.org/doi/10.1103/PhysRevLett.107.172301). v3 has minor
changes to match published version
(http://www.phenix.bnl.gov/phenix/WWW/info/pp1/128/PhysRevLett.107.172301)
Plain text data tables for points plotted in figures are publicly available
at http://www.phenix.bnl.gov/phenix/WWW/info/data/ppg128_data.htm
Serum Activity of Platelet-Activating Factor Acetylhydrolase Is a Potential Clinical Marker for Leptospirosis Pulmonary Hemorrhage
Pulmonary hemorrhage has been recognized as a major, often lethal, manifestation of severe leptospirosis albeit the pathogenesis remains unclear. The Leptospira interrogans virulent serogroup Icterohaemorrhagiae serovar Lai encodes a protein (LA2144), which exhibited the platelet-activating factor acetylhydrolase (PAF-AH) activity in vitro similar to that of human serum with respect to its substrate affinity and specificity and thus designated L-PAF-AH. On the other hand, the primary amino acid sequence of L-PAF-AH is homologous to the α1-subunit of the bovine brain PAF-AH isoform I. The L-PAF-AH was proven to be an intracellular protein, which was encoded unanimously and expressed similarly in either pathogenic or saprophytic leptospires. Mongolian gerbil is an appropriate experimental model to study the PAF-AH level in serum with its basal activity level comparable to that of human while elevated directly associated with the course of pulmonary hemorrhage during severe leptospirosis. Mortality occurred around the peak of pulmonary hemorrhage, along with the transition of the PAF-AH activity level in serum, from the increasing phase to the final decreasing phase. Limited clinical data indicated that the serum activity of PAF-AH was likely to be elevated in the patients infected by L. interrogans serogroup Icterohaemorrhagiae, but not in those infected by other less severe serogroups. Although L-PAF-AH might be released into the micro-environment via cell lysis, its PAF-AH activity apparently contributed little to this elevation. Therefore, the change of PAF-AH in serum not only may be influential for pulmonary hemorrhage, but also seems suitable for disease monitoring to ensure prompt clinical treatment, which is critical for reducing the mortality of severe leptospirosis
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