1,125 research outputs found

    Multiplicity Distributions and Charged-neutral Fluctuations

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    Results from the multiplicity distributions of inclusive photons and charged particles, scaling of particle multiplicities, event-by-event multiplicity fluctuations, and charged-neutral fluctuations in 158⋅A\cdot A GeV Pb+Pb collisions are presented and discussed. A scaling of charged particle multiplicity as Npart1.07±0.05N_{part}^{1.07\pm 0.05} and photons as Npart1.12±0.03N_{part}^{1.12\pm 0.03} have been observed, indicating violation of naive wounded nucleon model. The analysis of localized charged-neutral fluctuation indicates a model-independent demonstration of non-statistical fluctuations in both charged particles and photons in limited azimuthal regions. However, no correlated charged-neutral fluctuations are observed.Comment: Talk given at the International Symposium on Nuclear Physics (ISNP-2000), Mumbai, India, 18-22 Dec 2000, Proceedings to be published in Pramana, Journal of Physic

    First case of childhood Takayasu arteritis with renal artery aneurysms

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    Takayasu arteritis is a large vessel systemic granulomatous vasculitis characterized by stenosis or obliteration of large and medium sized arteries. It commonly involves elastic arteries such as the aorta and its main branches. Renal artery involvement is rare and has not been reported in a child. We report a 12-year-old boy with Takayasu arteritis who developed severe hypertension, proteinuria, microscopic hematuria and renal dysfunction. Conventional angiography demonstrated aneurysms of both renal arteries and multiple microaneurysms of the superior mesenteric artery. This case report illustrates that the children with Takayasu arteritis can develop renal involvement resulting in hematuria, proteinuria and even renal failure

    Novel Regulation of CCL2 Gene Expression by Murine LITAF and STAT6B

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    Inflammation is a multifaceted process: beneficial as a defense mechanism but also detrimental depending on its severity and duration. At the site of injury, inflammatory cells are activated by a cascade of mediators, one of which is LITAF, a transcription regulator known to upregulate TNF-α. We previously showed that human LITAF forms a complex with human STAT6B, which translocates into the nucleus to upregulate cytokine transcription. To dissect the molecular implications of this complex, a murine model was developed and interactions between mouse STAT6B (mSTAT6B) and mouse LITAF (mLITAF) were analyzed. Both mLITAF and mSTAT6B expression were MyD88- and TLR ligand-dependent. Furthermore, mLITAF was found to mediate LPS-induced CCL2 gene transcription with the cooperation of mSTAT6B leading to CCL2 protein expression. In LITAF-deficient mice, mLITAF-mediated CCL2 production in macrophages was significantly reduced compared to the wild-type control animals. Mice knockdown for mSTAT6B by 6BsiRNA1 tail vein injection resulted in a decrease in serum TNF-α and CCL2 production. mLITAF/mSTAT6B complex is proposed to play a role in LPS-induced CCL2 expression and possibly other cytokines
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