Hepatic steatosis and pancreatitis associated with the use of stavudine in a patient with HIV infection

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Title:	Hepatic steatosis and pancreatitis associated with the use of stavudine in a patient with HIV infection
Authors:	Lai, HY;Chen, JH;Tsai, PP;Ho, MW;Shen, WC
Contributors:	附設醫院放射線部;China Med Univ Hosp, Dept Radiol, Taichung 404, Taiwan;China Med Univ Hosp, Dept Internal Med, Taichung 404, Taiwan
Date:	2004
Issue Date:	2010-09-24 14:31:11 (UTC+8)
Publisher:	AMER ROENTGEN RAY SOC
Abstract:	2-Benzyloxybenzaldehyde (CCY1a) inhibited the formyl-Met-Leu-Phe (fMLP)-induced elevation of cytosolic [Ca2+] ([Ca2+](i)) in rat neutrophils. The late plateau phase, but not the initial Ca2+ spike, of the fMLP-induced [Ca2+](i) change was inhibited by CCY1a. In the absence of external Ca2+, CCY1a had no appreciable effect on either the fMLP- or cyclopiazonic acid (CPA)-induced [Ca2+](i) elevation. CCY1a failed to inhibit [Ca2+](i) changes induced by N-ethylmaleimide, GEA3162, ionomycin or sphingosine, but slightly inhibited the Ca2+ signals elicited by ATP or interleukin-8 (IL-8). In a classical Ca2+ readdition protocol, addition of CCY1a after cell activation strongly inhibited the [Ca2+](i) response to fMLP, whilst that to CPA was only slightly reduced. CCY1a nearly abrogated the fMLP-stimulated Mn2(+) influx but was less effective on the CPA-induced response. CCY1a attenuated the levels of tyrosine-phosphorylated bands in the 70-85 kDa molecular mass range. CCY1a had no effect on the basal [Ca2+](i) level, the pharmacologically isolated plasma membrane Ca2+-ATPase activity or on the mitochondrial membrane potential. Thus, CCY1a blocks fMLP-induced Ca2+ entry into neutrophils probably by blocking the relevant Ca2+ channel directly or, alternatively, indirectly through the attenuation of tyrosine phosphorylation of some cellular proteins.
Relation:	AMERICAN JOURNAL OF ROENTGENOLOGY 183(6):1605-1607
Appears in Collections:	[China Medical University Hospital] Jurnal articles

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