Early promoted : a memoir of the Rev. William Spiller Cox by Edward W Cox

http://www.archive.org/details/earlypromotedame00coxwuoft

Letter to Gershom Cox, dated January 29, 1844

This is a letter from Phoebe Palmer and her husband written on January 29, 1844 to Gershom Cox.

Temporal modelling of short-term rainfall using Cox processes

We study two marked point process models based on the Cox process. These models are used to describe the probabilistic structure of the rainfall intensity process. Mathematical formulation of the models is described and some second-moment characteristics of the rainfall depth, and aggregated processes are considered. The derived second-order properties of the accumulated rainfall amounts at different levels of aggregation are used in order to examine the model fit. A brief data analysis is presented. Copyright © 1998 John Wiley & Sons, Ltd.

Cox-2 Promotes Chromogranin A Expression and Bioactivity: Evidence for a PGE2-Dependent Mechanism and the Involvement of a Proximal cAMP-Responsive Element.

Abstract The prostanoid biosynthetic enzyme cyclooxygenase-2 (Cox-2) is upregulated in several neuroendocrine tumors. The aim of the current study was to employ a neuroendocrine cell (PC12) model of Cox-2 over-expression to identify gene products that might be implicated in the oncogenic and/or inflammatory actions of this enzyme in the setting of neuroendocrine neoplasia. Expression array and real-time PCR analysis demonstrated that levels of the neuroendocrine marker chromogranin A (CGA) were 2-fold and 3.2-fold higher, respectively, in Cox-2 over-expressing cells (PCXII) vs their control (PCMT) counterparts. Immunocytochemical and immunoblotting analyses confirmed that both intracellular and secreted levels of CGA were elevated in response to Cox-2 induction. Moreover, exogenous addition of prostaglandin E2 (1u�­M), mimicked this effect in PCMT cells, while treatment of PCXII cells with the Cox-2 selective inhibitor NS-398 (100 nM) reduced CGA expression levels, thereby confirming the biospecificity of this finding. Levels of neurone specific enolase (NSE) were similar in the two cell lines, suggesting that the effect of Cox-2 on CGA expression was specific and not due to a global enhancement of neuroendocrine marker expression/differentiation. Cox-2-dependent CGA upregulation was associated with significantly increased chromaffin granule number and intracellular and secreted levels of dopamine. CGA promoter-driven reporter gene expression studies provided evidence that prostaglandin E2-dependent upregulation required a proximal cAMP-responsive element (CRE; -71 - -64 bp). This study is the first to demonstrate that Cox-2 upregulates both CGA expression and bioactivity in a neuroendocrine cell line and has major implications for the role of this polypeptide in the pathogenesis of neuroendocrine cancers in which Cox-2 is upregulated.

The Influence of COX-2 Single Nucleotide Polymorphisms on Abdominal Aortic Aneurysm Development and the Associated Inflammation

Introduction: Cyclooxygenase (COX)-2 influences cardiovascular disease and serum concentration of high-sensitivity C-reactive protein (hsCRP). The study purpose was to determine the influence of single nucleotide polymorphisms (SNPs) of the COX-2 gene on abdominal aortic aneurysm (AAA) development and serum hsCRP concentrations. Patients and Methods: Patients with AAA and disease-free controls were recruited. High-sensitivity C-reactive protein was measured by an enzyme-linked immunosorbent assay (ELISA) test. The distributions of COX-2 SNPs were investigated (rs20417 and rs4648307). The influence of the COX-2 SNPs on the hsCRP serum concentration was assessed.Results: A total of 230 patients with AAA and 279 controls were included. No difference was found in the genotype distribution of the COX-2 SNPs rs20417 (P = .26) and rs4648307 (P = .90). They did not influence the hsCRP concentration (P = .24 and P = .61, respectively). Haplotype analysis of COX-2 SNPs revealed no difference. Conclusion: These COX-2 SNPs do not play any role in AAA development and do not influence serum hsCRP. These results differentiate AAA development from atherosclerotic diseases.