Although there had been some improvement of treatment results by the combination of concurrent chemoradiotherapy with esophagectomy, the overall prognosis for patients with esophageal cancer remained poor. Selection of optimal treatment strategy for individual patients would be improved by an objective biomarker that can predict prognosis accurately. The aim of this prospective study was to evaluate whether serum concentration of C-reactive protein (CRP) can be used as a prognostic factor to predict the survival of esophageal cancer patients treated with radiotherapy. Between Nov 2002 and July 2007, patients undergoing radiotherapy for newly diagnosed esophageal cancer were eligible for inclusion into this study. Serum CRP concentration was measured prospectively before the initiation of treatment. The relationship between the serum CRP levels and clinicopathological parameters were analyzed retrospectively. The prognosis factors of esophageal cancer were statistically determined. A total of 123 patients consisting of 120 males and 3 females were enrolled in this study. 81 patients (65.9%) had high CRP levels (greater than 5 mg/L). Patients with CRP levels higher than 5 mg/L had a shorter overall survival (P < 0.001). The 2-year survival was 78.4% for patients with CRP < 5 mg/L compared with 7.8% with CRP¡Ù5 mg/L. Hypoalbuminemia (albumin< 3.5g/dL) was significantly related to shorter survival in univariate analysis. Multivariate analysis demonstrated that higher serum CRP concentration and hypoalbuminemia were both independent prognostic factors for esophageal cancer. Pretreatment serum CRP and albumin levels are easily measurable biomarkers and are significant prognostic factors for esophageal cancer. They can be used in combination with the conventional staging system to predict survival and stratify patients with esophageal cancer treated with radiotherapy more accurately.

No description available.

Thesis (M.S.)--Montana State University--Bozeman, 2006. / Typescript. Chairperson, Graduate Committee: Mary P. Miles. Includes bibliographical references (leaves 63-66).

Thesis (M.S.)--University of Florida, 2004. / Typescript. Title from title page of source document. Document formatted into pages; contains 43 pages. Includes Vita. Includes bibliographical references.

El texto completo de este trabajo no está disponible en el Repositorio Académico UPC por restricciones de la casa editorial donde ha sido publicado. / Revisión por pares

Cartas al Editor

C-reactive protein (CRP) is an evolutionarily conserved protein, a component of the innate immune system, and an acute phase protein in humans. In addition to its raised level in blood in inflammatory states, CRP is also localized at sites of inflammation including atherosclerotic lesions, arthritic joints and amyloid plaque deposits. Results of in vivo experiments in animal models of inflammatory diseases indicate that CRP is an anti-pneumococcal, anti-atherosclerotic, anti-arthritic and an anti-amyloidogenic molecule. The mechanisms through which CRP functions in inflammatory diseases are not fully defined; however, the ligand recognition function of CRP in its native and non-native pentameric structural conformations and the complement-activating ability of ligand-complexed CRP have been suggested to play a role. One tool to understand the structure-function relationships of CRP and determine the contributions of the recognition and effector functions of CRP in host defense is to employ site-directed mutagenesis to create mutants for experimentation. For example, CRP mutants incapable of binding to phosphocholine are generated to investigate the importance of the phosphocholine-binding property of CRP in mediating host defense. Recombinant CRP mutants can be expressed in mammalian cells and, if expressed, can be purified from the cell culture media. While the methods to purify wild-type CRP are well established, different purification strategies are needed to purify various mutant forms of CRP if the mutant does not bind to either calcium or phosphocholine. In this article, we report the methods used to purify pentameric recombinant wild-type and mutant CRP expressed in and secreted by mammalian cells.

Turmeric extract or active component curcumin may have anti-inflammatory effects in people with chronic inflammatory diseases. The effect of turmeric or curcumin on a wide range of inflammatory markers has not been evaluated in a systematic review. We performed a systematic review of randomized controlled trials (RCTs)evaluating the effects of oral turmeric or curcumin on inflammatory markers (CRP, hsCRP, IL-1, IL-6, TNF)in patients with a wide range of chronic inflammatory diseases. Pubmed, EMBASE, Scopus, the Web of Science, and the Cochrane library were evaluated until June 2018. Random effects meta-analyses with inverse variance methods and stratified by turmeric or curcumin were performed. Effects were expressed as mean differences (MD)and their 95% confidence intervals (CI). Risk of bias of RCTs was evaluated with the Cochrane tool. Nineteen RCTs were identified; included patients had rheumatic diseases, advanced chronic kidney disease with hemodialysis, metabolic syndrome, and cardiovascular diseases. Turmeric was the intervention in 5 RCTs (n = 356)and curcumin/curcuminoids in 14 RCTs (n = 988). Follow up times ranged between 4 and 16 weeks. One RCT had high risk of bias. In comparison to controls, turmeric or curcumin did not significantly decrease levels of CRP (MD -2.71 mg/L, 95%CI -5.73 to 0.31, p = 0.08, 5 studies), hsCRP (MD -1.44 mg/L, 95%CI -2.94 to 0.06, p = 0.06, 6 studies), IL-1 beta (MD -4.25 pg/mL, 95%CI -13.32 to 4.82, p = 0.36, 2 studies), IL-6 (MD -0.71 pg/mL, 95%CI -1.68 to 0.25, p = 0.15), and TNF alpha (MD -1.23 pg/mL, 95%CI -3.01 to 0.55, p = 0.18, 7 studies). There were no differences between turmeric and curcumin interventions. High heterogeneity of effects was observed for all markers across studies, except hsCRP. Other inflammatory markers such as IL-1 alpha, TNF beta, IL-17, and IL-22 had scarce data. Turmeric or curcumin did not decrease several inflammatory markers in patients with chronic inflammatory diseases. / Revisión por pares

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Diss. (sammanfattning) Stockholm : Karolinska institutet, 2007. / Härtill 4 uppsatser.