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Score of 0 = 0 , 1 = 13 , 2 = 38 , 3 = 63 , 4 = 88 ). Agreement between the visual algorithm and planimetry was compared using BlandAltman analysis. Results: The study population consisted of 101 patients with chronic MI (infarct age 5.3 ?6.5 years) of which 70 (69 ) were men, age 63.7 ?2.3 years, left ventricular (LV) ejection fraction 52.4 ?15.5 , and LV mass 154.7 ?51.3 g. Of the 101 patients,
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Low CNKSR1 expression (p = 0.3666). Pancreatic tumors with nuclear in addition to cytoplasmic CNKSR1 staining (32/107) showed increased nuclear phospho-ERK expression compared to tumor with cytoplasmic CNKSR1 staining only (p = 0.017). Conclusion: CNKSR1 expression is increased in pancreatic tissue specimens and was found to be an independent prognostic marker of overall survival. CNKSR1 may help
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S. Increased CNKSR1 expression levels were observed in tumor tissues compared to matched normal tissue by Wilcoxon matchedpairs signed rank test (** p = 0.004)Table 1 presents demographic and clinical characteristics of the pancreatic cancer patient specimens used for clinical outcome associations (SEER, UMD, and NIH). Table 2 presents the demographics and tumor characteristics by CNKSR1 expressio
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Osclerotic plaque volume in the superficial femoral artery when compared to those already treated with statin given ezetimibe. Reverse vessel wall remodeling was noted among PAD patients newly treated with statins compared to those with ezetimibe added to preexisting statin therapy. Thus the degree and/or mechanism of LDL lowering rather than the final LDL achieved may be important in halting athe
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Authors�� contributions LEH done the sample preparation, fIFNG boosting as well as sequencing, way of measuring of the plasma power of IFN-��, set up genotyping techniques and also the article. LLC designed the research, participated in the study layout along with dexterity along with caused the particular planning with the manuscript. Each writers examine along with accredited the last manuscript
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Signals from integrins through FAK and Akt (Fig. 5A). Resistance to anoikis can be mediated through the IGF signal transduction pathway. IGFs activate the PI3-kinase/Akt, and the Grb2/Ras/MAP-kinase signal transduction pathways both of which have been implicated in anoikis resistance.Signal transduction pathway that mediates the anti-anoikic effect of IGF-The importance of the PI3-kinase/Akt pathw