Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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Chronic kidney disease (CKD) is higher in elderly, but mortality outweighs the risk of end-stage renal disease (ESRD). Our aim was to identify prognostic markers for ESRD or death in elderly CKD, within a competing-risk analysis. This is a longitudinal study of consecutive newly referred patients with CKD ages 65 years, followed until the time of the first event (ESRD or death), using a competing-risk analysis. ⋯ The independent predictors for ESRD with competing risk of death were: lower age (sHR=0.94; p=0.009), creatinine≥1.6 mg/dL (sHR=3.26, p=0.006), hemoglobin <11 g/dL (sHR=2.15, p=0.027), peripheral vascular disease (sHR=3.45, p=0.001) and having one or more hospitalizations (sHR=1.56, p=0.031). Elderly referred patients with CKD are near threefold more likely to die than progress to ESRD. A competing-risk framework based on available clinical and laboratory data may discriminate between those outcomes and could be used as a decision-making tool.
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The incidence of gastric cancer is declining in western countries but continues to represent a serious health problem worldwide, especially in Asia and among Asian Americans. This study aimed to investigate ethnic disparities in stage-specific gastric cancer, including differences in incidence, treatment and survival. The cohort study was analyzed using the data set of patients with gastric cancer registered in the Surveillance, Epidemiology, and End Results (SEER) program from 2004 to 2013. ⋯ Significant differences were found in OS and CSS between groups (p<0.001); OS was highest among Asians/Pacific Islanders. Multivariate analysis revealed that age, race, grade, stage, location, and second primary cancer were valid prognostic factors for survival. Marked ethnic disparities exist in age-adjusted incidence of primary gastric cancer, with significant differences between races in age, gender, histological type, grade, AJCC stage, location, second cancer, treatment and survival.
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The aim of this study is to investigate the role of tumor necrosis factor-α (TNF-α) in apoptosis and autophagy of mouse osteoblast MC3T3-E1 cells, as well as the crosstalk between autophagy and apoptosis. Mouse osteoblast MC3T3-E1 cells were cultured in vitro and treated with 5-fluorouracil (5-FU), rapamycin, 3-methyl adenine (3-MA) and TNF-α either alone or in combination, respectively. MTT assays were used to monitor the cell viability upon different treatments. ⋯ In addition, TNF-α caused an induction of apoptotic marker cleaved caspase-3. TNF-α-mediated induction of cleaved caspase-3 was downregulated by rapamycin, but upregulated by 3-MA, respectively. TNF-α induced both autophagy and apoptosis in osteoblasts, and upregulated autophagy protects the cell by reducing TNF-α-induced apoptosis.
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Multiple sclerosis (MS) is an autoimmune, demyelinating disease of the central nervous system (CNS). It predominantly affects young women and is one of the most common causes of disability in young adults. MS is characterized by formation of white matter lesions in the CNS as a result of inflammation, demyelination, and axonal loss. ⋯ MS is a major contributor to healthcare costs and it is critical that healthcare providers be aware of the availability and benefits of DMTs. It is imperative that prompt and adequate treatment be established on diagnosis. Changes in therapy should be considered when there is evidence of disease activity as well as accumulation of disability or safety or tolerability concerns.
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High levels of the antioxidant enzyme, glutathione peroxidase (GPx), have been associated with improved outcomes following acute coronary syndromes (ACS), suggesting a protective role. How GPx levels are altered with coronary disease is not clearly established. This study examined GPx activity, protein, and mRNA levels in healthy controls, patients with stable coronary artery disease (CAD), and patients with ACS. ⋯ Levels of oxLDL were also significantly higher in patients with ACS (61.9±22.2 U/L) than in patients with stable CAD (47.8±10.4 U/L, p<0.05) and healthy controls (48.9±11.9 U/L, p<0.05). Levels of oxLDL, GPx activity, protein, and mRNA are all significantly higher in patients with ACS compared with patients with stable CAD and healthy controls. These findings suggest that GPx may be upregulated in response to a change in oxidative stress during an ACS.