The red blood cell distribution width (RDW) is a simple and widely available parameter obtained from a complete blood cell count test and is usually used in the analysis of anemia. Recently, studies have discovered the association between RDW and the host inflammatory response of cancer patients. We aimed to determine the prognostic value of RDW in colorectal cancer (CRC) patients. 5315 total patients with stage I-II CRC from the Chang Gung Memorial Hospital between 2001 and 2018 were enrolled. The study cohort was divided into two groups using RDW = 13.8 as the cutoff value as determined by receiver operating curve. High RDW had worse overall survival (OS), disease-free survival (DFS), and cancer-specific survival (CSS), and was also independently related to older age, more advanced tumor stage, lower albumin level, lower hemoglobin level, and more co-morbidities including diabetes, hypertension, and chronic kidney disease. We performed a propensity-score matched analysis to balance the heterogeneity between the two groups and to reduce the influence of confounding factors that may have compromised the prognosis. High RDW remained a negative predictor of OS (HR = 1.49, 95% CI: 1.25–1.78), as well as DFS and CSS. In conclusion, this is the first report using propensity matching to demonstrate the relationship between RDW and the prognosis of early-stage CRC patients.
24Background 25 Sleep and physical activity are modifiable behaviors that play an important role in preventing 26 overweight, obesity, and metabolic health problems. Studies of the association between 27 concurrent objective measures of sleep, physical activity, and metabolic risk factors among 28 adolescents are limited. 29 Objective 30The aim of the study was to examine the association between metabolic risk factors and 31 objectively measured school day physical activity and sleep duration, quality, onset, and 32 variability in adolescents. 34 We measured one school week of free-living sleep and physical activity with wrist actigraphy 35 in 252 adolescents (146 girls), aged 15.8±0.3 years. Metabolic risk factors included body mass 36 index, waist circumference, total body and trunk fat percentage, resting blood pressure, and 37 fasting glucose and insulin levels. Multiple linear regression adjusted for sex, parental 38 education, and day length was used to assess associations between metabolic risk factors and 39 sleep and activity parameters. 33 Materials and Methods40 Results 41On average, participants went to bed at 00:22±0.88 hours and slept 6.2±0.7 hours/night, with 42 0.83±0.36 hours of awakenings/night. However, night-to-night variability in sleep duration 43 (0.87±0.57 hours) and bedtime (0.79±0.58 hours) was considerable. Neither average sleep 44 duration nor mean bedtime was associated with any metabolic risk factors. However, greater 45 night-to-night variability in sleep duration was associated with higher total body (β=1.9±0.9 3 46 %/h, p=0.03) and trunk fat percentage (β=1.6±0.7 %/h, p=0.02), poorer sleep quality (more 47 hours of awakening) was associated with higher systolic blood pressure (β=4.9±2.2 mmHg/h, 48 p=0.03), and less physical activity was associated with higher trunk fat percentage (p=0.04) and 49 insulin levels (p=0.01). 50 Conclusion 51Greater nightly variation in sleep, lower sleep quality, and less physical activity was associated 52 with a less favorable metabolic profile in adolescents. These findings support the idea that, 53 along with an adequate amount of sleep and physical activity, a regular sleep schedule is 54 important to the metabolic health of adolescents. 55 56 57 58 59 60 61 62 63 64 65 66 67 68 69 4 70 71The prevalence of overweight in the world has nearly tripled from 1975-2016, with over 72 39% of adults and 18% of children and adolescents being overweight or obese [1]. Greater total 73 body and central adiposity is associated with increased risk of cardio-metabolic comorbidities, 74 such as hypertension and diabetes [2, 3]. Prevalence of metabolic syndrome is high among 75 obese children and adolescents and increases with higher central obesity [4]. Along with diet, 76 sleep and physical activity have been identified as important modifiable risk factors implicated 77 in the development of overweight, obesity, and metabolic health problems [5]. 78 The importance of adequate sleep for health and daily functioning in adolescents is well 79 established [...
CIL-102 (1-[4-(furo[2,3-b]quinolin-4-ylamino) phenyl]ethanone) is a major active agent of Camptotheca acuminata’s alkaloid derivative, and its anti-tumorigenic activity, a valuable biological property of the agent, has been reported in many types of cancer. In this study, we researched the novel CIL-102-induced protein for either the induction of cell apoptosis or the inhibition of cell migration/invasiveness in colorectal cancer cells (CRC) and their molecular mechanism. Firstly, our data showed that CIL-102 treatment not only increased the cytotoxicity of cells and the production of Reactive Oxygen Species (ROS), but it also decreased cell migration and invasiveness in DLD-1 cells. In addition, many cellular death-related proteins (cleavage caspase 9, cleavage caspase 3, Bcl-2, and TNFR1 and TRAIL) and JNK MAPK/p300 pathways were increased in a time-dependent manner. Using the proteomic approach with a MALDI-TOF-TOF analysis, CIL-102-regulated differentially expressed proteins were identified, including eight downregulated and 11 upregulated proteins. Among them, upregulated Endoplasmic Reticulum resident Protein 29 (ERP29) and Fumarate Hydratase (FUMH) by CIL-102 were blocked by the inhibition of ROS production, JNK activity, and p300/CBP (CREB binding protein) signaling pathways. Importantly, the knockdown of ERP29 and FUMH expression by shRNA abolished the inhibition of cell migration and invasion by CIL-102 in DLD-1 cells. Together, our findings demonstrate that ERP29 and FUMH were upregulated by CIL102 via ROS production, JNK activity, and p300/CBP pathways, and that they were involved in the inhibition of the aggressive status of colorectal cancer cells.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.