Objective: To examine the association between cardiometabolic risk factors and visceral adipose tissue (VAT) measurements using a dual-energy X-ray absorptiometry (DXA) based approach. Design and Methods: An analysis of cross-sectional relationships between DXA VAT measured using CoreScan (GE Healthcare) and cardiometabolic indicators was conducted on a sample of 939 subjects (541 females and 398 males; average age, 56 years; average BMI, 26 kg/m 2 ) who had previously undergone a total body DXA scan as well as measurements of key cardiometabolic risk factors. Results: Sex-specific, age-adjusted multivariable regression analysis showed that for both men and women, DXA VAT was significantly associated with increased odds of hypertension, impaired fasting glucose, metabolic syndrome, and type 2 diabetes (P < 0.001). After additional model adjustment for BMI and waist circumference, the odds ratio (per SD change in VAT) for type 2 diabetes was 2.07 for women and 2.25 for men. Similarly, the odds ratio for metabolic syndrome for women was 3.46 and for men was 1.75. Conclusions: VAT measured using DXA showed a significant association with cardiometabolic risk factors and disease. These relationships persist after statistical adjustment for age, BMI, and waist circumference. DXA VAT may provide a new accessible option for quantifying VAT-related cardiometabolic risk.
ObjectiveThe psychological condition of healthcare workers since the COVID-19 pandemic has attracted the attention of many studies. However, few have reported on psychosocial problems of primary healthcare workers in the COVID-19 pandemic. This study aimed to examine the mediating roles of social support and resilience in COVID-19-related work stress and symptoms of anxiety and depression.MethodsA total of 840 primary healthcare workers in 17 community health centers in Guangzhou, China, were recruited from May to July 2021. Data on demographic characteristics, COVID-19-related work stress, social support, resilience, anxiety and depression were collected. A structural equation model was used for mediation analysis.ResultsMore than half of participants reported mild or more severe (at least borderline abnormal) symptoms of anxiety (68.1%) and depression (55.6%). Social support and resilience mediate the association between COVID-19-related work stress and symptoms of anxiety and depression, respectively. Furthermore, the association between work stress and symptoms of anxiety and depression was also mediated by an accumulation of social support and resilience. The indirect effect of COVID-19-related work stress on anxiety and depression through resilience was much greater than other indirect effects.ConclusionAnxiety and depression were prevalent among primary healthcare workers. This study highlights the psychological impact of the COVID-19-related psychosocial work environment on primary healthcare workers. There is an urgent need to improve working conditions for primary healthcare workers in the COVID-19 and to implement intervention strategies aimed at increasing individual resilience alongside the establishment of external supportive work environments.
Objective: A new tool to quantify visceral adipose tissue (VAT) over the android region of a total body dual-energy x-ray absorptiometry (DXA) scan has recently been reported. The measurement, CoreScan, is currently available on Lunar iDXA densitometers. The purpose of the study was to determine the precision of the CoreScan VAT measurement, which is critical for understanding the utility of this measure in longitudinal trials. Design and Methods: VAT precision was characterized in both an anthropomorphic imaging phantom (measured on 10 Lunar iDXA systems) and a clinical population consisting of obese women (n ¼ 32). Results: The intrascanner precision for the VAT phantom across 9 quantities of VAT mass (01,800 g) ranged from 28.4 to 38.0 g. The interscanner precision ranged from 24.7 to 38.4 g. There was no statistical dependence on the quantity of VAT for either the inter-or intrascanner precision result (p ¼ 0.670). Combining inter-and intrascanner precision yielded a total phantom precision estimate of 47.6 g for VAT mass, which corresponds to a 4.8% coefficient of variance (CV) for a 1 kg VAT mass. Our clinical population, who completed replicate total body scans with repositioning between scans, showed a precision of 56.8 g on an average VAT mass of 1110.4 g. This corresponds to a 5.1% CV. Hence, the in vivo precision result was similar to the phantom precision result. Conclusions: The study suggests that CoreScan has a relatively low precision error in both phantoms and obese women and therefore may be a useful addition to clinical trials where interventions are targeted towards changes in visceral adiposity.Obesity (2013) 21, E134-E136.
Although there are considerable evidences of PBI effects on some immune indicators, the effect sizes are modest and it is still premature to conclude whether PBIs have effects on immune functions among cancer patients. There is a clear need for much more rigorous efforts in this area and future researches should pay particular attention to intervention dose and focus, sample size and comparable immune measures.
UBIAD1 plays critical roles in physiology including vitamin K and CoQ10 biosynthesis as well as pathophysiology including dyslipimedia-induced SCD (Schnyder’s corneal dystrophy), Parkinson’s disease, cardiovascular disease and bladder carcinoma. Since the subcellular localization of UBIAD1 varies in different cell types, characterization of the exact subcellular localization of UBIAD1 in specific human disease is vital for understanding its molecular mechanism. As UBIAD1 suppresses bladder carcinoma, we studied its subcellular localization in human bladder carcinoma cell line T24. Since fluorescent images of UBIAD1-EGFP in T24, human prostate cancer cell line PC-3, human embryonic kidney cell line HEK293 and human hepatocyte cell line L02 are similar, these four cell lines were used for present study. Using a combination of fluorescent microscopy and immunohistochemistry, it was found that UBIAD1 localized on the Golgi and endoplasmic reticulum (ER), but not on the plasma membrane, of T24 and HEK293 cells. Using scanning electron microscopy and western blot analysis, we found that UBIAD1 is enriched in the Golgi fraction extracted from the L02 cells, verifying the Golgi localization of UBAID1. Site-directed mutagenesis showed that the RPWS motif, which forms an Arginine finger on the UBIAD1 N terminus, serves as the Golgi retention signal. With both cycloheximide and brefeldin A inhibition assays, it was shown that UBIAD1 may be transported from the endoplasmic reticulum (ER) to the Golgi by a COPII-mediated mechanism. Based upon flow cytometry analysis, it is shown that mutation of the RPWS motif reduced the UBIAD1-induced apoptosis of T24 cells, indicating that the proper Golgi localization of UBIAD1 influences its tumor suppressant activity. This study paves the way for further understanding the molecular mechanism of UBIAD1 in human diseases.
Vitamin K2 has been shown to exert remarkable anticancer activity. However, the detailed mechanism remains unclear. Here, our study was the first to show that Vitamin K2 significantly promoted the glycolysis in bladder cancer cells by upregulating glucose consumption and lactate production, whereas inhibited TCA cycle by reducing the amounts of Acetyl-CoA. Moreover, suppression of PI3K/ AKT and HIF-1α attenuated Vitamin K2-increased glucose consumption and lactate generation, indicating that Vitamin K2 promotes PI3K/AKT and HIF-1α-mediated glycolysis in bladder cancer cells. Importantly, upon glucose limitation, Vitamin K2-upregulated glycolysis markedly induced metabolic stress, along with AMPK activation and mTORC1 pathway suppression, which subsequently triggered AMPK-dependent autophagic cell death. Intriguingly, glucose supplementation profoundly abrogated AMPK activation and rescued bladder cancer cells from Vitamin K2-triggered autophagic cell death. Furthermore, both inhibition of PI3K/AKT/HIF-1α and attenuation of glycolysis significantly blocked Vitamin K2-induced AMPK activation and subsequently prevented autophagic cell death. Collectively, these findings reveal that Vitamin K2 could induce metabolic stress and trigger AMPK-dependent autophagic cell death in bladder cancer cells by PI3K/AKT/HIF-1α-mediated glycolysis promotion. Cancer cells, including bladder carcinoma cells, display the altered metabolism, compared to normal cells 1. One of the most metabolic shifts in cancer cells is the aberrant glucose metabolism. Unlike the normal cells, most cancer cells exhibit the remarkably increased glucose uptake and glycolysis rate to meet their rapid proliferation and metastasis 2. Moreover, numerous studies indicate that the glycolysis is usually uncoupled from the tricarboxylic acid (TCA) cycle and oxidative phosphorylation (OXPHOS) in cancer cells. Therefore, pyruvate, the end product of glycolysis, is mainly diverted to lactate production, with the reduction of mitochondrial TCA cycle and OXPHOS 3. This metabolic shift is well-known as the Warburg effect. However, in tumor microenvironment, the nutrients including glucose are limited. Excessively increasing glycolysis will inevitably result in intracellular metabolic stress and trigger cancer cell death due to energy depletion 4. Therefore, in nutrient-deficient tumor microenvironment, the method of promoting glycolysis to induce metabolic stress and activate cell death appears to be a novel strategy for cancer treatment. Phosphatidylinositide-3-kinase (PI3K) and AKT are usually hyper-activated in cancer cells. There are accumulating evidences indicating that activation of PI3K and AKT plays a pivotal role in the regulation of aerobic glycolysis in cancer cells 5-7. The activated PI3K/AKT can directly promote the shift to the aerobic glycolysis, rendering cancer cells more reliance on glucose consumption for lactate generation 8,9. Although activation of PI3K and AKT could directly stimulate the aerobic glycolysis by positive regulation of some glycol...
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.