This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Objective To investigate that whether an association between marital status and the female breast cancer risk exists. Methods The MEDLINE, EMBASE and PsycINFO databases were searched from their inception to July 2019. The Newcastle-Ottawa Scale was used to rate the methodological quality of included studies. Study data were pooled using random-effects meta-analyses to compare the breast cancer risk between unmarried, widowed, divorced or lifelong single women and married women. This study is registered with PROSPERO (number CRD42018112368). Results Forty-nine publications were included in the meta-analysis. Compared with married women, unmarried and lifelong single women had an elevated risk of breast cancer, and the pooled ORs of case-control studies were 1.20 (95% CI: 1.07 to 1.35) and 1.24 (95% CI: 1.05 to 1.45), respectively. In the subgroup analyses under these two comparisons, hospital-based estimates and multivariate-adjusted estimates demonstrated a strong association, while population-based estimates and age-adjusted estimates produced nonsignificant results. The pooled OR of cohort studies examining the effect of being a lifelong single woman was 1.10 (95% CI: 1.04 to 1.16). Heterogeneity was moderate to substantial across case-control studies (I 2 : 46% to 82%), which may be partially explained by differences in geographic
BackgroundPatients with cancer are vulnerable to depression or other depressive conditions. The aim of this paper was to evaluate the efficacy and safety of Chinese herbal medicine (CHM) for the treatment of depression or depressive symptoms in cancer patients.MethodsCENTRAL, MEDLINE, EMBASE, PsycINFO, CNKI, VIP, SinoMed, and online clinical trial registry websites were searched for relevant RCTs until May 2017. The methodological quality of each included study was assessed with the “risk of bias” tool. Review Manager 5.3.5 was used to analyze the data.ResultsWe identified 18 RCTs that included data from 1441 participants. Twelve different types of Chinese herbal preparations were investigated by these studies, and they showed a better therapeutic effect in most comparisons when measured in terms of depression rating scale scores, with SMDs (95% CI) of − 2.30 (− 3.54, − 1.05) (CHM versus no treatment), − 0.61 (− 1.03, − 0.18) (CHM versus antidepressants), and − 0.55 (− 1.07, − 0.02) (CHM plus psychological treatments versus psychological treatments), or when measured in terms of treatment response rate, with RRs (95% CI) of 1.65 (1.19, 2.29) (CHM versus no treatment), 1.15 (1.03, 1.28) (CHM versus psychological treatments), 1.32 (1.07, 1.63) (CHM plus antidepressants versus antidepressants), and 1.70 (1.02, 2.85) (CHM plus psychological treatments versus psychological treatments). Compared with antidepressants, these CHMs showed borderline superiority for improving the response rate, with an RR (95% CI) of 1.08 (0.93, 1.26). Subgroup analysis based on psychiatric diagnosis (depression versus depressive symptoms) did not modify the direction of these estimates and neither could it explain the high level of heterogeneity. Patients in the CHM group experienced fewer adverse events of cardiac toxicity (P = 0.02), functional gastrointestinal disorders (P = 0.008), sleep disturbances (P = 0.02), blurred vision (P = 0.02) and fatigue (P = 0.03) than the patients in the no treatment group or the antidepressants group.ConclusionsAccording to the investigation of the twelve herbal preparations, the CHM intervention appears to alleviate depressive symptoms in cancer patients, either alone or combined with antidepressants or psychological treatments. However, a high risk of bias and high heterogeneity made the mean estimates uncertain. Well-designed trials with comprehensive and transparent reporting are warranted in the future.Electronic supplementary materialThe online version of this article (10.1186/s12906-019-2441-8) contains supplementary material, which is available to authorized users.
The endothelial dysfunction induced by oxidized low-density lipoprotein (ox-LDL) plays an important role in the pathogenesis of atherosclerosis, which can lead to oxidative stress and inflammation. The role of autophagy in the process of atherosclerosis has drawn increasing attention. The human umbilical vein endothelial cells (HUVECs), whose Ras-related C3 botulinum toxin substrate 1 (Rac1) and Rac3 was knockdown, were used to detect whether the possible molecular mechanisms of Rac1 and Rac3 for anti-inflammatory in endothelial cells was effected by downregulation of autophagy. The HUVECs were incubated with ox-LDL. The inflammatory factors and autophagy proteins were evaluated to ascertain and compare the effect of Rac1 and Rac3 on autophagy. Then, 3-methyladenine (3-MA) as an inhibiter of autophagy was used to detect whether the effect of Rac1 and Rac3 was related to autophagy. ox-LDL-induced cell dysfunction in HUVECs was determined by testing the formation of foam cells, the expression of nuclear factor (NF)-κB and nucleotidebinding oligomerization domain (NOD)-like receptor protein 3 and NF-κB p65 and other inflammatory factors, the release of reactive oxygen species by oxidative stress and the dysfunction of the cytomembrane. And ApoE −/− mice on a high-fat diet were used as an animal model to detect the effect of Rac1 and Rac3 in vivo. The resultsshowed that when Rac1 and Rac3 were decreased in HUVECs, the cell dysfunction caused by ox-LDL was inhibited. If 3-MA was used to inhibit autophagy in Rac1 and Rac3 knockdown cells, the injury induced by ox-LDL on the cells was recovered.These results indicated that the effect of Rac1 and Rac3 was combined with ox-LDL, which was related to inhibition of autophagy. The effect of Rac3 was more significant than that of Rac1. atherosclerosis, autophagy, endothelial dysfunction, Rac1, Rac3Abbreviations: 3-MA, 3-methyladenine; ApoE, apolipoprotein E; AS, atherosclerosis; CE, cholesterol esterification; DMEM, Dulbecco's modified Eagle's media; DOX, doxycycline; ELISA, enzyme-linked immunosorbent assay; FBS, fetal bovine serum; FITC, fluorescein isothiocyanate; H&E stain, hematoxylin and eosin stain; HDL-C, high-density lipid cholesterol; HUVECs, human umbilical vein endothelial cells; IL-1β, interleukin-1β; LDH, lactic dehydrogenase; LDL-C, low-density lipid cholesterol; MMP, mitochondria membrane potential; NLRP3, nuclear factor (NF)-κB and nucleotide-binding oligomerization domain (NOD)-like receptor protein 3; ox-LDL, oxidized low-density lipoprotein; PBS, phosphate buffered saline; Rac, Ras-related C3 botulinum toxin substrate; ROS, reactive oxygen species; shRNA, small hairpin RNA; siRNA, small inhibitor RNA; TC, total cholesterol; TG, triglycerides; VCAM-1, vascular cell adhesion molecule-1.
PI3K is a downstream target of multiple cell-surface receptors, which acts as a crucial modulator of both cell polarization and survival. PI3K/AKT signaling pathway is commonly involved in cancer, atherosclerosis, and other diseases. However, its role in cardiovascular diseases, especially in atherosclerosis, remains to be further investigated. To determine the effect of PI3K/AKT signaling pathway on cellular inflammatory response and oxidative stress, PI3K inhibitor (GDC0941) and AKT inhibitor (MK2206) were used. First, THP-1 cells were incubated with ox-LDL (100 µg/ml) to establish an in vitro atherosclerosis model. The inflammatory factors and foam cell formation were then evaluated to ascertain and compare the effects of PI3K and AKT inhibition. ApoE -/mice fed a high-fat diet were used to assess the roles of PI3K and AKT in aortic plaque formation. Our results showed that the inhibition of PI3K or AKT could suppress the activation of NLRP3, decreased the expression levels of p-p65/p65 and reduced the production of MitoROS in THP-1 cells. Inhibition of PI3K or AKT could also reduced atherosclerosis lesion and plaque area, and decreased the levels of NLRP3 and IL-1β in ApoE -/mice. The effect of PI3K inhibition was more significant than AKT. Therefore, PI3K inhibition can retard the progress of atherosclerosis. Besides, there may be other AKT-independent pathways that regulate the formation of atherosclerosis.
Urologic cancers, particularly kidney, bladder, and prostate cancer, have a growing incidence and account for about a million annual deaths worldwide. Treatments, including surgery, chemotherapy, radiotherapy, hormone therapy, and immunotherapy are the main therapeutic options in urologic cancers. Immunotherapy is now a clinical reality with marked success in solid tumors. Immunological checkpoint blockade, non-specific activation of the immune system, adoptive cell therapy, and tumor vaccine are the main modalities of immunotherapy. Immunotherapy has long been used to treat urologic cancers; however, dose-limiting toxicities and low response rates remain major challenges in the clinic. Herein, nanomaterial-based platforms are utilized as the “savior”. The combination of nanotechnology with immunotherapy can achieve precision medicine, enhance efficacy, and reduce toxicities. In this review, we highlight the principles of cancer immunotherapy in urology. Meanwhile, we summarize the nano-immune technology and platforms currently used for urologic cancer treatment. The ultimate goal is to help in the rational design of strategies for nanomedicine-based immunotherapy in urologic cancer.
The effect of probiotics on serum lipid levels in non-obese healthy adults with hyperlipidemia: a systematic review and meta-analysis of randomized controlled trials El efecto de los probióticos sobre los niveles de lípidos séricos en adultos sanos no obesos con hiperlipidemia: revisión sistemática y metaanálisis de ensayos controlados y aleatorizados
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.