Background: Depression, as an independent risk factor, can lead to a substantially increased risk of coronary heart disease (CHD). The overall body of evidence involving depression and CHD is not consistent. Therefore, we performed an update meta-analysis to evaluate the association between depression and the risk of patients with CHD.Methods: Studies were identified through a comprehensive literature search of the PubMed, Embase, and the Cochrane Library database from its inception to 28 September 2021 for titles/abstracts with restricted to English language articles. The literature was screened according to the inclusion and exclusion criteria. Along with data extraction, we evaluated the quality of eligible studies using the Newcastle-Ottawa Scale (NOS). The primary outcome was fatal or non-fatal CHD. We calculated relative risk (RR) with 95% confidence intervals (CIs) using a random-effects models. The protocol was registered in the PROSPERO registration (registration number CRD42021271259).Results: From 9,151 records, we included 26 prospective cohort studies published from 1998 to 2018, consisting of 402,597 patients. Either in depression-exposured group or non-depression-exposured group, the mean age of all participants ranged from 18 to 99 years. Moreover, the NOS scores of these studies are eventually indicated that the quality of these eligible studies was reliable. In general, the pooled results showed that patients with depression had a higher risk of CHD compared to patients without depression (RR = 1.21, 95% CI: 1.14–1.29). Additionally, the funnel plot appeared to be asymmetry, indicating there existing publication bias for the pooled results between depression and CHD. A sensitivity analysis was used to assess the stability of the relationship between depression and CHD that indicating the results robust (RR = 1.15, 95% CI: 1.09–1.21).Conclusion: Depression may increase risk of CHD. Future studies on the share pathogenic mechanisms of both depression and CHD may develop novel therapies.

Background: Osteoporosis, a systemic skeletal disease characterized by low bone mass and increased fracture risk, poses significant social and economic challenges globally, while type 2 diabetes mellitus (T2DM), a prevalent metabolic disorder, has been linked to complex effects on bone health, including contradictory findings on its relationship with osteoporosis and fracture risk. Methods: We searched PubMed, Embase, Cochrane, and Web of Science Library to identify observational studies investigating whether people with T2DM have a higher risk of osteoporosis or fracture than people without diabetes. The time limit for literature retrieval was from the establishment of the database until March 2023. The quality of the studies was assessed using the Newcastle-Ottawa Scale and Agency for Healthcare Research and Quality checklist. The meta-analysis was conducted using Stata 15, and a random-effects model was used if I² was > 50%. The Egger test was used to assess publication bias. Results: The results demonstrated that people with T2DM have a higher risk of osteoporosis. (relative risk, 1.841; 95% confidence interval, 1.219–2.780; P = .004). Similar results were demonstrated for fractures (relative risk, 1.21; 95% confidence interval, 1.09–1.31; P < .001). However, the results of the subgroup analysis showed no significant correlation between T2DM and fractures in univariate analysis, cross-sectional studies, Asia, Europe, Oceania, and vertebral fractures. However, a significant correlation was found in other subgroup analyses. Conclusions: Osteoporosis and fractures are significantly associated with T2DM.

Studies of molecular mechanisms and related gene functions have long been restricted by limited genome editing technologies in malaria parasites. Recently, a simple and effective genome editing technology, the CRISPR/Cas (clustered regularly interspaced short palindromic repeats/CRISPR-associated) system, has greatly facilitated these studies in many organisms, including malaria parasites. However, due to the special genome feature of malaria parasites, the manipulation and gene editing efficacy of the CRISPR/Cas system in this pathogen need to be improved, particularly in the human malaria parasite, Plasmodium falciparum. Herein, based on the CRISPR/Cas9 system, we developed an integrating strategy to generate a Cas9i system, which significantly shortened the time for generation of transgenic strains in P. falciparum. Moreover, with this Cas9i system, we have successfully achieved multiplexed genome editing (mutating or tagging) by a single-round transfection in P. falciparum. In addition, we for the first time adapted AsCpf1 (Acidaminococcus sp. Cpf1), an alternative to Cas9, into P. falciparum parasites and examined it for gene editing. These optimizations of the CRISPR/Cas system will further facilitate the mechanistic research of malaria parasites and contribute to eliminating malaria in the future.

Background. Ursolic acid (UA) is an antitumor component derived from Chinese herbal medicine; this study is to observe the effects of UA on epithelial-mesenchymal transition (EMT) in gastric cancer. Methods. (1) In vitro experiments: 25μmol/L and 50μmol/L UA were applied to BGC-823, AGS, MGC-803, and HGC-27 cells; MTT staining, Transwell assay, and flow cytometry were used to assess cell proliferation, cell migration, and apoptosis, respectively. Western blot was performed to detect the expressions of N-Cadherin, Vimentin, Snail, Twist, Axl, p-Axl, IKK, p-IKK, NF-κB, and p-NF-κB. (2) In vivo experiments: Ten BALB/c-nu mice were used to establish gastric cancer xenograft model. Five were orally given UA for 4 weeks and five were given normal saline. Expressions of N-Cadherin and Snail were examined by immunohistochemical assay; expressions of N-Cadherin, Snail, Twist, Axl, p-Axl, IKK, and p-IKK were detected by Western blot. Results. (1) UA inhibited cell proliferation in BGC-823 and HGC-27 cells in dose-dependent manners. (2) UA inhibited cell migration in BGC-823, AGS, and MGC-803 cells while inducing apoptosis in BGC-823 cells. (3) UA significantly decreased the expressions of N-Cadherin, Vimentin, Snail, Twist p-Axl, p-IKKα/β, and p-NF-κB in BGC-823 and MGC-803 cells. (4) UA distinctly decreased the expressions of N-Cadherin, Snail, p-Axl, and p-IKKα/β in gastric cancer xenograft model rats. Conclusion. UA can effectively inhibit the proliferation and migration and induce apoptosis of gastric cancer cells. The antitumor effect of UA is conducted by EMT inhibition, which may be associated with the regulation of Axl/NF-κB signaling pathway.