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Background To systematically review the epidemiologic relationship between periodontitis and type 2 diabetes mellitus (T2DM). Methods Four electronic databases were searched up until December 2018. The manual search included the reference lists of the included studies and relevant journals. Observational studies evaluating the relationship between T2DM and periodontitis were included . Meta-analyses were conducted using STATA. Results A total of 53 observational studies were included. The Adjusted T2DM prevalence was significantly higher in periodontitis patients (OR = 4.04, p  = 0.000), and vice versa (OR = 1.58, p = 0.000). T2DM patients had significantly worse periodontal status, as reflected in a 0.61 mm deeper periodontal pocket, a 0.89 mm higher attachment loss and approximately 2 more lost teeth (all p  = 0.000), than those without T2DM. The results of the cohort studies found that T2DM could elevate the risk of developing periodontitis by 34% ( p  = 0.002). The glycemic control of T2DM patients might result in different periodontitis outcomes. Severe periodontitis increased the incidence of T2DM by 53% ( p  = 0.000), and this result was stable. In contrast, the impact of mild periodontitis on T2DM incidence (RR = 1.28, p  = 0.007) was less robust. Conclusions There is an evident bidirectional relationship between T2DM and periodontitis. Further well-designed cohort studies are needed to confirm this finding. Our results suggest that both dentists and physicians need to be aware of the strong connection between periodontitis and T2DM. Controlling these two diseases might help prevent each other’s incidence.

Transected axons are unable to regenerate after spinal cord injury (SCI). Glial scar is thought to be responsible for this failure. Regulating the formation of glial scar post-SCI may contribute to axonal regrow. Over the past few decades, studies have found that the interaction between immune cells at the damaged site results in a robust and persistent inflammatory response. Current therapy strategies focus primarily on the inhibition of subacute and chronic neuroinflammation after the acute inflammatory response was executed. Growing evidences have documented that mesenchymal stem cells (MSCs) engraftment can be served as a promising cell therapy for SCI. Numerous studies have shown that MSCs transplantation can inhibit the excessive glial scar formation as well as inflammatory response, thereby facilitating the anatomical and functional recovery. Here, we will review the effects of inflammatory response and glial scar formation in spinal cord injury and repair. The role of MSCs in regulating neuroinflammation and glial scar formation after SCI will be reviewed as well.

It is often difficult to regain neurological function following spinal cord injury (SCI). Neuroinflammation is thought to be responsible for this failure. Regulating the inflammatory response post-SCI may contribute to the recovery of neurological function. Over the past few decades, studies have found that macrophages/microglia are one of the primary effector cells in the inflammatory response following SCI. Growing evidence has documented that macrophages/microglia are plastic cells that can polarize in response to microenvironmental signals into M1 and M2 macrophages/microglia. M1 produces pro-inflammatory cytokines to induce inflammation and worsen tissue damage, while M2 has anti-inflammatory activities in wound healing and tissue regeneration. Recent studies have indicated that the transition from the M1 to the M2 phenotype of macrophage/microglia supports the regression of inflammation and tissue repair. Here, we will review the role of the inflammatory response and macrophages/microglia in SCI and repair. In addition, we will discuss potential molecular mechanisms that induce macrophage/microglia polarization, with emphasis on neuroprotective therapies that modulate macrophage/microglia polarization, which will provide new insights into therapeutic strategies for SCI.

To elucidate the biological mechanism of yellow rind formation on watermelon, the characteristics of soil bacterial community structure in rhizosphere and endophytic bacteria in stem of yellow rind watermelon were analyzed. Based on high-throughput sequencing technology, plant stem and rhizosphere soil samples, which collected from yellow and green rind watermelons were used in this paper, respectively. The structural characteristics of the endophytic bacteria in stems and soil bacterial communities in rhizospheres of yellow and green rind watermelons were comparative studied. Firstly, significant different proportions of some dominant bacteria and abundances could be detected between yellow and rind watermelons. Meanwhile, although different abundances of endophytic bacteria could be found, but no significant differences were observed between yellow and green rind watermelons. Moreover, Gemmatimonadota, Myxococcota, WPS-2, norank_f_Gemmatimonadaceae and Bradyrhizobium were the soil dominant bacterial genera in rhizosphere of green rind watermelon. All above results suggest that differences of rhizospheric and endophytic bacteria are exactly recruited as “workers” by different watermelon phenotypes relating to rind color formations.

The occurrence of osteoarthritis (OA) is highly correlated with the reduction of joint lubrication performance, in which persistent excessive inflammation and irreversible destruction of cartilage dominate the mechanism. The inadequate response to monotherapy methods, suboptimal efficacy caused by undesirable bioavailability, short retention, and lack of stimulus-responsiveness, are few unresolved issues. Herein, we report a pH-responsive metal-organic framework (MOF), namely, MIL-101-NH 2 , for the co-delivery of anti-inflammatory drug curcumin (CCM) and small interfering RNA (siRNA) for hypoxia inducible factor (HIF-2α). CCM and siRNA were loaded via encapsulation and surface coordination ability of MIL-101-NH 2 . Our vitro tests showed that MIL-101-NH 2 protected siRNA from nuclease degradation by lysosomal escape. The pH-responsive MIL-101-NH 2 gradually collapsed in an acidic OA microenvironment to release the CCM payloads to down-regulate the level of pro-inflammatory cytokines, and to release the siRNA payloads to cleave the target HIF-2α mRNA for gene-silencing therapy, ultimately exhibiting the synergetic therapeutic efficacy by silencing HIF-2α genes accompanied by inhibiting the inflammation response and cartilage degeneration of OA. The hybrid material reported herein exhibited promising potential performance for OA therapy as supported by both in vitro and in vivo studies and may offer an efficacious therapeutic strategy for OA utilizing MOFs as host materials.

Background Eukaryotic Initiation Factor 5A1 (EIF5A1) is a translation factor, and its pro-tumorigenic role has been extensively documented across various cancer types. However, its specific function in bladder cancer (BLCA) remains unclear. Methods We integrated proteomics and transcriptomics data with clinical data from BLCA patients to investigate the correlation between EIF5A1 expression and BLCA, as well as its potential clinical applications. Transcriptomic data were employed to explore the downstream signaling pathways regulated by EIF5A1. Furthermore, ChIP analysis and luciferase reporter assays were conducted to identify the upstream transcription factors regulating EIF5A1. Results EIF5A1 expression is significantly upregulated in cancer tissues and cells and is strongly associated with poor prognosis. Silencing EIF5A1 in BLCA cells significantly reduced invasiveness, and proliferative capacity. Mechanistic studies identified YAP/TEAD4 as a transcription factor that regulates EIF5A1, influencing mitochondrial-mediated apoptosis by activating the JAK2/STAT3 signaling pathway, thereby promoting BLCA progression. Conclusion Our research demonstrates that EIF5A1 is upregulated in BLCA and associated with poor prognosis. We identified TEAD4 as a potential transcriptional regulator of EIF5A1 and showed that EIF5A1 expression is associated with changes in JAK2/STAT3 signaling and mitochondrial apoptosis in BLCA.

Sweet taste receptors (STRs) play an important role in glucose metabolism, and type 2 diabetic rats have abnormal expressions of STRs in multiple tissues. Astragalus polysaccharides (APS) has shown a significant therapeutic effect on type 2 diabetes mellitus (T2DM), but its mechanism needs to be further clarified. T2DM rat model was induced by intraperitoneal streptozotocin injection and treated with APS for 8 weeks. Daily indicators of experimental rats were observed, and expression levels of STRs and genes related to glycolipid metabolism were determined by real-time quantitative PCR and western blot. The present study revealed that APS alleviated the symptoms of T2DM rats, improved HOMA-IR and promoted insulin secretion. Gene expression analysis found that APS significantly increased the expressions of signaling molecules in STRs pathways, including taste receptor family 1 member 2 (T1R2), α-gustducin (Gα) and transient receptor potential cation channel subfamily member 5 (TRPM5), and reversed the expressions of genes related to glucolipid metabolism, including glucose transporters 2 and 4 (GLUT2 and GLUT4), pyruvate carboxylase (PC), fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC) in the liver of T2DM rats. However, APS had no influences on the expressions of genes, including glycogen synthase kinase-3 beta (GSK-3β), pyruvate kinase (PK) and phosphoenolpyruvate carboxykinase (PEPCK) in the liver of T2DM rats. These results suggested that the physiological roles of STRs in the liver were involved with glucose transport and metabolism. APS alleviated T2DM rats by activating the STRs pathway, and promoted glucose transport and lipogenesis.

Background The importance of the lipid-related biomarkers has been implicated in the pathological process and prognosis of acute myocardial infarction (AMI). Our work was conducted to discuss and compare the predictive ability of the neutrophil to high-density lipoprotein cholesterol (HDL-C) ratio (NHR) with other existing prognostic indices, for instance, the monocyte to HDL-C ratio (MHR) and the low-density lipoprotein cholesterol (LDL-C) to HDL-C ratio (LDL-C/HDL-C) in elderly patients with AMI. Methods Our population was 528 consecutive elderly AMI patients (65–85 years) who were enrolled from Tongji Hospital and grouped according to the cutoff points which were depicted by the receiver operating characteristic (ROC). The Kaplan-Meier curves were plotted with the survival data from the follow-up to investigate the difference between cutoff point-determined groups. Moreover, we assessed the impact of NHR, MHR, LDL-C/HDL-C on the long-term mortality and recurrent myocardial infarction (RMI) with Cox proportional hazard models. Results Mean duration of follow-up was 673.85 ± 14.32 days (median 679.50 days). According to ROC curve analysis, NHR ≥ 5.74, MHR ≥ 0.67, LDL-C/HDL-C ≥ 3.57 were regarded as high-risk groups. Kaplan-Meier analysis resulted that the high-NHR, high-MHR and high-LDL-C/HDL-C groups presented higher mortality and RMI rate than the corresponding low-risk groups in predicting the long-term clinical outcomes (log-rank test: all P  < 0.050). In multivariate analysis, compared with MHR and LDL-C/HDL-C, only NHR was still recognized as a latent predictor for long-term mortality (harzard ratio [HR]: 1.96, 95% confidence interval [CI]: 1.02 to 3.75, P  = 0.044) and long-term RMI (HR: 2.23, 95% CI: 1.04 to 4.79, P  = 0.040). Furthermore, the positive correlation between NHR and Gensini score ( r  = 0.15, P  < 0.001) indicated that NHR was relevant to the severity of coronary artery to some extent. Conclusions NHR, a novel laboratory marker, might be a predictor of the long-term clinical outcomes of elderly patients with AMI, which was superior to MHR and LDL-C/HDL-C.

Background The relationship between vasectomy and the risk of prostate cancer (PCa) remains unclear, with observational studies reporting inconsistent results. To clarify this ambiguity, we embarked on a comprehensive investigation comprising both a meta-analysis and a Mendelian randomization (MR) study. This dual approach aimed to thoroughly examine not only the association but also the causality between undergoing a vasectomy and the subsequent risk of PCa. Methods Our systematic review meticulously examined cohort studies published until January 2024, employing a random effects model for the computation of relative risks (RR) and their 95% confidence intervals (CI). For MR Analysis, we leveraged aggregated data from the IEU Open GWAS database, investigating the correlation between genetic predisposition to vasectomy and PCa. We chose single nucleotide polymorphisms (SNPs) of European descent as instrumental variables (IVs) for this analysis. The primary method for calculating the odds ratios (ORs) and their 95% CIs was inverse variance weighting (IVW). Through sensitivity analysis, we confirmed the robustness of our findings. Results Our investigation synthesized data from 19 cohort studies, encompassing over four million participants. The combined analysis revealed a statistically significant link between vasectomy and an elevated risk of PCa across any grade (RR = 1.09; 95%CI: 1.05–1.14; P  = 0.001; I² = 83.3%). This association was observed for both localized PCa (RR = 1.08; 95% CI: 1.04–1.13; P  < 0.001; I² = 48.8%) and advanced PCa (RR = 1.07; 95% CI: 1.01–1.13; P  = 0.016; I² = 0%). Nonetheless, the discovery cohort MR Analysis indicated no genetic causal link between vasectomy and PCa (OR = 0.067; 95%CI = 0.002–1.535; P  = 0.09). A validation set in the Finnish population confirmed the robustness of the results. This conclusion remained consistent even after controlling for variables such as prostate-specific antigen (PSA) testing and body mass index (BMI), suggesting that while a statistical association exists, the genetic evidence does not support a causal relationship. Conclusion The cumulative analysis indicates a possible elevated risk of PCa in patients who have had a vasectomy. However, MR Analysis has not confirmed a direct causal link between vasectomy and PCa. This suggests that the association observed may not stem from direct causation, allowing for the continued consideration of vasectomy as a viable long-term contraceptive choice. Further research is imperative to uncover any factors that could potentially link vasectomy to an increased risk of prostate cancer, aiming to provide a more comprehensive understanding of the implications.

Background Digital leadership might be an innovative approach to decreasing the elevated rates of anxiety and depression symptoms among medical professionals, while also enhancing their psychological well-being. This emerging pathway may offer promising strategies to support the mental health of medical professionals. This study seeks to investigate the association among digital leadership, organizational identity, family-work conflict, and anxiety and depression symptoms, and further to uncover the underlying moderating mechanisms interplay. Methods A cross-sectional online survey with 657 valid data were collected from four tertiary hospitals in Harbin, Heilongjiang Province, China, with a response rate of 69.3%. The statistical analysis was conducted employing IBM SPSS Statistics 22.0. Hierarchical regression analysis was performed to scrutinize the pertinent factors associated with anxiety and depression symptoms among medical professionals, while also evaluating the moderating influence of organizational identity and family-work conflict on the nexus among those. Results The prevalence of anxiety and depression symptoms among medical professionals was 50.1%. Anxiety and depression symptoms were negatively correlated with digital leadership ( r = -0.278, p  < 0.01) and organizational identity (r  = − 0.318, p  < 0.01), and positively correlated with family-work conflict (r  = 0.445, p  < 0.01). Organizational identity ( β  = − 0.938, p  < 0.05) and family-work conflict (β  = 0.698, p  < 0.05) moderate the relationship between digital leadership and anxiety and depression symptoms; The results of the simple slope analysis indicated that high organizational identity and low family-work conflict strengthened the effect of digital leadership on anxiety and depression symptoms among Chinese medical professionals. Conclusions The prevalence of anxiety and depression symptoms among medical professionals was noted to be high. This study posits that strengthening digital leadership could apparently improve anxiety and depression symptoms among medical professionals. Moreover, it highlights the moderating role of organizational identity and family-work conflict in the relationship between digital leadership and anxiety and depression symptoms. These discoveries underscore the significance of implementing support and interventions to enhance the mental well-being of medical professionals, encompassing the cultivation of organizational identity, reduction of family-work conflict, and acknowledgment of the potential role of digital leadership in addressing mental health challenges.