Association between dysglycemia and the Charlson Comorbidity Index among hospitalized patients with diabetes

AimInpatient dysglycemia has been linked to short-term mortality, but longer-term mortality data are lacking. Our aim was to evaluate the association between inpatient dysglycemia and one-year mortality risk.MethodsRetrospective chart review of adults with diabetes hospitalized between 2015 and 2019. The Charlson Comorbidity Index (CCI) was used to estimate 1-year mortality risk, stratified into low (CCI ≤ 5) and high risk (CCI ≥6). Simple and multivariable logistic regression was used to evaluate the association between dysglycemic measures and high mortality risk.ResultsAmong 22,639 unique admissions, BG ≥ 180, ≥300, ≤70, <54 and <40 mg/dL were associated with adjusted odds of 1.43 (95 % CI, 1.33, 1.54), 1.58 (95 % CI, 1.48, 1.68), 2.16 (95 % CI, 2.01, 2.32), 2.58 (95 % CI, 2.32, 2.86), and 2.56 (95 % CI, 2.19, 2.99) for high mortality risk, respectively. Older age and Black race were positively associated with hyperglycemia and hypoglycemia. Myocardial infarction, congestive heart failure (CHF), and moderate to severe liver disease were most strongly associated with hyperglycemia, while renal disease, CHF, peripheral vascular disease, and peptic ulcer disease were most strongly associated with hypoglycemia.ConclusionsInpatient hypoglycemia and hyperglycemia were both positively associated with higher one-year mortality risk, with stronger magnitude of association observed for hypoglycemia. The association appears to be mediated mainly by presence of diabetes-related complications.     

Actin binding proteins,actin cytoskeleton and spermatogenesis – Lesson from toxicant models

Actin cytoskeleton is crucial to support spermatogenesis in the mammalian testis. However, the molecular mechanism(s) underlying changes of actin cytoskeletal organization in response to cellular events that take place across the seminiferous epithelium (e.g., self-renewal of spermatogonial stem cells, germ cell differentiation, meosis, spermiogenesis, spermiation) at specific stages of the epithelial cycle of spermatogenesis remain largely unexplored. This, at least in part, is due to the lack of suitable study models to identify the crucial regulatory proteins and to investigate how these proteins work in concert to support actin dynamics. Much of the information on the role of actin binding proteins in the literature, namely the actin bundling proteins, actin nucleation proteins and motor proteins, are either findings based on genetic models or morphological analyses. While this information is helpful to delineate the function of these proteins to support spermatogenesis, they are not helpful to identify the regulatory signaling proteins, the signaling pathways and the cascade of events to modulate actin cytoskeleton dynamics. Recent studies based on the use of toxicant models, both in vitro and in vivo, however, have bridged this gap by identifying putative regulatory and signaling proteins of actin cytoskeleton. Herein, we summarize and critically evaluate these findings. We also provide a hypothetical model by which actin cytoskeletal dynamics in Sertoli cells are regulated, which in turn supports spermatid transport across the seminiferous epithelium, and at the blood-testis barrier (BTB) during the epithelial cycle of spermatogenesis.     

Decline in skeletal muscle mass is associated with cognitive decline in type 2 diabetes mellitus

AimsTo examine the longitudinal association between skeletal muscle mass (SMM) loss and cognitive decline over time in type 2 diabetes mellitus (T2DM).MethodsWe conducted a prospective cohort study of 453 patients from SMART2D cohort with follow-up intervals of 1.6 to 6.4 years. Baseline and follow-up measurements included bio-impedance analysis (BIA) measure of skeletal muscle mass index (SMI) and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) measure of cognitive function. We examined the association between annual rate of SMI and RBANS scores using linear regression, adjusting for demographics, education, depression, clinical co-variables and presence of apolipoprotein E4 (APOE) _?4 allele.ResultsThe mean age of participants was 60.3 ± 7.4 years. Compared to patients with Tertile 1 SMI change, the group with greater SMI decline (Tertile 3 SMI change) experienced 0.30 decline in RBANS total score (95%CI ?0.57 to ?0.03; p = 0.030) in the adjusted analysis. RBANS scores for subdomains in immediate memory and visuo-spatial/construction were lower in Tertile 3 SMI change group with corresponding coefficients ?0.54 (95%CI ?1.01 to ?0.06; p = 0.026), and ?0.71 (95%CI ?1.30 to ?0.12; p = 0.019) respectively.ConclusionIn patients with T2DM, BIA measure of muscle mass loss over time was independently associated with cognitive decline globally and in the domains of memory and visuo-spatial/construction.     

Mmu-miR-92a-2-5p targets TLR2 to relieve Schistosoma japonicum-induced liver fibrosis

According to conservative estimates, >230 million people are infected with schistosomiasis,which becomes one of the most common parasitic diseases. This study focuses on investigating in vivo and in vitro effects of mmu-miR-92a-2-5p in Schistosoma japonicum-induced liver fibrosis by targeting TLR2. Through bioinformatic analysis, the overexpression of TLR2 and the down-regulation of mmu-miR-92a-2-5p were revealed in the progression of S. japonicum-induced liver fibrosis. BALB/C mice were taken advantage to construct normal control and schistosomiasis liver fibrosis (SLF) model. The mice in model groups were transfected recombinant lentivirus (Lenti-mmu-miR-92a-2-5p or Lenti-NC) to alter the expression of mmu-miR-92a-2-5p in vivo. HE and Masson staining were employed to observe the pathological changes and collagenous fibrosis. QRT-PCR showed that mmu-miR-92a-2-5p was decreased while TLR2 was elevated in the infected groups. However, lenti-mmu-miR-92a-2-5p group could inhibit liver fibrosis. Then the effect of mmu-miR-92a-2-5p on S. japonicum-induced liver fibrosis including cell apoptosis rates, proliferation and proteins related to liver fibrosis was examined in NIH-3T3 mouse embryonic fibroblasts. Moreover, the association between mmu-miR-92a-2-5p and TLR2 was detected by dual-luciferase reporter gene assay and the expression of cytokines IL-4, IFN-γ and TNF-α in SLF model was detected by ELISA. Further, the knockout of TLR2 in C57BL/6J mice was used to confirm the association between mmu-miR-92a-2-5p and TLR2. Thus, these findings demonstrated that mmu-miR-92a-2-5p inhibited S. japonicum-induced liver fibrosis by targeting TLR2 in vitro and in vivo.     

a-1, 2岩藻糖基转移酶II在肺鳞癌组织中的表达及对肺鳞癌细胞增殖的影响

目的：探讨a-1，2岩藻糖基转移酶II（FUT2）在肺鳞癌中的表达情况及其对肺鳞癌细胞增殖的影响。方法：应用UALCAN数据库分析FUT2在临床肺鳞癌患者组织中的差异表达及其与肺鳞癌患者临床TNM分期、年龄及性别因素的相关性；采用瞬时转染技术，将FUT2的shRNA质粒转染进H226细胞株中构建FUT2低表达的肺鳞癌细胞模型；利用CCK-8、平板克隆及Western blot实验检测FUT2对肺鳞癌细胞的生长、单克隆细胞团形成及PCNA蛋白表达的影响。结果：FUT2在肺鳞癌尤其是肺鳞癌TNM早中期呈现高表达趋势（P＜0.05），而与年龄和性别无关。低表达FUT2可以抑制肺鳞癌细胞的生长速率和单克隆细胞团的形成数，同时，可以抑制肺鳞癌细胞PCNA蛋白的表达水平，差异均有统计学意义（P＜0.05）。结论：FUT2在肺鳞癌中高表达且促进肺鳞癌细胞的增殖能力，有望成为肺鳞癌的早期诊断指标。     

后路枕骨髁螺钉技术研究进展

正枕骨、寰椎和枢椎共同构成了枕颈部活动的结构功能单位,即枕颈交界区~([1-2])。炎症、创伤、肿瘤及畸形等因素会导致枕颈交界区失稳,从而引起颈脊髓或神经根的损伤、麻痹及难以忍受的疼痛,甚至危及生命~([3-4])。后路内固定融合技术是治疗枕颈部失稳的重要手段,目前常用术式为枕骨螺钉技术,该技术较钢丝固定技术有更好的生物力学稳定