The relationship between mean platelet volume lymphocyte ratio and collateral circulation in patients with chronic total coronary occlusion.

Objective: To correlate mean platelet volume lymphocyte ratio (MPVLR) and coronary collateral circulation (CCC) in patients with chronic total occlusion (CTO). Materials and methods: A total of 643 patients who were hospitalized at a single large academic medical center from January 2020 to October 2021 and had CTO lesions in at least one major coronary artery confirmed by coronary angiography were retrospectively analyzed. Patients were divided according to the Rentrop criteria into poorly formed CCC (Rentrop grade 0-1, n = 235) and well-formed CCC (Rentrop grade 2-3, n = 408) groups. Mean platelet volume lymphocyte ratio (MPVLR) was calculated from routine laboratory data (MPV divided by lymphocyte count). The clinical data of the two groups were compared, and relationships between MPVLR and CCC formation were analyzed. Results: The MPVLR of patients with poorly formed CCC was significantly higher than that of patients with well-formed CCC (7.82 ± 3.80 vs. 4.84 ± 1.42, P < 0.01). The prevalence of diabetes mellitus and C-reactive protein levels were significantly higher in the poor CCC group than in the good CCC group (P < 0.01), while the proportions of patients with CTO or multivessel lesions in the right coronary artery were significantly lower in the poor CCC group than in the good CCC group (P < 0.01). Multivariate logistic regression analysis identified MPVLR (OR: 2.101, 95% CI: 1.840-2.399, P < 0.01), C-reactive protein level (OR: 1.036, 95% CI: 1.008-1.064, P < 0.05), a history of diabetes mellitus (OR: 2.355, 95% CI: 1.532-3.621, P < 0.01), and right coronary CTO ratio (OR: 0.313, 95% CI: 0.202-0.485, P < 0.01) as independent risk factors for CCC formation. The area under the ROC curve of MPVLR for predicting poorly formed CCC was 0.82 (95% CI: 0.784-0.855, P < 0.01), the best cut-off point was 6.02 and the sensitivity and specificity of MPVLR for predicting poorly formed CCC were 72.3 and 82.4%, respectively. Conclusion: In patients with coronary CTO, MPVLR was negatively correlated with CCC and a high MPVLR level was an independent predictor of poorly formed CCC.

A Comparative Study of the Clinical Benefits of Rivaroxaban and Warfarin in Patients With Non-valvular Atrial Fibrillation With High Bleeding Risk.

OBJECTIVE: To compare the clinical benefits of rivaroxaban and warfarin in patients with non-valvular atrial fibrillation (NVAF) with high bleeding risk. METHODS: A retrospective study was conducted on patients with high bleeding risk NVAF who were hospitalized at the First Affiliated Hospital of Zhengzhou University between May 31, 2016 and May 31, 2019 and took at least rivaroxaban and warfarin. The clinical benefits of both drugs were assessed by efficacy benefit and safety risk. The primary efficacy benefit was a composite end point for stroke (both ischemic and hemorrhagic) and systemic embolism. The secondary efficacy end points were death and myocardial infarction (MI). The principal safety end point was the composite end point of fatal bleeding and critical organ bleeding. RESULTS: A total of 1,246 patients with high bleeding risk were enrolled, including 787 patients in the rivaroxaban group and 459 patients in the warfarin group. Results of the primary efficacy benefit endpoint were obtained from 104 patients (13.2%) in the rivaroxaban group and 88 (19.2%) patients in the warfarin group (hazard ratio [HR]: 0.681; 95% confidence interval [CI]: 0.512-0.906; P < 0.001 for non-inferiority). The principal safety end points were observed in 49 (6.23%) patients in the rivaroxaban group and in 55 (11.98%) patients in the warfarin group (HR: 0.469 in the rivaroxaban group; 95% CI: 0.314-0.702; P < 0.001). With respect to secondary efficacy and benefit endpoints, 28 (3.56%) patients in the rivaroxaban group and 22 (4.79%) patients in the warfarin group died, with an HR of 0.760 (95% CI: 0.435-1.329; P = 0.336); 32 (4.07%) patients in the rivaroxaban group; and 26 (5.66%) patients in the warfarin group had MI, with an HR of 1.940 (95% CI: 0.495-1.069, P = 0.254) in the rivaroxaban group. CONCLUSIONS: Rivaroxaban is non-inferior to warfarin in the prevention of stroke and systemic embolism in patients with high blood NVAF. Rivaroxaban is superior to warfarin in reducing fatal bleeding and bleeding in critical organs. CLINICAL TRIAL REGISTRATION: Chinese Clinical Trials Registry, identifier ChiCTR2100052454.

Characterization, isolation, and culture of spermatogonial stem cells in Macaca fascicularis.

Spermatogonial stem cells (SSCs) have great applications in both reproductive and regenerative medicine. Primates including monkeys are very similar to humans with regard to physiology and pathology. Nevertheless, little is known about the isolation, the characteristics, and the culture of primate SSCs. This study was designed to identify, isolate, and culture monkey SSCs. Immunocytochemistry was used to identify markers for monkey SSCs. Glial cell line-derived neurotrophic factor family receptor alpha-1 (GFRA1)-enriched spermatogonia were isolated from monkeys, namely Macaca fascicularis (M. fascicularis), by two-step enzymatic digestion and magnetic-activated cell sorting, and they were cultured on precoated plates in the conditioned medium. Reverse transcription-polymerase chain reaction (RT-PCR), immunocytochemistry, and RNA sequencing were used to compare phenotype and transcriptomes in GFRA1-enriched spermatogonia between 0 day and 14 days of culture, and xenotransplantation was performed to evaluate the function of GFRA1-enriched spermatogonia. SSCs shared some phenotypes with rodent and human SSCs. GFRA1-enriched spermatogonia with high purity and viability were isolated from M. fascicularis testes. The freshly isolated cells expressed numerous markers for rodent SSCs, and they were cultured for 14 days. The expression of numerous SSC markers was maintained during the cultivation of GFRA1-enriched spermatogonia. RNA sequencing reflected a 97.3% similarity in global gene profiles between 0 day and 14 days of culture. The xenotransplantation assay indicated that the GFRA1-enriched spermatogonia formed colonies and proliferated in vivo in the recipient c-KitW/W (W) mutant mice. Collectively, GFRA1-enriched spermatogonia are monkey SSCs phenotypically both in vitro and in vivo. This study suggests that monkey might provide an alternative to human SSCs for basic research and application in human diseases.

[Curcumin inhibits iron overload-induced hepatocytic apoptosis and nuclear factor-κB activity].

OBJECTIVE: Iron is an essential micronutrient for human beings but its overload induces various diseases of liver, the main body storage site for iron, such as liver fibrosis. Curcumin is a natural polyphenol derived from turmeric and has been used widely. Its pharmacological action has attracted great attention in recent years. The apoptosis of rat cultured hepatocytes was induced by FeNTA (ferric nitrilotriacetate)-induced Iron overload. The present study was to examine the effect of curcumin at low concentrations on FeNTA-induced apoptosis of hepatocytes and elucidate the underlying mechanisms. METHODS: After the incubation of hepatocytes with 100 µmol/L FeNTA in the presence or absence of 1 - 10 µmmol/L of curcumin, a series of analyses were performed, including the analyses of hepatocytic apoptosis, the expressions of proteins relating with the regulations of cell apoptosis, caspase-3 activity, the production of reactive oxygen species (ROS) and nuclear factor NF-κB activity. RESULTS: Curcumin reduced the FeNTA-induced hepatocytic apoptosis by 46.65% and significantly down-regulated the protein levels of Bcl-2 and Bcl-XL. In contrast, it had no effect on the protein levels of Bax and Bad. The curcumin treatment reduced FeNTA-caused production of ROS and caspase-3 activity by 45.01% and 59.71% respectively. And the NF-κB activity was also inhibited. CONCLUSION: Curcumin at low concentrations reduces iron overload-caused hepatocytic apoptosis and NF-κB activity, the key regulatory transcription factor for the inflammation-related gene expression in cultured hepatocyte.