Effects of a long-term operation wetland for wastewater treatment on the spatial pattern and function of microbial communities in groundwater.

Constructed wetlands have been used globally for wastewater treatment owing to low energy inputs and operating costs. However, the impact of their long-term operation on groundwater microbial communities is still unclear. This study aims to investigate the effects and further reveal the linkage between a large-scale surface flow constructed wetland (in operation for 14 years) and groundwater. Changes in the characteristics of groundwater microbial communities and their potential influencing factors were studied based on hydrochemical analysis, Illumina MiSeq sequencing, and multivariate statistical analysis methods. Results show that the long-term operation wetland significantly elevated groundwater nutrient levels and increased the risk of ammonia nitrogen pollution compared to background values. An apparent heterogeneity of microbial communities exhibited in the vertical direction and a similarity in the horizontal direction. Wetland operations substantially altered the structure of microbial communities at 3, 5, and 12 m depths, particularly a reduced abundance of denitrifying and chemoheterotrophic functional genera. The formation and evolution of groundwater microbial community structure mainly subjected to the contributions of dissolved oxygen (33.70%), total nitrogen (21.40%), dissolved organic carbon (11.09%), and pH (10.60%) variations resulted from the wetland operation and largely differed in depths. A combined effect of these factors on the groundwater should be concerned for such a long-term running wetland system. This study provides a new insight into the responses of groundwater microbial community structure driving by wetland operation and a better understanding of corresponding variation of microbial-based geochemical processes.

Left atrial morpho-functional remodeling in atrial fibrillation assessed by three dimensional speckle tracking echocardiography and its value in atrial fibrillation screening.

BACKGROUND: Three dimensional speckle tracking echocardiography (3D STE) is a novel technique combining 3D echocardiography and speckle tracking analysis. 3D STE software dedicated to the left atrium (LA) was recently available. Our study aimed to assess (1) atrial fibrillation (AF) related LA morpho-functional remodeling using 3D STE and (2) value of LA function parameters in identifying paroxysmal AF (PAF). METHODS: One hundred thirty-nine PAF, 109 persistent AF (Per-AF) and 59 non-AF subjects underwent 3D STE. LA phasic volumes and total LA emptying fraction (LAEF) were obtained and used to calculate passive (pLAEF) and active LA emptying fraction (aLAEF) based on atrial contraction. LA longitudinal and circumferential strain representing reservoir (LASr/LASrc), conduit (LAScd/LAScdc) and pump (LASct/LASctc) function were also assessed. RESULTS: 3D STE was found to have good reproducibility. Increase of LA volumes and decrease of parameters representing LA reservoir and pump function were independently associated with AF as well as AF burden. The correlations between LA emptying fraction and LA circumferential strain representing the same function were always stronger than those with LA longitudinal strain (p < 0.001). Minimal LA volume, LAEF, aLAEF, LASrc and LASctc can be used to accurately differentiate PAF from non-AF subjects (AUC > 0.8) with great sensitivity and specificity. CONCLUSIONS: Assessing LA remodeling in AF using 3D STE was feasible. AF and AF burden were independently associated with LA enlargement and impairment of reservoir and pump function but not conduit function. LA function parameters can indicate underlying PAF and thus can guide AF screening strategy.

The different risk factors for isolated diastolic hypertension and isolated systolic hypertension: a national survey.

BACKGROUND: Hypertension is highly prevalent and is one of the modifiable risk factors for cardiovascular outcomes. Isolated diastolic hypertension (IDH), however, tends to be ignored due to insufficient recognition. We sought to depict the clinical manifestation of IDH and isolated systolic hypertension (ISH) to find a more efficient way to improve the management. METHODS: Patients with primary hypertension aged over 18 years were investigated from all over the country using convenience sampling during 2017-2019. IDH was defined as systolic blood pressure (SBP) < 140 mmHg and diastolic blood pressure (DBP) ≥90 mmHg. ISH was defined as SBP ≥ 140 mmHg and DBP < 90 mmHg. RESULTS: A total of 8548 patients were screened, and 8475 participants were included. The average age was 63.67 ± 12.78 years, and males accounted for 54.4%. Among them, 361 (4.3%) had IDH, and 2096 had ISH (24.7%). Patients with IDH (54.84 ± 13.21 years) were much younger. Aging turned out to be negatively associated with IDH but positively associated with ISH. Multivariate logistic regression analysis showed BMI was a significant risk factor for IDH (OR 1.30, 95%CI 1.05-1.61, p = 0.018), but not for ISH (OR 1.05, 95%CI 0.95-1.16, p = 0.358). Moreover, smoking was significantly associated with IDH (OR 1.36, 95%CI 1.04-1.78, p = 0.026) but not with ISH (OR 1.04, 95%CI 0.90-1.21, p = 0.653). CONCLUSIONS: Patients with IDH were much younger, and the prevalence decreased with aging. BMI and smoking were remarkably associated with IDH rather than ISH. Keeping fit and giving up smoking might be particularly efficient in the management of young patients with IDH. TRIAL REGISTRATION: NCT03862183 , retrospectively registered on March 5, 2019.

Inhibition of TRPA1 Promotes Cardiac Repair in Mice After Myocardial Infarction.

Recent studies have shown that TRPA1, a nonselective cation channel with high permeability to calcium, is expressed in many tissues of the cardiovascular system and is involved in the pathogenesis of many cardiovascular diseases. However, the role of TRPA1 in cardiac repair after myocardial infarction (MI) has not been clearly defined. The aim of this study was to confirm whether inhibition of TRPA1 could attenuate MI-induced cardiac ischemia injury. The C57BL/6 mice were subjected to ligation of the left anterior descending coronary artery and treated with TRPA1-specific inhibitor HC-030031 (HC) for 4 weeks. Echocardiography was performed to assess cardiac function. The results showed that HC significantly attenuated MI-induced cardiac dysfunction 4 weeks after MI. Similarly, HC reduced cardiac fibrosis and cell apoptosis after MI and significantly increased angiogenesis in the border zone of the infarct. In vitro, we found that HC promoted the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Importantly, HC treatment decreased phosphatase and tensin homolog expression and augmented the expression of phosphorylated Akt in the myocardium post MI and HUVECs. However, treatment of HUVECs with a PI3K inhibitor, LY294002, before HC administration almost completely abolished HC-induced migration in HUVECs. In conclusion, we demonstrate that the inhibition of TRPA1 promotes angiogenesis after MI, thereby alleviating myocardial ischemia injury via mechanisms involving inhibition of phosphatase and tensin homolog expression and subsequent activation of the PI3K/Akt signaling.

A stricter control of low-density lipoprotein is necessary for thrombosis reduction in "lower thrombosis risk" patients with atrial fibrillation: a multicenter retrospective cohort study.

Patients with atrial fibrillation (AF) are associated with increased thrombotic events. Our previous case-control study showed low-density lipoprotein cholesterol (LDL-C) was an independent predictor of ischemic stroke in AF patients. To investigate the risks of thrombosis in relation to LDL-C among AF patients at different stroke risks by long-time follow-up. Atrial fibrillation patients without history of thrombosis enrolled from five hospitals were classified into low-risk (LR) and high-risk (HR) group according to CHA2DS2VASc score and followed up with a median period of 26 months. Univariate and multivariate logistic regression analysis were performed in each group. The best cut-off value calculated by receiver operating characteristic (ROC) analysis was used to divide patients into low LDL-C (L-LDL) and high LDL-C (H-LDL) subgroups. Propensity score matching (PSM) and inverse probability of treatment weighted (IPTW) were utilized in both subgroups, after which Kaplan-Meier curves for thrombosis were performed. Univariate and multivariate analysis showed LDL-C was significantly related to thrombosis in LR, but less significantly in HR group. The best cut-off value was 2.155 mmol/L in LR and 2.795 mmol/L in HR group. Lower LDL-C was associated with decreased thrombosis in both groups by PSM and IPTW. Kaplan-Meier curves displayed that H-LDL subgroup was at higher thrombosis risk with significant difference at 24th month in LR patients. LDL-C independently predicts thrombosis with different cut-off values in AF patients at different risks. A stricter control of LDL-C level is necessary for thrombosis reduction in patients with lower score.

miR-221-3p inhibits oxidized low-density lipoprotein induced oxidative stress and apoptosis via targeting a disintegrin and metalloprotease-22.

Oxidized low-density lipoprotein (ox-LDL)-induced oxidative stress and apoptosis are considered as a critical contributor to atherosclerosis. MicroRNAs (miRNAs) have been reported versatile functions in all biological processes via directly suppressing target messenger RNA at a posttranscriptional level. Although miRNA-221 has been implied to be involved in the regulation of atherosclerosis, the underlying mechanism remains unclear. Here, we showed that ox-LDL treatment remarkably suppressed the expression of miR-221-3p in a concentration-dependent and time-dependent manner. Transfection of miR-221-3p mimic significantly reduced the foam cell formation and expression of lipid biomarkers, while transfection of the miR-221-3p inhibitor showed completely opposite effects. Moreover, miR-221-3p was also found to inhibit the process of cell apoptosis in macrophages. A disintegrin and metalloprotease-22 (ADAM22) is predicted as a direct target of miR-221-3p, and silencing AMAM22 resulted in a reduced foam cell formation and cell apoptosis. Furthermore, silencing AMAM22 restored the stimulatory effect of the miR-221-3p inhibitor in ox-LDL-induced foam cell formation and apoptosis. These findings suggest that miR-221-3p inhibits ox-LDL and apoptosis via directly targeting ADAM22.

The association of metabolic syndrome components and chronic kidney disease in patients with hypertension.

BACKGROUND: Hypertension is a highly prevalent disease and the leading cause of chronic kidney disease (CKD). Metabolic syndrome could also be the risk factor for CKD. We sought to study the association between metabolic syndrome components and the prevalence of CKD in patients with hypertension. METHODS: We carried out a multi-center cross-sectional study from Apr. 2017- Apr. 2018 in 15 cities in China. RESULTS: A total of 2484 patients with hypertension were enrolled. Among them, 56% were male and the average age was 65.12 ± 12.71 years. The systolic BP/diastolic BP was 142 ± 18/83 ± 12 mmHg. Metabolic syndrome components turned out to be highly prevalent in patients with hypertension, ranging from 40 to 58%. The prevalence of chronic kidney disease reached 22.0%. Multi-variate logistic analysis revealed that elevated triglyceride (TG) (OR = 1.81, 95% CI 1.28-2.57, p < 0.01), elevated fasting blood glucose (FBG) (OR = 1.43, 95% CI 1.00-2.07, p = 0.05) and hypertension grades (OR = 1.20, 95% CI 1.00-1.44, p = 0.05) were associated with the prevalence of CKD. In sub-group analysis, elevated TG remained strongly associated with CKD in both diabetes (OR = 2.10, 95%CI 1.22-3.61, p < 0.01) and non-diabetes (OR = 1.53, 95% CI 1.09-2.16, p = 0.01). In sub-group analysis of hypertension grades, there was also a graded trend between elevated TG and CKD from controlled blood pressure (BP) to hypertension grade 2 (OR = 1.81, 95%CI 1.06-3.11, p = 0.03; OR = 1.85, 95%CI 1.00-3.43, p = 0.05; OR = 2.81, 95% CI 1.09-7.28, p = 0.03, respectively). CONCLUSION: Elevated TG, elevated FBG and hypertension grades were significantly associated with the prevalence of CKD in patients with hypertension. Particularly, elevated TG was strongly associated with CKD, independent of diabetes and hypertension grades.

Urocortin-2 suppression of p38-MAPK signaling as an additional mechanism for ischemic cardioprotection.

Urocortin-2 (UCN2) is cardioprotective in ischemia/reperfusion injury (I/R) through short-lived activation of ERK1/2. Key factors involved in I/R, e.g. apoptosis, mitochondrial damage, p38 kinase, and Bcl-2 family, have not been well-investigated in UCN2-induced cardioprotection. We assessed the role of p38-MAPK in anti-apoptotic Bcl-2 signaling and mitochondrial stabilization as a putative mechanisms in UCN2-induced cardioprotection. Isolated hearts from adult Sprague-Dawley rats and cultured H9c2 cells were subjected to I/R protocols with or without 10 nM UCN2 treatment. The effect of a specific p38 inhibitor SB202190 was tested in H9c2 cells. Cardiac function, LDH release, and mitochondrial membrane potential (MMP) were used to assess the degree of myocardial injury in hearts and H9c2 cells. Post-perfusion, hearts were collected for Western blot analyses or mitochondria/cytosol isolation to analyze p38 activation and Bcl-2 family members. UCN2 treatment improved rate-pressure product (58 ± 5 vs. 31 ± 4 % of Baseline; P < 0.05) and decreased LDH release (20 ± 9 vs. 90 ± 40 mU/ml LDH, P < 0.01) at the end of 60 min reperfusion. UCN2 reduced phospho-p38 levels and Bax activation. UCN2 increased the expression of Bcl-2 and inhibited the accumulation of p-Bim. With additional experiments, it was confirmed that UCN2 increases the phosphorylation of ERK1/2 in the early phase of UCN2 treatment and increases the overshot recovery of ERK1/2 phosphorylation during reperfusion. UCN2 and SB202190 partially prevented the loss of MMP induced by I/R. However, combined treatment with UCN2 and SB202190 did not provide additive benefit. UCN2 is cardioprotective in I/R in association with reduced phosphorylation of p38 together with the increased ERK1/2 activation and increased Bcl-2 family member pro-survival signaling. These changes may stabilize cardiac mitochondria, similar to p38 inhibitors, as part of a pro-survival mechanism during I/R.

Salidroside attenuates myocardial ischemia-reperfusion injury via PI3K/Akt signaling pathway.

To investigate the cardioprotective effects of salidroside on myocardial ischemia-reperfusion injury (IRI) in rabbits and the underlying action mechanisms in PI3K/Akt signaling pathway, a rabbit ischemia/reperfusion model was created by ligating the left anterior descending coronary arterial branch for 30 min and by releasing the ligature to allow reperfusion for 120 min. Salidroside or salidroside+PI3K inhibitor (LY294002) was administered via intracoronary injections at the onset of reperfusion. Apoptosis of cardiomyocytes was assessed by terminal dUTP nick-end labeling assay, and the expression of apoptosis-related proteins was observed by immunohistochemistry. The expressions of total Akt and phosphorylated Akt (p-Akt) were detected by western blot analysis. The results showed that intracoronary injection of salidroside at the onset of reperfusion markedly reduced the apoptosis of cardiomyocytes, significantly increasing Bcl-2 and p-Akt proteins expressions and decreasing Bax and caspase-3 expressions in the hearts subjected to ischemia followed by 120-min reperfusion. However, the anti-apoptotic effect induced by salidroside was inhibited by LY294002, which blocked the activation of Akt. These results suggested that intracoronary administration of salidroside at the onset of reperfusion could significantly reduce the IRI-induced apoptosis of cardiomyocytes, and this protective mechanism seemed to be mediated by the PI3K-Akt signaling pathway.

[Response of Organic Carbon Loss to Soil Erosion and Its Drivers: A Meta-analysis].

Soil erosion is the main driving force of soil organic carbon (SOC) loss and plays an important role in the global carbon cycle. It is helpful to understand the mechanism of SOC loss under soil erosion by evaluating the main driving factors of SOC loss under soil erosion and their influence degree. Therefore, based on 24 cases published in domestic and foreign journals from 2007 to 2021, this study investigated the effects of soil erosion on SOC loss in China under different climatic factors (climate types, rainfall, and rainfall intensity) and soil factors (soil types, bulk density, and aggregate size) by using Meta-analysis. The results showed that:① compared with that under no erosion disturbance, the SOC content under erosion decreased significantly (overall decreased 16.0%), showing obvious negative response characteristics. ② Under the erosion background, the negative response degree of SOC to different factors was as follows:rainfall intensity (65.0%)>mean annual rainfall (24.3%)>soil types (21.4%)>bulk density (20.2%)>aggregate size (16.5%)>climate types (9.1%). ③ Principal component analysis showed that climate was the dominant factor affecting SOC loss, and rainfall intensity was again shown to be the key factor. In this study, the characteristics and influencing factors of SOC loss under soil erosion in China were analyzed, which provided theoretical reference for the systematic understanding of the role of soil erosion in the carbon cycle.

Tafolecimab in Chinese patients with non-familial hypercholesterolemia (CREDIT-1): a 48-week randomized, double-blind, placebo-controlled phase 3 trial.

Background: Tafolecimab, a fully human proprotein convertase subtilisin/kexin type 9 (PCSK9) monoclonal antibody developed for the treatment of hypercholesterolemia, demonstrated robust lipid-lowering efficacy and favorable safety in previous short-term studies. We aimed to assess the long-term efficacy and safety of tafolecimab in Chinese non-familial hypercholesterolemia (non-FH) patients. Methods: Non-FH patients at high or very-high cardiovascular risk with screening low-density lipoprotein cholesterol (LDL-C) level ≥1.8 mmol/L or non-FH patients with screening LDL-C level ≥3.4 mmol/L and on stable lipid-lowering therapy for at least 4 weeks, were randomized in a 2:2:1:1 ratio to receive subcutaneous tafolecimab 450 mg Q4W, tafolecimab 600 mg Q6W, placebo 450 mg Q4W, or placebo 600 mg Q6W, respectively, in the 48-week double-blind treatment period. The primary endpoint was the percent change from baseline to week 48 in LDL-C levels. Findings: A total of 618 patients were randomized and 614 patients received at least one dose of tafolecimab (n = 411) or placebo (n = 203). At week 48, tafolecimab induced significant reductions in LDL-C levels (treatment differences versus placebo [on-treatment estimand]: -65.0% [97.5% CI: -70.2%, -59.9%] for 450 mg Q4W; -57.3% [97.5% CI: -64.0%, -50.7%] for 600 mg Q6W; both P < 0.0001). Significantly more patients treated with tafolecimab achieved ≥50% LDL-C reductions, LDL-C < 1.8 mmol/L, and LDL-C < 1.4 mmol/L than placebo group at both dose regimens (all P < 0.0001). Furthermore, tafolecimab significantly reduced non-HDL-C, apolipoprotein B, and lipoprotein(a) levels. The most commonly-reported treatment emergent adverse events in the tafolecimab groups included upper respiratory infection, urinary tract infection and hyperuricemia. Interpretation: Tafolecimab dosed at 450 mg Q4W and 600 mg Q6W was safe and showed superior lipid-lowering efficacy versus placebo, providing a novel treatment option for Chinese hypercholesterolemia patients. Funding: This study was sponsored by Innovent Biologics, Inc.

Characteristics of various forms of phosphorus and their relationships in the sediments of Haizi Lake, China.

The phosphorus (P) distribution in the sediments of Haizi Lake from the middle reach of the Yangtze River region, China, was investigated using a sequential chemical extraction procedure. P forms and concentrations of sediment samples taken at 25 sites over the whole lake were measured. The relationships between various forms of P in sediments and dissolved P in the overlying water were also discussed. Results showed that the concentrations of total P (TP) in the sediments ranged from 404 to 670 mg kg⁻¹, with an average of 503 mg kg⁻¹. The exchangeable P (Ex-P), Al-bound P (Al-P), Fe-bound P (Fe-P), occluded P (Oc-P), authigenic carbonate fluorapatite + biogenic apatite + CaCO3-associated P (ACa-P), detrital apatite + other inorganic P (De-P) and organic P (Or-P) accounted for, on average, 0.52, 0.04, 10.9, 32.0, 7.4, 20.1 and 29.0% of TP, respectively. Relevance analysis indicated that Oc-P, ACa-P and De-P, as the majority forms of inorganic P, were less correlated to others. The significant correlations between Ex-P, Al-P, Fe-P, Or-P and TP suggested the probability of reciprocal transformation. It was suggested that Ex-P, Al-P, Fe-P, Or-P and TP in the sediments might be released easily to the water interface, resulting in sustained lake eutrophication.

Social support as a mediator of the relationship between forgiveness and post-traumatic growth in hemodialysis patients: A structural equation modeling approach.

Background: Post-traumatic growth (PTG) refers to the positive psychological changes experienced with individuals after struggling with highly challenging life circumstances. Forgiveness can facilitate positive outcomes such as reduced distress, anxiety, and depression. Many studies have tested the relationships among forgiveness, social support, and PTG; however, a mechanism of social support has not been completely explored in hemodialysis patients. Objective: To test the relationship between forgiveness and post-traumatic growth and verify the mediating factor of social support on the relationship between forgiveness and PTG in hemodialysis patients. Materials and methods: In a descriptive cross-sectional study using convenience sampling from March to May 2021, 497 hemodialysis patients from nine hospitals filled out the Perceived Social Support Scale (PSSS), Heartland Forgiveness Scale (HFS), Post-traumatic Growth Inventory (PTGI), and general information. Data were analyzed using SPSS, and structural equation modeling was used to explore the relationships among forgiveness, social support, and PTG. Results: Forgiveness was significantly positively associated with PTG (P < 0.01). The proposed model provided a good fit to the data. Social support was found to play a partial mediating role between forgiveness and PTG (a*b = 0.122, BCa 95% CI: 0.078∼0.181). Conclusion: The results imply that forgiveness significantly directly and indirectly is related to PTG. Forgiveness in hemodialysis patients should be detected and effectively managed to ameliorate positive effects on PTG. It is necessary for nurses to consider implementing forgiveness interventions with an emphasis on building social support strategies to help hemodialysis patients enhance their PTG.

Effects of active vitamin D on insulin resistance and islet ß-cell function in non-diabetic chronic kidney disease patients: a randomized controlled study.

PURPOSE: The purpose of the study is to observe the effects of active vitamin D supplementation on insulin resistance and islet ß-cell function (HOMA-ß) in patients with non-diabetic chronic kidney disease (NDCKD). METHODS: A total of 134 patients with NDCKD who met the inclusion criteria were enrolled in the prospective controlled study and categorized as such: 60 patients in the non-dialysis (ND) group; 36, hemodialysis (HD) group; and 38, peritoneal dialysis (PD) group. Each group was divided into two equal-numbered subgroups for vitamin D supplementation. Those in the experimental subgroups received calcitriol 0.5 ug/day orally, and were followed-up for 6 months. A total of 117 patients were followed-up, including 57 patients in the ND group; 29, HD group; and 31, PD group. Changes in the insulin resistance index (HOMA-IR) and HOMA-ß index were calculated and compared at the time of enrollment and after 1, 3, and 6 months of intervention. RESULTS: (1) Mean HOMA-IR value: In the ND group, mean HOMA-IR value of the experimental group significantly decreased compared with that of the control group after 3 months of intervention (P = 0.02). In the HD and PD groups, there was no statistical difference between the experimental and control groups (P > 0.05). (2) Mean HOMA-ß index: In the ND group, mean HOMA-ß index of the experimental group was higher than that of the control group after 1 month of active vitamin D treatment (P = 0.03), and, with an extended intervention time, the index gradually increased (P < 0.001). In the HD group, mean HOMA-ß index of the experimental group was higher than that of the control group after 3 months of active vitamin D treatment (P = 0.01). Among PD patients, mean HOMA-ß index of the patients in the experimental group was higher than that of the control group after 6 months of active vitamin D treatment (P = 0.02). CONCLUSIONS: Active vitamin D supplementation improved insulin resistance and HOMA-ß after 6 months in ND patients, but only improved HOMA-ß in the dialysis patients, with no significant effect on insulin resistance.

Is There a Diabetes-Kidney-Heart Continuum? Perspectives From the Results of the Cardiovascular and Renal Outcome Clinical Trials With SGLT2 Inhibitors.

Heart failure is associated with a substantial risk of mortality and morbidity. Findings from recent cardiovascular outcome trials have shown promise for sodium-glucose cotransporter-2 (SGLT2) inhibitors in preventing heart failure in patients with type 2 diabetes mellitus (T2DM). Notably, the benefits of SGLT2 inhibitors were consistent despite the presence of risk factors like atherosclerosis. Increasing evidence suggests that SGLT2 inhibitors may confer their cardioprotective effects through multiple mechanisms, ranging from improving cardiac and vascular performance to metabolism. The reduction of heart failure risk by SGLT2 inhibitors may also be attributed to the preservation of renal function. Indeed, renal insufficiency is a frequent comorbidity of patients with heart failure and T2DM; hence, the natriuretic and kidney protective effects offered by SGLT2 inhibitors may contribute to limiting adverse cardiac outcomes. In this article, we discuss the latest findings from the cardiovascular and renal outcome trials, paying special attention to the interlink between heart and kidney function, and how effective treatment of heart failure-irrespective of T2DM diagnosis-may require agents that offer both cardiac and renal protection.

The Integrated Management of Hypertension in General Hospitals and Community Hospitals.

PURPOSE: We sought to investigate and improve the integrated management of hypertension in general and community hospitals in China. PATIENTS AND METHODS: We carried out a cross-sectional study in 90 centers from 15 cities in China from 2017 to 2018. Patients with primary hypertension were included. RESULTS: Of the total 4286 patients included, 43.2% of them controlled blood pressure (BP) below 140/90 mmHg while only 11.5% controlled BP below 130/80 mmHg. The control rate of low-density lipoprotein-C (LDL-C) in patients with concomitant coronary artery disease (CAD), diabetes (DM), and chronic kidney disease (CKD) was 24.7%, 49.4%, and 40.6%, respectively. Thirty-one percent of the DM patients had HbA1c levels greater than 8% while 21.7% of the non-DM patients had HbA1c≥6.5%. The control rate of body mass index (BMI) was 54.4% in men and 59.8% in women. As compared to patients from community hospitals, patients from general hospitals had poorer control of BP<140/90 mmHg (OR 0.63, 95% CI 0.55-0.73, p<0.001), comparatively better attainment of LDL-C, particularly <1.8 mmol/L in CAD (OR 3.25, 95% CI 2.02-5.24, p<0.001), similar control of HbA1c < 8.0% in diabetes (OR 0.64, 95% CI 0.41-1.00, p=0.052) and comparatively worse achievement of BMI<25 kg/m2 (OR 0.72, 95% CI 0.63-0.83, p<0.001). CONCLUSION: The integrated management of hypertension needs to be improved. Besides LDL-C, the management of BP, blood glucose (BG), and BMI need to be strengthened in not only community hospitals but also general hospitals.

Salidroside Attenuates Doxorubicin-Induced Cardiac Dysfunction Partially Through Activation of QKI/FoxO1 Pathway.

Doxorubicin (DOX) is an effective chemotherapy. However, its usage has been associated with adverse effects. Salidroside (SAL) is an antioxidative drug, which confers protective effects against several diseases. Salidroside can attenuate cardiac dysfunction induced by DOX. Quaking (QKI) is identified as a protective factor that can inhibit cardiotoxicity medicated by DOX through the regulation of cardiac circular RNA expression. The present study investigated the role of QKI on the protective effect of SAL in the DOX-induced cardiotoxicity model. Results indicated that SAL attenuated DOX-induced adverse effects, including cardiac dysfunction, weight loss, and reactive oxygen species (ROS) production, and decreased the expression of BAX, caspase 3, and FoxO1. Also, it increased the Mn-SOD2 and QKI expression in vivo and in vitro. Furthermore, QKI knockdown suppressed anti-cardiotoxicity mediated by SAL. In conclusion, the results of the current study show that salidroside attenuates doxorubicin-induced cardiac dysfunction through activation of QKI/FoxO1 pathway.

Effects of Radix et Rhizoma Rhodiolae Kirilowii on expressions of von Willebrand factor, hypoxia-inducible factor 1 and vascular endothelial growth factor in myocardium of rats with acute myocardial infarction.

OBJECTIVE: To investigate the effects of Radix et Rhizoma Rhodiolae Kirilowii on angiogenesis and expressions of hypoxia-inducible factor 1alpha (HIF-1alpha), hypoxia-inducible factor 1beta (HIF-1beta) and vascular endothelial growth factor (VEGF) in myocardium of rats with acute myocardial infarction (AMI), to elucidate the possible mechanism of Radix et Rhizoma Rhodiolae Kirilowii in promoting angiogenesis, and to investigate that whether or not salidroside could be considered as the effective component of Radix et Rhizoma Rhodiolae Kirilowii with regard to the effects mentioned above. METHODS: Thirty-six male Wistar rats had the anterior descending branch of coronary artery ligated as AMI model. Rats were fed with normal saline (untreated group), Radix et Rhizoma Rhodiolae Kirilowii solution (Radix et Rhizoma Rhodiolae Kirilowii group) or salidroside solution (salidroside group) from 7 days before until 7 days after the operation, with twelve rats in each group. All rats were sacrificed 7 days after the operation. Immunohistochemical assay (IHC) was used for detecting the expression of von Willebrand factor (vWF); TaqMan real-time quantitative polymerase chain reaction (PCR) assay was employed for detection of the levels of HIF-1alpha, HIF-1beta and VEGF mRNAs; Western blot analysis was used for detection of the corresponding protein levels. RESULTS: Results of IHC index showed that both at infarct border zone and non-infarct zone, the expressions of vWF were significantly increased in Radix et Rhizoma Rhodiolae Kirilowii group as compared with the untreated group (P<0.05). The expressions of HIF-1alpha, HIF-1beta and VEGF mRNAs and the expressions of HIF-1alpha and VEGF proteins were significantly increased in the Radix et Rhizoma Rhodiolae Kirilowii group as compared with the untreated group (P<0.01). The level of HIF-1beta protein in the Radix et Rhizoma Rhodiolae Kirilowii group was also higher than that in the untreated group but the difference was not statistically significant (P>0.05). All the expression levels, including those of vWF, HIF-1alpha, HIF-1beta and VEGF, in the salidroside group were higher than those in the untreated group while lower than those in the Radix et Rhizoma Rhodiolae Kirilowii group. CONCLUSION: Radix et Rhizoma Rhodiolae Kirilowii may promote angiogenesis in myocardium of rats with AMI through elevating the expressions of HIF-1alpha, HIF-1beta, and VEGF. Salidroside may be one of the effective components in Radix et Rhizoma Rhodiolae Kirilowii, which increases the expressions of HIF-1alpha, HIF-1beta and VEGF during ischemia or hypoxia.

Salidroside prevents tumor necrosis factor-α-induced vascular inflammation by blocking mitogen-activated protein kinase and NF-κB signaling activation.

Vascular inflammation is a key factor in the pathogenesis of atherosclerosis. Salidroside is an important active ingredient extracted from the root of the Rhodiola rosea plant, which has been reported to have antioxidative, anti-cancer, neuroprotective and cardioprotective effects. However, the effects of salidroside on vascular inflammation have not been clarified. The purpose of the present study was to investigate the protective effects of salidroside against tumor necrosis factor (TNF)-α-induced vascular inflammation in cardiac microvascular endothelial cells (CMECs), a specific cell type derived from coronary micro-vessels. Over a 24-h period, salidroside did not exert any significant cytotoxicity up to a dose of 100 µM. Additionally, salidroside decreased the expression levels of the cell adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-stimulated CMECs, thus suppressing monocyte-to-CMEC adhesion. Salidroside also decreased the production of inflammatory cytokines such as interleukin (IL)-1ß, IL-6 and monocyte chemotactic protein 1 (MCP-1) in TNF-α-induced CMECs, as well as suppressing TNF-α-activated mitogen-activated protein kinase (MAPK) and NF-κB activation. Since MAPKs and NF-κB both serve notable roles in regulating the expression of VCAM-1, IL-1ß, IL-6 and MCP-1, the present study provided a preliminary understanding of the mechanism underlying the protective effects of salidroside. Overall, salidroside alleviated vascular inflammation by mediating MAPK and NF-κB activation in TNF-α-induced CMECs. These results indicated that salidroside may have potential applications as a therapeutic agent against vascular inflammation and atherosclerosis.

[Preliminary investigation on Paragonimus in Lvchun county of Yunnan province].

69 crabs were collected from Daxing, Gekui and Niukong townships of Lvchun county, Yunnan Province in 2006 and excysted metacercariae were only obtained from crabs of Niukong. The infection rate was 27.6% (8/29) with an average metacercaria number of 2.25 each crab. No encysted metacercariae were found. The excysted metacercariae were morphologically identified as Paragonimus proliferus.