Heart rate deceleration and acceleration capacities associated with circadian rhythm of blood pressure in essential hypertension.

BACKGROUND: This study aimed to investigate the potential association between the circadian rhythm of blood pressure and deceleration capacity (DC)/acceleration capacity (AC) in patients with essential hypertension. METHODS: This study included 318 patients with essential hypertension, whether or not they were being treated with anti-hypertensive drugs, who underwent 24-hour ambulatory blood pressure monitoring (ABPM). Patients were categorized into three groups based on the percentage of nocturnal systolic blood pressure (SBP) dipping: the dipper, non-dipper and reverse dipper groups. Baseline demographic characteristics, ambulatory blood pressure monitoring parameters, Holter recordings (including DC and AC), and echocardiographic parameters were collected. RESULTS: In this study, the lowest DC values were observed in the reverse dipper group, followed by the non-dipper and dipper groups (6.46 ± 2.06 vs. 6.65 ± 1.95 vs. 8.07 ± 1.79 ms, P < .001). Additionally, the AC gradually decreased (-6.32 ± 2.02 vs. -6.55 ± 1.95 vs. -7.80 ± 1.73 ms, P < .001). There was a significant association between DC (r = .307, P < .001), AC (r=-.303, P < .001) and nocturnal SBP decline. Furthermore, DC (ß = 0.785, P = .001) was positively associated with nocturnal SBP decline, whereas AC was negatively associated with nocturnal SBP (ß = -0.753, P = .002). By multivariate logistic regression analysis, deceleration capacity [OR (95% CI): 0.705 (0.594-0.836), p < .001], and acceleration capacity [OR (95% CI): 1.357 (1.141-1.614), p = .001] were identified as independent risk factors for blood pressure nondipper status. The analysis of ROC curves revealed that the area under the curve for DC/AC in predicting the circadian rhythm of blood pressure was 0.711/0.697, with a sensitivity of 73.4%/65.1% and specificity of 66.7%/71.2%. CONCLUSIONS: Abnormal DC and AC density were correlated with a blunted decline in nighttime SBP, suggesting a potential association between the circadian rhythm of blood pressure in essential hypertension patients and autonomic nervous dysfunction.

Triglyceride-glucose index as a marker of adverse cardiovascular prognosis in patients with coronary heart disease and hypertension.

BACKGROUND: The triglyceride-glucose (TyG) index has been proposed as a potential predictor of adverse prognosis of cardiovascular diseases (CVDs). However, its prognostic value in patients with coronary heart disease (CHD) and hypertension remains unclear. METHODS: A total of 1467 hospitalized patients with CHD and hypertension from January 2021 to December 2021 were included in this prospective and observational clinical study. The TyG index was calculated as Ln [fasting triglyceride level (mg/dL) × fasting plasma glucose level (mg/dL)/2]. Patients were divided into tertiles according to TyG index values. The primary endpoint was a compound endpoint, defined as the first occurrence of all-cause mortality or total nonfatal CVDs events within one-year follow up. The secondary endpoint was atherosclerotic CVD (ASCVD) events, including non-fatal stroke/transient ischemic attack (TIA) and recurrent CHD events. We used restricted cubic spline analysis and multivariate adjusted Cox proportional hazard models to investigate the associations of the TyG index with primary endpoint events. RESULTS: During the one-year follow-up period, 154 (10.5%) primary endpoint events were recorded, including 129 (8.8%) ASCVD events. After adjusting for confounding variables, for per standard deviation (SD) increase in the TyG index, the risk of incident primary endpoint events increased by 28% [hazard ratio (HR) = 1.28, 95% confidence interval (CI) 1.04-1.59]. Compared with subjects in the lowest tertile (T1), the fully adjusted HR for primary endpoint events was 1.43 (95% CI 0.90-2.26) in the middle (T2) and 1.73 (95% CI 1.06-2.82) in highest tertile (T3) (P for trend = 0.018). Similar results were observed in ASCVD events. Restricted cubic spline analysis also showed that the cumulative risk of primary endpoint events increased as TyG index increased. CONCLUSIONS: The elevated TyG index was a potential marker of adverse prognosis in patients with CHD and hypertension.

Bioinformatics analysis of potential common pathogenic mechanisms for systemic lupus erythematosus and acute myocardial infarction.

BACKGROUND: Systemic lupus erythematosus (SLE) patients have a higher risk of acute myocardial infarction (AMI) compared to the general population. However, the underlying common mechanism of this association is not fully understood. This study aims to investigate the molecular mechanism of this complication. METHODS: Gene expression profiles of SLE (GSE50772) and AMI (GSE66360) were obtained from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (DEGs) in SLE and AMI were identified, and functional annotation, protein-protein interaction (PPI) network analysis, module construction, and hub gene identification were performed. Additionally, transcription factor (TF)-gene regulatory network and TF-miRNA regulatory network were constructed for the hub genes. RESULTS: 70 common DEGs (7 downregulated genes and 63 upregulated genes) were identified and were mostly enriched in signaling pathways such as the IL-17 signaling pathway, TNF signaling pathway, lipid metabolism, and atherosclerosis. Using cytoHubba, 12 significant hub genes were identified, including IL1B, TNF, FOS, CXCL8, JUN, PTGS2, FN1, EGR1, CXCL1, DUSP1, MMP9, and ZFP36. CONCLUSIONS: This study reveals a common pathogenesis of SLE and AMI and provides new perspectives for further mechanism research. The identified common pathways and hub genes may have important clinical implications for the prevention and treatment of AMI in SLE patients.

ST-segment elevation predicts the occurrence of malignant ventricular arrhythmia events in patients with acute ST-segment elevation myocardial infarction.

BACKGROUND: ST-segment elevation (STE) represents a repolarization dispersion marker underlying arrhythmogenesis in ST-segment elevation myocardial infarction (STEMI); however, its value for predicting malignant ventricular arrhythmia events (MVAEs) remains uncertain. METHODS: In total, 285 patients with STEMI and those with or without MVAEs who presented within 6 h of symptom onset were enrolled. The relationships between STE and clinical characteristics of MVAEs (defined as ventricular tachycardia or ventricular fibrillation) were analyzed using t-test, chi-square test, binary multivariate logistic regression, and receiver operating characteristic curve analysis. RESULTS: Patients with STEMI and MVAEs had a shorter time from symptom onset to balloon time (p = 0.0285) and greater STE (p < 0.01) than those without MVAEs. The symptom-to-balloon time, age, and STE were associated with MVAEs after stepwise regression analysis in all cases. Only STE was significantly associated with the occurrence of MVAEs (all, p < 0.01). The area under the curve (AUC) of STE for predicting MVAEs was 0.905, and the cut-off value was 4.5 mV. When only infarct-related arteries were included in the analysis, the AUC of the left anterior descending artery was 0.925 with a cut-off value of 4.5 mV, that of the right coronary artery was 0.915 with a cut-off value of 4.5 mV, and that of the left circumflex artery was 0.929 with a cut-off value of 4.0 mV. CONCLUSIONS: In patients with STEMI presenting within 6 h of symptom onset, age, symptom-to-balloon time, and STE were the main predictors for MVAEs. However, among these, STE was the strongest predictor for MVAEs and was an index for repolarization dispersion of cardiomyocytes in infarcted and non-infarcted areas.

Outcome of Impella 2.5 use in patients undergoing Percutaneous Coronary Intervention in Henan, China: a case series.

BACKGROUND: Acute myocardial infarction (AMI) complicated by cardiogenic shock (AMI-CS) or heart failure is associated with an unacceptably high in-hospital mortality of 33%-55% and a lost chance to accept PCI (Percutaneous Coronary Intervention). AIM: The aim of the study was to find out whether percutaneous hemodynamic support device Impella 2.5 improves prognosis of high-risk PCI patients or not. METHODS: This study was a case series involving six patients who underwent a Left Ventricular Assist Device (LVAD, Impella 2.5, Abiomed, Danvers, MA) implantation after suffering from AMI with a very low ejection fraction and acute heart failure. The clinical experience and outcomes of the patients are hereby discussed. RESULTS: All PCI procedures were safely completed under LVAD support. The hemodynamic parameters of all patients improved clinically over the next 30 days and following 12 months after Impella insertion except in two patients, of which one patient (Case number 6) died 4 days post-Impella protected PCI procedure due to acute left ventricle heart failure with cardiogenic shock and pulmonary oedema; and another one died at 12 months after Impella protected PCI procedure (Case number 4) due to decompensated heart failure and infected pneumonia. CONCLUSION: Percutaneous hemodynamic support is favorable and feasible during high risk Percutaneous Coronary Intervention (PCI). A bigger study is needed to substantiate the claims of the current study.

GAS5/METTL14/ESR1 genetic variants are related to the susceptibility of coronary heart disease.

The prevention and treatment of coronary heart disease (CHD) is a difficult problem to be solved urgently. Genetic factors play a crucial role in CHD development. This study aimed to investigate the association of GAS5/METTL14/ESR1 polymorphisms with CHD susceptibility. We carried out a case-control study that included 506 patients and 506 healthy subjects to detect the correlation between GAS5/METTL14/ESR1 polymorphisms and CHD risk in a Chinese population. Odds ratios (OR) and 95% confidence intervals (CI) were computed to assess the associations. Our study showed that GAS5 rs17359906 (OR 2.32, p = 0.020) and rs75315904 (OR 0.41, p = 0.039) were related to the risk of CHD in females. ESR1 rs6927072 (OR 1.76, p = 0.007) and rs4870061 (OR 0.74, p = 0.036) correlated with CHD risk in age ≤ 60 years. GAS5 rs17359906 (OR 0.10, p = 0.032) and ESR1 rs3020308 (OR 2.73, p = 0.041) were associated with an increased susceptibility to CHD in smokers. We also found that METTL14 rs4834698 (OR 1.57, p = 0.044) and ESR1 rs4870061 (OR 0.62, p = 0.040) were associated with CHD susceptibility in non-drinkers. Besides, METTL14 rs17050450 (OR 0.48, p = 0.029) and ESR1 rs3853248 (OR 1.61, p = 0.018) had the susceptibility of CHD patients with diabetes. Our study indicated that GAS5/METTL14/ESR1 polymorphisms were associated with CHD risk, which might provide a new understanding of CHD in a Chinese population.

Nomogram predicting the probability of spontaneous stone passage in patients presenting with acute ureteric colic.

OBJECTIVES: To develop a nomogram that could predict spontaneous stone passage (SSP) in patients presenting with acute ureteric colic who are suitable for conservative management. SUBJECT/PATIENTS: A 2517 patient dataset was utilised from an international multi-centre cohort study (MIMIC, A Multi-centre Cohort Study Evaluating the role of Inflammatory Markers In Patients Presenting with Acute Ureteric Colic) of patients presenting with acute ureteric colic across 71 secondary care hospitals in the United Kingdom, Ireland, Australia, and New Zealand. Inclusion criteria mandated a non-contrast CT-KUB. METHODS: SSP was defined as the 'absence of the need for intervention'. The model was developed using logistic regression and backwards selection (to achieve lowest AIC) in a subset from 2009-2015 (n=1728) and temporally validated on a subset from 2016-2017 (n=789). RESULTS: Of the 2517 patients, 1874 had SSP (74.5%). Mean age (±[SD]) was 47 (±14.7) years and 1892 were male (75.2%). At the end of the modelling process, gender: male (OR 0.8, 95%CI 0.64-1.01, p=0.07), neutrophil count (OR 1.03, 95%CI 1.00-1.06, p = 0.08), hydronephrosis (OR 0.79, 95%CI 0.59-1.05, p=0.1), hydroureter (OR 1.3, 95%CI 0.97-1.75, p =0.08), stone size >5-7mm (OR 0.2, 95%CI 0.16-0.25, p<0.0001), stone size >7mm (OR 0.11, 95%CI 0.08-0.15, p<0.001), middle ureter stone position (OR 0.59, 95%CI 0.43-0.81, p=0.001), upper ureter stone position (OR 0.31, 95%CI 0.25-0.39, p<0.001) ), medical expulsive therapy use (OR 1.36, 95%CI 1.1 - 1.67, p = 0.001), oral NSAID use (OR 1.3, 95%CI 0.99 - 1.71, p=0.06), and rectal NSAID use (OR1.17, 95%CI 0.9 - 1.53, p=0.24) remained. Concordance-statistic (C-statistic) was 0.77 (95%CI 0.75 - 0.80) and a nomogram was developed based on these. CONCLUSION: The presented nomogram is available to use as an online calculator via www.BURSTurology.com and could allow clinicians and patients to make a more informed decision on pursuing conservative management versus early intervention.

Renal Interstitial Fibrosis Is Reduced in High-Fat Diet-Induced Obese Pigs following Renal Denervation from the Intima and Adventitia of the Renal Artery.

BACKGROUND: This study aims to compare whether 2 different routes of renal denervation (RDN) from the intima and adventitia of the renal artery can reduce renal fibrosis in a pig model of hypertension induced by a high-fat diet and to explore possible molecular mechanisms. METHODS: Twenty-four Bama miniature pigs were randomly divided into a control group (normal diet, n = 6) or a hypertension model group (high-fat diet, n = 18). The model group was randomly divided into the intima-RDN group (n = 6), the adventitia-RDN group (n = 6), or the renal arteriography-only group (sham group, n = 6). All animals were fed separately. The model group was fed a high-fat diet after the operation, and the control group was fed conventionally for 6 months. After 6 months, renal artery angiography was performed again to observe the condition of the renal arteries, after which all animals were euthanized. The blood pressure and blood biochemical results of each group were evaluated 6 months after the operation; kidney tissue morphology and collagen fiber content were examined by hematoxylin-eosin staining and Masson staining; superoxide dismutase activity and the malondialdehyde content of kidney tissue were assessed by a biochemical enzyme method; the protein expression level of transforming growth factor-ß 1 (TGF-ß1), α-smooth muscle actin (α-SMA), and Smad3 was assessed by Western blot, and electron microscopy was used to examine changes in the kidney microstructure. RESULTS: After 6 months of a high-fat diet, the blood lipid levels of the model group were significantly higher compared to baseline and to that of the control group during the same period (all showed p < 0.05); the blood lipid levels of the control group did not change significantly from baseline (p > 0.05). The degree of glomerular damage caused by hyperlipidemia in the intima-RDN group and the adventitia-RDN group was significantly lower than that of the sham and control groups, and the renal fibrosis area percentage was also significantly lower (p < 0.05). Electron microscopy showed that both the intima-RDN group and the adventitia-RDN group had a more even distribution of chromosomes and less mitochondrial swelling compared with the sham group. CONCLUSION: RDN from the adventitia of the renal artery and RDN from the intima of the renal artery have the similar advantages of delaying high-fat-induced renal fibrosis. The antifibrotic effect of RDN may be related to inhibition of the TGF-ß1/Smad3 pathway.

Preliminary Study of Genome-Wide Association Identified Novel Susceptibility Genes for Hemorheological Indexes in a Chinese Population.

Background: Genome-wide association studies for various hemorheological characteristics have not been reported. We aimed to identify genetic loci associated with hemorheological indexes in a cohort of healthy Chinese Han individuals. Methods: Genotyping was performed using Applied Biosystems Axiom™ Precision Medicine Diversity Array in 838 individuals, and 6,423,076 single nucleotide polymorphisms were available for genotyping. The relations were examined in an additive genetic model using mixed linear regression and combined with identical by descent matrix. Results: We identified 38 genetic loci (p < 5 × 10-6) related to hemorheological traits. In which, LOC102724502-OLIG2 rs28371438 was related to the levels of nd30 (p = 8.58 × 10-07), nd300 (p = 1.89 × 10-06), erythrocyte rigidity (p = 1.29 × 10-06), assigned viscosity (p = 6.20 × 10-08) and whole blood high cut relative (p = 7.30 × 10-08). The association of STK32B rs4689231 for nd30 (p = 3.85 × 10-06) and nd300 (p = 2.94 × 10-06) and GTSCR1-LINC01541 rs11661911 for erythrocyte rigidity (p = 9.93 × 10-09) and whole blood high cut relative (p = 2.09 × 10-07) was found. USP25-MIR99AHG rs1297329 was associated with erythrocyte rigidity (p = 1.81 × 10-06) and erythrocyte deformation (p = 1.14 × 10-06). Moreover, the association of TMEM232-SLC25A46 rs3985087 and LINC00470-METTL4 rs9966987 for fibrinogen (p = 1.31 × 10-06 and p = 4.29 × 10-07) and plasma viscosity (p = 1.01 × 10-06 and p = 4.59 × 10-07) was found. Conclusion: These findings may represent biological candidates for hemorheological indexes and contribute to hemorheological study.

Distribution of phosphorus forms in surface soils of typical peatlands in northern Great Khingan Mountains and its potential to reconstruct paleo-vegetations.

Phosphorus was one of the nutrient limitations to vegetations in wetland ecosystem. In peatland, organic phosphorus is accumulated as vegetation residues in anaerobic conditions, affecting the contents of phosphorus pools for long time. It is unclear that different vegetations affect the contents of phosphorus and whether successions of vegetations could reflected by sedimentation of phosphorus forms. Phosphorus forms from six surface soils plots and four dominant vegetations in the north of the Great Khingan mountains were detected to investigate the differences of phosphorus forms of soil between different vegetations. Phosphorus forms and macrofossil were also detected in a 77-cm peat core (1-cm intervals) in TQ. A fingerprinting historical vegetations were reconstructed by phosphors forms to reflect successions of vegetations during 2200 cal yr BP in TQ area. The results showed that the main phosphorus forms in peatland were NaOH-Po and conc. HCl-Po. The percentages of inorganic phosphorus forms of trees were generally higher than other vegetations. Moss was more conducive for accumulation of organic phosphorus. NaHCO3-Pi, NaOH-Pi, conc. HCl-Po and Pi were selected into linear discrimination analysis. The vegetations reconstructed by phosphorus forms were strongly correlated with the pollen records of moss, herbs and shrubs, as well as with macrofossils in herbs. The fingerprinting of vegetations by phosphorus has potential geochemical reference to reflect the successions of vegetation in peatland.

MicroRNA-532-5p-programmed cell death protein 4 (PDCD4) axis regulates angiotensin II-induced human umbilical vein endothelial cell apoptosis and proliferation.

BACKGROUND: This study was carried out to investigate the effect of microRNA miR-532-5p on the proliferation of hypertension endothelial cells. METHODS: Angiotensin II (Ang II)-treated human umbilical vein endothelial cells (HUVECs) and primary human aortic endothelial cells (HAECs) were used as cell models to imitate the pathological changes in endothelial cells under hypertensive conditions. The expression levels of miR-532-5p and programmed cell death protein 4 (PDCD4) were detected by Quantitative Real-time PCR (qRT-PCR). The effects of miR-532-5p and PDCD4 on the proliferation of HUVECs and HAECs treated with Ang II were detected by Methyl Thiazolyl Tetrazolium (MTT) assay. The effects of miR-532-5p and PDCD4 on the apoptosis and cell cycle of HUVECs and HAECs treated with Ang II were detected by flow cytometry. Western blot was used to detect the expression levels of PDCD4, apoptosis-related proteins and cycle-related proteins in HUVECs and HAECs treated with Ang II. Bioinformatics analysis and Luciferase gene reporter assay were used to assess the relationship between miR-532-5p and PDCD4. RESULTS: The expression levels of miR-532-5p were reduced, while the expression levels of PDCD4 were raised in Ang II-treated HUVECs and HAECs. MiR-532-5p mimic and si-PDCD4 restrained the apoptosis, promoted the proliferation of Ang II-treated HUVECs and HAECs and caused S-phase arrest of cells. PDCD4 was identified as a potential target for miR-532-5p. Knockdown of PDCD4 significantly affected apoptosis and proliferation of Ang II-treated HUVECs. MiR-532-5p regulates apoptosis and proliferation of Ang II-induced HUVECs and HAECs. In addition, overexpression of PDCD4 attenuated the effect of miR-532-5p on the proliferation of Ang II-treated HUVECs and HAECs. CONCLUSION: MiR-532-5p inhibited the expression of PDCD4, thereby inhibiting apoptosis and promoting proliferation of Ang II-treated HUVECs and HAECs.

The IDENTIFY study: the investigation and detection of urological neoplasia in patients referred with suspected urinary tract cancer - a multicentre observational study.

OBJECTIVE: To evaluate the contemporary prevalence of urinary tract cancer (bladder cancer, upper tract urothelial cancer [UTUC] and renal cancer) in patients referred to secondary care with haematuria, adjusted for established patient risk markers and geographical variation. PATIENTS AND METHODS: This was an international multicentre prospective observational study. We included patients aged ≥16 years, referred to secondary care with suspected urinary tract cancer. Patients with a known or previous urological malignancy were excluded. We estimated the prevalence of bladder cancer, UTUC, renal cancer and prostate cancer; stratified by age, type of haematuria, sex, and smoking. We used a multivariable mixed-effects logistic regression to adjust cancer prevalence for age, type of haematuria, sex, smoking, hospitals, and countries. RESULTS: Of the 11 059 patients assessed for eligibility, 10 896 were included from 110 hospitals across 26 countries. The overall adjusted cancer prevalence (n = 2257) was 28.2% (95% confidence interval [CI] 22.3-34.1), bladder cancer (n = 1951) 24.7% (95% CI 19.1-30.2), UTUC (n = 128) 1.14% (95% CI 0.77-1.52), renal cancer (n = 107) 1.05% (95% CI 0.80-1.29), and prostate cancer (n = 124) 1.75% (95% CI 1.32-2.18). The odds ratios for patient risk markers in the model for all cancers were: age 1.04 (95% CI 1.03-1.05; P < 0.001), visible haematuria 3.47 (95% CI 2.90-4.15; P < 0.001), male sex 1.30 (95% CI 1.14-1.50; P < 0.001), and smoking 2.70 (95% CI 2.30-3.18; P < 0.001). CONCLUSIONS: A better understanding of cancer prevalence across an international population is required to inform clinical guidelines. We are the first to report urinary tract cancer prevalence across an international population in patients referred to secondary care, adjusted for patient risk markers and geographical variation. Bladder cancer was the most prevalent disease. Visible haematuria was the strongest predictor for urinary tract cancer.

Understanding angiogenesis and the role of angiogenic growth factors in the vascularisation of engineered tissues.

Tissue engineering is a rapidly developing field with many potential clinical applications in tissue and organ regeneration. The development of a mature and stable vasculature within these engineered tissues (ET) remains a significant obstacle. Currently, several growth factors (GFs) have been identified to play key roles within in vivo angiogenesis, including vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF), FGF and angiopoietins. In this article we attempt to build on in vivo principles to review the single, dual and multiple GF release systems and their effects on promoting angiogenesis. We conclude that multiple GF release systems offer superior results compared to single and dual systems with more stable, mature and larger vessels produced. However, with more complex release systems this raises other problems such as increased cost and significant GF-GF interactions. Upstream regulators and pericyte-coated scaffolds could provide viable alternative to circumnavigate these issues.

Delta QRS distinguishes Ito -mediated J waves from pseudo J waves produced by conduction delay on body surface electrocardiographic.

BACKGROUND: On surface electrocardiographic (ECGs), it is difficult to differentiate Ito -mediated J waves, a repolarization phenomenon seen in J wave syndromes (JWS) from terminal QRS deflections that mimic J waves (pseudo J waves) in intraventricular conduction delay (IVCD), an abnormality in depolarization. We hypothesize that the difference between the "maximum QRS duration" inclusive of J point or terminal QRS deflections and the minimum QRS duration identified across a 12-lead ECG is significantly larger in Ito -mediated J waves, and can serve as a marker to make this distinction. METHODS: A retrospective analysis was performed on adults with ECGs consisting of one of the four following manifestations: J waves associated with hypothermia and early repolarization, and pseudo J waves associated with right bundle branch block (RBBB) and non-specific intraventricular conduction delay (NS-IVCD). All ECGs were assessed individually and the maximum and minimum discrete QRS deflections on 12-lead tracings, defined as "QRSmax " and QRSmin , were identified. The difference between "QRSmax " and QRSmin , designated as ∆QRS, was calculated and compared across the studied populations. RESULTS: A total of 60 patients consisting of 15 patients in each arm were included in the study. ΔQRS was significantly larger in the hypothermia and early repolarization groups, compared to RBBB and NS-IVCD (p < .0001), with the following mean ∆QRS: hypothermia 54.3 ± 13.7 ms, early repolarization pattern 47.3 ± 15.3 ms, RBBB 19.3 ± 6.5 ms, and NS-IVCD 16.0 ± 6.6 ms. CONCLUSION: ∆QRS may serve as a reliable ECG parameter for distinguishing Ito -mediated J waves from pseudo J waves produced by delayed intraventricular conduction.

Response of Calamagrostis angustifolia to burn frequency and seasonality in the Sanjiang Plain wetlands (Northeast China).

Fire is an important disturbance in many wetlands, which are key carbon reservoirs at both regional and global scales. However, the effects of fire on wetland vegetation biomass and plant carbon dynamics are poorly understood. We carried out a burn experiment in a Calamagrostis angustifolia wetland in Sanjiang Plain (Northeast China), which is widespread wetland type in China and frequently exposed to fire. Using a series of replicated experimental annual burns over a three-year period (spring and autumn burns carried out one, two or three times over three consecutive years), together with a control unburned treatment, we assessed the effect of burn seasonality and frequency on aboveground biomass, stem density, and carbon content of aboveground plant parts and ground litter. We found that burning promoted plant growth and hence plant biomass in burned sites compared to the unburned control, with this effect being greatest after three consecutive burn years. Autumn burns promoted higher stem density and more total aboveground biomass than spring burns after three consecutive burn years. Burning increased stem density significantly, especially in twice and thrice burned plots, with stem densities in September over 2000 N/m2, which was much higher than in the control plots (987 ± 190 N/m2). Autumn burns had a larger effect than spring burns on total plant biomass and litter accumulated (e.g. 1236 ± 295 g/m2 after thrice autumn burns compared 796.2 ± 66.6 g/m2 after thrice spring burns), except after two burn treatments. With time since burning, total biomass loads increased in spring-burned plots, while autumn-burned plots showed the opposite trend, declining towards values found at unburned plots in year three. Our results suggest that, at short fire return intervals, autumn burns lead to a more pronounced increase in aboveground biomass and carbon accumulation than spring burns; however, the effects of spring burns on biomass and carbon accumulation are longer lasting than those observed for autumn burns.

[Association of RAGE gene polymorphisms with MHR ratio and heart rate variability among patients with coronary heart disease].

OBJECTIVE: To assess the association of polymorphisms of receptor of advanced glycation end products (RAGE) gene, monocyte to high-density lipoprotein cholesterol ratio (MHR) and variability of heart rate among patients with coronary heart disease (CHD). METHODS: 120 patients with CHD and 120 healthy individuals were respectively selected as the observation group and the control group. Allelic and genotypic differences of -429T>C, 1704G>T, 82G>S, MHR ratio and heart rate variability between the two groups and patients with different severity were analyzed. The correlation between their genotypes and MHR ratio and heart rate variability was analyzed. RESULTS: The 82G>S polymorphism of the RAGE gene and the allelic difference between the two groups and patients with different severity were statistically significant (P< 0.05). Compared with the control group and patients with mild to moderate phenotype, monocyte, total cholesterol, triglyceride, low density lipoprotein, MHR, low frequency in the observation group and patients with severe symptoms were significantly higher, while their high density lipoprotein, standard deviation of NN intervals (SDNN), standard deviation average of NN intervals (SDANN), root mean square successive differences, percentage of differences exceeding 50ms between adjacent normal number of intervals (PMN50), high frequency (HF) were significantly lower. The gene frequencies of G-Gly-T, T-Gly-T, G-Ser-T and G-Gly-C were correlated with SDNN, SDANN, rMSSD, PMN50, HF and MHR, but negatively correlated with low frequency. CONCLUSION: Polymorphisms of the RAGE gene in patients with coronary heart disease are associated with the MHR ratio and heart rate variability, which can be used as markers for the diagnosis and efficacy evaluation.

MicroRNA-2861 and microRNA-5115 regulates myocardial ischemia-reperfusion injury through the GPR30/mTOR signaling pathway by binding to GPR30.

Myocardial ischemia-reperfusion (I/R) injury, a major contributor to morbidity and mortality, represents a combination of intrinsic cellular response to ischemia and the extrinsic acute inflammatory response. In the present study, microarray analysis of GSE67308 and GSE50885 identified differentially expressed GPR30 and upstream regulatory miR-2861 and miR-5115 in myocardial I/R. Furthermore, GPR30 was confirmed as a common target gene of miR-2861 and miR-5115, and miR-2861 and miR-5115 inhibited GPR30 expression. Poor expression of GPR30 was identified in the myocardial I/R injury mouse model. Overexpressed GPR30 led to alleviated the pathological conditions, diminished myocardial infarct size and apoptosis of myocardial tissue in mice. Moreover, miR-2861 and miR-5115 were found to be highly expressed in the myocardial I/R injury mouse model and to subsequently accelerate the disease progression. Notably, PR30 curtailed the development of myocardial I/R injury through activation of the mTOR signaling pathway. The key findings suggested that miR-2861 and miR-5115 blocked the activation of the GPR30/mTOR signaling pathway by targeting GPR30, thereby accelerating myocardial I/R injury in mice.

MMP9, CXCR1, TLR6, and MPO participant in the progression of coronary artery disease.

Coronary artery disease (CAD) is the most frequent cardiovascular disease, which is induced by the decreased myocardial blood supply. The present study is conducted to understand the mechanisms of CAD. The GSE98583, GSE69587, and GSE71226 datasets from the Gene Expression Omnibus database were obtained. The differentially expressed genes (DEGs) were analyzed by the limma package, then the DEGs appeared in two or three datasets were selected as the coregulated genes using the VENNY tool, followed by enrichment analysis using DAVID tool. Protein-protein interaction (PPI) network, microRNA-transcription factor-target regulatory network, and drug-gene network were visualized. Finally, quantitative PCR and dual-luciferase reporter assay were conducted to validate the expression of key genes and the target relationship. There were 221 coregulated genes in GSE98583, GSE69587, and GSE71226. Besides, four pathways and 23 functional terms for co-upregulated genes, and 11 functional terms for co-downregulated genes were enriched. The degrees of PPI network nodes matrix metallopeptidase 9 (MMP9), C-X-C motif chemokine receptor 1 (CXCR1), toll-like receptor 6 (TLR6), and myeloperoxidase (MPO) were relatively higher. Moreover, MPO could interact with MMP9, CXCR1, and TLR6 in the PPI network. In the regulatory network, TLR6 and MMP9 separately were targeted by miR-3960 and v-rel avian reticuloendotheliosis viral oncogene homolog A (RELA). Additionally, MMP9, CXCR1, and MPO were involved in the drug-gene network. The expression of MMP9, CXCR1, TLR6, and MPO were significantly upregulated in CAD samples than control, and miR-3960 could bind to TLR6 to inhibit its expression. CXCR1 and MPO might be involved in the progression of CAD. Besides, miR-3960 might function in the pathogenesis of CAD through targeting TLR6, and RELA might exert its role in CAD via targeting MMP9.

Y-box protein 1 promotes hypoxia/reoxygenation- or ischemia/reperfusion-induced cardiomyocyte apoptosis via SHP-1-dependent STAT3 inactivation.

Cardiomyocyte apoptosis induced by hypoxia and ischemia plays important roles in heart dysfunction after acute myocardial infarction (AMI). However, the mechanism of apoptosis induction remains unclear. A previous study reported that Y-box protein 1 (YB1) is upregulated after myocardial hypoxia/reoxygenation or ischemia/reperfusion (H/R or I/R, respectively) injury; however, whether YB1 is associated with H/R-induced cardiomyocyte apoptosis is completely unknown. In the present study, we investigated the roles of YB1 in H/R-induced cardiomyocyte apoptosis and the possible underlying molecular mechanisms. In vitro, H/R treatment upregulated the YB1 expression in H9C2 cells, whereas YB1 knockdown inhibited H/R-induced cardiomyocyte apoptosis and induced H9C2 cell proliferation via Src homology region 2 domain-containing phosphatase 1 (SHP-1)-mediated activation of signal transducer and activator of transcription 3 (STAT3). In vivo, YB1 knockdown ameliorated AMI, reducing infarct size, cardiomyocyte apoptosis, and oxidative stress, via SHP-1-mediated inactivation of STAT3. Additionally, YB1 knockdown inhibited H/R- or I/R-induced oxidative stress in vitro and in vivo. H/R and I/R increase YB1 expression, and YB1 knockdown ameliorates AMI injury via SHP-1-dependent STAT3 inactivation.

Atherosclerosis-associated endothelial cell apoptosis by miRNA let7-b-mediated downregulation of HAS-2.

MicroRNAs (miRNAs) play essential roles in the regulation and pathophysiology of various types of human diseases including atherosclerosis. Increasing numbers of miRNAs have been identified to be important regulators in the progression of atherosclerosis by regulating gene expression. However, functional miRNAs and the underlying mechanisms involved in atherosclerosis need fully elucidation. In the present study, the function of miRNA let-7b was investigated in human aortic endothelial cells (HAECs). The results showed that downregulation of let-7b in the high-fat diet mice and HAECs was inversely correlated with the expression level of HAS-2. upregulation of let-7b significantly reduced apoptosis of HAECs. The results also revealed that HAS-2 was a target gene of let-7b and HAS-2 reduction reversed the antiapoptotic effect of let-7b through regulation of the P13K/Akt pathway. These results together suggest the potential of regulating the let-7b expression and endothelial apoptosis against development and progression of atherosclerosis.