Coronary heart disease (CHD) is a lipid-driven inflammatory disease increasing in individuals. Lipoprotein(a) (Lp[a]) has an interdependence with systemic metabolism and inflammation to increase the risk of CHD. Our study aims to examine the coronary lesion and plaque characteristic in older CHD patients with elevated Lp(a) level by using untargeted metabolomics and proteomics assay. We included 285 consecutive individuals ≥ 65 years who took coronary artery CT scanning, collected blood samples and underwent percutaneous coronary angiography. After restricted exclusion, the enrolled age-matched individuals were randomly divided into two separated cohorts. For the testing cohort, plasma samples of 40 controls and 45 CHD patients were conducted with untargeted metabolomics and proteomics. Another validation cohort including 64 controls and 60 CHD patients was used to verify the link between differential plasma mediators and coronary stenosis and plaque characteristics. Compared with an averaged Lp(a) level of 98.9 nmol/L in controls with age ≥ 65 years, mean level of Lp(a) up to 188.4 nmol/L in age-matched CHD patients. The metabolome analyses revealed that differential plasma metabolites would be involved in the pathophysiological regulation of fatty acid transport, fatty-acid-CoA ligase and lipid transport related to lipid plaque progress. We found that plasma levels of β-Muricholic acid, 23-Nordeoxycholic acid, Docosahexaenoic acid, 7-Ketodeoxycholic acid, LPC (18:0) and LPA 16:1 were significantly altered in CHD group. Then proteomics assays showed positive immune response indicating by enhanced interleukin-18 (IL-18), immunoglobulin lambda joining 3 (IGLJ3) and immunoglobulin heavy variable 3 (IGHV3) levels in CHD patients compared to controls. Among these, β-muricholic acid, 23-nordeoxycholic acid, LPA 16:1 and IL-18 were correlated with coronary stenosis severity. Moreover, the levels of β-muricholic acid, IL-18 and IGLJ3 were associated with low-density noncalcified plaque burden in older CHD patients. We also observed plasma levels of β-muricholic acid, 23-nordeoxycholic acid, 7-Ketodeoxycholic acid and IL-18 altered in older CHD patients with chronic total occlusion (CTO) lesion. Our study demonstrated an altered profiling of plasma metabolites and proteins, and their correlation with coronary stenosis severity and plaque burden in older CHD individuals with elevated Lp(a) level, which may provide potential biomarkers in older CHD patients. Plasma metabolome and proteomics profiling was totally different in older CHD patients. Altered lipid-driven plasma metabolites and proteins were associated with coronary stenosis and plaque burden. Differential metabolites and proteins exhibited potential values linked to coronary stenosis severity and CTO lesion.

BACKGROUND:Blood glucose and serum albumin have been associated with cardiovascular disease prognosis, but the impact of admission-blood-glucose-to-albumin ratio (AAR) on adverse outcomes in critical ill coronary artery disease (CAD) patients was not investigated. METHODS:Patients diagnosed with CAD were non-consecutively selected from the MIMIC-IV database and categorized into quartiles based on their AAR. The primary outcome was 1-year mortality, and secondary endpoints were in-hospital mortality, acute kidney injury (AKI), and renal replacement therapy (RRT). A restricted cubic splines model and Cox proportional hazard models assessed the association between AAR and adverse outcomes in CAD patients. Kaplan-Meier survival analysis determined differences in endpoints across subgroups. RESULTS:A total of 8360 patients were included. There were 726 patients (8.7%) died in the hospital and 1944 patients (23%) died at 1 year. The incidence of AKI and RRT was 63% and 4.3%, respectively. High AAR was markedly associated with in-hospital mortality (HR = 1.587, P = 0.003), 1-year mortality (HR = 1.502, P < 0.001), AKI incidence (HR = 1.579, P < 0.001), and RRT (HR = 1.640, P < 0.016) in CAD patients in the completely adjusted Cox proportional hazard model. Kaplan-Meier survival analysis noted substantial differences in all endpoints based on AAR quartiles. Stratified analysis and interaction test demonstrated stable correlations between AAR and outcomes. CONCLUSIONS:The results highlight that AAR may be a potential indicator for assessing in-hospital mortality, 1-year mortality, and adverse renal prognosis in critical CAD patients.

Background Genetic variation plays an extremely important pathogenic role in the development of venous thromboembolism (VTE). Genetic protein S (PS) deficiency caused by PROS1 gene mutation is an important risk factor for hereditary thrombophilia.Case introduction In this case, we report a 28-year-old male patient who developed a severe pulmonary embolism during his visit. The patient had experienced one month of chest pains, coughing and hemoptysis symptoms. CTPA confirmed an acute pulmonary embolism with multiple filling defects in both pulmonary arteries. Ultrasound showed no thrombosis in the veins of both lower limbs. The patient's father and grandfather have a history of lower limb venous thrombosis. The patient was diagnosed with acute pulmonary embolism and pneumonia. The serum PS level significantly decreased (detection result: 10%, normal range: 77-143). Gene sequencing revealed a heterozygous missense mutation in PROS1 c.76+2_76+3del (base deletion), and further testing revealed that the genetic variation originated from his father. The patient was treated with heparin anticoagulant therapy, catheter thrombus aspiration, and catheter thrombolysis. After treatment, the patient's chest pain symptoms were relieved, and there were no symptoms such as difficulty breathing. On the 7th day of admission, the patient was transferred to a general hospital for further treatment.Conclusion Hereditary thrombophilia caused by mutations in the PROS1 (c.76+2_76+3del) gene is extremely rare. In clinical practice, heparin and rivaroxaban treatment are beneficial.

Atrial fibrillation (AF) is the most common sustained arrhythmia to affect 1% of the global population and increases with age. Atrial fibrosis is a crucial substrate for promoting structural remodeling to cause atrial arrhythmogenesis. Bone morphogenic protein 2 (BMP2) has been reported to be involved in cardiac fibrogenesis. However, its role in modulating atrial fibrosis to affect AF development remains unknown. Our study aimed to investigate the expression of BMP2 under different AF conditions and the effect of BMP2 on the progression of atrial fibrosis using an angiotensin II (Ang II) rat model and an ex vivo cardiac fibroblast model. The qRT-PCR and Western blot assay showed increased BMP2 mRNA and protein levels in the atria of chronic AF patients and the right atria of a tachypacing rabbit model. In contrast, the levels of BMP2 receptor mRNA were comparable. The AF incidence of the Ang II rat was higher than that of a control rat, which was reduced by BMP2 treatment. Masson staining demonstrated an anti-fibrogenic impact on BMP2-subjected rat atria compared to only Ang II-treated rat atria. RNA-sequencing indicated the potential function of blocking NLRP3-associted inflammasome activation in BMP2-treated rat atrial tissues. In vitro, transfecting BMP2 shRNA into neonatal rat atrial fibroblasts upregulated the mRNA levels of NLRP3/Caspase-1/p20/ASC and the secretion of IL-1β and IL-6. In contrast, recombinant BMP2 protein attenuated the increased levels of the NLRP3 inflammasome pathway induced by Ang II. In summary, BMP2 opposes atrial fibrosis to alleviate AF susceptibility by inhibiting the activation of the inflammasome in atrial fibroblasts.

Background:Atrial fibrillation (AF) is the most common cardiac arrhythmia with severe clinical sequelae, but its genetic characteristic implicated in pathogenesis has not been completely clarified. Accumulating evidence has indicated that circulating exosomes and their carried cargoes, such as long non-coding RNAs (lncRNAs), involve in the progress of multiple cardiovascular diseases. However, their potential role as clinical biomarkers in AF diagnosis and prognosis remains unknown.Methods:Herein, we conducted the sequence and bioinformatic analysis of circulating exosomes harvested from AF and sinus rhythm patients.Results:A total of 53 differentially expressed lncRNAs were identified, and a total of 6 significantly changed lncRNAs (fold change > 2.0), including NR0046235, NR003045, NONHSAT167247.1, NONHSAT202361.1, NONHSAT205820.1 and NONHSAT200958.1, were verified by qRT-PCR in 215 participants. Moreover, these circulating exosome lncRNA levels were different between paroxysmal and persistent AF patients, which were dramatically associated with abnormal hemodynamics and atrial diameter. Furthermore, we observed that the area under ROC curve (AUC) of six lncRNAs combination for diagnosis of persistent AF was 80.34%. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) enrichment pathway analysis indicated these exosome lncRNAs mainly concerning response to chemokine-chemokine receptor interaction, which induced activated inflammation and structural remodeling. In addition, increased plasma levels of CXCR3 ligands, including CXCL4, CXCL9, CXCL10 and CXCL11, were accumulated in AF patient tissues.Conclusion:Our study provides the transcriptome profile revealing pattern of circulating exosome lncRNAs in atrial structural remodeling, which bring valuable insights into improving prognosis and therapeutic targets for AF.

Coronary artery perforation (CAP) poses a significant challenge for interventional cardiologists. Management of CAP depends on the location and severity of the perforation. The conventional method for addressing the perforation of large vessels involves the placement of a covered stent, while the perforation of distal and collateral vessels is typically managed using coils, autologous skin, subcutaneous fat, microspheres, gelatin sponge, thrombin or other substances. However, the above techniques have certain limitations and are not applicable in all scenarios. Our team has developed a range of innovative strategies for effectively managing CAP. This article provides an insightful review of the various tips and tricks for the treatment of CAP.

Objective: Hyperlipidemia is closely related to premature acute myocardial infarction (AMI). The present study was performed to explore the correlation between various blood lipid components and the risk of premature AMI. Methods: This is a cross-sectional retrospective study. Consecutive patients with acute ST-segment elevation myocardial infarction (STEMI), who completed coronary angiography from October 1, 2020 to September 30, 2022 in our hospital, were enrolled and divided into premature AMI group (male<55 years old, female<65 years old) and late-onset AMI group. Total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), non-HDL-C, lipoprotein (a) (Lp (a)), apolipoprotein B (ApoB), apolipoprotein A-1 (ApoA-1), non-HDL-C/HDL-C and ApoB/ApoA-1 were analyzed. The correlation between the above blood lipid indexes and premature AMI was analyzed and compared by logistic regression, restricted cubic spline and receiver operating characteristic curve (ROC). Results: A total of 1 626 patients with STEMI were enrolled in this study, including 409 patients with premature AMI and 1 217 patients with late-onset AMI. Logistic regression analysis showed that the risk of premature AMI increased significantly with the increase of TG, non-HDL-C/HDL-C, non-HDL-C, ApoB/ApoA-1, TC and ApoB quintiles; while LDL-C, ApoA-1 and Lp (a) had no significant correlation with premature AMI. The restricted cubic spline graph showed that except Lp (a), LDL-C, ApoA-1 and ApoB/ApoA-1, other blood lipid indicators were significantly correlated with premature AMI. The ROC curve showed that TG and non-HDL-C/HDL-C had better predictive value for premature AMI. Inconsistency analysis found that the incidence and risk of premature AMI were the highest in patients with high TG and high non-HDL-C/HDL-C. Conclusion: TG, non-HDL-C/HDL-C and other blood lipid indexes are significantly increased in patients with premature AMI, among which TG is the parameter, most closely related to premature AMI, and future studies are needed to explore the impact of controlling TG on incidence of premature AMI.

Background and objectives The hemodynamic evaluation of coronary stenoses undergoes a transition from wire-based invasive measurements to image-based computational assessments. However, fractional flow reserve (FFR) values derived from coronary CT angiography (CCTA) and angiography-based quantitative flow ratio have certain limitations in accuracy and efficiency, preventing their widespread use in routine practice. Hence, we aimed to investigate the diagnostic performance of FFR derived from the integration of CCTA and invasive angiography (FFRCT-angio) with artificial intelligence assistance in patients with stable coronary artery disease (CAD). Methods Forty stable CAD patients with 67 target vessels (50%-90% diameter stenosis) were included in this single-center retrospective study. All patients underwent CCTA followed by coronary angiography with FFR measurement within 30 days. Both CCTA and angiographic images were combined to generate a three-dimensional reconstruction of the coronary arteries using artificial intelligence. Subsequently, functional assessment was performed through a deep learning algorithm. FFR was used as the reference. Results FFRCT-angio values were significantly correlated with FFR values (r = 0.81, P < 0.001, Spearman analysis). Per-vessel diagnostic accuracy of FFRCT-angio was 92.54%. Sensitivity and specificity in identifying ischemic lesions were 100% and 88.10%, respectively. Positive predictive value and negative predictive value were 83.33% and 100%, respectively. Moreover, the diagnostic performance of FFRCT-angio was satisfactory in different target vessels and different segment lesions. Conclusions FFRCT-angio exhibits excellent diagnostic performance of identifying ischemic lesions in patients with stable CAD. Combining CCTA and angiographic imaging, FFRCT-angio may represent an effective and practical alternative to invasive FFR in selected patients.

2019冠状病毒病(COVID-19)暴发是国际关注的突发公共卫生事件,COVID-19常导致严重的呼吸衰竭,部分患者会出现急性心肌损伤和高血压等心血管疾病,且COVID-19与病毒受体血管紧张素转换酶2(ACE2)密切相关.本文就COVID-19相关心血管疾病发病率、ACE2介导的相关作用机制及最新的诊治方法作一综述.

Purpose/Objective(s) Immune checkpoint inhibitors (ICI) demonstrated antitumor activity has been increasingly used as first-line or second-line treatments for patients with advanced hepatocellular carcinoma (HCC). In the meanwhile, radiotherapy is turning into a crucial component of multidisciplinary treatment for HCC. Mounting evidence suggests local radiotherapy including SBRT might promote immunogenic tumor cell death and could enhance immunotherapeutic effects in several cancers. However, evidence on advanced HCC is few. Here we report the efficacy and safety of combined SBRT and immunotherapy in patients of BCLC stage C HCC in our center. Materials/Methods This is a retrospective analysis of twenty-nine patients with advanced HCC, previously treated with sorafenib or lenvatinib, who received SBRT and anti-PD1 antibody concomitantly or sequentially. Here we report their treatment responses both in-field and outside the radiation field according to RECIST1.1 criteria, progression-free survival (PFS), overall survival (OS), and toxicities. Results The median age was 55.1 years (range, 25-75), 90% of patients were male, eighty percent had hepatitis B virus and all patients' Child-Pugh score ≤ B7. Among these patients, twenty-one (70%) had portal vein tumor thrombosis (PVTT), four (13.3%) had inferior vena cava tumor thrombosis and nineteen (63.3%) had extrahepatic metastasis. Eight patients had both extrahepatic metastases and PVTT. 86.2% of patients were also treated with second-line targeted therapy. Tumors treated with SBRT located in liver (52.7%), lung (33.3%), bone (11.2%) and retroperitoneal lymph nodes (2.8%). SBRT administration was a median of 40Gy (range, 25-60) and 5 fractions (range, 3-6). The median follow-up was 16.5 months (range, 6-58). The in-field ORRs were 82.8% and the DCR were 100% (CR 20.7%, PR 62.1%, four bone lesions and one lymph nodes were SD). The out-field ORRs were 27.6% and the DCR were 86.2%. The median PFS was 7 months (95% CI, 1-24 months). Six months PFS rate was 53.3% and 1-year PFS rate was 32.6%. At the time of data cutoff, the median duration of OS has not reached. 1-year OS rate was 62.1% and 2-years OS rate was 50.5%. The prognosis of patients with PVTT was worse than those patients without PVTT (2-years OS rate 35.07% vs 88.89%; p=0.04). Treatment-related AEs consisted of platelet count decrease in four patients, alanine/aspartate aminotransferase increase in five patients and myocarditis in one patient. No SBRT-related grade 3 or higher adverse events occurred. Conclusion Our experience suggests that combined SBRT and second line ICI with or without targeted drug can be a safe and effective therapy for BCLC stage C HCC. Further prospective trials are warranted.

High energy FRagment Separator (HFRS), an essential part of High Intensity heavy-ion Accelerator Facility (HIAF), is used to produce, separate and identify the Radioactive Ions Beams (RIBs). The target area in the pre-separator of HFRS can produce very strong secondary radiation, which seriously threatens the radiation safety of the environment, public and personnel. In this work, the FLUKA code is used to complete the radiation shielding calculation and design of the target area. Firstly, the secondary radiation produced by 25 different typical beam–target combinations are compared. The parameter of 78Kr in fast extraction mode is determined as the basis for the radiation shielding design based on its strongest secondary radiation. Then, the secondary neutron spectrum and the induced radioactivity of the production target and the beam dump are analyzed. The results show that the maximum neutron energy is close to 3 GeV, and special attention should be paid to high-energy neutrons in shielding design, as well as the maximum residual dose rates on the surface of the production target and the beam dump are 3.93 × 107 μSv/h and 9.58 × 107 μSv/h, respectively, after one month of continuous irradiation. Furthermore, the radiation shielding design is completed using the Q235 steel compact shielding together with the ordinary concrete and sand soil, based on the Monte Carlo simulations and the relevant dose limits. Finally, the radiation effects under this shielding scheme are analyzed. The results show that the shielding design meets the relevant design goals and can provide reliable radiation protection for the environment, public and personnel.

Objective: To observe the changes of fetal umbilical vein (UV) Doppler parameters in pregnant women with preeclampsia (PE) and analyze their pre-dictive values for maternal PE. Methods: Forty-six patients with PE who underwent systematic ultrasound examination in our hospital from December 2017 to May 2021 were included as the subjects, which were divided into two groups according to the severity of the disease (23 cases in each group). And 120 normal pregnant women who underwent health examination in our hospital during the same period were enrolled as the control group. Color Doppler ultrasonography was used to monitor the umbilical vein flow (QUV), left portal vein flow (QLPV), venous catheter flow (QDV), left portal vein (LPV) shunt rate and venous catheter (DV) shunt rate. And the sensitivity and specificity of the related indexes were calculated and analyzed according to the gold standard for clinical diagnosis of PE. Results: As the severity of PE increased, the fetal QUV, QLPV and LPV shunt rates decreased, and the QDV and DV shunt rates increased, with statistically significant differences compared with the control group (P < 0.05). The specificity and sensitivity of the combination of fetal QUV, QLPV, QDV, LPV shunt rate and DV shunt rate in predicting PE were higher than those of the indexes used alone (P < 0.05). Conclusion: The fetal umbilical vein Doppler parameters QUV, QLPV, QDV, LPV shunt rate, and DV shunt rate have some value in predicting PE, but their combination showed greater value, as well as higher diagnostic and clinical significance.

Coronary artery perforation （CAP） remains an infrequent but potentially lifethreatening complication during percutaneous coronary intervention （PCI）.Although the prevalence of CAP is about 0.2%-0.9%in relatively low risk PCI,the incidence could up to 9%in complex clinical scenarios such as severe coronary calcification,chronic total occlusions and rotational atherectomy. [1]

While EGFR mutant NSCLC patients are initially responsive to EGFR targeted therapies, resistant disease inevitably emerges. In nearly half of resistance cases, tumors lack secondary EGFR mutations such as T790M and are refractory to 2nd- and 3rd-generation EGFR tyrosine kinase inhibitors (TKI). We and others have also observed that EGFR-independent resistant tumor cells may undergo a histologic and functional transformation through epithelial-to-mesenchymal transition (EMT) (Byers et al., 2013; Chung et al., 2011; Uramoto et al., 2010; Zhang et al., 2012), which can occur concurrently with other genomic alterations. The lack of treatment regimens with efficacy against EGFR-independent EGFR TKI resistance remains a major clinical challenge. We investigated transcriptomic and proteomic alterations that occur in NSCLC cells with acquired resistance to EGFR TKIs that occurs independent of EGFR and c-Met and screened >1,300 compounds to identify targetable vulnerabilities. T790M-negative EGFR TKI resistance was associated with evidence of a mesenchymal transition along with increased activation of the YAP/FOXM1 transcriptional program and a broad-spectrum multidrug resistance phenotype. EGFR TKI resistant cells displayed increased expression of spindle assembly checkpoint (SAC) proteins PLK1, Aurora kinases, survivin, and KSP, and expression of these proteins was dependent on the YAP/FOXM1 axis. Consistent with recent reports (Bertran-Alamillo et al., 2019; Shah et al., 2019), EGFR TKI resistant cells were found to be sensitive to aurora kinase inhibitors. We further determined that EGFR TKI resistant cells were likewise highly sensitive to inhibitors of components of the spindle assembly checkpoint (SAC) pathway including PLK1, KSP, and survivin, and treatment with these agents resulted in the accumulation of cells in the G2/M phase of the cell cycle and mitotic catastrophe. Using a patient-derived model of T790M negative EGFR TKI resistance, we observed that treatment with SAC component inhibitors, alisertib, ispinesib, or volasertib significantly inhibited tumor growth compared with vehicle-treated tumors. Analysis of NSCLC clinical data revealed that FOXM1 expression correlated with expression of SAC components including PLK1, Aurora kinases, KSP, and survivin. Moreover, in EGFR mutant NSCLC patients, high FOXM1 expression was associated with a worse clinical outcome compared to EGFR mutant NSCLC patients with low expression of FOXM1. In resistant models, targeting of YAP reduced FOXM1 expression and expression of SAC components. In conclusion, we provide novel insights into the molecular alterations associated with EGFR TKI resistance and demonstrate that upregulation of SAC components in EGFR TKI resistant cells occurs through the activation of the YAP/FOXM1 pathway. These results support the future targeting of these pathways in NSCLC patients with EGFR-independent resistance to EGFR-targeted agents.

Abstract Previous studies have revealed associations of meteorological factors with tuberculosis (TB) cases. However, few studies have examined their lag effects on TB cases. This study was aimed to analyse nonlinear lag effects of meteorological factors on the number of TB notifications in Hong Kong. Using a 22-year consecutive surveillance data in Hong Kong, we examined the association of monthly average temperature and relative humidity with temporal dynamics of the monthly number of TB notifications using a distributed lag nonlinear models combined with a Poisson regression. The relative risks (RRs) of TB notifications were >1.15 as monthly average temperatures were between 16.3 and 17.3 °C at lagged 13–15 months, reaching the peak risk of 1.18 (95% confidence interval (CI) 1.02–1.35) when it was 16.8 °C at lagged 14 months. The RRs of TB notifications were >1.05 as relative humidities of 60.0–63.6% at lagged 9–11 months expanded to 68.0–71.0% at lagged 12–17 months, reaching the highest risk of 1.06 (95% CI 1.01–1.11) when it was 69.0% at lagged 13 months. The nonlinear and delayed effects of average temperature and relative humidity on TB epidemic were identified, which may provide a practical reference for improving the TB warning system.

Percutaneous coronary intervention（PCI）of chronic total occlusion（CTO）represents the most technically challenging procedure in contemporary interventional cardiology.（[1]） B lunt lesions and presence of proximal side branch are con-

No-reflow phenomenon is common in patients with acute coronary syndrome（ACS） after percutaneous coronary intervention（PCI）, and it is strongly associated with adverse clinical prognosis. Previous studies have shown that heavy thrombus burden could predict the development of no-reflow in PCI.[1,2] Manual and mechanical thrombus aspiration

Background Whether chronic obstructive sleep apnea (OSA) could promote epicardial adipose tissue (EAT) secretion of profibrotic adipokines, and thereby contribute to atrial fibrosis, and the potential therapeutic effects of metoprolol remain unknown. Methods and Results A chronic OSA canine model was established by repeatedly clamping the endotracheal tube for and then reopening it for 4 hours every other day for 12 weeks. In a metoprolol treatment group, metoprolol succinate was administered daily for 12 weeks. The EAT infiltration and left atrial fibrosis were examined. The expressions of adipokines secreted by EAT and hypoxic 3T3‐L1 adipocytes were detected. The changes in collagen synthesis, transforming growth factor‐β1 expression, and cell differentiation and proliferation in cardiac fibroblasts induced by hypoxic 3T3‐L1 adipocyte‐derived conditioned medium were further analyzed. Chronic OSA induced infiltration of EAT into the left atrium. OSA enhanced the profibrotic effect of EAT on the adjacent atrial myocardium. Moreover, OSA induced profibrotic cytokine secretion from EAT. We also found that hypoxia induced adipokine secretion in cultured adipocytes, and the medium conditioned by the hypoxic adipocytes increased collagen and transforming growth factor‐β1 protein expression and cell proliferation of cardiac fibroblasts. More importantly, metoprolol attenuated infiltration of EAT and alleviated the profibrotic effect of EAT by inhibiting adipokine secretion. Metoprolol also inhibited hypoxia‐induced adipokine secretion in adipocytes and thereby blocked the hypoxic adipocyte–derived conditioned medium–induced fibrotic response of cardiac fibroblasts. Conclusions Chronic OSA enhanced the profibrotic effect of EAT on the neighboring atrial myocardium by stimulating the secretion of profibrotic adipokines from EAT, which was significantly attenuated by metoprolol. This study gives insights into mechanisms underlying OSA‐induced atrial fibrillation and also provides experimental evidence for the protective effects of metoprolol.

Allogeneic hematopoietic stem cell transplantation has been accepted as one of the most effective therapy to treat hematological malignancies at home and abroad. The biological characteristics of immune cell subsets are different from each other, and donor cell chimerism after allogeneic hematopoietic stem cell transplantation can be complicated. Therefore, analyzing of donor-type chimerism in lineage-specific immune cell populations plays a significant role in estimating engraftment,predicting disease prognosis and improving survival rate because of its high sensibility and specificity. We reviewed the clinical significance of supervising chimerism in lineage-specific immune cell populations after allogeneic hematopoietic stem cell transplantation.

>In order to improve the success rate of chronic total occlusion (CTO) percutaneous coronary intervention (PCI),retrograde approach has been attracted more attention. Recent study reported the collateral perforation rate was 6.9%in retrograde CTO PCI. [1,2] Collateral related perforations were higher in patients with the epicardial collateral than that with the septal collateral.131 Several techniques have been developed to deal with the collateral branch perforation. Here, we described the treatment of epicardial collateral branch perforation by absorbable suture segments embolization through microcatheter during retrograde CTO PCI.