Patent foramen ovale(PFO), a congenital structural lesion that allows shunting of blood from the right to the left atrium, has been increasingly recognized as the main cause of cryptogenic stroke. The mechanism of PFO-related cryptogenic stroke is attributed to paradoxical embolism into the arterial system via PFO. A large number of domestic and foreign studies have confirmed the efficacy and safety of percutaneous PFO closure in the secondary prevention of a series of diseases including cryptogenic stroke and migraine. Percutaneous PFO closure is a mature and safe operation overall, but its corresponding complications are still unavoidable. We mainly introduce PFO closure and its related complications in this paper, aiming to enhance clinicians' understanding of this operation and its complications, so as to reduce some unnecessary troubles in clinical work.

Doxorubicin is an effective anthracycline chemotherapeutic drug, which is widely used in single or combined chemotherapy for various malignant tumors. However, the cardiotoxicity caused by doxorubicin has limited its clinical application. Despite a large amount of research investment, no suitable target has been found to reduce cardiotoxicity caused by doxorubicin while guaranteeing the effect of chemotherapy. Recent studies have found that non-coding RNA is related to doxorubicin-induced cardiomyopathy. Further explaining the relationship between the two may provide new strategies for the diagnosis, prevention and treatment of doxorubicin-induced cardiotoxicity.

Objective:To investigate the protective effect of dihydromyricetin (DHM) on doxorubicin (DOX)-induced myocardial injury and its mechanism.Methods:Twenty-four healthy male SD rats were divided into 4 groups: control group, DOX group, DOX+DHM100 group and DOX+DHM200 group. Echocardiography was used to measure cardiac function. At the end of the 6th week, the rats were anesthetized and sacrificed, and the pathological changes of the cardiac tissues were observed by HE staining, Masson staining and WGA staining. Cardiomyocyte apoptosis was observed by TUNEL staining, and protein levels of NLRP3, caspase-1, IL-1β, bax and bcl-2 were detected by Western blot and immunohistochemistry.Results:Compared with the control group, the left ventricular ejection fraction and left ventricular fractional shortening decreased significantly in DOX group, while left ventricular internal dimension at systole and left ventricular internal dimension at diastole increased. In DOX+DHM group, both left ventricular ejection fraction and left ventricular fractional shortening increased, while left ventricular internal dimension at systole and left ventricular internal dimension at diastole decreased ( P<0.05). Furthermore, DOX group showed significant myocardial injury histologically, while DOX+DHM group significantly inhibited DOX-induced myocardial injury in rats. Meanwhile, cardiomyocyte hypertrophy was found in the DOX group, while the cardiomyocyte hypertrophy was notably inhibited in the DOX+DHM group. Compared with the control group, the apoptotic rates of cardiomyocytes and the levels of bax/bcl-2　ratio were significantly increased in DOX group, which were significantly alleviated in the DOX+DHM group ( P<0.05). In addition, the levels of NLRP3, caspase-1 and IL-1β were increased as compared with control group, while the levels of the above indicators were remarkably reversed in DOX+DHM group as compared with DOX group ( P<0.05). Conclusion:DHM alleviates DOX-induced myocardial injury in rats by inhibiting NLRP3 inflammasome and reducing cardiomyocyte apoptosis.

Objective: To investigate the impact of homocysteine inducible endoplasmic reticulum(ER) protein with ubiquitin like domain 1 protein (Herpud1) in the homocysteine (Hcy) -induced phenotypic switching of vascular smooth muscle cells (VSMCs). Methods: VSMCs were derived from thoracic aortic artery of male Sprague Dawley rats and cultured VSMCs (4-7 passage) were treated with various concentrations of Hcy (0, 100, 500 and 1 000 μmol/L) and applied to immunofluorescence to observe the morphological changes of VSMCs via SM-actin staining. Western blot was used to detect the expression of VSMCs phenotypic markers, including Osteopontin, Calponin and smooth muscle myosin heavy chain (SM-MHC) and the expression of endoplasmic reticulum stress (ERS) related proteins, including C/EBP-homologous protein (CHOP), inositol-requiring kinase 1 (IRE-1) and glucose regulating protein 78 (GRP78) in the absence and presence of non-selective inhibitor of ERS, 4-phenylbutyric acid (4-PBA, 2 mg/ml). The Herpud1 mRNA and protein levels were determined in Hcy-stimulated VSMCs treated with 4-PBA or transfected with specific siRNA targeting Herpud1. Results: Compared with the control group, SM-actin staining results showed that the shape of VSMCs treated with different concentrations of Hcy for 24 hours changed from long fusiform into round form, arrangement of myofilament became irregular and the most significant alteration was found in the 500 μmol/L Hcy group. After intervention of 24 hours, various concentration of Hcy increased protein expression of Osteopontin, and reduced Calponin and SM-MHC protein expressions in VSMCs (all P<0.05). In addition, the results showed that Hcy increased the expression of CHOP, IRE-1 and GRP78 in a dose-dependent manner, which could be reversed by 4-PBA treatment (all P<0.05). However, 4-PBA inhibited Hcy induced upregulation of Osteopontin and downregulation of Calponin and SM-MHC, suggesting that ERS was involved in Hcy-induced phenotypic switching of VSMCs. Herpud1 protein was mostly expressed in the cytoplasm and was also expressed in the nucli, both in the control, Hcy and Hcy+4-PBA groups. Moreover, Hcy increased mRNA and protein levels of Herpud1 (P<0.05), whereas treatment with 4-PBA could significantly reduce Hcy-induced upregulation of Herpud1 (P<0.05). Furthermore, knockdown of Herpud1 abrogated the effects of Hcy on VSMCs phenotype markers. Conclusion Herpud1 plays an important role in Hcy-induced phenotypic switching of VSMCs.

Doxorubicin is a major culprit in chemotherapy-induced cardiotoxicity,which is the chief limiting factor in delivering optimal chemotherapy to cancer patients.Although extensive efforts have been devoted,no chemical synthesized drugs or natural compounds are available to prevent the harmful action of doxorubicin without reducing its anti-cancer efficacy.Accumulative experimental evidence has shown that polyphenols can prevent doxorubicin-induced cardiotoxicity largely due to their anti-cancer and cardio protective properties.We elaborated on the potential mechanisms associated with doxorubicin-induced cardiotoxicity and reviewed published literatures about the protective effects of polyphenols on doxorubicin-induced cardiotoxicity to provide novel strategies for the study of cardioprotective drugs.

Objective From the perspective of traditional Chinese medicine (TCM) syndrome differentiation to investigate the blood glucose control strategies of patients with different etiological factors and treated by mechanical ventilation.Methods One hundred and twenty-six mechanical ventilation patients admitted to the Department of Intensive Care Unit (ICU) of Hangzhou Third People's Hospital from February 2016 to February 2017 were enrolled, they were divided into a heart failure group (64 cases) and a pneumonia group (62 cases) according to the cause of disease. Altogether 4 cases due to death, giving up the treatment or being transferred to other hospital were excluded in each group, thus, 60 cases in heart failure group and 58 cases in pneumonia group were finally enrolled. Both groups received at least 4 days of formal blood glucose monitoring and control program. The differences in TCM syndromes, the number of patients necessary to use insulin to control the blood glucose, the daily use of insulin dosage, the incidence of hypoglycemia and prognosis of patients were compared between the two groups.Results According to TCM syndrome differentiation, deficiency was the primary syndrome in the heart failure group, while in the pneumonia group, excess was the primary syndrome, the proportion of deficiency syndrome in heart failure group was significantly higher than that in the pneumonia group [63.33% (38/60) vs. 31.03% (18/58),P < 0.05]. Within 4 days, the incidence of hyperglycemia [50.0% (29/58) vs. 13.3% (8/60)], daily insulin dose (U/d: 85.35±6.35 vs. 20.13±8.20) in pneumonia group were higher than those in the heart failure group (bothP < 0.05). The incidence of hypoglycemia in heart failure group was higher than that in pneumonia group [16.67% (10/60) vs. 3.45% (2/58),P < 0.01].Conclusions It is necessary to use different blood glucose control strategies in patients with heart failure and pneumonia to undergo mechanical ventilation, and the TCM syndrome differentiation can provide theoretical references.

Through taking patient as the center,doctor-patient friendliness concept is actively learned from,the information service,the full range of volunteer service,humanized hospice,fine process of transformation,standardized window service,electronic medical ethics appraisal,persistent humanistic management,three-dimensional health promotion and other eight core work,patient satisfaction is improved,and harmony between doctors and patients is promoted.

AIM:To investigate whether Chinese yellow wine has influences on homocysteine ( Hcy )-induced dysfunction in rat endothelial progenitor cells (EPCs).METHODS:Rat bone marrow was extracted to harvest mononucle-ar cells ( MNCs) by density gradient centrifugation .The MNCs were plated on fibronectin-coated culture dishes , and were induced into EPCs by EGM-2 complete medium supplemented with cell growth factor .The adherent cells were collected 7 d later for all studies .EPCs were characterized as adherent cells double positive for DiI-ac-LDL uptaking and lectin binding by direct fluorescent staining under a laser scanning confocal microscope .The viability, migration, apoptosis and in vitro vasculogenic activity of the EPCs were determined by MTT assay , Transwell chamber assay , apoptosis kit and in vitro vas-culogenesis kit, respectively.RESULTS:Compared with control group, the viability, migration and in vitro vasculogenic capacity of the EPCs in Hcy group were significantly decreased (P<0.01).Compared with Hcy group, yellow wine group and red wine group both significantly improved the viability , migration and in vitro vasculogenic capacity of Hcy-induced EPCs (P<0.01).Compared with control group, yellow wine group and red wine group both significantly improved the a-bove-mentioned functions of EPCs (P<0.05).However, no significant difference of apoptosis in all groups was observed . CONCLUSION:Hcy may result in dysfuction of EPCs .Treatment with yellow wine improves Hcy-induced EPC functions .

ABSTRACT:Objective To verify whether rosuvastatin can inhibit homocysteine (Hcy)‐induced rat aortic vascular smooth muscle cell (VSMC ) phenotype transformation and its potential mechanism .Methods The primary culture and identification of rat VSMCs were conducted , using VSMCs in passage4‐7 for the following experiments .The VSMCs were divided into 4 groups:control group ,Hcy (100μmol/L) group ,Hcy+ rosuvastatin group ,and Hcy+ rapamycin group .MTT was used to investigate the proliferation of VSMCs .Transwell chambers and wound healing were employed to test the migration ability of VSMCs . ICC was used to detect the VSMCs'morphology .Western blotting was used to investigate the expressions of SM‐actin ,SM‐MHC ,calponin ,OPN ,and p‐P70S6K1 in VSMCs of each group .Results Compared with those in control group , the proliferation and migration ability of VSMCs were significantly increased in Hcy modulation group (P< 0 .01) .The expressions of SM‐MCH and calponin increased but those of OPN and p‐P70S6K1 decreased in Hcy group compared with control group (P<0 .01) .The expression of SM‐actin did not significantly differ between the groups .Compared with those in Hcy modulation group , the proliferation and migration ability of VSMCs were significantly decreased in rosuvastatin and rapamycin groups ( P<0 .01) .The expressions of SM‐MCH and calponin increased while OPN and p‐P70S6K1 expressions decreased in rosuvastatin and rapamycin groups compared with Hcy group ( P< 0 .01 ) . Conclusion Hcy can induce the dedifferentiation of VSMCs ,and rosuvastatin can inhibit this effect of Hcy .Its potential mechanism may be realized via the mTOR/P70S6K1 signal pathway .