Analysis of Results of Continuous Invasive Arterial Blood Pressure Monitoring in Postoperative Patients.

Objective: In patients with postoperative circulatory instability, the exploration of invasive arterial blood pressure (IABP) monitoring is of great significance because it can provide real-time cardiovascular function information and help medical staff to better assess and manage the patient's circulatory status. To explore the value of IABP monitoring for patients with postoperative circulatory instability in the postanesthesia care unit (PACU). Methods: From January to December 2021, 160 postoperative patients with circulatory instability were randomly divided into a control group and a study group (80 patients in each group). A random number sequence is generated through a random number table, and random numbers are distributed to different patients to achieve random grouping. SPSS was used for data processing and statistical analysis, t test was used for continuous variables, chi-square test was used for count data, and the significance level was P < .05.We compared various parameters, such as systolic blood pressure (SBP), PACU observation time, arterial partial pressure of oxygen (PaO2), total hospitalization time, heart rate (HR), arterial partial pressure of carbon dioxide (PaCO2), re-intubation rate, mean arterial pressure (MAP), adverse events, and blood oxygen saturation (SaO2), between the two groups. Flow cytometry was used to analyze changes in immune lymphocyte subsets in the patient's peripheral blood. Results: During the postoperative observation period, there were no significant differences in SBP, PaCO2, HR, SaO2, MAP, and PaO2 between the two groups (P > .05)The study group showed higher SBP, SaO2, MAP, and PaO2, and lower HR and PaCO2 compared to the control group (P < .05). The study group also had shorter PACU observation time, total hospitalization time, and a lower re-intubation rate compared to the control group (P < .05). There was no significant difference in the overall incidence of adverse events between the two groups (7.50% vs 3.75%) (P > .05). The study group showed significantly higher proportions of lymphocytes, CD3+ T cells, CD3+ CD4+ T cells, and CD3+ CD4+/CD3+ CD8+ ratio compared to the control group (P < .05). This change may reflect the patients with a positive response of the immune system, help to resist disease progress and infection. Conclusion: IABP monitoring can continuously, dynamically and accurately collect arterial blood pressure data of patients with postoperative circulatory instability, contributing to the recovery of immune competence in patients to help formulate the best clinical treatment and intervention plan. The dynamic and accurate arterial blood pressure data collection provided by IABP monitoring contributes not only to immune competence recovery but also to overall patient management and treatment planning.

Effect of long-term nursing intervention on quality of life and social support of patients with coronary heart disease after percutaneous coronary intervention.

OBJECTIVE: To assess the effect of long-term nursing intervention on the quality of life and social support of patients after percutaneous coronary intervention (PCI). METHODS: A randomised controlled trial was designed. A total of 60 patients with coronary heart disease treated with PCI were randomly divided into the control group and the intervention group. The patients in the control group received routine nursing care, while the patients in the intervention group received long-term nursing intervention. The Simplified Quality of Life Scale-Quality of Life Scale, the Coronary Heart Disease Self-Management Scale, and the Social Support Rating Scale were used to collect and analyse the data. RESULTS: After the intervention, the scores for quality of life, social support and self-management in the intervention group were higher than those in the control group, and the differences were statistically significant (p < 0.05). CONCLUSION: Long-term nursing intervention can improve the quality of life and sense of social support of patients with coronary heart disease after PCI.

Urine N-terminal pro-B-type natriuretic peptide and plasma proenkephalin are promising biomarkers for early diagnosis of cardiorenal syndrome type 1 in acute decompensated heart failure: a prospective, double-center, observational study in real-world.

BACKGROUND: Patients with acute decompensated heart failure (ADHF) show cardiorenal syndrome type 1 (CRS-1) are more likely to have a poor outcome. However, the current criteria often lead to delayed CRS-1 diagnosis. Therefore, we evaluated the predictive value of plasma proenkephalin (pPENK) and urine NT-proBNP (uNT-proBNP) for early diagnosis of CRS-1 and vulnerable-phase prognosis in ADHF patients. METHODS: The plasma NT-proBNP (pNT-proBNP), pPENK, and uNT-proBNP were measured in 121 ADHF patients on admission. The plasma neutrophil gelatinase-associated lipocalin (pNGAL) was chosen as the reference. Logistic regression was used to determine the predictors of CRS-1. The area under the receiver operating curves (ROCs) was calculated to assess the early diagnostic value of pNGAL, pPENK, and uNT-proBNP/uCr for CRS-1. To evaluate the prognostic risk of factors for the 90-d outcomes of all ADHF patients, the Cox regression was performed and the cumulative risk curve was plotted. RESULTS: We found that pPENK [OR 1.093 (95% CI 1.022-1.169), p = 0.010; AUROC = 0.899 (95% CI 0.831-0.946)] and uNT-proBNP/uCr ratio [OR 1.015 (95% CI 1.003-1.028), p = 0.012; AUROC = 0.934 (95% CI 0.874-0.971)] could independently predict the occurrence of CRS-1 in hospitalized patients with ADHF. The pPENK [HR 1.014 (95% CI 1.000-1.042), p = 0.044] and uNT-proBNP/uCr ration [HR 0.998 (95% CI 0.997-1.000), p = 0.045] were also independent predictors of the risk of HF readmission or all-cause death 90 d after discharge in ADHF patients. CONCLUSIONS: The newly found pPENK and noninvasive test of uNT-proBNP/uCr ratio (pg/nmol) on admission may be two promising novel predictive biomarkers for early diagnosis of CRS-1 occurrence and vulnerable-phase outcomes in ADHF patients.

circ-Sirt1 controls NF-κB activation via sequence-specific interaction and enhancement of SIRT1 expression by binding to miR-132/212 in vascular smooth muscle cells.

NF-κB-mediated inflammatory phenotypic switching of vascular smooth muscle cells (VSMCs) plays a central role in atherosclerosis and neointimal formation. However, little is known about the roles of circRNAs in the regulation of NF-κB signaling. Here, we identify the involvement of circ-Sirt1 that was one of transcripts of SIRT1 host gene in VSMC inflammatory response and neointimal hyperplasia. First, in the cytoplasm, circ-Sirt1 directly interacts with and sequesters NF-κB p65 from nuclear translocation induced by TNF-α in a sequence-dependent manner. The inhibitory complex of circ-Sirt1-NF-κB p65 is not dependent on IκBα. Second, circ-Sirt1 binds to miR-132/212 that interferes with SIRT1 mRNA, and facilitates the expression of host gene SIRT1. Increased SIRT1 results in deacetylation and inactivation of the nuclear NF-κB p65. These findings illustrate that circ-Sirt1 is a novel non-coding RNA regulator of VSMC phenotype.

Analysis of factors affecting students going to school toilets in a rural primary school in China.

BACKGROUND: Several factors may affect students going to school toilets, but a few studies have analyzed the reasons for students using toilets. This study aimed to use a structural equation model to understand the factors that impacted children's toilet behavior. METHODS: This study was performed in 12 rural nonboarding primary schools (6 schools in the northern and 6 schools in the southern regions of China). All students of the third and sixth grades (761 students) were examined. A questionnaire on students' toilet behavior was used. The questionnaire included 33 perceptual items based on 5 factors: toilet facilities, cleanliness, hygiene practices, peer relationship, and experience. The questionnaire also covered the frequency of voiding and defecating by themselves. The exploratory factor analysis, confirmatory factor analysis, and pathway analysis were used to analyze the causes of students' toilet behavior. RESULTS: A statistically significant correlation coefficient of 0.300 indicated that cleanliness impacted the toilet frequency of students. The visual experience of the overall cleanliness of the toilet had the most significant impact on students' toilet behavior (path coefficient, 0.81). Washing facilities and convenient handwashing had the least impact on toilet use (path coefficient, 0.52). CONCLUSION: Cleanliness was the primary consideration for students' toilet use on campus. The visual experience of the overall cleanliness of toilets had the most significant impact when students used toilets. No pre-survey was conducted to test the reliability and validity of the questionnaire. Using self-reported data might be associated with potential recall errors.

LncRNA MIAT/miR-133a-3p axis regulates atrial fibrillation and atrial fibrillation-induced myocardial fibrosis.

Atrial fibrillation (AF) is a commonly encountered heart arrhythmia and a risk factor for cardiovascular system. The purpose of the present study was to explore the role of long non-coding RNA myocardial infarction-associated transcript (MIAT) in AF and AF-induced myocardial fibrosis and the possible mechanisms involved in this process. We successfully induced an AF rat model. Expression of MIAT presented a dramatic increase, while microRNA (miR)-133a-3p presented a dramatic decrease in atrium tissues of rats with AF induction. In addition, we also found that MIAT was highly expressed and miR-133a-3p was significantly reduced in peripheral blood leukocyte of AF patients. For biological function exploration of MIAT/miR-133a-3p axis, MIAT was knocked down using small hairpin RNA (shRNA) lentivirus injection and the rescue experiments were performed simultaneously by inhibiting miR-133a-3p using anti-miR-133a-3p lentivirus injection in rats with AF. MIAT downregulation significantly alleviated AF, increased atrial effective refractory period (AERP), and reduced the duration of AF as well as cardiomyocytes apoptosis. Whereas these effects of MIAT downregulation on AF were reversed by anti-miR-133a-3p administration. Luciferase reporter revealed that miR-133a-3p was directly regulated by MIAT. Moreover, MIAT knockdown effectively reduced AF-induced atrial fibrosis by detecting reduced collagen in the right atria and inhibited expression of fibrosis-related gene expression of collagen I, collagen III, connective tissue growth factor (CTGF) and transforming growth factor-ß1 (TGF-ß1) in rats with AF, these findings were in contrast with the findings for rats with inhibition of miR-133a-3p. In conclusion, our study demonstrated the role of MIAT downregulation in alleviating AF and AF-induced myocardial fibrosis, and the functional regulatory pathway of MIAT targeting miR-133a-3p.

Effects and Mechanisms of Vitamin C Post-Conditioning on Platelet Activation after Hypoxia/Reoxygenation.

BACKGROUND: Platelet activation occurs upon ischemia/reperfusion and is related to the generation of reactive oxygen species (ROS) during this process. Vitamin C (VC) is a powerful antioxidant. VC scavenges ROS, reduces platelet activation, and attenuates reperfusion injury. However, the effects of VC on platelets undergoing hypoxia/reoxygenation (H/R) remain unclear. OBJECTIVES: Herein, we evaluated the effects of VC on platelets in vitro following H/R and the related mechanisms. METHOD: Fresh platelets were collected from 67 volunteers at the Blood Center of Hebei Province. Platelets were diluted with saline to a concentration of 2.00 × 1011/L. Aggregation and the curve slope were evaluated within 4 h with a whole-blood impedance analyzer. To determine the optimal experimental time, platelets were treated with hypoxia or reoxygenation for different times, and impedance aggregometry was carried out by measuring changes in electrical impedance induced by arachidonic acid (0.5 mM) and adenosine diphosphate (10 µM), thereby establishing the H/R model. Three antioxidants (VC, melatonin, and probucol) were used to treat platelets after H/R, and impedance aggregometry was used to determine their effects on platelet aggregation. The influence of VC on apoptosis-related indicators was detected. ROS and the mitochondrial membrane potential were observed by inverted fluorescence microscopy and flow cytometry, respectively. Related protein levels were detected by Western blotting. RESULTS: ROS scavengers inhibited platelet activation and aggregation in a concentration-dependent manner. VC post-conditioning scavenged ROS, downregulated cytochrome C, Bax, and caspase-9 proteins, and upregulated Bcl-2 protein. These effects collectively blocked platelet apoptosis and inhibited platelet aggregation. CONCLUSIONS: VC inhibited platelet aggregation by blocking apoptosis. Thus, VC may have applications in the treatment of platelet-related diseases.

[Reliability and validity of SF-36 scale for evaluating the quality of life of Tuva adults in the Xinjiang Uygur Autonomous Region].

OBJECTIVE: To assess the reliability and validity of SF-36 scale in measuring quality of life of Tuva adults in Xinjiang Uygur Autonomous Region. METHODS: A total of 437 Tuva adults were selected by multistage sampling method, in Tuva families lived in Baihaba Village Habahe county and Kanasi and Hemu Villages Buerjin County in Artay Xinjiang Uygur Autonomous Region in 2016, including 100 males and 50 females, the three age groups 18-29, 30-49, 50 and above accounted for 30. 66%, 54. 00% and 15. 33% respectively. SF-36 scale was be used to measure the quality of life. The scale's reliability was assessed by internal consistency reliability and half-fold reliability, and the validity was assessed by set validity, discriminate validity and structural validity. RESULTS: The Cronbach's α coefficient of the SF-36 scale was 0. 838, and all of the Cronbach's α coefficients were more than 0. 750 after corresponding dimensions were deleted. The Spearman-Brown coefficient was 0. 828. The achievement ratio of aggregation tests and discrimination tests were 100% and 99. 59%, respectively. Thirty-five items were included in EFA. Seven common factors were extracted through maximum balanced rotation method, and the cumulative contribution rate was 68. 97%. Eight-dimensional data were included in EFA, and two common factors were extracted with a cumulative contribution rate of 66. 44%. The fitting degree of confirmatory factor analysis model is invalid. CONCLUSION: SF-36 has showed a good reliability, set validity and discrimination validity in evaluating the quality of life of Tuva adults in Xinjiang, but its structural validity needs to be improved.

High levels of serum ß2-microglobulin predict severity of coronary artery disease.

BACKGROUND: The identification of new risk factors for coronary artery disease (CAD) is increasingly sought in an effort to tackle this threatening disease. ß2-microglobulin (B2M) is reported to associate with peripheral arterial disease and adverse cardiovascular outcomes. However, the association between B2M and cardiovascular disease remains under-researched. This study evaluated the effects of B2M on CAD without renal dysfunction. METHODS: One thousand seven hundred sixty-two subjects (403 non-CAD subjects and 1,359 CAD subjects) were investigated. Fasting samples were collected to determine B2M level. The Gensini and SYNTAX scores were used to assess the severity of CAD. RESULTS: CAD subjects were significantly higher in serum B2M level comparing with non-CAD subjects (1.25 ± 0.46 vs 1.14 ± 0.28 mg/L, p < 0.001). Serum B2M level was a risk factor of CAD after adjusting potential confounders (Odds Ratio (OR) = 2.363, 95% confidence interval (CI): 1.467-3.906, p = 0.001). Receiver operating characteristics (ROC) showed B2M level moderately predicted diagnosis of CAD (the area under the ROC curve (AUC) = 0.608, 95% CI: 0.577-0.639, p < 0.001). Furthermore, serum B2M level was positively associated with Gensini score system, SYNTAX score system and the number of disease vessels (NDV ≥ 2). CONCLUSIONS: The significant association between serum B2M and CAD suggests that B2M could be a biomarker for CAD.

Atorvastatin Protects Myocardium Against Ischemia-Reperfusion Injury Through Inhibiting miR-199a-5p.

OBJECTIVE: This study aimed to evaluate the protective effects of atorvastatin against myocardial ischemia/reperfusion (I/R) injury in cardiomyocytes and its possible underlying mechanism. METHOD: Direct cytotoxic effect of OGD/R on cardiomyocytes with and without atorvastatin pretreatment was evaluated. Effects of atorvastatin on expression of GSK-3ß and miR-199a-5p were determined using RT-PCR and Western blot. In addition, GSK-3ß expression with miR-199a-5p upregulation and downregulation was detected using RT-PCR, Western blot, and immunohistochemistry. RESULTS: Pretreatment with atorvastatin significantly improved the recovery of cells viability from OGD/R (p<0.05). In addition, the atorvastatin pretreatment significantly increased GSK-3ß expression both in mRNA level and protein level and decreased miR-199a-5p expression in mRNA level (p<0.05). Upregulation and downregulation of miR-199a-5p respectively decreased and increased GSK-3ß expression both in mRNA level and protein level. CONCLUSION: These results suggested that atorvastatin provides the cardioprotective effects against I/R injury via increasing GSK-3ß through inhibition of miR-199a-5p.

Atorvastatin protects vascular smooth muscle cells from TGF-ß1-stimulated calcification by inducing autophagy via suppression of the ß-catenin pathway.

BACKGROUND: Arterial calcification is a major event in the progression of atherosclerosis. It is reported that statins exhibit various protective effects against vascular smooth muscle cell (VSMC) inflammation and proliferation in cardiovascular remodeling. Although statins counteract atherosclerosis, the molecular mechanisms of statins on the calcium release from VSMCs have not been clearly elucidated. METHODS: Calcium content of VSMCs was measured using enzyme-linked immunosorbent assay (ELISA). The expression of proteins involved in cellular transdifferentiation was analyzed by western blot. Cell autophagy was measured by fluorescence microscopic analysis for acridine orange staining and transmission electron microscopy analysis. The autophagic inhibitors (3-MA, chloroquine, NH4Cl and bafilomycin A1) and ß-catenin inhibitor JW74 were used to assess the effects of atorvastatin on autophagy and the involvement of ß-catenin on cell calcification respectively. Furthermore, cell transfection was performed to overexpress ß-catenin. RESULTS: In VSMCs, atorvastatin significantly suppressed transforming growth factor-ß1 (TGF-ß1)-stimulated calcification, accompanied by the induction of autophagy. Downregulation of autophagy with autophagic inhibitors significantly suppressed the inhibitory effect of atorvastatin on cell calcification. Moreover, the beneficial effect of atorvastatin on calcification and autophagy was reversed by ß-catenin overexpression. Conversely, JW74 supplement enhanced this effect. CONCLUSION: These data demonstrated that atorvastatin protect VSMC from TGF-ß1-stimulated calcification by inducing autophagy through suppression of the ß-catenin pathway, identifying autophagy induction might be a therapeutic strategy for use in vascular calcification.

Regulations of Citrus Pectin Oligosaccharide on Cholesterol Metabolism: Insights from Integrative Analysis of Gut Microbiota and Metabolites.

(1) Background: Recently, academic studies are demonstrating that the cholesterol-lowering effects of pectin oligosaccharides (POSs) are correlated to intestinal flora. However, the mechanisms of POS on cholesterol metabolisms are limited, and the observations of intestinal flora are lacking integrative analyses. (2) Aim and methods: To reveal the regulatory mechanisms of POS on cholesterol metabolism via an integrative analysis of the gut microbiota, the changes in gut microbiota structure and metabolite composition after POS addition were investigated using Illumina MiSeq sequencing and non-targeted metabolomics through in vitro gut microbiota fermentation. (3) Results: The composition of fecal gut flora was adjusted positively by POS. POS increased the abundances of the cholesterol-related bacterial groups Bacteroidetes, Bifidobacterium and Lactobacillus, while it decreased conditional pathogenic Escherichia coli and Enterococcus, showing good prebiotic activities. POS changed the composition of gut microbiota fermentation metabolites (P24), causing significant changes in 221 species of fermentation metabolites in a non-targeted metabolomics analysis and promoting the production of short-chain fatty acids. The abundances of four types of cholesterol metabolism-related metabolites (adenosine monophosphate, cyclic adenosine monophosphate, guanosine and butyrate) were significantly higher in the P24 group than those in the control group without POS addition. (4) Conclusion: The abovementioned results may explain the hypocholesterolemic effects of POS and promotion effects on cholesterol efflux of P24. These findings indicated that the potential regulatory mechanisms of citrus POS on cholesterol metabolism are modulated by cholesterol-related gut microbiota and specific metabolites.

miR-421-Mediated Suppression of FGF13 as a Novel Mechanism Ameliorating Cardiac Hypertrophy by Inhibiting Endoplasmic Reticulum Stress.

Pathological cardiac hypertrophy is an independent risk factor for heart failure. Currently, clinical treatments offer limited effectiveness, and both mortality and morbidity from cardiac hypertrophy and heart failure continue to be significant. Therefore, it is extremely urgent to find new intervention targets to prevent and alleviate pathological cardiac hypertrophy. In this study, we explored FGF13 expression and its upstream regulators in hypertrophic hearts. Firstly, we observed an increase in FGF13 expression levels in human hypertrophic myocardium tissues, as well as in mouse models of TAC-induced hypertrophy and in neonatal rat cardiomyocyte (NRCM) models induced by isoproterenol (ISO). Moreover, these elevated levels of FGF13 were shown to positively correlate with hypertrophic markers, including ANP and BNP. By using both gain-of-function and loss-of-function approaches in an in vitro hypertrophy model, we demonstrated that FGF13 knockdown could inhibit endoplasmic reticulum stress (ERS), thereby ameliorating cardiomyocyte hypertrophy. Meanwhile, we investigated the upstream regulators of FGF13 in hypertrophic hearts, and a dual-luciferase reporter assay confirmed that FGF13 is a direct target of miR-421. Overexpression of miR-421 decreased the protein level of FGF13 and ameliorated ISO-induced cardiomyocyte hypertrophy via modulating ER stress. In contrast, overexpression of FGF13 attenuated the ameliorative effect of miR-421 on ISO-induced cardiomyocyte hypertrophy. Taken together, the present results suggested that miR-421 ameliorated ISO-induced cardiomyocyte hypertrophy by negatively regulating FGF13 expression. This finding may offer a novel approach for the treatment of cardiac hypertrophy.

Atorvastatin suppresses aldosterone-induced neonatal rat cardiac fibroblast proliferation by inhibiting ERK1/2 in the genomic pathway.

UNLABELLED: Excessive proliferation of cardiac fibroblasts plays a critical role in myocardial remodeling and the development of chronic heart failure, and the inhibition of cardiac fibroblast proliferation may help in the prevention of heart failure. Recent studies indicate that aldosterone promotes fibroblast proliferation and that ERK1/2 is critically involved in this process. However, whether aldosterone promotes p-ERK1/2 expression in cardiac fibroblasts via the classic genomic or rapid nongenomic pathway is not fully understood, and the effect of statins on both of these pathways is poorly studied. In this study, we investigated the role of the ERK1/2 pathway in the antiproliferative effects of atorvastatin, in the context of aldosterone-induced cardiac fibroblast proliferation. METHODS: : 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and 5-bromo-2'-deoxyuridine assays and flow cytometry analysis were used to examine the inhibitory effects of atorvastatin on aldosterone-induced cardiac fibroblast proliferation and cell cycle progression. Confocal microscopy in conjunction with immunofluorescence and Western blot analysis were used to detect protein expression level. RESULTS: : Atorvastatin effectively inhibited aldosterone-induced cardiac fibroblast proliferation and blocked cell cycle progression by arresting the cells at the G0/G1 phase. Aldosterone-induced cyclin D1 and cyclin E2 expression was markedly suppressed by atorvastatin. In addition, atorvastatin significantly blocked the aldosterone-induced p-ERK1/2 expression in the genomic pathway but had no effect on the nongenomic pathway of the aldosterone-induced p-ERK1/2 expression. CONCLUSIONS: : ERK1/2 is essential for cardiac fibroblast proliferation induced by aldosterone. Atorvastatin effectively suppressed aldosterone-induced cardiac fibroblast proliferation and cell cycle progression, which were associated with the inhibition of the p-ERK1/2 expression in the genomic pathway and subsequent cyclin D1 and cyclin E2 expression.

Brachial-ankle pulse wave velocity increasing with heart rate accelerates.

Pulse wave velocity (PWV) indicates the degree of vascular stiffness. This study aimed to explore the association between heart rate (HR) and brachial-ankle (ba)-PWV in patients with pacemaker implantation. This retrospective observational study included patients who underwent permanent pacemaker implantation at the Second Hospital of Hebei Medical University between December 2018 and December 2021. All patients were pacemaker-dependent, and the ba-PWV values were collected during HR setted from 60 to 100 bpm. A total of 68 patients (34 males, aged 65.97 ± 9.90 years) were included in this study. There were significant difference of ba-PWV and diastolic blood pressure (DBP) among different HR (both P < 0.001). After adjusted systolic blood pressure (SBP), DBP, age, and sex, the generalized estimating equation showed ba-PWV was independently associated with HR, with increased HR showed higher coefficient: 70 bpm: ß = 42.26 (95% CI: 15.34-69.18, P = 0.002), 80 bpm: ß = 84.16 (95% CI: 52.48-115.84, P < 0.001), 90 bpm: ß = 129.27 (95% CI: 52.48-115.84, P < 0.001), and 100 bpm: 186.31 (95% CI: 137.02-235.59, P < 0.001). The results demonstrate that changes in HR may affect the ba-PWV, the ba-PWV values tend to be higher when HR accelerates.

Integrin beta 3-overexpressing mesenchymal stromal cells display enhanced homing and can reduce atherosclerotic plaque.

BACKGROUND: Umbilical cord (UC) mesenchymal stem cell (MSC) transplantation is a potential therapeutic intervention for atherosclerotic vascular disease. Integrin beta 3 (ITGB3) promotes cell migration in several cell types. However, whether ITGB-modified MSCs can migrate to plaque sites in vivo and play an anti-atherosclerotic role remains unclear. AIM: To investigate whether ITGB3-overexpressing MSCs (MSCsITGB3) would exhibit improved homing efficacy in atherosclerosis. METHODS: UC MSCs were isolated and expanded. Lentiviral vectors encoding ITGB3 or green fluorescent protein (GFP) as control were transfected into MSCs. Sixty male apolipoprotein E-/- mice were acquired from Beijing Vital River Lab Animal Technology Co., Ltd and fed with a high-fat diet (HFD) for 12 wk to induce the formation of atherosclerotic lesions. These HFD-fed mice were randomly separated into three clusters. GFP-labeled MSCs (MSCsGFP) or MSCsITGB3 were transplanted into the mice intravenously via the tail vein. Immunofluorescence staining, Oil red O staining, histological analyses, western blotting, enzyme-linked immunosorbent assay, and quantitative real-time polymerase chain reaction were used for the analyses. RESULTS: ITGB3 modified MSCs successfully differentiated into the "osteocyte" and "adipocyte" phenotypes and were characterized by positive expression (> 91.3%) of CD29, CD73, and CD105 and negative expression (< 1.35%) of CD34 and Human Leukocyte Antigen-DR. In a transwell assay, MSCsITGB3 showed significantly faster migration than MSCsGFP. ITGB3 overexpression had no effects on MSC viability, differentiation, and secretion. Immunofluorescence staining revealed that ITGB3 overexpression substantially enhanced the homing of MSCs to plaque sites. Oil red O staining and histological analyses further confirmed the therapeutic effects of MSCsITGB3, significantly reducing the plaque area. Enzyme-linked immunosorbent assay and quantitative real-time polymerase chain reaction revealed that MSCITGB3 transplantation considerably decreased the inflammatory response in pathological tissues by improving the dynamic equilibrium of pro- and anti-inflammatory cytokines. CONCLUSION: These results showed that ITGB3 overexpression enhanced the MSC homing ability, providing a potential approach for MSC delivery to plaque sites, thereby optimizing their therapeutic effects.

Interrupted sleep by ambulatory blood pressure monitoring does not affect blood pressure.

BACKGROUND: For the past 20 years, many hypertension guidelines have strongly recommended the practical use of ambulatory blood pressure monitoring (ABPM) to the diagnosis and management of hypertension. However, whether different sleep conditions during ABPM will affect blood pressure (BP) fluctuations and lead to inaccurate measurement results is a concern of clinicians. METHOD: This was a prospective cohort study in the real-world setting. The participants were recruited between June 2018 and June 2019 in Hebei Province, China. There are three types of sleep during ABPM: undisturbed sleep, disturbed sleep and severely disturbed sleep. The people were divided into three groups according to their sleep types during ABPM. The primary outcome is 24-h mean BP, circadian rhythm of BP and variation coefficient of 24-h BP. Comparisons between groups are tested by Kruskal-Wallis H test. RESULTS: In total 1154 people completed the study. There was no significant difference in 24-h mean BP and circadian rhythm of BP among the three groups. There are statistically significant differences among the three groups in the variation coefficient of 24-h BP for the general population and noninsomnia population. There was no significant difference in mean BP, circadian rhythm of BP and variation coefficient of BP among the three groups for the insomnia people. CONCLUSION: Regardless of the insomniac or noninsomniac population, sleep conditions during ABPM do not affect BP value and BP rhythm. For noninsomniac people, the sleep situation during ABPM may affect the BP variation coefficient.

DLEU2 modulates proliferation, migration and invasion of platelet-derived growth factor-BB (PDGF-BB)-induced vascular smooth muscle cells (VSMCs) via miR-212-5p/YWHAZ axis.

DLEU2 has been proved to act as an oncogene in a variety of cancers, but its role in cardiovascular diseases is dearth of research. Thus, this study mainly discussed the effect and possible mechanism of DLEU2 on platelet-derived growth factor-BB (PDGF-BB)-triggered vascular smooth muscle cell (VSMC) injury. To obtain authentic results, the expressions of target genes in atherosclerosis serum were determined by reverse transcription quantitative PCR (RT-qPCR) and the protein levels were evaluated by Western blot. PDGF-BB was used to simply simulate the biological characteristics of VSMCs in vitro. The effect of DLEU2 on the biological behavior of PDGF-BB-induced VSMCs was analyzed by gain- and loss-of-function assays. Bioinformatics analysis, dual luciferase reporter assay, and Pearson correlation method were conducted to determine the relationship between target genes. The role of DLEU2/miR-212-5p/ YWHAZ (tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein zeta) axis in PDGF-BB-induced VSMCs was verified by rescue experiments. As a result, DLEU2 and YWHAZ were up-regulated, and miR-212-5p was down-regulated in atherosclerosis serum. Overexpressed DLEU2 facilitated the biological behavior of PDGF-BB-induced VSMCs, whilst siDLEU2 did the opposite. Moreover, overexpressed DLEU2 promoted proliferating cell nuclear antigen (PCNA) expression but repressed α-smooth muscle actin (α-SMA) and Calponin expressions, while it also enhanced YWHAZ expression via suppressing miR-212-5p. MiR-212-5p mimic and siYWHAZ reversed the effects of overexpressed DLEU2 on above biological characteristics and protein expressions in PDGF-BB-induced VSMCs, while the regulatory effect of miR-212-5p mimic was partially offset by overexpressed YWHAZ. Collectively, DLEU2 modulates PDGF-BB-induced VSMC injury via miR-212-5p/YWHAZ axis in atherosclerosis.

CTRP3 is a coronary artery calcification biomarker and protects against vascular calcification by inhibiting ß-catenin nuclear translocation to prevent vascular smooth muscle cell osteogenic differentiation.

BACKGROUND: Coronary artery calcification (CAC) is an important risk factor for cardiovascular events and has been shown to be correlated with serum adiponectin levels. However, it remains unknown whether C1 tumor necrosis factor-related protein 3 (CTRP3) (homologous to adiponectin) is associated with CAC, and whether CTRP3 affects the osteoblastic differentiation of vascular smooth muscle cells. Here, we analyzed the association between CTRP3 expression and CAC. METHODS: A case-control study was conducted involving 119 patients with coronary heart disease to identify the predictive value of CTRP3 for CAC. Additionally, mouse aortic smooth muscle cells transfected for ß-catenin overexpression were subjected to treatment with CTRP3 and the ß-catenin inhibitor JW74. The calcium content in smooth muscle cells was determined. Western blotting was performed to measure the expression levels of different osteoblastogenic proteins in vascular smooth muscle cells obtained from different treatment groups. RESULTS: The serum CTRP3 levels were significantly lower in patients with CAC than in those without CAC, and even lower in patients with both CAC and diabetes mellitus. CTRP3 played roles as a protective factor and potential predictor in CAC. CTRP3 inhibited the osteogenic differentiation of vascular smooth muscle cells induced under high glucose and lipid conditions by inhibiting the nuclear translocation of ß-catenin. CONCLUSIONS: CTRP3 may serve as a valuable screening biomarker and a novel therapeutic target in CAC, particularly in diabetes patients.

Physical optimization of cell proliferation and differentiation using spinner flask and microcarriers.

The traditional breeding industry has been increasingly saturated and caused environmental pollution, disease transmission, excessive resource use, and methane emission; however, it still cannot meet the needs of the growing population. To explore other alternatives, researchers focused on cell agriculture and cell-based meat, especially large-scale cell culture. As a prerequisite for production, large-scale culture technology has become an important bottleneck restricting cell-based meat industrialization. In this study, the single-factor variable method was adopted to examine the influence of Cytodex1 microcarrier pretreatment, spinner flask reaction vessel, cell culture medium, serum and cell incubation, and other influencing factors on large-scale cell cultures to identify the optimization parameters suitable for 3D culture environment. Collagen and 3D culture were also prospectively explored to promote myogenesis and cultivate tissue-like muscle fibers that contract spontaneously. This research lays a theoretical foundation and an exploratory practice for large-scale cell cultures and provides a study reference for the microenvironment of myoblast culture in vitro, a feasible direction for the cell therapy of muscular dystrophy, and prerequisites for the industrialized manufacturing of cell-based meat. Graphical summary: Research on large-scale myoblast culture using spinner flasks and microcarriers. For cell culture, the microcarriers were pretreated with UV and collagen. Cell seeding condition, spinner flask speed, resting time, and spinner flask culture microenvironment were then optimized. Finally, two culture systems were prepared: a culture system based on large-scale cell expansion and a culture system for myogenesis promotion and differentiation.