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1.
Cell Biol Int ; 2021 Oct 17.
Artigo em Inglês | MEDLINE | ID: mdl-34658101

RESUMO

Myocardial ischemia reperfusion (MIR) injury negatively affects the prognosis of acute myocardial infarction (AMI), while effective suppression of MIR injury remains a largely unmet clinical need. Interferon regulatory factors (IRF) are key players in chronic cardiac disorders such as cardiac remodeling. However, their roles in acute MIR injury remain largely unknown. In current study, microarray data indicated that IRF1 expression was consistently changed in human ischemic heart and ischemic reperfused mouse heart. Western blot analysis confirmed the expression alterations of IRF1 in ischemic reperfused mouse heart. Cardiac-specific IRF1 knockdown significantly decreased infarct size, improved cardiac function, and suppressed myocardial apoptosis after MIR injury. Conversely, cardiac-specific IRF1 overexpression significantly promoted MIR injury. Further investigation revealed that IRF1 transcriptionally regulated the expression of inducible nitric oxide synthase (iNOS), and augmented oxidative stress. Taken together, we presented the first direct evidence that IRF1 served as a mediator of MIR injury, and IRF1 may represent a potential therapeutic target for alleviating MIR injury. This article is protected by copyright. All rights reserved.

2.
ACS Biomater Sci Eng ; 2021 Sep 08.
Artigo em Inglês | MEDLINE | ID: mdl-34494831

RESUMO

Porous inorganic materials play an important role in adsorbing targeted analytes and supporting efficient reactions in analytical science. The detection performance relies on the structural properties of porous materials, considering the tunable pore size, shape, connectivity, etc. Herein, we first clarify the enhancement mechanisms of porous materials for bioanalysis, concerning the detection sensitivity and selectivity. The diagnostic applications of porous material-assisted platforms by coupling with various analytical techniques, including electrochemical sensing, optical spectrometry, and mass spectrometry, etc., are then reviewed. We foresee that advanced porous materials will bring far-reaching implications in bioanalysis toward real-case applications, especially as diagnostic assays in clinical settings.

3.
Hepatology ; 2021 Sep 21.
Artigo em Inglês | MEDLINE | ID: mdl-34545586

RESUMO

BACKGROUND & AIMS: Nonalcoholic steatohepatitis (NASH) has become a worldwide epidemic, which is a common clinical condition predisposing to advanced liver diseases. A large and growing unmet therapeutic need for this condition reflects incomplete understanding of its pathogenesis. In current study, we identified a transcription factor Zinc Fingers and Homeoboxes 2 (ZHX2) in hepatocytes as a protective factor against steatohepatitis. APPROACH & RESULTS: We found that hepatic ZHX2 was significantly suppressed in NASH models and steatotic hepatic cells. Hepatocyte-specific ablation of ZHX2 exacerbated NASH-related phenotypes in mice, including lipid accumulation, enhanced inflammation, and hepatic fibrosis. Conversely, hepatocyte-specific overexpression of ZHX2 significantly alleviated the progression of NASH in an experimental setting. Integrated analysis of transcriptomic profiling and chromatin immunoprecipitation sequencing data demonstrated that the Phosphatase and Tensin Homologue (PTEN) was a target gene of ZHX2 in hepatocyte. ZHX2 bound to the promoter of PTEN gene and subsequently promoted the transcription of PTEN, which mediated the beneficial role of ZHX2 against NASH. CONCLUSION: In conclusion, current findings unfolded a protective role of ZHX2 against NASH progression by transcriptionally activating PTEN. These findings shed light on the therapeutic potential of targeting ZHX2 for treating NASH and related metabolic disorders.

4.
Artigo em Inglês | MEDLINE | ID: mdl-34541852

RESUMO

The nitrate electroreduction reaction (NO3--ERR) is an efficient and green approach for nitrate remediation, which requires a highly active and selective electrocatalyst. In this work, porous and amorphous cobalt phosphide nanoshuttles (CoP PANSs) are successfully synthesized by using Mg2+ ion-doped calcium carbonate nanoshuttles (Mg-CaCO3 NSs) as the initial reaction precursor via precipitation transformation and a high-temperature phosphidation strategy. Various physical characterizations show that CoP PANSs have porous architecture, amorphous crystal structure, and big surface area. Electrochemical measurements reveal for the first time that CoP PANSs have outstanding electroactivity for NO3--ERR in a neutral electrolyte. At an applied potential of -0.5 V vs reversible hydrogen electrode, CoP PANSs can achieve a high Faraday efficiency (94.24 ± 2.8%) and high yield rate (19.28 ± 0.53 mg h-1 mgcat-1) for ammonia production, which exceeds most reported values at various electrocatalysts for NO3--ERR. Thus, the present result indicates that cobalt phosphide nanomaterials have promising application for NO3--ERR.

5.
Medicine (Baltimore) ; 100(33): e26875, 2021 Aug 20.
Artigo em Inglês | MEDLINE | ID: mdl-34414939

RESUMO

BACKGROUND: Elevated homocysteine (Hcy) levels showed increasing significance as the predisposing factor for the pathogenesis of atherosclerotic sequelae, including cardiovascular mortality, coronary artery disease, and stroke. There is increasing evidence linking plasma Hcy levels and heart failure (HF). The association between the elevated level of plasma Hcy and HF was examined by meta-analysis and systematic review in this study. METHODS: The PubMed and ScienceDirect databases until April 2020 were utilized to collect previous literature on plasma Hcy levels and the potential relation to HF. The pooled effects were evaluated depending on standardized mean differences (SMDs) with 95% confidence intervals (CIs), and the calculation was performed using Stata 12 software. Potential sources of heterogeneity were assessed with subgroup analysis and sensitivity analysis. RESULTS: A total of 12 research projects including 5506 subjects were selected. For pooled effect, the results confirmed that patients with HF had higher Hcy levels than the control subjects (SMD,1.148 and 95%CI, [0.715, 1.581]). Based on the classification of New York Heart Association (NYHA), the Hcy levels for the group of NYHA I or II (SMD, 1.484 and 95% CI, [0.442, 2.527]) and the group of NYHA III or IV (SMD, 3.361 and 95% CI, [1.902, 4.820]) were significantly increased compared to controls, while the increase was more intensive for the group of NYHA III or IV. Subgroup analyses revealed similar results. CONCLUSION: Our meta-analysis identified that plasma Hcy levels were significantly elevated in HF patients compared to control subjects, which is positively related to the advancement of NYHA class.


Assuntos
Insuficiência Cardíaca/sangue , Insuficiência Cardíaca/complicações , Homocisteína/sangue , Humanos
6.
Artigo em Inglês | MEDLINE | ID: mdl-34461299

RESUMO

BACKGROUND & AIMS: Cirrhotic cardiomyopathy is a major complication and cause of morbidity in end-stage primary biliary cholangitis (PBC). However, it is unclear whether there is clinically silent myocardial involvement at the early stage of PBC before cirrhosis and cardiac manifestations. This prospective, three-center, multi-modality cardiac imaging study on the early identification of myocardial impairment in PBC (EARLY-MYO-PBC) was designed to identify silent myocardial impairment in PBC patients without cardiac manifestations. METHODS: A total of 112 subjects (56 with PBC and 56 age- and sex-matched controls) undergoing cardiovascular magnetic resonance (CMR) were enrolled. Demographic, serologic, and cardiac imaging data were prospectively collected. All participants had no cardiac discomfort or previous heart disease and had normal electrocardiographic findings. RESULTS: Subclinical myocardial involvement, as evidenced by cardiac morphologic, functional, and tissue characterization changes on CMR, including hyperdynamic left ventricular (LV) ejection fraction (median, 75% in PBC patients vs 69% in controls, P = .029), subclinical myocardial edema by T2-short tau inversion recovery (21% vs 2% in controls, P = .001), elevated extracellular matrix indices (30% vs 26% in controls, P < .001), and impaired myocardial viability by positive late gadolinium enhancement (LGE) (36%), was detected in PBC patients. Importantly, a mid-wall "stripe" at the LV septum was identified as a PBC-specific LGE pattern that differs from other known cardiomyopathies. In multivariate analysis, gp210 positivity (odds ratio [OR] = 9.909, P = .010), lower hemoglobin (OR = 0.919, P = .004), and body mass index (OR = 0.638, P = .005) were independent predictors of cardiac abnormalities in PBC. CONCLUSIONS: This study demonstrates clinically silent cardiac impairment with specific CMR patterns in PBC, allowing optimal screening for early myocardial impairment and potentially timely therapies. (Trial registration no.: NCT03545672).

7.
Nat Commun ; 12(1): 4721, 2021 08 05.
Artigo em Inglês | MEDLINE | ID: mdl-34354057

RESUMO

G protein-coupled receptors (GPCRs) are the most common proteins targeted by approved drugs. A complete mechanistic elucidation of large-scale conformational transitions underlying the activation mechanisms of GPCRs is of critical importance for therapeutic drug development. Here, we apply a combined computational and experimental framework integrating extensive molecular dynamics simulations, Markov state models, site-directed mutagenesis, and conformational biosensors to investigate the conformational landscape of the angiotensin II (AngII) type 1 receptor (AT1 receptor) - a prototypical class A GPCR-activation. Our findings suggest a synergistic transition mechanism for AT1 receptor activation. A key intermediate state is identified in the activation pathway, which possesses a cryptic binding site within the intracellular region of the receptor. Mutation of this cryptic site prevents activation of the downstream G protein signaling and ß-arrestin-mediated pathways by the endogenous AngII octapeptide agonist, suggesting an allosteric regulatory mechanism. Together, these findings provide a deeper understanding of AT1 receptor activation at an atomic level and suggest avenues for the design of allosteric AT1 receptor modulators with a broad range of applications in GPCR biology, biophysics, and medicinal chemistry.


Assuntos
Receptor Tipo 1 de Angiotensina/química , Receptor Tipo 1 de Angiotensina/metabolismo , Regulação Alostérica , Sítio Alostérico , Sítios de Ligação/genética , Desenho de Fármacos , Humanos , Cadeias de Markov , Simulação de Dinâmica Molecular , Mutagênese Sítio-Dirigida , Conformação Proteica , Receptor Tipo 1 de Angiotensina/genética , Transdução de Sinais , beta-Arrestinas/metabolismo
8.
Ying Yong Sheng Tai Xue Bao ; 32(6): 2180-2190, 2021 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-34212624

RESUMO

Due to its vulnerability and anthropogenic disturbance, ecological problems in karst areas are prominent, such as vegetation destruction, soil erosion, and rocky desertification. Comprehensive analysis of ecological vulnerability and influencing factors in karst areas can provide scientific support for regional ecological restoration and environmental governance. With Guangnan County, a typical karst region in southeastern Yunnan, as an example, we constructed a karst regional eco-environmental vulnerability assessment index system from the perspective of natural and factitious factors. We used SPCA to assess the ecological vulnerability in 2000, 2010 and 2018. We further analyzed the temporal and spatial variations and explored its influencing factors by using geographic detectors. From 2000 to 2018, the changes of overall fragility were small, but the degree of fragility had been intensifying. The grade of ecological vulnerability was mainly slight fragile. The area with mild, moderate and severe fragility was increasing, while the area of extremely fragile showed no change. Guangnan County had a higher ecological vulnerability in the south of "Zhetu-Liancheng-Yangliujing-Banbang", and lower in the north. The spatial agglomeration effect of vulnerability was strong in this county. The north part of Guangnan was vulnerable low-low agglomeration areas, while the southwest and southeast parts were in high-fragility-high agglomeration areas. The implementation of ecological engineering was conducive to the improvement of regional ecological fragility, while the disturbance of human activities further deteriorated ecological fragility. The area proportion of rocky desertification and stratum lithology had stronger influence on ecological fragility of the karst area. The most important influencing factor of the karst ecological fragility was the development of karst carbonate rocks.


Assuntos
Conservação dos Recursos Naturais , Ecossistema , China , Política Ambiental , Atividades Humanas , Humanos
9.
J Am Heart Assoc ; 10(15): e021707, 2021 08 03.
Artigo em Inglês | MEDLINE | ID: mdl-34325521

RESUMO

Background Abdominal aortic aneurysm (AAA) is a life-threatening vascular disorder characterized by chronic inflammation of the aortic wall, which lacks effective pharmacotherapeutic remedies and has an extremely high mortality. Nuclear receptor NR4A1 (Nur77) functions in various chronic inflammatory diseases. However, the influence of Nur77 on AAA has remained unclear. Herein, we sought to determine the effects of Nur77 on the development of AAA. Methods and Results We observed that Nur77 expression decreased significantly in human and mice AAA lesions. Deletion of Nur77 accelerated the development of AAA in mice, as evidenced by increased AAA incidence, abdominal aortic diameters, elastin fragmentation, and collagen content. Consistent with genetic manipulation, pharmacological activation of Nur77 by celastrol showed beneficial effects against AAA. Microscopic and molecular analyses indicated that the detrimental effects of Nur77 deficiency were associated with aggravated macrophage infiltration in AAA lesions and increased pro-inflammatory cytokines secretion and matrix metalloproteinase (MMP-9) expression. Bioinformatics analyses further revealed that LOX-1 was upregulated by Nur77 deficiency and consequently increased the expression of cytokines and MMP-9. Moreover, rescue experiments verified that LOX-1 notably aggravated inflammatory response, an effect that was blunted by Nur77. Conclusions This study firstly demonstrated a crucial role of Nur77 in the formation of AAA by targeting LOX-1, which implicated Nur77 might be a potential therapeutic target for AAA.

10.
Adv Sci (Weinh) ; 8(18): e2101333, 2021 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-34323397

RESUMO

Although mass spectrometry (MS) of metabolites has the potential to provide real-time monitoring of patient status for diagnostic purposes, the diagnostic application of MS is limited due to sample treatment and data quality/reproducibility. Here, the generation of a deep stabilizer for ultra-fast, label-free MS detection and the application of this method for serum metabolic diagnosis of coronary heart disease (CHD) are reported. Nanoparticle-assisted laser desorption/ionization-MS is used to achieve direct metabolic analysis of trace unprocessed serum in seconds. Furthermore, a deep stabilizer is constructed to map native MS results to high-quality results obtained by established methods. Finally, using the newly developed protocol and diagnosis variation characteristic surface to characterize sensitivity/specificity and variation, CHD is diagnosed with advanced accuracy in a high-throughput/speed manner. This work advances design of metabolic analysis tools for disease detection as it provides a direct label-free, ultra-fast, and stabilized platform for future protocol development in clinics.

11.
Aging (Albany NY) ; 13(12): 16062-16071, 2021 06 13.
Artigo em Inglês | MEDLINE | ID: mdl-34120891

RESUMO

Neural stem cells play pivotal roles during prenatal development and throughout life. Here, we report that Paired immunoglobulin-like receptor B (PirB) functions as a suppressor during brain neurogenesis in the adult mouse. PirB expression increased with age during development, and its deficiency promoted neural stem cell proliferation and differentiation in vivo and in vitro. Furthermore, we detected an increase in Type 1 neural stem cells in PirB-deficient mice compared to their wild-type littermates. PirB deficiency promoted stemness marker gene expression of Sox2 and KLF4 by activating Akt1 phosphorylation. These findings suggest that PirB inhibits the self-renewal and differentiation capacities of neural stem cells. Thus, PirB may have the potential to serve as a therapeutic target for treatment of reduced neurogenesis in adults due to aging or other pathological conditions.


Assuntos
Hipocampo/citologia , Células-Tronco Neurais/metabolismo , Receptores Imunológicos/metabolismo , Envelhecimento/metabolismo , Animais , Diferenciação Celular , Autorrenovação Celular , Camundongos Endogâmicos C57BL , Células-Tronco Neurais/citologia , Fosforilação , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais
12.
Biomed Pharmacother ; 140: 111779, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34062415

RESUMO

Doxorubicin (DOX) is a widely used antitumor drug that causes severe cardiotoxicity in patients; no effective strategy yet exists to address this problem. We previously reported that 8-formylophiopogonanone B (8-FOB), a natural isoflavone in Ophiopogon japonicas, antagonizes paraquat-induced hepatotoxicity. Here, we explored the mechanisms underlying DOX-induced cardiotoxicity as well as whether 8-FOB can alleviate DOX-induced cardiotoxicity. Acute cardiotoxicity was established by injecting C57BL/6J mice with a single dose of DOX (20 mg/kg, intraperitoneal). To elucidate the mechanisms underlying DOX-induced cardiotoxicity, differentially expressed genes between hearts from DOX-treated and control mice were identified from the Gene Expression Omnibus (GEO) database via GEO2R. Using the Cytoscape software plugin cytoHubba, five hub genes associated with DOX-induced cardiotoxicity were identified: CD68, PTEN, SERPINE1, AIF1, and HMOX1. However, of these, only HMOX1 protein expression levels were significantly increased after DOX treatment. We also confirmed that HMOX1-dependent myocardial inflammation and fibrosis were closely associated with DOX-induced cardiotoxicity. More importantly, 8-FOB protected against DOX-cardiotoxicity by ameliorating cardiac injury and dysfunction, reducing cardiac fibrosis and inflammatory cytokine release, and inhibiting HMOX1 expression. In conclusion, our results suggest that inhibition of HMOX1-dependent myocardial inflammatory insults and fibrosis is essential for 8-FOB to ameliorate DOX-caused cardiotoxicity.


Assuntos
Antineoplásicos , Cardiotônicos/uso terapêutico , Cardiotoxicidade/tratamento farmacológico , Doxorrubicina , Heme Oxigenase-1/antagonistas & inibidores , Isoflavonas/uso terapêutico , Proteínas de Membrana/antagonistas & inibidores , Animais , Cardiotônicos/farmacologia , Cardiotoxicidade/genética , Cardiotoxicidade/metabolismo , Cardiotoxicidade/patologia , Citocinas/genética , Fibrose , Heme Oxigenase-1/genética , Heme Oxigenase-1/metabolismo , Inflamação/tratamento farmacológico , Inflamação/genética , Inflamação/metabolismo , Inflamação/patologia , Isoflavonas/farmacologia , Masculino , Proteínas de Membrana/genética , Proteínas de Membrana/metabolismo , Camundongos Endogâmicos C57BL , Miocárdio/metabolismo , Miocárdio/patologia
13.
Hepatobiliary Pancreat Dis Int ; 20(4): 352-360, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-34024736

RESUMO

BACKGROUND: Hepatic ischemia-reperfusion (I/R) injury (IRI) represents a crucial challenge in liver transplantation. Fisetin has anti-inflammatory, anti-aging and anti-oxidative properties. This study aimed to examine whether fisetin mitigates hepatic IRI and examine its underlying mechanisms. METHODS: Sham or warm hepatic I/R operated mice were pretreated with fisetin (5, 10 or 20 mg/kg). Hepatic histological assessments, TUNEL assays and serum aminotransferase measurements were performed. An in vitro hypoxia/reoxygenation (H/R) model using RAW264.7 macrophages pretreated with fisetin (2.5, 5 or 10 µmol/L) was also used. Serum and cell supernatant concentrations of interleukin-1ß (IL-1ß), IL-18 and tumor necrosis factor-α (TNF-α) were determined by enzyme-linked immunosorbent assay (ELISA). Protein levels of p-GSK3ß, p-AMPK and NLR family pyrin domain-containing 3 (NLRP3)-associated proteins were detected by Western blotting. RESULTS: Compared with the I/R group, fisetin pretreatment reduced pathological liver damage, serum aminotransferase levels, serum concentrations of IL-1ß, IL-18 and TNF-α in the murine IRI model. Fisetin also reduced the expression of NLRP3 inflammasome-associated proteins (NLRP3, cleaved caspase-1, IL-1ß and IL-18) in I/R-operated liver. The experiments in vitro showed that fisetin decreased the release of IL-1ß, IL-18 and TNF-α, and reduced the expression of NLRP3 inflammasome-associated proteins in H/R-treated RAW264.7 cells. Moreover, fisetin increased the expressions of p-GSK3ß and p-AMPK in both models, indicating that its anti-inflammatory effects were dependent on GSK3ß/AMPK signaling. The anti-inflammatory effects of fisetin were partially inhibited by the AMPK specific inhibitor compound C. CONCLUSIONS: Fisetin showed protective effects against hepatic IRI, countering inflammatory responses through mediating the GSK3ß/AMPK/NLRP3 inflammasome pathway.

14.
J Am Heart Assoc ; 10(10): e018455, 2021 05 18.
Artigo em Inglês | MEDLINE | ID: mdl-33969692

RESUMO

Background Liver X receptor (LXR) belongs to the metabolic nuclear receptor superfamily, which plays a critical regulatory role in vascular physiology/pathology. However, effects of systemic LXR activation on established vulnerable plaques and the potential isotype-specific role involved remain unclear. Methods and Results The 8-week-old male apolipoprotein E-/- mice went through carotid branch ligation and renal artery constriction, combined with a high-fat diet. Plaques in the left carotid artery acquired vulnerable features 4 weeks later, confirmed by magnetic resonance imaging scans and histological analysis. From that time on, mice were injected intraperitoneally daily with PBS or GW3965 (10 mg/kg per day) for an additional 4 weeks. Treatment with LXR agonists reduced the lesion volume by 52.61%, compared with the vehicle group. More important, a profile of less intraplaque hemorrhage detection and necrotic core formation was found. These actions collectively attenuated the incidence of plaque rupture. Mechanistically, reduced lesional apoptosis, enhanced efferocytosis, and alleviated endoplasmic reticulum stress are involved in the process. Furthermore, genetic ablation of LXRα, but not LXRß, blunted the protective effects of LXR on the endoplasmic reticulum stress-elicited C/EBP-homologous protein pathway in peritoneal macrophages. In concert with the LXRα-predominant role in vitro, activated LXR failed to stabilize vulnerable plaques and correct the acquired cellular anomalies in LXRα-/- apolipoprotein E-/- mice. Conclusions Our results revealed that LXRα mediates the capacity of LXR activation to stabilize vulnerable plaques and prevent plaque rupture via amelioration of macrophage endoplasmic reticulum stress, lesional apoptosis, and defective efferocytosis. These findings might expand the application scenarios of LXR therapeutics for atherosclerosis.

15.
Blood Cells Mol Dis ; 89: 102568, 2021 07.
Artigo em Inglês | MEDLINE | ID: mdl-33862368

RESUMO

Liver X receptor ß (LXRß), a nuclear receptor involved in important cellular processes such as cholesterol, glucose and fatty acid metabolism, was suggested to be involved in platelet aggregation but its detailed roles are not clear. In the present study, we evaluated the contribution of LXRß to platelet functions and production. In the systemic collagen-epinephrine thrombosis mouse model, LXRß-deficient mice showed increased area of blood clots compared with control wide-type littermates. The aggregation of LXRß-deficient platelets in response to ADP was stronger than that of control mice platelets. More importantly, the number of platelets in blood of LXRß-deficient mice was significantly higher than that of wild-type mice, especially for female mice. Knockdown of LXRß expression in human megakaryoblastic Dami cells also enhanced cell polyploidization, formation of proplatelets and production of platelet-like particles. Increase in expression levels of proteins related to oxidative phosphorylation such as NADH:ubiquinone oxidoreductase core subunit V1 (Ndufv1) was observed in LXRß-knockdown Dami cells. The levels of Ndufv1 in LXRß-deficient mice platelets were also higher than that of wild-type mice. Taken together, our findings suggested LXRß might participate in control of platelet production from megakaryocytes by regulating mitochondrial metabolism.


Assuntos
Plaquetas/citologia , Receptores X do Fígado/metabolismo , Megacariócitos/citologia , Animais , Plaquetas/metabolismo , Linhagem Celular , Células Cultivadas , Feminino , Técnicas de Silenciamento de Genes , Humanos , Receptores X do Fígado/genética , Masculino , Megacariócitos/metabolismo , Camundongos , Camundongos Knockout , Agregação Plaquetária , Contagem de Plaquetas
16.
Brain Res Bull ; 173: 14-21, 2021 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-33892085

RESUMO

CIP2A is an oncoprotein that is overexpressed in multiple solid tumours and some malignant haematologic disorders. However, its function in glioma is poorly understood. In this study, our results demonstrated that the expression of CIP2A was higher in glioma tissues than in normal tissues. Using tissue microarrays for immunohistochemistry, we found that the intensity of CIP2A expression was higher in high-grade gliomas (grade III-IV) than in low-grade gliomas (grade I-II). In addition, we found that depletion of CIP2A inhibited glioma cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) in vitro. Taken together, our findings revealed that CIP2A was involved in glioma progression, indicating that CIP2A could be used as a potential therapeutic target in the future.

17.
Pacing Clin Electrophysiol ; 44(4): 595-600, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33533037

RESUMO

BACKGROUND: To establish a novel time-saving and safe suture method for cardiac implantable electronic device (CIED) implantation. METHODS: From January 2017 to April 2020, a total of 1317 patients scheduled for CIED procedure were consecutively enrolled in this study. Wound closure of all patients were prospectively assigned either to low-density suture spacing single layer suture group (single-layer group) or traditional two layer suture group (two-layer group). The effects of two closure methods on wound healing and pocket related complications were compared. RESULTS: There were no significant differences in age, gender, BMI, comorbid diseases (diabetes, hypertension, coronary heart disease, and chronic kidney disease), and antiplatelet or anticoagulant drug use between the two groups. The number of suture stitches in the single-layer group was significantly less than that in the two-layer group [3.03(3-4) vs. 7.17(7-10), p < .001], the suture time in the single-layer group was significantly shorter than that in the two-layer group [190.57(167-256) s vs. 493.36(452-655) s, p < .001], and the incidence of clinically significant hematoma in the single-layer group was comparable to that in the two-layer group (0.7% vs. 0.3%, p = .742). Additionally, there were no significant differences in the incidence of pocket infection, dehiscence and keloid between the two groups. CONCLUSION: Novel single-layer suture with low-density suture spacing is feasible and associated with a low incidence of wound dehiscence or infection for CIED implantation.

18.
Chem Commun (Camb) ; 2021 Feb 05.
Artigo em Inglês | MEDLINE | ID: mdl-33543740

RESUMO

A hollow Ni framework (HNF) is designed and prepared to utilize the exterior and interior surface active sites of a Ni-based binder-free and support-free electrode. Furthermore, the more efficient Ni-B active sites are then in situ introduced on the surface of HNF. This micro/nano structure engineering, together with the surface boron modulation, results in a synergistically enhanced catalytic effect for the HER performance.

19.
Am Heart J ; 234: 101-110, 2021 04.
Artigo em Inglês | MEDLINE | ID: mdl-33465369

RESUMO

BACKGROUND: Double kissing (DK) crush approach for patients with coronary bifurcation lesions, particularly localized at distal left main or lesions with increased complexity, is associated with significant reduction in clinical events when compared with provisional stenting. Recently, randomized clinical trial has demonstrated the net clinical benefits by intravascular ultrasound (IVUS)-guided implantation of drug-eluting stent in all-comers. However, the improvement in clinical outcome after DK crush treatment guided by IVUS over angiography guidance for patients with complex bifurcation lesions have never been studied in a randomized fashion. TRIAL DESIGN: DKCRUSH VIII study is a prospective, multicenter, randomized controlled trial designed to assess superiority of IVUS-guided vs angiography-guided DK crush stenting in patients with complex bifurcation lesions according to DEFINITION criteria. A total of 556 patients with complex bifurcation lesions will be randomly (1:1 of ratio) assigned to IVUS-guided or angiography-guided DK crush stenting group. The primary end point is the rate of 12-month target vessel failure, including cardiac death, target vessel myocardial infarction, or clinically driven target vessel revascularization. The secondary end points consist of the individual component of primary end point, all-cause death, myocardial infarction, and in-stent restenosis. The safety end point is the incidence of definite or probable stent thrombosis. An angiographic follow-up will be performed for all patients at 13 months and clinical follow-up will be continued annually until 3 years after the index procedure. CONCLUSIONS: DKCRUSH VIII trial is the first study designed to evaluate the differences in efficacy and safety between IVUS-guided and angiography-guided DK crush stenting in patients with complex true bifurcation lesions. This study will also provide IVUS-derived criteria to define optimal DK crush stenting for bifurcation lesions at higher complexity.


Assuntos
Angiografia Coronária/métodos , Doença das Coronárias/terapia , Stents Farmacológicos , Intervenção Coronária Percutânea/métodos , Ultrassonografia de Intervenção/métodos , Causas de Morte , Doença das Coronárias/diagnóstico por imagem , Doença das Coronárias/mortalidade , Doença das Coronárias/patologia , Reestenose Coronária/etiologia , Trombose Coronária/etiologia , Stents Farmacológicos/efeitos adversos , Humanos , Infarto do Miocárdio/etiologia , Revascularização Miocárdica , Estudos Prospectivos
20.
J Magn Reson Imaging ; 53(2): 516-526, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-32841481

RESUMO

BACKGROUND: Acute myocardial infarction (AMI) is a disease with high morbidity and mortality worldwide and the evaluation of myocardial injury and perfusion status following myocardial ischemia and reperfusion is of clinical value. PURPOSE: To assess the diagnostic utility of simplified perfusion fraction (SPF) in differentiating salvage and infarcted myocardium and its predictive value for left ventricular remodeling in patients with reperfusion ST-segment elevation myocardial infarction (STEMI). STUDY TYPE: Prospective. POPULATION: Forty-one reperfused STEMI patients and 20 healthy volunteers. FIELD STRENGTH/SEQUENCE: 3.0T MRI. The MR examination included cine, T2 -short tau inversion recovery (T2 -STIR), first pass perfusiong (FPP),phase sensitive inversion recovery (PSIR), and diffusion-weighted imaging (DWI). ASSESSMENT: SPF values among different myocardium regions (infarcted, salvaged, remote, and MVO) and stages of reperfused STEMI patients as well as normal controls were measured. The diagnostic utility of SPF values in differentiating salvaged and infarcted myocardium was assessed. STATISTICAL ANALYSIS: Independent t-test and the Mann-Whitney U-test. Logistic regression. RESULTS: SPF values in healthy controls were not significantly different than SPF values in the remote myocardium of patients (40.09 ± 1.47% vs. 40.28 ± 1.93%, P = 0.698). In reperfusion STEMI patients, SPF values were lower in infarcted myocardium compared to remote and salvaged myocardium (32.15 ± 2.36% vs. 40.28 ± 1.93%, P < 0.001; 32.15 ± 2.36% vs. 36.68 ± 2.71%, P < 0.001). SPF values of infarcted myocardium showed a rebound increase from acute to convalescent stages (32.15 ± 2.36% vs. 34.69 ± 3.69%, P < 0.001). When differentiating infarcted and salvaged myocardium, SPF values demonstrated an area under the curve (AUC) of 0.89 (sensitivity 85.4%, specificity 80.5%, cutoff 34.42%). Lower SPF values were associated with lower odds ratio (OR = 0.304) of left ventricular remodeling after adjusting for potential confounders with a confidence interval (CI) of 0.129-0.717, P = 0.007. DATA CONCLUSION: SPF might be able to differentiate salvaged and infarcted myocardium and is a strong predictor of left ventricular remodeling in reperfused STEMI patients. Level of Evidence 2 Technical Efficacy Stage 2.


Assuntos
Infarto do Miocárdio , Infarto do Miocárdio com Supradesnível do Segmento ST , Humanos , Imagem Cinética por Ressonância Magnética , Infarto do Miocárdio/diagnóstico por imagem , Miocárdio , Perfusão , Valor Preditivo dos Testes , Estudos Prospectivos , Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico por imagem , Função Ventricular Esquerda
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