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1.
FEBS J ; 2024 Jun 14.
Artigo em Inglês | MEDLINE | ID: mdl-38872483

RESUMO

Discoidin, CUB, LCCL domain-containing 2 (DCBLD2) is a type I transmembrane protein with a similar structure to neuropilin, which acts as a co-receptor for certain receptor tyrosine kinases (RTKs). The insulin receptor is an RTK and plays a critical role in endothelial cell function and glycolysis. However, how and whether DCBLD2 regulates insulin receptor activity in endothelial cells is poorly understood. Diabetes was induced through treatment of Dcbld2 global-genome knockout mice and endothelium-specific knockout mice with streptozotocin. Vascular ultrasound, vascular tension test, and hematoxylin and eosin staining were performed to assess endothelial function and aortic remodeling. Glycolytic rate assays, real-time PCR and western blotting were used to investigate the effects of DCBLD2 on glycolytic activity and insulin receptor (InsR)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway in endothelial cells. Co-immunoprecipitation was used to assess the effects of DCBLD2 on insulin receptor endocytosis and recycling. Membrane and cytoplasmic proteins were isolated to determine whether DCBLD2 could affect the localization of the insulin receptor. We found that Dcbld2 deletion exacerbated endothelial dysfunction and vascular remodeling in diabetic mice. Both Dcbld2 knockdown and Dcbld2 deletion inhibited glycolysis and the InsR/PI3K/Akt signaling pathway in endothelial cells. Furthermore, Dcbld2 deletion inhibited insulin receptor recycling. Taken together, Dcbld2 deficiency exacerbated diabetic endothelial dysfunction and vascular remodeling by inhibiting the InsR/PI3K/Akt pathway in endothelial cells through the inhibition of Rab11-dependent insulin receptor recycling. Our data suggest that DCBLD2 is a potential therapeutic target for diabetes and cardiovascular diseases.

2.
Biochem Pharmacol ; 225: 116329, 2024 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38821375

RESUMO

Calcium signaling abnormality in cardiomyocytes, as a key mechanism, is closely associated with developing heart failure. Fibroblast growth factor 13 (FGF13) demonstrates important regulatory roles in the heart, but its association with cardiac calcium signaling in heart failure remains unknown. This study aimed to investigate the role and mechanism of FGF13 on calcium mishandling in heart failure. Mice underwent transaortic constriction to establish a heart failure model, which showed decreased ejection fraction, fractional shortening, and contractility. FGF13 deficiency alleviated cardiac dysfunction. Heart failure reduces calcium transients in cardiomyocytes, which were alleviated by FGF13 deficiency. Meanwhile, FGF13 deficiency restored decreased Cav1.2 and Serca2α expression and activity in heart failure. Furthermore, FGF13 interacted with microtubules in the heart, and FGF13 deficiency inhibited the increase of microtubule stability during heart failure. Finally, in isoproterenol-stimulated FGF13 knockdown neonatal rat ventricular myocytes (NRVMs), wildtype FGF13 overexpression, but not FGF13 mutant, which lost the binding site of microtubules, promoted calcium transient abnormality aggravation and Cav1.2 downregulation compared with FGF13 knockdown group. Generally, FGF13 deficiency improves abnormal calcium signaling by inhibiting the increased microtubule stability in heart failure, indicating the important role of FGF13 in cardiac calcium homeostasis and providing new avenues for heart failure prevention and treatment.


Assuntos
Sinalização do Cálcio , Fatores de Crescimento de Fibroblastos , Insuficiência Cardíaca , Microtúbulos , Miócitos Cardíacos , Animais , Masculino , Camundongos , Ratos , Células Cultivadas , Fatores de Crescimento de Fibroblastos/metabolismo , Fatores de Crescimento de Fibroblastos/genética , Insuficiência Cardíaca/metabolismo , Insuficiência Cardíaca/genética , Camundongos Endogâmicos C57BL , Camundongos Knockout , Microtúbulos/metabolismo , Microtúbulos/efeitos dos fármacos , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/efeitos dos fármacos , Ratos Sprague-Dawley
3.
Artigo em Inglês | MEDLINE | ID: mdl-38818580

RESUMO

Fibroblast growth factor (FGF) isoform 13, a distinct type of FGF, boasts significant potential for therapeutic intervention in cardiovascular dysfunctions. However, its impact on regulating fibrosis remains unexplored. This study aims to elucidate the role and mechanism of FGF13 on cardiac fibrosis. Here, we show that following transverse aortic constriction (TAC) surgery, interstitial fibrosis and collagen content increase in mice, along with reduced ejection fraction and fractional shortening, augmented heart mass. However, following Fgf13 deletion, interstitial fibrosis is decreased, ejection fraction and fractional shortening are increased, and heart mass is decreased, compared with those in the TAC group. Mechanistically, incubation of cardiac fibroblasts with transforming growth factor ß (TGFß) increases the expressions of types I and III collagen proteins, as well as α-smooth muscle actin (α-SMA) proteins, and enhances fibroblast proliferation and migration. In the absence of Fgf13, the expressions of these proteins are decreased, and fibroblast proliferation and migration are suppressed, compared with those in the TGFß-stimulated group. Overexpression of FGF13, but not FGF13 mutants defective in microtubule binding and stabilization, rescues the decrease in collagen and α-SMA protein and weakens the proliferation and migration function of the Fgf13 knockdown group. Furthermore, Fgf13 knockdown decreases ROCK protein expression via microtubule disruption. Collectively, cardiac Fgf13 knockdown protects the heart from fibrosis in response to haemodynamic stress by modulating microtubule stabilization and ROCK signaling pathway.

4.
ACS Appl Mater Interfaces ; 15(48): 56293-56304, 2023 Dec 06.
Artigo em Inglês | MEDLINE | ID: mdl-37976105

RESUMO

In this work, we synthesized polydopamine nanoparticles (PDNPs-M, M = I, II, III, and IV) with uniform particle sizes but varying l-arginine (Arg) contents (0%, 0.53%, 3.73%, and 6.62%) through a one-pot synthesis approach. Thin-film nanocomposite (TFN) membranes were fabricated via in situ interfacial polymerization (IP). The effects of the PDNPs-M chemical structure on the IP process and the consequent impacts on the structure and properties of the polyamide (PA) selective layer were investigated. The hydrophilicity and dispersibility of PDNPs-M exhibited an upward trend with the Arg content. Furthermore, Arg doping contributes to a denser and smoother PA layer. Among the TFC and TFN membranes, TFN-PDNPs-IV exhibited a water permeability of 3.89 L·m-2·h-1·bar-1 (55.1% higher than that of TFC-0) with a NaCl rejection rate of 98.8%, signifying superior water/salt selectivity. Additionally, TFN-PDNPs-IV exhibited regular pressure stability, commendable acid/alkali stability, and enhanced antifouling properties. These findings highlight the significant impact of nanoparticle hydrophilic functional groups on the structural and functional attributes of TFN membranes, offering a promising approach for developing advanced reverse osmosis membranes.

5.
World J Stem Cells ; 15(9): 931-946, 2023 Sep 26.
Artigo em Inglês | MEDLINE | ID: mdl-37900938

RESUMO

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.

6.
Arterioscler Thromb Vasc Biol ; 43(12): e491-e508, 2023 12.
Artigo em Inglês | MEDLINE | ID: mdl-37795615

RESUMO

BACKGROUND: APN (adiponectin) and APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1) are potent vasculoprotective molecules, and their deficiency (eg, hypoadiponectinemia) contributes to diabetic vascular complications. However, the molecular mechanisms that govern their vasculoprotective genes as well as their alteration by diabetes remain unknown. METHODS: Diabetic medium-cultured rat aortic endothelial cells, mouse aortic endothelial cells from high-fat-diet animals, and diabetic human aortic endothelial cells were used for molecular/cellular investigations. The in vivo concept-prove demonstration was conducted using diabetic vascular injury and diabetic hindlimb ischemia models. RESULTS: In vivo animal experiments showed that APN replenishment caused APPL1 nuclear translocation, resulting in an interaction with HDAC (histone deacetylase) 2, which inhibited HDAC2 activity and increased H3Kac27 levels. Based on transcriptionome pathway-specific real-time polymerase chain reaction profiling and bioinformatics analysis, Angpt1 (angiopoietin 1), Ocln (occludin), and Cav1 (caveolin 1) were found to be the top 3 vasculoprotective genes suppressed by diabetes and rescued by APN in an APPL1-dependent manner. APN reverses diabetes-induced inhibition of Cav1 interaction with APPL1. APN-induced Cav1 expression was not affected by Angpt1 or Ocln deficiency, whereas APN-induced APPL1 nuclear translocation or upregulation of Angpt1/Ocln expression was abolished in the absence of Cav1 both in vivo and in vitro, suggesting Cav1 is upstream molecule of Angpt1/Ocln in response to APN administration. Chromatin immunoprecipitation-qPCR (quantitative polymerase chain reaction) demonstrated that APN caused significant enrichment of H3K27ac in Angpt1 and Ocln promoter region, an effect blocked by APPL1/Cav1 knockdown or HDAC2 overexpression. The protective effects of APN on the vascular system were attenuated by overexpression of HDAC2 and abolished by knocking out APPL1 or Cav1. The double knockdown of ANGPT1/OCLN blunted APN vascular protection both in vitro and in vivo. Furthermore, in diabetic human endothelial cells, HDAC2 activity is increased, H3 acetylation is decreased, and ANGPT1/OCLN expression is reduced, suggesting that the findings have important translational implications. CONCLUSIONS: Hypoadiponectinemia and dysregulation of APPL1-mediated epigenetic regulation are novel mechanisms leading to diabetes-induced suppression of vasculoprotective gene expression. Diabetes-induced pathological vascular remodeling may be prevented by interventions promoting APPL1 nuclear translocation and inhibiting HDAC2.


Assuntos
Diabetes Mellitus , Angiopatias Diabéticas , Lesões do Sistema Vascular , Animais , Humanos , Camundongos , Ratos , Proteínas Adaptadoras de Transdução de Sinal/genética , Proteínas Adaptadoras de Transdução de Sinal/metabolismo , Adiponectina/metabolismo , Diabetes Mellitus/genética , Angiopatias Diabéticas/genética , Angiopatias Diabéticas/prevenção & controle , Angiopatias Diabéticas/metabolismo , Células Endoteliais/metabolismo , Epigênese Genética , Lesões do Sistema Vascular/genética
7.
J Electrocardiol ; 81: 176-185, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37741272

RESUMO

PURPOSE: The current study was conducted to investigate the electrocardiographic (ECG) characteristics of idiopathic premature ventricular contractions (PVCs) originating from the aortic sinus cusp (ASC) and establish a novel ECG criterion to discriminate PVCs originating from the right coronary cusp (RCC), left coronary cusp (LCC), and the left and right coronary cusp junction (LRJ). METHODS: A retrospective analysis was performed on a total of 133 patients with idiopathic PVCs who underwent successful mapping and ablation. The sites of origin (SOO) were confirmed using fluoroscopy and a three-dimensional mapping system during radiofrequency catheter ablation (RFCA). Among the patients, 69 had PVCs originating from the LCC, 39 from the RCC, and 25 from the LRJ. Characteristics of surface 12­lead electrocardiograms (ECGs) recorded during PVCs were analyzed. Q-, R-, S, and R'-wave amplitudes were measured in lead I, and the lead I R-wave indexes (IRa, IRb, IRc, IRd, and IRe) were derived by employing multiplication, subtraction, sum, and division operations on these ECG measurements. Notably, IRb and IRe demonstrated usefulness as ECG indexes for discriminating PVCs originating from RCC, LCC, and LRJ in the ASC. RESULTS: The R- and S-wave amplitudes in lead I exhibited statistically significant differences among the three groups (P < 0.001 and P < 0.001, respectively). In discriminating PVCs originating from the RCC from the other two groups, IRb showed the largest area under the curve (AUC) of 0.813, as assessed by receiver operating characteristic (ROC) analysis, with a cutoff value of ≤0.5 indicating PVCs of RCC origin. The sensitivity and specificity were 80.3% and 78.7%, respectively. For discriminating PVCs arising from the LCC from those in the LRJ group, IRe exhibited the largest AUC of 0.801, with an optimal cutoff value of 0. An IRe value >0 indicated PVCs originating from the LRJ, while an IRe value ≤0 indicated PVCs originating from the LCC. The sensitivity and specificity of the IRe index were 84.0% and 70.7%, respectively. CONCLUSION: Lead I R-wave indexes provided simple and useful ECG criteria for discriminating PVCs originating from the LCC, RCC, and LRJ in the left ventricular outflow tract (LVOT).


Assuntos
Carcinoma de Células Renais , Ablação por Cateter , Neoplasias Renais , Seio Aórtico , Taquicardia Ventricular , Complexos Ventriculares Prematuros , Humanos , Estudos Retrospectivos , Seio Aórtico/cirurgia , Carcinoma de Células Renais/cirurgia , Eletrocardiografia/métodos , Ablação por Cateter/métodos , Neoplasias Renais/cirurgia
8.
J Opt Soc Am A Opt Image Sci Vis ; 40(9): 1724-1732, 2023 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-37707009

RESUMO

The camera function of a smartphone can be used to quantitatively detect urine parameters anytime, anywhere. However, the color captured by different cameras in different environments is different. A method for color correction is proposed for a urine test strip image collected using a smartphone. In this method, the color correction model is based on the color information of the urine test strip, as well as the ambient light and camera parameters. Conv-TabNet, which can focus on each feature parameter, was designed to correct the color of the color blocks of the urine test strip. The color correction experiment was carried out in eight light sources on four mobile phones. The experimental results show that the mean absolute error of the new method is as low as 2.8±1.8, and the CIEDE2000 color difference is 1.5±1.5. The corrected color is almost consistent with the standard color by visual evaluation. This method can provide a technology for the quantitative detection of urine test strips anytime and anywhere.

9.
J Int Med Res ; 51(7): 3000605231187946, 2023 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-37523148

RESUMO

A man in his late 60s with a history of angina pectoris developed low back pain during cardiac catheterization. During this episode of back pain, ST segment elevations were noted on the electrocardiogram. The patient reported relief of the pain immediately after implantation of two drug-eluting stents, and the ST segments on the electrocardiogram normalized. The probable mechanisms of low back pain during cardiac catheterization in this patient are briefly outlined.


Assuntos
Stents Farmacológicos , Dor Lombar , Masculino , Humanos , Dor Lombar/diagnóstico , Dor Lombar/etiologia , Angina Pectoris/complicações , Eletrocardiografia , Angiografia Coronária
10.
BMC Cardiovasc Disord ; 23(1): 323, 2023 06 24.
Artigo em Inglês | MEDLINE | ID: mdl-37355592

RESUMO

BACKGROUND: Hydration is currently the main measure to prevent contrast-induced nephropathy (CIN). We aimed to compare the preventive effect of preprocedure and postprocedure hydration on CIN in patients with coronary heart disease undergoing elective percutaneous coronary intervention (PCI). METHODS: A retrospective study included 198 cases of postprocedure hydration and 396 cases of preprocedure hydration using propensity score matching. The incidence of CIN 48 h after PCI and adverse events within 30 days after contrast media exposure were compared between the two groups. Logistic regression analysis was used to analyse the risk factors for CIN. RESULTS: The incidence of CIN in the postprocedure hydration group was 3.54%, while that in the preprocedure hydration group was 4.8%. There was no significant difference between the two groups (p = 0.478). Multivariate logistic regression analysis showed that diabetes mellitus, baseline BNP and cystatin C levels, and contrast agent dosage were independent risk factors for CIN. There was no significant difference in the incidence of major adverse events between the two groups (3.03% vs. 2.02%, p = 0.830). CONCLUSIONS: Postprocedure hydration is equally effective compared to preoperative hydration in the prevention of CIN in patients with coronary heart disease undergoing elective PCI.


Assuntos
Doença das Coronárias , Nefropatias , Intervenção Coronária Percutânea , Humanos , Intervenção Coronária Percutânea/efeitos adversos , Estudos Retrospectivos , Meios de Contraste/efeitos adversos , Nefropatias/induzido quimicamente , Nefropatias/diagnóstico , Nefropatias/epidemiologia , Doença das Coronárias/etiologia
11.
Ultrason Sonochem ; 95: 106399, 2023 May.
Artigo em Inglês | MEDLINE | ID: mdl-37060709

RESUMO

Sediment erosion frequently occurs in areas with high incidences of cavitation. The collaborative impact of abrasion and cavitation presents a host of challenges, threats, and damages to hydraulic engineering. However, little is known about the synergistic wear mechanism, and research conclusions remain inconsistent. In this work, relevant studies on synergistic erosion have been collected, classified, and analyzed. Presently, research on synergistic wear primarily operates at the macro and micro levels. The microscopic level enables the visualization and quantification of the process by which particles gain momentum from bubbles, the trajectory of particle acceleration, and the mechanism that triggers strong interactions between bubble-particle. At the macro level, erosion is understood as the summation of damage effects on the wall that is caused by the interaction between a plethora of bubbles of varying scales and numerous particles. The synergistic bubble-particle effect is reflected in the dual inhibiting or promoting mechanism. Furthermore, while numerical simulations could be realized by coupling cavitation, multiphase flow, and erosion models, their accuracy is not infallible. In the future, the dual role of particles, and particles driven by micro-jets or shock waves should be fully considered when establishing a combined erosion model. In addition, enhancing the influence of flow field and boundary parameters around bubbles and utilizing FSI would improve the predictive accuracy of erosion location and erosion rate. This work helps to elucidate the combined wear mechanism of hydraulic machinery components in sediment-laden flow environments and provides a theoretical basis for the design, manufacture, processing, and maintenance of hydraulic machinery.

12.
Circulation ; 147(15): 1162-1179, 2023 04 11.
Artigo em Inglês | MEDLINE | ID: mdl-36883479

RESUMO

BACKGROUND: Myocardial insulin resistance is a hallmark of diabetic cardiac injury. However, the underlying molecular mechanisms remain unclear. Recent studies demonstrate that the diabetic heart is resistant to other cardioprotective interventions, including adiponectin and preconditioning. The "universal" resistance to multiple therapeutic interventions suggests impairment of the requisite molecule(s) involved in broad prosurvival signaling cascades. Cav (Caveolin) is a scaffolding protein coordinating transmembrane signaling transduction. However, the role of Cav3 in diabetic impairment of cardiac protective signaling and diabetic ischemic heart failure is unknown. METHODS: Wild-type and gene-manipulated mice were fed a normal diet or high-fat diet for 2 to 12 weeks and subjected to myocardial ischemia and reperfusion. Insulin cardioprotection was determined. RESULTS: Compared with the normal diet group, the cardioprotective effect of insulin was significantly blunted as early as 4 weeks of high-fat diet feeding (prediabetes), a time point where expression levels of insulin-signaling molecules remained unchanged. However, Cav3/insulin receptor-ß complex formation was significantly reduced. Among multiple posttranslational modifications altering protein/protein interaction, Cav3 (not insulin receptor-ß) tyrosine nitration is prominent in the prediabetic heart. Treatment of cardiomyocytes with 5-amino-3-(4-morpholinyl)-1,2,3-oxadiazolium chloride reduced the signalsome complex and blocked insulin transmembrane signaling. Mass spectrometry identified Tyr73 as the Cav3 nitration site. Phenylalanine substitution of Tyr73 (Cav3Y73F) abolished 5-amino-3-(4-morpholinyl)-1,2,3-oxadiazolium chloride-induced Cav3 nitration, restored Cav3/insulin receptor-ß complex, and rescued insulin transmembrane signaling. It is most important that adeno-associated virus 9-mediated cardiomyocyte-specific Cav3Y73F reexpression blocked high-fat diet-induced Cav3 nitration, preserved Cav3 signalsome integrity, restored transmembrane signaling, and rescued insulin-protective action against ischemic heart failure. Last, diabetic nitrative modification of Cav3 at Tyr73 also reduced Cav3/AdipoR1 complex formation and blocked adiponectin cardioprotective signaling. CONCLUSIONS: Nitration of Cav3 at Tyr73 and resultant signal complex dissociation results in cardiac insulin/adiponectin resistance in the prediabetic heart, contributing to ischemic heart failure progression. Early interventions preserving Cav3-centered signalsome integrity is an effective novel strategy against diabetic exacerbation of ischemic heart failure.


Assuntos
Insuficiência Cardíaca , Resistência à Insulina , Traumatismo por Reperfusão Miocárdica , Estado Pré-Diabético , Camundongos , Animais , Caveolina 3/genética , Caveolina 3/metabolismo , Adiponectina/metabolismo , Adiponectina/farmacologia , Cloretos/metabolismo , Cloretos/farmacologia , Traumatismo por Reperfusão Miocárdica/metabolismo , Miócitos Cardíacos/metabolismo , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/metabolismo
13.
Med Phys ; 50(9): 5609-5620, 2023 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-36970887

RESUMO

BACKGROUND: Image registration technology has become an important medical image preprocessing step with the wide application of computer-aided diagnosis technology in various medical image analysis tasks. PURPOSE: We propose a multiscale feature fusion registration based on deep learning to achieve the accurate registration and fusion of head magnetic resonance imaging (MRI) and solve the problem that general registration methods cannot handle the complex spatial information and position information of head MRI. METHODS: Our proposed multiscale feature fusion registration network consists of three sequentially trained modules. The first is an affine registration module that implements affine transformation; the second is to realize non-rigid transformation, a deformable registration module composed of top-down and bottom-up feature fusion subnetworks in parallel; and the third is a deformable registration module that also realizes non-rigid transformation and is composed of two feature fusion subnetworks in series. The network decomposes the deformation field of large displacement into multiple deformation fields of small displacement by multiscale registration and registration, which reduces the difficulty of registration. Moreover, multiscale information in head MRI is learned in a targeted manner, which improves the registration accuracy, by connecting the two feature fusion subnetworks. RESULTS: We used 29 3D head MRIs for training and seven volumes for testing and calculated the values of the registration evaluation metrics for the new algorithm to register anterior and posterior lateral pterygoid muscles. The Dice similarity coefficient was 0.745 ± 0.021, the Hausdorff distance was 3.441 ± 0.935 mm, the Average surface distance was 0.738 ± 0.098 mm, and the Standard deviation of the Jacobian matrix was 0.425 ± 0.043. Our new algorithm achieved a higher registration accuracy compared with state-of-the-art registration methods. CONCLUSIONS: Our proposed multiscale feature fusion registration network can realize end-to-end deformable registration of 3D head MRI, which can effectively cope with the characteristics of large deformation displacement and the rich details of head images and provide reliable technical support for the diagnosis and analysis of head diseases.


Assuntos
Algoritmos , Processamento de Imagem Assistida por Computador , Processamento de Imagem Assistida por Computador/métodos , Imageamento por Ressonância Magnética , Diagnóstico por Computador
14.
Front Psychol ; 14: 1103003, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-36874874

RESUMO

Introduction: Physical activity interventions improve cognitive performance, especially visuospatial working memory (VSWM). However, evidence on the effects of these interventions in children, adolescents, and older adults remains scant. This meta-analysis aimed to identify the effects of physical activity on VSWM improvement in healthy individuals and the best exercise intervention program to improve VSWM capacity. Methods: We searched for randomized controlled trials (RCTs) of exercise interventions targeting VSWM in healthy individuals from Web of Science, MEDLINE, BIOSIS Previews, PubMed, China National Knowledge Infrastructure, and Wanfang Data (Chinese) databases, from inception to August 20, 2022. Results: Among 21 articles (1,595 healthy participants), the heterogeneity test statistic was I2 = 32.3%, p = 0.053. The mean quality scores of the included articles were 6.9 points (reaction time [RT] studies) and 7.5 points (Score studies). Moreover, 28 RCTs were included (10 RT studies and 18 Score studies), and the subgroup analysis found significant effects for elderly participants, children, interventions involving a higher level of cognitive engagement, low and moderate exercise intensity, chronic exercise, exercise duration ≥60 min, and exercise period ≥90 days. Physical activity had a small but significant positive impact on VSWM in healthy individuals. Current evidence confirms the effects of physical activity on VSWM capacity only in children and seniors but not in young adults. Other age groups, including adolescents and middle-aged adults, have not been studied. Prescription of interventions involving high-level cognitive engagement, low and moderate exercise intensity, chronic exercise, exercise for >30 min per session, and exercise for more than 3 months is recommended for children and seniors. Discussion: Future RCTs would be to fill the gap in studies on adolescents and middle-aged adults, and report detailed exercise intervention programs about different age groups.Systematic Review Registration: PROSPERO (https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022354737). INPLASY (https://doi.org/10.37766/inplasy2022.8.0053).

15.
J Cardiovasc Dev Dis ; 9(10)2022 Sep 20.
Artigo em Inglês | MEDLINE | ID: mdl-36286265

RESUMO

Coronary artery calcification (CAC) increases the risk of acute coronary syndrome. This study examined the correlation between C1q/TNF-related protein 9 (CTRP9) and CAC and explored CTRP9 as a biomarker for prognosis. We divided 275 patients with coronary heart disease into four groups. In order to balance the baseline confounding factors, propensity score matching (PSM) was performed to match CAC patients with non-CAC patients in a 1:1 ratio. Optical coherence tomography (OCT) calcification scoring was performed in 126 patients with CAC. Moreover, 140 patients who underwent OCT were followed-up for 9 months for analysis of the correlation between CTRP9 levels and clinical prognosis. Based on OCT calcification scores, 126 patients with CAC were divided into the 0-2 and 3-4 groups. Plasma CTRP9 levels were significantly lower in the type 2 diabetes mellitus (T2DM), CAC and CAC with T2DM groups than in the control group. CTRP9 played roles as a protective factor and potential predictor in CAC severity. The AUC of the OCT calcification score 3-4 group predicted by the plasma CTRP9 level was 0.766. During the follow-up period, the cumulative event-free survival rate was significantly lower in the low-level CTRP9 (L-CTRP9) group than in the high-level (H-CTRP9) group, and the incidence of major endpoint events was significantly higher in the L-CTRP9 group than in the H-CTRP9 group. CTRP9 can be a valuable biomarker for CAC occurrence and severity and can predict patients' clinical prognosis.

16.
Front Pharmacol ; 13: 962596, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36110551

RESUMO

Immune checkpoint inhibitors (ICIs) are the most notable breakthrough in tumor treatment. ICIs has been widely used in tumor patients, but its wide range of immune-related adverse events (irAEs) should not be ignored. irAEs can be involved in any organ system, including immune-related cardiotoxicity. Although the cardiotoxicity induced by immune checkpoint inhibitors is rare, it is extremely lethal and has attracted increasing attention. PD-1 and PD-L1 are expressed in human cardiomyocytes, so the application of PD-1/PDL-1 inhibitors can cause many adverse reactions to the cardiovascular system. This review summarizes the latest epidemiological evidence on the cardiovascular toxicity of programmed cell death protein-1(PD-1)/programmed cell death ligand-1(PD-L1) inhibitors and the clinical manifestations, as well as the potential pathological mechanisms. These updates may provide a novel perspective for monitoring early toxicity and establishing appropriate treatment for patients with ICI-related cardiotoxicity.

17.
Ren Fail ; 44(1): 1486-1497, 2022 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-36000917

RESUMO

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.


Assuntos
Síndrome Cardiorrenal , Insuficiência Cardíaca , Biomarcadores , Síndrome Cardiorrenal/diagnóstico , Diagnóstico Precoce , Encefalinas , Insuficiência Cardíaca/complicações , Insuficiência Cardíaca/diagnóstico , Humanos , Peptídeo Natriurético Encefálico , Fragmentos de Peptídeos , Prognóstico , Estudos Prospectivos , Precursores de Proteínas
18.
Entropy (Basel) ; 24(5)2022 Apr 29.
Artigo em Inglês | MEDLINE | ID: mdl-35626514

RESUMO

In this paper, three iterative methods (Stokes, Newton and Oseen iterative methods) based on finite element discretization for the stationary micropolar fluid equations are proposed, analyzed and compared. The stability and error estimation for the Stokes and Newton iterative methods are obtained under the strong uniqueness conditions. In addition, the stability and error estimation for the Oseen iterative method are derived under the uniqueness condition of the weak solution. Finally, numerical examples test the applicability and the effectiveness of the three iterative methods.

19.
Circ Res ; 131(2): e34-e50, 2022 07 08.
Artigo em Inglês | MEDLINE | ID: mdl-35611695

RESUMO

BACKGROUND: Despite significantly reduced acute myocardial infarction (MI) mortality in recent years, ischemic heart failure continues to escalate. Therapeutic interventions effectively reversing pathological remodeling are an urgent unmet medical need. We recently demonstrated that AdipoR1 (APN [adiponectin] receptor 1) phosphorylation by GRK2 (G-protein-coupled receptor kinase 2) contributes to maladaptive remodeling in the ischemic heart. The current study clarified the underlying mechanisms leading to AdipoR1 phosphorylative desensitization and investigated whether blocking AdipoR1 phosphorylation may restore its protective signaling, reversing post-MI remodeling. METHODS: Specific sites and underlying molecular mechanisms responsible for AdipoR1 phosphorylative desensitization were investigated in vitro (neonatal and adult cardiomyocytes). The effects of AdipoR1 phosphorylation inhibition upon APN post-MI remodeling and heart failure progression were investigated in vivo. RESULTS: Among 4 previously identified sites sensitive to GRK2 phosphorylation, alanine substitution of Ser205 (AdipoR1S205A), but not other 3 sites, rescued GRK2-suppressed AdipoR1 functions, restoring APN-induced cell salvage kinase activation and reducing oxidative cell death. The molecular investigation followed by functional determination demonstrated that AdipoR1 phosphorylation promoted clathrin-dependent (not caveolae) endocytosis and lysosomal-mediated (not proteasome) degradation, reducing AdipoR1 protein level and suppressing AdipoR1-mediated cytoprotective action. GRK2-induced AdipoR1 endocytosis and degradation were blocked by AdipoR1S205A overexpression. Moreover, AdipoR1S205E (pseudophosphorylation) phenocopied GRK2 effects, promoted AdipoR1 endocytosis and degradation, and inhibited AdipoR1 biological function. Most importantly, AdipoR1 function was preserved during heart failure development in AdipoR1-KO (AdipoR1 knockout) mice reexpressing hAdipoR1S205A. APN administration in the failing heart reversed post-MI remodeling and improved cardiac function. However, reexpressing hAdipoR1WT in AdipoR1-KO mice failed to restore APN cardioprotection. CONCLUSIONS: Ser205 is responsible for AdipoR1 phosphorylative desensitization in the failing heart. Blockade of AdipoR1 phosphorylation followed by pharmacological APN administration is a novel therapy effective in reversing post-MI remodeling and mitigating heart failure progression.


Assuntos
Insuficiência Cardíaca , Infarto do Miocárdio , Traumatismo por Reperfusão Miocárdica , Adiponectina/metabolismo , Animais , Insuficiência Cardíaca/metabolismo , Humanos , Isquemia/metabolismo , Camundongos , Camundongos Knockout , Infarto do Miocárdio/patologia , Traumatismo por Reperfusão Miocárdica/metabolismo , Miócitos Cardíacos/metabolismo , Fosforilação , Receptores de Adiponectina/genética , Receptores de Adiponectina/metabolismo
20.
Entropy (Basel) ; 24(4)2022 Mar 25.
Artigo em Inglês | MEDLINE | ID: mdl-35455117

RESUMO

In this paper, four stabilized methods based on the lowest equal-order finite element pair for the steady micropolar Navier-Stokes equations (MNSE) are presented, which are penalty, regular, multiscale enrichment, and local Gauss integration methods. A priori properties, existence, uniqueness, stability, and error estimation based on Fem approximation of all the methods are proven for the physical variables. Finally, some numerical examples are displayed to show the numerical characteristics of these methods.

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