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BACKGROUND:Cardiac hypertrophy is an adaptive response of the heart to physiological and pathological stimuli such as pressure overload.It is of compensatory significance in the early stage,but if the stimulation continues,it can cause cardiomyopathy leading to heart failure.MicroRNAs are involved in the regulation of cardiac hypertrophy.However,the role of miR-20a in pressure overload-induced cardiac hypertrophy has not been reported. OBJECTIVE:To investigate the role of miR-20a in pressure overload-induced cardiac hypertrophy and the underlying mechanisms. METHODS:Transverse aortic constriction was used to induce cardiac hypertrophy in vivo and angiotensin Ⅱ was used to induce H9c2 cell models of cardiac hypertrophy in vitro.MiR-20a was overexpressed in vivo by intramyocardial injection of miR-20a overexpressing adenovirus and in vitro by transfecting miR-20a mimic into H9c2 cells.Cardiac hypertrophy was assessed by measuring heart weight/body weight ratio,cell surface area,and myocardial fibrosis.The expression levels of atrial natriuretic peptide,brain natriuretic peptide,β-myosin heavy chain and miR-20a were detected by real-time fluorescence quantitative PCR.Mitochondrial fission was detected by MitoTracker.The downstream target genes of miR-20a were predicted by RNAhybrid software. RESULTS AND CONCLUSION:(1)The expression level of miR-20a was significantly decreased in both hypertrophic cardiomyocytes and hearts(P<0.05).(2)At the animal level,overexpression of miR-20a significantly inhibited transverse aortic constriction-induced cardiac hypertrophy,including decreasing the upregulated expression level of hypertrophic marker genes(P<0.05),reduced the enlarged heart volume,reducing the increased heart weight/body weight ratio(P<0.01),reducing the increased myocardial cross-sectional area(P<0.05),and attenuating fibrosis(P<0.01).(3)At the cellular level,overexpression of miR-20a significantly inhibited angiotensin Ⅱ-induced cardiomyocyte hypertrophy,including decreasing the upregulated expression levels of atrial natriuretic peptide(P<0.05),brain natriuretic peptide(P<0.01)and β-myosin heavy chain(P<0.05),reducing the increased protein/DNA ratio(P<0.01),and suppressing the increased cell surface area(P<0.05).(4)Overexpression of miR-20a significantly inhibited angiotensin Ⅱ-induced mitochondrial fission(P<0.05).(5)The results of RNAhybrid software analysis showed that miR-20a and the mRNA 3'untranslated region of cAMP-dependent protein kinase inhibitor alpha were well complementary and the predicted binding sites were highly conserved.(6)In conclusion,miR-20a is significantly down-regulated in pressure overload-induced cardiac hypertrophy.Overexpression of miR-20a inhibits cardiac hypertrophy at both the cellular level and animal level and attenuates angiotensin Ⅱ-induced mitochondrial fission.
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BACKGROUND@#Immunoneoadjuvant therapy opens a new prospect for local advanced lung cancer. The aim of our study was to explore the safety and feasibility of robotic-assisted bronchial sleeve resection in patients with locally advanced non-small cell lung cancer (NSCLC) after neoadjuvant chemoimmunotherapy.@*METHODS@#Data of 13 patients with locally advanced NSCLC that underwent bronchial sleeve resection after neoadjuvant chemoimmunotherapy during August 2020 and February 2021 were retrospectively included. According to the surgical methods, patients were divided into thoracotomy bronchial sleeve resection (TBSR) group and robot-assisted bronchial sleeve resection (RABSR) group. Oncology, intraoperative, and postoperative data in the two groups were compared.@*RESULTS@#The two groups of patients operated smoothly, the postoperative pathology confirmed that all the tumor lesions achieved R0 resection, and RABSR group no patient was transferred to thoracotomy during surgery. Partial remission (PR) rate and major pathological remissions (MPR) rate of patients in the TBSR group were 71.43% and 42.86%, respectively. Complete pathological response (pCR) was 28.57%. They were 66.67%, 50.00% and 33.33% in RABSR group, respectively. There were no significant differences in operative duration, number of lymph nodes dissected, intraoperative blood loss, postoperative drainage time and postoperative hospital stay between the two groups, but the bronchial anastomosis time of RABSR group was relatively short. Both groups of patients had a good prognosis. Successfully discharged from the hospital and post-operative 90-d mortality rate was 0.@*CONCLUSIONS@#In patients with locally advanced central NSCLC after neoadjuvant chemoimmunotherapy can achieve the tumor reduction, tumor stage decline and increase the R0 resection rate, bronchial sleeve resection is safe and feasible. Under the premise of following the two principles of surgical safety and realizing the tumor R0 resection, robot-assisted bronchial sleeve resection can be preferred.
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Humanos , Carcinoma de Pulmón de Células no Pequeñas/cirugía , Neoplasias Pulmonares/cirugía , Terapia Neoadyuvante , Neumonectomía/métodos , Estudios Retrospectivos , Robótica , Toracotomía , Resultado del TratamientoRESUMEN
Objective To investigate the feasibility of our new found 3-dimensional contrast-enhanced ultrasound 3D-CEUS registration system as an early assessment of the therapeutic response to radio frequency ablation for liver cancer Methods Twenty-seven patients with 28 lesions accepted 3D-CEUS before and after radio frequency ablation RFA the therapeutic respond to which would be assessed with 3D-CEUS registration system recording the rate of successful registration The CT was considered as the reference standard Results Ten cases 35 7% were successful matched with auto-registration and 24 cases 85 7% were succesful matched with interactive-registration relatively All cases were considered as complete ablated which were confirmed by CECT with 100% accuracy There were two cases achieving ablation margins ≥5 mm without local tumor progression LTP and nineteen cases achieving 0 -4 mm ablation margin with 3 LTP 3-month 6-month and 1-year later Conclusions The 3D-CEUS interactive-registration system can easily assess the therapeutic response of RFA in liver cancer immediately with high accuracy.
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RATIONALE: Necrosis is one of the main forms of cardiomyocyte death in heart disease. Recent studies have demonstrated that certain types of necrosis are regulated and programmed dependent on the activation of receptor-interacting serine/threonine-protein kinase (RIPK) 1 and 3 which may be negatively regulated by Fas-associated protein with death domain (FADD). In addition, microRNAs and long noncoding RNAs have been shown to play important roles in various biological processes recently. OBJECTIVE: The purpose of this study was to test the hypothesis that microRNA-103/107 and H19 can participate in the regulation of RIPK1- and RIPK3-dependent necrosis in fetal cardiomyocyte-derived H9c2 cells and myocardial infarction through targeting FADD. METHODS AND RESULTS: Our results show that FADD participates in H2O2-induced necrosis by influencing the formation of RIPK1 and RIPK3 complexes in H9c2 cells. We further demonstrate that miR-103/107 target FADD directly. Knockdown of miR-103/107 antagonizes necrosis in the cellular model and also myocardial infarction in a mouse ischemia/reperfusion model. The miR-103/107-FADD pathway does not participate in tumor necrosis factor-α-induced necrosis. In exploring the molecular mechanism by which miR-103/107 are regulated, we show that long noncoding RNA H19 directly binds to miR-103/107 and regulates FADD expression and necrosis. CONCLUSIONS: Our results reveal a novel myocardial necrosis regulation model, which is composed of H19, miR-103/107, and FADD. Modulation of their levels may provide a new approach for preventing myocardial necrosis.
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Proteína de Dominio de Muerte Asociada a Fas/metabolismo , MicroARNs/metabolismo , Infarto del Miocardio/metabolismo , Daño por Reperfusión Miocárdica/metabolismo , Miocitos Cardíacos/metabolismo , Animales , Modelos Animales de Enfermedad , Relación Dosis-Respuesta a Droga , Proteína de Dominio de Muerte Asociada a Fas/genética , Células HEK293 , Humanos , Peróxido de Hidrógeno/toxicidad , Masculino , Ratones Endogámicos C57BL , MicroARNs/genética , Infarto del Miocardio/genética , Infarto del Miocardio/patología , Infarto del Miocardio/prevención & control , Daño por Reperfusión Miocárdica/genética , Daño por Reperfusión Miocárdica/patología , Daño por Reperfusión Miocárdica/prevención & control , Miocitos Cardíacos/efectos de los fármacos , Miocitos Cardíacos/patología , Necrosis , Oligonucleótidos/administración & dosificación , Proteínas Serina-Treonina Quinasas/metabolismo , Interferencia de ARN , ARN Largo no Codificante/genética , ARN Largo no Codificante/metabolismo , Ratas , Proteína Serina-Treonina Quinasas de Interacción con Receptores/metabolismo , Transducción de Señal , Transfección , Factor de Necrosis Tumoral alfa/toxicidadRESUMEN
<p><b>OBJECTIVE</b>To evaluate whether glycation of high-density lipoprotein (HDL) increases cardiovascular risk in patients with type 2 diabetes mellitus by altering its anti-atherogenic property.</p><p><b>DATA SOURCES</b>Data cited in this review were obtained mainly from Pubmed and Medline in English from 2000 to 2013, with keywords "glycation", "HDL", and "atherosclerosis". Study selection Articles regarding glycation of HDL and its role in atherogenesis in both humans and experimental animal models were identified, retrieved and reviewed.</p><p><b>RESULTS</b>Glycation alters the structure of HDL and its associated enzymes, resulting in an impairment of atheroprotective functionality and increased risks for cardiovascular events in type 2 diabetic patients.</p><p><b>CONCLUSION</b>Glycation of HDL exerts a deleterious effect on the development of cardiovascular complications in diabetes.</p>