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Objective:To investigate the diagnostic value of bronchial arteriography CT (BA-ACT) combined with bronchoscopy (BS) in bronchial Dieulafoy′s disease (BDD), and the role of bronchial artery embolization (BAE) in the treatment of BDD.Methods:Retrospective analysis was made on the clinical data of 5 patients suspected of being BDD treated by BS in Guangzhou First People′s Hospital or Guangzhou Thoracic Hospital from January 2008 to January 2018 due to hemoptysis. Bronchial arteriography (BAG) and BA-ACT were performed during the operation of interventional embolization. BAG rotary acquisition data were post-processed according to BS findings, and BA-ACT reconstruction images of the diseased bronchi and bronchial arteries were obtained. BS reexamination and clinical follow-up observation were carried out after embolization to analyze the effect of embolization.Results:There were one BDD lesion for the five patients respectively, and the BAG lacked characteristic manifestations. Bronchoscopy revealed BDD foci to present as papillary (case 1-case 3), nodular (case 4), or lirellate (case 5) subbronchial submucosal protrusion lesions. On the BA-ACT reconstruction plot, the BDD lesions of papillary, nodular and carination manifested correspondingly as a bronchial artery branches locally " pointed arch" shaped (cases 1-case 4) or " bead-like" (case 5) fold and protruding toward the bronchial lumen. The BDD lesions of the cases 1-case 4 retraction and disappearance after one BAE were observed by BS examination, and no hemoptysis recurrence during the follow-up period (54-91 months). The ridge like BDD lesion of the case 5 remained unchanged after BAE, and hemoptysis recurred at 71 months after the first BAE; the uncollapsed foci were supplied by two collateral vessels that confirmed by second BAG and BA-ACT, and no hemoptysis for 71 months followed up after second BAE.Conclusions:BA-ACT combined with BS enables a locative and qualitative diagnosis of BDD, and BAE is a very effective treatment method for BDD.
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Objective To explore the risk factors for patients with massive hemoptysis in tuberculosis and to provide a strategy for clinical treatment for tuberculosis massive hemoptysis (TMH). Methods Chi-square test and multivariate logistics analysis were applied to analyze the medical data of 241 cases of TMH. Results Chi-squared test showed that eleven factors were found to be significantly correlated with TMH. Longer disease course (≥3 months), lung lesions range ≥ 3 lung fields, pulmonary tuberculosis cavity, a higher smoking index (≥400 cigarettes per year) and clinical treatment were risk factors for TMH. Patients aged 45 years or older accompanied with bronchiectasia, pulmonary fungal infection, diabetes or hepatopathy had higher probabilities of developing massive hemoptysis. Multivariate analysis showed lung lesions range over 3 lung fields (OR = 2.447,P = 0.015), pulmonary tuberculosis cavity (OR = 2.486, P = 0.004), bronchial asthma (OR =3.192,P = 0.002), pulmonary fungal infection (OR = 3.896, P = 0.005) and hepatopathy (OR = 3.101, P =0.006) were final risk factors for TMH. Conclusion Multiple factors contributed to patients with massive hemoptysis in tuberculosis. Lung lesions range over 3 lung fields, pulmonary tuberculous cavities, bronchial asthma, lung fungal infection and hepatopathy might be the independent risk factors for TMH.
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AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.
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AIM:To investigate the effect of miR-214 on cardiomyocyte hypertrophy and the expression of the potential target genes . METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular car-diomyocytes (NMVCs).Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Wes-tern blotting, respectively.RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-in-duced hypertrophic cardiomyocytes .Dual luciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly in-creased in the hypertrophic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hy-pertrophy-related genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .
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AIM:To determine circular RNA (circRNA) profiles in the diabetic mouse myocardium , and to investigate the effect of circRNA_000203 on fibrotic phenotypes in cardiac fibroblasts .METHODS:Masson trichrome stai-ning was performed on the myocardium of the diabetic db /db mice and the non diabetic db/m control mice .circRNA ex-pression profile in the diabetic myocardium was detected by circRNAs microarray .The expression of circRNA_000203 was determined by real time fluorescence quantitative PCR ( RT-qPCR ) .Recombinant circRNA_000203 adenovirus was pre-pared for enforced the expression of circRNA_000203 in mouse cardiac fibroblasts.The expression of Col1a2, Col3a1andα-SMA was determined in circRNA_000203-modified cardiac fibroblasts , respectively .RESULTS:Masson trichrome stai-ning showed that fibrosis was increased in the diabetic mouse myocardium .The results of circRNA array detection revealed that circRNAs were dysregulated in the diabetic myocardium .circRNA_000203 was up-regulated in the diabetic myocardi-um.Significant over-expression of circRNA_000203 was achieved in the cardiac fibroblasts after infection with the recombi-nant circRNA_000203 adenovirus.The mRNA and protein expression of Col1a2, Col3a1 and α-SMA was significantly in-creased in the cardiac fibroblasts with over-expression of circRNA_000203.CONCLUSION:circRNA_000203 is up-regu-lated in the diabetic mouse myocardium .It has pro-fibrotic effect on the cardiac fibroblasts .
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AIM:To investigate the effect of microRNA-214 ( miR-214) on cardiomyocyte hypertrophy and the expression of the potential target genes .METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular cardiomyocytes ( NMVCs) .Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Western blot , respectively .RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-induced hypertrophic cardiomyocytes .Dual lu-ciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly increased in the hypertro-phic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hypertrophy-re-lated genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .
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Objective To investigate the clinical efficacy of bronchoscopic MMC topical spraying for the treatment of tuberculous cicatricial stenosis of the central airway. Methods 45 patients with t tuberculous cicatricial stenosis of the central airway were randomly divided into a control group (14 patients), treatment group 1 (group1, 15 patients), or treatment group 2 (group 2, 16 patients), who received bronchial balloon dilatation alone, bronchial balloon dilatation combined with topical MMC spraying for one time, and for twice, respectively . The clinical efficacy was observed by using the MRC score and measuring airway diameter at the time points before treatment, end of treatment, and 3, 6, and 12 months after treatment, respectively. Results For the MRC scores at different time points, the MRC scores in group 2 (0.06 ± 0.25) and group 1 (0.33 ± 0.617) were significantly lower than those in the control group at 3 months after treatment (P 0.05). Conclusions Bronchial balloon dilatation combined with topical MMC spraying has certain short-term and long-term efficacy for improving dyspnea and maintaining the airway diameter after dilatation.
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Objective To explore the clinical features of transbronchial tuberculous mediastinal lymph-adenitis and value of bronchoscopic interventional therapy. Methods The clinical data of 50 patients who had been diagnosed as tuberculous mediastinal lymphadenitis and had received bronchoscopic interventional therapy in our hospital during the period from January 2008 to January 2013 were retrospectively analyzed. The bronchoscopic change , improvement in symptoms , and time to sputum smear and culture conversion were used to assess the therapeutic effect. The patients were followed up for six months. Results The mean age of the patients was (35 ± 15) years and the male to female ratio was 1:1.2. The lesions occurred mostly at the right middle lobe in 24% (12/50) of the patients. The total effectiveness rate was up to 98% (49/50) after chemotherapy and bronchoscopic interventional therapy. The major complication associated with interventional therapy was hemoptysis (8%, 4/50). After follow-up of 6 months , 49 patients with active lesions were stable , with smooth bronchial mucosa and no obvious obstruction by granulation and caseous necrosis tissues. Conclusions The relavent clinical symptoms of transbronchial tuberculous mediastinal lymphadenitis is mainly caused by tuberculosis inflammation which destroys and blocks the airway. The fiber bronchoscopic therapy with forceps clip and drug infusion has a definite effect and fewer complications.