Objective To analyze the clinical characteristics,diagnosis and the surgical treatment experience of the pulmonary sequestration.Methods The clinical data from 26 patients with pulmonary sequestration undergoing surgical operation were reviewed and analyzed retrospectively.Results Pulmonary sequestration was diagnosed in 16 out of 26 patients before the operation with the diagnosis rate of 61.5%(16/26).Pre-operation chest X-ray and plain CT-scan were performed in 26 cases.Enhancement CT scanning and CTA imaging were performed in 8 cases, magnetic resonance imaging were performed in 5 cases.21 patients with intralobar sequestration underwent lobectomy and 8 patients with extralobar sequestration underwent local lesion resection.Abnormal supply arteries were intraoprat-ibely found in 21 cases originating from the thoracic main artery,3 cases from the celiac artery,2 cases from the dia-phragm artery.Smooth recovery was achieved in all patients.No peri-operative death occurred.Symptoms disappeared were followed-up for 6 months.Conclusion Enhancement CT scanning,CTA imaging and magnetic resonance ima-ging ( MRI) may improve the diagnosis of pulmonary sequestration.Operation is a safe and effective method for the treatment of pulmonary sequestration.But intraoperative abnormal blood supply arteries should be paid attention to the treatment and prevention of intraoperative and postoperative bleeding.

Objective To summarize the clinical experience of T3-4 thoracic sympathectomy in the treatment of primary hyperhidrosis.Methods The clinical data of 80 patients with primary hyperhidrosis who underwent T3-4 thoracic sympathectomy were analyzed retrospectively.Results The operation was successfully performed on all patients.The symptom of palmar hyperhidrosis vanished in all patients,the operative time was (42.5 ± 15.7) min,the length of stay in hospital was (3.9 ± 0.6) d.No death and Horner syndrome occurred.All the patients were followed up for 6-24 months,compensatory hyperhidrosis was found in 26 patients,and no recurrence was found.Conclusion T3-4 thoracic sympathectomy is a safe and effective minimally invasive treatment for primary hyperhidrosis.

Objective: To investigate the effect of targeted silencing of DNA methyltransferase 3A(DNMT3A) on collagen deposition, proliferation and migration activity of mouse lung fibroblasts(PFs). Methods: In order to ensure the proliferation and migration activity of primary fibroblasts, the lung tissues of neonatal C57 suckling mice were taken, PFs were extracted after being sheared, and the morphology was observed and identified under the microscope. PFs cells were activated by 5 ng/ml TGF-β1for 24 h after cell attachment, and DNMT3A silencing model was constructed by small interfering RNA; The experiment was divided into control group, TGF-β1group, TGF-β1+ siRNA-NC group and TGF-β1+ siRNA-DNMT3A group. The protein expressions of DNMT3A, α-smooth muscle actin(α-SMA) and Collagen Ⅰ were detected by Western blot; Real time quantitative reverse transcription polymerase chain reaction(RT-qPCR) was used to detect the mRNA expression changes ofDNMT3A,α-SMAandCollagenⅠ. The proliferation ability of PFs was detected by CCK-8 and EdU staining; the migration ability of PFs was detected by scratch test and Transwell migration test. Results: Compared with the control group, TGF-β1induced the increase of DNMT3A in the activated PFs cell group(P<0.01), the protein and mRNA levels of fibrosis and proliferation related indicators α-SMA and Collagen Ⅰ also increased(allP<0.05), and the proliferation and migration ability of PFs increased(allP<0.000 1). Compared with the siRNA-NC group, the protein expression levels of DNMT3A(P<0.000 1) and related indicators α-SMA(P<0.01) and Collagen Ⅰ(P<0.01) significantly decreased in the DNMT3A silencing group by Western blot, and the mRNA levels ofDNMT3A,α-SMAandCollagenⅠby RT-qPCR also decreased(allP<0.001), and the proliferation(P<0.01) and migration ability(P<0.05) of PFs cells decreased compared with the control group. Conclusion Silencing DNMT3A can inhibit the deposition of collagen and the proliferation of PFs. DNMT3A can promote the proliferation and migration of PFs, and then promote the activation of PFs and the development of pulmonary fibrosis. This process may be regulated by DNA methylation modification.

Objective : To investigate the role of N-methyladenosine(m6 A) demethylase ALKBH5 in the prolifera- tion and activation of cardiac fibroblasts( CFs) in rats． Methods : The CFs taken from SD rats in 1 to 3 days were isolated by differential adhesion and observed under microscope．After cells were adherently grown to appropriate density，the cells were induced by TGF-β1 for modeling．The model cells were divided into the overexpression of ALKBH5 group infected by lentivirus and the negative control group for 24－48 hours. RT-qPCR was used to detect mRNA expression of ALKBH5，α-smooth muscle actin( α-SMA) ，type I collagen ( Collagen Ⅰ ) and proliferating cell nuclear antigen (PCNA) ．The expression of ALKBH5、α-SMA、Collagen Ⅰ and PCNA were assayed by West- ern blot．The cell proliferation activity was tested by CCK-8 assay and EdU. Results : Compared with the control group，the protein and mRNA of ALKBH5 were reduced in the model group active by TGF-β1．Meanwhile，the bi- omarkers of activation，such as PCNA，α-SMA and Collagen Ⅰ , increased significantly．Besides，the protein and mRNA of PCNA、α-SMA and Collagen Ⅰ were lower in overexpression of ALKBH5 group than those of the negative control group．CCK-8 assay and EdU suggested that the proliferation viability of CFs was reduced evidently in over- expression of ALKBH5 group，compared with the negative control group． Conclusion Overexpression of ALKBH5 can inhibit the proliferation of CFs，suggesting that ALKBH5 may be a key regulatory point in the development of myocardial fibrosis.