ABSTRACT
We investigated the endemic situation of alveolar echinococcosis (AE) in Nileke County,Yili Prefecture,Xinjiang and its genetic diversity of Echinococcus multilocularis.Human AE cases in the county were retrospectively investigated including their location and surrounding ecological conditions.Sequence detection and analysis of nad2,cob gene fragments of AE mtDNA from patients was used to identify genotype variation.Results showed that a total of 48 AE cases were diagnosed and the first AE patient was identified in 1989 in the county.The 45.8％ of AE cases were found in the recent 5 years (2011-2015) and annual prevalence was 1.7 per 100 000.The patients were distributed along the Kashgar River,particularly intensive in Wulasitai Township.The 38.6％ of the patients were aged arranged 35-44 years old,64.6％ were male and 95.8％ were farmers and herdsmen.AE cases were confirmed further and there was only one haplotype by sequencing analysis from 11 AE clinical patients in the county.It suggests that Nileke County is AE foci,and alveolar echinococcosis with sequences conserved is an emerging disease in the county.
ABSTRACT
Objective To evaluate the feasibility and effectiveness of secundum atrial septal defect(ASD)occlusion with the septal occluder through right-chest small incision. Methods The clinical data of 140 secundum ASD patients (47 males and 93 females) aged 3-63 years who were treated in our center from August 2004 to July 2014 were retrospectively analyzed. The diameter of ASD was 6 to 36 mm. Under general anesthesia, all patients underwent intraoperative transtsophageal echocardiography (TEE), during which no associated cardiac deformity was found. All patients received ASD occlusion via a small incision (3-4 cm) at the right anterior chest. The occluders were released with the help of TEE. Results The atrial septal defect closure was successfully completed in 134 cases. Six cases received surgical closure of ASD after the failure of occlusion. The reasons of conversion included postoperative dislodgement of occlusion device (n=2, both were central type with large size) and technically unsuitable for occlusion (n=4, in whom residual shunt was found in 2 case, sieve pore type in 1 case, and intraoperative dislodgement in 1 case). All of these 6 patients were treated surgically under cardiopulmonary bypass. No dislocation of the device or atrial shunt was found within 3 to 48 months after the operation. Conclusion Occlusion via small chest incision of ASD under TEE guidance without cardiopulmonary bypass is a safe, minimally invasive, effective, and convenient treatment and worth clinical application.
Subject(s)
Adolescent , Adult , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , Anesthesia, General , Cardiopulmonary Bypass , Echocardiography , Heart Septal Defects, Atrial , General Surgery , Retrospective Studies , Septal Occluder Device , Treatment OutcomeABSTRACT
<p><b>OBJECTIVE</b>To investigate the effect of liver X receptor agonist T0901317 on transforming growth factor-β1 (TGF-β1)-induced expression of α-smooth muscle actin (α-SMA) in normal human lung fibroblasts.</p><p><b>METHODS</b>Primary normal human lung fibroblast isolated from the lung specimens of lung cancer patients by explant culture technique were identified with immunostaining for vimentin and keratin. The cells in passages 4 to 10 were treated with T0901317 and/or TGF-β1, and RT-PCR, Western blotting and immunofluorescence assay were used to detect α-SMA expression in the fibroblasts.</p><p><b>RESULTS</b>Lung fibroblast expressed vimentin but not keratin. The results of RT-PCR, Western blotting and immunofluorescence assay all showed that normal human lung fibroblasts constitutively expressed α-SMA under baseline condition, and TGF-β1 at 5 ng/ml induced a significant upregulation of α-SMA both at the mRNA and protein levels. Liver X receptor agonist T0901317 (5 µg/ml) significantly inhibited TGF-β1-induced upregulation of α-SMA expression.</p><p><b>CONCLUSION</b>Liver X receptor agonist T0901317 can inhibit the upregulation of α-SMA in normal human lung fibroblasts induced by TGF-β1, suggesting the potential value of liver X receptor agonist in the treatment of lung fibrosis.</p>