Objective We investigated the effect of rhIL-10 on reperfusion injury and acute rejection in rats after liver transplantation. Methods ACI (RTI a) rats and LEW (RTI 1) rats were used as donors and recipients. The dose of rhIL-10 was 0,2,10,and 50??g?kg -1?d -1. Results rhIL-10 at a dosage of 10??g?kg -1?d -1 significantly prolonged recipient′s survival time (13.1?1.0?d vs. 9.4?0.7d,P

Objective To evaluate the modularized operative process during video-assisted thoracoscopic esophagectomy for esophageal cancer.Methods The clinical data of 45 patients with esophageal cancer who were admitted to the Daping Hospital from December 2011 to December 2012 were retrospectively analyzed.The influence of modularized operative process on the intra-and post-operative condition and short-term complications after videoassisted thoracoscopic esophagectomy + esophagogastric anastomosis were analyzed to investigate the efficacy and value of modularized operative process.Patients received video-assisted thoracoscopic and laparoscopic resection of esophageal carcinoma or thoracoscopic resection of esophageal carcinoma + gastric mobilization.Thoracoscopic esophageal mobilization and mediastinal lymph nodes dissection were done according to the modularized operative process:(1) Pulmonary ligament mobilization and groups 8L and 9 lymph nodes dissection.(2) Mobilization of the esophagus under the arcus venae azygos.(3) Mobilization of esophagus above the arcus venae azygos.(4) Transection of the arcus venae azygos.(5) Complete removal of thorax esophgus.(6) Ligation of thoracic duct.(7) Dissection of groups 4,5,7,10 and 2L lymph nodes.All the patients were followed up via phone call or mail till February 2013.Patients received thoracoabdominal computed tomography and gastrofiberscopy to detect tumor recurrence or metastasis every 3 months within the first year after the operation,and they were re-examinated every half year at 1 year later.Results Of the 45 patients,29 received video-assisted thoracoscopic and laparoscopic resection of esophageal carcinoma and 16 received video-assisted thoracoscopic resection of esophageal carcinoma + gastric mobilization.The length of the tumor was (4.2 ± 2.5) cm.The numbers of patients in AJCC T1,T2,T3 and T4 stages were 7,14,15 and 9,and the number of patients with AJCC N0,N1,N2,N3 stages were 23,13,7,2,respectively.The intrathoracic operation time,total operation time,volume of intraoperative blood loss,number of lymph node resected and postoperative duration of hospital stay were (72 ± 13)minutes,(249 ± 39) minutes,(183 ± 62) ml,27 ± 7,(18 ± 7) days,respectively.Two patients were transferred to open surgery.No patient died postoperatively,and 11 complications were detected after the operation.Six patients were complicated with cervical anastomotic fistula,4 with anastomotic stricture and 3 with hoarseness.Forty-five patients were followed for 1.5-14.0 months with the median follow-up time of 8 months.One patient died of upper gastrointestinal hemorrhage at postoperative month 12,and 1 died of multi-organ dysfunction syndrome at postoperative month 8.The remaining 43 patients survived.Conclusions The modularized operative process for thoraeoscopic esophagectomy is safe and effective,its short-term efficacy is satisfactory.

We report a complete genomic sequence of rare isolates (minor genotype) of the SARS-CoV from SARS patients in Guangdong, China, where the first few cases emerged. The most striking discovery from the isolate is an extra 29-nucleotide sequence located at the nucleotide positions between 27,863 and 27,864 (referred to the complete sequence of BJ01) within an overlapped region composed of BGI-PUP5 (BGI-postulated uncharacterized protein 5) and BGI-PUP6 upstream of the N (nucleocapsid) protein. The discovery of this minor genotype, GD-Ins29, suggests a significant genetic event and differentiates it from the previously reported genotype, the dominant form among all sequenced SARS-CoV isolates. A 17-nt segment of this extra sequence is identical to a segment of the same size in two human mRNA sequences that may interfere with viral replication and transcription in the cytosol of the infected cells. It provides a new avenue for the exploration of the virus-host interaction in viral evolution, host pathogenesis, and vaccine development.
Base Sequence ; China ; Cluster Analysis ; Gene Components ; Genetic Variation ; Genome, Viral ; Genotype ; Molecular Sequence Data ; Phylogeny ; Reverse Transcriptase Polymerase Chain Reaction ; SARS Virus ; genetics ; Sequence Analysis, DNA ; Severe Acute Respiratory Syndrome ; genetics

Coronary restenosis is an important cause of poor long-term prognosis in patients with coronary heart disease. Here, we show that lysine methyltransferase SMYD2 expression in the nucleus is significantly elevated in serum- and PDGF-BB-induced vascular smooth muscle cells (VSMCs), and in tissues of carotid artery injury-induced neointimal hyperplasia. Smyd2 overexpression in VSMCs (Smyd2-vTg) facilitates, but treatment with its specific inhibitor LLY-507 or SMYD2 knockdown significantly inhibits VSMC phenotypic switching and carotid artery injury-induced neointima formation in mice. Transcriptome sequencing revealed that SMYD2 knockdown represses the expression of serum response factor (SRF) target genes and that SRF overexpression largely reverses the inhibitory effect of SMYD2 knockdown on VSMC proliferation. HDAC3 directly interacts with and deacetylates SRF, which enhances SRF transcriptional activity in VSMCs. Moreover, SMYD2 promotes HDAC3 expression via tri-methylation of H3K36 at its promoter. RGFP966, a specific inhibitor of HDAC3, not only counteracts the pro-proliferation effect of SMYD2 overexpression on VSMCs, but also inhibits carotid artery injury-induced neointima formation in mice. HDAC3 partially abolishes the inhibitory effect of SMYD2 knockdown on VSMC proliferation in a deacetylase activity-dependent manner. Our results reveal that the SMYD2-HDAC3-SRF axis constitutes a novel and critical epigenetic mechanism that regulates VSMC phenotypic switching and neointimal hyperplasia.