Endothelial progenitor cells(EPCs)are the precursor cells of vascular endothelial cells.EPCs are in bone marrow,peripheral blood and cord blood.They participate in the process of angiogenesis after birth.The stimulation of exogenous and endogenous factors mobilizes bone marrow-derived EPCs into peripheral blood,and participates in the revascularization of ischemic tissue and the process of re-endothelialization of the injured blood vessels.The decreased mmahers and quality of EPCs in blood circulation are one of the most important factors of unfavourable prognosis after ischemic stroke.The transplantation of EPCs may provide a novel therapeutic strategy for the treatment of ischemic cerebrovascular disease.

Objective To investigate the associations of aquaporin-4 (AQP4) promoter polymorphisms with anti-AQP4 antibody and genetic susceptibility to multiple sclerosis (MS) and neuromyelitis optica (NMO) in Southern Chinese population.Methods The polymorphisms of AQP4promoter 0 and 1 were analyzed by PCR and DNA sequencing in 18 NMO,38 MS,13 recurrent myelitis (RM),6 recurrent optic neuritis (RON)patients and 39 healthy controls. Results Fourteen polymorphism loci were observed in AQP4-promoter 0,while 6 ones were observed in AQP4-promoter 1.Among them,the incidence rate of polymorphism at position - 1003 bp (A-G) of AQP4-promoter 0 in anti-AQP4 antibody-positive patients was significantly higher than that in anti-AQP4 antibody-negative patients and controls (former:13/18 vs 20/45,P =0.046; latter:13/18 vs 10/39,P =0.001 ).The incidence rates of polymorphism at position between -401 bp and -400 bp ( C inserted) of AQP4-promoter 1 in anti-AQP4 antibody-positive and -negative patients were significantly higher than that in controls( former:5/16 vs 0/28,P =0.008; latter:8/38 vs 0/28,P =0.027 ). The incidence rates of polymorphism at position - 1003 bp (A-G) of AQP4-promoter 0 and position between -401 bp and -400 bp ( C inserted)of AQP4-promoter 1 in patients with NMO and MS were significantly higher than that in controls( NMO:11/18 vs 10/39,P =0.010;4/15 vs 0/28,P =0.020; MS:19/38 vs 10/39,P =0.027;8/34 vs 0/28,P =0.018).Conclusions Polymorphisms loci were observed in AQP4-promoter 0 and AQP4-promoter 1,which may have an influence on the susceptibility to MS and NMO.Polymorphism at position - 1003 bp ( A-G) of AQP4-promoter 0 may be related to the emergence of anti-AQP4 antibody in patients with NMO and MS.

Objective To compare the efficiency of original neuromyelitis optica(NMO)-IgG assay of detecting NMO-IgG with a new anti-aquaporin-4(AQP4)assay of detecting AQP4,and to explore the accuracy of the method in the diagnosis of NMO and multiple sclerosis(MS).Methods The sera were obtained from 44 patients with NMO and 46 patients with MS and were tested by both NMO-IgG and antiAOP4 assays.NMO-IgG was identified by original NMO-IgG assay with a substrate from mouse brain.AntiAQIP4 was detected by anti-AQP4 antibody assay.The results from the two assays were statistically analyzed to compare accuracy and specificity of the methods.Results The results of the two assays were concordant in 45 testing negative cases and 36 positive cases(Kappa=0.798.P=0.000).The McNemar test showed that the positive rate of the two assays were not significantly different(P=1.000).The NMO-IgG assay showed 77.3% sensitivity,87% specificity,82.2% diagnosis accuracy,85%positive predictive value,87% negative predictive value.and 74.3%Younden index. The anti-AOP4 antibody assay showed 88.6% sensitivity,95.7%specificity,92.2% diagnosis accuracy,98.1% positive predictive value,89.8% negative predictive value.and 84.3% Younden index.Conclusions This study demonstrated that NMO-IgG and AQP4 antibody detection have high sensitivity and specificity to detect NMO and MS.Anti-AQP4 detected by anti-AQP4 antibody assay may be more useful for NMO diagnosis.

To obtain a primary overview of gene diversity and expression pattern in Lycoris longituba, 4,992 ESTs (Expressed Sequence Tags) from L. longituba bud were sequenced and 4,687 cleaned ESTs were used for gene expression analysis. Clustered by the PHRAP program, 967 contigs and 1,343 singlets were obtained. Blast search showed that 179 contigs and 227 singlets (totally 1,066 ESTs) had homologues in GenBank and 3,621 ESTs were novel.
Base Composition ; Computational Biology ; Expressed Sequence Tags ; Flowering Tops ; genetics ; Gene Expression Regulation, Plant ; Genetic Variation ; Lycoris ; genetics

H1 gene inactivation.Demethylation agent inhibits human pancreatic cancer cell line growth in association with ARH1 re-expression and reduced p-stat3 expression.

OBJECTIVETo investigate the effects of activation of the GLP-1 receptor on the p38MAPK signaling pathway in hepatic stellate cells (HSCs).

METHODSHSCs were isolated and identified according to morphological features; the levels of GLP-1R protein were determined by western blotting.The HSCs were randomly divided into a control grouP (normal saline treatment) and experimental grouP(liraglutide treatment); after 120 hours, the expression of p38MAPK mRNA was examined by RT-PCR and of phosphorylated (p)-p38MAPK protein was detected by western blotting.

RESULTSGLP-1R proteins were detected in the HSCs. Compared with the control group, the experimental group showed significantly decreased p38MAPK mRNA and p-p38MAPK protein (both P < 0.01).

CONCLUSIONThe p38MAPK signaling pathway could be down-regulated when GLP-1R is activated in HSCs.

Cells, Cultured ; Glucagon-Like Peptide 1 ; analogs & derivatives ; pharmacology ; Glucagon-Like Peptide-1 Receptor ; Hepatic Stellate Cells ; metabolism ; Humans ; Liraglutide ; MAP Kinase Signaling System ; RNA, Messenger ; Receptors, Glucagon ; metabolism ; p38 Mitogen-Activated Protein Kinases ; metabolism

It has been demonstrated that APPL1 (adaptor protein, phosphotyrosine interacting with PH domain and leucine zipper 1) is involved in the regulation of several growth-related signaling pathways and thus closely associated with the development and progression of some cancers. Diallyl trisulfide (DAT), a garlic-derived bioactive compound, exerts selective cytotoxicity to various human cancer cells through interfering with pro-survival signaling pathways. However, whether and how DAT affects survival of human hepatocellular carcinoma (HCC) cells remain unclear. Herein, we tested the hypothesis of the involvement of APPL1 in DAT-induced cytotoxicity in HCC HepG2 cells. We found that Lys 63 (K63)-linked polyubiquitination of APPL1 was significantly decreased whereas phosphorylation of APPL1 at serine residues remained unchanged in DAT-treated HepG2 cells. Compared with wild-type APPL1, overexpression of APPL1 K63R mutant dramatically increased cell apoptosis and mitigated cell survival, along with a reduction of phosphorylation of STAT3, Akt, and Erk1/2. In addition, DAT administration markedly reduced protein levels of intracellular TNF receptor-associated factor 6 (TRAF6). Genetic inhibition of TRAF6 decreased K63-linked polyubiquitination of APPL1. Moreover, the cytotoxicity impacts of DAT on HepG2 cells were greatly attenuated by overexpression of wild-type APPL1. Taken together, these results suggest that APPL1 polyubiquitination probably mediates the inhibitory effects of DAT on survival of HepG2 cells by modulating STAT3, Akt, and Erk1/2 pathways.

Objective To explore the impact of MR imaging T2 fluid-attenuated inversion-recovery sequence (MRI T2Flair) excision extension and postoperative chemotherapy in prognosis of patients with glioblastoma (GBM). Methods A retrospective study of clinical data and treatment efficacy of 17 patients with GBM, admitted to our hospital from April 2012 to August 2016, was performed. All patients were performed tumor resection by using awake anesthesia, neuroimage navigation, and intraoperative direct electrical stimulation. The impacts of the resection extent of T2Flair lesions and adjuvant chemotherapy on the prognosis of glioblastoma were analyzed. Results T1 enhanced lesions in these 17 patients were totally resected. The median follow-up duration was 18 months (8 months to 52 months). Median survival time was 20 months; the survival time of patients with resection ranges of 0%-10%, 10%-25% and more than 25% were 19, 22 and 24 months, respectively, without statistical differences (P>0.05). The patients adopted less than 6 courses chemotherapy had a 19-month-long median survival time, and those adopted 6 courses or more courses chemotherapy had a 33-month-long median survival time, with statistically significant difference (P<0.05). Conclusion When T1 enhanced lesions are totally resected, the resection extent of T2Flair lesions has no influence on patients survival time; however, patients accepted 6 or more courses of chemotherapy have a better survival.

Objective:To explore the selection of surgical methods for different sites of symptomatic Rathke's cleft cyst (RCC) and the clinical efficacies of these patients.Methods:Forty-seven patients with symptomatic RCC, admitted to our hospital from January 2016 to December 2019, were chosen in our study; 21 patients with intrasellar symptomatic RCC accepted surgery via unilateral nasal approach at the right side, 19 patients with intra-suprasellar symptomatic RCC accepted surgery via bilateral nasal approach, 3 patients with suprasellar symptomatic RCC accepted endonasal transsphenoidal surgery under endoscope, and 4 patients with suprasellar symptomatic RCC accepted craniotomy via pterion approach. The clinical efficacies and complications of patients accepted different surgical methods were compared. All patients were followed up for 3-36 months to observe the recurrence.Results:The postoperative symptoms of the patients were effectively improved, including headache relief ratio of 27/31, vision loss improvement ratio of 5/5, high prolactin relief ratio of 11/13, pituitary function improvement ratio of 9/18. Complications occurred in 6 patients, presenting as diabetes insipidus. Four patients recurred during follow-up.Conclusion:Intrasellar and intra-suprasellar symptomatic RCC accepted surgery via endoscopic transnasal transsphenoidal approach are safe and effective; selection of surgical methods for suprasellar symptomatic RCC should be determined according to the sizes and growth directions of cysts.

Objective:To evaluate deep learning for differentiating invasion depth of colorectal adenomas under image enhanced endoscopy (IEE).Methods:A total of 13 246 IEE images from 3 714 lesions acquired from November 2016 to June 2021 were retrospectively collected in Renmin Hospital of Wuhan University, Shenzhen Hospital of Southern Medical University and the First Hospital of Yichang to construct a deep learning model to differentiate submucosal deep invasion and non-submucosal deep invasion lesions of colorectal adenomas. The performance of the deep learning model was validated in an independent test and an external test. The full test was used to compare the diagnostic performance between 5 endoscopists and the deep learning model. A total of 35 videos were collected from January to June 2021 in Renmin Hospital of Wuhan University to validate the diagnostic performance of the endoscopists with the assistance of deep learning model.Results:The accuracy and Youden index of the deep learning model in image test set were 93.08% (821/882) and 0.86, which were better than those of endoscopists [the highest were 91.72% (809/882) and 0.78]. In video test set, the accuracy and Youden index of the model were 97.14% (34/35) and 0.94. With the assistance of the model, the accuracy of endoscopists was significantly improved [the highest was 97.14% (34/35)].Conclusion:The deep learning model obtained in this study could identify submucosal lesions with deep invasion accurately for colorectal adenomas, and could improve the diagnostic accuracy of endoscopists.