Objective: To determine plasma levels of soluble tumor necrosis factor-related apoptosis inducing ligand (sTRAIL) and its soluble death receptor (sDR4, sDR5) in essential hypertension (EH) patients with left ventricular hypertrophy (LVH). Methods: Enzyme linked immunosorbent assay (ELISA) was used to measure plasma levels of sTRAIL, sDR4 and sDR5 in 50 EH + LVH patients (EH + LVH group), 50 EH patients without LVH (EH group) and 50 healthy subjects (healthy control group), and the results were compared and analyzed among three groups. Results: ① Compared with healthy control group and EH group, there were significant increase in plasma levels of sTRAIL [(0.95±0.11) ng/ml vs. (1.12±0.86) ng/ml vs. (1.74±1.19) ng/ml], sDR4[(2.38±0.32) pg/ml vs. (5.63±1.05) pg/ml vs. (8.72±1.14) pg/ml] and sDR5[(< 6 pg/ml) vs. (39.19±8.23) pg/ml vs. (78.21±11.2) pg/ml] in EH + LVH group, P<0.01 all; and levels of sDR4 and sDR5 in EH group were significantly higher than those of healthy control group (P<0.01 both), but there was no significant difference in sTRAIL level between the two groups (P>0.05); ② Pearson correlation analysis indicated that there were significant positive correlation among levels of sTRAIL, sDR4 and sDR5 in EH + LVH patients (r=0.325~0.410, P<0.05 or <0.01). Conclusion: Plasma levels of sTRAIL, sDR4 and sDR5 may be valuable indexes for prediction of left ventricular hypertrophy in patients with hypertension.

To analyze the potential limitations of hospital-level research projects management by summarizing its performance status from 2008 to 2011,including but not limited to lack of time for conducting research,insufficient financial funds,inadequate funding application,inadequate supervision.Thus,since 2014,our hospital has adopted some new measurements for projects management,including full-time research,hierarchical management,full mobilization,the establishment of reward and punishment measures,which significantly improved the quality of hospital-level research projects,and the rate of longitudinal follow-up project,research enthusiasm of medical staff,and sustainable development of hospital science and technology.

AIM: To determine whether the eukaryotic initiation factor-4E (eIF-4E) inhibition facilitates the degradation of heparanase mRNA and alters heparanase protein expression in human colon adenocarcinoma cell line, LS-174T. METHODS: A 20-mer antisense s-oligodeoxynucleotide (asODN) targeted against the translation start site of eIF-4E mRNA were introduced into LS-174T cells by lipid-mediated DNA-transfection. eIF-4E protein and mRNA levels were detected by Western blot and RT-PCR, respectively. The mRNA levels of heparanase were determined by Northern blot. The alterations of heparanase expression were confirmed by Western blot analysis. RESULTS: The 20-mer asODN against eIF-4E specifically and significantly inhibited eIF-4E protein expression. Following eIF-4E inhibition, a significant reduction of heparanase mRNA was observed on Northern blot, and at the same time, heparanase protein expression significantly decreased as well. CONCLUSIONS: The results indicate that the inhibition of eIF-4E strongly reduces the stability of heparanase mRNA in colon adenocarcinoma cell line, LS-174T and resultes in an apparent reduction in the expression of heparanase protein. [

OBJECTIVES To analyse the diagnosis and treatment of 24 hereditary nonpolyposis colorectal cancer (HNPCC) kindreds and report mismatch repair gene mutations. METHODS The diagnosis, treatment and follow-up of 24 HNPCC kindreds were reviewed retrospectively, cancer incidence and spectrum were recorded. Clinical characteristics and treatment were analyzed. Peripherial blood and genomic DNA were extracted from family members who had provided informed consent. PCR and SSCP were used to screen coding regions of the hMLH1 and hMSH2 genes. Variant bands were sequenced by 377 DNA sequencer after purification. RESULTS One hundred and 25 malignant neoplasms were diagnosed in 75 patients (multiple cancers in 24) with an average age of 51 years in 24 pedigrees. The onset of the disease occurred earlier than expected with the passing of each generation within large kindreds. The neoplasm mainly included colonic cancer (63 patients), rectal cancer(21), stomach cancer(13), endometric cancer(7), and esophageal cancers(6). 84% patients received radical operations. Of 64 patients with colorectal cancer 16 had metachronous colorectal cancer. 24% colorectal patients developed metachronous cancer within 10 years after initial operation and received re-operation. In 3 detected families with germline hMSH2 and hMLH1 mutations resulting in truncated protein, 12 carriers were found. CONCLUSIONS The main characteristics of hereditary nonpolyposis colorectal cancer include early onset and frequence of cancer; predominance of colorectal cancer, especially right-sided colonic cancer; frequency of multiple primary cancer, especially colorectal cancer; and age anticipation in large HNPCC pedigrees. Segmental resection of colorectal cancer is not suitable for colorectal cancer patient in HNPCC kindred. Intensive follow-up is important for all patients and possible gene carriers.
Adaptor Proteins, Signal Transducing ; Adult ; Aged ; Carrier Proteins ; Colorectal Neoplasms, Hereditary Nonpolyposis ; diagnosis ; genetics ; therapy ; DNA-Binding Proteins ; Female ; Humans ; Male ; Middle Aged ; MutL Protein Homolog 1 ; MutS Homolog 2 Protein ; Mutation ; Neoplasm Proteins ; genetics ; Nuclear Proteins ; Proto-Oncogene Proteins ; genetics

OBJECTIVETo investigate the correlation between tissue factor (TF) expression and hepatic metastasis and prognosis in rectal cancer.

METHODSTF expression was retrospectively studied by immunohistochemical method in specimens of 40 rectal cancer, 3 hepatic metastasis and 6 benign adenoma with relation to their clinicopathologic data.

RESULTS1. TF expression was detected in 20 (50%) of the 40 primary rectal cancer specimens and all the 3 hepatic metastatic specimens, but not in the 6 benign adenoma or normal mucosa of rectum, 2. Significant correlation was observed between TF expression and synchronic hepatic metastasis (P = 0.002) and heterochronic hepatic metastasis (P = 0.001) and 3. TF was a risk factor for the prognosis of primary rectal cancer (P = 0.024).

CONCLUSIONTissue factor expression may play a role in the process of developing hepatic metastasis. It may be considered as a new clinical indicator for monitor of hepatic metastasis and prognosis of primary rectal cancer.

Adenoma ; metabolism ; pathology ; Humans ; Immunohistochemistry ; methods ; Liver Neoplasms ; metabolism ; secondary ; Logistic Models ; Predictive Value of Tests ; Proportional Hazards Models ; Rectal Neoplasms ; metabolism ; pathology ; Rectum ; metabolism ; Retrospective Studies ; Staining and Labeling ; methods ; Thromboplastin ; biosynthesis

Objective To evaluate the clinical efficacy and safety of preoperative endovascular embolization of Solid Hemangioblastomas.Methods The data bases including Wan Fang,CNKI(China National Knowledge Infrastructure),VIP Database,PubMed、Medline、Springer were searched for the related studies.Two independent surgeons assessed trails for eligibility and quality,and all data marching the standards were abstracted for Meta-analysis by RevMan 5.3.Results 8 randomized controlled trails(RCT)were included.Selected analysis of embolized and non-embolized groups of Solid Hemangioblastomas were observed for variables of clinical efficacy in surgery time,number of blood loss and transfusions,complete resection,there were statistical difference.(P＜0.000 01,WMD=-1.18,95％CI[-1.16,-0.71];P＜0.000 01,WMD=-464.17,95％CI[-492.17,-437.24];P＜0.000 01,WMD=-238.81,95％CI[-282.84,-194.77];P＜0.006,RR=1.17,95％CI[1.05,1.31]).Conclusion The preoperative endovascular embolization is beneficial for Hemangioblastomas because it can shorten the time of surgery,diminish the necessity of intra-operative blood loss and transfusion,it also raises the ratio of complete resection of Solid Hemangioblastomas.

In vitro studies have established the prevalent theory that the mitochondrial kinase PINK1 protects neurodegeneration by removing damaged mitochondria in Parkinson's disease (PD). However, difficulty in detecting endogenous PINK1 protein in rodent brains and cell lines has prevented the rigorous investigation of the in vivo role of PINK1. Here we report that PINK1 kinase form is selectively expressed in the human and monkey brains. CRISPR/Cas9-mediated deficiency of PINK1 causes similar neurodegeneration in the brains of fetal and adult monkeys as well as cultured monkey neurons without affecting mitochondrial protein expression and morphology. Importantly, PINK1 mutations in the primate brain and human cells reduce protein phosphorylation that is important for neuronal function and survival. Our findings suggest that PINK1 kinase activity rather than its mitochondrial function is essential for the neuronal survival in the primate brains and that its kinase dysfunction could be involved in the pathogenesis of PD.