Adult ; Aneurysm, Dissecting ; complications ; diagnosis ; Aortic Aneurysm ; complications ; diagnosis ; Diagnostic Errors ; Female ; Humans ; Myocardial Infarction ; complications ; diagnosis

5 days.Blood gas analysis and blood pressure were determined at admitted day.Meanwhile,peripheral white blood cells at d1,3,5,and blood glucose were measured every day,respectively.GCS at d1,3,5 and hyperglycemia scorce(HS) were evaluated.Results Of the 82 studied patients,36 cases died.Univariate analysis showed that hypotension,lower GCS,higher peripheral white blood cells and HS were the independent death risk factors(Pa0.05).In multivariate logistic regression,the factors significantly associated with an increase in mortality were hypotension,lower GCS and higher HS.Conclusion Lower GCS,higher HS and hypotension are associated with poor outcome of children with severe trauma brain injury.

OBJECTIVETo investigate the effect of decreased expression of high mobility group Box-1 on the proliferation and apoptosis of HepG2 cells.

METHODSThree specific siRNAs of HMGB1 were designed and synthesized, and were transiently transfected into HepG2 cells by Lipofectamine 2000. The HMGB1 expression in HepG2 cells was detected by RT-PCR and Western blotting respectively. The proliferation activity in vitro was assessed by MTT assay. In situ apoptosis was evaluated by terminal deoxynucleotidyl transferase-deoxyuridine triphosphate nick end labeling (TUNEL) assay.

RESULTSAll of these specific HMGB1-siRNAs (1, 2, 3) efficiently and specifically inhibited the expression of the HMGB1 gene, and the levels of HMGB1 mRNA were 1.147+/-0.024, 1.014+/-0.042, 0.435+/-0.055, respectively, in HMGB1-siRNAs transfection group, which were significantly lower than that in Lipofectamine 2000 alone group (1.411+/-0.065, P < 0.01). Correspondingly, all of these specific HMGB1-siRNAs (1, 2, 3) could efficiently and specifically inhibit the expression of the HMGB1 protein, and the levels of HMGB1 protein were 0.369+/-0.035, 0.340+/-0.028, 0.097+/-0.020, respectively, in HMGB1-siRNAs transfection group, which were significantly lower than that in Lipofectamine 2000 alone group (0.553+/-0.051, P < 0.01). Of the 3 specific HMGB1-siRNAs, HMGB1-siRNA-3 (siRNAH3) had the highest inhibition rate (80%). The proliferation of HepG2 cells was markedly inhibited by siRNAH3 transfection. Compared to mock-transfection, siRNAH3 transfection dramatically suppressed the proliferation of HepG2 cells (P < 0.01). Moreover, siRNAH3 can induce apoptosis (P < 0.01).

CONCLUSIONsiRNA targeting HMGB1 mRNA can specifically reduce HMGB1 gene and protein expression. siRNAH3 can effectively suppress the proliferation and induce apoptosis of HepG2 cells.

Apoptosis ; Cell Proliferation ; HMGB1 Protein ; genetics ; Hep G2 Cells ; Humans ; RNA, Small Interfering

Objective To investigate the lipid-regulating effect and safety of combined statin and bezafibrate therapy in acute coronary syndrome (ACS) patients complicating with dyslipedemia.Methods One hundred and four hospitalized patients with established ACS and increased serum triglycerides (TG) levels and/or low serum levels of high density lipoprotein cholesterol (HDL-C) were selected.Except for conventional therapy,the patients were randomly divided into 2 groups:control group (n =52),treated with atorvastatin 20 mg qn or other statin equivalent to 20 mg atorvastatin ; treatment group (n =52),treated with the same dose statin plus bezafibrate 200 mg bid.The serum levels of total cholesterol (TC),TG,lowdensity lipoprotein cholesterol (LDL-C) and HDL-C were assessed before and after 6 and 12 weeks treatment,side effects and adverse events were recorded.Results After 6 weeks treatment,the serum levels of TC,TG and LDL-C in two groups were significantly reduced compared to baseline (all P ＜ 0.05),which were further declined after 12 weeks treatment,and the reduction was more significant in treatment group(29.8％,38.0％ and 36.1％,respectively) than in control group (14.7％,9.8％ and 26.7％,respectively) (all P ＜ 0.05).After treatment,the serum levels of HDL-C in the two groups were significantly higher than the baseline levels,especially after 12 weeks treatment (all P ＜ 0.05),and the elevations of HDL-C levels in control group and in treatment group were 19.3％ and 24.2％,respectively,but there were no significant difference between the two groups (P ＞ 0.05).After 12 weeks,the rates reaching to target goals of LDL-C,TG,HDL-C,and non-HDL-C levels in the treatment group (69.2％,88.5％,92.3％,46.2％ and 65.4％,respectively) were significantly higher than those in the control group (34.6％,65.4％,46.2％,7.7％ and 42.3％,respectively,all P ＜ 0.05).No serious side effects were observed in the two groups during the treatment period.Conclusion The combined statin and bezafibrate treatment is safe and could increase the ratios of reaching target lipid levels in ACS patients complicating with increased TG and (or) decreased HDL-C.

BACKGROUNDResistin, a newly discovered cysteine-rich hormone secreted mainly by adipose tissues, has been proposed to form a biochemical link between obesity and type 2 diabetes. However, the resistin receptor has not yet been identified. This study aimed to identify resistin binding proteins/receptor.

METHODSThree cDNA fragments with the same 11 bp 5' sequence were found by screening a cDNA phage display library of rat multiple tissues. As the reading frames of the same 11 bp 5' sequence were interrupted by a TGA stop codon, plaque lift assay was consequently used to prove the readthrough phenomenon. The stop codon in the same 11 bp 5' sequence was replaced by tryptophan, and the binding activity of the coded peptide [AWIL, which was designated as resistin binding peptide (RBP)] with resistin was identified by the confocal microscopy technique and the affinity chromatography experiment. pDual GC-resistin and pDual GC-resistin binding peptide were co-transfected into 3T3-L1 cells to confirm the function of resistin binding peptide.

RESULTSThree cDNA fragments with the same 11 bp 5' sequence were found. The TGA stop codon in reading frames of the same 11 bp 5' sequence was proved to be readthroughed. The binding activity of RBP with resistin was consequently identified. The expression of the resistin binding peptide in 3T3-L1 preadipocytes expressing pDual GC-resistin significantly inhibited the adipogenic differentiation.

CONCLUSIONRBP could effectively rescue the promoted differentiation of resistin overexpressed 3T3-L1 preadipocyte.

3T3-L1 Cells ; Adipocytes ; cytology ; drug effects ; Amino Acid Sequence ; Animals ; Base Sequence ; Carrier Proteins ; isolation & purification ; pharmacology ; Cell Differentiation ; drug effects ; Mice ; Molecular Sequence Data ; Peptide Library ; Rats ; Resistin ; antagonists & inhibitors ; metabolism

OBJECTIVETumor necrosis factor alpha-stimulated gene-6 (TSG-6 gene) differentially expressed in adipose tissue of obese and normal human subjects or rats. To explore the relationship between the differential expression of TSG-6 and adipocyte differentiation, adipogenesis and obesity, the present study aimed to investigate the changes of TSG-6 gene expression during 3T3-L1 preadipocyte differentiation and to analyze the regulative role of TNF-alpha on TSG-6 gene expression in matured 3T3-L1 adipocytes.

METHODS3T3-L1 preadipocytes were cultured in vitro and differentiated into the matured adipocytes. TNF-alpha in different concentrations (0.1 ng/ml, 1.0 ng/ml, 10.0 ng/ml) was added into the culture medium of fully differentiated adipocytes (day 10) for various times (0.5 h, 2 h, 6 h, 12 h, 24 h). Total RNA from these adipocytes was extracted and the levels of TSG-6 gene mRNA expression were evaluated by RT-PCR.

RESULTS(1) In preadipocytes, the level of TSG-6 gene mRNA expression remained low. In the presence of dexamethasone (Dex), MIX and insulin, with the 3T3-L1 preadipocytes being differentiated into the matured adipocytes, the level of TSG-6 gene mRNA expression was upregulated and reached the higher level in fully differentiated adipocytes. There is a significant difference between any two detected phases in the levels of TSG-6 gene mRNA expression (P < 0.05), except that the levels of TSG-6 gene mRNA expression did not increase obviously on day 0 to day 2, day 3 to day 5, day 4 to day 6 and day 7 to day 10 (P > 0.05). (2) Treatment of day 10 3T3-L1 adipocytes with TNF-alpha of different concentrations (0.1 ng/ml, 1.0 ng/ml, 10.0 ng/ml) resulted in a significant decrease in the level of TSG-6 gene mRNA expression. The inhibition effect of TNF-alpha on TSG-6 gene mRNA expression generally tended to be reinforced with the increasing concentrations of TNF-alpha and the elongation of time course, except for the period of 6 - 24 h after the stimulation of 10.0 ng/ml TNF-alpha. When 0.1 ng/ml TNF-alpha was applied, the level of TSG-6 gene expression decreased by 33.73% at 6 h, 97.39% at 12 h. While 1.0 ng/ml TNF-alpha was used, the level of TSG-6 gene expression decreased by 78.68% at 6 h, which remained until 24 h. At a concentration of TNF-alpha up to 10.0 ng/ml, the level of TSG-6 gene expression decreased by 96.27% at 2 h. TSG-6 gene expression was almost fully inhibited.

CONCLUSION(1) TSG-6 gene may be involved in adipocyte differentiation and adipogenesis. (2) TNF-alpha can downregulate the mRNA expression of TSG-6 gene in matured adipocytes. The inhibitory effect of TNF-alpha on TSG-6 gene expression is generally dose-correlated.

3T3-L1 Cells ; Adipocytes ; cytology ; drug effects ; metabolism ; Animals ; Cell Adhesion Molecules ; genetics ; Cell Differentiation ; drug effects ; genetics ; Dose-Response Relationship, Drug ; Gene Expression ; drug effects ; Mice ; RNA, Messenger ; drug effects ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo compare the effect of 5-fluorouracil (5-FU) portal vein infusion (PVI) for 7 days after radical resection, with intraluminal chemotherapy during operation for eliminating liver metastasis and elevating long-term prognosis in colorectal cancer.

METHODS162 colorectal cancer patients with radical resection were divided into portal vein chemotherapy group (group A, 82 cases) and intraluminal chemotherapy group (group B, 80 cases) randomly. In group A, 5-fluorouracil were infused with 1g per day constantly for 7 days after operation through portal vein catheters, which placed into greater omental vein and fixed on the abdominal wall. In group B, intraluminal chemotherapy was given and 5-fluorouracil 0.5 g was injected into the greater omental vein during operation.

RESULTSThe short-term complications and long-term effect in the two groups were compared by statistical software SPSS 8.0. Group A had more operative complications, and no statistical differences was found in hospital time and survival rate of the two groups. The 5-year survival rate is 76.7% (group A: 74.3%, group B: 79.2%), and the liver metastasis rate is 19.8%. There is no significant difference between the two group-survival curves. Multiple variable analysis suggested that Dukes' stage was the prognosis factor (P < 0.05).

CONCLUSIONSThe present study demonstrated that the two chemotherapy methods play an important role in preventing liver metastasis and improving the survival rate, and the intraluminal chemotherapy would be easier and simpler. The result should be further improved by using combined chemotherapy.

Adult ; Aged ; Antimetabolites, Antineoplastic ; administration & dosage ; Chemotherapy, Adjuvant ; Chemotherapy, Cancer, Regional Perfusion ; methods ; Colorectal Neoplasms ; drug therapy ; mortality ; therapy ; Combined Modality Therapy ; Female ; Fluorouracil ; administration & dosage ; Follow-Up Studies ; Humans ; Infusions, Intravenous ; Male ; Middle Aged ; Portal Vein ; Survival Rate ; Treatment Outcome

OBJECTIVETo analyze the long- term results of radical resection for rectal cancer and the factors influencing the operative results.

METHODSFrom January 1990 to December 1999, clinical data of 689 patients who underwent radical resection for rectal cancer were analyzed retrospectively.

RESULTSThe overall operative mortality was 0.7%, the follow- up rate was 96.7%, the median survival rate was 67.4 months. The 1-, 3-, 5- and 10-year survival rate after operation was 89.9%, 77.3%, 69.6% and 63.3% respectively. Univariate analysis showed that the survival rate was related with the first onset symptom, tumor location, infiltrated circumference of intestine, T staging, Dukes staging, histological type, extent of lymph node metastasis and operative approaches. Multivariate analysis showed that tumor location, histological type, invasive depth and Dukes staging were independent prognostic factors.

CONCLUSIONSThe long-term efficacy after radical resection for rectal cancer is correlated with tumor location, histological type, invasive depth and Dukes staging.

Adult ; Aged ; Aged, 80 and over ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Neoplasm Staging ; Rectal Neoplasms ; mortality ; pathology ; surgery ; Rectum ; pathology ; Regression Analysis ; Retrospective Studies ; Survival Rate ; Treatment Outcome

Objective To explore the effects of p53 up-regulated modulator of apoptosis (PUMA)-α protein on the apoptosis and fibrosis of human peritoneal mesothelial cells (HPMCs) induced by high glucose.Methods HPMCs were induced by 50mmol/L D type glucose or mannitol for 72 hours respectively,flow cytometry was employed to detect the rate of apoptotic cells,and theexpression levels of apoptosis-and fibrosis-related proteins were detected by Western blotting.The untreated HPMCs were transfected with Lenti-PUMA-α,and the treated cells were transfected with shRNA-PUMA-α,the number of apoptotic cells and the expression levels of apoptosis-and fibrosis-related proteins were detected with the methods mentioned above.Results Flow cytometry showed that the rate of apoptotic HPMCs increased after being induced by high glucose for 72 hours,and Western blotting revealed that the expression levels of pro-apoptotic and pro-fibrotic related proteins increased,but the arrestins of apoptosis and fibrosis-related proteins decreased.Up-regulation of PUMA-α promoted apoptosis and fibrosis,while down-regulation of PUMA-α alleviated apoptosis and fibrosis of HPMCs.Conclusion High glucose may accelerate apoptosis and fibrosis of HPMCs by up-regulating the expression of PUMA-α.