Objective To investigate the regularity and significance of serum interleukin-6(IL-6) levels in the patients with sepsis.Methods Forty sepsis patients with APACHEⅡ scores over 12 and 30 normal controls were involved in the study.The IL-6 levels in serum were detected with radio-immunity analysis assay and the correlations among the IL-6 levels,the prognosis and APACHEⅡ score were investigated.Results In the patients with sepsis,the average level of IL-6 in serum was(152.02?55.77) pg/ml,which was significantly higher than that of the control group [(85.79?30.96) pg/ml](P

Objective To investigate the preoperative management and the clinical effeciency of Lichtenstein tension-free hernioplasty in adult patients with inguinal incarcerated hernia.Methods Clinical data of 86 patients with inguinal incarcerated hernia were analyzed retrospectively.Hernia was repaired with Lichtenstein tension free after reposition.Results There were 59 male patients and 27 female patients with median age of (63 ± 18) years.There were 8 patients with liver cirrhosis.The operation was performed successfully in all patients.Segmental bowel resection with end-to-end anastomosis was performed in 38 emergency cases.Operative time was 20-120 min,with an average time of 54 min.The postoperative hospitalization was 5-17 d,with an average of 8 d.There were 7 cases of skin ecchymosis at the scrotum,there were no intestinal perforation,hepatic encephalopathy and upper gastrointestinal hemorrhage after operation.In early series of 24 cases without drainage tube left in place,there were 10 cases of fat liquefaction,10 cases of hydrops of hernial sac,6 cases of seroma and 3 cases of wound infection after operation.After 12 to 48 months of follow-up,there was no mortality after 2 years,no hernia recurrence.Conclusions Tension free repair in the treatment of incarcerated inguinal hernia is safe and feasible.

Adult ; Aged ; Aged, 80 and over ; Apoptosis Regulatory Proteins ; genetics ; metabolism ; Carcinoma, Non-Small-Cell Lung ; genetics ; metabolism ; Exons ; genetics ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Diseases ; genetics ; metabolism ; Lung Neoplasms ; genetics ; metabolism ; Male ; Middle Aged ; Mutation ; Proto-Oncogene Proteins ; genetics ; metabolism ; RNA, Messenger ; metabolism

OBJECTIVETo investigate the role of long non-coding RNA growth arrest-specific transcript 5 (lncRNA-GAS5) in breast cancer progression and epithelial-mesenchymal transition (EMT) of the cancer cells.

METHODSReal-time quantitative PCR (qRT-PCR) was used to detect the expression of lncRNA-GAS5 in 37 pairs of breast cancer and adjacent non-tumor tissues and in parental MCF-7 cells and paclitaxel-resistant MCF-7 (MCF-7/PR) cells, and the correlation of lncRNA-GAS5 expression with the clinical stage and lymph node metastasis of breast cancer was investigated. The expressions of the genes related with cell cycle and EMT at both the mRNA and protein levels were detected using qRT-PCR, Western blotting and immunohistochemistry. The changes in the biological behaviors and morphology of breast cancer cells with either lncRNA-GAS5 knockdown or overexpression were observed. Nude mouse models were established bearing breast cancer xenografts derived from MCF-7/PR cells or MCF-7/PR cells over-expressing lncRNA-GAS5, and the inhibitory effect of paclitaxel on tumor growth was evaluated.

RESULTSThe transcriptional levels of lncRNA-GAS5 were significantly lower in breast cancer tissues than in the adjacent non-tumor tissues (P<0.05), and decreased lncRNA-GAS5 expression was significantly correlated with TNM stage and lymph node metastasis of breast cancer (P<0.05). lncRNA-GAS5 expression was also significantly lowered in paclitaxel-resistant breast cancer cells and showed a positive correlation with P21 expression and a negative correlation with CDK6. MCF-7 cells during EMT presented with a lowered expression of lncRNA-GAS5, whereas lncRNA-GAS5 over-expression strongly suppressed MCF-7/PR cell migration and invasion, and increased the susceptibility of the cells to paclitaxel. In the tumor-bearing nude mouse models, lncRNA-GAS5 overexpression in the tumor cells obviously enhanced the inhibitory effect of paclitaxel on tumor growth and lung metastasis by reversing the EMT marker proteins.

CONCLUSIONA decreased expression of lncRNA-GAS5 promotes lung metastasis of breast cancer by inducing EMT, suggesting the potential of lncRNA-GAS5 as a therapeutic target in breast cancer.

Objective:Pin1 plays an important role in the pathogenesis of cardiovascular disease,our study aims to investigate the effects of Pin1 silencing by siRNA on H9c2 apoptosis induced by hypoxia/reoxygenation.Methods:H9c2 cells were cultured and subjected to a hypoxia/reoxygenation (H/R) condition in vitro,mimicking ischemic/reperfusion injury in vivo.The mRNA and protein expression of Pin1 were detected by RT-qPCR and Western blot.H9c2 cells were divided into control group,H/R group,H/R+Pin1 siRNA group,H/R+scramble siRNA group.MTT and flow cytometry with Annexin V-FITC/PI staining were respectively performed to detect cell viability and apoptosis.The expression of Bax and Bcl-2 were measured by Western blot.The activity of Caspase-3 was detected by automatic biochemistry analytic instrument.Results:The mRNA and protein levels of Pin1 were highly expressed in the cells of H/R group.Transfection with Pin1 siRNA strikingly inhibited the expression of Pin1.Compared with H/R group,Pin1 siRNA markedly increased cell viability,decreased the cell apoptosis and the Caspase-3 activity.Furthermore,the increased Bcl-2,decreased Bax and the ratio of Bcl-2 to Bax were observed in Pin1 siRNA group (P<0.05) compared with H/R group.Conclusion:Downregulation of Pin1 protects hypoxia/reoxygenation-injured H9c2 cells from apoptosis,which is possibly through the upregulation of Bcl-2 and downregulation of Bax and Caspase-3 activity.

OBJECTIVETo investigate changes in apoptosis-related ligands in serum in rats with severe scald and the effect of intensive insulin therapy on the changes.

METHODSOne hundred and fifty Wistar rats were randomly divided into 3 groups: sham burn (SB), scald (S) and treatment (T) groups. Rats in S and T groups were inflicted with 40% TBSA full-thickness burn, followed by intraperitoneal injection with 40 mL/kg of isotonic saline for resuscitation. Rats in T group were subcutaneously injected insulin in a dose of 0.25 U/100 g 24 hours after burn injury, and every 12 hours for 5 days (0.25, 0.50, 0.75, 1.00, 1.25 U/100 g each day, respectively) to control the level of blood glucose between 3 and 6 mmol/L. Rats in SB group were sham scalded at 37 degrees C without resuscitation. Blood was drawn from abdominal aorta on 1, 4, 7, 10, 14 post burn day (PBD) for determination of serum levels of TNF-alpha, soluble Fas ligand (sFasL) and soluble Fas receptor (sFas) by enzyme-linked immunosorbent assay (ELISA), and insulin by radioimmunity assay (RIA).

RESULTSThe serum level of TNF-alpha in S group peaked on 1 PBD (30.9 +/- 8.7) ng/L, which showed statistically significant difference when compared with that of SB and T groups (12.7 +/- 2.8) ng/L, (16.8 +/- 4.7) ng/L, respectively, P < 0.01), then lowered gradually to become similar to that of SB group on 7 PBD. The level of TNF-alpha in T group increased gradually, but was obviously lower than that of S group on 1, 4, 7 PBD (P < 0.01). The level of sFasL in S (on 7-14 PBD) and T (4-10 PBD) groups was significantly higher than that in SB group (P < 0.05), then lowered to normal level. The levels of sFas on 4-10 PBD in T group were obviously higher than that in S and SB group (P < 0.05). Ratio of sFasL to sFas in serum of S group was higher than that in SB group on 7, 10 PBD, which was higher than that in T group on 7 PBD (P < 0.05). There was significant decrease in serum level of insulin in S group compared with that of SB group on 4-10 PBD (P < 0.05). The level of insulin in T group increased on 1 PBD, peaked on 4 PBD (327 +/- 15 microU/mL), which was significantly higher than that in SB and S groups (42 +/- 15, 28 +/- 10 microU/mL, respectively, P < 0.01), then decreased gradually to normal level.

CONCLUSIONSInsulin may inhibit apoptosis after burn by down-regulating secretion of apoptotic ligands.

Animals ; Apoptosis ; Blood Glucose ; analysis ; Burns ; blood ; drug therapy ; Fas Ligand Protein ; blood ; Insulin ; therapeutic use ; Male ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; blood ; fas Receptor ; blood

OBJECTIVETo investigate changes in proliferative activity of myoblasts in skeletal muscle and potential role of phosphorylated Akt on it, so that a better understanding in mechanisms of skeletal muscle atrophy after burn injury will be got.

METHODSOne hundred and twenty Wistar rats were randomly divided into 2 groups: control and severe thermal injury group. Rats in severe thermal injury group were subjected to a 40% total body surface area full-thickness scald injury, and Tibialis Anterior (TA) muscles were collected on 0, 1, 4, 7, 10, 14 days post-injury. After muscle mass determined, immunohistochemical double staining was used for detection of Proliferative Cell Nuclear Antigen (PCNA) of myoblasts. Protein expression of total Akt and phosphorylated Akt was determined by Western Blot.

RESULTSBurn injury induced significant reduction of TA muscle mass and maximal reduction of it appeared by 4 days after injury (P < 0.01). Proliferative activity of myoblasts decreased significantly from the first day post-injury (P < 0.01) and increased slowly to basal level of controls after 7 days post-injury. The phosphorylated Akt was undetectable in both of controls and injured samples before 4 days but increased significantly after 7 days post-injury (P < 0.01), though total Akt expression had no significant alteration at any time points (P > 0.05).

CONCLUSIONSDecrease in proliferative activity of myoblasts may be one of the contributors of significant atrophy of skeletal muscle after burn injury. Effect of phosphorylated Akt on proliferation attenuated in early stage and increased significantly in later stage after burn injury may partly explain the changes in proliferative activity of myoblasts.

Animals ; Burns ; metabolism ; pathology ; Cell Proliferation ; Disease Models, Animal ; Male ; Muscle, Skeletal ; metabolism ; pathology ; Myoblasts ; metabolism ; pathology ; Phosphorylation ; Proto-Oncogene Proteins c-akt ; metabolism ; Random Allocation ; Rats ; Rats, Wistar

OBJECTIVETo study the efficacy of hepatitis B immunoglobulin (HBIG) combining hepatitis B vaccine in high risk infants born to HBsAg positive mothers through a follow-up study program.

METHODS184 infants (4 twin pairs) born to HBsAg carrier mothers who were consecutively recruited from December 2002 to August 2004 were followed. Major HBV serologic markers in all infants were detected by enzyme-linked immunosorbent assay (ELISA) when they were at birth, at 7th, at 24th and at 36th months.

RESULTS7 of the 184 infants were HBsAg positive at birth, making the transplacental intrauterine infection rate of HBV as 3.80% (7/184). 125 infants were followed up at 7th months and 108 infants were followed up at 24th and 36th months. Only 2 of the 7 infants born to HBsAg-positive and HBeAg-positive mothers were persistently sera positive for HBsAg, making the chronic infection rate of HBV as 28.57%. The other 140 infants were HBsAg negative during t he follow-up period. The rate o f detectable anti-HBs i ninfants was 7.02% at birth. After infants were immunized by HBIG combining hepatitis B vaccine, the anti-HBs-positive rate reached 92% at 7th months, and gradually descended thereafter. 72.04% of the infants at 24th and 60% at 36th months showed detectable levels of anti-HBs. There was significant correlation between the produce of anti-HBs in infants and HBsAg-positive at birth while HBsAg-positive and HBeAg-positive in mothers did not relate to the produce of anti-HBs in their infants. Of 39 infants born to HBsAg-positive and HBeAg-positive mothers, 25 showed detectable levels of HBeAg. During the follow-up peirod, HBeAg was still detectable in 2 infants who were also HBsAg positive and the others all became HBeAg-negative but no infant became HBeAg-positive.

CONCLUSIONThe efficacy of HBIG combining hepatitis B vaccine in high risk infants was fine.

Adult ; Enzyme-Linked Immunosorbent Assay ; Female ; Follow-Up Studies ; Hepatitis B Antibodies ; immunology ; Hepatitis B Vaccines ; immunology ; therapeutic use ; Hepatitis B e Antigens ; immunology ; Humans ; Immunoglobulins ; immunology ; therapeutic use ; Infant, Newborn ; Pregnancy ; Young Adult

OBJECTIVETo detect the expression and variation of p53 gene during tree shrews' hepatocarcinogenesis induced by hepatitis B virus (HBV) and aflatoxin B1 (AFB1).

METHODSTree shrews were divided into four groups: the tree shrews were infected with HBV and fed with AFB1 in group A, only infected with HBV in group B, fed with AFB1 alone in group C, and normal control in group D. All the tree shrews were performed liver biopsy every 15 weeks. The tissues of liver and tumor were detected by immunohistochemistry and molecular biotechnologies.

RESULTS(1) The incidence of hepatocellular carcinoma (HCC) in group A (66.7%) was higher than that in Group B and C (30%). HCC appearance in group A was earlier than that in group C (120.0 weeks +/-16.6 weeks vs 153.3 weeks +/-5.8 weeks, t = 3.336, P<0.01). (2) Mutated p53 protein was not found before the 75th week of the experiment in each group. (3) At the 105th week, the expression rates of mutated p53 protein were 78.6%, 60% and 71.4% in group A, B and C respectively, which were much higher than that (10%) in group D (x2 > or = 5.03, P<0.05). An abnormal band of p53 gene was detected in both group A and C. (4) The mutation points of p53 gene in liver cancer of tree shrew were at codon 275, 78 and 13. The nucleotide sequence and amino acids sequence of tree shrew's wild-type p53 showed 91.7% and 93.4% homology with those of human p53 respectively.

CONCLUSIONSThere is a remarkable synergistic effect between HBV and AFB1 on HCC. Mutated p53 protein is expressed before HCC occurrence, which promotes the development and progress of HCC. HBV and AFB1 may synergistically induce p53 gene mutation.

Aflatoxin B1 ; toxicity ; Animals ; Carcinoma, Hepatocellular ; genetics ; Cocarcinogenesis ; Gene Expression Regulation, Neoplastic ; Genetic Variation ; Hepatitis B ; virology ; Hepatitis B virus ; Liver Neoplasms, Experimental ; genetics ; Point Mutation ; RNA, Neoplasm ; analysis ; Tumor Suppressor Protein p53 ; genetics ; Tupaiidae

BACKGROUNDTo study the anti-SARS virus activities of different recombinant human interferons on the cell culture system.

METHODSAnti-SARS virus activities of interferons were determined by using CPE inhibition test in human skeletal muscle sarcoma (Rda) cell culture.

RESULTSThe average minimum amount of interferon alpha 2b, alpha 1b, beta 1b or omega 1b to inhibit 50% CPE in Rda cell culture was (160.5+/-129.5) IU/ml, (149.0+/-71.7) IU/ml, (69.5+/-61.5) IU/ml, (87.3+/-47.1) IU/ml, respectively or (0.6+/-0.5) ng/ml, (10.6+/-5.1) ng/ml, (3.5+/-3.1) ng/ml, (0.9+/-0.5) ng/ml, respectively.

CONCLUSIONAll the tested recombinant interferons showed anti-SARS virus activities on the Rda cell culture with different sensitivities.

Antiviral Agents ; pharmacology ; Cell Line, Tumor ; Humans ; Interferon Type I ; pharmacology ; Interferon-alpha ; pharmacology ; Recombinant Proteins ; SARS Virus ; drug effects ; Severe Acute Respiratory Syndrome ; drug therapy ; virology