Objective: To search for a satisfactory method for establishing Stanford B type aortic dissection model in canine. Methods: Totally 12 adult dogs were used in the present study. The proximal descending aorta was clamped partially and laterally after a left thoracotomy; half circumference of the aorta, including the media and adventitia,was cut open transversely, with the intima kept intact. The aortic wall was then separated inferiorly, laterally and superiorly at a special dissecting space with a unique dissecting device. Then the intima at the same site was also cut open transversely and the two ends of the distal intimal flap were sutured to the adjacent aorta to allow blood entry. The distal adventitia and media were sutured to the proximal aorta to close the incision. Follow-up was carried out with pigtail catheter guided digital subtraction angiography (DSA) using omnipaque (16-18 ml/s) via either of the common iliac arteries and color Doppler ultrasound. Results: Formation and distal extension of aortic dissections were observed immediately after the procedure and were further confirmed by intra-operative color Doppler ultrasound, DSA, and post-operative biopsy at different time points. Conclusion: The present two-end intimal flap suturing method can be used for establishing Stanford B type aortic dissection model in canine; the model is similar to human Stanford B type aortic dissection.

Objective：A retrospective study was conducted to evaluate the efficiency of postoperative radiotherapy for completely resected, pathologically Stage Ⅲ a (N2) non-small cell lung cancer (NSCLC). Methods：From January 1989 to December 1993, among the patients with NSCLC who underwent radical surgery in the authors’hospital, there were 119 patients with completely resected, pathologically Stage Ⅲ a(N2)NSCLC. A total of 55 cases of these patients received postoperative radiotherapy with dose of 46-62 gray in mediastinum and hilus (S＋ RT group), except other 64 cases (S group). The survival rates and local control rates were analyzed and compared by the life table and Log-rank. Results：The clinical characters of patients such as age, sex, pathologic type were similar between two groups. The 1,3,5-year survival rates were 80.0％ , 32.7％ , 25.5％ respectively in S＋ RT group and 76.4％ , 36.4％ , 23.0％ respectively in S group, with no significant difference between two groups（ P >0.05） . The median time of local recurrence was 21 months in S＋ RT group and 12 months in S group, with significant difference between two groups(P<0.05） . The 1,3,5-year local control rates were 94.0％ , 78.5％ , 69.0％ respectively in S＋ RT group in contrast to 83.1％ , 58.3％ , 50.6％ respectively in S group(P< 0.05). The metastasis rates were similar in two groups （ P>0.05） . Conclusion：Postoperative radiotherapy can increase the local control rates and prolong the time of local recurrence for the patients with completely resected, pathologically Stage Ⅲ a (N2) NSCLC, but the survival rate can not be improved.

This study is to investigate the protection effect of schisandrin B (Sch B) against oxidation stress of HK-2 cells induced by cisplatin and the mechanisms involved. HK-2 cells were cultured and divided into different groups: solvent control group, cisplatin exposure group, positive group, Sch B treatment group. Cell viability and toxicity were evaluated by MTT and LDH assay. GSH level and SOD enzymes activities were also measured. DCFH-DA as fluorescence probe was used to detect ROS level by fluorescence microplate reader. Nrf2 translocation was detected by Western blotting. Real time Q-PCR was used to detect expressions of NQO1, HO-1 and GCLC mRNA level. The results showed that Sch B could significantly inhibit the decline of cell viability induced by cisplatin treatment (P < 0.05) and the protective effect was in a dose dependent manner. Furthermore, Sch B treatment significantly inhibited the increase of ROS level induced by cisplatin and reversed the decrease of GSH level (P < 0.05). When Sch B concentration was up to 5 micromol x L(-1), SOD enzyme activities were also enhanced significantly compared with that of the cisplatin group (P < 0.05). It was shown that Sch B could cause nuclear accumulation of Nrf2 in association with downstream activation of Nrf2 mediated oxidative response genes such as GCLC, NQO1 and HO-1. These results suggested Sch B could protect against the oxidative damage of HK-2 cells induced by cisplatin via the activation of Nrf2/ARE signal pathway.
Antineoplastic Agents ; toxicity ; Antioxidants ; isolation & purification ; pharmacology ; Cell Line ; Cell Survival ; drug effects ; Cisplatin ; toxicity ; Cyclooctanes ; isolation & purification ; pharmacology ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Glutathione ; metabolism ; Heme Oxygenase-1 ; genetics ; metabolism ; Humans ; Kidney Tubules, Proximal ; cytology ; metabolism ; L-Lactate Dehydrogenase ; metabolism ; Lignans ; isolation & purification ; pharmacology ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; NF-E2-Related Factor 2 ; genetics ; metabolism ; Polycyclic Compounds ; isolation & purification ; pharmacology ; RNA, Messenger ; metabolism ; Reactive Oxygen Species ; metabolism ; Schisandra ; chemistry ; Signal Transduction ; Superoxide Dismutase ; metabolism

Objective To explore the associations between fasting serum lipids and high-sensitivity C-reactive protein ( hsCRP).Methods Serum triglyceride ( TG),high-density lipoprotein cholesterol (HDL-C) and hsCRP were measured in residents of Chengdu,China.Subjects with potential factors which might influence lipids and hsCRP were excluded,580 subjects [ mean age ( 62.3 ± 6.6 ) years ; male:58.7％ ] were finally recruited by random sampling methods.Results There was a weak positive relationship between TG and hsCRP ( r =0.108,P =0.01 ) and a weak negative relationship between HDLC and hsCRP (r =- 0.197,P ＜ 0.001 ),this was also true in the sub-group with BMI ＜ 24 kg/m2 ( r =0.236,-0.140 respectively,all P ＜0.001 ).In subjects with BMI ＜24 kg/m2,the hsCRP concentration was significantly higher in subjects with higher TG or lower HDL-C ( all P ＜ 0.05 ).hsCRP increased in proportion with the degree of dyslipidemia.After adjusting for gender,age,TC,LDL-C,fasting blood glucose,systolic blood pressure,diastolic blood pressure,history of hypertension and diabetes,smoking and alcohol drinking,logistic regression analysis showed that the odds ratio for increased hsCRP was 1.970 in subjects with either increased TG or lower HDL-C (P =0.105) and 9.098 in subjects with both higher TG or lower HDL-C levels (P =0.031 ).However,the observed relationship between TG,HDL-C and hsCRP in subjects with BMI ＜ 24 kg/m2 could not be observed in subjects with subjects with BMI ＞ 24 kg/m2despite significant more cardiovascular risk factors in these subjects.Conclusions A weak positive correlation between TG and hsCRP as well as a weak negative correlation between HDL-C and hsCRP was evidenced in the whole cohort suggesting dyslipidemia might be related to enhanced inflammatory status.However,this relationship is not observed in subjects with BMI ＞ 24 kg/m2 despite existence of more cardiovascular risk factors in these subjects.

The aim of this study is to investigate the protection effect of tanshinone IIA (Tan) against triptolide (TP)-induced liver injury and the mechanisms involved. Acute liver injury was induced by intraperitoneal injection of TP (1 mg x kg(-1)) in mice. The activities of AST, ALT and LDH in serum and the levels of GSH, GST, GSH-PX, SOD, CAT and MDA in liver tissue were detected. The histopathological changes of liver tissues were observed after HE staining. Nrf2 translocation in liver tissue was detected by Western blotting, and real-time PCR was used to measure the expression levels of GCLC, NQO1 and HO-1 mRNA. The results showed that pretreatment with Tan significantly prevented the TP induced liver injury as indicated by reducing the activities of AST, ALT and LDH (P < 0.01). Tan pretreatment also prevented TP-induced oxidative stress in the mice liver by inhibiting MDA and restoring the levels of GSH, GST, SOD and CAT (P < 0.05). Parallel to these changes, pretreatment with Tan could attenuate histopathologic changes induced by TP. Furthermore, the results indicated that Tan pretreatment caused nuclear accumulation of Nrf2 as well as induction of mRNA expression of antioxidant response element (ARE)-driven genes such as GCLC, NQO1 and HO-1. These results indicated that Tan could protect against TP-induced acute liver injury via the activation of Nrf2/ARE pathway.
Animals ; Antioxidant Response Elements ; drug effects ; Chemical and Drug Induced Liver Injury ; metabolism ; pathology ; Diterpenes ; toxicity ; Diterpenes, Abietane ; pharmacology ; Drugs, Chinese Herbal ; pharmacology ; Epoxy Compounds ; toxicity ; Glutamate-Cysteine Ligase ; genetics ; metabolism ; Heme Oxygenase-1 ; genetics ; metabolism ; Liver ; metabolism ; pathology ; Male ; Membrane Proteins ; genetics ; metabolism ; Mice ; Mice, Inbred C57BL ; NAD(P)H Dehydrogenase (Quinone) ; genetics ; metabolism ; NF-E2-Related Factor 2 ; metabolism ; Phenanthrenes ; toxicity ; RNA, Messenger ; metabolism ; Signal Transduction ; drug effects

OBJECTIVETo investigate the association between CYP1A1 gene polymorphisms and susceptibility of nasopharyngeal carcinoma in Cantonese nuclear families through family-based association study.

METHODSA total of 457 Cantonese nuclear families,consisting of 2134 members, were recruited as subjects. Each family included two parents and at least one offspring with nasopharyngeal carcinoma. Two single nucleotide polymorphisms (SNP) in CYP1A1 named m1 (rs4646903) and m2 (rs1048943), were genotyped by PCR-RFLP assay and verified by directly sequencing. The genotype data were analyzed with family-based association test (FBAT) software to check the linkage and association between the two genetic markers and susceptibility of nasopharyngeal carcinoma.

RESULTSFBAT analysis showed that the minor allele frequencies (MAF) of the two SNP were 0.442 (C) and 0.339 (G) respectively. For m1 polymorphism in CYP1A1 gene was not significantly associated with nasopharyngeal carcinoma in our study population whether stratified with VCA-IgA or not (without stratification: chi2 = 2.399, P = 0.301; with stratification: low-titer group (VCA-IgA <1:80), MAF = 0.457 (C), chi2 = 1.221, P = 0.543; high-titer group (VCA-IgA > or = 1:80), MAF = 0.427 (C), chi2 =2.832, P = 0.243) . For m2 polymorphism, when VCA-IgA <1:80, the G allele showed decreased transmission under additive and dominant model (MAF = 0.347 (G); Zadditive = -2.120, Padditive = 0.034; Zdominant = - 2.303, Pdominant = 0.021) and a boundary P value was got with global statistic (chi2 = 5.394, P = 0.067) . Haplotype TG (0.057), constructed by m1 and m2, might decrease nasopharyngeal carcinoma risk (Z= -2.002, P=0.045). A boundary P value was also got with global statistic (chi2 =7.067, P=0.070).

CONCLUSIONThere was no statistical significance between m1 polymorphism and susceptibility of nasopharyngeal carcinoma in Cantonese nuclear families. And this study showed that m2 polymorphism might associated with the decrease of nasopharyngeal carcinoma in Cantonese nuclear families.

Cytochrome P-450 CYP1A1 ; genetics ; Female ; Gene Frequency ; Genetic Predisposition to Disease ; Genotype ; Haplotypes ; Humans ; Nasopharyngeal Neoplasms ; genetics ; Polymorphism, Single Nucleotide

Circulating microRNAs are robustly present in plasma or serum and have become a research focus as biomarkers for tumor diagnosis and prognosis. Centrifugation is a necessary procedure for obtaining high-quality blood supernatant. Herein, we investigated one-step and two-step centrifugations, two centrifugal methods routinely used in microRNA study, to explore their effects on plasma microRNA quantification. The microRNAs obtained from one-step and two-step centrifugations were quantified by microarray and TaqMan-based real-time quantitative polymerase chain reaction (Q-PCR). Dynamic light scattering was performed to explore the difference underlying the two centrifugal methods. The results from the microarray containing 1,347 microRNAs showed that the signal detection rate was greatly decreased in the plasma sample prepared by two-step centrifugation. More importantly, the microRNAs missing in this plasma sample could be recovered and detected in the precipitate generated from the second centrifugation. Consistent with the results from microarray, a marked decrease of three representative microRNAs in two-step centrifugal plasma was validated by Q-PCR. According to the size distribution of all nanoparticles in plasma, there were fewer nanoparticles with size >1,000 nm in two-step centrifugal plasma. Our experiments directly demonstrated that different centrifugation methods produced distinct quantities of plasma microRNAs. Thus, exosomes or protein complexes containing microRNAs may be involved in large nanoparticle formation and may be precipitated after two-step centrifugation. Our results remind us that sample processing methods should be first considered in conducting research.
Biomarkers ; blood ; Centrifugation ; methods ; Humans ; MicroRNAs ; blood ; Microarray Analysis ; Nanoparticles ; Plasma ; chemistry ; Real-Time Polymerase Chain Reaction

To investigate the effect of cyclin G1 antisense oligodeoxynucleotide (ASON) with liposomal transfection on mediating proliferation of HL-60 cell, the cyclin G1 ASON with liposomal transfection was used in vitro in co-culture with HL-60 cell, the protein and mRNA expression levels of cyclin G1 were measured by immunocytochemistry assay and RT-PCR. The cell apoptosis was detected by electron microscopy, in situ cell apoptosis detection kit (POD), DNA gel electrophoresis and flow cytometry (FCM). The results showed that in the cyclin G1 ASON group the protein and mRNA expression of cyclin G1 were significantly inhibited as compared with sense oligodeoxynucleotide (SON) group and blank group. When the ASON concentration increased, the proliferation ratio of HL-60 cell and CFU of HL-60 were also significantly inhibited. There was apoptosis of HL-60 cell. In conclusion, cyclin G1 ASON can specifically inhibit its protein and mRNA expression levels as well as the HL-60 cell proliferations and can accelerate the apoptosis of leukemia cells with concentration-dependent effect of ASON.
Apoptosis ; drug effects ; Cell Division ; drug effects ; Cyclin G ; Cyclin G1 ; Cyclins ; antagonists & inhibitors ; genetics ; Flow Cytometry ; HL-60 Cells ; cytology ; drug effects ; Humans ; Liposomes ; Microscopy, Electron ; Oligonucleotides, Antisense ; pharmacology ; Transfection

OBJECTIVETo study the inhibition effect of cyclin G(1) antisense oligodeoxynucleotides (ASON) on the growth of HL-60 cells in nude mice.

METHODS(1) Nude mice were divided into control group, sense oligodeoxynucleotides (SON) group and ASON group. After (60)Co radiation, with HL-60 cells SON group and ASON group were subcutaneously innoculated; (2) The weight and volume of tumors were continually measured; (3) The morphology of tumor cells was observed by microscope; (4) The protein and mRNA expression levels of cyclin G(1) were determined by flow cytometry (FCM) and reverse transcription polymerase chain reaction (RT-PCR); (5) The cell apoptosis was detected by electron microscopy and FCM.

RESULTS(1) The inhibition rate of tumor in ASON group was 69.4%. In ASON group, the wight and volume of tumor were significantly lower than those in SON group and control group. (2) The HL-60 cells in ASON group showed morphologically smaller nuclei, less mitosis, less heteromorphosis and apoptosis.

CONCLUSIONThe cyclin G(1) ASON can inhibit the growth of HL-60 cells in nude mice and induce apoptosis.

Animals ; Apoptosis ; genetics ; Cell Division ; genetics ; Cyclin G ; Cyclin G1 ; Cyclins ; genetics ; metabolism ; Female ; Flow Cytometry ; HL-60 Cells ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Oligonucleotides ; genetics ; metabolism ; Oligonucleotides, Antisense ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection ; Xenograft Model Antitumor Assays ; methods

Aged ; Female ; Humans ; Hypertriglyceridemia ; blood ; epidemiology ; Male ; Middle Aged ; Prevalence ; Uric Acid ; blood