Résumé
<p><b>BACKGROUND</b>Liver transplantation is the most effective treatment for patients with end-stage liver failure, however infection after transplantation is a serious clinical complication. The purpose of this research was to investigate the molecular epidemiology and the influence of multidrug-resistant Gram-positive infection in patients, following liver transplantation, to provide reference for clinical treatment and prevention of Gram-positive bacterial infection.</p><p><b>METHODS</b>We isolated and detected bacteria from phlegm, throat swabs, urine, wound or wound secretions, blood, and fecal samples from 221 liver transplant patients in our hospital from January 2007 to April 2010. All isolated bacterial strains were identified and tested by minimal inhibitory concentration (MIC) drug-sensitive detection using the BioMerieux ATB bacterial identification instrument and repetitive extragenic palindromic-polymerase chain reaction (REP-PCR) detection of bacterial homology. Risk factors were calculated by multivariate Logistic regression analysis.</p><p><b>RESULTS</b>We collected 250 specimens from 221 patients hospitalized following liver transplantation surgery, of which 29 patients developed multiple infections. Sixty-five Gram-positive bacterial strains were isolated from different specimens from 53 infectious patients. We detected 29 multidrug-resistant Gram-positive strains from 29 patients (44.62%), including 20 Staphylococcus aureus (S. aureus) strains (68.97%) and nine Enterococcus strains (31.03%). All 20 S. aureus strains were highly resistant to aminoglycosides (gentamicin), cephalosporins (cefoxitin), quinolones (ciprofloxacin and levofloxacin), lincomycins (clindamycin), penicillin, and erythromycin. The resistance rate reached 100% in some cases. The S. aureus strains were highly sensitive to vancomycin and oxazolidinone (linezolid), with MIC50 < 2 µg/ml for both. The nine Enterococci strains were also highly resistant to aminoglycosides, quinolones, and penicillins, and highly sensitive to vancomycin (MIC50 < 2 µg/ml) and oxazolidinone (MIC50 < 1 µg/ml). Using REP-PCR detection, S. aureus was divided into five genotypes with 14 B-type strains. Enterococcus was divided into 11 genotypes, with two D-type strains, two G-type strains, and two K-type strains. The risk factors for Gram-positive bacterial infection in patients following liver transplantation were preoperative use of antibiotics (OR = 3.949, P = 0.004), high intra-operative blood input (OR = 1.071, P = 0.005), and postoperative renal failure (OR = 5.427, P = 0.043).</p><p><b>CONCLUSIONS</b>S. aureus and Enterococcus were the main pathogens causing infection following liver transplantation in patients with drug-resistant Gram-positive bacterial infection. The isolated strains were resistant to multiple antibiotics. B-type S. aureus strains were predominant. Reasonable use of antibiotics, decreasing intra-operative blood input, and preventing post-operative renal failure may reduce Gram-positive bacterial infections and the appearance of drug-resistant strains following liver transplantation.</p>
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Adulte , Femelle , Humains , Mâle , Adulte d'âge moyen , Antibactériens , Pharmacologie , Multirésistance bactérienne aux médicaments , Génétique , Bactéries à Gram positif , Génétique , Virulence , Infections bactériennes à Gram positif , Épidémiologie , Microbiologie , Transplantation hépatique , Tests de sensibilité microbienne , Épidémiologie moléculaireRésumé
<p><b>OBJECTIVE</b>To explore the expression of gut-enriched Kruppel-like factor 4(KLF4) in gastric cancer, and its association with prognosis.</p><p><b>METHODS</b>Surgical specimens were collected from 264 patients undergoing radical surgery between 2004 and 2009 in the Affiliated Qianfoshan Hospital, Shandong University. KLF4 mRNA level of specimens was detected by real-time PCR. KLF4 protein expression was measured by immunohistochemistry on tissue microarray, which contained primary gastric cancer, corresponding para-cancerous tissue, and paired lymph node metastases.</p><p><b>RESULTS</b>Real-time PCR revealed that mRNA level of KLF4 was down-regulated in gastric cancer compared with paired normal gastric mucosa. Immunohistochemistry on tissue microarray showed gastric cancer tissues had significantly lower KLF4 levels compared with paired normal gastric tissues. By univariate and multivariate analysis, KLF4 was a significant predictor of survival and recurrence.</p><p><b>CONCLUSION</b>KLF4 expression is significantly down-regulated in gastric cancer, and is an independent predictor of survival and recurrence.</p>
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Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Femelle , Humains , Mâle , Adulte d'âge moyen , Tube digestif , Métabolisme , Facteurs de transcription Krüppel-like , Métabolisme , Pronostic , Tumeurs de l'estomac , Diagnostic , MétabolismeRésumé
<p><b>OBJECTIVE</b>To investigate the effects of artificial liver support system(plasma exchange combined with continuous veno - venous hemodiafiltration, PE + CVVHDF) on Gc globulin in patients with liver failure.</p><p><b>METHODS</b>81 patients with liver failure were divided into 4 groups according to the treatment protocols and indicators such as liver function and clinical symptoms. Totally 29 effective cases and 14 ineffective cases in the ALSS group versus 15 effective cases and 23 ineffective cases in the medical group were included. Finally the changes of Gc globulin were observed in four subgroups before and after treatment. The correlation between Gc globulin and IL-10, IL-4, IL-18, TNFa, endotoxin, NO, sVCAM-1and sICAM-1were analyzed by Pearson correlation analysis.</p><p><b>RESULTS</b>The effectiveness rate was 67.44% in ALSS group and 34.21% in the medical treatment (P less than 0.01). Gc globulin, one of liver cell protection proteins was notably increased following the artificial liver treatment as compared with the increase in the medical treatment (P less than 0.01). The time-response curve of Gc globulin level had a significant upward trend in the effective group as compared to no significant rise in the ineffective group. Moreover, the Gc globulin was negatively correlated with IL-4, IL-18, TNFa, SVCAM-1, SICAM-1 and NO. In contrast, no correlation existed between Gc globulin and IL-10. The treatment with artificial liver can improve the outcome of the patients with liver failure. The level of Gc globulin was correlated with the curative effect and thus may be used as a potential indicator for curative effect forcast in the patients with liver failure.</p>
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Sujet âgé , Femelle , Humains , Mâle , Molécules d'adhérence cellulaire , Sang , Cytokines , Sang , Défaillance hépatique , Sang , Chirurgie générale , Thérapeutique , Foie artificiel , Monoxyde d'azote , Sang , Résultat thérapeutique , Protéine de liaison à la vitamine D , Sang , MétabolismeRésumé
<p><b>OBJECTIVE</b>To evaluate the relationship of hypoxia-inducible factor (HIF)-1alpha expression with chemotherapy response in gastric cancer and its clinical outcome.</p><p><b>METHODS</b>Leucovorin (CF) and 5-fluorouracil (5-FU) in combination with oxaliplatin (L-OHP) were used in 52 patients with gastric carcinoma (GC) at advanced stage. CF 200 mg/m(2) was intravenous drop for 2 h at day 1 and day 14. 5-FU 1500 mg/m(2) was continuously intravenous drop for 46 h at day 1 and day 14. L-OHP 85 mg/m(2) was intravenous drop for 2 h at day 1 and day 14. Four-week was one cycle. All the patients received 4 cycles of chemotherapy at least. Chemotherapy response and clinical outcome were evaluated. Immunohistochemistry was used to examine the protein expressions of HIF-1alpha, P-gp and MRP4 by tissue microarray in GC. Twenty-seven normal gastric tissue samples were used as control group.</p><p><b>RESULTS</b>The positive expression rates of HIF-lalpha, P-gp and MRP4 in tumor samples were 53.9%, 51.9% and 57.7% respectively, which were significantly higher than those in normal gastric tissues (0, 18.5% and 14.8% respectively) (P<0.05). In cases with positive expression of HIF-lalpha, the response rate was 14.3%; whereas in cases with negative expression of HIF-1alpha, the response rate was 50.0%. There was significant difference between two groups (P<0.05). In patients of HIF-1alpha positive expression,the median progression-free survival time was 4.7 months,the median survival time was 8.8 months, and 1-year, 2-year survival rates were 37.5% and 21.5% respectively. In patients of HIF-1alpha negative expression, the median progression-free survival time was 8.4 months, the median survival time was l2.6 months, and 1-year, 2-year survival rates were 51.2% and 33.5% respectively. There were significant differences between two groups (P<0.05).</p><p><b>CONCLUSION</b>HIF-1alpha expression may be a useful indicator to predict the chemotherapy response and clinical outcome in gastric carcinoma.</p>
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Adulte , Sujet âgé , Femelle , Humains , Mâle , Adulte d'âge moyen , Traitement médicamenteux adjuvant , Sous-unité alpha du facteur-1 induit par l'hypoxie , Métabolisme , Pronostic , Tumeurs de l'estomac , Traitement médicamenteux , Métabolisme , Anatomopathologie , Taux de survieRésumé
<p><b>OBJECTIVE</b>To investigate the mechanism of DDP-resistance in gastric cancer cell line SGC7901/DDP mediated by phosphate(p)-JNK.</p><p><b>METHODS</b>The p-JNK expression was blocked by the JNK inhibitor SP600125. The drug sensitivity was detected by MTT. Cell apoptosis rate was measured by flow cytometry. The expression of p-JNK and P-glycoprotein (P-gp) was examined by Western blot. The expression of both proteins were detected in a tissue microarray containing 168 spots of cancer tissue and 27 spots of normal gastric tissue by SP immunohistochemistry. Pearson method was used to analyze the correlation between p-JNK and P-gp.</p><p><b>RESULTS</b>The drug sensitivity and cell apoptosis rate significantly increased (P<0.01), and the protein expression levels of p-JNK and P-glycoprotein were down-regulated after the inhibition of p-JNK by SP600125 in both SGC7901(p-JNK: 1.17+/-0.03 vs 0.38+/-0.071, P-gp: 0.21+/-0.01 vs 0.06+/-0.01) and SGC7901/DDP (p-JNK: 2.56+/-0.14 vs 1.02+/-0.12, P-gp: 0.77+/-0.05 vs 0.52+/-0.06 )cells(all P<0.01). The protein expression rates of p-JNK and P-glycoprotein were 45.8% and 51.8% respectively in gastric cancer tissue, which were significantly higher than those in normal gastric tissue 7.4% and 18.5% (P<0.01). The correlation of protein expression of p-JNK and P-gp was positive (P<0.01).</p><p><b>CONCLUSION</b>JNK anti-apoptosis pathway with the regulation of P-gp expression plays an important role in the DDP-resistance of gastric cancer, which may be a novel target for reversing multidrug resistance.</p>
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Humains , Glycoprotéine P , Métabolisme , Apoptose , Lignée cellulaire tumorale , Cisplatine , Métabolisme , Pharmacologie , Multirésistance aux médicaments , Résistance aux médicaments antinéoplasiques , Régulation de l'expression des gènes tumoraux , JNK Mitogen-Activated Protein Kinases , Métabolisme , Transduction du signal , Tumeurs de l'estomac , Traitement médicamenteux , MétabolismeRésumé
<p><b>OBJECTIVE</b>To investigate the mechanism that mda-7/IL-24 selectively kills hepatocellular carcinoma (HCC) HepG2 cells in vitro.</p><p><b>METHODS</b>HCC cell line HepG2 and normal liver cell line L02 were infected with Ad.mda-7. The expression of mda-7/IL-24 was detected by RT-PCR and ELISA, respectively. The apoptotic effects were confirmed by Hoechst staining and flow cytometry assay, respectively. Furthermore, Bcl-2 family proteins, cytochrome C, Smac/DIABLO and caspase-9 were determined by Western blot.</p><p><b>RESULTS</b>The exogenous mda-7/IL-24 gene was expressed in HepG2 and L02 cells infected with Ad.mda-7. Ad.mda-7 induced apoptosis in HepG2 but not in L02 cells in vitro. The induction of tumor cell apoptosis is correlated with the increasing expression of Bax and decreasing expression of Bcl-2 and Bcl-xL genes, then facilitated the releasing of cytochrome C and Smac/DIABLO from mitochondria to cytoplasm and increasing the expression of caspase-9, eventually, resulted in apoptosis.</p><p><b>CONCLUSION</b>Ad.mda-7 selectively induces growth inhibition and apoptosis in hepatocellular carcinoma HepG2 cells but not in normal L02 hepatocytes in vitro, and the mechanism might involve the decrease of Bcl-2 and Bcl-xL and increase of Bak expression, facilitating the release of cytochrome C and Smac/DIABLO from mitochondria in HCC cells.</p>
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Humains , Adenoviridae , Génétique , Apoptose , Caspase-9 , Métabolisme , Cytochromes c , Métabolisme , Cellules HepG2 , Hépatocytes , Biologie cellulaire , Interleukines , Génétique , Métabolisme , Protéines et peptides de signalisation intracellulaire , Métabolisme , Mitochondries , Métabolisme , Protéines mitochondriales , Métabolisme , Protéines proto-oncogènes c-bcl-2 , Métabolisme , Transfection , Protéine Bax , Métabolisme , Protéine bcl-X , MétabolismeRésumé
<p><b>OBJECTIVE</b>To refine the loss of heterozygosity (LOH) on chromosome 5p15 and screen new tumor suppressor gene(s) in colorectal tumorigenesis.</p><p><b>METHODS</b>Samples of colorectal cancer and normal tissue of 83 cases were collected in this study. Sixteen polymorphic microsatellite markers were analyzed on chromosome 5 and another 6 markers on chromosome 5p15 by PCR. PCR products were electrophoresed on an ABI 377 DNA sequencer. Genescan 3.1 and Genotype 2.1 software were used for LOH scanning and analysis.</p><p><b>RESULTS</b>Two distinct regions of frequent allelic deletions at D5S416 on 5p15 and D5S428-D5S410 on 5q were detected. Another 6 polymorphic microsatellite markers were applied to 5p15 and the minimal region of frequrent loss of heterozygosity was established on 5p15 spanning the D5S416 locus.</p><p><b>CONCLUSION</b>A critical and precise location of 5p deletions, 5p15.2-5p15.3, has been detected, which may contain one or more unknown tumor suppressor gene(s) related to colorectal cancer.</p>
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Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Femelle , Humains , Mâle , Adulte d'âge moyen , Cartographie chromosomique , Méthodes , Chromosomes humains de la paire 5 , Génétique , Tumeurs colorectales , Génétique , Délétion de gène , Perte d'hétérozygotie , Répétitions microsatellites , Réaction de polymérisation en chaîneRésumé
<p><b>BACKGROUND</b>As a model for both multistep and multipathway carcinogenesis, colorectal neoplastic progression provides paradigms for researching both oncogenes and tumor suppressor genes (TSGs). However, the mechanism of colorectal cancer (CRC) is not completely understood, and many genes may be involved in the colorectal carcinogenesis. The purpose of this study was to screen for the potential TSGs on chromosome 1q31.1-32.1 in Chinese patients with sporadic colorectal cancer, to explore whether colorectal cancer in the Chinese population has unique genetic alterations and determine whether other putative TSGs exist and contribute to colon carcinogenesis.</p><p><b>METHODS</b>Six polymorphic microsatellite markers, at a density of approximately one marker in every 1.6 cM, were chosen for refined loss of heterozygosity (LOH) mapping of 1q31.1-32.1. Eighty-three colorectal cancer patients' tumor and normal DNA were analyzed via polymerase chain reaction (PCR) for these microsatellite markers. PCR products were eletrophoresed on an ABI 377 DNA sequencer. Genescan 3.1 and Genotype 2.1 software were used for LOH scanning and analysis. On the basis of refined LOH mapping results, we undertook a microarray-based expression screening to identify tumor association genes in 19 of the CRC cases.</p><p><b>RESULTS</b>The average LOH frequency of 1q31.1-32.1 was 24.41%, with the highest frequency of 36.73% (18/49) at D1S2622, and the lowest of 16.42% (11/67) at D1S412. A minimal region of frequent deletion was located within a 2 cM genomic segment at D1S413-D1S2622. There was no significant association between LOH of any marker in the studied regions and the clinicopathological data (patient sex, age, tumor size, growth pattern, or Dukes stage). On the basis of refined mapping results, we chose 25 genes located in the D1S413-D1S2622 (1q31.3-32.1) region and presented a microarray-based high throughput screening approach in 19 sporadic CRC cases to identify candidate CRC related tumor suppressor genes. This study found 4 significantly down-expressed genes, including CSRP1, LMOD1, PPP1R12B and CFHL3. There was no significant association between expression levels of CFHL3, CSRP1, LMOD1, PPP1R12B and the clinicopathological data. By database searching, CSRP1 was hypothesized to be a colorectal cancer related tumor suppressor gene.</p><p><b>CONCLUSIONS</b>Through detailed deletion mapping, we found that the 1q31.3-32.1 region might harbor one or more colorectal cancer related tumor suppressor gene (s). And by microarray-based high-throughput screening of candidate genes located in this region and by subsequent database searching, we present the first evidence that CSRP1 might be involved in the progression of CRC.</p>
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Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Femelle , Humains , Mâle , Adulte d'âge moyen , Asiatiques , Chromosomes humains de la paire 1 , Génétique , Tumeurs colorectales , Génétique , Gènes suppresseurs de tumeur , Physiologie , Perte d'hétérozygotie , Génétique , Répétitions microsatellites , Génétique , Séquençage par oligonucléotides en batterie , Réaction de polymérisation en chaîneRésumé
<p><b>OBJECTIVE</b>To investigate the effect of melanoma differentiation associated gene-7/interleukin-24 (mda-7/IL-24) on the hepatocellular carcinoma cell lines and normal liver cell line in vitro.</p><p><b>METHODS</b>Hepatocellular carcinoma cell lines HepG2, SMMC7721, Hep3B, MHCC97L, M6 and normal liver cell line L02 were infected with Ad.mda-7. The gene expression of mda-7/IL-24 in these cell lines was confirmed by RT-PCR and ELISA assay. MTT assay and flow cytometry were used to study tumor cell proliferation and cell cycle in vitro. Hoechst staining and cytometry assay after Annexin-V and PI staining were studied to indicate the apoptosis effect.</p><p><b>RESULTS</b>It was confirmed by RT-PCR that the exogenous mda-7/IL-24 gene expressed in all of these cells. The mda-7/IL-24 protein product was confirmed by assaying the supernatant with ELISA. MTT and apoptosis test indicated mda-7/IL-24 can induce the hepatocellular carcinoma cell lines growth suppression, apoptosis in vitro but not in normal liver cell line L02, cell cycle test revealed mda-7/IL-24 can block cancer cell lines in G2/M but not in L02.</p><p><b>CONCLUSIONS</b>mda-7/IL-24 selectively induces growth suppression, apoptosis in hepatocellular carcinoma lines but not in normal liver cell in vitro.</p>
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Humains , Adenoviridae , Génétique , Apoptose , Génétique , Physiologie , Carcinome hépatocellulaire , Génétique , Anatomopathologie , Cycle cellulaire , Génétique , Physiologie , Lignée cellulaire , Lignée cellulaire tumorale , Prolifération cellulaire , Vecteurs génétiques , Hépatocytes , Biologie cellulaire , Interleukines , Génétique , Physiologie , Tumeurs du foie , Génétique , Anatomopathologie , TransfectionRésumé
<p><b>OBJECTIVE</b>To study the blood pressure (BP) changes in the liver transplant recipients.</p><p><b>METHODS</b>A total of 206 patients without preoperation hypertension received liver transplantation in our hospital from February 2001 to July 2005. The BP level and serum immunosuppressant concentration at preoperation and various time points post operation were determined.</p><p><b>RESULTS</b>Compared with the preoperation, the average systolic and diastolic pressure was significantly increased at the 2 week, 1, 2, 4 and 6 months post operation. The mobility of hypertension increased significantly after liver transplantation, with the highest mobility (46.49%) at the 1st month post operation. There was no linear correlation between the immunosuppressant (FK506) concentration and the BP level at any time point.</p><p><b>CONCLUSION</b>There was a high hypertension incidence after liver transplantation. Although the use of immunosuppressive drugs accompanied with the BP increase, there was no linear correlation between the immunosuppressant concentration and the BP level post operation.</p>
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Femelle , Humains , Mâle , Adulte d'âge moyen , Pression sanguine , Études de suivi , Hypertension artérielle , Immunosuppresseurs , Transplantation hépatique , Complications postopératoires , Études rétrospectivesRésumé
<p><b>BACKGROUND</b>Because of the lack of brain death laws in China, the proportion of cadaveric organ donation is low. Many patients with end-stage liver disease die waiting for a suitable donor. Living donor liver transplantation (LDLT) would reduce the current discrepancy between the number of patients on the transplant waiting list and the number of available organ donors. We describe the early experience of LDLT in the mainland of China based on data from five liver transplant centers.</p><p><b>METHODS</b>Between January 2001 and October 2003, 45 patients with end-stage liver disease received LDLT at five centers in China. The indication and timing, surgical techniques and complications, nonsurgical issues including rejection, infection, and advantages of LDLT in the series were reviewed. Actuarial patient and graft survival rates were calculated by using the Kaplan-Meier product-limit estimate. Statistical analysis was completed by using SPSS 10.0.</p><p><b>RESULTS</b>All LDLT recipients were cirrhotic patients, except for one man with fulminant hepatic failure. Among the 45 cases of LDLT, 35 (77.8%) were performed in one center (the First Affiliated Hospital of Nanjing Medical University). The overall 1 and 3 year survival rate of the recipients was 93.1% and 92.0%, respectively. Of the 45 LDLT donors, there were 3 cases of biliary leakage, 2 subphrenic collections, 1 fat liquefaction around the incision and 1 biliary peritonitis after T tube removal. All donors recovered completely.</p><p><b>CONCLUSIONS</b>LDLT provides an excellent approach to addressing the problem of donor shortage in China even though the operation is complicated, uncompromising and difficult with respect to the safety of the donors and receptors. Despite early technical hurdles having been overcome, perfection of technique is still necessarily. At present, LDLT is a good choice for the patients with irreversible liver disease.</p>
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Adolescent , Adulte , Enfant , Enfant d'âge préscolaire , Humains , Transplantation hépatique , Donneur vivantRésumé
<p><b>OBJECTIVE</b>To screen the candidate TSGs on 22q13 involved in sporadic colorectal cancer.</p><p><b>METHODS</b>The DNA samples of 83 cases with colorectal carcinoma and normal tissues were analyzed using eight fluorescent labeled polymorphic microsatellite markers by PCR. PCR products were electrophoresed on an ABI 377 DNA sequencer. Genescan 3.7 and Genotype 3.7 software was used for LOH scanning and analysis. Comparison between LOH frequency and clinicopathological factors were performed by chia2 test.</p><p><b>RESULTS</b>The prevalence of LOH was 35.58%, and the average hereditary distance was 1.9 cM. The highest frequency of LOH (D22S1160 locus) and the lowest (D22S1170 locus) were 64.71% and 20%, respectively. Two obvious LOH regions were detected: One between D22S1171 locus and D22S274 locus (about 2.7 cM); another between D22S1160 and D22S1149 locus (about 1.8 cM). Furthermore,significant differences were observed between the frequency of LOH on D22S1171 locus and tumors location (P=0.020), the frequency of LOH on D22S114 locus and liver metastasis (P=0.008), the frequency of LOH on D22S1160 locus and lymph node metastasis (P=0.016). No significant differences were found between LOH on other loci and those factors above. Gene function screening revealed that ARHGAP8 and PPARA gene were involved in carcinogenesis.</p><p><b>CONCLUSIONS</b>Two obvious high frequency LOH regions are detected by refined deletion mapping. One locates between D22S1171 locus and D22S274 locus (about 2.7 cM); another locates between D22S1160 and D22S1149 locus (about 1.8cM), ARHGAP8 and PPARA gene may be TSGs which contribute to carcinogenesis and progression of sporadic CRC on 22q13 region.</p>
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Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Femelle , Humains , Mâle , Adulte d'âge moyen , Chromosomes humains de la paire 22 , Tumeurs colorectales , Génétique , Anatomopathologie , Gènes suppresseurs de tumeur , Perte d'hétérozygotie , Réaction de polymérisation en chaîne , Délétion de séquenceRésumé
To assess the effect of prostaglandin E_1(PGE_1)on renal blood flow and serum endothelin of liver recipients.Methods PGE_1 was administered in 38 liver recipients at the dose of 0.6?g?kg~(-1)?h~(-1)during liver transplantation and every day after operation.The effects of PGE_1 on serum endothelin concentration and creatinine(Cr)were observed and these indexes were compared with those in the control group(n=18).The renal blood flow resistance indexes(RI)were measured by Doppler ultrasound.Results Cr and RI were significantly lower in PGE1=treated group than those in the control group.PGE_1-treated group also showed a significantly lower serum endothelin concen- tration.Conclusion Administration of PGE_1 in liver recipients can significantly improve the early re- nal function by reducing serum endothelin concentration and dilating renal blood vessels.
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<p><b>OBJECTIVE</b>To summarize the initial experience of simultaneous pancreas kidney transplantation (SPK) with portal venous and enteric drainage.</p><p><b>METHODS</b>Between Jane 2001 and Jane 2003, SPK were performed in 5 patients. Systemic venous-enteric drainage (SED) was used in the first 2 patients and portal venous-enteric drainage (PED) in the last 3 cases. All patient were immunosuppressed with quadruple therapy, which included anti-CD25 mAb (Zenapax/Simulect) induction therapy, FK506, mycophenolate mofetil (MMF), and prednisone baseline therapy. The complications were analyzed.</p><p><b>RESULTS</b>Serum glucose and renal function of the 5 cases were normal and no further insulin was needed within 7 days post-operation. No technique complications such as duodenal fistula and thrombosis were observed, One episode of acute rejection of kidney allograft occurred in one patient with SED, and resolved with a bolus corticosteroids. One case with SED and one with PED were died of sepsis and FK506 toxicity 4 weeks after transplantation. The death occurred with functioning pancreas graft. No latter complications were observed in the 3 survived patients with excellent graft functions.</p><p><b>CONCLUSIONS</b>Both methods of SED and PED can be performed successfully and with no latter complications. But with its potential physiologic and immunologic advantages, PED might be a standard procedure for SPK.</p>
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Adulte , Femelle , Humains , Mâle , Diabète de type 1 , Chirurgie générale , Néphropathies diabétiques , Chirurgie générale , Drainage , Méthodes , Études de suivi , Intestins , Chirurgie générale , Transplantation rénale , Méthodes , Transplantation pancréatique , Méthodes , Veine porte , Chirurgie générale , Transplantation homologue , Résultat thérapeutique , Urémie , Chirurgie généraleRésumé
<p><b>OBJECTIVE</b>To investigate the relation between p16 gene expression and the carcinogenesis and progress of hepatitis B virus (HBV) related hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>In 35 specimens of HCC tissue and the adjacent liver tissue, the integration of HBV X gene was detected by polymerase chain reaction (PCR) and Southern blot. The point mutation of exon-1alpha, 2 and 3 of p16 gene were detected by PCR-single strand conformation polymorphism (SSCP). The expression of p16 mRNA and p16 protein was detected by RT-PCR and Western blot.</p><p><b>RESULTS</b>The integration of X gene correlated with the expression loss of p16 mRNA and p16 protein in HCC (P < 0.05). The expression loss rates of p16 protein in HCC and adjacent tissues were 62.9% (22/35) and 40.0% (14/35) with significant difference (P < 0.05). The expression loss of p16 protein in HCC correlated with the differentiation degrees of HCC and the infiltration of tumor cells (P < 0.05).</p><p><b>CONCLUSION</b>The integration of X gene correlates with the expression loss of p16 protein. The alteration of p16 gene, playing an important role in all stages of hepatocarcinogenesis, correlates with the progress and invasion of hepatocellular carcinoma.</p>