Re: In vivo tension sustained by fascial sling in pubovaginal sling surgery for female stress urinary incontinence.
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Publications and source records attributed to Wen-Chi Chen.
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OBJECTIVE: To evaluate whether polymorphism of the interleukin-4 gene exon 3, and of the interleukin-1beta gene exon 5 and promoter region, are associated with transitional cell carcinoma (TCC) of the urinary bladder, as cytokines are hypothesized to be important in cancer formation. PATIENTS, SUBJECTS AND METHODS: The study included 138 patients with TCC of urinary bladder and 105 healthy controls living in the same area. Each genetic polymorphism was typed using polymerase chain reaction-based restriction analysis. Genotype distribution and allelic frequencies between patients and controls were compared. RESULTS: There were significant differences in genotype and allelic distribution of intron 3 RP1/RP2 polymorphism (P < 0.001), but no significant difference in genotype distribution or allelic frequencies of the interleukin-1beta gene polymorphism between patients with bladder cancer and controls. CONCLUSION: The interleukin-4 gene intron 3 polymorphism is associated with bladder cancer and is a potential genetic marker in screening for the possible causes of bladder cancer.
OBJECTIVE: This prospective, randomized, controlled, head-to-head study was conducted to compare the efficacies of esomeprazole- and pantoprazole-based triple therapies for Helicobacter pylori eradication. METHODS: From January 2002 to October 2003, 200 H. pylori-infected patients were randomly assigned to undergo twice daily treatment with esomeprazole 40 mg (n = 100) or pantoprazole 40 mg (n = 100) combined with clarithromycin 500 mg and amoxicillin 1 g for 1 wk (ECA and PCA groups, respectively). Follow-up endoscopy was performed at 8 wks after the end of treatment to assess the treatment response. RESULTS: Intention-to-treat analysis demonstrated a significantly higher eradication rate for the ECA group than for the PCA group (94%vs 82%, respectively, p= 0.009). Per-protocol analysis also showed similar results (97%vs 84%, p= 0.003). Both groups had similar frequencies of adverse events (15%vs 24%) and drug compliance (97%vs 96%). Multivariate analysis disclosed that the use of esomeprazole (OR: 1.56, 95% CI, 1.11-2.19) and good compliance 7.39 (95% CI, 1.27-42.95) were independent predictors of treatment success. Alcohol drinking was an independent predictor of eradication failure (OR: 0.18; 95% CI, 0.06-0.54). CONCLUSION: Esomeprazole-based triple therapy demonstrated a higher eradication rate than pantoprazole-based regimen. The differences in eradiation efficacies between the two study groups may be related to the more powerful acid inhibition effect and stronger anti-H. pylori activity of esomeprazole compared to pantoprazole.
INTRODUCTION: Inflammation might be one of the causes of stone disease. The function of the transporter associated with antigen-processing protein (TAP) is related to immune response and inflammation. Our aim was to investigate the relationship between stone disease and 5 polymorphic sites of the TAP gene (TAP1-1, 1-2, 2-1, 2-2, 2-3). MATERIALS AND METHODS: We compared the frequencies of 5 polymorphisms in the TAP gene between 208 patients with recurrent calcium oxalate stone and 210 healthy controls. The polymorphism was detected by polymerase chain reaction-based restriction analysis. RESULTS: Significant differences in the frequency of the polymorphism at the TAP2-2 site were detected between normal individuals and calcium stone disease patients (p<0.0001). The distribution of the genotype AA homozygote was higher in stone patients (33.3%) than in the control group (16.3%). The odds ratio for the A allele compared with the G allele was 2.097 (95% CI 1.571-2.802). CONCLUSIONS: We conclude that the TAP2-2 MspI polymorphism might be associated with calcium stone disease.
INTRODUCTION: E-cadherin (CDH-1) is a cell-cell adhesive molecule which maintains cell integrity and communication between the intracellular and extracellular world. CDH-1 may therefore be related to carcinogenesis. A polymorphism located at the 3'-UTR of the CDH-1 gene is associated with stone disease; however, its relationship to prostate cancer has not been reported. We aimed to study whether there is an association between the 3'-UTR polymorphism and prostate cancer. MATERIALS AND METHODS: We collected 96 patients with prostate cancer and 114 normal controls for this study. The polymorphism of the CDH-1 gene was studied by polymerase chain reaction-based restriction analysis. RESULTS: There was a significant difference in genotype distribution of the CDH-1 gene polymorphism between cancer patients and normal controls (p < 0.001). The distribution of the CDH-1 gene CC genotype in prostate cancer patients (51.0%) was higher than in the controls (10.5%). The odds ratio for the CDH-1 'C' allele was 2.896 (95% CI = 1.908-4.396). There was no significant difference according to age, pathological grading, clinical staging, and responsiveness to hormonal therapy among patients. Only 3 patients (3.1%) had a history of urolithiasis. CONCLUSIONS: The CDH-1 gene 3'-UTR C/T polymorphism is associated with prostate cancer. The 'CC' homozygote indicates a relatively higher risk for developing prostate cancer than other genotypes.
Cyclooxygenase may be important in the pathogenesis of smoking-related cancer because it activates carcinogens and is highly inducible in inflammation. Benzo[a]pyrene (B[a]P) is one of the most common ingredients of cigarette smoke and benzo[a]pyrene diol epoxide (BPDE) is a metabolic product of B[a]P. Cigarette smoking-induced inflammation has been found in several tissues and in association with cyclooxygenase-2 (COX-2) expression. The contribution of COX-2 to peripheral inflammation is well documented, however, little is known about its role in brain inflammation. We studied COX-2 expression following treatment with BPDE in the cortical cells of Sprague-Dawley rats in vivo, as well as in DI TNC1 rat astrocytes and rat pheochromocytoma PC-12 cells (neurons) cultured in vitro. Our data showed that BPDE increases levels of COX-2 mRNA and protein in cortical cells of Sprague-Dawley rats. BPDE also increases levels of COX-2 mRNA in PC-12 and DI TNC1 cells. Induction of COX-2 protein was only found in DI TNC1 cells. Gel shift assay and western blot revealed increased NF-kappaB binding activity and protein level after treatment with BPDE. Experiments were performed to define the signaling mechanism by which BPDE induces COX-2, and suggested that BPDE-mediated COX-2 induction increases the risk of brain inflammation.
Carcinosarcoma is a malignancy that occurs very rarely in the renal pelvis; thus, only a very limited number of cases has been documented. These tumors are composed of both carcinomatous and sarcomatous elements. We report here a case of a carcinosarcoma composed of well-differentiated, keratinizing, squamous carcinoma cells and high-grade sarcoma cells. Differently from the cases described so far, this carcinosarcoma of the renal pelvis was characterized by the quick recurrence, following complete surgical resection, as a highly disseminated high-grade sarcoma.
Urokinase is thought to be involved in the formation of oral cancer, although there is a lack of genetic evidence. Our aim was to study single nucleotide polymorphisms in order to investigate the possibility. A total of 130 oral cancer patients and 105 controls were studied. Polymerase chain reaction (PCR) based restriction analysis was used to identify the C/T polymorphism of the urokinase gene, which is located on the 3'-untranslated region (3'-UTR) of chromosome 10. There was a significant difference in the distribution of the urokinase gene 3'-UTR C/T polymorphism frequency between cancer patients and the normal control group (P < 0.05). The "T" allele was prominent in the cancer group. The odds ratio for the risk of the "T" allele in cancer patients was 2.71 (95% CI = 1.325 approximately 5.562). The cancer patients were further categorized according to gender and whether or not they were habitual smokers or betel nut chewers. These clinical parameters were then compared with tumor cell differentiation and tumor progression. No significant differences were found. Therefore, the urokinase gene 3'-UTR "T" allele is associated with oral cancer and may play a role in oral cancer formation. However, we did not find the relationship between tumor progression and this polymorphism.
INTRODUCTION: Genetic factors in the immune system are widely suspected to have a role in the etiology of glaucoma. In this study, we evaluated the association between primary open-angle glaucoma (POAG) and the transporter associated with antigen processing (TAP) gene polymorphisms. The TAP gene polymorphisms we evaluated were TAP1-1 codon 333 A/G (Ile-Val), TAP1-2 codon 637 (Asp-Gly), TAP2-1 codon 379 (Val-Ile), TAP2-2 codon 665 (Thr-Ala) and codon 687 (Stop-Gln), and TAP2-3 codon 565 (Ala-Tht). Due to the lack of predictive markers for glaucoma, many glaucoma patients are only diagnosed when their visual acuity and visual field has irreversibly deteriorated. Our aim was to confirm whether or not the TAP1 and TAP2 genes can be used to identify suspectability to glaucoma. METHODS: Sixty-six patients with POAG and 105 healthy volunteers were enrolled in this case-control study. We resolved the TAP1 and TAP2 gene polymorphisms by PCR-based analysis. RESULTS: There was a significant difference in the distribution of TAP1-1 codon 333 and TAP1-2 codon 637 gene polymorphisms (p = 0.0375 and 0.01, respectively) between POAG patients and healthy controls. However, there was no significant difference between the two groups in TAP2-1 codon 370, TAP2-2 codon 665, and TAP2-3 codon 565 (p = 0.273, 0.19, and 0.131, respectively). In TAP1-1 codon 333, there was a significant difference between the "GG" homozygote and "GA" heterozygote (OR 4.32; 95% CI 1.336, 13.969). In TAP1-2 codon 637, there was a significant difference between the "GG" homozygote and "GA" heterozygote (OR 15; 95% CI 1.733, 129.860). There was also a significant difference between "GG" homozygote and "AA" homozygote (OR 10.8; 95% CI 1.286, 91.880). Therefore, TAP1-1 codon 333 and TAP1-2 codon 637 gene polymorphisms were useful genetic markers of POAG. The prevalence of the TAP1-2 "GG" homozygote differs significantly between POAG patients and healthy controls, although in the alleles of the both TAP genes, there were no significant differences between the two groups. CONCLUSION: The immune system acts as an arbiter to help determine whether under stress a neuronal cell will survive or sacrifice itself to injuries. TAP1-1 and TAP1-2 play an important role in the immune system. TAP1-1 and TAP1-2 gene polymorphisms may, by way of post-transcriptional changes and altered regulation of gene expression, be involve the immune system in the development of POAG.
BACKGROUND: The value of band ligation for prevention of the first episode of variceal bleeding has not been fully evaluated. This study compared the efficacy and safety of band ligation vs. treatment with a beta-blocker for the prophylactic prevention of first bleeding in patients with cirrhosis and high-risk esophageal varices. METHODS: A total of 100 patients with cirrhosis and endoscopically determined high-risk esophageal varices but no history of bleeding were randomized to band ligation (50 patients) or treatment with nadolol (50 patients). In the ligation group, two to 4 elastic bands were deployed during each session. Ligation was repeated at intervals of 3 to 4 weeks until variceal obliteration was achieved. In the nadolol group, the dose of the drug, administered once daily, was sufficient to reduce the pulse rate by 25%. RESULTS: In the ligation group, variceal obliteration was achieved in 41 patients (82%), at a mean of 2.7 (1.1) ligation sessions. In the nadolol group, the mean daily dose of nadolol administered was 60 (20) mg. During follow-up (median approximately 22 months), 10 patients (20%) in the ligation group and 16 (32%) in the nadolol group had upper-GI bleeding (p=0.23). Esophageal variceal bleeding occurred in 5 patients (10%) in the ligation group and 9 (18%) in the nadolol group (p=0.31). By multivariate Cox analysis, Child-Pugh class was the only factor predictive of variceal bleeding. Minor complications were noted in 9 patients (18%) in the ligation group and 4 (8%) in the nadolol group (p=0.35). No serious complication was encountered. Twelve patients in the ligation group and 11 in the nadolol group died (p=0.62). One patient in the ligation group and 3 in the nadolol group died from uncontrollable variceal hemorrhage. CONCLUSIONS: Variceal ligation is as effective and as safe as treatment with nadolol for prevention of first variceal bleeding in patients with cirrhosis.
BACKGROUND: It remains unresolved whether the prognosis is worse for patients who present with actively bleeding varices at endoscopy compared with those in whom variceal bleeding has stopped. METHODS: Patients with acute esophageal variceal bleeding were enrolled in this study and were divided into two groups: an active bleeding group and an inactive bleeding group. All patients had band ligation shortly after endoscopic examination and underwent elective ligation procedures until the varices were obliterated. Patients were followed for 1 year or until death. Short- and long-term prognoses were compared. RESULTS: The active bleeding group included 54 patients and the inactive bleeding included 251 patients. Initial hemostasis was achieved in 93% in the active group and 99% in the inactive group ( p = not significant). The rate of recurrent variceal bleeding within 30 days was 24% in the active bleeding group vs. 12% in the inactive bleeding group ( p = 0.01); the mortality rates were 18% and 8%, respectively ( p = 0.03 in a single statistical test; however, Bonferroni correction for the multiple testing of data removed this significance). The rate of recurrent variceal bleeding within 1 year was 37% in the active bleeding group and 27% in the inactive bleeding group ( p = 0.06); the mortality rates were 22% and 21%, respectively ( p = not significant). CONCLUSIONS: Whether variceal bleeding is active or inactive at endoscopy, variceal ligation is equally effective for control of bleeding. The rates of recurrent bleeding and mortality at 1 month were significantly higher among patients with active bleeding. However, the mortality rate was similar for both groups at 1 year.
PURPOSE: Glaucomatous neuropathy is a type of cell death by apoptosis. Apoptosis is a genetically controlled form of cell death, and one of its primary regulatory steps is the activation of the tumour suppressor protein p53, of which p21 is an effector protein. The association between p21 codon 31 polymorphism and primary open-angle glaucoma (POAG) patients was evaluated in this study. METHODS: The study included 58 POAG patients and a control group of 59 healthy volunteers. Polymerase chain reaction-based analysis was used to resolve the p21 codon 31 polymorphism. RESULTS: The genotype frequencies of p21 codon 31 polymorphism were statistically different (p < 0.05) between the two groups. The Arg allele of the p21 codon 31 polymorphism was more frequently found in POAG patients than in healthy individuals (odds ratio: 2.389, 95% confidence interval: 1.14-5.01). CONCLUSION: This study suggests that an association exists between the Arg allele of the p21 codon 31 polymorphism and POAG in the Chinese population.
OBJECTIVE: A polymorphism of gene p53 codon 72 is associated with various cancer formations. Tumor necrosis factor-alpha (TNF-alpha) one of the cytokines secreted by macrophages in response to inflammation and is also related to cancer formation. We aimed to evaluate the association between prostate cancer and the polymorphisms of the TNF-alpha gene promoter -308 and p53 gene codon 72. PATIENTS AND METHODS: In our study, a normal control group of 126 healthy people and 96 patients with prostate cancer were examined. The polymorphism (G/A) of TNF-alpha gene was detected by polymerase chain reaction (PCR)-based restriction analysis (Nco I endonuclease) and the polymorphism of p53 gene was detected by two PCRs (one for proline and one for arginine form). RESULTS: There was a significant difference in the distribution of codon 72 polymorphism the p53 gene between prostate cancer patients and the normal controls (p < 0.001). The proline form of p53 gene codon 72 was significantly higher than the arginine form, with an odds ratio of 2.606 (95% CI = 1.052-6.455). This difference was also revealed in the tumor staging (p = 0.035) as the proline form was significantly higher in the metastasis group of prostate cancer. There were no statistical differences in the distribution of -308 polymorphism of the TNF-alpha gene between cancer patients and the control subjects (p = 1.0). CONCLUSION: Prostate cancer appears to be associated with the p53 gene codon 72 polymorphisms, but not with the TNF-alpha gene. The proline form of p53 gene codon 72 might be a more significant risk factor for the development of metastasis than the arginine form.
A total of 95 patients with Graves' disease (GD) and 105 normal healthy controls were enrolled in this study to determine how a single site polymorphism of the transporter associated with antigen processing 1 (TAP1) gene contributes to the pathogenesis of GD. The polymorphism was detected using polymerase chain reaction (PCR)-based restriction analysis. Associations between GD and the two-site polymorphisms of the TAP1 gene at codons 333 and 637 were evaluated. No significant differences were revealed comparing GD patients and normal individuals for the distributions of genotypes and allelic variants at codon 333 (p=0.253 and p=0.891, respectively). By contrast, the distributions for the AA homozygote at codon 637 were reduced and those for the GA heterozygote were increased comparing the two groups (p<0.0001). The allelic analysis also demonstrated lower A and higher G allele frequencies (p=0.0008; OR=2.745, 95% CI=1.482-5.085) comparing the GD patients with the normal healthy controls. This shows that the single-site polymorphism of the TAP1 gene at codon 637 may be an indicator for predicting development of GD.
Head injury often occurs in accidents, with severe consequences affecting not only the injured individual but his/her entire family. The purpose of this paper is to describe a case of nursing care provided to the family of a head injury patient using the family resiliency model. From June 26 to July 10, 2002, one of the authors took care of the head injury patient as a primary nurse, then assessed the family in accordance with the five factors influencing the family crisis adaptation process identified in the family resiliency model. The major stressors for the family included the unknown prognosis for the patient, the lack of family income, and not knowing how to talk with the children about their father's condition. Three nursing problems were identified, as follows: the family's knowledge deficit concerning head injury treatment, compromised family coping, disruption of family life and lack of coping resources. Applying various nursing interventions (i.e. education, family conferences, and play therapy), the authors guided the family towards an understanding of the disease treatment plan and the stresses they were facing. Finally, family members were able to participate in the rehabilitation plan for the patient and to find the resources to solve the family problems. This demonstrated that the resiliency model is a good tool for assessing families in crisis and planning nursing care in order to facilitate the family's successful bonadaptation.
BACKGROUND: Endoscopic and pharmacological treatments significantly reduce recurrent esophageal variceal bleeding and improve the prognosis of cirrhotic patients. This study was aimed to evaluate the incidence, risk factors, treatment and prognosis of hepatocellular carcinoma after esophageal variceal bleeding. METHODS: Patients with esophageal variceal bleeding underwent endoscopic or pharmacological treatments to arrest acute bleeding or prevent rebleeding. Concurrently, patients were followed by periodic serum alpha-fetoprotein examinations and ultrasonography, aiming at early detection and possible treatment of hepatocellular carcinoma. RESULTS: Hepatocellular carcinoma developed in 79 of 370 patients (21.4%) during the 10-year follow-up. The cumulative incidence of hepatocellular carcinoma was 21.1% at the end of the third year, 39.3% at the end of the fifth year and 53.0% at the end of the tenth year. Small tumors (< or = 3 cm) were found in 64 patients (81.0%, monofocal tumors in 46 patients). Age, hepatitis B virus, hepatitis C virus, and alpha-fetoprotein level > 20 ng/mL were factors associated with the risk of hepatocellular carcinoma development by multivariate analysis using Cox regression. Tumors were actively treated in 37 of 49 Child-Pugh A and B patients (75.5%) and 2 of 30 Child-Pugh C patients (6.7%). The median survival of all patients was 2.5 (range, 0.5 to 10.0) years. Development of hepatocellular carcinoma and serum bilirubin level were significantly associated with mortality in Child-Pugh A and B patients. CONCLUSIONS: Patients with esophageal variceal bleeding had a high risk of developing hepatocellular carcinoma. Surveillance on hepatocellular carcinoma could detect most tumors with small size. Hepatocellular carcinoma had an adverse impact on the survival of patients without advanced cirrhosis.
Growth factor-related genes regulate cell growth, differentiation and apoptosis in the kidney in response to cellular injury. One of the theories of stone formation is that cellular injury, and thus growth factors, play a role. We therefore investigated the association between growth factor genes and calcium oxalate stone disease. The most frequently seen polymorphism of the vascular endothelial growth factor (VEGF) gene is Bst U I C/T, which is located upstream at the -460th nucleotide. Other growth factor-related gene polymorphisms include the cytochrome P450c17alpha enzyme (CYP17) gene MspA I C/T polymorphism at the 5'-UTR promoter region, the epidermal growth factor receptor (EGFR) gene Bsr I polymorphism (A to T) at position 2,073, and the insulin-like growth factor-2 (IGF-2) gene Apa I A/G at exon 9. All four polymorphisms were used as genetic markers in this study in the search for an association between stone disease and growth factor related genes. A normal control group of 230 healthy people, and 230 patients with calcium oxalate stone, were examined. The polymorphism was seen following polymerase chain reaction based restriction analysis. The result revealed a significant difference between normal individuals and stone patients (P=0.0003, Fisher's exact test) in the distribution of the VEGF gene polymorphism as well as an odds ratio of 1.30 (95% confidence interval=0.993-1.715) per copy of the "T" allele. Whereas, the IGF-2, EGFR and CYP17 gene polymorphisms did not reveal a significant association with stone disease. We conclude that the VEGF gene Bst U I polymorphism is a suitable genetic marker of urolithiasis.
OBJECTIVE: To investigate the correlation of the androgen receptor gene microsatellite polymorphism (CAG trinucleotide repeat polymorphism on exon 1) with bone mineral density and their relationship to osteoporosis in postmenopausal women. STUDY DESIGN: A number of 168 of 477 postmenopausal women were randomly recruited. The androgen receptor gene microsatellite polymorphism was determined using polymerase chain reaction-based microsatellite analysis. Bone mineral density of the lumbar spine and proximal femur was measured using dual-energy X-ray absorptiometry. RESULTS: The AR genotype was classified from "9" to "32" according to the number of CAG trinucleotide repeats they contained to represent "signposts". After adjustment for potential confounding factors such as age, height, weight, years since menopause, and daily calcium intake, subjects with genotype 20+ (n=64) had lower bone mineral density values and a significantly greater risk for osteoporosis (OR 4.2, 95% CI 1.0-17.2) when compared with subjects with genotype 20- (n=104) at the femoral neck. CONCLUSION: The present study suggests that the androgen receptor gene microsatellite polymorphism may be a candidate genetic marker for risk of osteoporosis in postmenopausal women.