ABSTRACT
We performed a retrospective, case-control study to evaluate whether the urine flow acceleration (UFA, mL/s(2)) is superior to maximum uroflow (Qmax, mL/s) in diagnosing bladder outlet obstruction (BOO) in patients with benign prostatic hyperplasia (BPH). In this study, a total of 50 men with BPH (age: 58±12.5 years) and 50 controls (age: 59±13.0 years) were included. A pressure-flow study was used to determine the presence of BOO according to the recommendations of Incontinence Control Society (ICS). The results showed that the UFA and Qmax in BPH group were much lower than those in the control group [(2.05±0.85) vs. (4.60±1.25) mL/s(2) and (8.50±1.05) vs. (13.00±3.35) mL/s] (P<0.001). According to the criteria (UFA<2.05 mL/s(2), Qmax<10 mL/s), the sensitivity and specificity of UFA vs. Qmax in diagnosing BOO were 88%, 75% vs. 81%, 63%. UFA vs. Omax, when compared with the results of P-Q chart (the kappa values in corresponding analysis), was 0.55 vs. 0.35. The prostate volume, post void residual and detrusor pressure at Qmax between the two groups were 28.6±9.8 vs. 24.2±7.6 mL, 60.4±1.4 vs. 21.3±2.5 mL and 56.6±8.3 vs. 21.7±6.1 cmH2O, respectively (P<0.05). It was concluded that the UFA is a useful urodynamic parameter, and is superior to Qmax in diagnosing BOO in patients with BPH.
Subject(s)
Humans , Male , Middle Aged , Case-Control Studies , Prostatic Hyperplasia , Retrospective Studies , Urinary Bladder Neck Obstruction , Diagnosis , Urine , PhysiologyABSTRACT
We performed a retrospective, case-control study to evaluate whether the urine flow acceleration (UFA, mL/s(2)) is superior to maximum uroflow (Qmax, mL/s) in diagnosing bladder outlet obstruction (BOO) in patients with benign prostatic hyperplasia (BPH). In this study, a total of 50 men with BPH (age: 58±12.5 years) and 50 controls (age: 59±13.0 years) were included. A pressure-flow study was used to determine the presence of BOO according to the recommendations of Incontinence Control Society (ICS). The results showed that the UFA and Qmax in BPH group were much lower than those in the control group [(2.05±0.85) vs. (4.60±1.25) mL/s(2) and (8.50±1.05) vs. (13.00±3.35) mL/s] (P<0.001). According to the criteria (UFA<2.05 mL/s(2), Qmax<10 mL/s), the sensitivity and specificity of UFA vs. Qmax in diagnosing BOO were 88%, 75% vs. 81%, 63%. UFA vs. Omax, when compared with the results of P-Q chart (the kappa values in corresponding analysis), was 0.55 vs. 0.35. The prostate volume, post void residual and detrusor pressure at Qmax between the two groups were 28.6±9.8 vs. 24.2±7.6 mL, 60.4±1.4 vs. 21.3±2.5 mL and 56.6±8.3 vs. 21.7±6.1 cmH2O, respectively (P<0.05). It was concluded that the UFA is a useful urodynamic parameter, and is superior to Qmax in diagnosing BOO in patients with BPH.
ABSTRACT
Objective: To investigate the mechanism responsible for lost sensibility of tyrosine aminotransferase (TAT) to dexamethasone(Dex) in human hepatoma cell line SMMC-7721 through examining the cDNA sequence of TAT and the status of glucocorticoid receptor (GR) pathway. Methods: The TAT cDNA fragment containing the full length of coding sequence was amplified by reverse transcription polymerase chain reaction (RT-PCR) and was sequenced. The expression of TAT mRNA was determined by real-time quantitative PCR to observe the influence of Dex on expression of TAT mRNA in SMMC-7721 cells. The experiement with HepG2 cells was performed as the control. Reporter genes (GRE-tk-LUC and GRE-MMTV-CAT) were transiently transfected into SMMC-7721 cells by electroporation. The induction effieiencies of LUC and CAT genes expression by Dex were examined and compared between SMMC-7721 cells and HepG2 cells. Results: The results showed that there was a same-sense mutation (Gln576Gln) in TAT cDNA sequence. TAT mRNA could be induced by Dex, with the maximal induction level being 2.22-folds in SMMC-7721 cells, which was significantly lower than that in HepG2 cells (15.1-fold increase, P<0.01). Dex induced the expression of LUC and CAT genes in SMMC-7721 cells as well as the HepG2 cells. Conclusion: The induction efficiency of Dex for expression of TAT mRNA is decreased in SMMC-7721 cells, which might be due to the unchanged activity of TAT.
ABSTRACT
Objective:To investigate the mechanism responsible for lost sensibility of tyrosine aminotransferase(TAT)to dexam- ethasone(Dex)in human hepatoma cell line SMMC-7721 through examining the cDNA sequence of TAT and the status of glucocorticoid receptor(GR)pathway.Methods:The TAT cDNA fragment containing the full length of coding sequence was amplified by reverse transcription-polymerase chain reaction(RT-PCR)and was sequenced.The expression of TAT mRNA was determined by real-time quantitative PCR to observe the influence of Dex on expression of TAT mRNA in SMMC-7721 cells.The experiement with HepG2 cells was performed as the control.Reporter genes(GRE-tk-LUC and GRE-MMTV-CAT)were transiently transfected into SMMC-7721 cells by electroporation.The induction efficiencies of LUC and CAT genes expression by Dex were examined and compared between SMMC-7721 cells and HepG2 cells.Results:The results showed that there was a same-sense mutation(Gln576Gln)in TAT cDNA se- quence.TAT mRNA could be induced by Dex,with the maximal induction level being 2.22-folds in SMMC-7721 cells,which was signifi- cantly lower than that in HepG2 cells(15.1-fold increase,P