OBJECTIVES To compare the efficacy of two α1‐adrenoceptor antagonists, α1A‐adrenoceptor‐selective tamsulosin hydrochloride and α1D‐adrenoceptor‐selective naftopidil, in the treatment of lower urinary tract symptoms (LUTS) with benign prostatic hyperplasia (BPH). PATIENTS AND METHODS Thirty‐four patients (mean age 72.4 years, sd 4.3, range 66–79) with LUTS (International Prostate Symptom Score, IPSS >8) secondary to BPH were enrolled in a randomized crossover study. Seventeen patients were initially prescribed naftopidil 50 mg for 4 weeks, followed by tamsulosin 0.2 mg for 4 weeks (group A); another 17 were initially prescribed tamsulosin 0.2 mg, followed by naftopidil 50 mg (group B). Patients changed to the alternative treatment after a 1‐week washout period. Efficacy criteria were improvement in LUTS (IPSS), quality of life (QoL), uroflowmetry, and pressure‐flow study (PFS) values based on the treatment with each agent. RESULTS At baseline there were no significant differences between the groups in IPSS, QoL, uroflowmetry values or PFS values, except for the volume at maximum desire to void. After treatment with each agent, the IPSS and QoL were significantly improved and the reduction in bladder outlet obstruction confirmed by PFS. Naftopidil was significantly more effective than tamsulosin in relieving nocturia. The increases from baseline (before treatment) to the endpoint (after treatment with each agent) in the volume at first desire and maximum desire to void were significantly higher with naftopidil than with tamsulosin. Involuntary contractions disappeared in two patients with relief of nocturia with naftopidil, but not with tamsulosin. The decrease in other symptoms of the IPSS, QoL, increase in uroflowmetry values and changes in other PFS values were similar for both agents. CONCLUSIONS The two agents provided similar efficacy in the treatment of LUTS with BPH. However, naftopidil was better than tamsulosin for nocturia. The disappearance of involuntary contraction and the greater increase in first‐desire volume with naftopidil may be associated with the relief of nocturia. The α1D‐adrenoceptor antagonist is effective in alleviating both voiding and storage symptoms. The α1D‐adrenoceptor antagonist may be more effective than the α1A‐adrenoceptor antagonist in LUTS with BPH.
The a3.83 complex was reconstituted from a and (3 subunits of the thermophilic bacterium PS3 F1-ATPase (TFI) and then isolated. It is less stable at high and low temperatures than TFi?, and the complex dissociates into subunits during native polyacrylamide gel electrophoresis. The a_3%3 complex has about 20% of the ATPase activity of TF1. Its enzymic properties are similar to those of the native TFI, exhibiting similar cooperative kinetics as a function of ATP concentration, similar substrate specificity for nucleotide triphosphates, and the presence of two peaks in its temperatureactivity proffle. Differing from TFI, the ATPase activity of the a3(33 complex is insensitive to Nj-inhibition, its divalent cation specificity is less stringent, and its optimum pH shifts to the alkaline side. The addition of the y subunit to the a3P3 complex leads to the formation ofthe a3_33y complex, indicating that the a3.83 complex is an intermediate in the process of assembly of the holoenzyme from each subunit. These results definitely show that the essential structure for eliciting the ATPase activity of Fj-ATPase is trimeric aj pairs and that the kinetic cooperativity of the FI-ATPase is an inherent property of this trimeric structure but is not due to the presence of single-copy subunits. In this sense, the a433 complex is the catalytic core of Fl-ATPase.In energy-transducing membranes of bacteria, mitochondria, and chloroplasts, ATP synthases catalyze ATP synthesis coupled with proton flow (1-3). These enzymes are composed of an integral membrane protein sector, F0, and a peripheral protein sector, F1. F1 has an ATP-hydrolyzing activity, and its molecular weight is about 380,000. The subunit structure of the Fj-ATPase is a3f33'y8e. The were expressed in the E. coli DK-8 strain, a mutant with a deletion of FoF1 genes, which was given to us by M. Futai, and were isolated individually as described (17, 18). The isolated subunits were stored in 75% ammonium sulfate suspension at 40C. Prior to use, the a and ( subunits were applied to an HPLC gel permeation column (G3000SWxl, Tosoh, Tokyo) and were eluted at room temperature with 50 mM Tris sulfate buffer (pH 7.0) containing 200 mM Na2SO4 at a flow rate 0.5 ml/min. The purified subunits were mixed, incubated at 30'C for 15 min in the same buffer, and the mixture was reapplied to the same gel permeation column.The a3,3 complex was eluted at 14.7 min and was prepared freshly for each experiment.Assays of ATP Hydrolytic Activity.
Activation of blood cells during hemodialysis is considered to be a significant determinant of biocompatibility of the hemodialysis membrane because it may affect patient health adversely through microvascular inflammation and oxidative stress. This study found very different cell activation among various polysulfone (PSf) hemodialysis membranes. For example, CX‐U, a conventional PSf membrane, induced marked adhesion of platelets to its surface and increased surface expression of activated CD11b and production of reactive oxygen species (ROS) by neutrophils; while NV‐U, a hydrophilic polymer‐immobilized PSf membrane, caused little platelet adhesion and slight CD11b expression and ROS production by neutrophils. Analysis of the molecular mechanisms of the above phenomena on CX‐U and NV‐U indicated that anti‐integrin GPIIb/IIIa antibody blocked platelet adhesion, and that the combination of anti‐CD11b (integrin α subunit of Mac‐1) and anti‐integrin αvβ3 antibodies blocked ROS production by neutrophils. Plasma‐derived fibrinogen, a major ligand of GPIIb/IIIa, Mac‐1, and αvβ3 on membranes, was thus analyzed and found to be more adsorbed to CX‐U than to NV‐U. Moreover, comparison between five PSf membranes showed that the number of adherent platelets and neutrophil ROS production increased with increasing fibrinogen adsorption. These results suggested that fibrinogen, adsorbed on membranes, induced GPIIb/IIIa‐mediated platelet activation and Mac‐1/αvβ3‐mediated neutrophil activation, depending on the amount of adsorption. In conclusion, the use of biocompatible membranes like NV‐U, which show lower adsorption of fibrinogen, is expected to reduce hemodialysis‐induced inflammation and oxidative stress by minimizing cell activation.
SummaryTo serologically determine the association of microbial superantigens and the pathogenesis of Kawasaki disease (KD), we conducted a case-control study. Serum IgG and IgM antibodies against staphylococcal enterotoxin A (SEA), SEB, SEC, toxic shock syndrome toxin-1 (TSST-1), and streptococcal pyrogenic exotoxin A (SPEA) were measured by an enzyme-linked immunosorbent assay in 293 serum samples from 65 KD patients on clinical days 1-28 and 120 control samples. The administration of immunoglobulin products, which contain high concentrations of IgG antibodies against all the superantigens, directly elevated antitoxin IgG antibodies in KD patients. In contrast, antitoxin IgM antibodies were not detected in immunoglobulin products. Actually, we found a significant elevation of IgM antibodies against SEA in KD patients in the first (median titre: 0·020, P < < < < 0·01 versus control), second (0·024, P < < < < 0·001), third (0·030, P < < < < 0·001) and fourth (0·038, P < < < < 0·001) weeks, compared to the controls (0·015). Significant differences of IgM antibodies were also true for SEB, TSST-1, and SPEA throughout the first to fourth weeks, and for SEC throughout the second to fourth weeks. The prevalence of KD patients having high IgM titres (> > > > mean + + + + 2SD of control values) to the 5 superantigens was increased with the clinical weeks, and reached 29-43% of KD subjects at the fourth week. This is the first study that describes kinetics of IgM antibodies against superantigens and clarifies the serological significance throughout the clinical course of KD. Our results suggest that multiple superantigens involve in the pathogenesis of KD.
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