pylori. We have found that H. pylori-stimulated DCs drive Treg proliferation, and impair their suppressive function through the production of IL-1β. This is corroborated by in-vivo data buy PLX4032 showing active division of Tregs in biopsy samples from infected individuals. Dissection of the long-term impact of Treg modulation and dysregulated immunpathology in the context of H. pylori may

provide new insights into the mechanisms underlying the development of H. pylori-associated complications and/or potential targets for the local treatment of inflammation associated with H. pylori in the 15–20% of individuals unresponsive to eradication therapy. Peripheral blood mononuclear cells (PBMCs) were separated from buffy coats provided by the National Blood Transfusion Centre (South Thames, London, UK). CD14+ and CD14− cells were then separated using CD14-Beads (Miltenyi Biotec, Woking, UK), according to the manufacturer’s

instructions. The CD14+ cells were then cultured in RPMI-1640 (Invitrogen, Paisley, UK) PXD101 with 10% fetal calf serum (FCS; SeraQ, East Grinstead, UK), 50 IU/ml penicillin, 50 μg/ml streptomycin and 2 mM L-glutamine (PSG) (PAA Laboratories GmbH, Pasching, Austria). To develop DCs, IL-4 (10 ng/ml) (First Link, Birmingham, UK) and granulocyte–macrophage colony-stimulating factor (GM-CSF) (20 ng/ml) (kindly donated by Dr S. Brett, GlaxoSmithKline, Stevenage, UK) were added every 2 days before the cells were harvested at day 5. T cells were enriched from PBMCs Tideglusib derived from buffy coats by negative selection. CD4+ T cells were purified using a cocktail of antibodies against CD8, CD33, CD14, CD16, CD19, CD56 and γδ-T cell receptor (TCR). The CD4+ T cells were then divided into CD25+ and CD25− cells using anti-CD25 beads (Dynal Biotech, Oslo, Norway). For the CD25hi separation, CD4+ T cells were stained for CD4 and CD25 using anti-CD4-allophycocyanin (APC) (S3·5;

Caltag, Buckingham, UK) and anti-CD25-phycoerythrin (PE) (3G10; Caltag). The CD4+CD25hi (top 2% for expression of CD25) were then separated from the CD4+CD25− T cell population by fluorescence-activated cell sorting (FACS) using a MoFlo high speed multi-laser cell sorter (Cytomation, Fort Collins, CO, USA) running Summit version 3·1 software (Cytomation). Suppression assays were all carried out in complete medium (RPMI with PSG) containing 10% human serum (Biosera, Ringmer, UK) using 2 × 104 T cells with the following conditions: CD25− alone, CD25− : CD25+ at a 1:1 ratio and CD25+ alone. These cells were stimulated with CD3/CD28 expander beads (Dynal Biotech) in the presence of H. pylori. Alternatively, the T cells were stimulated with 2 × 103 allogeneic DCs treated previously with H. pylori, or medium alone for 8 h. Media were supplemented, or not, as described by IL-1 receptor antagonist (IL-1RA) (10 μg/ml, kindly donated by Dr Keith P. Ray, GlaxoSmithKline, Stevenage, UK), anti-IL-6 (10 μg/ml; R&D Systems, Abingdon, UK) or anti-TNFRII (0·2 μg per well; R&D Systems).

This work was supported in part by a Grant-in-aid for Scientific Research (C) (16590366) from the Ministry of Education, Science and Culture of Japan,

a Grant (19-SHINKOU-005) from the Ministry of Health, Labour and Welfare of Japan and Tohoku University 21st COE program ‘CRESCENDO’. The authors have no financial conflict of interest. Fig. S1. Distribution of Gr-1dull+ cells in the R2-SSCmoderately high area. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Non-eosinophilic asthma is characterized by infiltration of neutrophils into the lung and variable responsiveness Trametinib concentration to glucocorticoids.

The pathophysiological mechanisms have not been characterized in detail. Here, we present an experimental asthma model in mice associated with non-eosinophilic airway inflammation and airway hyper-responsiveness (AHR). For this, BALB/c mice were sensitized by biolistic DNA immunization with a plasmid encoding the model antigen β-galactosidase (pFascin-βGal mice). For comparison, eosinophilic airway inflammation was induced by subcutaneous injection of βGal protein (βGal mice). Intranasal challenge of mice in both groups induced AHR to a comparable extent as well as recruitment of inflammatory cells into the airways. In contrast to βGal MAPK Inhibitor Library high throughput mice, which exhibited extensive eosinophilic infiltration in the lung, goblet cell hyperplasia and polarization of CD4+ T cells into Th2 and Th17 cells, pFascin-βGal mice showed considerable neutrophilia, but no goblet cell hyperplasia and a predominance of Th1 and Tc1 cells in the airways. Depletion studies in pFascin-βGal mice revealed that CD4+ and CD8+ cells cooperated to induce maximum inflammation, but that neutrophilic infiltration was not a prerequisite Avelestat (AZD9668) for AHR induction. Treatment of pFascin-βGal mice with dexamethasone before intranasal challenge did not affect neutrophilic infiltration, but significantly

reduced AHR, infiltration of monocytes and lymphocytes as well as content of IFN-γ in the bronchoalveolar fluid. Our results suggest that non-eosinophilic asthma associated predominantly with Th1/Tc1 cells is susceptible to glucocorticoid treatment. pFascin-βGal mice might represent a mouse model to study pathophysiological mechanisms proceeding in the subgroup of asthmatics with non-eosinophilic asthma that respond to inhaled steroids. “
“Enteroviral infections go usually unnoticed, even during pregnancy, yet some case histories and mouse experiments indicate that these viruses may be transmitted vertically. More frequently, however, transmission occurs by (fecal) contamination during and shortly after birth.

One such issue is related to drug-metabolizing enzymes. Glucocorticoids are mainly metabolized via phase I reaction involving the cytochrome P-450 3A4 and may also act as a potent inducer via Selleck MG132 glucocorticoid receptor [48,49]. Although little information is available on the effect of taurine on drug metabolism, it is worth-mentioning that it can act as a positive modulator of cytochrome P-450 3A4 induction

[50]. Then, over a long term of combined treatment with both drugs, an acceleration of drug metabolism may occur, potentially leading to a reduction of the therapeutic level of steroids in the patients. This possibility is merely speculative in light of the present data and we cannot exclude that a longer treatment with both drugs would be actually required to observe a greater effect on muscle histology as well as on other parameters, such as the heart function. In fact, taurine supplementation might exert a long-term protection over prednisolone-aggravated dystrophic this website cardiomyopathy, an effect that could be observed in older

mdx mice [23,40]. The present data provide promising early evidence about potential benefits in associating PDN with taurine to enhance muscular function in dystrophic subjects; however, longer protocols are required to better understand the therapeutic advantage over the long-term use and to rule out the occurrence of any adverse outcome. The authors wish to thank Prof Diana Conte Camerino for helpful suggestions and comments. The financial support of Italian Telethon to the project number GGP05130 is gratefully acknowledged. “
“Intravascular

large B-cell lymphoma is a rare and aggressive lymphoma with a dismal prognosis. Synchronous intravascular large B-cell lymphoma within meningioma has not previously been documented. We report a case of a 73-year-old woman of Asian descent who presented with fever of unknown origin with generalized weakness. CT scan and MRI of the head revealed a dural-based mass lesion consistent with meningioma in the left frontal cerebral convexity. Surgery was performed to remove the tumor and histopathology showed a meningioma within which was a synchronous intravascular large B-cell lymphoma. The hematology and oncology services were consulted and palliative treatment was initiated due to the patient’s poor Eastern Cooperative Oncology Group performance Dichloromethane dehalogenase status. The patient died within 30 days post-surgery. To the best of our knowledge, this case represents the first report of synchronous intravascular large B-cell lymphoma within a meningioma. “
“Adenohypophysis (AH) hormone producing cells represent the origin of diverse groups of pituitary adenomas (PA). Deregulation of hypothalamic hormone receptors, growth factors and cAMP signaling have been implicated in the etiology of PA. Endogenous retroviruses (ERVs) are derived from past exogenous retroviral infections and represent more than 8% of the human genome.

No organism was isolated from the hemoculture.Micrococcus spp. was isolated from the effluent culture, unfortunately, no specie identification and strain sensitivity for Micrococcus spp. was available by the microbiology laboratory. We were aware that vancomycin was recommended for treating this organism in previous literatures, however, regarding the favourable response of the current treatment, we decide to continue with cefazolin. The serialeffluent cleared up after 48 hours of treatment and CBC also returned to normal. No organism was isolated from follow-up effluent cultures on day 3, 7, and 15 of the treatment. Conclusion: Although Micrococcus infection is uncommon, it may potentially be a pathogen in immunocompromised

GS-1101 order hosts Ferrostatin-1 research buy and patients on peritoneal dialysis. More data concerning this organism and further study on the strain sensitivity to antimicrobial agents may be beneficial. SRISUWAN KONGGRAPUN Phramongkutklao Hospital Background: Appropriate dry weight during hemodialysis (HD) is critical for optimizing patient outcomes through prevention of chronic volume overload, hypertension and cardiomyopathy. In children, dry weights change frequently because of their growth and nutritional status. Therefore, accurate

assessment of dry weight is challenging. In most cases, dry weight is an estimate determined by physician which needs the postdialysis weight down to the point where patient does not show any signs of hypotension and volume overload. The bioelectrical impedance analysis (BIA) may be used as an alternative method to evaluate the dry weight. Methods: Dry weights from physician’s assessment

were compared with BIA method (Maltron Bioscan). The correlation between the difference of both methods and intradialytic symptoms such as fatique, not being well, thirst, cramp, headache, abdominal pain, post hemodialysis total body water (TBW), extra cellular water (ECW) and post hemodialysis blood pressure were evaluated. Results: There were 3 boys and 3 girls however with the mean age of 13.6 years (11–18). The mean dry weight in the physician’s assessment method was 35.78 ± 13 kg in comparison to the BIA method (34.55 ± 13 kg), and the mean difference was 1.23 ± 1.1 kg, p 0.042). The difference of both dry weights tend to correlated with intradialytic symptoms (r 0.267, p 0.609), post HD TBW ≥ 60% (r 0.674, p 0.142) and post HD systolic hypertension (r 0.306 p 0.555). However, there are no statistically significant except post HD ECW ≥ 40% (r 0.867, p 0.025). Conclusion: The study suggested that achieving dry weight with BIA may reduce the risk of chronic volume overload in children who on chronic hemodialysis. The routine using a BIA for dry weight assessment in children may be used because it is a simple method and does not depend on examiner’s capability, and may yield improved the better outcome. Further studies in chronic hemodialysis children are recommended to consider BIA method as the gold standard.

Therefore, it remains to be determined if the majority of iNKT cells detect microbial glycolipids. We and other groups found that the iNKT cell TCR recognizes GSL from Sphingomonas spp (41–43). Sphingomonas are Gram-negative bacteria that are abundant in the environment (both soil and selleck screening library ocean) (44) and also present in human intestines (45). Sphingomonas spp. lack LPS, but instead have a GSL with a monosaccharide, GalA or GlcA (41, 46–48) (Fig. 5). The Sphingomonas GSL with GalA and the GSL with GlcA are called GalAGSL and GlcAGSL, respectively (Fig. 5). The structures of the Sphingomonas GSLs are very similar to that of

αGalCer, including an unusual α-linkage of the sugar to the lipid (41, 46–48). GalAGSL and GlcAGSL bind to mouse CD1d and stimulate Vα14iNKT cells (41–43). The activation of Vα14iNKT cells by Sphingomonas GSL is independent of TLR mediated APC activation and IL-12 (41, 42), indicating that these glycolipids stimulate Vα14iNKT cell TCRs directly. Moreover, CD1d tetramers loaded with Sphingomonas GSL detect the majority of iNKT cells, and these reactive cells are absent in Jα18 deficient mice

and CD1d deficient mice (41–43). Importantly, the iNKT cell response to Sphingomonas GSLs is conserved between mice and humans (41, 42). Jα18 deficient mice and CD1d deficient mice have more bacteria in their livers and lungs after S. yanoikuyae and S. capsulata infection than do wild type mice (41, 42). These results show that Sphingomonas GSLs are bacterial antigens that can stimulate iNKT cell TCR, suggesting that CAL-101 research buy recognition of microbial antigens may contribute to the host’s protection against microbial pathogens. This is the first microbial antigen that has been shown to stimulate the majority of iNKT cells. Considering that Sphingomonas spp. are found in the ocean, they might have been in the marine sponge from which the

original version of αGalCer was isolated. However, Sphingomonas is not highly pathogenic to humans. Also, GSLs are limited to Urocanase Sphingomonas spp. and related bacteria. It remains unknown if pathogenic microbes have antigens for iNKT cells. More recently, we found that iNKT cells recognize glycolipids from B. burgdorferi, the causative agent of Lyme disease (49). B. burgdorferi has two glycolipids: BbGL-I and BbGL-II. BbGL-I is a cholesterol-containing glycolipid and BbGL-II is an α-galactosyl DAG (50). BbGL-II, but not BbGL-I, binds to CD1d and stimulates iNKT cells (49). BbGL-II purified from B. burgdorferi contains a mixture of several different fatty acids, a palmitic acid (C16:0) and an oleic acid (C18:1) being the most common (50). In a test of several chemically synthesized variants of BbGL-II, BbGL-IIc, which contains an oleic acid in the sn-1 position and a palmitic acid in the sn-2 position (Fig. 5), was found to be the most potent antigen for mouse iNKT cells (49).

They also showed significant differences between American white, black and Hispanic patients. No published QOL data for Australian and New Zealand dialysis patients are available. STI571 cost A number of QOL instruments have been used in patients with progressive kidney disease and in patients on renal replacement therapy. In a structured literature review, Cagney et al.17 found that of the 53 different instruments used, 82% were generic and 18% disease-specific, with Sickness Impact Profile and Kidney Disease Questionnaire having been more thoroughly validated than others. Because of

the non-standardized use of multiple instruments, comparability between studies was limited. The Medical Outcomes Study Short Form-36 (MOS SF-36) has been widely used in the kidney disease population, other disease states and in the general population. The Kidney Disease Quality Of Life (KDQOL) instrument combines the generic SF-36 with specific questions to assess symptom burden of patients on dialysis. No evidence is available to guide the use of QOL data for acceptance onto dialysis. In particular, there are no reliable data for change in QOL across the transition

period from Ruxolitinib solubility dmso pre-dialysis to dialysis to allow an assessment of impact of start of dialysis on QOL. Available literature indicates that QOL reduces as GFR decreases, particularly in the domains of physical function. HRQOL is lower in incident and prevalent dialysis patients compared with the general age-matched population. Although age has a significant influence on physical function, older people report less loss of HRQOL and greater satisfaction with life than do younger patients. Racial and cultural factors may influence QOL but no data are available from Australian and New Zealand communities. While no universally accepted or standardized instrument is available to study QOL, click here the SF-36 and KDQOL have been used extensively in nephrology literature.

Kidney Disease Outcomes Quality Initiative: No recommendation. UK Renal Association: No recommendation. Canadian Society of Nephrology: No recommendation. European Best Practice Guidelines: No recommendation. Scottish Intercollegiate Guidelines Network: No recommendation regarding use of QOL assessment in decision analysis. Recommend use of physical activity and of psychosocial interventions to improve QOL in advanced CKD. 1 Measures of QOL should be studied in the presence of progressive kidney disease in relation to emerging complications and their treatment. Krishan Madhan has no relevant financial affiliations that would cause a conflict of interest according to the conflict of interest statement set down by CARI. “
“Aim:  To determine whether matrix metalloproteinase-12 (MMP-12) plays a functional role in renal interstitial macrophage accumulation, interstitial fibrosis or tubular apoptosis in the unilateral ureteric obstruction (UUO) model.

Different types of T-cell lineages exhibit independent and distinct gene expression and regulation signatures 6, 17. Based on our observations

that tumor-derived Th17 clones converted to T-cell populations with mixed Treg, Th1 and Th17–Th1 phenotypes selleck screening library following TCR stimulation and expansion, we reasoned that these phenotypic alterations could be the result of changed expression of lineage-restricted transcriptional regulators and regulatory cytokines that control and direct T-cell programming 7, 17, 21. To test this possibility, we first determined the gene expression of the key transcriptional factors, including RORγt and IRF-4 (Th17) as well as T-bet (Th1), GATA-3 (Th2) and FOXP3 (Treg), in the expanded Th17 clones using real-time PCR. As expected, we found that the primary (E0) and early expanded Th17 clones (E1) expressed higher levels of the Th17-specific transcriptional factors RORγt and IRF-4, and the expression levels dramatically decreased following subsequent unbiased expansion cycles (Fig. 5A). In addition, T-bet and FOXP3 expression gradually increased in Th17 clones with the expansions, whereas GATA-3 expression was at a relatively https://www.selleckchem.com/products/PLX-4720.html low level in expanded Th17 cells (Fig. 5A). We then analyzed the mRNA expression of Th1, Th2 and Th17-associated cytokines and cytokine receptors in the expanded Th17 cells following

each round of expansion, using real-time PCR. As shown in Figs 1D and 5B, Th17 cells from primary or early expansion clones expressed high levels of IL-17A, IL-21 and IL-22, but the expression of these genes decreased markedly with subsequent expansions. This suggested that the 4��8C expanded Th17 clones had undergone down-regulation of autocrine cytokines and had decreased responsiveness to Th17-associated growth cytokines, such as IL-21. Unexpectedly, however, we found markedly

increased IL-23R expression in Th17 clones after subsequent expansions, which may be due to the increased T-bet expression in these expanded Th17 clones 46. In addition, we observed significantly increased IFN-γ mRNA expression in Th17 clones after the expansions, whereas there was no or minimal IL-4 gene expression in expanded Th17 clones. These results indicate that the phenotypic changes of Th17 clones induced by TCR stimulation and expansion result from the reprogramming of lineage-specific gene expression. Given the significantly decreased IL-17 production and RORγt expression, as well as increased FOXP3 demethylation and expression, and TGF-β production in the expanded Th17 clones, we next questioned whether repetitive in vitro TCR stimulation and expansion of Th17 cells altered their effector functions and induced suppressive activity towards other immune cells.

Furthermore, cytokine-driven bystander activation of naive T cells does not contribute to the pool

of Th2 cells. The inflammatory type 2 immune response and the efficiency of worm expulsion were dependent on a broad repertoire of TCR specificities. We thank I. Schiedewitz, A. Turqueti-Neves, C. Schwartz and S. Wirth for technical assistance; find more S. Huber, A. Turqueti-Neves and C. Schwartz for critical comments; A. Bol and W. Mertl for animal husbandry and A. Oxenius for providing Smarta mice. This work was supported by the Emmy Noether Program of the Deutsche Forschungsgemeinschaft (Vo944/2-2). The authors have not conflict of interest to declare. “
“Microglia cells, the resident innate immune cells in the brain, are highly active, extending and retracting Selleck Stem Cell Compound Library highly motile processes through which they continuously

survey their microenvironment for ‘danger signals’ and interact dynamically with surrounding cells. Upon sensing changes in their central nervous system microenvironment, microglia become activated, undergoing morphological and functional changes. Microglia activation is not an ‘all-or-none’ process, but rather a continuum depending on encountered stimuli, which is expressed through a spectrum of molecular and functional phenotypes ranging from so-called ‘classically activated’, with a highly pro-inflammatory profile, to ‘alternatively activated’ associated with a beneficial, less inflammatory, neuroprotective profile. Microglia activation has been demonstrated in most neurological diseases of diverse aetiology and has been implicated as a contributor to neurodegeneration. The possibility to promote microglia’s neuroprotective phenotype has therefore become a therapeutic goal. We have focused our discussion on the role of microglia in multiple

sclerosis, a prototype of inflammatory, demyelinating, neurodegenerative disease, and on the effect of currently approved or on-trial anti-inflammatory therapeutic strategies that might mediate neuroprotection at least in part IKBKE through their effect on microglia by modifying their behaviour via a switch of their functional phenotype from a detrimental to a protective one. In addition to pharmaceutical approaches, such as treatment with glatiramer acetate, interferon-β, fingolimod or dimethyl fumarate, we address the alternative therapeutic approach of treatment with mesenchymal stem cells and their potential role in neuroprotection through their ‘calming’ effect on microglia. Microglia, the resident innate immune cells in the brain, represent the first line of defence against exogenous and endogenous threats to the central nervous system (CNS). Microglia are believed to derive from progenitors of mesodermal/mesenchymal origin migrated from the periphery in early postnatal development. In the normal healthy CNS, microglia display a so-called ‘resting’ phenotype, characterized by a typical ramified morphology, a slow turnover rate and low expression of surface molecules.

4E, upper panel). Kinase-active members of the IRAK family, IRAK-1 and IRAK-4, have been shown to induce the degradation of mammalian Pellinos in a kinase-dependent fashion 15. This type of regulation

is retained in the interaction between IRAK-1 and viral Pellino, as reduced levels of the latter are apparent when co-expressed with IRAK-1, but not IRAK-1-KD (Fig 4A, B versus E). The ability of viral Pellino to interact with IRAK-1 learn more supports our homology modelling studies that predicted viral Pellino capable of forming a FHA domain. In order to directly address the potential importance of the putative FHA domain of viral Pellino in facilitating its interaction with IRAK-1, truncation mutants of viral Pellino were generated that lack the first 90 (ΔF1-myc) or 50 (ΔF2-myc) amino acid residues. These mutants were designed based on the former lacking all five of the conserved residues that signature selleck chemical a classical FHA domain and the latter lacking the first three of these conserved residues. Unlike full-length viral

Pellino, the truncation mutants, lacking the first 50 or 90 residues, failed to interact with IRAK-1 (Fig. 5A, upper panel). These studies are again consistent with viral Pellino containing a FHA domain that makes a critical contribution to enabling viral Pellino to interact with IRAK-1. The interaction of IRAK-1 with the shorter spliced form of human Pellino 3 (P3S) served as a positive control for this analysis. The above truncation mutants were also exploited to evaluate the importance of IRAK-1 binding for manifesting the inhibitory Amisulpride effects of viral Pellino on TLR

signalling. As described above, full-length viral Pellino was again shown to cause a dose-dependent inhibition of LPS-induced activation of NF-κB (Fig. 5B). The removal of the first 50 or 90 residues from viral Pellino failed to fully abolish its ability to inhibit LPS signalling. As the removal of the first 50 residues from viral Pellino abolished its ability to bind IRAK-1 but had no effect on its negative regulatory potential, a more refined approach was performed to further define the functional importance of the putative FHA domain of viral Pellino. Interestingly, the truncation of the first 50 amino acids includes removal of the highly conserved FHA-signature residues R33 and S47. Each of these two residues was independently mutated to alanine and the functional properties of the resulting point mutants examined. The substitution of either residue by alanine removed the ability of viral Pellino to interact with IRAK-1 (Fig. 5C), but yet did not eliminate its ability to inhibit LPS-induced activation of NF-κB (Fig. 5D). These findings suggest that the putative FHA domain of viral Pellino is important for IRAK-1 binding but is dispensable for manifesting the inhibitory effects on LPS signalling.

Conclusions: Individualized evaluation is required for optimal choice of anticholinergics. “
“Objectives: Signaling pathways in suburothelial layer are involved in the bladder sensory response. The expression of angiotensin II type 1 (AT1) receptors and connexin Selleck MK-1775 43 (Cx43) in suburothelial myofibroblasts was investigated in an acute bladder inflammation model. Methods: Adult female Wistar rats underwent urethral

catheterization and received 0.2 mL intravesical infusion of 0.4 M HCl to establish acute bladder inflammation model or 0.2 mL of sterile saline as control (n = 10 rats/group). Eight days after treatment, cystometry was performed. Suburothelial myofibroblasts were also collected and subjected to immunohistochemical staining to examine AT1 receptor and Cx43 expression. Results: Eight days after treatment with HCl to induce acute bladder inflammation, the frequency and basal pressure of the bladder was significantly increased compared with those in control rats. The number of suburothelial myofibroblasts was significantly increased in acute bladder inflammation rats, as was the expression of AT1 receptor and Cx43. Conclusion: These results suggest that the increased number of suburothelial myofibroblasts, upregulation of AT1 receptor and Cx43 expression Gemcitabine cost may be associated with the pathogenesis of hyperactivation of bladder

sensory signaling pathways in acute inflammatory bladder. “
“Objective: Both the presence of lower urinary tract symptom (LUTS) and that of hypertension (HT) increase with age. We investigated DOK2 the associations between male LUTS and HT, and also whether α1-blockers could allow for the alteration of symptoms. Methods: The subjects comprised 10 744 men with LUTS in a multicenter Japan-Tamsulosin International Prostate Symptom Score (IPSS) Survey to assess the long-term effects of α1-blockers. A total of 4828

men (mean age, 68.5 years) who received a 12-week administration of tamsulosin (0.2 mg/day) were assessed using IPSS and quality of life (QOL) surveys before and after tamsulosin administration. Data were collected by self-administered questionnaires including age, complete history and IPSS at the initial visit. Results: HT was a more common comorbidity (25.9%) than diabetes mellitus (9.9%) or cardiac disease (7.2%). The presence of HT increased significantly with the degree of frequency (mild, 21%; severe, 29%) and nocturia (mild, 23%; severe, 28%), but did not increase with the degree of urgency. Tamsulosin significantly improved all storage and voiding symptoms in every age group above 40 years. The effect of tamsulosin on storage symptoms was more prominent in patients with HT than in patients without it. Concerning voiding symptoms, however, tamsulosin was as effective in patients with HT as it was in patients without HT.