Interestingly, our data further revealed that functional responses to non-specific pro-inflammatory cytokine stimulation were comparable among HC and asymptomatic Tx patients. Conversely, EBV-specific stimulation resulted in different

levels of IFN-γ and CD107a responses in these same cohorts, indicating a role of recall EBV-antigen stimulation in shaping anti-viral NK-cell function independently of Type-1 promoting cytokine stimulation. Indeed, recent reports have demonstrated that although still acknowledged as members of innate immunity, NK cells also possess nearly all the features of adaptive T-cell immunity 22, 23. Using a murine cytomegalovirus (MCMV) model of viral infection, long-lived MCMV-specific memory NK cells displayed enhanced capacity to produce IFN-γ and degranulate upon re-encounter AZD4547 ic50 with murine CMV, as compared with the resting NK cells from naïve mice 22, 23. The Ly49H receptor was responsible for this NK-cell MCMV-cognate recognition, and appeared not to recognize other viral antigens 22. Future work is therefore needed to elucidate

whether viral (including EBV) recognition by human NK cells is mediated by a single common receptor or by multiple viral antigen-specific receptors. Our results have further identified significant and broad (IFN-γ and CD107a) DZNeP functional impairment of NK cells from PTLD patients both in response to non-specific and to EBV antigen-specific stimulation. NK cells from asymptomatic HVL carriers displayed similar trends, suggesting Galeterone a progressive loss of NK-cell functions (exhaustion) in these patients that parallels

the increased EBV-antigenic load, and with cytotyoxicity being affected early. These NK-cell functional data resemble the functional features of exhausted viral-specific CD8+ T cells identified during chronic high viral load infections, with IFN-γ being the last function maintained by Ag-specific T cells 24. Furthermore, our results identified the decreased expression of NKp46 and NKG2D and concomitant up-regulation of PD-1 on NK cells from EBV viremic PTLD patients as potential regulatory mechanisms responsible for the NK-cell functional abnormalities. The decreased expression of activating NCRs was previously described in chronic viremic (HIV- and HCV-) patients, and was shown to lead to significant NK-cell functional impairment of cytolytic activity and IFN-γ release 25, 26. In another study, down-regulation of NKG2D activation pathways provided Kaposi’s sarcoma-associated herpesvirus with a mechanism for evasion of NK-cell efficient viral clearance 27. The mechanisms leading to decreased NK-cell triggering receptors on NK cells from viremic patients are not entirely clear.

In our study, high levels of cytokines were observed in all the animals after treatment. This has been shown earlier that patients with kala-azar usually show expansion of parasite-specific lymphocytes, and long-term T-cell responses are maintained even after clinical cure [29]. However, compared with chemotherapy, immunotherapy and immunochemotherapy, maximum absorbance in Th1 cytokine levels (IFN-γ and IL-2) and minimum levels of Th2 cytokines (IL-10, IL-4) were observed in animals treated with immunochemotherapy. Moreover, maximum levels of Th1 cytokines and minimum levels of Th2 cytokines were produced by cisplatin + 78 kDa + MPL-A.

This is in accordance to a study which stated that restoration of cell-mediated immunity to the parasite is necessary for an effective pentavalent antimonial therapy [30]. Our results are in correspondence to a study carried out by Musa et al., [20] who this website observed that the healing process in PKDL patients was due to modulation of patient’s immune system tipping the Th1/Th2 immune response to a pure Th1 response. Moreover, the dogs that were given immunochemotherapy showed a significantly increased percentage of T helper lymphocytes, that is, ATM inhibitor cancer the percentage of CD4/TcRαβ + and CD4/CD45RA+ cells increased significantly which are associated with disease remission [31]. Erythromycin To conclude, the present study puts an insight

into the use of immunochemotherapy with a combination of drug and vaccine formulation. As the standard antileishmanials used to treat leishmaniasis are met with various side effects; therefore, low dose of cisplatin in combination with L. donovani specific 78 kDa antigen along with adjuvant MPL-A can prove to be a good alternative for the treatment for visceral leishmaniasis. However, more studies are required to test the combination in higher animal models before it is tested in VL patients. The authors acknowledge the support provided by the PURSE Grant of Department

of Science and Technology, and University Grant Commission, Fellowship programme, India. The authors have no competing interests. Both the authors have materially participated in the research work and article preparation. Jyoti Joshi and Sukhbir Kaur conceived and designed the experiments. JJ performed the experiments and helped by SK to analyse the data. SK contributed reagents/materials for the experiment. JJ wrote the paper. SK gave necessary suggestions and finally approved the manuscript to be submitted for publication. “
“This study tested the hypothesis that pregnant female baboons exhibit increased levels of various inflammatory mediators in serum resulting from ligature-induced periodontitis, and that these profiles would relate to periodontal disease severity/extent in the animals.

3C–H). this website In the GD cases, we observed a small number of Gli3-IR nuclei and GFAP-IR cytoplasmic processes of the tumor cells within and around the nodules (Fig. 3I–M). In both ND and GD cases, immunoelectron microscopy demonstrated Gli3-IR at the inner membrane of the nuclear envelope with nuclear chromatin nearby, and inside the

nucleus (Fig. 4). Several clinical and histological characteristics, including age at onset, sex, risk evaluation factors proposed by Laurent et al.,[22] histological type, Ki-67 labeling index, and Gli3-IR, showed no significant relationship with the OS rate, whereas induction of chemoradiation was significantly correlated with longer OS (Table 1). With regard to EFS rate, Gli3-IR in the tumor was significantly MDV3100 molecular weight (P < 0.05) associated with a favorable patient outcome. Being male and having DNMB tended to be associated with a favorable outcome, but not to a significant degree (P < 0.1) (Table 1). Evaluation of differences in the profiles of each histopathological group is summarized in Table 2. Both the OS and EFS rates in the ND group were significantly higher than those in the other groups (Fig. 6 and Table 2). The GD group showed outcomes as equally poor as those of the DF group. It was found that the Ki-67 labeling index in the DF group tended to be higher than those in the ND and GD groups,

although the inter-group differences were not significant (Table 2). The findings of this study indicated that neuronal differentiation is associated with Gli3 expression in MB cells, and that this feature predicts a favorable outcome for patients with MB. In the present study, all patients in the ND group showed

a favorable course (Fig. 6 and Table 2). Previous reports have indicated that patients with MB accompanied by neuronal differentiation[24, 25] and those with MBEN[8, 9] show good progress, being consistent with our findings. On the other hand, the association between glial differentiation in the tumor and patient prognosis has been unclear; the three patients in the GD group (Fig. 3I–M) showed miserable courses (Table 2), whereas some previous reports have D-malate dehydrogenase indicated that patients with MB showing glial differentiation progressed well.[24, 25] Some previous reports have indicated that patients with DNMB did not show significant longer survival than those with CMB.[16, 17] Consistent with this, the difference on the 10-year OS rates of patients with CMB and those with DNMB was not significant (Table 2). Apparently, a large proportion of DNMB cases exhibited features of neuronal differentiation and Gli3 expression (Table 2). Therefore, combination of desmoplastic/nodular histological characteristics, NeuN indicating neuronal differentiation, and Gli3 expression, is useful for predicting a favorable outcome.

This pathway may also regulate the analogous processes of neurite extension and tumor cell invasion. “
“Please cite this paper as: Nunez, Trach, Burnett, Handa, Dyke, Callahan, and Smith (2011). Vasoactive Properties of Keratin-Derived Compounds. Microcirculation18(8), 663–669. Objective:  Keratin proteins have been utilized as biomaterials for decades, and are currently under investigation for a variety of tissue regeneration and trauma applications. It has been suggested that

certain keratins may have the capacity to act as a colloid in fluid resuscitation applications, providing viscosity and oncotic properties that PI3K inhibitor may be beneficial during acute ischemic events. Oxidized selleck keratin derivatives, also known as keratoses, show good blood and cardiovascular compatibility and thus are the subject of this study. Methods:  The effects of keratose compounds will be assessed using a topload i.v. infusion model and

observation of changes in the microvasculature of the cremaster muscle of rats. Results:  Keratose resuscitation fluid (KRF) administration resulted in significant vasodilation in the cremaster muscle. This effect was blocked with pretreatment of l-NA to inhibit NO. Another keratin fraction, alpha-keratose, which is the primary viscosic compound, was not found to induce vasodilation. Conclusions:  The apparent mechanism of vasodilation was found to be NO-mediated and isolated to a particular purified fraction, the KAP. “
“Microcirculation (2010) 17, 1–10. doi: 10.1111/j.1549-8719.2009.00010.x Objectives:  Knowledge of glomerular structural and hemodynamic changes in vivo is still limited under diabetic conditions. In this study, we examined the alterations in glomerular structure and permeability of macromolecules and the effects of telmisartan using a confocal laser microscope. Methods:  Diabetes was induced by injecting streptozotocin. After 4 and 8 weeks, the filtration and

permeability of differently sized compounds across the glomerular capillaries were visualized using a confocal laser microscope by injecting 500-kilodalton and 40-kilodalton dextran. At 7 weeks, some diabetic rats were treated P-type ATPase with telmisartan for 1 week. The permeation of the 40-kilodalton dextran across the glomerular capillaries into Bowman’s space was quantified. Glomerular volume, diameters of the afferent and efferent arterioles, and glomerular permeability were compared. Results:  Glomerular volume was significantly increased in the diabetic rats, and there was heterogeneity in the glomerular volumes. The diameter ratio of the afferent to efferent arterioles significantly increased, and there was increased glomerular permeability in the diabetic rats compared with the control rats. Telmisartan treatment reduced glomerular permeability without affecting glomerular volume.

Administration of EPO only slightly increased eNOS expression at day 10, when compared with controls. EPO induced angiogenesis and increased hematocrit. Finally, EPZ-6438 price EPO significantly reduced leukocytic inflammation in arterioles in all EPO receiving mice. EPO preconditioning effectively reduces skin necrosis

predominantly by capillary maintenance and reperfusion, as well as improved tissue regeneration. Thus, EPO preconditioning might represent a promising, non-invasive approach to reduce complications in ischemically challenged skin. “
“The formation of new blood vessels from existing vasculature, angiogenesis, is facilitated through a host of different signaling processes. Members of the TGF-β superfamily, TGF-β1, TGF-β3, and BMP9, are key propagators of both inhibition and initiation of angiogenesis. HHT, characterized by AVM and capillary bed defects, is caused by germline mutations in the ENG and ACVRL1/ALK1 genes, respectively. Clinical symptoms include epistaxis and GI hemorrhage. The membranous receptors endoglin and ALK1 activate proliferation and migration of endothelial cells during

the angiogenic process via the downstream intracellular SMAD signaling pathway. Endothelial cell senescence or activation is dependent on the type of cytokine, ligand concentration, cell–cell interaction, Selleck Ponatinib and a multitude of other signaling molecules. Endoglin and ALK1 receptor levels in tumor vasculature correlate inversely with prognosis in humans, whereas in mice, endoglin deficiency decelerates tumor progression. Therefore, endoglin and ALK1 have been identified as potential therapeutic targets for antibody treatment in various cancers. Early phase clinical trials in humans are

currently underway to evaluate the efficacy and safety of biological therapy targeting endoglin/ALK1-mediated cells signaling. “
“Please cite this paper as: Unekawa M, Tomita M, Tomita Y, Toriumi H and Suzuki N. Sustained Decrease and Remarkable Increase in Red Blood Cell Velocity in Intraparenchymal Capillaries Associated With Potassium-Induced Cortical Spreading Depression. Microcirculation 19: 166–174, 2012. Objectives:  To examine changes in red crotamiton blood cell (RBC) velocity in intraparenchymal capillaries of rat cerebral cortex in response to KCl-induced cortical spreading depression (CSD). Methods:  In isoflurane-anesthetized rats, the velocity of fluorescently labeled RBCs flowing in capillaries in layer I was measured with a high-speed camera laser-scanning confocal fluorescence microscope, with simultaneous monitoring of DC potential, the electroencephalogram (EEG), partial pressure of oxygen (PO2), and cerebral blood flow (CBF). Results:  After KCl application, a transient deflection of DC potential (i.e., CSD) repeatedly appeared concomitantly with depression of EEG, and was propagated in the distal direction. PO2 transiently decreased and CBF was slowly elevated.

3 (IV.3) and (3) medium containing F(ab)’2 goat anti-mouse IgG (GAM). Alternatively, cells were treated with anti-dinitrophenol (DNP) IgE (Sigma-Aldrich) and incubated on ice for 30 min followed by addition of DNP-BSA (Invitrogen, www.selleckchem.com/products/BI6727-Volasertib.html Carlsbad, CA, USA) to stimulate serotonin release. Following stimulation, cells were placed at 37 °C for 30 min to allow secretion to proceed. Secretion was terminated by addition of 100 μl ice-cold medium and placement of cells on ice. After supernatants were removed from each well, cells were lysed by addition of phosphate-buffered saline (PBS) containing 1% sodium dodecyl sulphate (SDS). The 3H-serotonin in

supernatants and lysates was determined by liquid scintillation counting. Serotonin release is calculated as the percent of the total serotonin available for secretion (serotonin release mediated by the calcium ionophore A23187). AZD1152-HQPA supplier For inhibition assays, cells were preincubated with medium containing either 25 μg/ml piceatannol or 10 nm wortmannin (Sigma) for 15 min at 37 °C. These specific Syk and PI3K inhibitors were chosen for consistency with previous observations. Phagocytosis assay.  5 × 105 cells were plated per well in 6-well tissue culture dishes. The following day, the medium was replaced with fresh complete medium containing 1 × 108 IgG-opsonized sheep red blood cells (EA). After 30 min at 37 °C, externally bound EA were lysed by exposure

for 1 min to cold hypotonic saline. Washed cells were fixed in Wright-Giemsa stain, and phagocytosis of EA was assessed in at least 300 cells by light microscopy. For inhibition studies, cells were preincubated for 15 min at 37 °C with either 25 μg/ml piceatannol or 10 nm wortmannin. Statistical analysis.  Statistics were performed using Students t-test. To create a model system to investigate FcγRIIA tirggered serotonin secretion, wildtype FcγRIIA or mutants of FcγRIIA were stably transfected into RBL-2H3 cells. FACS analysis with anti-FcγRII Calpain monoclonal antibody (IV.3) and FITC-conjugated goat anti-mouse

secondary antibody demonstrated that the selected cell lines transfected with FcγRIIA-wt or the various mutant FcγRIIA plasmids expressed quantitatively equivalent levels of FcγRII on the surface (Fig. 1). When stimulated with FcγRII-specific mAb IV.3 F(ab)’2/GAM F(ab)’2 (IV.3 + GAM), FcγRIIA-transfected RBL cells preloaded with 3H-serotonin released an average of 21% of total available radioactive serotonin (Fig. 2A). This release represents an almost 7-fold increase over what is observed for RBL-2H3 cells into which FcγRIIA had not been transfected (<4%, Fig. 2A). Less than 4% of total available serotonin is also released after mock stimulation of WT RBL-2H3 cells. This baseline release is considered due to general cell “leakiness”. Mock-stimulated FcγRIIA transfected RBL-2H3 cells also released baseline levels of serotonin (∼3%), indicating that cell surface expression of FcγRIIA by itself does not increase release of serotonin (Fig.

Interestingly, in the present study, the VLP internalization mechanism was observed to be different for NK cells: VLPs entered rapidly within large macropinocytosis vacuoles, independently of the clathrin and caveolae pathways (Figs. 4 and 5). RhoGTPase assays suggest the involvement of filopodia during find more VLP uptake (activation of the Cdc42, Fig. 5B) and a concurrent reduction of lamellipodia (inhibition of Rac1 Fig. 5C) 34, as observed by electron microscopy (Fig. 4G and H), and not membrane blebbing, described for host-cell entry of other viruses 24. Interaction of NK cells with VLPs was correlated with CD16 expression and experiments

with CD16 blocking antibody or co-immunoprecipitation confirmed the importance of this receptor for this interaction (Fig. 6A–F). Moreover, VLP internalization induced transient down-modulation of CD16, but no change in NKp46 expression, a receptor involved in Newcastle disease virus binding 35 (data not shown). Our findings are in agreement with those showing that binding of HPV–VLPs is mediated by CD16 on DCs 36 and that uptake of HPV–VLPs by DCs from FcγRIII-deficient mice is strongly reduced compared with wild-type mice 17. CD16 has been shown to be involved in macropinocytosis in Target Selective Inhibitor Library cost macrophages 37 and in γδ T cells 38. Moreover, transduction of CD16 into a CD8+ T-cell clone was sufficient to increase HPV–VLP entry into these cells (Supporting

Information Fig. 5B).

To exclude an interaction with CD16 mediated by antibodies, we checked the absence of antibodies reacting against VLPs in the human and bovine sera used in culture medium (data not shown). We also performed some experiments without serum and obtained similar results (data not shown). NK cells play a key role in immune responses by exocytosis of cytotoxic granules, and CD16 is a major receptor capable of triggering NK cytotoxicity 21. We showed that VLPs induced cytotoxic activity of NK cells expressing CD16 (Figs. 2A–C and 7A, B). In addition selleck chemicals llc to killing infected cells, this process could liberate granulysin, present in cytotoxic granules, which works as an alarmin and activates DCs 39. Besides this degranulation activity, through binding of CD16, NK cells are able to activate adaptive immune responses by the secretion of soluble factors such as IFN-γ and TNF-α 40. We showed that VLP stimulation induced the secretion of these cytokines in NK and NK92 CD16+ cells but not in NK92 CD16− cells (Fig. 7). VLPs were produced in insect cells infected with baculovirus coding for HPV16 L1. Because insect baculovirus contaminants have been reported to play a role in the immunogenicity induced by VLPs 41, we used a lysate of insect cells infected with WT baculovirus as a negative control and did not observe cytotoxic activity or cytokine production in this culture condition.

After blocking FcR, cells were incubated with appropriately diluted antibodies. Acquisition was performed using a FACSort or a LSRII (BD Biosciences, Mountain View, CA, USA) and data analysis was conducted

using FlowJo software (Tree Star, Ashland, OR, USA). Comparisons of two groups of data were analyzed by two-tailed Student’s t-test using GraphPad Prism 4.0. (GraphPad, San Diego, CA, USA). This project has been funded in whole or in part with federal funds from the National Cancer selleck screening library Institute, National Institutes of Health, under contract HHSN261200800001E. This Research was supported (in part) by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. R. H. is supported by International Training Program of Japan Society for the Promotion of Science. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. Government. The authors thank Dr. Teresa Born and Dr. John E Sims EX 527 purchase at Amgen Inc. for providing

anti-mouse TNF antibody and isotype control Mu IgG, and Dr O. M. Zack Howard, Dr. Hong Lou, Dr Hongchuan Li and Dr Gonzalo M. de la Rosa for help in this study. Conflict of interest: The authors declare no financial or commercial conflict of interest. “
“The activation-induced cytidine deaminase (AID) mediates somatic hypermutation and class switch recombination of the Ig genes by directly deaminating cytosines to uracils. As AID causes a substantial amount of off-target mutations, its activity has been associated with lymphomagenesis and clonal evolution of B-cell malignancies. Although it has been shown that AID is

expressed in B-cell chronic lymphocytic leukemia (CLL), a clear analysis of in vivo AID activity in this B-cell malignancy remained elusive. In this study performed on primary human CLL samples, we report that, despite the presence of a dominant VDJ heavy chain region, a substantial intraclonal diversity was observed at VDJ as well as at IgM switch regions (Sμ), showing ongoing AID activity in vivo during disease progression. This AID-mediated heterogeneity was higher in CLL subclones expressing CD86, which we identified as the proliferative CLL fraction. Finally, CD86 expression selleck correlated with shortened time to first treatment and increased γ-H2AX focus formation. Our data demonstrate that AID is active in CLL in vivo and thus, AID likely contributes to clonal evolution of CLL. “
“The ontogenic relationship between pro-inflammatory populations of interleukin-17 (IL-17A)- and/or IL-22-producing T cells and other T-cell subsets is currently unclear in humans. To appreciate T helper cell-lineage commitment, we combined cytokine production profiles of in vitro expanded T-cell clones with T-cell receptor (TCR) clonotypic signatures.

Voriconazole was continued for 6 months after transplant as secondary prophylaxis. find protocol After 15 months of follow-up, the patient is alive and well, and in complete remission of his underlying disease. Triazoles have the potential for improving the cure rate of Fusarium infections but both surgery and shortening the duration of neutropenia by GTXs

are important factors in optimising the results. “
“Necrotising external otitis (NEO) is a destructive, potentially fatal, infection usually seen in elderly diabetics or the immunocompromised. The commonest causative organism is Pseudomonas but immunocompromised patients are additionally susceptible to opportunistic infections. Here we describe the first reported case of NEO caused by a previously unknown human pathogen –Aspergillus wentii. A review of the literature reveals that fungal NEO is associated with a high rate of cranial nerve palsies suggesting that infections are not being treated rapidly enough to prevent morbidity. Fungal infection should be considered early in immunocompromised patients and microbiological

diagnosis should be obtained wherever possible. “
“Kodamaea ohmeri was isolated from a 38-year-old HIV seropositive woman with pseudomembranous oral candidiasis. The isolate was identified by the API 20 C yeast identification system and confirmed by sequence analysis. Antifungal susceptibility testing done by E-test showed that the isolate was susceptible to voriconazole, amphotericin B and caspofungin. “
“The unusual case of a 29-year-old woman with tinea manus caused by infection due to Trichophyton erinacei Selleckchem MG 132 is described. The patient presented with marked erosive inflammation of the entire fifth finger of her right hand. Mycological and genomic diagnostics resulted

in identification of T. erinacei as the responsible pathogen, which had been transmitted by a domestic African pygmy hedgehog, Atelerix albiventris. Upon prolonged treatment with topical and systemic antifungal agents skin lesions slowly resolved. This case illustrates that the increasingly popular keeping of extraordinary Interleukin-2 receptor pets such as hedgehogs may bear the risk of infections with uncommon dermatophytes. “
“Trichophyton violaceum is an anthropophilous dermatophyte endemic to parts of Africa and Asia, sporadic in Europe. It is an emerging pathogen in Italy due to immigration. We report 36 cases of infections due to T. violaceum, diagnosed in the last 5 years by mycological examination. The source of contagion was 13 children adopted from orphanages. “
“The frequency of mucosal infections caused by Candida glabrata has increased significantly. Candida glabrata infections are often resistant to many azole antifungal agents, especially fluconazole. The purpose of this study was to compare the efficacies of posaconazole (PSC) and fluconazole (FLC) in the treatment of experimental C.

Spontaneous contractions and possible consequent afferent nerve firing might participate in the generation of overactive bladder syndrome. Overactive bladder

syndrome (OAB) is characterized by urgency, with or without urgency incontinence, usually with frequency and nocturia.1 The urothelium has been the main focus of bladder sensation research in the past two decades. The urothelium acts as a sensor and excretes many substances that can act on suburothelial afferent nerves and the detrusor muscle.2,3 Adenosine triphosphate (ATP) or acetylcholine (ACh) is released from the urothelium by bladder distension (bladder filling) and may act on purinergic or muscarinic receptors on afferent nerves located in the urothelium and suburothelium, VX770 and this action was believed to evoke afferent nerve firing, resulting in the bladder filling sensation.2,3 However, experiments using in vitro bladder-nerve preparation raised doubts about this notion. Stretching of the bladder wall elicited afferent nerve firing near the urothelium, but this firing was not inhibited 3 MA by a purinergic receptor antagonist.4 More recently,

the role of the mucosa (i.e. the urothelium and suburothelium) in the generation of spontaneous contractions (SCs) of the bladder wall has become the center of attention in basic research of the bladder filling sensation.5–7 Studies Succinyl-CoA have demonstrated that small phasic increases in intravesical pressure during the filling phase of the micturition

cycle evoke afferent nerve firing.8 This type of bladder contraction during the filling phase is considered to be derived from spontaneous contractile activity in the bladder wall. The discovery of cells that resemble interstitial cells of Cajal (ICCs) in the gut9 has given rise to the hypothesis that these cells may be pacemakers in the bladder as their counterparts in the gut and that such cells play an important role in bladder sensation.10 As a result of these recent studies, the role of SCs of the bladder in bladder sensation has become an interesting and exciting target of basic research in bladder sensation. The human bladder was historically considered to be a simple reservoir of urine that does not contract during the filling phase. A phasic increase in intravesical pressure on cystometrogram (CMG) is recognized as an abnormal cystometric finding i.e. detrusor overactivity (DO), a phenomenon that may be associated with OAB in humans.1 However, a clinical study using ambulatory cystometry identified involuntary detrusor activity in healthy volunteers as well as in patients with OAB.11 Cystometric parameters discriminating between normal bladders and OAB indicate the duration of involuntary detrusor activity and the volume at which involuntary activity occurs.