0 for Windows. This study was supported by the Public Welfare & Safety Research program (20110020963) through the National Research Foundation of Korea (NRF)

funded by the Ministry of Education, Science and Technology. The authors declare no financial or commercial conflicts of interest. Disclaimer: Supplementary materials have been peer-reviewed but not copyedited. “
“The parasitic gastrointestinal nematode Nippostrongylus brasiliensis induces massive expansion of T helper type 2 (Th2) cells in the lung and small intestine. Th2 cells are a major source of interleukin-4 and interleukin-13, two cytokines that appear essential for rapid worm expulsion. It is unclear whether all Th2 cells induced during infection are pathogen-specific because Th2 cells might PLX4032 solubility dmso also be induced by parasite-derived superantigens or cytokine-mediated bystander activation. Bystander Th2 polarization could explain the largely unspecific B-cell response during primary infection. Furthermore, it is not known whether protective immunity Torin 1 in vitro depends on a polyclonal repertoire of T-cell receptor (TCR) specificities. To address these unresolved issues, we performed adoptive transfer experiments and analysed the TCR-Vβ repertoire before and after infection of mice with the helminth N. brasiliensis.

The results demonstrate that all Th2 cells were generated by antigen-specific rather than superantigen-driven or cytokine-driven

activation. Furthermore, we show that worm expulsion was impaired in mice with a limited repertoire of TCR specificities, indicating that a polyclonal T-cell response is required for protective immunity. Protective immunity against gastrointestinal nematodes is mediated by the cytokines interleukin-4 (IL-4) and IL-13 which are mainly produced by T helper type 2 (Th2) cells, basophils and mast cells.1 Infection of mice with the nematode Nippostrongylus brasiliensis leads to massive accumulation of Th2 cells in the lung and intestine.2 Reverse transcriptase Similarly, high frequencies of Th2 cells are found in several tissues after infection with Heligmosomoides polygyrus, even though this parasite remains localized to the small intestine.3 It is not well understood why helminths in general are such potent Th2 inducers. Secreted products from N. brasiliensis have been shown to contain large glycoproteins that promote Th2 cell differentiation by polarized activation of dendritic cells.4,5 A Th2-inducing component of Schistosoma mansoni egg antigen was recently identified as Omega-1, a T2 ribonuclease that reduces the contact time between dendritic cells and T cells and stimulates dendritic cells for Th2 cell activation.6,7 Other Th2-inducing factors from helminths include complex glycans and proteases.8,9 However, receptors on antigen-presenting cells that recognize these Th2-inducing factors remain largely unknown.

Bacillus cereus ATCC14579 was employed as a control strain for phenotypic identification and detection of the virulence genes. Staphylococcus aureus ATCC29213 was used as the control strain for susceptibility testings and detection of the virulence genes. Bacteria were stored at −70 °C

in heart infusion broth (Nissui Pharmaceutical) containing 20% glycerol. Subsequently bacteria were inoculated on heart infusion agar plates (Nissui Pharmaceutical) and incubated at 36.5 °C overnight. Genotyping of the isolates was performed by PFGE, as described previously Alectinib (Maslow et al., 1994). In brief, a treated agarose gel block containing bacteria was digested with 25 U of Smal for 20 h at 25 °C and subjected to electrophoresis on 1.0% agarose gel, employing a contour-clamped homogeneous

electric field system (CHEF DR III, Bio-Rad Laboratories, Tokyo, Japan) at 6.0 V cm−2 for 18.5 h with pulse times ranging from 1.0 to 14.0 s. The gel was stained with 0.5 μg mL−1 ethidium bromide LY294002 supplier and analyzed under UV light with quantity one sw software (Bio-Rad Laboratories). For genotyping, the PFGE patterns were interpreted as described elsewhere (Tenover et al., 1995), after analysis of the patterns was performed using fingerprinting ii software (version 3.0) (Bio-Rad Laboratories). Genomic DNA from B. cereus isolates and ATCC14579 was prepared using a DNeasy blood & tissue kit (Qiagen, Tokyo, Japan). To detect the virulence genes, polymerase chain reaction (PCR) assays were performed with specific primer pairs for the cereulide (ces) gene (Ehling-Schulz

et al., 2005), the nonribosomal peptide synthetase (NRPS) gene associated with cereulide production (Kyei-Poku et al., 2007), the enterotoxin FM (entFM) gene, the enterotoxin S (entS) gene (Asano et al., 1997), the enterotoxin T (bceT) gene (Agata et al., 1995), the hemolytic enterotoxin complex (hblACD) genes (Mäntynen & Lindström, 1998; Kyei-Poku et al., 2007), the nonhemolytic enterotoxin (NHE) complex (nheBC) genes (Rivera et al., 2000), the hly-II gene, the cytK gene Clomifene (Fagerlund et al., 2004), the immune inhibition A (inA) gene, the piplc gene (Guttmann & Ellar, 2000), the sph gene (Hsieh et al., 1999), and the vegetative insecticidal protein 3A (vip3A) gene (Zahner et al., 2005). The PCR conditions such as temperatures, times, and the number of cycles were described in each reference. Amplification was carried out with KOD-dash enzyme (Toyobo, Osaka, Japan) and a thermal cycler (Dice gradient; Takara Bio, Ohtsu, Japan). Bacillus cereus ATCC14579 was used as a positive control for amplification of the entFM, entS, bceT, hblACD, hly-II, cytK, and piplc genes, although no standard strain as a positive control for the ces, NRPS, nheBC, inA, sph, and vip3A genes was available.

The association of HCMV infection with increased proportions of NKG2C+ cells has been reported in chronic lymphocytic leukaemia patients [30], solid organ and hematopoietic transplant recipients [31-33], a primary T-cell immunodeficiency [34], as well as in individuals coinfected by other pathogens, for example, HIV-1 [35-37], hantavirus [38], chikungunya [39], HBV, and HCV [40]. Moreover, NKG2C+ NK cells expanded in response to HCMV-infected fibroblasts in vitro, and it was hypothesized that the CD94/NKG2C activating KLR might recognize HCMV-infected cells [41]. Altogether, these observations are reminiscent of the pattern of

response to murine CMV (MCMV) specifically mediated by the Ly49H+ NK-cell subset [42] and, on that basis, it has been speculated that the CD57+ selleck chemicals NKG2C+ subset might represent “memory” NK cells [32]. Interestingly, a complete deletion of the NKG2C gene has been reported in Japanese and European blood donors with ∼4% homozygosity and 32–34% heterozygosity rates [43, 44]; yet, whether

this genetic trait may influence the NK-cell selleck inhibitor response to HCMV is unknown. In the present study, the relationship between congenital HCMV infection, NKG2C genotype, and NKR distribution was addressed. An immunophenotypic study was carried out in blood samples from children with evidence of past HCMV infection, either congenital symptomatic (n = 15), asymptomatic (n = 11), or postnatal selleck kinase inhibitor (n = 11), and from noninfected children (n = 20). NKR expression (i.e., NKG2C, NKG2A, LILRB1, and CD161) was assessed by flow cytometry in NK (CD56+CD3−) and T cells (CD3+). Despite some differences in age distribution, both the proportions and the absolute numbers of NK and T cells were comparable in all four study groups (Table 1). Children with symptomatic congenital infection displayed higher proportions of NKG2C+ and lower percentages of NKG2A+ NK cells than asymptomatic or noninfected groups (Fig. 1). In contrast, the distributions of NKG2C+ and NKG2A+ NK cells were comparable in children with congenital symptomatic and postnatal infection. Remarkably, both the relative and absolute numbers

of LILRB1+ NK cells were markedly increased in symptomatic congenital infection, whereas no significant differences in the proportions of CD161+ NK cells were perceived (Fig. 1). Age, clinical features, and the proportions of NKG2C+ and LILRB1+ NK cells corresponding to cases of symptomatic congenital infection are displayed as Supporting Information Table 1. Multivariate analysis indicated that the immunophenotypic differences observed were independent of age. Studies in dizygotic twins further illustrated the impact of congenital symptomatic infection on the NKR repertoire (Table 2). In a first pair (TP1, 22 months old), only the HCMV-positive symptomatic boy displayed a marked increase of NKG2C+ and LILRB1+ NK cells as well as reduced proportions of NKG2A+ cells, compared to his noninfected sister.

Initial investigations include full blood count, inflammatory markers [C-reactive protein (CRP) and erythrocyte sedimentation

rate (ESR)], renal see more function such as epidermal growth factor receptor (eGFR) and serology to include anti-glomerular basement membrane antibodies. Inflammatory markers provide a non-specific tool for assessing inflammatory activity and monitoring treatment. Urinalysis detects proteinuria and haematuria which can be assessed further for red cell casts indicating active renal inflammation or a quantification of protein loss with a 24-h urine collection or protein : creatinine ratio. Urine infection should also be excluded. Liver function should be assessed prior to starting disease-modifying agents such as methotrexate. Ovarian function may

be assessed prior to cyclophosphamide in women of child-bearing age with measurements of follicle stimulating hormone (FSH), luteinizing hormone (LH) [30] or anti-Müllerian hormone (AMH) levels [31] to provide information prior to fertility counselling. Characteristic autoantibodies are formed towards enzymes and bactericidal proteins within the cytoplasmic granules of neutrophils and monocytes in a substantial proportion of patients with systemic vasculitis manifesting as Wegener’s granulomatosis, microscopic CH5424802 molecular weight polyangiitis and Churg–Strauss syndrome, as well as in patients with limited forms of these conditions. These include renal-limited necrotizing crescentic glomerulonephritis, subglottic stenosis and retrobulbar pseudotumour [15,32]. However, there is a cohort of patients with the same diseases who never manifest ANCA, which may represent an independent disease entity [33]. ANCA are demonstrated by a combination of indirect immunofluorescence (IIF) screening techniques using whole leucocyte smears as substrate to certify the neutrophil-specific reactivity, followed by a form of solid phase assay using isolated autoantigen as target [e.g. enzyme-linked immunosorbent assay (ELISA)][34]. Thus the mere identification of neutrophil-specific autoantibodies (NSA) by IIF does not

directly Evodiamine indicate the presence of ANCA [35]. ANCA divide into two main classes: C-ANCA or classical cytoplasmic ANCA (Fig. 1) and P-ANCA or perinuclear-staining ANCA (Fig. 2). The classical granular staining pattern (C-ANCA), seen initially by IIF in rapidly progressive glomerulonephritis patients and Wegener’s granulomatosis patients, indicated clearly that the autoantigen was located in granules of neutrophils and monocytes, and the nature of the proteinase 3 (PR3) antigen was revealed [36] as well as its surface expression [37]. As is the case with other IIF screening techniques, the autoantigen may differ even if the staining pattern is the same. International collaborative studies have helped define the diagnostic value of combining ANCA by IIF and antigen-specific ELISA using PR3 and myeloperoxidase (MPO) antigens [38].

Although the V6-V8 region also generated a single minor band in type strains analyses (Fig. 1c), this

non-specific minor band also appeared in each lane of the DGGE gels for subgingival bacterial community analysis and could easily be distinguished from other specific bands (Fig. 2). selleck screening library Finally, the DGGE patterns of V3-V5 (position 341–926 in E. coli) and V6-V8 (position 968–1401) showed great similarity in both number of bands in each sample and the Cs between baseline and 6 weeks after mechanical debridement (Fig. 3), suggesting that those two regions may be suitable for analyzing periodontal communities. In addition, the reproducibility of the DGGE analysis of the V3-V5 and V6-V8 regions was very high, with low variation between gels, further

indicating that DGGE is a useful tool for bacterial community analysis. Interestingly, the V3-V5 and V6-V8 amplicons retarded at quite different positions of the gels (Figs 1 and PS-341 in vivo 2), suggesting the nucleotide sequencing and DNA structure may largely reflect separation of the DNA fragment on the DGGE gels. Without gel extraction from the DGGE gels and further DNA amplification and sequencing, it is not possible to speculate whether different target regions of 16S rDNA would finally result in different species identification in DGGE analysis of the same sample. However, the present data suggest that when DGGE analysis is applied to subgingival microbial communities, the target regions of the 16S rDNA should be carefully considered. This work was supported in part by the Science and Technology Commission

of Shanghai (08DZ2271100) and Shanghai Leading Academic Discipline Project (S30206-fzd03). The authors would like to thank Prof. Yoichiro Miyake and Dr. Hiromichi Yumoto from the University of Tokushima for their thoughtful suggestions, and Dr. Yinqi Bai from BGI-Shenzhen for his kind help in UPGMA analysis. “
“Foxp3 specifies the Treg cell lineage and is indispensable for immune tolerance. Accordingly, rare Foxp3 mutations cause lethal autoimmunity. The mechanisms precipitating more prevalent human autoimmune diseases are poorly understood, but involve a combination of genetic and environmental factors. Many autoimmune diseases associate with a partial Treg-cell dysfunction, yet mouse models reflecting such complex pathophysiological processes are rare. Around 95% of Foxp3+ Ribonucleotide reductase Treg cells can be specifically depleted in bacterial artifical chromosome (BAC)-transgenic Depletion of REGulatory T cells (DEREG) mice through diphtheria toxin (DT) treatment. However, Treg-cell depletion fails to cause autoimmunity in adult DEREG mice for unclear reasons. By crossing Foxp3GFP knock-in mice to DEREG mice, we introduced additional genetic susceptibility that does not affect untreated mice. Strikingly, DT treatment of DEREG × Foxp3GFP mice rapidly causes autoimmunity characterized by blepharitis, tissue damage, and autoantibody production.

Unlike its human counterpart, the appendix of other mammals such as the rabbit has been recognized to play a pivotal role in systemic and mucosal immunity

this website [1–3]. The lifetime risk of appendicitis has been estimated to be 8·7% in men and 6·7% in women [4], making it the most common human abdominal emergency requiring surgical intervention. Uncertainty has persisted about the causality of acute appendicitis, although the most popular theory posits luminal obstruction and incarceration of secretions, leading to increased intraluminal pressure, culminating in mucosal ischaemia and bacterial overgrowth. Potential causes of appendiceal obstruction include lymphoid hyperplasia, faecoliths and malignancy [5]. Mortality due to acute appendicitis is around 0·3%, rising to 1·7% if perforation is present [6]. Although acute appendicitis can occur at any age, the peak age of incidence of appendicitis without perforation selleck is in the second and third decades [7]. There has been a paucity of immunological data from appendicitis, in contrast to histopathological data. Similarly, the immunopathology and complex interactions between genetic predisposition, bacterial flora and the intestinal immune system in inflammatory bowel diseases (comprised of ulcerative colitis and Crohn’s disease)

have not been elucidated satisfactorily. The critical role of appendicitis followed by appendicectomy in ameliorating or preventing development of human ulcerative colitis [8–10] and Crohn’s disease [9,11] has been demonstrated reproducibly,

despite controversies surrounding that role in Crohn’s disease [12]. However, the protective effect is limited to patients having surgery before 20 years of age [10]. Additionally, studies in three different murine models including the T cell receptor-α mutant colitis model [13], the dextran sulphate sodium-induced colitis model [14] and the adoptive T lymphocyte transfer colitis model [15] have demonstrated that removal of the caecum prevented the development of experimental colitis. We recently developed a murine model of appendicitis by constructing a pouch and ligature – occluding the murine equivalent of find more the human appendix, the caecal patch, followed by appendicectomy (removal of the murine caecal patch) [16]. The appendiceal histopathology in this appendicitis model closely resembles human appendicitis and reveals an age-dependent protection against trinitrobenzene sulphonic acid (TNBS)-induced colitis offered by appendicitis and appendicectomy [16]. Appendicitis per se or appendectomy per se was not protective. This protection offered by appendicitis followed by appendicectomy was dependent upon appendiceal interleukin (IL)-10-producing CD4+ and CD8+ regulatory T lymphocytes which proliferated in the appendix and migrated to the distal colon (Ng et al., submitted).

As surprising as it may appear, the presence of bacteria in the gut lumen contributes to the integrity of the intestinal epithelial barrier [26]. This is achieved by a series of molecular events induced

by the gut microbiocenosis. One event is increased synthesis of pIgR (epithelial polymeric immunoglobulin receptor), which provides the translocation of sIgA (secretory IgA) DAPT in vivo from LP in the intestinal lumen [27] (Fig. 1). sIgA, a valuable local defence tool, prevents unwanted antigens from adhering to the intestinal mucosa. pIgR-deficient mice that lack sIgA and sIgM exhibit an altered barrier function of the intestinal epithelium, but are also more prone to gaining oral tolerance [28]. This argues for a dual function of a competent intestinal mucosa, ensuring both protection against harmful agents and acceptance of small amounts of certain antigens which induce the development of Tregs. Another event triggered by some species of commensal bacteria is the abrogation of polyubiquitination, necessary for IκB-α degradation [29]. IκB-α is the molecule that controls the activity of nuclear factor (NF)-κB, acting as its suppressor. IκB-α degradation is dependent on both phosphorilation and polyubiquitination. A longer life of IκB-α due to suppressed polyubiquitination will result in reduced Selleckchem EPZ6438 proinflammatory activity of NF-κB. The barrier function of the enterocytes is completed by anti-microbial peptides (AMP)

and mucin proteins production [30]. We must specify that AMPs are produced mainly by Paneth cells, and intestinal mucus is the major result of goblet cell activity. Enterocytes produce mucin proteins, which compose the glycocalix, and anti-microbial factors such as β-defensins and hepatocarcinoma–intestine–pancreas/pancreatitis-associated protein (HIP/PAP) [31]. β-defensins bind to the microbial cell membrane and, once embedded, form pore-like membrane defects that allow efflux of ions and nutrients. HIP/PAP is a member of the C-type lectin family and has a promising potential for PD184352 (CI-1040) tissue regeneration and protection against apoptosis and cellular stress, being already tested as an agent for the therapy of acute

liver failure in humans [32]. Human β-defensin-1 (HBD-1) is expressed constitutively in enterocytes, while HBD-2 and HBD-3 are induced by microbial products and inflammatory cytokines [33,34]. Inducible expression of HBD-2 and HIP/PAP proteins in enterocytes was shown to be influenced by Toll-like receptor (TLR)- or myeloid differentiation primary response gene 88 (MyD88)-dependent signalling [35,36]. β-defensins may also chemoattract immature DCs [37] and have direct effects on DC function by inducing up-regulation of co-stimulatory molecules and DC maturation [38]. Enterocytes possess specialized receptors of the pathogen recognition receptors (PRR) family, such as TLRs and nucleotide oligomerization domain (NOD)-like receptors.

However, during the terminal X-396 stages of synapse development, which is marked by close approximation of the cytolytic granules to the interface, there was clear

molecular remodeling at the IS. In YTS-721.221 conjugates, IQGAP1 and F-actin were partitioned away from the IS immediately prior to degranulation in the mature synapses (Fig. 9, compare A with B). Furthermore, this partitioning of F-actin and IQGAP1 was limited to those image planes that correlated with juxta-positioning of the cytolytic granules at the synapse (Supporting Information Fig. 1). This analysis was further extended to pNK cells. We observed striking similarities between pNK-mediated K562 killing and YTS-mediated 721.221 killing mechanism. In pNK target conjugates, IQGAP1 and F-actin levels decreased from the synapse as the granules approached the IS. Both species of proteins were clearly excluded from the IS immediately prior to final degranulation stage (Fig. 9D). The partitioning was strictly limited to the regions occupied by the granules (indicated by * in Fig. 9D and Supporting Information Fig. 2).

Hence, in NK cells both of these molecules appear to be under strict spatial and temporal regulation which is coordinated with the positioning of cytolytic granules relative to the IS. These observations highlight the mechanistic similarities between the different NK cells and further

our suggested role of IQGAP1 in NK-cell function. The rationale for undertaking the Nivolumab present study was to determine if IQGAP1 was required for NK effector functions. Previous studies on cytotoxic T cells indicated that IQGAP1 underwent marked distributional changes as the IS matured 10. However, neither the requirement for, nor the specific role(s) of IQGAP1 in the cytotoxic process were clear from these studies. The results of the present investigation clearly demonstrate an obligate requirement for IQGAP1 in Cediranib (AZD2171) NK-mediated cytotoxicity. It appears that IQGAP1 plays critical roles in multiple aspects of the events required for this process including granule reorientation and reorganization at the NKIS. IQGAP1 is a multidomain protein with the potential to interact with cytoskeletal structural elements as well as several regulators of cytoskeletal organization. Importantly, the ability of IQGAP1 to simultaneously interact, through its N- and C-terminal regions, respectively, with F-actin filaments and microtubules, provides a potential mechanism to link these cytoskeleton elements 18, 19, 30. Indeed, IQGAP1 has been implicated in a diverse range of functional and morphological changes that are dependent on cytoskeletal patterning. These include lamellipodia, adherens junctions, pseudopodia, and the formation of phagocytic cups 15, 22, 31–33.

This may suggest that while high levels of FoxP3 expression are required to prevent Th2 differentiation, a reduced level of FoxP3 expression is still sufficient to prevent the emergence of Th1 and potentially Th17 responses. Indeed, mature Tregs

in which FoxP3 expression has been ablated (due to an induced cre-mediated deletion of a floxed FoxP3 allele) develop a capacity to produce considerable amounts of IL-2, tumour necrosis factor (TNF)-α, IFN-γ and IL-17 [36]. Furthermore, upon transfer to lymphopenic hosts, Tregs in which FoxP3 had been deleted failed to show suppressive function, but rather contributed to inflammation and predominated among tissue infiltrating lymphocytes. Any scientific readout is only as robust as the assay used to achieve it, and the assays used to measure suppressive potential in vitro and in vivo have different strengths and weaknesses. selleck inhibitor This must be borne in mind because, like many biological phenomena, Treg activity in vivo cannot always be predicted accurately from their behaviour in vitro and vice versa [37–39]. The techniques used to interrogate Treg activity HIF inhibitor have changed over time, reflecting our changing understanding of how Tregs function. The initial identification of the role of Tregs in preventing autoimmunity came from observations of autoimmune pathology in mice lacking CD25+ T cells [13]. Subsequently, assaying the capacity of CD25+

Tregs to suppress the proliferation of their CD25– counterparts in vitro became the gold standard measurement of suppressive potential (see below [40]) and antibody-mediated depletion of CD25+ T cells in vivo was adopted as an imperfect but practical strategy to assess the role GPCR & G Protein inhibitor of Tregs in models of infection, allergy and autoimmunity [41–44]. These in vitro and in vivo experiments identified many of the suppressive pathways utilized by Tregs– IL-2 deprivation [40], expression of CTLA-4 and glucocorticoid-induced TNF receptor-related protein

(GITR) [45,46], cell contact-dependent suppression [40], production of anti-inflammatory cytokines such as IL-10, TGF-β and IL-35 [31,47–51] and the expression of enzymes promoting tryptophan catabolism and adenosine production [52–54]. Throughout this time the role of Tregs was seen primarily as preventing the activation and differentiation of autoreactive T cells and the main arena for suppressive activity was considered to be the draining lymph node during naive T cell priming [39,55,56]. Their potential to modulate ongoing responses, or to display suppressive activity at sites of inflammation, was harder to address using such assays, although promising findings have been reported [57–59]. On this point, it is important to remember that Tregs can have controlling effects on inflammation through actions on a range of immune cell populations, not simply T cells.

Our findings are compatible with those of the empirical studies discussed above. With regard to feature of the patient’s history, our findings confirm those of Ito et al. (2000),[17] recurrent UTI and a history of allergy of some kind was reported in 28 and

19% of cases, respectively, compared to 28 and 20% in our study. This finding suggested that medical history of IC patients in Taiwan is similar to that in Japan. Our study is different from the study conducted by Choe et al. (2011)[18] with regard to the study method. All of our patients were diagnosed check details based on the physician-assigned diagnoses with cystoscopic finding treated as the major criteria, complemented by the symptoms, including frequency and pain, noted in the NIDDK criteria. However, the method

of Choe et al. was performed by telephone interview using O’Leary-Sant IC Symptom and https://www.selleckchem.com/products/pci-32765.html Problem (OLS) index. Therefore, it may be unsuitable to compare the two patient groups. Interstitial cystitis patients in Taiwan have lower economic status but lower impact on QOL than Western patients. However, the sexual-related pain and sleeping disorder were higher than previously thought and deserve our attention for improving QOL of the patients. In order to know if there is any difference of characteristic between the IC patients in Taiwan and in other countries, further research on epidemiology should be conducted. This is what we should strive to achieve in the future. We thank Dr Wei-Chih Chen for assisting us in writing this manuscript. The authors have no conflicts of interest. “
“Objectives: While detrusor-sphincter dyssynergia (DSD) occurs in conjunction

with lesions between Dolutegravir concentration the brainstem and the sacral cord, it is not well known whether sacral/peripheral lesions contribute to DSD. We studied the relationship between DSD and sacral/peripheral lesions. Methods: One hundred and forty-four patients with diverse neurologic etiologies underwent urodynamic study and analysis of motor unit potentials in the external sphincter muscles, 117 of whom were able to void during a urodynamic test. Sacral/peripheral lesion (SPL) is defined as neurogenic change in motor unit potentials. Detrusor overactivity (DO) is defined as involuntary detrusor contractions during the filling phase, which commonly occurs in lesions above the sacral cord. We considered DO as a putative indicator of supra-sacral lesion. Results: DSD was found in 44 (30.6%), SPL in 71 (49.3%), and DO in 83 (57.6%) of 144 patients, respectively. The incidence of DSD was the same in the SPL positive group (31%) and the SPL negative group (30.1%). By contrast, within the subgroup of patients without DO, the incidence of DSD was significantly more common in the SPL positive group (41.4%) than in the SPL negative group (25.0%) (P < 0.05).