Associations with other components were generally weak or null, except for the association of nocturia Proteasome inhibitor with increased odds of hypertension (adjusted OR 2.00, 95% CI 1.27–3.14) and increased triglycerides (adjusted OR 1.64, 95% CI 1.07–2.51), and mild LUTS (AUASI 2–7) and mild incomplete emptying with a waist circumference greater than 102 cm. Kupelian et al.24 hypothesized that possible pathophysiological mechanisms to explain the relationship of voiding rather than storage symptoms with MS of BACH survey

data the influence of hyperglycemia on the parasympathetic neurons in the pelvic ganglion. Chronic hyperinsulinemia induced peripheral neuropathy resulting in increased bladder neck obstruction and reduced bladder contractility.7,25 Increased glucose levels are likely to be accompanied by hyperinsulinemia which results in an increase in insulin-like growth factor (IGF). IGF is involved in prostate growth.26 In the Baltimore Longitudinal Study on Aging (BLSA) cohort, men with elevated fasting glucose were three times more likely to have BPH than men with normal glucose levels.27 Increased fasting glucose and diabetes were also associated with the presence of LUTS in this cohort study. Other studies including

the NHANES III cohort (Rohrmann et al.28), Flint Men’s Health Study,29 and a case-control study by Neuhouser et al. (LUTS-MS30) also demonstrated the association of IGF with the risk of LUTS in men. C-reactive protein (CRP), a well-known inflammatory GSK458 concentration marker, is known to have an association

Astemizole with cardiovascular diseases. Kupelian et al.31 assessed the relationship between CRP level and LUTS, and found a statistical significant association between CRP levels and overall LUTS among both men and women. There was a dose-response relationship between CRP levels and associated LUTS. However, Hong et al.32 studied the relationship between CRP and overactive bladder (OAB) in women without MS and found no significant correlation between CRP level and OAB symptoms. Many studies support the association of CRP and LUTS, but further research should be conducted to differentiate the significance of inflammatory process with or without MS in the development of LUTS. The prevalence of MS is increasing all over the world and Korea is not an exception. Most of the studies of MS and LUTS in Korea are risk analyses of BPH. Jang et al.33 analyzed the association of MS and BPH in 1412 men. They found that there was a significant correlation between each MS factor and prostate volume. Koo et al.34 also reported that MS is associated with prostate volume-related factors, but not with voiding dysfunction in Korean men aged 60 years or older. Among the subcategories of MS, they reported that obesity is the factor most strongly related to prostate volume. Yim et al.35 studied the correlation of prostate volume with MS and its related parameters.

Others contend that flow Selleck Stem Cell Compound Library crossmatching adds important information on the strength of donor-specific antibody reactivity and should be considered in the context of donor-specific antibody results and CDC crossmatching to help develop an overall opinion on the likelihood of immune complications. The area remains controversial and no clear recommendation can be made at this

time. A 65-year-old man who has end-stage renal failure as a result of ANCA vasculitis has been on dialysis for 4 months. He has had three blood transfusions in the past. His wife has been assessed as a possible renal donor for him. Their immune compatibility is defined below. Is it safe to proceed with transplantation? (Table 5) Proceeding with transplantation in the setting of a negative CDC and flow crossmatch is generally considered as low risk and is reasonable without a desensitization protocol. The issue here is the HLA A23 DSAb detected by Luminex antigen-coated beads (Luminex). Despite the lack of reaction on crossmatching the presence of a DSAb may have prognostic significance for the transplanted kidney and should be further considered before proceeding.23,24 Many transplant units screen all patients on their cadaveric waiting list for anti-HLA antibodies using Luminex and if positive the specificity of the anti-HLA Abs are defined. This means that the transplant clinician can perform a ‘virtual crossmatch’ at the time of a cadaveric renal

transplant PLX4032 purchase offer as well as in the live donor transplant setting. While outcomes for DSAb positive transplants are inferior to DSAb negative transplants a decision to proceed with a DSAb-positive, CDC crossmatch-negative transplant, in a highly sensitized recipient, may in some cases be in the patient’s best interests. Virtual crossmatching refers to the comparison of the anti-HLA antibodies of the recipient, as defined by Luminex, with the HLA of the donor.25 If there is a DSAb present this would represent a positive virtual crossmatch. Antibodies are defined against HLA class I and II antigens. Synthetic

microspheres (beads) coated with HLA antigens are commercially available for this testing. Beads may be coated with multiple HLA antigens for Baf-A1 nmr screening purposes or a single HLA antigen for defining specificity of antibodies more precisely (see Fig. 3). For the virtual crossmatch, multiple beads each coated with a single HLA antigen are mixed with recipient serum. Anti-HLA antibodies present bind to the beads and are detected by an isotype-specific (e.g. IgG) detection antibody via flow cytometry. Unique fluorochromes within the beads mark the HLA antigen specificity of each bead (reviewed in26). This technique is as sensitive as flow crossmatching and provides the specificity of the antibody.27 It has long been established that the presence of antibodies that react with human leucocytes portend worse long-term graft survival.

However, eosinophils were not able to ingest non-opsonized yeasts (eosinophils plus opsonized C. neoformans versus eosinophils plus non-opsonized C. neoformans, P < 0·05). C. neoformans phagocytosis was blocked by anti-FcγRII and anti-CD18 mAbs (Fig. 1b), suggesting that both receptors are involved in this phenomenon. Flow cytometric analysis of MHC class II surface expression demonstrated that the ingestion of opsonized yeasts

stimulated the increase of both the percentage and the mean fluorescence intensity (MFI) of MHC class II on eosinophils (Fig. 2a) (eosinophil plus opsonized C. neoformans versus eosinophil plus non-opsonized C. neoformans; P < 0·02). According to the observations for C. neoformans Lumacaftor cell line phagocytosis, MHC class II expression by eosinophils incubated with opsonized yeasts

was completely inhibited by FcγRII and CD18 (Fig. 2b). Furthermore, the increased expression of MHC class II on eosinophils treated with opsonized C. neoformans was significantly higher in cultures with GM-CSF than in its absence (60% versus 20%; P < 0·02) (Fig. 2b). We further analyzed buy MG-132 the expression of MHC class I, CD80 and CD86 on the surface of eosinophils incubated with opsonized or non-opsonized C. neoformans, in the presence or absence of GM-CSF. Figure 3a demonstrates that in the presence of GM-CSF, opsonized C. neoformans drastically increased the percentage and MFI of MHC class I expression on eosinophils (eosinophil plus opsonized C. neoformans versus eosinophil plus non-opsonized C. neoformans; P < 0·01). Moreover, opsonized C. neoformans significantly up-regulated the surface expression of CD80 and CD86 on these cells (eosinophil plus opsonized C. neoformans versus eosinophil plus non-opsonized C. neoformans; P < 0·05). Similar results were observed in cultures performed in the absence of GM-CSF (Fig. 3b). Therefore, in contrast to that observed for MHC class II, opsonized

C. neoformans up-regulated the expression of MHC class I and costimulatory molecules, regardless of the presence of GM-CSF O-methylated flavonoid in the medium. The levels of IFN-γ, TNF-α and IL-12p40 were also quantified in the supernatants of eosinophils obtained 24 hr after culture with opsonized or non-opsonized C. neoformans in the presence or absence of GM-CSF. Figure 4 shows the production of cytokines in cultures containing GM-CSF, revealing that in the presence of opsonized C. neoformans, eosinophils secreted significant amounts of IFN-γ, TNF-α and IL-12p40, compared to cells incubated in medium alone or with non-opsonized yeasts (P < 0·03). In contrast, Th2 cytokines (such as IL-4, IL-10 and IL-13) were not detected in these culture supernatants. Almost the same results were obtained in the absence of GM-CSF (data not shown). In order to evaluate the production of fungicidal molecules by GM-CSF-stimulated eosinophils incubated with opsonized C.

An effective way of visualizing the receptor-binding motif is by using sequence logos. Sequence logos were introduced by Schneider and Stephens14 to graphically represent the sequence motif contained in a set of aligned sequences, where at each position, the frequency of all amino acids is displayed as a stack of letters. The height of a column in the logo is given as the information content in bits of the alignment at that particular position, and the relative height of individual letters is proportional to the frequency of the corresponding amino

acid at that position. Alvelestat In this paper, we use such sequence logos to display the HLA-DP and HLA-DQ binding specificities identified by NNAlign. The five HLA-DP allelic variants were chosen by Wang et al.7 to cover a high percentage of the human population. Only considering the β-chain, more polymorphic than the α-chain and the main determinant for HLA-DP binding,15,16 the allele choice provides coverage of about 92% of the average population at the DPB1 locus.9 The sequence motifs identified by NNAlign for the five HLA-DP molecules are shown in Fig. 1. In general, all variants share a common pattern characterized by anchors at positions P1 and P6, with strong preferences for phenylalanine (F) and

other aromatic or hydrophobic amino acids. Additionally, some molecules appear to ICG-001 clinical trial have a hydrophobic many preference at P9 especially for leucine (L). This P9 anchor was previously described for DPB1*04:02,17 but here we observe it also

for other variants such as DPA1*02:01-DPB1*01:01 and DPA1*02:01-DPB1*05:01. In some instances, and notably for DPA1*03:01-DPB1*04:02, the residues at position P7 appear to have influence on the binding specificity of the molecule. This has not been described in previous reports. Another small exception to the P1–P6 hydrophobic/aromatic pattern is observed in the allelic variant DPA1*02:01-DPB1*05:01, where the positively charged amino acids R and K are moderately preferred at P1 together with hydrophobic ones, as was also previously noted.9 Taken as a whole, there appears to be a large overlap in the peptide-binding specificities of the five DP molecules, characterized by strong hydrophobic/aromatic anchors at P1 and P6, with the few exceptions noted above. Consistent with these observations, previous studies have found considerable overlaps in the peptide repertoires that can bind different DP alleles, and suggested the existence of a DP supertype encompassing the most common variants.9,17 Greenbaum et al.,18 on the basis of shared binding repertoires, suggested the presence of two DP supertypes: a ‘main DP’ supertype (composed of DPB1*01:01, 05:01 and 04:02) and a DP2 supertype (DPB1*02:01 and 04:01).

CDPs further differentiate into classical DCs (cDCs) and plasmacytoid DCs (pDCs). Here, we studied the impact of histone acetylation AZD6738 cell line on DC development in C57BL/6 mice by interfering with histone acetylation and deacetylation, employing histone deacetylase (HDAC) inhibitors. We observed that commitment of MPPs into CDPs was attenuated by HDAC inhibition and that pDC development was specifically blocked. Gene expression profiling revealed that HDAC inhibition prevents establishment of a DC-specific gene expression repertoire. Importantly,

protein levels of the core DC transcription factor PU.1 were reduced in HDAC inhibitor-treated cells and consequently PU.1 recruitment at PU.1 target genes Fms-like tyrosine kinase 3 (Flt3), interferon regulatory factor 8 (IRF8),

and PU.1 itself was impaired. Thus, our results demonstrate that attenuation of PU.1 expression by HDAC inhibition causes reduced expression of key DC regulators, which results in attenuation of DC development. We propose that chromatin modifiers, such as HDACs, are required for establishing Selleck Tanespimycin a DC gene network, where Flt3/STAT3 signaling drives PU.1 and IRF8 expression and DC development. Taken together, our study identifies HDACs as critical regulators of DC lineage commitment and development. “
“Neutrophils are the primary cells contributing to initial defense against Rucaparib order mycobacteria. Yet, little is known about the potential of various mycobacterial strains to stimulate neutrophils. This study was focused to compare the differential capacity of vaccine strains, Mycobacterium bovis bacillus Calmette–Guerin (BCG) and

Mycobacterium indicus pranii (Mw), and laboratory strain H37Rv to activate and enhance neutrophil functions. The expression of phenotypic markers like Fcγ receptor, toll-like receptor (TLR), and chemokine receptor; secretion of pro-inflammatory cytokines; and the rate of apoptosis were studied in infected neutrophils. Increased expression of CD32, CD64, TLR4, and CXCR3; increased TNF-α secretion; and downregulation of early apoptosis were observed in H37Rv-infected neutrophils. Among the vaccine strains, BCG increased the expression of only CD32 on neutrophils, while Mw was comparatively ineffective. To understand the paracrine role of neutrophils, the supernatants from infected neutrophils were used to stimulate monocytes and T helper cells. The secretory molecules from all infected neutrophils increased the expression of CCR5 on monocytes, whereas only H37Rv-infected supernatant increased the expression of CCR7 on monocytes and CD69 on T cells. Thus, H37Rv was more effective in activating neutrophils and in turn stimulating monocytes and T cells. By comparison, vaccine strains were less effective in modulating neutrophil functions.

Furthermore, the chronic infection stage of T. congolense is dominated by anti-inflammatory cytokines, such as IL-4, IL-10 [24] and possibly also TGF-β. Indeed, to limit inflammatory pathogenicity and premature death of the host, Plasmodium species induce a similar switch to an anti-inflammatory environment, whereby TGF-β plays an essential role [39], suggesting that a comparable mechanism might be important during Trypanosoma infections. Besides IL-4, also various M1- and M2-associated stimuli induce Cldn2 mRNA, and thus, its association with classical or alternative macrophage activation is less clear. In vivo, macrophage

Cldn2 induction levels during parasitic infections are minor compared with the high claudin-2 mRNA levels observed Carfilzomib order in TAMs. In comparison with the full

set of genes tested and published in TS/A TAM [25], claudin-2 situates amongst the top 30% in terms of fold upregulation compared to PEM. The mechanisms underlying the strong association of claudin-2 mRNA with TAM remain unclear. Possibly, the complex mixture of stimuli present within the tumour microenvironment is more appropriate for optimal Cldn2 induction, as opposed to the herein Osimertinib tested triggers in vitro. Hence, while Cldn2 is not appropriate to distinguish between bona fide CAMs or AAMS, this tight junction–associated gene could be used as a tumour-associated macrophage marker. IL-4 was identified as most potent Cldn11 inducer in all macrophage types tested, and this effect was nearly absent in STAT6-deficient macrophages. In agreement with our findings, Cldn11 was listed before as IL-4-inducible gene in mouse BMDM [22]. Importantly, IFN-γ and LPS did

not affect Cldn11 expression levels. Hence, claudin-11 behaves like a typical marker gene for mouse AAMs. This conclusion is corroborated in vivo, where claudin-11 mRNA is only significantly induced in typical IL-4/IL-13-induced AAMs isolated during the chronic stage of T. crassiceps helminth infections, but not in TAMs or macrophages from Trypanosoma-infected filipin mice. In this respect, Cldn11 seems to be a marker gene for AAMs that develop in a polarized Th2 cytokine environment and not for M2 that develop in a more complex environment like a tumour. Overall, we identified the tight junction component claudin-11 as a novel IL-4-induced gene in AAMs. Cldn1 is mainly associated with TGF-β-activated macrophages, and hence, Cldn1 expression could be used as a tracer for TGF-β-exposed macrophages. Finally, Cldn2 can be induced in macrophages by various stimuli in vitro and is abundantly expressed in vivo by tumour-associated macrophages. The authors thank Ella Omasta, Marie-Thérèse Detobel, Nadia Abou, Lea Brys and Eddy Vercauteren for their technical aid. This work was supported by a doctoral grant from ‘FWO-Vlaanderen’ to J.V.d.B and K.M.

16,31,32 The up-regulation of β-tubulin-specific IL-10 production by splenocytes suggests the possibility that hASCs may induce IL-10-producing Treg cells31,33 in EAHL mice. We therefore examined the possibility that this suppression was mediated by the production of Treg cells in vivo. We found a significantly elevated percentage of CD4+ CD25+ Foxp3+ cells from EAHL mice exposed to hASCs compared with the PBS control groups. Also, these hASC-induced Treg cells potently inhibited the proliferative response of autoreactive T cells in vitro, and these effects were significantly abrogated

by anti-IL-10 antibodies. Therefore, hASC treatment might induce IL-10-secreting click here β-tubulin-specific CD4+ CD25+ Foxp3+ Treg cells in mice with EAHL that mediate T-cell tolerance. In summary, the present study demonstrated that hASCs display a therapeutic potential and suggests that hASCs may provide a novel therapeutic approach for AIED. Mechanistically, our results indicate that the hASCs inhibit the Th1/Th17 cell responses through the generation of IL-10-secreting Treg cells with the capacity to suppress autoreactive T-cell responses, thereby maintaining self-tolerance. We thank RNL-bio (Korea) for providing

the funding for this research project. The authors declare no financial conflicts of interest. “
“Because regulatory T (Treg) cells play an important role in modulating the immune system response against Roxadustat Sclareol both endogenous and exogenous antigens, their control is critical to establish immunotherapy against autoimmune disorders, chronic viral infections and tumours. Ribavirin (RBV), an antiviral reagent used with interferon, is known to polarize the T helper (Th) 1/2 cell balance toward Th1 cells. Although the immunoregulatory mechanisms of RBV are not fully understood, it has been expected that RBV would affect T reg cells to modulate the Th1/2 cell balance. To confirm this hypothesis, we investigated whether RBV

modulates the inhibitory activity of human peripheral CD4+ CD25+ CD127− T cells in vitro. CD4+ CD25+ CD127− T cells pre-incubated with RBV lose their ability to inhibit the proliferation of CD4+ CD25− T cells. Expression of Forkhead box P3 (FOXP3) in CD4+ CD25− T cells was down-modulated when they were incubated with CD4+ CD25+ CD127− T cells pre-incubated with RBV without down-modulating CD45RO on their surface. In addition, transwell assays and cytokine-neutralizing assays revealed that this effect depended mainly on the inhibition of interleukin-10 (IL-10) produced from CD4+ CD25+ CD127− T cells. These results indicated that RBV might inhibit the conversion of CD4+ CD25− FOXP3− naive T cells into CD4+ CD25+ FOXP3+ adaptive Treg cells by down-modulating the IL-10-producing Treg 1 cells to prevent these effector T cells from entering anergy and to maintain Th1 cell activity.

Furthermore, compared with uninfected controls, BGJ398 purchase patients co-infected with S. mansoni and S. haematobium produce significantly greater amounts of immunoregulatory IL-10 when stimulated with 0-3 h RP but not with the control ligand zymosan. Although the sample sizes in each of our three groups (un-infected, S. mansoni-infected, and S. mansoni and S. haematobium co-infected) were limited, this initial investigation showing

a significant 0–3 h RP-specific up-regulation of IL-10 in co-infected patients highlights the potential importance of E/S products released from the invasive stage of the parasite in schistosome-infected humans. This provides justification for further larger studies of human immune responsiveness to cercarial E/S antigens. By collecting WB culture supernatants 24 h after stimulation, we specifically targeted the early production of cytokines released by innate immune cells in WB such as monocytes. We had previously shown using murine macrophages that 0–3 h RP induces abundant IL-10 within 24 h, as well as IL-12p40 and IL-6, and that cytokine production was largely dependent upon functional TLR4 [8]. Helminth E/S products, such as 0–3 h RP, are known to have greater stimulatory activity with regard to innate cytokine NVP-BEZ235 nmr production than preparations dominated by somatic components (e.g. soluble whole cercariae) [8], which may be more relevant to stimulation of the acquired immune response. We compared

the cytokine response to 0–3 h RP with zymosan pheromone (derived from the yeast Saccharomyces) as a control ligand as like 0–3 h RP, it is biochemically heterogeneous and enriched for glycosylated proteins [9]. Zymosan, like 0–3 h RP, also stimulates innate immune cells to drive CD4+ lymphocytes

towards a Th2 phenotype [25]. Schistosome infection status at the time of sample collection from individuals in the endemic region was the major factor in determining whether stimulation of WB cells using 0–3 h RP enhances levels of IL-10. Co-infection with S. mansoni and S. haematobium was associated with the highest production of 0–3 h RP-specific IL-10 relative to uninfected participants. This was not observed in response to the control ligand zymosan or in spontaneous IL-10 production by un-stimulated WB (data not shown). The production of IL-10 can be usefully expressed as ratio compared with production of pro-inflammatory TNFα. As a precedent for this, urinary tract morbidity in S. haematobium-infected patients was linked to a lower ratio of IL-10: TNFα production as part of the acquired immune response [28]. Here, we found that the ratio of 0–3 h RP-specific IL-10: TNFα was higher in infected than in uninfected individuals, supporting the hypothesis that cercarial E/S stimulates a regulatory immune phenotype through enhancement of innate/early IL-10 production relative to the production of the pro-inflammatory cytokine TNFα [5, 27]. The higher ratio of IL-10: TNFα in subjects co-infected with S.

We thank the NIH/NCRR Resource Erlotinib ic50 for Nonhuman Primate Immune Reagents (Emory University, Atlanta, GA) for the macaque recombinant proteins; the NIH Division of Veterinary Resources (Bethesda, MD) for providing macaque blood samples; Dr Bernard A.P. Lafont (Laboratory of Molecular Microbiology, NIAID/NIH) for providing 721.221 cells; Drs Alison E. Hogg and L. Jean Patterson (Vaccine Branch, NCI/NIH) for helpful discussions; and Katherine M. McKinnon (Vaccine Branch Flow Cytometry Core, NCI/NIH) for expert advice. This research was supported by the Intramural Research Program of

the NIH, National Cancer Institute. Figure  S1. CD8α- macaque NK cells represent 35 percent of CD3-CD8α+ lymphocytes and express both CD56 and CD16. “
“Experimental autoimmune thyroiditis (EAT) is commonly induced by thyroglobulin (Tg) or Tg peptides in mice genetically susceptible to thyroiditis. In the present study, we investigated the immunogenic and pathogenic potential of a novel 20mer human Tg peptide, p2208 (amino acids 2208–2227), in mouse strains classified as low (LR) or high (HR) responders in EAT. The peptide was selected for its content in overlapping binding motifs for MHC class II products, associated with either resistance (Ab), or susceptibility

(As, Ek) to EAT. We therefore immunized LR BALB/c (H-2d) and C57BL/6 (H-2b) strains, as well as HR CBA/J (H-2k) enough and SJL/J (H-2s) mice with 100 nmol of p2208 in adjuvant PD-0332991 chemical structure and collected their sera, lymph nodes and thyroid glands for further analysis. The p2208 peptide was found to contain B-cell and cryptic T-cell epitope(s) in two of the

four strains examined, one LR and one HR. Specifically, it elicited direct EAT in C57BL/6 mice (two of seven mice, infiltration index 1–3), as well as in SJL/J mice (two of six mice, infiltration index 1–2). Such an EAT model could provide insights into the immunoregulatory cascades taking place in resistant hosts. “
“An oral delivery system based on ApxIIA#5-expressed on Saccharomyces cerevisiae was studied for its potential to induce immune responses in mice. Murine bone marrow-derived dendritic cells (DCs) stimulated in vitro with ApxIIA#5-expressed on S. cerevisiae upregulated the expression of maturation and activation markers, leading to production of tumor necrosis factor-α, interleukin (IL)-1β, IL-12p70 and IL-10. Presentation of these activated DCs to cluster of differentiation CD4+ T cells collected from mice that had been orally immunized with the ApxIIA#5-expressed on S. cerevisiae elicited specific T-cell proliferation.

Looking closely at LUTS, as compared with the control subjects, the drug-naïve depressive patients had significantly more cases of urinary urgency (20.9% of women; 25.9% of men), nighttime frequency (15.2, 30.0%), urinary incontinence (9.1% women); retardation in initiating urination (13.1% men), prolongation/weak stream (23.0% men), intermittency (9.8% men), and sensation of residuals (12.1, 19.7%) P < 0.01, 0.05 (Fig. 1). The quality of life (QOL) index for the drug-naïve, depressive patients was also significantly higher (9.5, 8.3%). Therefore, both storage and evacuation symptoms are common; however, among these, OAB is the most striking feature of LUTS in major depression.

A comparison of age (those 49 years old and under and those 50 years old and over)

in the control group showed higher incidence of bladder dysfunction with age (without significance). In the depressive patients nighttime frequency, prolongation/weak LY294002 AZD4547 nmr stream (P < 0.01), urinary urgency, incontinence (P < 0.05), and QOL disturbance (P < 0.01) were more common in older patients. A comparison of sex in the control group showed nighttime frequency to be more common in men (P < 0.05). In the depressive patients, nighttime frequency and retardation in initiating urination (p < 0.05) were more common in men. A comparison of disease duration showed no difference for any category of bladder dysfunction. Considering the effect of previous antidepressant treatment, no difference was found in the frequency of urinary urgency or delayed start between the drug-naïve group and the medicated group, who were taking tricyclic antidepressants (imipramine hydrochloride, amoxapine, etc.), tetracyclic antidepressants (mianserin hydrochloride, etc.), selective serotonin reuptake inhibitors (SSRIs) (paroxetine

hydrochloride, fluvoxamine maleate, etc.), serotonin noradrenaline reuptake inhibitors (SNRI) (milnacipran hydrochloride, etc.), and others (benzodiazepine derivative, etc.). Among patients visiting urology clinics because of LUTS, psychogenic bladder dysfunction (PUD) has been well documented, and includes symptoms of OAB and voiding difficulty/retention (also called paruresis[26] or bashful bladder syndrome).[27] TCL We reported on 16 PUD patients in a previous study.[28] The age of this previous study sample was relatively young (mean 37 years [15–69 years]), which is almost the same as that in the depression cohort described above (mean 42 years). The sex ratio was female dominant (6 men to 10 women). All of these features were consistent with previous findings.[29, 30] The most common precipitating factors to trigger LUTS were traffic accidents in three cases (in two cases, LUTS appeared just after the accident; in the other LUTS appeared 3 months after the accident) and an inability to cope with families in three cases, followed by divorcing parents in two cases.