To further examine whether Gal-1–induced HepG2 cell polarization affects the structural and/or functional integrity of BC, we evaluated the immunolocalization of MDR1 and MRP2 on cells cultured for 48 hours in the absence or presence of rGal-1. Both MDR1 and MRP2 localized exclusively to the apical membrane surface, indicating that sorting and transport of MDR1 and MRP2 toward the apical membrane operates properly even in the presence of rGal-1 stimulation (Fig. 6A). Expression levels of these canalicular proteins were not altered by rGal-1 (Supporting Information Fig. 2A). Furthermore, when we double-stained

Gal-1–treated cells for Rapamycin in vivo MRP2 and actin, the structures stained with TRITC-phalloidin

were also immunostained for MRP2 (Fig. 6B), indicating that Gal-1 promotes the polarized phenotype through the formation of apical lumens. To evaluate the functional integrity of BC in rGal-1–treated cells, MRP2 secretory function was further examined. Both the transfer and secretion of glutathione methylfluorescein occurred in the presence of rGal-1 (Fig. 6B) at the same levels as in control cells (Supporting Information Fig. 2C). Therefore, Gal-1 can accelerate HepG2 cell polarization while maintaining BC structure and functional integrity. To examine the signaling pathways triggered by Gal-1 in HepG2 cells during polarization, compound screening assay we exposed cells to rGal-1 in the presence of specific pharmacological inhibitors. Interestingly, in the presence of wortmmanin or PD98059, rGal-1 effects were significantly attenuated compared with control values after 48 hours (Fig. 7A), suggesting involvement of PI3K and ERK1/2-mediated signaling pathways in this galectin effects. Because activation of PKA has been also implicated in the biogenesis of the BC,20, 21 we next explored whether this pathway was also involved in Gal-1–mediated enhancement of BC formation. When HepG2 cells were cultured in the presence 上海皓元医药股份有限公司 of both H89 and rGal-1, development of BC was significantly reduced compared with HepG2 cells cultured in the presence of Gal-1 alone (Fig. 7A). These results indicate

that Gal-1 promotes HepG2 cell polarization through PI3K, ERK1/2 MAPK, and/or PKA signaling pathways. To further confirm signaling pathways activation in HepG2 cells, we finally assessed ERK1/2 and Akt phosphorylation (Fig. 7B). When cells were incubated in serum-free medium in the presence of soluble rGal-1 for 1 minute, a rapid ERK1/2 phosphorylation was observed, which was sustained up to 5 minutes and declined after 10 minutes of rGal-1 exposure. However, no Akt phosphorylation was detected in cells treated with rGal-1 for up to 60 minutes of incubation (Fig. 7B).Therefore, Gal-1 triggers HepG2 cell adhesion and polarization through activation of upstream signaling pathways involving PI3K, MEK ERK1/2, and PKA.

Thirty-seven percent reported a seasonal predilection of the cluster periods, and 58% a diurnal periodicity of attacks. Eighty percent often or always had headache attacks during sleep, the most frequent time interval being at 12:00-4:00 am. Shift workers were significantly

more likely to see lack of sleep as a cluster attack trigger than daytime workers. Chronic insomnia and shift work seem to be common among Arctic cluster headache patients. The small number of subjects included in this study implies that conclusions should be drawn with caution, but the findings support the idea of cluster headache BMN 673 cost as a circadian rhythm disorder. “
“Cluster headache (CH) and irritable bowel syndrome (IBS) are pain disorders that possess relationships with circadian rhythms. However, they have not been compared to assess similarities that could yield pathophysiologic insights. A young male adult with periodic episodes of abdominal pain highly reminiscent of CH is described. Since childhood, he experienced GDC-0068 mouse severe attacks featuring excruciating, abdominal pain accompanied

by prominent restlessness, lasting 30-120 minutes, occurring in the evening and in discrete 2- to 8-week periods, interspersed with remissions where typical triggers did not lead to attacks. Although all of the patient’s symptoms fell within the spectrum of IBS, the semiology was highly evocative of CH, based on the attack duration, restlessness, periodicity, and selective vulnerability to particular triggers only during

attack periods. A subset of patients thought to have IBS may feature similar attack profiles and could suggest the importance of the hypothalamus in its pathophysiology, akin to CH. “
“Migraine MCE公司 is a neurovascular disorder, and although the pathophysiology of migraine has not been fully delineated, much has been learned in the past 50 years. This knowledge has been accompanied by significant advancements in the way migraine is viewed as a disease process and in the development therapeutic options. In this review, we will focus on 4 mediators (nitric oxide, histamine, serotonin, and calcitonin gene-related peptide) which have significantly advanced our understanding of migraine as a disease entity. For each mediator we begin by reviewing the preclinical data linking it to migraine pathophysiology, first focusing on the vascular mechanisms, then the neuronal mechanisms. The preclinical data are then followed by a review of the clinical data which support each mediator’s role in migraine and highlights the pharmacological agents which target these mediators for migraine therapy. “
“Objectives.— To evaluate the role of neuroimaging and to estimate the prevalence of significant and treatable intracranial lesions in children and adolescents with recurrent headaches. Background.

These data suggest RES iron may be detrimental in the early stages of NAFLD and may contribute to the initiation of fibrogenesis, but this finding should be confirmed in a larger cohort. Disclosures: Kris V. Kowdley – Advisory Committees or Review Panels: Abbott, Gilead, Merck, Novartis, Vertex; Grant/Research Support: Abbott, Beckman, Boeringer Ingelheim, BMS, Gilead Sciences, Ikaria, Janssen, Merck, Mochida, Vertex The following people have nothing to disclose: David E. Kleiner, Laura Wilson, Patricia H. Belt, James E. Nelson Background: Nonalcoholic

fatty liver disease (NAFLD) presents a high prevalence and diverse outcomes. Little is known about inflammatory and apoptosis mechanisms underlying the progression of NAFLD and its association with critical features as Kupffer cells and hepatocellular ballooning. Recently, PNPLA3 and bile Crizotinib datasheet check details acids have been associated in chronic liver disease progression. Aim: Investigate the expression of Na+/tauro-cholate

cotransporter pump (NTCP) and PNPLA3 in NAFLD progression and the association of inflammatory and apoptosis markers in liver biopsies of patients with NAFLD. Methods: 117 human liver biopsies of NAFLD patients were collected from 2009 to 2012 and classified according to disease spectrum (66 steatosis (S), 40 steatohepatitis (NASH) and 11 cirrhosis (C)). Biopsies were analyzed by immunohistochemistry in a tissue microarray for expression of CD68 as a kupffer cell bio-marker, CD163 as a marker of monocyte macrophage; therefore inflammatory and apoptosis markers were evaluated. RT-PCR real time was carried out for NTCP and PNPLA3 gene expression. H&E staining was employee to identify hepatocellular ballooning. Results. 117 patients, 51/49% (women/men) with a mean age of 52.4±14 years. 40% of the population had metabolic syndrome, 65% were overweight or obese, 24% diabetes,

73% hypertriglyceridemia, 38% hypercholesterolemia and 38% hypertension, and elevated AST, ALT and GGT in 54%, 56% and 65 %, respectively. NTCP expression was significantly up-regulated in C vs. S (P <0.01). A strong up-regu-lation was observed in PNPL3 medchemexpress vs. NTCP expression (p<0.05) according to liver injury degree. Regarding to inflammatory and apoptosis markers, an increase in CD68 expression between S vs. NASH (77% vs 100%), S vs. C (77% vs 36%) and NASH vs. C (100% vs 36%) (P <0.01) was shown. In NASH stage CD68+, CD1 63+ and positive hepatocellular ballooning were significantly associated with inflamatory and apoptosis biomarkers (Table 1). Conclusion. NTCP as an important regulator of bile acids transport seems to play a major role in the progression of NAFLD and presents an important asociation with PNPLA3 in terms of NAFLD stages.

4-6 In contrast, the case-control study by Lok et al., which addresses the role of OBI and previous HBV exposure in U.S. HCC patients with chronic HCV infection, found no association between previous HBV exposure or OBI and HCC in patients with histologically advanced chronic HCV infection.23 The aim of this study, using patients enrolled in the Hepatitis Antiviral Long-term Treatment against Cirrhosis (HALT-C) study who Metabolism inhibitor had failed to achieve a sustained virological response after previous interferon (IFN) treatment with or without ribavirin, was to compare the prevalence of OBI in a cohort of HBsAg-negative U.S. patients with histologically

advanced chronic hepatitis C and assess the contribution of OBI to the development of HCC. Briefly, MAPK Inhibitor Library manufacturer the investigators identified 91 HCC patients and 182 controls matched for degree of fibrosis, treatment assignment in the HALT-C study (i.e., pegylated IFN versus no treatment), and duration of follow-up. Serum

samples were tested for HBV serological markers and HBV DNA levels. Frozen liver samples obtained from 28 HCC cases and 55 controls were examined for HBV DNA levels using real-time PCR and primer sets amplifying within the surface and polymerase genes. Despite the relatively low population prevalence of HBV exposure in the United States, serum anti-HBc, used as a marker of previous HBV infection, was positive in 41.8% HCC cases and 45.6% of controls (P = 0.54); anti-HBc alone was positive in 16.5% of HCC cases and 24.7% of controls. HBV DNA was detected in the serum of 1 control subject and zero HCC patients. Three of the twenty-eight (10.7%) HCC cases and 13 of 55 (23.6%) controls tested for tissue HBV

DNA had evidence of 上海皓元 HBV DNA in their liver. Thus, there was no evidence of an association between OBI and development of HCC in these patients with chronic HCV infection unresponsive to IFN-based therapy. The U.S. and Hong Kong studies are not directly comparable because of the differences in HBV and HCV epidemiology between the two study populations. Although prior treatment was not addressed in the Hong Kong study, patients in the U.S. study had received prior treatment for chronic HCV infection and it is unclear whether either the presence of HCV infection or therapy for HCV infection may have affected baseline low levels of HBV in OBI patients. The exclusion of patients who responded to prior HCV therapy may also have been responsible for unrecognized bias in the results. It is also possible that more OBI-positive samples would have been identified if the U.S. study had utilized more sophisticated HBV assays, particularly those for intrahepatic HBV DNA, cccDNA, and HBV pgRNA. The U.S.

2). Consistent Selleck EX 527 with previous work on this species (Fewell & Page Jr, 1999), the distribution of task sharing in excavation of observed pairs was significantly lower than that predicted from the extent of intrinsic variation in excavation behavior displayed by queens when founding colonies alone (2011: predicted median = 0.55, observed median = 0.19, P < 0.01; 2012: predicted = 0.44, observed = 0.27, P < 0.05; Supporting Information Fig. S1), with the largest

excess in the most extreme level of excavation skew, where one queen performed little or no excavation while the behavior of the excavation specialist was either slightly but significantly lower (2011: t44 = 2.25, P < 0.05) or not significantly different (2012: t62 = 0.61, P = 0.54) from that of solitary queens (Fig. 2). Relative performance of excavation behavior was significantly predicted by patterns of queen–queen aggression during the first 15 min of pair formation

(t50 = 2.02, P < 0.05; Fig. 1c), but not by relative size differences (t50 = −0.24, P = 0.81; Fig. 1b). Both paired queens survived to brood collection in 6 of 28 colonies in 2011 and in 14 of 35 colonies in 2012. In contrast to excavation, Ivacaftor purchase total productivity in colonies with two surviving queens was significantly higher than productivity in single nests (main effect of queen number, F1,60 = 23.51, P < 0.001), with the two nest types not differing significantly in average per capita productivity (Student's t-test, t57 = 1.38, P = 0.17; Fig. 3). As with excavation, however, the allocation of offspring in paired nests was significantly more skewed toward a single queen than that predicted by the

distribution of productivity values from single queens (predicted median = 0.60, observed median = 0.40, P < 0.01; Supporting Information Fig. S2). This was caused by both a significant increase in reproduction by HF queens (t38 = 2.05, P < 0.05) and by a reduction in reproduction by the LF queen (t46 = 5.39, P < 0.001) relative to single queens (Fig. 3). Reproductive role was not significantly associated with relative size (t13 = 0.52, P = 0.61; Fig. 4a), relative social dominance (t13 = 0.39, P = 0.71; Fig. 4b) or excavation role (t13 MCE = 0.49, P = 0.63; Fig. 4c). Social life involves a complex interplay between individual behavior and patterns expressed at the level of the group as a whole, with the potential for complex group-level patterns and collective behavior from relatively simple individual decision rules (Camazine et al., 2001). Critically, higher level patterns emerge whenever individuals form interactive groups, which may or may not be adaptive but in many cases mimic the properties of socially adapted taxa (Parrish et al., 2002). Our experimental results support the notion that self-organization can produce reproductive division of labor, as predicted by an emergent property model.

RESULTS: There were 213 patients with no anemia, 230 with mild anemia and 209 with marked anemia. Patients with marked anemia (compared to mild or no anemia) were older in years (54.9 +/− 9.8 vs 53.7 +/− 10.2 vs 52.7 +/− 10.2: p=0.032), more likely to be male (71.3% vs 68.2% vs 56.3%:p=0.003), had a lower GFR at LT (67.8 +/− 36.7 vs 78.0 +/− 40.0 vs 84.5 +/− 42.6: p<0.001) and were more likely to have pre-LT diabetes (31.7% vs 21.8% vs 15.5%: p<0.001). There were marked differences in patient survival and development of renal insufficiency

over time using Kaplan-Meier find more analysis. Patients with marked anemia had 5 year survival of 73.7% compared to 83.7% in the mild anemia group and 91.4% in the no anemia group (p<0.001). Differences in severe RI were even more pronounced. Patients with marked anemia had rates of severe RI at 3 and 5 years of 28.7% and 35.1% compared to 10.4% and 13.2% for mild anemia and 8.8% and 11.4% for no anemia (p<0.001). In multivariate analysis, marked anemia three months after LT was significantly associated with both death and severe RI. Compared to no anemia, the presence of marked anemia was associated with severe RI with

a hazard ratio (HR) of 2.39 (CI 1.46-3.91: Alectinib concentration p<0.001). In multivariate analysis, other variables associated with severe RI were GFR at LT (HR 1.01 per ml/ min: p<0.001) female sex (HR 2.47: p<0.001) and diabetes before LT (HR 1.97: p=0.003). Marked anemia (vs no anemia) was associated with patient death with a HR of 2.16 (CI 1.283.63: p=0.004). CONCLUSIONS: The presence of marked anemia three months after

LT is common and is an early, significant and independent predictor of poor patient outcomes after LT including death and the development of severe renal insufficiency. The use of this variable along with other proven MCE variables, should help identity patients for aggressive renal sparing measures. Disclosures: Dilip Moonka – Advisory Committees or Review Panels: Gilead; Grant/Research Support: Bristol-Myers Squibb, Genentech; Speaking and Teaching: Merck, Genentech, Gilead The following people have nothing to disclose: Wadih Chacra, Mohammad Elbatta, Aishwarya Kuchipudi, Alexander Weick, Charlotte Burmeister, George Divine Introduction: Everolimus, a mammalian target of rapamycin (mTOR) inhibitor, is a ‘tolerance-sparing’ immunosuppressant used in solid organ transplantation. mTOR regulates diverse functions of professional antigen-presenting cells, in particular dendritic cells (DCs), and has important roles in the activation of conventional T cells and the function and proliferation of regulatory T cells (Treg). Aim: currently, no data are available concerning the impact of everolimus on DC and Treg in stable liver transplant patients. Therefore, the aim of this pilot study was to analyze peripheral blood DC subsets and Treg in 10 liver transplant patients exposed to everolimus (mTOR).

(HEPATOLOGY 2010;52:1758-1768) Chronic cholestatic liver diseases such as primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are characterized by impaired biliary secretion of bile acids

and other potentially harmful cholephiles. Intrahepatic accumulation of endogenous hydrophobic bile acids, together with cytokine- and chemokine-mediated inflammatory bile ductular and liver parenchymal see more injury, may contribute to development of fibrosis and cirrhosis in chronic cholestatic disorders. The ratio of toxic to less toxic bile acids correlates with severity of liver injury.1 The hydrophilic C24 bile acid, ursodeoxycholic acid (UDCA) improves biochemical and histological features in PBC, halts progression to cirrhosis in the majority of patients with PBC, Selleck EPZ015666 normalizes life expectancy in two-thirds of patients with PBC2-5 and currently represents the only approved therapy for PBC.6 In PSC, its therapeutic long-term benefit remains so far unclear although serum liver tests and surrogate markers of long-term prognosis improved during UDCA treatment in pilot trials.6 Mechanisms of action of UDCA in cholestatic disorders have not yet been fully resolved.7 Stimulation of impaired hepatocellular secretion by mainly

posttranscriptional mechanisms, detoxification of bile, antiapoptotic effects in hepatocytes and cholangiocytes, and stimulation of cholangiocyte HCO secretion may contribute to the beneficial effect observed during UDCA treatment in cholestatic disorders.7 NorUDCA is a C23 homolog of UDCA. C23 bile acids are found only in trace amounts in human bile.8 They are poorly conjugated with taurine and glycine in liver, and their pharmacokinetic properties differ from their naturally occurring C24 homologs.8NorUDCA has recently been shown to exert therapeutic effects superior to those of UDCA in

multidrug resistance protein 2 (Mdr2)/ATP-binding cassette b4 (Abcb4) knockout mice, a murine model of nonsuppurative, sclerosing cholangitis.9, 10 The mechanisms of action of norUDCA MCE in Mdr2−/− mice remain obscure.10NorUDCA is a potent (hyper-)choleretic bile acid as a result of cholehepatic shunting.8, 10 Whether this property may explain, at least in part, the anticholestatic, anti-inflammatory, and antifibrotic effects of norUDCA in Mdr2−/− mice9, 10 still remains unresolved. Most importantly, it is unclear whether norUDCA, like UDCA, may exert anticholestatic effects at the level of the hepatocyte.7, 11 Lithocholic acid conjugates are the most potent cholestatic agents among the major human bile acids.12 Taurolithocholic acid (TLCA)-induced cholestasis is an established experimental model of hepatocellular cholestasis.

The average percentage of infected hepatocytes in the 18 biopsies ranged from 1.3% to 53.9%. There was a significant positive correlation between the proportion of infected hepatocytes and the viral load in the serum and

the liver, but not with the HCV genotype. HCV positive cells occurred in clusters. A quantitative analysis of the spatial relationship between HCV RNA and interferon stimulated gene (ISG) mRNA expression in the subset of patients with an induced endogenous IFN system revealed a significant correlation. ISG signal intensity was lowest in uninfected cells with uninfected neighbors, intermediate in uninfected cells with at least one HCV positive neighbor, and highest in HCV positive cells. Conclusion: Over 20 years after Small molecule library the cloning and identification of HCV, we have developed the first highly sensitive, specific and reproducible in situ detection systems that allows to identify HCV infected cells in liver biopsies in patients with viral loads as low as 1 0E4 IU/ml. A quantitative analysis of the number and spatial distribution of HCV infected cells and ISG expression revealed a number of fundamental question concerning HCV-host

interactions: HCV infects only hepatocytes. The percentage of infected hepatocytes varies from 1 to 54 %, and correlates with serum viral load. HCV infected cells appear in clusters, favoring a model of cell to cell transmission. Finally, the positive correlation of HCV RNA Sotrastaurin ic50 signals 上海皓元 with ISG mRNA expression in patients with induced ISG expression reveals that HCV is the central driver of ISG induction. Disclosures: The following people have nothing to disclose: Stefan F Wieland, Zuzanna Makowska, Benedetta Campana, Diego Calabrese, Michael T. Dill, Josan Chung, Francis V. Chisari, Markus H. Heim Background: Combination therapy using peg-interferon (IFNa), ribavirin (RBV) and protease

inhibitor has improved the sustained antiviral response of chronic hepatitis C virus (HCV)1a infection. However, the treatment response has not improved significantly among patients who are prior non-responders to IFN-a and RBV and the mechanism of HCV resistance is not well understood. Aim: A persistent HCV replication cell culture model was developed to examine the impact of high-level viral replication on IFN-α and RBV treatment induced viral clearance. Methods: A persistent HCV infected cell culture model was established by using pJFH-delta V3-Rluc clone. HCV replication was confirmed by measuring the core and NS5A-Rluc protein expression by Western blotting and Renilla luciferase activity. Endoplasmic reticulum (ER) stress response due to HCV infection was measured by measuring ATF6 Firefly luciferase activity and autophagy induction was confirmed by measuring LC3II, p62 and Beclin 1 protein levels by Western blotting and immunocytochemical staining.

The average percentage of infected hepatocytes in the 18 biopsies ranged from 1.3% to 53.9%. There was a significant positive correlation between the proportion of infected hepatocytes and the viral load in the serum and

the liver, but not with the HCV genotype. HCV positive cells occurred in clusters. A quantitative analysis of the spatial relationship between HCV RNA and interferon stimulated gene (ISG) mRNA expression in the subset of patients with an induced endogenous IFN system revealed a significant correlation. ISG signal intensity was lowest in uninfected cells with uninfected neighbors, intermediate in uninfected cells with at least one HCV positive neighbor, and highest in HCV positive cells. Conclusion: Over 20 years after Palbociclib concentration the cloning and identification of HCV, we have developed the first highly sensitive, specific and reproducible in situ detection systems that allows to identify HCV infected cells in liver biopsies in patients with viral loads as low as 1 0E4 IU/ml. A quantitative analysis of the number and spatial distribution of HCV infected cells and ISG expression revealed a number of fundamental question concerning HCV-host

interactions: HCV infects only hepatocytes. The percentage of infected hepatocytes varies from 1 to 54 %, and correlates with serum viral load. HCV infected cells appear in clusters, favoring a model of cell to cell transmission. Finally, the positive correlation of HCV RNA Etoposide signals MCE公司 with ISG mRNA expression in patients with induced ISG expression reveals that HCV is the central driver of ISG induction. Disclosures: The following people have nothing to disclose: Stefan F Wieland, Zuzanna Makowska, Benedetta Campana, Diego Calabrese, Michael T. Dill, Josan Chung, Francis V. Chisari, Markus H. Heim Background: Combination therapy using peg-interferon (IFNa), ribavirin (RBV) and protease

inhibitor has improved the sustained antiviral response of chronic hepatitis C virus (HCV)1a infection. However, the treatment response has not improved significantly among patients who are prior non-responders to IFN-a and RBV and the mechanism of HCV resistance is not well understood. Aim: A persistent HCV replication cell culture model was developed to examine the impact of high-level viral replication on IFN-α and RBV treatment induced viral clearance. Methods: A persistent HCV infected cell culture model was established by using pJFH-delta V3-Rluc clone. HCV replication was confirmed by measuring the core and NS5A-Rluc protein expression by Western blotting and Renilla luciferase activity. Endoplasmic reticulum (ER) stress response due to HCV infection was measured by measuring ATF6 Firefly luciferase activity and autophagy induction was confirmed by measuring LC3II, p62 and Beclin 1 protein levels by Western blotting and immunocytochemical staining.

M.A. Edens (Isala Clinics, Zwolle, the Netherlands) for help with the statistical analyses. (a)  Conception and Design (a)  Drafting the Manuscript (a)  Final Approval of the Completed Manuscript “
“Sexual pain

and chronic headaches are both complex conditions with associated high disability. Little research has examined whether Birinapant in vitro there is a relationship between the 2. The aim of this survey-based study was to explore the frequency of sexual pain in a population of women being treated for chronic headache. Peripheral aims included exploring the number of patients receiving treatment for sexual pain and the association between sexual pain and libido, and history of abuse. Patients

presenting to an ambulatory chronic headache clinic were administered a short 10-item survey. Forty-four percent of patients reported that they had pelvic region or genital pain brought on by sexual activity. Only half of these patients had ever discussed their pelvic pain with a health care provider, and 31% of these patients had not received treatment. Almost all patients would be interested in treatment if available. Seventy-five percent of patients indicated a change in libido. Chronic headaches and sexual pain are both conditions that RXDX-106 clinical trial have a significant impact on patients and the health care system, 上海皓元 and they do coexist. More research is needed to look at the relationship between these conditions in addition to epidemiology, symptomatology, evaluation, and treatments. Chronic

pelvic pain (CPP) is a complex condition that can have a significant impact on quality of life.[1] Individuals with CPP face physical, psychological, and social challenges. Women with CPP experience interference in physical activities,[2] higher levels of depression and anxiety,[3] and disruptions in work and sexual relationships.[4, 5] CPP is a multifaceted condition often coexisting with gynecological and nongynecological causes of pain including interstitial cystitis, endometriosis, and irritable bowel syndrome.[6] Because of the multifaceted nature of this condition and difficulty in its diagnosis, a multidisciplinary diagnostic and treatment approach is key for providing quality health care.6-9 A common type of CPP is sexual pain, which can manifest in a variety of ways including dyspareunia (ie, painful intercourse), post-coital pain (ie, pain following intercourse), and vaginismus (ie, painful spasm of the vagina).[5] Little research has explored the epidemiology or health care costs of sexual pain among women.