Gregg Duester (Sanford-Burnham Medical Research Institute, La Jolla, CA). The mice were bred in a MAPK Inhibitor Library chemical structure specific pathogen-free facility (Bio Model System Park; KAIST, Daejeon, Korea). All animal experiments were approved by KAIST Institutional Animal Care and Use Committee. To induce liver fibrosis, 8- to 10-week-old mice were treated with 0.4 mL/kg carbon tetrachloride (CCl4) diluted in olive oil via intraperitoneal injection three times per week for 2 weeks. Twenty-four

hours after the last injection of CCl4, 1 × 106 whole BMCs or control medium were transferred to mice via the tail vein. Twelve or 24 hours after infusion of BMCs, mice were sacrificed. Human BMCs were harvested from patients with HBV-induced liver cirrhosis for autologous BMC infusion in Severance Hospital (Seoul, Korea). Some BMCs were used for in vitro experiments with the patients’ consent. Serum data were obtained from patients treated with autologous BMC infusion between November 2006 and February 2008. The protocol for the clinical trial conformed to the ethical guidelines of the Declaration of Helsinki and was approved

by the Institutional Review Board of Severance Hospital in the Yonsei University Health www.selleckchem.com/screening/protease-inhibitor-library.html System. Data are expressed as the mean ± SEM. To compare values, a Student t test or analysis of variance was performed. For blood samples of patients, a Wilcoxon signed-rank test with Bonferroni correction was used to compare the values of paired samples. P < 0.05 was considered statistically significant. All other materials and methods are described in the Supporting Information. To investigate early events following infusion of BMCs in fibrotic liver, mice with CCl4-induced liver

fibrosis were sacrificed at 12 and 24 hours after infusion with BMCs from GFP+ mice via the tail vein. At 12 and 24 hours, serum levels of alanine aminotransferase, aspartate aminotransferase, triglyceride, albumin, cholesterol, and glucose were not changed compared with those of vehicle-infused mice (Fig. 1A and selleck inhibitor Supporting Fig.1A). However, collagen fibers and α-smooth muscle actin (α-SMA)–positive HSCs in liver tissues of BMC-infused mice were decreased compared with those of vehicle-infused mice at 12 and 24 hours (Fig. 1B and Supporting Fig. 1B), which were confirmed by western blotting (Fig. 1C) and quantitative RT-PCR (qRT-PCR) analyses (Fig. 1D) in isolated HSCs. In contrast, relative messenger RNA (mRNA) levels in HSCs for TGF-β1, IL-6, and monocyte chemoattractant protein-1 (MCP-1) were decreased only at 24 hours in BMC-infused mice but not in vehicle-infused mice, whereas there was no significant difference in IL-10 mRNA expression in HSCs (Supporting Fig. 1C). More surprisingly, most migrated GFP+ BMCs were in close contact with activated HSCs in the fibrotic septa within 24 hours (Fig. 1E and Supporting Fig. 1D).

05). Conclusion: Conclusions: The results suggest that oxymatrine, cisplatin and oxaliplatin would have inhibiting effect on cell proliferation in human hepatocelluar carcinoma cell line Bel-7404, which would be strengthened and attain synergism when oxymatrine worked combinedly with cisplatin or oxaliplatin and oxaliplatin

was superior to cisplatin whether it worked separately or combinedly. Its mechanism may be related to the blocking of cell cycle at G0/G1 phase and inducing cell apoptosis. Key Word(s): 1. oxymatrine; 2. HCC cell Bel-7404; 3. cisplatin; 4. oxaliplatin; Presenting Author: WUHUA GUO Additional Authors: FC WANG, ZY XIE, JX ZHANG Corresponding Author: WUHUA GUO Affiliations: the second affiliated hospital of nanchang university Objective: TACE oriented comprehensive therapy is a popular choice for treatment of hepatocelluar carcinoma, especially the unresectable primary liver cancer. In this research, CT-guided SB203580 datasheet microwave ablation was applied for patients with incompletely treated hepatocellular carcinoma (HCC) after transcatheter arterial chemoembolization (TACE). The article is to evaluate the efficacy and safety for this therapy. Methods: 37 patients with single or multi nodular HCC were treated with TACE combined with microwave ablation. All patients were firstly treated with TACE 1 or 2 times. Then CT-guided microwave ablations

were performed to treat the masses incompletely treated according to CT/MRI. All patients were evaluated for complete tumor ablation rate, local recurrence-free rate, overall survival rate, and complications. Results: The times of procedure BI 2536 molecular weight were 137 and 82 for TACE and microwave ablation respectively in all 37 cases of HCC. The complete tumor ablation rate was 65.3% (32/49). One-, 2-, 3-, and 4-year overall survival

rates were 91.9% (34/37), 70.0% (26/37), 16.2% (6/37), and 5.4% (2/37), respectively. Complications were observed in 4 patients, one with descending duodenum perforation (Tumor infiltrated duodenal, abscess formation within the tumor 15 days after ablation. The patient selleck screening library didn’t have the clinical manifestations of acute peritonitis.), and the other with right pleural effusion. Conclusion: The strategy of TACE combined with microwave ablation could be effective and safe for the treatment of HCC. CT-guided microwave ablations would be an ideal companion for TACE especially incompletely treated masses. Key Word(s): 1. HCC; 2. Ablatin; 3. TACE; Presenting Author: XIULAN PENG Corresponding Author: XIULAN PENG Affiliations: Renmin Hospital of Wuhan University Objective: Purpose Hepatocellular carcinoma (HCC) is one of the most common malignant tumor. The molecular mechanism of HCC is poorly understood. Our previous study have shown that upregulation of Ezrin-radixin-moesin-binding phosphoprotein-50 (EBP50) could inhibit malignant biological characteristics of HCC, We aimed to confirm the function of EBP50 in human hepatocellular carcinoma.

These levels were almost double those in previous reports. In line with these findings was the observation of decreased serum iron levels, reflecting iron consumption for increased hemoglobin and erythropoietic cell output.[21] This demand for systemic iron was followed by a compensatory increase in transferrin

levels observed at day 4 in our study. It cannot be ruled out that these findings are a result of the combination of exercise, which could alter muscle iron accumulation and myoglobin homeostasis, and hypoxia. However, most of the findings in this study are in agreement with previous literature from both humans and experimental animals using an experimental setting without physical exertion.[4, 19] In previous studies, mediators of iron homeostasis Kinase Inhibitor Library in vivo have been investigated independently under high-altitude conditions. Hypoxia caused an increase of circulating IL-6,[23] whereas serum hepcidin levels were suppressed under these conditions.[1, 21, 24] In line with these findings, the measured IL-6 serum levels in our study were increased, indicating a subtle systemic inflammatory response, which could be slightly attenuated as expected by treatment with dexamethasone. Suppression of hepcidin expression represents the mechanistic link between

hypoxia and the observed changes in systemic iron availability. However, hepcidin suppression at high altitude is not driven by a reduction in iron selleck stores.[25] Despite the up-regulation of IL-6 as an activator of HAMP gene expression, click here the clearance of serum hepcidin levels under hypoxic conditions indicates a dominant-negative regulatory (iron-independent) impact of hypoxia-induced erythropoiesis over inflammatory cytokines. This could be based either on

direct hypoxia-mediated effects on hepcidin expression, or be a consequence of hypoxia-induced erythropoiesis and iron consumption for heme synthesis with a subsequent decrease of circulating iron levels.[32] Our data are in concert with the report of Huang et al.[26] which showed that the erythropoietic drive might inhibit both inflammatory and iron-sensing pathways in mice. Nonetheless, cytokines such as IL-6 can promote iron retention in macrophages by hepcidin-independent pathways, which would also result in low serum iron levels.[27] Such changes are always paralleled by increased circulating ferritin levels. However, the opposite, namely, decreased serum ferritin levels, were observed in our study, thus ruling out IL-6-mediated iron retention under hypoxic conditions. This response to hypoxia was even present in subjects with elevated baseline transferrin saturation or ferritin levels. However, we cannot exclude the presence of a genetic predisposition for later clinically relevant hemochromatosis (e.g., C282Y homozygotes) in these subjects.

4C). Altogether, our results demonstrate that B7-H4 on activated HSC inhibits the generation of cytokine-producing T cells. We investigated the influence of B7-H4-expressing HSC on recall Venetoclax responses of previously primed effector CD8+ T cells. Effector T cells upon re-encountering cognate antigen are capable of producing IFNγ. We generated CD8+ T cell blasts

or effector CD8+ T cells by pulsing P14 splenocytes with 1 μg/mL gp33 peptide and subsequently purifying them after 6 days of expansion. They were then cocultured with gp33 peptide-pulsed B7-H4 knockdown and control AHSC for 6 hours. As shown, IFNγ production is reduced after stimulation with B7-H4-expressing AHSC compared to B7-H4 knockdown AHSC (Fig. 5A). CD8+ T cell blasts or effector CD8+ T cells were also generated using anti-CD3/CD28 and restimulated with anti-CD3/CD28 in the presence of B7-H4-Ig or control-Ig. The addition of B7-H4-Ig reduces IFNγ production in a dose-dependent manner, whereas high levels of IFNγ +CD8+ T cells are seen with treatment with control-Ig (Fig. 5B). These results indicate

that B7-H4 on AHSC attenuates the recall effector T cell response. CD8+ T cells that are stimulated by B7-H4 silenced HSC exhibit a highly activated phenotype with a high frequency of CD44hi cells, even before cell division has ensued (Fig. 6A). Thus, in concordance with previous reports,22, 23 B7-H4 inhibits or delays T cell activation. To show whether HSC were capable of selleck compound processing and presenting antigen and whether inhibition of T cells by B7-H4 on infected HSC still occurred, AHSC were infected with 5 plaque-forming signaling pathway units (pfu)/mL of vaccinia virus expressing gp33 epitope of LCMV for 24 hours. Subsequent to vaccinia infection expressing gp33, AHSC were then transfected with B7-H4 siRNA or control siRNA. Two days post-transfection, P14 transgenic CD8+ T cells were added and the level of activation based on CD44 expression was evaluated. Our results demonstrate that in the absence of B7-H4, the vaccinia-gp33-infected HSC induce T cell

activation efficiently as compared to the control siRNA treatment (Fig. 6B). However, it is important to note that similar to stimulation with peptide pulsed HSC, the effect of B7-H4-mediated inhibition of T cell activation and proliferation is dose-dependent. To elucidate the mechanism of B7-H4 inhibition of T cells, we assessed the early signaling pathway and phosphorylation state of various signal transduction molecules on T cells. T cell activation is associated with mitogen activated protein kinase (MAPK) signaling through extracellular signal-regulated kinase (ERK)1/2. We evaluated the initiation of MAPK signaling by way of the presence of phosphorylated ERK molecules in T cells with and without B7-H4-Ig. Phosphorylated ERK1/2 could be detected in T cells with control-Ig as early as 5-15 minutes after stimulation.

[51] In the context of early activation

of the inflammasome in ASH and a significant protection from all www.selleckchem.com/products/Metformin-hydrochloride(Glucophage).html components of alcoholic liver disease observed in mice deficient in inflammasome components or IL-1 signaling, the available data suggested differential role of inflammasomes in the pathogenesis of ASH and NASH. In search for mechanisms that would explain this discrepancy, we investigated the cellular source of activated inflammasome and IL-1β. Both in ASH and NASH, the baseline levels of caspase-1 protein or pro-Casp-1, ASC, Nlrp3, and pro-IL-1b mRNA were substantially higher in liver immune cells, compared to hepatocytes.[66, 67] Specific for ASH, analysis of liver immune cells or primary hepatocytes isolated from alcohol-fed mice showed that alcohol increased the active fragment of caspase-1 and IL-1β only in liver immune cells but not in primary hepatocytes. As these data suggested that liver immune cells were the predominant cell type that activates caspase-1 and IL-1β in ASH, we generated ITF2357 solubility dmso caspase-1-chimeric mice using a combination of clodronate-mediated Kupffer cell depletion, irradiation, and bone marrow transplantation. Using this model, we confirmed our hypothesis

that caspase-1 expressed in Kupffer cells was involved in alcohol-induced liver inflammation, steatosis, and injury, and we did not find any evidence for a pathogenic role for caspase-1 in liver parenchymal cells in the development of ASH.[67] In addition to Kupffer cell-specific

inflammasome activation in ASH,[67] we observed that activation of the inflammasome occurred also in isolated hepatocytes in NASH.[66] Specifically, primary hepatocytes isolated from the MCD-fed mice had increased expression of NALP3, ASC, caspase-1, and pro-IL-1b mRNA.[49, 66] Taking into account that fatty livers had elevated the expression of inflammasome components and that this process occurred in hepatocytes which accumulate lipids, we tested whether fatty acids exert any effects on inflammasome in hepatocytes. We observed that in vitro treatment of primary mouse hepatocytes with palmitoic acid, a learn more saturated fatty acid, resulted in upregulation of the inflammasome component NALP3, priming of caspase-1 for subsequent activation by LPS and induction of IL-1β secretion. Using the pan-caspase inhibitor Z-VAD, we demonstrated that these events were caspase dependent, and we also showed that they were caused by saturated fatty acids, whereas non-saturated fatty acids had no effect. We further showed that hepatocytes exposed to palmitoic acid produced inflammasome-mediated danger signals, which in turn activated liver macrophages in a caspase-dependent manner.[66] Taken together, our findings have outlined several differences in inflammasome/IL-1 signaling between ASH and NASH.

The patient was hospitalised on several occasions over the next 12 months for the diagnosis of sigmoid diverticulosis and caecal CD respectively. Multiple CT scans and colonoscopies revealed ongoing caecal inflammation and patchy inflammation in the sigmoid MLN0128 supplier colon. The dual diagnosis of caecal CD and diverticulitis of the sigmoid colon was suggested. Mycobacterium tuberculosis (TB) was considered as a differential diagnosis however

acid fast bacilli were not detected on biopsy, the chest X-ray was normal and the quantiferon gold was negative. Due to the recurrent sigmoid diverticulitis accompanied by caecal CD a colectomy was performed. The unexpected diagnosis of colonic TB was only made following histological assessment of the surgical specimen. Numerous acid fast bacilli (Figure 1) and areas of granulomatous inflammation (Figure 2) were evident. The CT scans taken preoperatively show sigmoid diverticuli and colonic inflammation. This was confirmed at operation—the patient was suffering from both diverticulosis and intestinal

TB. CD and intestinal TB both may cause segmental and granulomatous disease of the intestine. Several recent case series help distinguish the two conditions and guide investigation. Importantly, Talazoparib in vitro TB is not simply a right-sided disease, with 30% of cases involving the left hemicolon. Radiological and endoscopic features of both conditions may be similar, and organisms selleck screening library are rarely stained or cultured successfully from biopsy specimens (< 10%). Diagnosis may only be possible in some cases following surgical resection or with anti-tuberculous agents causing a resolution of clinical and radiological disease. Recent advances in medical diagnostic technology hold promise in differentiating intestinal TB and CD. Polymerase

Chain Reaction (PCR) may detect mycobacterial DNA in endoscopic biopsy specimens. A large case series reports a sensitivity of 65%, and a specificity > 95% for intestinal TB where biopsies were taken at colonoscopy. Interferon—gamma release assays (IGRAs), such as QuantiFERON-TB Gold, are now used widely to screen for latent TB. It is not often appreciated however that Interferon Y—assays have been thoroughly tested and validated in cases of active tuberculosis, both pulmonary (and to a lesser extent) extrapulmonary. A sensitivity of 65–95%, with a specificity of approximately 90% has been demonstrated in cases of active TB. Contributed by “
“We read with interest the article by Al-Harthy et al.1 and believe that it provides important additional insights into the prevalence of fatigue in patients with primary biliary cirrhosis (PBC). The finding in a North American population of PBC-40 fatigue domain scores comparable to those in our previous United Kingdom–based studies2, 3 underlines the importance of this symptom in this patient group.

During each observation period, all marked bees were allowed to leave and enter the nest at will; the departure and arrival time for each bee was recorded. A completed trip outside the nest is referred

to as a foraging bout. Outside these observation periods, shutters were closed. Males and newly emerged queens were never allowed to leave the colonies, to prevent any non-native bees from establishing themselves as a result of our experiments. The mass of all workers was measured on each departure from and arrival to the nest (see Ings et al., 2005b for methods). One hour before the end of the daily observation period, further workers were prevented from leaving the nest, thus

minimizing the chances of foragers returning to the nest outside the observation period. Bees that returned outside observation periods were returned to their colony the see more next morning. Before placement in the field, all colonies were fed pollen and artificial nectar ad libitum. The colonies were also fed in the field during poor weather when no observations took place. In experiments conducted in Sardinia and Germany in 2001, three sets (blocks) of observations were carried out consecutively (for further details see Ings et al., 2005b). Each block consisted of one colony from each of the three populations: B. t. sassaricus, B. t. terrestris and B. t. canariensis (an additional Proteasome inhibitor block, i.e. three more colonies, was observed in Sardinia 2000). New colonies were used for each block. All three colonies within each block were placed simultaneously in the field within 5 m of each other. Observations

began immediately and were carried out simultaneously on all three populations. All colonies were monitored continuously between 08:00–19:00 h during dry weather. The total duration of observations varied between selleck blocks depending upon the weather and ranged from 4 to 16 days. One colony of each population (B. t. canariensis and B. t. dalmatinus) was placed on the roof of the Fogg Building, Queen Mary University of London in 2004 and 2005. In 2004, both colonies were monitored continuously between 1000–1700 h on 20 days (between 2 July and 3 August 2004) during dry weather. In 2005, both colonies were monitored continuously between 07:00–21:00 h for 10 consecutive days (20–29 May 2005). Colonies were kept inside the building overnight to protect them from harsh weather conditions. Observations began 10 min after the colonies were placed outside each day. Outside the stated observation hours, colonies were replaced by empty nest boxes to provide returning workers with overnight shelter. Empty nest boxes were also placed outside for two days after the observation period and checked regularly for returning foragers.

Disclosures: Mark S. Sulkowski – Advisory Committees or Review Panels: Merck, AbbVie, Idenix, Janssen, Gilead, BMS, Pfizer; Grant/Research Support: Merck, AbbVie, BIPI, Vertex, Janssen, Gilead, BMS Susanna Naggie – Advisory Committees or Review Panels: Vertex Pharmaceuticals, Boehinger Ingelheim, Gilead, Abbott, Merck; Consulting: Achillion; Grant/ Research Support: Vertex Pharmaceuticals, BVD-523 nmr Anandys, Scynexis, Medtronic, Gilead, AbbVie, BMS, Jenssen, Merck, Achillion The following people have nothing to disclose: Zobair Younossi, Maria Stepanova, Sharon L. Hunt Introduction: Hepatitis B constitutes a major health burden especially in countries where endemicity

of CHB is high and resources are limited. One of the known complications is renal failure which can be due to a variety of reasons. Telbivudine has been shown

to improve renal function (glomerular filtration rate) and is potentially useful for renoprotection in CHB cirrhotic patients. The impact on overall CHB treatment, avoidance of renal replacement therapy peri and post-transplant are not known at this time. Methods: We performed a markov modeling with cost-utility analysis to estimate the potential of routine telbivudine use in CHB cirrhotic patients assuming that the renoprotection effect is preserved in cirrhotic patient and post-transplant Barasertib supplier setting. The base case population is a 60 year old newly diagnosed CHB cirrhosis patient presenting with first liver decompensation. Comparison is made between tenofovir; lamivudine/adefovir add on salvage; telbivudine/ tenofovir addon salvage or telbivudine/tenofovir combination. HBV DNA suppression, resistance rates and progression to liver failure and transplant were taken from best published data. Renal replacement therapy needs pre and peritransplant were estimated based on projection selleck kinase inhibitor by glomerular filtration rate and rationalized against actual reported rates. Results: The use of telbivudine reduced the need for dialysis by 38% in the pre and peritransplant setting. Progression to chronic renal failure post-transplant was reduced by 54% and avoided the need for

renal replacement and or renal transplant by 27%. Telbivudine with tenofovir add on salvage was the most cost effective strategy with ICER of USD16500 /QALY. The use of LAM/ADV was dominated while tenofovir was extendedly dominated. Telbivudine with tenofovir combination provided the most efficacious use with reduction in both Hep B recurrence and renal complications but was still cost-effective with ICER 41600/QALY. ICER was most sensitive to cost of telbivudine, rate of GFR deterioration post-transplant, impact of telbivudine on GFR, use of HBIG and cost of renal replacement therapy. Conclusion: Telbivudine potentially may have renoprotective role in CHB cirrhotic patients who progress to liver failure and require liver transplantation.

Bile acids are known

to be involved in hepatocyte cell survival pathways. In this regard, hydrophobic bile acids have been reported to be cytotoxic and to induce apoptosis in hepatocytes.35 In contrast, hydrophilic bile acids such as ursodeoxycholic acid (UDCA) and conjugates have been reported to prevent apoptosis possibly through activation of the AKT and ERK1/2 signaling pathways.36, 37 Conjugates of UDCA have been shown to activate the ERK1/2 and AKT signaling pathways in primary hepatocytes in culture.36, 37 The current data suggest that activation of these signaling pathways by TUDCA may be through the S1P2 in primary hepatocytes (Fig. 4). Other laboratories have reported that bile acids may increase the cellular c-AMP that prevents

apoptosis.38 Everolimus in vivo The movement of ABC transporters in hepatocytes from intracellular locations to the canalicular membrane as well as their activity may also be partially controlled by the activation of PI3 kinase through the S1P2.39-41 The data suggest that activation of S1P2 may have effects on survival pathways and movement of ABC transporters in primary hepatocytes. Our current study strongly suggests that the S1P2 is the major GPCR activated by TCA and other conjugated bile acids in hepatocytes. This conclusion is based on the following lines of experimentation: 1. Screening of individual GPCRs in the lipid-activated phylogenetic family showed that only S1P2 was significantly activated by TCA in HEK293 cells (Fig. 1). These selleck kinase inhibitor cells lack a bile acid transporter; hence, TCA, a highly hydrophilic bile acid, must activate cell signaling pathways by binding to cell surface receptors. In addition, S1P2 mRNA is highly expressed in mouse, rat, and human hepatocytes (Supporting Fig. 2). In contrast, TGR5/M-BAR mRNA level is very low compared with S1P2 in primary hepatocytes. All these data point to S1P2 as another GPCR activated by bile acids. TCA rapidly activates the ERK1/2 and

AKT signaling pathways in primary rat hepatocytes and following intestinal infusion into a biliary diverted rat.14, 26 In addition, TCA is also an excellent activator of FXR in primary rat hepatocytes and in vivo models.26 Our current model suggests that both the selleck compound ERK1/2 and the AKT pathways are activated by TCA through S1P2. These data indicate that S1P2 may play an important role in the regulation of hepatic glucose, bile acid, and lipid metabolism through coordinate activation of ERK1/2, AKT and FXR. In this regard, we have observed that S1P2−/− mice have fatty livers compared with wild-type control mice (unpublished data). In summary, TCA activated the S1P2 in rodent hepatocytes and in vivo causing activation of both the ERK1/2 and AKT pathways in primary hepatocytes. Activation of the AKT pathway appears to be essential for optimal activation of the nuclear receptor FXR by conjugated bile acids.

These results demonstrate that reactive oxygen species can activate proCT expression from the CGRP gene in trigeminal glia by a paracrine regulatory mechanism. We propose that this glial recruitment pathway may occur following cortical spreading depression and neurogenic inflammation to increase CGRP nociceptive actions in migraine. “
“(Headache 2010;50:769-778) Background.— Electronic medical records (EMRs) are used in large healthcare centers to increase efficiency and accuracy of documentation. These databases may be utilized for clinical research or to describe clinical practices such as medication usage. Methods.— We conducted

a retrospective analysis of EMR data from a headache CDK inhibitor clinic to evaluate clinician prescription use and dosing patterns of topiramate. The study cohort comprised 4833 unique de-identified records, which were used to determine topiramate dose and persistence of treatment. Results.— Within the cohort, migraine was the most common headache diagnosis (n = 3753, 77.7%), followed by tension-type headache (n = 338, 7.0%) and cluster or trigeminal autonomic cephalalgias (n = 287, 5.9%). Physicians prescribed Selleckchem GPCR Compound Library topiramate more often for subjects with migraine and idiopathic intracranial hypertension (P < .0001) than for those with other conditions,

and more often for subjects with coexisting conditions including obesity, bipolar disorder, and depression. The most common maintenance dose of topiramate was 100 mg/day; however, approximately 15% of subjects received either less than 100 mg/day or more than 200 mg/day. More than a third of subjects were prescribed topiramate for

more than 1 year, and subjects with a diagnosis of migraine were prescribed topiramate for a longer period of time than those without migraine. Conclusions.— Findings from our study find more using EMR demonstrate that physicians use topiramate at many different doses and for many off-label indications. This analysis provided important insight into our patient populations and treatment patterns. “
“(Headache 2011;51:246-261) Objective.— To identify prognostic factors from the history and physical examination in women with tension-type headache (TTH) who are likely to experience self-perceived clinical improvement following a multimodal physical therapy session including joint mobilization and muscle trigger point (TrP) therapies. Background.— No definitive therapeutic intervention is available for TTH. It would be useful for clinicians to have a clinical prediction rule for selecting which TTH patients may experience improved outcomes following a multimodal physical therapy program. Methods.— Women diagnosed with pure TTH by 3 experienced neurologists according to the International Headache Society criteria from different neurology departments were included.