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 LY2606368 supplier 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 DAPT price have a significant impact on patients and the health care system, 4��8C 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.

Lastly, the negative correlation found between pAkt and PD-1 suggests a relationship between metabolism and exhaustion and therefore may affect T cell activity. JA HOLMES,1 SK ROBERTS,2 W SIEVERT,3 GJ DORE,4 M MCCAUGHAN,5 DJ CRAWFORD,6 W CHENG,7 M WELTMAN,8 S BONANZINGA,9 K VISVANATHAN,1 PV DESMOND,1 DS BOWDEN,9 G MATTHEWS,4 AJ THOMPSON1 1St Vincent’s Hospital, University of Melbourne, Australia, 2Alfred Hospital, Melbourne, YAP-TEAD Inhibitor 1 cost Australia, 3Monash Medical Centre and Centre of Inflammatory Diseases, Monash

University, Melbourne, Australia, 4Kirby Institute for Infection and Immunity in Society, University of New South Wales, Sydney, Australia, 5Royal Prince Alfred Hospital, Sydney, Australia, 6Greenslopes Hospital, Brisbane, Australia, 7Royal Perth Hospital, Perth, Australia, 8Nepean Hospital, Sydney, Australia, 9Victorian

Infectious Diseases Reference Laboratory, Melbourne, Australia Background: Two functional variants in the JAK inhibitor inosine triphosphatase (ITPA) gene resulting in ITPase deficiency are strongly associated with protection from ribavirin (RBV)-induced haemolytic anaemia1. On-treatment anaemia is associated with higher sustained virological response (SVR) rates during peg-interferon (pIFN) plus RBV therapy2,3, however despite these associations, ITPA genotype has not been associated with SVR1,2,4. To study this apparent discrepancy further, we examined the relationships between ITPA genotype, on-treatment anaemia SVR and RBV levels (where available) in a large cohort of HCV-1 patients from the CHARIOT study. Methods: 564 of 871 participants enrolled in the CHARIOT study consented to future biomarker testing. Participants were randomised to receive 180 mcg or 360 mcg pIFN subcutaneously weekly for the first 12 weeks plus RBV, then 180 mcg pIFN plus RBV for the remaining treatment duration. ITPA genotyping (rs7270101 and rs1127354) was performed on stored serum (TaqMan allelic discrimination kit) and predicted ITPase activity was calculated as previously described1,4. Relationships between ITPase activity, on-treatment Hb PLEK2 reduction, RBV levels and SVR were tested using regression modelling,

survival analyses and LOWESS plots. Results: ITPase deficiency was present in 190/546 (35%) patients and was strongly associated with protection from anaemia (Hb <100 g/L) and Hb reduction >30 g/L during treatment (p < 0.0001 for both). ITPase deficiency was also associated with longer time to and fewer RBV dose reductions within the first 12 weeks of therapy (p = 0.05). Anaemia and Hb reduction were independently associated with SVR (p = 0.043 and p < 0.0001, respectively). ITPase activity was not associated with SVR (p = 0.28). Using multivariable logistic regression modelling, independent predictors of SVR were age, fibrosis stage and nadir Hb. The estimated local probability of SVR was then plotted against nadir Hb for patients with ITPase wild-type vs deficiency.

Conclusion: S1P may play an important role in the pathophysiology of portal hypertension with Rho kinase activation by way of S1P2. The S1P2 antagonist merits consideration as a novel therapeutic agent for portal hypertension. (HEPATOLOGY 2012) Portal hypertension is a major

complication of liver cirrhosis, being a leading cause of death or cause for liver transplantation.1, 2 The management of patients with portal hypertension is still a clinical problem; nonselective beta-adrenergic blockers, the most commonly used pharmacological treatment for portal hypertension, have significant limitations due to adverse events and unpredictable response.3 Furthermore, the mean decrease in portal vein pressure in response to beta-adrenergic blockers is only ≈15%.4 Therefore, it is clear that new treatment strategies are needed to improve the prognosis of patients SB525334 mw with advanced portal hypertension. It is well known that the HCS assay enhanced pressure of the portal vein is caused by the increased intrahepatic vascular resistance. Fibrosis and regenerative nodule formation are classical

mechanisms that account for the increased intrahepatic vascular resistance in cirrhosis. Furthermore, recent data suggest that sinusoidal remodeling could also be involved in portal hypertension, characterized by the increased density of contractile hepatic stellate cells wrapping around sinusoidal endothelial cells.2 Previous evidence suggests a pivotal role of sinusoidal vasoconstriction in the pathophysiology of portal hypertension, where hepatic stellate cells operate as contractile machinery in response to vasoconstrictors.5

Among the various potential vasoconstrictors, we have focused on sphingosine 1-phosphate (S1P), a lipid mediator, which elicits a wide variety of cell responses.6 Recent investigation has revealed that S1P acts through at least five high-affinity G-protein-coupled receptors referred to as S1P1-5,7, 8 among which S1P1-3 are expressed in hepatic stellate cells.9 S1P stimulates contractility in rat hepatic stellate cells in culture; the stimulation new of contractility is C3 exotoxin-sensitive,9 and is abrogated by the S1P2 antagonist.10 Then we observed that S1P enhances portal vein pressure in an ex vivo model of isolated perfused rat livers by way of S1P2 with Rho activation.10 These findings prompted us to examine whether the antagonism of S1P2 could reduce portal vein pressure in an in vivo model of portal hypertension. BDL, bile duct ligation; S1P, sphingosine 1-phosphate; X-Gal, 5-bromo-4-chloro-3-indolyl-β-D-galactopyranoside. Male Sprague-Dawley rats were purchased from Japan SLC (Shizuoka, Japan). The conventional S1P2-deficient mice (S1P mice) and LacZ-knockin mice at the S1P2 locus (S1P mice) were generated as described.11 Wildtype mice (S1P mice) were used as littermate controls.

Psychological activity is

driven by psychological factors. Psychological factors are inevitably important causes of some mental illness and physical illness, which will inevitably lead to the establishment of discipline systems of the disorder caused by psychological factors, such as the digestive disorder caused by psychological factors. After the term “psychosomatic” was introduced in 1818, by the German psychiatrist Johann Heinroth, in his research paper on insomnia, in 1948, the American psychiatrists Dunbar gave a systematic discussion of “psychosomatic”, in his book Synopsis of Psychosomatic Diagnosis and Treatment. With intensive study and continuous practice of the psychosomatic relationship, in 1980, these selleck screening library diseases were officially named as “psychosomatic diseases” by the American Academy of Psychosomatic Medicine [3]. And so far it is still a mainstream concept of the medical profession. However, we believe that the “psychosomatic diseases” should become a

thing of the past. Why? First, let’s look at the concept of “psychosomatic diseases”: psychosomatic disease refers to the physical functional disease or physical organic disease in which psychological and social factors plays important roles in the occurrence and development of disease.[4]. Then, how could we name the mental illnesses caused by psychological factors? Obviously, such concept is not comprehensive enough. However, we believe that the introduction of psychosomatic disease is of historical significance, for it indicates that Selleck MK-1775 psychology is one of the disease causes, and reveals that psychosomatic diseases are universal and this understanding is important. Nonetheless, Fenbendazole it has a lot of problems. For example, under the

guidance of the original psychology, psychiatrists confuse “mental” with “psychological”, and non-psychiatrists believe that psychology is under the charge of psychiatry. These ideas make the transformation of medical model become a slogan that cannot be understood. Therefore, we must establish the system of general medical psychology, in order to promote the transformation of medical model, thereby making it a medical revolution. Methods: The disorder caused by psychological factors refers to physical or mental illnesses whose occurrence and development mainly attribute to psychological factors. It includes not only the physical functional and organic diseases caused by psychological factors, but also the mental functional and organic diseases caused by psychological factors. In fact, it has already been found that psychological factors are closely related to physical health. A clear understanding of the relationship between “psychological” and “mental” is the basis for understanding the disorder caused by psychological factors, that is, psychology is consciousness-related functions of the brain, and part of the mental symptoms is the partial manifestation of the psychology. Both are relatively easy to identify.

Fig. 2E shows the serum cytokine levels. Compared with

WT mice, IL-6−/− mice had similar levels of serum TNF-α and interferon-γ (IFN-γ), whereas IL-10−/− mice had higher levels of these cytokines in both the STD and HFD groups. Serum levels of IFN-γ were further elevated in IL-10−/−IL-6−/− Temozolomide dKO mice versus IL-10−/− mice after HFD feeding. Finally, serum levels of IL-6 were higher in IL-10−/− mice than those in WT mice. As expected, IL-6 levels were not detected in IL-6−/− and IL-10−/−IL-6−/− dKO mice. Four lines of mice were also fed an ETOH diet and pair-fed for 4 weeks, and analyzed similarly to the studies shown in Fig. 2. In general, findings similar to the HFD model were seen in the ETOH feeding model and are described in Supporting Fig. 4. As shown in Fig. 3A,B, IL-10−/− mice were resistant to HFD-induced steatosis and serum ALT elevation compared with WT mice, which was partially restored in IL-10−/−STAT3Hep−/− dKO mice. This suggests that enhanced hepatic STAT3 activation is responsible Selleck Bioactive Compound Library for the reduced steatosis and liver injury in IL-10−/− mice after HFD feeding. Furthermore, Fig. 3C,D shows that hepatic

mRNA levels of several inflammatory markers and cytokines were highest in IL-10−/−STAT3Hep−/− mice, followed by IL-10−/− mice and WT mice in both the STD and HFD-fed groups. Serum levels of TNF-α, IFN-γ, and IL-6 were also higher in IL-10−/−STAT3Hep−/− mice than those in IL-10−/− mice (Fig. 3E). Experiments similar to the HFD model described in Fig. 3 were also performed in the ETOH model. Similar changes, albeit to a lesser extent, were observed in the ETOH model (Supporting Fig. 5). To further understand the mechanisms by which IL-10−/− mice are prone to inflammatory response but resistant to steatosis induced by HFD or ETOH diet, we examined Farnesyltransferase the activation of STAT3 (pSTAT3) and pSTAT1, which play an important role in controlling steatosis and liver inflammation.31 Because the HFD model induces more dramatic phenotypes compared

with the ETOH model, the studies on the underlying mechanisms were predominately focused in this HFD model. As shown in Fig. 4A, in both the STD and HFD groups, hepatic levels of pSTAT3 were lower in IL-6−/− mice but higher in IL-10−/− versus WT mice. Compared with IL-10−/− mice, IL-10−/−IL-6−/− mice had significantly lower levels of hepatic activated pSTAT3 expression, while expression of STAT3 was comparable in these two groups. Additionally, expression of pSTAT1 and STAT1 protein was higher in the HFD-fed group versus the STD group, with the greatest expression in IL-10−/− IL-6−/− mice. As expected, an additional deletion of hepatocyte STAT3 markedly reduced the expression of pSTAT3 and STAT3 in IL-10−/−STAT3Hep−/− mice compared with WT and IL-10−/− mice (Fig. 4B). Interestingly, expression of STAT1 protein was higher in these dKO mice compared with other groups (Fig. 4B).

The agent used for TACE embolism is deposited in the tumor, thus creating greater acoustic impedance than liver tissue.[20] Deposition of iodinated oil not only has a positioning function, but also has a synergistic effect of temperature rise similar to HIFU. Therefore, it provides a strong thermogenic buy LDK378 action promoting the therapeutic effects of HIFU. Major differences of MR-

and US-guided HIFU therapy from other interventional therapies are its complete noninvasiveness of treatment with very low complication rates. After HIFU ablation, most patients have a favorable general condition and stable vital signs. An increased transaminase level was seen in most patients with larger tumors,21 as in our study, and an elevated transaminase level was observed in all patients; however, the results returned to normal within 2 weeks of therapy. Only three patients had a fever with temperature >39°C for 5 days after HIFU ablation. Skin-burn was a relatively common complication after HIFU: about 4.1% patients had serious skin burn in Jin et al.’s study,[9] especially in those patients whose tumor was located superficially. However, there was no skin burn observed in our

study. We also found a new complication that was not reported before in the adult population. Two patients were found to have mild malformation of ribs at follow-up. The potential mechanism may be interpreted as direct injury by high-energy US waves or indirect injury by elevated temperature of surrounding tissues. No rib fracture was seen in our series. We considered HIFU ablation in children with hepatoblastoma a safe procedure without serious complications. However, the number of our cases was limited and larger enough series are critical to draw a convincing conclusion. In conclusion,

our experience of the 12 cases, although small in number, suggests the advantages HIFU combined with TACE. HIFU has great developmental prospects for treating hepatoblastoma as a noninvasive treatment method with advantages of accurate location, noninvasive “resection,” radioactive decontamination, and low complication rates. However, HIFU for pediatric tumor is still in its beginning and requires further study and large-scale randomized clinical trails to confirm our observations and to further determine the role of HIFU. “
“While a certain international consensus has been reached regarding the diagnosis and treatment of autoimmune hepatitis (AIH), there are some unique clinical characteristics of AIH in Japan.

Although FasL is shown to induce Bid-independent apoptosis in hepatocytes cultured on collagen, the sensitizing effect of TNFα is clearly dependent on Depsipeptide chemical structure Bid. Moreover, both c-Jun N-terminal kinase activation and Bim, another B cell lymphoma 2 homology domain 3 (BH3)–only protein, are crucial mediators of TNFα-induced apoptosis sensitization. Bim and Bid activate the mitochondrial amplification loop and induce cytochrome c release, a hallmark of type II apoptosis. The mechanism of TNFα-induced sensitization is supported by a mathematical model that correctly reproduces the biological

findings. Finally, our results are physiologically relevant because TNFα also induces sensitivity to agonistic anti-Fas–induced liver damage. Conclusion: Our data suggest that TNFα can cooperate with FasL to induce hepatocyte apoptosis by activating the BH3-only proteins Bim and Bid. (HEPATOLOGY 2011.) Enhanced apoptosis is critically involved in many acute and chronic liver diseases, and hepatocytes are the main cell type undergoing massive cell death during liver injury. This process is regulated by a complex network of soluble and cell-associated apoptotic and inflammatory signals.1 It is therefore increasingly important to obtain insight into the mechanistic interplay of these signals to define new therapeutic strategies.

In the liver, apoptosis http://www.selleckchem.com/products/cobimetinib-gdc-0973-rg7420.html is mainly initiated by the death receptor ligands Fas ligand (FasL; CD95L) and tumor necrosis factor α (TNFα).2 After

ligand binding, death receptors recruit the adaptor Fas-associated death domain (FADD) and procaspase-8 to their intracellular face, and this forms the death-inducing signaling complex (DISC).3 By this assembly, procaspase-8 is autoprocessed and activated, and it can then trigger two different apoptotic signaling pathways. In so-called type I cells, such as lymphocytes, active caspase-8 directly cleaves and activates procaspase-3 to induce efficient cell death execution.4 In type II cells, such as hepatocytes, apoptosis induction first requires caspase-8–mediated cleavage of Bid into its truncated form [truncated Bid (tBid)]. tBid belongs to the subclass of B cell lymphoma 2 homology domain 3 (BH3)–only B selleck inhibitor cell lymphoma 2 (Bcl2) family members (e.g., Bim, p53–up-regulated modulator of apoptosis, and Noxa), which sense apoptotic stimuli and convey the death signals for B cell lymphoma 2–associated X protein (Bax) and B cell lymphoma 2 homologous antagonist/killer (Bak) activation on mitochondria. Although it is still unclear how this activation occurs,5 it has become well accepted that Bax and Bak are essential for mitochondrial membrane permeabilization (MOMP) and the release of apoptogenic factors such as cytochrome c and second mitochondria-derived activator of caspases (Smac)/diablo homolog (Diablo).

Age for herring and sprat was determined using length-at-age regression models that are derived during routine pelagic trawl surveys for stock assessment (Saunders et al. 2010). Carbon and nitrogen isotope composition of whale skin was determined using continuous flow elemental analysis isotope ratio mass spectrometry (CF-EA-IRMS) at the University of Southampton using a EuroVector EA 3000 (EA) combined

with a PDZ Europa Scientific 20-20 (IRMS). Isotope ratios are presented in delta notation as parts per thousand differences from an internal standard (ACROS L-Glutamic Acid) according to the following equation: δYX = [(Rsample/Rstandard) − 1] GSK2118436 × 10−3, where R denotes the heavier:lighter isotope ratio and Y is the atomic mass of the stable isotope X (δ13C or δ15N). Internal standards calibrated with International Atomic Energy Agency IAEA (Vienna, Austria), i.e., Vienna Pee Dee Belemnite (for C), atmospheric N2 (for N), were routinely analyzed between samples in order to determine instrument precision. Based on the two standard deviations of these standards, the analytical precision of two runs at separate laboratories was similar 0.4‰ and 0.2‰ for nitrogen, and 0.2‰ and 0.1‰ for carbon for Southampton and University Palbociclib molecular weight of California

Davis respectively. Prey items (fish muscle and homogenized krill) were analyzed at UC Davis by CF-EA-IRMS using a PDZ Europa ANCA-GSL (EA) combined with a PDZ Europa 20-20 (IRMS). The analytical precision at Southampton, calculated as the standard deviation of routinely measured bovine liver and glutamic acid standards, was 0.40‰ for nitrogen, and 0.20‰ for carbon. At the UC Davis laboratory, this was 0.15‰ and 0.06‰ for nitrogen and carbon, respectively. In exoskeletons of crustaceans such as krill, carbonates (CaCO3) are derived from isotopically heavy HCO3− ions from the environment, find more and

are thus a nondietary fraction and must also be removed as their enriched 13C affects whole-body δ13C values (Søreide et al. 2006). Lipids are depleted in 13C, thus altering the δ13C values of tissues. The elemental carbon to nitrogen ratio (C:N) is a useful proxy for lipid content (McConnaughey and McRoy 1979) and was used to assess lipid effects on isotopic values in light of those previously published species- and tissue-specific values for lean tissue. Lipid-free C:N values for whole zooplankton (range) are 3.30–4.03 for marine zooplankton (Kiljunen et al. 2006, Søreide et al. 2006), (± SD) 3.6 ± 0.1 for M. norvegica (Bentaleb et al. 2011) and 3.3 ± 0.1 for white muscle in sprat and herring of (Kiljunen et al. 2006, Caut et al. 2011). These were used as a threshold lipid-free and/or carbonate-free values for each species, which if exceeded indicated that all δ13C values for that species should be corrected arithmetically (i.e., lipid-normalized) to correct for the presence of isotopically lighter lipid (Table 1).

The liver chemistry profile was available in 20 patients and cholestatic in 9 patients (45%). All control cases showed normal expression for GS, CK7 and BerEP4. In 93% of NRH cases, there Vismodegib mouse was an abnormal zone 2 expression of GS (p<0.001). Moreover, a weak panacinar GS staining in all NRH cases

was seen (p<0.001). Ductular reaction was present in 88% of HNR cases with no significant bile duct injury with CK19 staining. Aberrant CK7 expression was present in all cases of NRH (p<0.001). There was no correlation between CK7 expression and cholestatic chemistry profile. BerEP4 was overexpressed in 47% of HNR cases. All cases with diffuse BerEP4 staining also showed extensive CK7 expression (p<0.01). Conclusions: We identified 1) A distinctive immunohistochemical GS staining pattern in NRH; 2) An aberrant expression of CK7 in all NRH cases that does not correlate with cholestatic chemistry profile; 3) CK7 reactivity staining in NRH that seems to correlate with BerEP4 overexpression. As this latter finding suggests that activation of hepatic progenitor cells may be involved in the pathogenesis of NRH, the formers could be helpful in the morphologic diagnosis of NRH. Disclosures: The following people have nothing to disclose: Marie-Christine Guilbert, Genevieve Soucy, Dominique

Trudel, Bich N. Nguyen Introduction: Gene profiling studies have revealed molecular subclasses of hepatocellular carcinoma (HCC) characterized by pathway deregulations associated with specific cellular and/or clinical phenotypes, which have

potential to inform clinical decision making as well as therapeutic development. Clinical surrogates of such molecular Stem Cell Compound Library clinical trial subclasses will enable more flexible clinical application of the findings. Here we aimed at elucidating correlation of histopathologic features with the molecular subclasses as potential surrogate indicators of underlying molecular deregulations. Methods: Histopathologic features of HCC correlated with HCC molecular subclasses (S1, S2, and S3) [Cancer Res 2009:69;7385] were identified in 99 HCC tumors (training set) by using multivariable logistic regression, and a predictive scoring system was developed. learn more The score was evaluated in an independent set of 96 HCC tumors (validation set). Molecular pathways associated with the key histopathologic features were determined by Gene Set Enrichment Analysis. Results: In the training set (S1: 30%, S2: 21%, S3: 48%), thin, thick trabecular, compact, and pseudoglandular architecture were observed in 54%, 24%, 24% and 14% of samples, respectively. Classical clear cell (CC), steatohepatitic clear cell (SH-CC), and fatty change were seen in 9%, 19% and 10%, respectively. Multivariable logistic regression showed: a) CC (OR 4.6, p=0.04) and thick trabecular (OR 3.8, p=0.02) were significantly associated with S2 tumors; b) Edmondson grade 1/2 (OR 8.6, p=0.008) and thin trabecular (OR 2.5, p=0.05) correlated with S3 tumors.

Key Word(s): 1. ulcerative colitis; 2. ß-arrestin 2; 3. insulin like growth factor-I (IGF-I); 4. extracellular signal-related kinase (ERK) Presenting Author: LI TAO Additional Authors: XIANYI LIN, JIN TAO Corresponding Author: LI TAO Affiliations: Compound Library price The Third Affiliated Hospital of Sun Yat-Sen University, The Third Affiliated Hospital of Sun Yat-Sen University Objective: To investigate the process of mocusal injury and repair of ulcerative colitis in mice and the key role of p-Smad3 in this process. Methods: Mice were exposed to 3% dextran sulfate sodium (DSS) for 5 days and followed by water for 4 weeks.

Mice were divided into six groups: control group that were allowed to drink only water, injury group that exposed to 3%DSS for 5 days and recover groups which drunk water for 1,2,3,4 weeks after DSS removed. General health condition was recorded daily. Related markers of apoptosis and proliferation were detected. The expression of TGF-β and p-Smad3 were measured to observe the change of TGF-β signaling pathway in this process. Results: The disease activity index of mice was increased after DSS treatment and returned to nomal at 2 weeks of DSS removed. The histological

score was increased significantly at injury group and began to decrease at 2 weeks of recovery. The apoptotic index was risen to the maximal level at injury group and came back to nomal level at 3 weeks. However, the proliferation index was reduced Birinapant cell line to the minimal level at injury group, then started to increase to reach at the peak at 3 weeks. TGF-β expression was increased at all learn more of the experimental group, while the activation of Smad3 was inhibited at injury group, the began to be reactivated at 1 week after DSS removal. Conclusion: Smad3 phosphorylation promotes the repair of colonic mucosa of ulcerative colitis in mice. Key Word(s): 1. ulcerative

colitis; 2. recovery; 3. proliferation; 4. TGF-ß; 5. Smad3 Presenting Author: WIDYARINI TEKY Additional Authors: ARITANTRI DAMAYANTI, PAULUS KUSNANTO, TRI YULI PRAMANA, TANTORO HARMONO Corresponding Author: WIDYARINI TEKY Affiliations: Gastroenterology and Hepatology Division, Gastroenterology and Hepatology Division, Resident of Internal Medicine, Resident of Internal Medicine Objective: To determine the descriptive profile of IBD at Dr. Moewardi Hospital Surakarta. Methods: A retrospective descriptive study of IBD patients at Dr Moewardi Hospital Surakarta between mei 2011 and mei 2014. Variables taken from medical record. Results: We found 109 patients IBD, Normal 0 false false false IN X-NONE X-NONE UC (ulcerative colitis) 96,3%, CD (chron’s disease) 62,4% Normal 0 false false false IN X-NONE X-NONE with m ale 62,4%, female 37.6%. The mean age:UC 50,7 ± 13.4 years old, CD 44,5 ± 8.5 years old. High class economy 63.3% and low class economy 36.7%. Senior high school graduated 48.6%, junior high school 26.6%, elementary school 12.8%, university 11%, no school 9%.