003; Table 2). However, the only Hector’s dolphin population that could be excluded as a source was the

South Coast for one of the dolphins, check details Che12NZ02 (P = 0.002). As in the Structure results, GeneClass2 assigned CheNI10-03 and CheNI10-24 to the West Coast South Island with high likelihoods (Table 2). GeneClass2 also provided high assignment likelihoods for Che12NZ02 to the West Coast South Island, and for Che09WH01 and Che11NZ06 to the East Coast South Island population, although they did not exceed the high confidence threshold of 0.01 (Table 2). Again similar to the Structure results, Che05NZ20 showed a more ambiguous assignment among the Hector’s dolphin populations with a moderate likelihood of 0.6189 to the West Coast, followed by 0.2353 to the East Coast. Our findings demonstrate the fundamental concept of genetic monitoring—observing changes in demographic and genetic parameters over time. The genetic monitoring of the Maui’s ICG-001 nmr dolphin resulted in the unexpected discovery of four Hector’s dolphins within the Maui’s dolphin distribution on the northwest coast of the North Island between 2010 and 2012. The presence of these Hector’s dolphins would not have been evident without the extensive baseline of genetic diversity initiated by Pichler (2002) and updated by Hamner et al. (2012) to include individuals sampled between 1988 and 2007. This

reference sample set was intentionally time-limited so as to minimize the potential for generational changeover, assuming an estimated 20 yr maximum lifespan of Hector’s and Maui’s dolphins (Slooten and Lad 1991), while maximizing the number of contemporary samples across the distribution of the species. In light of the unexpected discovery of the Hector’s dolphins among Maui’s medchemexpress dolphins,

we reexamined genotypes of two Hector’s dolphins sampled on the southwest coast of the North Island in 2005 and 2009. These dolphins sampled at Peka Peka Beach (Che05NZ20) and Wellington Harbour (Che09WH01), were found between the distributions of the two subspecies. Although the sample from Peka Peka Beach (Che05NZ20) was collected in 2005, within the 1988–2007 time period used for the baseline, it was excluded from the genetic baseline as an outlier, given that it was a neonate found beachcast in an area extralimital to the known distribution of either subspecies. However when considered together, the six Hector’s dolphins sampled on the North Island pose several nonexclusive scenarios: (A) several independent events occurred where one or more dolphins dispersed from known population(s) on the South Island to the North Island; (B) a single stochastic event occurred, where several Hector’s dolphins dispersed together as a group from a known population on the South Island to the North Island; or (C) a small population of previously unsampled Hector’s dolphins exists along the southern North Island or northern South Island, several of which dispersed into the Maui’s dolphin distribution.

Tuber late blight development caused by the different P. infestans genotypes on the tuber cultivars was evaluated at 10°C storage temperature using whole-tuber subperidermal inoculation. The washed, SB203580 cell line surface-disinfested tubers were inoculated by removing a 5-mm-diameter potato plug using a sterile cork borer and placing 2 × 10−5 ml of sporangia suspension (delivering zoospores released from approximately 20 sporangia per inoculation) with

a hypodermic syringe and needle at the apical end of the tuber approximately 1 cm from the dominant sprout to a maximum depth of 1 cm. The potato plug was returned to close the wound, and it was sealed with petroleum jelly. A complete randomized block design with three experimental repeats consisted of 10

tubers per cultivar, six different cultivars and 12 different isolates representing four genotypes. A total of three replicates were inoculated for each of the cultivar–isolate combination. Ten control tubers per cultivar were inoculated with cold (4°C) sterile distilled H2O. After inoculation, tubers were placed in the dark in sterilized, covered plastic crates and returned to controlled environment chambers [Percival Incubator (Model I-36LLVL; Geneva Scientific, LLC, Fontana, WI, USA)]. The chambers were set at 10°C BI2536 and 95% humidity, and the sample tubers were incubated for 30 days until evaluation. Tubers of three different cultivars with different responses to P. infestans were obtained from MSU potato breeding programme to evaluate periderm susceptibility. The three cultivars with different tuber blight ratings were Atlantic (S), Jacqueline Lee (MR) and Stirling (R) (Kirk 上海皓元医药股份有限公司 et al. 2009). Tubers were prepared as described above. Tubers were submerged in a sporangial suspension containing approximately 1 × 104 total sporangia/ml for 48 h at 18°C. After inoculation, tubers were placed in the dark in sterilized, covered plastic crates with damp towels to maintain high humidity and then placed in controlled environment chambers

at 10°C. The experimental design encompassed two different P. infestans genotypes (US-8F and Pi10-012), three cultivars and 12 tubers per cultivar. Arbitrary samples of three tubers per genotype–cultivar combination were sampled at 3, 6, 10 and 15 days postinoculation for evaluation. The experiment was conducted four times, and the replicates were analysed together, blocking by repeat. At each time, the number of eyes and the number of lenticels infected were assessed under the dissecting microscope at 20 ×  magnification (Olympus SZX10; Olympus America Inc., Lake Success, NY, USA) and light microscope at 200 ×  magnification (Olympus CX22; Olympus America Inc.). A digital image analysis technique (Niemira et al. 1999; Kirk et al. 2001b) was used to assess tuber tissue infection. The image files were analysed using SigmaScan V3.0 (Jandel Scientific, San Rafael, CA, USA).

Physico-theology proposed that not only had God provided the natural world for man’s enjoyment and edification, its perfection – the way particular species seemed so well suited to particular environments – was evidence of God’s existence. In The Wisdom of God, Ray focused on ultimate causes, asking remarkably perceptive

questions. Why, for example, do birds produce hard-shelled eggs instead of live young like mammals? Why do certain birds lay only a single egg, while others produce a clutch of ten or more? Why do different bird species have specific breeding seasons? These are questions that continue to interest biologists today. However, Ray did more than simply RXDX-106 nmr pose intriguing questions; he suggested answers, many of which – as subsequent research demonstrated – were extraordinarily accurate. Selleckchem Trametinib Basically, Ray was interested in adaptations, and because he was a religious man, saw God as the mechanism by which they had arisen. Physico-theology was extremely popular, so popular in fact that in the early 1800s, William Paley (1743–1805) borrowed extensively from Ray’s book to produce his own version, entitled Natural Theology (Paley, 1802). An Anglican minister, Paley is best known now for his metaphor concerning the watch. ‘Suppose I had found

a watch’… he says ‘its several parts are framed and put together for a purpose … the inference we think is inevitable, that the watch must have had a maker – that there must have existed, at some time and at some place or other, an artificer or artificers who formed it for the purpose which we find it actually to answer, who comprehended its construction and designed its use …. The hinges in the wings of an medchemexpress earwig, and the joints of its antennae, are as highly wrought,

as if the Creator had nothing else to finish. We see no signs of diminution of care by multiplicity of objects, or of distraction of thought by variety. We have no reason to fear, therefore, our being forgotten, or overlooked or neglected’. As is now obvious, Paley was the basis for the idea of intelligent design. When Charles Darwin was an undergraduate at Cambridge studying for the church between 1828 and 1831, Paley’s Natural Theology was required reading. Darwin loved it, later recalling that it provided: ‘as much delight as did Euclid. The careful study of these works, without attempting to learn any part by rote, was the only part of the Academical Course which, as I then felt and as I still believe, was of the least use to me in the education of my mind. I did not at that time trouble myself about Paley’s premises; and taking these on trust I was charmed and convinced of the long line of argumentation’.

Adacolumn selective granulocytapheresis (GCAP) has been associated with clinical efficacy 3-MA cell line in patients with UC. In the present study

we sought the effect of sequential GCAP procedures in peripheral blood APCs in patients with UC and the effect on soluble cytokines. Methods:  We used multiparametric flow cytometry to quantify peripheral blood APCs and serum cytokines in 210 samples obtained from seven patients with steroid-dependent or steroid resistant UC undergoing GCAP treatment. Samples were drawn before, after 30 and 60 min of each session. Results:  Each GCAP session resulted in a dramatic tenfold reduction of peripheral blood CD16-mDC (P < 0.01), pDC decreased twofold (P = 0.05) but CD11c-mDC remained unchanged. This depletion was reached after 30 min and maintained

at 60 min. The depletion of CD16-mDC and monocytes was associated with a reduction of serum tumor necrosis factor levels and a raise in interleukin-10 levels, although no statistical difference was reached. Conclusion:  The effect of GCAP in peripheral blood APC consisted mainly on a significant depletion of tumor necrosis factor-α secreting CD16-mDC. This finding could suggest a potential mechanism of GCAP beneficial effect that must be confirmed in larger series. “
“End-stage liver disease and hepatocellular carcinoma from chronic hepatitis C (HCV) remain as the most common indications MG-132 cost for liver transplantation (LT) in the Western world. Unfortunately, HCV infection universally 上海皓元 persists into the post-transplant period, threatening graft and patient survival. Unlike chronic HCV in the immunocompetent population, the natural history of chronic HCV in the LT population has a more accelerated course, with 10%-30% of LT recipients progressing to cirrhosis within 5 years of

transplantation and more than 40% within 10 years. The median interval of developing cirrhosis is 9.5 years from transplantation, as compared to 30 years from infection in immunocompetent persons.[1] Undoubtedly, recipients with recurrent HCV have a lower graft and patient survival than their noninfected counterparts.[2] Various factors associated with aggressive HCV recurrence after LT have been identified (Fig. 1). Donor age >40 years,[3] higher HCV RNA levels at time of transplantation and in the early posttransplant period,[1, 3] and use of corticosteroid pulses or antilymphocyte antibody preparations, such as OKT3, for treatment of acute cellular rejection have predicted fibrosis progression and, consequently, graft and patient survival.[1, 3, 4] Underlying all these factors is the recipient’s immune response, which exerts its actions through both innate and adaptive mechanisms.

20 These in vivo studies suggest that HSCs could present a new therapeutic target in the treatment of liver metastases. Although the role of TGF-β in cancer biology is complex and involves both tumor suppression and tumor promotion, depending on the stage of malignant progression, overexpression of TGF-β is generally accepted to be associated with metastasis and poor prognosis.39, 48 In mouse models, TGF-β pathway antagonists (1D11, a mouse monoclonal pan-TGF-β neutralizing antibody; LY2109761, a chemical inhibitor of both TGF-β

receptor I (TβRI) and TβRII; and TβRII:Fc fusion protein) inhibited metastases

in multiple organs, including the liver.49-51 Because TGF-β is one of the most potent cytokines for HSC activation and tumor desmoplasia, anti–TGF-β pathway therapy may provide HM781-36B research buy therapeutic benefits by targeting both tumor cells and tumor stroma. Currently, several agents that target TGF-β signaling are being Ensartinib manufacturer tested in phase 1 and 2 trials in patients with metastatic malignant tumors. These include GC1008, a human TGF-β–neutralizing monoclonal antibody capable of neutralizing all three TGF-β isoforms; AP12009, an antisense molecule against TGF-β2; and LY2157299, a newly developed inhibitor of TβRI kinase.52 Thus, TGF-β antagonists may have potential for clinical use in the prevention of liver metastases, in part through inhibiting effects on the liver microenvironment. The approved anticancer drugs imatinib mesylate (Gleevec, formerly referred to as STI571 or CGP57148B),

sunitinib, and sorafenib are small molecules that specifically target multiple protein tyrosine kinases, including PDGF receptors. These drugs may inhibit the desmoplastic reaction and tumor–stroma interactions in the liver. Indeed, numerous studies using experimental liver fibrosis animal models have already demonstrated that these drugs inhibited MCE HSC activation and liver fibrosis in vivo.31, 53-55 These small molecules are currently approved to treat cancer in patients, making it feasible to test whether they help prevent or reduce metastatic liver diseases through their inhibiting effects on desmoplasia. In summary, HSCs are postulated as a component of the prometastatic liver microenvironment. Tumor cells induce HSC activation, and activated HSCs in turn stimulate tumor growth. Bidirectional interactions between tumors and HSCs may function as an “amplification loop” to further enhance metastatic growth in the liver.

Thus, confinement of domestic cats might reduce the spatial extent of cat impact on native prey populations on oceanic islands. Negative impacts of introduced cats Felis catus have been reported on islands worldwide (Medina et al., 2011),

and cats have caused irreversible damage to populations of many native species (Fitzgerald & Turner, 2000). To assess the impacts of cats on native biodiversity, it is important to understand where cats find their prey and what species they consume. Cats feed on a wide variety of prey (Van Aarde, 1980) and hence are considered generalist predators, exploiting prey species according to their abundance (Fitzgerald & Karl, 1979). Native species on oceanic islands are particularly vulnerable to cat predation because 17-AAG of their lack of anti-predator behaviour. Conservation of island biodiversity therefore requires knowledge of whether cats prefer to consume native species that are easy to capture, or whether they consume species at random in proportion to their relative abundance. Although the diet of introduced cats on islands has been extensively investigated (Bonnaud et al., 2011), we are not aware of a study of cat diet that SCH 900776 datasheet simultaneously

measured the availability of prey. Simultaneous monitoring of diet and prey abundance is important to assess the role of cats as generalist predators and thus their impact on native species. The impact of cats on native biodiversity also depends on the spatial extent over which prey is encountered. This is a particular concern for domestic (owned and fed by humans) cat populations (van Heezik

et al., 2010; Horn et al., 2011), which coexist with feral cats (not owned by humans) on most inhabited islands where cats have been introduced. Domestic cats frequently kill wild prey and medchemexpress can have impacts on the environment similar to feral cats (Loss, Will & Marra, 2013). Although domestic cats generally receive supplementary food from humans, their urge to hunt and kill influences their home-range size (Barratt, 1997). Data on spatial movements might therefore be informative to identify which native species may be affected by domestic cats. Previous attempts at assessing cat impacts suggest that home-range size varies with sex, neuter status (whether a domestic cat has been neutered or not), and seasonal prey availability (Barratt, 1997; Edwards et al., 2001). However, most studies did not account for seasonal variation in home-range size or differences between individuals (Lilith, Calver & Garkaklis, 2008). Because sterilization and confinement would offer management tools to reduce the impacts of domestic cats on native species, more information is required on how neuter and confinement status affect home-range size and thus the spatial extent of cat impacts on native wildlife.

01, and 6.4 ± 1 in Pkd2cKO mice treated with 60 mg/kg/daily, P < 0.01) (Fig. 1C). Consistent with the increase in liver cysts, the liver/body weight ratio of Pkd2cKO mice was also significantly higher in sorafenib-treated animals (Pkd2cKO vehicles: 0.058 versus 0.0762 in mice treated with 20 mg/kg/day, P < 0.01, and 0.079 in mice treated with 60 mg/kg/day, P < 0.01) (Supporting Fig. 1). Previous studies have shown that the growth of liver cysts is dependent upon an increased

proliferation and a decreased apoptosis of cystic cholangiocytes.7, 8, 21 Consistent with the increased volume of liver cysts, the immunohistochemical expression of Ki67, a nuclear antigen present RO4929097 only in the nuclei of proliferating cells,22 was significantly CB-839 cell line increased in mice treated with sorafenib (Pkd2cKO vehicles: 6.8 ± 1% versus 11 ± 2% in Pkd2cKO mice treated with 20 mg/kg/day, P < 0.01, and 10.5 ± 2.1 in Pkd2cKO mice treated with 60 mg/kg/day, P < 0.01) (Fig. 2A). Apoptosis was assessed by measuring the immunohistochemical expression of CC3.7, 8 The number of CC3-positive cells in the liver cyst epithelium was significantly decreased in mice treated with sorafenib (Supporting Fig. 2) (Pkd2cKO vehicles: 11.0 ± 0.8% versus 8.2 ± 0.8% in Pkd2cKO mice treated with 20 mg/kg/day, P < 0.01, and 7.9 ± 0.7 in Pkd2cKO mice treated with 60 mg/kg/day; P <

0.01). These data suggest that sorafenib increases liver cyst growth through increased cell proliferation and decreased apoptosis in the liver cystic epithelium. Cyst proliferation in Pkd2cKO mice is sustained by a PKA-dependent Raf/MEK/ERK1/2 pathway.7 ERK1/2 is downstream of Raf and therefore should be inhibited by sorafenib. On the contrary,

the expression of phosphorylated ERK1/2 (pERK1/2) was significantly increased in cholangiocytes lining the cysts in mice treated with sorafenib, with respect to untreated Pkd2cKO mice (Pkd2cKO vehicles: 3 ± 0.7% versus 4.9 ± 1.1% in Pkd2cKO mice treated with 20 mg/kg/day, P < 0.01, and 5.2 ± 1 in Pkd2cKO mice treated with 60 mg/kg/day; P < 0.01) (Fig. 2B). No differences in the percentage of pERK1/2 positive hepatocytes were observed (Pkd2cKO vehicles: 2.2 ± 0.8% versus 2.8 ± 0.97% in Pkd2cKO mice treated with 20 mg/kg/day, P value not significant). These data suggest that increased proliferation in cystic MCE公司 cells in sorafenib-treated Pkd2cKO mice is a consequence of increased ERK1/2 signaling. In apparent contrast to our in vivo data, Yamaguchi et al.23 reported that sorafenib inhibits ERK1/2 activation and cell proliferation in kidney cells isolated from cysts of ADPKD patients. To clarify whether sorafenib has inhibitory effects on isolated PC2-defective cholangiocytes, we measured cell proliferation (by MTS and BrdU assays) and the levels of phosphorylated ERK1/2 in cholangiocytes isolated from normal controls and from liver cyst epithelial cells of Pkd2cKO mice, as described.

SBP was associated with hepatic encephalopathy (HE) in 93(57.7%), Dactolisib Variceal bleed (VB) in 16(9.9%), septic shock in 60(37.2%) requiring ventilator support in 47(29.2%) with median hospital stay of 7(range 4-14) days with a high mortality (n=43, 26.7%); predominantly due to sepsis (83.7%), Variceal bleed (11.7%). The predictors

of poor survival were presence of HE, Child-C status, MELD >24, persistence of SBP on D3 and D7, low ascitic fluid glucose <92mg/dl%, culture positivity for ascitic fluid (p<0.05). Reduction in ascitic fluid neutrophil count by 13% on D3, was the only predictor associated with improved survival (p<0.05). Conclusions:- The clinical presentation, advanced liver disease, low ascitic fluid glucose with culture positivity at the baseline and the neutrophil count reduction but not the base line ascitic fluid TLC or reduction at 48hr predict the resolution of SBP and overall outcome. The response tap at 48 hr showing neutrophil NVP-BGJ398 nmr count reduction by 13% is associated with better outcome Disclosures: The following people have nothing to disclose: Ashok K. Choudhury, Ankur Jindal, Chandan K. Kedarisetty, Tanmay S. Vyas, Ajeet S. Bhadoria, Shiv K. Sarin Purpose : To analyze the impact of TIPS with covered stents on survival of patients with

“severe” portal hypertension compared to a control group treated medically. To assess complications associated with implantation of the TIPS. Material and methods : 344 consecutive patients were hospitalized for decompensated cirrhosis (Child-Pugh B 60% / C 40%) from 01/2008 to 12/2012. Covered stent was implanted in 98 patients for refractory ascites or recurrent gastrointestinal

bleeding. Assessment of median survival (MS) with and without TIPS, MS according to Child-Pugh score and after matching 1:1 (n=130) for age, Child-Pugh score, MELD score, presence of hepatocellular carcinoma HCC, to a control group having a first decompensation. Results :TIPS implantation was successful in 100% of rates. The mean portosystemic pressure gradient decreased from 18.5±4.5 mmHg to 5.8±2.6 mmHg. MS of patients with TIPS (n=98) was 29.4 months [22-38.6] vs. 12.9 months [10.2-18.3] without TIPS (n=246), p=0.0015 ; MS of child-pugh B patients with TIPS (n=69) was 38.6 months [29.4-48.7] vs. 19.1 months [14.1-35.3] without TIPS (n=137), p=0.0183; 上海皓元医药股份有限公司 MS of child-pugh C patients with TIPS (n=29) was 17.4 months [10.1-25.3] vs. 8 months [6.2-11.2] without TIPS (n=109), p=0.22. TIPS was a prognostic variable associated with survival in univariate analysis (p=0.015). HCC, alcoholic hepatitis were more frequent in patients without TIPS (respectively 31% vs. 8%, p <.0001, 17% vs. 10%, p=0.05). After matching 1:1 for age (61 ±10), Child-Pugh score (B 66%, C 34%), MELD score (17.0±4.2) and presence of HCC (9%), esophageal varices grade 2 or 3 (p=0.003), refractory ascites (p=0.01), an increase in the portosystemic gradient (p=0.

SBP was associated with hepatic encephalopathy (HE) in 93(57.7%), find more Variceal bleed (VB) in 16(9.9%), septic shock in 60(37.2%) requiring ventilator support in 47(29.2%) with median hospital stay of 7(range 4-14) days with a high mortality (n=43, 26.7%); predominantly due to sepsis (83.7%), Variceal bleed (11.7%). The predictors

of poor survival were presence of HE, Child-C status, MELD >24, persistence of SBP on D3 and D7, low ascitic fluid glucose <92mg/dl%, culture positivity for ascitic fluid (p<0.05). Reduction in ascitic fluid neutrophil count by 13% on D3, was the only predictor associated with improved survival (p<0.05). Conclusions:- The clinical presentation, advanced liver disease, low ascitic fluid glucose with culture positivity at the baseline and the neutrophil count reduction but not the base line ascitic fluid TLC or reduction at 48hr predict the resolution of SBP and overall outcome. The response tap at 48 hr showing neutrophil Aloxistatin datasheet count reduction by 13% is associated with better outcome Disclosures: The following people have nothing to disclose: Ashok K. Choudhury, Ankur Jindal, Chandan K. Kedarisetty, Tanmay S. Vyas, Ajeet S. Bhadoria, Shiv K. Sarin Purpose : To analyze the impact of TIPS with covered stents on survival of patients with

“severe” portal hypertension compared to a control group treated medically. To assess complications associated with implantation of the TIPS. Material and methods : 344 consecutive patients were hospitalized for decompensated cirrhosis (Child-Pugh B 60% / C 40%) from 01/2008 to 12/2012. Covered stent was implanted in 98 patients for refractory ascites or recurrent gastrointestinal

bleeding. Assessment of median survival (MS) with and without TIPS, MS according to Child-Pugh score and after matching 1:1 (n=130) for age, Child-Pugh score, MELD score, presence of hepatocellular carcinoma HCC, to a control group having a first decompensation. Results :TIPS implantation was successful in 100% of rates. The mean portosystemic pressure gradient decreased from 18.5±4.5 mmHg to 5.8±2.6 mmHg. MS of patients with TIPS (n=98) was 29.4 months [22-38.6] vs. 12.9 months [10.2-18.3] without TIPS (n=246), p=0.0015 ; MS of child-pugh B patients with TIPS (n=69) was 38.6 months [29.4-48.7] vs. 19.1 months [14.1-35.3] without TIPS (n=137), p=0.0183; medchemexpress MS of child-pugh C patients with TIPS (n=29) was 17.4 months [10.1-25.3] vs. 8 months [6.2-11.2] without TIPS (n=109), p=0.22. TIPS was a prognostic variable associated with survival in univariate analysis (p=0.015). HCC, alcoholic hepatitis were more frequent in patients without TIPS (respectively 31% vs. 8%, p <.0001, 17% vs. 10%, p=0.05). After matching 1:1 for age (61 ±10), Child-Pugh score (B 66%, C 34%), MELD score (17.0±4.2) and presence of HCC (9%), esophageal varices grade 2 or 3 (p=0.003), refractory ascites (p=0.01), an increase in the portosystemic gradient (p=0.

SBP was associated with hepatic encephalopathy (HE) in 93(57.7%), Buparlisib cell line Variceal bleed (VB) in 16(9.9%), septic shock in 60(37.2%) requiring ventilator support in 47(29.2%) with median hospital stay of 7(range 4-14) days with a high mortality (n=43, 26.7%); predominantly due to sepsis (83.7%), Variceal bleed (11.7%). The predictors

of poor survival were presence of HE, Child-C status, MELD >24, persistence of SBP on D3 and D7, low ascitic fluid glucose <92mg/dl%, culture positivity for ascitic fluid (p<0.05). Reduction in ascitic fluid neutrophil count by 13% on D3, was the only predictor associated with improved survival (p<0.05). Conclusions:- The clinical presentation, advanced liver disease, low ascitic fluid glucose with culture positivity at the baseline and the neutrophil count reduction but not the base line ascitic fluid TLC or reduction at 48hr predict the resolution of SBP and overall outcome. The response tap at 48 hr showing neutrophil BAY 57-1293 count reduction by 13% is associated with better outcome Disclosures: The following people have nothing to disclose: Ashok K. Choudhury, Ankur Jindal, Chandan K. Kedarisetty, Tanmay S. Vyas, Ajeet S. Bhadoria, Shiv K. Sarin Purpose : To analyze the impact of TIPS with covered stents on survival of patients with

“severe” portal hypertension compared to a control group treated medically. To assess complications associated with implantation of the TIPS. Material and methods : 344 consecutive patients were hospitalized for decompensated cirrhosis (Child-Pugh B 60% / C 40%) from 01/2008 to 12/2012. Covered stent was implanted in 98 patients for refractory ascites or recurrent gastrointestinal

bleeding. Assessment of median survival (MS) with and without TIPS, MS according to Child-Pugh score and after matching 1:1 (n=130) for age, Child-Pugh score, MELD score, presence of hepatocellular carcinoma HCC, to a control group having a first decompensation. Results :TIPS implantation was successful in 100% of rates. The mean portosystemic pressure gradient decreased from 18.5±4.5 mmHg to 5.8±2.6 mmHg. MS of patients with TIPS (n=98) was 29.4 months [22-38.6] vs. 12.9 months [10.2-18.3] without TIPS (n=246), p=0.0015 ; MS of child-pugh B patients with TIPS (n=69) was 38.6 months [29.4-48.7] vs. 19.1 months [14.1-35.3] without TIPS (n=137), p=0.0183; medchemexpress MS of child-pugh C patients with TIPS (n=29) was 17.4 months [10.1-25.3] vs. 8 months [6.2-11.2] without TIPS (n=109), p=0.22. TIPS was a prognostic variable associated with survival in univariate analysis (p=0.015). HCC, alcoholic hepatitis were more frequent in patients without TIPS (respectively 31% vs. 8%, p <.0001, 17% vs. 10%, p=0.05). After matching 1:1 for age (61 ±10), Child-Pugh score (B 66%, C 34%), MELD score (17.0±4.2) and presence of HCC (9%), esophageal varices grade 2 or 3 (p=0.003), refractory ascites (p=0.01), an increase in the portosystemic gradient (p=0.