Multiple marker combinations improved sensitivity for eCCA The m

Multiple marker combinations improved sensitivity for eCCA. The most discriminant marker pair was CYP26C1

and LOC645323, which exhibited sensitivity of 83% for eCCA at a specificity of 95% (AUC 0.92). Conclusion: Novel methylation markers for CCA were identified by RRBS and validated in both iCCA Ridaforolimus supplier and eCCA. Further studies are now indicated to validate the performance of these aberrantly methylated markers in comparison to brush cytology, and in minimally invasive media such as bile, blood and stool. Disclosures: William R. Taylor – Patent Held/Filed: Exact Sciences Tracy C. Yab – Patent Held/Filed: Exact Sciences Lewis R. Roberts – Grant/Research Support: Bristol Myers Squibb, ARIAD Pharmaceuticals, BTG, Wako Diagnostics, Inova Diagnostics, Gilead Sciences David Ahlquist – Advisory Committees or Review Panels: exact sciences; Consulting: exact sciences; Grant/Research Support: exact sciences; Stock Shareholder: exact sciences John B. Kisiel – Grant/Research Support: Exact Sciences The following people have nothing to disclose: Mohammed M. Aboelsoud, Patrick H. Foote, Douglas W. Mahoney, Thomas C. Smyrk Background: Biliary tract cancers (BTCs) encompass intrahepatic and extrahepatic cholangiocarcinoma ITF2357 concentration and gallbladder carcinoma (ICC, EHCC and GBC); EHCCs subdivided into perihilar and distal cholangiocarcinoma (Perihilar-CC and Distal-CC). Cholangiocytes

constitutively expressed cytokeratin 19 (CK 19) and upregulated serum CK 19 fragment (CYFRA 21-1)

had been reported in ICC; however, clinical significance of CYFRA 21-1 in BTCs remained inconclusive. Method: CYFRA 21-1, CA 19-9 and CEA were quantitated preoperatively, on postoperative 7th day (POD7) and during follow-up in 134 consecutive BTCs patients (41 ICC, 32 GBC, 31 Perihilar-CC and 30 Distal-CC) and 52 patients with benign biliary diseases. The receiver operator characteristic (ROC) curves of biomarkers were analyzed. Level of CYFRA 21-1 was correlated with patients’ clinicopathologic features and follow-up data. Results: Serum CYFRA 21-1 was significantly upregulated in BTCs and expressional difference of CYFRA 21-1 existed among BTCs subtypes. Based on the old maximal Youden’s index, cutoff value of CYFRA 21-1 was selected: 2.61 ng/mL for BTCs (sensitivity, 74.6%; specificity, 84.6%); 3.27 ng/mL both for ICC (75.6%; 96.2%) and GBC (93.7%; 96.2%); 2.27 ng/mL for Perihilar-CC (71.0%; 71.2%) and 2.61 ng/mL for Distal-CC (63.3%; 84.6%). Diagnostic capacity of CYFRA 21-1 varied among BTCs subtypes: GBC or ICC > Distal-CC or Perihilar-CC. When compared with CA19-9 and CEA, CYFRA 21-1 showed better discrimination performance in GBC and ICC; combination of these biomarkers wasn’t superior to CYFRA 21-1 alone in diagnosing BTCs or either BTCs subtypes. CYFRA 21-1 was correlated with BTCs tumor stage, including tumor number, adjacent organ invasion and TNM stage. Serum CYFRA 21-1 declined significantly on POD7 after curative resection and reelevated when tumor recurred.

3 To better put into perspective what will happen to our patients

3 To better put into perspective what will happen to our patients with advanced NASH, it is logical to compare it to HCV, a disease with a well-established natural history. In a small prospective cohort study of Australian patients published in HEPATOLOGY nearly a decade ago, Hui and colleagues compared 23 patients with NASH-derived cirrhosis to 23 patients with untreated HCV-derived cirrhosis and 23 nonresponders with HCV-derived cirrhosis. The authors found that patients with NASH

cirrhosis experienced less hepatic decompensation, but a similar mortality to their HCV cirrhosis counterparts.4 In this issue of HEPATOLOGY, Bhala et al. extend their findings to a multinational prospective cohort study that includes patients from Italy, the United States, the United Kingdom, and Australia. They investigated the long-term outcome of patients with NASH or HCV and advanced fibrosis (stage 3 or 4). GPCR & G Protein inhibitor They compared 247 patients with NASH to 264 patients LY2109761 with HCV (nonresponders or untreated) in the analysis and followed them for a mean of 85.6 and 74.9 months, respectively. The findings demonstrate

that whereas the HCV cohort had more liver-related morbidity and incident HCC than the NASH cohort, rates of CV events and overall mortality were no different. Importantly, the current study differs from prior work in that it included patients with stage 3 fibrosis, in addition to those with compensated

cirrhosis. This is a timely study that sheds light on some aspects of the natural history of NAFLD. However, it has limitations that should be considered when interpreting the results. Given the heterogeneity of what we currently refer to as NASH, it is unlikely that any study would be generalizable to the entire NASH population. Ethnic differences in the susceptibility to develop NAFLD or progressive liver injury are well documented.5 For example, Hispanics and Asians (particularly the Indian subcontinent and southeast Asia), are at increased risk for advanced NASH, whereas African Liothyronine Sodium Americans are relatively protected despite the presence of similar metabolic risk factors.6-8 Although the current study is a multinational study from four countries (Australia, Italy, the United States, and the United Kingdom), 92% of the patients with NASH were Caucasian. Thus, as the authors concede, it is not clear whether these findings are applicable to other races. Although this is a potential weakness of the study, one could argue that given the heterogeneity of the NASH population at large, studies of ethnic-specific cohorts are important. It is known that HCV treatment response deters the rate of decompensation and the development of HCC.9 Thus, the natural history of the HCV group chosen by Bhala et al. was at less risk of being influenced by external factors such as viral clearance.

38 Furthermore, only patients with PBC and serum AMA react with H

38 Furthermore, only patients with PBC and serum AMA react with HiBEC Abs, yet patients with PBC without detectable AMA still have biliary damage. This suggests that biliary damage in PBC may not only be mediated by autoantibodies but also be cell-mediated responses, which would not have been detected in the experimental approach used here. Data from this study reinforces the hypothesis of apoptosis-related learn more immune tolerance as a mechanism in the initiation and perpetuation in PBC. Clearly, the etiology of PBC is unknown. However, both genetic susceptibility and environmental factors contribute to the onset

of disease. Interestingly, a number of candidate gene studies have reported critical PF-6463922 concentration links involving both MHC and non-MHC genes.39-44 More recently, genome-wide case–control association studies in PBC have identified a significant association with IL-12A (interleukin-12A), IL-12RB2 (interleukin-12

receptor, beta2 subunit), and STAT4 (signal transducer and activator of transcription 4) polymorphisms.45, 46 Interestingly, IL-12A polymorphism is associated with celiac disease47 and multiple sclerosis,48 and STAT4 polymorphism is also found in patients with SLE and rheumatoid arthritis.49 The association of these pleiotropic immune function–related genes in PBC and other autoimmune diseases illustrates that multiple genes are shared between clinical immune-related diseases, and the immune-mediated pathogenesis may be secondary upon breaking of tolerance by environmental xenobiotics.50 The challenge is to translate these genetic differences with functional human immunopathology. The pattern of antigens found within ABs is determined not by disease but rather by the evolutional characters of each cell type. Given this perspective, no cell that is subject of an autoimmune attack is really an innocent victim. Rather, development of disease, whether systemic or organ-specific, isometheptene is largely dependent

on the genetics and/or environment-induced susceptibility of each individual to the loss of tolerance of a specific apotope. Thus, in the case of PBC, autoimmunity does not target epithelial cells of the bronchia or mammary glands, despite the failure of these epithelial cells to completely clear all self-antigens under the same experimental conditions. HiBECs are targeted and destroyed for the selective presence of special apoptotic antigens—PDC-E2 and sometimes others—that are sensitive to the preexisting immunologic defect in patients with PBC. In addition to the three known mitochondrial autoantigens in PBC, we identified another mitochondrial enzyme, DECR1, as exclusively intact within HiBEC ABs. DECR1 was also immunologically recognized by antibodies in a small number of serum samples from patients with PBC.

A life expectancy of 10 years is predicted for patients with a se

A life expectancy of 10 years is predicted for patients with a serum bilirubin level <2.0 mg/dL, 5 years for 2.0–3.0 mg/dL, and 1 year for >6.0 mg/dL. Recommendations: Total bilirubin, prothrombin (INR), albumin, and the serum creatinine level, which are essential to calculate the MELD score, should be measured when considering liver transplantation. (LE 2b (2a in part), GR A) Patients with PBC should be referred to transplant hepatologists when serum total bilirubin level is >5 mg/dL. To encourage the patients to prepare for liver transplantation, an earlier and appropriate explanation of liver transplantation is desirable. (LE 4,

GR B) Although there is no completely curative treatment for PBC, ursodeoxycholic acid (UDCA) is currently considered the first-line treatment for the disease. UDCA delays the progression of PBC, although it does Autophagy Compound Library concentration not have a significant benefit for PBC at the advanced stage. The SRT1720 chemical structure clinical usefulness of UDCA is evaluated according to the following factors: (i) improvement of serum biochemical markers, such as ALP, GGT, AST, ALT and total bilirubin; (ii) histological improvement of cholangitis, liver inflammation and liver fibrosis; and (iii) delay in the disease progression until end-stage liver disease, death, or liver transplantation. The following Paris

and Barcelona criteria are useful for evaluating the clinical outcome of UDCA treatment. Resveratrol (i) Paris criteria: total bilirubin ≤1.0 mg/dL, ALP ≤3 × the upper normal limit (UNL), and AST ≤ 2 × UNL at 1 year after introduction of UDCA. (ii) Barcelona criteria: decrease of ALP ≥40% at 1 year after introduction of UDCA. Liver transplantation is the only therapeutic approach for patients in the advanced stage when medical treatment shows little improvement. Prevention and treatment strategies for comorbid autoimmune

diseases, cholestasis, and cirrhosis-related symptoms and complications are required. Although the term cirrhosis is included in the name PBC, most patients (70–80%) with PBC have little clinical and histological evidence of liver cirrhosis. Patients should be informed accordingly to prevent misunderstanding of their prognoses. Currently, patients are likely to be diagnosed at earlier stages and disease progression is likely to be delayed by UDCA. Therefore, the prognosis of patients with aPBC, as long as they remain asymptomatic, is equivalent to that in the general population. No restrictions are necessary in daily life for patients with aPBC. By contrast, some restrictions in daily life and nutritional education are required for patients with sPBC, depending on symptoms, expected future complications, and disease severity. Extensive clinical trials including randomized clinical trials (RCT) and meta-analyses were carried out for UDCA after the first report by Poupon et al.

We evaluated the safety and efficacy of Biotest-HCIG, a human hep

We evaluated the safety and efficacy of Biotest-HCIG, a human hepatitis C immune globulin to prevent HCV recurrence by neutralizing remaining HCV reservoirs in patients on pre-LT HCV AVT at the time of LT. Methods: In this phase 3, open-label randomized study, wait-listed patients with chronic HCV infection (all genotypes) treated with any AVT and who achieved HCV RNA <100 IU/ml prior to LT were eligible. In total, 84 patients will be randomized 1:1:1 to Biotest-HCIG (200 mg/kg or 300 mg/kg given on the day

of LT and for 10 weeks post-LT) or observation. The primary endpoint is post-LT sustained Akt inhibitor virologic response (pTVR), defined as HCV RNA <43 IU/ml at 12 wks

post-LT treatment. Post-transplant immunosuppression is site-specific. Results: To date, 17 subjects (all male, median age 59 yrs, 100% genotype 1, 94% with hepatocellular carcinoma, 12% with living donors) have undergone LT. Pre-LT AVT was telaprevir/peginterferon/ribavirin (RBV) (12%), sofosbuvir/RBV (76%) or sofosbuvir/simeprevir (12%) given for a median of 51 days (range 14-164 days) pre-LT with all patients achieving HCV RNA <43 IU/mL pre-LT (71% also undetectable). With median post-LT follow-up of 8 wks, post-LT HCV recurrence has been documented in 2 patients - at wk 2 (control) and wk 3 (200 mg Biotest-HCIG) post-LT. Overall, 11/12 (92%) of Biotest-HCIG-treated patients have maintained undetectable HCV RNA compared to 4/5 (80%) of controls (Table). Among 4 patients who were Clomifene viremic at the time of LT and randomized to Biotest-HCIG, all have undetectable HCV RNA at median 9 wks follow-up. Biotest-HCIG-related side effects were infrequent and there were no discontinuations

due to adverse events. Conclusion: Biotest-HCIG is safe and well-tolerated. To date, HCV recurrence rates in patients on pre-LT AVT are lower in Biotest-HCIG-treated patients compared with controls (8% vs 20%) and all patients viremic at LT who received Biotest-HCIG have undetectable HCV RNA. These preliminary results suggest Biotest-HCIG may be beneficial as an adjuvant therapy for HCV patients on AVT undergoing LT. Disclosures: Norah Terrault – Advisory Committees or Review Panels: Eisai, Biotest; Consulting: BMS, Merck; Grant/Research Support: Eisai, Biotest, Vertex, Gilead, AbbVie, Novartis, Merck Sanjaya K. Satapathy – Advisory Committees or Review Panels: Gilead Elizabeth C. Verna – Advisory Committees or Review Panels: Gilead; Grant/ Research Support: Salix, Merck Thomas D. Schiano – Advisory Committees or Review Panels: vertex, salix, merck, gilead, pfizer; Grant/Research Support: massbiologics, itherx Sher Linda – Grant/Research Support: Biotest John M.

26, 27 Liver is a sinusoid-enriched organ and thus may contain ni

26, 27 Liver is a sinusoid-enriched organ and thus may contain niche cells capable of sustaining HSCs. Still, in this study, the formal possibility cannot be excluded that these cells were blood HSPCs adherent to Gemcitabine chemical structure the endovascular compartment of the liver, which could not be perfused out. Moreover, after LT, either donor HSPCs generate mature HSCs inside grafted liver or circulate to recipient BM for hematopoiesis. These possibilities remain to be determined in future studies. The authors thank the Liver Transplantation Center at Queen Mary hospital of the University of Hong

Kong for outstanding clinical liver transplantation care. The authors also thank Ms. Kammy Yik, Banny Lam, and Waiyee Ho for data organization of LT donors and recipients. The authors also thank Dr. Mo Yang at the Department of Pediatrics and Adolescent Medicine of the University of Hong Kong for his useful help on the experiment. The authors also thank Ms Amy Lam selleck products and Mr. Jimmy Chen of Applied Biosystems for their technical support. “
“Surgery in the patient

with cirrhosis is problematic, as encephalopathy, ascites, sepsis and bleeding are common in the postoperative period. Accurate preoperative assessment and planning, and careful postoperative management have the potential to reduce the frequency and severity of such complications, and reduce the length of hospital stay, but there is little literature evidence to prove this. Operative mortality and other risks correlate

with the severity of the liver disease, co-morbidities and the type of surgery. The Child-Turcott-Pugh Gefitinib price (CTP) score or model for end-stage liver disease (MELD) score may be used to determine the severity of the liver disease, but must also take into account recent changes in the patient’s condition. Surgery that does not involve opening the peritoneum may have slightly better outcomes, as the risk of ascitic leak, sepsis and difficult fluid management are reduced. Mortality rates range from 10% in CTP-A patients to 82% in CTP-C patients. The presence of portal hypertension is an important negative predictor, especially in abdominal surgery, as refractory ascites may occur. Careful monitoring in the postoperative period and early intervention of complications are essential. Hepatic resections in cirrhosis are associated with other considerations such as leaving sufficient liver tissue to prevent liver failure, and are beyond the scope of this review. Surgical procedures in patients with liver cirrhosis carry a significant risk of complications and have a high mortality. Accurate preoperative risk stratification can be difficult, and occasionally the patient is only found to have cirrhosis at the time of surgery. Even when the patient has previously diagnosed liver disease, the severity may easily be miscalculated as many of the tools we use are imprecise. The literature in this field is sparse, and outdated with respect to contemporary surgical technology.

Primary human hepatocyte cultures were transfected with genomic R

Primary human hepatocyte cultures were transfected with genomic RNAs of HCV genotypes 1a, 1b, and 2a (1 μg/106 cells) using FuGENE6 (Roche). On day 6 postinfection, the small RNA (≤200-nucleotide) fraction was enriched from HCV-infected cell RNA using a mirVana isolation CHIR-99021 in vitro kit (Ambion). Four micrograms of each sample together with positive control (synthetic Arabidopsis thaliana mir-157a, which is not present in the human genome) was spiked in and was hybridized to the microarray slide (BioMicro

System). After 16 hours, the hybridized microarray was washed with a standard sodium citrate solution to remove unhybridized probes. After 3 hours of Klenow exonuclease-1 incubation, exo(-) Klenow enzyme was added to extend the miRNAs hybridized to the chip-attached templates in a primer extension step. During this step, biotinylated dATP was

incorporated as a final portion of the extension through the designed polythymidine region. Detection of this template-hybridized miRNA was performed using streptovidin-conjugated Alexa-fluor-555, which binds to the biotinylated stretch of A’s at the 3′-end of the captured miRNA. Fluorescence data sets were collected using GenePix 4000 scanner (Axon). Details of the procedure are described in Yeung et al.14 Primary hepatocytes were transfected with HCV1a genomic RNA (1 μg/106 cells) in triplicate. Parallel cultures were transfected with DLC-1 complementary DNA (cDNA) expression vector (50 ng/106 cells for 6 hours) prior to transfection with HCV 1a genomic RNA. Six days posttransfection, the cells were released with 0.05%

trypsin treatment and were resuspended at 104/100 μL in (phosphate-buffered selleck saline containing 2% fetal bovine serum) processed for Ki67 immunostaining (BD Biosciences) according Methane monooxygenase to the manufacturer’s instructions. Primary human hepatocytes were transfected with HCV genotypes 1a, 1b, and 2a (1 μg/106 cells) as described.12 Virus released in the culture medium was filtered through 0.25-μm filters from infected cells.12 Viral RNA replication was evaluated at indicated times after infection as outlined above, and the efficiency of virus released in the culture media was validated using the World Health Organization’s HCV standards (Acrometrix, Benicia, CA). Primary human hepatocyte culture was cotransfected with luciferase reporter containing DLC-1 3′ untranslated region (UTR) (50 ng/106 cells), miR-141 (50 nM/106 cells, antagomir) or miR-141 (50 nM/106 cells, Mimic) using Lipofectamine 2000 (Invitrogen). Luciferase assays (Promega) were performed on the third day after transfection according to the manufacturer’s instructions. The results are given as the mean ± SE. Statistical analysis of the data was performed using the Student t test, Fisher’s exact test, or otherwise as described. To assess virus infection-associated changes in host gene expression, we analyzed alterations in miRNAs in primary human hepatocytes infected with HCV genotypes 1a, 1b, and 2a (Supporting Information Fig. 1).

6, 7 Several studies suggest that a primary function of HBx in th

6, 7 Several studies suggest that a primary function of HBx in the HBV life cycle is to promote viral gene expression.8-10 Perhaps most compelling is the recent finding that primary human hepatocytes infected with HBx-deficient HBV particles show normal levels of cccDNA but essentially no viral gene expression.11 The underlying mechanism whereby HBx promotes viral messenger RNA (mRNA) synthesis remains elusive. In cell culture, HBx behaves as a pleiotropic transactivator capable of stimulating a variety

of cellular and Anti-infection Compound Library molecular weight viral promoters.12, 13 Although typically modest, the transactivation activity of HBx is likely biologically relevant. It is conserved among the HBx proteins encoded by HBV, woodchuck hepatitis virus, and ground squirrel hepatitis virus.8 Furthermore, the ability of HBx to stimulate reporter gene expression and HBV replication correlate.10, 14 The current explanation for the pleiotropic transactivation effects of HBx is that the protein Sunitinib can interact with numerous cellular proteins and has functions in both the cytoplasm and the nucleus of cells. Thus, HBx has been

proposed to activate diverse signal transduction pathways in the cytoplasm,12 whereas in the nucleus it is believed to function by way of direct interaction with transcription factors15, 16 (and references therein), components of the basal transcription machinery (reviewed12, 17), as well as DNA- and histone-modifying enzymes.18-20 That HBx may have so many activities is puzzling, especially because the HBx gene largely

overlaps the polymerase gene on the viral genome, a situation that has likely limited its potential to evolve multiple functions. In the present study we provide an alternative explanation for the pleiotropic transactivation properties of HBx. Previous work has established that HBx and WHx bind to host cell protein UV-damaged DNA binding protein 1 (DDB1) and Bacterial neuraminidase likely function as viral substrate-recruiting subunits of the DDB1-containing E3 ubiquitin ligase complex.14, 21 We show here that through its interaction with the E3 ligase, HBx up-regulates luciferase reporter and HBV gene expression by a mechanism that operates selectively on extrachromosomal DNA templates irrespective of the nature of the promoter sequences and cognate activators. cccDNA, covalently closed circular DNA; DDB1, UV-damaged DNA binding protein 1; GFP, green fluorescent protein; HBV, hepatitis B virus; HBx, hepatitis B virus X. GFP-HBx, GFP-HBx(R96E),22 GFP-SV5V,23 and the HBx(R96E)-DDB1 fusions14, 23 have been described and are all expressed at detectable levels.14, 22, 23 GFP-WHx was generated by amplifying the woodchuck WHx coding region by polymerase chain reaction (PCR) from a WHV genomic construct (OHVCGA prototype). The proteins were produced from the episomal vectors KEBOB-PL24 in Fig. 1A and EBS-PL24 in Figs.

Tumor histology was abstracted by cancer registrars


Tumor histology was abstracted by cancer registrars.

The first preference was to obtain this information EX 527 supplier from pathology reports, followed by other sources. Stage, histological confirmation, and first-course primary-site surgery data were all available for 1998-2008. Incidence trends by stage and histological confirmation were examined for the years from 1992 through 2008. Linear regression models were used to fit trend data (Joinpoint software, version 3.3.1; IMS, Silver Spring, MD).13 Annual percent change (APC) in regression-line slopes were considered statistically significant when the trend differed from zero (P < 0.05). Incidence trends were examined by histological confirmation, stage, and reported first-course surgical and ablative therapy. Five-year cause-specific survival was estimated during the most recent decade of surveillance with follow-up of vital status (1998-2007). Cause-specific survival was selected because life tables were Selleck Gefitinib unavailable for most racial and ethnic groups included in this analysis, and because life tables may not reflect mortality differentials between HCC cases and the population related to screening, socioeconomic status, or health behavior.14 Cause of death was

defined as cancer, with other causes of death censored at time of death. Survival analyses were restricted to 16,020 of 18,894 reported HCC cases (85%) diagnosed in SEER-13 registries during the most recent decade of surveillance (1998-2007). Cases were excluded from survival analysis because HCC was a second or later primary cancer diagnosis (n = 2,409; 13%), case information was limited to death certificate or autopsy reports (n = 418; 2%), or because the case was alive without information on survival time (n = 47; <0.5%). For historical context, 5-year cause-specific survival of HCC cases diagnosed in SEER-9 registries was calculated for 1975-1977. Overall, race- and ethnicity-specific survival and

95% confidence intervals (CIs) were estimated by first-course therapies in descending order of survival: liver transplantation, Uroporphyrinogen III synthase RFA of tumors less than 3 cm (potentially curative5), resection, local tumor destruction, all cases, and cases with no reported surgery. Stage distributions were presented by group, based on “reason no surgery performed,” “SEER historic stage A,” and “first-course primary-site surgery.” Among 1,249 cases with local tumor destruction, 75 (6%) underwent resection. Their 38% 5-year survival was similar to all cases with local tumor destruction (35%). Groups were combined for analysis. Of 21,390 HCCs diagnosed during 1998-2008, 4,727 (22%) reported liver surgery or local tumor destruction (Table 1). Interventions were reported more often among localized (39%) than regional (16%) or distant/unstaged cases (4%).

“Scent marking is commonly described as a territorial beha

“Scent marking is commonly described as a territorial behaviour, and scent marks might deter potential intruders from entering occupied areas. Conspecific neighbours present both a reproductive and a territorial threat, thus, determining which, if any, of these threats shapes scent-marking behaviour is difficult. Banded mongooses Mungos mungo provide a rare clear separation between reproductive rivals (found within groups) and territorial rivals (neighbouring groups), because immigration into social groups is

extremely rare, and mating occurs almost exclusively within groups. This situation offers an opportunity to assess the relative importance of territorial defence and intra-group competition for mates in shaping scent-marking behaviour. We combined detailed behavioural observations of scent marking, chemical analyses of scent composition and discrimination experiments in the MK-1775 solubility dmso field, and found little evidence for

higher rates of scent marking in overlapping areas, a lack of group specificity of scents and a failure of individuals to discriminate between the scents of different groups. Although scent may fulfill some role in territorial demarcation and defence, these results suggest that scent marks and scent-marking patterns are also involved in communicating within social groups. “
“Livestock predation by Asiatic lions Panthera leo persica in and around Gir Protected Area (Gir PA) in western India results in conflict with people and has important implications for the conservation of this species. A Transmembrane Transporters modulator 5-year study was undertaken to document diet and predation patterns based on direct observations of radio-collared lions,

opportunistically located carcasses and scat analysis. Magnitude of livestock predation was assessed based on interviews of resident pastoralists in 20 settlements. Lions made one kill in every 4 days and the diet primarily consisted of large prey. Wild prey, mainly chital Axis axis, represented 80% of the lion’s diet within Gir PA based on scat analysis. Within the protected area, though enough lions predominantly consumed wild prey in proportion to their availability, they were yet responsible for majority of livestock loss to the resident communities. The proportion of wild and domestic animals killed by lions varied between seasons: significantly more wild ungulates were killed during summer when prey were concentrated around waterholes. Domestic animals were the major prey outside the protected area. Thus, despite high proportion of wild prey in the diet, lions still considerably depended on livestock. Our study defines focal areas of lion–human conflict and suggests better husbandry practices. Population decline, crisis management, stabilization, precarious recovery and sustained recovery have been described as five stages of species restoration (Linklater, 2003).