Herein, we show that α4 integrin did not work in Con A-induced hepatitis but rather exacerbated symptoms perhaps by blocking MDSCs.

MDSCs are a heterogeneous family of cells that are in various stages of myeloid cell differentiation.[37] In mice, MDSCs are phenotypically characterized as CD11b+GR1+ coexpressing cells that represent a mononuclear CD49d+ MDSC subpopulation which strongly suppresses T-cell proliferation and activation through inducible NOS in tumor-bearing mice[28] but also in T-cell-mediated diseases. Importantly, our results show that Con A causes the recruitment R428 mw of monocytic MDSCs into the liver, which can be inhibited by anti-α4 integrin leading to increased IFN-γ production Y27632 in CD3 T cells. Although we previously blocked exogenous Th1 trafficking to the liver with anti-α4 integrin, the net effect of inhibiting α4 integrin recruitment of

endogenous cells including MDSCs caused more injury and increased recruitment of some cell types. Moreover MDSCs may stimulate Treg function and expansion[38] and Tregs are potent inhibitors of monocytic cells including effector T cells.[39, 40] Although blocking α4 integrin did not modify the number of Tregs in Con A-induced injured liver, we cannot exclude the possibility that a reduced number of MDSCs might cause a failure in stimulating Tregs and subsequent inhibitory cytokine production. Interestingly a 2-fold higher proportion of Tregs physiologically resides in the liver of VAP-1-deficient mice than of wild-type mice, which is augmented further in acute inflammation derived by Con A, suggesting that increased Tregs could also be contributing to benefits in VAP-1-deficient mice. Although SSAO inhibition alone did little to reduce inflammation blocking SSAO and adhesion

of VAP-1 was optimal. It has been reported that an SSAO inhibitor of VAP-1 reduced the recruitment of Gr-1+CD11b+ myeloid cells into tumor vasculature and attenuated the growth of tumor indicating that the SSAO activity of VAP-1 may be responsible for the recruitment of at least some leukocytes into the tumor.[41] In conclusion, VAP-1 plays a critical role in recruitment Fenbendazole of CD4 Th2 cells and inhibition of or lack of VAP-1 causes a decline in IL-4-producing T cells and subsequent improvement of the disease state. In various disease states ranging from sepsis to viral and autoimmune hepatitis, a very significant number of lymphocytes are recruited into the liver sinusoids. The strategy of inhibiting an inappropriate accumulation of inflammatory cells in liver microvasculature could improve the pathological state of a number of inflammatory diseases. Our data suggest that targeting VAP-1 has promise for the development of a potential antiinflammatory therapy. Anti-α4 integrin exacerbates the injury derived by Con A, which may be due to the inhibition of monocytic MDSCs, or indirect effects upon Tregs.

6 Despite the clear-cut association

between low bone mass and jaundice in patients with chronic cholestatic diseases,7-9 and the experimental find more evidence of skeletal fragility in bile duct–ligated rats,10 the influence of bilirubin on osteoporosis in patients with liver disease has been questioned because of some contradictory results concerning low bone mass and Gilbert’s syndrome, a mild clinical condition characterized by increased circulating levels of unconjugated bilirubin.11, 12 The effects of bilirubin on osteoblasts have only been assessed in one study which was mainly focused on the consequences on cell viability.5 However, no other effects have been explored including cell differentiation and mineralization and the regulation of some osteoblast-related genes, particularly those from the osteoprotegerin

(OPG)/receptor activator of nuclear factor-κB ligand (RANKL) system, which are the key regulators of osteoblast-induced osteoclastogenesis. Therefore, in this study, we evaluated the consequences of high bilirubin concentrations on cell viability, differentiation, mineralization, and gene expression in osteoblasts. DMEM, Dulbecco’s modified Eagle medium; FBS, fetal bovine serum; HAM F-12, MYO10 Ham’s formula-12 nutrient mixture; HBSS, Hank’s balance salt solution; mRNA, messenger RNA; OPG, osteoprotegerin; Silmitasertib molecular weight PCR, polymerase chain reaction; RANKL, receptor activator of nuclear factor-κB ligand; RUNX2, runt-related transcription factor 2; SD, standard deviation. Dulbecco’s modified Eagle medium (DMEM), Ham’s formula-12 nutrient mixture (HAM F-12), Hank’s balanced salt solution

(HBSS), fetal bovine serum (FBS), L-glutamine, and trypsin were purchased from Invitrogen (Grand Island, NY); insulin–transferrin–selenium, dihydroxyvitamin D3 (vitamin D), bilirubin, ascorbic acid, α-naphthylphosphate acid, and fast blue were from Sigma Chemical Co. (St. Louis, MO); penicillin–streptomycin was obtained from LabClinics (Barcelona, Spain). Bilirubin (Sigma) stock solution of 1600 μM was prepared just before use by dissolving it into 10 mL 0.1 N NaOH under dim light, as described.13, 14 The bilirubin solution was passed through a sterile filter (0.22 μm pore size) and adjusted to pH 7.2-7.4 with 0.1 N HCl if necessary. The bilirubin stock solution was added to a final concentration of 10 to 1000 μM in the culture medium. The cell cultures were kept in dark conditions to prevent light degradation of the bilirubin. Control cells were treated with vehicle (NaOH 0.1 N).

The current studies used a high trans-fat, high fructose diet to promote murine NAFLD with fibrosis,18 revealing that L-Fabp−/− mice not only exhibit attenuated steatosis with decreased LD accumulation but are also protected against steatosis-associated fibrogenesis. Several elements of these findings merit additional discussion. Little is known about the expression of genes related to FA uptake and metabolic channeling during HSC activation. Earlier studies in freshly isolated rat HSCs revealed expression

of mRNAs encoding Brain-Fabp (B-Fabp, Fabp7), L-Fabp, as well as retinol binding protein selleck chemicals (Rbp), with decreased expression upon culture in vitro.23 The current findings in murine HSCs confirm some but not all of those findings (specifically, B-Fabp was undetectable in our hands) but also demonstrate that L-Fabp depletion temporally accompanies LD depletion from cultured WT murine HSCs and that HSCs isolated from L-Fabp−/− mice SB525334 contain

fewer LDs. Importantly, Ad-L-Fabp expression both increased the accumulation of FA and neutral lipid and also suppressed the expression of profibrogenic genes in passaged HSCs. These findings imply that the expression of L-Fabp both promotes LD accumulation and also inhibits HSC activation in vitro. The underlying mechanisms and pathways remain to be defined, but we speculate that L-Fabp Osimertinib in vitro regulates the uptake and retention of lipid mediators and signaling molecules in HSCs, analogous to functions described for L-Fabp in liganding PPARα in isolated hepatocytes.24 Other studies have established a role for L-Fabp in the metabolic channeling of FA in enterocytes for complex lipid assembly.25 The findings in TFF-fed mice revealed a striking shift in LD accumulation in L-Fabp−/− mice with decreased expression of several LD-associated genes

including Plin4, Plin5, and Cidec, each of which has been shown to be modulated as downstream targets of either Pparα26 or Pparγ27, 28 in murine liver. Our a priori hypothesis, based on the role of L-Fabp in HSC activation in vitro, was that L-Fabp−/− mice would display enhanced susceptibility to high-fat diet-induced liver injury and fibrosis. Instead we found that L-Fabp−/− mice exhibited reduced fibrogenesis, which correlated with decreased hepatic steatosis. This discrepancy may reflect the complex intracellular crosstalk and lipid signaling that occurs in vivo between hepatocytes and HSCs and highlights the importance of in vivo models in understanding complex systems. Moreover, since germline deletion of L-Fabp has been shown to alter intestinal FA trafficking,12, 14, 15 it is unclear whether the absence of L-Fabp in the intestinal mucosa may also alter the progression of experimental NAFLD.

Clinical outcomes were predefined in the HALT-C Trial protocol and included death due to any cause, liver-related death, HCC, and hepatic decompensation (ascites, hepatic encephalopathy, variceal hemorrhage, or spontaneous bacterial peritonitis); we also collected data on liver transplantation. Two definitions

of HCC were adopted in the HALT-C Trial: “definite” HCC and “presumed” HCC. Definite HCC was defined by histologic confirmation or a new, ≥2-cm mass lesion on imaging with AFP levels increasing to >1000 ng/mL. Presumed HCC was defined as a new mass lesion on ultrasound in the absence of histology and AFP < 1000 ng/mL click here in conjunction with one of the following characteristics: (1) two liver imaging studies showing a mass lesion with characteristics of HCC, (2) progressively enlarging lesion on ultrasound and leading to death, or (3) one additional imaging study showing a mass lesion with characteristics of HCC that either increased in size over time or was accompanied by increasing AFP levels.11 An outcome committee, whose

members consisted of a rotating panel of three clinical site investigators blinded to study participant and clinical site, reviewed and adjudicated the validity of each clinical outcome. For the current analysis, we assessed overall mortality (i.e., death from any cause) or liver transplantation, and liver-related morbidity and mortality. Death from any cause or liver transplantation was defined U0126 as any patient who died (of any cause) or had undergone liver transplantation. The four categories of liver-related morbidity and mortality were: (1) Any liver-related clinical outcome: all patients in whom decompensated liver disease (ascites, variceal bleeding, hepatic encephalopathy, or spontaneous bacterial peritonitis) or HCC (presumed or definite) developed, or who had undergone liver transplantation, or died from conditions related to liver disease. For the calculation of

the cumulative Buspirone HCl incidence of any liver-related outcomes, patients were censored at the time when the first outcome developed. (2) Decompensated liver disease: all patients whose first clinical outcome was decompensated liver disease. (3) HCC: all patients in whom, at any time during the study, definite or presumed HCC developed. (4) Liver-related death or liver transplantation: any patient who died as the result of a liver-related cause, based on the opinion of the clinical site principal investigator, or who had undergone liver transplantation. Statistical analyses were performed at the Data Coordinating Center (New England Research Institute, Watertown, MA) with SAS software, release 9.1 (SAS Institute Inc., Cary, NC). The chi-squared and analysis of variance tests were used to determine categorical and continuous variables that were significantly different between the SVR group and the two comparison groups (NR and BT/R).

The boundaries and HRs for high-risk tertiles were CA Cloral ≤9.47 mL kg−1 min−1 (HR, 6.52), PHM ≤94.5 (HR, 4.97), spleen volume ≥5.93 mL kg−1 (HR, 4.16), and CA shunt ≥46% (HR, 3.98) (Table 3). By ROC analyses, c statistics were 0.84

for CA Cloral, 0.79 for CA shunt, 0.79 for PHM, and 0.78 for spleen volume. Baseline prevalence of PCI-32765 mouse cirrhosis (Ishak fibrosis stage 5 or 6) was higher and platelet count lower in the patients who subsequently experienced clinical outcomes (Table 2). Therefore, we tested the independence of QLFTs in predicting clinical outcomes by including these two factors as covariates. Interestingly, histologic stage dropped from significance in the prediction of clinical outcomes in models with AP Cl, CA Cloral, CA shunt, PHM, and spleen volume. Each QLFT, except spleen volume, retained significance in predicting clinical outcome in models of the QLFT with platelet count and histologic stage (Table 3). We further tested

the independence of QLFTs in models of each QLFT with the HALT-C laboratory score, which is derived from platelet count, bilirubin, Decitabine clinical trial albumin, and AST:ALT ratio. MBT, CA Cloral, PHM, and spleen volume remained significant, and CA shunt approached significance in these models (Table 3). Figure 3 displays the results for the serial QLFTs. The percentages of patients above and below QLFT cutoffs who experienced clinical outcomes during Rebamipide the 2-year intervals after QLFT studies at baseline, month

24, and month 48 are shown. AP Cl, caffeine kelim, CA Cloral, CA shunt, PHM, and spleen volume performed best. Eleven to thirty percent of patients characterized as high risk by QLFTs experienced their initial clinical outcomes in the 2-year intervals between testing periods. Pooled relative risks (RRs) for initial clinical outcomes, based on these QLFT cutoffs, were (RR [95% CI]) AP Cl 7.25 (2.98-17.63), caffeine kelim 5.63 (2.66-11.90), GEC 3.08 (1.73-5.49), MEGX15min 2.48 (1.33-4.61), MBT 5.43 (2.18-13.55), CA shunt 7.62 (3.77-15.42), CA Cloral 14.09 (6.03-32.95), PHM 14.47 (6.24-33.55), and spleen volume 6.07 (3.10-11.89). Sensitivities (pooled) of the serial QLFTs in identifying patients who developed outcomes were CA Cloral 86%, PHM 83%, AP Cl 80%, CA shunt 79%, caffeine kelim 76%, MBT 75%, spleen volume 72%, GEC 57%, and MEGX15min 51%. Perhaps even more important, characterization of a patient as low risk by QLFT cutoffs was associated with a very low risk for clinical outcome. The negative predictive values (pooled) for clinical outcome of QLFT cutoffs defining low risk were CA Cloral 98.4%, PHM 98.2%, AP Cl 97.6%, CA shunt 97.6%, caffeine kelim 97.1%, MBT 97.4%, spleen volume 97.0%, GEC 95.3%, and MEGX15min 95.0%. At each testing period, the mean values for QLFTs (except GEC) were significantly worse in the group of patients experiencing subsequent clinical outcomes.

Also, the data show that there is a decrease in Oct4 mRNA after plating. Similarly, Nanog’s mRNA was 15-fold in normal rat liver, again indicating a drop in Nanog levels after plating. These data for Oct4 and Nanog mRNA in Fig. 7A support their high protein levels seen at day 0 (2 hours after plating) in the selleck chemicals llc initial experiment (Fig. 2). Hepatocytes cultured with growth factors brought

back these levels, in contrast to hepatocytes cultured without the growth factors. The present data signify the fact that even though the expression of these reprogramming factors in cultures with GF is not comparable to MESC, the level of expression is nevertheless important for the proliferation and normal survival of these hepatocytes in culture. We also found that these reprogramming factors are up-regulated after PHx Everolimus purchase as seen by qRT-PCR, western blot, and IHC. In fact, the expression of REST and Oct4 is close to that of MESC,

whereas that of Myc is more than that in MESC (Fig. 7D,E). In view of our results with hepatocytes in culture, it is reasonable to speculate that they may play a role in liver regeneration in vivo as well. The fact that primary hepatocytes express these reprogramming factors but are not acting as stem cells is intriguing. The mechanism(s) that inhibit hepatocytes from behaving like stem cells in spite of expressing reprogramming factors is unknown and it probably relates to relative levels of expression. On the other hand, previous studies have shown that hepatocytes can transdifferentiate to biliary epithelial cells in vivo.21 Other studies have also shown that mouse22 and rat hepatocytes have a high capacity of clonal growth in recolonization of liver of mice with FAH deficiency.23-25 In these studies it was estimated that one mouse hepatocyte was check capable of generating 50 mouse livers. It is conceivable that the coordinated and growth factor-induced expression of REST and the reprogramming factors underlies the capacity

of hepatocytes for such high clonal growth, documented in several models of liver recolonization.26-28 It is also possible, however, that the expression of reprogramming factors may occur in other cell types under normal growth conditions. Our studies should prompt further investigation of both of these possibilities. We thank John Stoops for assistance with the partial hepatectomy experiments. Additional Supporting Information may be found in the online version of this article. “
“Background and Aim:  Although narrow-band imaging (NBI) is used increasingly in clinical situations, the significance of each NBI finding has not been investigated. The primary endpoint of the present study was to identify the significant NBI findings to diagnose esophageal mucosal high-grade neoplasia. Methods:  Between August 2007 and January 2009, we detected 59 new superficial esophageal lesions. The video images of NBI were recorded digitally.

However, tumor cell numbers in MC38CCL2 KD-inoculated mice were comparable to controls by day 13 (Fig. 5A), mirroring the

lack of difference in CD11b/Gr1mid recruitment at this time point. Likewise, fewer MC38GFP+ cells were detected in CCR2 KO mice compared with controls (Fig. 5B), although the differences were not as striking. Overall, decreased accumulation of CD11b/Gr1mid and CD11b/Gr1low cells in liver metastases caused a substantial reduction in tumor burden. In an attempt to deplete the CD11b/Gr1mid and CD11b/Gr1low subsets, CD11b-DTR mice bearing a human diphtheria toxin receptor https://www.selleckchem.com/products/Bortezomib.html (DTR) transgene driven by a CD11b promoter were used. Here, conditional ablation of CD11b+ cells can be achieved by diphtheria toxin (DT) administration.18

DT was administered to CD11b-DTR mice on day 7 and 9 after MC38GFP+ inoculation, a time when metastatic colonies had formed, and mice were sacrificed on day 11. DT administration markedly depleted CD11b/Gr1mid and CD11b/Gr1low cells in the liver compared with treatment with PBS (Supporting Fig. 4A) and had little effects on levels of T (CD3+) or B (CD19+) cells (Supporting Fig. 4B). Neutrophils were shown to be unaffected by DT in CD11b-DTR mice19 and numbers of CD11b/Gr1high cells were similarly unaffected (Supporting Fig. 4A). Livers of control mice had large metastatic colonies, whereas metastases were much smaller in DT-treated mice (Supporting Fig. 4C) and correspondingly, markedly fewer MC38GFP+ tumor cells were detected in livers of DT-treated mice (Fig. learn more 5C). Administration of DT to wild-type C57BL/6 mice did not deplete CD11b/Gr1mid cells, affect the number of MC38GFP+ cells in the liver, or the formation of liver metastases compared with controls (Supporting Fig. 4D-F). Tumor cell proliferation was assessed by staining liver tissue sections of CD11b-DTR mice after DT or PBS treatment. A pronounced two-fold reduction in both bromodeoxyuridine out incorporation (BrDu) and Ki67-positive cells (Fig. 5D,E) were observed

after DT treatment compared with controls. Overall, depletion of the CD11b/Gr1mid and CD11b/Gr1low subsets minimized metastatic growth, causing an appreciable reduction in tumor burden. We considered the possibility that CD11b+ cell depletion could instigate an adaptive immune response leading to decreased tumor burden. However, T cell and B cell numbers were comparable between DT-treated CD11b-DTR mice and controls (Supporting Fig. 4B). We also assessed myeloid infiltrates 14 days after MC38GFP+ inoculation in SCID mice (Supporting Fig. 5) and found myeloid subsets similar to those observed in wild-type C57BL/6 mice (Fig. 5F). Taken together, these findings suggest that accumulation of the CD11b/Gr1mid and CD11b/Gr1low subsets and decreased tumor growth after their depletion did not involve an adaptive immune response.

Key Word(s): 1. Autoimmune Hepatitis; 2. Diagnosis; Presenting Author: FENG LI Additional Authors: JI-YAO WANG Corresponding Author: FENG LI Affiliations: Department of Gastroenterology, Zhongshan Hospital affiliated to Fudan University Objective: To analyze the clinical manifestations and histological features of drug-induced auto-immune hepatitis (DI-AIH) in China. Methods: The medical records of patients with auto-immune hepatitis (AIH), who were

diagnosed by liver biopsy in Zhongshan hospital affiliated to Fudan University, shanghai, China, from January 2008 to June 2011, were analyzed retrospectively. The patients, with a further diagnosis as DI-AIH because of a definitive NSC 683864 history of medicine prior to the seizure of disease, were identified, and their medical records were further analyzed. Results: Among 16 patients with AIH, 5 patients (31.25%) were identified with a definitive drug history and diagnosed as DI-AIH. All of the patients were female, and the mean ages were 48.00 ± 7.52 years. Prior to the seizure of liver disease, they all took TCM herbal decoction or preparation to treat other diseases.

Two patients also took antibiotics (Azithromycin and Erythromycin) simultaneously. The most common presenting symptoms were anepithymia and fatigue. The levels of alanine aminotransferase and aspartate aminotransferase were significantly increased, accompanying with the increased levels of total bilirubin and conjugated bilirubin. The level of globulin and the percentage BVD-523 price of γ-globulin were markedly increased in all below of the patients, but the positive antinuclear antibody was only found in one patient (20%). Liver cirrhosis was found in one patient (20%). The typical AIH histological features were found in all the patients. And eosinophils infiltration in lobular parenchyma and hepatocytes microbubbles vacuolar degeneration,

which indicated drug-induced liver injury, were found in one patient. Conclusion: In China, the TCM herbal decoction or preparation and macrolides antibiotics might be the main cause for DI-AIH. There were no special clinical characteristics for the diagnosis of DI-AIH, so the diagnosis had to base on the combination of clinical manifestations, laboratory examination and histological features. Key Word(s): 1. Autoimmune hepatitis; 2. Drug-induced; 3. Clinical features; 4. Histological feature; Presenting Author: YINGQIAO ZHU Additional Authors: YANG BAI, DONGXUAN WANG Corresponding Author: YINGQIAO ZHU Affiliations: ultrasound department Objective: Accurate quantification of liver fibrosis is essential for therapeutic decision-making and follow-up of chronic liver diseases. Previous researchers used fiber-scan conducted liver fibrosis check.

“
“(Headache 2011;51:734-743) Background.— Neck muscle nociception mediated by nitric oxide may play a role in the pathophysiology of tension-type headache. Objective.— The present study addresses the involvement of neuronal nitric oxide synthase (nNOS) in the facilitation of neck muscle nociception after local application of nerve growth factor (NGF). Methods.— After administration of NGF into semispinal neck muscles, the impact of neck muscle noxious input on brainstem processing was monitored by the jaw-opening reflex in anesthetized mice. The modulatory effect of preceding and subsequent administration of an inhibitor of neuronal nitric oxide synthase on central facilitation

was addressed in a controlled study. Results.— With preceding i.p. application of saline or 0.096 mg/kg of Bioactive Compound Library the specific nNOS inhibitor Nω-propyl-L-arginine

(NPLA), NGF induced a sustained reflex facilitation within 60 minutes. IWR-1 price Preceding injection of 0.96 mg/kg or 1.92 mg/kg NPLA completely prevented the potentially facilitatory effect of NGF. Subsequent administration of 0.96 mg/kg NPLA did not affect established NGF-evoked reflex facilitation. Thus, NPLA prevents facilitation of brainstem processing by noxious myofascial input from neck muscles in a dose-dependent manner. Conclusion.— These findings suggest that nNOS is involved in the induction but not the maintenance of NGF-evoked facilitation of nociception in the brainstem. These results from an experimental animal model may support the idea of NOS and nNOS as potential targets for pharmacological treatment of tension-type headache. “
“To assess the decay of the conditioned pain modulation (CPM) response along repeated applications as a possible expression of subtle pronociception in migraine. One of the most explored mechanisms underlying the

pain modulation system is “diffuse noxious inhibitory controls,” which is measured psychophysically in the lab by the CPM paradigm. There PIK3C2G are contradicting reports on CPM response in migraine, questioning whether migraineurs express pronociceptive pain modulation. Migraineurs (n = 26) and healthy controls (n = 35), all females, underwent 3 stimulation series, consisting of repeated (1) “test-stimulus” (Ts) alone that was given first followed by (2) parallel CPM application (CPM-parallel), and (3) sequential CPM application (CPM-sequential), in which the Ts is delivered during or following the conditioning-stimulus, respectively. In all series, the Ts repeated 4 times (0-3). In the CPM series, repetition “0” consisted of the Ts-alone that was followed by 3 repetitions of the Ts with a conditioning-stimulus application. Although there was no difference between migraineurs and controls for the first CPM response in each series, we found waning of CPM-parallel efficiency along the series for migraineurs (P = .

This bias can be overcome by expressing prey intake as relative biomass and relative number of prey taken (Floyd, Mech, & Jordan, 1978). For estimating relative importance of the prey species, a correction factor developed for cougar Felis concolor (Ackerman, Lindzey & Hernker, 1984) was applied by assuming

that lion digestive physiology is similar to that of the cougar’s. The regression equation used is y=1.980+0.035x, where y is the biomass of prey consumed (kg) to produce a single field collectable scat and x is the average body weight of the prey species (kg). This relation was selleckchem used to convert frequency of prey occurrence in scats into relative biomass and number of prey consumed. Direct observations were made on 10 feeding events of six radio-collared lions, three males and three

females, to supplement opportunistic recordings of kills. Five sessions of continuous day–night observations ranging from 5–10 days, totaling 38 days, on three radio-collared males belonging to three different coalitions was carried out. A survey was conducted in all the 20 resident nesses and settlements within the intensive study area to obtain information on annual (2003–2004) livestock loss to lion predation. A total of 148 families were interviewed that included 1408 resident forest dwellers to collect information on number of families, number of individuals per family and livestock-holding in SAHA HDAC solubility dmso each household. Information on

livestock mortality was classified as loss due to predation and loss due to other natural causes and percentage loss due to predation was calculated. Data on 1215 lion attacks on livestock from January to December 2006 was obtained from Gujarat Forest Department to examine the time of attack. Selectivity indices, Amylase such as Jacobs index with values ranging from +1 (maximum preference) to −1 (maximum avoidance) indicate diet preference taking into account both proportion of kills and prey availability (Jacobs, 1974). Hayward & Kerley (2005) derived Jacobs index scores (D) for major lion prey species from Jacobs index preference equation (Jacobs, 1974): Prey preference was modelled for 2002–2006 (present study) by obtaining Jacobs index scores (D) for four major lion prey species of Gir, namely, chital, sambar, nilgai and wild pig from Hayward & Kerley (2005) and deriving predicted number of kills of each of these species based on proportional abundance of each prey species (Dave, 2008) and proportion of kills observed (Table 3). The accuracy of the model prediction was tested using the log-likelihood goodness of fit (G) test (Zar, 1999). Of 258 kills, livestock constituted 53% and wild prey 47%. Cattle were 31% of the total, chital 28%, buffalo 16%, sambar 10%, nilgai 3%, wild pig 6%, goat 3%, camel 2%, peafowl and chousinga 1%. Proportion of wild kills in summer was 67% (n=100), 35% (n=68) for monsoon and 38% (n=90) for winter.