3B). Eosinophils CX-4945 solubility dmso were abundant in areas juxtaposed to lesions in IL-10 KO animals; however, they were absent in IL-10 KO/PHIL mice, demonstrating that eosinophils were not critical in the development of hepatic necrosis. Results of ALT activity assays and hepatic leukocyte counts corroborated this interpretation (Fig. 3C,D). During infection, neutrophils were significantly increased in the livers of IL-10 KO animals in comparison with WT mice, with peak numbers (day 10) occurring just prior to the time of maximal lesion size (days 12-14; Fig. 4A). Numbers remained low in both WT and IL-4 KO mice, whereas those in IL-10/IL-4 KO animals initially rose but then fell, never achieving

the values observed in IL-10 KO mice. This was confirmed by flow cytometric analysis of hepatic leukocytes (data not shown). Additionally, the prevalence of neutrophils in the liver was suppressed by IL-10. For example, neutrophils represented 14% ± 1.7% of total leukocytes in IL-10 KO livers on day 12 versus 9% ± 1% in WT animals (P < 0.05). Loss of endogenous IL-4 decreased the prevalence to 2.7% ± 1.5% in IL-10/IL-4 KO mice. Activated neutrophils can release cytotoxic mediators, suggesting their potential participation in lesion development. We used expression

of CD11b and CD62L to determine if IL-10 and IL-4 influenced RG7204 supplier the neutrophil activation state in the liver. Infection resulted in a significant increase in the number of Ly6-G+F4/80− cells (markers of neutrophils) with an activated CD11b+CD62Llo phenotype in WT and IL-10 KO mice in comparison with naive animals (Fig. 4B). Upon infection, only the number of activated neutrophils in IL-10 KO mice differed significantly from that in WT animals. Taken together, the data suggested that IL-10 and IL-4 may have differential effects on neutrophil trafficking and activation state. To determine whether neutrophils

played a role in initial hepatocyte injury and/or subsequent development of hepatic necrosis, see more we depleted mice of neutrophils with one of two monoclonal antibodies. Figure 5A shows the effect of antibody administration on peripheral neutrophils. Both depleting antibodies reduced the prevalence of neutrophils to less than 2%. Control antibody-treated and neutropenic IL-10 KO mice had greater ALT values and hepatic leukocyte numbers than WT mice after infection (Fig. 5C,D). However, only control antibody-treated IL-10 KO mice developed hepatic necrosis (Fig. 5B). The number of CD4+α4β7+ cells was significantly increased in both control and depleted IL-10 KO mice in comparison with WT mice, corresponding to the elevated serum ALT activity in these animals (Fig. 5C,D). Thus, in the absence of IL-10 and in the presence of IL-4, neutrophils were necessary for the development of hepatic necrosis but were not required for the initiation of hepatocyte injury.

Amplification was performed for 40 cycles in a total volume of 16 μL, and products were detected using SYBR Green. The relative expression level of each target gene was determined by normalizing its mRNA level to the internal control gene GAPDH. Mann-Whitney’s two-tailed unpaired, one-way analysis of variance (ANOVA) followed by Bonferroni’s multiple-comparisons test, or Fisher’s exact test were used for different analyses, as appropriate. P values <0.05 were considered statistically significant. Because 5-month-old dnTGFβRII

mice develop IBD, we examined IL-23p19−/− dnTGFβRII mice for colitis at 24 weeks of age. Colonic hyperplasia, crypt abscesses, and epithelial ulcers were readily observed in Selleck Atezolizumab dnTGFβRII mice, but not in IL-23p19−/− mice (Fig. 1A). Colon weight and thickness, which correlates with severity of colitis, were significantly decreased in IL-23p19−/− dnTGFβRII mice, compared to age-matched dnTGFβRII mice (Fig. 1B). Colonic infiltration of total MNCs, as well as total and activated CD4 T cells, was significantly decreased in

IL-23p19−/− mice, compared to dnTGFβRII mice, whereas no differences were BVD-523 ic50 observed in the levels of infiltrating CD8 T-cell populations (Fig. 2). MPO+ cells appeared to accumulate around the ulcer region in dnTGFβRII

mice, whereas only a few of these cells were observed in the colon mucosal layer of IL-23p19−/− dnTGFβRII (Fig. 1A). In addition, a relatively higher incidence of dysplasia was observed in dnTGFβRII mice than selleck chemicals llc IL-23p19−/− mice (Fig. 1A,C). We next compared liver histology in IL-23p19−/− dnTGFβRII mice and dnTGFβRII mice at 24 weeks of age. There was no significant difference in the levels of inflammatory portal lymphoid cell infiltration and bile duct damage between the two mouse strains (Fig. 3A,B). In addition, the numbers of intrahepatic T cells, including the total CD8 T-cell population and activated CD8 T cells (defined by CD69+ and CD44+ phenotypes,1, 11 known to be pathogenic in liver disease of dnTGFβRII mice,13 did not differ significantly between the two mouse strains (Fig. 3C). These results indicate that the deficiency in IL-23p19 did not protect dnTGFβRII mice from developing liver disease. To address whether IL-23 has a role in autoantibody induction, serum levels of AMA and ANA as well as those for total IgG, IgM, and IgA were measured by ELISA. Levels of IgG in IL-23p19−/− dnTGFβRII mice was higher than in healthy B6 mice, but were comparable with those of dnTGFβRII mice (Fig. 4).

The overall LAR reported here supports the community structure SB203580 datasheet documented previously of three interacting social clusters (Elliser and Herzing 2012) because this type of LAR can be produced by a social system of permanent social units that associate temporarily (Whitehead 2008a). Combined with the fact that all sex class associations

leveled out above the null association rate, this indicates a community with distinct interacting social clusters along with differential association patterns due to sex. The detail of this study reveals how sex and age class interact in their influence on associations and social structure. The pattern of male associations was consistent with the rapid disassociation and constant companion model, where although there will be some rapid disassociation on a daily basis,

males remained with their preferred companions consistently over all time lags. Socio-ecological factors GDC-0068 ic50 determine female grouping and association patterns that in turn determine the options (regarding socio-sexual strategies, male associations/relationships and dispersal) left for males because they compete primarily for access to fertile females (Hill and Van Hooff 1994, Van Hooff and van Shaik 1994). The male spotted dolphins in this study show long-term strong associations between individuals and pair/trios of males, but are these male coalitions and/or alliances? de Waal and Harcourt (1992) define a coalition as a joining of forces by two or more parties

during a conflict of interests with other parties, and an alliance as an enduring cooperative relationship in which repeated coalitions are formed. Male alliances in primates, lions and dolphins are primarily attributed to increased access (directly or indirectly) to females (e.g., Packer et al. 1991, Watts 1998, Connor et al. 2000). Herzing (1996) described male coalitions (as defined above) of spotted dolphins consisting of three to four dolphins that chased and surrounded a female and eventually mated with her. This monopolization involves tending/following a female in apparent estrus, surrounding her, escorting her to the bottom during feeding bouts and fending click here off other male groups (Herzing and Johnson 1997; Herzing and Elliser, in press). The absolute duration of these behaviors is unknown, but females have been documented with the same male pair/trio during encounters (minutes to hours), multiple encounters in one day and in some cases across multiple days (DLH, unpublished data). Although this monopolizing behavior is not as overt as the herding by Shark Bay dolphins (Connor et al. 2000), or mate guarding in chimpanzees (Watts 1998), it seems to serve the same purpose: males cooperating to gain and maintain access to females.

The overall LAR reported here supports the community structure INCB018424 mw documented previously of three interacting social clusters (Elliser and Herzing 2012) because this type of LAR can be produced by a social system of permanent social units that associate temporarily (Whitehead 2008a). Combined with the fact that all sex class associations

leveled out above the null association rate, this indicates a community with distinct interacting social clusters along with differential association patterns due to sex. The detail of this study reveals how sex and age class interact in their influence on associations and social structure. The pattern of male associations was consistent with the rapid disassociation and constant companion model, where although there will be some rapid disassociation on a daily basis,

males remained with their preferred companions consistently over all time lags. Socio-ecological factors MG-132 ic50 determine female grouping and association patterns that in turn determine the options (regarding socio-sexual strategies, male associations/relationships and dispersal) left for males because they compete primarily for access to fertile females (Hill and Van Hooff 1994, Van Hooff and van Shaik 1994). The male spotted dolphins in this study show long-term strong associations between individuals and pair/trios of males, but are these male coalitions and/or alliances? de Waal and Harcourt (1992) define a coalition as a joining of forces by two or more parties

during a conflict of interests with other parties, and an alliance as an enduring cooperative relationship in which repeated coalitions are formed. Male alliances in primates, lions and dolphins are primarily attributed to increased access (directly or indirectly) to females (e.g., Packer et al. 1991, Watts 1998, Connor et al. 2000). Herzing (1996) described male coalitions (as defined above) of spotted dolphins consisting of three to four dolphins that chased and surrounded a female and eventually mated with her. This monopolization involves tending/following a female in apparent estrus, surrounding her, escorting her to the bottom during feeding bouts and fending selleck inhibitor off other male groups (Herzing and Johnson 1997; Herzing and Elliser, in press). The absolute duration of these behaviors is unknown, but females have been documented with the same male pair/trio during encounters (minutes to hours), multiple encounters in one day and in some cases across multiple days (DLH, unpublished data). Although this monopolizing behavior is not as overt as the herding by Shark Bay dolphins (Connor et al. 2000), or mate guarding in chimpanzees (Watts 1998), it seems to serve the same purpose: males cooperating to gain and maintain access to females.

2). The ALT level was elevated to 828 IU/mL, and the HBV DNA level was elevated to

3.18 × 107 IU/mL. Interestingly, this patient’s serum remained negative for HBsAg according to a radioimmunoassay throughout this exacerbation. Thus, this patient experienced an episode of HBsAg-negative hepatitis. The HBV DNA concentration was quantified with the Roche TaqMan HBV monitor (Roche Diagnostics, Basel, Switzerland). The detection limit of this test was 69 copies/mL. In this test, 5.82 copies/mL was equivalent to 1 IU/mL. Serum hepatitis markers, including Selleckchem EPZ015666 anti-HBs, HBeAg, and antibody to HBeAg (Ausria II and HBeAg radioimmunoassays, Abbott Laboratories, North Chicago, IL) and antibody to hepatitis D antigen (Formosa Biomedical Technology Corp., Taiwan), were assayed

with commercially available kits. HBsAg was also measured with another enzyme immunoassay when this was necessary (Enzygnost HBsAg 5.0, Dade Behring Marburg GmbH, Marburg, Germany). Serum antibody to hepatitis C virus levels were assayed with third-generation enzyme immunoassay kits (HCV EIA III, Abbott Laboratories). The quantitative assessment of HBsAg was performed with an automated chemiluminescent microparticle immunoassay (Architect HBsAg, Abbott Laboratories) according to the manufacturer’s instructions. For HBV DNA isolation, serum (100 μL) was mixed with 300 μL of a buffer [13.3 mmol/L trishydroxymethylaminomethane learn more hydrochloride (Tris-HCl), pH 8.0; 6.7 mmol/L ethylene diamine tetraacetic acid; 0.67% sodium dodecyl sulfate; and 133 mg/μL proteinase K] and incubated at 55°C for 4 hours. After phenol-chloroform extractions, DNA was precipitated with cold ethanol. The precipitate was dissolved in 20 μL of a Tris-HCl (10

mmol/L, pH 8.0)/ethylene diamine selleck inhibitor tetraacetic acid (1 mmol/L) buffer. PCR was performed for 30 cycles with a DNA thermal cycler (PerkinElmer Cetus, Norwalk, CT). The primers were called PS1 (5′-ATATTCTTGGGAACAAGAGC-3′, nucleotides 2828-2847, sense) and PS2 (5′-GGAATAACCCCATCTTTTTG-3′, nucleotides 867-848, antisense); all nucleotide sequences were numbered according to a reference sequence with GenBank accession number X02763. For the prevention of PCR-generated mutations, TaKaRa Ex Tag polymerase (Takara Shuzo Co., Shiga, Japan), which was capable of proofreading, was used with the PCR assay. A serum sample obtained from an HBsAg-negative normal subject and an aliquot of pure water were included as negative controls. The methods of cloning and sequencing were described previously.15 For each sample, seven clones with inserts were selected for sequence analysis with an automatic DNA sequencer (CEQ 2000, Beckman Instruments, Inc., Fullerton, CA). To further verify our sequence data resulting from direct sequencing, pyrosequencing was also performed.

2). The ALT level was elevated to 828 IU/mL, and the HBV DNA level was elevated to

3.18 × 107 IU/mL. Interestingly, this patient’s serum remained negative for HBsAg according to a radioimmunoassay throughout this exacerbation. Thus, this patient experienced an episode of HBsAg-negative hepatitis. The HBV DNA concentration was quantified with the Roche TaqMan HBV monitor (Roche Diagnostics, Basel, Switzerland). The detection limit of this test was 69 copies/mL. In this test, 5.82 copies/mL was equivalent to 1 IU/mL. Serum hepatitis markers, including this website anti-HBs, HBeAg, and antibody to HBeAg (Ausria II and HBeAg radioimmunoassays, Abbott Laboratories, North Chicago, IL) and antibody to hepatitis D antigen (Formosa Biomedical Technology Corp., Taiwan), were assayed

with commercially available kits. HBsAg was also measured with another enzyme immunoassay when this was necessary (Enzygnost HBsAg 5.0, Dade Behring Marburg GmbH, Marburg, Germany). Serum antibody to hepatitis C virus levels were assayed with third-generation enzyme immunoassay kits (HCV EIA III, Abbott Laboratories). The quantitative assessment of HBsAg was performed with an automated chemiluminescent microparticle immunoassay (Architect HBsAg, Abbott Laboratories) according to the manufacturer’s instructions. For HBV DNA isolation, serum (100 μL) was mixed with 300 μL of a buffer [13.3 mmol/L trishydroxymethylaminomethane HDAC inhibitor hydrochloride (Tris-HCl), pH 8.0; 6.7 mmol/L ethylene diamine tetraacetic acid; 0.67% sodium dodecyl sulfate; and 133 mg/μL proteinase K] and incubated at 55°C for 4 hours. After phenol-chloroform extractions, DNA was precipitated with cold ethanol. The precipitate was dissolved in 20 μL of a Tris-HCl (10

mmol/L, pH 8.0)/ethylene diamine check details tetraacetic acid (1 mmol/L) buffer. PCR was performed for 30 cycles with a DNA thermal cycler (PerkinElmer Cetus, Norwalk, CT). The primers were called PS1 (5′-ATATTCTTGGGAACAAGAGC-3′, nucleotides 2828-2847, sense) and PS2 (5′-GGAATAACCCCATCTTTTTG-3′, nucleotides 867-848, antisense); all nucleotide sequences were numbered according to a reference sequence with GenBank accession number X02763. For the prevention of PCR-generated mutations, TaKaRa Ex Tag polymerase (Takara Shuzo Co., Shiga, Japan), which was capable of proofreading, was used with the PCR assay. A serum sample obtained from an HBsAg-negative normal subject and an aliquot of pure water were included as negative controls. The methods of cloning and sequencing were described previously.15 For each sample, seven clones with inserts were selected for sequence analysis with an automatic DNA sequencer (CEQ 2000, Beckman Instruments, Inc., Fullerton, CA). To further verify our sequence data resulting from direct sequencing, pyrosequencing was also performed.

With Nutlin-3a in vivo sufficient nutrients, amino acids and insulin activate the mammalian target of rapamycin (mTOR) to down-regulate autophagy. The liver frequently serves as a model for the effects of starvation on autophagic function. Starvation-induced autophagy in mice decreases total hepatic protein content by 35% within 24 hours, 2 indicating that autophagy is a potent degradative pathway requiring strict regulation. Transcription

factor EB (TFEB) was first cloned from a human B-cell cDNA library by its ability to bind the adenoviral major late promoter. Sequence analysis demonstrated that TFEB has adjacent basic helix-loop-helix and leucine zipper domains, 3 which places it in the micropthalmia-transcription factor E (MiT/TFE) subfamily along with the genes, TFE3, TFEC, and MITF. 4 The function of TFEB remained unknown until Sardiello et al. 5 identified, by bioinformatics, a consensus DNA sequence in the promoters of 96 lysosomal genes termed the CLEAR (Coordinated Lysosomal Expression and Regulation) motif. The CLEAR element overlapped with the DNA target site for the MiT/TFE family, and expression studies demonstrated that TFEB specifically targeted the CLEAR motif to up-regulate genes essential for lysosomal biogenesis and function. 5 From these findings and knowledge of the existence of mTOR-independent

regulation of autophagy genes with starvation, 6 the present study by Settembre et al. 7 examined whether TFEB regulates autophagy. TFEB overexpression in several cell lines increased autophagosome formation and autophagic function, PS-341 clinical trial whereas a knockdown inhibited autophagy. 7 TFEB increased the expression of a number of autophagy genes containing a TFEB-binding site, and a subsequent study from the same laboratory confirmed and extended the list of TFEB-regulated autophagy genes. 8 In vivo TFEB overexpression also increased learn more autophagosome number and levels of lysosomal and autophagic TFEB target genes in liver. In vitro nutrient deprivation led to TFEB dephosphorylation at Ser142 and translocation to the nucleus to increase gene transcription. The mitogen-activated protein kinase (MAPK) extracellular

signal-regulated kinase 1/2 (ERK1/2) phosphorylated TFEB to maintain it in an inactive, cytosolic state. ERK1/2 is activated by growth factors, making it logical that this kinase down-regulates TFEB and autophagy in response to nutrients. Thus, the study demonstrates a central role for TFEB in controlling autophagosome formation, in addition to lysosomal biogenesis, to increase autophagy (Fig. 1). A weakness of the study is its reliance on ectopically expressed TFEB and failure to examine endogenous TFEB protein trafficking. The effects of mTOR signaling on TFEB were also not examined. Another recent study indicates that mTOR up-regulates TFEB. 9 Although TFEB phosphorylation regulated nuclear localization, Ser142 was not involved.

DCFDA fluorescence was measured with a multiwall fluorescence scanner (FLUOstar OPTIMA; BMG LABTECH, Ortenberg, Germany).6 Rac1 activity in HSCs was determined with

the Rac1 G-LISA activation assay kit (Cytoskeleton, Inc., BGJ398 mw Denver, CO). Briefly, WT or SOD1mu HSCs were treated by 10−6 M Ang II (Sigma-Aldrich) or vehicle (PBS) with 20 μM of NOX1/4 inhibitor or vehicle (PBS) for 24 hours. According to the manufacturer’s protocol, protein lysate was extracted and Rac1 activity was determined by luminescence intensity. Data are expressed as means ± standard error of the mean (SEM). Statistical differences between means were determined using Student t tests or analysis of variance on ranks, followed by a post-hoc test (Student-Newman-Keuls’ all pairwise comparison procedures), as appropriate. P values less than 0.05 were considered statistically significant. SOD1 messenger RNA (mRNA) levels were increased ZVADFMK in the livers of WT mice after CCl4-induced liver fibrosis (Fig. 1A). To investigate the cellular source of SOD1 in fibrotic liver, we measured mRNA expression of SOD1 in hepatocytes, macrophages/Kupffer cells, and HSCs isolated

from vehicle- or CCl4-treated mice. SOD1 expression was significantly increased in HSCs after CCl4 treatment, but not in hepatocytes or in macrophages (Fig. 1B). As detected by fluorescence microscopy, the number of SOD1- and desmin-positive HSCs was markedly increased in CCl4-treated liver, compared to vehicle control selleck compound (Fig. 1C,D). These results indicate that the up-regulation of SOD1 in HSCs is related to the development of liver fibrosis. In an effort to discover new, selective modulators of Nox enzymes, we developed cell-free assays using

membranes prepared from cells heterologously overexpressing a specific Nox enzyme isoform.23, 24 GKT137831 (Fig. 2A) is a potent Nox4 inhibitor (inhibition constant [Ki] =120 ± 30 nM) with an affinity similar to the irreversible, unspecific flavoprotein inhibitor, diphenyliodonium (DPI; Ki = 70 ± 10 nM) (Fig. 2B). As expected, DPI showed complete nonselectivity, and the same potency was recorded on all four Noxes probed (Fig. 2B). On the other hand, GKT137831 had a better potency, both on human Nox4 (Ki =140 ± 40 nM) and human Nox1 (Ki =110 ± 30 nM) and was found 15-fold less potent on Nox2 (Ki = 1,750 ± 700 nM) and 3-fold less potent on Nox5 (Ki =410 ± 100 nM). Moreover, GKT137831 did not significantly inhibit a highly specific NOX2-driven response (i.e., neutrophil oxidative burst up to 100 uM), as measured by flow cytometry in human whole blood.

If bile-duct stones are strongly suspected,

endoscopic retrograde cholangiopancreatography (ERCP) with transpapillary stone extraction is the method of choice. Endoscopic ultrasound and magnetic resonance cholangiopancreatography (MRCP) are less invasive diagnostic tools in patients with selleck chemicals llc intermediate probability of intraductal stones. Treatment comprises medical therapy for acute pain and/or bacterial infection and endoscopic interventions for common bile-duct stones, cholangitis, or biliary pancreatitis in selected patients. Laparoscopic cholecystectomy is the treatment of choice for symptomatic gallbladder stones and cholecystitis. It should also be performed after other complications of cholelithiasis (e.g., biliary pancreatitis, cholangitis) to prevent recurrence. “
“This chapter contains sections titled: Introduction Background The role of the gastrointestinal tract in ingestive behavior Gastrointestinal symptoms and disease in the obese patient Bariatric surgery – a primer for the gastroenterologist Considerations in

endoscopy Endoscopic treatments for obesity References “
“Hepatitis B virus (HBV) causes important human health problems. It has infected one-third of the world’s population and approximately 360 million people are chronic carriers. Worldwide, 0.5–1.2 million deaths are attributed to HBV infection annually. Therefore, AT9283 in vivo global control of HBV infection is important. HBV infection can be intervened by interrupting routes of transmission, treating the chronically infected, and preventing the susceptibles with immunoprophylaxis. All these measures are effective. Nevertheless, although pegylated interferons or nucleos(t)ide analogs are effective for the treatment of chronic hepatitis B, chronic carriage of HBV is not easy to eliminate, as revealed by the frequent persistence of hepatitis B surface antigen, despite satisfactory responses to these treatments. On the other hand, hepatitis B vaccination selleck chemicals has been shown to preclude HBV infection effectively.

This is particularly true for pre-exposure prophylaxis. Worthy of note is the universal vaccination of newborn infants. This is the most effective means of preventing HBV infection, especially for those born to HBV carrier mothers. To eliminate and eradicate hepatitis B, first, HBV in the chronically infected should be eradicated or strongly and efficiently suppressed, so that the infection does not spread rampantly. Second, all the transmission routes should be interrupted. Lastly, but most effectively, is to immunize all susceptibles. The difficulties and possible solutions of each approach are discussed. In conclusion, the existing means to prevent and treat HBV infection render our goal toward eliminating and eradicating hepatitis B possible, although it will take much time and effort to achieve this objective. Hepatitis B virus (HBV) is one of the most important human pathogens. It causes significant diseases spanning from fulminant hepatitis to end-stage liver disease.

Based on our dataset of 147 sequences, including 67 new sequences, we recovered four well-supported

deep clades within Buthus scorpions from the Maghreb and Southern Europe. This further strengthens the support for cryptic diversity in the Maghreb region. The broader sampling of the Maghreb permitted a better understanding of the phylogeographic structure in this area. Three clades were restricted to Morocco and appear to have originated at the Atlantic Coast of this country, while the fourth was found throughout the region. We propose a model with two colonizing events to explain the distribution patterns across the Strait Rapamycin datasheet of Gibraltar, with an initial colonization from North Africa to Iberia followed by a reinvasion of the Rif Mountains region in Morocco. “
“Dental enamel hypoplasia is a developmental defect in enamel caused by physiological stress during dental development. Previous analysis of enamel hypoplasia in sheep has demonstrated that variation in its frequency can be linked to nutrition levels, with animals suffering from malnutrition more susceptible

to enamel hypoplasia formation. Variation in enamel hypoplasia frequency has also been linked to climatic and ecological factors, leading to variation in the availability of fodder supplies and, consequently, variation in nutritional intake. In this paper, the occurrence of enamel hypoplasia in two modern sheep populations is, for the first time, correlated with known seasonal physiological and nutritional stress events. Using known age-at-death this website data, the dental development rates for sheep are reconstructed, allowing the position of enamel hypoplasia on the tooth crown to be linked to known periods of malnutrition and physiological stress. Both populations live under identical climatic conditions but with very different diets.

Clear differences are observed between the two populations, with peaks of enamel check details hypoplasia correlating with different seasonal periods of malnutrition as well as common physiological stressors linked to birth and weaning. This is the first time that a clear correlation has been made between seasonal variation in nutrition and the occurrence of hypoplastic enamel defects in caprine populations. As such, this study provides a baseline from which the nutritional impact of caprine foddering and husbandry practices can be determined in future archaeological studies. “
“Tigers are globally endangered and continue to decline due to poaching, prey depletion and habitat loss. In Nepal, tiger populations are fragmented and found mainly in four protected areas (PAs). To establish the use of standard methods, to assess the importance of prey availability and human disturbance on tiger presence and to assess tiger occupancy both inside and outside PAs, we conducted a tiger occupancy survey throughout the Terai Arc Landscape of Nepal.