Because of the large reduction in the number of donor DCs after elimination of the blood-migrating

DC subset and inhibition of systemic alloreactive T-cell generation in the recipient’s lymphoid organs, one might expect rejection to be delayed in the Irr(+) group. The question then arises: Why doesn’t preoperative irradiation of the graft liver selleck suppress rejection? Some of the possible effects of irradiation on the graft that promote rejection include the persistence of immunostimulatory factors and/or down-regulation of immunosuppressive factors. As for persistent stimulatory cells, the CD172a+CD11b+ DC subset is likely to be a central player. Other stimulatory factors may also be present that were not detected in our analysis. With respect to suppressive factors, there is a combination of fully MHC-incompatible strains that allows a rat liver to be spontaneously accepted. However, this tolerance is abrogated by donor irradiation17 in different rat strain combinations after different doses of Z-VAD-FMK irradiation (Supporting Table 2).24 These reports suggest the presence of some radiosensitive factors that promote liver graft-induced tolerance. Possible factors include

regulatory T cells,25 tolerogenic passenger cells,3, 26 and an apoptosis-inducing microenvironment in the liver27 that includes negative costimulatory molecules, such as B7-H1.28 In the present study, FoxP3+ regulatory T-cell responses were not different between the Irr(−) and Irr(+) groups (Supporting Fig. 3), indicating that graft irradiation did

not down-regulate the recipient’s regulatory T-cell response. Another study suggested that in the LT tolerant group, passenger leukocytes in the recipient’s lymphoid organs play a suppressive role by causing apoptosis of the Ergoloid recipient’s T cells in the graft.26 Accordingly, MHCIIlowCD11c+ immature DCs in mice29 have been suggested to be tolerogenic. We also found immature DCs in the liver of some rat strains. These DCs were MHCIIlow (Yu, unpublished data) and were not examined in this study. Concerning the liver microenvironment, the liver may facilitate CD8+ T-cell proliferation, leading to apoptosis30; however, we were not able to confirm changes in the expression of radiosensitive genes in the graft liver in this study. Our findings suggest that preoperative irradiation of the graft liver did not suppress rejection, because a radioresistant CD172a+CD11b+ DC subset generated a sufficient number of effector T cells. Immunosuppressive factors other than regulatory T cells might be down-regulated, but we did not observe them. Rat liver conventional DCs contain at least two immunogenic subsets that have distinct trafficking patterns and radiosensitivities. One subset comprises radiosensitive MHCII+CD103+CD172a+CD11b−CD86+ cells.

The study protocol was in compliance with the

Good Clinical Practice Guidelines and the 1975 Declaration of Helsinki and was approved by the Institutional Review Board. Each patient gave informed consent before participating in this trial. Patients were divided into two groups: 20 (25%) patients were allocated to a 12-week regimen of triple therapy (telaprevir [MP-424], PEG-IFN, and ribavirin) (the T12PR12 group), and 61 patients (75%) were assigned to a 24-week regimen of the same triple therapy for 12 weeks followed by dual therapy of PEG-IFN and ribavirin for 12 weeks (the T12PR24 group). All of 81 patients met the following inclusion and exclusion criteria: (1) diagnosis of chronic hepatitis

C. (2) HCV-1 confirmed by sequence analysis. (3) HCV RNA levels of ≥5.0 log IU/mL determined http://www.selleckchem.com/products/epz015666.html by the COBAS TaqMan HCV test (Roche Diagnostics, Tokyo, Japan). (4) Japanese (Mongoloid) ethnicity. (5) Age at study entry of 20-65 years. (6) Body weight ≥35 kg and ≤120 kg at the time buy Ruxolitinib of registration. (7) Lack of decompensated liver cirrhosis. (8) Negativity for hepatitis B surface antigen (HBsAg) in serum. (9) Negative history of HCC. (10) No previous treatment for malignancy. (11) Negative history of autoimmune hepatitis, alcohol liver disease, hemochromatosis, and chronic liver disease other than chronic hepatitis C. (12) Negative history of depression, schizophrenia or suicide attempts, hemoglobinopathies, angina pectoris, cardiac insufficiency, myocardial infarction or severe arrhythmia, uncontrollable hypertension, chronic renal dysfunction or creatinine clearance of ≤50 mL/minute at baseline, diabetes requiring treatment or fasting glucose level of ≥110 mg/dL, autoimmune disease, cerebrovascular either disorders, thyroidal dysfunction uncontrollable by medical treatment, chronic pulmonary disease, allergy to medication or anaphylaxis at baseline. (13) Hemoglobin level of ≥12 g/dL, neutrophil count ≥1500/mm3, and platelet count of ≥100,000/mm3 at baseline. Pregnant or breast-feeding

women or those willing to become pregnant during the study and men with a pregnant partner were excluded from the study. Furthermore, 72 of 81 patients were followed for at least 24 weeks after the completion of triple therapy. The treatment efficacy was evaluated by HCV-RNA negative at the end of treatment (end-of-treatment response) and 24 weeks after the completion of therapy (sustained virological response), based on the COBAS TaqMan HCV test (Roche Diagnostics). Telaprevir (MP-424; Mitsubishi Tanabe Pharma, Osaka, Japan) was administered at 750 mg or 500 mg three times a day at an 8-hour (q8) interval after the meal. PEG-IFNα-2b (PEG-Intron; Schering Plough, Kenilworth, NJ) was injected subcutaneously at a median dose 1.5 μg/kg (range: 1.3-2.

The study protocol was in compliance with the

Good Clinical Practice Guidelines and the 1975 Declaration of Helsinki and was approved by the Institutional Review Board. Each patient gave informed consent before participating in this trial. Patients were divided into two groups: 20 (25%) patients were allocated to a 12-week regimen of triple therapy (telaprevir [MP-424], PEG-IFN, and ribavirin) (the T12PR12 group), and 61 patients (75%) were assigned to a 24-week regimen of the same triple therapy for 12 weeks followed by dual therapy of PEG-IFN and ribavirin for 12 weeks (the T12PR24 group). All of 81 patients met the following inclusion and exclusion criteria: (1) diagnosis of chronic hepatitis

C. (2) HCV-1 confirmed by sequence analysis. (3) HCV RNA levels of ≥5.0 log IU/mL determined Cilomilast datasheet by the COBAS TaqMan HCV test (Roche Diagnostics, Tokyo, Japan). (4) Japanese (Mongoloid) ethnicity. (5) Age at study entry of 20-65 years. (6) Body weight ≥35 kg and ≤120 kg at the time BMS-907351 solubility dmso of registration. (7) Lack of decompensated liver cirrhosis. (8) Negativity for hepatitis B surface antigen (HBsAg) in serum. (9) Negative history of HCC. (10) No previous treatment for malignancy. (11) Negative history of autoimmune hepatitis, alcohol liver disease, hemochromatosis, and chronic liver disease other than chronic hepatitis C. (12) Negative history of depression, schizophrenia or suicide attempts, hemoglobinopathies, angina pectoris, cardiac insufficiency, myocardial infarction or severe arrhythmia, uncontrollable hypertension, chronic renal dysfunction or creatinine clearance of ≤50 mL/minute at baseline, diabetes requiring treatment or fasting glucose level of ≥110 mg/dL, autoimmune disease, cerebrovascular these disorders, thyroidal dysfunction uncontrollable by medical treatment, chronic pulmonary disease, allergy to medication or anaphylaxis at baseline. (13) Hemoglobin level of ≥12 g/dL, neutrophil count ≥1500/mm3, and platelet count of ≥100,000/mm3 at baseline. Pregnant or breast-feeding

women or those willing to become pregnant during the study and men with a pregnant partner were excluded from the study. Furthermore, 72 of 81 patients were followed for at least 24 weeks after the completion of triple therapy. The treatment efficacy was evaluated by HCV-RNA negative at the end of treatment (end-of-treatment response) and 24 weeks after the completion of therapy (sustained virological response), based on the COBAS TaqMan HCV test (Roche Diagnostics). Telaprevir (MP-424; Mitsubishi Tanabe Pharma, Osaka, Japan) was administered at 750 mg or 500 mg three times a day at an 8-hour (q8) interval after the meal. PEG-IFNα-2b (PEG-Intron; Schering Plough, Kenilworth, NJ) was injected subcutaneously at a median dose 1.5 μg/kg (range: 1.3-2.

Most of them were in middle to low educational level 116 (41,7%). 50,7% of the research subjects had normal body mass index. We had 11 subjects with positive result of I-FOBT with its prevalence 4%. Conclusion: Prevalence of positive result of I-FOBT was 4%. Further studies were needed

to be performed to estimate diagnostic study of I-FOBT in Indonesia. Key Word(s): 1. colorectal screening; 2. I-FOBT; 3. Indonesia; 4. prevalence; Presenting Author: ZUO-HUI YUAN Additional Authors: ZHI-JIE XU, KUN WANG, ZHI-WEI XIA, YING GE, LI-PING DUAN Corresponding Author: LI-PING DUAN Affiliations: Peking University Third Hospital Objective: To compare the characteristics between three-dimension high-resolution manometry (3D-HRM) and water-perfusion mamometry (WPM) in anorectal click here function www.selleckchem.com/products/PD-0325901.html evaluation. Methods: 63 subjects were enrolled in the study (46 chronic constipation patients and 17 healthy volunteers). All of them underwent anorectal manometry (ARM) by both 3D-HRM and WPM. WPM was performed using 8-channel water-perfusion catheter with side holes

spaced at 1-cm interval and diameter of 4.7 mm. 3D-HRM was performed using 256 (16*16)-channel solid-state catheter with diameter of 10 mm, displaying in topographic and three-dimension form using analysis software. Measurements of anal sphincter pressure at rest, during voluntary contraction, during forced defecation, and rectal sensory thresholds were compared. Results: Anal sphincter and rectal pressures recorded by 3D-HRM tended to be higher (anal resting pressure: 94.8 ± 26.3 Acyl CoA dehydrogenase vs 63.9 ± 21.4 mmHg, P = 0.000; anal squeezing pressure: 218.3 ± 61.1 vs 174.5 ± 50.9 mmHg, P = 0.000; defecation anal pressure: 76.4 ± 31.4 vs 44.5 ± 20.1 mmHg, P = 0.000; defecation rectal pressure: 43.7 ± 20.8

vs 35.1 ± 20.4 mmHg, P = 0.033) and urge defecation thresholds tended to be lower (128.6 ± 52.4 vs 157.7 ± 73.5 ml, P = 0.017) than those recorded with WPM. The two methods showed to be significantly correlated in the aspects of anal resting pressure (r = 0.575, P = 0.000), anal squeezing pressure (r = 0.610, P = 0.000), defecation anal pressure (r = 0.568, P = 0.000), anal relax ratio (r = 0.573, P = 0.000), first defecation threshold (r = 0.621, P = 0.000), urge defecation threshold (r = 0.595, P = 0.000) and maximal tolerated threshold (r = 0.663, P = 0.000). Also, there were weak correlations in the length of high pressure zone (r = 0.390, P = 0.002) and defecation rectal pressure (r = 0.419, P = 0.002). However, there was no correlation in minimum relaxation volume (MRV) for rectal anal inhibitory reflex (RAIR) (r = 0.156, P = 0.255) between the two methods. 3D-HRM could find paradoxical puborectalis contraction during defecation, but WPM could not provide the message. Conclusion: In addition to MRV, all pressure and sensory parameters were consistent between 3D-HRM and WPM, but 3D-HRM provided more detail information of anorectal anatomy.

47 ± 40.65 mg (during find more 6.52 ± 5.65 days)

in the HRS group. Conclusion: despite partial V2 agonist effects, clinically significant hyponatremia did not occur in our cohort of cirrhotic patients with variceal bleeding or hepatorenal syndrome. Disclosures: The following people have nothing to disclose: Ruth Bolier, Bart van Hoek, Hein W. Verspaget, Minneke Coenraad Background: Management of bleeding gastric varices (GV) is challenging. Cyanoacrylate (CYA) injection is the recommended treatment for bleeding GV, but has significant adverse effects. Diluted CYA with lipiodal results in higher prevalence of glue embolization and undiluted CYA sometimes causes fixation of injection needle resulting in fatal outcome. Transe-sophageal endoscopic ultrasound (EUS)-guided therapy of GV with combined coil and CYA injection has shown promising results. However, it is expensive and requires technical expertise. Combination of small amount

of undiluted CYA forming a nidus followed by large amount of lipiodal diluted CYA (UD CYA group) avoiding complications as fixation of needle and glue embolization may prove a better alternative Ulixertinib supplier for managing these patients. Therefore, we compared the safety, and efficacy of this new method with undiluted CYA (U CYA group) injection method. Methods: Thirty consecutive patients with bleeding GV between July, 2010 and June, 2014 were treated with CYA injection, 15 with UD CYA method and 15 with undiluted CYA (U CYA group). All patients in U CYA group had a thoracic CT scan for identifying glue embolism. Results: The GV obliteration rate was100% in UD CYA group

versus 93.3% in U CYA group. The rebleeding rate was 20% (3/15) in UD CYA group compared with 40% (6/15) in U CYA group (P=0.43). Meloxicam One patient in U CYA group had needle fixation and resulted in fatal bleeding after forceful needle extraction even after balloon tamponade. In UD CYA group one patient had fever and none had glue embolism. Conclusions: CYA therapy using U CYA or UD CYA is effective in bleeding GV. UD CYA method had fewer rebleeds and tended to have fewer adverse events compared with U CYA injection, however these differences were not statistically significant. A larger prospective, randomized trial is required to confirm our findings. Disclosures: The following people have nothing to disclose: Virendra Singh, Rajiv R. Singh, Navneet Sharma Aim: To assess the short- and long-term outcome of patients with gastric varices (GV) after balloon-occluded retrograde trans venous obliteration (B-RTO). Methods: One hundred thirteen consecutive patients with GV treated by B-RTO from December 1994 to March 2014 were retrospectively analyzed in this study. We analyzed factors associated with technical success (defined as complete clotting of targeted gastric vari-ces as observed by computed tomography) and long term survival. Results: Overall technical success was achieved in 125 of 130 (96%) treated patients.

Stool checking for parasites were performed before and after treatment, another 30 patients as a control group. Results: In vitro

experiments: Blastocystis hominis all died at the concentration of erythromycin RG7420 order of or more than 80 μg/ml after 72 h, optimal concentration was of 20 μg/ml; Pulsatilla soup of 6400 μg/ml 24 h and 72 h Blastocystis hominis all died, and the optimal concentration was 1600 μg/ml; Blastocystis hominis were completely eliminated at the concentrations more than 10 μg/ml + 1600 μg/ml in erythromycin plus Pulsatilla soup after 24 h and 72 h, the optimal concentration was erythromycin 10 μg/ml + Pulsatilla soup 1600 μg/ml. Clinic tests: the effective percentages of the erythromycin, Pulsatilla soup, erythromycin plus Pulsatilla soup are of 86.5%, 72.0%, and 94.0%, respectively, while the control group, no case conversed. Conclusion: Erythromycin, Pulsatilla soup made certain suppression role in treatment to infection of Blastocystis hominis. It can achieve a satisfactory effect if used both of them at the same time. Key Word(s): 1. Erythromycin; 2. Pulsatilla soup; 3. Blastocystis hominis; 4. drug effects; Presenting Author: ABDÜLKADIRGEYLANI ŞAHAN Additional Authors: SEYITHAN KAHRAMAN, ERSIN ACET, CENK SEZER, PD 332991 MUSTAFA SAĞCAN, HAKAN ŞIVGIN, ABDÜLKERIM YILMAZ Corresponding

Author: ABDÜLKADIRGEYLANI ŞAHAN Affiliations: Bahat Hospital; Bahat Hospital General Surgery Department; gaziosmanpaşa University internal medicine department; Gaziosmanpaşa University İnternal Medicine Department; Sivas Cumhuriyet University Gastroenterology Department Objective: Celiac disease can be defined as a small bowel disorder characterized by mucosal inflammation, villous atrophy, and crypt hyperplasia, which occur upon exposure to dietary gluten and which demonstrate improvement after withdrawal of gluten from the diet. However, the availability of serologic testing second for celiac disease and the common use of upper endoscopy has complicated the definition, since

these tests have identified patients who appear to have the disease but have variable degrees of histopathologic changes and/or symptoms. Thus, several categories of celiac disease have emerged. Whether these phenotypes are clinically useful remains to be determined.(1–3) All testing should be performed while patients are on a gluten-rich diet. No single test can confidently establish the diagnosis of celiac disease in every individual. As a result, the most important initial step in diagnosis is recognition of the many clinical features that can be associated with the disease. In this study, an atypical region for celiac disease wanted to show the involvement of the colon. We offer a series of thirty cases showed that celiac disease with colon mucosal non-spesific lenfoplasmocytic infiltration.

Ink4a/Arf−/− Dlk+ cells were transduced with either control enhanced green fluorescent protein (EGFP) or Bmi1 12-18 hours after purification. Enforced expression of Bmi1 was verified by western blot analysis (Fig. 4A). Exogenous Bmi1 in Ink4a/Arf−/− Dlk+ cells did not significantly increase colony number (Fig. 4B). Of note, however, the diameter of Bmi1-overexpressing colonies was significantly larger than that of the control colonies (Fig. 4C).

Furthermore, flow cytometric analyses showed that the percentage of Ink4a/Arf−/− Dlk+ cells labeled with EGFP was higher in Bmi1 cultures than in control cultures (22.6% ± 2.3%, 14.0% ± 1.2%, and 8.8% ± 0.7% versus 8.4% ± 1.1%, 3.4% ± 0.5%, and 2.1% ± 0.2% at days 7, 14, and 28 of culture, respectively) (Fig. selleck screening library 4D). We next carried out single-cell sorting of Dlk+ cells contained in primary colonies at days 14 and 28 of culture in order to evaluate their self-renewal capacity in terms of replating activity. Dlk+ cells overexpressing Bmi1 gave rise to

3.1-fold to 4.0-fold more secondary colonies than the control GS1101 (Fig. 5A). Secondary colonies were generated in a similar fashion to the original colonies. Immunocytochemical analyses demonstrated that the frequency of Alb+CK7+ bipotent cells was significantly higher in secondary colonies derived from Dlk+ cells collected from the primary Bmi1-transduced Ink4a/Arf−/− colonies at days 14 and 28 of culture (Fig. 5B,C). In contrast, Bmi1−/−Ink4a/Arf−/− Dlk+ cells behaved like Ink4a/Arf−/− Dlk+ cells (Supporting Fig. 5). Although loss of Bmi1 still affected the function of Ink4a/Arf−/− hepatic stem/progenitor cells to some extent, these findings indicate that Ink4a/Arf is the major target of Bmi1 in hepatic stem Thalidomide cells as in HSCs and NSCs. We then tested whether the loss of both Ink4a and Arf is enough for the transformation of hepatic stem cells. Considering

that a large number of cells were necessary for transplantations assays, these cells were allowed to form colonies in culture for 28 days. Immunocytochemical analyses showed that more than 90% of cells transduced with Bmi1 expressed both EGFP, a marker antigen for retrovirus integration, and Flag-tagged Bmi1 (Supporting Fig. 6). Subsequently, a total of 2 × 106 transduced cells were transplanted into the subcutaneous space of NOD/SCID mice (Fig. 5D). Although all the mice transplanted with Bmi1-transduced Ink4a/Arf−/− Dlk+ cells developed tumors, none of those transplanted with control Ink4a/Arf−/− Dlk+ cells did. Histological analyses revealed that the subcutaneous tumors consisted of both Alb+ parenchymal cells and a CK7+ glandular structure (Fig. 5D). The histological finding is consistent with our previous observation in tumors derived from Bmi1-transduced wild-type hepatic stem cells.3 These findings clearly indicate that repression of the Ink4a and Arf genes is not enough for Bmi1 to achieve its tumorigenic potential in hepatic stem cells.

We analyzed the prevalence, positions, and various characteristics of complex SVs in HBV. We further investigated clinical significance of complex SVs in HBV. Results: From the international database and published articles, we found six strains

of HBV with complex SVs. HBV genotype distribution was genotype A in two, genotype B in one, genotype D in one, and genotype E in two. All the complex SVs in HBV were observed in the region containing X open reading frame (ORF) and BCP. Patterns of complex SVs were deletion and duplication in two, deletion, insertion, and duplication in three, and deletion and insertion in one. Median deletion nucleotide length was 21 bases (range 8 -847 bases). In four strains with insertion, the median insertion nucleotide length was 23 bases (range 12-36 bases). In five strains with duplication, the median duplication nucleotide length was 31 selleck compound bases (range 20-67 bases). Two were found in patients with hepato-cellular carcinoma, and other

two Ku-0059436 datasheet were found in severe liver disease patients with post-renal transplantation. Conclusion: Novel genetic variants, complex SVs, were observed in six HBV strains. Complex SVs were observed in the region between X ORF and BCP. Complex SV in HBV was combination of canonical mutations. Though the cause and detailed mechanism still are not clear, it seems that this genetic variation is associated with severe liver disease, such as hepatocellular carcinoma or hepatic failure. (1) Fujiwara K, J Virology, 2005, 79(22), 14404. Disclosures: The following people have nothing to disclose: Kei Fujiwara, Noboru Shinkai, Shunsuke Nojiri, Mio Endo, Etsuko Iio, Takashi Joh Background and aim In clinical practice, serum HDV RNA level is used as a marker of viral replication. However, knowledge about its relationship to intrahepatic HDV markers is scant and there is no available data on the stability of HDV RNA in formalin-fixed paraffin-embedded liver samples (FFPE-LS). The aim of this

study was to Sitaxentan determine HDV RNA in FFPE-LS using a new technique and to compare the findings with HDV RNA levels in serum. Material and Methods Among 40 untreated CHD patients, 13 had FFPE-LS and a simultaneous serum sample testing positive for HDV RNA by qualitative assays. A patient with anti-HDV who tested negative for serum HDV RNA was also included. FFPE-LS were obtained between 1999 and 2012. Serum and liver HDV RNA were analyzed by quantitative realtime PCR. A new HDV RNA standard was used, and the sensitivity of the method was 10E3 to 10E6 copies HDV/uL. Results Liver HDV RNA was detected in 13/13 CHD patients (Table). The median liver HDV RNA level was 1.1×10E7 copies/mg (range 3.85×10E4-9.2×10E8). Retested serum HDV RNA yielded a median of 3.5×10E6 copies/uL (range 3.85×1 0E4-9.2×10E8). Serum and liver HDV RNA presented a good correlation (R2=0.89).

We analyzed the prevalence, positions, and various characteristics of complex SVs in HBV. We further investigated clinical significance of complex SVs in HBV. Results: From the international database and published articles, we found six strains

of HBV with complex SVs. HBV genotype distribution was genotype A in two, genotype B in one, genotype D in one, and genotype E in two. All the complex SVs in HBV were observed in the region containing X open reading frame (ORF) and BCP. Patterns of complex SVs were deletion and duplication in two, deletion, insertion, and duplication in three, and deletion and insertion in one. Median deletion nucleotide length was 21 bases (range 8 -847 bases). In four strains with insertion, the median insertion nucleotide length was 23 bases (range 12-36 bases). In five strains with duplication, the median duplication nucleotide length was 31 Venetoclax purchase bases (range 20-67 bases). Two were found in patients with hepato-cellular carcinoma, and other

two find more were found in severe liver disease patients with post-renal transplantation. Conclusion: Novel genetic variants, complex SVs, were observed in six HBV strains. Complex SVs were observed in the region between X ORF and BCP. Complex SV in HBV was combination of canonical mutations. Though the cause and detailed mechanism still are not clear, it seems that this genetic variation is associated with severe liver disease, such as hepatocellular carcinoma or hepatic failure. (1) Fujiwara K, J Virology, 2005, 79(22), 14404. Disclosures: The following people have nothing to disclose: Kei Fujiwara, Noboru Shinkai, Shunsuke Nojiri, Mio Endo, Etsuko Iio, Takashi Joh Background and aim In clinical practice, serum HDV RNA level is used as a marker of viral replication. However, knowledge about its relationship to intrahepatic HDV markers is scant and there is no available data on the stability of HDV RNA in formalin-fixed paraffin-embedded liver samples (FFPE-LS). The aim of this

study was to Baf-A1 molecular weight determine HDV RNA in FFPE-LS using a new technique and to compare the findings with HDV RNA levels in serum. Material and Methods Among 40 untreated CHD patients, 13 had FFPE-LS and a simultaneous serum sample testing positive for HDV RNA by qualitative assays. A patient with anti-HDV who tested negative for serum HDV RNA was also included. FFPE-LS were obtained between 1999 and 2012. Serum and liver HDV RNA were analyzed by quantitative realtime PCR. A new HDV RNA standard was used, and the sensitivity of the method was 10E3 to 10E6 copies HDV/uL. Results Liver HDV RNA was detected in 13/13 CHD patients (Table). The median liver HDV RNA level was 1.1×10E7 copies/mg (range 3.85×10E4-9.2×10E8). Retested serum HDV RNA yielded a median of 3.5×10E6 copies/uL (range 3.85×1 0E4-9.2×10E8). Serum and liver HDV RNA presented a good correlation (R2=0.89).

Thus, suckling bout duration in captive animals does not necessarily reflect evolutionary adaptation to an arid environment. Although suckling bout duration and frequency is not a good indicator of milk transfer (Cameron, 1998; Cameron et al., 1999), it can be useful to assess the amount of maternal care in current offspring (Mendl & Paul, 1989; Cassinello, 2001; Therrien et al., 2007; Pluháček et al., 2010a) and specifically the needs of the offspring (e.g. suckling frequency in Therrien et al., 2007). Our results suggested that suckling bout duration increased with intraspecific aggression rate among adult females of the

species (i.e. longest duration recorded in mountain zebras, followed by plains zebras and Grévy’s AZD2014 price zebras). A similar effect of relationships among adults, including aggression among female adults on maternal style, was recorded in interspecific comparisons of several macaque species (Kaufman & Rosenblum,

1969; Thierry, 1985; Maestripieri, 1994a,b). This has been given as a possible explanation for high-suckling frequency in studies on white-tailed deer Odocoileus virginianus and fallow deer (Lavigueur & Barrette, 1992; Therrien et al., 2007). In primates suckling duration is correlated with stress reduction (Gomendio, 1990; Clutton-Brock, 1991; Redondo, Gomendio & Medina, 1992), and in cattle with socialization with the dam (Das Neratinib concentration Niclosamide et al., 2000). Therefore, suckling bout duration and the time spent suckling can reflect the social needs of the foal, whereas termination and rejection seems to be affected by ecological adaptation. Because our results came from captive animals living in limited space,

the high aggression rate among mares could strengthen the social demands of the foal to the mother, in mountain zebras in particular. The artificial setting may also have affected the results likely by two factors: smaller space than in the wild and high-quality diet of predictable delivery. Our results dealing with suckling bout duration and frequency are a little different from those of Becker & Ginsberg (1990). In both studies the lowest suckling frequency and time spent suckling was observed in Grévy’s zebras. However, contrasting with the results of Becker & Ginsberg (1990) we recorded longer suckling bout duration in plains than in Grévy’s zebras. In our earlier study on captive plains zebras, we found that suckling bout duration was highly affected by the animal terminating the bout and by the pregnancy status of the nursing mare (Pluháček et al., 2010a); in this study we excluded pregnant mares and did separate analyses depending on the animal terminating the bout. These factors could have affected the results of Becker & Ginsberg (1990). Nevertheless, we cannot omit the effect of captivity as an explanation for the difference in suckling bout duration between our and their studies.