, 2007). However, one of our studied penguins (A5) did not exhibit a reduction in body angle and regularly surfaced at vertical speeds exceeding 2.2 m s −1. The second main hypothesis explaining delaying ascent is the use of buoyancy to travel horizontally (Sato et al., 2002). This would predict that penguins increase the horizontal component of the ascent phase after not encountering a prey patch, in order to prospect a bigger volume of the water column. Conversely, we could predict that penguins would minimize horizontal travelling after encountering a prey patch, in order to

maximize the probability of relocating the same patch. Indeed, we observed that ascent angles were higher and ascent flipper stroke frequency was lower after encountering prey, thus reducing horizontal travelling. check details However, as no data were available on the 3-D structure of the dives Palbociclib or on the surface locations between successive dives, we cannot confirm this hypothesis of horizontal travelling in the search of a new foraging patch. The present study indicates that king penguins exhibited higher vertical speed during transit times, linked with a steeper

body angle and a small increase in swimming speed following productive foraging during the preceding dive or during the current one. Similar results have been reported in two smaller penguin species performing shallower dives. In Adélie penguins, mean angles of ascent and subsequent descent are steeper after bottom phases where prey ingestions occurred (Ropert-Coudert et al., 2001); and in little penguins, mean descent angles were steeper after dives where prey pursuit occurred (Ropert-Coudert et al., 2006). Together, these results show that penguins are able to optimize 上海皓元医药股份有限公司 their diving behaviour by adjusting their transit. King penguins feed on myctophid fishes patchily distributed in dense monospecific shoals during the day (Perissinotto & McQuaid, 1992). When the penguin has fed successfully on a favourable patch, we can assume the preferred foraging option is to attempt to relocate the same patch before its dispersion

after returning to the surface. By shortening their post-dive interval and descending faster, the penguins increase their probability of encountering the same patch in the following dive. The fact that penguins ascended with a lower flipper stroke frequency after finding more prey during the bottom of the current dive was unexpected. Furthermore, this lower flipper stroke frequency seems not to handicap a faster ascent to the surface, which could be explained by higher buoyancy. We might hypothesize that penguins anticipated encountering prey and consequently increased respiratory air volume before submergence, which increased buoyancy up-thrust when ascending. Increased descent flipper stroke frequency after highly foraging dives, presumably to overcome this additional buoyancy, strongly supports this hypothesis.

, 2007). However, one of our studied penguins (A5) did not exhibit a reduction in body angle and regularly surfaced at vertical speeds exceeding 2.2 m s −1. The second main hypothesis explaining delaying ascent is the use of buoyancy to travel horizontally (Sato et al., 2002). This would predict that penguins increase the horizontal component of the ascent phase after not encountering a prey patch, in order to prospect a bigger volume of the water column. Conversely, we could predict that penguins would minimize horizontal travelling after encountering a prey patch, in order to

maximize the probability of relocating the same patch. Indeed, we observed that ascent angles were higher and ascent flipper stroke frequency was lower after encountering prey, thus reducing horizontal travelling. learn more However, as no data were available on the 3-D structure of the dives GS1101 or on the surface locations between successive dives, we cannot confirm this hypothesis of horizontal travelling in the search of a new foraging patch. The present study indicates that king penguins exhibited higher vertical speed during transit times, linked with a steeper

body angle and a small increase in swimming speed following productive foraging during the preceding dive or during the current one. Similar results have been reported in two smaller penguin species performing shallower dives. In Adélie penguins, mean angles of ascent and subsequent descent are steeper after bottom phases where prey ingestions occurred (Ropert-Coudert et al., 2001); and in little penguins, mean descent angles were steeper after dives where prey pursuit occurred (Ropert-Coudert et al., 2006). Together, these results show that penguins are able to optimize MCE their diving behaviour by adjusting their transit. King penguins feed on myctophid fishes patchily distributed in dense monospecific shoals during the day (Perissinotto & McQuaid, 1992). When the penguin has fed successfully on a favourable patch, we can assume the preferred foraging option is to attempt to relocate the same patch before its dispersion

after returning to the surface. By shortening their post-dive interval and descending faster, the penguins increase their probability of encountering the same patch in the following dive. The fact that penguins ascended with a lower flipper stroke frequency after finding more prey during the bottom of the current dive was unexpected. Furthermore, this lower flipper stroke frequency seems not to handicap a faster ascent to the surface, which could be explained by higher buoyancy. We might hypothesize that penguins anticipated encountering prey and consequently increased respiratory air volume before submergence, which increased buoyancy up-thrust when ascending. Increased descent flipper stroke frequency after highly foraging dives, presumably to overcome this additional buoyancy, strongly supports this hypothesis.

, 2007). However, one of our studied penguins (A5) did not exhibit a reduction in body angle and regularly surfaced at vertical speeds exceeding 2.2 m s −1. The second main hypothesis explaining delaying ascent is the use of buoyancy to travel horizontally (Sato et al., 2002). This would predict that penguins increase the horizontal component of the ascent phase after not encountering a prey patch, in order to prospect a bigger volume of the water column. Conversely, we could predict that penguins would minimize horizontal travelling after encountering a prey patch, in order to

maximize the probability of relocating the same patch. Indeed, we observed that ascent angles were higher and ascent flipper stroke frequency was lower after encountering prey, thus reducing horizontal travelling. Panobinostat mouse However, as no data were available on the 3-D structure of the dives AZD3965 ic50 or on the surface locations between successive dives, we cannot confirm this hypothesis of horizontal travelling in the search of a new foraging patch. The present study indicates that king penguins exhibited higher vertical speed during transit times, linked with a steeper

body angle and a small increase in swimming speed following productive foraging during the preceding dive or during the current one. Similar results have been reported in two smaller penguin species performing shallower dives. In Adélie penguins, mean angles of ascent and subsequent descent are steeper after bottom phases where prey ingestions occurred (Ropert-Coudert et al., 2001); and in little penguins, mean descent angles were steeper after dives where prey pursuit occurred (Ropert-Coudert et al., 2006). Together, these results show that penguins are able to optimize 上海皓元 their diving behaviour by adjusting their transit. King penguins feed on myctophid fishes patchily distributed in dense monospecific shoals during the day (Perissinotto & McQuaid, 1992). When the penguin has fed successfully on a favourable patch, we can assume the preferred foraging option is to attempt to relocate the same patch before its dispersion

after returning to the surface. By shortening their post-dive interval and descending faster, the penguins increase their probability of encountering the same patch in the following dive. The fact that penguins ascended with a lower flipper stroke frequency after finding more prey during the bottom of the current dive was unexpected. Furthermore, this lower flipper stroke frequency seems not to handicap a faster ascent to the surface, which could be explained by higher buoyancy. We might hypothesize that penguins anticipated encountering prey and consequently increased respiratory air volume before submergence, which increased buoyancy up-thrust when ascending. Increased descent flipper stroke frequency after highly foraging dives, presumably to overcome this additional buoyancy, strongly supports this hypothesis.

05) and it was not significantly different from that of the CE images. The detection rate of pink or orange color in AF

images was significantly higher for protruded intestinal-type EGCs than gastric adenomas (P = 0.005), depressed intestinal-type EGCs (P < 0.001), and diffuse-type EGCs (P = 0.027). Conclusions:  Autofluorescence videoendoscopy using the SAFE-3000 system for gastric neoplasias might be useful for diagnosing depressed intestinal-type early gastric cancers. The detection of orange or pink color in AF images may be efficacious in discriminating protruded intestinal-type early gastric cancers from gastric adenomas. "
“Knowing the Y-27632 mouse spontaneous outcome of hepatocellular carcinoma (HCC) is

important for designing randomized controlled trials (RCTs) of new therapeutic approaches; however, survival of patients in the absence of treatment is highly variable, and prognostic factors influencing outcomes are incompletely defined. The aims of this meta-analysis were to estimate the 1-year and 2-year survival rates of untreated HCC patients enrolled in RCTs of palliative treatments, and to identify prognostic factors. RCTs evaluating therapies for HCC with placebo or no-treatment arms were identified on MEDLINE through April 2009. Data were combined in a random effect model. Primary outcomes were 1-year and 2-year survival. Thirty studies met the inclusion criteria. The pooled estimates of the survival rates were 17.5% at 1 year (95% confidence interval [95%CI], Ruxolitinib 11%-27%; range, 0%-75%) and 7.3% at 2 years (95%CI, 3.9%-13%; range, 0%-50%). Heterogeneity among studies was highly significant (P < 0.0001) both for 1-year and 2-year survival, and persisted when RCTs were stratified according to all patient

and study features. Through meta-regression, impaired performance status, Child-Pugh B-C class, and presence of portal vein thrombosis were MCE公司 all independently associated with shorter survival. Ascites was strongly linked to a worse outcome in intermediate/advanced Barcelona Clinic Liver Cancer stages. Conclusion: This meta-analysis confirms the heterogeneity of behavior of untreated HCC and provides a sound basis for stratifying patients with HCC according to expected survival in future trials of new anti-cancer agents. (HEPATOLOGY 2010.) The extensive application of surveillance programs for early detection of small (<5 cm) hepatocellular carcinoma (HCC) has increased the number of tumors detected within the Milan criteria1 at Barcelona Clinic Liver Cancer (BCLC) stages 0 or A (very early or early),2 and potentially responsive to curative treatments, such as liver transplantation and percutaneous or surgical ablation.3, 4 Nonetheless, most patients with HCC (approximately 70%) are diagnosed at BCLC B (intermediate) and C (advanced) stages (approximately 50%) or BCLC D (end stage, approximately 20%).

05) and it was not significantly different from that of the CE images. The detection rate of pink or orange color in AF

images was significantly higher for protruded intestinal-type EGCs than gastric adenomas (P = 0.005), depressed intestinal-type EGCs (P < 0.001), and diffuse-type EGCs (P = 0.027). Conclusions:  Autofluorescence videoendoscopy using the SAFE-3000 system for gastric neoplasias might be useful for diagnosing depressed intestinal-type early gastric cancers. The detection of orange or pink color in AF images may be efficacious in discriminating protruded intestinal-type early gastric cancers from gastric adenomas. "
“Knowing the BYL719 price spontaneous outcome of hepatocellular carcinoma (HCC) is

important for designing randomized controlled trials (RCTs) of new therapeutic approaches; however, survival of patients in the absence of treatment is highly variable, and prognostic factors influencing outcomes are incompletely defined. The aims of this meta-analysis were to estimate the 1-year and 2-year survival rates of untreated HCC patients enrolled in RCTs of palliative treatments, and to identify prognostic factors. RCTs evaluating therapies for HCC with placebo or no-treatment arms were identified on MEDLINE through April 2009. Data were combined in a random effect model. Primary outcomes were 1-year and 2-year survival. Thirty studies met the inclusion criteria. The pooled estimates of the survival rates were 17.5% at 1 year (95% confidence interval [95%CI], signaling pathway 11%-27%; range, 0%-75%) and 7.3% at 2 years (95%CI, 3.9%-13%; range, 0%-50%). Heterogeneity among studies was highly significant (P < 0.0001) both for 1-year and 2-year survival, and persisted when RCTs were stratified according to all patient

and study features. Through meta-regression, impaired performance status, Child-Pugh B-C class, and presence of portal vein thrombosis were 上海皓元医药股份有限公司 all independently associated with shorter survival. Ascites was strongly linked to a worse outcome in intermediate/advanced Barcelona Clinic Liver Cancer stages. Conclusion: This meta-analysis confirms the heterogeneity of behavior of untreated HCC and provides a sound basis for stratifying patients with HCC according to expected survival in future trials of new anti-cancer agents. (HEPATOLOGY 2010.) The extensive application of surveillance programs for early detection of small (<5 cm) hepatocellular carcinoma (HCC) has increased the number of tumors detected within the Milan criteria1 at Barcelona Clinic Liver Cancer (BCLC) stages 0 or A (very early or early),2 and potentially responsive to curative treatments, such as liver transplantation and percutaneous or surgical ablation.3, 4 Nonetheless, most patients with HCC (approximately 70%) are diagnosed at BCLC B (intermediate) and C (advanced) stages (approximately 50%) or BCLC D (end stage, approximately 20%).

As shown in Fig. 1A, sALT levels increased as early as 1 hour of reperfusion, peaked at 6 hours, and decreased thereafter. To determine the function of PD-1/B7-H1 negative signaling in the acute phase of liver IRI in this model, WT mice treated with B7-H1Ig were subjected to 90 minutes of partial

liver warm ABT-199 molecular weight ischemia followed by 6 hours or 24 hours of reperfusion. Unlike WT mice given control Ig, those conditioned with B7-H1Ig were resistant against IR-mediated hepatocellular damage, as evidenced by reduced sALT levels (163 ± 30 U/L versus 845 ± 166 U/L [6 hours], P < 0.01; 65 ± 2 U/L versus 216 ± 113 U/L [24 hours], P < 0.05) (Fig. 1B). These data correlated with histological criteria of liver damage at the peak of 6 hours postreperfusion (Fig. 1C). Control livers revealed severe lobular edema, congestion, ballooning, and hepatocellular necrosis (Suzuki score 2.33 ± 0.29 [6 hours]). In contrast, the B7-H1Ig group showed well-preserved liver architecture and histological detail without edema, vacuolization, or necrosis (Suzuki score 0.33 ± 0.58 [6 hours], P < 0.01). To determine whether this effect was dependent on stimulation of PD-1/B7-H1, a separate group of WT mice was treated with anti–B7-H1 mAb. Indeed, PD-1/B7-H1 NVP-LDE225 molecular weight blockade re-created IR-triggered hepatocellular injury

and augmented liver damage compared with controls, as evidenced by increased sALT levels (1,497 ± 164 U/L [6 hours], 737 ± 264 U/L [24 hours], P < 0.05) (Fig. 1B), and deterioration of liver histology (Fig. 1C), reflected by the Suzuki score (3.83 ± 0.29 [6 hours], P < 0.01). We performed immunohistochemical staining of liver infiltrating cells at 6 hours of reperfusion following 90 minutes of warm ischemia. Treatment with B7-H1Ig diminished the number of cells per high-power field for T cells (0.5 ± 0.58 versus 2.0 ± 0.82, P < 0.05) ( Fig. 2A), neutrophils (2.0 ± 1.0 versus 53.7 ± 3.2, P < 0.001) (Fig. 2B), and macrophages (4.3 ± 1.0 versus 78.0 ± 2.0, P < 0.001) (Fig. 2) in the ischemic liver lobe compared with controls. Myeloperoxidase assay revealed that liver neutrophil activity was also

depressed in the treatment group compared with controls (0.03 ± 0.2 U/g versus 上海皓元医药股份有限公司 1.13 ± 0.3 U/g, P < 0.05) (Supporting Information Fig. 1). To assess the immunoregulatory mechanism of PD-1/B7-H1 activation, we contrasted intrahepatic T lymphocyte–related cytokine expression patterns in our model. B7-H1Ig significantly (P < 0.05) suppressed gene induction of Th1-type IFN-γ/granzyme B and largely abolished otherwise enhanced gene transcript levels of neutrophil/monocyte-derived proinflammatory chemokines (CXCL-1, CXCL-5, CCL-2, CXCL-10) and cytokines (TNF-α, IL-1β, IFN-β, IL-6) (P < 0.01) ( Fig. 3A,B). In contrast, Th2-type IL-10 but not IL-4 expression significantly (P < 0.01) increased after B7-H1Ig engagement (Fig. 3C).

As shown in Fig. 1A, sALT levels increased as early as 1 hour of reperfusion, peaked at 6 hours, and decreased thereafter. To determine the function of PD-1/B7-H1 negative signaling in the acute phase of liver IRI in this model, WT mice treated with B7-H1Ig were subjected to 90 minutes of partial

liver warm Tamoxifen datasheet ischemia followed by 6 hours or 24 hours of reperfusion. Unlike WT mice given control Ig, those conditioned with B7-H1Ig were resistant against IR-mediated hepatocellular damage, as evidenced by reduced sALT levels (163 ± 30 U/L versus 845 ± 166 U/L [6 hours], P < 0.01; 65 ± 2 U/L versus 216 ± 113 U/L [24 hours], P < 0.05) (Fig. 1B). These data correlated with histological criteria of liver damage at the peak of 6 hours postreperfusion (Fig. 1C). Control livers revealed severe lobular edema, congestion, ballooning, and hepatocellular necrosis (Suzuki score 2.33 ± 0.29 [6 hours]). In contrast, the B7-H1Ig group showed well-preserved liver architecture and histological detail without edema, vacuolization, or necrosis (Suzuki score 0.33 ± 0.58 [6 hours], P < 0.01). To determine whether this effect was dependent on stimulation of PD-1/B7-H1, a separate group of WT mice was treated with anti–B7-H1 mAb. Indeed, PD-1/B7-H1 selleck chemicals llc blockade re-created IR-triggered hepatocellular injury

and augmented liver damage compared with controls, as evidenced by increased sALT levels (1,497 ± 164 U/L [6 hours], 737 ± 264 U/L [24 hours], P < 0.05) (Fig. 1B), and deterioration of liver histology (Fig. 1C), reflected by the Suzuki score (3.83 ± 0.29 [6 hours], P < 0.01). We performed immunohistochemical staining of liver infiltrating cells at 6 hours of reperfusion following 90 minutes of warm ischemia. Treatment with B7-H1Ig diminished the number of cells per high-power field for T cells (0.5 ± 0.58 versus 2.0 ± 0.82, P < 0.05) ( Fig. 2A), neutrophils (2.0 ± 1.0 versus 53.7 ± 3.2, P < 0.001) (Fig. 2B), and macrophages (4.3 ± 1.0 versus 78.0 ± 2.0, P < 0.001) (Fig. 2) in the ischemic liver lobe compared with controls. Myeloperoxidase assay revealed that liver neutrophil activity was also

depressed in the treatment group compared with controls (0.03 ± 0.2 U/g versus 上海皓元 1.13 ± 0.3 U/g, P < 0.05) (Supporting Information Fig. 1). To assess the immunoregulatory mechanism of PD-1/B7-H1 activation, we contrasted intrahepatic T lymphocyte–related cytokine expression patterns in our model. B7-H1Ig significantly (P < 0.05) suppressed gene induction of Th1-type IFN-γ/granzyme B and largely abolished otherwise enhanced gene transcript levels of neutrophil/monocyte-derived proinflammatory chemokines (CXCL-1, CXCL-5, CCL-2, CXCL-10) and cytokines (TNF-α, IL-1β, IFN-β, IL-6) (P < 0.01) ( Fig. 3A,B). In contrast, Th2-type IL-10 but not IL-4 expression significantly (P < 0.01) increased after B7-H1Ig engagement (Fig. 3C).

The radiographical findings in arthropathy follow an expected sequence of events and are overall similar in different joints. Magnetic resonance imaging (MRI) has advantages over radiography based on its capability of visualizing soft tissue and cartilage changes in haemophilic joints. The recent development and standardization of MRI scoring systems for measuring soft tissue and cartilage abnormalities may enable the comparison of pathological joint findings in clinical trials conducted at different institutions across the world. The implementation of high-frequency transducers and colour/power

Doppler capabilities has provided new insights for clinical applications of ultrasonography (US) in haemophilic arthropathy. In spite of the imaging modality’s technical challenges such as operator-dependency, US has advantages over MRI. One of these advantages is its BMS-777607 research buy ability of differentiating synovium hypertrophy and hemosiderin deposition, which is not possible with MRI given the presence of susceptibility artefacts from extracellular hemosiderin on gradient-echo MR images. In addition to the aforementioned conventional PD0332991 imaging modalities, novel imaging techniques (blood oxygen level dependent, ultrasmall superparamagnetic iron-oxide contrast-enhanced, and T1 and T2 mapping MRI, ultrasound biomicroscopy,

microbubble contrast-enhanced US and positron emission tomography, among others) hold promise for early assessment of haemophilic arthropathy

in the future upon completion of their clinical validation. Joint disease affects 90% of severe haemophiliacs and contributes to most of the morbidity of this condition [1]. Ankles, knees and elbows are the joints most frequently involved [2]. Haemophilic arthropathy is caused by recurrent haemorrhagic episodes into the joint, which can be prevented by regular infusions of factor concentrate replacement known as medchemexpress prophylactic regimens [3]. Treatment includes continuous or on-demand clotting factor replacement and radionuclide or open synovectomy. The radiographical findings of haemophilic arthropathy depend on the stage of disease, the age of the patient at onset and the joint involved. These findings include joint effusion, soft tissue swelling, epiphyseal overgrowth, subchondral cysts, osseous erosion and secondary degenerative changes [4]. The pathogenetic mechanisms involved in haemophilic arthropathy are unknown, but most likely multifactorial [5]. Some authors [6–9] suggest that intra-articular blood has a precursor direct effect on cartilage, as a result of the iron-catalysed formation of destructive oxygen metabolites, subsequently affecting the synovium. Other authors [10,11] suggest that there is a hemosiderin-induced synovial triggering process. Nevertheless, most likely both processes occur in parallel, and while they influence each other, they probably do not depend on each other.

The radiographical findings in arthropathy follow an expected sequence of events and are overall similar in different joints. Magnetic resonance imaging (MRI) has advantages over radiography based on its capability of visualizing soft tissue and cartilage changes in haemophilic joints. The recent development and standardization of MRI scoring systems for measuring soft tissue and cartilage abnormalities may enable the comparison of pathological joint findings in clinical trials conducted at different institutions across the world. The implementation of high-frequency transducers and colour/power

Doppler capabilities has provided new insights for clinical applications of ultrasonography (US) in haemophilic arthropathy. In spite of the imaging modality’s technical challenges such as operator-dependency, US has advantages over MRI. One of these advantages is its Selleck Cabozantinib ability of differentiating synovium hypertrophy and hemosiderin deposition, which is not possible with MRI given the presence of susceptibility artefacts from extracellular hemosiderin on gradient-echo MR images. In addition to the aforementioned conventional Doxorubicin imaging modalities, novel imaging techniques (blood oxygen level dependent, ultrasmall superparamagnetic iron-oxide contrast-enhanced, and T1 and T2 mapping MRI, ultrasound biomicroscopy,

microbubble contrast-enhanced US and positron emission tomography, among others) hold promise for early assessment of haemophilic arthropathy

in the future upon completion of their clinical validation. Joint disease affects 90% of severe haemophiliacs and contributes to most of the morbidity of this condition [1]. Ankles, knees and elbows are the joints most frequently involved [2]. Haemophilic arthropathy is caused by recurrent haemorrhagic episodes into the joint, which can be prevented by regular infusions of factor concentrate replacement known as 上海皓元 prophylactic regimens [3]. Treatment includes continuous or on-demand clotting factor replacement and radionuclide or open synovectomy. The radiographical findings of haemophilic arthropathy depend on the stage of disease, the age of the patient at onset and the joint involved. These findings include joint effusion, soft tissue swelling, epiphyseal overgrowth, subchondral cysts, osseous erosion and secondary degenerative changes [4]. The pathogenetic mechanisms involved in haemophilic arthropathy are unknown, but most likely multifactorial [5]. Some authors [6–9] suggest that intra-articular blood has a precursor direct effect on cartilage, as a result of the iron-catalysed formation of destructive oxygen metabolites, subsequently affecting the synovium. Other authors [10,11] suggest that there is a hemosiderin-induced synovial triggering process. Nevertheless, most likely both processes occur in parallel, and while they influence each other, they probably do not depend on each other.

Results: The combined inhibition of p300 and PCAF HATs (compound EML-264) or stimulation

of hSirt1/2 HDAC activity (compound MC2791) resulted in an evident reduction of HBV replication that mirrored the decrease of pgRNA transcription. Potentiation of Ezh2 activity through the inhibition of JMJD3 histone demethylase with compound MC311 9 resulted in a >50% reduction of pgRNA transcription and a sharp increase in cccDNA bound H3 trimethylation at lysine 27 (H3K27me3). Conclusions: Altogether these results represent a proof of concept that small molecules / drugs that affect cccDNA Daporinad ic50 bound chromatin modifying enzymes can modulate HBV transcription and replication. Activation of hSirt1/2 and Ezh2 by small molecules can induce an “”active epigenetic suppression”" of HBV cccDNA minichromosome similar to that observed with

IFNα and provide the rationale to explore sequential treatments as a model for IFN sparing regimens in cellular or chimeric mice HBV replication systems. Disclosures: Massimo Levrero – Advisory Committees or Review Panels: BMS, Jansen, Gilead; Speaking and Teaching: MSD, Roche The following people have nothing to disclose: Gianna Aurora Palumbo, Laura Belloni, Sergio Valente, Dante Rotili, Natalia Pediconi, Antonello Mai Background: Patterns of hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)-negative, antibody to the hepatitis B core antigen (anti-HBc)-positive individuals undergoing hematopoietic stem cell transplantation (HSCT) have not been well described. Methods: Hydroxychloroquine mouse From October 201 1 onwards, we recruited HBsAg-negative, anti-HBc-positive Chinese patients with baseline undetectable serum HBV DNA (<10 IU/mL), undergoing either allogenic or autologous HSCT. For allogenic HSCT,

only recipients whose donors were HBsAg negative were recruited. Liver biochemistry, serum HBV DNA (Abbott MCE公司 RealTime HBV), HBsAg and antibody to HBsAg (anti-HBs) (Abbott Laboratories) were prospectively monitored every 4 weeks after HSCT up to 2 years from recruitment. Following guidelines from the European Association for the Study of the Liver, entecavir was started when detectable HBV DNA (≧10 IU/mL) was encountered. Results: At the time of writing, among 197 patients undergoing HSCT, 51 (25.9%) were HBsAg-neg-ative, anti-HBc-positive. After excluding allogenic HSCT recipients with HBsAg-positive donors (n=6) and patients with baseline detectable HBV DNA (n=2), 43 (48.9% male) patients were recruited. The median age and duration of follow-up were 46.5 (range 1 9.9-66.7) years and 47.6 (range 4-76) weeks respectively. 41 (95.4%) had detectable anti-HBs (range 11->1000 mIU/mL). 6 patients (14.0%) had detectable HBV DNA after a median follow-up period of 38 (range 16-68) weeks. The median HBV DNA level at reactivation was 24.5 (range 14-428) IU/mL. 5 patients (83.3%) remained HBsAg-negative at reactivation.