The abundances of the representative species in the pond increase

The abundances of the representative species in the pond increased during high-temperature LY2157299 seasons, whereas only C. raciborskii became dominant in the pond from summer to autumn in both 2009 and 2010. The high shade tolerance of C. raciborskii was likely one of the factors that enabled the cyanobacterium to grow during the summer when the transparency was low. Moreover, the heterocyst production of C. raciborskii was enhanced during summer when the concentration of dissolved inorganic nitrogen was low, implying that nitrogen fixation also played an important role in supporting the growth of C. raciborskii. Autumnal rainfall was a critical factor in the collapse of C. raciborskii

blooms. C. raciborskii formed blooms with relatively small trichomes, whereas larger trichomes dominated during winter. The dependence of the trade-off

between growth rate and trichome size on temperature was assumed to be an adaptation strategy of C. raciborskii. “
“Two Algal Turf Scrubber (ATS) units were deployed on the Great Wicomico River (GWR) for 22 months to examine the role of substrate in increasing algal productivity and nutrient removal. The yearly mean productivity of flat ATS screens was 15.4 g · m−2 · d−1. This was elevated to 39.6 g · m−2 · d−1 with a three-dimensional (3-D) screen, and to 47.7 g · m−2 · d−1 by avoiding high summer harvest temperatures. These methods enhanced nutrient removal (N, P) in algal biomass by 3.5 times. Eighty-six algal taxa (Ochrophyta [diatoms], Chlorophyta [green algae], and Cyan-obacteria [blue–green algae]) self-seeded from the GWR IMP dehydrogenase and demonstrated yearly cycling. selleck compound Silica (SiO2) content of the algal biomass ranged from 30% to 50% of total biomass; phosphorus, nitrogen, and carbon content of the total algal biomass ranged from 0.15% to 0.21%, 2.13% to 2.89%, and 20.0% to 25.7%, respectively. Carbohydrate content (at 10%–25% of AFDM) was dominated by glucose. Lipids (fatty acid methyl ester; FAMEs) ranged widely from 0.5% to 9% AFDM, with Omega-3 fatty acids a consistent component. Mathematical

modeling of algal produ-ctivity as a function of temperature, light, and substrate showed a proportionality of 4:3:3, resp-ectively. Under landscape ATS operation, substrate manipulation provides a considerable opportunity to increase ATS productivity, water quality amelioration, and biomass coproduction for fertilizers, fermentation energy, and omega-3 products. Based on the 3-D prod-uctivity and algal chemical composition demonstrated, ATS systems used for nonpoint source water treat-ment can produce ethanol (butanol) at 5.8× per unit area of corn, and biodiesel at 12.0× per unit area of soy beans (agricultural production US). “
“Algal and plant production of nonphosphorus lipids in place of phospholipids is a physiological response to low phosphorus (P) availability.

1D) A previous study has shown an inhibitory effect of MxA on th

1D). A previous study has shown an inhibitory effect of MxA on the nucleocytoplasmic export of HBV mRNA.11 We therefore checked the expression and the cytoplasmic/nuclear distribution of intracellular HBV RNAs in HepG2.2.15 cells. Results from real-time PCR demonstrated that neither the total RNAs nor its intracellular distribution was altered by MxA or each of the two mutants, as measured at 24 hours after transfection (Supporting Fig. 2A,B). Consistently, results of Western blot showed that the intracellular HBcAg protein level was not remarkably influenced (Supporting Fig. 2C). Taken together, these results suggest that in HepG2.2.15 cells, MxA GTPase activity independently inhibits HBV replication without altering

the cytoplasmic/nuclear HBV mRNA distribution Trametinib solubility dmso and HBcAg level, at least in the early stage of MxA expression. To investigate the mechanism underlying the anti-HBV effect of MxA, we observed the location of HBcAg, the core protein of HBV, in hepatoma cells expressing HBV plasmid and CFP-tagged MxA. Immunofluorescence images revealed that in HBV-transfected Huh7 cells without CFP-MxA expression, HBcAg was spread throughout the cytoplasm and the nucleus in a small punctate pattern (data not shown). Strikingly, in CFP-MxA–overexpressing cells, HBcAg colocalized

with CFP-MxA to generate large granular structures in the cytoplasm (Fig. 2A). To further verify the colocalization of MxA and HBcAg, we overexpressed the two proteins in a nonhepatoma cell type. In living Vero cells, YFP-HBcAg accumulated in the perinuclear region, overlapping with either the wild-type or the mutant CFP-MxA Etoposide cell line (Fig. 2B). Colocalization of MxA with HBcAg prompted us to look for evidence of their possible interaction. First, we determined whether MxA and HBcAg could undergo

coprecipitation. In Huh7 cells expressing Flag-MxA and YFP-HBcAg, immunoprecipitation of HBcAg using GFP antibody resulted in coprecipitation of Flag-MxA (Fig. 2C). The formation of the MxA-HBcAg complex was not dependent on the GTPase activity of MxA, because the Flag-L612K and Flag-K83A mutants of MxA were coimmunoprecipitated with YFP-HBcAg to a similar degree. We then tested whether exogenous HBcAg could interact with endogenous MxA, or exogenous MxA with endogenous HBcAg, because a previous study showed that in HBV-expressing HepG2.2.15 cells, IFN is unable to induce MxA expression.14 By treatment of Huh7 cells expressing Flag-HBcAg with IFNα, or transfection of HepG2.2.15 cells with Flag-MxA, we found that Flag-HBcAg coprecipitated IFNα-induced MxA (Fig. 2D), while Flag-MxA coprecipitated endogenous HBcAg (Fig. 2E), indicating a specific interaction between HBcAg and MxA. Finally, we performed fluorescence resonance energy transfer (FRET) experiments, which detect the proximity of interacting proteins. In living Vero cells expressing CFP-MxA and YFP-HBcAg, the proteins were first confirmed to colocalize to perinuclear structures.

pylori infection in the FD group was 497% [24] Another study lo

pylori infection in the FD group was 49.7% [24]. Another study looking at the

discriminatory value of the Rome III questionnaire in dyspeptic patients found that 136 of 191 (71%) patients had FD, and H. pylori infection was present in 70 (51%) [25]. The pathophysiology of FD is multifactorial. selleckchem Although the role of H. pylori in FD remains controversial, it is possible that immune mechanisms seen in other gut infections could be involved in the pathophysiology of dyspepsia. Li et al. [26] reported increased numbers of enterochromaffin cells and mast cells in the duodenum of patients with postinfectious and nonspecific FD compared with healthy controls, in addition to higher levels of chemicals such as histamine and tryptase derived from these cells. This suggests impaired ability of the immune system to terminate the inflammatory response after infection leading to release of potent chemicals that may be involved in the pathogenesis of postinfectious FD [27]. Suzuki et al. [28] have proposed that H. pylori-associated dyspepsia might be considered an organic disease and, as such, a disease entity separated from FD. While several randomized controlled

trials in Western populations have failed to show a significant advantage of H. pylori eradication in patients with FD, a study suggested that Asian patients benefit from treatment for H. pylori infection with as much as a 13-fold increased chance of symptom GDC-0941 mouse resolution following its eradication [29]. The Second Asia Pacific Consensus Guidelines strongly recommended H. pylori eradication in H. pylori-positive patients with FD [30]. A review of current practices in diagnosis and management of functional GI disorders in the Asia-Pacific (AP) region found 58% of doctors who attended the first Asia Pacific Conference in Tokyo in November 2010 checked H. pylori status

in their patients with FD, and when positive, about half (53%) of them opted for eradication therapy [31]. The past few years have seen increased focus on histological assessment and classification of gastritis to provide better correlation with the risk of malignant transformation. The Operative Link on Gastritis Cobimetinib in vitro Assessment (OLGA) classification was introduced in 2007 [32], and placed the histological phenotypes of gastritis on a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV). OLGA recommends at least five biopsy samples from: (1) the greater and lesser curvatures of the distal antrum (mucus-secreting mucosa), (2) the lesser curvature at the incisura angularis, where the earliest atrophic-metaplastic changes tend to occur, (3) the anterior and posterior walls of the proximal corpus (oxyntic mucosa).An article reviewed the histology reporting of gastritis and provides useful guidance on how to standardize gastritis histology reports in diagnostic practice [33].

Concomitantly, a 17-fold increase in the number of intrahepatic I

Concomitantly, a 17-fold increase in the number of intrahepatic IM (6.9E+5 vs 4.2E+4 cells /gram liver in uninfected control mice) is seen at 8 dpi, along with the influx in the liver of similar numbers of CD45+F4/80highCD11bhigh cells (6,3E+5 cells/ gr liver). Liver infiltration by both cell populations progressively diminishes with decreasing intrahepatic viral titers. After resolution of the biochemical hepatitis phase at 30dpi, classical KC reappear, and the double F4/80highCD1 1bhigh intrahepatic

cells have disappeared. In contrast to these phenotypic kinetics, repetitive R848 injections induces increases in the frequency of both IM (5-fold) and KC (2.4-fold) within 4 days, while no additional F4/80high CD1 1bhigh double+ cell population Opaganib mouse is observed. We are currently expanding these observations by functional and micro-array analysis on the

respective sorted cell populations. Conclusion: During LCMV-induced hepatitis, classical Kupffer cells are replaced by infiltrating inflammatory monocytes and later F4/80highCD1 1 bhigh cells, but reappear after resolution of the hepatitis flare. Therefore not KC, but rather IM and the F4/80highCD1 1bhigh cell population contribute to virus-induced liver inflammation. Disclosures: Gregory C. Fanning – Management Position: Tibotec, Tibotec, Tibotec, Tibotec Florence Herschke – Employment: Janssen Pharmaceutica Harry L. Janssen science – Consulting: Abbott, Bristol Myers Squibb, Debio, Gilead FDA-approved Drug Library molecular weight Sciences, Merck, Medtronic, Novartis, Roche,

Santaris; Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris Andre Boonstra – Grant/Research Support: BMS, Janssen Pharmaceutics, Merck The following people have nothing to disclose: Dowty Movita, Martijn D. van de Garde, Kim Kreefft, Bart L. Haagmans, Elina Zuniga, Thomas Vanwolleghem Background: Single-nucleotide polymorphism (SNPs) near IL28B gene is strongly associated to hepatitis C virus (HCV) clearance, both in acute infection and with IFN-based therapy. T cells also play a key role in natural HCV clearance. In this study, we hypothesized that IL28B genotype defines the level at which T cell costimulatory pathways are induced during acute hepatitis C (aHCV), thereby contributing to virological outcomes. To test this hypothesis, we examined the phenotype of circulating T cells in aHCV patients relative to IL28B genotypes. Method: Twenty one patients with aHCV were enrolled with IRB-approved informed consent between 2000–2012, and included based on available cryopreserved peripheral blood lymphocytes (PBL) collected within 24 weeks from clinical aHCV onset. aHCV was diagnosed by HCV viremia and acute ALT elevation with documented HCV seroconversion and/or 1 0-fold HCV-RNA fluctuation, excluding HIV-infected persons.

17 The first Denver successes were bolstered

by the openi

17 The first Denver successes were bolstered

by the opening in 1968 of a second clinical liver program by Roy Calne in Cambridge, England,133 following preclinical studies in outbred pigs.21,134 The early trials were described in my 1969 book titled, “Experience Ixazomib in Hepatic Transplantation”,22 based on our first 25 human liver replacements and eight performed elsewhere (four by Calne). Collateral support was provided with the use of the same immunosuppression regimen for the first successful human heart, lung, and pancreas transplantations (Table 5).135-137 However, the promise of the nonrenal procedures, and even of deceased donor kidney transplantation, was unfulfilled for the next 12 years because of immunosuppression-related

morbidity and mortality. Half or more of the liver recipients treated during this time died within the first FDA-approved Drug Library cell assay post-transplant year. The most encouraging observation was that many patients who survived to this milestone were quietly compiling years of good health thereafter (Fig. 7).64,155 Despite deepening suspicion that progress in the whole field of organ transplantation had permanently stalled, the new French and German liver teams of Henri Bismuth and Rudolf Pichlmayr joined the Denver-Cambridge (England) alliance in the early 1970s, followed later in the decade by the Dutch group of Rudi Krom. Much of the medical-scientific, logistic, and administrative framework of hepatic transplantation that exists today was developed by the five mutually supportive liver centers during the frustrating period between 1969

and 1979. Most of the indications for liver transplant candidacy Y-27632 datasheet were obvious, including inheritable disorders with a definitive biochemical explanation (e.g., Wilson’s disease23). The acid test of liver transplantation ultimately would help elucidate the mechanisms or pathophysiology of less well-understood inborn errors: e.g., the three diseases that were palliated by portacaval shunt (see above). Four patients with alpha-1-antitrypsin deficiency underwent liver transplantation between 1973-1977.138,139 Liver replacement for treatment of glycogen storage disorders,140,141 hyperlipoproteinemia,44, 45 and a growing panoply of other metabolic diseases awaited better immunosuppression. Improvements in therapy were heralded in 1979 by Roy Calne’s report of cyclosporine-based immunosuppression in 34 patients, including two liver recipients.33 The side effects of cyclosporine precluded its use as a single agent. However, when it was substituted for azathioprine in our two-drug or three-drug therapeutic algorithm that included dose-maneuverable prednisone,34 cyclosporine’s full potential was realized. Kidney recipients were the first to be treated, with liver recipients close behind. Eleven of our first 12 liver recipients treated in Colorado with cyclosporine-based immunosuppression during 1979-1980 survived for >1 year.

Burstein and collaborators55 found that sensory neurons in the ra

Burstein and collaborators55 found that sensory neurons in the rat posterior thalamus that were activated and sensitized by chemical stimulation of the cranial dura exhibited long-lasting hyperexcitability

to innocuous (brush, pressure) and noxious (pinch, heat) stimulation of the paws. Innocuous, extracephalic skin stimuli that did this website not produce neuronal firing at baseline (such as brush) became as effective as noxious stimuli (such as pinch) in eliciting large bouts of neuronal firing after sensitization was established. In migraine patients, functional MRI with BOLD analysis showed that brush and heat stimulation at the skin of the dorsum of the hand produced larger BOLD responses in the posterior thalamus of subjects undergoing a migraine attack with extracephalic allodynia than the corresponding responses registered when the same patients that were free of migraine and allodynia. The authors suggested that the spreading of multimodal allodynia and hyperalgesia beyond the locus of migraine headache is mediated by sensitized thalamic neurons that process nociceptive information from the cranial meninges together with sensory information from the skin of

the scalp, face, body, and limbs. The transformation of episodic migraine into chronic, daily headache has been attributed frequently to the excessive use buy LEE011 of abortive medication. Patients with this type of chronic headache (medication-overuse headache, MOH) exhibit abnormal glucose metabolism in brain areas belonging to the “pain network.”56 Fluorodeoxyglucose (FDG) PET data were obtained by Fumal and colleagues57 in patients during an analgesic-overuse headache and 3 weeks after withdrawal of the overused medication. Before withdrawal, several areas of abnormal metabolic activity were detected in association with MOH (ie, hypometabolism

in the bilateral thalamus, orbitofrontal cortex, anterior cingulate cortex, insula/ventral striatum, and right inferior parietal lobule; and hypermetabolism in the cerebellar vermis). Interestingly, the cerebellum displays an increased Adenosine triphosphate blood flow during migraine ictus. In addition, altered serotonergic transmission, decreased grey matter volume, reduced activity, and increased functional connectivity with dorsal anterior cingulate cortex were evidenced in the orbitofrontal cortex of migraineurs.58 In MOH, glucose uptake in dysmetabolic areas, recognized as being involved in pain processing, recovered to almost normal levels after the medication was withdrawn. The metabolic activity of the orbitofrontal cortex, however, was further reduced after medication withdrawal, indicating a role for this structure in the predisposition to analgesic overuse. Interestingly, this area also has been implicated in drive and compulsive behavior, including drug dependence and gaming addiction.59 In addition, PET studies using 18F-FDG demonstrated increased metabolism in the brainstem of patients with chronic migraine.

Serum levels of AST as markers

of hepatocyte injury were

Serum levels of AST as markers

of hepatocyte injury were measured 2 days after transplantation. Mice were prepared 1 hour after transplantation for intravital fluorescence microscopy as described16 on a Leica CLS 150× microscope. Microscopy sequences were captured by a camera and recorded by a video system for offline evaluation. Total RNA was extracted from liver tissue using TRIzol reagent. Quantitative real-time polymerase chain Protein Tyrosine Kinase inhibitor reaction amplification and data analysis were performed using an ABI Prism 7000 Sequence Detection System. Results were quantified as fold induction comparison with baseline after normalization to 18S RNA. Liver tissue was prepared for scanning electron microscopy 3

hours after transplantation: the graft was flushed with 3% polyvinylpyrrolidone in Hank’s balanced salt solution. The fixed liver tissues were cut into small pieces. The specimen were then washed with phosphate-buffered saline and stored at 4°C until further processing for scanning electron microscopy. Values are expressed as the mean ± SD. The data were analyzed using GraphPad Prism version 5 software. Differences between groups were evaluated using an unpaired t test. Differences RAD001 research buy were considered statistically significant at P < 0.05. To evaluate whether serotonin had an effect on SFS OLT and could improve liver regeneration, we performed 30% OLT. The recipient Amobarbital was treated with the serotonin agonist DOI or with saline, until grafts were harvested 48 hours after surgery. Ki-67 and PCNA staining were analyzed on liver sections by immunohistochemistry (Fig. 1A,B). Both showed significantly enhanced hepatocyte proliferation in DOI-treated

liver grafts when compared with control grafts. Fig. 1C,E (control) and Fig. 1D,F (DOI) demonstrate a strong induction of proliferation markers by DOI. Ischemia/reperfusion injury is inevitable in organ transplantation.17, 18 It may be particularly harmful and exacerbate the loss of function in liver grafts contributing to SFS syndrome.19 To test the impact of DOI on ischemia/reperfusion injury of SFS liver grafts, serum AST was tested 2 days after 30% OLT. AST levels were elevated in the recipient control group, whereas application of DOI significantly blunted tissue injury in recipients (Fig. 1G) (P = 0.027). Hematoxylin-eosin staining of embedded liver graft tissue disclosed diffuse microvesicular steatosis in the control (Fig. 1H). Few neutrophils and rare small foci of necrosis were present in control animals. SECs are highly susceptible to cold ischemic injury.18 Preservation of intact SECs is key for a successful OLT.20 In our model of partial OLT, all grafts are inherently exposed to a short period of cold ischemia. Therefore, we studied SEC on hematoxylin-eosin–stained biopsies and by scanning electron microscopy 3 hours after reperfusion.

We read the abstracts of these articles, extracted the published

We read the abstracts of these articles, extracted the published work that seemed to be relevant and useful for surveillance and diagnostic imaging, read the original articles, and finally selected articles, mainly English-language articles providing high-level evidence. For this second version, we extracted articles related to surveillance and diagnostic imaging for hepatocellular carcinoma published between 2003 and June 2007, again read the original articles, and finally selected

articles, mainly those providing high-level evidence. CQ4 In what patient subsets should regular hepatocellular carcinoma screening be performed? The risk factors for hepatocellular carcinoma are cirrhosis, chronic hepatitis C, chronic hepatitis B, male sex, advanced age, habitual alcohol consumption, obesity and diabetes mellitus. Smoothened Agonist order Among these, regular hepatocellular carcinoma screening is recommended in patients with type C chronic liver disease, type B chronic liver disease or non-viral cirrhosis. (grade B) Hepatocellular carcinoma is a cancer that has been observed to show marked regional clustering. Hepatitis B virus (HBV) and hepatitis C virus (HCV), and also several environmental factors, are considered to have a great impact on the risk of development of hepatocellular carcinoma. In Japan, approximately 85% of hepatocellular carcinoma patients have underlying type B or C chronic liver disease (Report of the 17th Nationwide

Follow-up Survey of Primary Liver Cancer in Japan). Besides these virus-related factors, buy DZNeP male sex, advanced age, heavy alcohol consumption, smoking, aflatoxin, obesity and diabetes mellitus have been reported as risk factors for development of liver C-X-C chemokine receptor type 7 (CXCR-7) cancer. These risk factors for hepatocellular carcinoma are discussed in further detail below. Persistent HBV infection is the most significant risk factor for development of liver cancer. HBV carriers have a

223-fold higher risk of carcinogenesis than non-carriers (LF072091 level 2a). Among HBV carriers, HBe antigen-positive persons are at a higher risk for carcinogenesis than HBe antigen-negative persons (relative risk: 6.3 times) (LF072052 level 3, LF038253 level 2a, LF072084 level 3, LF072065 level 3, LF038776 level 3, LF071987 level 3, LF071998 level 2a). Among the patients with type B chronic liver disease, those with cirrhosis are at higher risk. Persistent HCV infection is also as significant a risk factor for carcinogenesis as persistent HBV infection. Particularly in some developed countries, including Japan, it is the most common predisposing factor for development of liver cancer (LF072029 level 4). A characteristic feature of carcinogenesis attributable to hepatitis C is that liver cancer develops against a background of cirrhosis in the majority of cases (LF0357510 level 2a, LF0240411 level 2b). The annual incidence of HCV-related cirrhosis is extremely high, approximately 3–8%, although it varies among countries.

1 Although

twin and family studies suggest that genetic f

1 Although

twin and family studies suggest that genetic factors contribute to disease susceptibility and severity,2, 3 the cause of PBC remains poorly understood.4 Significant associations of genetic factors, including HLA alleles, tumor necrosis factor alpha,5–8 and cytotoxic T-lymphocyte AUY-922 antigen 4,8–14 with PBC have been reported. Among these, only HLA has consistently been associated with PBC susceptibility.15 The HLA-DRB1*08 family of alleles has been the most frequently described determinant for susceptibility to PBC16–21; HLA-DRB1*08:03 has been associated with PBC in the Japanese.22–26 However, HLA DQB1 alleles and haplotypes have not been fully investigated, and large cohort studies have indicated that HLA-DRB1*11 and DRB1*13 alleles are, in fact, protective against PBC.20, 21, 26 Because recent genome-wide studies of PBC have shown the strongest association signals in the HLA region,27–30 we sought to determine whether particular HLA alleles or haplotypes or DRB1 allele amino acid alignments were associated with susceptibility

to PBC or disease progression in the Japanese population. CI, confidence interval; HLA, human leukocyte antigen; OLT, orthotopic liver transplantation; OR, odds ratio; PBC, primary biliary cirrhosis. Clinical and biochemical features of 229 PBC patients who were enrolled for this study between January 2005 and September 2010 are shown in Table 1. The racial background of all patients was Japanese. HLA class I and II allelic genotypes from 523 healthy subjects obtained in a previous learn more study were available as controls.31 In addition, HLA class II allelic genotypes from 130 patients with chronic hepatitis C virus infection were adopted from another study as comparison cases having another liver disease.32 The diagnosis of PBC was based on criteria from the American Association for the Study of Liver Diseases.33 Serum antimitochondrial antibody was determined using indirect immunofluorescence, and a titer of ≥1:40 was considered to be positive.34 Our serological protocol did not include testing for particular antinuclear antibodies, such as IMP dehydrogenase ani-gp210 antibody reactivity, or antimitochondrial antibody titration. All patients

were negative for hepatitis B surface antigen, antibody to hepatitis B core antigen, antibody to hepatitis C virus, and antibody to human immunodeficiency virus. Patients were classified into two stages of PBC, based on their most recent follow-up: Early-stage patients were histologically Scheuer stage I or II35 or of unknown histological stage without liver cirrhosis, and late-stage patients were histologically Scheuer stage III or IV or clinically diagnosed with liver cirrhosis or hepatic failure.14 Liver cirrhosis was diagnosed by histological examination and/or characteristic clinical signs of advanced liver disease.36 All subjects provided written informed consent for this study, which was approved by the institutional ethics committee.

The direct causes of ALF included herbal medication in two patien

The direct causes of ALF included herbal medication in two patients, SAE of CHB in two, veno-occlusive AZD2281 manufacturer disease in one, extensive radiation-induced liver disease in one, and indeterminate in one. The mean ± standard deviation (SD) weight of the 44 explanted livers in the LT group was 850 ± 378 g. There was no difference in mean weight between the 12 patients with SAE of CHB and the 32 other patients (870

± 428 g versus 843 ± 366 g, P = 0.84). Pathological examination of the explants showed massive or submassive necrosis in all patients and moderate to marked hepatitis in 33 patients (75%). Bridging fibrosis was observed in 23 patients (52.3%), and no or minimal fibrosis in the remainder. No patients had definite features of cirrhosis. The proportion of patients selleck chemicals llc with bridging fibrosis did not differ significantly between patients with SAE of CHB and others

(66.7% versus 46.9%, P = 0.24). Overall patient survival was 42.7% (47 of 110 patients). All 11 patients with contraindications to LT died within 10 weeks of diagnosis (Fig. 3). Of the 55 patients in the no-LT group, 45 (82%) died while awaiting a graft, with a median time from diagnosis to death of 7 days (IQR 4-11 days). Of the 49 patients in the no-LT group who had grade 1 or 2 encephalopathy at enrollment, only six (12.2%) remained at encephalopathy grade 1 or 2, and all six recovered spontaneously. In contrast, 43 (87.8%) of these 49 patients progressed to grade 3 or 4, with only four (9.3%) recovering

spontaneously. All of the survivors (n = 10, 18%) in the no-LT group recovered fully and maintained normal liver function after a median follow-up period of 1,277 days (range, 855–1,841 days). Among the 56 patients who died without transplantation, the most common cause Sirolimus of death was cerebral edema (46%) followed by infection (43%). All patients in the LT group progressed to grade 3 or 4 encephalopathy before receiving LT. Four patients received liver grafts from deceased donors on days 2, 5, 6, and 10, respectively, after diagnosis. The median time from diagnosis to adult LDLT was 2.5 days (range, 0–26 days). The 1-year patient survival rate of the adult LDLT group was 85% (34 of 40 patients), significantly higher than that of the no-LT group (P < 0.01), but similar to that of the DDLT group (75%, P > 0.05; Fig. 3). The 1-year graft survival rate for the adult LDLT group was the same as the patient survival rate. Six adult LDLT patients, including one who received a dual-graft and one DDLT patient, died within 6 months as a result of brain edema (n = 2), systemic infection (n = 4), or bleeding (n = 1). One LDLT patient underwent a second transplantation for graft failure caused by acute cellular rejection, but later died of fungal pneumonia and sepsis. None of the 1-year survivors in the LT group (n = 37) died within a median follow-up period of 1,168 days (range, 465–1,989 days).