Disclosures: Kazuaki Chayama – Consulting: Abbvie;

Grant/Research Support: Dainippon Sumitomo, Chugai, Mitsubishi Īanabe, DAIICHI SANKYO, Toray, BMS, MSD; Speaking and Teaching: Chugai, Mitsubishi Īanabe, DAIIcHl SANKYO, KYORIN, Nihon Medi-Physics, BMS, Dainippon Sumitomo, MSD, ASKA, Astellas, AstraZeneca, Eisai, Olympus, GlaxoSmithKline, ZERIA, Bayer, Minophagen, Shinyaku, Takeda, AJINOMOTO, Meiji Seika, Toray The following people have nothing to disclose: Tsunehiro Ochi, Motoi Hashiba, Masafumi Ono, Hideyuki Hyogo, Yukio Ikeda, Kensuke Munekage, Nobuto Okamoto, Shinji Iwasaki, Yuichiro Eguchi, Toshiji Saibara Background/Aims: Gallstone disease and fatty liver are both prevalent diseases in the general populations and share the same risk factors AZD5363 supplier such as obesity and insulin resistance. However, association between gallstone disease and ultrasonographically diagnosed fatty liver has not been completely established. The aim of this study was to characterize the relationship between gallstone

disease and fatty liver in large population. Methods: A cross-sectional study with 24, 050 health check-up subjects was conducted. Gallstone disease was defined as the presence of gallstones on abdominal sonography or previous history of cholecystectomy. Fatty liver was diagnosed on the basis of typical ultrasonographic findings. Subjects positive for hepatitis B or C virus or check details with a history of other forms of hepatitis were excluded. Results: The mean age of the subjects was 48.7 ± 11.1 years and 54.5% were male. The prevalence of gallstone disease was 5.3% (n=1, 280). The prevalence of fatty liver increased with presence of gallstone disease (43.0% vs.31.3%, p <0.001). In the same manner, the prevalence of gallstone disease increased with presence of fatty liver (7.2% vs.4.4%, p <0.001). The gallstone disease was significantly associated with fatty liver after adjusted for age SPTLC1 and sex [odds ratio (OR) 1.50 95%

confidence interval (Cl) 1.331.69]. Multivariate regression analysis after adjustment for body mass index, waist circumference, total cholesterol, triglycerides, HDL cholesterol, HbA1 c, and systolic blood pressure showed that gallstone disease was statistically significantly associated with fatty liver (OR 1.23, 95% CI 1.06-1.42, p=0.007). These association was attenuated, however still statistically significant after adjusting for insulin resistance (OR 1.27 95% Cl 1.04-1.55, p=0.018). Conclusions: Patients with fatty liver have a high prevalence of gallstone disease. Gallstone disease is associated with fatty liver independently of known metabolic risk factors, especially insulin resistance.

Recognition of selleck compound this clinical feature implies that the pathophysiology of migraine is impressionable and may be why diagnosis and treatment are often delayed. “
“Cephalalgia alopecia is a rare and recently described headache syndrome in which recurrent, burning head and neck pain is associated with hair loss from areas of scalp affected by the pain. We here report the case of a 33-year-old woman with continuous unilateral occipital pain and colocalized alopecia, only responsive to onabotulinumtoxin A injections. We hypothesize whether this clinical phenotype

may correspond to either cephalalgia alopecia or nummular headache with trophic changes, conditions that might represent 2 manifestations of the same spectrum of disorders. “
“The nose offers an attractive noninvasive alternative for drug delivery. Nasal anatomy, with a large mucosal surface area and high vascularity, allows for rapid systemic absorption and other potential benefits. However, the complex nasal geometry, including the narrow anterior valve, poses a serious challenge to efficient drug delivery. This barrier, plus the inherent limitations of traditional nasal delivery mechanisms, has precluded achievement of the full potential of nasal delivery. Breath Powered bi-directional delivery, a simple but novel

nasal delivery mechanism, overcomes these barriers. This innovative mechanism has now been applied to the delivery of sumatriptan. Multiple studies of drug deposition, including comparisons of traditional SB203580 manufacturer Selleck Fludarabine nasal sprays to Breath Powered delivery, demonstrate significantly improved deposition to superior and posterior intranasal target sites beyond the

nasal valve. Pharmacokinetic studies in both healthy subjects and migraineurs suggest that improved deposition of sumatriptan translates into improved absorption and pharmacokinetics. Importantly, the absorption profile is shifted toward a more pronounced early peak, representing nasal absorption, with a reduced late peak, representing predominantly gastrointestinal (GI) absorption. The flattening and “spreading out” of the GI peak appears more pronounced in migraine sufferers than healthy volunteers, likely reflecting impaired GI absorption described in migraineurs. In replicated clinical trials, Breath Powered delivery of low-dose sumatriptan was well accepted and well tolerated by patients, and onset of pain relief was faster than generally reported in previous trials with noninjectable triptans. Interestingly, Breath Powered delivery also allows for the potential of headache-targeted medications to be better delivered to the trigeminal nerve and the sphenopalatine ganglion, potentially improving treatment of various types of headache.

(Fig. 5). Because peroxisome proliferator-associated receptor α (PPARα) is associated with lipid accumulation, we examined PPARα mRNA levels in ethanol- and pair-fed control and HIF-1α(Hep−/−) mice. To amplify the effect of ethanol feeding, we also applied an LPS challenge. LPS has been identified in the portal circulation after chronic alcohol intake in mice and men, and it contributes to the development of ALD.20 To our surprise, we found that PPARα was similarly suppressed by ethanol feeding in each of these experimental groups, indicating that the HIF-1α effect on lipid accumulation

was independent selleckchem of PPARα (Fig. 6A). Next, we examined adipocyte differentiation-related protein (ADRP), which has been associated with HIF-1α expression.21

We found that ADRP mRNA was significantly up-regulated with ethanol feeding alone (P < 0.05) (Fig. 6B). Although no cooperative effect of LPS injection and chronic ethanol was observed in ADRP mRNA expression 2 hours after LPS injection (Fig. 6B), by 18 hours there was a robust cooperative up-regulation of ADRP mRNA with chronic ethanol and LPS injection (P < 0.05) (Supporting Fig. 2). HIF-1α(Hep−/−) mice were protected from any up-regulation of ADRP with chronic ethanol alone or with chronic ethanol and LPS challenge (Fig. 6B; Supporting Fig. 2). These results indicated that ADRP may be implicated in the differential effect of HIF-1α on lipid accumulation. Thus, we examined the effect of constitutive HIF activation on the expression of ADRP in Selleck Dabrafenib HIF1dPA and in control Alb-Cre mice (Fig. 6C). We found a significant increase in ADRP expression with ethanol feeding in Alb-Cre mice, similar to that observed in WT mice (P < 0.02). Furthermore, we found that the presence of the HIF1dPA transgene up-regulated hepatic ADRP protein expression to a similar extent as ethanol feeding (P < 0.01) (Fig. 6D,E).

In order to further dissect the mechanism of HIF-1α regulation in hepatic lipid accumulation, we supplemented our in vivo work with an in vitro model of hepatic lipid accumulation. The chemokine MCP-1 has recently been demonstrated to result in lipid accumulation in the hepatocyte cell line Huh7.8 First, we examined MCP-1 expression levels in ethanol-fed control and HIF-1α(Hep−/−) Rutecarpine mice. We found that alcohol feeding alone resulted in a small, but significant up-regulation in MCP-1 serum levels (Fig. 7A). This corresponded to increased MCP-1 hepatic mRNA with chronic ethanol (Fig. 7B). LPS stimulation and ethanol cooperatively up-regulated MCP-1 in WT mice (Fig. 7C). LPS induced MCP-1 in HIF1α(Hep−/−) mice to an extent comparable to WT, but there was no further increase in HIF-1α(Hep−/−) with alcohol feeding (Fig. 7C). To evaluate mechanistic events, we next treated Huh7 cells with recombinant MCP-1 or with a plasmid containing the degradation-resistant HIF1dPA mutant.

This event requires that CREB becomes phosphorylated by PKA at Ser133 and acts at the major CRE within the HMGCR promoter region. Even though there was no further research for other regulatory proteins in the present study, our results also demostrated that activation of CREB by TSH in hepatocytes was found to contribute to increased gene expression of HMGCR. A unique experimental approach

in the present study was the use of surgically thyroidectomized rats that completely lost the ability to produce endogenous thyroid hormones and were subsequently treated with exogenous T4 to correct hypothyroidism and maintained a constant serum level of thyroid hormone as well as stably suppressed endogenous TSH through feedback selleck screening library from the pituitary gland. With this approach, we were able to alter the TSH levels in the body of the animal by administering exogenous TSH without

altering the thyroid hormone levels which would otherwise have occurred through stimulation of the normal thyroid gland by exogenous TSH. Consequently, under these controlled conditions, we were able to test a sole role of TSH in cholesterol metabolism. As a result, we were not only able to demonstrate a role of TSH in up-regulating hepatic HMGCR expression Target Selective Inhibitor Library in vivo but also a corresponding increase in serum TC. In this study, thyroidectomy with resulting hypothyroidism

itself caused elevated hepatic expression of HMGCR in rats. This is somewhat inconsistent with the results of Ness and Gertz, which showed lower expression of hepatic HMGCR in Tx rats.27 The explanation for this discrepancy might lie in differences in some of the experimental conditions, such as the duration of hypothyroidism and the types of foods (e.g., cholesterol contents) used to feed the animals. It is notable that in the studies of Ness and Gertz, the Tx animals were commercially obtained and likely had long-term hypothyroidism. Relatively long-term hypercholesterolemia that likely had occurred through other mechanisms, such as the TH deficiency-promoted down-regulation of LDLR in hepatocytes in such chronic hypothyroid conditions, could itself down-regulate Etomidate HMGCR through a negative feedback mechanism. It is well known that a high level of serum cholesterol, such as that seen after intake of foods rich in cholesterol, can dramatically decrease HMGCR expression in liver.28 In contrast, the elevated hepatic HMGCR expression seen in our Tx animals occurred in a relative acute phase of hypothyroidism in which the positive effect of elevated TSH was probably quick and strong so that it overwhelmed the negative effect of the early and therefore still relatively mild hypercholesterolemia on the expression of hepatic HMGCR.

Analysis of the MDL confirmed that North American captive Asian elephants belong to either the previously characterized α or β clade. An average

nucleotide diversity of 0.017 was observed for the Asian elephant mtDNA MDL fragment sequences. Regardless whether an individual possessed mtDNA α or β clade haplotype, all individuals belonged to one nuclear gene lineage for the two X-linked (BGN and PHKA2) and one Y-linked (AMELY) genes sequenced. Analysis of multilocus genotypes indicated an average observed and expected heterozygosities were 0.543 and 0.539 in wild-sourced and 0.579 and MK-1775 mouse 0.547 in the captive-born Asian elephants, respectively. No subdivision among the sampled individuals was detected, including data partitioned by mtDNA clades. Aside from parent–offspring dyads, no further relationships were detected among wild-sourced and captive-born Asian elephants (average relatedness value <0.000). "
“In theory, snails can come

in two enantiomorphs: either dextral (coiling clockwise) or sinistral (coiling counter-clockwise). In snail species where both forms are actually present, coiling direction is determined by a single gene with delayed maternal inheritance; there is no predictable relationship between a snail’s own coiling genotype and its actual coiling direction. Because of this genetic decoupling, it might be expected that dextral and sinistral individuals would be exact mirror images of one another. However, learn more indications exist that there is a subtle but detectable shape difference between dextral and sinistral individuals that derive from the same gene pool. In this paper, enough we attempt to detect such differences in 50 dextral and 50 sinistral individuals of Amphidromus inversus, a species of land snail that is consistently chirally dimorphic. Four out of 18 volunteers who measured the shells with Vernier calipers found that sinistrals are stouter to a significant degree. A

similar result was found by one out of five volunteers who measured the shells from photographs. These results do not allow distinguishing between real shape differences and a handling bias of sinistral as compared with dextral shells. However, when the same set of shells was subjected to a geometric morphometric analysis, we were able to show that sinistrals indeed exhibit a slight but significant widening and twisting of the shell near the palatal and parietal apertural areas. This result is surprising because species of the subgenus Amphidromus s. str. share a long history of chiral dimorphism, and the species would be expected to have been purged from disadvantageous interactions between direction of coil and general shell shape.

Treatment results were assessed 1 month after RFA by US with CEUS,31 plus CT or MRI, and AFP assay if pretreatment

levels were elevated. Results were classified as complete responses (CRs) Staurosporine ic50 (no enhancing tissue at the tumor site and normalization of AFP) or incomplete responses (IRs) (enhancing tissue at the tumor site, persistently elevated AFP levels, or both).6, 11, 29 An IR to laparoscopic RFA was classified as treatment failure (TF). When IR was observed after percutaneous RFA, the procedure was repeated within 15 days. An IR to the second treatment (assessed as described above) was classified as a TF. Patients with TF underwent selective transarterial chemoembolization (sTACE)3 and were then followed with the rest of the cohort. The protocol included abdominal US and CEUS, AFP assays, and Child-Pugh-related tests every 4 months (more frequently when needed) and CT or MRI every 6 months the first year after treatment and yearly thereafter (more frequently if US, CEUS or

AFP suggested recurrence).6, 11, 29 Local recurrence was diagnosed when enhancement reappeared within the ablation zone or ≤2.0 cm from its margins or when histology was positive for viable tumor.10-12, 18 US-guided biopsies were performed: (1) when the ablation zone remained unenhanced but failed to shrink during follow-up; (2) when it remained unenhanced but AFP levels were ≥400 ng/mL in the absence MI-503 nmr of other intra- or extrahepatic lesions (excluded by a diagnostic work-up that included US/CEUS, bone scintigraphy, hepatic angiography, and chest or site-specific roentgenography, CT/MRI).6, 27 Nonlocal recurrences comprised all intrahepatic regrowth >2.0 cm from the ablation zone and extrahepatic metastases. They were diagnosed by imaging modalities and AFP assay; US-guided biopsies were used when ambiguous findings emerged.6, 10-12, 27 Patients with nonlocal recurrences

were classified as having limited disease (reflected by a tumor that still met the study’s inclusion criteria) or advanced disease, i.e., intrahepatic HCC that was large (1-2 nodules >3.5 cm in diameter), massive (occupying an entire lobe or more), multifocal (≥3 nodules, any size), Branched chain aminotransferase or neoplastic vein thrombosis, or extrahepatic metastases. Recurrences in patients who still met all of the inclusion criteria were treated with RFA and managed as described above, with one exception: local recurrence was treated with a single RFA session. If this session did not produce a CR or the tumor subsequently reappeared at this site, the case was classified as a TF and managed as described above. If only inclusion criterion (1) was unmet at the time of recurrence, the patient underwent sTACE (for multifocal or massive forms)3 or RFA preceded by transarterial gelatin-sponge embolization of tumor (large forms).27 Otherwise, treatment was exclusively supportive. We analyzed follow-up data collected through September 30, 2008.

For the acute treatment of migraine, several triptans are available including sumatriptan, naratriptan, rizatriptan, zolmitriptan, frovatriptan,

eletriptan, and almotriptan.1-4 All triptans are available as oral tablets, or, some also as orally disintegrating tablets, and some of the triptans are also available in additional formulations including intranasal and STI571 manufacturer subcutaneous forms. The availability of multiple triptans and multiple formulations facilitates the tailoring of therapy to individual patients’ needs.[5] Results of randomized, double-blind, controlled studies establish the efficacy of triptans in the acute treatment of migraine.[6] However, triptan benefits demonstrated in clinical trials have not consistently been realized in clinical practice. Results of real-world studies demonstrate high rates of patient dissatisfaction with current migraine therapy.[7, 8] In one recent study,

for example, 42% of 183 migraineurs at 3 headache centers were dissatisfied with the degree of relief provided by their Fulvestrant manufacturer acute migraine medication – Vitamin B12 a triptan oral tablet for the majority of patients – and 37% were dissatisfied with the speed of relief.[8] Dissatisfaction with treatment is linked to a high rate of discontinuation of the triptans[9] and may be the cause of the low triptan utilization and high turnover in clinical practice.[10] The reasons for treatment failure in migraine often relate to incomplete or incorrect diagnosis; missing and therefore failing

to address important exacerbating factors; inadequate pharmacotherapy; inadequate nonpharmacologic treatment; and other factors such as the patient’s unrealistic expectations, failure to account for the influence of comorbid conditions, and the need for inpatient treatment ( Box).[11] These reasons, which have been comprehensively reviewed elsewhere,[11] also apply specifically to failure of triptan treatment. This paper explores the contribution of gastrointestinal manifestations of migraine – namely nausea (with or without vomiting) and gastroparesis – to triptan treatment failure. Gastrointestinal manifestations of migraine have been characterized as being among the greatest challenges affecting migraine care today.

05), also the protein expressions of Phospho-Akt, Phospho-mTOR in CD patients’ mucosal lymphocytes were higher than control (p < 0.05). The expression of both PTEN mRNA and protein in peripheral CD4+ T Cells and mucosal lymphocytes

were lower in CD patient than in control (p < 0.05). GDC-0449 nmr Conclusion: Activation of PI3K/Akt/mTOR pathway was seen in Crohn’s disease. PTEN down-regulation maybe the cause of PI3K/Akt/mTOR pathway activation, which may play a role in the pathogenesis of CD. Key Word(s): 1. Crohn’s disease; 2. PI3K/Akt/mTOR; 3. PTEN; 4. pathogenesis; Presenting Author: YUN QIU Additional Authors: HUMIN CHEN Corresponding Author: YUN QIU, HUMIN CHEN Affiliations: The first affiliated hospital of Sun Yat-sen University Objective: To conduct a meta-analysis evaluating the efficacy of infliximab for prevention of post-operative learn more (PO) recurrence of Crohn’s disease (CD). Methods: Selection of studies: Evaluating infliximab for prevention of PO recurrence of CD. Study quality: Independently assessed by two reviewers. Data synthesis: by “intention-to-treat”. Results: Four clinical trials met criteria were included. (ii)  Clinical remission: short-term (1 yr PO) was observed in 90% (18/20) of the IFX group vs. 38% (8/21) in the placebo group (OR 9.32; 95% CI 2.14∼40.59; RD 0.53; 95%

CI 0.29∼0.78; NNT = 2, P < 0.0001). Long-term (≥2 yr PO) was observed in 100% (20/20) of the IFX group vs. 48%(13/27) in the placebo group (OR 18.51; 95% CI 2.18∼156.87; RD 0.44; 95% CI 0.24∼0. 64; NNT = 2, P < 0.0001), the overall clinical remission was achieved in 95% (38/40) of the IFX group vs. 44%(21/48) in the placebo group (OR 12.05; 95% CI 3.60∼40.37; RD 0.48; 95% CI 0.33∼0. Bumetanide 64; NNT = 2, P < 0.0001) Conclusion: IFX may be effective for maintaining both short-term and long-term clinical remission in PO CD, reducing both PO-CR and PO-ER with no serious adverse events reported. Key Word(s): 1. Crohn's disease; 2. infliximab; 3. postoperative; 4.

recurrence; Presenting Author: YONG XIE Additional Authors: NANJIN ZHOU, MEIJUN ZHONG, PING WANG, ZHIRONG MAO, ZHIFA LV Corresponding Author: YONG XIE Affiliations: Digestive Disease Institute, the First Affiliated Hospital of Nanchang University, Nanchang, China.; Institute of Medical Sciences of Jiangxi province Objective: To observe the effect of intervention of Tim-3 signal pathway on different types of experimental colitis in mice, to provide the basis for using Tim-3 as the target for the treatment of IBD. Methods: 54 BALB/c mice were randomly allocated into six groups: ① Mice + IgG1(control); ② DSS model + IgG1; ③ TNBS model + IgG1; ④ Mice + Tim-3-Ab(control); ⑤ DSS model +Tim-3-Ab; ⑥ TNBS model + Tim-3-Ab. To observe the disease activity index (DAI), change of pathohistology, expression of Foxp3, MyD88, TLR4 and SIGIRR in colonic mucosa.

[22] Finally, a homozygous splice site mutation, IVS5+1 G>A, was reported in a Vietnamese family with HH.[23] This mutation, which causes skipping

of exon 5, has been reported with low frequency in the Vietnamese population (0.3% allele frequency[24]) as well as in Thailand.[25] Interestingly, the same mutation has been found in the Vietnamese population residing in the USA but with a much higher allele frequency of around 2%.[26] In spite of this frequency, only two homozygous individuals HSP inhibitor cancer have been reported, one of whom had iron overload, while the other did not, suggesting variable penetrance of this mutation similar to that seen for C282Y.[26] Juvenile hemochromatosis (JH) is the most severe form of HH, with symptomatic onset usually occurring within the first three decades of life. JH can arise from germline mutations in one of two genes, hemojuvelin (HJV) that accounts for approximately 90% of JH cases and is termed type 2a HH, or hepcidin that accounts for the remainder and is termed type 2b HH. In both disorders,

inheritance is autosomal recessive, and definitive diagnosis Crizotinib is only achieved via gene sequencing. Patients with JH typically present in their teenage years or 20s with symptoms that may include hypogonadotropic hypogonadism or associated reproductive problems, and/or cardiomyopathy.[27] Apart from the early age of onset, another feature of JH that differentiates it from HFE-HH is that clinically, males and females are affected in equal proportions.

Biochemical testing of these patients reveals elevations in both serum ferritin (typically over 1000 μg/L) and transferrin saturation (typically 80–100%). Other clinical features that may be present include arthropathy, diabetes mellitus, and liver fibrosis or cirrhosis. In a study of 29 patients with the disorder, characteristics of hypogonadism or cardiomyopathy were present in 96% and 35%, respectively.[27] It is these features of JH that contribute mainly to the associated morbidity and mortality. If not detected Phosphoglycerate kinase and treated in the early stages of symptomatic presentation, cardiac failure becomes a leading cause of death in this group. If identified early, however, effective treatment can significantly limit the progression of these symptoms and minimize morbidity and mortality. The treatment of JH typical requires initial aggressive phlebotomy to reduce accumulated iron stores, followed by phlebotomy guided by monitoring to maintain normal iron parameters; treatment is the same for both types 2a and 2b JH. Iron chelators may also be used to rapidly reduce iron stores, especially in those patients with cardiomyopathy where phlebotomy therapy may not be suitable. The gene for type 2a HH was originally mapped by linkage analysis to chromosome 1q.

IP was measured by lactulose and mannitol excretion ratio (LMR) in patients and 50 healthy controls (HC). Serum endotoxin levels were also assessed in 48 patients and 20 HC. Results:  Eighty patients (74 male), 41 (51.3%) Child B and 56 (70%) Child C, with a mean age of 40.7 ± 9.8 years were enrolled. IP was increased in 28 (35%) patients. LMR of patients was higher than HC (patients vs HC = 0.0238 [0.0010–1.557] vs 0.0166 [0.0018–0.720]; P = 0.007]. No significant difference was seen in the LMR of patients among various Child classes and etiologies. Serum endotoxin levels (GMU/mL) were higher in patients than HC (patients vs HC = 1.42 [0.68–2.13] ATM signaling pathway vs 0.994 [0.067–1.382]; P = 0.001), but comparable between

patients with abnormal and normal IP. At follow up, there was no significant difference in the incidence of complications like spontaneous bacterial

peritonitis, HRS, VB, HE and death between patients with abnormal and normal IP. Conclusion:  IP was increased in 35% of patients with LC; however, it was not associated with a higher incidence of disease-related selleck screening library complications. “
“Background: Graft local infusion and splenectomy have been established as pivotal strategies in ABO incompatible (ABO-I) living donor liver transplantation (LDLT). However, these procedures are associated with high rates of intraoperative and postoperative complications. Methods: From January 2012 to January 2013, 13 consecutive ABO-I LDLT patients were identified at National Cancer Center, Republic of Korea. Our protocol Fludarabine involved rituximab (300 mg/m2) at preoperative 2 weeks, followed by plasma exchange (target before LDLT: isoagglutinin titer ≤ 1:8), basiliximab (20 mg on operation day and postoperative day 4),

and intravenous immune globulin (0.8 g/day at postoperative day 1 and 4) without graft local infusion and splenectomy. Results: The 13 patients (10 males, three females) who underwent transplantation comprised liver cirrhosis (n=3) and hepatocellular carcinoma (n = 10). The median isoagglutinin antibody titer before plasma exchange was 1:32 (range, 1:4 – 1:256). All patients are alive without graft failure. There was no hyperacute rejection and antibody-mediated rejection. Mean duration of hospital stay was 13.2 days. There was no recurrence of hepatitis B virus (0/10 patients), but recurrence of hepatitis C virus (1/1 patient) and one positive CMV antigenemia (1/13 patients) after transplantation. No bacterial and fungal infections were observed. Complications included herpes zoster viral infection in one patient, postoperative bleeding in one patient and extrahepatic biliary stricture in three patients. Conclusions: The new simplified ABO-I LDLT protocol using rituximab, plasma exchange, basiliximab, and intravenous immune globulin without graft local infusion and splenectomy showed good graft outcomes without hyperacute, antibody mediated rejection, and serious infection.