Furthermore, the criteria were developed from hepatitis B-related FHF, thus there is hesitancy of utilization of the Clichy Criteria for non-hepatitis B patients. In contrast, a high or rising serum alpha-fetoprotein level is a reflection of liver regeneration, a favorable prognostic marker.8 Criteria of age, acuteness, etiology and severity of liver failure are also stated in the King’s College criteria.9 However, in the face of more advanced intensive care and potent antiviral therapeutic agents for viral hepatitis, other parameters

might be useful. A practical approach used by most clinicians is close monitoring of clinical parameters of progression of hepatic encephalopathy, coagulopathy and liver function tests. When a suitable donor is available, either deceased or living, the decision to go ahead with liver transplantation becomes imminent as development of complications from liver selleck products failure deprives the potential Tamoxifen concentration recipient of the chance of survival. In this article in the Journal of Gastroenterology and Hepatology, Takayama et al. show that

lower serum levels of platelet-derived growth factor-BB (PDGF-BB) and vascular endothelial growth factor (VEGF) were associated with FHF. Importantly, serum levels of PDGF-BB and VEGF were even lower in patients who did not recover from FHF. Among the 17 patients with FHF, five recovered spontaneously. Those categorized as having poor outcomes included six who had undergone liver transplantation and six who died without liver transplantation. The serum PDGF-BB and VEGF levels of these 12 patients who did not recover spontaneously were the lowest in the series.10 As already stated, FHF carries a high mortality without liver transplantation. Therefore, diagnostic tests with high negative predictive

value are most worthwhile. Although lower serum levels of PDGF-BB and VEGF were indicative of poor prognosis, quite a number of patients who had 上海皓元医药股份有限公司 low levels eventually had a good outcome.10 Thus, these parameters are restricted in guiding the clinical decision of liver transplantation. Nevertheless, when these factors, and in particular the trend of changes, are interpreted in conjunction with other parameters, the prediction of clinical course should be more accurate. The ideal site to study the most effective medical treatment for FHF is where liver transplantation is not available. This allows clearer delineation of clinical and laboratory indices of patients with irreversible FHF despite best medical treatment. In practice, such regions often are deficient in research and clinical facilities, and resources. Collaboration between centers that are able to provide laboratory support might enable studies in this important area. In summary, in contemporary clinical practice, use of standard criteria might still lead to some patients being transplanted who might have recovered.

The decline/decrease in these mutants was completely blocked/restored by a potent proteasome inhibitor, MG-132. This was consistent with the prediction by molecular modelling that

the mutant molecules would lose the native structure of wild-type molecule, leading to their instability and degeneration and ultimately to degradation. These mutants might have significantly altered conformations, resulting in the rapid degradation by the proteasome inside the synthesizing cells, and ultimately leading to FXIII deficiency. “
“A number of studies have been published on the benefits of prophylactic treatment in adults with haemophilia. However, in many countries, it is considered as optional due to financial constraints. RO4929097 cost This survey was carried out to examine the long-term effects of prophylaxis and the continuing benefit of the treatment into adulthood. Self-assessed health-related data and the EQ-5D questionnaire measuring health utility were collected from 124 men (26.9 ± 4.6 years) from Canada (N = 40), France (N = 14), Ireland (N = 17), the Netherlands (N = 16), Poland (N = 24) and the UK (N = 13). The respondents were split into four groups: On-Demand, <50% life BMN 673 concentration on prophylaxis, ≥50% life

on prophylaxis, Prophylaxis. Overall, long-term prophylaxis results in lower presence of target joints (P ≤ 0.001), occurrence of serious bleeding episodes (P ≤ 0.05), recurring bleeding episodes (P ≤ 0.01) and requirement for surgical procedures (P ≤ 0.05). Furthermore, health utility (P ≤ 0.01) in the On-demand group was significantly lower (P ≤ 0.01) compared to the ≥50% life on prophylaxis and the Prophylaxis

group. No significant differences between countries were found except between the Netherlands and Poland, with Poland showing the lowest health utility (P ≤ 0.01) and the most problems with mobility (P ≤ 0.05) and pain/discomfort (P ≤ 0.001). The Netherlands showed the highest health utility (0.915) followed by Canada (0.791), Ireland (0.786), UK (0.768), France (0.687) and Poland (0.629). The results demonstrate consistently higher quality of life of individuals who are on long-term prophylactic treatment when compared to on-demand treatment or intermittent prophylaxis and on -demand treatment. In haemophilia, prophylaxis for children with severe FVIII and FIX deficiencies MCE is recognized as the optimum standard of care [1-3]. However, the continuation of prophylactic therapy into adulthood is still closely scrutinized. In many countries, the clinical benefit is acknowledged, although given the limited resources not everywhere provides prophylaxis into adulthood. A number of studies have been published demonstrating the benefits of prophylactic treatment in adults [4-6]. This study was carried out to examine the long-term effects of prophylaxis and the continuing benefit of the therapy into adulthood. It is an expansion of the four-country survey reported in 2009 [7].

Bile acid coenzyme A (CoA):amino-acid N-acyltransferase (BAT) mRNA abundance was reduced in GW4064 treated mice (0.55 ± 0.10, P = 0.031), while bile acid CoA synthetase (BACS) mRNA abundance was not significantly changed with GW4064 treatment (0.86 ± 0.14, P = 0.61) (Fig. 3b). In addition, we found no difference in CSAD mRNA abundance in kidney between control and GW4064 treated mice Deforolimus solubility dmso (1.05 ± 0.12) (Fig. 3c). Previous data have implicated the nuclear receptor SHP in the regulation of CYP7A1 and CYP8B1 expression.[6-8] We found

CYP7A1 and CYP8B1 mRNA expression was increased in Shp−/− mice (5.90 ± 0.86, P = 0.0002, 2.23 ± 0.20, P = 0.0003, respectively, Fig. 4a). We also found that hepatic CSAD mRNA expression was increased in Shp−/− mice (8.49 ± 0.25, P < 0.0001, Fig. 4a), with no difference in hepatic CDO (Fig. 4a), BAT or BACS mRNA levels (0.96 ± 0.01, P = 0.33, and 0.91 ± 0.08, P = 0.45, respectively) (Fig. 4b). In addition, renal CSAD mRNA abundance was not altered (0.95 ± 0.11, P = 0.76) in Shp−/− mice (Fig. 4c). To explore the biochemical significance of the elevated levels of CSAD mRNA we measured hypotaurine concentrations, the immediate product of CSAD activity. We observed a 2.3-fold elevation in hepatic hypotaurine concentration in Shp−/− mice compared to WT controls (WT 46.4 nmol/g vs Shp−/− 108.5 nmol/g, P = 0.034) (Fig. 4d). However, we did not observe changes in either hepatic

(Fig. 4d) or serum (data not shown) taurine content in Shp−/− mice. The bile acid pool composition of Shp−/− mice has been I-BET-762 solubility dmso previously investigated and includes primarily an increase in cholate[7, 22] as well as a shift in the α-muricholate versus β-muricholate fraction.[22] Measurement of taurine conjugates in liver and serum revealed no difference in the fraction of bile acids that were taurine conjugated (Fig. 4e). However, 上海皓元医药股份有限公司 we observed increased concentrations of tauro-conjugated bile acids in serum (Fig. 4f)

but not in liver (data not shown). Fibroblast growth factor 15/19 is produced by ileal enterocytes and acts in the liver via FGF4 receptor (FGF4R)/β-klotho to regulate expression of the CYP7A1 gene[25, 26] Hepatic CYP7A1 and CYP8B1 mRNA levels were suppressed in FGF19-treated mice (0.06 ± 0.03, P = 0.0001, 0.50 ± 0.13, P = 0.005) compared to vehicle-injected control mice (Fig. 5a). By contrast, hepatic CSAD mRNA abundance was not altered by FGF19 treatment (1.03 ± 0.35, P = 0.94). In addition, CDO mRNA abundance in liver and CSAD mRNA abundance in kidney were no different in FGF19-treated mice (1.14 ± 0.12, P = 0.34, 0.98 ± 0.08, P = 0.25, respectively) (Fig. 5a,b). Excess cholesterol and/or oxysterols in the liver act via the nuclear receptor LXRα to increase CYP7A1 mRNA transcription, resulting in accelerated catabolism of cholesterol to bile acids.[27, 28] C57BL/6 mice were gavaged with T-0901317 (a synthetic LXR agonist) for 7 days.

In the present study, down-regulation of TAT was frequently detected in primary HCCs. Introduction of TAT gene into HCC cells could effectively inhibit their tumorigenicity, strongly suggesting that TAT plays a tumor suppressive role in the pathogenesis of HCC. CGH, comparative genomic hybridization; HCC, hepatocellular carcinoma; LOH, loss of heterozygosity; MSP, methylation-specific PCR; qPCR, quantitative real-time PCR; TAT, tyrosine SRT1720 datasheet aminotransferase; TMA, tissue microarray; TSG, tumor suppressor gene. Fifty primary HCC samples and their surrounding nontumor liver tissues were collected at the time of surgical

resections from the Cancer Center, Sun Yat-Sen University (Guangzhou, China). Samples used in this study were approved by the Committees for Ethical Review of Research Involving Human Subjects at Cancer Center, Sun Yat-Sen University. HCC cell lines QGY-7703, BEL7402, and PLC-8024 were obtained from the Institute of Virology, Chinese Academy of Medical Sciences (Beijing, China). Genomic DNA and total RNA from these samples were extracted as described.9 Details are described in the Supporting Materials and Methods. A 1401-bp probe of the TAT cDNA covering its whole coding region was synthesized by PCR (the primers are listed in Supporting Table 1). This probe was then labeled with 32P and

hybridized to the membrane transferred this website with HCC genomic DNA or total RNA by southern and northern MCE blot analyses as described.10 PCR was carried out for 28 cycles with genomic DNA from 50 HCC cases as a template. Five sets of primers used in the PCR are listed in Supporting Table 1. Details are described in the Supporting Materials and Methods.11 Details are described in the Supporting Materials and Methods. To study whether demethylation could restore TAT expression in QGY-7703 cells, 2 × 105 cells were treated with the DNA demethylating agent 5-Aza (Sigma-Aldrich, St. Louis, MO)

at the indicated concentration for 72 hours. Drugs and culture medium were refreshed every day during treatment. Genomic DNA was chemically modified with 2.4 mol/L of sodium metabisulfite for 4 hours as described.9 The bisulfite-modified DNA was amplified using primers for either methylated or unmethylated sequences of the 5′ CpG island of TAT. The primers for methylated and unmethylated TAT are listed in Supporting Table 1. MSP was performed with 36 cycles. To test the tumor-suppressive function of TAT, the full-length cDNA and mutant (deletion of 77 amino acids at C-terminal) of the gene was PCR amplified, cloned into pcDNA3.1/V5-His TOPO TA vector (Invitrogen, Carlsbad, CA), and transfected into HCC cell line QGY-7703 and BEL7402 cells. Stable TAT-expressing clones were selected for further study. Empty vector transfected QGY-7703 and BEL7402 cells (Vec-7703/Vec-7402) were used as control. MTT assay, foci formation assay, and colony formation in soft agar was carried out as described.

[43] OSTEOPONTIN PROTEIN WAS immunohistochemically labeled in 40–55% of HCC,[11, 44-46] and OPN mRNA was overexpressed in 55% of HCC.[12] The immunohistochemical staining

and RNA in situ analysis were observed in the cytoplasm of HCC cells, but not in nuclei.[11, 12, 44] OPN positive HCC cells were ZD1839 concentration scattered in the periphery of cancer nodules adjacent to stromal cells, or dispersed in the cancer nodules.[11, 46, 47] OPN protein and/or mRNA overexpression was significantly associated with large size,[12, 45] late tumor stage,[12, 48] poor differentiation,[12, 45, 46, 48] capsular infiltration,[11, 44, 45] vascular invasion,[44, 46] lymph node invasion[44] and intrahepatic metastasis[12, 13, 46] of HCC. Plasma OPN levels were significantly higher in patients with HCC than in patients with chronic liver diseases without HCC, and healthy controls.[47, 49] In patients after curative resection of hepatitis B virus (HBV)-related HCC, plasma OPN levels significantly

decreased after a transient fluctuation, and increased again at the time of tumor recurrence.[50] As a marker for the diagnosis of HCC in patients with cirrhosis, plasma OPN level had a greater area under curve (AUC) value than α-fetoprotein (AFP)[47, 49, 51] and protein induced by vitamin K absence/antagonist-II[47] by receiver–operator curve (ROC) analysis. Furthermore, the combination of OPN and AFP levels enhanced sensitivity and specificity in detecting HCC.[51] Moreover, plasma OPN levels were reported to be useful as a prognostic Palbociclib datasheet factor after liver resection

or transplantation in patients with HCC of tumor–node–metastasis (TNM) 上海皓元医药股份有限公司 stage I, II or III.[48, 52] In a prospective study, TNM stage and plasma OPN level measured prior to tumor resection were highly significant predictors of overall survival (OS) and disease-free survival (DFS) in patients with HCC in China.[48] Preoperative plasma OPN level and Edmondson’s grade were also identified as independent predictors for prognostic factor for OS and DFS in patients with TNM stage I of HBV-related HCC.[52] Increased expression of OPN protein in HCC was also shown to be an independent predictor of poor OS and/or poor DFS in patients undergoing liver transplantation[53] and resection of HCC.[44, 54, 55] Finally, a meta-analysis revealed high OPN expression in HCC predicted poor OS (hazard ratio, 1.37; 95% CI, 1.21–1.55) and DFS (hazard ratio, 1.62; 95% CI, 1.24–2.11) of HCC after liver resection, liver transplantation or transarterial chemoembolization.[56] It has been reported that OPN plays significant roles in the metastasis of HCC in vivo and in vitro. However, the effects of OPN on the growth of HCC cells were controversial. In nude mice, s.c.

Thief pigeons are worth further study. The second example of promiscuity was one Darwin (1871) cited in Descent. The information came from his cousin

William Darwin Fox and involved the two species of geese he kept. In one season, a male Chinese goose seduced a white domestic goose, causing her to abandon her domestic gander: when the female’s clutch hatched, it was immediately evident from the appearance of the goslings that both the Chinese gander and the white gander had fathered offspring: promiscuity and multiple paternity in a single, striking example. With such clear evidence in front of him, it is easy (with the benefit of hindsight) to ask how Darwin could have overlooked the potential for promiscuity and sperm competition. In this instance, I think Victorian prudery won out over science (Birkhead, 1997), but Smith (1998) selleck compound Ensartinib concentration offers

some other possibilities. He suggests that Darwin (and many of his successors) were psychologically predisposed to presume that females are monogamous. If so, the few explicit examples of female promiscuity that Darwin was aware of were then viewed as exceptions and could be ignored. Darwin may also have assumed pre-copulatory choice to preclude the necessity of female promiscuity. Finally, Smith (1998) suggests that during Darwin’s lifetime, knowledge of sexual reproduction was both amorphous and confused, creating an intellectual barrier that prevented Darwin from considering the implications of female promiscuity. As far as I am aware, there is no synthesis of what Darwin understood or did not understand about sexual reproduction in animals. He wrote extensively about the process of fertilization in plants, and so it is almost inconceivable that he did not have an interest in animal reproduction, and yet our understanding of Darwin’s knowledge of sexual reproduction remains MCE unclear. He knew a great deal about the reproductive anatomy of the barnacles

he spent so long dissecting. We also know from his notebooks (Barrett et al., 1987) that he had read Spallanzani’s (1769) ingenious study from the late 1700s that erroneously concluded that spermatozoa had no role in fertilization. As Smith (1998) points out, Spallazani’s account of fertilization must have confused Darwin, and continues: ‘Perhaps it was this confusion that pressed Darwin to his own fuzzy “gemmule” theory of inheritance [pangenesis], which despite its own vagaries at least restored a heritable male contribution to reproduction’. Smith then says: ‘Ideas about fertilisation and heredity remained extremely amorphous through the eighteenth and most of the nineteenth centuries …’. While it is certainly true that ideas about heredity remained amorphous, it is less clear why Darwin should have remained confused about sexual reproduction.

57 More recently, its utility as a sensitive and specific marker of intestinal inflammation in patients with chronic intestinal disease has been investigated.9,23,24,36,54,58–61 Several studies have indicated the usefulness of measuring lactoferrin in patients with IBD. For example, Sugi and colleagues57 investigated lactoferrin, polymorphonuclear neutrophil (PMN) elastase, and lysozyme together with myeloperoxidase in fecal material and whole-gut lavage fluid from IBD patients. They concluded that lactoferrin

was superior as a marker of intestinal inflammation. In contrast, Silberer et al.62 reported that only PMN elastase and calprotectin, but not lactoferrin, myeloperoxidase, or lysozyme, were able to differentiate chronic IBD from IBS, and were correlated with severity of inflammation, as determined

GSI-IX in vitro by ileocolonoscopy. In an another study, lactoferrin and calprotectin were shown to differentiate active IBD from inactive IBD and IBS in 80% of cases, compared to 74% for PMN elastase and 64% for CRP.9 Following these results, the authors suggested that using all three markers (lactoferrin, calprotectin, and PMN elastase) in a composite index might be an additional non-invasive tool for the management of patients with UC. In a further study of 215 patients, including 184 with known IBD, Kane et al.54 demonstrated that fecal lactoferrin was 86% sensitive and 100% specific in distinguishing IBD compared to Regorafenib healthy controls and patients with IBS. Significant differences were also seen between patients with active and inactive IBD, and those with inactive IBD had increased fecal lactoferrin levels compared to healthy controls and 上海皓元医药股份有限公司 patients with IBS. Furthermore, fecal lactoferrin concentrations were noted to differ between patients with CD and those with UC. In

contrast, another study found that fecal lactoferrin was unable to distinguish between active CD and UC.58 Using a rapid fecal latex agglutination test for the detection of lactoferrin, Fine and colleagues63 demonstrated that fecal lactoferrin was 90% sensitive in detecting inflammation in IBD and had a negative predictive value of 99%. Additionally, a recent pediatric study suggested that it is a sensitive and specific marker of inflammation in children with IBD, with the level correlating well with both clinical disease activity indices and ESR.24 Finally, the potential utility of fecal lactoferrin measurements in predicting patients who are at risk of relapse has been investigated.61 Although only performed with a small sample size, the results obtained in this investigation were promising, raising the possibility that elevations in lactoferrin might presage clinical flares. PK is a key enzyme in the glycolytic pathway and is expressed by all cells.64 In humans, PK exists in dimeric and tetrameric isotypes.

The progression of injury in these cells involved mitochondrial reactive oxygen and reactive nitrogen formation. APAP did not increase caspase activity above untreated control values and a pancaspase inhibitor did not protect against APAP-induced cell injury. Conclusion: These data suggest that key mechanistic features

of APAP-induced cell death are the same in human HepaRG cells, rodent in vivo models, and primary cultured mouse hepatocytes. Thus, HepaRG cells are a useful model to study mechanisms of APAP hepatotoxicity in humans. (HEPATOLOGY 2011) Acetaminophen (APAP) is a widely used over-the-counter http://www.selleckchem.com/products/AZD0530.html analgesic and antipyretic drug and is a common component of opioid-containing prescription formulations. Although safe at therapeutic levels, overdose of APAP causes liver injury and is the foremost cause of acute liver failure in the US and the UK.1 At therapeutic doses, >90% of the drug is glucuronidated or sulfated in the liver and subsequently excreted. The remainder is metabolized by cytochromes P450 (CYP450) to the electrophilic intermediate N-acetyl-p-benzoquinoneimine (NAPQI), which can be neutralized by conjugation with glutathione.2 However, after an overdose of APAP, formation of NAPQI exceeds the detoxification capacity of glutathione, resulting in covalent

binding to cellular proteins.3 Although the overall protein binding caused by an overdose of APAP or its isomer 3′-hydroxyacetanilide is similar and many adducted proteins have been identified, toxicity only occurred with APAP, which shows greater binding to mitochondrial proteins.3-6 The subsequent mitochondrial dysfunction leads Selleckchem Liproxstatin 1 to inhibition of mitochondrial respiration,7 ATP depletion,8 and formation of reactive oxygen8 and peroxynitrite9 (ROS and RNS) inside mitochondria. The oxidant stress is involved in activation of the c-jun-N-terminal kinase (JNK) pathway10 and eventually triggers the opening of the mitochondrial membrane permeability transition (MPT) pore,11 resulting in collapse of the mitochondrial membrane potential.11,

12 Mitochondrial matrix swelling and rupture of the outer membrane causes the 上海皓元医药股份有限公司 release of intermembrane proteins including cytochrome c, endonuclease G, and apoptosis-inducing factor (AIF).13 Only endonuclease G and AIF translocate to the nucleus and induce DNA fragmentation.14 The severe impairment of aerobic energy metabolism, massive ATP depletion, and nuclear DNA damage result in necrotic cell death.15 Despite the release of cytochrome c from mitochondria, no significant activation of caspases has been detected and apoptosis contributes less than 5% to the overall injury in mice.15-17 Most of our present knowledge of APAP hepatotoxicity has been learned from rodent studies in vivo and in primary culture.2, 13 However, notable differences exist in the time course of injury between rodents and humans.

Taken together, this is a startling trio of articles, and the accompanying references find more can help lead the interested reader to wider and varied possibilities in approaching our headache patients. “
“Migraine is subdivided into six major categories, of which the two most important are migraine without aura and migraine with aura. Additional subtypes of migraine include childhood periodic syndromes that are commonly precursors of migraine, retinal migraine, complications of migraine and probable migraine. In this chapter we present an overview of the second edition of the International Classification Headache Disorders (ICHD-2)

classification system of migraine, highlighting each of the diagnostic types and subtypes of migraine. “
“Non-steroidal anti-inflammatory drugs (NSAIDS) are commonly used

medications for many pain conditions, and can be very effective for the treatment of migraine. There are several reasons to consider using this class of medications: NSAIDs may be more effective deep into the headache attack, when the pain has spread throughout the head, and even into the neck and shoulders. This spread of pain is called central sensitization, in which the pain spreads as the attack progresses. Central sensitization is also associated with the dislike of light, noise, smells, touch, and movement so common at the peak of a migraine. NSAIDs are helpful with wake-up early morning headaches which CT99021 have likely progressed during the night, so that when someone with a migraine wakes up, the migraine is full-blown, and less responsive to a triptan. NSAIDs can be used be used to increase the effect of migraine-specific medications. They can be added to most medications already being taken for a migraine, possibly lowering the chance of the headache coming back, also called recurrence. Triptans do not work for all patients. It is estimated that triptan tablets 上海皓元医药股份有限公司 are ineffective in up to 40% of patients, and in these individual, NSAIDS may work better than triptans. Pain in migraine occurs through two pathways, inflammation

and blood vessels getting big (dilation). Triptans do not work against the inflammation, although they reverse the blood vessel dilation. NSAIDs block the inflammation. Therefore, taken together, NSAIDs and triptans can work together, and the whole can be greater than the sum of the parts. NSAIDs can generally be used in the setting of vascular disease. Unlike the usual migraine-specific medications such as triptans or dihydroergotamine (DHE), NSAIDs do not narrow arteries.. Individuals who have had a heart attack will still need to discuss NSAID use with their cardiologist, as NSAIDs are not entirely risk-free. Clinical trials of some NSAIDs have shown an increased risk of heart attacks and stroke, but this risk differs with different NSAIDs.

The process at high volume living donor liver TCs is variable within and across TCs. Applying the evidence that does exist, a standardized positioning protocol is being developed. Understanding and implementing optimal supine

patient positioning applies to many abdominal surgical patients, not only living liver donors. A standardized evidence-based approach has the potential to have wide-reaching impact, in an effort to reduce the incidence of neuropraxia. Disclosures: James V. Guarrera – Grant/Research Support: Organ Recovery Systems The following people have nothing to disclose: Daniela Ladner, Robert A. Fisher, Elizabeth A. Pomfret, Mary Ann Simpson, Donna Woods Methods: 15 donors (9 males & 6 females) with median age of 23 years (range: 18 to 45 years) undergoing right lobe donor hepatectomy for buy Crizotinib living related liver transplantation are included in the study. Peripheral venous blood samples were taken before surgery and 1, 3, 7, 14 and 42 post operative day (POD) after donor hepatectomy. HGF, IL-6, TNF α, Thrombopoietine, TGF β1, Interferon a and Interferon γ levels were detected. Sandwich ELISA assay were performed in the plasma after separation of cells. Paired sample t test was used for statistical analysis and p value of < 0.05 was considered significant. Results: The statistically significant observations (P<0.05) are described. HGF and TNF α levels increased transiently on POD

1 after donor hepatectomy. IL6 and Thrombopoietine levels increased after donor hepatectomy and remained elevated till POD 42. IFN α and IFN γ levels decreased on POD 1 and then increased to significant level at POD 14 and POD 42 click here respectively. TGF β1 levels increased at POD 42. Conclusion: The biological markers of liver regeneration have shown distinct patterns after right lobe donor hepatectomy. Disclosures: The following people have nothing to disclose: Shridhar Sasturkar, Shreya Sharma, Paul David, Shiv K. Sarin, Nirupma Trehanpati, Viniyendra Pamecha Objective: Compare the incidence and severity of post-operative complications of left lobe (LL) versus right lobe (RL) live liver donation (LLD) in a single

institution. Methods: Retrospectively analyzed LLD charts and evaluated patient demographics, 上海皓元 post-operative complications, and length of stay (LOS). We combined left lateral segment (LLS) resections with LL resections under the LL group. All the data was obtained from patients who underwent hepatectomies for LLD at our institution. We analyzed the post-operative complications in left versus RL living donor hepatectomies. Results: Post-operative complications using the Clavien-Dindo Classification. 58 living donor liver transplants (LDLTx) were done at our institution from 03/08-03/14. 29(50%) were male and the average age was 38.2(+/−10.5 years). 19(32.76%) were RL donations and 39(67.24%) were either LLS (n=17,29.31%) or LL donations(n=22,37.93%). The mean LOS was 7.05+/−2.66 days for right hepatectomies and 6.92+/−3.