47–49 In contrast, analysis of Il17f−/− suggests that this cytokine has a non-essential role in the development of arthritis, despite displaying similar pro-inflammatory properties as IL-17A in cultured RA synoviocytes.34,46 Likewise, the clinical symptoms of experimental autoimmune encephalomyelitis (EAE), a murine model

for MS, are reduced in il17a−/− mice and in mice treated with an anti-IL-17A blocking antibody.30,33,50,51 Conversely, akin to what was observed in the arthritis pre-clinical models, moderate improvement in recovery from EAE is seen in Il17f−/− mice.30 Interestingly, the detection of elevated levels of IL-17F in human MS patients unresponsive to interferon-β, suggests that IL-17F may play a more dominant role in inflammation than that predicted by the mouse system.52 Further investigation is required to understand

the role of IL-17F in MS. The contribution of IL-17A Fulvestrant in vitro DMXAA and IL-17F to IBD is unclear, as pre-clinical models have yielded inconsistent results. Studies using the dextran-sulphate-sodium-induced colitis model suggest that IL-17A has a protective role in the gut. Neutralization of IL-17A or genetic deficiency of il17a exacerbated disease in this model.30,53 However, dextran-sulphate-sodium-treated il17f−/− mice displayed reduced colitis.30 Conflicting results were observed using a second model of IBD, the CD45RBhi transfer model of colitis. One report corroborates a protective role for IL-17A whereas the other suggests that IL-17A and IL-17F are pathogenic in this model.53,54 Additional studies are needed to resolve this discrepancy, in particular, understanding how the intestinal microflora shape Th17 cell differentiation and secretion of IL-17A and IL-17F is necessary to understand the biology of these molecules in homeostatic and disease states. Interleukin-17A has also been implicated in inflammation associated with metabolic diseases. It is detected in T cells from Resminostat specimens of coronary atherosclerosis, and patients with acute coronary syndrome display elevated

levels of circulating Th17 cells and cytokines.55 Blockade of IL-17A decreases lesion size, lipid accumulation and cellular infiltration in the apoE−/− models of atherosclerosis. Similarly, il17a−/− mice fed a high-fat diet also develop fewer atherosclerotic lesions. Likewise, glucose homeostasis is impaired in il17a−/− mice, an effect attributed to IL-17A signalling in adipocytes.8 How IL-17A contributes to human atherosclerosis remains to be determined. The pre-clinical and clinical data substantiate a key role for IL-17A/F in host defence and inflammatory diseases, and rationalize the development of therapeutics to target this pathway. Multiple programmes targeting different aspects of the IL-17 pathway are in clinical development.

Upon aGVHD development in the group of mice receiving PBMC alone (positive control)

(days 12–15), target organs and sera were harvested from all groups for histological analysis, serum analysis and cell characterization. All experiments were repeated two or more times with five to seven mice per group on each occasion. Target organs (lung, liver and gut) were recovered from mice (days 12 or 15) and fixed in 10% (v/v) buffered formalin, processed for histology and embedded in paraffin wax. Five-μm tissue sections were stained by haematoxylin and eosin (H&E) and coded without reference to prior treatment, blinded and then examined by two independent observers. A semi-quantitative scoring system was used to assess abnormalities in the lung, liver and gastrointestinal tract (GI) tract [30-32]. Human bone marrow mesenchymal stem cells were generated as previously described [33] in collaboration with the Regenerative Sorafenib chemical structure Medicine Institute (REMEDI, NUI Galway, Ireland). Briefly, bone marrow

aspirates were taken from the iliac crest of healthy consenting adult donor patients according to an approved clinical protocol [34]. Human MSC batches used in this study conformed to the International Society for Cellular Therapy (ISCT) criteria [16] and were capable of differentiation to adipocytes, osteocytes and chondrocytes and were only used at low passage (3–8). Human MSC were cultured in complete Dulbecco’s modified Eagle’s medium (DMEM) (Invitrogen-Gibco, Dublin, Ireland) supplemented with 10 % (v/v) fetal bovine serum (FBS), 200 U/ml penicillin and 200 μg/ml streptomycin. In some instances, www.selleckchem.com/products/PLX-4720.html MSC were stimulated with recombinant human IFN-γ (500 U/ml) (Peprotech, London, UK) for 48 h and washed extensively with PBS prior to their use in vitro or in vivo. For in-vitro apoptosis, PBMC (0·5 × 106/ml) were co-cultured with MSC (1·5 × 105/ml) in complete RPMI (cRPMI) in the presence or absence of 500 μg/ml cisplatin (control) (Sigma-Aldrich, Arklow, Ireland). After 24 h, PBMC were recovered by gentle aspiration

from adherent MSC and apoptosis was detected by annexin V/propidium iodide (PI) staining (BD Biosciences, Oxford, RVX-208 UK), measured by flow cytometry using a BD fluorescence activated cell sorter (FACS)Calibur cytometer with CellQuest software (BD Biosciences). For in-vivo apoptosis, in order to optimize, first, the detection of apoptosis FAM-FLIVO™ green dye (Immunochemistry Technologies, Bloomington, MN, USA) was used. As a control for the detection of FLIVO in vivo, BALB/c mice were irradiated lethally with 12 Gy gamma irradiation. After 24 h, 8 μg (100 μl) of FAM-FLIVO™ green dye was injected per mouse and left to circulate for 1 h. After 1 h (or other times, not shown), the liver was harvested and isolated cells were analysed by flow cytometry to verify detectability of apoptosis in vivo.

Several of these genes (e.g. claudin-1) have also been implicated in the pathogenesis of epithelial–mesenchymal transition of tubular epithelial cells. Adriamycin also has effects that are not specific to the kidney and that are currently used therapeutically in the treatment of many types of cancers. Acute cellular changes include alterations FK228 supplier in DNA structure (intercalation, cross-linking or binding), inhibition of

topoisomerase 11, free radical generation causing DNA damage and lipid peroxidation, direct cell membrane effects, necrosis, apoptosis and promotion of senescence-like growth arrest. Delayed effects include reactive oxygen species generation causing mitochondrial DNA damage.5 Adriamycin also causes tubulotoxicity independent of its effects on glomeruli via

tubular cell chemokine release (CCL2 & CCL5) and oxidant injury via reactive oxygen species and/or Fas/FasL interactions. These and other organ effects (myelotoxicity,64 hepatotoxicity65 and cardiomyopathy66) may potentially contribute to Adriamycin-induced nephropathy. The most important factor in successful use of this model is the dose of Adriamycin. As there are variations in batch potency and species sensitivity, dose-finding studies are usually required to ascertain the exact dose required to induce the pathological changes required to test the investigator’s hypotheses. As little as 0.5 mg/kg difference in dose can mean the difference between success and failure, particularly in mice.

The intravenous route of Adenosine administration is preferable. Adriamycin nephropathy is a well-established DNA Damage inhibitor rodent model, which is analogous to human focal segmental glomerulosclerosis, characterized by reductions in glomerular filtration rate, proteinuria, glomerulosclerosis associated with changes in the glomerular filtration barrier, and tubulointerstitial fibrosis. The most common method of administration is intravenous via tail vein injection as it is most reproducible in inducing renal injury. Difficulties in using the model may arise due to a number of issues including batch variation and genetic variation in the rodent used. Notwithstanding these shortcomings, this model has facilitated the study of the pathophysiology and possible therapeutics of chronic proteinuric renal disease. The authors acknowledge the National Health and Medical Research Council of Australia for their support. “
“Mean corpuscular volume (MCV) is a measure of size of red blood cells. Recently a few studies showed an association of macrocytosis with all-cause mortality. We aimed to assess the relationship of MCV with cardiovascular (CV) morbidity and mortality in patients with chronic kidney disease (CKD), and the effect of MCV on endothelial function. This is an observational cohort study with a prospectively maintained cohort of patients with stage 1–5 CKD.

4B). Moreover, we did not detect a significant change in the frequency, absolute

number or phenotype of B cells during colitis development (Supporting Information Fig. 1). While these observations do not exclude a possible role for B cells in this process, buy PF-02341066 they also do not exclude a potential contribution for resident γδ T cells during T-cell-induced immune pathology in the gut. Flow cytometric analysis of draining mesLN of colitic mice showed a two-fold increase in accumulation of donor CD4+ TEFF cells in TCR-β−/− compared with RAG2−/− recipient mice; however, CD4+ TEFF cells accumulated at a similar rate in the LP of either recipients (Fig. 4C). Interestingly, when we examined frequencies of IFN-γ- and IL-17-secreting donor CD4+ T cells, we observed that RAG2−/− recipient mice harbored significantly fewer IL-17+ TEFF cells compared with TCR-β−/− mice, despite a slightly more elevated frequency in IFN-γ-secreting

TEFF cells. Over 50% of donor CD4+ T cells isolated from mesLN and LP of RAG2−/− recipients secreted IFN-γ, and only 10% were positive for IL-17, which is three times less compared with TCR-β−/− recipient Selleck Ivacaftor mice (Fig. 4D and E). Thus, γδ T cells resident in mesenteric sites of TCR-β−/− mice fuel Th17 responses and actively participate in intestinal inflammation. Our results show that TREG cells potently inhibit the expansion and accumulation of pro-inflammatory cytokine secreting donor CD4+ TEFF and host γδ T cells in T-cell-induced intestinal inflammation in TCR-β−/− mice. Interestingly, by 21 days post CD4+ TEFF cell transfer, co-transfer of TREG cells resulted in a two-fold reduction in the proportion of γδ T cells in mesLN compared with colitic mice receiving only TEFF cells (Fig. 5A and B). Furthermore, this decrease was more profound in the LP and reached an eight-fold reduction in the proportion of γδ T cells (Fig. 5B), suggesting that TREG cells impair the

accumulation of γδ T cells in the inflamed gut. To examine the proliferation of donor and host T cells in the presence and absence of TREG cells, the proportion of cycling RAS p21 protein activator 1 cells was determined by intracellular Ki-67 expression. Co-transfer of TREG cells significantly decreased the frequency and absolute numbers of cycling donor CD4+ TEFF and resident γδ T-cell populations in lymphoid organs as well as in the LP in recipient TCR-β−/− mice (Fig. 5C and D). Thus, TREG-cell transfer suppresses the expansion and accumulation of resident γδ T cells in the inflamed colon during development of T-cell-induced colitis. In order to show a direct inhibitory effect of TREG cells on γδ T cells, we performed an in vitro suppression assay where anti-CD3 pre-activated FACS sorted responder populations were co-cultured with titrated numbers of freshly isolated CD4+CD25+ TREG cells. At the highest 1:1 TREG to T responder ratio, TREG cells inhibited γδ T-cell proliferation by 75%, with a similar effect on control CD4+CD25− T responder cells (Fig. 6A).

Donor site morbidity was evaluated using the Constant–Murley test for the shoulder unit. Follow-up ranged from 6 to 35 months (mean 20.6 months). Good or excellent results in mouth opening

and cosmesis were achieved in eight patients, speech was assessed as intelligible or normal in all but one patient and mean ambulation time after surgery was 2.5 days. Results of Constant score ranged from 45 to 70 (mean 60.6), and the main limitation encountered was elevation of the arm above the Rapamycin research buy head, which was seen in all but one patient confirming the low impact of the technique on the shoulder system. Low morbidity, early ambulation time, possibility of simultaneous harvesting with the tumor resection, large musculocutaneous paddles in the chimeric version of the flap are advantages of the STFF and makes it a good choice in elderly patients, when other bone containing free flaps are not indicated because of the related morbidity, when other flaps are not available or when wide composite defects are approached. © 2014 Wiley Periodicals, Inc. Microsurgery, 2014. “
“In 1926, a physicist

at Harvard named William T. Bovie created an instrument, which revolutionized the medical profession—the unipolar electrocautery device. This incredible device could make surgical incisions and provide hemostasis as well. It came with a price, however, as it also created new risks and dangers in the operating room, such as electrical burns Selleckchem Panobinostat and fires. To resolve some of these problems, a bipolar electrocautery device was developed. The historical development and principles of both unipolar and bipolar electrocautery will be discussed in this article. © 2010 Wiley-Liss, Inc. Microsurgery, 2010. “
“Acellular nerve allograft is a new option for bridging nerve PAK5 defects that allows appropriate diameter

matching. The aim of the study was to compare the histologic and functional recovery of nerve defects treated with acellular nerve allograft versus cabled sural nerve autograft. Fifty-four Sprague–Dawley rats were divided into one of three experimental groups. A unilateral 10 mm sciatic nerve defect was created and repaired with an acellular nerve allograft (Group A), three cabled sural nerve autografts in antidromic orientation (Group B), and the newly created segmental defect in antidromic orientation (reversed autograft) (Group C). Two rats in each group we evaluated histologically at 6 weeks while the rest of the groups were tested histologically and functionally at 12 weeks. There were no differences in histomorphometry between the groups at 6 weeks, but at 12 weeks at mid-graft there were differences. Group C had the highest fiber count which was statistically greater when compared to Group A (P = 0.023) and when compared to Group B (P = 0.001).

In the mice infected with SB, infection and inflammation could be seen all the way to the periphery of the lungs next to the pleural membrane. In a recent study, using the traditional bead preparation providing a mean size beads of 60 µm, comparing mucoid and non-mucoid isotypes of P. aeruginosa, only the mucoid isolates had the ability to proceed to the very periphery of the lungs [14]. However, with the new procedure https://www.selleckchem.com/products/icg-001.html in bead preparation employed in the present study and using a non-mucoid

isolate, bacteria in the small beads could be identified in the alveoli of the lungs. Localization of pathogens in the lungs is of particular interest with respect to inflammation. In the larger airways

pathogens are caught primarily in the s-IgA-containing mucus and transported by the mucociliary escalator https://www.selleckchem.com/products/BMS-777607.html to the mouth without initiating inflammation. In addition, the ability to initiate inflammation in the larger airways is limited, as immunological cells are not located in the epithelial tissue of larger normal airways except for scanty lymphoid cells and specialized DCs. Recruitment of inflammation in the larger airways is also impaired due to limited blood supply and the distance from vascular lumen to airway lumen. In addition, the dominating class of antibodies in the upper airways is the non-opsonizing and complement non-activating secretory IgA secreted from the submucosal lymphoid aggregates in the conducting zones [6,15]. Similarly, the involvement of intraepithelial conventional CD11b– DCs (cDCs), lamina propia CD11Bhigh cDCs and plasmacytoid (pDCs) without danger signals add to this anti-inflammatory state of the immune system [16]. As the upper airways are significantly more exposed to intruders than the lower airways, this is a suitable arrangement to avoid constant irritation and inflammation of the upper airways. In contrast, professional immune cells, especially alveolar macrophages and supported by type II epithelial cells, are located

in the SB-3CT alveoli and with their PRRs they can rapidly recognize the PAMPs of pathogens being inhaled or aspirated to the periphery of the lungs [3,4,16,17]. The initiated inflammation follows within few hours, primarily with recruitment of PMNs, and influx of humoral factors such as complement, defensins and cytokines, as the alveolar lumen and vascular lumen is within a distance of a few µm. In chronic infection, IgG synthesized in the medulla of the regional lymph nodes and the bone marrow, and induced by different subsets of CD11Bhigh and CD11B– cDCs and pDCs induced by danger signals via the alveolar macrophages and type II alveolar epithelial cells, will also be present in the airway lumen resulting in opsonin activation of PMNs and complement activation, thereby further enhancing inflammation [6,7,15,16,17].

1% of the cases as either probable or possible, RUCAM attributed 69.5% of the cases to the equivalent probable or possible categories. These comparative results are displayed in a box and whisker plot (Fig. 2). There was considerable variability in the comparison of the RUCAM score to each level of the DILIN structured expert opinion scores, with RUCAM displaying lower levels of causality (Spearman’s MK0683 datasheet correlation, r = 0.42 in absolute value; P = 0.0001). A comparison of the agreement among the reviewers in

causality assessment between the structured expert opinion and RUCAM methods, restricted to the 187 patients who had received only a single drug, is shown in Table 6. Complete agreement (MAD = 0) was reached in 27% with expert opinion versus 19% with RUCAM (P = 0.08). The average MAD was 1.12 with the DILIN strategy and 1.18 with the RUCAM strategy. In order to adequately assess the relationship between the conclusions of the DILIN process and RUCAM, it should be possible to directly compare the results of the two different

assessment methods. Such a comparison is, however, compromised by the fact that, even though both systems use five levels of likelihood, the terminological differences hinder a direct comparison. In an effort to circumvent this problem, two different types of comparisons were undertaken. The first consisted of directly comparing the results of the two learn more approaches in a 5 × 5 table with the established terms for each of them, even though an individual term, such as possible, might not have the identical weight. Nevertheless, the comparison is based on the relative ranking on PtdIns(3,4)P2 the two ordinal scales. As shown in cross-tabulation (diagonal box) in Table 7, there was agreement in the relative ranking in 230 of the 557 reviews (41.3%). Moreover, scores fell within one category of each other in 479 reviews (86.0%). The majority of cases scored at DILIN’s highest causality category (definite) were scored at lower levels by RUCAM. Similarly, disagreements at DILIN’s second causality level (very likely)

were scored more often at lower causality levels by RUCAM. In contrast, disagreements at DILIN’s third and fourth causality levels (probable and possible) were scored more often at higher causality levels by RUCAM. Thus, RUCAM graded more cases in the middle ranges, whereas the DILIN process scored a greater number of cases in higher and lower likelihood categories. A second analysis took into account the fact that a score of probable or higher in both systems would probably signify a valid case of DILI. Thus, the comparison was collapsed into a 2 × 2 table, and the outcomes for both were separated into “yes = DILI” and “no = not DILI” (Table 8). Even at this most basic level, there was agreement in only 384 of the reviews (68.9%), as displayed in the cross-tabulation. In this analysis, the DILIN expert opinion process was more likely than RUCAM to ascribe the case to DILI [DILIN, 495/557 (88.

The adenomatous polyp is regarded as a marker of a neoplasm-prone colon. The incidence of new adenomas in series of surveillance colonoscopies ranges from 16% to 41% depending on individuals risk status. The incidence of adenomas/ carcinomas in patients with CRC undergoing surveillance colonoscopy see more is unknown. We audited consecutive surveillance colonoscopies

done in patients with CRC at Tata Memorial Hospital over 2 years (2012–2013). We evaluated the yield of polyps /cancers. Methods: 373 consecutive patients with CRC who had completed treatment underwent an unsedated surveillance colonoscopy after standard bowel preparation. Patient demographics and colonoscopy findings were reviewed. Data was collected prospectively and analysed. Results: The mean age was 52 years (range 15–82 yrs). There were 247 (66%) males. The site of primary tumor was in the anorectum in 186 and colon in 187 (50% each). The bowel preparation was graded subjectively as good in 22 (6%), fair in 267 (72%) and poor in 40 (11%). 327 (88%) subjects underwent a complete colonoscopy. Common reasons for incomplete colonoscopy were stenotic tumor/ stricture in 15 (4%), poor bowel preparation in 10 (2.7%) and abdomen discomfort/pain or excessive looping in 19 (5%). 18 subjects (5%) had metachronous tumors with one subject having 3 tumors. 24 (6.4%) had polyps

of which 4 (1.1%) had multiple polyps. 13 polyps (3.5%) were tubular adenomas, 11 (2.9%) were tubulovillous adenomas and 3 (0.8%) were hyperplastic polyps. Protease Inhibitor Library clinical trial 1 subject each had a non hodgkins lymphoma and a serrated adenoma. Conclusion: Of the subjects undergoing surveillance colonoscopy, 18 (5%) had a metachronous cancer in the colon and 24 (6.4%) had a polyp. 1 subject was diagnosed

to have a second tumor (lymphoma). 12% patients could not have a complete colonoscopy. Key Word(s): 1. colorectal cancer; 2. surveillance; 3. colonoscopy; 4. yield Presenting Author: LING FEI WU Additional Authors: WEI DENG, MENG QI XIANG, LI XUAN LIU, XIAO TAO ZHOU, PEI RUI CHEN, LING FEI WU Corresponding Author: LING FEI WU Affiliations: Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, Shantou University Med, Second Affiliated Hospital, GNA12 Shantou University Med Objective: The aim of the present study was to confirm whether long non-coding RNA MEG3 is downregulated, determine its possible mechanism of action and elucidate the role of MEG3 in human HCC. Methods: Differences in the expression of MEG3 and in the methylation status of the MEG3 promoter were analyzed in HCC tissues and HepG2 cell line using RT-PCR and methylation-specific PCR (MSP), respectively. CCK-8 assay and colony formation assays were used to assess the effect of MEG3 on cell proliferation; Flow cytometric analysis was used to evaluate the cell apoptosis. PcDNA 3.

We think that an explanatory strategy for building the Cox model, using time-dependent covariates and a propensity score to adjust for the potential confounding factors, would have enriched the study.3–5 In this way, instead of being FDA-approved Drug Library cost driven by significance tests, covariates would have entered and remained in the explanatory model as a result of their modification effect on the association of therapy and mortality.3 Moreover, they could have checked for confounding and likely interactions to explore whether the observed effect was the same in different subsets of patients, as the editorialists claimed. Besides, the use of time-dependent covariates would have allowed fine-tuning of the

beta-blocker therapy duration and would have better addressed its influence on outcomes.4 Finally, a propensity score, which defines the probability that an individual will receive a specific treatment based on his or her pretreatment characteristics, is useful for overcoming the imbalance

between check details groups when treatment assignment is not random.5 Specifically, in Serstè et al.’s study, the propensity score would have corrected the effect of beta-blockers for patient characteristics such as the presence of varices, which heavily conditions their prescription. With such an analysis, the focus of the model would have been the influence of beta-blockers on survival rather than the identification of factors influencing survival; hence, it would have offered more clues to the causal effect. The proposed approach would add robustness to the interesting results provided by Serstè et al. Agustín Albillos M.D., Ph.D.* ‡, Javier

Zamora M.D., Ph.D.† §, * Departments of Gastroenterology and Hepatology, Ramón y Cajal Institute of Health Research, University of Alcalá, Madrid, Spain, † Clinical Biostatistics, Ramón tuclazepam y Cajal University Hospital, Ramón y Cajal Institute of Health Research, University of Alcalá, Madrid, Spain, ‡ Network Centers for Biomedical Research in Hepatic and Digestive Diseases Carlos III Institute of Health, Madrid, Spain, § Epidemiology and Public Health, Carlos III Institute of Health, Madrid, Spain. “
“The hepatitis C virus (HCV) is a small, parenterally transmitted RNA virus that is acquired today almost exclusively by the use of unsterile needles. It occurs in sixdistinct genotypes, genotype 1 being the most prevalent in North America, Europe, and Japan. HCV causes an acute hepatitis that is clinically silent in most cases and persists in the majority (80%) of patients leading to chronic hepatitis. Chronic hepatitis C remains clinically silent, and progresses to cirrhosis in about 10% of patients within 20 years. Once cirrhosis is established, morbidity and mortality from hepatic decompensation and hepatocellular carcinoma ensues. Concomitant alcohol consumption, male gender, co-infection with HIV or HBV, and older age at time of infection accelerates the progression to cirrhosis.

The family of serotonin receptors is subdivided into seven subgroups. These receptors

have been grouped according to their genetic and structural similarities and also according to the intracellular signaling pathways associated with each receptor. Serotonin regulates hepatic function and response to injury, blood flow, and proliferation of hepatocyte.14 In further studies, we could not detect any negative impact of serotonin in a model of ischemia/reperfusion injury. In contrast, we identified a new role for serotonin in tissue repair following ischemic injury.15 We therefore hypothesize that serotonin rescues liver regeneration after implantation of a small graft without enhancing the inherent ischemic damage, and thereby prevents SFS syndrome. 5-HT, 5-hydroxytryptamine; Navitoclax 5-HT2B, serotonin receptor-2B; AST, aspartate aminotransferase; DOI, α-methyl-5-HT; IL-6, interleukin-6; OLT, orthotopic liver transplantation; PCNA, proliferating cell nuclear antigen; PTX, pentoxifylline; SEC, sinusoidal endothelial cell; SFS, small-for-size; TNF-α, tumor necrosis factor α. Male inbred C57BL/6 mice were purchased from Harlan, Netherlands, IL-6−/−

mice with C57BL/6 background were obtained from selleck chemicals Jackson Laboratory and used as syngeneic transplant donors and recipients. Animals were kept in accordance with the guidelines of the University of Zurich Animal Care Committee. The protocol of the study was approved by the Cantonal Veterinary office of Zurich. All mice were kept in a temperature-controlled environment

with a 12-hour light/dark cycle and with free access to food and tap water. We performed 30% partial OLTs in mice using techniques described previously.10 Some mice received a 25% OLT graft consisting of the right liver lobe. The recipient mice were divided into two groups: (1) α-methyl-5-HT (DOI, an agonist of the serotonin receptor and (2) a control group. DOI (1 mg/kg dissolved in saline) was given intravenously immediately following reperfusion of the partial enough liver graft. Subsequently, recipients were injected subcutaneously twice a day for 2 days postoperatively. In control recipients, the same amount of vehicle solution was administered. Recipients were sacrificed at 1 hour, 3 hours, 2 days, or 7 days postoperatively. Hepatic regeneration, aspartate aminotransferase (AST) levels in serum, transcript levels of 5-HT2 receptors, IL-6, TNF-α in liver grafts, histology, scanning electron microscopy, and intravital microscopy were evaluated. In separate series of experiments, the recipient survival rates of 7 days after transplantation were tested. Some animals were treated with an antagonist of the 5-HT2B receptor: SB206553 (3 mg/kg) was injected subcutaneously into the donor and recipient before surgery and twice a day for 2 days after transplantation. Tissues were immersion-fixed in 4% buffered formalin and embedded in paraffin wax, then sectioned, and stained with hematoxylin-eosin.