Ischemia and reperfusion injury (IRI) is an inevitable event in conventional organ transplant procedure and is associated with significant mortality and morbidity post-transplantation. We hypothesize that IRI is avoidable if the blood supply for the organ is not stopped, thus resulting in optimal transplant outcomes. Here we described the first case of a novel procedure called ischemia-free organ transplantation (IFOT) for patients with end-stage liver disease. The liver graft with severe macrovesicular steatosis was donated from a 25-year-old man. The recipient was a 51-year-old man with decompensated liver cirrhosis and hepatocellular carcinoma. The graft was procured, preserved, and implanted under continuous normothermic machine perfusion. The recipient did not suffer post-reperfusion syndrome or vasoplegia after revascularization of the allograft. The liver function test and histological study revealed minimal hepatocyte, biliary epithelium and vascular endothelium injury during preservation and post-transplantation. The inflammatory cytokine levels were much lower in IFOT than those in conventional procedure. Key pathways involved in IRI were not activated after allograft revascularization. No rejection, or vascular or biliary complications occurred. The patient was discharged on day 18 post-transplantation. This marks the first case of IFOT in humans, offering opportunities to optimize transplant outcomes and maximize donor organ utilization.

Background:The three microRNAs from miRNA cluster MC-let-7a-1ϳlet-7d are often down-regulated in human cancers. Results: We functionally characterized the promoter and investigated the transcriptional regulation of MC-let-7a-1ϳlet-7d. Conclusion: MYC oncoprotein could inhibit the transcription of MC-let-7a-1ϳlet-7d via binding to a noncanonical E-box. Significance: Understanding how MC-let-7a-1ϳlet-7d is regulated could shed light on identifying new molecular targets and designing novel treatment for cancers.

BackgroundInadequate liver regeneration (LR) is still an unsolved problem in major liver resection and small-for-size syndrome post-living donor liver transplantation. A number of microRNAs have been shown to play important roles in cell proliferation. Herein, we investigated the role of miR-26a as a pivotal regulator of hepatocyte proliferation in LR.Methodology/Principal FindingsAdult male C57BL/6J mice, undergoing 70% partial hepatectomy (PH), were treated with Ad5-anti-miR-26a-LUC or Ad5-miR-26a-LUC or Ad5-LUC vector via portal vein. The animals were subjected to in vivo bioluminescence imaging. Serum and liver samples were collected to test liver function, calculate liver-to-body weight ratio (LBWR), document hepatocyte proliferation (Ki-67 staining), and investigate potential targeted gene expression of miR-26a by quantitative real-time PCR and Western blot. The miR-26a level declined during LR after 70% PH. Down-regulation of miR-26a by anti-miR-26a expression led to enhanced proliferation of hepatocytes, and both LBWR and hepatocyte proliferation (Ki-67+ cells %) showed an increased tendency, while liver damage, indicated by aspartate aminotransferase (AST), alanine aminotransferase (ALT) and total bilirubin (T-Bil), was reduced. Furthermore, CCND2 and CCNE2, as possible targeted genes of miR-26a, were up-regulated. In addition, miR-26a over-expression showed converse results.Conclusions/SignificanceMiR-26a plays crucial role in regulating the proliferative phase of LR, probably by repressing expressions of cell cycle proteins CCND2 and CCNE2. The current study reveals a novel miRNA-mediated regulation pattern during the proliferative phase of LR.

BackgroundSoybean cyst nematode (SCN) is the most devastating pathogen of soybean. Our previous study showed that the plant growth-promoting rhizobacterium Bacillus simplex strain Sneb545 promotes soybean resistance to SCN. Here, we conducted a combined metabolomic and transcriptomic analysis to gain information regarding the biological mechanism of defence enhancement against SCN in Sneb545-treated soybean. To this end, we compared the transcriptome and metabolome of Sneb545-treated and non-treated soybeans under SCN infection.ResultsTranscriptomic analysis showed that 6792 gene transcripts were common in Sneb545-treated and non-treated soybeans. However, Sneb545-treated soybeans showed a higher concentration of various nematicidal metabolites, including 4-vinylphenol, methionine, piperine, and palmitic acid, than non-treated soybeans under SCN infection.ConclusionsOverall, our results validated and expanded the existing models regarding the co-regulation of gene expression and metabolites in plants, indicating the advantage of integrated system-oriented analysis.Electronic supplementary materialThe online version of this article (10.1186/s12870-018-1302-9) contains supplementary material, which is available to authorized users.

Although pathogens such as nematodes are known to hijack nutrients from host plants, the mechanisms whereby nematodes obtain sugars from plants remain largely unknown. To determine the effects of nematode infection on host plant sugar allocation, soluble sugar (fructose, glucose, sucrose) content was investigated using high-performance liquid chromatography with refractive index detection and was found to increase significantly in tomato (Solanum lycopersicum, Sl) leaves and roots during early infection by root-knot nematodes (RKNs). To further analyze whether sugar transporters played a role in this process, the expression levels of sucrose transporter (SUT/SUC), Sugars Will Eventually be Exported Transporter (SWEET), tonoplast monosaccharide transporter (TMT), and vacuolar glucose transporter (VGT) gene family members were examined by qRT-PCR analysis after RKN infection. The results showed that three SlSUTs, 17 SlSWEETs, three SlTMTs, and SlVGT1 were upregulated in the leaves, whereas three SlSUTs, 17 SlSWEETs, two SlTMTs, and SlVGT1 were induced in the roots. To determine the function of the sugar transporters in the RKN infection process, we examined post-infection responses in the Atsuc2 mutant and pAtSUC2-GUS lines. β-glucuronidase expression was strongly induced at the infection sites, and RKN development was significantly arrested in the Atsuc2 mutant. Taken together, our analyses provide useful information for understanding the sugar transporter responses during early infection by RKNs in tomato.