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Liver transplantation is the ultimate method for treating end-stage liver disease. With the increasing prevalence of obesity, the number of patients with non-alcoholic fatty liver, a common cause of chronic liver disease, is on the rise and may become the main cause of liver transplantation in the future. With the increasing gap between the number of donor livers and patients waiting for liver transplantation and the increasing prevalence of non-alcoholic fatty liver, the proportion of steatosis livers among non-standard donor organs is also increasing. Ischemia-reperfusion injury has historically been the focus of attention in the liver transplantation process, and severe ischemia-reperfusion injury leads to adverse outcomes of liver transplantation. Studies have shown that the production of reactive oxygen species and subsequent oxidative stress play a key role in the pathogenesis of hepatic ischemia and reperfusion injury and non-alcoholic fatty liver. Furthermore, the sensitivity of fatty liver transplantation to ischemia-reperfusion injury has been suggested to be related to the production of reactive oxygen species (ROS) and oxidative stress. In ischemia-reperfusion injury, Kupffer cell and macrophage activation along with mitochondrial damage and the xanthine/xanthine oxidase system promote marked reactive oxygen species production and the inflammatory response and apoptosis, resulting in liver tissue injury. The increased levels of ROS and lipid peroxidation products, vicious circle of ROS and oxidative stress along with mitochondrial dysfunction promoted the progress of non-alcoholic fatty liver. In contrast to the non-fatty liver, a non-alcoholic fatty liver produces more reactive oxygen species and suffers more serious oxidative stress when subjected to ischemia-reperfusion injury. We herein review the effects of reactive oxygen species on ischemia-reperfusion injury and non-alcoholic fatty liver injury as well as highlight several treatment approaches.

Hepatic ischemia reperfusion injury (IRI), a fascinating topic that has drawn a lot of interest in the last few years, is a major complication caused by a variety of clinical situations, such as liver transplantation, severe trauma, vascular surgery, and hemorrhagic shock. The IRI process involves a series of complex events, including mitochondrial deenergization, metabolic acidosis, adenosine-5'-triphosphate depletion, Kupffer cell activation, calcium overload, oxidative stress, and the upregulation of pro-inflammatory cytokine signal transduction. A number of protective strategies have been reported to ameliorate IRI, including pharmacological therapy, ischemic pre-conditioning, ischemic post-conditioning, and machine reperfusion. However, most of these strategies are only at the stage of animal model research at present, and the potential mechanisms and exact therapeutic targets have yet to be clarified. IRI remains a main cause of postoperative liver dysfunction, often leading to postoperative morbidity or even mortality. Very recently, it was reported that the activation of peroxisome proliferator-activated receptor γ (PPARγ), a member of a superfamily of nuclear transcription factors activated by agonists, can attenuate IRI in the liver, and FAM3A has been confirmed to mediate the protective effect of PPARγ in hepatic IRI. In addition, non-coding RNAs, like LncRNAs and miRNAs, have also been reported to play a pivotal role in the liver IRI process. In this review, we presented an overview of the latest advances of treatment strategies and proposed potential mechanisms behind liver IRI. We also highlighted the role of several important molecules (PPARγ, FAM3A, and non-coding RNAs) in protecting against hepatic IRI. Only after achieving a comprehensive understanding of potential mechanisms and targets behind IRI can we effectively ameliorate IRI in the liver and achieve better therapeutic effects.

Background Eimeria spp. are responsible for chicken coccidiosis which is the most important enteric protozoan disease resulting in tremendous economic losses in the poultry industry. Understanding the interaction between the avian cecal microbiota and coccidia is of interest in the development of alternative treatments that do not rely on chemotherapeutics and do not lead to drug resistance. Methods We utilized 16S rRNA gene sequencing to detect the dynamics of the cecal microbial community in AA broilers challenged with Eimeria tenella . Histopathological analysis of the cecum was also conducted. Results We found that microbial shifts occur during the infection. Lactobacillus , Faecalibacterium , Ruminococcaceae UCG-013, Romboutsia and Shuttleworthia decreased in abundance. However, the opportunistic pathogens Enterococcus and Streptococcus increased in abundance over time in response to the infection. Conclusions Eimeria tenella disrupts the integrity of the cecal microbiota and could promote the establishment and growth of potentially pathogenic bacteria. Defining bacterial populations affected by coccidial infection might help identify bacterial markers for intestinal disease as well as populations or species that could be beneficial in maintaining and restoring gut homeostasis during and after infection with E. tenella .

[...]developmental stages of B cells, that is B220+CD43+IgM−IgD− (pro‐B), B220+CD43−IgM−IgD− (pre‐B), B220+CD43−IgM+IgD− (immature B) and B220+CD43−IgM+IgD+ (mature B), were detected in mouse BM, intestinal lamina propria (LPL) and Peyer's patches (PPs) by flow cytometry. [...]the expression levels of CD40, CD80 and MHC‐Ⅱ on B cells were detected in mouse SPL, MLN and PPs. [...]we examined the Secretory Immunoglobulin A (SIgA) level in intestinal lavage fluid and serum IgM, IgA and Immunoglobulin G (IgG) by ELISA. [...]LGG intervention can promote the development and maturation of B lymphocytes, enhance the activation and antigen‐presentation ability of B lymphocytes, and regulate the secretion of immunoglobulin by B lymphocytes. [...]LGG can regulate the mucosal immunity and humoural immunity of mice.

BackgroundWith the increasing realization of the importance of gallbladder function, choledochoscopic gallbladder-preserving surgery has been advocated for benign gallbladder diseases. However, limited information is available regarding the use of endoscopic gallbladder-preserving surgery (EGPS) for patients with benign gallbladder diseases. The aim of this study was to evaluate the feasibility of EGPS for benign gallbladder diseases.MethodsBetween June 2020 and January 2021, 22 patients with gallbladder stones and/or gallbladder polyps were treated with EGPS. The main outcome measures included the rate of complications, residual gallbladder stones, and gallbladder stone recurrence.ResultsIn this study, transgastric EGPS was successfully performed in 22 patients (13 female, 9 male) with benign gallbladder diseases, and included 8 cases of multiple gallstones, 4 cases of gallbladder polyps with gallstones, 6 cases of multiple gallbladder polyps, 2 cases of single gallstone, and 2 case of singe gallbladder polyp. The median time of transgastric EGPS was 118 min. During hospitalization, 4 patients suffered localized peritonitis (4/22, 18.2%), and these patients successfully recovered after conservative medical treatment. None of the patients experienced massive bleeding, delayed bleeding, diffuse peritonitis, or any other serious complications. During the median follow-up of 4 months, 1 patient suffered residual gallstone, while no gallstone recurrence or deaths related to transgastric EGPS occurred in any patients.ConclusionsTransgastric EGPS appears to be a feasible treatment method in selected patients with benign gallbladder diseases. However, as it is a new technique, further studies are needed to explore the long-term effectiveness of transgastric EGPS.

Clinical islet transplantation has the potential to cure type 1 diabetes. Despite recent therapeutic success, it is still uncommon because transplanted islets are damaged by multiple challenges, including instant blood mediated inflammatory reaction (IBMIR), inflammatory cytokines, hypoxia/reperfusion injury, and immune rejection. The transplantation microenvironment plays a vital role especially in intraportal islet transplantation. The identification and targeting of pathways that function as “master regulators” during deleterious inflammatory events after transplantation, and the induction of immune tolerance, are necessary to improve the survival of transplanted islets. In this article, we attempt to provide an overview of the influence of microenvironment on the survival of transplanted islets, as well as possible therapeutic targets.

Although endoscopic resection is an accepted technique for upper gastrointestinal subepithelial tumors (SETs) originating from the muscularis propria (MP) layer, published data regarding its complications are highly variable and limited to small data series. This study aimed to analyze the safety of endoscopic resection in a large case series. A total of 726 consecutive patients with 733 upper gastrointestinal SETs originating from the MP layer underwent endoscopic resection from June 2005 to December 2014. The complete resection rate, perioperative perforation rate, and perioperative bleeding rate were the main outcome measurements. The complete resection rate was 97.1%. Ninety-four patients had complications (12.9%), including 88 with perioperative perforations (12.1%), 13 with perioperative bleeding (1.8%), 5 with localized peritonitis (0.7%), and one with delayed bleeding (0.1%). Eleven patients required surgery; the others were treated endoscopically. Risk factors for incomplete resection were extensive connection of the tumor to the MP layer (P=0.007) and extraluminal growth (P=0.048). Risk factors for perioperative perforation were larger tumor size (≤2.0 cm vs. 2.1-3.0 cm vs. >3.0 cm, P=0.021), extraluminal growth (P=0.046), and extensive connection (P<0.001). A risk factor for perioperative bleeding was larger tumor size (P=0.045). No residual or recurrent lesions were detected during the follow-up period (median: 28 months). Endoscopic resection is an effective and reasonably safe therapeutic method for treating/removing upper gastrointestinal SETs originating from the MP layer when managed by an experienced endoscopic team.

Numerous studies have shown Kinesin family member 20A (KIF20A) may play a critical role in the development and progression of cancer. However, the clinical value of KIF20A in nasopharyngeal carcinoma (NPC) is unknown. Here, we investigated the expression pattern of KIF20A in NPC and its correlation with clinicopathological features of patients. Real-time PCR and Western blotting were used to quantify KIF20A expression in NPC cell lines and clinical specimens compared with normal controls. KIF20A protein expression was also examined in archived paraffin embedded tumor samples from 105 patients with pathologically confirmed NPC by immunohistochemistry (IHC). Statistical analyses were applied to assess the associations between KIF20A expression and the clinicopathological features and survival outcomes. Effects on migration and invasion were assessed by wound healing and transwell invasion assays after KIF20A silencing. KIF20A was significantly overexpressed at both the mRNA and protein levels in NPC cell lines and human tumor tissues. 45/105 (42.9%) of NPC specimens expressed high levels of KIF20A among the KIF20A detectable cases. Statistical analysis revealed that high KIF20A expression was significantly associated with gender (P = 0.046), clinical stage (P<0.001), T category (P = 0.022), N category (P<0.001), distant metastasis (P = 0.001) and vital status (P = 0.001). Moreover, Higher KIF20A expression patients had shorter overall survival (OS) and progression-free survival (PFS) (P = 0.001 and P = 0.001; log-rank test). In multivariate analysis, KIF20A was an independent prognostic factor for OS and PFS in the entire cohort (P = 0.033, P = 0.008). Knock down of KIF20A expression significantly suppressed NPC cell's migration and invasion. KIF20A is overexpressed and may serve as an independent prognostic biomarker in NPC. Targeting KIF20A reduces migration and invasion of NPC cells.

Background and aimsCurrently, published data of endoscopic resection (ER) for giant (≥ 6 cm) gastric subepithelial tumors originating from the muscularis propria layer (MP-SETs) are extremely rare and limited to only case reports. The aim of this study was thus to assess the feasibility of using ER for giant (≥ 6 cm) gastric MP-SETs in a case series.MethodsBetween July 2013 and December 2020, a total of 23 patients with giant (≥ 6 cm) gastric MP-SETs were treated with ER in the endoscopic center of Taizhou hospital. The study assessed outcomes of en bloc resection, complete resection, total complications, and local residual/recurrence of tumors.ResultsThe mean procedure time was 112.2 min. En bloc resection was achieved in 22 tumors (95.7%). En bloc removal from the stomach and complete resection were achieved in 6 patients (26.1%). The rate of complete resection differed significantly depending on the minimum tumor diameter (P < 0.001). During hospitalization, 4 patients had complications, including localized peritonitis (3/23, 13.0%) and pulmonary infection (1/23, 4.3%). These 4 patients recovered successfully after conservative medical treatment. Histopathological examination revealed that 18 tumors were gastrointestinal stromal tumors (GISTs), and 5 tumors were leiomyoma. No patients were observed to have residual or recurrent tumors during the follow-up.ConclusionsAlthough ER for giant (≥ 6 cm) gastric MP-SETs was associated with several technical challenges and a relatively low complete resection rate, this technique was found to be a feasible therapeutic method for selected patients with a giant (≥ 6 cm) gastric MP-SETs when performed by an experienced endoscopic team.

Background and aimsAlthough endoscopic resection (ER) is already established as a minimally invasive technique for small (< 4.0 cm) upper gastrointestinal subepithelial tumors originating from the muscularis propria layer (MP-SETs), published data of ER for large (≥ 4.0 cm) upper gastrointestinal MP-SETs are extremely rare and limited to case reports. This retrospective study aimed to evaluate the feasibility and safety of ER for large (≥ 4.0 cm) upper gastrointestinal MP-SETs in a large case series.MethodsBetween June 2012 and December 2018, 101 patients with large (≥ 4 cm) upper gastrointestinal MP-SETs were enrolled in this study. The main outcome measures included complete resection, total complications, and local residual or recurrent tumor.ResultsThe rate of complete resection was 86.1%. Thirteen patients (12.9%) experienced complications including gas-related complications (6/101, 5.9%), localized peritonitis (4/101, 4.0%), esophageal/cardiac mucosal laceration (2/101, 2.0%), and delayed bleeding (1/101, 1.0%). These 13 patients recovered after endoscopic and conservative treatment. The independent risk factor for incomplete resection was tumor size (P = 0.005), and the independent risk factors for total complications were tumor size (P = 0.011) and tumor extraluminal growth (P = 0.037). During the median follow-up of 36 months, local residual tumor was detected in 1 patient. No local recurrence occurred in any patient.ConclusionsDespite being associated with a relatively low complete resection rate, ER is an alternative therapeutic method for large (≥ 4.0 cm) upper gastrointestinal MP-SETs when performed by an experienced endoscopist. This method is especially valuable for patients who are unwilling to undergo surgery.