Tracking tumor alteration in glioma through serum fibroblast activation protein combined with image.

PURPOSE: Detecting tumor progression of glioma continues to pose a formidable challenge. The role of fibroblast activation protein (FAP) in gliomas has been demonstrated to facilitate tumor progression. Glioma-circulating biomarkers have not yet been used in clinical practice. This study seeks to evaluate the feasibility of glioma detection through the utilization of a serum FAP marker. METHODS: We adopted enzyme-linked immunosorbent assay (ELISA) technique to quantify the relative FAP level of serum autoantibodies in a cohort of 87 gliomas. The correlation between preoperative serum autoantibody relative FAP levels and postoperative pathology, including molecular pathology was investigated. A series of FAP tests were conducted on 33 cases of malignant gliomas in order to ascertain their efficacy in monitoring the progression of the disease in relation to imaging observations. To validate the presence of FAP expression in tumors, immunohistochemistry was conducted on four gliomas employing a FAP-specific antibody. Additionally, the investigation encompassed the correlation between postoperative tumor burden, as assessed through volumetric analysis, and the relative FAP level of serum autoantibodies. RESULTS: A considerable proportion of gliomas exhibited a significantly increased level of serum autoantibody relative FAP level. This elevation was closely associated with both histopathology and molecular pathology, and demonstrated longitudinal fluctuations and variations corresponding to the progression of the disease The correlation between the rise in serum autoantibody relative FAP level and tumor progression and/or exacerbation of symptoms was observed. CONCLUSIONS: The measurement of serum autoantibody relative FAP level can be used to detect the disease as a valuable biomarker. The combined utilization of its detection alongside MR imaging has the potential to facilitate a more accurate and prompt diagnosis.

Non-SMC condensin I complex subunit H enhances proliferation, migration, and invasion of hepatocellular carcinoma.

Non-SMC condensing I complex subunit H (NCAPH) is a member of the Barr protein family and part of the condensin I complex. The upregulation of NCAPH is associated with poor prognosis in patients with colon cancer. However, the relationship between NCAPH and hepatocellular carcinoma (HCC) remains unclear. This study aimed to explore NCAPH expression in HCC tissues and to investigate NCAPH functions in HCC cells. In this study, we found that high expression of NCAPH in HCC indicated worse prognosis via bioinformatics analysis. Consistently, quantitative real-time polymerase chain reaction assays in 20 pairs of HCC specimens and the immunohistochemical analysis of 100 HCC tissues showed the upregulation of NCAPH. We established stable NCAPH-overexpressing and NCAPH knockdown cell lines. Cell Counting Kit-8 assays and colony formation assay were performed to analyze cell proliferation. Migration and invasion were analyzed by Transwell assays. Subcutaneous xenograft models were used to explore the role of NCAPH in tumor formation in vivo. Our results showed that NCAPH promoted tumor proliferation, migration, and invasion in vitro and in vivo. In conclusion, our findings indicate that NCAPH could serve as a novel prognostic biomarker and a potential therapeutic target for patients with HCC.

Deceased Donor Predictors for Pediatric Liver Allograft Utilization.

BACKGROUND: The number of pediatric deceased organ donors has recently declined, and the nonutilization of pediatric liver allografts has limited the development of liver transplantation. We determined the utilization rate of pediatric livers and identified risk factors for graft discard. METHODS: We used data from the Scientific Registry of Transplant Recipients database from January 1, 2000, to December 31, 2012. The trends of pediatric liver donors and utilization rates were analyzed. Donor risk factors that impacted the graft use of pediatric livers were measured. Logistic regression modelling was performed to evaluate graft utilization and risk factors. RESULTS: A total of 11,934 eligible pediatric liver donors were identified during this period. A total of 1191 authorized liver grafts did not recover or recovered without transplantation. Factors including pediatric donors >1 year of age (odds ratio [OR] = 2.956, 95% confidence interval [CI] 2.494-3.503, P < .001), nonhead trauma (OR = 2.243, 95% CI 1.903-2.642, P < .001), lack of heartbeat (OR = 7.534, 95% CI 5.899-9.623, P < .001), hepatitis B surface antigen positivity (OR = 4.588, 95% CI 1.021-20.625, P = .047), anti-hepatitis C virus positivity (OR = 4.691, 95% CI 1.352-16.280, P = .015), total bilirubin >1 mg/dL (OR = 1.743, 95% CI 1.469-2.068, P < .001), and blood urea nitrogen >21 mg/dL (OR = 1.941, 95% CI 1.546-2.436, P < .001) were significantly related to graft nonutilization. Steroids or diuretics administered prerecovery were significantly related to graft utilization (OR = 0.684, 95% CI 0.581-0.806, P < .001; OR = 0.744, 95% CI 0.634-0.874, P < .001; respectively). CONCLUSIONS: The pediatric liver allograft utilization rate and risk factors for nonutilization of grafts were determined.

Avoiding Ischemia Reperfusion Injury in Liver Transplantation.

Currently, ex situ machine perfusion is a burgeoning technique that provides a better preservation method for donor organs than conventional static cold preservation (0-4 °C). A continuous blood supply to organs using machine perfusion from procurement and preservation to implantation facilitates complete prevention of ischemia reperfusion injury and permits ex situ functional assessment of donor livers before transplantation. In this manuscript, we provide a step-by-step ischemia-free liver transplantation protocol in which an ex situ normothermic machine perfusion apparatus is used for pulsatile perfusion through the hepatic artery and continuous perfusion of the portal vein from human donor livers to recipients. In the perfusion period, biochemical analysis of the perfusate is conducted to assess the metabolic activity of the liver, and a liver biopsy is also performed to evaluate the degree of injury. Ischemia-free liver transplantation is a promising method to avoid ischemia-reperfusion injury and may potentially increase the donor pool for transplantation.

Comprehensive and combined omics analysis reveals factors of ischemia-reperfusion injury in liver transplantation.

AIM: To explore molecular mechanisms underlying liver ischemia-reperfusion injury (IRI). MATERIALS & METHODS: Four Gene Expression Omnibus datasets comprising liver transplantation data were collected for a comprehensive analysis. A proteomic analysis was performed and used for correlations analysis with transcriptomic. RESULTS & CONCLUSION: Ten differentially expressed genes were co-upregulated in four Gene Expression Omnibus datasets, including ATF3, CCL4, DNAJB1, DUSP5, JUND, KLF6, NFKBIA, PLAUR, PPP1R15A and TNFAIP3. The combined analysis demonstrated ten coregulated genes/proteins, including HBB, HBG2, CA1, SLC4A1, PLIN2, JUNB, HBA1, MMP9, SLC2A1 and PADI4. The coregulated differentially expressed genes and coregulated genes/proteins formed a tight interaction network and could serve as the core factors underlying IRI. Comprehensive and combined omics analyses revealed key factors underlying liver IRI, and thus having potential clinical significance.