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Background Patients with hepatocellular cancer (HCC) are known to have worse health‐related quality of life (HRQL) than the general population. However, the change in HRQL from before the diagnosis to after diagnosis remains unknown and is difficult to estimate. We aimed to compare HCC cases with matched controls to evaluate the differences in change in HRQL from before to after HCC diagnosis. Methods We performed propensity score‐matched analysis using the self‐reported HRQL data from the Surveillance, Epidemiology, and End Results registries (SEER) data linked with Medicare Health Outcomes Survey (MHOS) data (1998–2014). Cases were selected as Medicare beneficiaries (aged ≥65 years) who were diagnosed with HCC between their baseline assessment and follow‐up assessment. Matched controls were selected from the same data resource and the same time period to include subjects without cancer diagnosis by propensity scores. HRQL was assessed using the Medical Outcomes Study Short Form‐36 (SF‐36). Results The study included 62 subjects who developed HCC and 365 matched controls. Compared to their baseline HRQL scores, after diagnosis of HCC, subjects were more likely to report declines in scores related to the mental component of HRQL. When stratified by time since diagnosis, mental component remained significantly lower as the disease advanced. In contrast, only general health aspects of physical health worsened after HCC diagnosis. Conclusions Diagnosis of HCC has a profound negative impact on patients’ HRQL. Mental health component deteriorated significantly over time. The need of including mental health services within a multidisciplinary HCC care model is clearly evident. Patients with hepatocellular cancer are known to have worse quality of life (QOL), and the change in QOL from before the diagnosis to after diagnosis remains unknown. We report the change in QOL post‐diagnosis, as this information can inform clinicians on what to expect.

Major histocompatibility complex class I‐related chain A (MICA) is a highly polymorphic gene that modulates immune surveillance by binding to its receptor on natural killer cells, and its genetic polymorphisms have been associated with chronic immune‐mediated diseases. The progressive form of nonalcoholic fatty liver disease (NAFLD), nonalcoholic steatohepatitis (NASH), is characterized by accumulation of fat and inflammatory cells in the hepatic parenchyma, potentially leading to liver cell injury and fibrosis. To date, there are no data describing the potential role of MICA in the pathogenesis of NAFLD. Therefore, our aim was to assess the association between MICA polymorphism and NASH and its histologic features. A total of 134 subjects were included. DNA from patients with biopsy‐proven NAFLD were genotyped using polymerase chain reaction–sequence‐specific oligonucleotide for MICA alleles. Liver biopsies were assessed for histologic diagnosis of NASH and specific pathologic features, including stage of fibrosis and grade of inflammation. Multivariate analysis was performed to draw associations between MICA alleles and the different variables; P ≤ 0.05 was considered significant. Univariate analysis showed that MICA*011 (odds ratio [OR], 7.14; 95% confidence interval [CI], 1.24‐41.0; P = 0.04) was associated with a higher risk for histologic NASH. Multivariate analysis showed that MICA*002 was independently associated with a lower risk for focal hepatocyte necrosis (OR, 0.24; 95% CI, 0.08‐0.74; P = 0.013) and advanced fibrosis (OR, 0.11; 95% CI, 0.02‐0.70; P = 0.019). MICA*017 was independently associated with a higher risk for lymphocyte‐mediated inflammation (OR, 5.12; 95% CI, 1.12‐23.5; P = 0.035). Conclusion: MICA alleles may be associated with NASH and its histologic features of inflammation and fibrosis. Additional research is required to investigate the potential role of MICA in increased risk or protection against NAFLD.

Introduction: NASH is the progressive form of non-alcoholic fatty liver disease (NAFLD). Stage of fibrosis in NASH predicts mortality. Phosphoproteomic and MicroRNAs (miRs) technologies can elucidate pathways involved in the pathogenesis of NASH-related fibrosis. Methods: The study included liver tissue, serum and clinical data from patients with NAFLD. Hepatic phosphoproteins were measured using Reverse Phase Protein Microarrays (RPMA). Using sera and liver specimen, HTG EdgeSeq sequencing technology was used to sequence ~2200 miR on NextSeq®500 system. Correlations of phosphoproteins, miRNAs and hepatic fibrosis had been reported. In this analysis, we used Ingenuity Pathway Analysis (IPA) to elucidate interaction between signature miR, phosphoproteins and hepatic fibrosis. Results: The study included 43 biopsy-proven NASH and 23 non-NASH NAFLD.Random forest analysis revealed that hepatic miR-449b-3p, miR-1233-3p and miR-142-5p (all p<0.001) are associated with NASH-fibrosis. Also, miR-let7c-5p, miR-199a-5p and miR-6756-3p were independently associated with increased % hepatic collagen (p=<0.01). Using proteomic data (RPMA), ASK1 S83, the receptor tyrosine kinase, Met Y1234/1235, p38-MAPK T180/Y182, LIMK1T508/LIMK2 T505 are independently associated with increased % hepatic collagen (p=<0.01). IPA identified significant networks, top functions and canonical pathways of differentially expressed miRNA and phosphoproteins which were associated with NASH-fibrosis and collagen %. miR 200b-3p and miR-17-5p directly interacts with ASK-1, while miR34a-5p directly regulates Met and p38MAPK. The top most significantly associated canonical pathways with more of the miRNA and phosphoproteins include: the intrinsic signaling pathway of apoptosis, PI3K/AKT signaling, platelet derived growth factor (PDGF) signaling, Tec Kinase cytoskeletal signaling and principal signaling JAK/STAT pathway. Top casual models that significantly associated with NASHfibrosis include Epithelial-Mesenchymal Transition pathway (EMT) (Figure 1), CXCR1 known as (Interleukin 8 receptor alpha) and leucine rich repeat Kinase 2 (LRRK2). Conclusion: This analysis of miR and phosphoproteins suggests involvement of EMT pathway in NASH-fibrosis. This derangement may promote transformation of hepatocytes into myofibroblast and ultimately collagen producing stellate cells. These derangements may explain the mechanism underlying hepatic fibrosis in NASH.

The interfacial interaction between asphalt binder and mineral aggregate makes different components have different diffusion behavior. It influences the performance of interface and consequently that of the mix. In this research, the models of four asphalt components (asphaltene, resin, aromatics and saturate) and five minerals were constructed individually, and then the Al2O3-asphalt interface model was constructed by adding the asphalt layer and mineral layer together. The interfacial behavior at molecular scale was simulated by setting boundary conditions, optimizing the structure and canonical ensemble. The mean square displacement (MSD) and diffusion coefficient of particles were selected as indicators to study the diffusion of asphalt components on the surface of Al2O3. The results show that when the temperature was 65 °C, asphalt binder showed more viscosity, the diffusion speed of asphalt components ranked according to their molecular mass, which was saturate > aromatics > resin > asphaltene. At 25 °C and 165 °C, the resin had the fastest diffusion speed, which was nearly twice of asphaltene. The interaction between asphalt components and Al2O3 mineral surface can make the diffusion of asphalt components independent on temperature.

Individual effect of aging and rejuvenator recycling on basic properties of asphalt is readily recognized, but there is only limited understanding about whether the recycling of SBS- (styrene-butadiene-styrene-) modified asphalt is an inverse process of aging or not. To compare the effects of aging and rejuvenator on microproperties and molecular composition of SBS-modified asphalt, comprehensive performance tests and physical-chemistry experiments were conducted. The results of infrared spectroscopy tests demonstrate that the reticular crosslinking structure of asphalt was destroyed and SBS’s modification effect was gradually lost after aging. This can cause the strengthening of high-temperature performance and reduction of the low-temperature anticrack property of SBS-modified asphalt. Scanning electron microscope shows that the island structure of SBS-modified asphalt disappeared after aging. Energy spectrum analysis shows that the C (carbon) content of aged SBS-modified asphalt has decreased, while the O (oxygen) content and S (sulfur) content have increased obviously. Results of the fluorescence microscope, SEM, and rheological tests show that the epoxy functional group compounds of aliphatic glycidyl ether resin had high reactivity; the triblock molecular structure of SBS and the mechanical performance of SBS-modified asphalt were recovered.