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Bar code image recognition is a key technology in modern logistics management. An efficient identification system is built based on manifold learning and fuzzy SVM. By integrating the fractal image segmentation technology, it realizes high automatic classification and identification of bar code image. At first, the authors conduct the preprocessing of the collected code image, including three steps, tilt correction, image binarization based on globally dynamic threshold, and fractal segmentation technology. Then, a graph-based fuzzy support vector machine is proposed to realize the high accuracy classification and identification. Experimental results indicate that the accuracy of the proposed method is higher than other compared methods in both pure and noisy samples, reaching 96.6% and 94.5%. And no huge decrease exists when some noise is added to the pure dataset, and the percentage is only 2.1%, which is much lower than the drop of other methods. It shows that the proposed method can significantly promote the identification accuracy, the generalization, and robustness to noise.

Human herpes virus-6B (HHV-6B) was suggested as an important etiologic factor of mesial temporal lobe epilepsy, while the mechanism is still unknown. Here, we aimed to analyze antigens representing latent, early and late HHV-6B infection and the association with inflammatory cytokines in brain tissue and cerebral spinal fluid (CSF) from MTLE patients with HHV-6B-positivity.Nested polymerase chain reaction (nPCR), real-time PCR, immunohistochemistry (IHC) and suspension bead array for cytokines were performed.Nested polymerase chain reaction (nPCR) in brain tissue revealed HHV-6B DNA in 19 of 49 MTLE patients (39%) and 1 of 19 controls (5%) (P 0.001), but not in CSF. ICH showed HHV-6B early antigen (P41) positivity in 3 patients (6%), late antigen (gp116/54/64) positivity in 5 patients (10%), latent antigen (U94) positivity in 8 patients (16%), and multiple antigen (early and late or/and latent) positivity in 9 patients (18%). None of these HHV-6B related proteins were found positive in control brain tissue. PCR revealed significant up-regulation of IL-1a, IL-2 and IL-7 mRNA levels in the brain tissue from MTLE patients expressing early antigens compared to those expressing late, latent, multiple antigens, negative antigens and the controls. Suspension bead array of the CSF confirmed significant up-regulation of IL-1a and IL-7 protein expression from MTLE patients expressing early antigens compared to the other groups.Our finding suggests HHV-6B is a common etiologic agent of MTLE. Different virus life cycle may play an important modifying role in inflammatory biology that warrants further investigation. Though virus DNA is difficult detected in CSF, up-regulation of IL-1a and IL-7 in CSF indicates the two cytokines may be taken as indirect biomarker of HHV-6B infection.

Olefin selectivity and catalyst lifetime are two key metrics for industrial methanol-to-olefin catalysts. Currently, it is very difficult to obtain high olefin selectivity and long catalyst lifetime at the same time. Herein, a feasible strategy combining precoking and steaming to directionally construct the active naphthalenic species within the crystal center of the SAPO-34 catalyst has been developed, which can not only promote the lower olefin selectivity to ∼89% (ethylene and propylene) but also prolong the catalyst lifetime by ∼3.7-fold in the methanol-to-olefin conversion. Structured illumination microscopy

The development of non-precious metal catalysts for oxygen reduction reactions (ORR) is vital for promising clean energy technologies such as fuel cells, and zinc-air batteries. Herein, we present a stepwise synthesis of N-doped and carbon encapsulated BiOCl-CNTs heterostructures. Electrocatalytic ORR studies show that the optimized catalyst has a high half-wave potential (E1/2) of 0.85 V (vs. RHE), large limiting current density (-5.34 mA cm−2@0.6 V) in alkaline medium, and nearly perfect 4e− reduction characteristics, even surpassing commercial Pt/C. Meanwhile, the catalyst has exceptional durability (above 97.5 % after 40000 s) and strong resistance towards methanol poisoning. The good ORR activity also results in high-performance zinc-air batteries with a specific capacity (724 mAh g−1@10 mA cm−2), a high open-circuit potential of 1.51 V and a peak power density of 170.7 mW cm−2, as well as an ultra-long charge–discharge cycle stability (155 h), comparable with the Pt/C catalyst. The catalytic mechanism reveals that the excellent electrocatalytic performance originates from the synergistic effect of N doping, oxygen vacancies, and BiOCl sites.

Considerable toxic tellurium-containing wastewater has been discharged into water environment and constantly accumulates, due to the widespread applications but low utilization of tellurium, causing irreversible harm to the environment and human health, thus it is crucial to find an efficient strategy for tellurium separation. Herein, hierarchical porous magnesium oxide modified cellulose acetate membranes (MgO@CAM) were prepared via a facile physical blending and phase inversion method for tellurium separation. Diverse characterization methods and batch separation experiments were conducted to investigate the morphological structure of MgO@CAM, tellurium separation mechanism, and the separation behavior under different influencing factors. The results exhibit that MgO@CAM has a hierarchical porous structure and a hydroxyl-rich surface, which facilitates the separation of tellurium. Besides, MgO@CAM reveals eligible regeneration performance, good stability and thermal stability due to the hydrogen bonding and skeletal structure of cellulose acetate. The study on the effect of pH suggests that an acidic environment is more conducive to the separation of tellurium by MgO@CAM, and the prepared membranes show outstanding separation efficiency of tellurium, with a maximum of 97.6%. Furthermore, the membranes also achieve satisfactory separation efficiency of tellurium in the presence of multiple coexisting ions. Thomas dynamics indicate the practical application of MgO@CAM in tellurium separation. More importantly, prominent hydrophilic enables MgO@CAM to demonstrate excellent antifouling performance. Therefore, the preparation of hierarchical porous MgO@CAM provides an efficient and economic strategy for tellurium separation in wastewater and has promising applications in water treatment.

Background: Data regarding the additional effect on the recurrence of hepatic encephalopathy (HE) after oral L-carnitine administration are scarce. Objective: This study aimed to assess the additional effects of L-carnitine in patients who were receiving rifaximin for HE. Methods: This randomized study comprised a screening visit and a 12-week treatment period. Patients who fulfilled the eligibility criteria were randomized to either group A (additional rifaximin) or group B (additional L-carnitine and rifaximin). Group A received 1,200 mg/day of rifaximin. Group B received 1,500 mg/day of L-carnitine and rifaximin at 1,200 mg/day. The endpoints were the changes in the portal systemic encephalopathy (PSE) index and the admission rate from the baseline for the duration of the study in both groups. Results: Eighty-three patients were randomized to either group A (n = 42) or group B (n = 41). In group A, the PSE index decreased from 0.35 ± 0.09 at baseline to 0.27 ± 0.11 on the final evaluation day (p = 0.001). In group B, the PSE index decreased from 0.37 ± 0.09 at baseline to 0.24 ± 0.11 on the final evaluation day (p = 0.001). Although there was not a significant reduction in the PSE index in group A compared to that in group B (p = 0.202), the admission rates were 30.9% and 9.8% in groups A and B, respectively. Additional L-carnitine significantly reduced the admission rate (p = 0.028). Conclusion: L-Carnitine addition reduced the risk of hospitalization for patients who received rifaximin for HE.

To study the influence of flame-spreading behaviour in the ignition process of different charging structures in high-density charge chambers, a visualisation device was designed, and the ignition p...

Accruing research shows the implications of long non-coding RNAs (lncRNAs) in the progression of various autoimmune diseases including systemic lupus erythematosus (SLE). The present study aimed to identify the expression pattern of LINC00176 in SLE and to explore its effects on CD4+T cell adhesion in this context. The biological functions of LINC00176, WIF1 and WNT5a on CD4+T cells in SLE were evaluated via gain- and loss-of-function experiments, following delivery of pcDNA3-LINC00176, siRNA-LINC00176, pcDNA3-WIF1 and WNT-sFRP5 (an inhibitor for the WNT5a signaling pathway). High LINC00176 expression was evident in the CD4+T cells of SLE patients. Additionally, WIF1 was identified as a potential target gene of LINC00176, and was negatively regulated by LINC00176. The overexpression of LINC00176 could promote proliferation and adhesion of CD4+T cells in SLE. Such alternations were reversed following up-regulation of WIF1 or inhibition of the WNT5a signaling pathway. Taken together, the key findings of our study highlight the ability of LINC00176 to potentially promote the proliferation and adhesion of CD4+T cells in SLE by down-regulating WIF1 and activating the WNT5a signaling pathway, providing new insight and a theoretical basis for translation in SLE therapy.

BackgroundDiabetic kidney disease (DKD) is the primary cause of end-stage renal disease, raising a considerable burden worldwide. Recognizing novel biomarkers by metabolomics can shed light on new biochemical insight to benefit DKD diagnostics and therapeutics. We hypothesized that serum metabolites can serve as biomarkers in the progression of DKD.MethodsA cross-sectional study of 1,043 plasma metabolites by untargeted LC/MS among 89 participants identified associations between proteinuria severity and metabolites difference. Pathway analysis from differently expressed metabolites was used to determine perturbed metabolism pathways. The results were replicated in an independent, cross-sectional cohort of 83 individuals. Correlation and prediction values were used to examine the association between plasma metabolites level and proteinuria amount.ResultsDiabetes, and diabetic kidney disease with different ranges of proteinuria have shown different metabolites patterns. Cysteine and methionine metabolism pathway, and Taurine and hypotaurine metabolism pathway were distinguishable in the existence of DKD in DC (diabetes controls without kidney disease), and DKD with different ranges of proteinuria. Two interesting tetrapeptides (Asn-Met-Cys-Ser and Asn-Cys-Pro-Pro) circulating levels were elevated with the DKD proteinuria progression.ConclusionsThese findings underscore that serum metabolomics provide us biochemical perspectives to identify some clinically relevant physiopathologic biomarkers of DKD progression.

BackgroundThere are still differences in the prognostic factors of renal cell carcinoma with sarcomatoid dedifferentiation (sRCC). The aim of this study was to evaluate important predictors of survival in patients with sRCC.Patients and methodsA comprehensive search of PubMed, Embase, and Cochrane Library was conducted to identify eligible studies. The endpoints embraced overall survival (OS), cancer-specific survival (CSS), and progression-free survival (PFS). Hazard ratios (HRs) and related 95% confidence intervals (CIs) were extracted.ResultsA total of 13 studies were included for analyses. The pooled results showed that high European Cooperative Oncology Group performance score (HR 2.39, 95% CI 1.32–4.30; P = 0.004), high T stage (HR 2.18, 95% CI 1.66–2.86; P P P P P P = 0.010), and percentage sarcomatoid ≥50% (HR 2.35, 95% CI 1.57–3.52; P P P = 0.008) were associated with unfavorable CSS. High T stage (HR 1.93 95% CI 1.44–2.58; P ConclusionsA meta-analysis of available data identified important prognostic factors for CSS, OS, and PFS of sRCC, which should be systematically evaluated for patient counseling, risk stratification, and treatment selection.Systematic Review Registrationhttps://www.crd.york.ac.uk/PROSPERO/display_record.php?RecordID=249449.

Background: Lenvatinib is appropriate for reducing the production of nitric oxide (NO) and facilitating as block angiogenesis. However, to our knowledge, there are no data that support the correlation between NO and clinical response in patients who received lenvatinib therapy for HCC. Therefore, we investigated whether or not NO influence a therapeutic response and adverse events (AEs) after lenvatinib therapy for unresectable hepatocellular carcinoma (HCC).Methods: This study was conducted using previously collected data from another study. We enrolled 70 patients who received lenvatinib for advanced or unresectable HCC. NO was measured by converting nitrate (NO3–) to nitrite (NO2–) with nitrate reductase, followed by quantitation of NO2– based on Griess reagent. To determine whether lenvatinib influences NO in unresectable HCC, we evaluated the influence of maximal therapeutic response and SAE on the change rate of NO from baseline after administration of lenvatinib.Results: After lenvatinib administration, a change rate in the NO from 0.27 to 4.16 was observed. There was no difference between the clinical response to lenvatinib and the change rate of NO (P = 0.193). However, the change rate of NO was significantly higher in patients with AEs than in those without AEs (P = 0.013). When a reduction in NO rate of < 0.8 was defined as a clinically significant reduction of NO (CSRN), the CSRN group had significantly worse progression-free survival (PFS) and overall survival (OS) than the non-CSRN group (P = 0.040 and P = 0.005, respectively)ConclusionDecreased NO levels were associated with the occurrence of AEs and worse prognosis after lenvatinib administration. Change rate in serum NO can be used as predictive markers in patients receiving lenvatinib therapy for HCC.

Background Lenvatinib is appropriate for reducing the production of nitric oxide (NO) and facilitating as block angiogenesis. However, to our knowledge, there are no data that support the correlation between NO and clinical response in patients who received lenvatinib therapy for HCC. Therefore, we investigated the correlation between the change rate of NO levels and clinical responses including adverse events (AEs) after lenvatinib therapy for unresectable hepatocellular carcinoma (HCC). Methods This study was conducted using previously collected data from another study. We enrolled 70 patients who received lenvatinib for advanced or unresectable HCC. NO was measured by converting nitrate (NO3−) to nitrite (NO2−) with nitrate reductase, followed by quantitation of NO2− based on Griess reagent. To determine whether lenvatinib influences NO in unresectable HCC, we evaluated the influence of the change rate of NO from baseline after administration of lenvatinib on maximal therapeutic response and SAE. Results After lenvatinib administration, a change rate in the NO from 0.27 to 4.16 was observed. There was no difference between the clinical response to lenvatinib and the change rate of NO (p = 0.632). However, the change rate of NO was significantly lower in patients with AEs than in those without AEs (p = 0.030). When a reduction in NO rate of p = 0.029 and p = 0.005, respectively). Conclusion Decreased NO levels were associated with the occurrence of AEs and worse prognosis after lenvatinib administration. Change rate in serum NO can be used as predictive markers in patients receiving lenvatinib therapy for HCC.

Background: Human herpes virus-6B (HHV-6B) was suggested as an important etiologic factor of mesial temporal lobe epilepsy, while the mechanism is still unknown. Here, we aimed to analyze antigens representing latent, early and late HHV-6B infection and the association with inflammatory cytokines in brain tissue and cerebral spinal fluid (CSF) from MTLE patients with HHV-6B-positivity.Results: Nested polymerase chain reaction (nPCR) in brain tissue revealed HHV-6B DNA in 19 of 49 MTLE patients (39%) and 1 of 19 controls (5%) (PConclusions: Our finding suggests HHV-6B is a common etiologic agent of MTLE. Different virus life cycle may play an important modifying role in inflammatory biology that warrants further investigation. Though virus DNA is difficult detected in CSF, up-regulation of IL-1a and IL-7 in CSF indicates the two cytokines may be taken as indirect biomarker of HHV-6B infection.

To explore the mechanism of proteasome inhibitor MG132 in improving osteoporosis.Total of 32 female SD rats, weighing 220 to 250 g and 8 weeks old, were selected. They were randomly divided into 4 groups(n=8). Rats of group A and group B were cut off ovaris on both sides to make model of osteoporosis, and then they were given proteasome inhibitors MG132 and dimethyl sufoxide (DMSO) respectively. Group C was a sham group and rats were given MG132. Group D was a normal group and rats were given MG132 too. The rats were killed in batches at 6 and 12 weeks after administration, and the femoral neck tissues were obtained. Relevant data were analyzed, such as pathomorphological observation, micro-CT analysis, detection of 20S proteasome activity in tissues, and expression of Wnt and β-catenin.Morphological observation showed that the trabecular were slightly thinner, reticulated, and occasionally interrupted in group A, while the trabecular were obviously thinner and discontinuous in group B. And the trabecular were intact and arranged reticulated in group C and D. The analysis results of bone mineral density(BMD), bone surface(BS), bone volume/total volume(BV/TV) and trabecular thickness(Tb.Th) showed that group B was worse than other groups in all parameters at different time points(MG-132, a ubiquitin proteasome inhibitor, can regulate Wnt/β-catenin signaling pathway by inhibiting the degradation of β-catenin protein, and delaying the occurrence and development of osteoporosis.

Abdominal ultrasound in a 50-year-old Japanese man revealed a cystic lesion on the caudate lobe of the liver. Four-month follow-up imaging showed a rapid increase in the size of the cystic lesion. The patient underwent laparoscopic partial hepatectomy because of a suspicion and perceived risk that the lesion might be malignant. The initial histological diagnosis was a hepatic cyst. Eleven months later, computed tomography showed a giant cystic lesion in the abdominal cavity and multiple liver metastases. The patient underwent excision of the giant cystic lesion and a partial hepatectomy. Immunohistochemistry for the recurring lesion revealed undifferentiated embryonal sarcoma of the liver.

Podocyte injury plays a vital role in proteinuria and nephrotic syndrome. Calcineurin (CaN) inhibitors are effective in reducing proteinuria. However, their molecular mechanism is still not fully understood. Angiopoietin-like-4 (ANGPTL4) is a secreted protein that mediates proteinuria in podocyte-related nephropathy. In this study, we established a puromycin aminonucleoside (PAN)-induced minimal-change disease (MCD) rat model and a cultured podocyte injury model. We found that CaN inhibitors protected against PAN-induced podocyte injury, accompanied by an inhibition of Nfatc1 and Angptl4 both in vivo and in vitro. Nfatc1 overexpression and knockdown experiments indicated that Angptl4 was regulated by Nfatc1 in podocytes. ChIP assays further demonstrated that Nfatc1 increased Angptl4 expression by binding to the Angptl4 promoter. In addition, overexpression and knockdown of Angptl4 revealed that Angptl4 directly induced rearrangement of the cytoskeleton of podocytes, reduced the expression of synaptopodin, and enhanced PAN-induced podocyte apoptosis. Furthermore, in a cohort of 83 MCD and 94 membranous nephropathy (MN) patients, we found increased expression of serum ANGPTL4 compared to 120 healthy controls, and there were close correlations between serum ANGPTL4 and Alb, urinary protein, urinary Alb, eGFR, Scr, and BUN in MCD patients. No obvious correlation was found in MN patients. Immunofluorescence studies indicated that increased ANGPTL4 in MCD and MN patients was located mostly in podocytes. In conclusion, our results demonstrate that CaN inhibitors ameliorate PAN-induced podocyte injury by targeting Angptl4 through the NFAT pathway, and Angptl4 plays a vital role in podocyte injury and is involved in human podocyte-related nephropathy. © 2020 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

The rational design of non-precious-metal bifunctional catalysts of oxygen and hydrogen evolution reactions that generate a high current density and stability at low over potentials is of great significance in the field of water electrolysis. Herein, we report a facile and controllable method for the in-situ growth of urchin-like FeOOH–NiOOH catalyst on Ni foam (FeOOH–NiOOH/NF). X-ray photoelectron spectroscopy confirms that the proportion of Ni and Fe species with high valence state gradually increase with the extension of growth time. Electrochemical studies have shown that the optimized FeOOH–NiOOH/NF-24 h and −12 h catalysts demonstrate excellent electrochemical activity and stability in oxygen/hydrogen evolution reactions. Moreover, the cell voltage is reduced around 0.15 V at high current density (0.5–1.0 A cm−2) as compared to the state-of the art RuO2/NF(+)||Pt–C/NF(−) system, far better than most of the previously reported catalysts. The cost analyst revealed that using FeOOH–NiOOH/NF catalyst as both electrodes could potentially reduce the price of H2 around 7% compared with traditional industrial electrolyzers. These excellent electrocatalytic properties can be attributed to the unique urchin-like structure and the synergy between Ni and Fe species, which can not only provide more active sites and accelerate electron transfer, but also promote electrolyte transport and gas emission.

AIM Lenvatinib is an oral, multitargeted, tyrosine kinase inhibitor, which suppress tumor angiogenesis and tumor progression. It was non-inferior to sorafenib in overall survival in untreated advanced hepatocellular carcinoma (HCC). Sorafenib had a beneficial effect on portocollateral circulation with portal hypertension in translating and clinical studies. However, the hemodynamic effects of lenvatinib appear to be different from those of sorafenib because the efficacy of lenvatinib for vascular endothelial growth factor receptors and fibroblast growth factor receptors is different from that of sorafenib. This study was prospectively performed to evaluate the portal hemodynamic effect of lenvatinib in patients with advanced HCC using duplex Doppler ultrasonography. METHODS In total, 28 Child-Pugh class A or B patients with advanced HCC received lenvatinib depending on body weight daily for 2 weeks. Primary outcomes were changes in the hemodynamics of the portal venous system using duplex Doppler ultrasonography before and after the 2-week administration of lenvatinib. RESULTS The portal venous flow velocity (cm/s) significantly reduced (27 ± 12.1 vs. 22.6 ± 8.0, P = 0.019), while portal venous area (cm2 ) did not change after the 2-week administration (0.80 ± 0.36 vs. 0.82 ± 0.27, P = 0.665). Therefore, the congestion index (portal venous area/portal venous flow velocity), which reflects the pathophysiological hemodynamics of the portal venous system significantly worsened (0.037 ± 0.025 vs. 0.043 ± 0.024, P = 0.045). CONCLUSIONS Considering that this was a short-term study, because lenvatinib could be an agent that aggravates portal hypertension, it will be necessary to verify its clinical effects for portal hypertension in future studies.

Background Autotaxin (ATX) has been reported as a direct biomarker for estimating the evaluation of liver fibrosis. But available data on ATX as a useful biomarker for the complications of liver cirrhosis (LC) are scant. Aim To assess the clinical usefulness of ATX for assessing the complications of LC. Methods This multicenter, retrospective study was conducted at six locations in Japan. We include patients with LC, n = 400. The ATX level was evaluated separately in men and women because of its high level in female patients. To assess the clinical usefulness of ATX for the complications of LC, the area under the curve (AUC) of ATX assessing for the severe complications was analyzed in comparison with the model for end-stage liver disease score, albumin-bilirubin (ALBI) score, fibrosis-4 index, and aspartate aminotransferase-to-platelet ratio index. Results The mean age was 68.4 ± 11.4 years, 240 patients (60.0%) were male. A total of 213 (53.3%) and 187 (46.8%) patients were compensated and decompensated, respectively. The numbers of patients with varix rupture, hepatic ascites, and hepatic encephalopathy were 35 (8.8%), 131 (32.8%), and 103 (25.8%), respectively. The AUCs of ATX in men for hepatic encephalopathy, hepatic ascites, and varix ruptures were 0.853, 0.816, and 0.706, respectively. The AUCs of ATX in women for hepatic encephalopathy, hepatic ascites, and varix rupture were 0.759, 0.717, and 0.697, respectively. The AUCs of ATX in men were higher than those in women, as were all the other biomarkers used to detect encephalopathy and varix ruptures. However, for detecting ascites, the AUC of ALBI in men was more effective than using ATX. Conclusion ATX in men was more effective than any other biomarkers for detecting hepatic encephalopathy and varix ruptures.

Developing the earth-abundant transition metal-based bifunctional electrocatalysts for water splitting and renewable energy devices has attracted much attention. Herein, we report a 1 T-WS

Background: Data regarding the influence of patatin-like phospholipase domain-containing 3 (PNPLA3) polymorphism for patients with liver cirrhosis (LC) are scarce. Objective: This study assesses the role of the PNPLA3 polymorphism for the development of LC and its complications by the findings of genetic examinations. Methods: Patients with LC caused by virus (n = 157), alcohol (n = 104), nonalcoholic fatty liver disease (NAFLD) (n = 106), or autoimmune disease (n = 33) and without LC (n = 128) were enrolled. LC was composed of the presence and absence of complications, such as variceal bleeding, hepatic ascites, and hepatic encephalopathy. To assess the role of the PNPLA3 polymorphism, odds ratio (OR) for the rs738409 variant was calculated for the patients between (i) with LC and without LC in the entire cohort and (ii) the presence and absence of complications in the patients with LC. Results: There was a significant difference among the patients without LC and those with alcohol, NAFLD-related LC in the frequency of G alleles (p < 0.001, both). According to complications of LC, the OR for NAFLD-related cirrhosis significantly increased in the presence of the two mutated alleles (OR = 3.165; p = 0.046) when the wild type was used as the reference. However, there were no significant risks for the complications in the virus and alcohol-related cirrhosis unless there was a presence of G alleles. Conclusion: The PNPLA3 polymorphism was associated with the risk of NAFLD-related LC and its complications.

Tellurium is massively used as the main light-absorbing layer component in the manufacturing of CdTe thin-film solar cells, a critical component in the photovoltaic industry. However, the process of manufacturing and renewing components has produced large amounts of tellurium-containing wastewater that is difficult to degrade and poses a serious threat to the aquatic ecosystem and human health. Hence, to achieve the recovery of tellurium resources for reducing their damages, a win-win approach was employed to utilize waste lignin to construct functional copper-doped activated lignin (CAL) adsorbents for selective separation and recovery of tellurium from wastewater. CAL exhibited superior adsorption properties towards tellurium (248.45 mg/g), mainly attributed to the adsorption mechanism of coordination interactions. Kinetic and isotherm results elucidated that monolayer chemisorption dominated CAL adsorption process. Besides, CAL had a satisfactory regeneration capability with minimal loss adsorption capacity after six consecutive cycles, which also exhibited high antifouling properties. Meanwhile, CAL achieved high selectivity for tellurium adsorption under the simulated wastewater, revealing the potential of CAL for practical application in wastewater. Therefore, this work provides a promising environmental strategy for exploring the application of lignin-based materials for tellurium recovery from wastewater.

A partial emission liquid hydrogen circulation pump was developed to meet an application requirement of small flow and high head in a cryogenic system. Experimental study on prototype pump with liquid nitrogen based on the similarity theory for hydraulic performances such as head, power and efficiency curves were carried out in the cryogenic test platform, which was specially designed and constructed to test performance characteristics for cryogenic fluid in the absence of cavitation and aerial binding. By analyzing the experimental data on the basis of similarity conversion, the results demonstrated theoretically that the pump could achieve performance levels, that is, at the rated condition, head of 125 m, power of 210 W and efficiency of 45%, if liquid hydrogen was used as working fluid finally. To validate the liquid hydrogen pump design and clarify the pressure and velocity effect on internal flows of the pump, a numerical simulation on the Reynolds-averaged Navier-Stokes combined with the RNG k-e turbulence model accounts for three dimensional unsteady flows was applied for getting the pump hydrodynamic performances in all various conditions. Comparison of the performance curves of numerical simulation with test results showed that, at the rated condition point, the head, power and efficiency was 138.5 m, 220 W and 45% respectively. It was proved that the calculating results was in accordance with experimental data well. Feasibility of the model had been validated to a certain extent.

Background Hepatocellular carcinoma (HCC) is one of the most common malignancies, and its global morbidity and mortality are increasing. Previous studies confirmed that miR-342 was involved in the development and progression of malignant tumors. However, the relationship between miR-342 and Wnt/β-catenin signaling pathway in HCC remains unknown. Materials and methods Cell viability was detected by MTT assay. Immunofluorescence staining was used to detect Brdu-positive cells and Western blot was used to detect the apoptotic proteins. Furthermore, linear correlation analysis was used to investigate the possible relationship between miR-342 and the downstream genes of Wnt/β-catenin signaling pathway in the progression of HCC. Results Over-expression of miR-342 significantly reduced cell proliferation and obviously increased apoptosis in HCC, while silencing of miR-342 showed an opposite effect on HCC cell proliferation and apoptosis. In addition, we found that the CXCL12 was the target gene of miR-342. This study also demonstrated that miR-342 up-regulation suppressed Wnt/β-catenin signaling pathway by inhibiting CXCL12 expression. Conclusion Up-regulation of miR-342 inhibited cell proliferation and induced cell apoptosis in HCC by inhibiting Wnt/β-catenin signaling pathway, suggesting that miR-342 might act as a promising tumor gene therapeutic target for HCC patients.

BACKGROUND Hyperphosphatemia, hypocalcemia, and elevation of parathyroid hormone (PTH) are typical abnormalities of uremic patients with Secondary hyperparathyroidism (SHPT). However, metabolic imbalance associated with SHPT is not well understood. METHODS A total of 15 SHPT patients with an intact parathyroid hormone (iPTH) level > 600 pg/mL were set as preoperative (PR) group, 15 age- and gender-matched controls who had undergone parathyroidectomy plus forearm transplantation because of hyperparathyroidism and achieved an iPTH level

The role of mitochondrial dysfunction and its molecular mechanism in inflammation-induced acute liver failure (ALF) remain unknown. Despite the numerous studies performed to date, very few therapies are available for inflammation-induced ALF. Therefore, our study is aimed to explore the regulatory effects of mitochondrial stress and the Akt-Sirt3 pathway on the development of TNF-α-induced hepatocyte death and assess the therapeutic effects of melatonin on the damaged liver. Our results exhibited that TNF-α treatment induced hepatocyte damage in vitro; the effect of which was dose-dependently inhibited by melatonin. At the molecular level, TNF-α-treated hepatocytes expressed lower levels of Sirt3 and subsequently exhibited mitochondrial stress. Interestingly, melatonin treatment improved mitochondrial bioenergetics, reduced mitochondrial oxidative stress, reversed mitochondrial dynamics, and repressed mitochondrial apoptosis by reversing the decrease in Sirt3 expression after TNF-α challenge. In addition, we found that melatonin-regulated Sirt3 expression in a manner dependent on the Akt pathway. Blockade of the Akt pathway abolished the protective exerted by melatonin on mitochondria and hepatocyte under TNF-α treatment. In conclusion, TNF-α promotes hepatocyte apoptosis by inducing mitochondrial stress. However, melatonin significantly increases the activity of the Akt/Sirt3 axis and consequently maintains mitochondrial homeostasis, restoring hepatocyte viability in an inflammatory environment. Thus, the information compiled here might provide important perspectives for the use of melatonin in the clinic for preventive and therapeutic applications in patients with ALF based on its anti-inflammatory and mitochondria-protective effects.

The brain is a high energy-consuming organ that typically utilizes glucose as the main energy source for cerebral activity. When glucose becomes scarce under conditions of stress, ketone bodies, such as β-hydroxybutyrate, acetoacetate and acetone, become extremely important. Alterations in brain energy metabolism have been observed in psychostimulant abusers; however, the mode of brain metabolic programming in cocaine dependence remains largely unknown. Here, we profiled the metabolites and metabolic enzymes from brain nucleus accumbens (NAc) of mice exposed to cocaine. We found that cocaine modified energy metabolism and markedly activated ketogenesis pathway in the NAc. The expression of HMG-CoA synthase 2 (HMGCS2), a critical rate-limiting ketogenesis enzyme, was markedly up-regulated. After switching metabolic pathways from ketogenesis to glycolysis through activation of glucokinase, cocaine-evoked metabolic reprogramming regained homeostasis, and the cocaine effect was attenuated. Importantly, both the pharmacological and genetic inhibition of HMGCS2 significantly suppressed cocaine-induced ketogenesis and behavior. In conclusion, cocaine induces a remarkable energy reprogramming in the NAc, which is characterized by HMGCS2-driven ketogenesis. Such effect may facilitate adaptations to cocaine-induced energy stress in the brain. Our findings establish an important link between drug-induced energy reprogramming and cocaine effect, and may have implication in the treatment of cocaine addiction.

Recovery of the tellurium from wastewater is significance for both industrial applications and sustainable development due to the adverse impacts emanating from environmental pollution and strategic values in the photovoltaic industry. Herein, this study presents the recovery of tellurium from wastewater by flower-like structure ZnO-Ag@cellulose (ZAC) composites. For adsorbent preparation, lignocellulose was first extracted from waste wood debris by an alkaline extraction process. Then, the flower-like structure of ZAC composites were synthesized by a facile one-step hydrothermal method. The obtained materials are conducted under different parameters to investigate tellurium adsorption properties. The results indicate that the tellurium adsorption process is an exothermic reaction and fits well to the Freundlich model. Kinetic data are well described by pseudo-second-order model, indicating ZAC adsorption of tellurium is a chemical process. Besides, as-prepared ZAC exhibited excellent performance for tellurium elimination from wastewater with a maximum removal efficiency of 98.86%. The ZAC also shows outstanding antifouling performance in polluted environment and can still achieve the rate of 94.23% for tellurium. Moreover, the ZAC composite reveals high reusability and stability after six desorption-regeneration cycles. Importantly, the ZAC composite exhibits disinfection performance against E. coli and S. aureus with high killing efficiency. Therefore, this work not only demonstrates ZAC composite is efficient adsorbent with antifouling and antibacterial capability for tellurium recovery, but also provides an effective channel for promising candidates to decontaminate similar pollutants and practical applications of wastewater.

BackgroundTo compare perioperative, functional and oncological outcomes between transperitoneal robotic partial nephrectomy (TRPN) and retroperitoneal robotic partial nephrectomy (RRPN).MethodsA literature searching of Pubmed, Embase, Cochrane Library and Web of Science was performed in August, 2020. Pooled odds ratios (ORs) or weighted mean differences (WMDs) with 95% confidence intervals (CIs) were estimated using fixed-effect or random-effect model. Publication bias was evaluated with funnel plots. Only comparative studies with matched design or similar baseline characteristics were included.ResultsEleven studies embracing 2,984 patients were included. There was no significant difference between the two groups regarding conversion to open (P = 0.44) or radical (P = 0.31) surgery, all complications (P = 0.06), major complications (P = 0.07), warm ischemia time (P = 0.73), positive surgical margin (P = 0.87), decline in eGFR (P = 0.42), CKD upstaging (P = 0.72), and total recurrence (P = 0.66). Patients undergoing TRPN had a significant higher minor complications (P = 0.04; OR: 1.39; 95% CI, 1.01–1.91), longer operative time (P < 0.001; WMD: 21.68; 95% CI, 11.61 to 31.76), more estimated blood loss (EBL, P = 0.002; WMD: 40.94; 95% CI, 14.87 to 67.01), longer length of hospital stay (LOS, P < 0.001; WMD: 0.86; 95% CI, 0.35 to 1.37). No obvious publication bias was identified.ConclusionRRPN is more favorable than TRPN in terms of less minor complications, shorter operative time, less EBL, and shorter LOS. Methodological limitations of the included studies should be considered while interpreting these results.

Patatin-like phospholipase domain-containing 3 (PNPLA3) and transmembrane 6-superfamily member 2 (TM6SF2) polymorphisms have major impact for fibrosis due to steatohepatitis. However, there are scant data about correlations between cirrhosis-related complications and the polymorphisms of these genes. Therefore, we aimed to determine the role of the PNPLA3 and TM6SF2 polymorphisms in fibrosis progression for patients with liver cirrhosis. A multicenter study was performed at six hospitals in Japan enrolling 400 patients with liver cirrhosis caused by virus (n = 157), alcohol (n = 104), nonalcoholic fatty liver disease (NAFLD) (n = 106), or autoimmune disease (n = 33). These cirrhotic patients included those with complications of variceal bleeding, hepatic ascites, and/or hepatic encephalopathy and those without. To assess the role of the PNPLA3 and TM6SF2 polymorphisms in patients with cirrhosis related complications, we calculated the odds ratio and relative risk for the rs738409 and rs58542926 polymorphisms. We also accessed whether or not the interaction between these two polymorphisms contributed to cirrhosis related complications. As a result, the odds ratio for complications in the NAFLD group significantly increased in the presence of the rs738409 GG genotype when the CC genotype was used as the reference. There were no significant risks between complications and the presence of the rs738409 G allele in the virus or alcohol groups. There were no significant risks of complications in the frequency of the rs58542926 T polymorphism regardless of the etiology of liver cirrhosis. The interaction between the rs738409 and rs58542926 polymorphisms had the highest odds ratio of 2.415 for complications in the rs738409 GG + rs58542926 (CT+TT) group when rs738409 (CC+CG) + TM6SF2 CC was used as the reference in the NAFLD group although there was no statistically interaction between these gene polymorphisms (P=0.085).

We investigated whether or not nitric oxide synthase 3 (NOS3) rs2070744 genotypes can affect the response for lenvatinib treatment in patients with hepatocellular carcinoma (HCC). We evaluated the relation of the NOS3 rs2070744 genotypes to the tumor response, progression-free survival (PFS), and overall survival (OS) as the response for lenvatinib. We also examined the association between fibroblast growth factor receptor (FGFR) gene polymorphisms, a potential feature of lenvatinib, and the response. There were no significant differences between the studies for either PFS or OS, even though patients with the TT genotype had a longer mean PFS (hazard ratio [HR] 0.60; p = 0.069) and mean OS (HR 0.46; p = 0.075) than those with the TC/CC genotypes. However, patients with a single-nucleotide polymorphism (SNP) combination pattern of the NOS3 rs2070744 TC/CC and FGFR4 rs351855 CT/TT genotypes had a significantly shorter mean PFS (HR 2.56; p = 0.006) and mean OS (HR 3.36; p = 0.013) than those with the other genotypes. The NOS3 rs2070744 genotypes did not influence the clinical response. However, the SNP combination pattern of the NOS3 rs2070744 and FGFR4 rs351855 genotypes may be helpful as treatment effect predictors and prognostic factors for HCC patients treated with lenvatinib.

AIM Esophageal variceal ligation (EVL) is usually carried out to decrease the risk of hemorrhage. Several complications have been reported with the procedure, including bleeding from ligation-induced esophageal ulcers or heartburn. However, there is scant evidence for gastroesophageal reflux caused by EVL. The aim of this study was to assess 24-h pH monitoring in the esophagogastric junction before and after EVL and the bleeding rate for 18 months. METHODS We undertook this single-center prospective trial in Kitasato University Hospital (Sagamihara, Japan). We included patients with cirrhosis who were Child-Pugh classification A or B, without uncontrollable hepatocellular carcinoma, and had F2 or larger esophageal varices, and/or were red color sign (RC) positive. The study period was from July 2012 through September 2017 for 32 patients enrolled in this study and followed up until March 2019. RESULTS Baseline characteristics were: median Child-Pugh score, 6; and mean age, 64.3 years. Before and after EVL, the median 24-h under pH 4 holding time percentages of all patients were 0.6% (range, 0-5.6%) and 0.95% (range, 0-50.6%), respectively, without a significant difference (P = 0.107). We could not find any G3 or G4 adverse events during this study, and 75% of the patients who had already suffered from moderate gastroesophageal reflux became worse after EVL (P = 0.18) and required antacid therapies. There were no patients with hemorrhage from esophageal varices. CONCLUSIONS Esophageal variceal ligation for esophageal varices did not significantly change gastroesophageal reflux. Therefore, acid suppressive therapy might be unnecessary for patients who do not suffer from gastroesophageal reflux after EVL.

Accruing research shows the implications of long non-coding RNAs (lncRNAs) in the progression of various autoimmune diseases including systemic lupus erythematosus (SLE). The present study aimed to identify the expression pattern of LINC00176 in SLE and to explore its effects on CD4

Background: To make an accurate estimate of the response to thrombopoietin (TPO) receptor agonists for thrombocytopenia associated with chronic liver disease, we evaluated the influence of antiplatelet autoantibodies on the response to lusutrombopag in thrombocytopenic patients with liver disease. Methods: A prospective study was conducted at 2 hospitals. Thrombocytopenic patients with liver disease received oral lusutrombopag 3.0 mg once daily for up to 7 days. We analyzed changes in platelet counts from baseline to the maximum platelet count on days 9–14. The definition of clinical response was a platelet count of ≥5 × 104/μL with an increased platelet count of ≥2 × 104/μL from baseline. We assessed the correlation between the response to treatment drug and antiplatelet autoantibodies measured by anti-GPIIb/IIIa antibody-producing B cells. Results: Thirty patients received the trial drug. There were 25 responders and 5 nonresponders. The median change in platelet counts was 3.9 × 104/μL (95% CI 2.8–4.6, p < 0.0001). The correlation between change in platelet counts and the frequency of the anti-glycoprotein IIb/IIIa antibody-producing B cells was moderate (r = 0.414, 95% CI 0.064–0.674, p = 0.023). In multivariate analysis of factors affecting the change in platelet counts, the anti-GPIIb/IIIa antibody-producing B cells were identified as an independent factor (regression coefficient [B] = 0.089; CI 0.021–0.157, p = 0.013). Conclusion: Anti-GPIIb/IIIa antibody-producing B cells may be a predictor for TPO receptor agonists in patients with chronic liver disease.

Background Effective therapy for hepatocellular carcinoma (HCC) is currently an imperative issue, and sorafenib is a first-line drug for the treatment of HCC. However, the clinical benefit of sorafenib is often impaired by drug resistance. Accordingly, the present study was conducted to investigate the molecular mechanisms involving sorafenib resistance, with a focus on large tumor suppressor 2 (LATS2) and mitophagy. Methods HepG2 liver cancer cells were treated with sorafenib and infected with adenovirus-loaded LATS2 (Ad-LATS2). Cell death, proliferation and migration were measured via western blotting analysis, immunofluorescence and qPCR. Mitochondrial function and mitophagy were determined via western blotting and immunofluorescence. Results Our data indicated that LATS2 expression was repressed by sorafenib treatment, and overexpression of LATS2 could further enhance sorafenib-mediated apoptosis in HepG2 liver cancer cells. At the molecular level, mitochondrial stress was triggered by sorafenib treatment, as evidenced by decreased mitochondrial membrane potential, increased mitochondrial ROS production, more cyc-c release into the nucleus, and elevated mitochondrial pro-apoptotic proteins. However, in response to mitochondrial damage, mitophagy was activated by sorafenib treatment, whereas LATS2 overexpression effectively inhibited mitophagy activity and thus augmented sorafenib-mediated mitochondrial stress. Subsequently, we also demonstrated that the AMPK–MFN2 signaling pathway was involved in mitophagy regulation after exposure to sorafenib treatment and/or LATS2 overexpression. Inhibition of the AMPK pathway interrupted mitophagy and thus enhanced the antitumor property of sorafenib, similar to the results obtained via overexpression of LATS2. Conclusions Altogether, our findings revealed the importance of the LATS2/AMPK/MFN2/mitophagy axis in understanding sorafenib resistance mechanisms, with a potential application to increase the sensitivity response of sorafenib in the treatment of liver cancer.

A previous paper [J. Lumin. 177 (2016) 219] has studied Judd-Ofelt spectroscopic properties of Er3+ (0.5 at%)-doped Gd3(Al, Ga)5O12 garnet single-crystal, and reported the Judd-Ofelt intensity parameters Ω2 = 1.47 × 10−20 cm2, Ω4 = 1.38 × 10−20 cm2 and Ω6 = 1.19 × 10−20 cm2. We have performed a re-study on the Judd-Ofelt spectroscopic properties of a similar garnet single-crystal Er3+(20 at%)-doped Gd3(Al0.4Ga0.6)5O12, and obtained quite different values of Judd-Ofelt intensity parameters Ω2 = (0.34 ± 0.11) × 10−20 cm2, Ω4 = (0.48 ± 0.16) × 10−20 cm2 and Ω6 = (1.05 ± 0.17) × 10−20 cm2. The quite different Ωt values given by two studies are mainly due to remarkably different absorption characteristics of Er3+ in the crystals employed in two studies, and factors that lead to quite different absorption characteristics are discussed. Another reason is that the hypersensitive transition at 380 nm was excluded from the Judd-Ofelt calculation in that paper, resulting in deviation of their result. Instead, all of the Er3+ absorption bands were included in our calculation, allowing to obtain more accurate Ωt values. Quite different Ωt values lead to considerable differences of relevant spectroscopic parameters, such as radiative rates and lifetimes of typical Er3+ emissions, for which the difference from each other is as much as three times. In addition, visible, near-infrared and mid-infrared fluorescence spectra and lifetimes of Er3+ in the studied crystal were measured, and the emission characteristics are discussed.

Fabrication of an acid-resistant, biodegradable and recoverable highly efficient adsorbent to selectively recover tellurium resources from acidic wastewater for minimizing their threat still presents a significant challenge. Herein, a sheet-like magnetic FeS@Lignin-derived carbon (FeS@LC) nanocomposite with acid-resistant was obtained as an efficient adsorbent for tellurium separation through a simple two-step hydrothermal reaction. The results indicated that this FeS@LC fabricated with biodegradable lignin-derived carbon (LC) and highly reactive FeS revealed a superior adsorption capacity (148.36 mg/g) for tellurium. Isotherm and kinetic results suggested that the tellurium adsorption process was dominated by a monolayer chemisorption process. The thermodynamic parameters for tellurium adsorption on FeS@LC confirmed that the tellurium adsorption was exothermic and spontaneous. Precipitation, reduction, ion exchange, and surface complexation are regarded as the main adsorption mechanisms for tellurium purification. Besides, FeS@LC composites can selectively adsorb tellurium from a multitude of coexisting ions. Meanwhile, the FeS@LC maintained quick magnetic recyclable capability (10S) and excellent adsorption performance (108.87 mg/g) after five consecutive adsorption-desorption. Importantly, FeS@LC exhibited a superior stability and antifouling properties, facilitating its practical application in complex environments. Therefore, this work expands the application field of lignin-derived carbon-based materials, presenting a bright application for similar pollutants purification in wastewater.

Interleukin (IL)-35, a newly identified member of the IL-12 cytokine family, has been reported to suppress inflammation and induce immunotolerance. However, little is known regarding the role of IL-35 during chronic hepatitis C virus (HCV) infection. Herein, we measured the serum IL-35 concentration of 73 patients with hepatitis C and 22 healthy individuals, as well as further investigated the modulatory function of IL-35 on CD4+CD25+CD127dim/- regulatory T cells (Tregs) and on hepatocytes infected with HCV in cell culture (HCVcc). IL-35 expression was significantly increased in patients with chronic hepatitis C and was positively correlated with the levels of HCV RNA. Inhibition of viral replication led to decreases in the serum levels of IL-35. IL-35 stimulation not only elevated the percentage of Tregs but also robustly inhibited cellular proliferation and up-regulated the production of anti-inflammatory cytokines (e.g., IL-10 and IL-35) in a HCV-specific and non-specific manner, which indicates enhancement of the suppressive function of Tregs. Although IL-35 did not exert anti-HCV activity in HCVcc-infected Huh7.5 cells, it reduced inflammatory cytokine secretion from Huh7.5 cells. This was probably via inhibition of the STAT1 and STAT3 signaling pathways, which could suppress subsequent liver damage due to chronic hepatitis C. The current data suggested that IL-35 contributes to persistent HCV infection by inhibiting antiviral immune activity. Moreover, IL-35 might also protect against HCV-induced liver injury by down-regulating the expression of proinflammatory cytokines. Thus, the immunosuppressive properties of IL-35 might play contradictory roles in maintaining viral persistence and reducing the inflammatory responses in chronic HCV infection.

Previous studies have found that the primary pathogenesis of liver cancer progression is linked to excessive cancer cell proliferation and rapid metastasis. Although therapeutic advances have been made for the treatment of liver cancer, the mechanism underlying the liver cancer progression has not been fully addressed. In the present study, we explored the role of spliced X-box binding protein 1 (XBP1) in regulating the viability and death of liver cancer cells in vitro. Our study demonstrated that XBP1 was upregulated in liver cancer cells when compared to the primary hepatocytes. Interestingly, the deletion of XBP1 could reduce the viability of liver cancer cells in vitro via inducing apoptotic response. Further, we found that XBP1 downregulation was also linked to proliferation arrest and migration inhibition. At the molecular levels, XBP1 inhibition is followed by activation of the Mst1 pathway which promoted the phosphorylation of c-Jun N-terminal kinase (JNK). Then, the active Mst1-JNK pathway mediated mitochondrial reactive oxygen species (mROS) overproduction and then excessive ROS induced cancer cell death. Therefore, our study demonstrated a novel role played by XBP1 in modulating the viability of liver cancer cells via the Mst1-JNK-mROS pathways.

Interleukin (IL)-35 is a newly identified IL-12 cytokine family member, which has been demonstrated to induce immunotolerance by suppression of CD8+ T cells function in chronic viral hepatitis. However, the role of IL-35 in modulating CD8+ T cells activity in non-viral hepatitis-related hepatocellular carcinoma (HCC) was not fully elucidated. Forty-four patients with non-viral hepatitis-related HCC and 20 healthy individuals were enrolled. Serum IL-35 concentration was measured by ELISA. CD8+ T cells were purified from peripheral bloods and liver tissues. mRNA expression of cytotoxic/inhibitory molecules in CD8+ T cells with IL-35 stimulation was semi-quantified by real-time PCR. Direct and indirect contact co-culture systems of CD8+ T cells and HCC cell lines were set up. The modulatory function of IL-35 on peripheral and liver-resident CD8+ T cells was assessed by measurement of lactate dehydrogenase release and cytokine production in the co-culture supernatants. Serum IL-35 was notably elevated in HCC patients, while effective anti-tumor therapies down-regulated IL-35 concentration. Recombinant IL-35 stimulation suppressed cytotoxicity and proinflammatory cytokine secretion of peripheral and liver-resident CD8+ T cells in direct and indirect contact co-culture systems. This process was accompanied by reduction of perforin expression and interferon-γ production, as well as programmed death-1 and cytotoxic T-lymphocyte-associated protein 4 elevation in CD8+ T cells. The current data suggested that IL-35 inhibited both cytolytic and non-cytolytic function of CD8+ T cells to non-viral hepatitis-related HCC probably via repression of perforin expression. IL-35 might be considered to be one of the therapeutic targets for patients with HCC.

Background Effective therapy for hepatocellular carcinoma (HCC) is currently an imperative issue, and sorafenib is a first-line drug for the treatment of HCC. However, the clinical benefit of sorafenib is often impaired by drug resistance. Accordingly, the present study was conducted to investigate the molecular mechanisms involving sorafenib resistance, with a focus on large tumor suppressor 2 (LATS2) and mitophagy. Methods HepG2 liver cancer cells were treated with sorafenib and infected with adenovirus-loaded LATS2 (Ad-LATS2). Cell death, proliferation and migration were measured via western blotting analysis, immunofluorescence and qPCR. Mitochondrial function and mitophagy were determined via western blotting and immunofluorescence. Results Our data indicated that LATS2 expression was repressed by sorafenib treatment, and overexpression of LATS2 could further enhance sorafenib-mediated apoptosis in HepG2 liver cancer cells. At the molecular level, mitochondrial stress was triggered by sorafenib treatment, as evidenced by decreased mitochondrial membrane potential, increased mitochondrial ROS production, more cyc-c release into the nucleus, and elevated mitochondrial pro-apoptotic proteins. However, in response to mitochondrial damage, mitophagy was activated by sorafenib treatment, whereas LATS2 overexpression effectively inhibited mitophagy activity and thus augmented sorafenib-mediated mitochondrial stress. Subsequently, we also demonstrated that the AMPK–MFN2 signaling pathway was involved in mitophagy regulation after exposure to sorafenib treatment and/or LATS2 overexpression. Inhibition of the AMPK pathway interrupted mitophagy and thus enhanced the antitumor property of sorafenib, similar to the results obtained via overexpression of LATS2. Conclusions Altogether, our findings revealed the importance of the LATS2/AMPK/MFN2/mitophagy axis in understanding sorafenib resistance mechanisms, with a potential application to increase the sensitivity response of sorafenib in the treatment of liver cancer.