Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Background: s/Aims: Non-invasive models stratifying clinically significant portal hypertension (CSPH) are limited. Herein, we developed a new non-invasive model for predicting CSPH in patients with compensated cirrhosis and investigated whether carvedilol can prevent hepatic decompensation in patients with high-risk CSPH stratified using the new model. Methods: Non-invasive risk factors of CSPH were identified via systematic review and meta-analysis of studies involving patients with hepatic venous pressure gradient (HVPG). A new non-invasive model was validated for various performance aspects in three cohorts, i.e., a multicenter HVPG cohort, a follow-up cohort, and a carvediloltreating cohort. Results: In the meta-analysis with six studies (n=819), liver stiffness measurement and platelet count were identified as independent risk factors for CSPH and were used to develop the new “CSPH risk” model. In the HVPG cohort (n=151), the new model accurately predicted CSPH with cutoff values of 0 and –0.68 for ruling in and out CSPH, respectively. In the follow-up cohort (n=1,102), the cumulative incidences of decompensation events significantly differed using the cutoff values of <–0.68 (low-risk), –0.68 to 0 (medium-risk), and >0 (high-risk). In the carvediloltreated cohort, patients with high-risk CSPH treated with carvedilol (n=81) had lower rates of decompensation events than non-selective beta-blockers untreated patients with high-risk CSPH (n=613 before propensity score matching [PSM], n=162 after PSM). Conclusions Treatment with carvedilol significantly reduces the risk of hepatic decompensation in patients with high-risk CSPH stratified by the new model.

Enzyme-driven micro/nanomotors consuming in situ chemical fuels have attracted lots of attention for biomedical applications. However, motor systems composed by organism-derived organics that maximize the therapeutic efficacy of enzymatic products remain challenging. Herein, swimming proteomotors based on biocompatible urease and human serum albumin are constructed for enhanced antitumor therapy via active motion and ammonia amplification. By decomposing urea into carbon dioxide and ammonia, the designed proteomotors are endowed with self-propulsive capability, which leads to improved internalization and enhanced penetration in vitro. As a glutamine synthetase inhibitor, the loaded l-methionine sulfoximine further prevents the conversion of toxic ammonia into non-toxic glutamine in both tumor and stromal cells, resulting in local ammonia amplification. After intravesical instillation, the proteomotors achieve longer bladder retention and thus significantly inhibit the growth of orthotopic bladder tumor in vivo without adverse effects. We envision that the as-developed swimming proteomotors with amplification of the product toxicity may be a potential platform for active cancer treatment.

Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence rate and mortality worldwide. However, most patients are not suitable for radical treatment at the time of first diagnosis. As one of the important schemes for the treatment of HCC, one of the most representative drug is Sorafenib, which has certain survival benefits for HCC patients at different stages. However, the drug resistance of HCC to Sorafenib greatly limits its efficacy. So far, people have found that some natural substances, experimental agents and biological macromolecules can reverse the drug resistance of HCC to Sorafenib through tumor cell microenvironment, metabolism and other mechanisms. This article will summarize the above substances and their mechanism in order to provide research ideas for the improvement of Sorafenib′s treatment program.

Hepatocellular carcinoma (HCC) is the sixth most common malignant disease in the world and one of the main causes of cancer-related death. At present, the treatment of patients with advanced HCC is very limited, and as an important research direction of advanced cancer treatment in recent years, immunotherapy has achieved good results. Up to now, scholars have tested a variety of immunotherapy methods, and the use of immune checkpoint inhibitor (ICIs) in the treatment of advanced cancer has made considerable progress. However, immunotherapy is still incurable for HCC, and the benefit of treatment is limited to a small number of patients. In the current context of liver cancer, one of the key research directions of oncology is to understand the biomarkers that predict the clinical response of immunotherapy, so as to improve patient selection, maximize clinical benefits and avoid unnecessary toxicity. Compared with tumor and surrounding tissue biomarkers, peripheral blood biomarkers play a unique role in clinical research and use because of their advantages of non-invasive detection. In this review, we summarize the peripheral blood biomarkers that play a key role in predicting the clinical response and prognosis of HCC patients.

Objective: To analyze the clinical characteristics of cases of novel coronavirus pneumonia and a preliminary study to explore the relationship between different clinical classification and liver damage. Methods: Consecutively confirmed novel coronavirus infection cases admitted to seven designated hospitals during January 23, 2020 to February 8, 2020 were included. Clinical classification (mild, moderate, severe, and critical) was carried out according to the diagnosis and treatment program of novel coronavirus pneumonia (Trial Fifth Edition) issued by the National Health Commission. The research data were analyzed using SPSS19.0 statistical software. Quantitative data were expressed as median (interquartile range), and qualitative data were expressed as frequency and rate. Results: 32 confirmed cases that met the inclusion criteria were included. 28 cases were of mild or moderate type (87.50%), and four cases (12.50%) of severe or critical type. Four cases (12.5%) were combined with one underlying disease (bronchial asthma, coronary heart disease, malignant tumor, chronic kidney disease), and one case (3.13%) was simultaneously combined with high blood pressure and malignant tumor. The results of laboratory examination showed that the alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin (ALB), and total bilirubin (TBil) for entire cohort were 26.98 (16.88 ~ 46.09) U/L and 24.75 (18.71 ~ 31.79) U/L, 39.00 (36.20 ~ 44.20) g/L and 16.40 (11.34- ~ 21.15) mmol/L, respectively. ALT, AST, ALB and TBil of the mild or moderate subgroups were 22.75 (16.31- ~ 37.25) U/L, 23.63 (18.71 ~ 26.50) U/L, 39.70 (36.50 ~ 46.10) g/L, and 15.95 (11.34 ~ 20.83) mmol/L, respectively. ALT, AST, ALB and TBil of the severe or critical subgroups were 60.25 (40.88 ~ 68.90) U/L, 37.00 (20.88 ~ 64.45) U/L, 35.75 (28.68 ~ 42.00) g/L, and 20.50 (11.28 ~ 25.00) mmol/L, respectively. Conclusion The results of this multicenter retrospective study suggests that novel coronavirus pneumonia combined with liver damage is more likely to be caused by adverse drug reactions and systemic inflammation in severe patients receiving medical treatment. Therefore, liver function monitoring and evaluation should be strengthened during the treatment of such patients.

Chronic inflammation and tumor occurrence and development, recurrence and metastasis and immune escape and other key links have a far-reaching impact. The level of inflammation and immunity can be reflected by the markers of inflammatory response, including C-reactive protein, neutrophils, platelets, lymphocytes and their combinations in the blood, such as neutrophil to lymphocyte ratio, platelet to lymphocyte ratio, lymphocyte to monocyte ratio, systemic immune inflammation index and so on. At present, inflammatory index has been proved to be predictors of recurrence and survival in a variety of malignant tumors. Hepatocellular carcinoma (HCC), as a common invasive tumor, is often diagnosed in the late course of the disease, so patients often can not achieve a satisfactory prognosis. This article mainly reviews the clinical application of the above inflammatory response indexes in HCC.

Hepatocellular carcinoma is one of the pathological types of primary liver cancer, and its prognosis is often not ideal. The prognosis of patients with hepatocellular carcinoma is not only closely related to tumor load and general physical status, but also closely related to liver reserve function. Albumin-bilirubin grading (ALBI) is a new model reflecting liver reserve function. In many therapeutic measures, such as surgical resection, liver transplantation, transcatheter arterial chemoembolization, radiofrequency ablation and targeted therapy, its ability to predict the prognosis of patients with hepatocellular carcinoma has been proved to be no less than that of Child-Pugh grade, which is widely used in clinic, and its predictive performance will be further improved when combined with other indexes.Therefore, it has great application value in clinical practice. This article mainly reviews the clinical application of ALBI grade in patients with hepatocellular carcinoma and the progress of research results in recent years.

Objective To explore the effect of supplemental parenteral nutrition (SPN) combined with early enteral nutrition (EN) for enhanced recovery in postoperative liver cancer patients.Methods From June 2015 to June 2018,liver cancer patients admitted to our hospital were randomly divided into two groups with 47 patients receiving SPN combined with early EN in the study group and 45 patients receiving early EN in the control group.Results There were no significant difference in bilirubin recovery,liver enzyme recovery,postoperative exhaust and defecation time and complication rate between the two groups (P ＞ 0.05).In study group prealbumin (PAB) synthesis recovered faster (F =7.89,P =0.006),albumin use was significantly lower (t =-2.29,P =0.0024),and postoperative hospital stay was shorter (t =2.46,P =0.016).Conclusion In ERAS patients with liver cancer,the combination of SPN and early EN provide reasonable energy support to improve nutritional status and accelerate patient recovery.