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Background and aims: Hepatitis B virus-associated acute-on-chronic liver failure (HBV-ACLF) is a complicated syndrome with extremely high short-term mortality. Whether plasma exchange (PE) improves HBV-ACLF outcomes remains controversial. Here, PE-based non-bioartificial liver support system (NB-ALSS) effects on short-term HBV-ACLF patient outcomes were investigated. Materials and methods: HBV-ACLF patients from Chinese Acute-on-chronic Liver Failure (CATCH-LIFE) cohort receiving standard medical therapy (SMT) alone or PE-based NB-ALSS in addition to SMT were allocated to SMT and SMT+PE groups, respectively; propensity score matching (PSM) was used to eliminate confounding bias. Short-term (28/90-day and 1-year) survival rates were calculated (Kaplan-Meier). Results: In total, 524 patients with HBV-ACLF were enrolled in this study; 358 received SMT alone (SMT group), and the remaining 166 received PE-based NB-ALSS in addition to SMT (SMT+PE group). PSM generated 166 pairs of cases. In the SMT+PE group, 28-day, 90-day, and 1-year survival rates were 11.90, 8.00, and 10.90%, respectively, higher than those in the SMT group. Subgroup analysis revealed that PE-based NB-ALSS had the best efficacy in patients with ACLF grade 2 or MELD scores of 30-40 (MELD grade 3). In MELD grade 3 patients who received SMT+PE, 28-day, 90-day, and 1-year survival rates were improved by 18.60, 14.20, and 20.10%, respectively. According to multivariate Cox regression analysis, PE-based NB-ALSS was the only independent protective factor for HBV-ACLF patient prognosis at 28 days, 90 days, and 1 year (28 days, HR = 0.516, p = 0.001; 90 days, HR = 0.663, p = 0.010; 1 year, HR = 0.610, p = 0.051). For those who received SMT+PE therapy, PE-based NB-ALSS therapy frequency was the only independent protective factor for short-term prognosis (28-day, HR = 0.597, p = 0.001; 90-day, HR = 0.772, p = 0.018). Conclusions: This multicenter prospective study showed that the addition of PE-based NB-ALSS to SMT improves short-term (28/90 days and 1-year) outcomes in patients with HBV-ACLF, especially in MELD grade 3 patients. Optimization of PE-based NB-ALSS may improve prognosis or even save lives among HBV-ACLF patients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Chen, Li, Xu, Zheng, Li, Wang, Huang, Gao, Qian, Liu, Lu, Shang, Li, Wang, Zhang, Meng and Chinese Chronic Liver Failure (CLIF) Consortium.)

Type 1 autoimmune pancreatitis (AIP) or chronic sclerosing sialadenitis (Küttner's tumour) is an uncommon disorder that has recently been confirmed as an IgG4-related disease. Here, we describe a rare case of a 53-year-old male patient who primarily presented with pancreatic body mass, left neck mass and several lumps in his lower lip mimicking pancreatic cancer (PC) and neck metastasis. The patient underwent pancreatic body mass and labial gland lumps resection as well as an ultrasound-guided biopsy of the left neck mass. He was diagnosed with IgG4-related focal type of AIP (f-AIP) and Küttner's tumour by immunohistochemistry. The patient responded well to corticosteroid therapy and remains healthy with no signs of recurrence at one year follow-up. The differentiation of f-AIP from PC is very important to avoid unnecessary pancreatic resection.

Objective: To identified the beta(2)-glycoprotein I (beta(2)GPI)-bound receptor on the membrane of hepatocellular carcinoma cells, and to analyze its function., Methods: Through the beta(2)GPI-affinity chromatography column, the peptide-polysome-mRNA complex specially binding to beta(2)GPI stayed with the column and was separated from the whole polysome of liver cells. Then it was eluted and collected. With the cDNA synthesis kit and cDNA PCR kit, the corresponding cDNA was obtained and sequenced. RT-PCR was used to amplify annexin II, and flow cytometry was used to study the competitive binding of annexin II with beta(2)GPI to SMMC-7721 cells., Results: 1.1 kb cDNA fragment of the specific binding protein of beta(2)GPI on liver cell membrane was obtained. And the sequence of cDNA shared a high homology with human annexin II (98%). Annexin II was expressed on the membrane of the hepatocellular carcinoma cells of the line SMMC-7721, and 1 microl and 4 microl of annexin II caused the binding rate of beta(2)GPI-GFP with SMMC-7721 cells from 15.58% to 13.66% and 7.56% respectively., Conclusion: The receptor of beta(2)GPI on the membrane of hepatocellular carcinoma cells is annexin II, and beta(2)GPI may help HBV invade hepatic cells through combing with annexin II on the liver cell membrane.

Aim: To evaluate the receptor protein which can specifically bind to beta(2)GP I on the membrane of hepatocellular carcinoma (HCC) cell line SMMC-7721, and to study the biological function of the receptor., Methods: Through beta(2)GP I -affinity chromatography column, the peptid-polysome-mRNA complex, which can specially bind to beta(2)GP I, stayed with the column and was separated from the whole polysome of liver cells, and then eluted and collected. Using cDNA synthesis kit and cDNA PCR kit, the corresponding cDNA was obtained and sequenced. RT-PCR was used to amplify annexin II, and flow cytometry was used to study the competitive binding of annexin II with beta(2)GP I to SMMC-7721., Results: A total of 1.1 kb of the cDNA fragment of the specific binding protein of beta(2)GP I on liver cell membrane was obtained. The sequence of cDNA shared high homology with human annexin II (98%). Annexin II was expressed on the membrane of SMMC-7721, and could compete with beta(2)GP I for combining with SMMC-7721., Conclusion: The receptor for beta(2)GP I on membrane of SMMC-7721 cells is annexin II, which might bridge HBV to infect hepatocytes.

Objective: To explore the relations of ulcerative colitis (UC) to anti-beta2-glycoproteinI antibodies (abeta(2)GPI) and platelet activation status., Methods: Peripheral blood samples were collected from 56 UC patients, 34 males and 22 females, aged 43.5 (21 - 66), including 36 in active stage and 20 in remission stage, and 25 sex- and age-matched controls. The level of abeta(2)GPI was detected by ELISA. The platelet activation markers, platelet activation complex-1 (PAC-1) and P-selectin (CD62P) were detected by immunofluorescence staining and flow cytometry., Results: The A value of IgG abeta(2)GPI of the active UC group was 0.61 +/- 0.13, significantly higher than those of the remittent UC group and the control group (0.50 +/- 0.13 and 0.22 +/- 0.14, both P < 0.01), and there was a significant difference between the remittent UC group and the control group (P < 0.01). The A value of IgM abeta(2)GPI of the active and remittent UC groups were 0.43 +/- 0.13 and 0.38 +/- 0.12, both significantly higher than that of the control group (0.20 +/- 0.12, both P < 0.01), however, there was no significant difference between the active UC and remittent UC groups (P > 0.05). The PAC-I positive rate of the active UC and remittent UC groups were 30.6% +/- 7.6% and 19.6% +/- 7.8%, both significantly higher than that of the control group (6.3% +/- 1.7%, both P < 0.01), and there was a significant difference between the active and remittent groups too (P < 0.01). The CD62P positive rates of the active UC and remittent UC groups were 45.0% +/- 8.8% and 31.9% +/- 7.8% respectively, both significantly higher than that of the control group (9.2% +/- 2.7%, both P < 0.01), and there was a significant difference between the active and remittent groups too (P < 0.01). In the active UC group, more severe the state of illness, the higher the A value of IgG abeta(2)GPI, and the positive rates of PAC-I and CD62P, and these values were all positively correlated with the state of illness (F(abeta2GPI) = 3.679, P < 0.05, F(PAC-I(%)) = 5.346, P < 0.01, and F(CD62P(%)) = 5.418, P < 0.01 respectively)., Conclusion: The abeta(2)GPI level and the platelet activation state are closely correlated with the pathogenesis and development of UC.

Objective: To further study the binding character of hepatitis B surface antigen (HBsAg) and beta 2-glycoprotein I (beta2GP I) and to explore whether beta2GP I plays an important role in the hepatotropism of hepatitis B virus., Methods: Using Western blot technique, we observed the binding character of the HBsAg with reduced and non-reduced beta2GP I., Results: rHBsAgs with reduced and non-reduced beta2GP I showed identical binding activity., Conclusions: The binding activity of HBsAg is dependent on tandem residues, but not on conformational structures of beta2GP I. There is a specific binding between HBV and beta2GP I, which may play an important role in HBV infection and is one of the reasons of hepatotropism of HBV.