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Aim: The study was conducted to evaluate the feasibility and safety profile of hepatic arterial infusion chemotherapy with oxaliplatin, 5‐fluorouracil, and leucovorin (HAIC‐FOLFOX) as an alternative therapeutic choice for patients with advanced hepatocellular carcinoma (HCC) that is refractory to systemic treatment including immune checkpoint blockades or molecular targeting agents. Methods: Two hundred and forty five consecutive patients with advanced HCC who received HAIC‐FOLFOX treatment after systemic treatment failure were retrospectively reviewed in six institutions and their survival, tumor response, and tolerance were assessed. Results: The median overall survival (OS) and progression‐free survival of the 209 included participants were 10.5 months (95% confidence interval [CI], 8.1–12.9) and 6.0 months (95% CI, 5.1–6.9), respectively. According to Response Evaluation Criteria in Solid Tumors 1.1 criteria, the objective response rate was 21.1%, and the disease control rate was 64.6%. Multivariate analysis of risk factors of OS were albumin–bilirubin grade (2 and 3 vs. 1, hazard ratio [HR] 1.57; 95% CI, 1.05–2.34; p = 0.028), tumor number (>3 vs. 1–3, HR 2.18; 95% CI, 1.10–4.34; p = 0.026), extrahepatic spread (present vs. absent, HR 1.61, 95% CI, 1.06–2.45; p = 0.027), synchronous systemic treatment (present vs. absent, HR 0.55, 95% CI, 0.37–0.83; p = 0.004) and treatment response (responder vs. nonresponder, HR 0.30, 95% CI, 0.17–0.53; p < 0.001). Grade 3–4 adverse events (AEs) occurred in 59 (28.2%) HCC patients. All AEs were manageable, and deaths related to hepatic artery infusion chemotherapy treatment were not observed. Conclusions: Our findings support the effectiveness and safety of HAIC‐FOLFOX treatment for patients with advanced HCC who have failed systemic treatment. [ABSTRACT FROM AUTHOR]

Objective: To observe the therapeutical effects of esculentoside A (EsA) on rats with mesangial proliferative glomerulonephritis (MsPGN) induced by anti-Thy1.1 antibody and make a comparison of the effects between EsA and dexamethasone (DXM)., Methods: Wistar rats with MsPGN induced by anti-Thy1.1 serum (ATS) were randomly divided into 3 groups: EsA group, DXM group, and model group. Moreover, a normal group was used for comparison. The BUN, SCr, urinary protein and renal pathological changes were examined after 7 d treatment with EsA and DXM., Results: The urinary protein, cell count and mesangium area of glomerulus were significantly higher in all modeled groups than in normal group (P<0.001-0.05), and they were significantly lower in the treated groups than in untreated group (P<0.001-0.01)., Conclusion: The results suggest that EsA is effective for reducing the urinary protein excretion and inhibiting the proliferation process of glomerular mesangium and matrix in rats with MsPGN.

Objective: To probe into the pathogenesis of rat mesangial proliferative glomerulonephritis (MsPGN) induced by anti-Thy1 antibody., Methods: Anti-Thy1 serum was produced, and then intravenously injected into Wistar rats for establishing an experimental model of MsPGN. The control group received intravenous injection of normal saline. Urinary volume and urinary protein were examined every other day. The IL-1, IL-6 and TNF contents of serum were detected by radioimmunoassay. Pathologic morphology of renal section was observed with micrscope and BI2000 Image Analysis System. The rats of model group were killed on the 1st, 3rd, 5th and 7th days., Results: No significant difference was seen between the model group and control group in regard to the volume of urine and in-take water (P > 0.05). The levels of urinary protein, IL-1, IL-6 and TNF in model group were significantly higher than those in control group at all time points (P < 0.001-0.005). Glomerular mesangium cells and matrix in the model group were obviously proliferative, compared with those in control group., Conclusion: It is suggested that cytokine plays an important role in the onset of MsPGN.