Objective: To investigate the efficacy and safety of Yadanzi ® (Javanica oil emulsion injection) combined with chemotherapy for treatment of patients with advanced gastric cancer. Methods: From January 2011 to December 2012, we recruited 75 patients with advanced gastric cancer, who received javanica oil emulsion injection together with chemotherapy. After two cycles of treatment, efficacy and safety of the combined therapies were evaluated. Results: Overall response rate of 75 patients after treatment was 85.3% (CR+PR+SD). Treatment related side effects were recorded. No treatment related death occurred. Conclusions: Javanica oil emulsion injection combined with chemotherapy could be considered as a safe and effective regimen in treating patients with advanced gastric cancer. Further randomized clinical trials should be conducted to confirm whether the addition of Yadanzi ® to chemotheraphy could be associated with reduced toxicity, enhanced tolerability and improved quality of life for patients with advanced gastric cancer.

Background Gastric cancer (GC) is a malignant tumor with a significantly high mortality rate, yet, its pathogenesis is not fully understood. Bioinformatics predicted that LINC01224 is highly expressed in stomach adenocarcinoma (STAD), and showed that LINC01224 adsorbed miR‐193a‐5p to target CDK8. Therefore, this study intended to verify the effect of the LINC01224/miR‐193a‐5p/CDK8 axis on the biological behavior of gastric cancer. Methods Expressions of LINC01224, miR‐193a‐5p, CDK8, apoptosis‐, and EMT‐related genes were analyzed using the GEPIA website, RT‐qPCR, in situ hybridization, and Western blot as needed. Bioinformatics and dual luciferase assay were used to evaluate the relationship between LINC01224, miR‐193a‐5p, and CDK8. Functional experiments and rescue experiments (MTT assay, flow cytometry, wound healing assay, and Transwell) were conducted to detect the effects of the above genes on the biological characteristics of GC cells. Tumorigenesis assay was used to verify the results of in vitro experiments. Results LINC01224 adsorbed miR‐193a‐5p to target and upregulate CDK8. The expressions of LINC01224 and CDK8 were increased, while the expression of miR‐193a‐5p was decreased in GC. Overexpressed LINC01224 promoted cell viability, migration and invasion, accelerated tumor formation, attenuated apoptosis, inhibited the expressions of apoptosis‐related proteins, and promoted the expressions of EMT‐related proteins, whereas silenced LINC01224 led to the opposite effect. MiR‐193a‐5p inhibitor partially offset the effect of silenced LINC01224; interestingly, siCDK8 significantly reversed the effect of miR‐193a‐5p inhibitor on GC cells. Conclusion LINC01224 affects the biological behavior of gastric cancer by mediating miR‐193a‐5p to regulate CDK8.

Large granular lymphocytic leukemia (LGLL) is a chronic clonal lymphoproliferative disease of mature T or NK cells, and produces a variety of hematological abnormalities. Pure red cell aplasia (PRCA) is a rare haematological disease and is one of the most common complications of LGLL. LGLL-associated PRCA may represent a relatively indolent type and may be more common than reported, but its natural history and clinical course have not been well described. The ethnic origin of the patients is an important consideration in determining the relationship between PRCA and LGLL. Guidelines and progresses for management of LGLL-associated PRCA rely on accumulation of empirical experiences, integrative analyses of several cases and clinical trials. The purpose of this review is to evaluate occurrence, possible mechanisms, diagnosis, clinical features, treatments and outcomes of LGLL-associated PRCA.

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The Fuling (Poria cocos)-Guizhi (Cinnamomi ramulus) herb pair (FGHP) is a commonly used traditional Chinese herbal formula with coronary heart disease (CHD) treatment potential. However, the mechanism of FGHP in the treatment of CHD was still unclear. In this study, the action targets and underlying mechanism of FGHP against CHD were successfully achieved by combined network pharmacology prediction with experimental verification. 76 common targets were screened out by overlapping the chemical-protein data of FGHP and CHD-related targets. Then, two key targets were further selected for verification by using western blot analysis after analyzing PPI, GO function, and KEGG pathway. Results indicated FGHP could alleviate CHD syndromes and regulate inflammatory responses in acute myocardial ischemia rats, and the reduction of expression of TNF-α and IL-6 in myocardial tissue would be one of its possible underlying mechanisms. Our work demonstrated that network pharmacology combined with experimental verification provides a credible method to elucidate the pharmacological mechanism of FGHP against CHD.