Decitabine combined with CAG regimen in the treatment of elderly patients with acute myeloid leukemia.

OBJECTIVE: To analyze the efficacy and safety of decitabine combined with CAG ((cytarabine + aclacinomycin + granulocyte colony stimulating factor)) regimen and CAG regimen alone in the treatment of elderly acute myeloid leukemia. METHODS: 96 elderly patients with acute myeloid leukemia who were admitted to our hospital from July 2015 to July 2017 were randomly divided into an observation group and a control group, 48 cases in each group. The patients in the control group were treated with CAG regimen, while the patients in the observation group were treated with decitabine on the basis of the control group. The clinical curative effect, changes of immune indicators, occurrence of adverse reactions and survival rate at different time after treatment were compared between the two groups. RESULTS: The total effective rate of the observation group was significantly higher than that of the control group (P<0.05). After treatment, the indicators of cellular immunity in the two groups were significantly lower than those before treatment, and the indicators of cellular immunity in the observation group were significantly lower than those in the control group (P<0.05). There was no significant difference in the incidence of adverse reactions between the two groups (P>0.05). The 9-month survival rate and 1-year survival rate in the observation group were significantly higher than those in the control group (P<0.05). CONCLUSION: The combination of decitabine and CAG regimen is effective in the treatment of elderly patients with acute myeloid leukemia. The therapy can fully inhibit cellular immune function and improve long-term survival rate, and its safety has a small difference with that of CAG regimen alone. It is worth clinical promotion.

Decreased Serum miR-1296 may Serve as an Early Biomarker for the Diagnosis of Non-Alcoholic Fatty Liver Disease.

BACKGROUND: Circulating microRNA has become a candidate biomarker for many diseases. The purpose of this study was to investigate the significance of miR-1296 as a non-invasive biomarker in nonalcoholic fatty liver disease (NAFLD). METHODS: Serum samples were collected from normal people and NAFLD patients for biochemical detection. Serum microRNAs were isolated by the NucleoZOL method, and the stem-loop method was used to reverse transcribe the DNA. The relative quantification of miR-1296 was performed by SYBR Green method. Spearman's method was used to analyze the correlation between miR-1296 and serum biochemical parameters. RESULTS: By using 2-∆∆CT method, we found that, compared with the normal control group, the expression of serum miR-1296 increased in patients with normal lipid NAFLD and those with hyperlipidemia NAFLD. At the same time, the expression of microRNA-1296 in the NAFLD hyperlipidemia group increased more significantly than that in the NFALD group with normal lipid. Spearman's correlation assay demonstrated that the correlation between the expression of miR-1296 and blood lipids, including TC, TG, HDL-c, and LDL-c, was TC (r = 0.4951, p = 0.0013), TG (r = 0.054, p = 0.6425), HDL-C (r = 0.3435, p = 0.07522), and LDL-C (r = 0.3307, p = 0.0699. The data showed that miR-1296 was positively correlated with serum TC level. CONCLUSIONS: In summary, serum microRNA-1296 is a more sensitive marker of NAFLD than blood lipids, which provides a new method for noninvasive early screening of NAFLD.

Emodin relieved lipopolysaccharide-evoked inflammatory damage in WI-38 cells by up-regulating taurine up-regulated gene 1.

BACKGROUND: Neonatal pneumonia (NP) has a high fatality rate in neonatal illness. This research investigated the functions of emodin on lipopolysaccharide (LPS)-evoked inflammatory injury in WI-38 cells. METHODS: Cell counting kit-8 (CCK-8) assay and flow cytometry were utilized for examining the impacts of LPS and emodin on viability and apoptosis, respectively. Taurine up-regulated gene 1 (TUG1) level was altered through cell transfection and investigated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Moreover, RT-qPCR, western blot and enzyme-linked immunosorbent assay (ELISA) were utilized for investigating expressions of monocyte chemoattractant protein-1 (MCP-1) and interleukin (IL)-6. Western blot was carried out for investigating the levels of Bcl-2, Bax, pro-Caspase-3, cleaved-Caspase-3 and NF-κB and p38MAPK pathway-related proteins. RESULTS: LPS treatment restrained cell viability, enhanced apoptosis, and expressions of inflammation-related IL-6 and MCP-1. Emodin alleviated LPS-evoked inflammatory injury and restrained the NF-κB and p38MAPK pathways. Furthermore, emodin positively regulated TUG1 expression and TUG1 silencing could reverse the efficacy of emodin on IL-6 and MCP-1 expressions. Finally, TUG1 regulates the expression of inflammatory factors through NF-κB and p38MAPK pathways. CONCLUSION: Emodin alleviated LPS-evoked inflammatory injury by raising TUG1 expression via NF-κB and p38MAPK pathways in WI-38 cells.