CircFN1 promotes acute myeloid leukemia cell proliferation and invasion but refrains apoptosis via miR-1294/ARHGEF10L axis.

Previous studies have proved circFN1 is highly expressed in acute myeloid leukemia (AML) patients and AML cell lines. This study aims to investigate the impact of circFN1 on AML and its mechanism. Via real-time quantitative PCR to detect circFN1, miR-1294, ARHGEF10L expressions in clinical plasma samples and AML cell lines, AML cells were cultured in vitro and transfected with si-circFN1, pcDNA3.1-circFN1, and si-ARHGEF10L, respectively, or co-transfected pcDNA3.1-circFN1 + miR-1294 mimic and pcDNA3.1-circFN1 + si-ARHGEF10L. Using dual luciferase reporter experiment to detect the relationship between circFN1 and miR-1294, as well as miR-1294 and ARHGEF10L. CCK-8 was used to detect cell proliferation, Transwell to cell invasion, TUNEL staining and flow cytometry to detect cell apoptosis, RT-qPCR to circFN1 RNA, miR-1294, and ARHGEF10L expression levels in HL-60 cells, and western blot to ARHGEF10L protein expression level in HL-60 cells. We found highly expressed circFN1 and ARHGEF10L, as well as low-expressed miR-1294 in AML patients and AML cell lines. In contrast to si-NC group, si-circFN1 group could signally inhibit HL-60 cell proliferation and migration, but promote cell apoptosis; compared with mimic NC group, miR-1294 mimic group could visually inhibit HL-60 cell proliferation and migration, but promote cell apoptosis. miR-1294 was the target of circFN1, and ARHGEF10L was the target of miR-1294. Over-expressing miR-1294 or silencing ARHGEF10L could signally inhibit circFN1 promoting HL-60 cell proliferation and migration and repressing cell apoptosis. circFN1 promotes proliferation and invasion of AML cell and represses cell apoptosis via regulating miR-1294/ARHGEF10L axis, which provides new insight for molecular targeted-treatment for AML.

Relationships among lymphocyte subsets, cytokines, and the pulmonary inflammation index in coronavirus (COVID-19) infected patients.

We explored the relationships between lymphocyte subsets, cytokines, pulmonary inflammation index (PII) and disease evolution in patients with (corona virus disease 2019) COVID-19. A total of 123 patients with COVID-19 were divided into mild and severe groups. Lymphocyte subsets and cytokines were detected on the first day of hospital admission and lung computed tomography results were quantified by PII. Difference analysis and correlation analysis were performed on the two groups. A total of 102 mild and 21 severe patients were included in the analysis. There were significant differences in cluster of differentiation 4 (CD4+ T), cluster of differentiation 8 (CD8+ T), interleukin 6 (IL-6), interleukin 10 (IL-10) and PII between the two groups. There were significant positive correlations between CD4+ T and CD8+ T, IL-6 and IL-10 in the mild group (r2  = 0·694, r 2  = 0·633, respectively; P < 0·01). After 'five-in-one' treatment, all patients were discharged with the exception of the four who died. Higher survival rates occurred in the mild group and in those with IL-6 within normal values. CD4+ T, CD8+ T, IL-6, IL-10 and PII can be used as indicators of disease evolution, and the PII can be used as an independent indicator for disease progression of COVID-19.

"Five-Early" Model: The Magic Weapon against COVID-19.

BACKGROUND: COVID-19(2019 novel coronavirus disease)has brought tremendous pressure to the prevention and control of the national epidemic due to its concealed onset, strong infectivity and fast transmission speed. METHODS: In this retrospective study, 226 patients diagnosed with 2019 novel coronavirus pneumonia (NCP) in the Chongqing University Three Gorges Hospital were included. The patients' clinical data, including general information, initial symptoms at the onset, time of disease diagnosis, time to treatment in hospital, time of nucleic acid conversion to negative, disease classification, total time of hospitalization were collected. The clinical data of the mild and severe patients were compared. RESULTS: Fever, cough, sore throat, poor appetite andfatigue were the main symptoms of the diagnosed patients. The time of diagnosis was significantly shorter in the mild patients (4.96 ± 4.10 days) than severe patients (7.63 ± 9.17 days) (P=0.004). Mild patients had shorter time to treatment in hospital (6.09 ± 4.47 vs. 8.71 ± 9.04 days) and less time of nucleic acid conversion to negative (7.58 ± 2.51 vs. 11.6 ± 4.67 days) compared to the severe patients. CONCLUSION: The above results can be used as a quantitative basis for the "five-early"(early detection, early screening, early diagnosis, early isolation treatment, and early recovery) model. The government, the masses, and the hospitals' joint prevention and optimization of the "five-early" model will provide important scientific reference for further prevention and control of the epidemics.

Comparison of the Efficacy of Nilotinib and Imatinib in the Treatment of Chronic Myeloid Leukemia.

OBJECTIVE: To compare the efficacy of nilotinib and imatinib in the treatment of chronic myeloid leukemia (CML). STUDY DESIGN: Analytical study. PLACE AND DURATION OF STUDY: Department of Hematology, Chongqing Three Gorges Central Hospital, China, from January 2016 to January 2018. METHODOLOGY: Eighty patients with CML were randomly divided into the nilotinib group (treated with nilotinib) and the imatinib group (treated with imatinib), 40 patients in each group. The therapeutic effects of the two groups of patients were compared. RESULTS: After months of treatment, the neutrophilic granulocytes and neutrophilic metamyelocyte, serum interleukin (IL)-6 and IL-8 and α1-acid glycoprotein (AGP) levels in nilotinib group were lower than those in imatinib group (p=0.002, p<0.001, p=0.027, p=<0.001 and p=0.001, respectively); the proportion of patients with BCR-ABLIS <10% in nilotinib group and the proportion of patients with BCR-ABLIS <0.0032% were higher than those in imatinib group (p=0.032 and 0.043, respectively). During treatment period, there was no significant difference in the incidence of adverse reactions such as mild liver damage, nausea and vomiting, rash, musculoskeletal pain and edema between two groups (p = 0.556, 0.396, 0.576, 0.775 and 0.390, respectively). CONCLUSION: Nilotinib is superior to imatinib in the treatment of CML. There is no significant difference in the safety of the two drugs, and the adverse reactions can be tolerated.

Effects of magnesium isoglycyrrhizinate on AST, ALT, and serum levels of Th1 cytokines in patients with allo-HSCT.

This study aimed to investigate the protective effects of magnesium isoglycyrrhizinate (MGL) on aspartate aminotransferase (AST), alanine aminotransferase (ALT), and serum levels of T helper 1 (Th1) cytokines in patients with allogeneic hematopoietic stem cell transplantation (allo-HSCT). The study included 42 patients prepared for allo-HSCT, who were divided equally into MGL and reduced glutathione groups. The ALT and AST levels were detected 1day before pretreatment and transplantation, and 7, 14, and 21days after transplantation. The total days and times of fever, treatment time of patients in the laminar flow room, white blood cell (WBC) count, platelet (PTL) implantation time, and success rate of transplantation were recorded. The serum levels of Th1/Th2 cytokines were detected. MGL had a significant protective effect on AST 1day before transplantation and 7, 14, and 21days after transplantation, while ALT had a statistical difference only 7days after transplantation. MGL could shorten the duration of fever during transplantation and advance the WBC and PTL implantation time. Significant differences in Th1-like cytokines (P<0.05) and higher levels of Th2-like cytokines but with no statistical significance (P>0.05) were found in the MGL group compared with the control group. MGL had significant protective effects on AST after transplantation. MGL could reduce the duration of fever during transplantation, help the reconstruction and recovery of WBCs and PTLs, and regulate Th1 cytokines, revealing its protective effects on hepatic transaminases and graft versus host disease in allo-HSCT patients.