ATP-binding cassette protein E (ABCE1) has been annotated as an Rnase L inhibitor in eukaryotes. Previous study showed that the overexpression of ABCE1 was related with the occurrence and clinical stage of lung adenocarcinoma. As an initial investigation into the novel functions of ABCE1, siRNA-expressing vectors targeting sites of the ABCE1 gene were constructed from RNAi-Ready pSIREN-DNR-DsRed-Express vector. Cultured 95-D and NCI-H446 lung carcinoma cells were transfected with the siRNA-expressing vectors using FuGENE 6 and transfection efficiency was determined by using fluorescence microscopy. The expression level of ABCE1 protein was determined by Western blot and immunofluorescence staining. Cell viability was determined by MTT, cell cycle was analysed by flow cytometry.The apoptotic rate was observed by ELISA. Fluorescence microscopy showed a satisfactory transfection efficiency which was about 42.70%. Cell viability and the growth fraction were markedly suppressed, whereas the apoptosis was significantly increased in SiRNA-95-D and SiRNA-NCI-H446 cells than controls(P< 0.05). It can be concluded that the siRNA targeting ABCE1 gene shows a dramatic inhibitory effect on RNA transcription and protein expression and a promoting effect on the apoptosis in 95-D/NCI-H446 cells, which offers a reliable base for the further in vivo experiment.

Fatigue, which is one of the most commonly reported symptoms in cancer, can negatively impact the functional status and the health-related quality of life of individuals. Although awareness and
study of CRF have grown in recent years,the biological mechanisms and risk factors that induce CRF remain unclear.This paper systematically reviews the available evidence on the biological mechanisms and the risk factors to guide the development of targeted, individualized interventions for cancer-related fatigue.

Fatigue is commonly experienced in patients with advanced kidney disease and associated with poor outcomes. The purpose of this review was to discuss the prevalence, assessment methods and contributing factors of fatigue in patients with end-stage renal disease (ESRD), and also examined possible interventions to improve fatigue and concludes by defining some future research directions.

Objective:To quantify the plasma concentrations of inorganic arsenic (As(III) and As(V)) and methylated metabo-lites ( MMA and DMA) , and to detect the total amount of arsenic in blood cells and plasma by high performance liquid chromatogra -phy-hydridegeneration-atomic fluorescence spectrometry ( HPLC-HG-AFS) and HG-AFS methods to clarify the arsenic species in acute promyelocytic leukemia (APL) patients.Methods:The blood cells and plasma were digested by the mixture of HNO 3-H2O2 and ana-lyzed by HG-AFS.For the arsenic species , the plasma samples were prepared with perchloric acid to precipitate protein .The superna-tant was separated on an anion-exchange column in 6 min with isocratic elution using 13 mmol · L-1 CH3 COONa, 3 mmol · L-1 NaH2 PO4 , 4 mmol· L-1 KNO3 and 0.2 mmol· L-1 EDTA-2Na.Results:The methods provided linear range of 0.2-20 ng· ml-1 for total arsenic and 2.0-50 ng· ml-1 for four arsenic species (r>0.9950).The spiked recoveries ranged from 81.2％to 108.6％, and the coefficients of variation for intra-and inter-batch precision were less than 9.3％and 12.5％, respectively.The developed methods were applied successfully in the assay of total arsenic and arsenic species in 5 APL patients.Conclusion:The method is simple, fast and accurate , which can be applied in the assay of arsenic compounds in plasma and blood cells in APL patients .

Osteoporosis can be induced by various factors including prolonged glucocorticoid usage, diminished estrogen levels, secondary hyperparathyroidism, and alterations in the microenvironment of bone tissue. The bone metabolism imbalance(osteogenic-lipogenic imbalance) plays a crucial role in the development of osteoporosis. This imbalance is primarily driven by an increase in the differentiation of bone marrow mesenchymal stem cells into adipocytes and a decrease in their differentiation into osteoblasts, thus forming the core of the osteogenic-lipogenic imbalance observed in osteoporosis. The bone morphogenesis protein(BMP) plays a crucial role in the regulation of the osteogenic-lipid balance in osteoporosis. This regulatory function is accomplished through both the Smad-dependent and Smad-independent pathways. This review centers on the Smad-dependent and Smad-independent pathways facilitated by BMP, offering a comprehensive overview of the potential mechanisms through which BMP-2, 4, 6, 7, and 9 contribute to the regulation of osteogenesis and lipid metabolism in osteoporosis via these pathways. In order to present novel insights for the identification of efficacious targets for clinical anti-osteoporosis medications.