BackgroundThis study aimed to investigate the effect of deferoxamine (DFO) on leukemia in vitro, and to explore the underlying molecular mechanism.Material/MethodsK562 leukemia cells were treated with various concentrations of DFO (10, 50, and 100 μmol/l) with or without 10 μmol/l ferric chloride for 12 h. Then, total cellular iron was detected. CCK-8 kit and flow cytometry were used for cell viability and apoptosis detection. In addition, expression of apoptosis-related genes was determined by Western blotting and qRT-PCR, respectively.ResultsThe results suggested that DFO significantly inhibited K562 cell viability and induced cell apoptosis in a dose-dependent manner. We also found that the protein and mRNA levels of Bax, p53, and Fas dose-dependently increased in DFO-treated K562 cells, while the level of Bcl-2 markedly decreased in a dose-dependent manner. Moreover, the findings showed that ferric chloride eliminated these effects on K562 cells caused by DFO treatment.ConclusionsOur results indicate that DFO plays a protective role in leukemia via inhibiting leukemia cell viability and inducing cell apoptosis by the regulation of apoptosis-related genes expression.
Background: The present study aimed to use the targeted capture and sequencing technique to diagnose adult hereditary spherocytosis (HS). These results were compared with clinical features and laboratory examinations to explore the diagnosis of HS.Methods: Whole blood and clinical data from ten patients with HS were collected. Genomic DNA was extracted, and a library was prepared. Exomes of patients with ten HS-related genes encoding red cell membrane skeleton protein were captured and sequenced. Bioinformatics analyses were carried out throughout the 1000 Genomes Project, ExAC, dbSNP147, and 1000 Normal Han Population databases.Results: Gene mutations were found in 9 out of 10 cases of HS. Our data validation showed 90% specificity. Three types of gene mutations were found, including 6 cases of SPTB, 3 cases of ANK1, and 2 cases of SLC4A1. There were 4 mutation forms, including nonsense mutation, missense mutation, shear mutation, and code shift mutation, all of which were new, heterozygous mutations. These variations were predicted to be pathogenic in four databases.Conclusions: Our data demonstrate that targeted gene enrichment and sequencing methods were an efficient tool for determining genetic etiologies of red blood cell (RBC) membrane disorders and can facilitate accurate diagnosis and genetic counseling. They are also in good agreement with the clinical results.
Hereditary spherocytosis (HS) is often misdiagnosed due to lack of specific diagnostic methods. Our study summarized clinical characteristics and described the diagnostic workflow for mild and moderate HS in Chinese individuals, using data from 20 adults, 8 of whom presented a familial history for HS. We used scanning electron microscopy (SEM) to diagnose HS. We observed reduced eosin maleimide fluorescence activity (5.50 mean channel fluorescence (MCF) units) in the 10 cases of HS, which differed significantly when compared with 10 normal adults (15.50 units), iron deficiency anemia (15.50 MCF units), and megaloblastic anemia (12.00 MCF units) values (P < .05). Next generation sequencing results revealed that 9 out of 10 patients were found to have mutations in the spectrin alpha chain (SPTB), anchor protein (ANK1), and SLC4A1 genes. These mutations were not reported in the Human Gene Mutation Database (HGMD), 1000 human genome, ExAC, and dbSNP147 databases. Splenectomy proved to be beneficial in alleviating HS symptoms in 10 cases. It was found that for the diagnosis of HS, SEM and next generation gene sequencing method proved to be more ideal than red blood cell membrane protein analysis using sodium dodecyl sulfate polyacrylamide gel electrophoresis and western blotting.
Objective:To explore the effect of mother's own milk (MOM) feeding time on the risk of moderate and severe bronchopulmonary dysplasia (BPD) in infants with very low birth weight (VLBW).MethodsClinical data from 630 infants with VLBW were retrospectively analyzed. Participants were divided into the early mother's own milk (EMOM) feeding group (first mother's own milk feeding time ≤72 h after birth, n = 397) and the late mother's own milk (LMOM) feeding group (first mother's own milk feeding time >72 h after birth, n = 233). Differences in the incidence of moderate and severe BPD among the two groups were analyzed using the chi-square test. Effects of MOM feeding time on the incidence of moderate and severe BPD were evaluated using univariate and multivariate logistic regression analysis.ResultsThe incidences of moderate and severe BPD in the EMOM feeding group and the LMOM feeding group were 13.9% (55/397) and 21.0% (49/233), respectively (P = 0.019). Variate logistic regression analysis showed that the LMOM feeding group had an increased risk of moderate and severe BPD compared with the EMOM feeding group (OR = 1.656, 95% CI:1.083–2.532). The results of multivariate logistic regression analysis showed that the LMOM feeding group had an increased risk of moderate and severe BPD compared with the EMOM feeding group (OR = 1.894, 95% CI:1.127–3.185).ConclusionThe first time of MOM feeding within 72 h after birth and the persistence of mother's own milk feeding during hospitalization can reduce the incidence of moderate and severe BPD in infants with VLBW.
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