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The karyotype is highly important for diagnosis and prognosis in myelodysplastic syndrome (MDS). The objective of the present study was to investigate the cytogenetic characteristics of patients with MDS in China. The karyotypes of 665 Chinese patients with MDS were analyzed, and it was identified that 298 cases (298/665, 44.8%) had abnormal karyotypes. Among the 298 patients with abnormal karyotypes, the 75 patients with trisomy 8 (+8) constituted the most common subset (75/298, 25.2%). The incidence of abnormal karyotypes was significantly higher in patients who were ≥51 years old compared with those <51 years old, (54.8 vs. 34.7%, respectively; P<0.05). Based on World Health Organization (WHO) classification-based Prognostic Scoring System (WPSS) criteria, the incidence of poor-prognosis karyotypes was significantly higher (17.4 vs. 5.4%; P<0.05) in the older patient group, and based on the Revised International Prognostic Scoring System (IPSS-R) criteria, the incidence of poor-/very poor-prognosis karyotypes was also significantly higher (17.4 vs. 6.6%; P<0.05) in patients ≥51 years old compared with younger ones. Based on the WHO classification of MDS subtypes, the incidence of abnormal karyotypes in patients with high percentages of bone marrow (BM) blasts [excess blasts (EB)-I + EB-II, ≥5% blasts] was significantly higher than that in patients with low percentages of BM blasts (those with single lineage dysplasia + multilineage dysplasia, <5% blasts) (62.5 vs. 36.0%; P<0.05). The incidence of poor-prognosis karyotypes based on WPSS criteria was significantly higher in patients with high percentages of BM blasts than those with low percentages (22.0 vs. 6.9%, respectively; P<0.05), and the incidence of poor-/very poor-prognosis karyotypes based on IPSS-R criteria was also significantly higher (23.0 vs. 7.4%, respectively; P<0.05). These results demonstrate that +8 is the most common abnormal karyotype in Chinese patients with MDS. Age and the percentage of BM blasts are associated with the incidence of both abnormal karyotypes and karyotypes with poor prognosis. The results of cytogenetic abnormalities in this study will supplement the data on patients of MDS in China. [ABSTRACT FROM AUTHOR]

Dysregulation of angiogenesis can be caused by hypoxia, which may result in severe diseases of the heart, including coronary artery disease. Hypoxia-inducible factor 1 (HIF-1) modulates angiogenesis via the regulation of several angiogenic factors. However, the underlying mechanism of hypoxia-induced angiogenesis remains unknown. In the present study, it was hypothesized that long non-coding RNA?(lncRNA) non-coding RNA activated by DNA damage (NORAD) may serve a role in the process of angiogenesis via the regulation of microRNA (miR)-590-3p under hypoxic conditions. The effect of NORAD and miR- 590-3p on cell viability and properties associated with angiogenesis, including cell migration and tube formation in human umbilical vein endothelial cells (HUVEC s) under hypoxic conditions, were assessed. Potential downstream angiogenic factors of miR- 590-3p were also determined by molecular experiments. It was identified that NORAD expression was upregulated and miR- 590-3p expression was downregulated in hypoxia-exposed HUVEC s, and also in myocardial infarction (MI) left ventricle tissues in mice. Moreover, downregulation of NORAD expression resulted in decreased cell viability and angiogenic capacity, but further knocking down miR- 590-3p expression reversed these alterations, resulting in increased cell migration and tube formation in HUVEC s under hypoxic conditions for 24 h. It was demonstrated that NORAD overexpression also increased cell vitality and tube-formation capacity. Furthermore, NORAD was identified to bind with miR- 590-3p directly, and miR- 590-3p was shown to target certain proangiogenic agents, such as vascular endothelial growth factor (VEGF)A, fibroblast growth factor (FGF)1 and FGF2 directly. Therefore, the present results suggested that lncRNA NORAD may bind with miR- 590-3p to regulate the angiogenic ability of HUVEC s via the regulation of several downstream proangiogenic factors under hypoxia. Thus, the lncRNA NORAD/miR- 590-3p axis may be a novel regulatory pathway in the angiogenic mechanisms in HUVEC s, which highlights a potentially novel perspective for treating ischemia/hypoxia-induced angiogenic diseases. [ABSTRACT FROM AUTHOR]