Seventh Peoples Hospital of Zhengzhou
Seventh Peoples Hospital of Zhengzhou
Yuan D.-D.,Peking University |
Yuan D.-D.,Seventh Peoples Hospital of Zhengzhou |
Xiang Q.,Peking University |
Zhou Y.,Peking University
Chinese Pharmaceutical Journal | Year: 2014
OBJECTIVE: To explore the key points of work for clinical pharmacists in individualized anticoagulant therapy in patients with atrial fibrillation. METHODS: The pharmacists participated in the development of the regimen of warfarin anticoagulation and its supervision for prevention of embolism complications in one case of aged patient with non valvular disease combined with diabetes. RESULTS: The anticoagulant intensity and the combination regiment of warfarin with heparin were determined according to the characteristics of the patient. Patient self-monitoring and awareness of influencing factors were improved through the medical education by clinical pharmacists. CONCLUSION: Design of individualized medication regimen and medication supervision should be the breakthrough point of clinical pharmacists.
Yang J.,Zhengzhou University |
Lyu X.,Zhengzhou University |
Zhu X.,Zhengzhou University |
Meng X.,Seventh Peoples Hospital of Zhengzhou |
And 3 more authors.
Oncology Letters | Year: 2017
The chromosomal translocation t(7;11)(p15;p15) and the resulting nucleoporin 98-homeobox A9 (NUP98-HOXA9) gene fusion is rare but recurrent genetic abnormity in acute myeloid leukemia (AML). The present study describes a case of AML plus maturation (-M2) with multilineage dyspoiesis in a 30-year-old male in whom a 46,XY,t(7;11)(p15;p15) karyotype was detected through chromosome analysis. Subsequent molecular and sequencing analysis demonstrated a NUP98-HOXA9 fusion gene with a type I fusion between NUP98 exon 12 and HOXA9 exon 1b, and mutations in neuroblastoma V-Ras oncogene homolog and Wilms tumor 1. The patient achieved hematological complete remission (CR) following two courses of induction chemotherapy. However, the NUP98-HOXA9 fusion gene remained detectable during the hematological CR period and following intensive consolidation chemotherapy. The disease relapsed 11 months after diagnosis, and the patient became refractory, with complications from an infection causing eventual mortality. The present case and literature review suggest that patients with AML and t(7;11) may have unique biological and clinical characteristics, and a poor prognosis. © 2017, Spandidos Publications. All rights reserved.
Zhang S.,Seventh Peoples Hospital of Zhengzhou |
Zhao Y.,PLA Fourth Military Medical University |
Xu M.,PLA Fourth Military Medical University |
Yu L.,Seventh Peoples Hospital of Zhengzhou |
And 5 more authors.
PLoS ONE | Year: 2013
Cardiac microvascular endothelial cells (CMECs) dysfunction induced by hypoxia is an important pathophysiological event in myocardium ischemic injury, whereas, the underlying mechanism is not fully clarified. FoxO transcription factors regulate target genes involved in apoptosis and cellular reactive oxygen species (ROS) production. Therefore, the present study was designed to elucidate the potential role of FoxOs on the hypoxia-induced ROS formation and apoptosis in CMECs. Exposure to low oxygen tension stimulated ROS accumulation and increased apoptosis in CMECs within 6-24 h. Hypoxia also significantly increased the expressions of HIF-1α and FoxO3a. However, hypoxia decreased the phosphorylation of Akt and FoxO3a, correlated with increased nuclear accumulation. Conversely, the expression of FoxO1 was not significantly altered by hypoxia. After inhibition of HIF-1α by siRNA, we observed that hypoxia-induced ROS accumulation and apoptosis of CMECs were decreased. Meanwhile, knockdown of HIF-1α also inhibited hypoxia induced FoxO3a expression in CMECs, but did not affect FoxO1 expression. Furthermore, hypoxia-induced ROS formation and apoptosis in CMECs were correlated with the disturbance of Bcl-2 family proteins, which were abolished by FoxO3a silencing with siRNA. In conclusion, our data provide evidence that FoxO3a leads to ROS accumulation in CMECs, and in parallel, induces the disturbance of Bcl-2 family proteins which results in apoptosis. © 2013 Zhang et al.