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Update on Rivaroxaban 利伐沙班的最新进展
IF 3 Q2 Medicine Pub Date : 2010-01-01 DOI: 10.4137/CMBD.S5101
O. Moussa, D. Chattopadhyay, V. Bhattacharya
Anticoagulants are recommended for the prevention and treatment of venous thromboembolism (VTE). The new anticoagulants which target specific factors in the coagulation cascade offer the advantage that they can be administered orally. These drugs seek to offer safe anticoagulation without the need for regular monitoring and frequent dose adjustment. Some of these newer drugs are in the advanced stages of clinical trials or have already completed them and thereby aim to provide more options in the management of thromboembolism. In the present review we discuss the currently available evidence supporting the use of these new anticoagulants, in particular rivaroxaban.
抗凝剂被推荐用于预防和治疗静脉血栓栓塞(VTE)。针对凝血级联中的特定因子的新型抗凝剂具有口服给药的优势。这些药物寻求提供安全的抗凝,而不需要定期监测和频繁调整剂量。其中一些新药正处于临床试验的后期或已经完成,因此旨在为血栓栓塞的治疗提供更多的选择。在本综述中,我们讨论了目前可用的证据支持使用这些新的抗凝剂,特别是利伐沙班。
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引用次数: 1
Birth MCV and MCH are Quite Reliable Parameters for the Prediction of Alpha Thalassemia Trait 出生MCV和MCH是预测α地中海贫血性状的较为可靠的参数
IF 3 Q2 Medicine Pub Date : 2009-01-01 DOI: 10.4137/CMBD.S1927
Altaee Akram, Abu Saud Khalida, S. Sawsan, L. Charles
To assess some simple blood parameters at birth that can be used as a basis to suspect α-thalassemia minor (ATM), a prospective study involving 202 consecutive neonates with MCV of less than 95 fl or less were checked for Hb Barts by HPLC. The group was divided into two, one with an MCV of 90-95 (89 cases) and the other with an MCV below 90 (113 cases). For control, 104 consecutive neonates with an MCV ≥ 95 fl were similarly checked. It has been confirmed that an MCV that is below 90 fl, especially with and MCH of ≤30 pg is a strong indicator of the presence of ATM (109/113). On the other hand, MCV of 90 or more, especially with an MCH of 30 or more is a strong negative indicator for ATM (70/89). Firm diagnosis of ATM at birth can thus be secured in majority of neonates.
为了评估出生时一些简单的血液参数,以作为怀疑α-地中海贫血(ATM)的依据,一项前瞻性研究纳入了连续202例MCV小于或小于95 fl的新生儿,采用HPLC检测Hb Barts。分组分为两组,一组MCV在90-95之间(89例),另一组MCV在90以下(113例)。作为对照,连续104例MCV≥95 fl的新生儿进行类似检查。已经证实,MCV低于90 fl,特别是MCH≤30 pg时,是存在ATM的有力指标(109/113)。另一方面,MCV在90以上,特别是MCH在30以上,是ATM(70/89)的强烈负面指标。因此,在大多数新生儿中,可以在出生时确定ATM的诊断。
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引用次数: 0
Occurrence of Acute Myeloid Leukemia in Young Pregnant Women 年轻孕妇急性髓性白血病的发生
IF 3 Q2 Medicine Pub Date : 2008-01-01 DOI: 10.4137/CMBD.S823
J. Menezes, M. Emerenciano, F. Pimenta, Gilson Guedes Filho, I. Magalhães, M. Sant'ana, Marina Lipkin Vasquez, Llana Zalcberg Renault, M. Pombo-de-Oliveira
Although acute leukaemia is rare in pregnancy its importance lies in its life-threatening potential, both to the child and the mother. The possibility of vertical transmission of leukemic cells increases the attention devoted to these patients and their offspring. Three cases of pregnant young women (15-17 years of age) with AML are presented. This series of cases is the first report where gene abnormalities such as ITD mutations of the FLT3 gene and AML1/ETO fusion genes were screened in pregnant AML patients and their babies, so far. Unfortunately, very poor outcomes have been associated to similar cases described in literature, and the same was true to the patients described herein. Although very speculative, we think that the timing and possible similar exposures would be involved in all cases.
虽然急性白血病在怀孕期间很少见,但它的重要性在于它对孩子和母亲都有可能危及生命。白血病细胞垂直传播的可能性增加了对这些患者及其后代的关注。本文报道3例年轻孕妇(15-17岁)急性髓性白血病。这一系列病例是迄今为止首次在妊娠AML患者及其婴儿中筛查FLT3基因ITD突变和AML1/ETO融合基因等基因异常的报道。不幸的是,文献中描述的类似病例的预后非常差,本文所描述的患者也是如此。尽管这只是推测性的,但我们认为,所有案例都会涉及到时机和可能的类似风险敞口。
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引用次数: 5
Long Term Results after 3 Courses of ABVD plus Subtotal Nodal Radiotherapy in 188 Adult Patients with Stage I, II and IIIA Hodgin Lymphoma 188例成年I、II、IIIA期霍金淋巴瘤患者ABVD加次全淋巴结放疗3个疗程后的远期疗效
IF 3 Q2 Medicine Pub Date : 2008-01-01 DOI: 10.4137/CMBD.S357
P. Brice, M. André, P. Franchi-Rezgui, I. Biasoli, C. Hennequin
In patients with Hodgkin lymphoma (HL) a continued improvement in outcome with a high cure rate is observed but with an increased treatment-induced late effects. We report the long-term results from 188 (stage I to IIIA) patients treated during the period 1985-94 with 3 courses of ABVD-like chemotherapy and subtotal nodal radiotherapy. 10 year overall survival is of 88% and no secondary leukaemia was observed. The main long term toxicity was cardiac, mainly related to a mediastinal dose of 45 Grays in patients with partial remission. New strategies are aiming to reduce the mediastinal dose at 30 Grays after chemotherapy-induced complete remission.
在霍奇金淋巴瘤(HL)患者中,观察到高治愈率的结果持续改善,但治疗引起的晚期效应增加。我们报告了1985- 1994年期间188例(I期至IIIA期)患者接受abvd样化疗和次全淋巴结放疗的长期结果。10年总生存率为88%,未观察到继发性白血病。主要的长期毒性是心脏,主要与部分缓解患者的纵隔剂量45格雷有关。新的策略旨在减少化疗诱导的完全缓解后30 gray的纵隔剂量。
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引用次数: 0
Quantification of Drug-Induced mRNA in Human Whole Blood ex vivo 体外人全血药物诱导mRNA的定量分析
IF 3 Q2 Medicine Pub Date : 2008-01-01 DOI: 10.4137/CMBD.S507
M. Mitsuhashi, K. Endo, Kazuhiko Obara, H. Izutsu, T. Ishida, Norio Chikatsu, A. Shinagawa
Apoptosis was induced in heparinized human whole blood by 3 different ways (radiation, bleomycin, or etoposide), and various mRNA were quantified using the method we reported (Clin. Chem. 2006; 52:634-642). We found that cyclin-dependent kinase inhibitor 1A (p21) and p53 upregulated modulator of apoptosis (PUMA) were the most sensitive and universal mRNA markers of apoptosis in leukocytes. In order to define positive and negative responses, a synthetic RNA was spiked into the lysis buffer and the fold increase was calculated. As a result, 837/880 (95.1%) of data points stayed between 0.75 and 1.5 fold increase, and 874/880 (99.3%) were within 0.5-2.0 fold increase. When blood samples from 40 healthy adults were stimulated with 22 different drugs, more than 75% of the samples responded to bleomycin (1 μM), idarubicin (2 μM), vincristine (1 μM), daunorubicin (2 μM), cytarabine (10 μM), to induce p21 and/or PUMA mRNA, and approximately 25% showed no induction. Significant correlation was found between p21 and PUMA mRNA responses, and between daunorubicin and cytarabine, idarubicin, and vincristine for both p21 and PUMA. The quantification of drug-induced mRNA in whole blood will be considered as ex vivo, and is a suitable platform for biomarker screening as well as a model system for drug sensitivity tests in future.
采用放射、博来霉素和依托泊苷三种不同的方法诱导肝素化人全血细胞凋亡,并采用我们报道的方法定量测定各种mRNA (Clin。化学2006;52:634 - 642)。我们发现细胞周期蛋白依赖性激酶抑制剂1A (p21)和p53细胞凋亡上调调节剂(PUMA)是白细胞中最敏感和最普遍的细胞凋亡mRNA标志物。为了确定阳性和阴性反应,将合成RNA加入裂解缓冲液中,并计算倍增率。837/880(95.1%)个数据点在0.75 ~ 1.5倍之间,874/880(99.3%)个数据点在0.5 ~ 2.0倍之间。用22种不同的药物刺激40例健康成人的血液样本,超过75%的样本对博来霉素(1 μM)、阿达红霉素(2 μM)、长春新碱(1 μM)、柔红霉素(2 μM)、阿糖胞苷(10 μM)有诱导p21和/或PUMA mRNA的反应,约25%的样本没有诱导作用。p21和PUMA mRNA应答之间、柔红霉素与阿糖胞苷、依达红霉素和长春新碱对p21和PUMA的应答之间存在显著相关性。全血中药物诱导mRNA的定量将被认为是离体的,是生物标志物筛选的合适平台,也是未来药物敏感性试验的模型系统。
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引用次数: 8
A Disease Mechanism Underlying Bleeding in Wiskott-Aldrich Syndrome Wiskott-Aldrich综合征出血的发病机制
IF 3 Q2 Medicine Pub Date : 2008-01-01 DOI: 10.4137/CMBD.S536
S. Tsuboi
The Wiskott-Aldrich Syndrome (WAS) is an × chromosome-linked immunodeficiency disorder. The most common symptom in WAS is bleeding. Several clinical investigations indicate that low platelet counts and defective platelet aggregation are the major causes of bleeding in WAS patients. However, the molecular bases underlying these defects are unclear. This study focuses on the molecular mechanism of defective platelet aggregation of WAS patients. The gene responsible for WAS encodes WAS protein (WASP). The mutations or deletion of WASP causes various functional defects in hematopoietic cells. We previously showed that binding of WASP to calcium- and integrin-binding protein (CIB) is required for activation of platelet integrin, αIIbβ3. I here demonstrate that blocking WASP binding to CIB reduces binding of talin to the β3 cytoplasmic tail, resulting in impaired activation of αIIbβ3. Impaired αIIbβ3 activation causes defective platelet aggregation, resulting in bleeding. This finding suggests a potential disease mechanism underlying bleeding seen in WAS patients.
Wiskott-Aldrich综合征(WAS)是一种x染色体相关免疫缺陷疾病。WAS最常见的症状是出血。一些临床研究表明,血小板计数低和血小板聚集缺陷是WAS患者出血的主要原因。然而,这些缺陷背后的分子基础尚不清楚。本研究主要探讨WAS患者血小板聚集缺陷的分子机制。负责WAS的基因编码WAS蛋白(WASP)。WASP的突变或缺失会导致造血细胞的各种功能缺陷。我们之前的研究表明,血小板整合素αIIbβ3的激活需要WASP与钙和整合素结合蛋白(CIB)的结合。我在这里证明阻断WASP与CIB的结合减少了talin与β3细胞质尾部的结合,导致αIIbβ3的激活受损。αIIbβ3活化受损导致血小板聚集缺陷,导致出血。这一发现提示了WAS患者出血的潜在疾病机制。
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引用次数: 1
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Clinical Medicine Insights-Blood Disorders
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