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| 1 | 慢性淋巴细胞白血病诊治指南显示文摘流行病学
慢性淋巴细胞白血病(CLL)在西方国家很常见,占65岁以上白血病患者的65%.中位发病年龄65~70岁.30岁以下极为罕见,但20%~30%病例于55岁前发病,年发病率约3/10万.欧洲、澳大利亚、北美白人以及黑人的发病率是印度、中国及日本的20~30倍.男女之比约2:1.无确凿证据显示,接触化学物质和射线、饮食、吸烟、病毒感染和自身免疫性疾病为本病的高危因素,但患者一级和二级亲属淋巴系统恶性肿瘤发病率增高.许多家族尚存在患者后代发病年龄更早、病情更重的现象.经治和未治患者第二肿瘤发病率增高. | Oscier D Fegan C Hillman P Illide T Johnson S Maguir P Matutes M Milligan D 孙蕾 高举 | 2005 | 国外医学(输血及血液学分册)2005,28,1: | 6 |
| 2 | P2X4受体对活化的小胶质细胞的调控作用显示文摘小胶质细胞是中枢神经系统内的免疫细胞,当脑组织出现损伤时,小胶质细胞被激活,对脑组织起到保护作用。在自身免疫性脑脊髓炎模型大鼠和视神经脊髓炎患者体内,均观察到在脊髓炎性病灶及小胶质细胞内,P2X4受体表达上调。本课题组进行在体和离体实验,用LPS活化小胶质细胞,观察P2X4受体在小胶质细胞炎性反应中的作用。膜片钳检测显示,在LPS激活的小胶质细胞内,P2X4受体活性增加。P2X4受体阻断剂可显著降低小胶质细胞的膜皱缩、TNFα的分泌、细胞形态的改变及LPS导致的小胶质细胞死亡。在体研究显示,LPS髓内注射后会诱发炎性反应,迅速导致小胶质细胞丢失;给予P2X4受体阻断剂可显著减少小胶质细胞的丢失,而P2X4受体激活剂则可显著增加小胶质细胞的丢失。海马齿状回的小胶质细胞特别容易被LPS诱导的炎症反应激活。注射LPS后2 h,位于海马齿状回的小胶质细胞即被激活,大约24 h后死亡,P2X4受体阻断剂可减少LPS诱导的小胶质细胞活化和死亡。上述数据提示,P2X4受体对于小胶质细胞的激活和存活有重要的调控作用。 | Vázquez-Villoldo N Domercq M Martín A Llop J Gómez-Vallejo V Matute C | 2014 | 神经损伤与功能重建2014,9,1: | 4 |
| 3 | Analysis of the therapeutic evolution in the management of airway infantile hemangioma显示文摘AIM: To analyze the evolution in the management of airway infantile hemangioma(AIH) and to report the results from 3 pediatric tertiary care institutions.METHODS: A retrospective study of patients with diagnosis of AIH and treated in 3 pediatric tertiary care institutions from 1996 to 2014 was performed. RESULTS: Twenty-three patients with diagnosis of AIH were identified. Mean age at diagnosis was 6 mo(range, 1-27). Single therapy was indicated in 16 patients and 7 patients received combined therapy. Two therapeutic groups were identified: Group A included 14 patients who were treated with steroids, interferon, laser therapy and/or surgery; group B included 9 patients treated with oral propranolol. In group A, oral corticosteroids were used in 9 patients with a good response in 3 cases(no requiring other therapeutic option), the other patients required additional treatment options. Cushing syndrome was observed in 3 patients. One patient died of a fulminant sepsis. Open surgical excision and endoscopic therapy were performed in 11 patients(in 5 of them as a single treatment) with a response rateof 54.5%. Stridor persisted in 2 cases, and one patient died during the clinical course of bronchial aspiration. In group B, oral propranolol was used in 9 patients(in 8 of them as a single treatment) with a response rate of 100%, with an mean treatment duration of 7 mo(range, 5-10); complications were not observed. CONCLUSION: Our experience and the medical literature support the use of propranolol as a first line of treatment in AIH. | Grecia V Vivas-Colmenares Israel Fernandez-Pineda Juan Carlos Lopez-Gutierrez Miguel Angel Fernandez-Hurtado Maria Antonia Garcia-Casillas Jose Antonio Matute de Cardenas | 2016 | World Journal of Clinical Pediatrics2016,5,1: | 3 |
| 4 | 白质内的神经递质信号显示文摘脑白质是由许多有髓鞘的轴突组成,白质和灰质共同组成中枢神经系统,白质是中枢神经系统内信息快速传递的基础。有髓神经通路主要是由少突胶质细胞、星形胶质细胞及少量的小胶质细胞和少突胶质前体细胞构成。大部分白质内的神经递质信号主要存在于神经细胞胞体外,这提示这些神经递质除了具有完成神经元与神经元之间信息传递的功能外,还有其他生理功能。白质中的神经递质信号种类很多,已经证实的有谷氨酸能、嘌呤能(ATP和腺苷)、GABA能、甘氨酸能、肾上腺素能、胆碱能、多巴胺能、血清素能等信号递质,通过与各种离子型或代谢型受体结合发挥作用。轴突和胶质细胞都可以释放神经递质,也可以表达相应的受体。白质内神经递质信号的生理功能还需进一步研究,但研究已经证实谷氨酸和ATP介导的信号可激活胶质细胞上的钙离子通道,并调节轴突的传导功能。某项研究显示,在动作电位传播的过程中,轴突释放神经递质并与胶质细胞上的受体结合,通过少突胶质细胞来调节星形胶质细胞的稳态和髓鞘形成。星形胶质细胞也释放神经递质,与轴突上的受体相结合,增强动作电位的传播,维持信号电位沿长的轴突传播。白质内神经递质种类的多样性,提示它们有多种功能,对信号的传递有重要作用。白质内的神经递质信号现象很有可能也存在于大脑皮质和灰质,在这些部位的神经递质对于大脑的高级认知功能有更重要的作用。 | Butt AM Fern RF Matute C 唐颖馨 | 2014 | 神经损伤与功能重建2014,9,6: | 2 |
| 5 | Reinforcement's incidental effects on reproductive isolation between conspecifics显示文摘 | Biology Department Daniel R. MATUTE | 2016 | Current Zoology2016,62,2: | 2 |
| 6 | The classification of acute leukaemia显示文摘 | CATOVSKY D MATUTES E | 1992 | Leukemia1992,6,: | 1 |
| 7 | Eicosapentaenoic acid actions on adiposity and insulin resistance in control and high - fat - fed rats : Role of apoptosis, adiponectin and tumour necrosis factor - alpha 显示文摘 | Perez - Matute P Perez - Echarfi N Martinez JA | 2007 | Br J Nutr2007,97,2: | 1 |
| 8 | Outcome of biphenotypicacute leukemia显示文摘 | Killick S Matutes E Powles R L | 1999 | Haematologica1999,84,8: | 1 |
| 9 | Granulomatous slack skin disease-disease features and response to pentostatin 显示文摘 | Osuji N Fearfield L Matutes E | 2003 | Br J Haematol2003,123,2: | 1 |
| 10 | Mix and Match: Product Compatibility without Network Externalities 显示文摘 | MATUTES CARMEN REGIBEAU P | 1988 | RAND Journal of Economies1988,19,: | 1 |
| 11 | A classification of acute leukaemia for the 1990s显示文摘 | D. Catovsky E. Matutes V. Buccheri V. Shetty J. Hanslip N. Yoshida R. Morilla | 1991 | Annals of Hematology1991,,1: | 1 |
| 12 | The role of pentostatin in the treatment of T-cell malignancies: analysis of response rate in 145 patients according to disease subtype 显示文摘 | Mercieca J Matutes E Dearden C | 1994 | J Clin Oncol1994,12,12: | 1 |
| 13 | Lineage commitment in biphenotypic acute leukemia 显示文摘 | BUCCHERI V MATUTES E DYER M | 1993 | Leukemia1993,7,: | 1 |
| 14 | The immunological profile of B-cell disorders and proposal of a scoring system for the diagnosis of CLL显示文摘 | Matutes E Owusu-ankomah K Morillar | 1994 | Leukemia1994,8,: | 1 |
| 15 | The diagnostic value of CD123 in B-cell disorders with hairy or villous lymphocytes 显示文摘 | Del Giudice L Matutes E Monlla R | 2004 | Haemat Ologiea2004,89,3: | 1 |
| 16 | Chromosome abnormalities in hairy cell leukaemia varlant显示文摘 | Brito-Babapulle V Matutes E Oscier D | 1994 | Genes Chromosomes Cancer1994,10,: | 1 |
| 17 | Morphological and immunophenotypic Features of chronic lymphocytic leukemia 显示文摘 | Matutes E Polliaek A | 2000 | Rev Clin Exp Henaato12000,4,: | 1 |
| 18 | Corporate Social Responsibility as a Vehicle to Reveal the Corporate Identity: A Study Focused on the Websites of Spanish Financial Entities 显示文摘 | Bravo R Matute J Pina J M | 2012 | Journal of Business Ethics2012,107,2: | 1 |
| 19 | Contribution of in the diagnosis and classification of hae- mopoietie malignancies显示文摘 | Matutes E | 1995 | J Clin Pathol1995,48,3: | 1 |
| 20 | T-cell Prolymphocytic Leukemia 显示文摘 | Matutes E | 1998 | Cancer Control1998,5,1: | 1 |