白春学
主要研究方向为肺损伤和肺癌的分子发病机制和治疗。
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- 姓名:白春学
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学术头衔:
博士生导师
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学科领域:
内科学
- 研究兴趣:主要研究方向为肺损伤和肺癌的分子发病机制和治疗。
白春学 男,1951年4月生,吉林人。1982年获北京中国协和医科大学硕士学位,1989年获上海医科大学博士学位,1985年在日本进修结核病防治,1997~1998年在美国加州大学旧金山分校(UCSF)心血管研究所做博士后研究。从事内科呼吸专业,主要研究方向为肺损伤和肺癌的分子发病机制和治疗。现任复旦大学教授、博士生和博士后导师,上海市医学领军人才,上海市医学重点学科-复旦大学附属中山医院呼吸内科负责人、主任,中山医院肺部肿瘤综合诊疗中心主任。同时担任中华医学会呼吸分会常委,中国医师协会呼吸分会常委,中华医学会呼吸分会肺癌组副组长,世界卫生组织聘请为全球抗呼吸病联盟(GARD)会议顾问,美国胸科学会会员,日本结核病预防会名誉会员及国际防痨和肺病联合会会员,英国Taylor & Francis出版社《J Organ Dysfunction》杂志副主编,《世界感染》杂志副总编辑,《临床肺科杂志》副主编,《中华结核和呼吸杂志》和《国际呼吸杂志》杂志编委会常委,以及《中国呼吸和危重监护杂志》、《中国实用内科杂志》和《中国医刊》等多家杂志编委和特约编委。
目前承担复旦大学“985工程”科技创新平台建设项目、上海市医学重点学科卫生局重点项目、国家自然科学基金、卫生部、教委博士点、美国NIH和上海市科委重大科技攻关项目等多项课题。已发表论文160余篇, 其中SCI索引杂志论文20篇,影响因子累计50余分。主编《呼吸系统疾病诊断和鉴别诊断学》和《急性呼吸窘迫综合征》,参编多部专著和教科书。在国内和国际上最早研究肺水通道的生理功能;最早应用RNAi技术研究抗肺肿瘤药物,已获得“一种双链RNA及其用途”的专利(专利号:ZL03115489.1);最早研究联合应用血液净化和膜氧合器治疗ARDS, 已获得实用新型专利(专利号:ZL 2004 2 0091118.1);目前已研发成功具有自主知识产权的随弃式氧和pH生物光纤化学传感器,并开发出以其为基础的实时血气分析仪雏型,首次在体系列应用获得成功。本着“服务病人,造福社会”的宗旨,于2004年4月28日建立上海市ARDS协作网,2003年3月设立慢性阻塞性肺病专科门诊,2002年1月建立肺部肿瘤综合诊疗中心,使很多病人得到了科学有效的治疗。1991年国家教委和国务院学位委员会授予“为四化建设做出突出贡献的中国博士学位获得者”称号。2005年上海市优秀发明选拔赛一等奖,此外,还分别获得“国家医药卫生科技进步三等奖”两次和其它奖励多次。
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白春学, ZHANG Song, JIANG Shu-Juan, ZHANG Cai-Qing, WANG Hong-Mei, BAI Chun-Xue
,-0001,():
-1年11月30日
Solid tumor cells show a resistance to immunologic effector cells in vitro[1]. The resistance may be one reason why these tumors withstand immunotherapeutic approaches in humans. Dendritic cells play an important role in the immune response to tumor-associated antigens in humans. Dendritic cells in the periphery capture and process antigens,express lymphocyte costimulatory molecules, migrate to lympoid organs, and secrete cytokines to initiate immune response.
DC, CIK, cytokine., antitumor
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【期刊论文】肺腺癌SPC2A21细胞表皮生长因子受体表达水平对其增殖的影响
白春学, 张敏, 张新, 高磊, 毛翎, 陈杰
中华结核和呼吸杂志,2005,28(5):337-341,-0001,():
-1年11月30日
目的:探讨采用体外化学合成的针对表皮生长因子受体(EGFR)设计的双链RNA(double-stranded RNA, dsRNA),是否能诱导肺非小细胞肺癌(NSCLC)细胞出现序列特异性基因沉默,及抑制EGFR基因表达后NSCLC细胞的生物学特征。方法:体外合成EGFR序列特异性dsRNA(dsRNA-EGFR),结合脂质体2000转染肺腺癌SPC2A21细胞,用荧光显微镜及流式细胞仪测定转染细胞的EGFR受体数量;适时定量聚合酶链反应检测其EGFR基因表达水平。采用集落形成试验检测SPC2A21细胞的增殖和集落形成能力。建立裸鼠肿瘤模型,计算肿瘤抑制率。结果:dsRNA2EGFR可使EGFR在蛋白水平表达下降7113%、基因水平表达下降5010%, SPC2A21细胞集落形成下降6618%,并显著抑制在体肿瘤生长,肿瘤抑制率为7510%。结论:dsRNA2EGFR可序列特异性下调NSCLC细胞EGFR在基因及蛋白水平的表达,有效抑制肿瘤生长。
癌,, 非小细胞肺, 受体,, 表皮生长因子, RNA,, 双链, 生长抑制率
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白春学, Li Baia, Zubin Yub, Guisheng Qiana, Pin Qianc, Jinjun Jiangd, Guansong Wanga, Chunxue Baid, *
Respiratory Physiology & Neurobiology (2005) 1-9,-0001,():
-1年11月30日
Recently identified suppressors of cytokine signaling (SOCS) have been proposed as negative regulators of cytokine signaling, which have distinct mechanisms of inhibiting JAK-STAT pathway. In this study, using cultures of rat primary pulmonary vascular smooth muscle cells (PASMC), we found that hypoxia induced strongly STAT3 phosphorylation by up to four-fold. At the same time, mRNA for the endogenous cytokine signaling repressor SOCS3, but not SOCS1, was markedly induced in PASMC early as 2 h following hypoxic stimulation. Furthermore, forced expression of SOCS3 gene suppressed tyrosine phosphorylation of STAT3 and transcription of c-myc gene by more than 70% and 60% in PASMC under hypoxic conditions, respectively. Additionally, we showed here that hypoxia enhanced nearly two-fold increase of PASMC proliferation and overexpression SOCS3 gene downregulated hypoxia-induced PASMC proliferation by about 50%. The finding suggest that STAT3-dependent pathway is involved in the activation and proliferation of PASMC stimulated by hypoxia, and SOCS3 is a rapidly hypoxiainducible gene and acts to inhibit activation of cellular signaling pathway in a classical negative feedback loop.
Hypoxia, Pulmonary artery, Muscle, Smooth, Vascular, SOCS, Signal transduction
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白春学, Min Zhang, Xin Zhang, , Chun-Xue Bai, Xian-Rang Song, Jie Chen, Lei Gao, Jie Hu, Qun-Ying Hong, Malcolm J West and Ming Q Wei*
Genetic Vaccines and Therapy 2005, 3: 5,-0001,():
-1年11月30日
Lung cancer has emerged as a leading cause of cancer death in the world. Non-small cell lung cancer (NSCLC) accounts for 75–80% of all lung cancers. Current therapies are ineffective, thus new approaches are needed to improve the therapeutic ratio. Double stranded RNA (dsRNA) -mediated RNA interference (RNAi) has shown promise in gene silencing, the potential of which in developing new methods for the therapy of NSCLC needs to be tested. We report here RNAi induced effective silencing of the epidermal growth factor receptor (EGFR) gene, which is over expressed in NSCLC. NSCLC cell lines A549 and SPC-A1 were transfected with sequence- specific dsRNA as well as various controls. Immune fluorescent labeling and flow cytometry were used to monitor the reduction in the production of EGFR protein. Quantitative reverse-transcriptase PCR was used to detect the level of EGFR mRNA. Cell count, colony assay, scratch assay, MTT assay in vitro and tumor growth assay in athymic nude mice in vivo were used to assess the functional effects of EGFR silencing on tumor cell growth and proliferation. Our data showed transfection of NSCLC cells with dsRNA resulted in sequence specific silencing of EGFR with 71.31% and 71.78% decreases in EGFR protein production and 37.04% and 54.92% in mRNA transcription in A549 and SPC-A1 cells respectively. The decrease in EGFR protein production caused significant growth inhibition, i.e.: reducing the total cell numbers by 85.0% and 78.3%, and colony forming numbers by 63.3% and 66.8%. These effects greatly retarded the migration of NSCLC cells by more than 80% both at 24 h and at 48h, and enhanced chemo-sensitivity to cisplatin by four-fold in A549 cells and seven-fold in SPC-A1. Furthermore, dsRNA specific for EGFR inhibited tumor growth in vivo both in size by 75.06% and in weight by 73.08%. Our data demonstrate a new therapeutic effect of sequence specific suppression of EGFR gene expression by RNAi, enabling inhibition of tumor proliferation and growth. However, in vivo use of dsRNA for gene transfer to tumor cells would be limited because dsRNA would be quickly degraded once delivered in vivo. We thus tested a new bovine lentiviral vector and showed lentivector-mediated RNAi effects were efficient and specific. Combining RNAi with this gene delivery system may enable us to develop RNAi for silencing EGFR into an effective therapy for NSCLC.
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白春学, Hong Zhao, Xia Zhao, Chunxue Bai and Xiangdong Wang
Journal of Organ Dysfunction, 2005; 1: 32-44,-0001,():
-1年11月30日
The incidence of the pulmonary complications in patients with acute pancreatitis is up to 60%, from mild hypoxaemia without clinical or radiological abnormalities to severe acute lung injury. Although a number of reviews has described clinical evidence of pancreatitis-associated lung injury (PALI), there is still a lack of information on potential interorgan signalling involved in the development of PALI. The present review discusses the potential factors that have been considered as candidates responsible for interorgan signalling coupling pancreatitis to lung injury. Inflammatory mediators produced from the pancreas, leucocyte system and extrapancreatic organs may directly or indirectly contribute to the high concentration in the circulation, activate circulating leucocytes, initiate the inflammatory responses of pulmonary resident cells or induce acute lung injury. Circulating leucocytes have been suggested to play an important role in interorgan signalling during the development of PALI, by producing the inflammatory mediators, reactive oxygen species and proteinases, interacting with endothelial cells, communicating with pulmonary cells and compromising the lung tissue. Extrapancreatic organ fluid, e.g. liver, PAAF and gut, may also contribute to the interorgan signalling between the pancreas and lungs. There is still a great need to clarify the specificity, sensitivity and repeatability of these candidates for interorgan signalling in PALI.
acute pancreatitis, ARDS, cytokines, inflammation, leucocytes, lung injury
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白春学, Zhihong Chen, Rong Zhu, Li Bai, Chunxue Bai*
Respiratory Physiology & Neurobiology (2005) 1-7,-0001,():
-1年11月30日
The aquaporins (AQPs) are a family of homologous water channels expressed in many epithelial and endothelial cells, however no reliable and non-toxic inhibitors of AQPs have been reported yet. Our researchers have analyzed the changes of AQP5 expression induced by vector-based short hairpinRNA(shRNA) in the human airway submucosal gland cell line (SPC-A1) and observed its regulation on the expression of MUC5AC gene. Localizations of AQP5 and MUC5AC in SPC-A1cells were detected by Immunofluorescence. AQP5 mRNA was significantly reduced by 75.1% one day after transfection with specific shRNA, named shAQP5. However, the significant suppression of AQP5 protein did not appear until day 5 after transfection. MUC5AC mRNA was remarkably increased by 119.9% On day 3 after shAQP5 transfection, while comparable MUC5AC protein changes were not found in SPC-A1 cells with flow cytometry analysis. These results indicate that vector-based shRNA could be used as a potential tool to inhibit the expression ofAQP5. This is the first investigation providing evidence demonstrating the regulation of the mucin gene by AQP5 gene silencing.
AQP5, MUC5AC, shRNA, Submucosal gland cell, SPC-A1
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白春学, Xiao Sua, Yuanlin Songb, Jinjun Jianga, Chunxue Baia, *
Respiratory Physiology & Neurobiology 142(2004)1-11,-0001,():
-1年11月30日
A murine model of lipopolysaccharide (LPS)-induced acute lung injury (ALI) was used to evaluate whether aquaporin-1 (AQP1) is involved in lung inflammation and lung edema formation. Swiss strain mice (n=122) had LPS (5mg/kg) instilled intratracheally (IT), and were then treated with either 0.9% saline or dexamethasone (5mg/kg/day). Mice were euthanized at 2 days and 7 days after treatment. Inflammatory cytokines (TNF-α, IL-6), protein concentration in bronchoalveolar lavage (BAL) fluid, lung wet-to-dry weight ratio, histology, immunohistochemistry, and AQP1 Western blot were performed. Lung wet-to-dry weight ratio and lung vascular permeability were also measured in the AQP1 knockout mice (n=9) that received IT LPS (5mg/kg) at 2 days. Intratracheal instillation of LPS produced a severe lung injury at 2 days, characterized by elevation of TNF-α, IL-6 in the BAL fluid, and by histological changes consistent with increased lung vascular permeability and neutrophil infiltration. AQP1-immunoreactivity in the pulmonary capillary endothelium was reduced at 2 days and 7 days. Administration of dexamethasone improved LPS-induced ALI and retained expression of AQP1. However, depletion of AQP1 did not affect lung edema formation, lung vascular permeability, or lung histology. The results suggest that although AQP1 expression is decreased after lung injury, depletion of AQP1 does not alter lung inflammation and lung edema induced by LPS.
Channel,, aquaporin,, AQP1, Disease,, ARDS, Mammals,, mouse, Modulators,, IL-6,, TNF-α, Pharmacological agents,, lipopolysaccharide,, dexamethasone
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【期刊论文】RNA干扰技术抑制A549细胞表皮生长因子受体表达的研究
白春学, 张敏, 张新, 陈杰, MinQ. Wei
中华肿瘤杂志,2004,26(12):713-716,-0001,():
-1年11月30日
目的:探讨RNA干扰(RNAi)技术抑制非小细胞肺癌(NSCLC)细胞株A549细胞表皮生长因子受体(EGFR)表达后,对A549细胞生物学特性的影响。方法:体外化学合成EGFR 序列特异性双链RNA(dsRNA),用Lipofectamine 2000 转染A549细胞,采用Western blot技术和流式细胞仪检测EGFR的表达,并观察A549细胞周期、集落形成、化疗敏感性等生物学特性的改变。结果:序列特异性dsRNA-EGFR可显著抑制A549细胞EGFR表达;dsRNA-EGFR组细胞生长抑制率为85.0%,集落形成抑制率63.3%;细胞周期分析结果表明,dsRNA-EGFR组G0~G1期细胞数较对照组增加了12.7%,进入S期的细胞数较对照组减少了6.6%。转染dsRNA-EGFR后,可将A549细胞对顺铂的敏感性提高约4倍。结论:dsRNA-EGFR可有效抑制A549细胞EGFR的表达,并将更多的细胞阻滞在G0~G1期,抑制细胞增生,显著增加细胞对顺铂的敏感性。RNAi可能为NSCLC的基因治疗提供新策略。
表皮生长因子受体, RNA干扰, 双链RNA, 癌,, 非小细胞肺, 肺肿瘤
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白春学, Min Zhang, Chun-Xue Bai*, Xin Zhang, Jie Chen, Ling Mao, Lei Gao
2004; Vol. 1 Issue 1,-0001,():
-1年11月30日
RNA interference (RNAi) is a recently observed process by which double-stranded RNA (dsRNA) directs sequence-specific degradation of messenger RNA (mRNA) in animal and plant cells. In several model systems, RNAi had been developed into a useful tool for the investigation of gene function. In order to study the effectiveness of RNAi in mammalian cells, we introduced chemically synthetic 21-nucleotide small interference RNA (siRNA) duplexes into 293T/GFP cells, which were transduced by enhanced green fluorescence protein (EGFP) gene, by means of TransIT-TKO, Oligofectamine reagent, Lipofectamine 2000 respectively. The results demonstrated that EGFP expression was significantly and specifically inhibited by the corresponding dsRNA, but not by unrelated dsRNA. In three different vectors, Lipofectamine 2000 demonstrated the highest transfection efficiency with a 48h exposure. The decrease in EGFP fluorescence intensity was approximately 80%. Although TransIT-TKO and Oligofectamine displayed similar trends, the transfections were inefficient, and often toxic. The results also exhibited that siRNA inhibited the EGFP gene expression in a dose and time-dependent manner. Therefore, we concluded that the Lipofectamine 2000 was a better transfection reagent for RNAi. RNAi pathway seems operative in mammalian embryo cells. RNAi may be developed into a potential tool for gene therapy.
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【期刊论文】Role of aquaporin and sodium channel in pleural water movement
白春学, Jinjun Jiang, Jie Hu, Chunxue Bai*
Respiratory Physiology & Neurobiology (2003) 1-6,-0001,():
-1年11月30日
The role of the ENaC sodium channel and aquaporin-1 (AQP1) water channel on pleural fluid dynamics in mice was investigated. 0.25 ml of hypertonic or isosmolar fluid was infused into the pleural space in anesthetized wildtype and AQP1 null mice. Pleural fluid was sampled at specified times to quantify the osmolality and volume. The sodium channel activator terbutaline increased isosmolar fluid clearance by 90% while the sodium channel inhibitor amiloride decreased it by 15%, but had no effect on osmotically driven water transport. AQP1 deletion significantly decreased osmotic water transport in pleural space by twofold, but it had no effect on isosmolar fluid clearance. Pretreatment with dexamethasone increased pleural osmotic fluid entry by 25%, while intravenous injection of HgCl2 decreased osmotic pleural water movement by 43%. These results provided evidence for a role of a sodium channel in pleural fluid absorption; AQP1 plays a major role in osmotic liquid transport but it does not affect isosmolar fluid clearance.
Channel,, ENaC,, AQP1, Mammals,, mouse, Pharmacological agents,, amiloride,, terbutaline, Pleura,, fluid dynamics
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