NATURE MEDICINE
自然医学
ISSN: 1078-8956
自引率: 0.8%
发文量: 201
被引量: 85220
影响因子: 87.154
通过率: 暂无数据
出版周期: 月刊
审稿周期: 2.14
审稿费用: 0
版面费用: 暂无数据
年文章数: 201
国人发稿量: 18

投稿须知/期刊简介:

The journal publishes original research in all disciplines of biomedical science, according to editorial assessment of a paper's potential interest, impact, and implications for clinical medicine and the biomedical community. The journal favours submissions that represent a conceptual advance or an original approach to understanding the molecular basis of pathogenesis and therapy.

期刊描述简介:

The journal publishes original research in all disciplines of biomedical science, according to editorial assessment of a paper's potential interest, impact, and implications for clinical medicine and the biomedical community. The journal favours submissions that represent a conceptual advance or an original approach to understanding the molecular basis of pathogenesis and therapy.

最新论文
  • Cell identification and isolation on the basis of cytokine secretion: a novel tool for investigating immune responses.

    被引量:8 发表:2001

  • ORP150 protects against hypoxia/ischemia-induced neuronal death.

    :Oxygen-regulated protein 150 kD (ORP150) is a novel endoplasmic-reticulum-associated chaperone induced by hypoxia/ischemia. Although ORP150 was sparingly upregulated in neurons from human brain undergoing ischemic stress, there was robust induction in astrocytes. Cultured neurons overexpressing ORP150 were resistant to hypoxemic stress, whereas astrocytes with inhibited ORP150 expression were more vulnerable. Mice with targeted neuronal overexpression of ORP150 had smaller strokes compared with controls. Neurons with increased ORP150 demonstrated suppressed caspase-3-like activity and enhanced brain-derived neurotrophic factor (BDNF) under hypoxia signaling. These data indicate that ORP150 is an integral participant in ischemic cytoprotective pathways.

    被引量:65 发表:2001

  • CYP3A genetics in drug metabolism.

    被引量:31 发表:2001

  • Sir John Sulston.

    被引量:- 发表:2001

  • Induction of tumor lymphangiogenesis by VEGF-C promotes breast cancer metastasis.

    :Metastasis of breast cancer occurs primarily through the lymphatic system, and the extent of lymph node involvement is a key prognostic factor for the disease. Whereas the significance of angiogenesis for tumor progression has been well documented, the ability of tumor cells to induce the growth of lymphatic vessels (lymphangiogenesis) and the presence of intratumoral lymphatic vessels have been controversial. Using a novel marker for lymphatic endothelium, LYVE-1, we demonstrate here the occurrence of intratumoral lymphangiogenesis within human breast cancers after orthotopic transplantation onto nude mice. Vascular endothelial growth factor (VEGF)-C overexpression in breast cancer cells potently increased intratumoral lymphangiogenesis, resulting in significantly enhanced metastasis to regional lymph nodes and to lungs. The degree of tumor lymphangiogenesis was highly correlated with the extent of lymph node and lung metastases. These results establish the occurrence and biological significance of intratumoral lymphangiogenesis in breast cancer and identify VEGF-C as a molecular link between tumor lymphangiogenesis and metastasis.

    被引量:583 发表:2001

统计分析
是否有问题?您可以直接对期刊官方提问 提问

最近浏览

关于我们

zlive学术集成海量学术资源,融合人工智能、深度学习、大数据分析等技术,为科研工作者提供全面快捷的学术服务。在这里我们不忘初心,砥砺前行。

友情链接

联系我们

合作与服务

©2024 zlive学术声明使用前必读