主题:【求助】(已应助)求助两篇英文文献,多谢。

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Science 4 February 2005:
Vol. 307. no. 5710, pp. 720 - 724
DOI: 10.1126/science.1099593
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Mechanisms of Hair Graying: Incomplete Melanocyte Stem Cell Maintenance in the Niche
Emi K. Nishimura,1* Scott R. Granter,2 David E. Fisher1*

Hair graying is the most obvious sign of aging in humans, yet its mechanism is largely unknown. Here, we used melanocyte-tagged transgenic mice and aging human hair follicles to demonstrate that hair graying is caused by defective self-maintenance of melanocyte stem cells. This process is accelerated dramatically with Bcl2 deficiency, which causes selective apoptosis of melanocyte stem cells, but not of differentiated melanocytes, within the niche at their entry into the dormant state. Furthermore, physiologic aging of melanocyte stem cells was associated with ectopic pigmentation or differentiation within the niche, a process accelerated by mutation of the melanocyte master transcriptional regulator Mitf.

1 Department of Pediatric Hematology/Oncology, Melanoma Program in Medical Oncology, Dana-Farber Cancer Institute, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.
2 Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Address after 9 February 2005: Department of Dermatology, Hokkaido University Graduate School of Medicine, N15, W7, Sapporo 060-8638, Japan.


* To whom correspondence should be addressed. E-mail: emi_k_nishimura@yahoo.co.jp (E.K.N.); David_Fisher@dfci.harvard.edu (D.E.F.)
推荐答案:dong3626回复于2009/01/17
http://www.jsvs.org/en/index.htmlhttp://www.jstage.jst.go.jp/browse/jsvs/_vols
第二篇没有电子版。。
只有纸版的。。
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TOP > J-EAST > List of Journal Titles (J) > Journal of the Japanese Society of Internal Medicine(1999) > Molecular mechanism and clinic of aging. 3 Human progeria gene. Molecular mechanism and clinic of aging. 3 Human progeria gene.Accession number;99A0954122
Title;Molecular mechanism and clinic of aging. 3 Human progeria gene.
Author;MIKI TETSURO(Ehime Univ.)  MORISHIMA ATSUYUKI(Ehime Univ.)  NAKURA JUN(Ehime Univ.)   
Journal Title;Journal of the Japanese Society of Internal Medicine

Journal Code:F0916A

ISSN:0021-5384

VOL.88;NO.9;PAGE.1701-1705(1999) 
Figure&Table&Reference;FIG.1, TBL.2, REF.2
Pub. Country;Japan
Language;Japanese
Abstract;Werner's syndrome (W), one of hereditary progeria, is generally short stature with developing cataract, gray hair and hair removal from about 20 years old, and shows high frequency of malignant tumor. RNA of the cause gene of W is length of about 5.8kb, and it is acidic protein (DNA helicase) consisting of 1432 amino acids. In the causal gene mutation of W, a type, in which the translation of the protein has stopped due to single base substitution of the protein translation region during the translation and a type in which the abnormal splicing occurs due to the mutation of the connecting point of exon and intron in mRNA. The causal gene of Bloom's syndrome, a part of complementary group of Cokayne's syndrome and a part of complementary group of xeroderma pigmentosum except for W are protein with the helicase domain.
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