1.A post-classical theory of enamel biomineralization… and why we need one.
James P SIMMER ; Amelia S RICHARDSON ; Yuan-Yuan HU ; Charles E SMITH ; Jan Ching-Chun HU
International Journal of Oral Science 2012;4(3):129-134
Enamel crystals are unique in shape, orientation and organization. They are hundreds of thousands times longer than they are wide, run parallel to each other, are oriented with respect to the ameloblast membrane at the mineralization front and are organized into rod or interrod enamel. The classical theory of amelogenesis postulates that extracellular matrix proteins shape crystallites by specifically inhibiting ion deposition on the crystal sides, orient them by binding multiple crystallites and establish higher levels of crystal organization. Elements of the classical theory are supported in principle by in vitro studies; however, the classical theory does not explain how enamel forms in vivo. In this review, we describe how amelogenesis is highly integrated with ameloblast cell activities and how the shape, orientation and organization of enamel mineral ribbons are established by a mineralization front apparatus along the secretory surface of the ameloblast cell membrane.
Ameloblasts
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chemistry
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cytology
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Amelogenesis
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physiology
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Basement Membrane
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chemistry
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Crystallization
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Dental Enamel
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chemistry
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Dental Enamel Proteins
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secretion
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Humans
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Tooth Calcification
2.Identification of new genetic risk factors for prostate cancer.
Michelle GUY ; Zsofia KOTE-JARAI ; Graham G GILES ; Ali Amin Al OLAMA ; Sarah K JUGURNAUTH ; Shani MULHOLLAND ; Daniel A LEONGAMORNLERT ; Stephen M EDWARDS ; Jonathan MORRISON ; Helen I FIELD ; Melissa C SOUTHEY ; Gianluca SEVERI ; Jenny L DONOVAN ; Freddie C HAMDY ; David P DEARNALEY ; Kenneth R MUIR ; Charmaine SMITH ; Melisa BAGNATO ; Audrey T ARDERN-JONES ; Amanda L HALL ; Lynne T O'BRIEN ; Beatrice N GEHR-SWAIN ; Rosemary A WILKINSON ; Angela COX ; Sarah LEWIS ; Paul M BROWN ; Sameer G JHAVAR ; Malgorzata TYMRAKIEWICZ ; Artitaya LOPHATANANON ; Sarah L BRYANT ; null ; null ; null ; Alan HORWICH ; Robert A HUDDART ; Vincent S KHOO ; Christopher C PARKER ; Christopher J WOODHOUSE ; Alan THOMPSON ; Tim CHRISTMAS ; Chris OGDEN ; Cyril FISHER ; Charles JAMESON ; Colin S COOPER ; Dallas R ENGLISH ; John L HOPPER ; David E NEAL ; Douglas F EASTON ; Rosalind A EELES
Asian Journal of Andrology 2009;11(1):49-55
There is evidence that a substantial part of genetic predisposition to prostate cancer (PCa) may be due to lower penetrance genes which are found by genome-wide association studies. We have recently conducted such a study and seven new regions of the genome linked to PCa risk have been identified. Three of these loci contain candidate susceptibility genes: MSMB, LMTK2 and KLK2/3. The MSMB and KLK2/3 genes may be useful for PCa screening, and the LMTK2 gene might provide a potential therapeutic target. Together with results from other groups, there are now 23 germline genetic variants which have been reported. These results have the potential to be developed into a genetic test. However, we consider that marketing of tests to the public is premature, as PCa risk can not be evaluated fully at this stage and the appropriate screening protocols need to be developed. Follow-up validation studies, as well as studies to explore the psychological implications of genetic profile testing, will be vital prior to roll out into healthcare.
Genetic Predisposition to Disease
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genetics
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Genetic Testing
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Humans
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Kallikreins
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genetics
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Male
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Membrane Proteins
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genetics
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Prostatic Neoplasms
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diagnosis
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genetics
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Prostatic Secretory Proteins
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genetics
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Protein-Serine-Threonine Kinases
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genetics
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Risk Factors