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Wieslaw H. Trzeciak

Researcher at Poznan University of Medical Sciences

Publications -  82
Citations -  1584

Wieslaw H. Trzeciak is an academic researcher from Poznan University of Medical Sciences. The author has contributed to research in topics: Ectodermal dysplasia & Gene. The author has an hindex of 22, co-authored 82 publications receiving 1516 citations. Previous affiliations of Wieslaw H. Trzeciak include University of Texas Southwestern Medical Center & University of Texas at Austin.

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Molecular basis of non-syndromic tooth agenesis: mutations of MSX1 and PAX9 reflect their role in patterning human dentition.

TL;DR: This paper aims to review current literature about the molecular mechanisms responsible for selective tooth agenesis in humans and identify the genes associated with the non-syndromic form of tooth Agenesis.
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Studies on the synthesis of sterol carrier protein-2 in rat adrenocortical cells in monolayer culture. Regulation by ACTH and dibutyryl cyclic 3',5'-AMP

TL;DR: It is concluded that the synthesis ofSCP2 in rat adrenocortical cells is induced by ACTH and that the induction is mediated by cAMP and may involve increased levels of translatable mRNA encoding a higher molecular weight precursor form of SCP2, which presumably undergoes post-translational processing yielding the mature form.
Journal Article

Clinical features, treatment and genetic background of Treacher Collins syndrome.

TL;DR: Mutational spectra support the hypothesis that TCS results from haploinsufficiency of treacle, and current procedures of surgical treatment of TCS are discussed and novel findings concerning the genetic background are described.
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Novel mutation in the paired box sequence of PAX9 gene in a sporadic form of oligodontia.

TL;DR: The view that mutations in PAX9 could constitute a causative factor of oligodontia is supported, as a novel, heterozygous G151A transition in the sequence encoding the paired domain of the PAX9 protein was detected in a patient with permanent tooth agenesis.
Journal Article

Oxidative DNA damage and level of thiols as related to polymorphisms of MTHFR, MTR, MTHFD1 in Alzheimer's and Parkinson's diseases.

TL;DR: The results indicate that of the enzymes studied only polymorphisms of folate-dependent enzyme MTHFD1 have pointed to significant differences in intensity of turnover of circulating thiols between AD and PD patients.