Publications by authors named "Martin Udart"

Background: Against the background of increasing use of dental implants, and thus an increasing prevalence of implant-associated complications, a deeper understanding of the biomolecular mechanisms in the peri-implant tissue is needed. Peri-implant soft tissue is in direct contact with transmucosal dental implant abutments. The aim of this trial is to distinguish the biomolecular and histological interactions of various dental abutment materials with peri-implant soft tissue.

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Lasers are used in dentistry for a variety of indications. One of these is the disinfection of root canals or the sterilization of residual caries. Many studies have demonstrated the capacity to kill bacteria for lasers but the fundamental mechanism of the laser effect remains quite unclear.

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Deregulation of the cell-cycle G1-restriction point control via abnormalities of Rb-pathway components is a frequent event in the formation of cancer. The aim of this study was to evaluate numerical aberrations of the Cyclin D1 (CCND1, PRAD1, bcl-1) gene locus at chromosome 11q13 in basal cell carcinomas (BCCs) and squamous cell carcinomas (SCCs) of the skin and to compare it with the Cyclin D1 protein expression. Fluorescence in situ hybridization with DNA-probes specific for the Cyclin D1 gene locus and the centromere of chromosome 11 as well as immunostaining for Cyclin D1 protein was applied on 5 microm serial paraffin sections.

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Cyclin D1 (CCND1, PRAD1, bcl-1) is associated with progression through G1 and entry into S phase of the cell cycle, as a partner of cyclin-dependent kinases (CDKs). The aim of this study was to evaluate cytogenetic aberrations of the gene locus at chromosome 11q13 in cutaneous malignant melanoma. Fluorescence in situ hybridisation (FISH) was applied on metaphase spreads of short-term primary cell cultures as well as on 5 microm paraffin tissue sections of primary melanomas and melanoma metastases, and on melanoma cell lines (C32, WM 266-4, HT 144, RPMI 7951, SK MEL 28).

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Apoptosis is an important co-factor in the pathogenesis of a plethora of malignancies. Enhanced c-myc activation can result either in proliferation or apoptosis. Coexpression with antiapoptotic bcl-2, which abrogates the apoptotic function of c-myc might lead to an enormous growth advantage of cells.

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