Publications by authors named "Kerstin Peters"

Background: Self-assembling peptide (SAP) P-4 was introduced to treat initial caries lesions by means of guiding hydroxyapatite regeneration within the lesion. The objective of this study was to assess its effectiveness in a practical clinical setting.

Methods: Caries lesions in permanent teeth treated with monomeric and polymeric SAP P-4 from May 2015 through October 2020 were retrospectively analyzed at lesion and child levels by means of bite-wing radiography for changes in stage and cavitation and restoration.

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Fragility fractures are associated with a substantial mortality and morbidity. Because of the high prevalence of comorbidities and a high risk of complications the application of geriatric principles in the complex treatment of these patients is vital. The last years have seen a paradigm shift in the treatment of fragility fractures from an orthopedic disorder towards an orthogeriatric syndrome.

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The intensity and duration of endoplasmic reticulum (ER) stress converts the unfolded protein response (UPR) from an adaptive into a terminal response. The first regulates homeostasis, the latter triggers apoptosis. Cells that rapidly proliferate and possess developed secretory capabilities, such as leukemia cells, depend on an efficiently operating UPR to maintain proteostasis.

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Purpose: Despite proven antitumor activity of gemcitabine in chemoradiotherapy of advanced head and neck cancer, many authors refer to severe acute and late local and haematological toxicity. Fludarabine does imply nearly the same mechanisms of action as gemcitabine, inhibiting various enzymes involved in DNA replication. This investigation focuses on the combined effect of either fludarabine or gemcitabine and radiation on human squamous carcinoma cell lines in vitro, providing data for future decisions on head and neck chemoradiotherapy regimen.

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We have recently shown that the hematopoietic Granulocyte-Colony Stimulating Factor (G-CSF) is neuroprotective in rodent stroke models, and that this action appears to be mediated via a neuronal G-CSF receptor. Here, we report that the G-CSF receptor is expressed in rodent dopaminergic substantia nigra neurons, suggesting that G-CSF might be neuroprotective for dopaminergic neurons and a candidate molecule for the treatment of Parkinson's disease. Thus, we investigated protective effects of G-CSF in 1-methyl-4-phenylpyridinium (MPP+)-challenged PC12 cells and primary neuronal midbrain cultures, as well as in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease.

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