Retention force of polyetheretherketone and cobalt-chrome-molybdenum removable dental prosthesis clasps after artificial aging.

Objectives: To examine the retention force of removable dental prosthesis (RDP) clasps made from polyetheretherketone (PEEK) and cobalt-chrome-molybdenum (CoCrMo, control group) after storage in water and artificial aging.

Materials And Methods: For each material, 15 Bonwill clasps with retentive buccal and reciprocal lingual arms situated between the second pre- and first molar were manufactured by milling (Dentokeep [PEEKmilled1], NT digital implant technology; breCAM BioHPP Blank [PEEKmilled2], bredent), pressing (BioHPP Granulat for 2 press [PEEKpressed], bredent), or casting (remanium GM 800+ [CoCrMo], Dentaurum); N = 60, n = 15/subgroup. A total of 50 retention force measurements were performed for each specimen per aging level (initial; after storage [30 days, 37 °C] and 10,000 thermal cycles; after storage [60 days, 37 °C] and 20,000 thermal cycles) in a pull-off test.

Evolution of lung and kidney allograft function in patients receiving kidney after lung transplantation.

Calcineurin inhibitor (CNI) toxicity leads to end-stage renal disease in almost half of long-term survivors after lung transplantation, some of them receiving kidney transplants. Little is known about the outcomes of kidney and lung allograft function following kidney after lung transplantation (KALTPL) in the modern era. We retrospectively analyzed a group of 13 consecutive patients who received a KALTPL with respect to their renal and pulmonary function and immunological evolution over 2 years.

Mutation Update of the CLCN5 Gene Responsible for Dent Disease 1.

Dent disease is a rare X-linked tubulopathy characterized by low molecular weight proteinuria, hypercalciuria, nephrocalcinosis and/or nephrolithiasis, progressive renal failure, and variable manifestations of other proximal tubule dysfunctions. It often progresses over a few decades to chronic renal insufficiency, and therefore molecular characterization is important to allow appropriate genetic counseling. Two genetic subtypes have been described to date: Dent disease 1 is caused by mutations of the CLCN5 gene, coding for the chloride/proton exchanger ClC-5; and Dent disease 2 by mutations of the OCRL gene, coding for the inositol polyphosphate 5-phosphatase OCRL-1.