Publications by authors named "Tomke Cordts"

Progression of cystic kidney disease has been linked to activation of the mTORC1 signaling pathway. Yet the utility of mTORC1 inhibitors to treat patients with polycystic kidney disease remains controversial despite promising preclinical data. To define the cell intrinsic role of mTORC1 for cyst development, the mTORC1 subunit gene Raptor was selectively inactivated in kidney tubular cells lacking cilia due to simultaneous deletion of the kinesin family member gene Kif3A.

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Background: Primary anterolateral thigh (ALT) flap donor-site closure is crucial to achieve patient satisfaction, avoid burdensome secondary surgeries, and avert poor outcomes. Only vague maximum flap width recommendations have been suggested, which fall short of acknowledging individual patient habitus and thigh morphology. Therefore, we aimed at identifying a user-friendly preoperative calculation of maximum flap width for primary closure.

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Background: Chronic prevertebral soft tissue defects with exposed metal hardware following spinal surgery represent a challenging complication. Frequently patients underwent multiple previous operations due to wound complications. Surrounding soft tissues are often compromised due to malperfusion, severe subcutaneous scarring, previous local advancement flaps and therefore impair stable wound closure.

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Introduction: Full-thickness soft tissue defects of the back remain challenging clinical problems for reconstructive surgeons. Among a vast variety of local flap options, perforator-based local flaps gain increasing popularity lately. Because mostly heterogeneous patient cohort comparison of different perforator flaps is difficult and decision-making algorithms are lacking.

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Background: Burn-induced compartment syndrome is a severe sequela after circumferential burns of the extremities and is avoidable by immediate release of the underlying pressure under the eschar. Although the current gold standard is operative escharotomy, this procedure carries considerable morbidity. Our study evaluates the safety and effectiveness of immediate enzymatic debridement to prevent the need for operative escharotomy because of burn-induced compartment syndrome in selected patients.

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Purpose: The clinical course after major burns is characterized by microcirculatory changes and consecutive capillary leakage. However, current clinical monitoring does not properly assess microcirculation, whereas macrohemodynamic changes are continuously evaluated. Here, we assess if macrohemodynamic and microhemodynamic parameters after burn trauma are correlated in a rat model.

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A female patient with a critical soft tissue defect after elective knee replacement surgery was transferred to our department for reconstruction. As wounds were rapidly progressing, necrotizing fasciitis was initially suspected but eventually ruled out by histopathological analysis. A 50 × 15 cm defect was then reconstructed by means of a combined Parascapular and latissimus dorsi flap before, a couple days later, the patient developed tender pustules and ulcers involving the flap as well as the donor site.

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Background: Severe burns of hands and arms are complex and challenging injuries. The Standard of care (SOC) - necrosectomy with skin grafting - is often associated with poor functional or aesthetic outcome. Enzymatic debridement (ED) is considered one promising alternative but, until recently, results proved to be highly variable.

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The mTOR pathway orchestrates cellular homeostasis. The rapamycin-sensitive mTOR complex (mTORC1) in the kidney has been widely studied; however, mTORC2 function in renal tubules is poorly characterized. Here, we generated mice lacking mTORC2 in the distal tubule (Rictorfl/fl Ksp-Cre mice), which were viable and had no obvious phenotype, except for a 2.

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Mammalian target of rapamycin complex 1 (mTORC1) is a key regulator of cell metabolism and autophagy. Despite widespread clinical use of mTORC1 inhibitors, the role of mTORC1 in renal tubular function and kidney homeostasis remains elusive. By using constitutive and inducible deletion of conditional Raptor alleles in renal tubular epithelial cells, we discovered that mTORC1 deficiency caused a marked concentrating defect, loss of tubular cells, and slowly progressive renal fibrosis.

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