[Plastic Surgery in Palliative Care - Report on the Consensus Workshop of the 37th Annual Meeting of the German-language Group for Microsurgery of the Peripheral Nerves and Vessels (DAM) 2016 in Bochum]. / Plastische Chirurgie in der Palliation ­ Bericht des Consensus-Workshops im Rahmen der 37. Jahrestagung der Deutschsprachigen Gemeinschaft für Mikrochirurgie der peripheren Nerven und Gefäße (DAM) 2015 in Bochum.

Introduction: At the consensus meeting on "Plastic Surgery in the Palliative Situation" at the 37th Annual Meeting of the DAM 2015 in Bochum, treatment options were discussed with oncologists and palliative care anesthesiologists and recommendations were given. Methods: The literature was reviewed and the results of the expert-meeting options and limits of therapy were illustrated. The role of plastic surgery for palliative care patients was pointed out and recommendations given for successful cooperative treatment. Results: A rational combination of chemotherapy and surgery as well as early integration into a palliative care concept prolongs survival and improves the quality of life of patients in the palliative situation. Discussion: Plastic surgeons should regularily attend tumour boards to spread the knowledge of the value of reconstructive procedures in multidisciplinary treatment, in order to enhance the quality of live of the palliative patient. Participation in the preparation of the next treatment guidelines for palliative care would be desirable. Whenever patients are considered in a palliative situation, palliative care anesthesiologists should be involved.

Immunolesion-induced loss of cholinergic projection neurones promotes ß-amyloidosis and tau hyperphosphorylation in the hippocampus of triple-transgenic mice.

AIMS: Currently available animal models incompletely capture the complex pathophysiology of Alzheimer's disease (AD), typically involving ß-amyloidosis, neurofibrillary tangle formation and loss of basal forebrain cholinergic projection neurones (CPN). While age-dependent ß-amyloidosis and tau hyperphosphorylation are mimicked in triple-transgenic mice (3xTg), experimental induction of CPN loss in these mice is still lacking. Here, we introduce a more-complex animal model of AD by inducing cellular loss of CPN in an already existing transgenic background aiming to elucidate subsequent changes of hippocampal ß-amyloid (Aß) and tau pathology. METHODS: Twelve-month-old 3xTg mice intracerebroventricularly received the rabbit-anti-low affinity neurotrophin receptor p75-saporin, an immunotoxin specifically targeting forebrain CPN. After histochemical verification of immunolesion in immersion-fixed forebrains, markers of Aß and tau metabolism were analysed using quantitative Western blot analyses of hippocampi from these mice. In parallel, these markers and glial activation were investigated by multiple immunofluorescence labelling of perfusion-fixed hippocampi and confocal laser-scanning microscopy. RESULTS: Four months after immunolesion, the selective lesion of CPN was verified by disappearance of choline acetyltransferase and p75 immunolabelling. Biochemical analysis of hippocampi from immunolesioned mice revealed enhanced levels of Aß, amyloid precursor protein (APP) and its fragment C99. Furthermore, immunolesion-induced increase in levels of phospho-tau and tau with AD-like conformation were seen in 16-month-old mice. Immunofluorescence staining confirmed an age-dependent occurrence of hippocampal Aß-deposits and phospho-tau, and demonstrated drastic gliosis around Aß-plaques after immunolesion. CONCLUSION: Overall, this extended model promises further insights into the complexity of AD and contributes to novel treatment strategies also targeting the cholinergic system.