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"text": "\n171032\np53 Functions in Adipose Tissue Metabolism and Homeostasis.\n\nKrstic, J\n\nReinisch, I\n\nSchupp, M\n\nSchulz, TJ\n\nProkesch, A\n\nBeiträge in Fachzeitschriften\nISI:000449988100158\n30181511.0\n10.3390/ijms19092622\nPMC6165290\nAs a tumor suppressor and the most frequently mutated gene in cancer, p53 is among the best-described molecules in medical research. As cancer is in most cases an age-related disease, it seems paradoxical that p53 is so strongly conserved from early multicellular organisms to humans. A function not directly related to tumor suppression, such as the regulation of metabolism in nontransformed cells, could explain this selective pressure. While this role of p53 in cellular metabolism is gradually emerging, it is imperative to dissect the tissue- and cell-specific actions of p53 and its downstream signaling pathways. In this review, we focus on studies reporting p53's impact on adipocyte development, function, and maintenance, as well as the causes and consequences of altered p53 levels in white and brown adipose tissue (AT) with respect to systemic energy homeostasis. While whole body p53 knockout mice gain less weight and fat mass under a high-fat diet owing to increased energy expenditure, modifying p53 expression specifically in adipocytes yields more refined insights: (1) p53 is a negative regulator of in vitro adipogenesis; (2) p53 levels in white AT are increased in diet-induced and genetic obesity mouse models and in obese humans; (3) functionally, elevated p53 in white AT increases senescence and chronic inflammation, aggravating systemic insulin resistance; (4) p53 is not required for normal development of brown AT; and (5) when p53 is activated in brown AT in mice fed a high-fat diet, it increases brown AT temperature and brown AT marker gene expression, thereby contributing to reduced fat mass accumulation. In addition, p53 is increasingly being recognized as crucial player in nutrient sensing pathways. Hence, despite existence of contradictory findings and a varying density of evidence, several functions of p53 in adipocytes and ATs have been emerging, positioning p53 as an essential regulatory hub in ATs. Future studies need to make use of more sophisticated in vivo model systems and should identify an AT-specific set of p53 target genes and downstream pathways upon different (nutrient) challenges to identify novel therapeutic targets to curb metabolic diseases.\n\nKrstic, Jelena\n\nProkesch, Andreas\n\nReinisch, Isabel Nadine\n\n\n"
},
{
"text": "\n176913\nPresenilin-1 Established ER-Ca<sup>2+</sup> Leak: a Follow Up on Its Importance for the Initial Insulin Secretion in Pancreatic Islets and β-Cells upon Elevated Glucose.\n\nKlec, C\n\nMadreiter-Sokolowski, CT\n\nZiomek, G\n\nStryeck, S\n\nSachdev, V\n\nDuta-Mare, M\n\nGottschalk, B\n\nDepaoli, MR\n\nRost, R\n\nHay, J\n\nWaldeck-Weiermair, M\n\nKratky, D\n\nMadl, T\n\nMalli, R\n\nGraier, WF\n\nBeiträge in Fachzeitschriften\nNone\n31529929.0\n10.33594/000000158\nNone\nIn our recent work, the importance of GSK3β-mediated phosphorylation of presenilin-1 as crucial process to establish a Ca2+ leak in the endoplasmic reticulum and, subsequently, the pre-activation of resting mitochondrial activity in β-cells was demonstrated. The present work is a follow-up and reveals the importance of GSK3β-phosphorylated presenilin-1 for responsiveness of pancreatic islets and β-cells to elevated glucose in terms of cytosolic Ca2+ spiking and insulin secretion.\n Freshly isolated pancreatic islets and the two pancreatic β-cell lines INS-1 and MIN-6 were used. Cytosolic Ca2+ was fluorometrically monitored using Fura-2/AM and cellular insulin content and secretion were measured by ELISA.\n Our data strengthened our previous findings of the existence of a presenilin-1-mediated ER-Ca2+ leak in β-cells, since a reduction of presenilin-1 expression strongly counteracted the ER Ca2+ leak. Furthermore, our data revealed that cytosolic Ca2+ spiking upon administration of high D-glucose was delayed in onset time and strongly reduced in amplitude and frequency upon siRNA-mediated knock-down of presenilin-1 or the inhibition of GSK3β in the pancreatic β-cells. Moreover, glucose-triggered initial insulin secretion disappeared by depletion from presenilin-1 and inhibition of GSK3β in the pancreatic β-cells and isolated pancreatic islets, respectively.\n These data complement our previous work and demonstrate that the sensitivity of pancreatic islets and β-cells to glucose illustrated as glucose-triggered cytosolic Ca2+ spiking and initial but not long-lasting insulin secretion crucially depends on a strong ER Ca2+ leak that is due to the phosphorylation of presenilin-1 by GSK3β, a phenomenon that might be involved in the development of type 2 diabetes.\n © Copyright by the Author(s). Published by Cell Physiol Biochem Press.\n\nGottschalk, Benjamin\n\nGraier, Wolfgang\n\nKlec, Christiane\n\nKratky, Dagmar\n\nMadl, Tobias\n\nMadreiter-Sokolowski, Corina\n\nMalli, Roland\n\nRost, René\n\nWaldeck-Weiermair, Markus\n\n\n"
},
{
"text": "\n182083\nBrain Volume: An Important Determinant of Functional Outcome After Acute Ischemic Stroke.\n\nSchirmer, MD\n\nDonahue, KL\n\nNardin, MJ\n\nDalca, AV\n\nGiese, AK\n\nEtherton, MR\n\nMocking, SJT\n\nMcIntosh, EC\n\nCole, JW\n\nHolmegaard, L\n\nJood, K\n\nJimenez-Conde, J\n\nKittner, SJ\n\nLemmens, R\n\nMeschia, JF\n\nRosand, J\n\nRoquer, J\n\nRundek, T\n\nSacco, RL\n\nSchmidt, R\n\nSharma, P\n\nSlowik, A\n\nStanne, TM\n\nVagal, A\n\nWasselius, J\n\nWoo, D\n\nBevan, S\n\nHeitsch, L\n\nPhuah, CL\n\nStrbian, D\n\nTatlisumak, T\n\nLevi, CR\n\nAttia, J\n\nMcArdle, PF\n\nWorrall, BB\n\nWu, O\n\nJern, C\n\nLindgren, A\n\nMaguire, J\n\nThijs, V\n\nRost, NS\n\nMRI-GENIE and GISCOME Investigators and the International Stroke Genetics Consortium\n\nBeiträge in Fachzeitschriften\nISI:000540247200019\n32370856.0\n10.1016/j.mayocp.2020.01.027\nNone\nTo determine whether brain volume is associated with functional outcome after acute ischemic stroke (AIS).\n This study was conducted between July 1, 2014, and March 16, 2019. We analyzed cross-sectional data of the multisite, international hospital-based MRI-Genetics Interface Exploration study with clinical brain magnetic resonance imaging obtained on admission for index stroke and functional outcome assessment. Poststroke outcome was determined using the modified Rankin Scale score (0-6; 0 = asymptomatic; 6 = death) recorded between 60 and 190 days after stroke. Demographic characteristics and other clinical variables including acute stroke severity (measured as National Institutes of Health Stroke Scale score), vascular risk factors, and etiologic stroke subtypes (Causative Classification of Stroke system) were recorded during index admission.\n Utilizing the data from 912 patients with AIS (mean ± SD age, 65.3±14.5 years; male, 532 [58.3%]; history of smoking, 519 [56.9%]; hypertension, 595 [65.2%]) in a generalized linear model, brain volume (per 155.1 cm3) was associated with age (β -0.3 [per 14.4 years]), male sex (β 1.0), and prior stroke (β -0.2). In the multivariable outcome model, brain volume was an independent predictor of modified Rankin Scale score (β -0.233), with reduced odds of worse long-term functional outcomes (odds ratio, 0.8; 95% CI, 0.7-0.9) in those with larger brain volumes.\n Larger brain volume quantified on clinical magnetic resonance imaging of patients with AIS at the time of stroke purports a protective mechanism. The role of brain volume as a prognostic, protective biomarker has the potential to forge new areas of research and advance current knowledge of the mechanisms of poststroke recovery.\n Copyright © 2020. Published by Elsevier Inc.\n\nSchmidt, Reinhold\n\n\n"
},
{
"text": "\n185390\nPosterior fragment in ankle fractures: anteroposterior vs posteroanterior fixation.\n\nVidović, D\n\nElabjer, E\n\nMuškardin, IVA\n\nMilosevic, M\n\nBekic, M\n\nBakota, B\n\nBeiträge in Fachzeitschriften\nNone\n29122126.0\n10.1016/S0020-1383(17)30743-X\nNone\nThe aim of this study was to compare reduction quality and functional outcome of posterior malleolus fractures treated with indirect reduction and anteroposterior (AP) fixation or with direct reduction via a posterolateral approach and posteroanterior (PA) fixation.\n Forty-eight patients with trimalleolar fracture were enrolled in the study. Patients were randomised in two groups: indirect reduction and AP fixation (AP group) and direct reduction and PA fixation (PA group). Inclusion criteria were: posterior fragment involving more than 25% of the articular surface, displacement over 2mm and ankle instability. The quality of reduction was evaluated using postoperative plain radiographs. Residual displacement of the posterior fragment, articular step-off and/or articular surface gap were analysed. The reduction was considered excellent (<1mm), good (1-2mm) or poor (>2mm). Range of motion (ROM) was measured bilaterally, and the difference in dorsiflexion between the injured and uninjured side was considered as dorsiflexion restriction. Demographic data (age, sex), type of fracture (AO/ASIF classification) and complications were noted.\n Forty-six patients completed all follow-up examinations. There was no statistically significant difference in age (p = 0.41), sex (p = 0.29) or specific type of fracture (p = 0.83) distribution between the AP and PA groups. All fractures completely healed within 3 months. The overall complication rate was 8.7%. There was no statistically significant difference in complication rate between the two groups (p = 0.71). Radiological evaluation of the ankle showed there was significantly better quality of reduction with direct reduction via a posterolateral approach in the PA group. Excellent reduction was achieved in 79.2% and 45.5% of the PA and AP groups, respectively. The quality of reduction was significantly higher in the PA group compared with the AP group (p = 0.04). The mean restriction of dorsiflexion was lower in the PA group (5.96 ± 0.65°) compared with the AP group (6.45 ± 1.06°), but this difference did not reach statistical significance (p = 0.07).\n The direct reduction technique via a posterolateral approach and PA fixation enables higher quality of reduction and better functional outcome in the management of the posterior fragment compared with indirect reduction and percutaneous AP fixation.\n © 2017 Elsevier Ltd. All rights reserved.\n\n\n"
},
{
"text": "\n187331\nRiociguat for the treatment of pulmonary arterial hypertension.\n\nGhofrani, HA\n\nGaliè, N\n\nGrimminger, F\n\nGrünig, E\n\nHumbert, M\n\nJing, ZC\n\nKeogh, AM\n\nLangleben, D\n\nKilama, MO\n\nFritsch, A\n\nNeuser, D\n\nRubin, LJ\n\nPATENT-1 Study Group\n\nBeiträge in Fachzeitschriften\nNone\n23883378.0\n10.1056/NEJMoa1209655\nNone\nRiociguat, a soluble guanylate cyclase stimulator, has been shown in a phase 2 trial to be beneficial in the treatment of pulmonary arterial hypertension.\n In this phase 3, double-blind study, we randomly assigned 443 patients with symptomatic pulmonary arterial hypertension to receive placebo, riociguat in individually adjusted doses of up to 2.5 mg three times daily (2.5 mg-maximum group), or riociguat in individually adjusted doses that were capped at 1.5 mg three times daily (1.5 mg-maximum group). The 1.5 mg-maximum group was included for exploratory purposes, and the data from that group were analyzed descriptively. Patients who were receiving no other treatment for pulmonary arterial hypertension and patients who were receiving endothelin-receptor antagonists or (nonintravenous) prostanoids were eligible. The primary end point was the change from baseline to the end of week 12 in the distance walked in 6 minutes. Secondary end points included the change in pulmonary vascular resistance, N-terminal pro-brain natriuretic peptide (NT-proBNP) levels, World Health Organization (WHO) functional class, time to clinical worsening, score on the Borg dyspnea scale, quality-of-life variables, and safety.\n By week 12, the 6-minute walk distance had increased by a mean of 30 m in the 2.5 mg-maximum group and had decreased by a mean of 6 m in the placebo group (least-squares mean difference, 36 m; 95% confidence interval, 20 to 52; P<0.001). Prespecified subgroup analyses showed that riociguat improved the 6-minute walk distance both in patients who were receiving no other treatment for the disease and in those who were receiving endothelin-receptor antagonists or prostanoids. There were significant improvements in pulmonary vascular resistance (P<0.001), NT-proBNP levels (P<0.001), WHO functional class (P=0.003), time to clinical worsening (P=0.005), and Borg dyspnea score (P=0.002). The most common serious adverse event in the placebo group and the 2.5 mg-maximum group was syncope (4% and 1%, respectively).\n Riociguat significantly improved exercise capacity and secondary efficacy end points in patients with pulmonary arterial hypertension. (Funded by Bayer HealthCare; PATENT-1 and PATENT-2 ClinicalTrials.gov numbers, NCT00810693 and NCT00863681, respectively.).\n\nOlschewski, Horst\n\n\n"
},
{
"text": "\n187698\nRecombinant versus bovine hyaluronidase for oocyte denudation before intracytoplasmic sperm injection: a systematic review and meta-analysis\n\nTsampras, N\n\nKollmann, M\n\nCraciunas, L\n\nBeiträge in Fachzeitschriften\nISI:000646430400001\n33938350.0\n10.1080/01443615.2021.1893670\nNone\nThe removal of cumulus cells in a process called oocyte denudation is required in order to visualise, grade and manipulate the oocytes before injection. The objective of this study was to appraise critically the published randomised controlled trials (RCTs) comparing recombinant hyaluronidase with bovine hyaluronidase for oocyte denudation before intracytoplasmic sperm injection (ICSI). We performed a comprehensive literature search of the standard medical databases in order to identify the RCTs comparing oocyte denudation with recombinant hyaluronidase or bovine hyaluronidase before ICSI. Three RCTs involving 2445 oocytes collected from 200 women were analysed. There was substantial heterogeneity among the included RCTs. A meta-analysis from the available moderate to high quality trials found no statistical difference in terms of fertilisation rate, embryo quality and live birth rate between the use of recombinant or bovine hyaluronidase for oocyte denudation before ICSI.IMPACT STATEMENT What is already known on this subject? The removal of cumulus cells in a process called oocyte denudation is required in order to visualise, grade and manipulate the oocytes before injection. The long-established source of hyaluronidase has been represented by bovine testes, but concern has been raised regarding the possible negative effects over the fragile oocytes by mechanisms involving low enzyme purity, variable concentrations, trauma, prolonged exposure and integration of external DNA in the oocyte. Recombinant human hyaluronidase has been proposed as an alternative in order to counteract the possible negative effects of using animal derived products. What do the results of this study add? A meta-analysis from the available moderate to high quality trials found no statistical difference in fertilisation rate, embryo quality and live birth rate between the use of recombinant or bovine hyaluronidase for oocyte denudation before ICSI. What are the implications of these findings or clinical practice and/or further research? Future trials should be powered adequately in order to be able to identify the possible small differences between the study groups and they should be conducted according to the CONSORT guidelines as the absence of blinding for outcome assessors can induce detection bias.\n\nKollmann, Martina\n\n\n"
},
{
"text": "\n482\nClinical and histological features of poor prognosis in cutaneous metastatic melanomas.\n\nHofmann-Wellenhof, R\n\nWoltsche-Kahr, I\n\nSmolle, J\n\nKerl, H\n\nBeiträge in Fachzeitschriften\nISI:A1996UQ07700001\n8793653.0\n10.1111/j.1600-0560.1996.tb01467.x\nNone\nPatients with melanoma metastatic to the skin show variable prognosis. Though some may survive for quite a long time, some die of disseminated disease within 1 year of removal of cutaneous metastases. The aim of this study was to find out whether there are any histological criteria indicating particular poor outcome. Clinical and histological features of 344 melanoma lesions metastatic to the skin were assessed and their prognostic relevance was investigated. H&E stained histological slides were scanned for the presence of morphological criteria expressing certain tumor cell-stroma interactions: capsule formation (CAPSULE), formation of intratumoral septa (NEWSEPTA), simple invasion between collagen of reticular dermis (DERM-SIMPLE), or subcutis (SCSIMPLE), preservation of preexistent collagen (PRECOLL) or fatty tissue (PREFAT) and, finally, histological site of metastasis. Additionally, anatomical location of the metastases, time between removal of primary tumor and metastases age and sex of patients were recorded. The metastases were divided into two groups: lesions of patients who died within 1 year after resection (n = 59) and lesions from patients with a longer survival (n = 285). Metastases which were associated with death within one year were significantly more often found in male patients (54.2% versus 34.7%), in younger patients (mean age 51.1 +/- 14.1 years versus 58.8 +/- 15.3 years), had developed earlier after the primary tumor (mean time of 21.7 +/- 19.9 months versus 43.3 +/- 27.4 months) and were more often found at distant sites than in localregional sites (45.7% versus 30.5%), and were more often involved in the subcutis (74.5% versus 56.1%). From a histological point of view, DERMSIMPLE (80% versus 46%; p < 0.001) and PRECOLL (82.8% versus 57.6; p < 0.01) were more frequent in metastases of poor outcome. The same was true for SCSIMPLE (50% versus 25.6%; p < 0.01) and PREFAT (68.1% versus 46.8%; p < 0.05) in lesion with subcutaneous growth, whereas CAPSULE (54.5% versus 75%) was less frequently seen. In conclusion, melanoma deposits metastatic to the skin with particular poor outcome differ clinically and histologically from other cutaneous melanoma metastases. This should be taken into account in the design of therapeutic clinical trials.\n\nHofmann-Wellenhof, Rainer\n\nKerl, Helmut\n\nSmolle, Josef\n\n\n"
},
{
"text": "\n4175\nSupracondylar humerus fracture in childhood--an efficacy study. Results of a multicenter study by the Pediatric Traumatology Section of the German Society of Trauma Surgery--I: Epidemiology, effectiveness evaluation and classification\n\nWeinberg, AM\n\nMarzi, I\n\nGünter, SM\n\nWessel, L\n\nRiedel, J\n\nvon Laer, L\n\nBeiträge in Fachzeitschriften\nISI:000174860500004\n11995215.0\n10.1007%2Fs001130100314\nNone\nIn this retrospective study of the pediatric trauma group of German trauma society, issued to investigate the state of the art treatment of the supracondylar fracture of the humerus, 13 clinics took part. In this first part of our study we tested the epidemiology and effectivity of therapeutic interventions based on the classification of v. Laer. 886 fractures were included with an average patients age of 5.8 years (+/- 2.9). Causes of trauma was in 45% playing, followed by school/kindergarden and sports injuries. Fractures were initially classified according to v. Laer and showed following displacement: 35.4% Type I, 21.9% Type II, 18.1% Type III and 24.6% Type IV. 10 of the 886 cases (1.1%) were open fractures. Damages to nerves were described in 45 patients (5.1%) and only 7 (0.7%) had primary vessel lesions. 476 patients were treated by reduction of fragments, 72% using a closed technical approach and 28% using an open approach. 6% underwent a second resposition-maneuver, which was mainly observed after crossed Kirschner-wire in type-III-and-IV-fractures. Therapy was changed in 5.1% mostly of the cases were initially closed reduced and then fixed with a collar and cuff sling. 540 patients were seen at follow-up (61%). 81.1% of these patients showed symmetrical axis compared to the uninjured arm. A varus-deformity was noted in 11.7%, a valgus-deformity in 7.2%. Analysis of effectivity showed that the primarily used classification was not sufficient for prediction of the outcome after reposition and retention. Therefore the classification was modified based on 4 groups: Type I undisplaced, Type II displacement in one plane, Type III displacement in two planes and Type IV displacement in three spatial planes. Using this classification we could found that in group II 25% of reduction an 7% of retentions were ineffective. For group III and IV we found that > 20% of the retention proofed to be ineffective.\n\nWeinberg, Annelie-Martina\n\n\n"
},
{
"text": "\n63663\nLoss of active MEK1-ERK1/2 restores epithelial phenotype and morphogenesis in transdifferentiated MDCK cells.\n\nSchramek, H\n\nFeifel, E\n\nMarschitz, I\n\nGolochtchapova, N\n\nGstraunthaler, G\n\nMontesano, R\n\nBeiträge in Fachzeitschriften\nISI:000184549600019\n12900389.0\n10.1152/ajpcell.00463.2002\nNone\nConstitutive activation of the MAPK/ERK kinase (MEK)1-ERK2 signaling module in Madin-Darby canine kidney (MDCK)-C7 cells disrupts their ability to form cyst-like structures in collagen gels and induces an invasive, myofibroblast-like phenotype. However, the reversibility of these cellular events, as well as the relative role of both MEK isoforms (MEK1 and MEK2) and both ERK isoforms (ERK1 and ERK2) during these processes, has not yet been investigated. We now report that loss of constitutively active MEK1 (caMEK1) and, thus, loss of active ERK1/2 in C7caMEK1 cells is associated with increased MEK2 protein expression, reexpression of ERK1 protein, and epithelial redifferentiation of these cells. The morphological changes toward an epithelial phenotype in these revertant cell lines (C7rev4, C7rev5, C7rev7) are reflected by the upregulation of epithelial marker proteins, such as E-cadherin, beta-catenin, and cytokeratin, by the loss of alpha-smooth muscle actin expression, and by the ability of these epithelial revertants to form well-organized spherical cysts when grown in three-dimensional collagen gels. Further evidence for a role of the MEK1-ERK1/2 module in epithelial-mesenchymal transition was obtained from the analysis of two novel, spontaneously transdifferentiated MDCK-C7 cell clones (C7e1 and C7e2 cells). In these clones, increased MEK1/2-ERK1/2 phosphorylation, reduced MEK2 protein expression, and loss of ERK1 protein expression is associated with phenotypic alterations similar to those observed in transdifferentiated C7caMEK1 cells. C7e1 cells at least partially regained some of their epithelial characteristics at higher passages. In contrast, C7e2 cells maintained a transdifferentiated phenotype at high passage, were unable to generate cyst-like epithelial structures, and retained invasive properties when grown on a three-dimensional collagen matrix. We conclude that in renal epithelial MDCK-C7 cells, stable epithelial-to-mesenchymal transition (EMT) is associated with loss of ERK1 protein expression, reduced MEK2 protein expression, and increased basal ERK2 phosphorylation. In contrast, loss of active MEK1-ERK1/2 results in increased MEK2 protein expression and reexpression of ERK1 protein, concomitant with the restoration of epithelial phenotype and the ability to form cystic structures.\n\nMarschitz, Ingrid Christine\n\n\n"
},
{
"text": "\n86912\nChemokines and interleukin-18 are up-regulated in bronchoalveolar lavage fluid but not in serum of septic surgical ICU patients.\n\nMathiak, G\n\nNeville, LF\n\nGrass, G\n\nBoehm, SA\n\nLuebke, T\n\nHerzmann, T\n\nKabir, K\n\nRosendahl, R\n\nSchaefer, U\n\nMueller, C\n\nBohlen, H\n\nWassermann, K\n\nHoelscher, AH\n\nBeiträge in Fachzeitschriften\nISI:000167071100003\n11236899.0\n10.1097/00024382-200115030-00003\nNone\nOur objective was to investigate the levels of chemokines (MIP1-alpha, MCP-1, and Gro-alpha), Interleukin-18 (IL-18), and Interleukin (IL-6) in bronchoalveolar lavage (BAL) fluid and serum at the onset and ongoing states of sepsis as defined by the American College of Chest Physicians/Society of Critical Care Medicine in septic surgical ICU patients. Our summary background data was to understand the significance of compartmentalized inflammatory mediator production in an immunologically active organ (lung) in comparison with levels in the systemic circulation. The study group consisted of 20 septic patients and 10 non-septic patients on surgical ICU. At the onset of sepsis, both BAL fluid and serum samples were taken and levels of MIP-1alpha, MCP-1, GRO-alpha, IL-18, and IL-6 were measured by ELISA. Furthermore, over a subsequent 8-day period, levels of these mediators were determined in serum. In some experiments, IL-18 mRNA levels were determined in peripheral blood lymphocytes (PBL) of septic and non-septic patients. At the onset of sepsis, MIP-1alpha, MCP-1, GRO-alpha, IL-18, and IL-6 levels were significantly up-regulated in BAL fluid as compared with non-septic controls. In marked contrast, with the exception of IL-18 mRNA and IL-6 peptide, there was no increase in serum levels of inflammatory mediators determined both at the onset and during the ongoing states of sepsis. Based on the present data, monitoring levels of serum chemokines and IL-18 protein as markers of sepsis might be misleading since despite their non-detection in serum, they were highly up-regulated in the lung tissue compartment. These data might underscore the role of MIP-1alpha, MCP-1, GRO-alpha, and IL-18 in the mediation of local tissue damage. Furthermore, these findings raise the notion that mediator measurement in immunologically active organs might serve as pivotal indicators of sepsis prior to the actual fulfillment of specific clinical criteria that defines the patient as being septic.\n\nSchäfer, Ute\n\n\n"
},
{
"text": "\n120880\nLymphotoxin β receptor signaling promotes development of autoimmune pancreatitis.\n\nSeleznik, GM\n\nReding, T\n\nRomrig, F\n\nSaito, Y\n\nMildner, A\n\nSegerer, S\n\nSun, LK\n\nRegenass, S\n\nLech, M\n\nAnders, HJ\n\nMcHugh, D\n\nKumagi, T\n\nHiasa, Y\n\nLackner, C\n\nHaybaeck, J\n\nAngst, E\n\nPerren, A\n\nBalmer, ML\n\nSlack, E\n\nMacPherson, A\n\nManz, MG\n\nWeber, A\n\nBrowning, JL\n\nArkan, MC\n\nRülicke, T\n\nAguzzi, A\n\nPrinz, M\n\nGraf, R\n\nHeikenwalder, M\n\nBeiträge in Fachzeitschriften\nISI:000310459700049\n22863765.0\n10.1053/j.gastro.2012.07.112\nNone\nBACKGROUND AND AIMS: Little is known about the pathogenic mechanisms of autoimmune pancreatitis (AIP), an increasingly recognized, immune-mediated form of chronic pancreatitis. Current treatment options are limited and disease relapse is frequent. We investigated factors that contribute to the development of AIP and new therapeutic strategies. METHODS: We used quantitative polymerase chain reaction, immunohistochemical, and enzyme-linked immunosorbent analyses to measure the expression of cytokines and chemokines in tissue and serum samples from patients with and without AIP. We created a mouse model of human AIP by overexpressing lymphotoxin (LT)alpha and beta specifically in acinar cells (Ela1-LTab mice). RESULTS: Messenger RNA levels of LT alpha and beta were increased in pancreatic tissues from patients with AIP, compared with controls, and expression of chemokines (CXCL13, CCL19, CCL21, CCL1, and B-cell-activating factor) was increased in pancreatic and serum samples from patients. Upregulation of these factors was not affected by corticosteroid treatment. Acinar-specific overexpression of LT alpha beta (Ela1-LT alpha beta) in mice led to an autoimmune disorder with various features of AIP. Chronic inflammation developed only in the pancreas but was sufficient to cause systemic autoimmunity. Acinar-specific overexpression of LT alpha beta did not cause autoimmunity in mice without lymphocytes (Ela1-LTab/Rag1(-/-)); moreover, lack of proinflammatory monocytes (Ela1-LTab/Ccr2(-/-)) failed to prevent AIP but prevented early pancreatic tissue damage. Administration of corticosteroids reduced pancreatitis but did not affect production of autoantibodies, such as antipancreatic secretory trypsin inhibitor in Ela1-LTab mice. In contrast, inhibition of LT beta R signaling reduced chemokine expression, renal immune-complex deposition, and features of AIP in Ela1-LTab mice. CONCLUSIONS: Overexpression of LT alpha beta specifically in acinar cells of mice causes features of AIP. Reagents that neutralize LT beta R ligands might be used to treat patients with AIP.\n\nHaybäck, Johannes\n\nLackner, Karoline\n\n\n"
},
{
"text": "\n145178\nOncogenic human papillomavirus-associated nasopharyngeal carcinoma: an observational study of correlation with ethnicity, histological subtype and outcome in a UK population.\n\nRobinson, M\n\nSuh, YE\n\nPaleri, V\n\nDevlin, D\n\nAyaz, B\n\nPertl, L\n\nThavaraj, S\n\nBeiträge in Fachzeitschriften\nISI:000326167000001\n23938045.0\n10.1186/1750-9378-8-30\nPMC3751535\nNasopharyngeal carcinoma (NPC) accounts for 0.6% of all cancers worldwide with the highest prevalence in South East Asia, Southern China and Northern Africa but the disease is uncommon in Europe with an annual incidence in this region of less than 1 per 100 000. Although the Epstein-Barr virus (EBV) is a well known causative agent in NPC, recent reports have implicated oncogenic Human Papillomavirus (HPV) in a subgroup of these tumours. The recent striking rise of oropharyngeal carcinoma has been attributed to HPV, but little is known about the prevalence and clinical significance of the virus in NPC. The aim of this study was to determine the prevalence of oncogenic HPV in NPC from tissue archives of two head and neck cancer centres in the UK.\n Samples were available for 67 patients with clinically validated NPC. The detection of high-risk HPV was carried out by screening all cases for p16 using immunohistochemistry and HPV DNA by polymerase chain reaction (PCR) using GP5+/6+ primers. All cases with p16 over-expression or positive for HPV by PCR were then examined by high-risk HPV DNA in-situ hybridisation and genotype analysis by PCR.\n Eleven cases (11/67, 16.4%) showed concurrent over-expression of p16 and evidence of high-risk HPV DNA by in-situ hybridisation; the majority were HPV16 positive. Of these 11 cases, nine occurred in Whites and two in Blacks. Histologically, there were two keratinising squamous cell carcinoma and nine non-keratinising carcinomas (eight differentiated and one undifferentiated). None of the HPV-positive cases showed any co-infection with EBV. There was no statistically significant difference in overall survival outcome between patients with HPV-positive and HPV-negative NPC.\n The results of this study show that oncogenic HPV is associated with a subgroup of NPCs and is more likely to occur in Whites. However, unlike oropharyngeal carcinoma there was no significant difference in overall survival between patients with HPV-positive and HPV-negative NPC.\n\nPosch-Pertl, Laura\n\n\n"
},
{
"text": "\n172262\nSarcopenic Obesity: Time to Meet the Challenge.\n\nBarazzoni, R\n\nBischoff, S\n\nBoirie, Y\n\nBusetto, L\n\nCederholm, T\n\nDicker, D\n\nToplak, H\n\nVan Gossum, A\n\nYumuk, V\n\nVettor, R\n\nBeiträge in Fachzeitschriften\nISI:000454455800003\n30016792.0\n10.1159/000490361\nPMC6189532\nThe prevalence of overweight and obesity has reached epidemic proportions worldwide due to increasingly pervasive obesogenic lifestyle changes. Obesity poses unprecedented individual, social, and multidisciplinary medical challenges by increasing the risk for metabolic diseases, chronic organ failures, and cancer as well as complication rates in the presence of acute disease conditions. Whereas reducing excess adiposity remains the fundamental pathogenic treatment for obese individuals, complex metabolic and lifestyle abnormalities as well as weight reduction therapies per se may also compromise the ability to preserve muscle function and mass, especially when chronic disease co-exists with obesity. Emerging evidence indicates that low muscle mass and quality have a strong negative prognostic impact in obese individuals and may lead to frailty, disability, and increased morbidity and mortality. Awareness of the importance of skeletal muscle maintenance in obesity is however low among clinicians and scientists. The term 'sarcopenic obesity' has been proposed to identify obesity with low skeletal muscle function and mass, but its utilization is largely limited to the aging patient population, and consensus on its definition and diagnostic criteria remains insufficient. Knowledge on prevalence of sarcopenic obesity in various clinical conditions and patient subgroups, on its clinical impacts in patient risk stratification, and on effective prevention and treatment strategies remain therefore dramatically inadequate. In particular, optimal dietary options and medical nutritional support strategies to preserve muscle mass in obese individuals remain largely undefined. The European Society for Clinical Nutrition and Metabolism (ESPEN) and the European Association for the Study of Obesity (EASO) recognize and indicate obesity with altered body composition due to low skeletal muscle function and mass (sarcopenic obesity) as a scientific and clinical priority for researchers and clinicians. ESPEN and EASO therefore call for coordinated action aimed at reaching consensus on its definition, diagnostic criteria, and optimal treatment with particular regard to nutritional therapy. We are convinced that achievement of these goals has a strong potential to reduce the burden of morbidity and mortality in the rapidly increasing obese patient population.\n © 2018 The Author(s) Published by S. Karger GmbH, Freiburg.\n\nToplak, Hermann\n\n\n"
},
{
"text": "\n6154\nEffects of prostaglandin E1 metabolites on the induction of arterial thromboresistance.\n\nSinzinger, H\n\nNeumann, I\n\nO'Grady, J\n\nRogatti, W\n\nPeskar, BA\n\nBeiträge in Fachzeitschriften\nISI:000075011200001\n9653766.0\n10.1016%2FS0090-6980%2898%2900025-2\nNone\nProstaglandin (PG) E1 has been shown to induce arterial thromboresistance in experimental animals and in man. It is known to be degraded in vivo to metabolites which have comparable (13, 4-dihydro-PGE1) or no (15-keto-PGE1, 15-keto-13, 4-dihydro-PGE1) biological activity. It was the goal of this study to examine whether 13, 4-dihydro-PGE1 and its derivatives might share biological activity in rendering the arterial wall less thrombogenic. Using a cross-perfusion technique the aorta and iliac artery surface were exposed to a donor rabbits' blood. We examined the intact endothelial lining and a surface which had been deendothelialized before by means of a Fogarty catheter. Donor animals and/or receiver animals were treated daily for 1 week with 13, 4-dihydro-PGE1, PGE1, 15-keto-PGE1, 15-keto-13, 4-dihydro-PGE1, or the vehicle only, respectively. From the group of the receiver animals, a subgroup of 6 animals each was treated for the same period of time with either 13, 4-dihydro-PGE1, PGE1, 15-keto-PGE1, 15-keto-13, 4-dihydro-PGE1, or the vehicle. Immediately after the last administration of the respective PG or solvent, native blood from a donor rabbit was circulated [30 mL/min. under in vivo flow conditions (60 Hz)] over an arterial segment of a receiver animal. Deposition of 111Indium-oxine labeled autologous platelets per surface unit was quantitatively assessed. In vitro perfusion data were morphometrically analysed. In animals pretreated with 13, 4-dihydro-PGE1 the thromboresistance was almost comparable to that achieved with PGE1. In contrast, pretreatment of the donor animals (platelet) had only minor effects on the thromboresistance. The other compounds showed no effects. In vitro perfusion of human saphenous vein segments revealed PGE1 and 13, 4-dihydro-PGE1 again to be of comparable potency, while 15-keto-PGE1 and 15-keto-13, 4-dihydro-PGE1 were only active at concentrations being several orders of magnitude higher. Not only PGE1 but also its in vivo formed metabolite PGE0 may play an important role in inducing improvement of haemostatic balance via the vascular wall rather than the platelets. The other metabolites, however, are unlikely to exhibit an effect at biologically relevant concentrations.\n\nPeskar, Bernhard\n\n\n"
},
{
"text": "\n112368\nAssessing the clinical benefit of nuclear matrix protein 22 in the surveillance of patients with nonmuscle-invasive bladder cancer and negative cytology: a decision-curve analysis.\n\nShariat, SF\n\nSavage, C\n\nChromecki, TF\n\nSun, M\n\nScherr, DS\n\nLee, RK\n\nLughezzani, G\n\nRemzi, M\n\nMarberger, MJ\n\nKarakiewicz, PI\n\nVickers, AJ\n\nBeiträge in Fachzeitschriften\nISI:000292056200011\n21692050.0\n10.1002/cncr.25903\nPMC3334293\nBACKGROUND: Several studies have demonstrated that abnormal levels of nuclear matrix protein 22 (NMP22) are associated with bladder cancer and have led to the approval of NMP22 as a urinary biomarker by the US Food and Drug Administration. Nonetheless, the clinical significance of NMP22 remains unclear. The objective of this study was to use decision analysis to determine whether NMP22 improves medical decision-making. METHODS: The current study included 2222 patients who had a history of nonmuscle-invasive bladder cancer and current negative cytology. The authors developed models to predict cancer recurrence or progression to muscle-invasive disease using voided NMP22 levels, cystoscopy, age, and sex. Clinical net benefit was calculated by summing the benefits (true-positives), subtracting the harms (false-positives), and weighting these values by the threshold probability at which a patient or clinician would opt for cytoscopy. RESULTS: After cystoscopy, 581 patients (26%) had cancer identified. The NMP22 level was associated significantly with bladder cancer recurrence and progression (P < .001 for both). The use of NMP22 in a model with age and sex was associated with better patient outcomes than performing cystoscopy on everyone and produced threshold probabilities > 8% for recurrence and > 3% for progression. Only offering cystoscopy to those who had a risk > 15% reduced the number of cystoscopies by 229 while missing only 25 cancer recurrences per 1000 men with negative cytology. The current study was limited by its multicenter design. CONCLUSIONS: For clinicians who would perform a cystoscopy at a threshold of 5% for recurrence or 1% for progression, NMP22 did not aid clinical decision-making. For less risk-averse clinicians who would only perform a cystoscopy at a threshold probability >thinsp;8% for recurrence or > 3% for progression, NMP22 helped to indicate which patients required cystoscopy and which could be spared this procedure. Cancer 2011;117:2892-7. (C) 2071 American Cancer Society.\n\n\n"
},
{
"text": "\n119400\nLevosimendan versus milrinone in neonates and infants after corrective open-heart surgery: A pilot study.\n\nLechner, E\n\nHofer, A\n\nLeitner-Peneder, G\n\nFreynschlag, R\n\nMair, R\n\nWeinzettel, R\n\nRehak, P\n\nGombotz, H\n\nBeiträge in Fachzeitschriften\nISI:000308537800017\n22622649.0\n10.1097/PCC.0b013e3182455571\nNone\nObjective: Low cardiac output syndrome commonly complicates the postoperative course after open-heart surgery in children. To prevent low cardiac output syndrome, prophylactic administration of milrinone after cardiopulmonary bypass is commonly used in small children. The aim of this study was to compare the effect of prophylactically administered levosimendan and milrinone on cardiac index in neonates and infants after corrective open-heart surgery. Design: Prospective, single-center, double-blind, randomized pilot study. Setting: Tertiary care center, postoperative pediatric cardiac intensive care unit. Patients: After written informed consent, 40 infants undergoing corrective open-heart surgery were included. Interventions: At weaning from cardiopulmonary bypass, either a 24-hr infusion of 0.1 mu g/kg/min levosimendan or of 0.5 mu g/kg/min milrinone were administered. Cardiac output was evaluated at 2, 6, 9, 12, 18, 24, and 48 hrs after cardiopulmonary bypass using a transesophageal Doppler technique (Cardio-QP, Deltex Medical, Chichester, UK). Cardiac index was calculated from cardiac output and the patients' respective body surface area. Results: Intention-to-treat data of 39 patients (19 in the levosimendan and 20 in the milrinone group) were analyzed using analysis of variance for repeated measurements for statistics. Analysis of variance revealed for both, cardiac index and cardiac output, similar results with no significant differences of the factors group and time. A significant interaction for cardiac output (p = .005) and cardiac index (p = .007) was found, which indicates different time courses of cardiac index in the two groups. Both drugs were well tolerated; no death or serious adverse event occurred. Conclusions: In our small study, postoperative cardiac index over time was similar in patients with prophylactically administered levosimendan and patients with prophylactically given milrinone. We observed an increase in cardiac output and cardiac index over time in the levosimendan group, whereas cardiac output and cardiac index remained stable in the milrinone group. This pilot study has primarily served to obtain experience using the new drug levosimendan in neonates and infants and to initiate further multicenter trials in pediatric patients. (Pediatr Crit Care Med 2012; 13:542-548)\n\n\n"
},
{
"text": "\n120510\nImpact of FTO genotypes on BMI and weight in polycystic ovary syndrome: a systematic review and meta-analysis.\n\nWojciechowski, P\n\nLipowska, A\n\nRys, P\n\nEwens, KG\n\nFranks, S\n\nTan, S\n\nLerchbaum, E\n\nVcelak, J\n\nAttaoua, R\n\nStraczkowski, M\n\nAzziz, R\n\nBarber, TM\n\nHinney, A\n\nObermayer-Pietsch, B\n\nLukasova, P\n\nBendlova, B\n\nGrigorescu, F\n\nKowalska, I\n\nGoodarzi, MO\n\nGIANT Consortium\n\nStrauss, JF\n\nMcCarthy, MI\n\nMalecki, MT\n\nBeiträge in Fachzeitschriften\nISI:000308354600012\n22801903.0\n10.1007/s00125-012-2638-6\nPMC3433670\nFTO gene single nucleotide polymorphisms (SNPs) have been shown to be associated with obesity-related traits and type 2 diabetes. Several small studies have suggested a greater than expected effect of the FTO rs9939609 SNP on weight in polycystic ovary syndrome (PCOS). We therefore aimed to examine the impact of FTO genotype on BMI and weight in PCOS. A systematic search of medical databases (PubMed, EMBASE and Cochrane CENTRAL) was conducted up to the end of April 2011. Seven studies describing eight distinct PCOS cohorts were retrieved; seven were genotyped for SNP rs9939609 and one for SNP rs1421085. The per allele effect on BMI and body weight increase was calculated and subjected to meta-analysis. A total of 2, 48 women with PCOS were included in the study; 762 were TT homozygotes, 1, 53 had an AT/CT genotype, and 533 were AA/CC homozygotes. Each additional copy of the effect allele (A/C) increased the BMI by a mean of 0.19 z score units (95% CI 0.13, 0.24; p = 2.26 x 10(-11)) and body weight by a mean of 0.20 z score units (95% CI 0.14, 0.26; p = 1.02 x 10(-10)). This translated into an approximately 3.3 kg/m(2) increase in BMI and an approximately 9.6 kg gain in body weight between TT and AA/CC homozygotes. The association between FTO genotypes and BMI was stronger in the cohorts with PCOS than in the general female populations from large genome-wide association studies. Deviation from an additive genetic model was observed in heavier populations. The effect of FTO SNPs on obesity-related traits in PCOS seems to be more than two times greater than the effect found in large population-based studies. This suggests an interaction between FTO and the metabolic context or polygenic background of PCOS.\n\nLerchbaum, Elisabeth\n\nObermayer-Pietsch, Barbara\n\n\n"
},
{
"text": "\n121827\nIncidence of inflammatory bowel disease in the province of Styria, Austria, from 1997 to 2007: a population-based study.\n\nPetritsch, W\n\nFuchs, S\n\nBerghold, A\n\nBachmaier, G\n\nHögenauer, C\n\nHauer, AC\n\nWeiglhofer, U\n\nWenzl, HH\n\nBeiträge in Fachzeitschriften\nISI:000315367100005\n22542057.0\n10.1016/j.crohns.2012.03.012\nNone\nThe incidence of inflammatory bowel disease (IBD) varies widely between different countries. This large variation is also observed for the incidence of its main two forms, ulcerative colitis (UC) and Crohn's disease (CD). Controversy exists whether IBD incidence is increasing, especially in western countries. Currently no data are available for Austria. This study therefore aimed to evaluate for the first time the incidence of IBD over an eleven-year period in Styria, a province of Austria with a population of 1.2 million.\n All patients with an initial diagnosis of IBD between 1997 and 2007, who were Styrian residents, were eligible for this retrospective study. Data were acquired from electronically stored hospital discharge reports and individual reports by patients and physicians. According to population density Styria was divided into two rural and one urban area.\n Throughout the study period 1527 patients with an initial diagnosis of IBD were identified. The average annual incidence was 6.7 (95% CI 6.2-7.1) per 100, 00 persons per year for CD and 4.8 (95% CI 4.5-5.2) for UC. The average annual incidence increased significantly (p<0.01) for both diseases during the 11 year study period. Median age at initial diagnosis was 29 years (range 3-87) for CD and 39 years (range 3-94) for UC. At diagnosis, 8.5% of all IBD patients were <18 years of age. The incidence of both CD and UC was significantly higher in the urban area than in rural areas (CD: 8.8, 95% CI 7.8-9.8 versus 5.5, 95% CI 4.7-6.4 and 5.9, 95% CI 5.3-6.7; [p<0.001]; UC: 5.8, 95% CI 5.1-6.6 versus 4.0, 95% CI 3.4-4.7 and 4.7, 95% CI 4.1-5.4; [p=0.04]).\n We observed an overall increase in the incidence of ulcerative colitis and Crohn's disease in a part of Austria during an eleven year period. IBD was more predominant in the largest urban area than in rural areas.\n Copyright © 2012 European Crohn's and Colitis Organisation. Published by Elsevier B.V. All rights reserved.\n\nBachmaier, Gerhard\n\nBerghold, Andrea\n\nHauer, Almuthe\n\nHoegenauer, Christoph\n\nPetritsch, Wolfgang\n\n\n"
},
{
"text": "\n123753\nWhat is the optimal number of implants for fixed reconstructions: a systematic review.\n\nHeydecke, G\n\nZwahlen, M\n\nNicol, A\n\nNisand, D\n\nPayer, M\n\nRenouard, F\n\nGrohmann, P\n\nMühlemann, S\n\nJoda, T\n\nBeiträge in Fachzeitschriften\nISI:000309915600022\n23062144.0\n10.1111/j.1600-0501.2012.02548.x\nNone\nObjectives To assess the 5-year and 10-year survival and complication rates of implant-supported fixed reconstructions in partially and totally edentulous patients with regard to the optimal number and distribution of dental implants. Material and Methods This review was designed as a systematic review of the literature. A search strategy was developed and executed using an electronic and selective hand search for English-language articles in Dental Journals limited to human clinical trials. Search terms were grouped into categories for problem intervention outcome. For articles retrieved by this search, abstracts were screened by two reviewers based on the inclusion criteria. Selected articles were then obtained in full texts. Finally, the selection based on inclusion/exclusion criteria was repeated for the full-text articles. Results Of the 210 titles retrieved by the search, 51 were selected for full-text review based on the information given in the abstract. From the full-text articles, a total of nine studies were included for this systematic review. In meta-analysis, prosthetic survival rates over 5 and 10 years for partial Fixed Dental Prostheses (FDPs) on two to four implants were estimated as 98.9% (95% CI: 98.599.2%) and as 97.8% (95% CI: 96.998.4%) respectively. A survival rate for maxillary Full-Arch Fixed Dental Prostheses (FAFDPs) on four to six implants after 5 years was assessed as 97.5% (95% CI: 94.198.9%) and a survival rate after 10 years as 95.0% (95% CI: 88.597.9%). The result for the survival rates in case of mandibular FAFDPs on four to six implants after 5 years was 97.9% (95% CI: 96.398.8%) and after 10 years 95.9% (95% CI: 92.897.7%). Specific implant-to-replaced-unit-ratios were not available in any of the studies. Conclusion For implant-supported FAFDPs, using 46 implants is a well-documented treatment option with high estimated 5-year survival of the construction. It is unclear whether three implants for supporting a FAFDP will achieve similar survival rates. The RCTs needed that report implant-to-replaced-units-ratios for partial FDPs and include 3 vs. 46 implants for supporting a FAFDP in the mandible.\n\nPayer, Michael\n\n\n"
},
{
"text": "\n139218\nQuantitative 3D soft tissue analysis of symmetry prior to and after unilateral cleft lip repair compared with non-cleft persons (performed in Cambodia).\n\nSchwenzer-Zimmerer, K\n\nChaitidis, D\n\nBerg-Boerner, I\n\nKrol, Z\n\nKovacs, L\n\nSchwenzer, NF\n\nZimmerer, S\n\nHolberg, C\n\nZeilhofer, HF\n\nBeiträge in Fachzeitschriften\nISI:000261254200001\n18701312.0\n10.1016/j.jcms.2008.05.003\nNone\nThe aim of this study was to evaluate the clinical application of three-dimensional (3D) imaging and morphological analysis with subsequent individual therapy planning and postoperative 3D symmetry control in comparison with data from non-cleft persons.\n This was a prospective study using a 3D surface-imaging and evaluation system in cleft patients and non-cleft persons. The pre- and postoperative 3D facial profiles were recorded from the patients using a 3D laser scanner. The preoperative 3D image was analyzed qualitatively and quantitatively for an individual therapy planning. On the basis of ratios and scores, based on empirical regions of interest, the technique of cleft repair was designed individually. The postoperative result was evaluated regarding symmetry. The surgically created soft tissue shift was defined quantitatively and visualized with vectors. The postoperative symmetry was compared with 3D data from a group of non-cleft persons of the same ethnical group.\n Eleven patients (mean age 13.8 years, median 13, minimum 2, maximum 41 years) with either a unilateral isolated cleft lip, a cleft lip and alveolus or a complete unilateral cleft lip, alveolus and palate and 25 non-cleft persons (8 children between 4 and 12 years, 17 adults (9 men, 8 women) between 18 and 50 years). All these persons investigated were Asians of Khmer origin.\n The analysis permitted quantitative 3D evaluation. The 3D anthropometric data of the non-cleft Khmer persons were collected and named the gold standard of symmetry in this ethnical group. All postoperative 3D images reached symmetrical values within the range of the normal cohort. Soft tissue shifts from pre- to postoperative sites could be visualized.\n A new method for registration was described enabling follow-up registration in patients when growing older. This 3D soft tissue analysis can be a useful tool in quantitative analysis and objective follow-up control in cleft patients. It offers deeper insight into the complex morphology to be treated and could contribute to individualisation of surgical procedures.\n\n\n"
}
]
}