@article{EngelmannRoethEberbecketal.2018,
  author    = {Engelmann, Ulrich M. and Roeth, Anjali A.J. and Eberbeck, Dietmar and Buhl, Eva Miriam and Neumann, Ulf Peter and Schmitz-Rode, Thomas and Slabu, Ioana},
  title     = {Combining Bulk Temperature and Nanoheating Enables Advanced Magnetic Fluid Hyperthermia Efficacy on Pancreatic Tumor Cells},
  series = {Scientific Reports},
  volume    = {8},
  journal   = {Scientific Reports},
  number    = {1},
  publisher = {Springer Nature},
  address   = {Cham},
  issn      = {2045-2322},
  doi       = {10.1038/s41598-018-31553-9},
  pages     = {Article number 13210},
  year      = {2018},
  abstract  = {Many efforts are made worldwide to establish magnetic fluid hyperthermia (MFH) as a treatment for organ-confined tumors. However, translation to clinical application hardly succeeds as it still lacks of understanding the mechanisms determining MFH cytotoxic effects. Here, we investigate the intracellular MFH efficacy with respect to different parameters and assess the intracellular cytotoxic effects in detail. For this, MiaPaCa-2 human pancreatic tumor cells and L929 murine fibroblasts were loaded with iron-oxide magnetic nanoparticles (MNP) and exposed to MFH for either 30 min or 90 min. The resulting cytotoxic effects were assessed via clonogenic assay. Our results demonstrate that cell damage depends not only on the obvious parameters bulk temperature and duration of treatment, but most importantly on cell type and thermal energy deposited per cell during MFH treatment. Tumor cell death of 95\% was achieved by depositing an intracellular total thermal energy with about 50\% margin to damage of healthy cells. This is attributed to combined intracellular nanoheating and extracellular bulk heating. Tumor cell damage of up to 86\% was observed for MFH treatment without perceptible bulk temperature rise. Effective heating decreased by up to 65\% after MNP were internalized inside cells.},
  language  = {en}
}
@article{ConzenAlbannaWeissetal.2018,
  author    = {Conzen, Catharina and Albanna, Walid and Weiss, Miriam and K{\"u}rten, David and Vilser, Walthard and Kotliar, Konstantin and Z{\"a}ske, Charlotte and Clusmann, Hans and Schubert, Gerrit Alexander},
  title     = {Vasoconstriction and Impairment of Neurovascular Coupling after Subarachnoid Hemorrhage: a Descriptive Analysis of Retinal Changes},
  series = {Translational Stroke Research},
  journal   = {Translational Stroke Research},
  number    = {9},
  publisher = {Springer Nature},
  address   = {Cham},
  issn      = {1868-601X},
  doi       = {10.1007/s12975-017-0585-8},
  pages     = {284 -- 293},
  year      = {2018},
  abstract  = {Impaired cerebral autoregulation and neurovascular coupling (NVC) contribute to delayed cerebral ischemia after subarachnoid hemorrhage (SAH). Retinal vessel analysis (RVA) allows non-invasive assessment of vessel dimension and NVC hereby demonstrating a predictive value in the context of various neurovascular diseases. Using RVA as a translational approach, we aimed to assess the retinal vessels in patients with SAH. RVA was performed prospectively in 24 patients with acute SAH (group A: day 5-14), in 11 patients 3 months after ictus (group B: day 90 ± 35), and in 35 age-matched healthy controls (group C). Data was acquired using a Retinal Vessel Analyzer (Imedos Systems UG, Jena) for examination of retinal vessel dimension and NVC using flicker-light excitation. Diameter of retinal vessels—central retinal arteriolar and venular equivalent—was significantly reduced in the acute phase (p < 0.001) with gradual improvement in group B (p < 0.05). Arterial NVC of group A was significantly impaired with diminished dilatation (p < 0.001) and reduced area under the curve (p < 0.01) when compared to group C. Group B showed persistent prolonged latency of arterial dilation (p < 0.05). Venous NVC was significantly delayed after SAH compared to group C (A p < 0.001; B p < 0.05). To our knowledge, this is the first clinical study to document retinal vasoconstriction and impairment of NVC in patients with SAH. Using non-invasive RVA as a translational approach, characteristic patterns of compromise were detected for the arterial and venous compartment of the neurovascular unit in a time-dependent fashion. Recruitment will continue to facilitate a correlation analysis with clinical course and outcome.},
  language  = {en}
}
@article{QuittmannMeskemperAbeletal.2018,
  author    = {Quittmann, Oliver J. and Meskemper, Joshua and Abel, Thomas and Albracht, Kirsten and Foitschik, Tina and Rojas-Vega, Sandra and Str{\"u}der, Heiko K.},
  title     = {Kinematics and kinetics of handcycling propulsion at increasing workloads in able-bodied subjects},
  series = {Sports Engineereing},
  volume    = {21},
  journal   = {Sports Engineereing},
  number    = {21},
  publisher = {Springer Nature},
  address   = {Cham},
  issn      = {1460-2687},
  doi       = {10.1007/s12283-018-0269-y},
  pages     = {283 -- 294},
  year      = {2018},
  abstract  = {In Paralympic sports, biomechanical optimisation of movements and equipment seems to be promising for improving performance. In handcycling, information about the biomechanics of this sport is mainly provided by case studies. The aim of the current study was (1) to examine changes in handcycling propulsion kinematics and kinetics due to increasing workloads and (2) identify parameters that are associated with peak aerobic performance. Twelve non-disabled male competitive triathletes without handcycling experience voluntarily participated in the study. They performed an initial familiarisation protocol and incremental step test until exhaustion in a recumbent racing handcycle that was attached to an ergometer. During the incremental test, tangential crank kinetics, 3D joint kinematics, blood lactate and ratings of perceived exertion (local and global) were identified. As a performance criterion, the maximal power output during the step test (Pmax) was calculated and correlated with biomechanical parameters. For higher workloads, an increase in crank torque was observed that was even more pronounced in the pull phase than in the push phase. Furthermore, participants showed an increase in shoulder internal rotation and abduction and a decrease in elbow flexion and retroversion. These changes were negatively correlated with performance. At high workloads, it seems that power output is more limited by the transition from pull to push phase than at low workloads. It is suggested that successful athletes demonstrate small alterations of their kinematic profile due to increasing workloads. Future studies should replicate and expand the test spectrum (sprint and continuous loads) as well as use methods like surface electromyography (sEMG) with elite handcyclists.},
  language  = {de}
}