@article{ZouWangNeffeetal.2017,
  author    = {Zou, Jie and Wang, Weiwei and Neffe, Axel T. and Xu, Xun and Li, Zhengdong and Deng, Zijun and Sun, Xianlei and Ma, Nan and Lendlein, Andreas},
  title     = {Adipogenic differentiation of human adipose derived mesenchymal stem cells in 3D architectured gelatin based hydrogels (ArcGel)},
  series = {Clinical hemorheology and microcirculation : blood flow and vessels},
  volume    = {67},
  journal   = {Clinical hemorheology and microcirculation : blood flow and vessels},
  number    = {3-4},
  publisher = {IOS Press},
  address   = {Amsterdam},
  issn      = {1386-0291},
  doi       = {10.3233/CH-179210},
  pages     = {297 -- 307},
  year      = {2017},
  abstract  = {Polymeric matrices mimicking multiple functions of the ECM are expected to enable a material induced regeneration of tissues. Here, we investigated the adipogenic differentiation of human adipose derived mesenchymal stem cells (hADSCs) in a 3D architectured gelatin based hydrogel (ArcGel) prepared from gelatin and L-lysine diisocyanate ethyl ester (LDI) in an one-step process, in which the formation of an open porous morphology and the chemical network formation were integrated. The ArcGel was designed to support adipose tissue regeneration with its 3D porous structure, high cell biocompatibility, and mechanical properties compatible with human subcutaneous adipose tissue. The ArcGel could support initial cell adhesion and survival of hADSCs. Under static culture condition, the cells could migrate into the inner part of the scaffold with a depth of 840 +/- 120 mu m after 4 days, and distributed in the whole scaffold (2mm in thickness) within 14 days. The cells proliferated in the scaffold and the fold increase of cell number after 7 days of culture was 2.55 +/- 0.08. The apoptotic rate of hADSCs in the scaffold was similar to that of cells maintained on tissue culture plates. When cultured in adipogenic induction medium, the hADSCs in the scaffold differentiated into adipocytes with a high efficiency (93 +/- 1\%). Conclusively, this gelatin based 3D scaffold presented high cell compatibility for hADSC cultivation and differentiation, which could serve as a potential implant material in clinical applications for adipose tissue reparation and regeneration.},
  language  = {en}
}
@article{TangSullivanHongetal.2019,
  author    = {Tang, Alan T. and Sullivan, Katie Rose and Hong, Courtney C. and Goddard, Lauren M. and Mahadevan, Aparna and Ren, Aileen and Pardo, Heidy and Peiper, Amy and Griffin, Erin and Tanes, Ceylan and Mattei, Lisa M. and Yang, Jisheng and Li, Li and Mericko-Ishizuka, Patricia and Shen, Le and Hobson, Nicholas and Girard, Romuald and Lightle, Rhonda and Moore, Thomas and Shenkar, Robert and Polster, Sean P. and Roedel, Claudia Jasmin and Li, Ning and Zhu, Qin and Whitehead, Kevin J. and Zheng, Xiangjian and Akers, Amy and Morrison, Leslie and Kim, Helen and Bittinger, Kyle and Lengner, Christopher J. and Schwaninger, Markus and Velcich, Anna and Augenlicht, Leonard and Abdelilah-Seyfried, Salim and Min, Wang and Marchuk, Douglas A. and Awad, Issam A. and Kahn, Mark L.},
  title     = {Distinct cellular roles for PDCD10 define a gut-brain axis in cerebral cavernous malformation},
  series = {Science Translational Medicine},
  volume    = {11},
  journal   = {Science Translational Medicine},
  number    = {520},
  publisher = {American Assoc. for the Advancement of Science},
  address   = {Washington},
  issn      = {1946-6234},
  doi       = {10.1126/scitranslmed.aaw3521},
  pages     = {14},
  year      = {2019},
  abstract  = {Cerebral cavernous malformation (CCM) is a genetic, cerebrovascular disease. Familial CCM is caused by genetic mutations in KRIT1, CCM2, or PDCD10. Disease onset is earlier and more severe in individuals with PDCD10 mutations. Recent studies have shown that lesions arise from excess mitogen-activated protein kinase kinase kinase 3 (MEKK3) signaling downstream of Toll-like receptor 4 (TLR4) stimulation by lipopolysaccharide derived from the gut microbiome. These findings suggest a gut-brain CCM disease axis but fail to define it or explain the poor prognosis of patients with PDCD10 mutations. Here, we demonstrate that the gut barrier is a primary determinant of CCM disease course, independent of microbiome configuration, that explains the increased severity of CCM disease associated with PDCD10 deficiency. Chemical disruption of the gut barrier with dextran sulfate sodium augments CCM formation in a mouse model, as does genetic loss of Pdcd10, but not Krit1, in gut epithelial cells. Loss of gut epithelial Pdcd10 results in disruption of the colonic mucosal barrier. Accordingly, loss of Mucin-2 or exposure to dietary emulsifiers that reduce the mucus barrier increases CCM burden analogous to loss of Pdcd10 in the gut epithelium. Last, we show that treatment with dexamethasone potently inhibits CCM formation in mice because of the combined effect of action at both brain endothelial cells and gut epithelial cells. These studies define a gut-brain disease axis in an experimental model of CCM in which a single gene is required for two critical components: gut epithelial function and brain endothelial signaling.},
  language  = {en}
}
@article{UlyanenkovBaumbachDarowskietal.1999,
  author    = {Ulyanenkov, A. and Baumbach, Tilo and Darowski, Nora and Pietsch, Ullrich and Wang, K. H. and Forchel, Alfred and Wiebach, T.},
  title     = {Investigation of the in-plane strain distribution in free-standing GaAs/InGaAs/GaAs single quantum well surface nanostructures on GaAs[001]},
  year      = {1999},
  language  = {en}
}
@article{WangNaolouMaetal.2017,
  author    = {Wang, Weiwei and Naolou, Toufik and Ma, Nan and Deng, Zijun and Xu, Xun and Mansfeld, Ulrich and Wischke, Christian and Gossen, Manfred and Neffe, Axel T. and Lendlein, Andreas},
  title     = {Polydepsipeptide Block-Stabilized Polyplexes for Efficient Transfection of Primary Human Cells},
  series = {Biomacromolecules : an interdisciplinary journal focused at the interface of polymer science and the biological sciences},
  volume    = {18},
  journal   = {Biomacromolecules : an interdisciplinary journal focused at the interface of polymer science and the biological sciences},
  publisher = {American Chemical Society},
  address   = {Washington},
  issn      = {1525-7797},
  doi       = {10.1021/acs.biomac.7b01034},
  pages     = {3819 -- 3833},
  year      = {2017},
  abstract  = {The rational design of a polyplex gene carrier aims to balance maximal effectiveness of nucleic acid transfection into cells with minimal adverse effects. Depsipeptide blocks with an M (n) similar to 5 kDa exhibiting strong physical interactions were conjugated with PEI moieties (2.5 or 10 kDa) to di- and triblock copolymers. Upon nanoparticle formation and complexation with DNA, the resulting polyplexes (sizes typically 60-150 nm) showed remarkable stability compared to PEI-only or lipoplex and facilitated efficient gene delivery. Intracellular trafficking was visualized by observing fluorescence-labeled pDNA and highlighted the effective cytoplasmic uptake of polyplexes and release of DNA to the perinuclear space. Specifically, a triblock copolymer with a middle depsipeptide block and two 10 kDa PEI swallowtail structures mediated the highest levels of transgenic VEGF secretion in mesenchymal stem cells with low cytotoxicity. These nanocarriers form the basis for a delivery platform technology, especially for gene transfer to primary human cells.},
  language  = {en}
}
@article{XieXuWangetal.2022,
  author    = {Xie, Dongjiu and Xu, Yaolin and Wang, Yonglei and Pan, Xuefeng and H{\"a}rk, Eneli and Kochovski, Zdravko and Eljarrat, Alberto and M{\"u}ller, Johannes and Koch, Christoph T. and Yuan, Jiayin and Lu, Yan},
  title     = {Poly(ionic liquid) nanovesicle-templated carbon nanocapsules functionalized with uniform iron nitride nanoparticles as catalytic sulfur host for Li-S batteries},
  series = {ACS nano},
  volume    = {16},
  journal   = {ACS nano},
  number    = {7},
  publisher = {American Chemical Society},
  address   = {Washington},
  issn      = {1936-0851},
  doi       = {10.1021/acsnano.2c01992},
  pages     = {10554 -- 10565},
  year      = {2022},
  abstract  = {Poly(ionic liquid)s (PIL) are common precursors for heteroatom-doped carbon materials. Despite a relatively higher carbonization yield, the PIL-to-carbon conversion process faces challenges in preserving morphological and structural motifs on the nanoscale. Assisted by a thin polydopamine coating route and ion exchange, imidazoliumbased PIL nanovesicles were successfully applied in morphology-maintaining carbonization to prepare carbon composite nanocapsules. Extending this strategy further to their composites, we demonstrate the synthesis of carbon composite nanocapsules functionalized with iron nitride nanoparticles of an ultrafine, uniform size of 3-5 nm (termed "FexN@C "). Due to its unique nanostructure, the sulfur-loaded FexN@C electrode was tested to efficiently mitigate the notorious shuttle effect of lithium polysulfides (LiPSs) in Li-S batteries. The cavity of the carbon nanocapsules was spotted to better the loading content of sulfur. The well-dispersed iron nitride nanoparticles effectively catalyze the conversion of LiPSs to Li2S, owing to their high electronic conductivity and strong binding power to LiPSs. Benefiting from this well-crafted composite nanostructure, the constructed FexN@C/S cathode demonstrated a fairly high discharge capacity of 1085 mAh g(-1) at 0.5 C initially, and a remaining value of 930 mAh g(-1 )after 200 cycles. In addition, it exhibits an excellent rate capability with a high initial discharge capacity of 889.8 mAh g(-1) at 2 C. This facile PIL-to-nanocarbon synthetic approach is applicable for the exquisite design of complex hybrid carbon nanostructures with potential use in electrochemical energy storage and conversion.},
  language  = {en}
}
@article{TungMaringXuetal.2022,
  author    = {Tung, Wing Tai and Maring, Janita A. and Xu, Xun and Liu, Yue and Becker, Matthias and Somesh, Dipthi Bachamanda and Klose, Kristin and Wang, Weiwei and Sun, Xianlei and Ullah, Imran and Kratz, Karl and Neffe, Axel T. and Stamm, Christof and Ma, Nan and Lendlein, Andreas},
  title     = {In vivo performance of a cell and factor free multifunctional fiber mesh modulating postinfarct myocardial remodeling},
  series = {Advanced Functional Materials},
  volume    = {32},
  journal   = {Advanced Functional Materials},
  number    = {31},
  publisher = {Wiley},
  address   = {Weinheim},
  issn      = {1616-301X},
  doi       = {10.1002/adfm.202110179},
  pages     = {17},
  year      = {2022},
  abstract  = {Guidance of postinfarct myocardial remodeling processes by an epicardial patch system may alleviate the consequences of ischemic heart disease. As macrophages are highly relevant in balancing immune response and regenerative processes their suitable instruction would ensure therapeutic success. A polymeric mesh capable of attracting and instructing monocytes by purely physical cues and accelerating implant degradation at the cell/implant interface is designed. In a murine model for myocardial infarction the meshes are compared to those either coated with extracellular matrix or loaded with induced cardiomyocyte progenitor cells. All implants promote macrophage infiltration and polarization in the epicardium, which is verified by in vitro experiments. 6 weeks post-MI, especially the implantation of the mesh attenuates left ventricular adverse remodeling processes as shown by reduced infarct size (14.7\% vs 28-32\%) and increased wall thickness (854 mu m vs 400-600 mu m), enhanced angiogenesis/arteriogenesis (more than 50\% increase compared to controls and other groups), and improved heart function (ejection fraction = 36.8\% compared to 12.7-31.3\%). Upscaling as well as process controls is comprehensively considered in the presented mesh fabrication scheme to warrant further progression from bench to bedside.},
  language  = {en}
}
@misc{XieJiaRollsetal.2021,
  author    = {Xie, Chao and Jia, Tianye and Rolls, Edmund T. and Robbins, Trevor W. and Sahakian, Barbara J. and Zhang, Jie and Liu, Zhaowen and Cheng, Wei and Luo, Qiang and Zac Lo, Chun-Yi and Schumann, Gunter and Feng, Jianfeng and Wang, He and Banaschewski, Tobias and Barker, Gareth J. and Bokde, Arun L.W. and B{\"u}chel, Christian and Quinlan, Erin Burke and Desrivi{\`e}res, Sylvane and Flor, Herta and Grigis, Antoine and Garavan, Hugh and Gowland, Penny and Heinz, Andreas and Hohmann, Sarah and Ittermann, Bernd and Martinot, Jean-Luc and Paill{\`e}re Martinot, Marie-Laure and Nees, Frauke and Papadopoulos Orfanos, Dimitri and Paus, Tom{\´a}š and Poustka, Luise and Fr{\"o}hner, Juliane H. and Smolka, Michael N. and Walter, Henrik and Whelan, Robert},
  title     = {Reward versus nonreward sensitivity of the medial versus lateral orbitofrontal cortex relates to the severity of depressive symptoms},
  series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  journal   = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe},
  number    = {3},
  issn      = {1866-8364},
  doi       = {10.25932/publishup-55788},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-557882},
  pages     = {13},
  year      = {2021},
  abstract  = {BACKGROUND: The orbitofrontal cortex (OFC) is implicated in depression. The hypothesis investigated was whether the OFC sensitivity to reward and nonreward is related to the severity of depressive symptoms. METHODS: Activations in the monetary incentive delay task were measured in the IMAGEN cohort at ages 14 years (n = 1877) and 19 years (n = 1140) with a longitudinal design. Clinically relevant subgroups were compared at ages 19 (high-severity group: n = 116; low-severity group: n = 206) and 14. RESULTS: The medial OFC exhibited graded activation increases to reward, and the lateral OFC had graded activation increases to nonreward. In this general population, the medial and lateral OFC activations were associated with concurrent depressive symptoms at both ages 14 and 19 years. In a stratified high-severity depressive symptom group versus control group comparison, the lateral OFC showed greater sensitivity for the magnitudes of activations related to nonreward in the high-severity group at age 19 (p = .027), and the medial OFC showed decreased sensitivity to the reward magnitudes in the high-severity group at both ages 14 (p = .002) and 19 (p = .002). In a longitudinal design, there was greater sensitivity to nonreward of the lateral OFC at age 14 for those who exhibited high depressive symptom severity later at age 19 (p = .003). CONCLUSIONS: Activations in the lateral OFC relate to sensitivity to not winning, were associated with high depressive symptom scores, and at age 14 predicted the depressive symptoms at ages 16 and 19. Activations in the medial OFC were related to sensitivity to winning, and reduced reward sensitivity was associated with concurrent high depressive symptom scores.},
  language  = {en}
}
@article{XieJiaRollsetal.2021,
  author    = {Xie, Chao and Jia, Tianye and Rolls, Edmund T. and Robbins, Trevor W. and Sahakian, Barbara J. and Zhang, Jie and Liu, Zhaowen and Cheng, Wei and Luo, Qiang and Zac Lo, Chun-Yi and Schumann, Gunter and Feng, Jianfeng and Wang, He and Banaschewski, Tobias and Barker, Gareth J. and Bokde, Arun L.W. and B{\"u}chel, Christian and Quinlan, Erin Burke and Desrivi{\`e}res, Sylvane and Flor, Herta and Grigis, Antoine and Garavan, Hugh and Gowland, Penny and Heinz, Andreas and Hohmann, Sarah and Ittermann, Bernd and Martinot, Jean-Luc and Paill{\`e}re Martinot, Marie-Laure and Nees, Frauke and Papadopoulos Orfanos, Dimitri and Paus, Tom{\´a}š and Poustka, Luise and Fr{\"o}hner, Juliane H. and Smolka, Michael N. and Walter, Henrik and Whelan, Robert},
  title     = {Reward versus nonreward sensitivity of the medial versus lateral orbitofrontal cortex relates to the severity of depressive symptoms},
  series = {Biological Psychiatry: Cognitive Neuroscience and Neuroimaging},
  volume    = {6},
  journal   = {Biological Psychiatry: Cognitive Neuroscience and Neuroimaging},
  number    = {3},
  publisher = {Elsevier Science},
  address   = {Amsterdam},
  issn      = {2451-9022},
  doi       = {10.1016/j.bpsc.2020.08.017},
  pages     = {259 -- 269},
  year      = {2021},
  abstract  = {BACKGROUND: The orbitofrontal cortex (OFC) is implicated in depression. The hypothesis investigated was whether the OFC sensitivity to reward and nonreward is related to the severity of depressive symptoms. METHODS: Activations in the monetary incentive delay task were measured in the IMAGEN cohort at ages 14 years (n = 1877) and 19 years (n = 1140) with a longitudinal design. Clinically relevant subgroups were compared at ages 19 (high-severity group: n = 116; low-severity group: n = 206) and 14. RESULTS: The medial OFC exhibited graded activation increases to reward, and the lateral OFC had graded activation increases to nonreward. In this general population, the medial and lateral OFC activations were associated with concurrent depressive symptoms at both ages 14 and 19 years. In a stratified high-severity depressive symptom group versus control group comparison, the lateral OFC showed greater sensitivity for the magnitudes of activations related to nonreward in the high-severity group at age 19 (p = .027), and the medial OFC showed decreased sensitivity to the reward magnitudes in the high-severity group at both ages 14 (p = .002) and 19 (p = .002). In a longitudinal design, there was greater sensitivity to nonreward of the lateral OFC at age 14 for those who exhibited high depressive symptom severity later at age 19 (p = .003). CONCLUSIONS: Activations in the lateral OFC relate to sensitivity to not winning, were associated with high depressive symptom scores, and at age 14 predicted the depressive symptoms at ages 16 and 19. Activations in the medial OFC were related to sensitivity to winning, and reduced reward sensitivity was associated with concurrent high depressive symptom scores.},
  language  = {en}
}
@article{LevermannWinkelmannNowickietal.2014,
  author    = {Levermann, Anders and Winkelmann, Ricarda and Nowicki, S. and Fastook, J. L. and Frieler, Katja and Greve, R. and Hellmer, H. H. and Martin, M. A. and Meinshausen, Malte and Mengel, Matthias and Payne, A. J. and Pollard, D. and Sato, T. and Timmermann, R. and Wang, Wei Li and Bindschadler, Robert A.},
  title     = {Projecting antarctic ice discharge using response functions from SeaRISE ice-sheet models},
  series = {Earth system dynamics},
  volume    = {5},
  journal   = {Earth system dynamics},
  number    = {2},
  publisher = {Copernicus},
  address   = {G{\"o}ttingen},
  issn      = {2190-4979},
  doi       = {10.5194/esd-5-271-2014},
  pages     = {271 -- 293},
  year      = {2014},
  abstract  = {The largest uncertainty in projections of future sea-level change results from the potentially changing dynamical ice discharge from Antarctica. Basal ice-shelf melting induced by a warming ocean has been identified as a major cause for additional ice flow across the grounding line. Here we attempt to estimate the uncertainty range of future ice discharge from Antarctica by combining uncertainty in the climatic forcing, the oceanic response and the ice-sheet model response. The uncertainty in the global mean temperature increase is obtained from historically constrained emulations with the MAGICC-6.0 (Model for the Assessment of Greenhouse gas Induced Climate Change) model. The oceanic forcing is derived from scaling of the subsurface with the atmospheric warming from 19 comprehensive climate models of the Coupled Model Intercomparison Project (CMIP-5) and two ocean models from the EU-project Ice2Sea. The dynamic ice-sheet response is derived from linear response functions for basal ice-shelf melting for four different Antarctic drainage regions using experiments from the Sea-level Response to Ice Sheet Evolution (SeaRISE) intercomparison project with five different Antarctic ice-sheet models. The resulting uncertainty range for the historic Antarctic contribution to global sea-level rise from 1992 to 2011 agrees with the observed contribution for this period if we use the three ice-sheet models with an explicit representation of ice-shelf dynamics and account for the time-delayed warming of the oceanic subsurface compared to the surface air temperature. The median of the additional ice loss for the 21st century is computed to 0.07 m (66\% range: 0.02-0.14 m; 90\% range: 0.0-0.23 m) of global sea-level equivalent for the low-emission RCP-2.6 (Representative Concentration Pathway) scenario and 0.09 m (66\% range: 0.04-0.21 m; 90\% range: 0.01-0.37 m) for the strongest RCP-8.5. Assuming no time delay between the atmospheric warming and the oceanic subsurface, these values increase to 0.09 m (66\% range: 0.04-0.17 m; 90\% range: 0.02-0.25 m) for RCP-2.6 and 0.15 m (66\% range: 0.07-0.28 m; 90\% range: 0.04-0.43 m) for RCP-8.5. All probability distributions are highly skewed towards high values. The applied ice-sheet models are coarse resolution with limitations in the representation of grounding-line motion. Within the constraints of the applied methods, the uncertainty induced from different ice-sheet models is smaller than that induced by the external forcing to the ice sheets.},
  language  = {en}
}