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We review recent progress in the field of light responsive soft nano-objects. These are systems the shape, size, surface area and surface energy of which can be easily changed by low-intensity external irradiation. Here we shall specifically focus on microgels, DNA molecules, polymer brushes and colloidal particles. One convenient way to render these objects photosensitive is to couple them via ionic and/or hydrophobic interactions with azobenzene containing surfactants in a non-covalent way. The advantage of this strategy is that these surfactants can make any type of charged object light responsive without the need for possibly complicated (and irreversible) chemical conjugation. In the following, we will exclusively discuss only photosensitive surfactant systems. These contain a charged head and a hydrophobic tail into which an azobenzene group is incorporated, which can undergo reversible photo-isomerization from a trans-to a cis-configuration under UV illumination. These kinds of photo-isomerizations occur on a picosecond timescale and are fully reversible. The two isomers in general possess different polarity, i.e. the trans-state is less polar with a dipole moment of usually close to 0 Debye, while the cis-isomer has a dipole moment up to 3 Debye or more, depending on additional phenyl ring substituents. As part of the hydrophobic tail of a surfactant molecule, the photo-isomerization also changes the hydrophobicity of the molecule as a whole and hence its solubility, surface energy, and strength of interaction with other substances. Being a molecular actuator, which converts optical energy in to mechanical work, the azobenzene group in the shape of surfactant molecule can be utilized in order to actuate matter on larger time and length scale. In this paper we show several interesting examples, where azobenzene containing surfactants play the role of a transducer mediating between different states of size, shape, surface energy and spatial arrangement of various nanoscale soft-material systems.
Unravelling the spatiotemporal evolution of the Cenozoic Andean (Altiplano-Puna) plateau has been one of the most intriguing problems of South American geology. Despite a number of investigations, the early deformation and uplift history of this area remained largely enigmatic. This paper analyses the Paleogene tectono-sedimentary history of the Casa Grande Basin, in the present-day transition zone between the northern sector of the Puna Plateau and the northern part of the Argentine Eastern Cordillera. Our detailed mapping of synsedimentary structures records the onset of regional contractional deformation during the middle Eocene, revealing reactivation of Cretaceous extensional structures and the development of doubly vergent thrusts. This is in agreement with records from other southern parts of the Puna Plateau and the Eastern Cordillera. These observations indicate the existence of an Eocene broken foreland setting within the region, characterized by low-lying compressional basins and ranges with spatially disparate sectors of deformation, which was subsequently subjected to regional uplift resulting in the attainment of present-day elevations during the Neogene.
Plant roots control uptake of water and nutrients and cope with environmental challenges. The root epidermis provides the first selective interface for nutrient absorption, while the endodermis produces the main apoplastic diffusion barrier in the form of a structure called the Casparian strip. The positioning of root hairs on epidermal cells, and of the Casparian strip around endodermal cells, requires asymmetries along cellular axes (cell polarity). Cell polarity is termed planar polarity, when coordinated within the plane of a given tissue layer. Here, we review recent molecular advances towards understanding both the polar positioning of the proteo-lipid membrane domain instructing root hair initiation, and the cytoskeletal, trafficking and polar tethering requirements of proteins at outer or inner plasma membrane domains. Finally, we highlight progress towards understanding mechanisms of Casparian strip formation and underlying endodermal cell polarity.
To cope with the already large, and ever increasing, amount of information stored in organizational memory, "forgetting," as an important human memory process, might be transferred to the organizational context. Especially in intentionally planned change processes (e.g., change management), forgetting is an important precondition to impede the recall of obsolete routines and adapt to new strategic objectives accompanied by new organizational routines. We first comprehensively review the literature on the need for organizational forgetting and particularly on accidental vs. intentional forgetting. We discuss the current state of the art of theory and empirical evidence on forgetting from cognitive psychology in order to infer mechanisms applicable to the organizational context. In this respect, we emphasize retrieval theories and the relevance of retrieval cues important for forgetting. Subsequently, we transfer the empirical evidence that the elimination of retrieval cues leads to faster forgetting to the forgetting of organizational routines, as routines are part of organizational memory. We then propose a classification of cues (context, sensory, business process-related cues) that are relevant in the forgetting of routines, and discuss a meta-cue called the "situational strength" cue, which is relevant if cues of an old and a new routine are present simultaneously. Based on the classification as business process-related cues (information, team, task, object cues), we propose mechanisms to accelerate forgetting by eliminating specific cues based on the empirical and theoretical state of the art. We conclude that in intentional organizational change processes, the elimination of cues to accelerate forgetting should be used in change management practices.
Lifestyle-related disorders, such as the metabolic syndrome, have become a primary risk factor for the development of liver pathologies that can progress from hepatic steatosis, hepatic insulin resistance, steatohepatitis, fibrosis and cirrhosis, to the most severe condition of hepatocellular carcinoma (HCC). While the prevalence of liver pathologies is steadily increasing in modern societies, there are currently no approved drugs other than chemotherapeutic intervention in late stage HCC. Hence, there is a pressing need to identify and investigate causative molecular pathways that can yield new therapeutic avenues. The transcription factor p53 is well established as a tumor suppressor and has recently been described as a central metabolic player both in physiological and pathological settings. Given that liver is a dynamic tissue with direct exposition to ingested nutrients, hepatic p53, by integrating cellular stress response, metabolism and cell cycle regulation, has emerged as an important regulator of liver homeostasis and dysfunction. The underlying evidence is reviewed herein, with a focus on clinical data and animal studies that highlight a direct influence of p53 activity on different stages of liver diseases. Based on current literature showing that activation of p53 signaling can either attenuate or fuel liver disease, we herein discuss the hypothesis that, while hyper-activation or loss of function can cause disease, moderate induction of hepatic p53 within physiological margins could be beneficial in the prevention and treatment of liver pathologies. Hence, stimuli that lead to a moderate and temporary p53 activation could present new therapeutic approaches through several entry points in the cascade from hepatic steatosis to HCC.
Two decades ago, sphingosine 1-phosphate (S1P) was discovered as a novel bioactive molecule that regulates a variety of cellular functions. The plethora of S1P-mediated effects is due to the fact that the sphingolipid not only modulates intracellular functions but also acts as a ligand of G protein-coupled receptors after secretion into the extracellular environment. In the plasma, S1P is found in high concentrations, modulating immune cell trafficking and vascular endothelial integrity. The liver is engaged in modulating the plasma S1P content, as it produces apolipoprotein M, which is a chaperone for the S1P transport. Moreover, the liver plays a substantial role in glucose and lipid homeostasis. A dysfunction of glucose and lipid metabolism is connected with the development of liver diseases such as hepatic insulin resistance, non-alcoholic fatty liver disease, or liver fibrosis. Recent studies indicate that S1P is involved in liver pathophysiology and contributes to the development of liver diseases. In this review, the current state of knowledge about S1P and its signaling in the liver is summarized with a specific focus on the dysregulation of S1P signaling in obesity-mediated liver diseases. Thus, the modulation of S1P signaling can be considered as a potential therapeutic target for the treatment of hepatic diseases.