Wissensstandsanalyse zum Verbraucher- und Ernährungsverhalten bei ökologischen Lebensmitteln mit Einbezug der Außer-Haus-Verpflegung

Die vorliegende Studie enthält einen umfassenden Überblick zur nationalen wie internationalen Verbraucherforschung für Öko-Lebensmittel. Insgesamt wurden 562 Publikationen basierend auf 338 wissenschaftlichen Studien aus dem Zeitraum Januar 2000 bis Juni 2011 zu den Themengebieten Determinanten des Verbraucherverhaltens, Verbrauchersegmentierung, Produkt-, Preis-, Kommunikations- und Distributionspolitik sowie Außer-Haus-Verzehr analysiert und hinsichtlich ihrer Datengrundlage und Methodik bewertet. Die Betrachtung der einschlägigen englisch- und deutschsprachigen Literatur lieferte Erkenntnisse zum Wissensstand über die Verbraucherforschung für Öko-Lebensmittel und ermöglichte die Identifizierung relevanter Forschungslücken für Deutschland, die richtungsweisend für die zukünftige Forschung ist. Insgesamt ergab sich eine hohe Publikationsdichte insbesondere in den letzten vier Jahren. Zu den zahlenmäßig am häufigsten behandelten Themengebieten gehören die Determinanten des Verbraucherverhaltens, die Produktpolitik sowie die Preispolitik. Dennoch sind auch hier viele gänzlich unbearbeitete Fragestellungen, bspw. zu den Geschmackspräferenzen unterschiedlicher Verbraucher-gruppen, zu umweltfreundlichen Verpackungen sowie zur Preiskenntnis und Preispsychologie des Konsumenten, zu finden. Darüber hinaus konnten innovative Aspekte der Trendforschung zum Thema Öko-Lebensmittel ausgemacht werden. Andere Themengebiete wie zum Beispiel Kommunikationspolitik und Außer-Haus-Verzehr sind bisher kaum untersucht. Die Status-Quo-Analyse wurde mit den Ergebnissen aus einer Online-Befragung und einem Experten-Workshop ergänzt, um die Relevanz der identifizierten Forschungslücken einzuschätzen und den Forschungsbedarf aus Praktiker- und Expertensicht zu ermitteln. Aus dieser umfassenden Analyse konnten konkret Empfehlungen für zukünftige Forschungsschwerpunkte in Deutschland abgeleitet werden

Canagliflozin and renal outcomes in type 2 diabetes and nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to <90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

Urokinase-induced signaling in human vascular smooth muscle cells is mediated by PDGFR-β

Urokinase (uPA)-induced signaling in human vascular smooth muscle cells (VSMC) elicits important cellular functional responses, such as cell migration and proliferation. However, how intracellular signaling is linked to glycolipid-anchored uPA receptor (uPAR) is unknown. We provide evidence that uPAR activation by uPA induces its association with platelet-derived growth factor receptor (PDGFR)-β. The interaction results in PDGF-independent PDGFR-β activation by phosphorylation of cytoplasmic tyrosine kinase domains and receptor dimerization. Association of the receptors as well as the tyrosine kinase activity of PDGFR-β are decisive in mediating uPA-induced downstream signaling that regulates VSMC migration and proliferation. These findings provide a molecular basis for mechanisms VSMC use to induce uPAR- and PDGFR-directed signaling. The processes may be relevant to VSMC function and vascular remodeling

Visual-auditory integration for visual search: a behavioral study in barn owls

Barn owls are nocturnal predators that rely on both vision and hearing for survival. The optic tectum of barn owls, a midbrain structure involved in selective attention, has been used as a model for studying visual- auditory integration at the neuronal level. However, behavioral data on visual- auditory integration in barn owls are lacking. The goal of this study was to examine if the integration of visual and auditory signals contributes to the process of guiding attention towards salient stimuli. We attached miniature wireless video cameras on barn owls' heads (OwlCam) to track their target of gaze. We first provide evidence that the area centralis (a retinal area with a maximal density of photoreceptors) is used as a functional fovea in barn owls. Thus, by mapping the projection of the area centralis on the OwlCam's video frame, it is possible to extract the target of gaze. For the experiment, owls were positioned on a high perch and four food items were scattered in a large arena on the floor. In addition, a hidden loudspeaker was positioned in the arena. The positions of the food items and speaker were changed every session. Video sequences from the OwlCam were saved for offline analysis while the owls spontaneously scanned the room and the food items with abrupt gaze shifts (head saccades). From time to time during the experiment, a brief sound was emitted from the speaker. The fixation points immediately following the sounds were extracted and the distances between the gaze position and the nearest items and loudspeaker were measured. The head saccades were rarely towards the location of the sound source but to salient visual features in the room, such as the door knob or the food items. However, among the food items, the one closest to the loudspeaker had the highest probability of attracting a gaze shift. This result supports the notion that auditory signals are integrated with visual information for the selection of the next visual search target

Loss of urokinase receptor sensitizes cells to DNA damage and delays DNA repair.

DNA damage induced by numerous exogenous or endogenous factors may have irreversible consequences on the cell leading to cell cycle arrest, senescence and cell death. The DNA damage response (DDR) is powerful signaling machinery triggered in response to DNA damage, to provide DNA damage recognition, signaling and repair. Most anticancer drugs induce DNA damage, and DNA repair in turn attenuates therapeutic efficiency of those drugs. Approaches delaying DNA repair are often used to increase efficiency of treatment. Recent data show that ubiquitin-proteasome system is essential for signaling and repair of DNA damage. However, mechanisms providing regulation of proteasome intracellular localization, activity, and recruitment to DNA damage sites are elusive. Even less investigated are the roles of extranuclear signaling proteins in these processes. In this study, we report the involvement of the serine protease urokinase-type plasminogen activator receptor (uPAR) in DDR-associated regulation of proteasome. We show that in vascular smooth muscle cells (VSMC) uPAR activates DNA single strand break repair signaling pathway. We provide evidence that uPAR is essential for functional assembly of the 26S proteasome. We further demonstrate that uPAR mediates DNA damage-induced phosphorylation, nuclear import, and recruitment of the regulatory subunit PSMD6 to proteasome. We found that deficiency of uPAR and PSMD6 delays DNA repair and leads to decreased cell survival. These data may offer new therapeutic approaches for diseases such as cancer, cardiovascular and neurodegenerative disorders

Urokinase Receptor Counteracts Vascular Smooth Muscle Cell Functional Changes Induced by Surface Topography

© Ivyspring International Publisher. This is an open-access article distributed under the terms of the Creative Commons Licens

uPAR is required for MMS-induced PSMD6 phosphorylation.

<p>A. SiCo and uPARsi human VSMC were treated with 1.2(A) and serine phosphorylation (B) was assessed using Duolink proximity ligation assay. The right panels show the number of Duolink PLA signals per cell quantified using ImageJ software. DraQ5 was used as nuclear stain. C. Serine phosphorylation of PSMD6 was assessed by immunoprecipitation. PSMD6 from lysates of control and MMS-stimulated cells was immunoprecipitated. P-Ser was detected by western blotting. The lower panel shows loading controls.</p

uPAR regulates PSMD6 recruitment to 26S proteasome and its activity.

<p>A. SiCo and uPARsi human VSMC were treated with 1.2</p