Studie zu den Herausforderungen der klassischen Hotellerie im Berner Oberland

Die Hotellerie in Bergregionen wird seit einigen Jahren mit neuen Herausforderungen konfrontiert. Dazu gehören unter anderem die politische und wirtschaftliche Lage, der Klimawandel und die damit verbundene Abnahme der Gäste im Winter sowie der technische Fortschritt und die kleinen Strukturen in der Schweizer Hotelbranche. Zudem prophezeit der wachsende Geschäftstourismus sowie der Trend zu kürzeren Reisen Schweizer Städten eine positivere Entwicklung im Vergleich zu den Bergregionen

Cytotoxic effect of Agaricus bisporus and Lactarius rufus β-d-glucans on HepG2 cells

AbstractThe cytotoxic activity of β-d-glucans isolated from Agaricus bisporus and Lactarius rufus fruiting bodies was evaluated on human hepatocellular carcinoma cells (HepG2). NMR and methylation analysis suggest that these β-d-glucans were composed of a linear (1→6)-linked and a branched (1→3), (1→6)-linked backbone, respectively. They both decreased cell viability at concentrations of up to 100μgmL−1, as shown by MTT assay. The amount of LDH released and the analysis of cell morphology corroborated these values and also showed that the β-d-glucan of L. rufus was more cytotoxic to HepG2 cells than that of A. bisporus. The treatment of HepG2 cells with L. rufus and A. bisporus β-d-glucans at a dose of 200μgmL−1 for 24h promoted an increase of cytochrome c release and a decrease of ATP content, suggesting that these polysaccharides could promote cell death by apoptosis. Both β-d-glucans were tested against murine primary hepatocytes at a dose of 200μgmL−1. The results suggest that the L. rufus β-d-glucan was as cytotoxic for hepatocytes as for HepG2 cells, whereas the A. bisporus β-d-glucan, under the same conditions, was cytotoxic only for HepG2 cells, suggesting cell selectivity. These results open new possibilities for use of mushroom β-d-glucans in cancer therapy

Daily Fermented Whey Consumption Alters the Fecal Short-Chain Fatty Acid Profile in Healthy Adults

FUNDING: This study was funded by A.Vogel Bioforce AG, Roggwil, Switzerland. NS was co-funded by the School of Medicine, Medical Sciences and Nutrition (University of Aberdeen) and A.Vogel Bioforce AG. The Rowett Institute (University of Aberdeen) receives financial support from the Scottish Government Rural and Environmental Sciences and Analytical Services (RESAS). ACKNOWLEDGMENTS: We thank all the volunteers which contributed their time and efforts into enrolling and completing the trial. Further, we are grateful for the staff at the Human Nutrition Unit and Analytical Services at the Rowett Institute for supporting the research and assisting when needed. We would like to thank Brennan Martin at the Center for Genome Enabled Biology of Medicine for his assistance in DNA sequencingPeer reviewedPublisher PD

Population-based reference values for the 1-min sit-to-stand test

Objectives: To determine reference values for the 1-min sit-to-stand (STS) test in an adult population. Methods: Cross-sectional study nested within a nationwide health promotion campaign in Switzerland. Adults performed the STS test and completed questions on demographics and health behavior. Results: 6,926 out of 7,753 (89.3 %) adults were able to complete the STS test. The median number of repetitions ranged from 50/min (25-75th percentile 41-57/min) in young men and 47/min (39-55/min) in young women aged 20-24years to 30/min (25-37/min) in older men and 27/min (22-30/min) in older women aged 75-79years. Conclusions: The reference values support the interpretation of 1-min STS test performance and identification of subjects with decreased lower body muscular strength and enduranc

Population-based reference values for the 1-min sit-to-stand test

Abstract Objectives To determine reference values for the 1-min sit-to-stand (STS) test in an adult population. Methods Cross-sectional study nested within a nationwide health promotion campaign in Switzerland. Adults performed the STS test and completed questions on demographics and health behavior

Integration of a peer practitioner in a hospital unit for patients with psychotic disorders: an exploratory qualitative study

IntroductionStudies on the integration of peer mental health practitioners (PMHP) in hospitals are sparse, despite significant benefits being reported for patients and professionals. The integration of PMHP requires the consideration of several parameters and a change in the culture of care. This study aims to understand the impact of the integration of a PMHP in a hospital unit caring for patients with psychiatric disorders.MethodsA qualitative content analysis of three focus groups with the interdisciplinarity team were conducted. A consulting PMHP was integrated into the entire research process.ResultsData analysis revealed five main themes: the importance of integration, benefits for patients linked to the identification process, benefits for the team and institution, potentials risks, and perspectives.DiscussionThe study was conducted in a hospital setting with patients suffering from severe psychiatric disorders associated with behavioral disturbances. The benefits reported in the results outline the feasibility of PMHP integration in an acute psychiatric care setting. Nevertheless, further formalization of the PMHP role is required to minimize possible areas of tension between respective fields of activity of each professional

Landscape of DNA methylation on the marsupial x

DNA methylation plays a key role in maintaining transcriptional silence on the inactive X chromosome of eutherian mammals. Beyond eutherians, there are limited genome wide data on DNA methylation from other vertebrates. Previous studies of X borne genes in various marsupial models revealed no differential DNA methylation of promoters between the sexes, leading to the conclusion that CpG methylation plays no role in marsupial X-inactivation. Using reduced representation bisulfite sequencing, we generated male and female CpG methylation profiles in four representative vertebrates (mouse, gray short-tailed opossum, platypus, and chicken). A variety of DNA methylation patterns were observed. Platypus and chicken displayed no large-scale differential DNA methylation between the sexes on the autosomes or the sex chromosomes. As expected, a metagene analysis revealed hypermethylation at transcription start sites (TSS) of genes subject to X-inactivation in female mice. This contrasted with the opossum, in which metagene analysis did not detect differential DNA methylation between the sexes at TSSs of genes subject to X-inactivation. However, regions flanking TSSs of these genes were hypomethylated. Our data are the first to demonstrate that, for genes subject to X-inactivation in both eutherian and marsupial mammals, there is a consistent difference between DNA methylation levels at TSSs and immediate flanking regions, which we propose has a silencing effect in both groups.This work was funded by Australian Research Council Discovery Projects DP0987091 and DP1094868

Oxidative stress induces degradation of mitochondrial DNA

Mitochondrial DNA (mtDNA) is located in close proximity of the respiratory chains, which are the main cellular source of reactive oxygen species (ROS). ROS can induce oxidative base lesions in mtDNA and are believed to be an important cause of the mtDNA mutations, which accumulate with aging and in diseased states. However, recent studies indicate that cumulative levels of base substitutions in mtDNA can be very low even in old individuals. Considering the reduced complement of DNA repair pathways available in mitochondria and higher susceptibility of mtDNA to oxidative damage than nDNA, it is presently unclear how mitochondria manage to maintain the integrity of their genetic information in the face of the permanent exposure to ROS. Here we show that oxidative stress can lead to the degradation of mtDNA and that strand breaks and abasic sites prevail over mutagenic base lesions in ROS-damaged mtDNA. Furthermore, we found that inhibition of base excision repair enhanced mtDNA degradation in response to both oxidative and alkylating damage. These observations suggest a novel mechanism for the protection of mtDNA against oxidative insults whereby a higher incidence of lesions to the sugar–phosphate backbone induces degradation of damaged mtDNA and prevents the accumulation of mutagenic base lesions

Automated white matter fiber tract identification in patients with brain tumors

We propose a method for the automated identification of key white matter fiber tracts for neurosurgical planning, and we apply the method in a retrospective study of 18 consecutive neurosurgical patients with brain tumors. Our method is designed to be relatively robust to challenges in neurosurgical tractography, which include peritumoral edema, displacement, and mass effect caused by mass lesions. The proposed method has two parts. First, we learn a data-driven white matter parcellation or fiber cluster atlas using groupwise registration and spectral clustering of multi-fiber tractography from healthy controls. Key fiber tract clusters are identified in the atlas. Next, patient-specific fiber tracts are automatically identified using tractography-based registration to the atlas and spectral embedding of patient tractography. Results indicate good generalization of the data-driven atlas to patients: 80% of the 800 fiber clusters were identified in all 18 patients, and 94% of the 800 fiber clusters were found in 16 or more of the 18 patients. Automated subject-specific tract identification was evaluated by quantitative comparison to subject-specific motor and language functional MRI, focusing on the arcuate fasciculus (language) and corticospinal tracts (motor), which were identified in all patients. Results indicate good colocalization: 89 of 95, or 94%, of patient-specific language and motor activations were intersected by the corresponding identified tract. All patient-specific activations were within 3mm of the corresponding language or motor tract. Overall, our results indicate the potential of an automated method for identifying fiber tracts of interest for neurosurgical planning, even in patients with mass lesions

Morbillivirus Glycoprotein Expression Induces ER Stress, Alters Ca2+ Homeostasis and Results in the Release of Vasostatin

Although the pathology of Morbillivirus in the central nervous system (CNS) is well described, the molecular basis of neurodegenerative events still remains poorly understood. As a model to explore Morbillivirus-mediated CNS dysfunctions, we used canine distemper virus (CDV) that we inoculated into two different cell systems: a monkey cell line (Vero) and rat primary hippocampal neurons. Importantly, the recombinant CDV used in these studies not only efficiently infects both cell types but recapitulates the uncommon, non-cytolytic cell-to-cell spread mediated by virulent CDVs in brain of dogs. Here, we demonstrated that both CDV surface glycoproteins (F and H) markedly accumulated in the endoplasmic reticulum (ER). This accumulation triggered an ER stress, characterized by increased expression of the ER resident chaperon calnexin and the proapoptotic transcription factor CHOP/GADD 153. The expression of calreticulin (CRT), another ER resident chaperon critically involved in the response to misfolded proteins and in Ca2+ homeostasis, was also upregulated. Transient expression of recombinant CDV F and H surface glycoproteins in Vero cells and primary hippocampal neurons further confirmed a correlation between their accumulation in the ER, CRT upregulation, ER stress and disruption of ER Ca2+ homeostasis. Furthermore, CDV infection induced CRT fragmentation with re-localisation of a CRT amino-terminal fragment, also known as vasostatin, on the surface of infected and neighbouring non-infected cells. Altogether, these results suggest that ER stress, CRT fragmentation and re-localization on the cell surface may contribute to cytotoxic effects and ensuing cell dysfunctions triggered by Morbillivirus, a mechanism that might potentially be relevant for other neurotropic viruses