In the last decades, there has been rising interest in public health research in the importance of the built environment for a healthy and active life in old age, but little attention has been paid to less densely populated areas. This study aimed to explore the impact of the built environment on walking for transport in the context of an older population living in communities of less then 100,000 inhabitants. Within the project AFOOT-Securing urban mobility of an aging population, a cross-sectional postal survey was carried out from May to September 2019 in older adults (≥65 years) in the Metropolitan Region Northwest, Germany. Self-reported data from 2189 study participants were analyzed. Logistic and linear regression models were used to examine the associations between the built environment and walking for transport. Any walking and frequent walking were positively associated with nearly all built environment attributes, even after adjustment for demographic and health covariates. The amount of walking in minutes per week was associated only with residential density. Moderating effects of gender, age, and use of walking aids were identified. Improving the built environment appears to be a promising opportunity to motivate and enable older adults to walk for transport.Malnutrition among heart-transplant patients may affect survival. The aim was to investigate the survival and nutrition status among male and female heart transplant patients who underwent transplantation, before and 1 year after surgery based on the nutritional risk index (NRI). The medical records of ninety heart-transplant patients (2009-2014) from the King Faisal Specialist Hospital, Riyadh, were reviewed. The assessment included demographic data, anthropometric measurements, and NRI calculation. Moreover, postoperative data included the length of stay and survival. Paired t-test and survival analysis by Kaplan-Meier (KM) curves were used. A total of 90 patients (males 77.78%) were included. The prevalence of malnutrition in the preoperative phase by NRI was 60% (7.78% as severe; 40% as moderate, and 12.22% mild NRI scores). After 1 year, body mass index (BMI) and NRI increased significantly (p less then 0.001). Furthermore, NRI was significantly different between men and women (p less then 0.01), while KM survival curves were insignificantly different (p = 0.67). Recipients with postoperative moderate or severe nutritional risk (NRI less then 97.5) had significantly shorter survival in the first-year post-transplantation (HR = 0.82; 95% CI, 0.75-0.89; p less then 0.001). Our findings indicate that the NRI after 1 year of transplant correlated significantly with mortality. Besides, there was no significant gender difference regarding survival; however, malnutrition and low survival were more prominent among women.Removal of biofilms is extremely pivotal in environmental and medicinal fields. Therefore, reporting the new-enzymes and their combinations for dispersal of infectious biofilms can be extremely critical. Herein, for the first time, we accessed the enzyme "protease from bovine pancreas type-I (PtI)" for anti-biofilm properties. We further investigated the anti-biofilm potential of PtI in combination with α-amylase from Bacillus sp. (αA). PtI showed a very significant biofilm inhibition effect (86.5%, 88.4%, and 67%) and biofilm prevention effect (66%, 64%, and 70%), against the E. coli, S. aureus, and MRSA, respectively. However, the new enzyme combination (Ec-PtI+αA) exhibited biofilm inhibition effect (78%, 90%, and 93%) and a biofilm prevention effect (44%, 51%, and 77%) against E. coli, S. aureus, and MRSA, respectively. The studied enzymes were found not to be anti-bacterial against the E. coli, S. aureus, and MRSA. In summary, the PtI exhibited significant anti-biofilm effects against S. aureus, MRSA, and E. coli. Ec-PtI+αA exhibited enhancement of the anti-biofilm effects against S. aureus and MRSA biofilms. Therefore, this study revealed that this Ec-PtI+αA enzymatic system can be extremely vital for the treatment of biofilm complications resulting from E. coli, S. aureus, and MRSA.Astrocytes, the most abundant cell type in the brain, are non-excitable cells and play critical roles in brain function. Mature astrocytes typically exhibit a linear current-voltage relationship termed passive conductance, which is believed to enable astrocytes to maintain potassium homeostasis in the brain. We previously demonstrated that TWIK-1/TREK-1 heterodimeric channels mainly contribute to astrocytic passive conductance. However, the molecular identity of astrocytic passive conductance is still controversial and needs to be elucidated. Here, we report that spadin, an inhibitor of TREK-1, can dramatically reduce astrocytic passive conductance in brain slices. A series of gene silencing experiments demonstrated that spadin-sensitive currents are mediated by TWIK-1/TREK-1 heterodimeric channels in cultured astrocytes and hippocampal astrocytes from brain slices. Our study clearly showed that TWIK-1/TREK-1-heterodimeric channels can act as the main molecular machinery of astrocytic passive conductance, and suggested that spadin can be used as a specific inhibitor to control astrocytic passive conductance.Cerebral cavernous malformations (CCMs) are vascular malformations that can be the result of the deficiency of one of the CCM genes.  https://www.selleckchem.com/products/ly333531.html  Their only present treatment is surgical removal, which is not always possible, and an alternative pharmacological strategy to eliminate them is actively sought. We have studied the effect of the lack of one of the CCM genes, CCM3, in endothelial and non-endothelial cells. By comparing protein expression in control and CCM3-silenced cells, we found that the levels of the Epidermal Growth Factor Receptor (EGFR) are higher in CCM3-deficient cells, which adds to the known upregulation of Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) in these cells. Whereas VEGFR2 is upregulated at the mRNA level, EGFR has a prolonged half-life. Inhibition of EGFR family members in CCM3-deficient cells does not revert the known cellular effects of lack of CCM genes, but it induces significantly more apoptosis in CCM3-deficient cells than in control cells. We propose that the susceptibility to tyrosine kinase inhibitors of CCM3-deficient cells can be harnessed to kill the abnormal cells of these lesions and thus treat CCMs pharmacologically.