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Agnes Kalibata: altering foodstuff systems.
PURPOSE Recently, efforts have been made to quantify frailty among older adults with intellectual disability (ID). Medication exposure is associated with frailty among older adults without ID. However, there is little research on this association among older adults with ID. The aim of this study was to examine specifically in people with ID the association between frailty and medication exposure, including anticholinergic and sedative medication exposure. METHODS Data were drawn from Wave 2 (2013/2014) of the Intellectual Disability Supplement to the Irish Longitudinal Study on Ageing (IDS-TILDA), a nationally representative study of older adults with ID in Ireland. A modified version of Fried's frailty phenotype was constructed. Drug burden measures were polypharmacy, Drug Burden Index (DBI), Anticholinergic Cognitive Burden (ACB) and Sedative Load Model. Multinomial logistic regression was used to calculate odds ratios (ORs) and identify associations between frailty and drug burden. RESULTS This study included 570 participants with ID. Excessive polypharmacy (use of ≥10 medications) was significantly associated with being pre-frail (P = .017; OR = 2.56; 95% confidence interval [CI] 1.19-5.50) and frail (P  .05). CONCLUSIONS This is the first study to examine frailty and its association with medication use including anticholinergic and sedative medication burden among older adults with ID. Further research is required to investigate frailty as measured by other frailty models in relation to medication burden in older adults with ID. © 2020 John Wiley & Sons Ltd.Diabetic wound infection is a frequent complication that may result in limb amputation. To develop new treatment strategies in response to increasing bacterial resistance, animal models are needed. We created a diabetic mouse model with chronically infected wounds. Diabetes was induced using streptozotocin, and wounds were performed using a biopsy punch, and then infected with a clinical strain of Staphylococcus aureus. Chronification was reached by delaying healing thanks to chemical products (aminotriazole and mercaptosuccinic acid). Overall survival, as well as clinical, bacteriological and immunological data in skin, blood and spleens were collected at days 1, 7, and 14 after wounding. After a transient bacteremia proved by bacteria presence in spleen and kidneys in the first days after wounding, infected mice showed a chronic infection, with a bioburden impairing the healing process, and bacteria persistence compared to control mice. Infected mice showed gradual increasing skin levels of IL-17A compared to control mice that resulted in an IL-17/IFN-γ inbalance, pointing out a localized Th17 polarization of the immune response. Whether infected or not, the skin level of IL-10 decreased dramatically at days 1 and 7 after wounding, with an increase observed only in the control mice at day 14. After a decrease at day 1 in both groups, spleen IL-10 showed a rather steady level at days 7 and 14 in the control group compared with the decrease observed in the infected group. The spleen IL-10/IFN-γ ratio showed a systemic inflammatory response with Th1 polarization. Therefore, this model provides useful data to study wound healing. It is easy to reproduce, affordable and offers clinical and biological tools to evaluate new therapeutics. © 2020 by the Wound Healing Society.We report the first bottom-up synthesis of NBN-doped zigzag-edged GNRs (NBN-ZGNR1 and NBN-ZGNR2) through surface-assisted polymerization and cyclodehydrogenation based on two U-shaped molecular precursors with an NBN unit preinstalled at the zigzag edge. The resultant zigzag-edge topologies of GNRs are elucidated by high-resolution scanning tunneling microscopy (STM) in combination with noncontact atomic force microscopy (nc-AFM). Scanning tunneling spectroscopy (STS) measurements and density functional theory (DFT) calculations reveal that the electronic structures of NBN-ZGNR1 and NBN-ZGNR2 are significantly different from those of their corresponding pristine fully-carbon-based ZGNRs. Additionally, DFT calculations predict that the electronic structures of NBN-ZGNRs can be further tailored to be gapless and metallic through one-electron oxidation of each NBN unit into the corresponding radical cations. This work reported herein provides a feasible strategy for the synthesis of GNRs with stable zigzag edges yet tunable electronic properties. © 2020 The Authors. Published by Wiley-VCH Verlag GmbH & Co. KGaA.BACKGROUND Achalasia is an esophageal motility disorder with unknown etiology. MLT-748 nmr Previous findings indicate that immune-mediated inflammatory process causes inhibitory neuronal degeneration. This study was designed to evaluate levels of serological cytokines and chemokines in patients with achalasia. METHODS We collected information from forty-seven patients with achalasia who underwent peroral endoscopic myotomy. Control samples were collected from forty-seven age- and sex-matched healthy people. The concentrations of serological cytokines and chemokines were analyzed by Luminex xMAP immunoassay. Serological and clinical data were compared between groups. KEY RESULTS Compared with healthy controls, achalasia patients had significantly increased concentrations of eleven cytokines and chemokines, namely, TGF-ß1 (P less then .001), TGF-ß2 (P less then .001), TGF-ß3 (P less then .001), IL-1ra (P less then .001), IL-17 (P = .005), IL-18 (P less then .001), IFN-γ (P less then .001), MIG (P less then .001), PDGF-BB (P less then .001), IP-10 (P = .003), and SCGF-B (P less then .001). Gene ontology (GO) and network functional enrichment analysis revealed regulation of signaling receptor activity and receptor-ligand activity were the most related pathways of these cytokines and chemokines. Levels of twelve cytokines and chemokines were significantly increased in type III compared with I/II achalasia, namely, TGF-ß2, IL-1ra, IL-2Ra, IL-18, MIG, IFN-γ, SDF-1a, Eotaxin, PDGF-BB, IP-10, MCP-1, and TRAIL. CONCLUSIONS AND INFERENCES Patients with achalasia exhibited increased levels of serological cytokines and chemokines. Levels of cytokines and chemokines were significantly increased in type III than in type I/II achalasia. Cytokines and chemokines might contribute to the inflammatory development of achalasia. © 2020 John Wiley & Sons Ltd.
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