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Corruption has found very fertile ground in the health sector. Many studies demonstrate the negative relationship between sustainability and corruption. However, relatively little is known at this time about how to prevent corruption in healthcare organizations (HCOs), and thus to recover the important sustainability of the entire healthcare system. After noticing this gap in the literature, the authors’ aim in undertaking this study was twofold: first, to analyze the current state of knowledge about how Italian HCOs adopt corruption prevention plans in compliance with the National Plan issued by the National Anti-Corruption Authority; second, to identify some clusters of HCOs which represent different adoption patterns of corruption prevention interventions and to classify these HCOs. For these purposes, the authors studied 68 HCOs along 13 dimensions that characterized the corruption prevention plans. The empirical results showed that the HCOs were not fully compliant with the anti-corruption legislation. At the same time, the authors identified three clusters of HCOs with different patterns of anti-corruption prevention interventions. The clusters that adopted some specific interventions seemed to be more sustainable than others.

The leaves of Aster yomena (Kitam.) Honda have long been used as a traditional herb for treating disorders including coughs, asthma, and insect bites. According to recent studies, A. yomena leaf extracts have several pharmacological properties, including anti-inflammatory, antioxidant, and anti-asthmatic activities. However, little information is available regarding their anti-obesity effect. In this study, we investigated the inhibitory effect of the ethanol extracts of A. yomena leaves (EEAY) on adipocyte differentiation and adipogenesis using 3T3-L1 preadipocytes. When 3T3-L1 preadipocytes were treated with various concentrations of EEAY (ranging from non-toxic), the number of lipid droplets, lipid content, and triglyceride production, the typical characteristics of adipocytes, were suppressed in a concentration-dependent manner. During this process, EEAY significantly reduced the expression of adipogenic transcription factors, including peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding protein α and β, and sterol regulatory element-binding protein-1c. In addition, EEAY was also found to potently inhibit the expression of adipocyte-specific genes, including adipocyte fatty acid-binding protein and leptin. In particular, EEAY treatment effectively enhanced the activation of the AMP-activated protein kinase (AMPK) signaling pathway; however, the co-treatment with compound C, an inhibitor of AMPK, significantly restored the EEAY-induced inhibition of pro-adipogenic transcription factors and adipocyte-specific genes. These results indicate that EEAY may exert an anti-obesity effect by controlling the AMPK signaling pathway, suggesting that the leaf extract of A. yomena may be a potential anti-obesity agent.

Pour obtenir un aperçu spécifique des rôles que les micro-organismes pourraient jouer dans la stéatose hépatique non alcoolique (NAFLD), certaines bactéries intestinales et lactiques et une levure (Anaerostipes caccae, Bacteroides thetaiotaomicron, Bifidobacterium longum, Enterococcus fecalis, Escherichia coli, Lactobacillus acidophilus, Lactobacillus fermentum, Lactobacillus plantarum, Weissella confusa, Saccharomyces cerevisiae) ont été caractérisées par une chromatographie liquide haute performance pour la production d'éthanol lorsqu'elles sont cultivées sur différents glucides : hexoses (glucose et fructose), pentoses (arabinose et ribose), disaccharides (lactose et lactulose) et inuline. Les quantités les plus élevées d'éthanol ont été produites par S. cerevisiae, L. fermentum et W. confusa sur le glucose et par S. cerevisiae et W. confusa sur le fructose. En raison de la mannitol-déshydrogénase exprimée dans L. fermentum, la production d'éthanol sur le fructose a été significativement réduite (P < 0,05). Le pyruvate et le citrate, deux accepteurs d'électrons potentiels pour la régénération du NAD+/NADP+, ont considérablement réduit la production d'éthanol avec de l'acétate produit à la place dans L. fermentum cultivé sur glucose et W. confusa cultivé sur glucose et fructose, respectivement. Dans les boues fécales préparées à partir des matières fécales de quatre volontaires en surpoids, on a constaté que l'éthanol était produit lors de l'ajout de fructose. L'ajout d'A. caccae, L. acidophilus, L. fermentum, ainsi que de citrate et de pyruvate, respectivement, a aboli la production d'éthanol. Cependant, l'ajout de W. confusa a entraîné une augmentation significative (P < 0,05) de la production d'éthanol. Ces résultats indiquent que des micro-organismes comme W. confusa, une bactérie lactique hétéro-fermentaire, négative à la mannitol-déshydrogénase, peuvent favoriser la NAFLD par l'éthanol produit à partir de la fermentation du sucre, tandis que d'autres bactéries intestinales et des bactéries lactiques homo- et hétéro-fermentaires mais positives à la mannitol-déshydrogénase peuvent ne pas favoriser la NAFLD. En outre, nos études indiquent que les facteurs alimentaires interférant avec le microbiote gastro-intestinal et le métabolisme microbien peuvent être importants dans la prévention ou la promotion de la NAFLD. Para obtener información específica sobre los roles que podrían desempeñar los microorganismos en la enfermedad del hígado graso no alcohólico (NAFLD, por sus siglas en inglés), algunas bacterias intestinales y del ácido láctico y una levadura (Anaerostipes caccae, Bacteroides thetaiotaomicron, Bifidobacterium longum, Enterococcus fecalis, Escherichia coli, Lactobacillus acidophilus, Lactobacillus fermentum, Lactobacillus plantarum, Weissella confusa, Saccharomyces cerevisiae) se caracterizaron por cromatografía líquida de alto rendimiento para la producción de etanol cuando se cultivaron en diferentes carbohidratos: hexosas (glucosa y fructosa), pentosas (arabinosa y ribosa), disacáridos (lactosa y lactulosa) e inulina. Las cantidades más altas de etanol fueron producidas por S. cerevisiae, L. fermentum y W. confusa en glucosa y por S. cerevisiae y W. confusa en fructosa. Debido a la manitol-deshidrogenasa expresada en L. fermentum, la producción de etanol en fructosa se redujo significativamente (P < 0.05). El piruvato y el citrato, dos aceptores de electrones potenciales para la regeneración de NAD+/NADP+, redujeron drásticamente la producción de etanol con acetato producido en su lugar en L. fermentum cultivado en glucosa y W. confusa cultivado en glucosa y fructosa, respectivamente. En suspensiones fecales preparadas a partir de heces de cuatro voluntarios con sobrepeso, se encontró que el etanol se producía tras la adición de fructosa. La adición de A. caccae, L. acidophilus, L. fermentum, así como citrato y piruvato, respectivamente, abolió la producción de etanol. Sin embargo, la adición de W. confusa resultó en un aumento significativo (P < 0.05) de la producción de etanol. Estos resultados indican que microorganismos como W. confusa, una bacteria de ácido láctico hetero-fermentativa, negativa para manitol-deshidrogenasa, pueden promover NAFLD a través del etanol producido a partir de la fermentación de azúcar, mientras que otras bacterias intestinales y bacterias de ácido láctico homo- y hetero-fermentativas pero positivas para manitol-deshidrogenasa pueden no promover NAFLD. Además, nuestros estudios indican que los factores dietéticos que interfieren con la microbiota gastrointestinal y el metabolismo microbiano pueden ser importantes para prevenir o promover la EHGNA. To gain some specific insight into the roles microorganisms might play in non-alcoholic fatty liver disease (NAFLD), some intestinal and lactic acid bacteria and one yeast (Anaerostipes caccae, Bacteroides thetaiotaomicron, Bifidobacterium longum, Enterococcus fecalis, Escherichia coli, Lactobacillus acidophilus, Lactobacillus fermentum, Lactobacillus plantarum, Weissella confusa, Saccharomyces cerevisiae) were characterized by high performance liquid chromatography for production of ethanol when grown on different carbohydrates: hexoses (glucose and fructose), pentoses (arabinose and ribose), disaccharides (lactose and lactulose), and inulin. Highest amounts of ethanol were produced by S. cerevisiae, L. fermentum and W. confusa on glucose and by S. cerevisiae and W. confusa on fructose. Due to mannitol-dehydrogenase expressed in L. fermentum, ethanol production on fructose was significantly (P < 0.05) reduced. Pyruvate and citrate, two potential electron acceptors for regeneration of NAD+/NADP+, drastically reduced ethanol production with acetate produced instead in L. fermentum grown on glucose and W. confusa grown on glucose and fructose, respectively. In fecal slurries prepared from feces of four overweight volunteers, ethanol was found to be produced upon addition of fructose. Addition of A. caccae, L. acidophilus, L. fermentum, as well as citrate and pyruvate, respectively, abolished ethanol production. However, addition of W. confusa resulted in significantly (P < 0.05) increased production of ethanol. These results indicate that microorganisms like W. confusa, a hetero-fermentative, mannitol-dehydrogenase negative lactic acid bacterium, may promote NAFLD through ethanol produced from sugar fermentation, while other intestinal bacteria and homo- and hetero-fermentative but mannitol-dehydrogenase positive lactic acid bacteria may not promote NAFLD. Also, our studies indicate that dietary factors interfering with gastrointestinal microbiota and microbial metabolism may be important in preventing or promoting NAFLD. لاكتساب بعض الأفكار المحددة حول الأدوار التي قد تلعبها الكائنات الحية الدقيقة في مرض الكبد الدهني غير الكحولي (NAFLD)، تميزت بعض بكتيريا حمض الأمعاء واللاكتيك وخميرة واحدة (Anaerostipes caccae، Bacteroides thetaiotaomicron، Bifidobacterium longum، Enterococcus fecalis، Escherichia coli، Lactobacillus acidophilus، Lactobacillus fermentum، Lactobacillus plantarum، Weissella confusa، Saccharomyces cerevisiae) بتصوير سائل عالي الأداء لإنتاج الإيثانول عند زراعته على كربوهيدرات مختلفة: hexoses (الجلوكوز والفركتوز)، pentoses (الأرابينوز والريبوز)، disaccharides (اللاكتوز واللاكتولوز)، و inulin. تم إنتاج أعلى كميات من الإيثانول بواسطة S. cerevisiae و L. fermentum و W. confusa على الجلوكوز و S. cerevisiae و W. confusa على الفركتوز. بسبب نازعة هيدروجين المانيتول المعبر عنها في L. fermentum، انخفض إنتاج الإيثانول على الفركتوز بشكل كبير (P < 0.05). قلل البيروفات والسيترات، وهما مستقبلان محتملان للإلكترون لتجديد NAD +/NADP+، بشكل كبير من إنتاج الإيثانول مع الأسيتات المنتجة بدلاً من ذلك في L. fermentum المزروع على الجلوكوز و W. confusa المزروع على الجلوكوز والفركتوز، على التوالي. في الملاط البرازي الذي تم تحضيره من براز أربعة متطوعين يعانون من زيادة الوزن، وجد أن الإيثانول يتم إنتاجه عند إضافة الفركتوز. إضافة A. caccae، L. acidophilus، L. fermentum، وكذلك السترات والبيروفات، على التوالي، ألغت إنتاج الإيثانول. ومع ذلك، أدت إضافة W. confusa إلى زيادة كبيرة في إنتاج الإيثانول (P < 0.05). تشير هذه النتائج إلى أن الكائنات الحية الدقيقة مثل W. confusa، وهي بكتيريا حمض اللاكتيك السلبية غير المتجانسة، قد تعزز NAFLD من خلال الإيثانول المنتج من تخمير السكر، في حين أن البكتيريا المعوية الأخرى وبكتيريا حمض اللاكتيك الإيجابية غير المتجانسة ولكن غير المتجانسة قد لا تعزز NAFLD. أيضًا، تشير دراساتنا إلى أن العوامل الغذائية التي تتداخل مع الكائنات الحية الدقيقة في الجهاز الهضمي والتمثيل الغذائي الميكروبي قد تكون مهمة في منع أو تعزيز NAFLD.

Background:  We previously found that activation of the glial cell line‐derived neurotrophic factor (GDNF) pathway in the ventral tegmental area (VTA) reduces ethanol‐drinking behaviors. In this study, we set out to assess the contribution of endogenous GDNF or its receptor GFRα1 to the regulation of ethanol‐related behaviors.Methods:  GDNF and GFRα1 heterozygote mice (HET) and their wild‐type littermate controls (WT) were used for the studies. Ethanol‐induced hyperlocomotion, sensitization, and conditioned place preference (CPP), as well as ethanol consumption before and after a period of abstinence were evaluated. Blood ethanol concentration (BEC) was also measured.Results:  We observed no differences between the GDNF HET and WT mice in the level of locomotor activity or in sensitization to ethanol‐induced hyperlocomotion after systemic injection of a nonhypnotic dose of ethanol and in BEC. However, GDNF and GFRα1 mice exhibited increased place preference to ethanol as compared with their WT littermates. The levels of voluntary ethanol or quinine consumption were similar in the GDNF HET and WT mice, however, a small but significant increase in saccharin intake was observed in the GDNF HET mice. No changes were detected in voluntary ethanol, saccharin or quinine consumption of GFRα1 HET mice as compared with their WT littermates. Interestingly, however, both the GDNF and GFRα1 HET mice consumed much larger quantities of ethanol after a period of abstinence from ethanol as compared with their WT littermates. Furthermore, the increase in ethanol consumption after abstinence was found to be specific for ethanol as similar levels of saccharin intake were measured in the GDNF and GFRα1 HET and WT mice after abstinence.Conclusions:  Our results suggest that endogenous GDNF negatively regulates the rewarding effect of ethanol and ethanol‐drinking behaviors after a period of abstinence.

Aims The aim of this study was to determine whether the sequential application of povidone iodine-alcohol (PVI) followed by chlorhexidine gluconate-alcohol (CHG) would reduce surgical wound contamination to a greater extent than PVI applied twice in patients undergoing spinal surgery. Patients and Methods A single-centre, interventional, two arm, parallel group randomised controlled trial was undertaken, involving 407 patients who underwent elective spinal surgery. For 203 patients, the skin was disinfected before surgery using PVI (10% [w/w (1% w/w available iodine)] in 95% industrial denatured alcohol, povidone iodine; Videne Alcoholic Tincture) twice, and for 204 patients using PVI once followed by CHG (2% [w/v] chlorhexidine gluconate in 70% [v/v] isopropyl alcohol; Chloraprep with tint). The primary outcome measure was contamination of the wound determined by aerobic and anaerobic bacterial growth from samples taken after disinfection. Results The detection of viable bacteria in any one of the samples taken after disinfection (culture-positive) was significantly lower in the group treated with both PVI and CHG than in the group treated with PVI alone (59 (29.1%) versus 85 (41.7%), p = 0.009; odds ratio 0.574; 95% confidence interval, 0.380 to 0.866). Conclusions Antisepsis of the skin with the sequential application of PVI and CHG more effectively reduces the contamination of a surgical wound than PVI alone. Cite this article: Bone Joint J 2017;99-B:1354–65.

ABSTRACTPrenatal ethanol exposure causes a variety of cognitive deficits that have a persistent impact on quality of life, some of which may be explained by ethanol-induced alterations in interneuron function. Studies from several laboratories, including our own, have demonstrated that a single binge-like ethanol exposure during the equivalent to the third trimester of human pregnancy leads to acute apoptosis and long-term loss of interneurons in the rodent retrosplenial cortex (RSC). The RSC is interconnected with the hippocampus, thalamus, and other neocortical regions and plays distinct roles in visuospatial processing and storage, as well as retrieval of hippocampal-dependent episodic memories. Here we used slice electrophysiology to characterize the acute effects of ethanol on GABAergic neurotransmission in the RSC of neonatal mice, as well as the long-term effects of neonatal ethanol exposure on parvalbumin-interneuron mediated neurotransmission in adolescent mice. Mice were exposed to ethanol using vapor inhalation chambers. In postnatal day (P) 7 mouse pups, ethanol unexpectedly failed to potentiate GABAAreceptor-mediated synaptic transmission. Binge-like ethanol exposure of P7 mice expressing channel rhodopsin in parvalbumin-positive interneurons enhanced the peak amplitudes, asynchronous activity and total charge, while decreasing the rise-times of optically-evoked GABAAreceptor-mediated inhibitory postsynaptic currents in adolescent animals. These effects could partially explain the learning and memory deficits that have been documented in adolescent and young adult mice exposed to ethanol during the third trimester-equivalent developmental period.

BackgroundWe previously showed that, by activating innate immune receptors Toll‐like 4 (TLR4), adolescent intermittent ethanol (EtOH) exposure causes neuroinflammation, myelin damage, and behavioral dysfunctions. Recent findings reveal that clinically used opioid antagonists naltrexone (NT) and naloxone (NX) inhibit opioid‐induced TLR4 signaling and that NT, NX, and nalmefene (NF), the 6‐methylene derivative of NX, are able to reduce alcohol drinking escalation.MethodsNF (0.1 mg/kg, intraperitoneally) was injected 1 hour prior to EtOH (3 g/kg, intraperitoneally) following intermittent treatment in female (PND35) adolescent mice. Inflammatory molecules, myelin proteins, and apoptotic markers were assessed in the prefrontal cortex (PFC) and striatum/nucleus accumbens (STR/NAcc). The effect of NF on alcohol drinking preference was evaluated in both the wild‐type and TLR4 knockout (KO) adolescent mice. Using astroglial cells, the inhibitory potential of NT, NX, and NF on lipopolysaccharide (LPS), or the EtOH‐triggered TLR4 response, was compared.ResultsOur findings indicate that NF prevents the up‐regulation of cytokines (IL‐1β, IL‐17A, TNF‐α), chemokines (MCP‐1, MIP‐1, KC), and pro‐inflammatory mediators (iNOS, COX‐2), along with myelin damage and apoptotic events, in both PFC and STR/NAcc. NF also abolishes EtOH‐induced escalation of alcohol preference/consumption, but has no effect when administered to TLR4‐KO mice. In vitro experiments indicate that NX and NF inhibit TLR4 activation upon LPS or EtOH stimulation. Immunofluorescence studies and lipid rafts isolation show that NF is able to prevent TLR4 translocation to lipid rafts/caveolae in astrocytes.ConclusionsThese results suggest that NF prevents neuroinflammation and brain damage by blocking the TLR4 response and also support the role of central pro‐inflammatory immune signaling in the modulation of alcohol consumption/addiction.