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This study assessed the hand hygiene performance in French nursing homes using the consumption of alcohol-based hand rubs (AHRs) as a surrogate. Nursing homes from the 17 French regions were contacted to collect their AHR consumption and occupancy in 2018 and 2019. A total of 1290 nursing homes from 15 French regions participated in the survey. The estimated median number of hand hygiene actions per resident-day was 1.48 (interquartile range: 1.04-2.03) in 2018 and 1.60 (1.10-2.26) in 2019. A significantly higher AHR consumption was observed in public nursing homes with an infection control team or link nurse.

AbstractThe co‐occurrence of chronic pain and alcohol use disorders (AUDs) involves complex interactions between genetic and neurophysiological aspects, and the research has reported mixed findings when they both co‐occur. There is also an indication of a gender‐dependent effect; males are more likely to use alcohol to cope with chronic pain problems than females. Recently, a new conceptualization has emerged, proposing that the negative affective component of pain drives and maintains alcohol‐related behaviors. We studied in a longitudinal fashion alterations in alcohol drinking patterns and pain thresholds in a mouse model of chronic neuropathic pain in a sex‐dependent manner. Following partial denervation (spared nerve injury [SNI]), stimulus‐evoked pain responses were measured before chronic alcohol consumption, during drinking, during a deprivation phase, and following an episode of excessive drinking. During the course of alcohol drinking, we observed pronounced sex differences in pain thresholds. Male mice showed a strong increase in pain thresholds, suggesting an analgesic effect induced by alcohol over time, an effect that was not observed in female mice. SNI mice did not differ from sham‐operated controls in baseline alcohol consumption. However, following a deprivation phase and the reintroduction of ethanol, male SNI mice but not female mice showed more pronounced excessive drinking than controls. Finally, we observed decreased central ethanol sensitivity in male SNI mice but not in females. Together with our finding, that ethanol is able to decrease a pain‐induced negative affective memory we come to following conclusion. We propose that a lower sensitivity to the intoxicating effects of alcohol together with the ability of alcohol to reduce the negative affective component of pain may explain the higher co‐occurrence of AUD in male chronic pain patients.

ABSTRACTA novel design for a high temperature SOFC, based on lamellar electrode-electrolyte segments obtained by solidification of an oxidic eutectic melt on an electrolyte substrate is presented. Such “composite” electrodes contain NiO or MnO - 8Y-ZrO2 lamellae, which after reduction / oxidation yield electrode-electrolyte lamellae with 1–2 μm width and a vertical dimension of> 100 μm, depending upon the amount of eutectic melt solidified on a polycrystalline substrate. The nucleation of the eutectic on a polycrystalline substrate followed by a semi-directional crystallization of the two phases yields a gradient of 3-phase boundaries over the height of such an electrode, with the number of 3-phase boundaries increasing towards the substrate.

Anaphylactic reactions to ethanol are rare with only seven cases reported in the literature. All previous cases have occurred following ingestion of alcoholic beverages or food to which an alcoholic beverage has been added. To date there are no cases in the literature of ethanol-induced anaphylaxis caused by the accumulation of endogenous ethanol in overripe fruit.We report a patient with ethanol-induced anaphylaxis who developed anaphylaxis following ingestion of overripe, but not fresh rock melon (Cucumis melo). The patient is a 24-year-old, previously well woman who experienced five episodes of acute anaphylaxis following ingestion of various alcoholic beverages and, on one occasion, following ingestion of overripe rock melon to which no ethanol was added. Ethanol-induced anaphylaxis was confirmed on blinded challenge; however, challenge with freshly prepared rock melon was negative. The patient declined further challenges.Ingestion of overripe fruits may cause anaphylaxis in patients with ethanol-induced anaphylaxis. These patients should therefore, be advised to avoid ingestion of overripe fruits.

Abstract Aims Alcohol use alters the reward signaling processes contributing to the development of addiction. We studied the effects of alcohol use disorder (AUD) on brain regions and blood of deceased women and men to examine sex-dependent differences in epigenetic changes associated with AUD. We investigated the effects of alcohol use on the gene promoter methylation of GABBR1 coding for GABAB receptor subunit 1 in blood and brain. Methods We chose six brain regions associated with addiction and the reward pathway (nucleus arcuatus, nucleus accumbens, the mamillary bodies, amygdala, hippocampus and anterior temporal cortex) and performed epigenetic profiling of the proximal promoter of the GABBR1 gene of post-mortem brain and blood samples of 17 individuals with AUD pathology (4 female, 13 male) and 31 healthy controls (10 female, 21 male). Results Our results show sex-specific effects of AUD on GABBR1 promoter methylation. Especially, CpG −4 showed significant tissue-independent changes and significantly decreased methylation levels for the AUD group in the amygdala and the mammillary bodies of men. We saw prominent and consistent change in CpG-4 across all investigated tissues. For women, no significant loci were observed. Conclusion We found sex-dependent differences in GABBR1 promoter methylation in relation to AUD. CpG-4 hypomethylation in male individuals with AUD is consistent for most brain regions. Blood shows similar results without reaching significance, potentially serving as a peripheral marker for addiction-associated neuronal adaptations. Further research is needed to discover more contributing factors in the pathological alterations of alcohol addiction to offer sex-specific biomarkers and treatment.

It has been estimated that more than 80% of alcoholics are also nicotine dependent and that, vice versa, the rate of alcoholism is substantially increased by a factor of 4-10 in the nicotine-dependent population. However, the cause for this very high degree of comorbidity is still largely unknown. At the molecular and cellular level, both drugs have very different mechanisms of action. Nicotine specifically activates ligand-gated ion channels in the brain, which are normally gated by acetylcholine, while alcohol interacts with various neurotransmitter receptors. Despite this diversity, both drugs seem to engage the endogenous opioid system as a modulator of some of its pharmacological effect. An acute exposure to nicotine or alcohol leads to a release of opioid peptides in specific brain regions, thus resulting in an activation of their corresponding receptors. If the brain is exposed repeatedly or chronically to these drugs, adaptive changes in the level and expression of opioid peptides and receptors occur. These adaptive changes are thought to contribute to the homeostatic or allostatic adaptations of the brain, which have been associated with drug dependence. This review summarizes pharmacological and genetic studies in animal models and in humans that have addressed the role of specific opioid peptides and receptors in various stages of the addiction process.

Abstract In order to achieve a perfect bottom-up electroplated Cu filling with a minimal surface thickness, 2-mercaptopyridine (2-MP) was investigated as a new leveler for replacing Janus Green B (JGB) for bottom-up copper filling. Electrochemical impedence results indicate that 2-MP has a stronger suppression for Cu deposition than JGB. With the addition of 2-MP, the filling capability of the electroplating solution is improved significantly with the Cu thickness on surface decreasing from ∼16 μm to ∼10 μm. The interaction mechanisms of 2-MP, bis(3-sulfopropyl) disulfide (SPS), Cl − and tri-block copolymer of PEG and PPG with ethylene oxide terminal blocks (EPE) in the plating solution are studied by galvanostatic measurements (GMs). The acceleration effect of SPS and the inhibition effect of 2-MP on copper deposition occur in the presence of EPE, and the convection-dependent adsorption (CDA) behavior of additives usually occurs with the injection of four additives at optional concentrations. Further, it was found that when 1.0 ppm 2-MP, 1.0 ppm SPS and 200 ppm EPE were injected into the basic electrolyte, the potential difference ( Δ h) value of the electrolyte became positive, and the bottom-up electroplated copper filling was obtained in the electrolyte in absence of Cl − . The interaction mechanisms of three additives for bottom-up filling have been investigated by GMs.

Abstract Recently, the oxygen potential dependence of the signal of a potentiometric CO 2 sensor, based on a cation conductor with carbonate as gas sensitive layer, has been interpreted as caused by electronic transference through the electrolyte. Though this interpretation is quite correct, the relationships on the basis of which the effect of electronic conductivity has been discussed are wrong and so are the conclusions on the electronic conduction parameter of the electrolyte material under consideration, i.e. of the lithium ion conductor Li 3 PO 4 + SiO 2 (5 mol%). In what follows, the questionable points will be corrected and the role of the electronic conductivity for the understanding of the behaviour of a CO 2 sensor will be re-examined.

AbstractThirty‐four alcoholics were treated with acupuncture to the ear and the body in a randomized single‐blind placebo‐controlled design over 14 days. Orthodox points and placebo needles to orthodox points were used daily for a total of 10 treatments starting on the first day of admission as add‐on therapy to standard medication with carbamazepine. The primary outcome was the Clinical Institute Withdrawal Assessment (CIWA‐Ar‐scale) assessed on days 1‐6, 9 and 14. No initial differences were found regarding sociodemographic data, drinking history and alcohol‐related data, indicating successful randomization. Longitudinal analysis of the Clinical Institute Withdrawal Assessment (CIWA‐Ar‐scale) data showed that patients assigned to acupuncture had a general tendency towards better outcome results and significantly fewer withdrawal symptoms on day 14 (Wilcoxon‐W=177.500, Z=‐2.009, p = 0.045). No significant differences were found in the Beck Depression Inventory (BDI), State‐Trait Anxiety Inventory (STAI X1 and X2) and Eigenschaftswoerterliste (EWL S60). We conclude that acupuncture as an adjunctive treatment to carbamazepine medication shows promise for the treatment of alcohol withdrawal symptoms. Further investigation of this treatment modality appears to be warranted.

Abstract: Five groups of NMRI mice were fed ethanol or sucrose in a nutritionally adequate liquid diet for 9 days. The dietary fat consisted of olive oil with the fatty acid composition 18:1 77%, 18:2 10%, 18:0 and 16:0 12%. The ethanol treated groups received 5% w/v ethanol (E) or isocaloric sucrose (S). Two groups (S‐ and E‐) received the diet without supplement. In two groups (S+ and E +) 7% of the fat was exchanged for arachidonic acid (20:4). In a fifth group (IE +) treated with ethanol and arachidonic acid the diet also contained indomethacin (10 mg/1). The mean intake of ethanol was about 20 g/kg/day. After 9 days animals were killed and liver lipids analyzed after Folch extraction. The post mortem accumulation of prostaglandin E2 in the kidney was measured by GC‐MS. Dietary 20:4 was found to protect mice against fatty liver caused both by a high fat diet alone and in combination with ethanol. The liver triglycerides were 30.7 + 4.3 (S ‐), 46.1+6.9 (E ‐), 6.8 + 0.4 (S +) and 19.4 ±1.8 (E +). Prostaglandin levels in the kidney were depressed by ethanol treatment. Indomethacin gave variable degrees of PG synthesis inhibition. The degree of liver triglyceride accumulation in the IE+ group was inversely propotional to the degree of PG synthesis. The data suggest a role for liver 20:4 cyclooxyganase metabolites in fatty liver caused by high fat diets and ethanol.