•Electrokinetic remediation was performed with a constant voltage.•Maximum mass removal for manganese and zinc was 31.88% and 17.95%, respectively.•Effect of interaction between electric field and ...acidification was proven.•Significant mass removal was observed in every experiment for manganese.
The scope of this work is to determine the effect of initial acidity and electric field intensity on the Electrokinetic Remediation of manganese and zinc from mine tailings from a Chilean copper mine. To achieve this objective, experiments were carried out focusing on the effect of the applied electric field (1 and 2 V cm−1), the H2SO4 concentration during pretreatment (1 and 2 mol L−1) and the interaction between these factors in manganese and zinc concentration. From the obtained results, manganese and zinc can be removed from the analyzed tailings, with the maximum net removal 31.88% and 17.95%, respectively. The enhancement of electromigration was proven by an Analysis of Variance with a significance level of 10% for the soluble and total metal concentration in the cathodic zone, where total concentration was increased to 24% and 11% for zinc and manganese, respectively.
Background:
Several studies have revealed widening of inequalities in life expectancy, but little is known about the recent changes in health expectancy nationally and between socioeconomic groups. ...This study examines dynamics of national and education-specific life expectancy and health expectancies at age 50 years in Denmark from 2004/2007 to 2015.
Methods:
Nationwide register data on education and mortality were linked and combined with Danish health data from the Survey of Health, Ageing and Retirement in Europe and changes in life expectancy and three health expectancy indicators were estimated by Sullivan’s method.
Results:
From 2004 to 2015, national life expectancy at age 50 years increased by 2.4 years for men and 2.1 years for women. Simultaneously, after an initial rapid improvement from 2004 to 2007, the pace of progress in health expectancy decreased. From 2007 to 2015, the difference in life expectancy at age 50 years between men with long and short education increased from 4.3 to 5.0 years. For women, the corresponding increase in the life expectancy gap was less pronounced from 3.5 to 3.8 years. The educational gap in lifetime without long-term illness decreased from 4.6 years to 3.1 years for men and from 6.1 years to 4.6 years for women. On the contrary, the educational gap increased for lifetime without activity limitations and in self-rated good health.
Conclusions:
Previously observed improvements in health expectancy in Denmark slowed down despite continuing progress in life expectancy. This worrying change coincides with persistent educational inequalities in life expectancy and health expectancy and is a challenge to a sustainable social and health development in the future.
To evaluate the pharmacodynamics of compounds in clinical development for nonalcoholic steatohepatitis (NASH) in obese mouse models of biopsy-confirmed NASH.
Male wild-type C57BL/6J mice (DIO-NASH) ...and Lep
(
-NASH) mice were fed a diet high in trans-fat (40%), fructose (20%) and cholesterol (2%) for 30 and 21 wk, respectively. Prior to treatment, all mice underwent liver biopsy for confirmation and stratification of liver steatosis and fibrosis, using the nonalcoholic fatty liver disease activity score (NAS) and fibrosis staging system. The mice were kept on the diet and received vehicle, liraglutide (0.2 mg/kg, SC, BID), obeticholic acid (OCA, 30 mg/kg PO, QD), or elafibranor (30 mg/kg PO, QD) for eight weeks. Within-subject comparisons were performed on changes in steatosis, inflammation, ballooning degeneration, and fibrosis scores. In addition, compound effects were evaluated by quantitative liver histology, including percent fractional area of liver fat, galectin-3, and collagen 1a1.
Liraglutide and elafibranor, but not OCA, reduced body weight in both models. Liraglutide improved steatosis scores in DIO-NASH mice only. Elafibranor and OCA reduced histopathological scores of hepatic steatosis and inflammation in both models, but only elafibranor reduced fibrosis severity. Liraglutide and OCA reduced total liver fat, collagen 1a1, and galectin-3 content, driven by significant reductions in liver weight. The individual drug effects on NASH histological endpoints were supported by global gene expression (RNA sequencing) and liver lipid biochemistry.
DIO-NASH and
-NASH mouse models show distinct treatment effects of liraglutide, OCA, and elafibranor, being in general agreement with corresponding findings in clinical trials for NASH. The present data therefore further supports the clinical translatability and utility of DIO-NASH and
-NASH mouse models of NASH for probing the therapeutic efficacy of compounds in preclinical drug development for NASH.
A patient on maintenance hemodialysis asked his physician if it would be safe for him to run a marathon. For healthy persons, studies show that it is relatively safe. Very few data are available on ...patients on hemodialysis performing out of center endurance exercise. To address this question, we conducted a clinical study to investigate the electrolyte derangements during different running distances. Our main concern was development of hyperkalemia. We present a case of an anuric hemodialysis patient, who ran eight different runs with a maximum distance of 32.2 km. Blood was analyzed before and after the runs. We did not find severe hyperkalemia at any point. According to this study, we found no signs of increased risk.
•Surprisingly, recent papers claim higher sonochemical production of H2 under pure CO2.•Modeling considerations of the sonolytic formation of H2 under different saturation gases are ...highlighted.•Dissolved gases affect the sonochemical production of H2 through physical and chemical pathways.•For CO2-saturated water, degassing bubbles are formed instead of transient cavitation.•CO2 effects on sonolytic production of H2 in recent papers are mostly due to wrong procedures.
Although most of researchers agree on the elementary reactions behind the sonolytic formation of molecular hydrogen (H2) from water, namely the radical attack of H2O and H2O2 and the free radicals recombination, several recent papers ignore the intervention of the dissolved gas molecules in the kinetic pathways of free radicals, and hence may wrongly assess the effect of dissolved gases on the sonochemical production of hydrogen. One may fairly ask to which extent is it acceptable to ignore the role of the dissolved gas and its eventual decomposition inside the acoustic cavitation bubble? The present opinion paper discusses numerically the ways in which the nature of dissolved gas, i.e., N2, O2, Ar and air, may influence the kinetics of sonochemical hydrogen formation. The model evaluates the extent of direct physical effects, i.e., dynamics of bubble oscillation and collapse events if any, against indirect chemical effects, i.e., the chemical reactions of free radicals formation and consequently hydrogen emergence, it demonstrates the improvement in the sonochemical hydrogen production under argon and sheds light on several misinterpretations reported in earlier works, due to wrong assumptions mainly related to initial conditions. The paper also highlights the role of dissolved gases in the nature of created cavitation and hence the eventual bubble population phenomena that may prevent the achievement of the sonochemical activity. This is particularly demonstrated experimentally using a 20 kHz Sinaptec transducer and a Photron SA 5 high speed camera, in the case of CO2-saturated water where degassing bubbles are formed instead of transient cavitation.
The bromodomain and extraterminal (BET) domain family of proteins binds to acetylated lysines on histones and regulates gene transcription. Recently, BET inhibitors (BETi) have been developed that ...show promise as potent anticancer drugs against various solid and hematological malignancies. Here we show that the structurally novel and orally bioavailable BET inhibitor RVX2135 inhibits proliferation and induces apoptosis of lymphoma cells arising in Myc-transgenic mice in vitro and in vivo. We find that BET inhibition exhibits broad transcriptional effects in Myc-transgenic lymphoma cells affecting many transcription factor networks. By examining the genes induced by BETi, which have largely been ignored to date, we discovered that these were similar to those induced by histone deacetylase inhibitors (HDACi). HDACi also induced cell-cycle arrest and cell death of Myc-induced murine lymphoma cells and synergized with BETi. Our data suggest that BETi sensitize Myc-overexpressing lymphoma cells partly by inducing HDAC-silenced genes, and suggest synergistic and therapeutic combinations by targeting the genetic link between BETi and HDACi.
Abstract
Objectives
Widowhood is a stressful life event with one of the most profound negative effects on health and longevity. Immigrant populations are growing and aging throughout Western nations, ...and marginalization and cultural differences may make some immigrants especially vulnerable to the stressors of widowhood. However, studies have yet to systematically explore whether the widowhood effect differs between immigrant and native-born individuals.
Methods
Using Danish population register data from 1980 to 2014, this study assesses whether the relationship between widowhood and mortality differs between immigrants from 10 countries and native-born Danes aged 50 and older at 0–2, 3–5, and 6 and more years post-widowhood.
Results
We find that immigrant men are at higher risk of dying in the first 2 years after experiencing widowhood than Danish-born men, but these mortality differences dissipate over longer periods. Immigrant women have a higher risk of having died 3 and more years after a spouse’s death than Danish women. Patterns vary further by country of origin.
Discussion
The results suggest that some immigrants may suffer more from widowhood than native-born individuals, giving insight into how immigration background may influence the health effects of negative life events. They also underscore the potential vulnerabilities of aging immigrant populations to stressors encountered in older age.
Health impact assessment (HIA) of exposure to air pollution is commonly based on city level (fine) particle concentration and may underestimate health consequences of changing local traffic. Exposure ...to traffic-related air pollution can be assessed at a high resolution by modelling levels of nitrogen dioxide (NO2), which together with ultrafine particles mainly originate from diesel-powered vehicles in urban areas. The purpose of this study was to estimate the health benefits of reduced exposure to vehicle emissions assessed as NO2 at the residence among the citizens of Copenhagen Municipality, Denmark.
We utilized residential NO2 concentrations modelled by use of chemistry transport models to calculate contributions from emission sources to air pollution. The DYNAMO-HIA model was applied to the population of Copenhagen Municipality by using NO2 concentration estimates combined with demographic data and data from nationwide registers on incidence and prevalence of selected diseases, cause specific mortality, and total mortality of the population of Copenhagen. We used exposure-response functions linking NO2 concentration estimates at the residential address with the risk of diabetes, cardiovascular diseases, and respiratory diseases derived from a large Danish cohort study with the majority of subjects residing in Copenhagen between 1971 and 2010. Different scenarios were modelled to estimate the dynamic impact of NO2 exposure on related diseases and the potential health benefits of lowering the NO2 level in the Copenhagen Municipality.
The annual mean NO2 concentration was 19.6 μg/m3 and for 70% of the population the range of exposure was between 15 and 21 μg/m3. If NO2 exposure was reduced to the annual mean rural level of 6 μg/m3, life expectancy in 2040 would increase by one year. The greatest gain in disease-free life expectancy would be lifetime without ischemic heart disease (1.4 years), chronic obstructive pulmonary disease (1.5 years for men and 1.6 years for women), and asthma (1.3 years for men and 1.5 years for women). Lowering NO2 exposure by 20% would increase disease-free life expectancy for the different diseases by 0.3–0.5 years. Using gender specific relative risks affected the results.
Reducing the NO2 exposure by controlling traffic-related air pollution reduces the occurrence of some of the most prevalent chronic diseases and increases life expectancy. Such health benefits can be quantified by DYNAMO-HIA in a high resolution exposure modelling. This paper demonstrates how traffic planners can assess health benefits from reduced levels of traffic-related air pollution.
•Nitrogen oxide concentration can serve as a proxy of exposure to traffic-related air pollution.•The annual mean nitrogen oxide concentration is 19.6 μg/m3 in Copenhagen.•One-year gain in life expectancy by lowering nitrogen oxide exposure to rural level•Marked increase in disease-free life expectancies by reducing nitrogen oxide exposure
Abstract In addition to a prominent role in glycemic control, glucagon-like peptide 1 (GLP-1) receptor agonists exhibit neuroprotective properties. There is mounting experimental evidence that GLP-1 ...receptor agonists, including liraglutide, may enhance synaptic plasticity, counteract cognitive deficits and ameliorate neurodegenerative features in preclinical models of Alzheimer’s disease (AD), predominantly in the context of β-amyloid toxicity. Here we characterized the effects of liraglutide in a transgenic mutant tau (hTauP301L) mouse tauopathy model, which develops age-dependent pathology-specific neuronal tau phosphorylation and neurofibrillary tangle formation with progressively compromised motor function (limb clasping). Liraglutide (500 µg/kg/day, s.c., q.d., n =18) or vehicle ( n =18) was administered to hTauP301L mice for 6 months from the age of three months. Vehicle-dosed wild-type FVB/N mice served as normal control ( n =17). The onset and severity of hind limb clasping was markedly different in liraglutide and vehicle-dosed transgenic mice. Clasping behavior was observed in 61% of vehicle-dosed hTauP301L mice with a 55% survival rate in 9-month old transgenic mice. In contrast, liraglutide treatment reduced the clasping rate to 39% of hTauP301L mice, and fully prevented clasping-associated lethality resulting in a survival rate of 89%. Stereological analyses demonstrated that hTauP301L mice exhibited hindbrain-dominant neuronal accumulation of phosphorylated tau closely correlated to the severity of clasping behavior. In correspondence, liraglutide treatment significantly reduced neuronal phospho-tau load by 61.9±10.2% ( p <0.001) in hTauP301L mice, as compared to vehicle-dosed controls. In conclusion, liraglutide significantly reduced tau pathology in a transgenic mouse tauopathy model.
Recent studies indicate that glucagon-like peptide 1 (GLP-1) receptor agonists, currently used in the management of type 2 diabetes, exhibit neurotrophic and neuroprotective effects in amyloid-β (Aβ) ...toxicity models of Alzheimer's disease (AD). We investigated the potential pro-cognitive and neuroprotective effects of the once-daily GLP-1 receptor agonist liraglutide in senescence-accelerated mouse prone 8 (SAMP8) mice, a model of age-related sporadic AD not dominated by amyloid plaques. Six-month-old SAMP8 mice received liraglutide (100 or 500 μg/kg/day, s.c.) or vehicle once daily for 4 months. Vehicle-dosed age-matched 50% back-crossed as well as untreated young (4-month-old) SAMP8 mice were used as control groups for normal memory function. Vehicle-dosed 10-month-old SAMP8 mice showed significant learning and memory retention deficits in an active-avoidance T-maze, as compared to both control groups. Also, 10-month-old SAMP8 mice displayed no immunohistological signatures of amyloid-β plaques or hyperphosphorylated tau, indicating the onset of cognitive deficits prior to deposition of amyloid plaques and neurofibrillary tangles in this AD model. Liraglutide significantly increased memory retention and total hippocampal CA1 pyramidal neuron numbers in SAMP8 mice, as compared to age-matched vehicle-dosed SAMP8 mice. In conclusion, liraglutide delayed or partially halted the progressive decline in memory function associated with hippocampal neuronal loss in a mouse model of pathological aging with characteristics of neurobehavioral and neuropathological impairments observed in early-stage sporadic AD.
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