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The potential impacts of climate change on human health in sub-Saharan Africa are wide-ranging, complex, and largely adverse. The region's Indigenous peoples are considered to be at heightened risk given their relatively poor health outcomes, marginal social status, and resource-based livelihoods; however, little attention has been given to these most vulnerable of the vulnerable. This paper contributes to addressing this gap by taking a bottom-up approach to assessing health vulnerabilities to climate change in two Batwa Pygmy communities in rural Uganda. Rapid Rural Appraisal and PhotoVoice field methods complemented by qualitative data analysis were used to identify key climate-sensitive, community-identified health outcomes, describe determinants of sensitivity at multiple scales, and characterize adaptive capacity of Batwa health systems. The findings stress the importance of human drivers of vulnerability and adaptive capacity and the need to address social determinants of health in order to reduce the potential disease burden of climate change.

During an extraordinary event, like the COVID19 pandemic, very rapid changes in consumption profiles and customers behaviors were recorded. This paper investigates the impact of the lockdown on load and production in the distribution system of Terni. From a DSO point of view, no relevant issues were encountered to be faced. The distributed power generation from renewable resources did not affect relevant issues, maintaining the typical annual generation profiles. A domestic consumption increase was replaced by more relevant decrease of industrial processes and commercial activities absorptions. More than 25,000 domestic users increased their consumptions in April 2020 and the overall consumption of domestic customers in March was 1,05 times higher than the 2015 respectively consumption. The power flows at primary substations reveal a relevant electric demand reduction for each point of connection with the high voltage transmission system; especially bar 1 and 2 of the most relevant Terni primary substation, recorded a 15.3% decrease with respect to March 2019, and a 24.25% decrease with respect to April 2019.

To investigate the structural development of the colloid phases generated during lipolysis of a lipid-based formulation in an in vitro lipolysis model, which simulates digestion in the small intestine.Small-Angle X-Ray scattering (SAXS) coupled with the in vitro lipolysis model which accurately reproduces the solubilizing environment in the gastrointestinal tract and simulates gastrointestinal lipid digestion through the use of bile and pancreatic extracts. The combined method was used to follow the intermediate digestion products of a self nano emulsified drug delivery system (SNEDDS) under fasted conditions. SNEDDS is developed to facilitate the uptake of poorly soluble drugs.The data revealed that a lamellar phase forms immediately after initiation of lipolysis, whereas a hexagonal phase is formed after 60 min. The change of the relative amounts of these phases clearly demonstrates that lipolysis is a dynamic process. The formation of these phases is driven by the lipase which continuously hydrolyzes triglycerides from the oil-cores of the nanoemulsion droplets into mono- and diglycerides and fatty acids. We propose that this change of the over-all composition of the intestinal fluid with increased fraction of hydrolyzed nanoemulsion induces a change in the composition and effective critical packing parameter of the amphiphilic molecules, which determines the phase behavior of the system. Control experiments (only the digestion medium) or the surfactant (Cremophor RH 40) revealed the formation of a lamellar phase demonstrating that the hexagonal phase is due to the hydrolysis of the SNEDDS formulation.The current results demonstrate that SAXS measurements combined with the in vitro dynamic lipolysis model may be used to elucidate the processes encountered during the digestion of lipid-based formulations of poorly soluble drugs for oral drug delivery. Thus the combined methods may act as an efficient screening tool.

AbstractAlcohol (ethanol) use is almost normative by late adolescence, in most western countries. It is important to identify factors that distinguish those who progress from alcohol initiation to sustained use of the drug, from those that keep a controlled pattern of drinking. The factors precipitating this transition may change across development. This study analyzed associations between behavioral endophenotypes and ethanol intake at three developmental periods. Exp. 1 measured ethanol drinking at postnatal day 18, via an intraoral infusion procedure, in male or female pre‐weanling rats screened for anxiety response in the light‐dark box test and for distance traveled in a novel open field. Exp. 2 measured, in juvenile/adolescent or young adult rats, the association between shelter seeking, exploratory/risk‐taking behaviors, anxiety or hedonic responses, and ethanol intake. Ethanol intake in pre‐weanlings was explained by distance traveled in a novel environment, whereas anxiety responses, measured in the multivariate concentric square field apparatus (MSCF), selectively predicted ethanol intake at adolescence, but not at adulthood. Those juvenile/adolescents with lower mean duration of visit to areas of the MSCF that evoke anxiogenic responses exhibited heightened ethanol intake. These findings suggest that the association between anxiety and ethanol intake may be specifically relevant during adolescence.

Objective: Positron Emission Tomography (PET) with F-18-Fluoro-deoxy-glucose (FDG) emerged as a prognostic tool to predict treatment outcome in Hodgkin Lymphoma (HL). Moreover, a FDG-PET adapted strategy is currently assessed in clinical trial to minimize the toxic effect while maintaining the efficacy of treatment in HL. Purpose was to analyze the quantitative parameters to support the prognostic role of FDG-PET today based on the semi-quantitative Deauville 5-point Scale (D5-PS). Methods: This retrospective study included 53 patients diagnosed with advanced-stage HL between 2009 and 2014, enrolled in the PET response-adapted clinical trial HD 0607. FDG-PET was performed at baseline (PET0) and after two cycles of chemotherapy (PET2). Analysis was based on two main approaches: on the single lesion presenting the higher FDG uptake and on the five hottest lesions. Different metabolic parameters were analyzed. Patients were classified into responders and nonresponders. Optimal cut-offs were derived from Receiver Operating Characteristic (ROC) curves. Results were correlated with Progression Free Survival (PFS) using Kaplan-Meier. Results: A 71% threshold in SUVmax reduction (?SUVmax) was found to be the best cutoff quantitative parameter able to identify responders vs. non-responders, also with a multivariate analysis, joining clinical data with SUVmax. After a mean follow-up of 34.2 months (95% CI, 26.2 to 39.1), the median PFS for non-responders was 8 months vs. not reached for responders. These results were superimposable to that obtained by an independent group of reviewers using the D5-PS. Conclusion: Semi-quantitative analysis by ?SUVmax outperforms qualitative assessment by D5-PS in predicting treatment outcome in ABVD-treated advanced-stage HL.

Although neurokinin 1 receptor antagonists prevent ethanol (EtOH)-induced gastric lesions, the mechanisms by which EtOH releases substance P (SP) and SP damages the mucosa are unknown. We hypothesized that EtOH activates transient receptor potential vanilloid 1 (TRPV1) on sensory nerves to release SP, which stimulates epithelial neurokinin 1 receptors to generate damaging reactive oxygen species (ROS). SP release was assayed in the mouse stomach, ROS were detected using dichlorofluorescein diacetate, and neurokinin 1 receptors were localized by immunofluorescence. EtOH-induced SP release was prevented by TRPV1 antagonism. High dose EtOH caused lesions, and TRPV1 or neurokinin 1 receptor antagonism and neurokinin 1 receptor deletion inhibited lesion formation. Coadministration of low, innocuous doses of EtOH and SP caused lesions by a TRPV1-independent but neurokinin 1 receptor-dependent process. EtOH, capsaicin, and SP stimulated generation of ROS by superficial gastric epithelial cells expressing neurokinin 1 receptors by a neurokinin 1 receptor-dependent mechanism. ROS scavengers prevented lesions induced by a high EtOH dose or a low EtOH dose plus SP. Gastric lesions are caused by an initial detrimental effect of EtOH, which is damaging only if associated with TRPV1 activation, SP release from sensory nerves, stimulation of neurokinin 1 receptors on epithelial cells, and ROS generation.

AbstractDefects in the ubiquitin‐proteasome system have been implicated in Parkinson's Disease (PD). Recently, a rat model of PD was developed using a synthetic proteasome inhibitor (PSI), (Z‐lle‐Glu(OtBu)‐Ala‐Leu‐al). We attempted to transfer this model to mouse studies, where genetics can be more readily investigated due to the availability of genetically modified mice. We treated C57BL/6 (B6) mice with six intraperitoneal injections of 6 mg/kg PSI in 50 μl of 70% ethanol over a 2‐week‐period. We found significant decreases in nigrostriatal dopamine in PSI‐treated mice compared with saline‐treated mice. However, we observed similar decreases in the ethanol‐treated vehicle control group. Administration of ethanol alone led to significant long‐term alterations in dopamine levels. Ethanol significantly eclipses the effects of PSI in the dopamine system, and therefore is a confounding vehicle for this model. © 2006 Movement Disorder Society

Background:  Genetic variation in ethanol metabolism may have an influence on both alcohol drinking habits and the susceptibility to health effects of alcohol drinking. Such influences are likely to bias exposure‐disease associations in epidemiologic studies of health effects of alcohol drinking. In a Caucasian population, we examined the association of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genetic variants with alcohol drinking habits, biomarkers of alcohol exposure, and risk factors for cardiovascular disease.Methods:  The study population consisted of 1,216 Danish men and women aged 15–77 years participating in a health examination in 1998. The health examination included a self‐administered questionnaire (alcohol drinking habits), a physical examination (blood pressure), and various blood tests [alanine aminotransferase (ALAT), erythrocyte mean corpuscular volume (E‐MCV), and lipids]. ADH and ALDH gene variants were determined by standard techniques. Data were analyzed by regression analyses adjusted for relevant confounders.Results:  Self‐reported alcohol drinking was significantly associated with increasing levels of ALAT, E‐MCV, high‐density lipoprotein cholesterol, and blood pressure. The ALDH1b ala69val variant was associated with nondrinking and total alcohol intake. The ALDH2 promoter variant was associated with binge‐drinking, and the ALDH1b1 ala69val polymorphism was associated with diastolic blood pressure. We did not find any statistically significant interactions between any of the gene variants and alcohol consumption in relation to the various outcomes.Conclusions:  In this Caucasian population sample, we found evidence to support that genetic variation in ethanol metabolism may influence drinking habits, but no statistically significant gene‐environment interactions. More large‐scale epidemiologic studies are needed to confirm theses results and to further investigate genetic susceptibility to the effects of alcohol drinking.