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Cultural heritage of a country represents an array of monuments, historic buildings, arts and crafts, indigenous skills and traditions. The emerging threats to the cultural resources by way of decay, loss or destruction, has become a prime concern today. Heritage has become one of the vital components of tourism industry. It is being considered as cultural capital. The process of valuation of this capital is very complex since Heritage is basically a nonmarketed good. Different techniques used for valuating environmental resources which are similar in nature to Heritage, have led to the development of economic valuation models especially for valuation of Heritage as cultural assets. This economic approach has helped to derive the real value of heritage sites by way of consumer’s surplus and consumer’s willingness to pay for the use of cultural heritage assets and sustain sites for future generations.

Alcohol binge drinking allows the translocation of bacterial lipopolysaccharide (LPS) from the gut to the blood, which activates the peripheral immune system with consequences in neuroinflammation. A possible access/direct signaling of LPS to/in the brain has not yet been described under alcohol abuse conditions. Apolipoproteins are compounds altered by alcohol with high affinity to LPS which may be involved in its transport to the brain or in its elimination. Here, we explored the expression of small components of LPS, in its free form or bound to apolipoproteins, in the brain of female and male rats exposed to alcohol binges. Animals received ethanol oral gavages (3 g/kg every 8 h) for 4 days. LPS or its components (Lipid A and core), LPS-binding protein, corticosterone, lipoproteins (HDL, LDL), apolipoproteins (ApoAI, ApoB, and ApoE), and their receptors were measured in plasma and/or in nonperfused prefrontal cortex (PFC) and cerebellum. Brain LipidA-apolipoprotein aggregates were determined by Western blotting and confirmed by co-immunoprecipitation. In animals exposed to alcohol binges: 1) plasma LPS-binding protein was elevated in both sexes; 2) females showed elevations in plasma ApoAI and corticosterone levels; 3) Lipid A formed aggregates with ApoAI in the female PFC and with ApoB in males, the latter showing Toll-like receptor 4 upregulation in PFC but not females. These results suggest that small bacterial components are present within the brain, forming aggregates with different apolipoproteins, depending on the sex, after alcohol binge intoxications. Results may have implications for the crosstalk between alcohol, LPS, and neuroinflammation.

OBJECTIVEThis study investigated whether preceding ethanol intake impairs glucose response to low-dose glucagon in individuals with type 1 diabetes.RESEARCH DESIGN AND METHODSThis was a randomized, crossover, placebo-controlled study in 12 insulin pump–treated individuals (median [interquartile range] age, 37 [31–51] years; HbA1c, 57 [51–59] mmol/mol or 7.3% [6.8–7.5]; and BMI, 23.9 [22–25] kg/m2). During two overnight study visits, a 6 p.m. dinner (1 g carbohydrates/kg) was served with diet drink (placebo) or diet drink and ethanol (0.8 g/kg). After 8–9 h, ethanol was estimated to be metabolized, and a subcutaneous (s.c.) insulin bolus was given to induce mild hypoglycemia. When plasma glucose (PG) was ≤3.9 mmol/L, 100 µg glucagon was given s.c., followed by another s.c. 100 µg glucagon 2 h later. Primary end point was incremental peak PG induced by the first glucagon bolus.RESULTSEthanol was undetectable before insulin administration at both visits. The insulin doses (mean ± SEM: 2.5 ± 0.4 vs. 2.7 ± 0.4 IU) to induce hypoglycemia (3.7 ± 0.1 vs. 3.9 ± 0.1 mmol/L) did not differ and caused similar insulin levels (28.3 ± 4.6 vs. 26.1 ± 4.0 mU/L) before glucagon administration on ethanol and placebo visits (all, P > 0.05). The first glucagon bolus tended to cause lower incremental peak PG (2.0 ± 0.5 vs. 2.9 ± 0.3 mmol/L, P = 0.06), lower incremental area under the curve (87 ± 40 vs. 191 ± 37 mmol/L × min, P = 0.08), and lower 2-h PG level (3.6 ± 1.0 vs. 4.8 ± 0.4 mmol/L, P = 0.05) after ethanol compared with placebo. The second glucagon bolus had similar responses between visits, but PG remained 1.8 ± 0.7 mmol/L lower after ethanol compared with placebo.CONCLUSIONSThe ability of low-dose glucagon to treat mild hypoglycemia persisted with preceding ethanol intake, although it tended to be attenuated.

The Nuclear Energy Agency organised its third workshop on ‘Science and values in radiological protection’ in November 2012 in Tokyo. One of the issues addressed, non-cancer effects, had also been addressed in the first two science and values workshops (Helsinki, Finland, 2008; Vaux-de-Cernay, France, 2009), but presented several new elements of relevance to International Commission on Radiological Protection discussions of the evolution of the system of radiological protection. Radiological protection science, both epidemiological and biological, now suggests that stroke and heart disease may well be caused by radiation exposure at doses of the order of 0.5 Gy or less. Further, it is possible that such detriments may be caused by either chronic or acute exposures. While significant uncertainties remain, the need to consider non-cancer detriment in risk assessment and in the development of protection strategies is now a significant scientific and ethical question. This paper will present the results of the Nuclear Energy Agency science and values workshop discussion of non-cancer risks, and of the questions and possible future directions raised during the workshop.

Nitric oxide (NO) mediated transmission in the dorsal raphe nucleus (DRN) has been shown to be involved in the modulation of anxiety-like behaviors. We investigated whether inhibition of nitric oxide synthase (NOS) in the DRN would prevent anxiety-like behavior induced by ethanol withdrawal. Male Wistar rats were treated with ethanol 2-6% (v/v) for a period of 21 days. Ethanol withdrawal was induced by abrupt discontinuation of the treatment. Experiments were performed 48 h after ethanol discontinuation. Rats with a guide cannula aimed at the DRN received intra-DRN injections of the non-selective NOS inhibitor NG-nitro-l-arginine methyl ester (l-NAME), selective neuronal NOS (nNOS) inhibitor N(ω)-propyl-l-arginine (NPLA), or selective inhibitor of inducible NOS (iNOS) N-([3-(aminomethyl)phenyl] methyl) ethanimidamidedihydrochloride (1400W). Five minutes later, the animals were tested in the elevated plus maze (EPM). Plasma ethanol levels were determined by gas chromatography. There was a reduction in plasma ethanol levels 48 h after ethanol withdrawal. Rats from the ethanol withdrawal group showed decreased exploration of the open arms of the EPM with no change in the exploration of enclosed arms. Intra-DRN treatment with l-NAME (100 nmoles/0.2 μL) and 1400W (1 nmol/0.2 μL), but not NPLA (10 nmoles/0.2 μL) in the DRN attenuated the decrease in the exploration of the open arms of the EPM induced by ethanol withdrawal. The major new finding of the present study is that iNOS in the DRN plays a role in the anxiety-like behavior induced by ethanol withdrawal.

Death practices are a highly individual and sensitive, but also strongly social and socially regulated issue. Passing rituals and types of burials have developed over centuries, and their significant environmental cost is rarely discussed. In this paper, we propose an intervention that aims to open up the conversation about green passing practices and help reduce the environmental impact of current death practices in the United Kingdom. We used the multilayered installation design approach, leveraging activity theory and installation theory to identify relevant stakeholders and entry points for intervention. We then developed a holistic intervention strategy subsumed under the green passer Initiative, which proposes intervention into burial practices at the physical, social, and embodied level. We illustrate the intervention strategy with three ideal-type journeys of future green passers and outline relevant implications for policy makers, researchers, and the general public.

The storage phosphor plate (SPP) is a reusable radiation image detector, widely used in diagnostic computed radiography, x‐ray crystallography and radioactive tracer studies. When exposed to ionizing radiation, the SPP stores a latent image until it is scanned with a red reading laser which causes blue photostimulated luminescent (PSL) photons to be emitted. The mechanism of formation of the latent image is still poorly understood, especially for megavoltage photon beams. In order to gain insight into this mechanism and aid applications to high‐energy beam dosimetry, the authors have directly determined the SPP generation efficiency, , the energy required to produce one quantum of emitted PSL when it is irradiated by and photon beams. This was done in four steps: 1. The SPP, in a water‐equivalent plastic (WEP) phantom, was exposed to a or beam, which had been calibrated to give a known absorbed dose to water in a water phantom at the position of the sensitive layer of the SPP. 2. Monte Carlo simulations were used to calculate the ratio of the dose to the sensitive layer in the WEP phantom to the dose to water at the same position in a water phantom. 3. A bleaching experiment was used to determine the number of photons emitted by a plate given a known dose. 4. The generation efficiency was calculated from the number of photons and the dose. This method is much more direct than previous calculations for kilovoltage x‐ray beams based on quantum noise analysis. W was found, within experimental uncertainty, to be for and for , independent of dose. The values for kilovoltage x‐ray beams determined previously agree, within their large uncertainty, with these values for megavoltage beams.