Ghost Projection

Ghost imaging is a developing imaging technique that employs random masks to image a sample. Ghost projection utilizes ghost-imaging concepts to perform the complementary procedure of projection of a desired image. The key idea underpinning ghost projection is that any desired spatial distribution of radiant exposure may be produced, up to an additive constant, by spatially-uniformly illuminating a set of random masks in succession. We explore three means of achieving ghost projection: (i) weighting each random mask, namely selecting its exposure time, according to its correlation with a desired image, (ii) selecting a subset of random masks according to their correlation with a desired image, and (iii) numerically optimizing a projection for a given set of random masks and desired image. The first two protocols are analytically tractable and conceptually transparent. The third is more efficient but less amenable to closed-form analytical expressions. A comparison with existing image-projection techniques is drawn and possible applications are discussed. These potential applications include: (i) a data projector for matter and radiation fields for which no current data projectors exist, (ii) a universal-mask approach to lithography, (iii) tomographic volumetric additive manufacturing, and (iv) a ghost-projection photocopier.Comment: 32 pages, 15 figure

The Impact of Public Law of Privatization, Deregulation, Outsourcing, and Downsizing: A Canadian Perspective

Globalization and Governance: The Prospects for Democracy, Symposiu

The Impact of Public Law of Privatization, Deregulation, Outsourcing, and Downsizing: A Canadian Perspective

Globalization and Governance: The Prospects for Democracy, Symposiu

Universal mask for hard X rays

The penetrating power of X rays underpins important applications such as medical radiography. However, this same attribute makes it challenging to achieve flexible on-demand patterning of X-ray beams. One possible path to this goal is ``ghost projection'', a method which may be viewed as a reversed form of classical ghost imaging. This technique employs multiple exposures, of a single illuminated non-configurable mask that is transversely displaced to a number of specified positions, to create any desired pattern. An experimental proof-of-concept is given for this idea, using hard X rays. The written pattern is arbitrary, up to a tunable constant offset, and its spatial resolution is limited by both (i) the finest features present in the illuminated mask and (ii) inaccuracies in mask positioning and mask exposure time. In principle, the method could be used to make a universal lithographic mask in the hard-X-ray regime. Ghost projection might also be used as a dynamically-configurable beam-shaping element, namely the hard-X-ray equivalent of a spatial light modulator. The underpinning principle can be applied to gamma rays, neutrons, electrons, muons, and atomic beams. Our flexible approach to beam shaping gives a potentially useful means to manipulate such fields.Comment: Revised for resubmission to Optica; numerous clarifications throughout the paper; Sec. 4 (numbered item 2) and Supplement 1 Sec. 2 significantly extended; all figures and ancillary movies unchange

Phagocytosis of Cholesteryl Ester Is Amplified in Diabetic Mouse Macrophages and Is Largely Mediated by CD36 and SR-A

Type 2 diabetes (T2D) is associated with accelerated atherosclerosis, which accounts for approximately 75% of all diabetes-related deaths. Here we investigate the link between diabetes and macrophage cholesteryl ester accumulation. When diabetic (db/db) mice are given cholesteryl ester intraperitoneally (IP), peritoneal macrophages (PerMΦs) recovered from these animals showed a 58% increase in intracellular cholesteryl ester accumulation over PerMΦs from heterozygote control (db/+) mice. Notably, PerMΦ fluid-phase endocytosis and large particle phagocytosis was equivalent in db/+and db/db mice. However, IP administration of CD36 and SR-A blocking antibodies led to 37% and 25% reductions in cholesteryl ester accumulation in PerMΦ. Finally, in order to determine if these scavenger receptors (SRs) were part of the mechanism responsible for the increased accumulation of cholesteryl esters observed in the diabetic mouse macrophages, receptor expression was quantified by flow cytometry. Importantly, db/db PerMΦs showed a 43% increase in CD36 expression and an 80% increase in SR-A expression. Taken together, these data indicate that direct cholesteryl ester accumulation in mouse macrophages is mediated by CD36 and SR-A, and the magnitude of accumulation is increased in db/db macrophages due to increased scavenger receptor expression

Mitochondrial Uncoupling Protein-2 (UCP2) Mediates Leptin Protection Against MPP+ Toxicity in Neuronal Cells

Mitochondrial dysfunction is involved in the pathogenesis of neurodegenerative diseases, including Parkinson’s disease (PD). Uncoupling proteins (UCPs) delink ATP production from biofuel oxidation in mitochondria to reduce oxidative stress. UCP2 is expressed in brain, and has neuroprotective effects under various toxic insults. We observed induction of UCP2 expression by leptin in neuronal cultures, and hypothesize that leptin may preserve neuronal survival via UCP2. We showed that leptin preserved cell survival in neuronal SH-SY5Y cells against MPP+ toxicity (widely used in experimental Parkinsonian models) by maintaining ATP levels and mitochondrial membrane potential (MMP); these effects were accompanied by increased UCP2 expression. Leptin had no effect in modulating reactive oxygen species levels. Stable knockdown of UCP2 expression reduced ATP levels, and abolished leptin protection against MPP+-induced mitochondrial depolarization, ATP deficiency, and cell death, indicating that UCP2 is critical in mediating these neuroprotective effects of leptin against MPP+ toxicity. Interestingly, UCP2 knockdown increased UCP4 expression, but not of UCP5. Our findings show that leptin preserves cell survival by maintaining MMP and ATP levels mediated through UCP2 in MPP+-induced toxicity

Contribution of international ecotourism to comprehensive economic development and convergence in the Central American and Caribbean region

Drawing on the positive experience from Costa Rica, the study examines whether international ecotourism makes a significant contribution to comprehensive economic development for the Central American and Caribbean region and contributes to comprehensive economic convergence. Following a standard empirical growth model, a dynamic panel regression model is estimated using time-series data from 1995 until 2012 for a cross section of seven countries. The interaction of international tourism and various established sustainability indicators is employed allowing ecotourism to be consistently quantified across countries, while numerous country-specific structural characteristics are controlled for. The estimation results show that international ecotourism has a statistically significant positive effect on both traditional economic development (real GDP per capita) and comprehensive economic development (adjusted net savings; ANS per capita), which is a measure of a society’s potential future well-being, thus providing evidence in support of the tourism-led growth hypothesis and pointing towards an important role for ecotourism in driving comprehensive economic convergence

Enhanced Lipid Oxidation and Maintenance of Muscle Insulin Sensitivity Despite Glucose Intolerance in a Diet-Induced Obesity Mouse Model

<div><p>Background</p><p>Diet-induced obesity is a rising health concern which can lead to the development of glucose intolerance and muscle insulin resistance and, ultimately, type II diabetes mellitus. This research investigates the associations between glucose intolerance or muscle insulin resistance and tissue specific changes during the progression of diet-induced obesity.</p><p>Methodology</p><p>C57BL/6J mice were fed a normal or high-fat diet (HFD; 60% kcal fat) for 3 or 8 weeks. Disease progression was monitored by measurements of body/tissue mass changes, glucose and insulin tolerance tests, and <i>ex vivo</i> glucose uptake in intact muscles. Lipid metabolism was analyzed using metabolic chambers and <i>ex vivo</i> palmitate assays in intact muscles. Skeletal muscle, liver and adipose tissues were analyzed for changes in inflammatory gene expression. Plasma was analyzed for insulin levels and inflammatory proteins. Histological techniques were used on muscle and liver cryosections to assess metabolic and morphological changes.</p><p>Principal Findings/Conclusions</p><p>A rapid shift in whole body metabolism towards lipids was observed with HFD. Following 3 weeks of HFD, elevated total lipid oxidation and an oxidative fiber type shift had occurred in the skeletal muscle, which we propose was responsible for delaying intramyocellular lipid accumulation and maintaining muscle’s insulin sensitivity. Glucose intolerance was present after three weeks of HFD and was associated with an enlarged adipose tissue depot, adipose tissue inflammation and excess hepatic lipids, but not hepatic inflammation. Furthermore, HFD did not significantly increase systemic or muscle inflammation after 3 or 8 weeks of HFD suggesting that early diet-induced obesity does not cause inflammation throughout the whole body. Overall these findings indicate skeletal muscle did not contribute to the development of HFD-induced impairments in whole-body glucose tolerance following 3 weeks of HFD.</p></div