A role for vitamin D in the regulation of immune function was first proposed after the identification of Vitamin D receptors in lymphocytes. It has since been recognized that the active form of ...vitamin D, 1α,25(OH)₂D₃, has direct affects on naïve and activated helper T cells, regulatory T cells, activated B cells and dendritic cells. There is a growing body of literature linking vitamin D (serum 25(OH)D, oral intake and surrogate indicators such as latitude) to various immune-related conditions, including allergy, although the nature of this relationship is still unclear. This review explores the findings of epidemiological, clinical and laboratory research, and the potential role of vitamin D in promoting the inappropriate immune responses which underpin the rise in a broad range of immune diseases.
Since March 2003, measurements of surface ozone have been made at the British Antarctic Survey Clean Air Sector Laboratory (CASLab) at Halley station in coastal Antarctica. Detailed measurements of ...boundary layer meteorology, as well as standard meteorological parameters, are also measured at the CASLab. Combining these data allows us to probe the transport pathway of air masses during ozone depletion events (ODEs). ODEs were observed at Halley on several occasions during Antarctic spring 2003. On some occasions, extremely rapid loss of ozone was observed (loss of 16 ppbv in 1 min on one occasion), which was associated with regional‐scale transport. For each such event during 2003, the air mass originated in the southern Weddell Sea, an area of vigorous sea‐ice production. On other occasions the development of the event and its recovery were strongly associated with the build‐up and decline of a stable boundary layer. In these cases, air masses had had recent contact with a nearby open water lead where sea‐ice production is known to occur. The data presented here are entirely consistent with the idea that halogens responsible for ozone loss are derived during new sea‐ice formation from an associated surface such as brine slush or frost flowers.
Low vitamin D and insufficient sun exposure are additive independent risk factors for the development of multiple sclerosis (MS). The usual measure of vitamin D status, serum 25-hydroxy vitamin D ...25(OH)D, is also a marker of recent exposure to the UVB rays of sunshine. The main evidence for a protective effect for MS development of higher 25(OH)D comes from observational studies, but this study design cannot separate out whether 25(OH)D is acting as a marker of vitamin D status, sun exposure, or both. In light of a lack of definitive outcomes in MS patients after trials of vitamin D supplementation and the ability of narrowband UVB to induce vitamin D, as well as other immune-regulatory molecules in skin, the Phototherapy for Clinically Isolated Syndrome (PhoCIS) trial was established to investigate the benefits of narrowband UVB, in addition to supplemented vitamin D, on MS development in individuals with Clinically Isolated Syndrome. We propose that the PhoCIS trial provides a fresh approach to re-defining the reported associations of 25(OH)D levels with MS development and progression.
It has been shown that NOx is produced photochemically within the snowpack of polar regions. If emitted to the atmosphere, this process could be a major source of NOx in remote snowcovered regions. ...We report here on measurements made at the German Antarctic station, Neumayer, during austral summer 1999, aimed at detecting and quantifying emissions of NOx from the surface snow. Gradients of NOx measured, and fluxes calculated using local meteorology measurements. On the 2 days of flux measurements, the derived fluxes showed continual release from the snow surface, varying between ∼0 and 3 × 108 molecs/cm²/s. When not subject to turbulence, the variation was coincident with the uv diurnal cycle, suggesting rapid release once photochemically produced. Scaling the diurnal average of Feb. 7th (1.3 × 108 molecs/cm²/s) suggests an annual emission over Antarctica of the order 0.0076TgN.
Background: Patients with spinal cord injuries (SCIs) are at a greater risk for the development of cardiovascular diseases (CVDs) than able-bodied individuals due to the high risk of endothelial ...dysfunction. Summary: For instance, patients with SCIs lose autonomic control of the heart and vasculature, which results in severe fluctuations in blood pressure. These oscillations between hypotension and hypertension have been shown to damage blood vessel endothelial cells and may contribute to the development of atherosclerosis. Furthermore, the loss of skeletal muscle control results in skeletal muscle atrophy and inward remodeling of the conduit arteries. It has been shown that blood vessels in the legs are chronically exposed to high shear, while the aorta experiences chronically low shear. These alterations to shear forces may adversely impact endothelial vasodilatory capacity and promote inflammatory signaling and leukocyte adherence. Additionally, microvascular endothelial vasodilatory capacity is impaired in patients with an SCI, and this may precede changes in conduit artery endothelial function. Finally, due to immobility and a loss of skeletal muscle mass, patients with SCIs have a higher risk of metabolic disorders, inflammation, and oxidative stress. Key Messages: Collectively, these factors may impair endothelium-dependent vasodilatory capacity, promote leukocyte adhesion and infiltration, promote the peroxidation of lipids, and ultimately support the development of atherosclerosis. Therefore, future interventions to prevent CVDs in patients with SCIs should focus on the management of endothelial health to prevent endothelial dysfunction and atherosclerosis.
Silver nanowires grow from highly Ag+‐loaded zeolitesat the impact of the electron beam from a transmission electron microscope. Both bent, polycrystalline (see Figure), and straight single crystal ...wires (15 to 150 nm wide, and up to tens of μm long) can be obtained. Their formation can be rationalized as the reduction of Ag+ within the zeolite, accumulation of Ag metal in mesopores, and finally the breaching of the crystallite surface (see the collage of images on the inside front cover).
Obesity and cigarette smoking are both important risk factors for insulin resistance, cardiovascular disease, and cancer. Smoking reduces appetite, which makes many people reluctant to quit. Few ...studies have documented the metabolic impact of combined smoke exposure (se) and high-fat-diet (HFD). Neuropeptide Y (NPY) is a powerful hypothalamic feeding stimulator that promotes obesity. We investigated how chronic se affects caloric intake, adiposity, plasma hormones, inflammatory mediators, and hypothalamic NPY peptide in animals fed a palatable HFD. Balb/c mice (5 wk old, male) were exposed to smoke (2 cigarettes, twice/day, 6 days/wk, for 7 wk) with or without HFD. Sham-exposed mice were handled similarly without se. Plasma leptin, hypothalamic NPY, and adipose triglyceride lipase (ATGL) mRNA were measured. HFD induced a 2.3-fold increase in caloric intake, increased adiposity, and glucose in both sham and se cohorts. Smoke exposure decreased caloric intake by 23%, with reduced body weight in both dietary groups. Fat mass and glucose were reduced only by se in the chow-fed animals. ATGL mRNA was reduced by HFD in se animals. Total hypothalamic NPY was reduced by HFD, but only in sham-exposed animals; se increased arcuate NPY. We conclude that although se ameliorated hyperphagia and reversed the weight gain associated with HFD, it failed to reverse fat accumulation and hyperglycemia. The reduced ATGL mRNA expression induced by combined HFD and se may contribute to fat retention. Our data support a powerful health message that smoking in the presence of an unhealthy Western diet increases metabolic disorders and fat accumulation.
The innate immune inflammatory response to lipopolysaccharide (LPS, an endotoxin) is essential for lung host defense against infection by gram-negative bacteria but is also implicated in the ...pathogenesis of some lung diseases. Studies on genetically altered mice implicate granulocyte-macrophage colony-stimulating factor (GM-CSF) in lung responses to LPS; however, the physiological effects of GM-CSF neutralization are poorly characterized. We performed detailed kinetic and dose-response analyses of the lung inflammation response to LPS in the presence of the specific GM-CSF-neutralizing antibody 22E9. LPS instilled into the lungs of BALB/c mice induced a dose-dependent inflammation comprised of intense neutrophilia, macrophage infiltration and proliferation, TNF-alpha and matrix metalloproteinase release, and macrophage inflammatory protein-2 induction. The neutralization of anti-GM-CSF in a dose-dependent fashion suppressed these inflammatory indexes by 85% when given before or after LPS or after repeat LPS challenges. Here we report for the first time that the physiological expression of Toll-like receptor-4 in lung is reduced by anti-GM-CSF. We observed that lower Toll-like receptor-4 expression correlated with a similar decline in peak TNF- levels in response to endotoxin. Consequently, sustained expression of key inflammatory mediators over 24 h was reduced. These data expand the understanding of the contribution of GM-CSF to innate immune responses in lung and suggest that blocking GM-CSF might benefit some lung diseases where LPS has been implicated in etiology.
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