A Preliminary Report on Unique Hail and Tornadic Storm Observations in Central Illinois and Eastern Indiana on 3 April 1974

published or submitted for publicationis peer reviewedOpe

Detection of Optically Faint GEO Debris

There have been extensive optical surveys for debris at geosynchronous orbit (GEO) conducted with meter-class telescopes, such as those conducted with MODEST (the Michigan Orbital DEbris Survey Telescope, a 0.6-m telescope located at Cerro Tololo in Chile), and the European Space Agency's 1.0-m space debris telescope (SDT) in the Canary Islands. These surveys have detection limits in the range of 18th or 19th magnitude, which corresponds to sizes larger than 10 cm assuming an albedo of 0.175. All of these surveys reveal a substantial population of objects fainter than R = 15th magnitude that are not in the public U.S. Satellite Catalog. To detect objects fainter than 20th magnitude (and presumably smaller than 10 cm) in the visible requires a larger telescope and excellent imaging conditions. This combination is available in Chile. NASA's Orbital Debris Program Office has begun collecting orbital debris observations with the 6.5-m (21.3-ft diameter) "Walter Baade" Magellan telescope at Las Campanas Observatory. The goal is to detect objects as faint as possible from a ground-based observatory and begin to understand the brightness distribution of GEO debris fainter than R = 20th magnitude

Searching for Optically Faint GEO Debris

We report on results from a search for optically faint debris (defined as R > 20th magnitude, or smaller than 10 cm assuming an albedo of 0.175)) at geosynchronous orbit (GEO) using the 6.5-m Magellan telescope "Walter Baade" at Las Campanas Observatory in Chile. Our goal is to characterize the brightness distribution of debris to the faintest limiting magnitude possible. Our data was obtained during 6 hours of observing time during the photometric nights of 26 and 27 March 2011 with the IMACS f/2 instrument, which has a field of view (fov) of 0.5 degrees in diameter. All observations were obtained through a Sloan r filter, and calibrated by observations of Landolt standard stars. Our primary objective was to search for optically faint objects from one of the few known fragmentations at GEO: the Titan 3C Transtage (1968-081) fragmentation in 1992. Eight debris pieces and the parent rocket body are in the Space Surveillance Network public catalog. We successfully tracked two cataloged pieces of Titan debris with the 6.5-m telescope, followed by a survey for unknown objects on similar orbits but with different mean anomalies. To establish the bright end of the debris population, calibrated observations were acquired on the same field centers, telescope rates, and time period with a similar filter on the 0.6-m MODEST (Michigan Orbital DEbris Survey Telescope), located 100 km to the south of Magellan at Cerro Tololo Inter-American Observatory, Chile. We will show the calibrated brightness distributions from both telescopes, and compare the observed brightness distributions with that predicted for various population models of debris of different sizes

An optical survey for space debris on highly eccentric and inclined MEO orbits

Optical surveys for space debris in high-altitude orbits have been conducted since more than ten years. Originally these efforts concentrated mainly on the geostationary region (GEO). Corresponding observation strategies, processing techniques and cataloguing approaches have been developed and successfully applied. The ESA GEO surveys, e.g., resulted in the detection of a significant population of small-size debris and later in the discovery of high area-to-mass ratio objects in GEO-like orbits. Comparably less experience (both, in terms of practical observation and strategy definition) is available for eccentric orbits that (at least partly) are in the MEO region, in particular for the Molniya-type orbits. Different survey and follow-up strategies for searching space debris objects in highly-eccentric MEO orbits, and to acquire orbits which are sufficiently accurate to catalog such objects and to maintain their orbits over longer time spans were developed. Simulations were performed to compare the performance of different survey and cataloguing strategies. Eventually, optical observations were conducted in the framework of an ESA study using ESA’s Space Debris Telescope (ESASDT) the 1-m Zeiss telescope located at the Optical Ground Station (OGS) at the Teide Observatory at Tenerife, Spain. Thirteen nights of surveys of Molniya-type orbits were performed between January and August 2013. Eventually 255 surveys were performed during these thirteen nights corresponding to about 47 h of observations. In total 30 uncorrelated faint objects were discov- ered. On average one uncorrelated object was found every 100 min of observations. Some of these objects show a considerable brightness variation and have a high area-to-mass ratio as determined in the orbit estimation process

Circulating Retinol-Binding Protein-4 Concentration Might Reflect Insulin Resistance–Associated Iron Overload

OBJECTIVES—The mechanisms behind the association between retinol-binding protein-4 (RBP4) and insulin resistance are not well understood. An interaction between iron and vitamin A status, of which RBP4 is a surrogate, has long been recognized. We hypothesized that iron-associated insulin resistance could be behind the impaired insulin action caused by RBP4

IGFBP3 Colocalizes with and Regulates Hypocretin (Orexin)

Background: The sleep disorder narcolepsy is caused by a vast reduction in neurons producing the hypocretin (orexin) neuropeptides. Based on the tight association with HLA, narcolepsy is believed to result from an autoimmune attack, but the cause of hypocretin cell loss is still unknown. We performed gene expression profiling in the hypothalamus to identify novel genes dysregulated in narcolepsy, as these may be the target of autoimmune attack or modulate hypocretin gene expression. Methodology/Principal Findings: We used microarrays to compare the transcriptome in the posterior hypothalamus of (1) narcoleptic versus control postmortem human brains and (2) transgenic mice lacking hypocretin neurons versus wild type mice. Hypocretin was the most downregulated gene in human narcolepsy brains. Among many additional candidates, only one, insulin-like growth factor binding protein 3 (IGFBP3), was downregulated in both human and mouse models and coexpressed in hypocretin neurons. Functional analysis indicated decreased hypocretin messenger RNA and peptide content, and increased sleep in transgenic mice overexpressing human IGFBP3, an effect possibly mediated through decrease

An Inflammatory Cascade Leading to Hyperresistinemia in Humans

BACKGROUND: Obesity, the most common cause of insulin resistance, is increasingly recognized as a low-grade inflammatory state. Adipocyte-derived resistin is a circulating protein implicated in insulin resistance in rodents, but the role of human resistin is uncertain because it is produced largely by macrophages. METHODS AND FINDINGS: The effect of endotoxin and cytokines on resistin gene and protein expression was studied in human primary blood monocytes differentiated into macrophages and in healthy human participants. Inflammatory endotoxin induced resistin in primary human macrophages via a cascade involving the secretion of inflammatory cytokines that circulate at increased levels in individuals with obesity. Induction of resistin was attenuated by drugs with dual insulin-sensitizing and anti-inflammatory properties that converge on NF-κB. In human study participants, experimental endotoxemia, which produces an insulin-resistant state, causes a dramatic rise in circulating resistin levels. Moreover, in patients with type 2 diabetes, serum resistin levels are correlated with levels of soluble tumor necrosis factor α receptor, an inflammatory marker linked to obesity, insulin resistance, and atherosclerosis. CONCLUSIONS: Inflammation is a hyperresistinemic state in humans, and cytokine induction of resistin may contribute to insulin resistance in endotoxemia, obesity, and other inflammatory states

Growth Hormone Protects Against Ovariectomy-Induced Bone Loss in States of Low Circulating Insulin-like Growth Factor (IGF-1)*

Early after estrogen loss in postmenopausal women and ovariectomy (OVX) of animals, accelerated endosteal bone resorption leads to marrow expansion of long bone shafts that reduce mechanical integrity. Both growth hormone (GH) and insulin-like growth factor (IGF-1) are potent regulators of bone remodeling processes. To investigate the role of the GH/IGF-1 axis with estrogen deficiency, we used the liver IGF-1-deficient (LID) mouse. Contrary to deficits in controls, OVX of LID mice resulted in maintenance of cortical bone mechanical integrity primarily owing to an enhanced periosteal expansion affect on cross-sectional structure (total area and cortical width). The serum balance in LID that favors GH over IGF-1 diminished the effects of ablated ovarian function on numbers of osteoclast precursors in the marrow and viability of osteocytes within the cortical matrix and led to less endosteal resorption in addition to greater periosteal bone formation. Interactions between estrogen and the GH/IGF-1 system as related to bone remodeling provide a pathway to minimize degeneration of bone tissue structure and osteoporotic fracture. © 2010 American Society for Bone and Mineral Researc

Weight and metabolic effects of cpap in obstructive sleep apnea patients with obesity

<p>Abstract</p> <p>Background</p> <p>Obstructive sleep apnea (OSA) is associated with obesity, insulin resistance (IR) and diabetes. Continuous positive airway pressure (CPAP) rapidly mitigates OSA in obese subjects but its metabolic effects are not well-characterized. We postulated that CPAP will decrease IR, ghrelin and resistin and increase adiponectin levels in this setting.</p> <p>Methods</p> <p>In a pre- and post-treatment, within-subject design, insulin and appetite-regulating hormones were assayed in 20 obese subjects with OSA before and after 6 months of CPAP use. Primary outcome measures included glucose, insulin, and IR levels. Other measures included ghrelin, leptin, adiponectin and resistin levels. Body weight change were recorded and used to examine the relationship between glucose regulation and appetite-regulating hormones.</p> <p>Results</p> <p>CPAP effectively improved hypoxia. However, subjects had increased insulin and IR. Fasting ghrelin decreased significantly while leptin, adiponectin and resistin remained unchanged. Forty percent of patients gained weight significantly. Changes in body weight directly correlated with changes in insulin and IR. Ghrelin changes inversely correlated with changes in IR but did not change as a function of weight.</p> <p>Conclusions</p> <p>Weight change rather than elimination of hypoxia modulated alterations in IR in obese patients with OSA during the first six months of CPAP therapy.</p

The role of the small intestine in the development of dietary fat-induced obesity and insulin resistance in C57BL/6J mice

<p>Abstract</p> <p>Background</p> <p>Obesity and insulin resistance are two major risk factors underlying the metabolic syndrome. The development of these metabolic disorders is frequently studied, but mainly in liver, skeletal muscle, and adipose tissue. To gain more insight in the role of the small intestine in development of obesity and insulin resistance, dietary fat-induced differential gene expression was determined along the longitudinal axis of small intestines of C57BL/6J mice.</p> <p>Methods</p> <p>Male C57BL/6J mice were fed a low-fat or a high-fat diet that mimicked the fatty acid composition of a Western-style human diet. After 2, 4 and 8 weeks of diet intervention small intestines were isolated and divided in three equal parts. Differential gene expression was determined in mucosal scrapings using Mouse genome 430 2.0 arrays.</p> <p>Results</p> <p>The high-fat diet significantly increased body weight and decreased oral glucose tolerance, indicating insulin resistance. Microarray analysis showed that dietary fat had the most pronounced effect on differential gene expression in the middle part of the small intestine. By overrepresentation analysis we found that the most modulated biological processes on a high-fat diet were related to lipid metabolism, cell cycle and inflammation. Our results further indicated that the nuclear receptors Ppars, Lxrs and Fxr play an important regulatory role in the response of the small intestine to the high-fat diet. Next to these more local dietary fat effects, a secretome analysis revealed differential gene expression of secreted proteins, such as Il18, Fgf15, Mif, Igfbp3 and Angptl4. Finally, we linked the fat-induced molecular changes in the small intestine to development of obesity and insulin resistance.</p> <p>Conclusion</p> <p>During dietary fat-induced development of obesity and insulin resistance, we found substantial changes in gene expression in the small intestine, indicating modulations of biological processes, especially related to lipid metabolism. Moreover, we found differential expression of potential signaling molecules that can provoke systemic effects in peripheral organs by influencing their metabolic homeostasis. Many of these fat-modulated genes could be linked to obesity and/or insulin resistance. Together, our data provided various leads for a causal role of the small intestine in the etiology of obesity and/or insulin resistance.</p