994 research outputs found
Chronic pancreatitis: An international draft consensus proposal for a new mechanistic definition
No full textA definition of chronic pancreatitis (CP) is needed for diagnosis and distinguishing CP from other disorders. Previous definitions focused on morphology. Advances in epidemiology, genetics, molecular biology, modeling and other disciplines provide new insights into pathogenesis of CP, and allow CP to be better defined
Whitcomb, David C.
No full textSee entry in Butler County, volume 1, page 39: https://digital.archives.alabama.gov/digital/collection/voter1867/id/109
Optical dilution and feedback cooling of a gram-scale oscillator to 6.9 mK
No full textWe report on the use of a radiation pressure induced restoring force, the optical spring effect, to optically dilute the mechanical damping of a 1 g suspended mirror, which is then cooled by active feedback (cold damping). Optical dilution relaxes the limit on cooling imposed by mechanical losses, allowing the oscillator mode to reach a minimum temperature of 6.9 mK, a factor of ~40 000 below the environmental temperature. A further advantage of the optical spring effect is that it can increase the number of oscillations before decoherence by several orders of magnitude. In the present experiment we infer an increase in the dynamical lifetime of the state by a factor of ~200.Thomas Corbitt, Christopher Wipf, Timothy Bodiya, David Ottaway, Daniel Sigg, Nicolas Smith, Stanley Whitcomb, and Nergis Mavalval
Profiling Microdissected Epithelium and Stroma to ModelGenomic Signatures for Cervical Carcinogenesis Accommodating for Covariates.
No full textPathogenetics of chronic pancreatitis
No full textChronic pancreatitis is a condition that is associated with the progressive inflammation of the pancreas which over time gives rise to irreversible morphological changes accompanied by impairment of both exocrine and endocrine functions (Majumder and Chari 2016). Over the last 20 years, molecular genetics has played an increasingly important role in elucidating the aetiology of chronic pancreatitis. The dawn of the new era in the genetic analysis of autosomal dominant hereditary pancreatitis (OMIM #167800) was heralded by the mapping of a disease locus to the long arm of chromosome 7 (Le Bodic et al. 1996; Pandya et al. 1996; Whitcomb et al. 1996b) and the subsequent identification of a gain-of-function missense mutation (i.e., p.Arg122His) in the cationic trypsinogen gene (PRSS1; OMIM #276000) (Whitcomb et al. 1996a). Thereafter, a steady stream of chronic pancreatitis susceptibility (or protective) variants in different genes has been reported. The analysis of variants in four specific genes, all highly expressed in human pancreatic acinar cells [PRSS1, PRSS2 (encoding anionic trypsinogen; OMIM #601564), SPINK1 (encoding pancreatic secretory trypsin inhibitor; OMIM #167790) and CTRC (encoding chymotrypsin C, which specifically degrades all human trypsinogen/trypsin isoforms (OMIM #601405) (Szmola and Sahin-Tóth 2007))] has firmly established the importance of a homeostatic balance between the activation and inactivation of trypsinogen within the pancreas, thereby defining a trypsin-dependent pathway in the pathogenesis of chronic pancreatitis. Whereas gain-of-function missense mutations and copy number variants in PRSS1 (Le Maréchal et al. 2006; Whitcomb et al. 1996a) and loss-of-function variants in SPINK1 (Witt et al. 2000) and CTRC (Masson et al. 2008b; Rosendahl et al. 2008) predispose to chronic pancreatitis, loss-of-function variants in PRSS1 (Boulling et al. 2015; Chen et al. 2003; Derikx et al. 2015; Whitcomb et al. 2012) and PRSS2 (Witt et al. 2006) protect against the disease
Chronic Pancreatitis, Type 3c Diabetes, and Pancreatic Cancer Risk
No full textAbout half of all patients with chronic pancreatitis (CP) develop diabetes mellitus (DM) due to the loss of islet cell mass, not just beta cells as in Type 1 DM (T1DM), or due to insulin resistance, as in Type 2 DM (T2DM). Patients with DM from loss of islets due to pancreatic disease or resection are diagnosed with pancreatogenic or Type 3c DM (T3cDM). Patients with T3cDM also lose counter-regulatory hormones, such as glucagon and pancreatic polypeptide, and experience maldigestion associated with pancreatic exocrine insufficiency. Patients with T3cDM are therefore more susceptible to hypoglycemia and a mismatch (asynchrony) between food ingestion and nutrient absorption. At the same time, the use of incretin therapy is likely useless, since maldigestion leads to the release of higher levels of hind gut hormones, including GLP1. Thus, T3cDM caused by CP or destruction of the islets involves a special class of potential risks and comorbidity that may be overlooked if the CP has not been diagnosed. Further, because CP is also associated with pancreatic ductal adenocarcinoma, better classification of patients with DM is needed to determine if PDAC is associated with DM or with undetected CP that gave rise to T3cDM that was previously misclassified as T1DM to T2DM.Image: Cathedral of Learning at University of Pittsburgh. Pittsburgh, PA, USA. (Author: Kevin Albright, Wikimedia Commons
An all-optical trap for a gram-scale mirror
No full textWe report on a stable optical trap suitable for a macroscopic mirror, wherein the dynamics of the mirror are fully dominated by radiation pressure. The technique employs two frequency-offset laser fields to simultaneously create a stiff optical restoring force and a viscous optical damping force. We show how these forces may be used to optically trap a free mass without introducing thermal noise, and we demonstrate the technique experimentally with a 1 g mirror. The observed optical spring has an inferred Young's modulus of 1.2 TPa, 20% stiffer than diamond. The trap is intrinsically cold and reaches an effective temperature of 0.8 K, limited by technical noise in our apparatus.Thomas Corbitt, Yanbei Chen, Edith Innerhofer, Helge Müller-Ebhardt, David Ottaway, Henning Rehbein, Daniel Sigg, Stanley Whitcomb, Christopher Wipf, and Nergis Mavalval
Riley's Rubaiyat embellished with comments and illustrations
No full textRiley's Rubaiyat embellished with handwritten comments from the author as well as additional illustrations and autograph by Charles M. Relyea. Transcription included
Asahel Curtis letter to David Whitcomb regarding the Mount Olympus National Park articles published in the New York Herald, March 31, 1937
No full textCurtis' letter to David Whitcomb calls attention to the inaccurate information printed in the New York Herald regarding the new proposed boundaries of the Wallgren bill (H.R. 4724). He also discusses the large portion of pulpwood that is included in the boundaries of the current bill. He writes , "My criticism is that there is still too large an area of this type included in the present bill. This country is not of National Park character and was so classed in a report by the representatives of the National Park Service. I read their report to the Public Lands Committee and it is included in the hearings. Our old friend Mather would not have accepted it for park purposes."Asahel Curtis, prominent Seattle photographer of the early twentieth century, was brother to famed photographer, Edward S. Curtis. Asahel Curtis was a founding member of the Mountaineers, a mountain-climbing group which also promoted the preservation of wilderness areas. Curtis was active in the affairs of the club for the first several years after its founding in 1906. His involvement in the Seattle-Tacoma Rainier National Park Committee (later the Rainier National Park Advisory Board) strained his relations with the Mountaineers. The committee was formed by community business interests to take advantage of the park's tourism potential. Curtis, through the committee, sought to promote greater accessibility to the park by building roads to increase tourism. His opposition to the expansion of the Olympic National Park in the late 1930's as a representative of the Seattle Chamber of Commerce and the timber industry, led to a further deterioration of relations with the Mountaineers.
The Olympic National Park was first created by President Grover Cleveland in 1897, naming it the Olympic Forest Reserve. In 1909 President Theodore Roosevelt designated the area Mount Olympus National Monument to protect the summer range and breeding grounds of the Olympic elk. In 1915, conceding to the protests and mindful of the increasing need for timber with the advent of World War I, President Woodrow Wilson reduced the Monument by half. On February 15, 1937 Representative Mon C. Wallgren of Washington introduced the second of three bills to establish the “Mount Olympus National Park”. The proposed bill (H.R. 4724) would have reduced the size of the proposed park by about 142,000 acres and eliminate the originally proposed areas in the Bogachiel, Queets and Quinault drainages on the west side. The bill failed. In 1938 Congress signed a bill designating 898,000 acres as Olympic National Park thanks in large part to the enthusiastic support of President Franklin D. Roosevelt. Two years later, in 1940, Roosevelt added an additional 300 square miles to the park
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