841 research outputs found
Eucaryotic gene inactivation by sequence-specific promoter methylation and the release of the transcription block
No full textDoerfler W, Langner KD, Knebel D, et al. Eucaryotic gene inactivation by sequence-specific promoter methylation and the release of the transcription block. In: Kahl G, ed. Architecture of Eukaryotic Genes. Weinheim, New York: VHC; 1988: 409-418
Die Form der Realität
No full textKaldewey D. Die Form der Realität. In: Langner R, Luks T, Schlimm A, Straube G, Thomaschke D, eds. Ordnungen des Denkens. Debatten um Wissenschaftstheorie und Erkenntniskritik. Verhandlungen mit der Gegenwart. Vol 2. Münster: LIT Verlag; 2007: 25-26
Collaborating in virtual teams
Get PDFAbstract. This paper describes some early results from observin
Joule heating in nanowires
Get PDFWe study the effect of Joule heating from electric currents flowing through ferromagnetic nanowires on the temperature of the nanowires and on the temperature of the substrate on which the nanowires are grown. The spatial current density distribution, the associated heat generation, and diffusion of heat is simulated within the nanowire and the substrate. We study several different nanowire and constriction geometries as well as different substrates: (thin) silicon nitride membranes, (thick) silicon wafers, and (thick) diamond wafers. The spatially resolved increase in temperature as a function of time is computed. For effectively three-dimensional substrates (where the substrate thickness greatly exceeds the nanowire length), we identify three different regimes of heat propagation through the substrate: regime (i), where the nanowire temperature increases approximately logarithmically as a function of time. In this regime, the nanowire temperature is well-described analytically by You et al. [APL89, 222513 (2006)]. We provide an analytical expression for the time tc that marks the upper applicability limit of the You model. After tc, the heat flow enters regime (ii), where the nanowire temperature stays constant while a hemispherical heat front carries the heat away from the wire and into the substrate. As the heat front reaches the boundary of the substrate, regime (iii) is entered where the nanowire and substrate temperature start to increase rapidly. For effectively two-dimensional substrates (where the nanowire length greatly exceeds the substrate thickness), there is only one regime in which the temperature increases logarithmically with time for large times. We provide an analytical expression, valid for all pulse durations, that allows one to accurately compute this temperature increase in the nanowire on thin substrate
Lipoprotein profiles in Miniature Schnauzer dogs with idiopathic hypertriglyceridemia and hypercortisolism
No full textMiniature Schnauzer dogs (MSs) are predisposed to both idiopathic hypertriglyceridemia (iHTG) and hypercortisolism (HCort). To our knowledge, the lipoprotein profiles of MSs with iHTG have not been compared to those with HCort. We analyzed cholesterol and triglyceride concentrations and lipoprotein fractions in 4 groups of MSs: normotriglyceridemia (NTG) without concurrent disease (Healthy-NTG), HCort and NTG (HCort-NTG), HCort and HTG (HCort-HTG), and iHTG. Lipoprotein fractions were assessed by lipoprotein electrophoresis and compared between groups. Fifty-one plasma samples were analyzed. Twenty-five dogs had NTG (16 Healthy-NTG, 9 HCort-NTG) and 26 dogs had HTG (7 iHTG, 19 HCort-HTG). Dogs with iHTG or HCort-HTG had significantly higher cholesterol concentrations than Healthy-NTG dogs. Dogs with HCort-HTG had higher cholesterol than HCort-NTG dogs. There was a significantly higher low-density lipoprotein (LDL) percentage in iHTG and HCort-HTG dogs than HCort-NTG dogs. HCort-HTG dogs also had lower high-density lipoproteins (HDL) than HCort-NTG dogs. It was not possible to readily distinguish MSs with iHTG from MSs with HCort-HTG or Healthy-NTG using lipoprotein electrophoresis fractions. The diagnosis of iHTG remains a diagnosis by exclusion
M[agnifico]. D[omino]. P[atre]. G[regorio]. W[ibmperger]. R[ectore]. / G[eorgio]. C[hristophoro]. L[angner]. N[otaro]
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National Inventors Council visit to Cleveland factory
No full textGroup photograph of the National Inventors Council visiting a Cleveland factory. Front row, left to right: Lawrence Langner, Dr. Fredrick M. Feiker, Dr. William D. Coolidge, Com. H. A. Phelps, Dr. George W. Lewis, George W. Codrington, Orville Wright, Charles F. Kettering, Admiral H. G. Bowen, Hon. Conway P. Coe, Commissioner of Patents. 2nd row: J. C. Green, Dr. Fin Sparre, Rear Admiral J. D. Beuret, Major General W. H. Tschappat, Colonel L. B. Lent, Watson Davis, George Baekeland.https://corescholar.libraries.wright.edu/special_ms1_photographs/2744/thumbnail.jp
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U.S. Support Program tasks
Get PDFIn the fall of 1993, President Clinton announced before the United Nations General Assembly, that the US would voluntarily offer excess fissile material of weapons origin to International Atomic Energy Agency (IAEA) safeguards. There are presently five US Support Program tasks at work. Three are complete, and two are underway. Reports are available from two of the completed SP-1s; a draft is in preparation for the third. These tasks are: (1) plutonium scrap multiplicity counter at Hanford; (2) calorimeter authentication at Hanford; (3) large neutron multiplicity counter at Rocky Flats; (4) calorimeter authentication at Rocky Flats; and (5) safeguards approach support at the APSF, SRS. The status of the first four tasks above is described here. Information on the work at Savannah River is contained in a separate paper
KRAS mutation testing for predicting response to anti-EGFR therapy for colorectal carcinoma: proposal for an European quality assurance program
No full textNovel therapeutic agents targeting the epidermal growth factor receptor (EGFR) have improved outcomes for patients with colorectal carcinoma. However, these therapies are effective only in a subset of patients. Activating mutations in the KRAS gene are found in 30-40% of colorectal tumors and are associated with poor response to anti-EGFR therapies. Thus, KRAS mutation status can predict which patient may or may not benefit from anti-EGFR therapy. Although many diagnostic tools have been developed for KRAS mutation analysis, validated methods and standardized testing procedures are lacking. This poses a challenge for the optimal use of anti-EGFR therapies in the management of colorectal carcinoma. Here we review the molecular basis of EGFR-targeted therapies and the resistance to treatment conferred by KRAS mutations. We also present guideline recommendations and a proposal for a European quality assurance program to help ensure accuracy and proficiency in KRAS mutation testing across the European Union
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