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Search Results: 1 - 10 of 3836 matches for " Tim Mefford "
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Charge Symmetry Breaking in 500 MeV Nucleon-Trinucleon Scattering
Tim Mefford,Rubin H. Landau
Physics , 1995, DOI: 10.1103/PhysRevC.52.1212
Abstract: Elastic nucleon scattering from the 3He and 3H mirror nuclei is examined as a test of charge symmetry violation. The differential cross-sections are calculated at 500 MeV using a microsopic, momentum-space optical potential including the full coupling of two spin 1/2 particles and an exact treatment of the Coulomb force. The charge-symmetry-breaking effects investigated arise from a violation within the nuclear structure, from the p-nucleus Coulomb force, and from the mass-differences of the charge symmetric states. Measurements likely to reveal reliable information are noted.
Stromal Genes Add Prognostic Information to Proliferation and Histoclinical Markers: A Basis for the Next Generation of Breast Cancer Gene Signatures
Dwain Mefford, Joel Mefford
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0037646
Abstract: Background First-generation gene signatures that identify breast cancer patients at risk of recurrence are confined to estrogen-positive cases and are driven by genes involved in the cell cycle and proliferation. Previously we induced sets of stromal genes that are prognostic for both estrogen-positive and estrogen-negative samples. Creating risk-management tools that incorporate these stromal signatures, along with existing proliferation-based signatures and established clinicopathological measures such as lymph node status and tumor size, should better identify women at greatest risk for metastasis and death. Methodology/Principal Findings To investigate the strength and independence of the stromal and proliferation factors in estrogen-positive and estrogen-negative patients we constructed multivariate Cox proportional hazards models along with tree-based partitions of cancer cases for four breast cancer cohorts. Two sets of stromal genes, one consisting of DCN and FBLN1, and the other containing LAMA2, add substantial prognostic value to the proliferation signal and to clinical measures. For estrogen receptor-positive patients, the stromal-decorin set adds prognostic value independent of proliferation for three of the four datasets. For estrogen receptor-negative patients, the stromal-laminin set significantly adds prognostic value in two datasets, and marginally in a third. The stromal sets are most prognostic for the unselected population studies and may depend on the age distribution of the cohorts. Conclusion The addition of stromal genes would measurably improve the performance of proliferation-based first-generation gene signatures, especially for older women. Incorporating indicators of the state of stromal cell types would mark a conceptual shift from epithelial-centric risk assessment to assessment based on the multiple cell types in the cancer-altered tissue.
Enumerating the gene sets in breast cancer, a "direct" alternative to hierarchical clustering
Dwain Mefford, Joel A Mefford
BMC Genomics , 2010, DOI: 10.1186/1471-2164-11-482
Abstract: Applied to four large breast cancer datasets, this alternative exploratory method detects more than thirty sets of co-regulated genes, many of which are conserved across experiments and across platforms. Many of these sets are readily identified in biological terms, e.g., "estrogen", "erbb2", and 8p11-12, and several are clinically significant as prognostic of either increased survival ("adipose", "stromal"...) or diminished survival ("proliferation", "immune/interferon", "histone",...). Of special interest are the sets that effectively factor "immune response" and "stromal signalling".The gene sets induced by the enumeration include many of the sets reported in the literature. In this regard these inventories confirm and consolidate findings from microarray-based work on breast cancer over the last decade. But, the enumerations also identify gene sets that have not been studied as of yet, some of which are prognostic of survival. The sets induced are robust, biologically meaningful, and serve to reveal a finer structure in existing breast cancer microarrays.After removing genes that exhibit little variance, the standard script for exploring microarray data applies two-way hierarchical clustering (HC), followed by a visual search for patterns displayed in a red-green heatmap [1,2]. For breast cancer in particular, this procedure has proven immensely productive. It can be credited with the discovery[3] (or rediscovery) [4] of the basal subtype, and, more broadly the identification of subtypes of breast cancer that hold out the potential to inform clinical practice [3,5-8]Despite its utility, the standard script suffers from several limitations, in particular the instability of the binary tree of the clusters found [9]. Perturbation and re-sampling techniques are available to gauge the robustness of the clusters defined by subtrees [10,11]. But, small changes in the selection of genes or choice of samples can result in disconcertingly large changes in the overall conf
Improved Diabetes Control and Pancreatic Function in a Type 2 Diabetic after Omeprazole Administration
I. N. Mefford,J. T. Mefford,C. A. Burris
Case Reports in Endocrinology , 2012, DOI: 10.1155/2012/468609
Abstract: A 43-year-old man with type 2 diabetes, opposed to insulin use and poorly responsive to oral agents added sequentially over 6 years, was placed on 40 mg omeprazole twice daily. A linear decline in daily fasting blood glucose was observed over the first two-month treatment, and his hemoglobin A1c was reduced from 11.9% to 8.2%, then sustained at 8.1% after four months. Glucose, insulin, and C-peptide response to a 2-hour glucose tolerance test were consistently improved across this time period, and calculated beta-cell mass increased by 67%. We believe these responses are consistent with activation or neogenesis of pancreatic beta cells, possibly through a gastrin-mediated mechanism.
Improved Diabetes Control and Pancreatic Function in a Type 2 Diabetic after Omeprazole Administration
I. N. Mefford,J. T. Mefford,C. A. Burris
Case Reports in Endocrinology , 2012, DOI: 10.1155/2012/468609
Abstract: A 43-year-old man with type 2 diabetes, opposed to insulin use and poorly responsive to oral agents added sequentially over 6 years, was placed on 40?mg omeprazole twice daily. A linear decline in daily fasting blood glucose was observed over the first two-month treatment, and his hemoglobin A1c was reduced from 11.9% to 8.2%, then sustained at 8.1% after four months. Glucose, insulin, and C-peptide response to a 2-hour glucose tolerance test were consistently improved across this time period, and calculated beta-cell mass increased by 67%. We believe these responses are consistent with activation or neogenesis of pancreatic beta cells, possibly through a gastrin-mediated mechanism. 1. Introduction Type 2 diabetes is a progressive disease characterized by both insulin resistance and increasing dysfunction of pancreatic beta cells, either through inactivation or apoptosis [1, 2]. Common treatments of type 2 diabetes may modify insulin sensitivity, increase insulin secretion, or in some cases either reduce beta-cell dysfunction or slow their degradation [3]. However, none of the current available agents are known to increase beta-cell population in humans. Meier et al. have demonstrated increased beta-cell activity in the human pancreas surrounding gastrinomas [4], and further studies have shown gastrin administration to induce pancreatic beta-cell neogenesis in animal models of diabetes [5, 6]. We previously observed in a retrospective analysis of our patient database a significant improvement in type 2 diabetes control in patients concurrently taking proton pump inhibitors (PPIs) [7]. These data are supported by similar observations that have since been made in three other independent data sets [8–10]. PPI administration has been shown to reverse diabetes in a murine model when combined with a dipeptidyl peptidase (DPP-4) inhibitor [11] and to markedly improve glycemic control in Psammomys obesus, a model for type 2 diabetes [12]. PPIs are known to induce hypergastrinemia [13], and such an effect has been hypothesized to mediate these observations. We now report a case study of a 43-year-old man with uncontrolled type 2 diabetes, treated consecutively and concurrently for several years with multiple oral agents, who had declined to be advanced to insulin use. In lieu of starting insulin administration and based on earlier observations in our database, the patient was placed on omeprazole 40?mg twice daily; measures of pancreatic insulin secretion and diabetes control were obtained across a four-month period. 2. Case Report 2.1. Patient Background A
The Covariate's Dilemma
Joel Mefford,John S. Witte
PLOS Genetics , 2012, DOI: 10.1371/journal.pgen.1003096
Abstract:
Angular Momentum Analysis of Spin 1/2 x 1/2 Scattering including Singlet-Triplet Mixing
T. Mefford,R. H. Landau
Physics , 1993,
Abstract: The angular momentum (partial wave) reduction of the Lippmann--Schwinger equation describing the interaction of two spin 1/2 particles is extended to the case in which the spin singlet and triplet states are coupled. A straight forward method for obtaining the angular momentum decomposition of the general potential is indicated. The derived formalism is needed to describe the interaction between two nonidentical spin--1/2 particles or between two nucleons when isospin symmetry is violated. The resulting modification of the Stapp phase--shift analysis is given.
Genetically complex epilepsies, copy number variants and syndrome constellations
Heather C Mefford, John C Mulley
Genome Medicine , 2010, DOI: 10.1186/gm192
Abstract: The International League Against Epilepsy defines an epileptic seizure as 'a transient occurrence of signs and/or symptoms due to abnormal excessive or synchronous neuronal activity in the brain' [1,2]. The condition is common, with prevalence around 1% and lifetime incidence around 3% [3]. Most epilepsies can be broadly and easily classified based on their pattern of electroclinical onset as either generalized ('originating at some point from within, and rapidly engaging, bilaterally distributed networks') or focal ('originating within networks limited to one hemisphere') [1]. Within each of these broad classifications are multiple distinct syndromes, more than half of which are considered to be 'genetic epilepsies'. In older terminology, genetic epilepsies were referred to as 'idiopathic epilepsies' [4]. Syndromes, and sometimes subsyndromes, are delineated when the seizures are defined by easily recognizable electroclinical features and similar enough to be regarded as a homogeneous group, distinct from other groups in the same classification level (Table 1). For example, genetic generalized epilepsies are frequently divided into their subsyndromes of childhood absence epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy and generalized tonic clonic seizures.There is a subset of epilepsy syndromes that are clearly monogenic, and traditional linkage studies in large families have been useful for identifying causative genes [5,6]. However, the vast majority of the genetic epilepsies are multifactorial, with an underlying genetic contribution that is polygenic, where few or usually none of the susceptibility genes have been identified. This multifactorial concept dates back to the early works of William Lennox [7] and was well established in the modern era with additional twin data [8]. It is important to note that epilepsy with complex genetics and complex epilepsy are distinct concepts. To the geneticist, complex epilepsy is epilepsy with complex genet
The phka1 deficient I/LnJ mouse exhibits endurance exercise deficiency with no compensatory changes in glycolytic gene expression  [PDF]
Ashley M. Mefford, Claci C. Ayers, Naomi S. Rowland, Nancy A. Rice
Open Journal of Molecular and Integrative Physiology (OJMIP) , 2013, DOI: 10.4236/ojmip.2013.32014
Abstract: During exercise, phosphorylase kinase (PhK) is the key regulatory enzyme responsible for maintaining glycogenolytic flux to sustain muscle contraction. The absence of PhK in skeletal muscle results in glycogen storage disease (GSD) Type IX which is characterized by muscle weakness and rapid fatigue upon exercise. In this study, we have used the phka1 deficient I/LnJ mouse model of GSD to investigate the physiological and genetic adaptations that occur in response to voluntary exercise. When quantified over training periods of either 1, 2, or 5 weeks, I/LnJ mice ran significantly less time/day and distance/day than agematched C57/Bl6 mice. Cumulatively after five weeks, adult I/LnJ mice ran ~1/2 the total time and distance of wild-type mice, 116 ± 6 hours and 211 ±23 kmversus 194 ± 3 hours and 418 ±4 km, respectively. After 5 weeks, C57/Bl6 mice demonstrated an increase in endurance as a result of aerobic training; this observed physiological adaptation was not present in I/LnJ mice. The decrease in total distance run by I/LnJ mice was not due to a reduction in speed; juvenile and adult I/LnJ mice ran ~75% - 80% as fast as C57/Bl6 mice. When transcription of glycolytic genes glucose transporter 4 (scla1), pyruvate dehydrogenase (pdha1), and phosphofructokinase (pfk) were quantified at the end of each training period, no significant differences in expression levels were found between mouse strains, suggesting that non-glycolytic mechanisms work to maintain the muscle function observed in the I/LnJ mice.
A Study on Configuration and Integration of Sub-Systems to System-of-Systems with Rule Verification  [PDF]
Tim Warnecke
Engineering (ENG) , 2015, DOI: 10.4236/eng.2015.710056
Abstract: Increasing complexity of today’s software systems is one of the major challenges software engineers have to face. This is aggravated by the fact that formerly isolated systems have to be interconnected to more complex systems, called System-of-Systems (SoS). Those systems are in charge to provide more functionality to the user than all of their independent sub-systems could do. Reducing the complexity of such systems is one goal of the software engineering paradigm called component-based software engineering (CBSE). CBSE enables the developers to treat individual sub-systems as components which interact via interfaces with a simulated environment. Thus those components can be developed and implemented independently from other components. After the implementation a system integrator is able to interconnect the components to a SoS. Despite this much-used approach it is possible to show that constraints, which are valid in an isolated sub-system, are broken after this system is integrated into a SoS. To emphasize this issue we developed a technique based on interconnected timed automata for modelling sub-systems and System-of-Systems in the model checking tool UPPAAL. The presented modelling technique allows it to verify the correctness of single sub-systems as well as the resulting SoS. Additionally we developed a tool which abstracts the complicated timed automata to an easy to read component based language with the goal to help system integrators building and verifying complex SoS.
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