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Search Results: 1 - 10 of 199691 matches for " N.;Campbell "
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African Biochemists Plan More Collaboration
Peter N. Campbell
The Scientific World Journal , 2000, DOI: 10.1100/tsw.2000.16
Abstract:
Finite temperature phase transition in the two-dimension Randomly Coupled Ferromagnet
N. Lemke,I. A. Campbell
Physics , 1999, DOI: 10.1088/0305-4470/32/45/304
Abstract: We show using extensive simulation results and physical arguments that an Ising system on a two dimensional square lattice, having interactions of random sign between first neighbors and ferromagnetic interactions between second neighbors, presents a phase transition at a non-zero temperature.
Two dimensional Ising spin glasses with non-zero ordering temperatures
N. Lemke,I. A. Campbell
Physics , 1996, DOI: 10.1103/PhysRevLett.76.4616
Abstract: We demonstrate numerically that for Ising spins on square lattices with ferromagnetic second neighbour interactions and random near neighbour interactions, two dimensional Ising spin glass order with a non-zero freezing temperature can occur. We compare some of the physical properties of these spin glasses with those of standard spin glasses in higher dimensions.
Stretched exponential behavior and random walks on diluted hypercubic lattices
N. Lemke,I. A. Campbell
Physics , 2011, DOI: 10.1103/PhysRevE.84.041126
Abstract: Diffusion on a diluted hypercube has been proposed as a model for glassy relaxation and is an example of the more general class of stochastic processes on graphs. In this article we determine numerically through large scale simulations the eigenvalue spectra for this stochastic process and calculate explicitly the time evolution for the autocorrelation function and for the return probability, all at criticality, with hypercube dimensions $N$ up to N=28. We show that at long times both relaxation functions can be described by stretched exponentials with exponent 1/3 and a characteristic relaxation time which grows exponentially with dimension $N$. The numerical eigenvalue spectra are consistent with analytic predictions for a generic sparse network model.
Síndrome de la bolsa de orina púrpura Purple urine bag syndrome
Santiago Emilio Campbell,Arturo Izquierdo,Sebastián Campbell,Lilia Erazo
Acta Medica Colombiana , 2011,
Abstract: Se presenta el caso de un paciente masculino de 62 a os remitido por oncología para estudio por presentar orina de color morado. Desde hace tres meses tiene sonda vesical permanente por retención urinaria posterior a una resección quirúrgica de una metástasis cerebral por tumor primario a nivel pulmonar, tiene pendiente radioterapia holoencefálica y posterior quimioterapia sistémica. La única medicación que tomaba de manera intermitente era omeprazol, refería además anorexia y náuseas. La bolsa urinaria contenía orina de color morado y a la extracción aparecía turbia. El análisis de la orina fue compatible con infección urinaria. El color de la orina en la bolsa fue motivo de una interesante discusión científica. Se discuten los mecanismos a través de los cuales la orina toma dicho color (Acta Med Colomb 2011; 36: 38-40). The case is presented of a 62-year-old male patient who was referred by the Oncology Department for evaluation of purple-colored urine. Over the past three months the patient has had an indwelling catheter because of urinary retention after surgical resection of a brain metastasis of a lung tumor. The patient is to be treated with holoencephalic radiotherapy and afterwards with systemic chemotherapy. The only current medication was omeprazole, which he took intermittently. He also complained of anorexia and nausea. The urinary bag contained purple-colored urine, which appeared turbid upon extraction. Urinalysis was consistent with urinary tract infection. The color of the urine gave rise to an interesting scientific discussion. The mechanisms are discussed through which urine takes a purple color (Med Colomb 2011; 36: 38-40).
Agency at Work: A Dynamic Interpretive Approach  [PDF]
Colin Campbell
Sociology Mind (SM) , 2012, DOI: 10.4236/sm.2012.24047
Abstract: Roy’s 1950s paper “Banana Time” is used as the basis for an exploration of the nature and relationship of agency and action. Roy’s activity in playing his “game of work” is shown to be a feature of individual conduct that, despite possessing subjective meaning, is largely neglected by contemporary sociologists, mainly because of its covert character. What an examination of this aspect of his conduct suggests is the need to revise the conventional observational approach to the definition of the unit act by recognising that there may well be an additional actor’s covert definition sitting within the accepted social definition and that it is therefore necessary to use the criterion of attentionality to identify the unit act. An analysis of Roy’s game of work also helps to shed light on the possible relationship between action and agency, revealing that while the power of agency enables individuals to act, it is also frequently necessary for individuals to act in order to maintain or restore their power of agency. Finally, a consideration of the function fulfilled by Roy’s game of work shows that a behaviourist-style stimulus-response analysis of conduct is not at odds either with voluntarism or the adoption of the actor’s standpoint. This is because Roy demonstrates how actors are themselves lay behaviourists, fully aware of how they need to manipulate stimuli in order to produce desired responses in themselves.
Postmodernism and Educational Research  [PDF]
Madelaine Campbell
Open Journal of Social Sciences (JSS) , 2018, DOI: 10.4236/jss.2018.67006
Abstract: Postmodernism is an elusive concept when we attempt to connect it to educational research methodologies. This paper is a review of the literature regarding postmodernist research methodologies in education.
The Role of Dicentric Chromosome Formation and Secondary Centromere Deletion in the Evolution of Myeloid Malignancy
Ruth N. MacKinnon,Lynda J. Campbell
Genetics Research International , 2011, DOI: 10.4061/2011/643628
Abstract: Dicentric chromosomes have been identified as instigators of the genome instability associated with cancer, but this instability is often resolved by one of a number of different secondary events. These include centromere inactivation, inversion, and intercentromeric deletion. Deletion or excision of one of the centromeres may be a significant occurrence in myeloid malignancy and other malignancies but has not previously been widely recognized, and our reports are the first describing centromere deletion in cancer cells. We review what is known about dicentric chromosomes and the mechanisms by which they can undergo stabilization in both constitutional and cancer genomes. The failure to identify centromere deletion in cancer cells until recently can be partly explained by the standard approaches to routine diagnostic cancer genome analysis, which do not identify centromeres in the context of chromosome organization. This hitherto hidden group of primary dicentric, secondary monocentric chromosomes, together with other unrecognized dicentric chromosomes, points to a greater role for dicentric chromosomes in cancer initiation and progression than is generally acknowledged. We present a model that predicts and explains a significant role for dicentric chromosomes in the formation of unbalanced translocations in malignancy. 1. Introduction Dicentric chromosomes, which have two centromeres, are a well-known feature of cancer cells, and the genome instability and evolution they induce are highly relevant to cancer biology [1, 2]. Although constitutional dicentric chromosomes are much rarer, in those that have been identified there is little evidence of this instability. Our studies have shown that the mechanisms by which dicentric chromosomes are stabilized include the loss of a centromere from a dicentric chromosome making it secondarily monocentric [3, 4], a previously little known mechanism which may be relatively common in cancer evolution. We review evidence that dicentric chromosomes have a greater role in oncogenesis than is currently acknowledged. During cell division the two centromeres of an unstable dicentric chromosome migrate towards opposite poles at anaphase, causing cycles of breakage and rejoining which create new chromosome arrangements, deletions, and amplifications. This is known as the bridge-fusion-breakage (BFB) cycle [5]. The gene copy number aberrations which are a byproduct of dicentric chromosome instability can create an increased risk of malignancy. Positive selection of these copy number changes can drive clonal evolution [6–10].
Gaucher Disease and Cancer: Concept and Controversy
Francis Y. M. Choy,Tessa N. Campbell
International Journal of Cell Biology , 2011, DOI: 10.1155/2011/150450
Abstract: Gaucher disease is an inherited disorder caused by a deficiency in the lysosomal hydrolase glucocerebrosidase. There is a wide spectrum of clinical presentations, with the most common features being hepatosplenomegaly, skeletal disease, and cytopenia. Gaucher disease has been classified into three broad phenotypes based upon the presence or absence of neurological involvement: Type 1 (nonneuronopathic), Type 2 (acute neuronopathic), and Type 3 (subacute neuronopathic). The two main treatment options include enzyme replacement therapy and substrate reduction therapy. Recently, discussion has escalated around the association of Gaucher disease and cancer, with conflicting reports as to whether Gaucher patients have an increased risk of malignancy. In this review, we present both the concept and controversy surrounding the association of Gaucher disease with cancer. 1. Introduction Gaucher disease is a panethnic autosomal recessive disorder characterized by a heterogeneous set of signs and symptoms caused by the defective hydrolysis of glucocerebroside. A deficiency in the enzyme glucocerebrosidase (glucosylceramidase, acid β-glucosidase) leads to the accumulation of glucocerebroside in the spleen, liver, and bone marrow. The resultant hepatosplenomegaly, haematological changes, and orthopaedic complications are the predominant symptoms [1]. Gaucher disease has been classified into three broad phenotypes. Type 1, the most common form, has no central nervous system involvement. Conversely, patients with Type 2 (acute neuronopathic disease) suffer from an aggressive form that leads to death perinatally or within the first few years of life. In Type 3 (subacute neuronopathic disease), patients show neurodegenerative symptoms but are able to survive through childhood to adulthood [2, 3]. The glucocerebrosidase gene is found on chromosome 1q21-22, consisting of 11 exons encoding a 497-amino-acid protein. A highly homologous pseudogene, located 16?kb downstream, complicates mutation analysis in this region. To date, nearly 300 mutations have been identified in Gaucher’s patients, including point mutations, deletions, insertions, splice site mutations, frame-shift mutations, and recombinant alleles [4–6]. Gaucher disease is the most common lysosomal storage disorder and the first to be successfully treated by enzyme replacement therapy [7]. In 1991, alglucerase (Ceredase, Genzyme Inc.), the placental derivative of glucocerebrosidase was FDA-approved. In 1994, the human recombinant-form imiglucerase (Cerezyme, Genzyme Inc.) received FDA approval. Alglucerase is
Gaucher disease and the synucleinopathies: refining the relationship
Tessa N Campbell, Francis YM Choy
Orphanet Journal of Rare Diseases , 2012, DOI: 10.1186/1750-1172-7-12
Abstract: Gaucher disease (OMIM 230800, 230900, 231000), the most common lysosomal storage disorder, is characterized by a spectrum of signs and symptoms caused by the defective hydrolysis of glucocerebroside. A deficiency in the enzyme glucocerebrosidase (GBA, glucosylceramidase, acid β-glucosidase, EC.3.2.1.45) leads to the accumulation of its glucocerebroside substrate in the liver, spleen, and bone marrow. The predominant symptoms are hepatosplenomegaly, haematological changes, and orthopaedic complications [1,2]. Gaucher disease has been classified into three phenotypes based upon the presence or absence of neurological involvement: Type 1 (non-neuronopathic; most common form), Type 2 (acute neuronopathic) and Type 3 (subacute neuronopathic) [3].The GBA gene, located on chromosome 1q21-22, is comprised of 11 exons encoding a 497 amino acid protein. Presently, nearly 300 mutations have been identified in Gaucher patients, including frame-shift mutations, point mutations, deletions, insertions, splice site mutations, and recombinant alleles [2,4,5]. For the purpose of genotype-phenotype correlations, many of these mutations have been classified as "null," "severe," or "mild" with respect to levels of glucocerebrosidase production. Null mutations, such as c.84dupG (84 GG), do not direct any enzyme production. Severe mutations, such as c.1448T > C (L444P), produce enzyme but, when inherited with a null or another severe mutation, are usually associated with Type 2 or 3 disease. Mild mutations, such as c.1226A > G (N370S), are those that are only associated with Type 1 disease [6].Gaucher disease is the first lysosomal storage disorder to be successfully treated by enzyme replacement therapy [7]. At present, alglucerase (Ceredase?, Genzyme Inc.), imiglucerase (Cerezyme?, Genzyme Inc.), and velaglucerase alfa (VPRIV?, Shire) have been FDA-approved for treatment of Gaucher patients [8,9]. Alternative therapies have also been developed. In 2003, substrate reduction/inhibition th
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