31 research outputs found
Recommended from our members
Traction and Troublesome Learning: A Praxis of Stuck Places For Course-Embedded Tutoring
While many composition theorists have tackled the question of how to encourage transfer beyond their introductory writing classes (see Perkins and Saloman; Wardle; Beaufort; Fallon, Lahar, and Susman; Blaauw-Hara), we also need to consider how embedded peer tutors develop their practices as they enter into disciplinary tutoring and, over time, gain traction while tutoring in different disciplines. Whereas in a first-year writing course we might gear our pedagogy to students’ development over a single semester but never fully know how they will transfer their learning into new disciplinary contexts, in an embedded tutoring program we mentor tutors who must transfer their learning and gain traction in new disciplines several different times during their semesters with us. Like Dara Rossman Regaignon, we define “traction” here as the process of engaging rigorously and in authentic ways, rather than passing smoothly over, the difficult analytic and rhetorical frameworks available in all disciplinary learning environments (121-22). We think that successful tutoring in an embedded tutoring program depends on such an engaged learning process. Not surprisingly, however, the experience of moving from class to class and gaining traction in the new one rarely happens smoothly for students or tutors. Instead, both frequently struggle as learning and practice become “troublesome,” and they get “stuck.” Building from the work of Jan H. F. Meyer and Ray Land on “troublesome knowledge” and Leslie Gourlay on “threshold practices,” we investigate how tutor development and student learning in an embedded tutoring program can be understood and cultivated in relation to the idea of liminality that shapes their paradigm for learning. In this context, we offer a rationale for and an analysis of “a praxis of stuck places” for tutor development and student learning in an embedded tutoring program (Lather qtd. in Meyer and Land 379).University Writing Cente
Sigmoid Neural Transfer Function Realised by Percolation
An experiment using the phenomenon of percolation has been conducted to demonstrate the implementation of neural functionality (summing and sigmoid transfer). A simple analog approximation to digital percolation is implemented. The device consists of a piece of amorphous silicon with stochastic bit-stream optical inputs, in which a current percolating from one end to the other defines the neuron output, also in the form of a stochastic bit stream. Preliminary experimental results are presented
Plasmodium knowlesi transmission:integrating quantitative approaches from epidemiology and ecology to understand malaria as a zoonosis
The public health threat posed by zoonotic Plasmodium knowlesi appears to be growing: it is increasingly reported across South East Asia, and is the leading cause of malaria in Malaysian Borneo. Plasmodium knowlesi threatens progress towards malaria elimination as aspects of its transmission, such as spillover from wildlife reservoirs and reliance on outdoor-biting vectors, may limit the effectiveness of conventional methods of malaria control. The development of new quantitative approaches that address the ecological complexity of P. knowlesi, particularly through a focus on its primary reservoir hosts, will be required to control it. Here, we review what is known about P. knowlesi transmission, identify key knowledge gaps in the context of current approaches to transmission modelling, and discuss the integration of these approaches with clinical parasitology and geostatistical analysis. We highlight the need to incorporate the influences of fine-scale spatial variation, rapid changes to the landscape, and reservoir population and transmission dynamics. The proposed integrated approach would address the unique challenges posed by malaria as a zoonosis, aid the identification of transmission hotspots, provide insight into the mechanistic links between incidence and land use change and support the design of appropriate interventions
Cytogenetics of human malignant melanoma
There has been a tremendous recent resurgence of interest in examining chromosomal abnormalities in human cancers (particularly solid tumors). This interest has been stimulated by the molecular examination of recurring chromosome abnormalities, and the recognition that they may pinpoint the location of growth regulatory sequences (e.g. cellular oncogenes). This finding coupled with the clear recognition that specific chromosome abnormalities can also have important diagnostic and prognostic implications, have caused this avenue of research to expand at a significant rate. The following brief review will summarize the current state of knowledge regarding recurring chromosome abnormalities in human malignant melanoma. A discussion of chromosome changes in pre-malignant skin lesions, primary melanoma, and metastatic melanoma is described. Brief descriptions of the potential clinical utility, and biologic relevance of chromosome abnormalities in this disorder are also discussed.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44500/1/10555_2004_Article_BF00049408.pd
PTEN/MMAC1 expression in melanoma resection specimens
PTEN/MMAC1, a tumour suppressor gene located on chromosome 10q23.3, has been found to be deleted in several types of human malignancies. As the chromosomal region 10q22-qter commonly is affected by losses in melanomas, we addressed this gene as tumour suppressor candidate in melanomas. Investigating PTEN/MMAC1 expression at mRNA level by semi-quantitative reverse transcription-polymerase chain reaction, we did not find a statistically significant down-regulation in melanoma resection specimens in comparison to acquired melanocytic nevi from which melanomas quite often are known to arise. Upon immunohistochemistry, PTEN/MMAC1 protein expression in melanomas was not lost. Sequencing the PTEN/MMAC1 cDNAs in 26 melanoma resection specimens (21 primary melanomas, five metastases), we detected three point mutations and two nucleotide deletions which did not represent genetic polymorphisms. With respect to the predicted protein sequences, all three point mutations were silent whereas the two frame shifts at the extreme C-terminus resulted in a loss of the putative PDZ-targeting consensus sequence. As loss of this motif possibly impairs localization and function of PTEN/MMAC1 in the two corresponding primary tumours, alterations of this tumour suppressor protein may participate in some melanomas
Refined physical map of the human PAX2/HOX11/NFKB2 cancer gene region at 10q24 and relocalization of the HPV6AI1 viral integration site to 14q13.3-q21.1
BACKGROUND: Chromosome band 10q24 is a gene-rich domain and host to a number of cancer, developmental, and neurological genes. Recurring translocations, deletions and mutations involving this chromosome band have been observed in different human cancers and other disease conditions, but the precise identification of breakpoint sites, and detailed characterization of the genetic basis and mechanisms which underlie many of these rearrangements has yet to be resolved. Towards this end it is vital to establish a definitive genetic map of this region, which to date has shown considerable volatility through time in published works of scientific journals, within different builds of the same international genomic database, and across the differently constructed databases. RESULTS: Using a combination of chromosome and interphase fluorescent in situ hybridization (FISH), BAC end-sequencing and genomic database analysis we present a physical map showing that the order and chromosomal orientation of selected genes within 10q24 is CEN-CYP2C9-PAX2-HOX11-NFKB2-TEL. Our analysis has resolved the orientation of an otherwise dynamically evolving assembly of larger contigs upstream of this region, and in so doing verifies the order and orientation of a further 9 cancer-related genes and GOT1. This study further shows that the previously reported human papillomavirus type 6a DNA integration site HPV6AI1 does not map to 10q24, but that it maps at the interface of chromosome bands 14q13.3-q21.1. CONCLUSIONS: This revised map will allow more precise localization of chromosome rearrangements involving chromosome band 10q24, and will serve as a useful baseline to better understand the molecular aetiology of chromosomal instability in this region. In particular, the relocation of HPV6AI1 is important to report because this HPV6a integration site, originally isolated from a tonsillar carcinoma, was shown to be rearranged in other HPV6a-related malignancies, including 2 of 25 genital condylomas, and 2 of 7 head and neck tumors tested. Our finding shifts the focus of this genomic interest from 10q24 to the chromosome 14 site
Analysis of the 10q23 chromosomal region and the PTEN gene in human sporadic breast carcinoma
We examined a panel of sporadic breast carcinomas for loss of heterozygosity (LOH) in a 10-cM interval on chromosome 10 known to encompass the PTEN gene. We detected allele loss in 27 of 70 breast tumour DNAs. Fifteen of these showed loss limited to a subregion of the area studied. The most commonly deleted region was flanked by D10S215 and D10S541 and encompasses the PTEN locus. We used a combination of denaturing gradient gel electrophoresis and single-strand conformation polymorphism analyses to investigate the presence of PTEN mutations in tumours with LOH in this region. We did not detect mutations of PTEN in any of these tumours. Our data show that, in sporadic breast carcinoma, loss of heterozygosity of the PTEN locus is frequent, but mutation of PTEN is not. These results are consistent with loss of another unidentified tumour suppressor in this region in sporadic breast carcinoma. © 1999 Cancer Research Campaig
Direct Fabrication of Microlenses on Arrays of Optoelectronic Semiconductor Devices
No abstract available