56 research outputs found
Digital transformations and the archival nature of surrogates
Large-scale digitization is generating extraordinary collections of visual
and textual surrogates, potentially endowed with transcendent long-term cultural
and research values. Understanding the nature of digital surrogacy is a substantial
intellectual opportunity for archival science and the digital humanities, because of
the increasing independence of surrogate collections from their archival sources.
The paper presents an argument that one of the most significant requirements for the
long-term access to collections of digital surrogates is to treat digital surrogates as
archival records that embody traces of their fluid lifecycles and therefore are worthy
of management and preservation as archives. It advances a theory of the archival
nature of surrogacy founded on longstanding notions of archival quality, the traces
of their source and the conditions of their creation, and the functional ββwork of the
archive.ββ The paper presents evidence supporting a ββsecondary provenanceββ
derived from re-digitization, re-ingestion of multiple versions, and de facto
replacement of the original sources. The design of the underlying research that
motivates the paper and summary findings are reported separately. The research has
been supported generously by the US Institute of Museum and Library Services.Institute for Museum and Library ServicesPeer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111825/1/J26 Conway Digital Transformations 2014-pers.pdfDescription of J26 Conway Digital Transformations 2014-pers.pdf : Main articl
Mitochondrial DNA Haplogroup Analysis Reveals no Association between the Common Genetic Lineages and Prostate Cancer in the Korean Population
Mitochondrial DNA (mtDNA) variation has recently been suggested to have an association with various cancers, including prostate cancer risk, in human populations. Since mtDNA is haploid and lacks recombination, specific mutations in the mtDNA genome associated with human diseases arise and remain in particular genetic backgrounds referred to as haplogroups. To assess the possible contribution of mtDNA haplogroup-specific mutations to the occurrence of prostate cancer, we have therefore performed a population-based study of a prostate cancer cases and corresponding controls from the Korean population. No statistically significant difference in the distribution of mtDNA haplogroup frequencies was observed between the case and control groups of Koreans. Thus, our data imply that specific mtDNA mutations/lineages did not appear to have a significant effect on a predisposition to prostate cancer in the Korean population, although larger sample sizes are necessary to validate our results
Foetal haemoglobin-blood cells (F-cells) as a feature of embryonic tumours (blastomas)
Tumour markers are important in the diagnosis and monitoring of many tumours. This study tested the hypothesis that an oncofoetal protein, foetal haemoglobin (HbF) is a potential tumour marker in embryonic tumours, useful for management. An immunohistochemical investigation of HbF blood cell (Fc) distribution was carried out in tumours and in bone marrow samples from 83 children and 13 adults with various embryonic tumours (blastomas), and in bone marrow samples of 24 leukaemia patients. In the three, main blastoma types, nephroblastoma (Wilms' tumour), neuroblastoma and retinoblastoma, where all the patients, except two, were children, around 80% of the tumour samples had Fc within proliferating blood vessels and spaces between tumour cells. In parallel, clusters of Fc, mostly F-erythroblasts (Feb), were distributed in the bone marrow of some of those patients and in the bone marrow of 79% of the leukaemia patients. Foetal haemoglobin, as well as being a potential prognostic cancer marker, is a potential indicator of DNA hypomethylation implicated in the development of these tumours, as well as in others previously noted for the presence of HbF
Lack of Association between Y-Chromosomal Haplogroups and Prostate Cancer in the Korean Population
The Y chromosome has recently been suggested to have an association with prostate cancer risk in human populations. Since this chromosome is haploid and lacks recombination over most of its length, haplotypes constructed from binary markers throughout the chromosome can be used for association studies. To assess the possible Y-chromosomal contribution to prostate cancer risk, we have therefore analyzed 14 Y-chromosomal binary markers in 106 prostate cancer cases and 110 controls from the Korean population. In contrast to previous findings in the Japanese population, no statistically significant difference in the distribution of Y-chromosomal haplogroup frequencies was observed between the case and control groups of Koreans. Thus, our data imply that the previously reported associations between Y-chromosomal lineages and a predisposition to, or protection against, prostate cancer might be explained by statistical fluctuations, or by genetic effects that are seen only in some environments
Risk factors and clinical outcomes of acute myeloid leukaemia with central nervous system involvement in adults
Epigenetic regulation of prostate cancer
Prostate cancer is a commonly diagnosed cancer in men and a leading cause of cancer deaths. Whilst the underlying mechanisms leading to prostate cancer are still to be determined, it is evident that both genetic and epigenetic changes contribute to the development and progression of this disease. Epigenetic changes involving DNA hypo- and hypermethylation, altered histone modifications and more recently changes in microRNA expression have been detected at a range of genes associated with prostate cancer. Furthermore, there is evidence that particular epigenetic changes are associated with different stages of the disease. Whilst early detection can lead to effective treatment, and androgen deprivation therapy has a high response rate, many tumours develop towards hormone-refractory prostate cancer, for which there is no successful treatment. Reliable markers for early detection and more effective treatment strategies are, therefore, needed. Consequently, there is a considerable interest in the potential of epigenetic changes as markers or targets for therapy in prostate cancer. Epigenetic modifiers that demethylate DNA and inhibit histone deacetylases have recently been explored to reactivate silenced gene expression in cancer. However, further understanding of the mechanisms and the effects of chromatin modulation in prostate cancer are required. In this review, we examine the current literature on epigenetic changes associated with prostate cancer and discuss the potential use of epigenetic modifiers for treatment of this disease
A novel method for banking stem cells from human exfoliated deciduous teeth: lentiviral TERT immortalization and phenotypical analysis
Prenatal diagnosis of a de novo tetrasomy 15q24.3β25.3: Case report and literature review
Microdissection, DOP-PCR, and comparative genomic hybridization of paraffin-embedded familial prostate cancers
Numerical chromosomal aberrations in prostate cancer: correlation with morphology and cell kinetics
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