A prototype system for handwritten sub-word recognition: Toward Arabic-manuscript transliteration

A prototype system for the transliteration of diacritics-less Arabic manuscripts at the sub-word or part of Arabic word (PAW) level is developed. The system is able to read sub-words of the input manuscript using a set of skeleton-based features. A variation of the system is also developed which reads archigraphemic Arabic manuscripts, which are dot-less, into archigraphemes transliteration. In order to reduce the complexity of the original highly multiclass problem of sub-word recognition, it is redefined into a set of binary descriptor classifiers. The outputs of trained binary classifiers are combined to generate the sequence of sub-word letters. SVMs are used to learn the binary classifiers. Two specific Arabic databases have been developed to train and test the system. One of them is a database of the Naskh style. The initial results are promising. The systems could be trained on other scripts found in Arabic manuscripts.Comment: 8 pages, 7 figures, 6 table

Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth

Prostate cancer is the most common cancer in men and it is estimated that over 350,000 men worldwide die of prostate cancer every year. There remains an unmet clinical need to improve how clinically significant prostate cancer is diagnosed and develop new treatments for advanced disease. Aberrant glycosylation is a hallmark of cancer implicated in tumour growth, metastasis, and immune evasion. One of the key drivers of aberrant glycosylation is the dysregulated expression of glycosylation enzymes within the cancer cell. Here, we demonstrate using multiple independent clinical cohorts that the glycosyltransferase enzyme GALNT7 is upregulated in prostate cancer tissue. We show GALNT7 can identify men with prostate cancer, using urine and blood samples, with improved diagnostic accuracy than serum PSA alone. We also show that GALNT7 levels remain high in progression to castrate-resistant disease, and using in vitro and in vivo models, reveal that GALNT7 promotes prostate tumour growth. Mechanistically, GALNT7 can modify O-glycosylation in prostate cancer cells and correlates with cell cycle and immune signalling pathways. Our study provides a new biomarker to aid the diagnosis of clinically significant disease and cements GALNT7-mediated O-glycosylation as an important driver of prostate cancer progression

Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth.

Prostate cancer is the most common cancer in men and it is estimated that over 350,000 men worldwide die of prostate cancer every year. There remains an unmet clinical need to improve how clinically significant prostate cancer is diagnosed and develop new treatments for advanced disease. Aberrant glycosylation is a hallmark of cancer implicated in tumour growth, metastasis, and immune evasion. One of the key drivers of aberrant glycosylation is the dysregulated expression of glycosylation enzymes within the cancer cell. Here, we demonstrate using multiple independent clinical cohorts that the glycosyltransferase enzyme GALNT7 is upregulated in prostate cancer tissue. We show GALNT7 can identify men with prostate cancer, using urine and blood samples, with improved diagnostic accuracy than serum PSA alone. We also show that GALNT7 levels remain high in progression to castrate-resistant disease, and using in vitro and in vivo models, reveal that GALNT7 promotes prostate tumour growth. Mechanistically, GALNT7 can modify O-glycosylation in prostate cancer cells and correlates with cell cycle and immune signalling pathways. Our study provides a new biomarker to aid the diagnosis of clinically significant disease and cements GALNT7-mediated O-glycosylation as an important driver of prostate cancer progression

Upregulation of GALNT7 in prostate cancer modifies O-glycosylation and promotes tumour growth

Prostate cancer is the most common cancer in men and it is estimated that over 350,000 men worldwide die of prostate cancer every year. There remains an unmet clinical need to improve how clinically significant prostate cancer is diagnosed and develop new treatments for advanced disease. Aberrant glycosylation is a hallmark of cancer implicated in tumour growth, metastasis, and immune evasion. One of the key drivers of aberrant glycosylation is the dysregulated expression of glycosylation enzymes within the cancer cell. Here, we demonstrate using multiple independent clinical cohorts that the glycosyltransferase enzyme GALNT7 is upregulated in prostate cancer tissue. We show GALNT7 can identify men with prostate cancer, using urine and blood samples, with improved diagnostic accuracy than serum PSA alone. We also show that GALNT7 levels remain high in progression to castrate-resistant disease, and using in vitro and in vivo models, reveal that GALNT7 promotes prostate tumour growth. Mechanistically, GALNT7 can modify O-glycosylation in prostate cancer cells and correlates with cell cycle and immune signalling pathways. Our study provides a new biomarker to aid the diagnosis of clinically significant disease and cements GALNT7-mediated O-glycosylation as an important driver of prostate cancer progression

Mark and Mike Wisnovsky Interview

This interview is an oral history conducted by Linfield College archivist Rachael Cristine Woody with Mark and Mike Wisnovsky of Valley View Winery. The interview took place at Valley View Winery on August 1, 2013 and covered topics including the Wisnovskys\u27 late father, Frank, different marketing strategies, and the necessity of continuous experimentation in the vineyard and winery. The interview offers extensive commentary on the necessity to choose and adapt to the market—in Valley View Winery\u27s case, making and selling wine for the local consumers. The Wisnovsky brothers provide examples of how they\u27ve tailored their choices to that strategy, including focusing on local sources, sustainable practices, and choosing to produce fruit-forward wines. For a shareable version of this video, please see the interview on YouTube

Notes on Avicenna's Concept of Thingness (ŠAY’IYYA)

In an article published in 1984, Jean Jolivet suggested that the origins of Avicenna’s distinction between essence and existence lay not in ancient Greek philosophy, as has generally been supposed, but in early Islamic dogmatic theology (kal®m), and specifically in the ninth- and tenth-century-CE debates between Muslim dogmatists (mutakallim‚n) over how the terms “thing” (say’) and “existent” (mawgud) relate to each other. The present article provides evidence that gives qualified support to Jolivet’s hypothesis.[...

Investigating the Cellular Effects of Mitochondrial DNA Damage Using Targeted Chemical Probes

Mitochondria are compartments within eukaryotic cells that produce energy to power cellular metabolism. Uniquely amongst mammalian organelles, mitochondria contain a small amount of their own genetic material (mtDNA), the proper maintenance and expression of which is essential for mitochondrial function. Mitochondrial DNA damage has been linked to several pathophysiological processes, but the cellular effects of mtDNA damage remain poorly understood. In order to better understand mtDNA damage, our group has pioneered the development of selective mitochondria-targeted DNA damaging agents using positively charged, hydrophobic delivery vectors known as mitochondria-penetrating peptides (MPPs). In my first study, an analogue of the commonly used anticancer drug cisplatin was conjugated to an MPP, yielding a mitochondria-targeted platinum DNA-damaging agent (mtPt) that induced specific damage to mtDNA. Using mtPt, I showed that selective mtDNA platinum damage induced apoptotic cell death associated with reactive oxygen species production, demonstrating that mtDNA damage is sufficient to mediate the cytotoxic activity of a platinum drug. In another work, I aimed to use mitochondria-targeted DNA damaging agents in a screen to characterize novel factors in mtDNA replication and repair. By knocking down expression of known DNA repair genes, and monitoring synergistic effects of gene knockdown on the activity of an mtDNA-oxidizing agent, I identified a series of genes with novel roles in mtDNA repair and replication. Included amongst these hits was DNA Polymerase θ (Polθ), a novel mtDNA polymerase. In a further study, I found that Polθ plays an essential role in facilitating mtDNA replication under conditions of oxidative stress. Finally, I conducted a genome-wide CRISPR screen to comprehensively identify genes whose knockout sensitizes cells to mitochondria-localized DNA damage. The hits of this screen were heavily enriched for genes involved in mitochondrial translation, implying the importance of mitochondrial protein synthesis in mediating an adaptive response to mtDNA damage. These studies demonstrate the application of mitochondria-targeted DNA damaging agents to the study of a wide range of significant areas in mitochondrial biology. Going forward, my thesis work shows mtDNA-damaging chemical probes to be essential tools for achieving better understanding of mtDNA damage in health and disease.Ph.D.2018-12-19 00:00:0