Thesis (M.S.)--West Virginia University, 2003. / Title from document title page. Document formatted into pages; contains xiv, 158 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 141).

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Traditionally ultrafine fibers below 1 dpf are produced by extrusion followed by mechanical drawing. A modified melt spinning apparatus with high-speed air nozzle was designed and fabricated to produce continuous polypropylene filaments by cold air drawing only. With this setup, the fiber is quenched and simultaneously attenuated by a symmetric cold air jet. Since the formation of fiber structure is highly dependent on the processing conditions, the new process will provide a unique operation window to study fiber attenuation and structural formation under high-speed cold air drawing. Based on computational fluid dynamics simulation results, a parametric study was carried out under different process conditions which include processing temperature, air velocity and polymer volume flow rate. Effects of changes in processing variables on the fiber diameter, molecular orientation, crystallinity, tensile strength and other properties were studied. Furthermore, a theoretical model was developed to analyze the non-isothermal fiber attenuation mechanisms. The new knowledge obtained in this study would likely yield a new process for producing innovative fiber products.

published_or_final_version / Mechanical Engineering / Doctoral / Doctor of Philosophy

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Pleural solitary fibrous tumours (pSFTs) are uncommon soft tissue tumours of the pleura. that may recur and contribute to the patients’ demise. We analyzed a group of benign and malignant pSFTs for copy number alterations and for common mutations in oncogenes and tumour-suppressor genes. Malignant SFTs demonstrated more copy number alterations, especially 8q (c-myc) gain, 10q (include PTEN) loss, and 13q (Rb1) loss. Mutations were rare in this limited study.

Pleural solitary fibrous tumours (pSFTs) are uncommon soft tissue tumours of the pleura. that may recur and contribute to the patients’ demise. We analyzed a group of benign and malignant pSFTs for copy number alterations and for common mutations in oncogenes and tumour-suppressor genes. Malignant SFTs demonstrated more copy number alterations, especially 8q (c-myc) gain, 10q (include PTEN) loss, and 13q (Rb1) loss. Mutations were rare in this limited study.

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