@article{lucovsky_phillips_2009, title={Strain-eliminating chemical bonding self-organizations within intermediate phase (IP) windows in chalcogenide, oxide and nitride non-crystalline bulk glasses and deposited thin film binary, ternary and quaternary alloys}, volume={355}, ISSN={["0022-3093"]}, DOI={10.1016/j.jnoncrysol.2009.04.044}, abstractNote={Transitions into, and out of intermediate phases (IPs) with minimal strain have been identified to date by Boolchand and co-workers, in bulk glasses, primarily by the extraordinary low values of the change in enthalpy, ΔHnr, associated with non-reversible heat flow, and by Lucovsky and coworkers in deposited thin films, and at dielectric–semiconductor interfaces by combining spectrographic characterizations, primarily synchrotron X-ray absorption and X-ray photoemission, and electrical measurements. This paper emphasizes chemical bonding self-organizations that minimize macroscopic strain within the IP windows, and identifies for the first time the necessary and sufficient conditions for IP windows to open, and to close, as a function of changes in the alloy composition. Percolation theory, and in particular competitive and synergistic double percolation provide a quantification of IP window first and second transition compositions that account for many of the experimentally determined IP window threshold transitions and IP window widths identified to date.}, number={37-42}, journal={JOURNAL OF NON-CRYSTALLINE SOLIDS}, author={Lucovsky, Gerald and Phillips, Jim C.}, year={2009}, month={Oct}, pages={1786–1791} }
 @article{lucovsky_phillips_2007, title={Chemical self-organization length scales in non- and nano-crystalline thin films}, volume={51}, ISSN={["1879-2405"]}, DOI={10.1016/j.sse.2007.06.001}, abstractNote={This paper identifies different length scales λs for strain-reducing chemical bonding self-organizations (CBSO) in non-crystalline and nano-crystalline thin films. CBSOs are differentiated spectroscopically, and explained by semi-empirical bond-constraint theory (SE-BCT). Non-crystalline thin film CBSOs are characterized by molecular scale, strain-reducing chemical ordering with λs > 0.6 nm, and extending to at most 1 nm. The non-random bonding results in reduced defect densities that are enabling for device applications. Nano-crystalline transition metal oxide thin films display qualitatively different properties in two distinct nano-scale regimes in which the length scale metric is defined by π-bond coupling between atoms in strings of neighboring primitive unit cells (PUCs): (i) type I with nano-grain dimensions and λs ∼ 2 nm (or <4 PUCs), and (ii) type 2 with nano-grain sizes and λs > 3–4 nm (>6 PUCs). There are also diphasic nano-crystalline/non-crystalline technologically important thin films in which strain percolation is also minimized by CBSOs that combine molecular and PUC scales of order. Representative non-crystalline, nano-crystalline and diphasic nano-crystalline/non-crystalline thin film materials with qualitatively different behaviors and degrees of phase stability/metastability are addressed.}, number={10}, journal={SOLID-STATE ELECTRONICS}, author={Lucovsky, G. and Phillips, J. C.}, year={2007}, month={Oct}, pages={1308–1318} }
 @article{lucovsky_phillips_2007, title={Defect reduction in non-crystalline and nano-crystalline thin films: chemical bonding self-organizations and minimization of macroscopic strain}, volume={9}, number={10}, journal={Journal of Optoelectronics and Advanced Materials}, author={Lucovsky, G. and Phillips, J. C.}, year={2007}, pages={2989–2995} }
 @article{lucovsky_baker_paesler_phillips_thorpe_2007, title={Intermediate phases in binary and ternary alloys. How far can we go with a semi-empirical bond-constraint theory?}, volume={9}, number={10}, journal={Journal of Optoelectronics and Advanced Materials}, author={Lucovsky, G. and Baker, D. A. and Paesler, M. A. and Phillips, J. C. and Thorpe, M. F.}, year={2007}, pages={2979–2988} }
 @article{lucovsky_baker_paesler_phillips_2007, title={Spectroscopic and electrical detection of intermediate phases and chemical bonding self-organizations in (i) dielectric films for semiconductor devices, and (ii) chalcogenide alloys for optical memory devices}, volume={353}, ISSN={["1873-4812"]}, DOI={10.1016/j.jnoncrysol.2007.01.041}, abstractNote={This paper presents a discussion of intermediate phases in thin film materials that have been incorporated into liquid crystal displays, LCDs, and optical memory thin film devices. The formation of intermediate phases in the a-Si3N4:H (a-Si:N:H) alloys used for gate dielectrics in thin film transistors, TFTs, of LCDs, and the a-Ge–Sb–Te (GST) alloys used for read-write optical writing and storage in optical memory discs are qualitatively different than those first addressed by the Boolchand group in Ge–Se bulk glass alloys. In the a-Si:N:H and a-GST thin films, the chemical self-organizations that suppress percolation of strain, involve chemically-ordered bonding arrangements that break bond bending constraints at the four-fold coordinated Si and Ge atoms in a-Si:N:H and a-GST, respectively. In the GST alloys, this results in over-coordinated and under-coordinated atomic constituents, or valence alternation pairs, VAPs, of charged defects. Finally, other technologically important systems in which broken constraints, and/or VAP defects are important in intermediate phase formation include group IVB (Ti, Zr and Hf) Si oxynitride alloys, and hydrogenated amorphous Si (a-Si:H).}, number={18-21}, journal={JOURNAL OF NON-CRYSTALLINE SOLIDS}, author={Lucovsky, G. and Baker, D. A. and Paesler, M. A. and Phillips, J. C.}, year={2007}, month={Jun}, pages={1713–1722} }
 @article{lucovsky_phillips_2004, title={Bond strain and defects at Si-SiO2 and internal dielectric interfaces in high-k gate stacks}, volume={16}, ISSN={["1361-648X"]}, DOI={10.1088/0953-8984/16/44/011}, abstractNote={The performance and reliability of aggressively-scaled field effect transistors are determined in large part by electronically-active defects and defect precursors at the Si–SiO2 and internal SiO2-high-k dielectric interfaces. A crucial aspect of reducing interfacial defects and defect precursors is associated with bond-strain-driven bonding interfacial self-organizations that take place during high temperature annealing in inert ambients. The interfacial self-organizations and intrinsic interface defects are addressed through an extension of bond constraint theory from bulk glasses to interfaces between non-crystalline SiO2 and (i) crystalline Si, and (ii) non-crystalline and crystalline alternative gate dielectric materials.}, number={44}, journal={JOURNAL OF PHYSICS-CONDENSED MATTER}, author={Lucovsky, G and Phillips, JC}, year={2004}, month={Nov}, pages={S5139–S5151} }
 @article{olby_blot_thibaud_phillips_dp o'brien_burr_berg_brown_breen_2004, title={Cerebellar cortical degeneration in adult American Staffordshire Terriers}, volume={18}, ISSN={["1939-1676"]}, DOI={10.1892/0891-6640(2004)18<201:CCDIAA>2.0.CO;2}, abstractNote={Journal of Veterinary Internal MedicineVolume 18, Issue 2 p. 201-208 Open Access Cerebellar Cortical Degeneration in Adult American Staffordshire Terriers Natasha Olby, Corresponding Author Natasha Olby Department of Clinical Sciences, North Carolina State University, Raleigh, NC College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606;e-mail: [email protected].Search for more papers by this authorStephane Blot, Stephane Blot Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJean-Laurent Thibaud, Jean-Laurent Thibaud Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJeff Phillips, Jeff Phillips Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorDennis P. O'Brien, Dennis P. O'Brien Department of Clinical Sciences, University of Missouri, Columbia, MOSearch for more papers by this authorJeanne Burr, Jeanne Burr Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorJason Berg, Jason Berg VCA County Animal Clinic, Yonkers, NYSearch for more papers by this authorTalmage Brown, Talmage Brown Department of Population Health and Pathobiology, North Carolina State University, Raleigh, NCSearch for more papers by this authorMatthew Breen, Matthew Breen Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC.Search for more papers by this author Natasha Olby, Corresponding Author Natasha Olby Department of Clinical Sciences, North Carolina State University, Raleigh, NC College of Veterinary Medicine, North Carolina State University, 4700 Hillsborough Street, Raleigh, NC 27606;e-mail: [email protected].Search for more papers by this authorStephane Blot, Stephane Blot Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJean-Laurent Thibaud, Jean-Laurent Thibaud Ecole Nationale Ve-terinaire d'Alfort, Paris, FranceSearch for more papers by this authorJeff Phillips, Jeff Phillips Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorDennis P. O'Brien, Dennis P. O'Brien Department of Clinical Sciences, University of Missouri, Columbia, MOSearch for more papers by this authorJeanne Burr, Jeanne Burr Department of Clinical Sciences, North Carolina State University, Raleigh, NCSearch for more papers by this authorJason Berg, Jason Berg VCA County Animal Clinic, Yonkers, NYSearch for more papers by this authorTalmage Brown, Talmage Brown Department of Population Health and Pathobiology, North Carolina State University, Raleigh, NCSearch for more papers by this authorMatthew Breen, Matthew Breen Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC.Search for more papers by this author First published: 28 June 2008 https://doi.org/10.1111/j.1939-1676.2004.tb00161.xCitations: 47AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Adult-onset cerebellar cortical degeneration recently has been reported in American Staffordshire Terriers. We describe the clinical and histopathologic features of this disease and examine its mode of inheritance in 63 affected dogs. The age at which neurologic deficits 1st were recognized varied from 18 months to 9 years, with the majority of dogs presented to veterinarians between 4 and 6 years of age. Time from onset of clinical signs to euthanasia varied from 6 months to 6.5 years, with the majority of affected dogs surviving from 2 to 4 years. Initial neurologic findings included stumbling, truncal sway, and ataxia exacerbated by lifting the head up and negotiating stairs. Signs progressed to obvious ataxia characterized by dysmetria, nystagmus, coarse intention tremor, variable loss of menace reaction, marked truncal sway, and falling with transient opisthotonus. With continued progression, dogs became unable to walk without falling repeatedly. Cerebellar atrophy was visible on magnetic resonance images and on gross pathology. Histopathologic findings included marked loss of Purkinje neurons with thinning of the molecular and granular layers and increased cellularity of the cerebellar nuclei. The closest common ancestor of the dogs was born in the 1950s and inheritance was most consistent with an autosomal recessive mode of transmission with a prevalence estimated at 1 in 400 dogs. This inherited disease is comparable to the group of diseases known as spinocerebellar ataxias in humans. Many spinocerebellar ataxias in humans are caused by nucleotide repeats, and this genetic aberration merits investigation as a potential cause of the disease in American Staffordshire Terriers. References 1 de Lahunta A. Abiotrophy in domestic animals: A review. 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Arch Neurol 2002; 59: 623–629. 27 Vuillaume I., Devos D., Schraen-Maschke S., et al. A new locus for spinocerebellar ataxia (SCA21) maps to chromosome 7p21.3-p15.1. Ann Neurol 2002; 52: 666–670. 28 Jardim LB, Silveira I., Pereira ML, et al. A survey of spinocerebellar ataxia in South Brazil–6new caseswith Machado-Joseph disease, SCA7, SCA8, or unidentified disease-causing mutations. J Neurol 2001; 248: 870–876. 29 Zhuchenko O., Bailey J., Bonnen P., et al. Autosomal dominant cerebellar ataxia (SCA6) associated with small polyglutamine expansions in the a1A-voltage dependent calcium channel. Nat Genet 1997; 15: 62–69. 30 Sinke RJ, Ippel EF, Diepstraten CM, et al. Clinical and molecular correlations in spinocerebellar ataxia type 6. Arch Neurol 2001; 58: 1839–1844. 31 Pujana MA, Corral J., Gratacos M., et al. Spinocerebellar ataxias in Spanish patients: Genetic analysis of familial and sporadic cases. Hum Genet 1999; 104: 516–522. 32 Gabsi S., Gouider-Khouja N., Belal S., et al. Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiency. Eur J Neurol 2001; 8: 477–481. 33 Van Swieten JC, Brusse E., de Graaf BM, et al. A mutation in the fibroblast growth factor 14 gene is associated with autosomal dominant cerebellar ataxia. Am J Hum Genet 2003; 77: 191–199. Citing Literature Volume18, Issue2March 2004Pages 201-208 ReferencesRelatedInformation}, number={2}, journal={JOURNAL OF VETERINARY INTERNAL MEDICINE}, author={Olby, N and Blot, S and Thibaud, JL and Phillips, J and DP O'Brien and Burr, J and Berg, J and Brown, T and Breen, M}, year={2004}, pages={201–208} }
 @article{phillips_2002, title={Four novel mutations in the PITX2 gene in patients with Axenfeld-Rieger syndrome}, volume={34}, ISSN={["1423-0259"]}, DOI={10.1159/000065602}, abstractNote={Mutational screening and sequence analysis of the PITX2 gene was performed in four families previously diagnosed with Rieger syndrome. The results of this analysis identified four novel mutations within the coding sequence of PITX2. These mutations were not identified in the sequence of 50 control individuals. Two mutations were found in the homeobox and would be expected to result in nonconservative amino acid changes within the second and third helixes. The remaining two mutations were found in the region downstream of the homeobox and are also predicted to result in missense mutations. In conclusion, mutations within the homeobox sequence and the adjacent coding sequence of PITX2 lead to various Rieger syndrome phenotypes characterized by a high incidence of glaucoma.}, number={5}, journal={OPHTHALMIC RESEARCH}, author={Phillips, JC}, year={2002}, pages={324–326} }