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1. On the global solvability of porous media equations with general (spatially dependent) advection terms

Author

Diehl, N. M. L., Fabris, L., and Zingano, P. R.

Subjects
Mathematics - Analysis of PDEs, 35K65 (primary), 35A01, 35K15
Abstract

We show that advection-diffusion equations with porous media type diffusion and integrable initial data are globally solvable under very mild conditions. Some generalizations and related results are also given., Comment: 7 pages, 2 eps figures. This is a quick communication of an important global existence result that is valid for a broad class of PME type equations

Published
2018

20. Population-specific frequencies for LRRK2 susceptibility variants in the Genetic Epidemiology of Parkinson's Disease (GEO-PD) Consortium

Author

Heckman, M. G., Soto Ortolaza, A. I., Aasly, J. O., Abahuni, N., Annesi, G., Bacon, J. A., Bardien, S., Bozi, M., Brice, A., Brighina, L., Carr, J., Chartier Harlin, M., Dardiotis, E., Dickson, D. W., Diehl, N. N., Elbaz, A., Ferrarese, C., Fiske, B., Gibson, J. M., Gibson, R., Hadjigeorgiou, G. M., Hattori, N., J. P. A., Boczarska Jedynak, M., Jasinska Myga, B., Jeon, B. S., Kim, Y. J., Klein, C., Kruger, R., Kyratzi, E., Lesage, S., Lin, C., Lynch, T., Maraganore, D. M., Mellick, G. D., Mutez, E., Nilsson, C., Opala, G., Park, S. S., Petrucci, S., Puschmann, A., Quattrone, A., Sharma, M., Silburn, P. A., Sohn, Y. H., Stefanis, L., Tadic, V., Theuns, J., Tomiyama, H., Uitti, R. J., Valente, Enza Maria, Broeckhoven, C. V., S. v., De, Vassilatis, D. K., Vilariño Güell, C., White, L. R., Wirdefeldt, K., Wszolek, Z. K., Wu, R., Hentati, F., Farrer, M. J., Ross, O. A., G. E., Of, Heckman, M, Soto Ortolaza, A, Aasly, J, Abahuni, N, Annesi, G, Bacon, J, Bardien, S, Bozi, M, Brice, A, Brighina, L, Carr, J, Chartier Harlin, M, Dardiotis, E, Dickson, D, Diehl, N, Elbaz, A, Ferrarese, C, Fiske, B, Gibson, J, Gibson, R, Hadjigeorgiou, G, Hattori, N, Ioannidis, J, Boczarska Jedynak, M, Jasinska Myga, B, Jeon, B, Kim, Y, Klein, C, Kruger, R, Kyratzi, E, Lesage, S, Lin, C, Lynch, T, Maraganore, D, Mellick, G, Mutez, E, Nilsson, C, Opala, G, Park, S, Petrucci, S, Puschmann, A, Quattrone, A, Sharma, M, Silburn, P, Sohn, Y, Stefanis, L, Tadic, V, Theuns, J, Tomiyama, H, Uitti, R, Valente, E, Van Broeckhoven, C, van de Loo, S, Vassilatis, D, Vilariño Güell, C, White, L, Wirdefeldt, K, Wszolek, Z, Wu, R, Hentati, F, Farrer, M, and Ross, O

Subjects
Molecular Epidemiology, Genotype, Parkinson's disease, LRRK2, Parkinson Disease, Protein Serine-Threonine Kinases, association study, Leucine-Rich Repeat Serine-Threonine Protein Kinase-2, Protein-Serine-Threonine Kinases, Polymorphism, Single Nucleotide, genetics [Protein-Serine-Threonine Kinases], Article, Genetics, Population, Gene Frequency, Haplotypes, genetics [Parkinson Disease], Humans, genetics, lrrk2, parkinson's disease, genetic association studies, population, genotype, haplotypes, hHumans, leucine-rich repeat serine-threonine protein kinase-2, molecular epidemiology, parkinson disease, polymorphism, single nucleotide, protein-serine-threonine kinases, gene frequency, genetic predisposition to disease, Genetic Predisposition to Disease, ddc:610, epidemiology [Parkinson Disease], LRRK2 protein, human, genetic, Genetic Association Studies
Abstract

Variants within the leucine-rich repeat kinase 2 gene are recognized as the most frequent genetic cause of Parkinson's disease. Leucine-rich repeat kinase 2 variation related to disease susceptibility displays many features that reflect the nature of complex, late-onset sporadic disorders like Parkinson's disease.The Genetic Epidemiology of Parkinson's Disease Consortium recently performed the largest genetic association study for variants in the leucine-rich repeat kinase 2 gene across 23 different sites in 15 countries.Herein, we detail the allele frequencies for the novel risk factors (p.A419V and p.M1646T) and the protective haplotype (p.N551K-R1398H-K1423K) nominated in the original publication. Simple population allele frequencies not only can provide insight into the clinical relevance of specific variants but also can help genetically define patient groups.Establishing individual patient-based genomic susceptibility profiles that incorporate both risk factors and protective factors will determine future diagnostic and treatment strategies.

Published
2013

21. Partielle Rotatorenmanschettenrupturen: Diagnostische Wertigkeit der MRT-Untersuchung sowie der klinischen Untersuchung

Author

Brockmeyer, M, Diehl, N, Schmitt, C, Mosser, P, Kohn, D, and Lorbach, O

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

Fragestellung: Aussagekraft der klinischen und kernspintomographischen Befunde hinsichtlich der Detektion einer Partialläsion der Rotatorenmanschette (RM) Methodik: Retrospektive Analyse von 334 Schulterarthroskopien von Anfang 2010 bis Ende 2012. Der präoperative klinische Untersuchungsbefund,[for full text, please go to the a.m. URL], Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2014)

Published
2014
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23. LRRK2 exonic variants and risk of multiple system atrophy

Author

Heckman, M. G., primary, Schottlaender, L., additional, Soto-Ortolaza, A. I., additional, Diehl, N. N., additional, Rayaprolu, S., additional, Ogaki, K., additional, Fujioka, S., additional, Murray, M. E., additional, Cheshire, W. P., additional, Uitti, R. J., additional, Wszolek, Z. K., additional, Farrer, M. J., additional, Sailer, A., additional, Singleton, A. B., additional, Chinnery, P. F., additional, Keogh, M. J., additional, Gentleman, S. M., additional, Holton, J. L., additional, Aoife, K., additional, Mann, D. M. A., additional, Al-Sarraj, S., additional, Troakes, C., additional, Dickson, D. W., additional, Houlden, H., additional, and Ross, O. A., additional

Published
2014
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24. Population-specific frequencies for LRRK2 susceptibility variants in the genetic epidemiology of Parkinson's disease (GEO-PD) consortium

Author

Heckman, M, Soto Ortolaza, A, Aasly, J, Abahuni, N, Annesi, G, Bacon, J, Bardien, S, Bozi, M, Brice, A, Brighina, L, Carr, J, Chartier Harlin, M, Dardiotis, E, Dickson, D, Diehl, N, Elbaz, A, Ferrarese, C, Fiske, B, Gibson, J, Gibson, R, Hadjigeorgiou, G, Hattori, N, Ioannidis, J, Boczarska Jedynak, M, Jasinska Myga, B, Jeon, B, Kim, Y, Klein, C, Kruger, R, Kyratzi, E, Lesage, S, Lin, C, Lynch, T, Maraganore, D, Mellick, G, Mutez, E, Nilsson, C, Opala, G, Park, S, Petrucci, S, Puschmann, A, Quattrone, A, Sharma, M, Silburn, P, Sohn, Y, Stefanis, L, Tadic, V, Theuns, J, Tomiyama, H, Uitti, R, Valente, E, Van Broeckhoven, C, van de Loo, S, Vassilatis, D, Vilariño Güell, C, White, L, Wirdefeldt, K, Wszolek, Z, Wu, R, Hentati, F, Farrer, M, Ross, O, Heckman, MG, Soto Ortolaza, AI, Aasly, JO, Bacon, JA, Dickson, DW, Diehl, NN, Gibson, JM, Hadjigeorgiou, GM, Ioannidis, JPA, Jeon, BS, Kim, YJ, Maraganore, DM, Mellick, GD, Park, SS, Silburn, PA, Sohn, YH, Uitti, RJ, Valente, EM, Vassilatis, DK, White, LR, Wszolek, ZK, Farrer, MJ, Ross, OA, FERRARESE, CARLO, Heckman, M, Soto Ortolaza, A, Aasly, J, Abahuni, N, Annesi, G, Bacon, J, Bardien, S, Bozi, M, Brice, A, Brighina, L, Carr, J, Chartier Harlin, M, Dardiotis, E, Dickson, D, Diehl, N, Elbaz, A, Ferrarese, C, Fiske, B, Gibson, J, Gibson, R, Hadjigeorgiou, G, Hattori, N, Ioannidis, J, Boczarska Jedynak, M, Jasinska Myga, B, Jeon, B, Kim, Y, Klein, C, Kruger, R, Kyratzi, E, Lesage, S, Lin, C, Lynch, T, Maraganore, D, Mellick, G, Mutez, E, Nilsson, C, Opala, G, Park, S, Petrucci, S, Puschmann, A, Quattrone, A, Sharma, M, Silburn, P, Sohn, Y, Stefanis, L, Tadic, V, Theuns, J, Tomiyama, H, Uitti, R, Valente, E, Van Broeckhoven, C, van de Loo, S, Vassilatis, D, Vilariño Güell, C, White, L, Wirdefeldt, K, Wszolek, Z, Wu, R, Hentati, F, Farrer, M, Ross, O, Heckman, MG, Soto Ortolaza, AI, Aasly, JO, Bacon, JA, Dickson, DW, Diehl, NN, Gibson, JM, Hadjigeorgiou, GM, Ioannidis, JPA, Jeon, BS, Kim, YJ, Maraganore, DM, Mellick, GD, Park, SS, Silburn, PA, Sohn, YH, Uitti, RJ, Valente, EM, Vassilatis, DK, White, LR, Wszolek, ZK, Farrer, MJ, Ross, OA, and FERRARESE, CARLO

Abstract

Variants within the leucine-rich repeat kinase 2 gene are recognized as the most frequent genetic cause of Parkinson's disease. Leucine-rich repeat kinase 2 variation related to disease susceptibility displays many features that reflect the nature of complex, late-onset sporadic disorders like Parkinson's disease.

Published
2013

25. Association of LRRK2 exonic variants with susceptibility to Parkinson's disease: a case-control study

Author

Ross, O, Soto Ortolaza, A, Heckman, M, Aasly, J, Abahuni, N, Annesi, G, Bacon, J, Bardien, S, Bozi, M, Brice, A, Brighina, L, Van Broeckhoven, C, Carr, J, Chartier Harlin, M, Dardiotis, E, Dickson, D, Diehl, N, Elbaz, A, Ferrarese, C, Ferraris, A, Fiske, B, Gibson, J, Gibson, R, Hadjigeorgiou, G, Hattori, N, Ioannidis, J, Jasinska Myga, B, Jeon, B, Kim, Y, Klein, C, Kruger, R, Kyratzi, E, Lesage, S, Lin, C, Lynch, T, Maraganore, D, Mellick, G, Mutez, E, Nilsson, C, Opala, G, Park, S, Puschmann, A, Quattrone, A, Sharma, M, Silburn, P, Sohn, Y, Stefanis, L, Tadic, V, Theuns, J, Tomiyama, H, Uitti, R, Valente, E, van de Loo, S, Vassilatis, D, Vilariño Güell, C, White, L, Wirdefeldt, K, Wszolek, Z, Wu, R, Farrer, M, FERRARESE, CARLO, Farrer, M., Ross, O, Soto Ortolaza, A, Heckman, M, Aasly, J, Abahuni, N, Annesi, G, Bacon, J, Bardien, S, Bozi, M, Brice, A, Brighina, L, Van Broeckhoven, C, Carr, J, Chartier Harlin, M, Dardiotis, E, Dickson, D, Diehl, N, Elbaz, A, Ferrarese, C, Ferraris, A, Fiske, B, Gibson, J, Gibson, R, Hadjigeorgiou, G, Hattori, N, Ioannidis, J, Jasinska Myga, B, Jeon, B, Kim, Y, Klein, C, Kruger, R, Kyratzi, E, Lesage, S, Lin, C, Lynch, T, Maraganore, D, Mellick, G, Mutez, E, Nilsson, C, Opala, G, Park, S, Puschmann, A, Quattrone, A, Sharma, M, Silburn, P, Sohn, Y, Stefanis, L, Tadic, V, Theuns, J, Tomiyama, H, Uitti, R, Valente, E, van de Loo, S, Vassilatis, D, Vilariño Güell, C, White, L, Wirdefeldt, K, Wszolek, Z, Wu, R, Farrer, M, FERRARESE, CARLO, and Farrer, M.

Abstract

Background The leucine-rich repeat kinase 2 gene (LRRK2) harbours highly penetrant mutations that are linked to familial parkinsonism. However, the extent of its polymorphic variability in relation to risk of Parkinson's disease (PD) has not been assessed systematically. We therefore assessed the frequency of LRRK2 exonic variants in individuals with and without PD, to investigate the role of the variants in PD susceptibility. Methods LRRK2 was genotyped in patients with PD and controls from three series (white, Asian, and Arab-Berber) from sites participating in the Genetic Epidemiology of Parkinson's Disease Consortium. Genotyping was done for exonic variants of LRRK2 that were identified through searches of literature and the personal communications of consortium members. Associations with PD were assessed by use of logistic regression models. For variants that had a minor allele frequency of 0.5% or greater, single variant associations were assessed, whereas for rarer variants information was collapsed across variants. Findings 121 exonic LRRK2 variants were assessed in 15 540 individuals: 6995 white patients with PD and 5595 controls, 1376 Asian patients and 962 controls, and 240 Arab-Berber patients and 372 controls. After exclusion of carriers of known pathogenic mutations, new independent risk associations were identified for polymorphic variants in white individuals (M1646T, odds ratio 1.43, 95% CI 1.15-1.78; p=0.0012) and Asian individuals (A419V, 2.27, 1.35-3.83; p=0.0011). A protective haplotype (N551K-R1398H-K1423K) was noted at a frequency greater than 5% in the white and Asian series, with a similar finding in the Arab-Berber series (combined odds ratio 0.82, 0.72-0.94; p=0.0043). Of the two previously reported Asian risk variants, G2385R was associated with disease (1.73, 1.20-2.49; p=0.0026), but no association was noted for R1628P (0.62, 0.36-1.07; p=0.087). In the Arab-Berber series, Y2189C showed potential evidence of risk association with PD (4.

Published
2011

33. SNCA,MAPT, andGSK3Bin Parkinson disease: a gene-gene interaction study

Author

Wider, C., primary, Vilariño-Güell, C., additional, Heckman, M. G., additional, Jasinska-Myga, B., additional, Ortolaza-Soto, A. I., additional, Diehl, N. N., additional, Crook, J. E., additional, Cobb, S. A., additional, Bacon, J. A., additional, Aasly, J. O., additional, Gibson, J. M., additional, Lynch, T., additional, Uitti, R. J., additional, Wszolek, Z. K., additional, Farrer, M. J., additional, and Ross, O. A., additional

Published
2010
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46. Immediate intraocular pressure changes following intravitreal injections of triamcinolone, pegaptanib, and bevacizumab.

Author

Bakri, S. J., Pulido, J. S., McCannel, C. A., Hodge, D. O., Diehl, N., and Hillemeier, J.

Subjects
INTRAOCULAR pressure, OPHTHALMIC drugs, TRIAMCINOLONE, BEVACIZUMAB, OPHTHALMOLOGICAL therapeutics
Abstract

PurposeTo assess the intraocular pressure (IOP) changes, within the first 30 min after intravitreal injection of 0.1 ml (4 mg) triamcinolone, 0.09 ml (0.3 mg) pegaptanib, and 0.05 ml (1.25 mg) bevacizumab.MethodsRecords of patients who received intravitreal triamcinolone, pegaptanib, and bevacizumab and who had their IOP measured post-injection were reviewed.ResultsA total of 212 injections were performed (76 bevacizumab in 63 patients, 42 triamcinolone in 41 patients, 94 pegaptanib in 74 patients). At 10 min, over 87% of eyes receiving each drug had an IOP of less than 35 mmHg. Three of the 42 eyes receiving intravitreal triamcinolone were treated with IOP-lowering drops for pressures of 44, 46, and 60 mmHg. No patients treated with intravitreal bevacizumab or pegaptanib received IOP-lowering drops. The number of eyes in each injection group that had an IOP rise >10 mmHg within 30 min after injection was 27.6% of eyes receiving bevacizumab, 33.3% of eyes receiving triamcinolone, and 36.2% of eyes receiving pegaptanib. At 10 min, eyes with glaucoma were less likely to have an IOP<35 mmHg, but this difference became less marked with time.ConclusionIn our series, most patients receiving intravitreal injections did not require IOP-lowering drops after injection, and none required a paracentesis.Eye (2009) 23, 181–185; doi:10.1038/sj.eye.6702938; published online 10 August 2007 [ABSTRACT FROM AUTHOR]

Published
2009
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47. PARTICULATE MATTER CHARACTERIZATION IN EQUESTRIAN RIDING ARENAS.

Author

Wheeler, E. F., Diehl, N. K., Zajaczkowski, J. L., and Brown, D.

Subjects
*AEROSOLS, *HORSE diseases, *DUST, *DUST control, *PARTICLE size distribution, *SCANNING electron microscopy, *HOOFS
Abstract

Particulate matter (PM) from hay and bedding contributes to respiratory disease in horses, but horses and handlers are also exposed to irritating levels of dust arising from the footing material used as the arena riding surface. Airborne total and respirable PM in two indoor equine riding arenas was quantitatively studied using gravimetric methods daring 5 to 10 h when the arenas were occupied by horse activity and over three sessions each to coincide with footing dust suppression management. Samplers were positioned approximately, 0.5 m above the arena surface, which consisted of inorganic, low-moisture, sand-soil footing in one arena and organic stall waste material footing in the second arena. Footing materials were characterized in terms of moisture content, elemental analysis, and particle size distribution. Qualitative evaluations of captured dust particle size and shape were performed using scanning electron microscopy, which determined that spherical fine particles dominated. Both total dust (0.600 mg m-3 with organic footing; 0.706 mg m-3 with inorganic footing) and respirable dust (0.327 mg m-3 with organic footing; 0.429 mg m-3 with inorganic footing) levels were lower than expected compared to data from stable dust studies. Dust detection did not vary systematically with dust suppression but rather was associated with the overall quality of the footing present in the arena. Dust detection in the arenas was best calculated according to the level of horse activity daring sampling. Total dust levels were O. 778 mg m-3 and 3.395 mg m-3 (organic and inorganic footing, respectively) when calculated based on time the arena was occupied by horses. Total dust levels were 2.5 to 3 times higher during times of horse activity faster than a walk than daring more sedentary, activity. Respirable particles were about half of the total dust during riding activity. When observing horses moving in an arena, it is readily apparent that dust is suspended in the air behind the tread of the horse's hooves, and its suspension is transient in nature. Horses in this study were apparently not exposed to a quantity of respirable dust particles in the riding arena comparable to that found in their stall environment. [ABSTRACT FROM AUTHOR]

Published
2006
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