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2. In-flight fatigue crack monitoring of an aircraft engine cowling

Author

Vaughn, Samuel Gordon, Eric v. K. Hill, Frank J. Radosta, Charles W. Bishop, Vaughn, Samuel Gordon, III, Vaughn, Samuel Gordon, Eric v. K. Hill, Frank J. Radosta, Charles W. Bishop, and Vaughn, Samuel Gordon, III

Subjects
Airplanes Motors Cowlings., Multivariate analysis., Composite materials., Neural networks (Computer science), Analyse multivariée., Composites., Réseaux neuronaux (Informatique), composite material., Airplanes Motors Cowlings, Composite materials, Multivariate analysis, Neural networks (Computer science)
Abstract

This research investigates the feasibility of implementing an in-flight fatigue crack monitoring system in an airplane to identify fatigue crack growth. An acoustic emission data acquisition system coupled with a Kohonen self organizing map neural network were used to perform the analysis. Fatigue cracking was responsible for ripping the top of a fuselage off an Aloha Airline’s Boeing 737-200 as it carried passengers over the Pacific Ocean, killing some aboard. This tragedy is perhaps a precursor of problems to come, as our nation’s aircraft age. These planes experience fatigue as they perform their daily routine of ferrying passengers from location to location. Fatigue can initiate cracking within the aircraft’s structure and at least damage a small expendable part of the plane, or at most damage a vital part of the airplane leading to disaster as happened to the Aloha Airline’s flight. In an attempt to curb this sort of devastation, this research involves the development of an in-flight fatigue crack monitoring system. Such a system would have the ability to identify possible crack sources before the crack would have the chance to cause significant damage. Advantages of this type of system would be first, an obvious safety cushion, and second, lower maintenance costs because routine parts replacement and inspection could be minimized.

Published
2024

5. The IRF5–TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share

Author

Kottyan, Leah C, Zoller, Erin E, Bene, Jessica, Lu, Xiaoming, Kelly, Jennifer A, Rupert, Andrew M, Lessard, Christopher J, Vaughn, Samuel E, Marion, Miranda, Weirauch, Matthew T, Namjou, Bahram, Adler, Adam, Rasmussen, Astrid, Glenn, Stuart, Montgomery, Courtney G, Hirschfield, Gideon M, Xie, Gang, Coltescu, Catalina, Amos, Chris, Li, He, Ice, John A, Nath, Swapan K, Mariette, Xavier, Bowman, Simon, Rischmueller, Maureen, Lester, Sue, Brun, Johan G, Gøransson, Lasse G, Harboe, Erna, Omdal, Roald, Cunninghame-Graham, Deborah S, Vyse, Tim, Miceli-Richard, Corinne, Brennan, Michael T, Lessard, James A, Wahren-Herlenius, Marie, Kvarnström, Marika, Illei, Gabor G, Witte, Torsten, Jonsson, Roland, Eriksson, Per, Nordmark, Gunnel, Ng, Wan-Fai, Anaya, Juan-Manuel, Rhodus, Nelson L, Segal, Barbara M, Merrill, Joan T, James, Judith A, Guthridge, Joel M, Scofield, R Hal, Alarcon-Riquelme, Marta, Bae, Sang-Cheol, Boackle, Susan A, Criswell, Lindsey A, Gilkeson, Gary, Kamen, Diane L, Jacob, Chaim O, Kimberly, Robert, Brown, Elizabeth, Edberg, Jeffrey, Alarcón, Graciela S, Reveille, John D, Vilá, Luis M, Petri, Michelle, Ramsey-Goldman, Rosalind, Freedman, Barry I, Niewold, Timothy, Stevens, Anne M, Tsao, Betty P, Ying, Jun, Mayes, Maureen D, Gorlova, Olga Y, Wakeland, Ward, Radstake, Timothy, Martin, Ezequiel, Martin, Javier, Siminovitch, Katherine, Sivils, Kathy L Moser, Gaffney, Patrick M, Langefeld, Carl D, Harley, John B, and Kaufman, Kenneth M

Subjects
Biological Sciences, Genetics, Autoimmune Disease, Biotechnology, Lupus, Aetiology, 2.1 Biological and endogenous factors, Inflammatory and immune system, Autoimmune Diseases, Bayes Theorem, Case-Control Studies, Cohort Studies, DNA-Binding Proteins, Haplotypes, Humans, Interferon Regulatory Factors, Lupus Erythematosus, Systemic, Male, Polymorphism, Single Nucleotide, Promoter Regions, Genetic, beta Karyopherins, UK Primary Sjögren's Syndrome Registry, Medical and Health Sciences, Genetics & Heredity
Abstract

Exploiting genotyping, DNA sequencing, imputation and trans-ancestral mapping, we used Bayesian and frequentist approaches to model the IRF5-TNPO3 locus association, now implicated in two immunotherapies and seven autoimmune diseases. Specifically, in systemic lupus erythematosus (SLE), we resolved separate associations in the IRF5 promoter (all ancestries) and with an extended European haplotype. We captured 3230 IRF5-TNPO3 high-quality, common variants across 5 ethnicities in 8395 SLE cases and 7367 controls. The genetic effect from the IRF5 promoter can be explained by any one of four variants in 5.7 kb (P-valuemeta = 6 × 10(-49); OR = 1.38-1.97). The second genetic effect spanned an 85.5-kb, 24-variant haplotype that included the genes IRF5 and TNPO3 (P-valuesEU = 10(-27)-10(-32), OR = 1.7-1.81). Many variants at the IRF5 locus with previously assigned biological function are not members of either final credible set of potential causal variants identified herein. In addition to the known biologically functional variants, we demonstrated that the risk allele of rs4728142, a variant in the promoter among the lowest frequentist probability and highest Bayesian posterior probability, was correlated with IRF5 expression and differentially binds the transcription factor ZBTB3. Our analytical strategy provides a novel framework for future studies aimed at dissecting etiological genetic effects. Finally, both SLE elements of the statistical model appear to operate in Sjögren's syndrome and systemic sclerosis whereas only the IRF5-TNPO3 gene-spanning haplotype is associated with primary biliary cirrhosis, demonstrating the nuance of similarity and difference in autoimmune disease risk mechanisms at IRF5-TNPO3.

Published
2015

16. Catatonia responsive to corticosteroids in a patient with an SCN2Avariant

Author

Senko, Kimberly, Saddoris, Kelsey L., Baus, Ella, Soe, Katherine, and Vaughn, Samuel E.

Abstract

Variants in SCN2Aare a known risk factor for developing autism spectrum disorder (ASD). Catatonia is a complex neuropsychiatric syndrome, which occurs at a higher rate in individuals with ASD. Catatonia has also been associated with COVID‐19 infection, though the majority of these cases are associated with increased serum inflammatory markers. We present a case of a 15‐year‐old female with ASD and corticosteroid responsive stuporous catatonia to explore the relationship between SCN2Avariants, ASD, COVID‐19 exposure, and treatment refractory catatonia. Despite a lack of significantly elevated serum or CSF inflammatory markers, this patient showed significant improvement following initiation of corticosteroid therapy. This case presents a novel approach to the work‐up and treatment of catatonia in individuals with SCN2Avariants independent of elevated inflammatory markers.

Published
2024
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20. The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.

Author

Kottyan, Leah C., Zoller, Erin E., Bene, Jessica, Lu, Xiaoming, Kelly, Jennifer A., Rupert, Andrew M., Lessard, Christopher J., Vaughn, Samuel E., Marion, Miranda, Weirauch, Matthew T., Namjou, Bahram, Adler, Adam, Rasmussen, Astrid, Glenn, Stuart, Montgomery, Courtney G., Hirschfield, Gideon M., Xie, Gang, Coltescu, Catalina, Amos, Chris, Li, He, Ice, John A., Nath, Swapan K., Mariette, Xavier, Bowman, Simon, Rischmueller, Maureen, Lester, Sue, Brun, Johan G., Gøransson, Lasse G., Harboe, Erna, Omdal, Roald, Cunninghame-Graham, Deborah S., Vyse, Tim, Miceli-Richard, Corinne, Brennan, Michael T., Lessard, James A., Wahren-Herlenius, Marie, Kvarnström, Marika, Illei, Gabor G., Witte, Torsten, Jonsson, Roland, Eriksson, Per, Nordmark, Gunnel, Ng, Wan-Fai, Anaya, Juan-Manuel, Rhodus, Nelson N., Segal, Barbara M., Merrill, Joan T., James, Judith A., Guthridge, Joel M., Hal Scofield, R, Alarcon-Riquelme, Marta, Bae, Sang-Cheol, Boackle, Susan A., Criswell, Lindsey A., Gilkeson, Gary, Kamen, Diane L, Jacob, Chaim O., Kimberly, Robert, Brown, Elizabeth, Edberg, Jeffrey, Alarcón, Graciela S., Reveille, John D., Vilá, Luis M., Petri, Michelle, Ramsey-Goldman, Rosalind, Freedman, Barry I., Niewold, Timothy, Stevens, Anne M., Tsao, Betty P., Ying, Jun, Mayes, Maureen D., Gorlova, Olga Y., Wakeland, Ward, Radstake, Timothy, Martin, Ezequiel, Martin, Javier, Siminovitch, Katherine, Moser Sivils, Kathy L., Gaffney, Patrick M., Langefeld, Carl D., Harley, John B., Kaufman, Kenneth M., Kottyan, Leah C., Zoller, Erin E., Bene, Jessica, Lu, Xiaoming, Kelly, Jennifer A., Rupert, Andrew M., Lessard, Christopher J., Vaughn, Samuel E., Marion, Miranda, Weirauch, Matthew T., Namjou, Bahram, Adler, Adam, Rasmussen, Astrid, Glenn, Stuart, Montgomery, Courtney G., Hirschfield, Gideon M., Xie, Gang, Coltescu, Catalina, Amos, Chris, Li, He, Ice, John A., Nath, Swapan K., Mariette, Xavier, Bowman, Simon, Rischmueller, Maureen, Lester, Sue, Brun, Johan G., Gøransson, Lasse G., Harboe, Erna, Omdal, Roald, Cunninghame-Graham, Deborah S., Vyse, Tim, Miceli-Richard, Corinne, Brennan, Michael T., Lessard, James A., Wahren-Herlenius, Marie, Kvarnström, Marika, Illei, Gabor G., Witte, Torsten, Jonsson, Roland, Eriksson, Per, Nordmark, Gunnel, Ng, Wan-Fai, Anaya, Juan-Manuel, Rhodus, Nelson N., Segal, Barbara M., Merrill, Joan T., James, Judith A., Guthridge, Joel M., Hal Scofield, R, Alarcon-Riquelme, Marta, Bae, Sang-Cheol, Boackle, Susan A., Criswell, Lindsey A., Gilkeson, Gary, Kamen, Diane L, Jacob, Chaim O., Kimberly, Robert, Brown, Elizabeth, Edberg, Jeffrey, Alarcón, Graciela S., Reveille, John D., Vilá, Luis M., Petri, Michelle, Ramsey-Goldman, Rosalind, Freedman, Barry I., Niewold, Timothy, Stevens, Anne M., Tsao, Betty P., Ying, Jun, Mayes, Maureen D., Gorlova, Olga Y., Wakeland, Ward, Radstake, Timothy, Martin, Ezequiel, Martin, Javier, Siminovitch, Katherine, Moser Sivils, Kathy L., Gaffney, Patrick M., Langefeld, Carl D., Harley, John B., and Kaufman, Kenneth M.

Abstract

Exploiting genotyping, DNA sequencing, imputation and trans-ancestral mapping, we used Bayesian and frequentist approaches to model the IRF5-TNPO3 locus association, now implicated in two immunotherapies and seven autoimmune diseases. Specifically, in systemic lupus erythematosus (SLE), we resolved separate associations in the IRF5 promoter (all ancestries) and with an extended European haplotype. We captured 3230 IRF5-TNPO3 high-quality, common variants across 5 ethnicities in 8395 SLE cases and 7367 controls. The genetic effect from the IRF5 promoter can be explained by any one of four variants in 5.7 kb (P-valuemeta = 6 × 10(-49); OR = 1.38-1.97). The second genetic effect spanned an 85.5-kb, 24-variant haplotype that included the genes IRF5 and TNPO3 (P-valuesEU = 10(-27)-10(-32), OR = 1.7-1.81). Many variants at the IRF5 locus with previously assigned biological function are not members of either final credible set of potential causal variants identified herein. In addition to the known biologically functional variants, we demonstrated that the risk allele of rs4728142, a variant in the promoter among the lowest frequentist probability and highest Bayesian posterior probability, was correlated with IRF5 expression and differentially binds the transcription factor ZBTB3. Our analytical strategy provides a novel framework for future studies aimed at dissecting etiological genetic effects. Finally, both SLE elements of the statistical model appear to operate in Sjögrens syndrome and systemic sclerosis whereas only the IRF5-TNPO3 gene-spanning haplotype is associated with primary biliary cirrhosis, demonstrating the nuance of similarity and difference in autoimmune disease risk mechanisms at IRF5-TNPO3.

Published
2015
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21. Lupus risk variants in the PXK locus alter B-cell receptor internalization

Author

Vaughn, Samuel E., primary, Foley, Corinne, additional, Lu, Xiaoming, additional, Patel, Zubin H., additional, Zoller, Erin E., additional, Magnusen, Albert F., additional, Williams, Adrienne H., additional, Ziegler, Julie T., additional, Comeau, Mary E., additional, Marion, Miranda C., additional, Glenn, Stuart B., additional, Adler, Adam, additional, Shen, Nan, additional, Nath, Swapan, additional, Stevens, Anne M., additional, Freedman, Barry I., additional, Tsao, Betty P., additional, Jacob, Chaim O., additional, Kamen, Diane L., additional, Brown, Elizabeth E., additional, Gilkeson, Gary S., additional, Alarcón, Graciela S., additional, Reveille, John D., additional, Anaya, Juan-Manuel, additional, James, Judith A., additional, Moser, Kathy L., additional, Criswell, Lindsey A., additional, Vilá, Luis M., additional, Alarcón-Riquelme, Marta E., additional, Petri, Michelle, additional, Scofield, R. Hal, additional, Kimberly, Robert P., additional, Ramsey-Goldman, Rosalind, additional, Binjoo, Young, additional, Choi, Jeongim, additional, Bae, Sang-Cheol, additional, Boackle, Susan A., additional, Vyse, Timothy J., additional, Guthridge, Joel M., additional, Namjou, Bahram, additional, Gaffney, Patrick M., additional, Langefeld, Carl D., additional, Kaufman, Kenneth M., additional, Kelly, Jennifer A., additional, Harley, Isaac T. W., additional, Harley, John B., additional, and Kottyan, Leah C., additional

Published
2015
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22. Genome-wide association analysis of eosinophilic esophagitis provides insight into the tissue specificity of this allergic disease

Author

Kottyan, Leah C, primary, Davis, Benjamin P, additional, Sherrill, Joseph D, additional, Liu, Kan, additional, Rochman, Mark, additional, Kaufman, Kenneth, additional, Weirauch, Matthew T, additional, Vaughn, Samuel, additional, Lazaro, Sara, additional, Rupert, Andrew M, additional, Kohram, Mojtaba, additional, Stucke, Emily M, additional, Kemme, Katherine A, additional, Magnusen, Albert, additional, He, Hua, additional, Dexheimer, Phillip, additional, Chehade, Mirna, additional, Wood, Robert A, additional, Pesek, Robbie D, additional, Vickery, Brian P, additional, Fleischer, David M, additional, Lindbad, Robert, additional, Sampson, Hugh A, additional, Mukkada, Vincent A, additional, Putnam, Phil E, additional, Abonia, J Pablo, additional, Martin, Lisa J, additional, Harley, John B, additional, and Rothenberg, Marc E, additional

Published
2014
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25. Natural fatal Sarcocystis falcatula infections in free-ranging eagles in North America.

Author

Wüinschmann, Arno, Rejmanek, Daniel, Conrad, Patricia A., Hall, Natalie, Cruz-Martinez, Luis, Vaughn, Samuel B., and Barr, Bradd C.

Subjects
SARCOCYSTOSIS in animals, GOLDEN eagle, BALD eagle, IMMUNOHISTOCHEMISTRY, POLYMERASE chain reaction, DISEASES
Abstract

The article discusses research on eagles that are affected by Sarcocystis falcatula infections. It references a study by Natalie Hall and colleagues, published in the 2010 issue of the "Journal of Veterinary Diagnostic Investigation." The researchers examined a golden eagle and three bald eagles in North America that are unable to fly. They found that the animals exhibit natural infections which can cause their death.

Published
2010
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26. Natural Fatal Sarcocystis FalcatulaInfections in Free-Ranging Eagles in North America

Author

Wünschmann, Arno, Rejmanek, Daniel, Conrad, Patricia A., Hall, Natalie, Cruz-Martinez, Luis, Vaughn, Samuel B., and Barr, Bradd C.

Abstract

Three bald eagles (Haliaeetus leucocephalus) and 1 golden eagle (Aquila chrysaetos) were admitted to rehabilitation facilities with emaciation, lethargy, and an inability to fly. Intravascular schizonts and merozoites were present in 2 bald eagles, mainly in the lung tissue, whereas the third bald eagle and the golden eagle had lymphohistiocytic encephalitis with intralesional schizonts and merozoites. In all eagles, protozoal tissue cysts were present in skeletal musculature or heart. The protozoal organisms were morphologically compatible with a Sarcocystissp. By immunohistochemistry, the protozoal merozoites were positive for Sarcocystis falcatulaantigen in all cases when using polyclonal antisera. Furthermore, the protozoa were confirmed to be most similar to S. falcatulaby polymerase chain reaction in 3 of the 4 cases. To the authors' knowledge, this report presents the first cases of natural infection in eagles with S. falcatulaas a cause of mortality.

Published
2010
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30. PXK and Lupus: Novel Immunobiology for a Lupus-Risk Gene

Author

Vaughn, Samuel

Subjects
Immunology, Lupus, PXK, B cells, BCR, fine-mapping
Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by multi-organ damage. There is a strong evidence for genetics playing an important role in the development of disease. Genetic association studies have begun to identify many SLE-associated genetic loci, yet for very few of these loci is the specific pathogenic mechanism of disease described. We undertook a genetic fine-mapping study of the PXK locus, which our group had previously identified as being associated with SLE. In the course of performing the fine-mapping study, we also developed a streamlined analytic approach. By using existing genetic analysis software suites, linking them with small Linux scripts and parallel processing multiple statistical models simultaneously, we were able to greatly facilitate our genetic analysis. For the PXK locus, we identify a 257kb haplotype associated with SLE. The strongest association was found at rs6445972 with P < 4.62 × 10-10, OR 0.81 (0.75–0.86). We confirmed this finding with Bayesian analysis, confirming a 95% credible set consisting of 172 variants. We found one association at the locus. In addition to the genetic fine-mapping results, we also demonstrate that PXK colocalizes with the B cell antigen receptor (BCR) following BCR-crosslinking. shRNA-mediated knockdown of PXK resulted in delayed BCR internalization. Cell lines derived from patients carrying the SLE-associated risk variant displayed a delay in BCR internalization. Given the role for BCR internalization in B cell fate determination and survival, our results support new candidate mechanisms for SLE-disease risk, including BCR trafficking and BCR-mediated B cell activation.

Published
2015

31. Ask a veterinarian.

Author

Vaughn, Samuel B.

Subjects
*FIREPLACES, *BIRDS
Abstract

The article provides answer to a question about health aspects of fireplace for birds.

Published
2016

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