Ultraviolet radiation intensity predicts the relative distribution of dermatomyositis and anti-Mi-2 autoantibodies in women.

OBJECTIVE: Because studies suggest that ultraviolet (UV) radiation modulates the myositis phenotype and Mi-2 autoantigen expression, we conducted a retrospective investigation to determine whether UV radiation may influence the relative prevalence of dermatomyositis and anti-Mi-2 autoantibodies in the US. METHODS: We assessed the relationship between surface UV radiation intensity in the state of residence at the time of onset with the relative prevalence of dermatomyositis and myositis autoantibodies in 380 patients with myositis from referral centers in the US. Myositis autoantibodies were detected by validated immunoprecipitation assays. Surface UV radiation intensity was estimated from UV Index data collected by the US National Weather Service. RESULTS: UV radiation intensity was associated with the relative proportion of patients with dermatomyositis (odds ratio [OR] 2.3, 95% confidence interval [95% CI] 0.9-5.8) and with the proportion of patients expressing anti-Mi-2 autoantibodies (OR 6.0, 95% CI 1.1-34.1). Modeling of these data showed that these associations were confined to women (OR 3.8, 95% CI 1.3-11.0 and OR 17.3, 95% CI 1.8-162.4, respectively) and suggests that sex influences the effects of UV radiation on autoimmune disorders. Significant associations were not observed in men, nor were UV radiation levels related to the presence of antisynthetase or anti-signal recognition particle autoantibodies. CONCLUSION: This first study of the distribution of myositis phenotypes and UV radiation exposure in the US showed that UV radiation may modulate the clinical and immunologic expression of autoimmune disease in women. Further investigation of the mechanisms by which these effects are produced may provide insights into pathogenesis and suggest therapeutic or preventative strategies.

Differential dynamic properties of scleroderma fibroblasts in response to perturbation of environmental stimuli.

Diseases are believed to arise from dysregulation of biological systems (pathways) perturbed by environmental triggers. Biological systems as a whole are not just the sum of their components, rather ever-changing, complex and dynamic systems over time in response to internal and external perturbation. In the past, biologists have mainly focused on studying either functions of isolated genes or steady-states of small biological pathways. However, it is systems dynamics that play an essential role in giving rise to cellular function/dysfunction which cause diseases, such as growth, differentiation, division and apoptosis. Biological phenomena of the entire organism are not only determined by steady-state characteristics of the biological systems, but also by intrinsic dynamic properties of biological systems, including stability, transient-response, and controllability, which determine how the systems maintain their functions and performance under a broad range of random internal and external perturbations. As a proof of principle, we examine signal transduction pathways and genetic regulatory pathways as biological systems. We employ widely used state-space equations in systems science to model biological systems, and use expectation-maximization (EM) algorithms and Kalman filter to estimate the parameters in the models. We apply the developed state-space models to human fibroblasts obtained from the autoimmune fibrosing disease, scleroderma, and then perform dynamic analysis of partial TGF-beta pathway in both normal and scleroderma fibroblasts stimulated by silica. We find that TGF-beta pathway under perturbation of silica shows significant differences in dynamic properties between normal and scleroderma fibroblasts. Our findings may open a new avenue in exploring the functions of cells and mechanism operative in disease development.

Houston History of Medicine Society 2008-2009 Schedule and Abstracts

The National Library of Medicine and the Continuing Legacy of Michael E. DeBakey, M.D. (Stephen B. Greenberg) The Legacy of William Osler: North America’s most famous physician (Robert E. Rakel) A Lady Alone: Elizabeth Blackwell: First American Woman Doctor (Linda Gray Kelley, Charlton) A Mariner with Crippling Arthritis and Bleeding Eyes: The Chronic Arthritis of Christopher Columbus (Frank C. Arnett) Generation C(affeine): A History of Caffeine Consumption and its Medical Implications (Student Essay Contest winners) (Priti Dangayach) Our Artificial Fitness? Relaxed Selection Leads to Medical Dependence (Student Essay Contest winners) Philip Boone Remembering John P. McGovern, M.D. (1921-2007) (Bryant Boutwell) Who Was Albert Schweitzer? (Bryant Boutwell) Disease, Doctors and the Duty to Treat in American History (Thomas R. Cole) Vaccinating Freedom: The African-American Experience of Smallpox Prophylaxis in Old Philadelphia, 1723-1923 (Dayle B. Delancey) The Royal Hemophilia (The Royal Hemophilia)

Connexin-43 in the osteogenic BM niche regulates its cellular composition and the bidirectional traffic of hematopoietic stem cells and progenitors

Connexin-43 (Cx43), a gap junction protein involved in control of cell proliferation, differentiation and migration, has been suggested to have a role in hematopoiesis. Cx43 is highly expressed in osteoblasts and osteogenic progenitors (OB/P). To elucidate the biologic function of Cx43 in the hematopoietic microenvironment (HM) and its influence in hematopoietic stem cell (HSC) activity, we studied the hematopoietic function in an in vivo model of constitutive deficiency of Cx43 in OB/P. The deficiency of Cx43 in OB/P cells does not impair the steady state hematopoiesis, but disrupts the directional trafficking of HSC/progenitors (Ps) between the bone marrow (BM) and peripheral blood (PB). OB/P Cx43 is a crucial positive regulator of transstromal migration and homing of both HSCs and progenitors in an irradiated microenvironment. However, OB/P Cx43 deficiency in nonmyeloablated animals does not result in a homing defect but induces increased endosteal lodging and decreased mobilization of HSC/Ps associated with proliferation and expansion of Cxcl12-secreting mesenchymal/osteolineage cells in the BM HM in vivo. Cx43 controls the cellular content of the BM osteogenic microenvironment and is required for homing of HSC/Ps in myeloablated animals

1977 UM Track Team

Top Row: Calvin Williams, Mike Boehmer, Tim Thomas, Dan Heikkinen, Greg Thomas, Scott Walters, Sam Angell, Mike Hetes.

3rd Row: asst. coach Greg Syphax, Doug Sweazey, Bruce McFee, Jim Baumgartner, Charles Crouther, Jay Anstaett, Gary Hicks, Warren T. Dobson, James Henry.

2nd Row; Bob Scheper, Arnett Chisholm, John Risk, Don Wheeler, Randy Foss, Lynn Dobosy, Scott Hurd, asst. coach Ron Warhurst

Front Row: Steve Elliott, Bill Donakowski, James Grace, co-captain Jeff McLeod, coach Jack Harvey, co-captain Greg Meyer, Andy Johnson, Dave Furst, Doug Hennigar.

School of Nursing Class of 1983

Top Row: Barbara A. Fleckenstein, Anne M. Phelan, Julie-Ann Gersin, Laura E. Kemper, Mary Ann McCulloch, Meryl I. Faber, Karen E. Morton, Jennifer S. Miller, Catherine A. Chichester, Dana R. Piper, Harold K. Lohwasser, Michelle A. Lyons, Julia C. Kelly, Deborah L. Rossman, Amy L. Keskey, John F. Nama, Linda Borucki, Michelle M. Bradley, Caroline M. Fischer, Lisa A. Kuhnlein

Row 2: Karen M. Pardo, Laura L. Price, Mollie A. McDonald, Jan M. Grable, Janna S. Nichols, Laura A. Quain, Patricia M. Battel, Claudia J. Koch, Maureen G. D'hondt, Trudy J. Tervo, Linda A. Walz, Cheryl K. Ebling, Patricia A. Merte, Lauri R. Klock, Maria A. Lomibao, Mary E. Eisenhauer, Ellen B. Malvern, Josephine A. Polesnak

Row 3: Yvonne D. Krisel, Rosemary T. Coyne, Janey A. Porterfield, Deborah A. Mulawa, Janet E. Lovelace, Susan P. O'brien, Margaret T. Perrone, Brenda K. Luckhardt, Terry A. Layher, Sharon A. Potonac, Susan K. Watson, Janet A. Servatowski

Row 4: Vivian A. Reeves, Tracey A. Weeks, Marilyn K. Morgan, Terrilynn Phillips, Susan S. Kirk, Robert J. Ziola, Fred Roberts, Karen S. Myron, Pamela M. Przybylski, Mary Jo F. Lafata, Janet A. Scapini, Mary J. Swails

Row 5: Julie E. Reitz, Julie A. Symons, Ave M. Reagor, Catherine A. Regan, Marsha A. Glass, Susan M. Derubeis, Judy L. Goode, Jennifer P. Wylie, Janet L. Nowak, Karen M. Ulfig, Cynthia E. West, Carol A. Czarnecki, Gloria J. Verdi, Lisa D. Singleton

Row 6: Cynthia Wiggins, Monica L. Babyak, Gail M. Ray, Karen S. Desloover, Ladonna L. Christian-Combs, Deborah J. Dunnaback, Deborah A. Cecchini, Nancy A. Neville, Julia H. Grove, Wendy A. Weinfurtner, Susan M. Twigg, Jolynne Vanotteren, Lori A. Clark, Susan T. Savidge

Row 7: Marianne Ojeda, Ann M. Tucker, Lisa A. Valiquette, Sharon J. Bergmann, Elizabeth A. Rice, Marjorie R. Hovis, Laura I. Berry, Janice B. Lindberg, Rhetaugh G. Dumas, Susan B. Steckel, Helen L. Erickson, Kathleen M. Oshea, Tricia A. Richardson, Cheryl L. Sanders, Ann L. Shcoene, Anita M. Bargardi, Constance S. Siler, Anne L. Scott

Row 8: Gassenie Thomas, Victoria L. cadagin, Sheryl A. Strace, Joyce I. Sourbeck, Mary S. Donald, Cindy Tollis, Miriam L. Allis, Julie J. Watson, Patricia A. Shefferly, Nina M. Squire, Carol J. Debrodt, Jennifer A. Dreps, Cynthia B. Stone, Martha A. House, Elizabeth A. Hull, Laurie J. Bommarito, Erin A. Swain, Lisa D. Davis

Row 9: Lisa W. Barak, Charlotte L. Allport, Karen J. Baker, Julie M. Sweet, Pamela R. Armfield, Kathleen A. Hornick, Marcianna M. Davis, Joann L. Holdridge, Barbara A. Black, Scott L. Baker, Lawrene S. Gardipee, Julie A. Hemsteger, Mary Ann Barz, Carla L. Arnett, Danielle L. Bonam, Janice S. Brady, Karen L. Eischer, Amy A. Hing, Marcia L. Hassig, Heidi G. Henn

School of Nursing Class of 1996

Top Row: Jessica M. Adair, Casey Arnett, Amy Lynn Babchek, Mary E. Bartlett, Rhonda Bass, Nancy Bidlack, Heather Bjerke, Stacy Bodrie, Dana Boonstra, Kellu Bowers, Pamela Bowser, Rachel L. Bradley, Michele Brotherton, Stacie Buckler, Hope Bufkin

Row 2: Saran Burnley, Jennifer Caraan, Barbara Carpenter, Nutrena Helene Watts, Aimee Schuman, Debra Jameson, Jennifer Jennings, Mary Cassette, Nikki Burns, Lisa Multhaupt, Jeffrey M. Adams, Christine Hepner, Julie Chamberlain, Andy Chan, Jennifer Choike

Row 3: Heather Chrisman, Abbey C. Clark, Renita Cobb, Amy Cotton, Cattleya Crossen, Kimberly Curl, Christy Debolt, Patricia DeLamielleure, Jennifer Dyer, Lisa L. Eliasom, Patricia Fowler Faling, Rita Fallone

Row 4: Richard Fisher, Rebecca J. Forbes, Tiffany Fowler, Karen R. Fritz, Debbie M. Fulton, Michelle J. Gaskill, Ellen M. Gavin, Emily Golin, Umeika Makita Griffith, Lydia D. Hampton, Natalie Michele Hoffman, Julie Holbird

Row 5: Kathryn A. Huffman, Tara Lynn Humphrey, Nicole Jaccques, Michelle C. Johnson, Bryan Wayne Kerridge, Violet H. Barkauskas, Beverly Jones, Ada Sue Hinshaw, Nola Pender, Susan Boehm, Noelle Kirouac, Sarah Kohn, Sherri Krajenta, Brian Kubinski, Stephanie L. Kuczera

Row 6: Heather Lange, Sang Hee Lee, Soya Lee, Natalie Lehrer, Kimberly Lilley, Elizabeth A. Lundy, Darcey Lutz-Guenther, Michelle J. Malicsi, Dawn Marteeny, Sheila Mendiola, Sharon Mitchell, Caryl S. Molton, Colette Montilla, Celeste Montone-Horne, Emily T. Mooney, Naima Moore

Row 7: Kami Nobis, Thresa M. Nugent, Michelle Ober, Nisha Patel, Stephanie Perrett, Holly Powers, Julie L. Pryor, Elizabeth K. Rachubinski, Anne Rammelkamp, Kathy Rarog, Erin Richards, Amy Roehrig, Catherine Ann Rosloniec, Tansey Rosset, Kimberly Sanders, Marla Sands, James C. Sausser

Row 8: Juana Sebree, Erin J. Showers, Prabhjyot Singh, Lynn Sinkel, Nicole LaDon Smith, Nicole M. Speck, Mickie Speers, Krista Stapleton, Karon Starr, Elizabeth Studley, Janice Brenda Supena, Rashelle Talbert,Kimberly Tocco, Edda Toting, Lisa Uren, Lori VanBergen

Row 9: Lisa VanStratton, kathleen Veenstra, Kristen Venadam, Rhonda E. Walkowe, Ching-Ru Bonny Wang, Deborah Webb, Ruthann Clausen Weiss, Debra R. White, Rochelle Whiteman, Tara Wilson, Jessica Wise, Sheryl Woloskie, Denice Annette Zakalata, Rebecca S. Zeiler

Hypermethylation of the 5 ' CpG island of the gene encoding the serine protease Testisin promotes its loss in testicular tumorigenesis

The Testisin gene (PRSS21) encodes a glycosylphosphatidylinositol (GPI)-linked serine protease that exhibits testis tissue-specific expression. Loss of Testisin has been implicated in testicular tumorigenesis, but its role in testis biology and tumorigenesis is not known. Here we have investigated the role of CpG methylation in Testisin gene inactivation and tested the hypothesis that Testisin may act as a tumour suppressor for testicular tumorigenesis. Using sequence analysis of bisulphite-treated genomic DNA, we find a strong relationship between hypermethylation of a 385 bp 50 CpG rich island of the Testisin gene, and silencing of the Testisin gene in a range of human tumour cell lines and in 100% (eight/eight) of testicular germ cell tumours. We show that treatment of Testisin-negative cell lines with demethylating agents and/or a histone deacetylase inhibitor results in reactivation of Testisin gene expression, implicating hypermethylation in Testisin gene silencing. Stable expression of Testisin in the Testisin-negative Tera-2 testicular cancer line suppressed tumorigenicity as revealed by inhibition of both anchorage-dependent cell growth and tumour formation in an SCID mouse model of testicular tumorigenesis. Together, these data show that loss of Testisin is caused, at least in part, by DNA hypermethylation and histone deacetylation, and suggest a tumour suppressor role for Testisin in testicular tumorigenesis.

ESTUDO COMPARATIVO ENTRE A ANÁLISE FACIAL SUBJETIVA E ANÁLISE CEFALOMÉTRICA DE TECIDOS MOLES NO DIAGNÓSTICO ORTODÔNTICO

O propósito deste estudo foi avaliar a concordância entre a Análise facial subjetiva, proposta por CAPELOZZA FILHO e a Análise Cefalométrica de Tecidos Moles, de ARNETT; McLAUGHLIN. Fotografias de frente e de perfil e telerradiografias em norma lateral padronizadas, de 50 indivíduos, com média de idade de 24 anos e 1 mês foram utilizadas para a avaliação. Verificou-se também nos indivíduos classificados como Padrão I, a correspondência dos valores médios e dos desvios-padrão das medidas obtidas, com os valores normativos da Análise Cefalométrica dos Tecidos Moles para os indivíd uos com harmonia facial. Constatou-se em indivíduos do Padrão I que os lábios sempre se encontram à frente da Linha Vertical Verdadeira, e que apesar de grandes variações do ponto pogônio, ainda é mantido o equilíbrio facial. Os resultados demonstraram que a Análise facial subjetiva eficiente na classificação do padrão facial.

Impacto de la resiliencia en pacientes con Artritis Reumatoide

Introducción: La artritis reumatoide (AR) es una enfermedad autoinmune-inflamatoria, que compromete las articulaciones diartrodiales. Tiene una importante repercusión sistémica que incluye la depresión; por lo tanto, tiene un severo impacto sobre la calidad de vida. Es posible que mecanismos de defensa, tales como la resiliencia, puedan amortiguar dicho impacto. Metodología: estudio de corte transversal, multicéntrico (análisis inicial dentro del grupo AR, con muestra no probabilística de 66 pacientes, posterior selección aleatoria simple de 16 pacientes de la muestra inicial y selección de 16 individuos sanos pareados). Posteriormente, se comparó la resiliencia entre sujetos con AR y sujetos sanos, mediante las escalas RS y CD-RISC25. Adicionalmente, se aplicaron las escalas EEAE, EADZ, SF-36 y PANAS. Los datos fueron evaluados mediante el coeficiente de correlación de Spearman, las pruebas U Mann-Whitney, Kruskall-Wallis, T de Student y análisis de varianza. Resultados: se encontraron diferencias significativas en las estrategias de afrontamiento no espirituales en grupos de resiliencia baja, media y alta; diferencias en las medianas de resiliencia en los grupos de depresión por EAZD en los pacientes. No se encontraron resultados significativos en las variables clínicas de la AR ni en la comparación con sujetos sanos. Conclusiones: el uso de estrategias de afrontamiento no espirituales y la ausencia de depresión, se asoció a mayores niveles de resiliencia en los pacientes con AR, por lo cual, los componentes emocionales y cognitivos se asocian a la resiliencia.

Factores asociados a respuesta de abatacept subcutaneo en artritis reumatoide

INTRODUCCION Dado que la artritis reumatoide es la artropatía inflamatoria más frecuente en el mundo, siendo altamente discapacitante y causando gran impacto de alto costo, se busca ofrecer al paciente opciones terapéuticas y calidad de vida a través del establecimiento de un tratamiento oportuno y eficaz, teniendo presentes aquellos predictores de respuesta previo a instaurar determinada terapia. Existen pocos estudios que permitan establecer aquellos factores de adecuada respuesta para inicio de terapia biológica con abatacept, por lo cual en este estudio se busca determinar cuáles son esos posibles factores. METODOLOGIA Estudio analítico de tipo corte transversal de 94 pacientes con diagnóstico de AR, evaluados para determinar las posibles variables que influyen en la respuesta a terapia biológica con abatacept. Se incluyeron 67 de los 94 pacientes al modelo de regresión logística, que son aquellos pacientes en que fue posible medir la respuesta al tratamiento (respuesta EULAR) a través de la determinación del DAS 28 y así discriminar en dos grupos de comparación (respuesta y no respuesta). DISCUSION DE RESULTADOS La presencia de alta actividad de la enfermedad al inicio de la terapia biológica, aumenta la probabilidad de respuesta al tratamiento respecto al grupo con baja/moderada actividad de la enfermedad; OR 4,19 - IC 95%(1,18 – 14.9), (p 0,027). La ausencia de erosiones óseas aumenta la probabilidad de presentar adecuada respuesta a la terapia biológica respecto aquellos con erosiones, con un OR 3,1 (1,01-9,55), (p 0,048). Niveles de VSG y presencia de manifestaciones extra-articulares son otros datos de interés encontrados en el análisis bivariado. Respecto a las variables o características como predictores de respuesta al tratamiento con abatacept, se encuentran estudios que corroboran los hallazgos de este estudio, respecto al alto puntaje del DAS 28 al inicio de la terapia (9, 12). CONCLUSIONES Existen distintas variables que determinan la respuesta a los diferentes biológicos para manejo de AR. Es imprescindible evaluar dichos factores de manera individual con el fin de lograr de manera efectiva el control de la enfermedad y así mejorar la calidad de vida del individuo (medicina personalizada). Existen variables tales como la alta actividad de la enfermedad y la ausencia de erosiones como predictores de respuesta en la terapia con abatacept.

Asociación entre la escala de riesgo Framingham y el puntaje de calcio coronario

Introducción: Entre las diferentes herramientas clínicas para evaluar la presencia de enfermedad coronaria mediante puntajes, la más usada es la Escala de Riesgo cardiovascular de Framingham. Desde hace unos años, se creó el puntaje de calcio coronario el cual mide el riesgo cardiovascular según la presencia de placas ateromatosas vistas por tomografía computarizada. Se evaluó la asociación entre la escala de Framigham y el puntaje de calcio coronario en una población de sujetos sanos asintomáticos. Metodología: Se realizó un estudio transversal para evaluar la asociación entre el puntaje de calcio coronario y la escala de Framingham en sujetos asintomáticos que se practicaron exámen médico preventivo en la Fundación Cardioinfantil- Instituto de Cardiología (FCI-IC) en el periodo comprendido entre 1 de Julio 2011 hasta el 31 de octubre de 2015. Resultados: Se evaluaron 262 pacientes en total. La prevalencia de riesgo cardiovascular fue bajo en un 77.86% de la población, medio en 18.70% y alto en 3.44%, según la escala de Framingham. El riesgo cardiovascular según el puntaje de Calcio coronario fue nulo 70.99%, bajo en 21.75%, medio en 4.19%, severo en 3.05%. Se encontró una asociación entre ambos puntajes para riesgo estadísticamente significativa (p0,00001) Discusión: El riesgo cardiovascular establecido por escala de Framingham se relaciona de forma significativa con la presencia de placas aterioscleróticas. El estudio demostró que en una muestra de sujetos asintomáticos, hay una alteración estructural coronaria temprana.

Cardiorespiratory fitness and cardiometabolic risk factors in schoolchildren from Colombia: The FUPRECOL Study

The objectives of this study are to investigate the association between cardiorespiratory fitness and cardiovascular risk factors in schoolchildren and to evaluate the degree of association between overall and abdominal adiposity and cardiorespiratory fitness. A total of 1,875 children and adolescents attending public schools in Bogota, Colombia (56.2% girls; age range of 9–17.9 years). A cardiovascular risk score (Z-score) was calculated and participants were divided into tertiles according to low and high levels of overall (sum of the skinfold thicknesses) and abdominal adiposity. Schoolchildren with a high level of overall adiposity demonstrated significant differences in seven of the 10 variables analyzed (i.e. systolic and diastolic blood pressure, triglycerides, triglycerides/HDL-c ratio, total cholesterol, glucose and cardiovascular risk score). Schoolchildren with high levels of both overall and abdominal adiposity and low cardiorespiratory fitness had the least favorable cardiovascular risk factors score. These findings may be relevant to health promotion in Colombian youth.