Search

Your search keyword '"Tau, Julia"' showing total 37 results
Start Over Author "Tau, Julia"
37 results on '"Tau, Julia"'

7. Tear Lysozyme in Sjögren´s syndrome, Meibomian gland dysfunction, and non-dry-eye

Author

Berra, Martín, Galperín, Gustavo, Berra, Federico, Marquez, Maria Isabel, Mandaradoni, Mariana, Tau, Julia, and Berra, Alejandro

Subjects
genetic structures, Lysozyme, Non-dry-eye, Síndrome de Sjögren, Sjogren’s syndrome, Disfunção da glân dula tarsal, sense organs, Meibomian gland dysfunction, eye diseases, Lisozima, Olho não seco
Abstract

Purpose: To evaluate the concentration of tear lysozyme in individuals with Sjogren´s syndrome, meibomian gland dysfunction, and non-dry-eye disease. Methods: Ninety subjects were recruited for this study, including 30 with Sjogren´s syndrome, 30 with meibomian gland dysfunction, and 30 with non-dry-eye disease. All subjects were referred to participate in the study based on a “dry eye” investigation. They underwent a complete ocular surface ophthalmic examination encompassing ocular surface disease index, biomicroscopy, tear break-up time, Schirmer test type I, conjunctival vital staining with fluorescein and lissamine green, tear lysozyme concentration, and impression cytology. Results: Clinical tests yielded the following results: ocular surface disease index Sjogren´s syndrome: 64.5 ± 22.6 meibomian gland dysfunction: 43.5 ± 21.4, non-dry-eye disease: 6.7 ± 4.3 (p=0.02 between groups); Schirmer I test (mm/5 min): Sjogren´s syndrome: 4.95 ± 2.25, meibomian gland dysfunction: 13.28 ± 1.53, non-dry-eye disease 13.70 ± 1.39 (p

Published
2021

10. Tear Lysozyme in Sjögren's syndrome, Meibomian gland dysfunction, and non-dry-eye.

Author

Berra, Martín, Galperín, Gustavo, Berra, Federico, Marquez, Maria Isabel, Mandaradoni, Mariana, Tau, Julia, and Berra, Alejandro

Subjects
MEIBOMIAN glands, SJOGREN'S syndrome, LYSOZYMES, EYE diseases, CYTOLOGY, DRY eye syndromes
Abstract

Copyright of Arquivos Brasileiros de Oftalmologia is the property of Arquivos Brasileiros de Oftalmologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2022
Full Text
View/download PDF

11. Impacto da poluição ambiental na superfície ocular de pacientes com síndrome de Sjögren

Author

Galperín, Gustavo Javier, Berra, Fabio Martín, Marquez, Maria Isabel, Mandaradoni, Mariana, Tau, Julia, and Berra, Alejandro

Subjects
NITROGEN DIOXIDE, CIENCIAS MÉDICAS Y DE LA SALUD, genetic structures, DIÓXIDO DE NITROGÊNIO, SUPERFÍCIE OCULAR, OCULAR SURFACE, Medicina Clínica, DRY EYE SYNDROMES, eye diseases, POLUIÇÃO DO AR, AIR POLLUTION, SÍNDROMES DO OLHO SECO, Sjögren’s syndrome, purl.org/becyt/ford/3.2 [https], Oftalmología, purl.org/becyt/ford/3 [https], sense organs, SJÖGREN'S SYNDROME, SÍNDROME DE SJÖGREN
Abstract

Purpose: To evaluate the effect of air pollution on the ocular surface of patients with Sjögren's syndrome. Methods: We investigated the ocular surfaces of thirty patients with Sjögren's syndrome and thirty healthy volunteers (control group) living in the Metropolitan Area of Buenos Aires. We used nitrogen dioxide as an indicator of exposure to air pollution. An ocular symptoms questionnaire was answered by all subjects, who also underwent a complete ocular surface ophthalmic examination-including an Ocular Surface Disease Index questionnaire, biomicroscopy, tear breakup time, Schirmer 1 test, corneal and conjunctival vital staining with fluorescein and lissamine green, tear lysozyme concentration, and impression cytology. Results: In almost all ocular surface test findings, we found a positive and significant correlation between higher levels of exposure to air pollution and higher levels of ocular surface damage in both the control group and Sjögren's syndrome patients. In Sjögren's syndrome patients, the Ocular Surface Disease Index questionnaire, tear breakup time, vital staining and impression cytology showed a significant correlation between high levels of air pollution and ocular surface disease. In the control group, the Ocular Surface Disease Index questionnaire, tear breakup time, and impression cytology showed a significant correlation between high levels of air pollution and ocular surface disease. Conclusions: Here we demonstrated that in patients with dry eye syndrome associated with Sjögren, abnormalities of the ocular surface and eye irritation related to air pollution are more severe than those in the control group. We believe that measuring air quality should be not only an integral part of the evaluation of ocular surface disease but also a therapeutic consideration. Objetivo: Avaliar o efeito da poluição do ar na superfície ocular de pacientes com síndrome de Sjögren. Métodos: Foram investigadas as superfícies oculares de trinta pacientes com síndrome de Sjögren e trinta voluntários saudáveis (grupo controle) residentes na Região Metropolitana de Buenos Aires. Usamos o dióxido de nitrogênio como um indicador de exposição à poluição do ar. Um questionário de sintomas oculares foi respondido por todos os indivíduos, que também foram submetidos a um exame oftalmológico completo da superfície ocular - incluindo um questionário do Índice da Doença da Superfície Ocular, biomicroscopia, tempo de ruptura do filme lacrimal, teste de Schirmer 1, coloração da córnea e conjuntiva com fluoresceína e lissamina verde, concentração de lisozima lacrimal e citologia de impressão. Resultados: Em quase todos os achados do teste de superfície ocular, encontramos uma correlação positiva e significativa entre níveis mais altos de exposição à poluição do ar e níveis mais elevados de danos na superfície ocular tanto no grupo controle quanto nos pacientes com síndrome de Sjögren. Em pacientes com síndrome de Sjögren, o questionário do Índice da Doença da Superfície Ocular, tempo de ruptura do filme lacrimal, coloração vital e citologia de impressão mostraram uma correlação significativa entre altos níveis de poluição do ar e doença da superfície ocular. No grupo controle, o questionário do Índice de Doenças da Superfície Ocular, tempo de ruptura do filme lacrimal e citologia de impressão mostraram uma correlação significativa entre altos níveis de poluição do ar e doença da superfície ocular. Conclusões: Aqui demonstramos que, pacientes com síndrome de olho seco associada a Sjögren, as anormalidades da superfície ocular e airritação ocular relacionadas à poluição do ar são mais graves do que aquelas no grupo controle. Acreditamos que a medição da qualidade do ar não deve ser apenas uma parte integral da avaliação da doença da superfície ocular, mas também uma consideração terapêutica. Fil: Galperín, Gustavo Javier. Hospital Oftalmológico Pedro Lagleyze; Argentina Fil: Berra, Fabio Martín. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Hospital Oftalmológico Pedro Lagleyze; Argentina Fil: Marquez, Maria Isabel. Bioquímica Ocular; Argentina Fil: Mandaradoni, Mariana. Hospital Nacional Professor Dr. Alejandro Posadas; Argentina Fil: Tau, Julia. Laboratorio de Investigaciones Oculares; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Berra, Alejandro. Laboratorio de Investigaciones Oculares; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina

Published
2018
Full Text
View/download PDF

12. Urban air pollution induces redox imbalance and epithelium hyperplasia in mice cornea

Author

Lasagni Vitar, Romina M., primary, Hvozda Arana, Ailen G., additional, Janezic, Natasha S., additional, Marchini, Timoteo, additional, Tau, Julia, additional, Martinefski, Manuela, additional, Tesone, Agustina I., additional, Racca, Lourdes, additional, Reides, Claudia G., additional, Tripodi, Valeria, additional, Evelson, Pablo A., additional, Berra, Alejandro, additional, Llesuy, Susana F., additional, and Ferreira, Sandra M., additional

Published
2019
Full Text
View/download PDF

13. A Pilot Cross-Sectional Study to Investigate the Biomarker Potential of Phosphorylated Neurofilament-H and Immune Mediators of Disability in Patients With 5 Year Relapsing-Remitting Multiple Sclerosis

Author

Herrera, María Inés, primary, Kölliker-Frers, Rodolfo Alberto, additional, Otero-Losada, Matilde, additional, Perez Lloret, Santiago, additional, Filippo, Macarena, additional, Tau, Julia, additional, Capani, Francisco, additional, and Villa, Andrés M., additional

Published
2019
Full Text
View/download PDF

17. Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin-2 Administration

Author

Romero, Juan Ignacio, primary, Holubiec, Mariana Inés, additional, Tornatore, Tamara Logica, additional, Rivière, Stéphanie, additional, Hanschmann, Eva-Maria, additional, Kölliker-Frers, Rodolfo Alberto, additional, Tau, Julia, additional, Blanco, Eduardo, additional, Galeano, Pablo, additional, Rodríguez de Fonseca, Fernando, additional, Lillig, Christopher Horst, additional, and Capani, Francisco, additional

Published
2017
Full Text
View/download PDF

19. Efecto del déficit de galectina-3 sobre la remodelación ventricular posoclusión coronaria en ratones

Author

Willensky, Luciana, Martínez Naya, Nadia L., Cassaglia, Pablo, Volberg, Verónica I., Tau, Julia, Aruanno, Eugenia, Morgunowsky Michell, Isaac, Morales, Celina, Gónzalez, Germán E., Willensky, Luciana, Martínez Naya, Nadia L., Cassaglia, Pablo, Volberg, Verónica I., Tau, Julia, Aruanno, Eugenia, Morgunowsky Michell, Isaac, Morales, Celina, and Gónzalez, Germán E.

Abstract

Background: Galectin-3 (Gal-3) is a lectin that regulates the immune response. However, its role in remodeling and ventricular function after myocardial infarction (MI) is unknown. Objective: The purpose of this study was to analyze whether Gal-3 deficit impairs remodeling and ventricular function after MI in mice. Methods: Male Gal-3 KO mice and their respective C57 controls underwent anterior descending coronary artery ligation or sham operation. Animals were then divided into four experimental groups: 1) C57 sham; 2) Gal-3 KO sham; 3) C57 MI and 4) Gal-3 KO MI. Seven days after surgery, an echocardiography was performed followed by euthanasia. Heart samples were collected to measure MI size and fibrosis using Masson’s trichrome and picrosirius red, respectively, and assess macrophage infiltration and IL-6 expression. Results: Left ventricular diameters were significantly increased in the C57 MI group compared with sham animals and the increase was even higher in the Gal-3 KO MI group. Moreover, ejection fraction decreased to 47%±2% in C57 MI and 37%±3% in Gal-3 KO MI mice (p<0.02), and infarct size increased from 39.4%±5% in C57 MI to 66.8%±5% in Gal-3 KO MI animals (p=0.002). Macrophage infiltration and fibrosis in the MI area were significantly reduced in Gal-3 KO MI mice (p<0.001 C57 MI vs. Gal-3KO MI) without changes of IL-6 concentration in the left ventricular free wall (p=ns). Conclusions: Gal-3 gene deletion is an important factor in repair kinetics, regulating macrophage infiltration and the degree of fibrosis in the infarct area, as well as early remodeling after MI., Galectina 3 (Gal-3) es una lectina que regula la respuesta inmune. Sin embargo, su rol en el remodelamiento y la función ventricular post-infarto de miocardio (IM) es desconocido. Estudiamos si el déficit de Gal-3 empeora el remodelamiento y la función ventricular post-IM en ratones. Se utilizaron ratones machos Gal-3 KO y su respectivo control C57 con ligadura de la coronaria descendente anterior o Sham. Se realizaron 4 grupos experimentales: C57 Sham, Gal-3 KO Sham, C57 IM y Gal-3 KO IM. A los 7 días post-cirugía, se les realizó ecocardiografía, autopsia, y se cuantificó el tamaño de IM y la fibrosis en cortes teñidos con tricrómico de Masson (TM) y picrosirius red (SR) respectivamente, y el infiltrado de macrófagos y la expresión de IL-6. Los diámetros del VI se incrementaron significativamente en el grupo C57 IM respecto al Sham y dicho incremento fue aun mayor en el grupo Gal-3 KO IM. Además, la fracción de eyección (FE) disminuyó desde 47 ± 2% a 37 ± 3% en en C57 IM y Gal-3 KO IM respectivamente (P< 0.02). El tamaño de IM aumentó desde 39,4 ± 5% en los ratones C57 IM a 66,8 ± 5% en Gal-3 KO (P= 0,002). El infiltrado de macrófagos y la fibrosis en el área de IM se redujeron en los animales Gal-3 KO IM (P< 0,001 C57 IM vs Gal-3 KO IM) mientras que la concentración de IL-6 en la pared libre del VI fue similar entre grupos (P=NS). En conclusión, la deleción de Gal-3 es un factor importante para la cinética del proceso reparativo regulando el infiltrado de macrófagos, el grado de fibrosis de la zona infartada, como así también en la evolución temprana del remodelamiento post-IM.

Published
2015

24. Effects of PUFAs in a Mouse Model of HSV-1 Chorioretinitis.

Author

Berra, Alejandro, Tau, Julia, Zapata, Gustavo, and Chiaradia, Pablo

Subjects
*CHORIORETINITIS, *UNSATURATED fatty acids, *SAFFLOWER oil, *TUMOR necrosis factors, *HIGH-fat diet, *HERPESVIRUSES, *ANIMALS, *BIOLOGICAL models, *CORN oil, *FISH oils, *HERPESVIRUS diseases, *IRIDOCYCLITIS, *MICE, *OMEGA-3 fatty acids, *OMEGA-6 fatty acids, *POLYMERASE chain reaction, *RNA, *TRANSFERASES, *UVEITIS, *VIRAL eye infections, *PHYSIOLOGY
Abstract

Purpose: To examine the effects of n-3 and n-6 polyunsaturated fatty acids (n-3 and n-6 PUFAs) in a murine model of herpetic chorioretinitis.Methods: BALB/c mice were fed on three high fat diets, which contained: Menhaden oil (rich in n-3 PUFAs); Safflower oil (rich in n-6 PUFAs); or Corn oil (rich in saturated fatty acids) as control group, 14 days previously and until 12 days following anterior chamber (AC) HSV-1 inoculation.Results: Mice fed on Menhaden oil present an early development of contralateral chorioretinitis by day 6 post-AC HSV-1 inoculation and also significant increase of RNA HSV-1 expression compared with Safflower and Corn oil groups. Furthermore, mice fed on Menhaden oil showed a significant decrease secretion of TNF-α, IFN-γ, IL-2 and IL-10 in splenic cells and both retinas.Conclusion: Our results showed that mice fed on Menhaden oil (n-3 PUFAs) presented an early development of contralateral chorioretinitis by day 6 post-AC HSV-1 inoculation and also a significant increase in RNA HSV-1 expression compared with animals fed on Safflower and Corn oils. This increase of HSV-1 could be associated with the higher development of chorioretinitis. [ABSTRACT FROM AUTHOR]

Published
2017
Full Text
View/download PDF

25. Expresión y rol del slpi (secretory leukocyte protease inhibitor) en la inmunidad innata del ojo asociado a procesos inflamatorios e infecciosos oculares

Author

Reviglio, Victor Eduardo, Sambuelli, Rubén Horacio, Berra, Alejandro, Grenat, Andrés R., Luján, Hugo Daniel, Tau, Julia, Reviglio, Victor Eduardo, Sambuelli, Rubén Horacio, Berra, Alejandro, Grenat, Andrés R., Luján, Hugo Daniel, and Tau, Julia

Abstract

En la terapia antimicrobiana, se pretende comprender y desarrollar sinergia con los mecanismos de defensa innatos del huésped, en el área oftalmológica, los relacionados a procesos oculares infecciosos tanto específicos como no específicos. Conservando y estimulando la presencia de los péptidos antimicrobianos, se obtendría una prevención e inhibición de los microorganismos responsables de los principales procesos infecciosos e inflamatorios oculares, que permitirá un tratamiento rápido y eficaz en el control del proceso patológico.De esta forma se podrá evitar secuelas devastadoras de dichas complicaciones que en un gran porcentaje llevan a la ceguera del paciente asociadas al diagnóstico tardío, inespecífico o asociado a resistencia a los antibióticos actuales.Los péptidos antimicrobianos y anti-inflamatorios prometen ser un método terapéutico eficaz, natural, libre de efectos secundarios y adversos en la terapia antimicrobiana e inmuno moduladora futura.Basados en estudios publicados realizados en animales, estos péptidos con capacidad antibacteriana se expresarían en tejidos oculares normales actuando como agentes antimicrobianos de la inmunidad innata del ojo y así también como regulador de la actividad inflamatoria. Estos péptidos antimicrobianos – anti inflamatorios podrían utilizarse para la prevención y tratamiento de procesos infecciosos oculares, en formulaciones simples o combinadas a otras sustancias antibióticas antimicrobianas en forma sinérgica.Secretory leukocyte protease inhibitor (SLPI), terminología anglosajona que se utilizo para definir a una proteína de 12 kDa de peso molecular cuya única función conocida hasta hace unos años era la de ser secretada por leucocitos para inhibir proteasas de la matriz extracelular. El objetivo es estudiar la presencia del péptido antimicrobiano SLPI en relación con el remodelado cicatrizal de la matriz extracelular de la cornea y otras estructuras intra oculares, como así también su expresión en relación a proce, Fil: Reviglio. Víctor Eduardo. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; Argentina, Fil: Sambuelli, Rubén Horacio. Universidad Católica de Córdoba. Facultad de Ciencias de la Salud; Argentina

Published
2012

26. Reply

Author

Berra, Martin, primary, Galperin, Gustavo, additional, Boscaro, Gabriela, additional, Zarate, Jorge, additional, Tau, Julia, additional, Chiaradia, Pablo, additional, and Berra, Alejandro, additional

Published
2013
Full Text
View/download PDF

28. Reply

Author

Galperín, Gustavo, primary, Berra, Martín, additional, Tau, Julia, additional, Boscaro, Gabriela, additional, Zarate, Jorge, additional, and Berra, Alejandro, additional

Published
2013
Full Text
View/download PDF

33. Impact of wildfire smoke in Buenos Aires, Argentina, on ocular surface.

Author

BERRA, MARTIN, GALPERÍN, GUSTAVO, DAWIDOWSKI, LAURA, TAU, JULIA, MÁRQUEZ, ISABEL, and BERRA, ALEJANDRO

Subjects
PHYSIOLOGICAL effects of smoke, FLUORESCEIN, ROSE bengal, ARTIFICIAL hyperemia, HYPEREMIA, CYTOLOGY, PARTICULATE matter, THERAPEUTICS
Abstract

Copyright of European Journal of Translational Myology is the property of PAGEPress and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Published
2015
Full Text
View/download PDF

34. Neuronal Damage Induced by Perinatal Asphyxia Is Attenuated by Postinjury Glutaredoxin-2 Administration

Author

Christopher Horst Lillig, Fernando Rodríguez de Fonseca, Mariana Inés Holubiec, Julia Tau, Tamara Maite Ayelén Logica Tornatore, Juan Ignacio Romero, Rodolfo Alberto Kölliker-Frers, Eduardo Blanco, Stéphanie Rivière, Eva-Maria Hanschmann, Pablo Galeano, Francisco Capani, [Ignacio Romero, Juan] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Ines Holubiec, Mariana] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Logica Tornatore, Tamara] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Riviere, Stephanie] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Alberto Kolliker-Frers, Rodolfo] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Capani, Francisco] UBA CONICET, Fac Med, Inst Invest Cardiol Prof Dr Alberto C Taquini INI, Marcelo T de Alvear 2270,C1122AAJ, Buenos Aires, DF, Argentina, [Hanschmann, Eva-Maria] Heinrich Heine Univ, Med Fac, Dept Neurol, Dusseldorf, Germany, [Hanschmann, Eva-Maria] Ernst Moritz Arndt Univ Greifswald, Univ Med Greifswald, Inst Med Biochem & Mol Biol, D-17475 Greifswald, Germany, [Lillig, Christopher Horst] Ernst Moritz Arndt Univ Greifswald, Univ Med Greifswald, Inst Med Biochem & Mol Biol, D-17475 Greifswald, Germany, [Tau, Julia] Univ Buenos Aires, Sch Med, Dept Pathol, Lab Ocular Invest, Buenos Aires, DF, Argentina, [Blanco, Eduardo] Univ Lleida, Fac Educ Psicol & Treball Social, Dept Pedag & Psicol, Avda Estudi Gen 4, Lleida 25001, Spain, [Galeano, Pablo] Fdn Inst Leloir, Av Patricias Argentinas 435,C1405BWE, Buenos Aires, DF, Argentina, [Rodriguez de Fonseca, Fernando] Univ Malaga, Hosp Reg Univ Malaga, Inst Invest Biomed Malaga, Unidad Gest Clin Salud Mental, Avda Carlos Haya 82, Malaga 29010, Spain, [Capani, Francisco] Univ Argentina JF Kennedy, Dept Biol, Buenos Aires, DF, Argentina, [Capani, Francisco] Univ Autonoma Chile, Santiago, Chile, Deutsche Forschungsgemeinschaft, Federal Ministry for Science and Education, MINCYT, German Academic Exchange Service DAAD, MINCYT (PROALAR program), National Scientific and Technical Research Council (CONICET, Argentina), Instituto de Salud Carlos III, Ministerio de Economia y Competitividad UE/ERDF, Fundacio 'La Marato de TV3', and University of Buenos Aires

Subjects
Cerebellar granule neurons, 0301 basic medicine, Male, Aging, Mixed disulfide, Redox control, Excitotoxicity, Pharmacology, medicine.disease_cause, Biochemistry, 0302 clinical medicine, Medicine, Neurons, lcsh:Cytology, Glutamate receptor, purl.org/becyt/ford/3.1 [https], General Medicine, Astrogliosis, Medicina Básica, Neurology, Anesthesia, Hypoxia-Ischemia, Brain, purl.org/becyt/ford/3 [https], Thioredoxin, medicine.symptom, Research Article, Perinatal Asphyxia, CIENCIAS MÉDICAS Y DE LA SALUD, Article Subject, Ischemic brain-damage, Neurociencias, Ischemia, Brain damage, Neuroprotection, Neurological reflexes, Neurologia, 03 medical and health sciences, Asphyxia, Cerebral-ischemia, Animals, lcsh:QH573-671, Glutaredoxins, Dopamine-induced apoptosis, Nf-kappa-b, business.industry, Cell Biology, medicine.disease, Perinatal asphyxia, Rats, Treatment, Disease Models, Animal, 030104 developmental biology, Animals, Newborn, Heat-shock-protein, Oxidative stress, Grx2, business, 030217 neurology & neurosurgery
Abstract

The general disruption of redox signaling following an ischemia-reperfusion episode has been proposed as a crucial component in neuronal death and consequently brain damage. Thioredoxin (Trx) family proteins control redox reactions and ensure protein regulation via specific, oxidative posttranslational modifications as part of cellular signaling processes. Trx proteins function in the manifestation, progression, and recovery following hypoxic/ischemic damage. Here, we analyzed the neuroprotective effects of postinjury, exogenous administration of Grx2 and Trx1 in a neonatal hypoxia/ischemia model. P7 Sprague-Dawley rats were subjected to right common carotid ligation or sham surgery, followed by an exposure to nitrogen. 1 h later, animals were injected i.p. with saline solution, 10 mg/kg recombinant Grx2 or Trx1, and euthanized 72 h postinjury. Results showed that Grx2 administration, and to some extent Trx1, attenuated part of the neuronal damage associated with a perinatal hypoxic/ischemic damage, such as glutamate excitotoxicity, axonal integrity, and astrogliosis. Moreover, these treatments also prevented some of the consequences of the induced neural injury, such as the delay of neurobehavioral development. To our knowledge, this is the first study demonstrating neuroprotective effects of recombinant Trx proteins on the outcome of neonatal hypoxia/ischemia, implying clinical potential as neuroprotective agents that might counteract neonatal hypoxia/ischemia injury Fil: Romero, Juan Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Holubiec, Mariana Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Tornatore, Tamara Logica. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Rivière, Stéphanie. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Hanschmann, Eva Maria. Heinrich Heine University; Argentina Fil: Kölliker Frers, Rodolfo Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina Fil: Tau, Julia. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Patología; Argentina Fil: Blanco, Eduardo. Universidad de Lleida; España Fil: Galeano, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Instituto de Investigaciones Bioquímicas de Buenos Aires. Fundación Instituto Leloir. Instituto de Investigaciones Bioquímicas de Buenos Aires; Argentina Fil: Rodríguez de Fonseca, Fernando. Universidad de Málaga; España Fil: Lillig, Christopher Horst. Heinrich Heine University; Alemania Fil: Capani, Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina. Universidad de Chile; Chile. Universidad Argentina "John F. Kennedy"; Argentina

Published
2017

35. Tear Lysozyme in Sjögren´s syndrome, Meibomian gland dysfunction, and non-dry-eye.

Author

Berra M, Galperín G, Berra F, Marquez MI, Mandaradoni M, Tau J, and Berra A

Subjects
Humans, Meibomian Glands, Muramidase, Tears, Dry Eye Syndromes diagnosis, Meibomian Gland Dysfunction, Sjogren's Syndrome complications
Abstract

Purpose: To evaluate the concentration of tear lysozyme in individuals with Sjogren´s syndrome, meibomian gland dysfunction, and non-dry-eye disease., Methods: Ninety subjects were recruited for this study, including 30 with Sjogren´s syndrome, 30 with meibomian gland dysfunction, and 30 with non-dry-eye disease. All subjects were referred to participate in the study based on a "dry eye" investigation. They underwent a complete ocular surface ophthalmic examination encompassing ocular surface disease index, biomicroscopy, tear break-up time, Schirmer test type I, conjunctival vital staining with fluorescein and lissamine green, tear lysozyme concentration, and impression cytology., Results: Clinical tests yielded the following results: ocular surface disease index Sjogren´s syndrome: 64.5 ± 22.6 meibomian gland dysfunction: 43.5 ± 21.4, non-dry-eye disease: 6.7 ± 4.3 (p=0.02 between groups); Schirmer I test (mm/5 min): Sjogren´s syndrome: 4.95 ± 2.25, meibomian gland dysfunction: 13.28 ± 1.53, non-dry-eye disease 13.70 ± 1.39 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease); tear break-up time (seconds): Sjogren´s syndrome: 3.97 ± 1.47, meibomian gland dysfunction: 3.95 ± 0.86, non-dry-eye disease: 7.25 ± 1.90 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease); Lissamine green score: Sjogren´s syndrome-dry-eye: 6.18 ± 2.14, meibomian gland dysfunction-dry-eye: 5.27 ± 1.27, non-dry-eye disease: 1.52 ± 0.97 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease); impression cytology score: Sjogren´s syndrome: 1.88 ± 0.92, meibomian gland dysfunction: 1.67 ± 0.56, non-dry-eye: 0.45 ± 0.44 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 meibomian gland dysfunction vs. non-dry-eye disease) and; tear lysozyme concentration (µg/mL): Sjogren´s syndrome: 751.25 ± 244.73, meibomian gland dysfunction: 1423.67 ± 182.75, non-dry-eye disease: 1409.90 ± 188.21 (p<0.01 Sjogren´s syndrome vs. non-dry-eye disease and p<0.01 Sjogren´s syndrome vs. meibomian gland dysfunction)., Conclusion: The concentration of lysozyme in the tears was lower in Sjögren's syndrome patients than in meibomian gland dysfunction and non-dry-eye disease groups. Hence, the lacrimal lysozyme could be considered as a simple, non-invasive, and economical biomarker to differentiate between Sjögren's syndrome dry eye disease and meibomian gland dysfunction dry eye disease.

Published
2021
Full Text
View/download PDF

36. Reply: To PMID 22081155.

Author

Galperín G, Berra M, Tau J, Boscaro G, Zarate J, and Berra A

Subjects
Animals, Eye Infections, Fungal radiotherapy, Fusariosis radiotherapy, Keratitis radiotherapy, Ultraviolet Therapy
Published
2013
Full Text
View/download PDF

37. [Crystalline keratopathy: an infrequent corneal infection produced by the Streptococcus mitis group].

Author

Galperín GJ, Boscaro G, Tau J, and Berra M

Subjects
Anti-Bacterial Agents therapeutic use, Combined Modality Therapy, Conjunctiva surgery, Equipment Contamination, Female, Humans, Keratitis diagnosis, Keratitis drug therapy, Keratitis surgery, Middle Aged, Streptococcal Infections diagnosis, Streptococcal Infections drug therapy, Streptococcal Infections surgery, Streptococcus mitis drug effects, Surgical Flaps, Surgical Wound Infection diagnosis, Sutures microbiology, Vancomycin therapeutic use, Keratitis microbiology, Keratoplasty, Penetrating, Streptococcal Infections microbiology, Streptococcus mitis isolation & purification, Surgical Wound Infection microbiology, Sutures adverse effects
Abstract

The objective of this report is to describe a case of crystalline keratopathy caused by the Streptococcus mitis group corresponding to a patient who attended hospital for discomfort in her right eye. The ophthalmological examination showed an interrupted stitch of 10-0 nylon suture without tension and with attached mucus secretions. The loose suture was removed under aseptic conditions. Moxifloxacin 0.5 % eye drops were topically indicated. The treated eye successfully epithelialized and evolved favorably. However, after 15 days, a white tree-shaped infiltrate developed. A corneal sample was taken in the operating room, threading the intrastromal path of the removed stitch with a 7-0 vicryl suture. Vancomycin 50 mg/ml drops were indicated. The infiltrate, which was stable for 45 days, later increased its size and tissue necrosis occurred with danger of corneal perforation. A bipedicle conjunctival flap was performed in the affected corneal area, which evolved favorably. After spontaneous conjunctival flap retraction, only corneal scarring and neovascularization outside the visual axis were observed.

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results