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Consensus recommendations on the management of multiple sclerosis patients in Argentina
No full textIntroduction
During the last 20 years, multiple sclerosis (MS) disease has seen major changes with new diagnostic criteria, a better identification of disease phenotypes, individualization of disease prognosis and the appearance of new therapeutic options in relapsing remitting as well as progressive MS. As a result, the management of MS patients has become more complex and challenging. The objective of these consensus recommendations was to review how the disease should be managed in Argentina to improve long-term outcomes in MS patients.
Methods
A panel of 36 experts in neurology from Argentina, dedicated to the diagnosis and care of MS patients, gathered both virtually and in person during 2018 and 2019 to carry out a consensus recommendation on the management of MS patients in Argentina. To achieve consensus, the methodology of “formal consensus-RAND/UCLA method” was used.
Results
Recommendations focused on diagnosis, disease prognosis, tailored treatment, treatment failure identification and pharmacovigilance process.
Conclusions
The recommendations of these consensus guidelines attempt to optimize the health care and management of patients with MS in Argentina.Fil: Cristiano, Edgardo. Hospital Italiano de Buenos Aires Centro de Esclerosis Múltiple de Buenos Aires; Argentina.Fil: Rojas, Juan Ignacio. Hospital Italiano de Buenos Aires. Centro de Esclerosis Múltiple de Buenos Aires; Argentina.Fil: Alonso, Ricardo. Hospital Ramos Mejía. Centro Universitario de Esclerosis Múltiple; Argentina. Hospital Universitario Sanatorio Güemes; Argentina.Fil: Alvez Pinheiro, Amelia. Hospital San Martín; Argentina.Fil: Bacile, Elizabeth A. Instituto Privado de Neurociencias Córdoba; Argentina.Fil: Balbuena Aguirre, María Eugenia. Hospital de Clinicas "Jose de San Martin" . Servicio de Neurologia. Seccion de Neuroinmunologia y Enfermedades Desmielinizantes; Argentina.Fil: Barboza, Andrés G. Hospital Central de Mendoza; Argentina.Fil: Bestoso, Santiago. Universidad Nacional del Nordeste. Facultad de Medicina. Hospital Escuela de Corrientes. Servicio de Neurología; Argentina.Fil: Burgos, Marcos. Hospital San Bernardo; Argentina.Fil: Cáceres, Fernando. Fundación Favaloro. Instituto de Neurociencias; Argentina. Fil: Carnero Contentti, Edgar. Hospital Alemán. Departmento de Neurosciencias. Unidad de Neuroinmunología; Argentina.Fil: Curbelo, María Celeste. Hospital Británico. Sección de Esclerosis Múltiple; Argentina. Policlinico Municipal "Sofía T. de Santamarina"; Argentina.Fil: Deri, Norma. Instituto de Asistencia Integral en Diabetes y Patologías Crónicas; Argentina. Hospital General de Agudos "Dr.. Juan A. Fernández"; Argentina.Fil: Fernandez Liguori, Nora. Hospital General de Agudos "Dr. Enrique Tornú"; Argentina. Fundación Sanatorio Güemes; Argentina.Fil: Gaitán, María Inés. Fleni. Departamento de Neurología; Argentina.Fil: Garcea, Orlando. Hospital Ramos Mejía. Centro Universitario de Esclerosis Múltiple; Argentina.Fil: Giunta, Diego Hernán. Hospital Italiano de Buenos Aires. Sección de Investigación Clínica; Argentina.Fil: Halfon, Mario Javier. Hospital Británico; Argentina. Hospital Prof. Dr. Bernardo A. Houssay; Argentina.Fil: Hryb, Javier Pablo. Hospital General de Agudos "Carlos G. Durand". Servicio de Neurología; Argentina.Fil: Jacobo, Miguel. Red Integral Asistencial al Paciente con Esclerosis Múltiple; Argentina.Fil: Kohler, Eduardo. Fundación Sinapsis; Argentina.Fil: Luetic, Geraldine G. Instituto de Neurociencias de Rosario; Argentina.Fil: Martínez, Alejandra Diana. Hospital Británico. Sección de Esclerosis Múltiple; Argentina.Fil: Míguez, Jimena S. Hospital Italiano de Buenos Aires. Centro de Esclerosis Múltiple de Buenos Aires; Argentina.Fil: Nofal, Pedro G. Hospital de Clínicas "Nuestra Sra. del Carmen"; Argentina.Fil: Patrucco, Liliana. Hospital Italiano de Buenos Aires Centro de Esclerosis Múltiple de Buenos Aires; Argentina.Fil: Piedrabuena, Raúl. Clinica Universitaria "Reina Fabiola"; Argentina. Instituto Modelo de Neurología "Lennox"; Argentina.Fil: Rotta Escalante, Roberto. Policlínico Bancario. Servicio de Neurología; Argentina.Fil: Saladino, María Laura. Fundación Favaloro. Instituto de Neurociencias; Argentina. Fil: Silva, Berenice Anabel. Hospital Ramos Mejía. Centro Universitario de Esclerosis Múltiple; Argentina.Fil: Sinay, Vladimiro. Fundación Favaloro. Instituto de Neurología Cognitiva; Argentina.Fil: Tkachuk, Verónica. Hospital de Clínicas "José de San Martín". Servicio de Neurología. Sección de Neuroinmunología y Enfermedades Desmielinizantes; Argentina.Fil: Villa, Andrés. Hospital Ramos Mejia. Sección Neuroinmunología; Argentina.Fil: Vrech, Carlos. Sanatorio Allende. Departamento de Enfermedades Desmielinizantes; Argentina.Fil: Ysrraelit, María Célica. Fleni. Departamento de Neurología; Argentina.Fil: Correale, Jorge. Fleni. Departamento de Neurología. Servicio de Neuroinmunología y Enfermedades Desmielinizantes; Argentin
Comparing cortical signatures of atrophy between late-onset and autosomal dominant Alzheimer disease
No full textDefining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone. Since late-onset Alzheimer disease (LOAD) participants tend to have age-related comorbidities, the younger-onset age in autosomal dominant AD (ADAD) may provide a more idealized model of cortical thinning in AD. To test this, the goals of this study were to compare the degree of overlap between the ADAD and LOAD cortical thinning maps and to evaluate the ability of the ADAD cortical signature regions to predict early pathological changes in cognitively normal individuals. We defined and analyzed the LOAD cortical maps of cortical thickness in 588 participants from the Knight Alzheimer Disease Research Center (Knight ADRC) and the ADAD cortical maps in 269 participants from the Dominantly Inherited Alzheimer Network (DIAN) observational study. Both cohorts were divided into three groups: cognitively normal controls (nADRC = 381; nDIAN = 145), preclinical (nADRC = 153; nDIAN = 76), and cognitively impaired (nADRC = 54; nDIAN = 48). Both cohorts underwent clinical assessments, 3T MRI, and amyloid PET imaging with either 11C-Pittsburgh compound B or 18F-florbetapir. To generate cortical signature maps of cortical thickness, we performed a vertex-wise analysis between the cognitively normal controls and impaired groups within each cohort using six increasingly conservative statistical thresholds to determine significance. The optimal cortical map among the six statistical thresholds was determined from a receiver operating characteristic analysis testing the performance of each map in discriminating between the cognitively normal controls and preclinical groups. We then performed within-cohort and cross-cohort (e.g. ADAD maps evaluated in the Knight ADRC cohort) analyses to examine the sensitivity of the optimal cortical signature maps to the amyloid levels using only the cognitively normal individuals (cognitively normal controls and preclinical groups) in comparison to hippocampal volume. We found the optimal cortical signature maps were sensitive to early increases in amyloid for the asymptomatic individuals within their respective cohorts and were significant beyond the inclusion of hippocampus volume, but the cortical signature maps performed poorly when analyzing across cohorts. These results suggest the cortical signature maps are a useful MRI biomarker of early AD-related neurodegeneration in preclinical individuals and the pattern of decline differs between LOAD and ADAD.Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Dincer, Aylin. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Gordon, Brian A. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Hari-Raj, Amrita.The Ohio State University College of Medicine; Estados Unidos.Fil: Keefe, Sarah J. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Flores, Shaney. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: McKay, Nicole S. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Paulick, Angela M. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Feldman, Rebecca L. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Shady Lewis, Kristine E. University of Kentucky College of Medicine. Sanders Brown Center on Aging & Alzheimer's; Estados Unidos.Fil: Hornbeck, Russ C. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Ances, Beau M. Washington University School of Medicine. Department of Radiology, Department of Neurology, Department of Psychiatry, Department of Pathology and Immunology, Division of Biostatistics; Estados Unidos.Fil: Berman, Sarah B. University of Pittsburgh School of Medicine. Department of Neurology and Clinical & Translational Science; Estados Unidos.Fil: Brickman, Adam M. Columbia University. College of Physicians and Surgeons. Taub Institute for Research on Alzheimer's Disease and the Aging Brain and Department of Neurology; Estados Unidos.Fil: Brooks, William S. Neuroscience Research Australiay; Australia. University of New South Wales. Prince of Wales Clinical School; Australia.Fil: Cash, David M. UCL Queen Square Institute of Neurology. Dementia Research Centre and UK Dementia Research Institute; Reino Unido.Fil: Chhatwal, Jasmeer P. Harvard Medical School. Massachusetts General Hospital. Department of Neurology; Estados Unidos.Fil: Farlow, Martin R. Indiana University School of Medicine. Department of Radiology and Imaging Science. Department of Neurology; Estados Unidos.Fil: La Fougère, Christian. German Center for Neurodegenerative Diseases (DZNE); Alemania. University Hospital of Tübingen. Department of Nuclear Medicine and Clinical Molecular Imaging; Alemania.Fil: Fox, Nick C. UCL Queen Square Institute of Neurology. Dementia Research Centre and UK Dementia Research Institute; Reino Unido
Parkin Pleiotropy: Extremely Atypical Phenotypes in Patients With Compound Heterozygous Mutations
No full textBackground: Parkin mutations are suspected in early-onset Parkinson's disease with early motor complications, and in pedigrees showing an autosomal recessive pattern. Some compound heterozygous mutations can present with various uncommon phenotypes.
Case report: Two siblings with the same mutations, one with atypical postural and action tremor, and the other with an axonal motor autonomic neuropathy. A woman with a 45-year history of slowly progressive parkinsonism with no motor complications.
Discussion: Due to the variability of phenotypes of Parkin mutations, testing should also be warranted in patients with atypical tremor syndromes or axonal polyneuropathy when more common causes have been ruled out.
Highlights: We report three patients with extremely atypical parkin mutation phenotypes: an atypical tremor syndrome, an axonal motor autonomic neuropathy, and a remarkably slowly progressive parkinsonism. This shows that parkin mutations may present with a highly variable phenotype, and should be considered in patients with such manifestations.Fil: Millar Vernetti, Patricio. Fleni. Departamento de Neurología. Servicio de Movimientos Anormales; Argentina.Fil: Merello, Marcelo. Fleni. Departamento de Neurología. Servicio de Movimientos Anormales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Pontificia Universidad Católica; ArgentinaFil: Rossi, Malco. Fleni. Departamento de Neurología. Servicio de Movimientos Anormales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Creation of the Argentina-Sports Concussion Assessment & Research Study (Arg-SCARS).
No full textFil: Russo, María Julieta. Fleni. Centro de Rehabilitación Adultos CR; Argentina.Fil: Salvat, Fernando. Fleni. Departamento de Neurología. Clínica del Dolor; Argentina.Fil: Sevlever, Gustavo Emilio. Fleni. Departamento de Neuropatología y Biología Molecular. Laboratorio de Enfermedades Neurodegenerativas; Argentina
Results in the treatment of intracranial hemangiopericytomas. Case series
No full textObjective: Intracranial hemangiopericytoma (HPC) is a rare central nervous system tumor characterized by its low incidence, high rate of local recurrence and risk of metastasis. The main objectives of this paper are two: to show the results in the treatment of HPC in our institution in the last 20years and to make a review of the literature on this topic.
Methods: Retrospective review that includes patients diagnosed with intracranial solitary fibrous tumor/hemangiopericytoma (SFT/HPC) that have undergone surgery from 1997 to 2017. It includes patients that had nuclear expression of STAT-6 (detected by immunohistochemistry) and gradeII/III histopathological diagnosis (defined by the World Health Organization in 2016). We collected demographic data, tumor characteristics, treatment and survival of these patients.
Results: A total of 19 patients fulfilled inclusion criteria. The median follow up was 96 months (12-230). The mortality rate was 21% (n=4). 57.9% of patients presented at least one tumor recurrence (n=11) (recurrences of 6%, 67% y 90% at 1, 5 and 10years). Five patients presented extracranial metastasis. Patients with tumors <6cm had greater survival (P<.05).
Conclusions: A series of patients undergoing SFT/HPC were presented according to the new WHO criteria. Size is a predictor of survival. Currently there are no validated criteria for surgical resection in this pathology. A classification with surgical guidance would be useful.Fil: Marcó del Pont, Francisco. Fleni. Departamento de Neurocirugía; Argentina.Fil: Lorefice, Fernando. Fleni. Departamento de Neurología; ArgentinaFil: Giovannini, Sebastián Juan María. Fleni. Departamento de Neurología; Argentina.Fil: Cervio, Andrés Eduardo. Fleni. Departamento de Neurocirugía; Argentina.Fil: Ries Centeno, Tomás. Fleni. Departamento de Neurocirugía; Argentina.Fil: Villalonga, Juan Francisco. Fleni. Departamento de Neurocirugía; Argentina.Fil: Caffaratti, Guido. Fleni. Departamento de Neurocirugía; Argentina
Adaptación creativa y longevidad; más que una función ejecutiva. Mirada integradora
No full textResumen no disponibleFil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.Fil: Iturry, Mónica. Hospital de Agudos Dr. Abel Zubizarreta; Argentina.Fil: Leis, Adriana. Sanatorio de la Trinidad Mitre; Argentina
Emerging PD-1 and PD-1L inhibitors-associated myopathy with a characteristic histopathological pattern
Get PDFBackground and objective: Drug-induced myopathy is among the most common causes of muscle disease. An association has recently been described between programmed death-1 (PD-1)/PD-1 ligand (PD-L1) inhibitors and immune-related adverse events (irAE) affecting the muscle. Here, we report the clinical and pathological findings of nine unrelated patients with PD-1 and PD-L1 inhibitors-associated myopathy.
Methods: We retrospectively analyzed 317 muscle biopsies performed for diagnostic purposes from January 2017 to June 2019. Patients were attended in two tertiary centers and muscle biopsies were performed and analyzed by two myology experts. Muscle biopsies were frozen in cooled isopenthane, cryostat sectioned and stained. Immunohistochemistry studies were also performed as a routine procedure in our lab.
Results: We identified 9 patients receiving anti-PD-1 or PD-L1 inhibitors consulting for either muscle weakness, asthenia, myasthenic-like syndrome or other muscle related-symptoms, along with biopsy-proven inflammatory myopathy. One had concomitant myocarditis. In most of the cases muscle biopsy showed a marked phenomenon of necrosis, macrophagy and muscle regeneration with perivascular inflammatory infiltrates with a large component of macrophagic cells. A tendency to perifascicular atrophy was also noticed. The expression of MHC class I antigens predominated in the perifascicular zones. Raised muscle enzymes were detected in 7 patients.
Conclusion: A characteristic clinic-pathological pattern, including a myasthenia gravis-like syndrome plus myositis was found in patients receiving PD-1 and PD-1 L inhibitors. A large component of macrophages resembling granulomas seems to be the pathological hallmark of the syndrome. Further information is required to understand the wide spectrum of immune-related adverse events involving the muscle during or after treatment with anti-PD-1 inhibitors, but the pathological picture seems to be characteristic.Fil: Antoniol, María Noelia. Fleni. Departamento de Medicina Interna. Sección de Reumatología; Argentina.Fil: Selva O’Callaghan, Albert. Hospital Vall d'Hebron. Internal Medicine Department. Systemic Autoimmune Diseases Unit; España.Fil: Grau, Josep María. Hospital Clínic de Barcelona. Internal Medicine Department. Muscle Research Unit; España. Universidad de Barcelona. Center for Biomedical Research on Rare Diseases; España.Fil: Padrosa, Joan. Hospital Clínic de Barcelona. Internal Medicine Department. Muscle Research Unit; España. Universidad de Barcelona. Center for Biomedical Research on Rare Diseases; España.Fil: Milisenda, José C. Hospital Clínic de Barcelona. Internal Medicine Department. Muscle Research Unit; España. Universidad de Barcelona. Center for Biomedical Research on Rare Diseases; España.Fil: Matas-García, Ana. Hospital Clínic de Barcelona. Internal Medicine Department. Muscle Research Unit; España. Universidad de Barcelona. Center for Biomedical Research on Rare Diseases; España.Fil: Prieto-González, Sergio. Hospital Clínic de Barcelona. Department of Autoimmune Diseases; España. Universitat de Barcelona; España.Fil: Cabrera, Carlos. Hospital Clínic de Barcelona. Medical Oncology Department; España.Fil: Reguart, Noemi. Hospital Clínic de Barcelona. Medical Oncology Department; España.Fil: Castrejón, Natalia. Hospital Clínic de Barcelona. Pathology Department; España.Fil: Solé, Manel. Hospital Clínic de Barcelona. Pathology Department; España.Fil: Ros, Javier. Hospital Universitari Vall d'Hebron. Medical Oncology Department; España.Fil: Trallero-Araguas, Ernesto. Hospital Universitari Vall d'Hebron. Rheumatology Unit; España.Fil: Vila-Pijoan, Gemma. Hospital Universitari Vall d'Hebron. Immunology Department; España
CoViD-19: perspectivas y vulnerabilidad
No full textLa enfermedad del coronavirus 2019 (CoViD-19: Coronavirus Disease 2019) es causada por el síndrome respiratorio
agudo severo coronavirus-2 (SARS-CoV-2: severe acute respiratory syndrome coronavirus 2) y se ha extendido
mundialmente como una pandemia. Es de resaltar que CoViD-19 superó el sistema de atención médica en muchos
países, debido a la rapidez de su propagación y a la falta de previsión a nivel sanitario, así como a la subvaloración
de su contagiosidad. Además, al ser una entidad nosológica nueva y desconocida, no existen aún tratamientos que
hayan demostrado ser científicamente efectivos y seguros; así como tampoco una vacuna que permita aniquilar la
pandemia. Por eso, la única respuesta hasta ahora ha sido tratar de limitar la propagación de la enfermedad a través
de buenas prácticas de higiene y distanciamiento social. Todo ello ha provocado el cierre de las principales partes
de la economía y un alto desempleo repentino, ocasionando consecuencias negativas y una recesión nunca vista.
Las estrategias más ampliamente adoptadas han involucrado el enfoque epidemiológico de fomentar las buenas
prácticas de higiene y el distanciamiento social, incluidas las órdenes de refugio en el lugar y cuarentena. Estas
estrategias han tenido diversos grados de éxito según el país. La frase común utilizada para describir el objetivo
de este enfoque epidemiológico es aplanar la curva, efecto que se logra a partir de la reducción de los contagios.
Este enfoque también fue una forma de ganar tiempo para aprender más sobre la enfermedad y encontrar formas
más efectivas de tratamiento, preparar a los sistemas de salud, es decir, desarrollar terapias y vacunas validadas.
Otro enfoque sería el de restablecer más rápidamente la economía y ayudaría así a toda la población a evitar los
profundos efectos adversos de una grave recesión o depresión para la sociedad y la salud; así, como, aumentaría
la inmunidad de la comunidad, lo que reduciría el riesgo para todos, incluidos los más susceptibles a resultados
adversos graves, y aquellos que desarrollan inmunidad podrían donar suero enriquecido con anticuerpos, lo que
podría proporcionar un tratamiento efectivo mientras se desarrollan y prueban las vacunas y tratamientos efectivos
para combatir la enfermedad. El balance entre las estrategias del enfoque epidemiológico para atenuar la curva de
contagio y el intento por reabrir una población y su economía serán la clave para un futuro venturoso.
Este artículo fue escrito con la esperanza de ayudar a los profesionales a comprender los problemas ocasionados
por CoViD-19.Fil: Perrone, Sergio Victor. Fleni. Servicio de Cardiología; Argentina. Instituto Argentino de Diagnóstico y Tratamiento; Argentina. Hospital de Alta Complejidad en Red “El Cruce” Néstor Kirchner; Argentina.Fil: Bevacqua, Raúl J. Hospital General de Agudos Dr. J. M. Ramos Mejía. División Cardiología; Argentina
Structural brain abnormalities in schizophrenia in adverse environments: examining the effect of poverty and violence in six Latin American cities
No full textBackground
Social and environmental factors such as poverty or violence modulate the risk and course of schizophrenia. However, how they affect the brain in patients with psychosis remains unclear.
Aims
We studied how environmental factors are related to brain structure in patients with schizophrenia and controls in Latin America, where these factors are large and unequally distributed.
Method
This is a multicentre study of magnetic resonance imaging in patients with schizophrenia and controls from six Latin American cities. Total and voxel-level grey matter volumes, and their relationship with neighbourhood characteristics such as average income and homicide rates, were analysed with a general linear model.
Results
A total of 334 patients with schizophrenia and 262 controls were included. Income was differentially related to total grey matter volume in both groups (P = 0.006). Controls showed a positive correlation between total grey matter volume and income (R = 0.14, P = 0.02). Surprisingly, this relationship was not present in patients with schizophrenia (R = −0.076, P = 0.17). Voxel-level analysis confirmed that this interaction was widespread across the cortex. After adjusting for global brain changes, income was positively related to prefrontal cortex volumes only in controls. Conversely, the hippocampus in patients with schizophrenia, but not in controls, was relatively larger in affluent environments. There was no significant correlation between environmental violence and brain structure.
Conclusions
Our results highlight the interplay between environment, particularly poverty, and individual characteristics in psychosis. This is particularly important for harsh environments such as low- and middle-income countries, where potentially less brain vulnerability (less grey matter loss) is sufficient to become unwell in adverse (poor) environments.Fil: Crossley, Nicolas. Pontificia Universidad Católica de Chile; Chile.Fil: Zugman, Andre. Universidade Federal de São Paulo; Brasil.Fil: Reyes-Madrigal, Francisco. Instituto Nacional de Neurología y Neurocirugía; México.Fil: Czepielewski, Leticia. Universidade Federal do Rio Grande do Sul; Brasil.Fil: Castro, Mariana Nair. Fleni. Instituto de Neurociencias FLENI-CONICET; Argentina. Fleni. Grupo de Investigación en Neurociencias Aplicadas a las Alteraciones de la Conducta; Argentina.Fil: Diaz-Zuluaga, Ana María. Universidad de Antioquía; Colombia.Fil: Pineda-Zapata, Julián. Instituto de Alta Tecnología Médica; Colombia.Fil: Reckziegel, Ramiro. Universidade Federal do Rio Grande do Sul; Brasil.Fil: Gadelha, Ary. Universidade Federal de São Paulo; Brasil.Fil: Jackowski, Andrea. Universidade Federal de São Paulo; Brasil.Fil: Noto, Cristiano. Universidade Federal de São Paulo; Brasil.Fil: Alliende Serra, Luz Maria. Pontificia Universidad Católica de Chile; Chile.Fil: Iruretagoyena, Bárbara. Pontificia Universidad Católica de Chile; Chile.Fil: Ossandon, Tomas. Pontificia Universidad Católica de Chile; Chile.Fil: Ramirez-Mahaluf, Juan Pablo. Pontificia Universidad Católica de Chile; Chile.Fil: Castañeda, Carmen Paz. Instituto Psiquiátrico Dr. José Horwitz Barak; Chile.Fil: Gonzalez-Valderrama, Alfonso. Instituto Psiquiátrico Dr. José Horwitz Barak; Chile.Fil: Nachar, Ruben. Instituto Psiquiátrico Dr. José Horwitz Barak; Chile.Fil: Guinjoan, Salvador Martín. Fleni. Grupo de Investigación en Neurociencias Aplicadas a las Alteraciones de la Conducta; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Fleni. Servicio de Psiquiatría; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Psiquiatría y Salud Mental; Argentina
PIWI-interacting RNAs are differentially expressed during cardiac differentiation of human pluripotent stem cells
Get PDFPIWI-interacting RNAs (piRNAs) are a class of non-coding RNAs initially thought to be restricted exclusively to germline cells. In recent years, accumulating evidence has demonstrated that piRNAs are actually expressed in pluripotent, neural, cardiac and even cancer cells. However, controversy remains around the existence and function of somatic piRNAs. Using small RNA-seq samples from H9 pluripotent cells differentiated to mesoderm progenitors and cardiomyocytes we identified the expression of 447 piRNA transcripts, of which 241 were detected in pluripotency, 218 in mesoderm and 171 in cardiac cells. The majority of them originated from the sense strand of protein coding and lncRNAs genes in all stages of differentiation, though no evidences of amplification loop (ping-pong) were found. Genes hosting piRNA transcripts in cardiac samples were related to critical biological processes in the heart, like contraction and cardiac muscle development. Our results indicate that these piRNAs might have a role in fine-tuning the expression of genes involved in differentiation of pluripotent cells to cardiomyocytes.Fil: La Greca, Alejandro. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Scarafía, María Agustina. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Hernández Cañás, María Clara. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Pérez, Nelba. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Castañeda, Sheila. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Colli, Carolina. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Miqueas Möbbs, Alan. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Santín Velazque, Natalia Lucía. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Neiman, Gabriel. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Garate, Ximena. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Aban, Cyntia. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Waisman, Ariel. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Moro, Lucía Natalia. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Sevlever, Gustavo Emilio. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Luzzani, Carlos. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina.Fil: Miriuka, Santiago Gabriel. Fleni. Laboratorio de Investigación Aplicada a las Neurociencias; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina