Epidemic Spread of SARS-CoV-2 Lineage B.1.1.7 in Brazil

The emergence of diverse lineages harboring mutations with functional significance and potentially enhanced transmissibility imposes an increased difficulty on the containment of the SARS-CoV-2 pandemic [...

MicroRNAs 145 and 148a Are Upregulated During Congenital Zika Virus Infection.

Submitted by Fábio Marques ([email protected]) on 2019-07-04T13:28:28Z No. of bitstreams: 1 MicroRNAs_Marcelo_Ribeiro-Alves_INI_Lapclin-AIDS_2019.pdf: 1352248 bytes, checksum: 0223da5170d1c175d5eb393366ef4edd (MD5)Approved for entry into archive by Regina Costa ([email protected]) on 2019-07-04T16:40:10Z (GMT) No. of bitstreams: 1 MicroRNAs_Marcelo_Ribeiro-Alves_INI_Lapclin-AIDS_2019.pdf: 1352248 bytes, checksum: 0223da5170d1c175d5eb393366ef4edd (MD5)Made available in DSpace on 2019-07-04T16:40:10Z (GMT). No. of bitstreams: 1 MicroRNAs_Marcelo_Ribeiro-Alves_INI_Lapclin-AIDS_2019.pdf: 1352248 bytes, checksum: 0223da5170d1c175d5eb393366ef4edd (MD5) Previous issue date: 2019Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Department of Microbiology, Immunology & Tropical Medicine, The George Washington University, Washington, DC, USA.Faculdade de Ciências Médicas de Campina Grande, Núcleo de Genética Médica, Centro Universitário UniFacisa, Campina Grande, Brasil.Instituto de Pesquisa Professor Amorim Neto, Campina Grande, Brasil.Serviço de Neurologia, Hospital Vera Cruz, Belo Horizonte, Brasil.Fundação Oswaldo Cruz. Instituto Fernandes Figueira. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Fernandes Figueira. Rio de Janeiro, RJ, Brasil.Fundação Oswaldo Cruz. Instituto Fernandes Figueira. Rio de Janeiro, RJ, Brasil.Laboratório de Neuropatologia, Instituto Estadual do Cérebro, Rio de Janeiro, Brasil.Faculdade de Ciências Médicas de Campina Grande, Núcleo de Genética Médica, Centro Universitário UniFacisa, Campina Grande, Brasil./ Instituto de Pesquisa Professor Amorim Neto, Campina Grande, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.Division of Infectious Diseases, Weill Cornell Medicine, New York City, NY, USA.Fundação Oswaldo Cruz. Instituto Nacional de Infectologia Evandro Chagas. Laboratório de Pesquisa Clínica em DST/AIDS. Rio de Janeiro, RJ, Brasil.Departamento de Genética, Instituto de Biologia, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil./ Departamento de Biologia Geral, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brasil

Stimulus dimensions of the cold pressor test and the associated patterns of cardiovascular response

Hemodynamics of the cold pressor response in relation to its pain and nonpain stimulus components were investigated in normotensive college men using the foot and forehead cold pressor tasks. Mechanisms of pain‐ and non‐pain‐related increases in blood pressure were analyzed as residual effects of concurrent changes in total peripheral resistance and cardiac output. The identified partial relationships suggested that the response pattern associated with pain included positive change both in cardiac output and in total peripheral resistance, whereas the nonpain‐related response was limited to an increase in total peripheral resistance. Analyses of individual differences in car‐diovascular responses to pain further indicated that pain‐related increments in blood pressure were mediated by a steeper rise in total peripheral resistance, an increase in heart rate, and an apparent increase in preload. At baseline, high reactors to pain manifested relatively elevated total perpheral resistance, diminished cardiac output, and an indication of a reduced inotropic state, suggesting that altered basal homeostasis may discriminate normotensive individuals displaying heightened cardiovascular reactivity to aversive cold stimulation

Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?

Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-β (Aβ) plaques — one of the hallmarks of AD — may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI