Impact and future of telemedicine amidst the COVID-19 pandemic: a systematic review of the state-of-the-art in Latin America / Impacto e futuro da telemedicina em meio à pandemia de COVID-19: uma revisão sistemática do estado da arte na América Latina

Abstract Significant progress has been made in using information and communication technologies in medicine, by impacting the quality of health-care delivery system and patient care, and paving the way for ground-breaking tools for e-health and clinical decision-support systems. This study investigates the extent to which the evolution of telemedicine applications has been used to support patient care in Latin America (LATAM) amidst the pandemic. Theoretically, the study applied the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology to identify the impact of telemedicine in the region. Practically, the paper provides a systematic mapping study of the different domain areas and methodological progress in Telemedicine that occurred during the pandemic, and applied a text mining technique to understand the intensities of the terms expressed by the analyzed studies. The results show that while telemedicine has not been extensively used, a greater percentage of the studies report that telemedicine was effective. Approximately 70% positive emotional valence score was found. The paper also provides an empirical discussion and recommendations for the next steps in ample adoption of telemedicine.

Resumo Foram feitos progressos significativos na utilização de tecnologias de informação e comunicação na medicina, com impacto no sistema de prestação de cuidados de saúde e nos cuidados aos doentes, e abrindo caminho a ferramentas inovadoras para sistemas eletrônicos de saúde e de apoio à decisão clínica. O presente estudo investiga até que ponto o crescimento das aplicações da telemedicina tem sido utilizado para apoiar os cuidados aos doentes na América Latina (LATAM) em meio da pandemia. Teoricamente, o estudo aplicou a metodologia Preferred Reporting Items for Systematic Reviews e Meta-Analyses (PRISMA) para identificar o impacto da telemedicina na região. Na prática, o artigo apresenta um estudo de mapeamento sistemático das diferentes áreas de domínio e progresso metodológico em telemedicina que ocorreram durante a pandemia, e aplicou uma técnica de text mining para compreender as intensidades dos termos expressos pelos pesquisas analisadss. Os resultados mostram que, embora a telemedicina não tenha sido amplamente utilizada, um maior percentual de estudos informa que a telemedicina foi eficaz. Foi encontrada uma pontuação de valência emocional positiva de aproximadamente 70%. O documento também traz uma discussão empírica para os próximos passos na adoção da telemedicina.

Impact and future of telemedicine amidst the COVID-19 pandemic: a systematic review of the state-of-the-art in Latin America.

Significant progress has been made in using information and communication technologies in medicine, by impacting the quality of health-care delivery system and patient care, and paving the way for ground-breaking tools for e-health and clinical decision-support systems. This study investigates the extent to which the evolution of telemedicine applications has been used to support patient care in Latin America (LATAM) amidst the pandemic. Theoretically, the study applied the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) methodology to identify the impact of telemedicine in the region. Practically, the paper provides a systematic mapping study of the different domain areas and methodological progress in Telemedicine that occurred during the pandemic, and applied a text mining technique to understand the intensities of the terms expressed by the analyzed studies. The results show that while telemedicine has not been extensively used, a greater percentage of the studies report that telemedicine was effective. Approximately 70% positive emotional valence score was found. The paper also provides an empirical discussion and recommendations for the next steps in ample adoption of telemedicine.

Ageist No More: Interprofessional Training for Undergraduate Healthcare Students.

Ageism seeps deep into our society, whether in law, policies, or healthcare practices it segregates individuals based on their age. The aim of this work was to evaluate the impact of an educational strategy in ageist attitudes against older adults in healthcare undergraduate students. A five-week intervention: Healthy environments and self-care for the older adults was implemented. To assess the impact of this strategy in ageist attitudes in participants, a simulated consultation with an older adult was conducted. Participants' perspectives on the experience were collected using an online survey. One hundred and thirty-eight undergraduate students from health programs were included. They highlighted growth in the understanding of the normal aging process and the prejudices that surround aging. During the role-play activity, participants identified communication, empathy, and professionalism as the abilities developed with this strategy and the need to show empathy and avoid prejudice against older adults in their clinical interactions. Educational interventions are a great tool to promote cultural changes, diminish prejudices and misconceptions of ageism in future healthcare professionals.

Transcriptome and Function of Novel Immunosuppressive Autoreactive Invariant Natural Killer T Cells That Are Absent in Progressive Multiple Sclerosis.

BACKGROUND AND OBJECTIVE: The aim of this study was to determine whether natural killer T (NKT) cells, including invariant (i) NKT cells, have clinical value in preventing the progression of multiple sclerosis (MS) by examining the mechanisms by which a distinct self-peptide induces a novel, protective invariant natural killer T cell (iNKT cell) subset. METHODS: We performed a transcriptomic and functional analysis of iNKT cells that were reactive to a human collagen type II self-peptide, hCII707-721, measuring differentially induced genes, cytokines, and suppressive capacity. RESULTS: We report the first transcriptomic profile of human conventional vs novel hCII707-721-reactive iNKT cells. We determined that hCII707-721 induces protective iNKT cells that are found in the blood of healthy individuals but not progressive patients with MS (PMS). By transcriptomic analysis, we observed that hCII707-721 promotes their development and proliferation, favoring the splicing of full-length AKT serine/threonine kinase 1 (AKT1) and effector function of this unique lineage by upregulating tumor necrosis factor (TNF)-related genes. Furthermore, hCII707-721-reactive iNKT cells did not upregulate interferon (IFN)-γ, interleukin (IL)-4, IL-10, IL-13, or IL-17 by RNA-seq or at the protein level, unlike the response to the glycolipid alpha-galactosylceramide. hCII707-721-reactive iNKT cells increased TNFα only at the protein level and suppressed autologous-activated T cells through FAS-FAS ligand (FAS-FASL) and TNFα-TNF receptor I signaling but not TNF receptor II. DISCUSSION: Based on their immunomodulatory properties, NKT cells have a potential value in the treatment of autoimmune diseases, such as MS. These significant findings suggest that endogenous peptide ligands can be used to expand iNKT cells, without causing a cytokine storm, constituting a potential immunotherapy for autoimmune conditions, including PMS.

ADAM12 is a costimulatory molecule that determines Th1 cell fate and mediates tissue inflammation.

A disintegrin and metalloproteinase (ADAM)12 was previously found to be expressed in T cells in the inflamed brain. However, the function of ADAM12 in T-cell responses in general and in tissue inflammation has not been examined. Here, we studied the role of ADAM12 in T-cell responses, fate determination on activation, and its functions in T cells to mediate tissue inflammation. We identified ADAM12 as a costimulatory molecule that is expressed on naive T cells and downregulated on stimulation. ADAM12 mimics CD28 costimulatory signaling to activate and induce the proliferation of T-helper 1 (Th1) cells. Monoclonal ADAM12 Fab antibodies trigger T-cell activation by amplifying TCR signaling to stimulate T-bet-mediated IFNγ production. Lack of genomic ADAM12 and its knockdown in T cells diminished T-bet and IFNγ production in Th1 cells, whereas other T cells, including Th17 cells, were unaffected. ADAM12 had similar functions in vivo on myelin antigen (MOG35-55)-induced T-cell activation. We found that genetic loss of ADAM12 profoundly alleviated Th1-mediated neuroinflammation and thus disease severity in experimental autoimmune encephalomyelitis, a model of multiple sclerosis. Transcriptomic profiling of MOG35-55-specific ADAM12-/- T cells revealed differentially expressed genes that are important for T-cell activation, proliferation, and costimulatory signaling and Th1 pathogenicity, consistent with their inability to cause T-cell-mediated skin inflammation in a model of adoptive delayed-type hypersensitivity. We conclude that ADAM12 is a T-cell costimulatory molecule that contributes to the pathogenesis of tissue inflammation and a potential target for the treatment of Th1-mediated diseases.

FoxA1 directs the lineage and immunosuppressive properties of a novel regulatory T cell population in EAE and MS.

The defective generation or function of regulatory T (Treg) cells in autoimmune disease contributes to chronic inflammation and tissue injury. We report the identification of FoxA1 as a transcription factor in T cells that, after ectopic expression, confers suppressive properties in a newly identified Treg cell population, herein called FoxA1(+) Treg cells. FoxA1 bound to the Pdl1 promoter, inducing programmed cell death ligand 1 (Pd-l1) expression, which was essential for the FoxA1(+) Treg cells to kill activated T cells. FoxA1(+) Treg cells develop primarily in the central nervous system in response to autoimmune inflammation, have a distinct transcriptional profile and are CD4(+)FoxA1(+)CD47(+)CD69(+)PD-L1(hi)FoxP3(-). Adoptive transfer of stable FoxA1(+) Treg cells inhibited experimental autoimmune encephalomyelitis in a FoxA1-and Pd-l1-dependent manner. The development of FoxA1(+) Treg cells is induced by interferon-ß (IFN-ß) and requires T cell-intrinsic IFN-α/ß receptor (Ifnar) signaling, as the frequency of FoxA1(+) Treg cells was reduced in Ifnb(-/-) and Ifnar(-/-) mice. In individuals with relapsing-remitting multiple sclerosis, clinical response to treatment with IFN-ß was associated with an increased frequency of suppressive FoxA1(+) Treg cells in the blood. These findings suggest that FoxA1 is a lineage-specification factor that is induced by IFN-ß and supports the differentiation and suppressive function of FoxA1(+) Treg cells.