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1.
World Neurosurg ; 183: e145-e152, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38092357

RESUMO

BACKGROUND: There exists a complex and ever-evolving relationship between social media and medicine. This study investigates the usage of X (formerly Twitter) among neurosurgeons and explores how virtual engagement potentially impacts this specialty. METHODS: The researchers examined X posts from the top fifty influential neurosurgeons over 6 months. Demographics and practice information were collected. Posts were categorized into 9 predetermined coding definitions. Descriptive statistics were used to summarize user characteristics. χ2 tests and two-tailed T-tests were employed to examine patterns of posting behavior. RESULTS: Most influencers practiced in an academic setting (89%) and 43% of them were age fifty or older. Only 15% identified as female. Cerebrovascular subspecialists accounted for 39% of the cohort. Reposting was the most popular type of posting, constituting 61% of all posts. The most common postcategory observed was "Professional Events" (31%), while "Patient Education" was the least common (0.8%). Private practice and general neurosurgeons infrequently posted about "Professional Events" (5.1%, P < 0.01 and 3.2%, P < 0.01, respectively). "Personal Thoughts" constituted the second most common category, with a notable increase among users younger than 50 (25%, P < 0.01), individuals who identified as female (62%, P < 0.01), those in private practice (69%, P < 0.01), and general neurosurgeons (86%, P < 0.01). CONCLUSIONS: Neurosurgeons of all ages use X to advance their careers and stay updated. However, the utilization of this influential platform likely varies depending on the current practice setting and individual career goals. Neurosurgeons on X appear to have the greatest influence within an academic context, particularly when promoting professional events.


Assuntos
Medicina , Neurocirurgia , Mídias Sociais , Humanos , Feminino , Neurocirurgiões , Procedimentos Neurocirúrgicos
3.
Hepatology ; 76(4): 1090-1104, 2022 10.
Artigo em Inglês | MEDLINE | ID: mdl-35083765

RESUMO

BACKGROUND AND AIMS: Within the next decade, NAFLD is predicted to become the most prevalent cause of childhood liver failure in developed countries. Predisposition to juvenile NAFLD can be programmed during early life in response to maternal metabolic syndrome (MetS), but the underlying mechanisms are poorly understood. We hypothesized that imprinted genes, defined by expression from a single parental allele, play a key role in maternal MetS-induced NAFLD, due to their susceptibility to environmental stressors and their functions in liver homeostasis. We aimed to test this hypothesis and determine the critical periods of susceptibility to maternal MetS. APPROACH AND RESULTS: We established a mouse model to compare the effects of MetS during prenatal and postnatal development on NAFLD. Postnatal but not prenatal MetS exposure is associated with histological, biochemical, and molecular signatures of hepatic steatosis and fibrosis in juvenile mice. Using RNA sequencing, we show that the Imprinted Gene Network (IGN), including its regulator Zac1, is up-regulated and overrepresented among differentially expressed genes, consistent with a role in maternal MetS-induced NAFLD. In support of this, activation of the IGN in cultured hepatoma cells by overexpressing Zac1 is sufficient to induce signatures of profibrogenic transformation. Using chromatin immunoprecipitation, we demonstrate that Zac1 binds the TGF-ß1 and COL6A2 promoters, forming a direct pathway between imprinted genes and well-characterized pathophysiological mechanisms of NAFLD. Finally, we show that hepatocyte-specific overexpression of Zac1 is sufficient to drive fibrosis in vivo. CONCLUSIONS: Our findings identify a pathway linking maternal MetS exposure during postnatal development to the programming of juvenile NAFLD, and provide support for the hypothesis that imprinted genes play a central role in metabolic disease programming.


Assuntos
Síndrome Metabólica , Hepatopatia Gordurosa não Alcoólica , Fatores de Transcrição , Animais , Proteínas de Ciclo Celular/genética , Proteínas de Ciclo Celular/metabolismo , Modelos Animais de Doenças , Redes Reguladoras de Genes/genética , Redes Reguladoras de Genes/fisiologia , Genes Supressores de Tumor/fisiologia , Síndrome Metabólica/complicações , Síndrome Metabólica/genética , Síndrome Metabólica/metabolismo , Camundongos , Hepatopatia Gordurosa não Alcoólica/complicações , Hepatopatia Gordurosa não Alcoólica/genética , Hepatopatia Gordurosa não Alcoólica/metabolismo , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Fator de Crescimento Transformador beta1
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