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2.
J Surg Educ ; 78(2): 485-491, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-32800767

RESUMO

OBJECTIVE: Clinical clerkships are a fundamental component of medical education where students' learning is aided by exposure to real patients in diverse practical settings. Countless programs use overnight call shifts as an essential part of their clerkships. There has been concerns about the negative effects these shifts have on students. The study aims to determine relations between call schedule, lecture attendance, and academic and clinical performance. METHODS: One hundred and eight medical students were followed during their surgery clerkship. Students on a Q3 schedule had an on-call shift once every 3 nights, while students on a Q4 schedule once every 4 nights. Their academic performance was evaluated using their exams grades, while their clinical performance was evaluated by their attending physicians. Burnout syndrome was measured using Maslach Inventory. RESULTS: A total of 108 medical students attended their surgical clerkship. Sixty-nine students were under the Q3 call schedule while 39 students in the Q4 call schedule. Mean lecture attendance for students in Q3 was 82.7% (17.3%) compared to 90% (11.2%) (p = 0.020). Final exam grades were different between groups, with Q3 scoring a mean 71.55 (9.3) compared to Q4 85.07 (9.8) (p = 0.001). Clinical performance score means were similar between groups (p = 0.777). Q4 had 74% and Q3 had 49.3% of the students with >90% of attendance (p = 0.008). Q4 had 2.6% students with <70% attendance compared to Q3 with 23.2% (p = 0.008). Students with >90% attendance regardless of call schedule, scored higher in both midterms and final exams (p = 0.002; p = 0.001). Burnout prevalence was higher in students on the Q3 schedule with 28.6% compared to 4.7% of those on the Q4 schedule (p = 0.003). CONCLUSIONS: Students with less call frequency were associated with an improvement in lecture attendance and academic performance, and a lower burnout syndrome rate, without impacting clinical performance. Students with higher attendance regardless of call schedules performed higher academically. Further studies should evaluate the impact on clinical performance and exposure more thoroughly.


Assuntos
Desempenho Acadêmico , Esgotamento Profissional , Estágio Clínico , Estudantes de Medicina , Esgotamento Profissional/epidemiologia , Humanos
3.
Int J Mol Sci ; 19(12)2018 Nov 22.
Artigo em Inglês | MEDLINE | ID: mdl-30467294

RESUMO

Heart failure (HF) is a cardiovascular syndrome characterized by maladaptive changes with an underlying inflammatory mediated pathogenesis. Nevertheless, current therapy is aimed at the heart workload and neurohormonal axis; thus, prognosis remains poor. To continue improving treatment, we rely on murine models for a better understanding of HF pathophysiology. Among them, pressure overload HF (PO-HF) animal models are a common strategy. Development of PO-HF is characterized by monocyte infiltration, which orchestrates a cascade of events leading to sustained inflammation and maladaptive changes. Here, we divide the PO-HF model progression into four phases and describe the inflammatory, structural, and gene expression profiles. This division is relevant due to its similarities with clinical hypertensive heart disease progression to HF. Evidence shows improvement in hemodynamic and other local parameters by altering the inflammatory response in a specific immune response at a specific point of time. Thus, it is relevant to focus on the time-dependent immune response interaction in order to provide more effective therapy. This review summarizes the pathogenesis of PO-HF murine models, highlighting the inflammatory events in a time frame view. By this approach, we expect to provide researchers with a better understanding of the intertwining time-dependent events that occur in PO-HF.


Assuntos
Linfócitos B/imunologia , Insuficiência Cardíaca/imunologia , Hipertensão/imunologia , Monócitos/imunologia , Linfócitos T/imunologia , Angiotensina II/administração & dosagem , Angiotensina II/efeitos adversos , Animais , Aorta/imunologia , Aorta/patologia , Linfócitos B/patologia , Cardiomegalia/imunologia , Cardiomegalia/patologia , Movimento Celular , Constrição Patológica/imunologia , Constrição Patológica/patologia , Citocinas/biossíntese , Citocinas/imunologia , Modelos Animais de Doenças , Fibrose Endomiocárdica/imunologia , Fibrose Endomiocárdica/patologia , Insuficiência Cardíaca/induzido quimicamente , Insuficiência Cardíaca/etiologia , Insuficiência Cardíaca/patologia , Humanos , Hipertensão/complicações , Hipertensão/patologia , Camundongos , Monócitos/patologia , Linfócitos T/patologia , Fatores de Tempo , Disfunção Ventricular Esquerda/imunologia , Disfunção Ventricular Esquerda/patologia
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