RESUMO
BACKGROUND: The task of writing multiple choice question examinations for medical students is complex, timely and requires significant efforts from clinical staff and faculty. Applying artificial intelligence algorithms in this field of medical education may be advisable. METHODS: During March to April 2023, we utilized GPT-4, an OpenAI application, to write a 210 multi choice questions-MCQs examination based on an existing exam template and thoroughly investigated the output by specialist physicians who were blinded to the source of the questions. Algorithm mistakes and inaccuracies, as identified by specialists were classified as stemming from age, gender or geographical insensitivities. RESULTS: After inputting a detailed prompt, GPT-4 produced the test rapidly and effectively. Only 1 question (0.5%) was defined as false; 15% of questions necessitated revisions. Errors in the AI-generated questions included: the use of outdated or inaccurate terminology, age-sensitive inaccuracies, gender-sensitive inaccuracies, and geographically sensitive inaccuracies. Questions that were disqualified due to flawed methodology basis included elimination-based questions and questions that did not include elements of integrating knowledge with clinical reasoning. CONCLUSION: GPT-4 can be used as an adjunctive tool in creating multi-choice question medical examinations yet rigorous inspection by specialist physicians remains pivotal.
Assuntos
Educação Médica , Avaliação Educacional , Humanos , Avaliação Educacional/métodos , Projetos Piloto , Inteligência Artificial , RedaçãoRESUMO
Hepatocellular carcinoma (HCC) is the third leading cause of cancer mortality worldwide and is considered to be the outcome of chronic liver inflammation. Currently, the main treatment for HCC is surgical resection. However, survival rates are suboptimal partially because of tumor recurrence in the remaining liver. Our aim was to understand the molecular mechanisms linking liver regeneration under chronic inflammation to hepatic tumorigenesis. Mdr2-KO mice, a model of inflammation-associated cancer, underwent partial hepatectomy (PHx), which led to enhanced hepatocarcinogenesis. Moreover, liver regeneration in these mice was severely attenuated. We demonstrate the activation of the DNA damage-response machinery and increased genomic instability during early liver inflammatory stages resulting in hepatocyte apoptosis, cell-cycle arrest, and senescence and suggest their involvement in tumor growth acceleration subsequent to PHx. We propose that under the regenerative proliferative stress induced by liver resection, the genomic unstable hepatocytes generated during chronic inflammation escape senescence and apoptosis and reenter the cell cycle, triggering the enhanced tumorigenesis. Thus, we clarify the immediate and long-term contributions of the DNA damage response to HCC development and recurrence.