ABSTRACT
OBJECTIVES: Artificial intelligence (AI)-based chatbots have demonstrated accuracy in a variety of fields, including medicine, but research has yet to substantiate their accuracy and clinical relevance. We evaluated an AI chatbot's answers to questions posed during a treatment planning conference. METHODS: Pathology residents, pathology faculty, and an AI chatbot (OpenAI ChatGPT [January 30, 2023, release]) answered a questionnaire curated from a genitourinary subspecialty treatment planning conference. Results were evaluated by 2 blinded adjudicators: a clinician expert and a pathology expert. Scores were based on accuracy and clinical relevance. RESULTS: Overall, faculty scored highest (4.75), followed by the AI chatbot (4.10), research-prepared residents (3.50), and unprepared residents (2.87). The AI chatbot scored statistically significantly better than unprepared residents (P = .03) but not statistically significantly different from research-prepared residents (P = .33) or faculty (P = .30). Residents did not statistically significantly improve after research (P = .39), and faculty performed statistically significantly better than both resident categories (unprepared, P < .01; research prepared, P = .01). CONCLUSIONS: The AI chatbot gave answers to medical questions that were comparable in accuracy and clinical relevance to pathology faculty, suggesting promise for further development. Serious concerns remain, however, that without the ability to provide support with references, AI will face legitimate scrutiny as to how it can be integrated into medical decision-making.
ABSTRACT
Background: Hyperhemolysis syndrome (HS) is a severe hemolytic transfusion reaction that can cause hemoglobin and hematocrit levels to drop below pretransfusion levels, leading to severe anemia. HS most commonly occurs in patients with a pre-existing hemoglobinopathy such as sickle cell disease (SCD) or beta-thalassemia. Methods: We report a case of HS, occurring in the absence of hemoglobinopathy, making the diagnosis challenging. The patient reported was also affected by a CIC-rearranged sarcoma. As part of the workup, the patient received a bone marrow biopsy for suspected hemophagocytic lymphohistiocytosis. Results: This provided a rare biopsy specimen to correlate reticulocytopenia with marked erythroid hyperplasia in the marrow, supporting the hypothesis of reticulocyte destruction as a contributing cause of anemia in these patients. This patient had demonstrable alloantibodies to the Jk(a) and P1 antigens as potential triggers for HS. Conclusions: It is vital that a diagnosis of HS be correctly made in these patients with severe anemia, as blood transfusions generally lead to worsening of their conditions.
ABSTRACT
Impaired social interaction is a key feature of several major psychiatric disorders including depression, autism, and schizophrenia. While, anatomically, the prefrontal cortex (PFC) is known as a key regulator of social behavior, little is known about the cellular mechanisms that underlie impairments of social interaction. One etiological mechanism implicated in the pathophysiology of the aforementioned psychiatric disorders is cellular stress and consequent adaptive responses in the endoplasmic reticulum (ER) that can result from a variety of environmental and physical factors. The ER is an organelle that serves essential roles in protein modification, folding, and maturation of proteins; however, the specific role of ER stress in altered social behavior is unknown. In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment. Reduced estrogen receptor beta (ERß) protein levels were found in the PFC of male mice following tunicamycin treatment. Pretreatment with an ERß specific agonist, ERB-041 significantly attenuated tunicamycin-induced deficits in social behavior, and activation of IRE1/XBP1 pathway in mouse PFC. Moreover, ERB-041 inhibited tunicamycin-induced increases in functional connectivity between PFC and hippocampus in male mice. Together, these results show that ERß agonist attenuates ER stress-induced deficits in social behavior through the IRE-1/XBP1 pathway.
