Background and Objectives: Sertraline is a selective serotonin reuptake inhibitor (SSRI) that is frequently prescribed during pregnancy to treat mood disorders. Studies indicate that chronic use of sertraline is associated with elevated liver enzymes, oxidative stress, and histological alterations in the liver. Folic acid, a recommended supplement currently used during the first trimester of pregnancy, has antioxidant and anti-inflammatory effects. Hence, folic acid might be a potential protective agent against sertraline-induced liver injury. The current study aimed to investigate the possible hepatotoxic effects of sertraline administration during pregnancy and early postpartum. In addition, we sought to evaluate the potential protective effects of folic acid supplementation in alleviating any sertraline-induced liver damage. Materials and Methods: Eighty pregnant albino rats were randomly divided into four groups: control, folic acid-treated, sertraline-treated, and folic acid–sertraline-treated. Each group was divided into rats euthanized immediately after giving birth (0 h) or 14 days postpartum. Biochemical, histological, and immunohistochemical evaluations of liver function and structure were conducted. Results: Administration of sertraline was associated with a significant increase in hepatic enzymes (ALT and AST) and disrupted lipid profile (elevated cholesterol, triglycerides, and LDL-c) compared to the control group. Increased apoptosis was evidenced by increased caspase 3 expression and histological alterations, including vacuolation and inflammatory infiltrates, in sertraline-treated rats. Folic acid supplementation effectively mitigated these effects by preserving liver architecture, normalizing biochemical markers (ALT, AST, and lipid profile changes), and reducing apoptotic activity (lower caspase 3 expression). Conclusions: Folic acid mitigated sertraline-induced hepatic damage in pregnant rats. This suggests the potential benefits of using folic acid during the whole duration of pregnancy in patients treated with sertraline.

Background: The medical internship is a critical period of intense learning and professional development. During this time, medical graduates must acquire and apply vast amounts of knowledge under significant cognitive and emotional strain. Novel methods, such as integrating behavioral neuroscience, which examines how the brain enables learning and memory, manages emotions, and guides decision-making, with educational psychology, which explores how people are motivated, regulate their own learning, and think about their thinking, may support a more effective, brain-aligned, and sustainable training environment. Aim: This study assessed the feasibility and efficacy of a curriculum integrating neurodidactic and psychological techniques to improve resilience and clinical performance among Saudi medical interns. Methods: This study used a pragmatic, quasi-experimental, single-cohort longitudinal design with pre- and post-intervention assessments. The research team co-developed a curriculum comprising a series of educational modules that incorporated evidence-based learning strategies, including retrieval practice, spaced repetition, and interleaving. The curriculum also featured multimedia cognitive-load design, metacognitive coaching, mindfulness, reappraisal drills, and team communication simulations. One hundred participants completed the study. To evaluate the intervention’s impact, we used validated Arabic-language surveys to assess cognitive engagement, emotional resilience, and perceived stress. Faculty members rated clinical competencies using workplace-based assessments (mini-CEX), and focus groups were conducted to gather qualitative feedback. Results: The implementation yielded significant positive outcomes, with notable elevations in cognitive engagement (+12.4, p < 0.001) and in emotional resilience (+8.7, p = 0.002). Perceived stress decreased from 48% to 32% (p = 0.008), while clinical competency scores improved significantly ( p < 0.001). Multivariable regression revealed that resilience increase was a strong predictor of improvements in clinical competency (R ² = 0.35, p < 0.001). Conclusion: This pragmatic, single−cohort curriculum was feasible to implement and was associated with improvements in cognitive engagement, emotional resilience, perceived stress, and clinical performance among Saudi medical interns, supporting further evaluation and potential broader adoption of such integrated programs in medical education.

Background and Objectives: Pulmonary fibrosis (PF) is an interstitial lung disease that leads to death and is characterized by excessive collagen deposition and tissue scarring. Bleomycin (BLM) is widely used to induce PF in rodent models, closely resembling human idiopathic pulmonary fibrosis. Ivermectin, a broad-spectrum antiparasitic agent, has recently attracted interest due to its reported anti-inflammatory and antifibrotic effects. The beneficial effects of ivermectin to treat PF may be attributed to suppressing the NLRP3 inflammasome. Ivermectin can cause acute toxicity, including convulsions, when overdosed in animals. In humans, it may induce neurological disorders, particularly in individuals with mutations in the ABCB1 gene. This study aimed to investigate the potential protective role of ivermectin against BLM-induced PF in rats. Materials and Methods: Forty adult male albino rats were randomly allocated into four groups (n = 10 each): control, ivermectin-treated (0.6 mg/kg, orally on days 0, 1, 7, and 8), BLM-treated (single intratracheal dose of 5 mg/kg), and BLM- and ivermectin-treated. Lung tissues were collected for histopathological analysis and Mallory trichrome staining to assess collagen deposition. Mast cell (MC) infiltration was assessed using toluidine blue. Immunohistochemistry for α-SMA and Ki-67 was used to evaluate myofibroblast and cell proliferation. Oxidative stress parameters, including serum total antioxidant capacity, lung glutathione and lung nitric oxide were measured. Results: Ivermectin treatment markedly attenuated BLM-induced lung fibrosis, showing reduced collagen accumulation, restoration of alveolar architecture, and decreased inflammatory cell infiltration. Immunohistochemical evaluation revealed decreased expression of α-SMA and Ki-67, while biochemical analyses demonstrated improved oxidative stress markers. Conclusions: Ivermectin significantly mitigates BLM-induced pulmonary fibrosis in rats through modulation of inflammation, suppression of myofibroblast proliferation, and reduction in oxidative stress and collagen deposition. These findings highlight ivermectin as a potential candidate for the management of fibrotic lung diseases, warranting further mechanistic and clinical investigations.