Mohammad Mahdi Heidari

Background: Bedside teaching (BST) is a crucial component of the clinical skills training program for medical students, where patients are used as educational examples. Understanding patients’ attitudes toward BST is essential for making informed choices and enhancing quality. Objectives: The present study aimed to investigate the attitudes of hospitalized patients toward various aspects of BST. Methods: A cross-sectional study was coanducted involving 250 patients admitted to Shahid Beheshti Hospital in Kashan, Iran. Patients’ attitudes toward BST and influencing factors were assessed using a translated and validated version of the Marwan Questionnaire. Results: The highest level of dissatisfaction was observed with diagnostic or therapeutic procedures performed without the supervising professor (19.4%), while the lowest dissatisfaction was with students reviewing medical records (5.1%). Women expressed significantly more dissatisfaction than men regarding examinations conducted without a teacher and diagnostic and therapeutic procedures, both with and without a teacher present. Conversely, men were more opposed to students’ presence in outpatient clinics (23.8% vs. 5.4%, P < 0.001) and during surgeries (12.7% vs. 4.5%, P = 0.04) compared to women. Conclusions: Overall, patients generally accept the presence of students, irrespective of gender, and the presence of a supervising professor enhances patients’ willingness to participate in BST.

Polycomb Repressive Complex 2 (PRC2) is a central regulator of gene expression via the trimethylation of histone H3 on lysine 27. This epigenetic modification plays a crucial role in maintaining cell identity and controlling differentiation, while its dysregulation is closely linked to cancer progression. PRC2 silences tumor suppressor genes, promoting cell proliferation, metastasis, epithelial-mesenchymal transition, and cancer stem cell plasticity. Enhancement of zeste homolog 2 (EZH2) overexpression or gain-of-function mutations have been observed in several cancers, including lymphoma, breast, and prostate cancers, driving aggressive tumor behavior and drug resistance. In addition to EZH2, other PRC2 components, such as embryonic ectoderm development (EED) and suppressor of zeste 12, are essential for complex stability and function. EED, in particular, enhances EZH2 activity and has emerged as a therapeutic target. Inhibitors like MAK683 and EED226 disrupt EED’s ability to maintain PRC2 activity, thereby reducing H3K27me3 levels and reactivating tumor suppressor genes. Valemetostat, a dual inhibitor of both EZH2 and EED, has shown promising results in aggressive cancers like diffuse large B-cell lymphoma and small-cell lung cancer, underlining the therapeutic potential of targeting multiple PRC2 components. PRC2’s role extends beyond gene repression, as it contributes to metabolic reprogramming in tumors, regulating glycolysis and lipid synthesis to fuel cancer growth. Furthermore, PRC2 is implicated in chemoresistance, particularly by modulating DNA damage response and immune evasion. Tazemetostat, a selective EZH2 inhibitor, has demonstrated significant clinical efficacy in EZH2-mutant cancers, such as non-Hodgkin lymphomas and epithelioid sarcoma. However, the compensatory function of enhancer of zeste homolog 1 (EZH1) in some cancers requires dual inhibition strategies, as seen with agents like UNC1999 and Tulmimetostat, which target both EZH1 and EZH2. Given PRC2’s multifaceted role in cancer biology, its inhibition represents a promising avenue for therapeutic intervention. The continued development of PRC2 inhibitors and exploration of their use in combination with standard chemotherapy or immunotherapy has great potential for improving patient outcomes in cancers driven by PRC2 dysregulation. Graphical abstract

Growth-associated protein 43 (GAP-43) is found in the axonal terminal of neurons in the limbic system, which is affected in people with Alzheimer’s disease (AD). We assumed GAP-43 may contribute to AD progression and serve as a biomarker. So, in a two-year follow-up study, we assessed GAP-43 changes and whether they are correlated with tensor-based morphometry (TBM) findings in patients with mild cognitive impairment (MCI). We included MCI and cognitively normal (CN) people with available baseline and follow-up cerebrospinal fluid (CSF) GAP-43 and TBM findings from the ADNI database. We assessed the difference between the two groups and correlations in each group at each time point. CSF GAP-43 and TBM measures were similar in the two study groups in all time points, except for the accelerated anatomical region of interest (ROI) of CN subjects that were significantly greater than those of MCI. The only significant correlations with GAP-43 observed were those inverse correlations with accelerated and non-accelerated anatomical ROI in MCI subjects at baseline. Plus, all TBM metrics decreased significantly in all study groups during the follow-up in contrast to CSF GAP-43 levels. Our study revealed significant associations between CSF GAP-43 levels and TBM indices among people of the AD spectrum.