Masoumeh Jorjani

Background. The higher education system of medical sciences in Iran requires competent and qualified educational leaders to enhance the quality of education, research, and social accountability. However, the process of selecting heads of educational departments and deans often lacks transparent, competitive, and competency-based mechanisms. This study aimed to identify the key competencies of educational leaders and to design context-specific, policy options for their selection in Iranian universities of medical sciences. Methods. This qualitative study was conducted in four phases using a mixed-methods design. In the first phase, a scoping review was performed to identify the competencies of educational leaders in national and international literature. In the second phase, qualitative data were collected through semi-structured interviews and focus group discussions with medical education experts and analyzed accordingly. In the third phase, the identified competencies were prioritized and weighted using the Delphi technique. In the fourth phase, findings from the previous phases were integrated, and policy options were developed based on the identified competency domains. Results. The competencies of educational leaders were categorized into four main domains: human resource management and development; organizational behavior and professional culture development; change management and educational innovation; and performance monitoring and evaluation. In the Delphi phase, these competencies were prioritized based on scientific, managerial, and professional ethics criteria. Emphasis was placed on selecting leaders through the participation of department members and requiring completion of relevant training programs. For each competency domain, a set of policy interventions was subsequently developed, including the establishment of a competency-based selection system, succession planning programs, continuous leadership development, and the implementation of data-driven performance evaluation systems. These interventions can be implemented as an integrated, phased policy package. Conclusion. Establishing a merit-based model for selecting educational leaders in Iranian universities of medical sciences is a strategic necessity. Designing and implementing a competency-based selection system as a priority action can facilitate the execution of complementary interventions and ultimately enhance transparency, accountability, and the quality of education within the national health system. Research Insights · Effective leadership of medical sciences universities is essential for improving educational, research, and organizational performance. It requires competencies beyond academic and scientific qualifications, including managerial, interpersonal, leadership, professional, and academic competencies. · Although existing evidence highlights the importance of these competencies, evidence on context-specific competencies and transparent, systematic criteria for selecting educational leaders in medical universities, particularly in Iran, remains limited. How these competencies can be translated into clear selection criteria remains insufficiently understood. · This study provides context-specific, evidence-informed, and merit-based policy options for selecting educational leaders in Iranian universities of medical sciences. The options organize the required competencies into a structured framework that can be applied to the selection process. · The proposed policy options can support Iranian universities of medical sciences in developing clearer and more systematic criteria for selecting educational leaders and in strengthening competency-based decision-making in educational leadership appointments.

Background: Studies have reported inconsistent findings regarding the potential effects of polycystic ovary syndrome (PCOS) on neurocognitive function. Objectives: This study aimed to investigate whether cognitive function, particularly spatial learning and memory, and hippocampal tissue are impaired in middle-aged rats with a history of PCOS. Methods: Spatial learning and memory, hippocampal histopathology, and the expression of genes including beta-secretase 1 (bace1), microtubule-associated protein tau (mapt), amyloid-beta precursor protein (app), nestin (nes), and doublecortin (dcx) in hippocampal tissue were compared between middle-aged PCOS rats and controls (n = 7/group). Results: During training (learning), middle-aged PCOS rats had significantly higher mean latency (22.04 (1.86, 42.22); P = 0.03) and duration (5.62 (1.41, 9.84); P = 0.009) than controls. However, memory performance did not differ significantly between PCOS rats and controls. PCOS rats had a significantly higher number of damaged neurons in the CA1 (24.25 ± 2.68 vs. 9.50 ± 0.64), CA2 (20.75 ± 1.03 vs. 8.25 ± 1.10), CA3 (20.50 ± 1.65 vs. 8.50 ± 1.04), and DG (28.25 ± 1.88 vs. 13.00 ± 1.29) regions of the hippocampus than controls (P < 0.05), and they showed mild hippocampal damage. In PCOS rats, bace1 gene expression was significantly increased in hippocampal tissue, whereas mapt gene expression was decreased compared with controls. The expression levels of the other genes did not differ significantly between the two groups. Conclusions: A history of PCOS during reproductive age may increase the risk of cognitive dysfunction, particularly impaired spatial learning, as well as hippocampal damage later in life.

Introduction: Evidence regarding age‐related variation in anti‐Müllerian hormone (AMH) and its associations with hormonal and metabolic parameters in women with polycystic ovary syndrome (PCOS), healthy women, and those with isolated PCOS features remains inconsistent. This study aimed to address these gaps using a cross‐sectional, population‐based approach. Methods: A total of 883 women aged 18–45 years were categorized into three groups: PCOS ( n = 124; Rotterdam criteria), suspicious (one PCOS criterion, n = 274), and healthy controls ( n = 485). The coefficient of determination (R ² ) assessed age‐related AMH variation. Linear regression evaluated associations between AMH and hormonal and metabolic profiles. Age‐stratified multivariable logistic regression, adjusted for BMI, parity, and physical activity, examined associations between AMH and type 2 diabetes (T2DM), hypertension, metabolic syndrome (MetS), and dyslipidemia. Results: Age explained nearly 40% of AMH variation in healthy women, but only 20% in those with PCOS. AMH was inversely correlated with BMI in healthy and suspicious groups, but not in PCOS. Among healthy women aged ≥ 35 years, higher AMH was associated with a 37% reduced likelihood of T2DM (OR: 0.63, 95% CI: 0.41–0.97). In contrast, among women with PCOS aged < 35 years, elevated AMH was associated with 2.6‐fold higher odds of MetS (OR: 2.6, 95% CI: 1.20–6.20). In the suspicious group, AMH correlated positively with free androgen index and prolactin. Conclusion: AMH declines less with age in women with PCOS than in healthy women. Higher AMH may be protective against T2DM in older healthy women but indicates elevated metabolic risk in younger women with PCOS, suggesting that AMH may serve as a life‐course biomarker for metabolic risk stratification and personalized preventive strategies in women's healthcare.

The selection and appointment of qualified managers in health sciences schools are critically important due to their substantial impact on the performance

Most individuals who suffer from spinal cord injury (SCI) experience neuropathic pain, which currently has no effective treatment. In this study, we examined how testosterone affects neuropathic pain resulting from SCI. We administered three different doses of testosterone (4, 8, 16 mg/kg, intraperitoneal) to male rats after an electrolytic lesion of the spinothalamic tract. We then conducted behavioral tests, including open field and von Frey tests, within 28 days post-SCI. On day 28 after SCI, we analyzed spinal tissue using western blot to measure the levels of ionized calcium binding adaptor molecule 1 (Iba1), glial fibrillary acidic protein (GFAP), phospho-extracellular signal-regulated kinase (p-ERK1/2), and p-P38 at the injury site. The results showed that testosterone significantly improved both motor activity and mechanical allodynia compared to the SCI-only group. Testosterone also inhibited microglia and astrocyte activation. Furthermore, testosterone significantly decreased p-P38 and p-ERK levels. The findings indicate that testosterone may alleviate SCI-induced neuropathic pain by inhibiting the activation of astrocytes and microglia, as well as suppressing MAPK signaling pathways.

Spinal cord injury (SCI) is a common neurological disease worldwide, often resulting in a substantial decrease in quality of life, disability, and in severe cases, even death. Unfortunately, there is currently no effective treatment for this disease. Nevertheless, current basic and clinical evidence suggests that vitamins, with their antioxidant properties and biological functions, may play a valuable role in improving the quality of life for individuals with SCI. They can promote overall health and facilitate the healing process. In this review, we discuss the mechanisms and therapeutic potential of vitamins in the treatment of SCI.

Spinal cord edema is a quick-onset phenomenon with long-term effects. This complication is associated with inflammatory responses, as well as poor motor function. No effective treatment has been developed against spinal edema, which urges the need to provide novel therapies. Astaxanthin (AST) is a fat-soluble carotenoid with anti-inflammatory effects and a promising candidate for treating neurological disorders. This study aimed to investigate the underlying mechanism of AST on the inhibition of spinal cord edema, astrocyte activation, and reduction of inflammatory responsesin a rat compression spinal cord injury (SCI) model. Male rats underwent laminectomy at thoracic 8–9, and the SCI model was induced using an aneurysm clip. After SCI, rats received dimethyl sulfoxide or AST via intrathecal injection. The effects of AST were examined on the motor function, spinal cord edema, integrity of blood-spinal cord barrier (BSCB), and expression of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), glial fibrillary acidic protein (GFAP), and aquaporin-4 (AQP4), and matrix metallopeptidase- 9 (MMP-9) post-SCI. We showed that AST potentially improved the recovery of motor function and inhibited the spinal cord edema via maintaining the integrity of BSCB, reducing the expression of HMGB1, TLR4, and NF-κB, MMP-9 as well as downregulation of astrocyte activation (GFAP) and AQP4 expression. AST improves motor function and reduces edema and inflammatory responses in the spinal tissue. These effects are mediated by suppression of the HMGB1/TLR4/NF-κB signaling pathway, suppressing post-SCI astrocyte activation, and decreasing AQP4 and MMP-9 expression. Graphical abstract

Astaxanthin (AST) is a lipid-soluble carotenoid with antioxidant and anti-inflammatory properties. Previous reports demonstrated the promising effects of AST on spinal cord injury (SCI)-induced inflammation and sensory-motor dysfunction. Macrophage migration inhibitory factor (MIF), as a cytokine, plays a critical role in the inflammatory phase of SCI. The aim of this study was to evaluate the effects of AST on post-SCI levels of MIF in serum and spinal cord. The possible correlation between MIF and mechanical pain threshold was also assessed. Adult male rats were subjected to a severe compression spinal injury and 30 min later were treated with AST (Intrathecal, 2 nmol) or vehicle. Neuropathic pain was assessed by von Frey filaments before the surgery, and then on days 7, 14, 21, and 28 post-SCI. Western blot and ELISA were used to measure the serum level and spinal expression of MIF following SCI in the same time points. AST treatment significantly attenuated the SCI-induced dysregulations in the serum levels and tissue expression of MIF. A negative correlation was observed between mechanical pain threshold and serum MIF level (r = −0.5463, P < 0.001), as well as mechanical pain threshold and spinal level of MIF (r = −0.9562; P < 0.001). AST ameliorates SCI-induced sensory dysfunction, probably through inhibiting MIF-regulated inflammatory pathways.

Nepeta menthoides Boiss . & Buhse and Melissa officinalis are extensively used in Persian medicine for the treatment of depression. Considering the active ingredients and main phenolic compounds of these plants and possible synergistic effects, this study examined the antidepressant and antioxidant activities of aqueous extract of N . menthoides (NM) and M . officinalis (MO) in reserpinized mice alone and combination. Mice were pretreated orally for 1‐week with normal saline (10 ml/kg), fluoxetine (20 mg/kg), imipramine (10 mg/kg), NM (50–100–200–400 mg/kg), MO (150–350–550–750 mg/kg), and combination (NM 50 with MO 150 mg/kg). The behavioral changes were evaluated using forced swim, tail suspension, and open field tests, 24 hr after reserpine injection (4 mg/kg) on eighth day. The amounts of active components in the extracts and catalase (CAT) as a brain oxidative stress were measured with enzyme‐linked immunosorbent assay. Data showed that this combination produced a synergistic action on behaviors and a significant increase in CAT activity. High‐performance liquid chromatography results showed that rosmarinic acid contents in MO and NM were 6.42 ± 1.1 and 11.03 ± 2.16 mg/g of dried extract, respectively. Total flavonoid and phenolic contents of MO were higher than NM. The findings suggest that the present combination produces an antidepressant‐like effect, which is possibly triggered by its antioxidant properties.

The effects of astaxanthin (AST) were evaluated on oxidative mediators, neuronal apoptosis, and autophagy in functional motor recovery after spinal cord injury (SCI). Rats were divided into three groups of sham, SCI + DMSO (dimethyl sulfoxide), and SCI + AST. Rats in the sham group only underwent a laminectomy at thoracic 8–9. While, the SCI + DMSO and SCI + AST groups had a compression SCI with an aneurysm clip. Then, this groups received an intrathecal (i.t.) injection of 5% DMSO and AST (10 μl of 0.005 mg/kg), respectively. The rat motor functions were assessed weekly until the 28th day using a combined behavioral score (CBS). Total antioxidant capacity (TAC), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were measured in spinal tissue to evaluate oxidative stress-related parameters. Besides, autophagy-related proteins (P62, LC3B, and Beclin1) and apoptosis-associated proteins (Bax and Bcl2) were determined using western blotting on the 1st and 7th days after surgery. Hematoxylin–eosin and Fluoro-Jade B staining were performed to detect the histological alterations and neuronal degeneration. As the result, treatment with AST potentially attenuated rat CBS scores (p < 0.001) towards a better motor performance. AST significantly reduced the spinal level of oxidative stress by increasing TAC, SOD, and GPx, while decreasing MDA (p < 0.001). Furthermore, AST treatment remarkably upregulated expression of LC3B (p < 0.001), and Beclin1 (p < 0.05) in the spinal cord, but downregulated P62 (p < 0.05) and the Bax/Bcl2 ratio (p < 0.001). Consequently, AST reduced SCI-induced histological alterations and neuronal degeneration (p < 0.001). In conclusion, AST can improve motor function after SCI by reducing oxidative stress/apoptosis and increasing neuronal autophagy.