Iranian Journal of

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Background: In this study, we investigated the diagnostic power of ultrasound in the diagnosis of malignancy in thyroid nodules in Iranian patients. For this purpose, we examined the relationship between ultrasound findings and pathology findings.
Methods: The present study is a retrospective study. The patients with a diagnosis of thyroid nodules who underwent ultrasound and FNA, were included in this study. To assess the relationship between the results of FNA and the ultrasound characteristics of nodules, we classified the results of FNA into malignant and benign groups and then compared ultrasound characteristics between the two groups. In cases which the FNA results were indeterminate (AUS/FLUS or FN/SFN), the postoperative pathology result was considered (if thyroid surgery was done and the result was available).
Results: In total, 201 nodules were included in this study. The results showed that hypoechogenicity, irregular/ill-defined margin, microcalcification, malignant flow pattern in Doppler sonography and concurrent cervical lymphadenopathy with suspicious features were significantly associated with malignant thyroid nodules. However, other ultrasound findings, such as the size and location of the nodule, presence of a cystic components within the nodule, the presence of a Halo sign, and the presence of a taller-than-wide shape, could not distinguish between benign and malignant nodules. Finally, the results of the present study showed that the accuracy of ultrasound in the diagnosis of malignancy in thyroid nodules is high.
Conclusion: This study suggests that the use of ultrasound can be very effective in diagnosing malignancy in thyroid nodules.

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Background: Aging is associated with Sarcopenia as well as oxidative stress (OS) caused by Ferroptosis. The aim of the present study was to investigate the effect of aerobic exercise training (AT) on OS caused by ferroptosis in sarcopenia model mice.
Methods: Twenty-one C57BL/6 mice (16-24 wks. age) sarcopenia model with an average weight (25-35 g), and 21 healthy mice (6-7 weeks age) were randomly assigned to the following (1) healthy-young control (HYC; n= 7), (2) aerobic training-young (ATY; n= 7), (3) healthy-old control (HOC; n= 7), (4) old control-sarcopenia model (OCS; n= 7), (5) aerobic training-healthy-old (ATHO; n= 7), (6) healthy-old sarcopenia model (HOS= 7). The intervention group underwent AT for eight weeks, five sessions per week at an intensity of 60-80% of aerobic capacity (VO2max). The expression of the glutathione peroxidase (GPX-4) and superoxide dismutase (SOD) genes was measured using Real Time PCR. The Malondialdehyde (MDA) and Fe²⁺concentration in the gastrocnemius muscle was also measured.
Results: It was observed that the enzymes gene expression of SOD and GPX-4 in the (OSC) was significantly decreased compared to the (HOC) (P= 0.001, P= 0.002, respectively), and the MDA and Fe²⁺ was significantly increased (P= 0.001; P= 0.002, respectively). Also, the of SOD and GPX-4 gene expression of enzymes in the ATY, ATHO was significantly increased compared to the HYC, and HOS (P= 0.001; P= 0.002, respectively), and the concentration of MDA and Fe²⁺ was significantly decreased (P= 0.001; P= 0.002, respectively).
Conclusion: Finally, it can be said that aerobic training reduces oxidative stress caused by ferroptosis in Sarcopenia by increasing the enzymes GPX and SOD gene expression and reducing the concentration of MDA and Fe²⁺.
 

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Background: Metabolic syndrome (MetS) is associated with a higher risk of cognitive dysfunction and brain structural alterations, yet the specific contributions of its components and underlying mechanisms remain unclear.
Methods: This narrative review integrates findings from neuroimaging, clinical, and molecular studies to provide a conceptual understanding of how MetS affects cognition. A non-systematic and targeted search was conducted up to June 2025 using terms such as metabolic syndrome, cognition, and magnetic resonance imaging (MRI). Studies were selected based on their relevance and conceptual contribution.
Results: Evidence converges on inflammation, oxidative stress, vascular injury, and insulin resistance as key mechanisms linking MetS to gray and white matter changes and cognitive impairment. Structural and functional MRI studies demonstrate disrupted brain connectivity and reduced hippocampal volume in individuals with MetS. Gender and genetic differences may also influence the strength of this association. The coexistence of metabolic syndrome and cognitive dysfunction is linked to reduced health-related quality of life.
Conclusion: The narrative synthesis highlights how metabolic and vascular factors jointly drive neurocognitive decline and underscores the need for longitudinal and mechanistic research.