Computed Tomography (CT) is vital for diagnosing and monitoring medical conditions. However, increased usage raises concerns about patient radiation exposure. Diagnostic Reference Levels (DRLs) aim to minimize radiation doses in CT imaging. This study examines CT DRLs in India compared to other countries to identify optimization opportunities. A literature review was conducted to gather data from published studies, guidelines, and regulatory authorities. Findings show significant international variations in CT DRLs, with differences up to 50%. In India, DRLs also vary significantly across states. For head CT exams, Indian DRLs are generally 20–30% lower than international standards (27–47 mGy vs. 60 mGy). Conversely, for abdominal CT scans, Indian DRLs are 10–15% higher (12–16 mGy vs. 13 mGy). Factors influencing DRL variations include equipment differences, imaging protocols, patient demographics, and regulatory conditions. Dose-optimization techniques like automatic exposure control and iterative reconstruction can reduce radiation exposure by 25–60% while maintaining image quality. Comparative data highlight best practices, such as the United Kingdom’s 30% reduction in CT doses from 1984 to 1995 via DRL implementation. This study suggests that adopting similar practices in India could reduce radiation doses by 20–40% for common CT procedures, promoting responsible CT usage and minimizing patient exposure.

Background: Diosgenin, a powerful compound found in fenugreek and Dioscorea villosa, has diverse pharmacological effects. This study examines the anticancer potential of diosgenin nanoparticles (Dio-NPs) against DMBA-induced breast cancer in mice in combination with tamoxifen. Methods: In the current investigation, characterization of Dio-NPs was performed, including their size, shape, zeta potential, UV-vis, and FT-IR spectra. Dio-NPs (120 mg/kg) and tamoxifen (2 mg/kg) were given to mice with DMBA-induced breast cancer, either alone or in combination, over 4 weeks. We measured inflammatory and oxidative stress markers, as well as gene expressions related to apoptosis, using ELISA and qRT-PCR. Additionally, molecular docking studies were conducted to assess the binding affinity of diosgenin with specific proteins. Molecular dynamics simulations were conducted on CDK4, AKT, and CDK6 proteins with diosgenin using GROMACS. The systems were solved, neutralized, and equilibrated under NVT and NPT ensembles. Simulations ran for 100 ns, and trajectories were analyzed for RMSD, RMSF, RG, SASA, and hydrogen bonds. Results: The IC₅₀ of Dio-NPs against MCF-7 cells was 47.96 ± 1.48 µg/mL. Dio-NPs had a zeta potential of −21.8 ± 0.6 mV and a size of 56.85 ± 3.19 nm and were uniform and spherical. The LD₅₀ of Dio-NPs was 2400 mg/kg. DMBA exposure increased WBCs, inflammatory markers, oxidative stress, and gene expression of CDK2, CDK4, CDK6, and Akt, while reducing Hb%, RBCs, PLTs, GSH, superoxide dismutase, and catalase levels. Dio-NPs and tamoxifen, both alone and combined, significantly reduced these effects. The combination treatment was more effective than individual treatments. Histological analyses supported these findings. Molecular docking showed diosgenin had a stronger binding affinity with the target proteins compared to tamoxifen. The simulations revealed that diosgenin effectively binds to CDK4, AKT, and CDK6, maintaining their stability and structural integrity. CDK4, AKT, and CDK6 showed consistent RMSD, RG, and SASA values, with moderate flexibility and stable hydrogen bonding patterns, suggesting their potential as therapeutic targets. Conclusions: Combining diosgenin and tamoxifen effectively inhibits breast cancer progression in DMBA-treated mice. This is primarily due to the reduction in expression of CDK2, CDK4, CDK6, and Akt proteins, which enhances the sensitivity of resistant breast cancer cells to tamoxifen.

Higher levels of cortisol can disrupt the normal patterns of cerebral glucose metabolism in the human brain. This study aims to investigate the effects of elevated cortisol levels on cerebral glucose metabolism in men and women across Alzheimer's disease spectrum. The data was derived from the publicly available Alzheimer's Disease Neuroimaging Initiative (ADNI) database. Eight hundred and twenty-two participants across varying diagnostic cognition status were included: 469 men (mean age of 74.14 ± 7.19 years) and 353 women (mean age of 72.31 ± 7.34 years). Main effect and interaction terms were used in generalized linear models to examine the association between elevated cortisol levels and cerebral glucose metabolism as measured by Fluorodeoxyglucose positron emission tomography (FDG-PET) in men and women across Alzheimer's disease spectrum. Sex-stratified analysis was conducted a priori based on established biological differences in HPA axis function between sexes. Elevated cortisol levels were negatively associated with brain glucose consumption in women, but not in men. Women with APOE4 alleles were at greater risk of brain hypometabolism. Diastolic blood pressure in men, but not women, was negatively associated with brain glucose consumption, an indication of higher vascular vulnerability in men. Notably, while sex-stratified analyses revealed these differential patterns, the formal cortisol ^* sex interaction term did not reach statistical significance ( p = 0.157), potentially due to limited statistical power for detecting interactions. Larger studies are warranted to confirm these sex-specific findings. These findings suggest that cortisol may represent a modifiable risk factor warranting further investigation, particularly in postmenopausal women who experience estrogen decline, a known neuroprotective mediator.

Background: The role of cerebrospinal fluid (CSF) transforming growth factor β (TGF-β) isoforms in Alzheimer’s disease (AD) remains unclear. We examined associations of CSF TGF-β1, TGF-β2, and TGF-β3 with AD biomarkers, neurodegeneration, cognition, and clinical progression. Methods: In 294 ADNI participants with baseline CSF TGF-β measurements, adjusted regression, and mixed-effect models were used to evaluate associations with CSF biomarkers, neuroimaging, cognitive outcomes, and conversion. False-discovery-rate correction was applied. Results: Higher baseline TGF-β1 was associated with higher CSF total tau (β = 52.68 pg/mL per 1 SD increase; q < 0.001) and p-tau (β = 5.68 pg/mL; q < 0.001). Higher TGF-β2 was associated with faster hippocampal volume loss (β = −45.42 mm³/year; q < 0.001). No isoform was robustly associated with FDG-PET decline, cognitive decline, clinical conversion, or time to conversion. Conclusions: CSF TGF-β1 and TGF-β2 show distinct associations with tau-related pathology and hippocampal neurodegeneration, respectively, but do not appear to be prognostic biomarkers of clinical progression in AD.