1.Radiation dose and establishment of a regression model for dose estimation in pediatric chest CT
Ziyu ZHAO ; Yu LIANG ; Yutong ZHANG ; Zifan WEI ; Xinxing MA
Chinese Journal of Radiological Health 2025;34(5):654-659
Objective To investigate the differences in radiation dose during chest CT examinations among children of different age groups and establish dose estimation regression models. Methods Chest CT data from 135 children aged 4 to 15 years were retrospectively collected from the First Affiliated Hospital of Soochow University between January 2022 and December 2023. The children were divided into three age groups: 4-5 years, 6-10 years and 11-15 years. CT scanning parameters (tube voltage, tube current, scan range) and dosimetry parameters including volume CT dose index (CTDIvol) dose length product (DLP), and size-specific dose estimate (SSDE) were recorded. The Kruskal-Wallis test was used to compare intergroup differences. A Pearson correlation analysis was performed to assess the relationship between age and dose indicators. Both linear and nonlinear regression models were constructed. Results Age showed a weak positive correlation with CTDIvol (r = 0.27), a moderate positive correlation with DLP (r = 0.60), and a moderate negative correlation with SSDE (r = −0.55). Linear regression analysis revealed that DLP increased with age (y = 117.85 + 9.81x, R2 = 0.36), while SSDE decreased with age (y = 12.4 − 0.18x, R2 = 0.32). Using orthogonal distance regression, the goodness-of-fit of the nonlinear models for DLP and SSDE significantly improved (R2 = 0.99 and 0.94, respectively). Conclusion In pediatric chest CT dose assessment, CTDIvol underestimates radiation dose compared to SSDE and fails to account for patient body size. The dose estimation models constructed with orthogonal distance regression outperform those established using the least squares method, demonstrating higher fitting accuracy, and can serve as a reference for personalized dose management in pediatric CT examinations.
2.Individualized plasticity autograft mimic with efficient bioactivity inducing osteogenesis.
Yan WEI ; Guixin ZHU ; Zifan ZHAO ; Chengcheng YIN ; Qin ZHAO ; Hudi XU ; Jinyang WANG ; Jinglun ZHANG ; Xiaoxin ZHANG ; Yufeng ZHANG ; Haibin XIA
International Journal of Oral Science 2021;13(1):14-14
Mineralized tissue regeneration is an important and challenging part of the field of tissue engineering and regeneration. At present, autograft harvest procedures may cause secondary trauma to patients, while bone scaffold materials lack osteogenic activity, resulting in a limited application. Loaded with osteogenic induction growth factor can improve the osteoinductive performance of bone graft, but the explosive release of growth factor may also cause side effects. In this study, we innovatively used platelet-rich fibrin (PRF)-modified bone scaffolds (Bio-Oss
Autografts
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Bone Regeneration
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Cell Differentiation
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Humans
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Mesenchymal Stem Cells
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Osteogenesis
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Tissue Engineering
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Tissue Scaffolds
3.Generation of a Hutchinson-Gilford progeria syndrome monkey model by base editing.
Fang WANG ; Weiqi ZHANG ; Qiaoyan YANG ; Yu KANG ; Yanling FAN ; Jingkuan WEI ; Zunpeng LIU ; Shaoxing DAI ; Hao LI ; Zifan LI ; Lizhu XU ; Chu CHU ; Jing QU ; Chenyang SI ; Weizhi JI ; Guang-Hui LIU ; Chengzu LONG ; Yuyu NIU
Protein & Cell 2020;11(11):809-824
Many human genetic diseases, including Hutchinson-Gilford progeria syndrome (HGPS), are caused by single point mutations. HGPS is a rare disorder that causes premature aging and is usually caused by a de novo point mutation in the LMNA gene. Base editors (BEs) composed of a cytidine deaminase fused to CRISPR/Cas9 nickase are highly efficient at inducing C to T base conversions in a programmable manner and can be used to generate animal disease models with single amino-acid substitutions. Here, we generated the first HGPS monkey model by delivering a BE mRNA and guide RNA (gRNA) targeting the LMNA gene via microinjection into monkey zygotes. Five out of six newborn monkeys carried the mutation specifically at the target site. HGPS monkeys expressed the toxic form of lamin A, progerin, and recapitulated the typical HGPS phenotypes including growth retardation, bone alterations, and vascular abnormalities. Thus, this monkey model genetically and clinically mimics HGPS in humans, demonstrating that the BE system can efficiently and accurately generate patient-specific disease models in non-human primates.
Animals
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Disease Models, Animal
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Female
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Gene Editing
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Humans
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Lamin Type A/metabolism*
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Macaca fascicularis
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Progeria/pathology*

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