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Hongxu Xian Yuan Liu Alexandra Rundberg Nilsson Raphaella Gatchalian Timothy R. Crother Warren G. Tourtellotte Yi Zhang German R. Aleman-Muench Gavin Lewis Weixuan Chen Sarah Kang Melissa Luevanos Dorit Trudler Stuart A. Lipton Pejman Soroosh John Teijaro Juan Carlos de la Torre Moshe Arditi Elsa Sanchez-Lopez 《Immunity》2021,54(7):1463-1477.e11
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Nelly Mauras Paul Mazaika Bruce Buckingham Stuart Weinzimer Neil H. White Eva Tsalikian Tamara Hershey Allison Cato Peiyao Cheng Craig Kollman Roy W. Beck Katrina Ruedy Tandy Aye Larry Fox Ana Maria Arbelaez Darrell Wilson Michael Tansey William Tamborlane Daniel Peng Matthew Marzelli Karen K. Winer Allan L. Reiss 《Diabetes》2015,64(5):1770-1779
Significant regional differences in gray and white matter volume and subtle cognitive differences between young diabetic and nondiabetic children have been observed. Here, we assessed whether these differences change over time and the relation with dysglycemia. Children ages 4 to <10 years with (n = 144) and without (n = 72) type 1 diabetes (T1D) had high-resolution structural MRI and comprehensive neurocognitive tests at baseline and 18 months and continuous glucose monitoring and HbA1c performed quarterly for 18 months. There were no differences in cognitive and executive function scores between groups at 18 months. However, children with diabetes had slower total gray and white matter growth than control subjects. Gray matter regions (left precuneus, right temporal, frontal, and parietal lobes and right medial-frontal cortex) showed lesser growth in diabetes, as did white matter areas (splenium of the corpus callosum, bilateral superior-parietal lobe, bilateral anterior forceps, and inferior-frontal fasciculus). These changes were associated with higher cumulative hyperglycemia and glucose variability but not with hypoglycemia. Young children with T1D have significant differences in total and regional gray and white matter growth in brain regions involved in complex sensorimotor processing and cognition compared with age-matched control subjects over 18 months, suggesting that chronic hyperglycemia may be detrimental to the developing brain. 相似文献
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Dysregulated TGF‐β signaling alters bone microstructure in a mouse model of Loeys‐Dietz syndrome 下载免费PDF全文
Ashvin K. Dewan Ryan E. Tomlinson Stuart Mitchell Brian C. Goh Rachel M. Yung Sarvesh Kumar Eric W. Tan Marie‐Claude Faugere Harry C. Dietz III Thomas L. Clemens Paul D. Sponseller 《Journal of orthopaedic research》2015,33(10):1447-1454
Loeys‐Dietz syndrome (LDS) is a connective tissue disorder characterized by vascular and skeletal abnormalities resembling Marfan syndrome, including a predisposition for pathologic fracture. LDS is caused by heterozygous mutations in the genes encoding transforming growth factor‐β (TGF‐β) type 1 and type 2 receptors. In this study, we characterized the skeletal phenotype of mice carrying a mutation in the TGF‐β type 2 receptor associated with severe LDS in humans. Cortical bone in LDS mice showed significantly reduced tissue area, bone area, and cortical thickness with increased eccentricity. However, no significant differences in trabecular bone volume were observed. Dynamic histomorphometry performed in calcein‐labeled mice showed decreased mineral apposition rates in cortical and trabecular bone with normal numbers of osteoblasts and osteoclasts. Mechanical testing of femurs by three‐point bending revealed reduced femoral strength and fracture resistance. In vitro, osteoblasts from LDS mice demonstrated increased mineralization with enhanced expression of osteoblast differentiation markers compared with control cells. These changes were associated with impaired TGF‐β1–induced Smad2 and Erk1/2 phosphorylation and upregulated TGF‐β1 ligand mRNA expression, compatible with G357W as a loss‐of‐function mutation in the TGF‐β type 2 receptor. Paradoxically, phosphorylated Smad2/3 in cortical osteocytes measured by immunohistochemistry was increased relative to controls, possibly suggesting the cross‐activation of TGF‐β–related receptors. The skeletal phenotype observed in the LDS mouse closely resembles the principal structural features of bone in humans with LDS and establishes this mouse as a valid in vivo model for further investigation of TGF‐β receptor signaling in bone. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1447–1454, 2015. 相似文献