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131.
Kurnia King Hans Elvioza Sidik Mohamad Sari Teny Tjitra Prihartono Joedo Sitorus Rita S. 《Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie》2021,259(9):2633-2641
Graefe's Archive for Clinical and Experimental Ophthalmology - To investigate retinal changes in β-thalassemia major patients and identify their association with systemic risk factors. In... 相似文献
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Cédric Delhaye Arnaud Sudre Gilles Lemesle Mohamad Koussa Thomas Modine 《Cardiovascular Revascularization Medicine》2012,13(3):201.e1-201.e3
Corevalve dislocation has been reported to significantly increase the perioperative risk for severe complications and poor outcomes. We describe the case of an 87-year-old man who was referred to our center for transcatheter aortic valve implantation and who experienced an original complication after Corevalve dislocation by subclavian approach. Indeed, during the attempt to retrieve the partially expanded and dislocated valve through the subclavian introducer sheath, we experienced a dislodgment of the valve from the housing sheath that led to a delivery catheter cone separation and systemic embolization. 相似文献
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Steven D Rhodes Xiaohua Wu Yongzheng He Shi Chen Hao Yang Karl W Staser Jiapeng Wang Ping Zhang Chang Jiang Hiroki Yokota Ruizhi Dong Xianghong Peng Xianlin Yang Sreemala Murthy Mohamad Azhar Khalid S Mohammad Mingjiang Xu Theresa A Guise Feng‐Chun Yang 《Journal of bone and mineral research》2013,28(12):2476-2489
Dysregulated transforming growth factor beta (TGF‐β) signaling is associated with a spectrum of osseous defects as seen in Loeys‐Dietz syndrome, Marfan syndrome, and Camurati‐Engelmann disease. Intriguingly, neurofibromatosis type 1 (NF1) patients exhibit many of these characteristic skeletal features, including kyphoscoliosis, osteoporosis, tibial dysplasia, and pseudarthrosis; however, the molecular mechanisms mediating these phenotypes remain unclear. Here, we provide genetic and pharmacologic evidence that hyperactive TGF‐β1 signaling pivotally underpins osseous defects in Nf1flox/?;Col2.3Cre mice, a model which closely recapitulates the skeletal abnormalities found in the human disease. Compared to controls, we show that serum TGF‐β1 levels are fivefold to sixfold increased both in Nf1flox/?;Col2.3Cre mice and in a cohort of NF1 patients. Nf1‐deficient osteoblasts, the principal source of TGF‐β1 in bone, overexpress TGF‐β1 in a gene dosage–dependent fashion. Moreover, Nf1‐deficient osteoblasts and osteoclasts are hyperresponsive to TGF‐β1 stimulation, potentiating osteoclast bone resorptive activity while inhibiting osteoblast differentiation. These cellular phenotypes are further accompanied by p21‐Ras–dependent hyperactivation of the canonical TGF‐β1–Smad pathway. Reexpression of the human, full‐length neurofibromin guanosine triphosphatase (GTPase)‐activating protein (GAP)‐related domain (NF1 GRD) in primary Nf1‐deficient osteoblast progenitors, attenuated TGF‐β1 expression levels and reduced Smad phosphorylation in response to TGF‐β1 stimulation. As an in vivo proof of principle, we demonstrate that administration of the TGF‐β receptor 1 (TβRI) kinase inhibitor, SD‐208, can rescue bone mass deficits and prevent tibial fracture nonunion in Nf1flox/?;Col2.3Cre mice. In sum, these data demonstrate a pivotal role for hyperactive TGF‐β1 signaling in the pathogenesis of NF1‐associated osteoporosis and pseudarthrosis, thus implicating the TGF‐β signaling pathway as a potential therapeutic target in the treatment of NF1 osseous defects that are refractory to current therapies. © 2013 American Society for Bone and Mineral Research. 相似文献
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Jamile F. Gonçalves Roselia M. Spanevello Amanda M. Fiorenza Cinthia M. Mazzanti Margarete D. Bagatini Cíntia S. da Rosa Lara V. Becker Pauline da Costa Fátima H. Abdalla Vera M. Morsch Maria Rosa C. Schetinger 《International journal of developmental neuroscience》2013
The purpose of the present investigation was to evaluate the hydrolysis of adenine nucleotides on synaptosomes and platelets obtained from rats exposed to cadmium (Cd) and treated with N-acetylcysteine (NAC). Rats received Cd (2 mg/kg) and NAC (150 mg/kg) by gavage every other day for 30 days. Animals were divided into four groups (n = 4–6): control/saline, NAC, Cd, and Cd/NAC. The results of this study demonstrated that NTPDase and 5′-nucleotidase activities were increased in the cerebral cortex synaptosomes of Cd-poisoned rats, and NAC co-treatment reversed these activities to the control levels. In relation to hippocampus synaptosomes, no differences on the NTPDase and 5′-nucleotidase activities of Cd-poisoned rats were observed and only the 5′-nucleotidase activity was increased by the administration of NAC per se. In platelets, Cd-intoxicated rats showed a decreased NTPDase activity and no difference in the 5′-nucleotidase activity; NAC co-treatment was inefficient in counteracting this undesirable effect. Our findings reveal that adenine nucleotide hydrolysis in synaptosomes and platelets of rats were altered after Cd exposure leading to a compensatory response in the central nervous system and acting as a modulator of the platelet activity. NAC was able to modulate the purinergic system which is interesting since the regulation of these enzymes could have potential therapeutic importance. Thus, our results reinforce the importance of the study of the ecto-nucleotidases pathway in poisoning conditions and highlight the possibility of using antioxidants such as NAC as adjuvant against toxicological conditions. 相似文献
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