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1.
Front Neurol ; 13: 1079737, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36588903

RESUMO

Introduction: Carpal tunnel syndrome (CTS) is a common compression neuropathy of the median nerve in the wrist. Early diagnosis of CTS is essential for selecting treatment options and assessing prognosis. The current diagnosis of CTS is based on the patient's clinical symptoms, signs, and an electromyography (EMG) test. However, they have some limitations. Recently, ultrasound has been adopted as an adjunct diagnostic tool for electromyography (EMG). Ultrasound is a non-invasive and cost-effective technique. It provides a dynamic display of morphological changes in the median nerve and an assessment of CTS etiology such as tenosynovitis, mass compression, and tendon disease. This study aimed to investigate the value of conventional ultrasound and real-time shear wave elastography (SWE) in evaluation of median neuropathy in patients with carpal tunnel syndrome (CTS) before and after surgery. Methods: First, the Boston Carpal Tunnel Questionnaire (BCTQ) was administered to patients with CTS. All subjects were measured at three levels: the distal 1/3 of the forearm, the carpal tunnel inlet, and the distal carpal tunnel using conventional ultrasound and SWE. Median nerve parameters were examined in patients with CTS 1 week after surgery. Results: The cross-sectional area (CSA) and stiffness of the median nerve at the carpal tunnel inlet and distal carpal tunnel were significantly higher in patients with CTS than in healthy controls (p < 0.001). The CSA and stiffness of the median nerve at the carpal tunnel inlet were statistically significantly significantly between pre- and postoperative patients with CTS (p < 0.001). The CSA and stiffness of the nerve in patients with CTS had a positive correlation with electrophysiology severity. Conclusions and discussion: Conventional ultrasound and elastography are valuable in the diagnosis of CTS and are useful in the clinical assessment of patient's nerve recovery after operation.

2.
Ann N Y Acad Sci ; 1425(1): 70-81, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29873092

RESUMO

The operations involved in preimplantation genetic testing (PGT) occur during the key stages of gametogenesis and early embryonic development, and the health of progeny following PGT (PGT-born) is worthy of attention. In order to fully assess the potential risk of abnormal glucose metabolism in adult PGT-born offspring and to evaluate possible mechanisms, we compared a mouse model of PGT (in vitro cultured embryos with biopsy, hereafter "PTG-born mice"), an in vitro embryo manipulation mouse model (in vitro cultured embryos without biopsy), and normal mice. PGT-born mice displayed increased fasting glucose, and decreased glycogen synthesis and glucose oxidative utilization in the liver. Moreover, PGT-born mice also displayed reduced expression of insulin receptor, AKT, and insulin-stimulated Akt phosphorylation (pAkt) in the liver. These results suggest a potential risk of insulin resistance in adult PGT-born mice. By analyzing the DNA methylation profiles of 7.5 days postconception (dpc) embryos, we identified differentially methylated genes associated with liver development between PGT-born and control groups; some of these genes are associated with glucose homeostasis and insulin response. These results suggest that abnormal methylation in embryos that develop after PGT may be a potential mechanism occurring during embryonic development that can influence the risk of liver-derived insulin resistance in adulthood.


Assuntos
Metilação de DNA , Desenvolvimento Embrionário/genética , Testes Genéticos/métodos , Resistência à Insulina/genética , Fígado/metabolismo , Diagnóstico Pré-Implantação/métodos , Animais , Embrião de Mamíferos/embriologia , Embrião de Mamíferos/metabolismo , Feminino , Regulação da Expressão Gênica no Desenvolvimento , Glucose/metabolismo , Glicogênio/biossíntese , Glicogênio/sangue , Glicogênio Sintase/genética , Glicogênio Sintase/metabolismo , Humanos , Camundongos Endogâmicos ICR , Gravidez , Receptor de Insulina/genética , Receptor de Insulina/metabolismo , Fatores de Risco
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