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1.
Diagn Cytopathol ; 52(7): 369-376, 2024 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-38595067

RESUMEN

BACKGROUND: Fine needle aspiration cytology (FNAC) is the most useful tool in the diagnosis of thyroid nodules. Liquid-based cytology (LBC) is replacing the conventional smear (CS) for evaluation of thyroid FNAC. In our institution, thyroid FNAC preparation was changed from CS to LBC SurePath in July 2016. This study aimed to compare the diagnostic value of SurePath with that of CS in thyroid lesions. METHODS: A total of 35,406 samples of thyroid FNAC (11,438 CS and 23,968 SurePath), collected from January 2010 to December 2022, were included in this study. We also examined the malignant rate using the surgical pathology diagnosis as the gold standard. RESULTS: The distribution of TBSRTC cytological categories was equivalent between CS and SurePath. The rate of nondiagnostic/unsatisfactory category was higher in CS compared to SurePath (43.4% vs. 22.3%; p < .05). After routine use of SurePath, the surgical resection rate was reduced from 12.0% to 8.6% (p < .05) and the malignant rate increased from 32.2% to 41.5% (p < .05). The sensitivities of CS and SurePath were 71.0% and 82.0%, respectively, and the specificities were 99.0% and 97.3%, respectively, whereas the positive predictive values were 97.8% and 96.8%, respectively, and the negative predictive values were 85.0% and 84.6%, respectively. Diagnostic accuracy of CS and SurePath were 88.5% and 89.7% respectively. CONCLUSION: SurePath can increase the sample adequacy, increase the sensitivity and reduce the workload and avoid unnecessary surgeries with similar accuracy to CS.


Asunto(s)
Glándula Tiroides , Neoplasias de la Tiroides , Nódulo Tiroideo , Humanos , Biopsia con Aguja Fina/métodos , Femenino , Masculino , Persona de Mediana Edad , Nódulo Tiroideo/patología , Nódulo Tiroideo/diagnóstico , Adulto , Glándula Tiroides/patología , Neoplasias de la Tiroides/patología , Neoplasias de la Tiroides/diagnóstico , Sensibilidad y Especificidad , Anciano , Citodiagnóstico/métodos , Citología
2.
Int J Cardiol ; 134(2): 169-75, 2009 May 15.
Artículo en Inglés | MEDLINE | ID: mdl-18597869

RESUMEN

BACKGROUND: Metformin has been reported to reduce cardiovascular complications in diabetic patients. The purpose of the present study was to investigate the anti-inflammatory effects of metformin on endothelial cells and the related molecular mechanisms. METHODS: Human umbilical vein endothelial cells (HUVEC) were used for the experiments. The effects of metformin on TNF-alpha-induced IL-6 production were investigated. Modulation of AMPK and related signal transduction pathways were also performed. RESULTS: TNF-alpha increased IL-6 secretion by HUVEC in a dose-dependent manner but inhibitors of NF-kappaB abolished the TNF-alpha-induced IL-6 production. Pre-treatment with metformin (100-1000 micromol/L) also inhibited TNF-alpha-induced IL-6 production, phosphorylation of IkappaB kinase (IKK) alpha/beta and IkappaB-alpha degradation. Metformin increased phosphorylation of AMP-activated kinase (AMPK) but wortmannin, a PI3K inhibitor, negated its effects on AMPK phosphorylation and TNF-alpha-induced IkappaB-alpha degradation. AICAR, a direct AMPK activator, had inhibitory effects on TNF-alpha-induced IL-6 production, similar to that of metformin. Transfection of siRNA against alpha1-AMPK eradicated the inhibitory effects of metformin on TNF-alpha-induced IL-6, implying the essential role of AMPK. CONCLUSIONS: Metformin had anti-inflammatory effects on endothelial cells and inhibited TNF-alpha-induced IKKalpha/beta phosphorylation, IkappaB-alpha degradation and IL-6 production in HUVEC. This effect was related to PI3K-dependent AMPK phosphorylation.


Asunto(s)
Proteínas Quinasas Activadas por AMP/metabolismo , Células Endoteliales/efectos de los fármacos , Quinasa I-kappa B/metabolismo , Interleucina-6/metabolismo , Metformina/farmacología , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Quinasas Activadas por AMP/genética , Antiinflamatorios/farmacología , Aterosclerosis/tratamiento farmacológico , Aterosclerosis/metabolismo , Aterosclerosis/patología , Células Cultivadas , Células Endoteliales/citología , Células Endoteliales/metabolismo , Activación Enzimática/efectos de los fármacos , Humanos , Hipoglucemiantes/farmacología , FN-kappa B/metabolismo , Fosforilación/efectos de los fármacos , ARN Interferente Pequeño , Transducción de Señal/efectos de los fármacos , Factor de Necrosis Tumoral alfa/metabolismo , Venas Umbilicales/citología
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