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1.
Zhonghua Yi Xue Za Zhi ; 100(43): 3402-3406, 2020 Nov 24.
Artículo en Chino | MEDLINE | ID: mdl-33238669

RESUMEN

Objective: To explore the imaging features in age-related cerebral small vessel disease (ArCSVD) with idiopathic normal pressure hydrocephalus (INPH). Methods: Ten cases of age-related cerebral small vessel disease (CSVD) with idiopathic normal pressure hydrocephalus admitted to the Third Affiliated Hospital of Sun Yat-sen University from December 2015 to March 2020 were retrospective analyzed, all patients met the inclusion and exclusion criteria, and completed the head Magnetic resonance angiography plain scan, T2 fluid attenuated inversion recovery and Susceptibility Weighted Imaging sequence. Deep marrow venous signs (DMVs), INPH severity (DESH score), cortical/subcortical and deep microhemorrhages (CMBs) statistics, paraventricular and deep white matter damage (WMH) severity and CSVD imaging burden score were acquired, and correlations of DMVs and DESH scores with CMBs, WMH and Burden scores were evaluated using Spearman correlation analysis. Results: DMVs and DESH scores were significantly and positively correlated (r=0.965 9, P<0.000 1). DMVs and DESH scores were not significantly correlated with cortical/subcortical CMBs and deep CMBs. Likewise, DMVs and DESH scores were not significantly correlated with deep WMH. The WMH score of paraventricular of the 10 cases was 3 points, and the Burden score was 4 points. Conclusion: DMVs may be an indicator of the severity of ArCSVD with INPH, due to the small sample size of the current study, more cases are needed for further verification.


Asunto(s)
Enfermedades de los Pequeños Vasos Cerebrales , Hidrocéfalo Normotenso , Sustancia Blanca , Enfermedades de los Pequeños Vasos Cerebrales/diagnóstico por imagen , Humanos , Hidrocéfalo Normotenso/diagnóstico por imagen , Imagen por Resonancia Magnética , Estudios Retrospectivos
2.
Eur Rev Med Pharmacol Sci ; 22(10): 3067-3073, 2018 05.
Artículo en Inglés | MEDLINE | ID: mdl-29863252

RESUMEN

OBJECTIVE: LIM homeobox domain 6 (LHX6) is emerging as a critical regulator in carcinogenesis and tumor progression. The previous study has reported the expression and function of LHX6 in breast cancer (BC). However, its mechanism underlying BC metastasis remains largely unclear. This study aimed to investigate the related mechanisms of the tumor-suppressive role of LHX6 in BC. PATIENTS AND METHODS: Quantitative Real-time PCR (qRT-PCR) and Western blotting were used to determine LHX6 mRNA levels and protein expressions in BC tissues and cell lines. LHX6 protein expression was also analyzed in BC tissues and matched normal breast tissues using immunohistochemistry (IHC). The biologic functions of LHX6 in BC were explored by CCK-8 assay, colony formation assay, and transwell assays in vitro. Finally, we investigated the effect of LHX6 up-regulation on PI3K/AKT/mTOR pathway by Western blot. RESULTS: Our results showed that LHX6 was lowly expressed at the mRNA and protein level in BC cancer tissues and cell lines. Ectopic expression of LHX6 in MDA-MB-231 and T-47D suppressed cell growth, migration, and invasion. Mechanistically, our further investigations revealed that the upregulation of LHX6 inhibited the activation of the PI3K/Akt/mTOR signaling pathway. CONCLUSIONS: We firstly provided evidence that LHX6 exerted its anti-tumor function on BC via suppressing activation of the PI3K/Akt/mTOR signaling, which eventually inhibited the progression of BC.


Asunto(s)
Neoplasias de la Mama/metabolismo , Movimiento Celular , Proliferación Celular , Proteínas con Homeodominio LIM/metabolismo , Proteínas del Tejido Nervioso/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , Serina-Treonina Quinasas TOR/metabolismo , Factores de Transcripción/metabolismo , Neoplasias de la Mama/patología , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Femenino , Humanos , Proteínas con Homeodominio LIM/genética , Invasividad Neoplásica , Proteínas del Tejido Nervioso/genética , Transducción de Señal , Factores de Transcripción/genética
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