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1.
BMC Neurol ; 20(1): 351, 2020 Sep 18.
Artículo en Inglés | MEDLINE | ID: mdl-32948136

RESUMEN

BACKGROUND: Oculomotor nerve palsy (ONP) is a common symptom of posterior communicating artery aneurysm (PcomAA) that can lead to impaired eye movement and pupil dilation. Currently, surgical clipping and endovascular embolization are the two most popular treatment methods for PcomAA-induced ONP; however, the recovery outcome between the two methods remains to be elucidated. METHODS: In the present study, we thoroughly compared the pretreatment factors and recovery outcome of the two treatments on 70 patients with PcomAA-induced ONP. The patients were separated into two groups based on the treatment that was received. Pretreatment factors, including age, sex, time period between ONP onset and treatment, ONP type, aneurysm diameter, status of subarachnoid hemorrhage and aneurysm rupture were recorded for each individual patient. Recovery outcome of the patients was assessed over a 12-month period. RESULTS: No significant differences were observed in any of the analyzed factors. Importantly, we revealed a significantly higher full recovery rate for the patients receiving the surgical clipping treatment than the ones that received the endovascular embolization treatment. In addition, we showed that patients' age was negatively correlated with the recovery extent in both treatment groups. CONCLUSIONS: The outcome of our study suggests that surgical clipping might be a better option to treat PcomAA-induced ONP.


Asunto(s)
Embolización Terapéutica/métodos , Procedimientos Endovasculares/métodos , Aneurisma Intracraneal/terapia , Enfermedades del Nervio Oculomotor/etiología , Recuperación de la Función , Adulto , Anciano , Femenino , Humanos , Aneurisma Intracraneal/complicaciones , Masculino , Persona de Mediana Edad , Estudios Retrospectivos , Instrumentos Quirúrgicos
2.
J Nutr Sci Vitaminol (Tokyo) ; 67(2): 84-90, 2021.
Artículo en Inglés | MEDLINE | ID: mdl-33952739

RESUMEN

Few studies have been performed to investigate the effect of vitamin D supplementation and T2DM in type 2 diabetic animal models. The present study aimed to explore the relationship between early 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and the incidence of T2DM and determine whether early 1,25(OH)2D3 supplementation was associated with inflammation in KK-Ay mice. The KK-Ay mice were divided into 4 vitamin D treatment groups, the low-dose vitamin D supplementation group (VDS-L, 1.5 µg/kg 1,25(OH)2D3), moderate-dose vitamin D supplementation group (VDS-M, 3.0 µg/kg 1,25(OH)2D3), high-dose vitamin D supplementation group (VDS-H, 6.0 µg/kg 1,25(OH)2D3) and the model control group (MC). C57BL/6J mice were used as the controls. The treatment period lasted for 9 wk. During this treatment period, fasting blood glucose (FBG) level of the mice was measured on a weekly basis. The levels of lipid profile, insulin and inflammation biomarkers were determined after 9 wk of 1,25(OH)2D3 intragastric gavage. After 9 wk of 1,25(OH)2D3 intragastric gavage, FBG level was significantly decreased in the vitamin D treatment groups compared with the MC group. The number of T2DM incidence in the VDS-L group (n=7), VDS-M group (n=5) and VDS-H group (n=3) was lower than those in the MC group (n=10) on week 9. Moreover, serum C-reactive protein (CRP) and interleukin-6 (IL-6) in the vitamin D treatment groups were significantly suppressed by 1,25(OH)2D3 administration compared with the MC group. Early 1,25(OH)2D3 supplementation could effectively lower the incidence of T2DM via ameliorating inflammation in KK-Ay mice.


Asunto(s)
Diabetes Mellitus Tipo 2 , Animales , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Suplementos Dietéticos , Incidencia , Inflamación/tratamiento farmacológico , Inflamación/prevención & control , Ratones , Ratones Endogámicos C57BL , Vitamina D/análogos & derivados
3.
Hum Cell ; 33(4): 1273-1280, 2020 Oct.
Artículo en Inglés | MEDLINE | ID: mdl-32779154

RESUMEN

Long non-coding RNAs (lncRNAs) are closely associated with tumorigenesis of various malignancies, including glioma. However, the roles of most lncRNAs in glioma remain undiscovered. The present study for the first time explored the roles of NFIA-AS2 in glioma. Based on informatic analyses by online database, lncRNA NFIA-AS2 in glioma tissues was overexpressed and further confirmed in glioma tissues and cells by quantitative real-time PCR (qRT-PCR). High expression of NFIA-AS2 was closely correlated with poor prognosis and might be an independent prognostic factor for PFS and OS. Functionally, silenced NFIA-AS2 could remarkably hinder glioma cell proliferation, migration and invasion, and cause the apoptosis. Mechanistic investigation disclosed that NFIA-AS2 interacted with miR-655-3p and inversely connected with miR-655-3p in glioma. Additionally, miR-655-3p was proved to regulate the expression of ZFX. Final rescue assay demonstrated that ZFX overexpression or miR-655-3p downregulation could neutralize the suppressive effects of NFIA-AS2 knockdown on glioma progression. In conclusion, this study firstly reported that NFIA-AS2 could promote the progression of glioma by targeting the miR-665-3p/ZFX axis, which highlighted that NFIA-AS2 could be a novel biomarker and therapeutic target for glioma patients.


Asunto(s)
Regulación Neoplásica de la Expresión Génica/genética , Expresión Génica/genética , Glioma/genética , Factores de Transcripción de Tipo Kruppel/genética , Factores de Transcripción de Tipo Kruppel/metabolismo , MicroARNs/metabolismo , Factores de Transcripción NFI/genética , ARN Largo no Codificante/genética , Apoptosis/genética , Línea Celular Tumoral , Movimiento Celular/genética , Proliferación Celular/genética , Progresión de la Enfermedad , Regulación hacia Abajo , Femenino , Glioma/terapia , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Terapia Molecular Dirigida , Factores de Transcripción NFI/metabolismo , Invasividad Neoplásica/genética , ARN Largo no Codificante/metabolismo , Regulación hacia Arriba/genética
4.
J Nutr Sci Vitaminol (Tokyo) ; 65(3): 211-218, 2019.
Artículo en Inglés | MEDLINE | ID: mdl-31257260

RESUMEN

The association of serum vitamin D deficiency and metabolic risk factors in Chinese adults with prediabetes (PreDM) has not been investigated. The present study aimed to investigate the association of serum vitamin D deficiency and metabolic risk factors in Chinese adults with PreDM. In this cross-sectional study, we stratified 412 PreDM patients into vitamin D sufficient, vitamin D insufficient and vitamin D deficient subgroups. The physical examination data was collected. Serum 25-hydroxyvitamin D3 [25(OH)D3] were measured by high performance liquid chromatography. The prevalence of vitamin D deficiency and insufficiency in PreDM patients were 30.58% and 26.70%, respectively. Compared with the vitamin D deficient group, the prevalence of metabolic syndrome, central obesity, hyperglycemia and hypertension were higher than those in the vitamin D insufficient or sufficient group (p<0.05). Moreover, the prevalence of dyslipidemia in the vitamin D deficient group was higher than those in the vitamin D sufficient group (p<0.05). We observed an inverse relationship between 25(OH)D3 levels and waist circumference, triglyceride, and serum uric acid (ß=-0.315; ß=-0.134; ß=-0.239), a positive relationship between 25(OH)D3 levels and high-density lipoprotein cholesterol (ß=0.197) after adjusting for age, sex and body mass index. Vitamin D deficiency is very common among PreDM patients in China and this deficiency is related to metabolic risk factors.


Asunto(s)
Estado Prediabético , Deficiencia de Vitamina D , Adulto , Anciano , China/epidemiología , HDL-Colesterol/sangre , Estudios Transversales , Femenino , Humanos , Masculino , Persona de Mediana Edad , Estado Prediabético/complicaciones , Estado Prediabético/epidemiología , Factores de Riesgo , Triglicéridos/sangre , Ácido Úrico/sangre , Vitamina D/sangre , Deficiencia de Vitamina D/complicaciones , Deficiencia de Vitamina D/epidemiología , Circunferencia de la Cintura , Adulto Joven
5.
Sci Technol Adv Mater ; 9(3): 035008, 2008 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-27878005

RESUMEN

Superhydrophobic surfaces were fabricated by the complex coating of silica nanoparticles with functional groups onto cotton textiles to generate a dual-size surface roughness, followed by hydrophobization with stearic acid, 1H, 1H, 2H, 2H-perfluorodecyltrichlorosilane or their combination. The wettability and morphology of the as-fabricated surfaces were investigated by contact angle measurement and scanning electron microscopy. Characterizations by transmission electron microscopy, Fourier transformation infrared spectroscopy, and thermal gravimetric analysis were also conducted.

6.
Oncol Lett ; 16(2): 1439-1448, 2018 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-30008822

RESUMEN

Gliomas are the most common type of malignant primary brain tumors in adults and exhibit a spectrum of aberrantly aggressive phenotypes. Despite advances in treatments during past decades, prognosis of the disease remains poor, with a median survival time of 12-14 months. Future studies on the molecular mechanism of the disease may provide the theoretical basis to identify new targets for effective therapies. The present study revealed that in glioblastoma cells, the overexpression of cytochrome P450, family 27, subfamily A, polypeptide 1 (CYP27A1) promoted proliferation, while silencing of CYP27A1 inhibited proliferation, without affecting migration and invasion. CYP27A1 protein was upregulated in glioblastoma tissues, indicating that CYP27A1 is an oncogene. The downregulation of specific microRNAs (miRNA) may contribute to the upregulation of oncogenes in glioblastoma. A common strategy was used to predict target miRNAs of CPY27A1 using the miRanda algorithm. miR-211 and miR-204 could target the 3'untranslated region of CPY27A1 mRNA. Additional studies confirmed that the overexpression of miR-204 inhibited CPY27A1 expression in glioblastoma cells. Finally, it was identified that miR-204 was downregulated in glioblastoma and that its overexpression inhibited proliferation, migration and invasion in glioblastoma cells. Thus, it was concluded that miR-204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma.

7.
Mol Med Rep ; 13(5): 4279-88, 2016 May.
Artículo en Inglés | MEDLINE | ID: mdl-27035789

RESUMEN

Glioblastoma is the most common type of primary brain tumor in adults, and is usually fatal in a short duration. Acquiring a better understanding of the pathogenic mechanisms of glioblastoma is essential to the design of effective therapeutic strategies. Grb2-associated binding protein 2 (GAB2) is a member of the daughter of sevenless/Gab family of scaffolding adapters, and has been reported to be important in the development and progression of human cancer. Previously, it has been reported that GAB2 is expressed at high levels in glioma, and may serve as a useful prognostic marker for glioma and a novel therapeutic target for glioma invasion intervention. Elucidating why GAB2 is overexpressed in glioma, and investigating how to downregulate it will assist in further understanding the pathogenesis and progression of the disease, and to offer novel targets for therapy. The present study used in situ hybridization to detect microRNA (miR)­197 expression levels and Targetscan to predict that the 3'-UTR of GAB2 was targeted by miR-197. Northern blotting and reverse transcription­quantitative polymerase chain reaction were also conducted in the current study. miR-197 is downregulated in glioblastoma tissues, compared with adjacent normal tissues, however it involvement continues to be detected in the disease. The results of the present study demonstrated that miR­197, as a tumor suppressor gene, inhibited proliferation by regulating GAB2 in glioblastoma cells. Furthermore, GAB2 was not only upregulated in glioma, but its expression levels were also associated with the grades of glioma severity. In addition, overexpression of GAB2 suppressed the expression of miR­197 in glioblastoma cells. Therefore, restoration of miR­197 and targeting GAB2 may be used, in conjunction with other therapies, to prevent the progression of glioblastoma.


Asunto(s)
Proteínas Adaptadoras Transductoras de Señales/biosíntesis , Neoplasias Encefálicas/metabolismo , Proliferación Celular , Glioblastoma/metabolismo , MicroARNs/biosíntesis , Proteínas de Neoplasias/biosíntesis , ARN Neoplásico/biosíntesis , Proteínas Adaptadoras Transductoras de Señales/genética , Adulto , Anciano , Neoplasias Encefálicas/genética , Neoplasias Encefálicas/patología , Femenino , Glioblastoma/genética , Glioblastoma/patología , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Proteínas de Neoplasias/genética , ARN Neoplásico/genética
8.
Oncol Rep ; 34(2): 868-76, 2015 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-26081814

RESUMEN

Glioblastoma is the most common primary malignancy of the adult central nervous system (CNS) and is associated with an exceptionally poor prognosis. Elucidation of the pathogenesis and molecular changes will help us to further understand the pathogenesis and progression of the disease and offer new therapeutic targets. FUS1 (TUSC2, tumor suppressor candidate 2) is a tumor-suppressor gene located on human chromosome 3p21. Restoration of FUS1 function in human non-small cell lung cancer (NSCLC) cells was found to significantly inhibit tumor cell growth and modulate the chemosensitivity of lung cancer cells. Yet, its role in human glioblastoma has rarely been addressed. In the present study, we demonstrated that low expression of FUS1 was detected in high-grade human glioma, implying that FUS1 expression is negatively associated with progression of the disease. Subsequent studies confirmed that FUS1 overexpression inhibited the proliferation, migration and invasion of human glioblastoma cells. In addition, we found that FUS1 overexpression significantly upregulated miR-197 expression in the glioblastoma cells. We also revealed that miR-197 suppressed the proliferation, migration and invasion of the cells as well as the silencing of miR-197 attenuated the biological functions of FUS1. Using human glioblastoma tissue samples, we demonstrated that miR-197 is negatively associated with metastasis. All the results demonstrated that FUS1 acts as a tumor-suppressor gene by upregulating miR-197 in human glioblastoma and implied that restoration of FUS1 and miR-197 could be new therapeutic strategies for glioblastoma.


Asunto(s)
Proliferación Celular/genética , Glioblastoma/genética , MicroARNs/biosíntesis , Proteínas Supresoras de Tumor/biosíntesis , Adulto , Anciano , Línea Celular Tumoral , Movimiento Celular/genética , Progresión de la Enfermedad , Femenino , Regulación Neoplásica de la Expresión Génica , Glioblastoma/patología , Humanos , Masculino , MicroARNs/genética , Persona de Mediana Edad , Invasividad Neoplásica/genética , Estadificación de Neoplasias , Proteínas Supresoras de Tumor/genética
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