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Yan X.-T.,First Affiliated Hospital Of Xian Jiaotong University
European Journal of Clinical Nutrition | Year: 2016

Background/Objectives:Effects of vitamin D deficiency in pregnancy have been associated with some adverse pregnancy outcomes. The objective of this study was to analyze the relationship between vitamin D deficiency in childbearing aged women and pregnancy loss (PL) in the first trimester.Subjects/Methods:This is a cross-sectional study. Plasma was collected from 60 nulliparous women with singleton at 7–9 weeks of gestation (30 with viable gestation and 30 with PL) and 60 non-gravid childbearing aged women (30 with a successful pregnancy history, and 30 with one or more spontaneous first-trimester PL history). Quantitation of serum 25-hydroxyvitamin D (25(OH)D) and 25-hydroxyvitamin D-1 alpha hydroxylase (CYP27B1) was assayed.Results:By pregnancy/non-gravid, normal pregnant women had higher 25(OH)D (49.32 μg/l) and CYP27B1 (82.00 pg/ml) than PL women (34.49 μg/l and 37.87 pg/ml, both P<0.01); the non-gravid women with a successful pregnancy history also had higher 25(OH)D (39.56 μg/l) and CYP27B1 (39.04 pg/ml) than women with PL history (12.30 μg/l and 12.35 pg/ml, both P<0.01). The 96.7% of non-gravid women with PL history and 43.3% of PL women had serum 25(OH)D concentrations below 30 μg/l. There was a strong association between low vitamin D levels and PL (odds ratio 1.71; 95% confidence interval: 1.2–2.4, P<0.001). The regression analyses showed that PL was significantly inversely correlated with 25(OH)D (P<0.01) and CYP27B1 levels (P<0.01).Conclusions:Vitamin D deficiency associated with PL in the first trimester of pregnancy. Decreased serum vitamin D levels among childbearing aged women with the failed clinical pregnancies history may predispose to increased risk for PL.European Journal of Clinical Nutrition advance online publication, 25 May 2016; doi:10.1038/ejcn.2016.83. © 2016 Macmillan Publishers Limited Source

He J.,First Affiliated Hospital Of Xian Jiaotong University
Oncology Letters | Year: 2015

Breast hamartoma is an uncommonly reported benign breast lesion of uncertain cause and pathogenesis. The diagnosis of breast hamartoma by a single method such as mammography, magnetic resonance imaging or sonography is inadequate. In the majority of cases, the breast hamartoma is excised a few years after it has occurred when it is not too big. In the present report, however, a particularly large lesion with a long history is described. Such a case has rarely been reported and shows the necessity of early surgery to reduce trauma as much as possible. Excision of hamartoma was successfully performed and an 11x9x3.5-cm tumor was completely excised. The present study also reviews the literature on breast hamartoma. © 2015, Spandidos Publications. All rights reserved. Source

Hu Y.-F.,Yanan University Affiliated Hospital | Lei X.,Yanan University Affiliated Hospital | Zhang H.-Y.,Yanan University Affiliated Hospital | Ma J.-W.,Yanan University Affiliated Hospital | And 5 more authors.
OncoTargets and Therapy | Year: 2015

Purpose: We aimed to investigate the expression of EGFR and the autophagy-related markers Beclin1 and LC3 in cervical cancer. Methods: Beclin1, LC3, and EGFR expression were analyzed in 80 samples of cervical squamous cell carcinoma (SCC), 40 samples of high-grade cervical intraepithelial neoplasia (CIN), and 40 samples of normal cervical tissues by immunohistochemistry. The protein expression rates were analyzed with χ2 and Fisher’s exact tests. Differences in overall survival (OS) were determined using the Kaplan–Meier method and log-rank tests. Results: Cervical cancer, high-grade CIN, and normal cervical epithelial cells expressed Beclin1 in 26.2%, 77.5%, and 82.5% of patients, respectively, and expressed LC3 in 28.8%, 70.0%, and 75.0% of patients, respectively. There was a significant difference between cervical SCC and high-grade CIN or normal cervical epithelial cells (P=0.000). Cervical cancer cells, high-grade CIN cells, and normal cervical epithelial cells expressed EGFR in 68.8%, 62.5%, and 12.5% of patients, respectively. There was a significant difference between cervical SCC or high-grade CIN and normal cervical epithelial cells (P=0.000). No significant association between Beclin1 or LC3 or EGFR expression and various clinicopathological parameters was observed in cervical SCC. There was no significant correlation between Beclin1, LC3, EGFR expression, and 5-year OS rates of cervical SCC patients. Beclin1- or LC3-negativity with EGFR-positivity in cervical SCC was associated with a higher Federation International of Gynecology and Obstetrics (FIGO) stage (P=0.011 and P=0.013, respectively) and pelvic lymph node metastasis (P=0.036 and P=0.092, respectively). The 5-year OS rates did not significantly differ between Beclin1- or LC3-positive and -negative patients with positive EGFR. Conclusion: Autophagy was downregulated and EGFR was upregulated in cervical SCC. Autophagy downregulation combined with EGFR upregulation promotes the progression of cervical SCC. © 2015 Hu et al. Source

Zhu M.,Ningxia Medical University | Zhang N.,Ningxia Medical University | He S.,First Affiliated Hospital Of Xian Jiaotong University | Yan R.,The Eighth Hospital of Xian | Zhang J.,First Affiliated Hospital Of Xian Jiaotong University
Clinical and Experimental Metastasis | Year: 2016

Mounting evidences has shown that miRNAs are involved in the development and progression of gastric cancer acts as tumor suppressor genes or oncogenes. In our previous studies, we have found that the up-regulation of miR-106a occurs frequently in human gastric cancer tissues compared with that of normal tissues. Here, we investigate the role of the ectopic expressed miR-106a in the progression and metastasis of gastric cancer in vitro and in vivo. FFPE samples have the priority to be included and qRT-PCR was used to detect the miR-106a expression. Human gastric cancer cells and immortalized gastric epithelial cell were selected and the miR-106a mimic and inhibitor were transfected. Cell growth was determined by MTT method. The flow cytometric analysis for cell apoptosis and transwell assays for evaluating the cell migration and invasion were conducted. Luciferase assay and western blot confirmed the direct binding site of miR-106a and its target. BALB/c nude mice were randomly divided to explore the implantation of gastric cancer cells transfected with miR-106a antagomir. Abnormal over-expression of miR-106a significantly promoted gastric cancer cell proliferation, metastasis, inhibited the cell apoptosis. Functional experiment ascertained that miR-106a interacted with FAS and mediated caspase3 pathway. Knockdown of miR-106a leaded to the attenuation of gastric cancer implantation capacity in vivo. Moreover, expression of TIMP2 was inversely associated with miR-106a in nodule tissues. Apoptotic body was also seen under electron microscope accompanied by silencing of miR-106a. Together, this data indicated that miR-106a may act as an oncogene and contribute to gastric cancer development. © 2016 Springer Science+Business Media Dordrecht Source

Zhang J.-Y.,First Affiliated Hospital Of Xian Jiaotong University | Deng Y.-N.,First Affiliated Hospital Of Xian Jiaotong University | Zhang M.,First Affiliated Hospital Of Xian Jiaotong University | Su H.,University of California at San Francisco | Qu Q.-M.,First Affiliated Hospital Of Xian Jiaotong University
Neurochemical Research | Year: 2016

SIRT3 is a member of Sirtuins family, which belongs to NAD+ dependent class III histone deacetylases. Emerging evidence suggests that SIRT3 plays a pivotal role in regulating mitochondrial function. Mitochondrial dysfunction is a main pathogenesis of Parkinson’s disease (PD). Here, we have investigated the protective effect of SIRT3 for PD cell model. The rotenone-induced human neuroblastoma SH-SY5Y cells damage was used as PD cell model. The lentiviral vectors were used to over-expression or knockdown SIRT3 expression. The cell viability was analyzed using MTT method. The apoptosis, reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were measured by flow cytometer. Superoxide dismutase (SOD) and glutathione (GSH) were detected by using automated microplate reader. The accumulation of α-synuclein was determined by immunofluorescence staining. SIRT3 knockdown significantly worsen rotenone-induced decline of cell viability (p < 0.01) and enhanced cell apoptosis (p < 0.01), exacerbated the decrease of SOD (p < 0.05) and GSH (p < 0.05), and augmented the accumulation of α-synuclein (p < 0.05). While SIRT3 overexpression dramatically increased cell viability (p < 0.01), and decreased cell apoptosis (p < 0.01), prevented the accumulation of α-synuclein (p < 0.05), suppressed the reducing of SOD (p < 0.05) and GSH (p < 0.01), decreased ROS generation (p < 0.05), and alleviated MMP collapse (p < 0.01) induced by rotenone. SIRT3 has neuroprotective effect in PD cell model and could be developed into a therapeutic agent for PD patients. © 2016 Springer Science+Business Media New York Source

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