The First Hospital of Yulin City

Yulin, China

The First Hospital of Yulin City

Yulin, China

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Wang R.,Xi'an Jiaotong University | Wang R.,The First Hospital of Yulin City | Zhang J.,Xi'an Jiaotong University | Qin Q.,Xi'an Jiaotong University | And 6 more authors.
Journal of Xi'an Jiaotong University (Medical Sciences) | Year: 2012

Objective: To detect the expression of Foxp3 in both peripheral blood mononuclears (PBMCs) and thyroid tissues of patients with autoimmune thyroid disease (AITD), including Graves' disease (GD) and Hashimoto's thyroiditis (HT) so as to evaluate the relationship between regulatory T cells (Treg) and pathogenesis of AITD. Methods: Foxp3 mRNA level was measured by real-time PCR from PBMCs and thyroid tissues of AITD patients and normal controls; Foxp3 protein expression was detected both by a standard immunohistochemical procedure from thyroid tissues and by western blot from PBMCs. Results: Foxp3 mRNA level in PBMCs from AITD patients significantly decreased compared with that in normal controls (P<0.05); Foxp3 protein expression was lower only in HT patients from PBMCs, but not in GD patients (P>0.05). Foxp3 mRNA and protein levels were higher in thyroid tissues of HT patients than in normal tissues (P<0.05), but did not differ significantly in thyroid tissues from GD patients (P>0.05). Conclusion: The lower expression of Foxp3 in AITD patients suggests that the decreased number of CD4 +CD25 +Foxp3 +Tregs or dysfunction of these cells may be involved in the development of AITD, especially in HT.


Jiang Z.,the First Hospital of Yulin City | Hao Y.,the First Hospital of Yulin City | Ding X.,the First Hospital of Yulin City | Zhang Z.,the First Hospital of Yulin City | And 3 more authors.
Tumor Biology | Year: 2016

A novel paradigm in tumor biology suggests that non-small cell lung cancer (NSCLC) growth is driven by lung cancer stem cell-like cells (LCSCs), but molecular mechanisms regulating tumorigenic and self-renewal potential of LCSCs are still unclear. Here, we aim to investigate biological function of SLC34A2 in regulating tumorigenicity of LCSCs and its underlying mechanisms. Our findings testified that CD166+ cells which were derived from fresh primary NSCLC samples displayed stem cell-like features. Fluorescence-activated cell sorting (FACS) analysis showed the presence of a variable fraction of CD166 cells in 15 out of 15 NSCLC samples. Significantly, CD166+ LCSCs from primary NSCLC tumors expressed high level of SLC34A2 which was required for CD166+ LCSCs tumorigenic and self-renewal potential. In NSCLC patient cohort, increased SLC34A2 expression correlated with histology, which suggests a potential role of SLC34A2 in CD166+ LCSCs. Furthermore, Wnt/β-catenin pathway and Bmi1 were found necessary for tumorigenicity and self-renewal capacity of CD166+ LCSCs by a series in vitro and in vivo experiments. Then, our study indicated that SLC34A2 regulated Bmi1 to promote tumorigenic and self-renewal potential of CD166+ LCSCs through Wnt/β-catenin pathway. In this study, the characterization of molecular basis of SLC34A2 in CD166+ LCSCs not only allows for better understanding of the mechanisms regulating tumorigenicity of this specific population of NSCLC cells but also provides insight into the gradual improvement of more effective cancer therapies against this disease. © 2016 International Society of Oncology and BioMarkers (ISOBM)


He S.,Ningxia Medical University | Guo X.,Health Elements | Tan W.,Health Elements | Su X.,Health Elements | And 3 more authors.
Biological Trace Element Research | Year: 2015

Selenium is an important trace element for human health. Previous studies have raised concern that dietary selenium intake may change energy metabolism. AMP-activated protein kinase (AMPK) is a sensor of energy status that controls cellular energy homeostasis. We aimed to determine the effect of selenium on the phosphorylation of AMPK pathway between Se-deficient and normal Sprague–Dawley rats. Twenty-four weaning rats were fed either a Se-deficient diet (0.02 mg Se/kg) or a standard diet (0.18 mg Se/kg). After 109 days, total serum levels of non-esterified fatty acid and total amino acids were significantly higher and the serum insulin concentration was significantly lower in Se-deficient rats than in healthy controls. Selenium concentration and the activity of glutathione peroxidase (GPx) in myocardial tissue were significantly lower in Se-deficient rats. Importantly, mRNA levels of acetyl-CoA carboxylase beta (ACACB), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and protein levels of p-AMPKα were increased in the Se-deficient group compared to normal controls (p < 0.05). In conclusion, our results suggest that selenium deficiency induces changes in metabolic and molecular parameters involved in energy metabolism in the AMPK pathway. © 2015 Springer Science+Business Media New York


PubMed | the First Hospital of Yulin City
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

A novel paradigm in tumor biology suggests that non-small cell lung cancer (NSCLC) growth is driven by lung cancer stem cell-like cells (LCSCs), but molecular mechanisms regulating tumorigenic and self-renewal potential of LCSCs are still unclear. Here, we aim to investigate biological function of SLC34A2 in regulating tumorigenicity of LCSCs and its underlying mechanisms. Our findings testified that CD166(+) cells which were derived from fresh primary NSCLC samples displayed stem cell-like features. Fluorescence-activated cell sorting (FACS) analysis showed the presence of a variable fraction of CD166 cells in 15 out of 15 NSCLC samples. Significantly, CD166(+) LCSCs from primary NSCLC tumors expressed high level of SLC34A2 which was required for CD166(+) LCSCs tumorigenic and self-renewal potential. In NSCLC patient cohort, increased SLC34A2 expression correlated with histology, which suggests a potential role of SLC34A2 in CD166(+) LCSCs. Furthermore, Wnt/-catenin pathway and Bmi1 were found necessary for tumorigenicity and self-renewal capacity of CD166(+) LCSCs by a series in vitro and in vivo experiments. Then, our study indicated that SLC34A2 regulated Bmi1 to promote tumorigenic and self-renewal potential of CD166(+) LCSCs through Wnt/-catenin pathway. In this study, the characterization of molecular basis of SLC34A2 in CD166(+) LCSCs not only allows for better understanding of the mechanisms regulating tumorigenicity of this specific population of NSCLC cells but also provides insight into the gradual improvement of more effective cancer therapies against this disease.


PubMed | the First Hospital of Yulin City, Xi'an Jiaotong University and Xian No1 Hospital
Type: Journal Article | Journal: International journal of ophthalmology | Year: 2015

To compare posterior capsule opacification (PCO) degree and visual functions after phacoemulsification in eyes implanted with 360-degree square edge hydrophilic acrylic intraocular lens (IOL) (570C C-flex, Rayner) and sharp edge hydrophobic acrylic IOL (Sensar AR40e, AMO) in diabetic patients.Sixty diabetic patients underwent uneventful phacoemulsification and randomly implanted one of the two IOLs. The PCO value was measured by retroillumination photographs and Evaluation of Posterior Capsule Opacification (EPCO) 2000 image-analysis software at 1, 6, 12, and 24mo after surgery. Visual acuity, and contrast sensitivity in photopic and mesopic conditions were also examined at each follow up time point. The incidence of eye that required Nd:YAG laser posterior capsulotomy were also compared.There was not any statistically significant difference in PCO scores between Rayner C-flex 570C group and Sensar AR40e group at each follow up time point. Visual acuity, Nd:YAG capsulotomy incidence and contrast sensitivity also had no significant difference during the 24mo follow-up.For diabetic patients, Rayner 570C C-flex and Sensar AR40e IOLs are same effective for prevent PCO. The 360-degree square edge design maybe is a good alternative technique to improve PCO prevention.


PubMed | Ningxia Medical University, the First Hospital of Yulin City and Xi'an Jiaotong University
Type: Journal Article | Journal: Biological trace element research | Year: 2016

Selenium is an important trace element for human health. Previous studies have raised concern that dietary selenium intake may change energy metabolism. AMP-activated protein kinase (AMPK) is a sensor of energy status that controls cellular energy homeostasis. We aimed to determine the effect of selenium on the phosphorylation of AMPK pathway between Se-deficient and normal Sprague-Dawley rats. Twenty-four weaning rats were fed either a Se-deficient diet (0.02mgSe/kg) or a standard diet (0.18mgSe/kg). After 109days, total serum levels of non-esterified fatty acid and total amino acids were significantly higher and the serum insulin concentration was significantly lower in Se-deficient rats than in healthy controls. Selenium concentration and the activity of glutathione peroxidase (GPx) in myocardial tissue were significantly lower in Se-deficient rats. Importantly, mRNA levels of acetyl-CoA carboxylase beta (ACACB), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1), and protein levels of p-AMPK were increased in the Se-deficient group compared to normal controls (p<0.05). In conclusion, our results suggest that selenium deficiency induces changes in metabolic and molecular parameters involved in energy metabolism in the AMPK pathway.

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