The Third Peoples Hospital Of Yunnan Province

Kunming, China

The Third Peoples Hospital Of Yunnan Province

Kunming, China

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PubMed | The Peoples Hospital of Wenshan Prefecture, Sun Yat Sen University, Kunming Medical University and the Third Peoples Hospital of Yunnan Province
Type: Journal Article | Journal: Journal of the renin-angiotensin-aldosterone system : JRAAS | Year: 2015

The renin-angiotensin-aldosterone system is important to the development of atrial fibrillation (AF). A lot of research has focused on the relationship between angiotensin-converting enzyme (ACE) insertion (I) /deletion (D) gene polymorphisms and AF, with inconsistent results. A meta-analysis was carried out to find the correlation between ACE I/D gene polymorphisms and AF.Data were extracted from articles published before September 2013 on ACE I/D polymorphisms and AF in Embase, PubMed, WanFangData, and China National Knowledge Infrastructure.The recessive model found that ACE I/D gene polymorphisms were related to AF (odds ratio (OR) = 1.61, 95% confidence interval (CI) = 1.16-1.72). Subgroup analysis showed a significant association in the recessive model for Asian (OR = 1.40, 95% CI = 1.19-1.80) and Caucasian (OR = 1.42, 95% CI = 1.01-1.99) populations.ACE I/D gene polymorphisms and AF are significantly related to ethnicity. Individuals with the ACE D/D genotype appear to be at higher risk of AF.


Yin Y.,The Third Peoples Hospital of Yunnan Province | Fan N.,The Third Peoples Hospital of Yunnan Province | Liu X.,The Third Peoples Hospital of Yunnan Province
Zhonghua Shiyan Yanke Zazhi/Chinese Journal of Experimental Ophthalmology | Year: 2015

Exfoliation syndrome (XFS), one of the most common causes of glaucoma, represents an age related, complex, multifactorial and late-onset disease worldwide. The etiopathogenesis involves both genetic and environmental factor. However, the exact etiopathogenesis of XFS is still unclear. The purpose of this review was to discuss the recent research progress of the molecular genetics of XFS. Some candidate genes linked to XFS include lysyl oxidase-like 1 (LOXL1) gene, clusterin (CLU) gene, contactin associated protein-like 2 (CNTNAP2) gene, apolipoprotein E (ApoE) gene, matrix metallo proteinases (MMPs) gene, glutathione S-transferase (GST) gene, transforming growth factor-β1, (TGF-β1) gene, tumor necrosis factor-α (TNF-α) gene and so on. These genes may be modifying genes for the development of XFS. Copyright © 2015 by the Chinese Medical Association.


Hu T.,Kunming Medical University | Hu T.,The Third Peoples Hospital of Yunnan Province | Zhang C.,Kunming Medical University | Zhang C.,Yunnan Provincial Maternal and Child Health Hospital | And 8 more authors.
BMC Cancer | Year: 2013

Background: Glucose-6-phosphate dehydrogenase (G6PD), elevated in tumor cells, catalyzes the first reaction in the pentose-phosphate pathway. The regulation mechanism of G6PD and pathological change in human melanoma growth remains unknown.Methods: HEM (human epidermal melanocyte) cells and human melanoma cells with the wild-type G6PD gene (A375-WT), G6PD deficiency (A375-G6PD{increment}), G6PD cDNA overexpression (A375-G6PD{increment}-G6PD-WT), and mutant G6PD cDNA (A375-G6PD{increment}-G6PD-G487A) were subcutaneously injected into 5 groups of nude mice. Expressions of G6PD, STAT3, STAT5, cell cycle-related proteins, and apoptotic proteins as well as mechanistic exploration of STAT3/STAT5 were determined by quantitative real-time PCR (qRT-PCR), immunohistochemistry and western blot.Results: Delayed formation and slowed growth were apparent in A375-G6PD{increment} cells, compared to A375-WT cells. Significantly decreased G6PD expression and activity were observed in tumor tissues induced by A375-G6PD{increment}, along with down-regulated cell cycle proteins cyclin D1, cyclin E, p53, and S100A4. Apoptosis-inhibited factors Bcl-2 and Bcl-xl were up-regulated; however, apoptosis factor Fas was down-regulated, compared to A375-WT cells. Moderate protein expressions were observed in A375-G6PD{increment}-G6PD-WT and A375-G6PD{increment}-G6PD-G487A cells.Conclusions: G6PD may regulate apoptosis and expression of cell cycle-related proteins through phosphorylation of transcription factors STAT3 and STAT5, thus mediating formation and growth of human melanoma cells. Further study will, however, be required to determine potential clinical applications. © 2013 Hu et al.; licensee BioMed Central Ltd.


He Y.,Harbin Medical University | Han L.,Harbin Medical University | Li W.,The Third Peoples Hospital of Yunnan Province | Shu X.,University of Houston | And 4 more authors.
Gene | Year: 2012

The calcium-sensing receptor (CaSR) is involved in maintaining calcium homeostasis via the regulation of parathyroid hormone (PTH) secretion. The associations between serum calcium concentrations, parathyroid hormone (PTH) level and CaSR polymorphism A986S have been studied, but results are inconsistent. Therefore, we performed a meta-analysis to clarify the role of this polymorphism on this topic. Weighted mean difference (WMD) and 95% confidence interval (CI) were calculated with random-effects model or fixed-effects model based on the heterogeneity analysis. Overall 2820, 1135 and 3149 healthy individuals were included for total calcium concentration, ionized calcium concentration and PTH level meta-analyses, respectively. Most of the individuals in this meta-analysis were healthy women. Healthy individuals with the AS. +. SS genotype had significantly higher total and ionized calcium concentrations than those with the AA genotype. However, there was no statistical significance concerning serum PTH level. The pooled WMD for total calcium concentration was 0.028 (95% CI: 0.012-0.045, P = 0.001); for ionized calcium concentration was 0.016 (95% CI: 0.013-0.020, P < 0.0001); and for PTH level was - 0.027 (95% CI: -0.360-0.306, P = 0.874). In conclusion, our meta-analysis indicates that the CaSR A986S polymorphism might be associated with total and ionized calcium concentrations in healthy individuals. © 2011 Elsevier B.V.


PubMed | Northwestern University, Harvard University and The Third Peoples Hospital of Yunnan Province
Type: Journal Article | Journal: Journal of Alzheimer's disease : JAD | Year: 2016

Microglia are immune cells of the brain that display a range of functions. Most of our knowledge about microglia biology and function is based on cells from the rodent brain. Species variation in the complexity of the brain and differences in microglia response in the primate when compared with the rodent, require use of adult human microglia in studies of microglia biology. While methods exist for isolation of microglia from postmortem human brains, none allow culturing cells to high passage. Thus cells from the same case could not be used in parallel studies and multiple conditions. Here we report a method, which includes use of growth factors such as granulocyte macrophage colony stimulating factor, for successful culturing of adult human microglia from postmortem human brains up to 28 passages without significant loss of proliferation. Such cultures maintained their phenotype, including uptake of the scavenger receptor ligand acetylated low density lipoprotein and response to the amyloid- peptide, and were used to extend in vivo studies in the primate brain demonstrating that inhibition of microglia activation protects neurons from amyloid- toxicity. Significantly, microglia cultured from brains with pathologically confirmed Alzheimers disease displayed the same characteristics as microglia cultured from normal aged brains. The method described here provides the scientific community with a new and reliable tool for mechanistic studies of human microglia function in health from childhood to old age, and in disease, enhancing the relevance of the findings to the human brain and neurodegenerative conditions.


PubMed | Kunming University, The First Peoples Hospital of Yunnan Province, Kunming Medical University, Southwest University and The Third Peoples Hospital of Yunnan Province
Type: Journal Article | Journal: Oncotarget | Year: 2016

Ectopic glucose-6-phosphate dehydrogenase (G6PD) expression may contribute to tumorigenesis in cervical cancer associated with high-risk human papillomavirus (HR-HPV 16 and 18) infections. Here, we demonstrate that microRNA-1 (miR-1) in association with AGO proteins targets G6PD in HR-HPV-infected human cervical cancer cells. miR-1 inhibited expression of a reporter construct containing a putative G6PD 3-UTR seed region and suppressed endogenous G6PD expression. Down-regulation of miR-1 increased G6PD expression in cervical cancer cells. Regression analysis revealed that miR-1 levels correlate negatively with the clinicopathologic features in HR-HPV 16/18-infected cervical cancer patients. miR-1 overexpression inhibited proliferation and promoted apoptosis in cervical cancer cells and reduced xenograft tumor growth in nude mice. Conversely, sponge-mediated miR-1 knockdown markedly increased viability and reduced apoptosis in cervical cancer cells and supported neoplasm growth. Restoration of G6PD expression partially reversed the effects of miR-1 overexpression both in vitro and in vivo. In addition, co-transfection of G6PD siRNA and miR-1 sponge partially reversed miR-1 sponge-induced reductions in cell viability and neoplasm growth. These results suggest that miR-1 suppresses the development and progression of HR-HPV 16/18-infected cervical cancer by targeting G6PD and may be a promising novel therapeutic candidate.


PubMed | The Third Peoples Hospital of Yunnan Province
Type: Journal Article | Journal: Journal of molecular neuroscience : MN | Year: 2015

Recent evidences revealed that the alteration of microRNAs (miRNAs) might be associated with neuroplasticity induced by voluntary running wheel (RW) exercise in mice suffered from traumatic brain injury (TBI). In the present study, we explored the possible role of miR21 involved in the cognitive improvement following voluntary RW in TBI mice. Firstly, in situ hybridization and quantitative real-time PCR (qRT-PCR) were employed to determine the hippocampal expression and location of miR21 in TBI mice with or without spontaneous RW. Either miR21-mimics/plenti-miR21 or miR21-agomir/miR21-sponge was employed to regulate the miR21 expression in vivo and in vitro. Acquisition of spatial learning and memory retention was assessed by Morris Water Maze (MWM) test. Golgi stain was also performed to evaluate the alteration of hippocampal dendrite. Our finding confirmed that the elevated miR21 level in hippocampal post-TBI was significantly reduced by spontaneous RW. Overexpression of miR21 in TBI mice with spontaneous RW induced deteriorations in spatial learning and memory retention by significant decreases in the somata size and branch points of the hippocampus neurons. In vitro transduction with miR21 also reduced the neurite extension and the area of cultured hippocampal neuron. However, miR21 down-regulation reversed these effects. The present data strongly suggest that miR21 is an important molecule that has been involved in neuroprotection induced by voluntary RW exercise post-TBI.


PubMed | CAS Kunming Institute of Zoology and The Third Peoples Hospital of Yunnan Province
Type: Journal Article | Journal: Journal of human genetics | Year: 2016

In the past decades, the Tai people are increasingly being focused by genetic studies. However, a systematic genetic study of the whole Tai people is still lacking, thus making the population structure as well as the demographic history of this group uninvestigated from genetic perspective. Here we extensively analyzed the variants of hypervariable segments I and II (HVS-I and HVS-II) of mitochondrial DNA (mtDNA) of 719 Tai samples from 19 populations, covering virtually all of the current Tai peoples residences. We observed a general close genetic affinity of the Tai people, reflecting a common origin of this group. Taken into account the phylogeographic analyses of their shared components, including haplogroups F1a, M7b and B5a, our study supported a southern Yunnan origin of the Tai people, consistent with the historical records. In line with their diverse cultures and languages, substantial genetic divergences can be observed among different Tai populations that could be attributable to assimilation of maternal components from neighboring populations. Our study further implied the advent of rice agriculture in Mainland Southeast Asia at 5 kya (kilo years ago) had greatly promoted the population expansion of the Tai people.


PubMed | The Third Peoples Hospital of Yunnan Province, Kunming Medical University and Kunming Childrens Hospital
Type: | Journal: Oncology reports | Year: 2017

Pediatric head and neck cancers account for overall 12% of all pediatric cancers. Despite recent advances in therapeutic modalities, children with tumor metastasis have poor prognosis. Therefore, there is an unmet need for new and effective treatment modalities for pediatric head and neck cancers. The present study describes a simple and efficient method for fabrication of cationic lipidpolymer hybrid nanoparticles(CLPNs) for codelivery of cisplatin(CDDP) and DNA(CDDP/DNA CLPNs) for the therapy of childhood head and neck cancers. CDDP/DNA CLPNs were prepared by the modified double emulsion solvent evaporation method with selfassembly. CDDPloaded CLPNs(CDDP CLPNs), CDDP-loaded polymeric nanoparticles(PNPs)(CDDP PNPs), and DNAloaded Lipofectamine2000(DNA LIPO) were also prepared for comparison. The results illustrated that the concentration of the cationic lipid has influence on the characteristics of CLPNs. Invitro anticancer effect, invitro transfection efficiency, invivo antitumor and gene delivery efficacy of CDDP/DNA CLPNs have advantages over other formulations tested. In conclusion, outstanding delivery ability of CLPNs for both CDDP and DNA could combine the therapeutic efficiency of both drug and gene for the treatment of pediatric rhabdomyosarcoma(RMS).


PubMed | Cancer Hospital of Yunnan Province, Kunming Medical University and The Third Peoples Hospital of Yunnan Province
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

The present study aimed to explore the association between single nucleotide polymorphisms (SNPs) in the hepatocyte nuclear factor4 (HNF4) gene and the incidence of type 2 diabetes in the Chinese Bai population in Dali city, China. The polymerase chain reactionrestriction fragment length polymorphism method was used to analyze four SNPs (rs4810424, rs1884613, rs1884614 and rs2144908) in the HNF4 gene in 44 patients with type 2 diabetes and 87 healthy controls in Chinese Bai individuals. The haploid type was subsequently built to assess its association with the incidence of type 2 diabetes in the Bai population in Dali city. No significant differences were observed between the genotype and allele frequencies of the four SNPs in the HNF4 gene and type 2 diabetes mellitus (P>0.05). However, the frequency of haplotype, CCTA, built by rs4810424, rs1884613, rs1884614 and rs2144908 was significantly higher in the type 2 diabetes mellitus group compared with the control group (2=8.34, P=0.004). The four polymorphisms, rs4810424, rs1884613, rs1884614 and rs2144908, in the HNF4 gene were not the susceptible loci for type 2 diabetes in the Bai population of Dali city, however, the haplotype, CCTA, built from the four SNPs may increase the risk of type 2 diabetes in this population.

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