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PubMed | Minzu Hospital of Guangxi Zhuang Autonomous Region, XING, Imperial College London, Peoples Hospital of Guangxi Autonomous Region and 2 more.
Type: Journal Article | Journal: Gene | Year: 2016

To assess the clinical relevance of IL8 gene polymorphisms in patients with sepsis and its association with systemic IL-8 levels.PCR and DNA sequencing were used to examine the polymorphism of IL8 in 152 patients with sepsis and in 199 healthy volunteers in China. The distribution frequencies of the genotype and allele were compared among different groups. The serum IL-8 was measured by ELISA and analyzed in relation to polymorphisms of IL8.The homozygote TT genotype and T allele of rs4073 (genotype: p=0.01, allele: p=0.002), the homozygote CC genotype and C allele (genotype: p=0.03, allele: p=0.003) of rs2227306, homozygote AA genotype and A allele of re1126647 (genotype: p=0.01, allele: p=0.002) were associated with susceptibility to sepsis in males. Serum IL-8 levels were significantly increased in patients with sepsis but showed no correlation with IL8 rs4073, rs2227306 and rs1126647 polymorphisms.The male population carrying the homozygote TT genotype and T allele of rs4073, the homozygote CC genotype and C allele of rs2227306 and homozygote AA genotype and A allele of rs1126647 are more susceptible to sepsis, suggesting there is a protective effect in females carrying these genotypes and alleles respectively. There was no association between rs4073, rs2227306 and rs1126647 polymorphisms and serum levels of IL-8 in patients with sepsis.


PubMed | Peoples Hospital of Guangxi Autonomous Region, Minzu Hospital of Guangxi Zhuang Autonomous Region, Youjiang Medical University for Nationalities and Imperial College London
Type: | Journal: BMC medical genetics | Year: 2015

Sepsis is now the leading cause of death in the non-cardiovascular intensive care unit (ICU). Recent research suggests that sepsis is likely to be due to an interaction between genetic and environmental factors. Genetic mutations of toll-like receptor 4 (TLR4) and cluster of differentiation 14 (CD14) genes are involved in the immune and (or) inflammatory response. These may contribute to the susceptibility to sepsis in patients. This study was designed to evaluate whether the TLR4 and cluster CD14 gene polymorphisms are associated with susceptibility to sepsis.The single nucleotide polymorphisms (SNPs) of TLR4 (rs10759932, rs11536889, rs7873784, rs12377632, rs1927907, rs1153879) and CD14 (rs2569190 and rs2563298) in patients with sepsis and control subjects in the Guangxi Province were analyzed by using the polymerase chain reaction-single base extension (PCR-SBE) and DNA sequencing methods.The rs11536889 polymorphism in TLR4 and rs2563298 polymorphism in CD14 were significantly associated with the risk of sepsis when compared to the control group. The frequencies of rs11536889 and rs2563298 polymorphisms in the group with sepsis were higher than that in the control group (OR = 1.430, 95% CI, 1.032-1.981, P<0.05; OR = 2.454, 95% CI, 1.458-4.130, P<0.05, respectively). Followed up haplotype analysis suggested that there were two haplotypes in which increased risk factors for sepsis were indicated.The rs11536889 polymorphism in TLR4 and rs2563298 polymorphism in CD14, and two haplotypes were associated with increased susceptibility to sepsis.


PubMed | Guangxi Medical University, Wuhan Asia Heart Hospital and Minzu Hospital of Guangxi Zhuang Autonomous Region
Type: Journal Article | Journal: Journal of cardiovascular pharmacology and therapeutics | Year: 2016

Cardiomyocyte apoptosis by coronary microembolization (CME) contributes to myocardial dysfunction, in which mitochondrial pathway and death receptor pathway are activated. Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) is a membrane protein involved in apoptosis. The study aimed to explore the role of LOX-1 in the activation of these 2 major apoptotic pathways.Twenty Bama miniature swine were randomized into 4 groups (n = 5 per group). The groups were Sham, CME, LOX-1 small-interfering RNA (siRNA), and control siRNA. Microspheres were injected into the left anterior descending artery of swine to establish CME model. Twelve hours after operation, cardiac function, serum c-troponin I level, microinfarct, and apoptotic index were examined. The levels of LOX-1, Bcl-2, Bax, cytochrome c as well as cleaved caspase 9, -8, and -3 were detected.Myocardial dysfunction, enhanced serum c-troponin I, microinfarct, and apoptosis were induced following CME. Moreover, CME induced increased expression of LOX-1, Bax, cytochrome c, cleaved caspase 9, -8, and -3 as well as decreased Bcl-2 expression levels. The LOX-1 siRNA reversed these effects by CME except cleaved caspase 8 expression, while the control siRNA had no effect.Coronary microembolization induces cardiomyocyte apoptosis via the LOX-1-dependent mitochondrial pathway and caspase 8-dependent pathway.


PubMed | Guangxi Medical University, Wuhan Asia Heart Hospital and Minzu Hospital of Guangxi Zhuang Autonomous Region
Type: Journal Article | Journal: The Canadian journal of cardiology | Year: 2015

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a membrane protein associated with apoptosis. Endoplasmic reticulum (ER) stress-induced apoptosis has been determined in several cardiovascular diseases. Mitogen-activated protein kinase (MAPK) signalling is involved in apoptosis. The aim of this study was to investigate whether LOX-1, ER stress, and MAPKs play a role in cardiomyocyte apoptosis after coronary microembolization (CME) and the exact mechanisms involved.Thirty swine were randomized into the following groups (n= 5 per group): sham, CME, CME+ LOX-1 small-interfering RNA (siRNA), CME+ control siRNA, CME+ JNK inhibitor, and CME+ p38 inhibitor. The CME model was established by injecting microspheres into the left anterior descending (LAD) artery, whereas swine in the sham group received normal saline instead. Twelve hours after the sham operation or CME, cardiac function, serum c-troponin I level, microinfarcts, and apoptotic index were determined. Relative expression levels of LOX-1, ER stress markers (glucose-regulated protein 78 [GRP 78], C/EBP homologous protein [CHOP], and cleaved caspase-12), cleaved caspase-3, c-Jun NH2-terminal protein kinases (JNK), p38, and extracellular signal-related protein kinases (ERK1/2) were measured.CME induced cardiac dysfunction, microinfarction, increased serum c-troponin I levels, and cardiomyocyte apoptosis. Additionally, the expression of LOX-1, ER stress markers, and cleaved caspase-3, and the phosphorylation of JNK, p38, and ERK1/2 were all enhanced. LOX-1 siRNA inhibited these effects except the phosphorylation of ERK1/2. Pretreatment with a JNK inhibitor or a p38 inhibitor attenuated the expression of ER stress markers and apoptosis.Our results indicated that CME induced cardiomyocyte apoptosis through the LOX-1-dependent ER stress pathway, in which the phosphorylation of JNK and p38 were involved. This might provide a new approach for the prevention and treatment of CME.


Su G.,Minzu Hospital of Guangxi Zhuang Autonomous Region | Tang Z.,Guangxi Chest Hospital | Mo Q.,Minzu Hospital of Guangxi Zhuang Autonomous Region | Wen W.,Minzu Hospital of Guangxi Zhuang Autonomous Region
Chinese-German Journal of Clinical Oncology | Year: 2013

Objective: The aim of our study was to investigate the expression of p53, p57(Kip2) and CD68 in esophageal squamous cell carcinoma (ESCC) and their correlation with the biological behavior of ESCC. Methods: The protein expressions of p53, p57(Kip2) and CD68 were detected in 51 cases of ESCC with S-P immunohistochemical method. Results: The total positive rate of those proteins was p53 64.71%, CD68 58.82% and p57(Kip2) 45.09% respectively in ESCC. The positive expression rate of p57(Kip2) was significantly lower in the positive p53 of ESCC than in the negative p53 (P < 0.05). The positive expression rate of p57(Kip2) was significantly lower in the positive CD68 of esophageal squamous cell carcinoma than in the negative (P < 0.05). The positive expression of p53 and CD68 were related to differentiate and TNM of ESCC, but p57(Kip2) was not related to TNM (P > 0.05). Conclusion: There are significant negative correlations between p57(Kip2) and p53, CD68 protein expression and related to biological behavior. Multy predictors are better guide to patients than single predictor. © 2013 Springer-Verlag Berlin Heidelberg.


Li F.,Southern Medical University | Zhou Y.,Minerva Foundation Institute for Medical Research | Hu R.-T.,Minzu Hospital of Guangxi Zhuang Autonomous Region | Hou L.-N.,Southern Medical University | And 5 more authors.
Nutrition and Cancer | Year: 2013

The findings of epidemiologic studies on the association between egg consumption and bladder cancer risk remain conflicting. We conducted a meta-analysis to clarify the potential association between egg consumption and bladder cancer risk. Four cohort studies and 9 case-control studies in the PubMed database through February 2012 were identified on egg consumption and risk of bladder cancer involving 2715 cases and 184,727 participants. Random-effects models were used to calculate the summary relative risk estimates (SRRE) based on the highest compared with the lowest category of egg consumption. In addition, we performed stratified analyses and sensitivity and dose-response analyses to examine the association. Overall, no significant association was observed between egg consumption and bladder cancer (SRRE = 1.11 95% CI: 0.90-1.35). However, increased risk of bladder cancer was detected in North/South America (SRRE = 1.40 95% CI: 1.05-1.86) and, moreover, fried egg intake positively associated with bladder cancer as well (SRRE = 2.04, 95% CI: 1.41-2.95). In conclusion, our findings suggest no significant association between egg consumption and bladder cancer risk, except for a possible positive relationship with the intake of fried eggs based on the limited number of studies. Additional studies, especially large prospective cohort studies, are warranted to confirm these findings. © 2013 Copyright Taylor and Francis Group, LLC.


Peng F.,Wuhan University | Wu H.,Huazhong University of Science and Technology | Zheng Y.,Minzu Hospital of Guangxi Zhuang Autonomous Region | Xu X.,Huazhong University of Science and Technology | Yu J.,Huazhong University of Science and Technology
Lasers in Medical Science | Year: 2012

Mesenchymal stem cells (MSCs) are promising for use in regenerative medicine. Low-level light irradiation (LLLI) has been shown to modulate various processes in different biological systems. The aim of our study was to investigate the effect of red light emitted from a lightemitting diode (LED) on bone marrow MSCs with or without osteogenic supplements. MSCs both with and without osteogenic supplements were divided into four groups, and each group was irradiated at doses of 0, 1, 2 and 4 J/cm 2. Cellular proliferation was evaluated using WST-8 and 5-ethynyl-2'-deoxyuridine (EdU) fluorescence staining. The alkaline phosphatase activity, mineralization, and expression of osteoblast master genes (Collαl, Alpl, Bglap and Runx2) were monitored as indicators of MSC differentiation towards osteoblasts. In groups without osteogenic supplements, red light at all doses significantly stimulated cellular proliferation, whereas the osteogenic phenotype of the MSCs was not enhanced. In groups with osteogenic supplements, red light increased alkaline phosphatase activity and mineralized nodule formation, and stimulated the expression of Bglap and Runx2, but decreased cellular proliferation. In conclusion, nonconherent red light can promote proliferation but cannot induce osteogenic differentiation of MSCs in normal media, while it enhances osteogenic differentiation and decreases proliferation of MSCs in media with osteogenic supplements. © Springer-Verlag London Ltd 2011.


Chen Y.,Minzu Hospital of Guangxi Zhuang Autonomous Region | Li H.,Southern Medical University | Wu D.,Minzu Hospital of Guangxi Zhuang Autonomous Region | Bi K.,Minzu Hospital of Guangxi Zhuang Autonomous Region | Liu C.,Southern Medical University
World Journal of Urology | Year: 2014

Purpose: Construction of three-dimensional (3D) model of renal tumor facilitated surgical planning and imaging guidance of manual image fusion in laparoscopic partial nephrectomy (LPN) for intrarenal tumors.Materials and methods: Fifteen patients with intrarenal tumors underwent LPN between January and December 2012. Computed tomography-based reconstruction of the 3D models of renal tumors was performed using Mimics 12.1 software. Surgical planning was performed through morphometry and multi-angle visual views of the tumor model. Two-step manual image fusion superimposed 3D model images onto 2D laparoscopic images. The image fusion was verified by intraoperative ultrasound. Imaging-guided laparoscopic hilar clamping and tumor excision was performed. Manual fusion time, patient demographics, surgical details, and postoperative treatment parameters were analyzed.Results: The reconstructed 3D tumor models accurately represented the patient’s physiological anatomical landmarks. The surgical planning markers were marked successfully. Manual image fusion was flexible and feasible with fusion time of 6 min (5–7 min). All surgeries were completed laparoscopically. The median tumor excision time was 5.4 min (3.5–10 min), whereas the median warm ischemia time was 25.5 min (16–32 min). Twelve patients (80 %) demonstrated renal cell carcinoma on final pathology, and all surgical margins were negative. No tumor recurrence was detected after a media follow-up of 1 year (3–15 months).Conclusions: The surgical planning and two-step manual image fusion based on 3D model of renal tumor facilitated visible-imaging-guided tumor resection with negative margin in LPN for intrarenal tumor. It is promising and moves us one step closer to imaging-guided surgery. © 2013, Springer-Verlag Berlin Heidelberg.


Zou W.,Minzu Hospital of Guangxi Zhuang Autonomous Region
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2013

In patients with diabetes, glucose fluctuations, insulin resistance, poor circulation, and likely immune damage can easily lead to infections. Splenic abscess is rare in diabetic patients and is associated with a high mortality rate. Type 2 diabetes causes increased risks of splenic abscess, and timely and effective treatment can lower the mortality rate. We report here a case of type 2 diabetes complicated by multiple splenic abscesses.


Xiang Y.H.,Minzu Hospital of Guangxi Zhuang Autonomous Region
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases | Year: 2012

To Investigate the influences of chronic intermittent hypoxia (CIH) and continuous hypoxia (CH) on renin angiotensin system (RAS) in serum and tissues of rats, and therefore to investigate the mechanism of CIH-induced hypertension and hypoxia induced pulmonary hypertension. Eighteen male Sprague-Dawley (SD) rats were divided into 3 groups: CIH group, CH group and control group (UC). CIH rats were subjected to alternating cycles of hypoxia (6% ∼ 8% O(2) in N(2) for 20 ∼ 25 s) and normoxia (21% O(2) in N(2) for 2 min) every 180 s for 7 h/d. CH rats were consistently given nitrogen (oxygen concentration 8% - 12% in the cabin, 7 h/d), while the UC rats were not treated. Systolic blood pressure (SBP) in the CIH rats at the end of 6th week was significantly elevated compared with baseline SBP (P < 0.001), and that in the CH and the UC rats (P < 0.05). At the end of 6th week, the expression of ACE and ACE2 in the renal arteriole was significantly different (P < 0.05), and the levels of AngII in serum and kidney tissues were increased. Ang-(1-7) was decreased in the CIH rats compared with the CH and the UC rats (P < 0.05). The levels of AngII in pulmonary tissues were increased, while the levels of Ang-(1-7) were decreased in the CH rats compared with the CIH and the UC rats (P < 0.05). SBP showed a positive correlation with AngII in serum and kidney tissues, and a negative correlation with Ang-(1-7) in serum and kidney tissues. There were significant differences in arterial wall thickness, WT%, and WA% of renal arterioles and pulmonary arterioles among the 3 groups. Wall thickness of pulmonary arterioles and kidney arterioles was positively correlated with AngII in pulmonary and kidney tissues (r = 0.386, 0.414, P < 0.05), and negatively correlated with Ang-(1-7) (r = -0.401, -0.394, P < 0.05). CIH and CH showed different effects on RAS in the serum and the tissues of rats. CIH mainly affected levels of RAS in the serum, kidney tissues and renal arterioles, and was closely related with blood pressure. CH mainly affected the levels of RAS in lung tissues and pulmonary small arteries, which may be related with pulmonary, hypertension and pulmonary arterial remodeling.

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