Guangzhou First Municipal Peoples Hospital
Guangzhou First Municipal Peoples Hospital
Luo L.,Jinan University |
Yin L.,Baoan District Hospital |
Liu Z.,Guangzhou First Municipal Peoples Hospital |
Xiang Z.,Longgang District Hospital
Journal of Trauma and Acute Care Surgery | Year: 2012
BACKGROUND: Posttraumatic pulmonary pseudocyst (PPP) is a complication of blunt chest trauma and poorly documented. A retrospective review of PPPs observed during the past 6 years in our hospitals is presented in this report. METHODS: We retrospectively studied the serial chest computed tomographic scans and clinical data of 33 consecutive patients with PPPs. RESULTS: Fifty-three PPPs from 33 patients were found. Thirty-six PPPs were located in the subpleural pulmonary parenchyma, whereas others were located in the pulmonary parenchyma near other harder structures. Follow-up examinations demonstrated that air-filled cavities and air-fluid cavities could turn into pulmonary hematomas and eventually resolved without specific treatment. The PPPs were resolved in 11 to 82 days. The resolving time of air-fluid cavity (mean, 47.5 days) was significantly longer than the resolving time of air-filled cavity (mean, 16.3 days; p = 0.001). Three patients died of acute respiratory distress syndrome or head trauma. No patient died of PPP. Twelve patients with serious pneumothorax, hemothorax, or both were cured with surgical hemostasis and/or drainage. Eighteen patients resolved without specific treatment. CONCLUSION: Computed tomography increased the frequency of PPP diagnosis and accurately demonstrated the characteristics of the lesions. Air-filled pseudocysts resolved more quickly than those containing fluid. The outcome of PPPs can be favorable without specific treatment. PPP does not require follow-up CT scan or intervention in the absence of complications. LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level V. © 2012 Lippincott Williams & Wilkins.
Zhou K.,Sun Yat Sen University |
Gao Q.,Sun Yat Sen University |
Zheng S.,Sun Yat Sen University |
Pan S.,Sun Yat Sen University |
And 5 more authors.
Molecular Human Reproduction | Year: 2013
Estrogen exerts vascular protective effects, but the underlying mechanisms remain to be understood fully. In recent years, hydrogen sulfide (H2S) has increasingly been recognized as an important signaling molecule in the cardiovascular system. VascularH2S is produced from L-cysteine, catalyzed by cystathionine γ-lyase (CSE). In our study, apolipoprotein E (ApoE)-deficient mice were ovariectomized and implanted with placebo(OVXmice) or 17b-estradiol (E2) pellets (OVX + E2 mice). Compared with OV Xmice, OVX + E2 mice showed increased plasma H2S levels (P = 0.012) and decreased aortic lesion area (P = 0.028). These effects were largely reversed when supplementing with the irreversible CSE inhibitor DL-propargylglycine (PPG) in the OVX + E2 + PPG mice. Meanwhile, the nitric oxide and prostacyclin-resistant responses to cumulative application of acetylcholine (ACh) were studied among all the three groups of femoral arteries. Compared with the arteries in the OVXgroup, the vasodilator sensitivity of arteries to ACh was increased in the OVX + E2 group and attenuated in the OVX + E2 + PPG group. E2 and estrogen receptor (ER) a agonist 4′,4′′,4′′′-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol rapidly increased H2S release in human endothelial cells, but not partially selective ERb agonist 2,3-bis-(4-hydroxyphenyl)-propionitrile. These effects were inhibited by ER antagonist ICI 182780 or by protein kinase G (PKG) inhibitor KT5823. Furthermore, endothelial PKG activity was increased by E2 (P = 0.003) and E2-induced vasodilation was inhibited by KT5823 (P = 0.009). In conclusion, the endothelial CSE/H2S pathway is activated by E2 through PKG, which leads to vasodilation. These actions may be relevant to estrogen's anti-atherogenic effect. © The Author 2012. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved.
Zhu K.,Sun Yat Sen University |
Chen J.,Sun Yat Sen University |
Lai L.,Guangzhou First Municipal Peoples Hospital |
Meng X.,Sun Yat Sen University |
And 4 more authors.
Radiology | Year: 2014
Purpose: To determine the safety and efficacy of transarterial chemoembolization (TACE) combined with sorafenib (hereafter, TACE-sorafenib) in patients with hepatocellular carcinoma (HCC) and portal vein tumor thrombus (PVTT). Materials and Methods: This study was approved by the institutional review board, and the requirement for informed consent was waived. The medical records of consecutive patients with HCC and PVTT who underwent TACE-sorafenib or TACE alone from January 2010 to December 2012 were retrospectively evaluated. Sorafenib (400 mg) was administered twice daily. Outcomes of patients who underwent TACE-sorafenib were compared with outcomes of patients who underwent TACE by using the Kaplan-Meier method according to types of PVTT: PVTT in the main portal vein (type A), PVTT in the first-order portal vein branch (type B), and PVTT in second- or lower-order portal vein branches (type C). Results: Ninety-one patients were included in the analysis; 46 patients underwent TACE-sorafenib and 45 underwent TACE. TACE-sorafenib showed significant survival benefits compared with TACE in patients with type B (median survival, 13 months vs 6 months; P = .002) or type C (median survival, 15 months vs 10 months; P = .003) PVTT. TACE-sorafenib and main PVTT were the independent prognostic factors for survival at uni- and multivariate analysis. Liver function after TACE-sorafenib worsened only in patients with main PVTT. Sorafenib-related adverse events of grade 3 or higher occurred in 16 patients (35%). Conclusion: TACE-sorafenib side effects were acceptable, and this treatment may improve overall survival in patients with HCC with first-order or lower-branch PVTT when compared with patients who underwent TACE alone. © RSNA, 2014.
He M.,Sun Yat Sen University |
Cheng Y.,Guangzhou first municipal peoples hospital |
Li W.,Sun Yat Sen University |
Liu Q.,Sun Yat Sen University |
And 3 more authors.
BMC Cancer | Year: 2010
Background: The elevated expression of vascular endothelial growth factor C (VEGF-C) is correlated with clinical cervical cancer metastasis and patient survival, which is interpreted by VEGF-C functions to stimulate angiogenesis and lymphatic genesis. However, the direct impact of VEGF-C on cervical cancer cell motility remains largely unknown.Methods: In this study, we investigated the effects of VEGF-C on actin cytoskeleton remodeling and on cervical cancer cell migration and invasion and how the actin-regulatory protein, moesin regulated these effects through RhoA/ROCK-2 signaling pathway.Results: On cervical carcinoma cell line SiHa cells, exposure of VEGF-C triggered remodeling of the actin cytoskeleton and the formation of membrane ruffles, which was required for cell movement. VEGF-C significantly enhanced SiHa cells horizontal migration and three-dimensional invasion into matrices. These actions were dependent on increased expression and phosphorylation of the actin-regulatory protein moesin and specific moesin siRNA severely impaired VEGF-C stimulated-cell migration. The extracellular small GTPase RhoA/ROCK-2 cascade mediated the increased moesin expression and phosphorylation, which was discovered by the use of Y-27632, a specific inhibitor of Rho kinase and by transfected constitutively active, dominant-negative RhoA as well as ROCK-2 SiRNA. Furthermore, in the surgical cervical specimen from the patients with FIGO stage at cervical intra-epithelial neoplasia and I-II cervical squamous cell carcinoma, the expression levels of moesin were found to be significantly correlated with tumor malignancy and metastasis.Conclusions: These results implied that VEGF-C promoted cervical cancer metastasis by upregulation and activation of moesin protein through RhoA/ROCK-2 pathway. Our findings offer new insight into the role of VEGF-C on cervical cancer progression and may provide potential targets for cervical cancer therapy. © 2010 He et al; licensee BioMed Central Ltd.
Hou G.,Sun Yat Sen University |
Lu H.,Sun Yat Sen University |
Chen M.,Guangzhou First Municipal Peoples Hospital |
Yao H.,Sun Yat Sen University |
Zhao H.,Sun Yat Sen University
Archives of Gerontology and Geriatrics | Year: 2014
Aging is a major factor associated with lumber intervertebral disc degeneration, and oxidative stress is known to play an essential role in the pathogenesis of many age-related diseases. In this study, we investigated oxidative stress in intervertebral discs of Wistar rats in three different age groups: youth, adult, and geriatric. Age-related intervertebral disc changes were examined by histological analysis. In addition, oxidative stress was evaluated by assessing nitric oxide (NO), superoxide dismutase (SOD), malondialdehyde (MDA), and advanced oxidation protein products (AOPPs). Intervertebral disc, but not serum, NO concentrations significantly differed between the three groups. Serum and intervertebral disc SOD activity gradually decreased with age. Furthermore, both serum and intervertebral disc MDA and AOPP levels gradually increased with age. Our studies suggest that oxidative stress is associated with age-related intervertebral disc changes. © 2014 Elsevier Ireland Ltd.
Liu J.,Sun Yat Sen University |
Cheng Y.,Guangzhou First Municipal Peoples Hospital |
He M.,Sun Yat Sen University |
Yao S.,Sun Yat Sen University
Gynecological Endocrinology | Year: 2014
Vascular endothelial growth factor C (VEGF-C) promotes cervical cancer metastasis, while the detailed mechanism remains obscure. Recent evidence shows that galectin-3 (Gal-3), a glycan binding protein, interacts with the VEGF receptors and reinforces their signal transduction. In this study, we investigated the role of Gal-3 in VEGF-C-induced cervical cancer cell invasion. On cervical carcinoma cell line SiHa cells, silencing of Gal-3 expression with specific siRNA largely impaired VEGF-C-enhanced cell invasion. Treatment with VEGF-C for 12-48 h enhanced Gal-3 protein expression, which was inhibited by the addition of NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC). Moreover, the silencing of NF-κB subunit p65 expression with specific siRNA attenuated VEGF-C-enhanced Gal-3 expression, suggesting that NF-κB is the key intermediate. Under VEGF-C stimulation, an enhanced interaction between VEGF receptor-3 (VEGF-R3) and Gal-3 was found, which may possibly lead to VEGF-R3 activation since exogenous Gal-3 induced VEGF-R3 phosphorylation in a dose- and time-dependent manner. In conclusion, our findings implied that VEGF-C enhanced cervical cancer invasiveness via upregulation of Gal-3 protein through NF-κB pathway, which may shed light on potential therapeutic strategies for cervical cancer therapy. © 2014 Informa UK Ltd.
Li S.,PLA Fourth Military Medical University |
Jin T.,Life Detection Systems |
Zhang J.,Life Detection Systems |
Lou H.,Guangzhou First Municipal Peoples Hospital |
And 4 more authors.
Cancer Epidemiology | Year: 2012
Introduction: Glioma is one of the most aggressive human tumors; however, little is known about its genetic risk factors. The role of heredity is likely to be explained by combinations of common low-risk variants. Previous studies have indicated that more than 100 single nucleotide polymorphisms (SNPs) are associated with the risk of glioma. Methods: To further investigate how and to what extent these SNPs contribute to glioma susceptibility in a Chinese population, we analyzed 43 SNPs of 226 glioma patients and 254 normal people in order to evaluate the associations between SNPs and the risk of glioma. Results: Overall, we found three protective alleles for glioma in patients: the allele " G" of rs1801275 in the IL4R gene by allele model (odds ratio [OR], 0.71; 95% confidence interval [CI], 0.50-0.99; P= 0.04) and dominant model (OR, 0.67; 95% CI, 0.46-0.99; P= 0.04) analysis respectively, the allele " T" of rs17748 in the TREH gene by recessive model (OR, 0.48; 95% CI, 0.23-1.01; P= 0.05) analysis, and the allele " G" of rs6470745 in CCDC26 gene by recessive model (OR, 0.48; 95% CI, 0.26-0.89; P= 0.02) analysis. Conclusion: This study provides evidence for three glioma susceptibility genes - TREH, IL4R and CCDC26 - in a Chinese population; this may shed light on molecular markers of glioma susceptibility and could therefore be used as a diagnostic and prognostic marker for glioma patients in clinical study. © 2012 Elsevier Ltd.
Yang H.,University of Kansas Medical Center |
Yang H.,Guangzhou Medical College |
Yang H.,Guangzhou First Municipal Peoples Hospital |
Bushue N.,University of Kansas Medical Center |
And 2 more authors.
Biochemical Pharmacology | Year: 2010
Fenretinide, a synthetic retinoid, is known to induce apoptosis in various cancer cells. However, the mechanism by which fenretinide induces apoptosis remains unclear. The current study examines the mechanisms of fenretinide-induced apoptosis in human hepatoma cells. The induction of Nur77 and the cytoplasmic distribution of Nur77 induced by fenretinide were positively correlated with the apoptotic effect of fenretinide in HCC cells. The sensitivity of Huh-7 cells was related to Nur77 translocation and targeting mitochondria, whereas the mechanism of resistance for HepG2 cells seemed due to Nur77 accumulating in the nucleus. The intracellular location of Nur77 was also associated with the differential capability of fenretinide-induced ROS generation in these two cell lines. In addition, the knockdown of Nur77 expression by siRNA greatly reduced fenretinide-induced apoptosis and cleaved caspase 3 in Huh- 7 cells. Therefore, our findings demonstrate that fenretinide-induced apoptosis of HCC cells is Nur77 dependent and that the intracellular localization of Nur77 dictates the sensitivity of the HCC cells to fenretinide-induced apoptosis. © 2009 Elsevier Inc. All rights reserved.
Lou H.,Guangzhou First Municipal Peoples Hospital
Nan fang yi ke da xue xue bao = Journal of Southern Medical University | Year: 2012
To investigate the clinical value of serum total procollagen type 1 aminoterminal propeptide (total P1NP), cross-linked C-terminal telopeptide of type I collagen (β-CTX) and 25(OH)D3 detection in evaluating the risks of fragile hip fracture in elderly patients with osteoporosis. Serum levels of total P1NP, β-CTX and 25(OH)D3 was measured in 68 elderly osteoporotic patients with fragile hip fracture and 68 age- and gender-matched osteoporotic controls without fragile hip fracture. In both groups, bone mineral density (BMD) was detected with dual X-ray absorptiometry. The serum levels of total P1NP and β-CTX were significantly higher and 25(OH)D3 level was significantly lower in fragile hip fracture group than in the control group (P<0.05), but the two groups showed no significant difference in lumbar or total hip BMD. Bivariate correlation analysis suggested that in fragile hip fracture group, serum 25(OH)D3 level was positively, while serum total P1NP and β-CTX levels were inversely correlated with lumbar and total hip BMD (P<0.05). In control group, 25(OH)D3 was not related to lumbar or total hip BMD, and serum total P1NP and β-CTX levels were inversely correlated with total hip BMD (P<0.05) but not related to lumbar BMD. In osteoporotic elderly patients with close BMD levels, high serum levels of total P1NP and β-CTX and low serum levels of 25(OH)D3 might independently indicate high fragile hip fracture risk, and detection of the three markers can help identify high-risk individuals.
Zhang Y.,Guangzhou First Municipal Peoples Hospital
Chinese Journal of Rehabilitation Medicine | Year: 2012
Objective: To compare the validity of Montreal cognitive assessment (MoCA) and mini-mental state examination (MMSE) in screening vascular cognitive impairment (VCI) and its main subtype vascular demantia (VaD) in cerebral vascular disease (CVD). Method: One hundred and twenty-seven patients from both neurology clinic and ward of hospital of traditional Chinese medicine of Guangdong province with cerebral vascular disease (CVD) meeting studying criterion were included. All the subjects were administered a neuropsychological tests battery, which included measurements in the following 5 cognitive domains: memory, executive abilities, attention, visuospatial, language, and were administered MoCA and MMSE as well. An operationalized criteria of cognitive deficits was used, results of every subjects' cognitive deficits and diagnostic criteria for vascular cognitive impairment-no dementia(VCIND) and VaD were combined as reference resources by neurology clinicians to diagnose VCIND and VaD. This diagnostic result was considered as the relative clinical gold standard to draw receiver operating curve(ROC) and to compare the validity of MoCA and MMSE in screening VCI in CVD. Result: One hundred and one subjects met the criteria of cognitive deficits, and 55 of them were diagnosed as VaD, 46 of them were VCIND, the other 26 subjects were cognitive normal. The discriminant validity in detecting VCI from CVD was the MoCA superior to the MMSE (receiver operating characteristic area under the curve (AUC): MoCA(0.956±0.0177)>MMSE(0.920±0.0233), Z=2.339, P=0.019); The discriminant validity in detecting VaD from VCD was similar for the MoCA and the MMSE (receiver operating characteristic AUC MoCA(0.945±0.0194)and MMSE (0.931±0.0248), Z=1.453, P=0.146). Conclusion: The MoCA possess adequate psychometric properties as a screening instrument in detecting VCI from CVD, and is superior to the MMSE, while they have the similar validity in detecting VaD from CVD.