463rd Hospital of PLA

Shenyang, China

463rd Hospital of PLA

Shenyang, China
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Zi Y.,Shanghai JiaoTong University | Zi Y.,463rd Hospital of PLA | Yin Z.,463rd Hospital of PLA | Xiao W.,Fudan University | And 4 more authors.
Molecular Neurobiology | Year: 2015

An increasing number of circulating micro-ribonucleic acids (microRNAs, miRNAs) have been discovered its potential as biomarkers to diagnose neurodegenerative diseases (NDs) by many researchers. However, there were obvious inconsistencies among previous studies, and thus we performed this meta-analysis to evaluate whether miRNA is an effective biomarker with high accuracy to diagnose the NDs. PubMed, MEDLINE, EMBASE, the Cochrane Library, and other related databases were used to search eligible articles. The data of sensitivity and specificity were employed to plot the summary receiver operator characteristic (SROC) curve and calculate the area under the SROC curve (AUC). I2 test were used to estimate the heterogeneity among different studies. In addition, the possible sources of heterogeneity were further explored by subgroup analyses and meta-regression. All analyses were performed by STATA 12.0 software. In this meta-analysis, eight publications with 459 NDs patients and 340 healthy controls were included to investigate the diagnostic performance of circulating miRNAs for NDs. The overall sensitivity and specificity, positive likelihood ratio (PLR), negative likelihood ration (NLR), and diagnostic odds ratio (DOR) were 0.83 (95 % confidence interval (CI) 0.77–0.88), 0.87 (95 % CI 0.83–0.89), 6.2 (95 % CI 4.9–7.9), 0.19 (95 % CI 0.14–0.27), 33 (95 % CI 20–52), and 0.91 (95 % CI: 0.88–0.93), respectively. The overall SROC curve was plotted with AUC of 0.91 (95 % CI 0.88–0.93), which indicated an excellent diagnostic performance of circulating miRNA for NDs. Subgroup analysis based on miRNA profile demonstrated that multiple-miRNA assay had higher diagnostic accuracy for NDs when compared with single-miRNA assay. In conclusion, the circulating miRNAs may be the potential biomarkers in the clinical diagnosis of NDs, and the diagnostic accuracy would be better by using multiple-miRNA assay. However, large-scale studies are still needed to explore the relation between the circulating miRNA dysregulation and the pathological mechanism of NDs. © 2014, Springer Science+Business Media New York.

PubMed | 463rd Hospital of PLA, Shanghai JiaoTong University, Shanghai Minhang District Hospital of Traditional Chinese Medicine and Shanghai University
Type: | Journal: Neuropeptides | Year: 2016

Fracture repair is a complex yet well orchestrated regenerative process involving numerous signaling and cell types including osteoblasts. Here we showed that NPY, a neurotransmitter with regulatory functions in bone homeostasis, may contribute to the post-fracture bone healing in patients with traumatic brain injury-fracture combined injuries. Our results suggested NPY levels were increased in patients with the combined injuries, accomplished by arising of bone healing markers, such as ALP, OC, PICP and ICTP, than in those with simple fractures, and NPY have direct actions on MSCs to promote their osteogenic differentiation. Our results provided clinical evidences for NPY participating in the bone healing process in a nonhypothalamic manner, most probably by directly promoting osteogenesis of mesenchymal stem cells.

Yang Y.,PLA Fourth Military Medical University | Jiang S.,PLA Fourth Military Medical University | Dong Y.,General Hospital of Shenyang Military Command | Dong Y.,463rd Hospital of PLA | And 9 more authors.
Journal of Pineal Research | Year: 2015

Silent information regulator 1 (SIRT1), a type of histone deacetylase, is a highly effective therapeutic target for protection against ischemia reperfusion (IR) injury (IRI). Previous studies showed that melatonin preserves SIRT1 expression in neuronal cells of newborn rats after hypoxia-ischemia. However, the definite role of SIRT1 in the protective effect of melatonin against cerebral IRI in adult has not been explored. In this study, the brain of adult mice was subjected to IRI. Prior to this procedure, the mice were given intraperitoneal with or without the SIRT1 inhibitor, EX527. Melatonin conferred a cerebral-protective effect, as shown by reduced infarct volume, lowered brain edema, and increased neurological scores. The melatonin-induced upregulation of SIRT1 was also associated with an increase in the anti-apoptotic factor, Bcl2, and a reduction in the pro-apoptotic factor Bax. Moreover, melatonin resulted in a well-preserved mitochondrial membrane potential, mitochondrial Complex I activity, and mitochondrial cytochrome c level while it reduced cytosolic cytochrome c level. However, the melatonin-elevated mitochondrial function was reversed by EX527 treatment. In summary, our results demonstrate that melatonin treatment attenuates cerebral IRI by reducing IR-induced mitochondrial dysfunction through the activation of SIRT1 signaling. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Qiu J.,Shenyang University | Li W.,General Hospital of Shenyang Military Command | Feng S.H.,463rd Hospital of PLA | Wang M.,463rd Hospital of PLA | He Z.Y.,Shenyang University
Genetics and Molecular Research | Year: 2014

Ginsenoside Rh2 (Rh2) is a ginseng derivative used in Chinese traditional medicine. We investigated whether Rh2 can help prevent Alzheimer's disease symptoms and examined underlying mechanisms. We injected Rh2 into tg2576 Alzheimer's disease model mice and looked for behavioral improvement and senile plaque reduction in brain slices. We measured amyloid precursor protein (APP) metabolism species changes, amyloid beta40 and 42 levels and β, γ secretase activity in primary hippocampal neurons. By living cell staining, we detected surface and endocytosed APP. We also measured cholesterol and lipid rafts in primary neurons. Rh2 treatment significantly improved learning and memory performance at 14 months of age; it also reduced brain senile plaques at this age. Based on in vitro experiments, we found that Rh2 treatment increased soluble APPα (sAPPα) levels, increased CTFα/β ratios, and reduced amyloid beta 40 and 42 concentrations. Surface APP levels dramatically increased. Based on living cell staining, we found that Rh2 inhibited APP endocytosis. Based on lipid removal and reload experiments, we found that Rh2 can modulate APP by reducing cholesterol and lipid raft levels. We concluded that Rh2 improves learning and memory function in Alzheimer's disease model mice, and that this improvement is accomplished by reducing amyloid beta secretion and APP endocytosis, which in turn is achieved by reducing cholesterol and lipid raft concentrations. © FUNPEC-RP.

Dong Y.,PLA Fourth Military Medical University | Dong Y.,463rd Hospital of PLA | Li Y.,463rd Hospital of PLA | Feng D.,PLA Fourth Military Medical University | And 8 more authors.
Brain Research | Year: 2013

Hypoxia-inducible factor 1α (HIF-1α) is a master regulator of cellular adaptation to hypoxia and has been proposed as a potent therapeutic target for cerebral ischemia. However, research on the expression and effects of HIF-1α in subarachnoid hemorrhage (SAH) is limited. The aim of the present study was to investigate the expression of HIF-1α in the hippocampus and its possible protective effect against hippocampal apoptosis and cognitive dysfunction in a rat model of SAH. Seventy-two Sprague-Dawley (SD) rats were randomly divided into the sham group, the SAH+vehicle group, and the SAH+YC-1 group. Immunohistochemical staining and western blotting analyses revealed that the expression of HIF-1α and its downstream effectors, vascular endothelial growth factor (VEGF), erythropoietin (EPO), and glucose transporter 1 (GLUT1), increased in the hippocampus 48 h after the induction of SAH. YC-1 blocked this upregulation. The number of active caspase-3-positive cells and the expression of active caspase-3 in the hippocampus significantly increased in the YC-1 group relative to the vehicle group. A cell death assay further revealed that DNA fragmentation was significantly increased at 48 h in the YC-1 group compared with the vehicle group. In Morris water maze (MWM) tests, the YC-1 group showed increased escape latency times and distances as well as reduced time spent and distance traveled in the target quadrant. These results indicate that hippocampal apoptosis increased and cognitive function deteriorated when HIF-1α was inhibited, suggesting that HIF-1α has a neuroprotective effect in SAH and may represent an effective therapeutic target. © 2013 Elsevier B.V. All rights reserved.

Dong Y.-S.,PLA Fourth Military Medical University | Dong Y.-S.,463rd Hospital of PLA | Wang J.-L.,PLA Fourth Military Medical University | Wang J.-L.,General Hospital of Guangzhou Military Command | And 6 more authors.
International Journal of Medical Sciences | Year: 2014

Quercetin has been demonstrated to play an important role in altering the progression of ischemic brain injuries and neurodegenerative diseases by protecting against oxidative stress. The effects of quercetin on brain damage after subarachnoid hemorrhage (SAH), however, have not been investigated. This study was designed to explore the effects of quercetin on oxidative stress and brain edema after experimental SAH using four equal groups (n = 16) of adult male Sprague- Dawley (SD) rats, including a sham group, an SAH + vehicle group, an SAH + quercetin10 group, and an SAH + quercetin50 group. The rat SAH model was induced by injection of 0.3 ml of non-heparinised arterial blood into the prechiasmatic cistern. In the SAH + quercetin10 and SAH + quercetin50 groups, doses of 10 mg/kg and 50 mg/kg quercetin, respectively, were directly administered by intraperitoneal injection at 30 min, 12 h, and 24 h after SAH induction. Cerebral tissue samples were extracted for enzymatic antioxidant determination, lipid peroxidation assay, caspase-3 activity and water content testing 48 h after SAH. Treatment with a high dose (50 mg/kg) of quercetin markedly enhanced the activities of copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px), and treatment with this dose significantly reduced the level of malondialdehyde (MDA). Caspase-3 and brain edema was ameliorated and neurobehavioral deficits improved in rats that received the high dose of quercetin. The findings suggest that the early administration of optimal dose of quercetin may ameliorate brain damage and provide neuroprotection in the SAH model, potentially by enhancing the activity of endogenous antioxidant enzymes and inhibiting free radical generation. © Ivyspring International Publisher.

Feng D.,PLA Fourth Military Medical University | Wang W.,PLA Fourth Military Medical University | Dong Y.,PLA Fourth Military Medical University | Dong Y.,463rd Hospital of PLA | And 7 more authors.
Neuroscience | Year: 2014

Early brain injury (EBI) after subarachnoid hemorrhage (SAH) is characterized by a reduction in excitatory amino acid transporter 2 (EAAT2) expression and severe amino acid excitotoxicity. The aim of this study was to explore the neuroprotective effect of ceftriaxone (CEF), a potent compound that up-regulates EAAT2, against EBI and the potential mechanisms using in vitro experiments and a rat model of SAH. Intracisternal treatment with CEF significantly improved neurological outcomes and alleviated extracellular glutamate accumulation after SAH. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining and Western blot analysis of cleaved caspase 3 showed that CEF decreased hippocampal neuronal apoptosis following SAH. Immunofluorescent staining and Western blotting revealed that CEF significantly reversed the down-regulation of EAAT2 expression following SAH. In Morris water maze (MWM) tests, CEF remarkably ameliorated the SAH-induced cognitive dysfunction in spatial learning memory and reference memory. CEF promoted the nuclear translocation of p65 as well as the activation of Akt in hippocampal astrocytes in vitro and in vivo. These findings suggest that CEF may exert significant protective effects against EBI following SAH by modulating the PI3K/Akt/NF-κB signaling pathway. © 2014 IBRO.

Dong Y.-S.,PLA Fourth Military Medical University | Dong Y.-S.,463Rd Hospital of PLA | Hou W.-G.,PLA Fourth Military Medical University | Li X.-L.,Life Detection Systems | And 7 more authors.
Tumor Biology | Year: 2014

Glioblastoma (GBM), a deadly brain tumor, is the most malignant glioma. It mainly occurs in adults and occurs significantly more in males than in females. We genotyped 19 tag single nucleotide polymorphisms (tSNPs) from 13 genes in a case - control study of the Han Chinese population to identify genetic factors contributing to the risk of GBM. These tSNPs were genotyped by Sequenom MassARRAY RS1000. Statistical analysis was performed using χ2 test and SNPStats, a website software. Using χ2 test, we found that the distribution of two tSNPs (rs2267130 in checkpoint kinase 2 (CHEK2), p=0.040; rs1695 in GSTP1, p=0.023) allelic frequencies had significant difference between cases and controls. When we analyzed all of the tSNPs using the SNPStats software, we found that rs1695 in GSTP1 decreased the risk of GBM in log-additive model (OR=0.56, 95% CI, 0.34-0.94, p=0.022). Besides, we found that there is an interaction between rs3212986 in excision repair cross-complementing group 1 (ERCC1) and gender under codominant and recessive models. The gene polymorphisms in CHEK2, GSTP1, and ERCC1 may be involved in GBM in the Han Chinese population. Since our sample size is small, further investigation needs to be performed. © International Society of Oncology and BioMarkers (ISOBM) 2014.

PubMed | 463rd Hospital of PLA, PLA Fourth Military Medical University and General Hospital of Shenyang Military Command
Type: Journal Article | Journal: Cell death and differentiation | Year: 2016

Testicular phagocytosis by Sertoli cells (SCs) plays an essential role in the efficient clearance of apoptotic spermatogenic cells under both physiological and pathological conditions. However, the molecular mechanism underlying this unique process is poorly understood. Herein, we report for the first time that -taxilin protein (TXLNA), a binding partner of the syntaxin family that functions as a central player in the intracellular vesicle traffic, was dominantly expressed in SCs. Induction of apoptosis in murine meiotic spermatocytes and haploid spermatids by busulfan treatment stimulated a significant increase of TXLNA in SCs at day (d) 14 and d 24 after busulfan treatment, respectively. Consistently, TXLNA expression was steadily upregulated when SCs were co-cultured with apoptotic germ cells (GCs). Moreover, using siRNA treatment, we found that ablation of endogenous TXLNA significantly impaired the phagocytotic capacity of SCs and thereby resulted in defective spermiogenesis and reduced fertility during the late recovery after testicular heat stress. Mechanistically, upregulation of TXLNA expression by apoptotic GCs was associated with the stabilization of ATP-binding cassette transporter 1 (ABCA1), a transporter-mediated lipid efflux from SCs and influencing male fertility. TXLNA acted as an upstream suppressor of ABCA1 ubiquitination and thus promoted ABCA1 stability and accumulation following GC apoptosis. We further provide in vitro evidence that epidermal growth factor receptor (EGFR)-mediated phosphorylation regulated ABCA1 ubiquitination and was enhanced by TXLNA deficiency during testicular phagocytosis. Taken together, the TXLNA/ABCA1 cascade may serve as an important feedback mechanism to modulate the magnitude of subsequent phagocytotic process of SCs in response to testicular injury.

PubMed | 463rd Hospital of PLA and Southern Medical University
Type: Journal Article | Journal: Genetics and molecular research : GMR | Year: 2015

The aim of this study was to understand the effect of autologous bone powder graft repair of partial mandibular defects of rabbits by the quantitative detection of bone formation. New Zealand rabbits (N = 18) were selected as the test objects, and subjected to bilateral partial mandibular defect induction. One side of the mandibular defect acted as the test group, upon which the autologous bone powder backfilling graft was performed; the other side was put aside and acted as the negative control group. All used an autogenous control. At the twelfth postoperative week, the animals were sacrificed, and semi-automatic image analysis was used to conduct bone histomorphometric detection. Immediately subsequent, quantitative detection of bone formation was performed in the test group. Fluorescent perimeter percent, mineralization apposition rate, and bone formation rate were selected as the dynamic indicators; and trabecular area percent, trabecular thickness, trabecular number, and trabecular separation degree were selected as the static indicators for single factorial variance testing. It was found that the values of P are less than 0.05 between the test group and the control group, indicating that the effect of autologous bone powder graft repair on partial mandibular defects in rabbits was positive.

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