Shenyang First Peoples Hospital

Shenyang, China

Shenyang First Peoples Hospital

Shenyang, China
SEARCH FILTERS
Time filter
Source Type

Sui Y.,University of Melbourne | Sui Y.,Shenyang First Peoples Hospital | Vermeulen R.,Karolinska Institutet | Vermeulen R.,Maastricht University | And 6 more authors.
Frontiers in Cellular Neuroscience | Year: 2013

Neurogenesis in the adult rodent brain is largely restricted to the subependymal zone (SVZ) of the lateral ventricle and subgranular zone (SGZ) of the dentate gyrus (DG). We examined whether cholecystokinin (CCK) through actions mediated by CCK1 receptors (CCK1R) is involved in regulating neurogenesis. Proliferating cells in the SVZ, measured by 5-bromo-2-deoxyuridine (BrdU) injected 2 hours prior to death or by immunoreactivity against Ki67, were reduced by 37% and 42%, respectively, in female (but not male) mice lacking CCK1Rs (CCK1R-/-) compared to wild-type (WT). Generation of neuroblasts in the SVZ and rostral migratory stream was also affected, since the number of doublecortin (DCX)-immunoreactive (ir) neuroblasts in these regions decreased by 29%. In the SGZ of female CCK1R-/- mice, BrdU-positive (+) and Ki67-ir cells were reduced by 38% and 56%, respectively, while DCX-ir neuroblasts were down 80%. Subsequently, the effect of reduced SVZ/SGZ proliferation on the generation and survival of mature adult-born cells in female CCK1R-/- mice was examined. In the OB granule cell layer (GCL), the number of neuronal nuclei (NeuN)-ir and calretinin-ir cells was stable compared to WT, and 42 days after BrdU injections, the number of BrdU+ cells co-expressing GABA- or NeuN-like immunoreactivity (LI) was similar. Compared to WT, the granule cell layer of the DG in female CCK1R-/- mice had a similar number of calbindin-ir cells and BrdU+ cells co expressing calbindin-LI 42 days after BrdU injections. However, the OB glomerular layer (GL) of CCK1R-/- female mice had 11% fewer NeuN-ir cells, 23% less TH-ir cells, and a 38% and 29% reduction in BrdU+ cells that co-expressed TH-LI or GABA-LI, respectively. We conclude that CCK, via CCK1Rs, is involved in regulating the generation of proliferating cells and neuroblasts in the adult female mouse brain, and mechanisms are in place to maintain steady neuronal populations in the OB and DG when the rate of proliferation is altered. © 2013 Sui, Vermeulen, Hökfelt, Horne and Stanic.


Zhu C.,Shenyang Seventh Peoples Hospital | Xu B.,Shenyang First Peoples Hospital | Sun X.,Shenyang University | Zhu Q.,Shenyang Medical College | And 3 more authors.
Molecular Neurobiology | Year: 2016

The majority of Alzheimer’s disease (AD) patients have a late onset, and chronic neuroinflammation, characterized by glial activation and secretion of pro-inflammatory cytokines and chemokines, plays a role in the pathogenesis of AD. The chemokine CCL11 has been shown to be a causative factor of cognitive decline in the process of aging, but little is known whether it is involved in the pathogenesis of AD. In the present study, we showed that CCR3, the receptor for CCL11, was expressed by hippocampal neurons and treatment of primary hippocampal neuronal cultures (14 days in vitro) with CCL11 resulted in activation of cyclin-dependent kinase 5 and glycogen synthase kinase-3β, associated with elevated tau phosphorylation at multiple sites. CCL11 treatment also induced the production of Aβ and dendritic spine loss in the hippocampal neuronal cultures. All these effects were blocked by the CCR3 specific antagonist, GW766994. An age-dependent increase in CCL11, predominantly expressed by the activated microglia, was observed in the cerebrospinal fluid of both APP/PS1 double transgenic mice and wild-type (WT) littermates, with a markedly higher level in APP/PS1 double transgenic mice than that in WT littermates. Deletion of CCR3 in APP/PS1 double transgenic mice significantly reduced the phosphorylation of CDK5 and GSK3β, tau hyperphosphorylation, Aβ deposition, microgliosis, astrogliosis, synaptic loss, and spatial learning and memory deficits. Thus, the age-related increase in CCL11 may be a risk factor of AD, and antagonizing CCR3 may bring therapeutic benefits to AD. © 2016 Springer Science+Business Media New York


PubMed | University of Wollongong, University of Melbourne and Shenyang First Peoples Hospital
Type: Journal Article | Journal: Restorative neurology and neuroscience | Year: 2015

Epilepsy is a prevalent neurological disorder with a high frequency of drug resistance. While significant advancements have been made in drug delivery systems to overcome anti-epileptic drug resistance, efficacies of materials in biological systems have been poorly studied. The purpose of the study was to evaluate the anti-epileptic effects of injectable poly(epsilon-caprolactone) (PCL) microspheres for controlled release of an anticonvulsant, phenytoin (PHT), in an animal model of epilepsy.PHT-PCL and Blank-PCL microspheres formulated using an oil-in-water (O/W) emulsion solvent evaporation method were evaluated for particle size, encapsulation efficiency, surface morphology and in-vitro drug release profile. Microspheres with the most suitable morphology and release characteristics weresubsequently injected into the hippocampus of a rat tetanus toxin model of temporal lobe epilepsy. Electrocorticography (ECoG)from the cerebral cortex were recorded for all animals. The number of seizure events, severity of seizures, and seizure duration were then compared between the two treatment groups.We have shown that small injections of drug-loaded microspheres are biologically tolerated and released PHT can control seizures for the expected period of time that is in accord with in-vitro release data.The study demonstrated the feasibility of polymer-based delivery systems incontrolling focal seizures.


Wang J.-E.,Shenyang First Peoples Hospital | Wang J.-E.,Shenyang University | Liu Y.-H.,Shenyang University | Liu Y.-H.,Shenyang Medical College | And 4 more authors.
Journal of Neuro-Oncology | Year: 2011

This study was performed to determine whether low frequency ultrasound (LFU) irradiation, Papaverine (PA) infusion and combination LFU irradiation with PA infusion opened the blood-tumor barrier (BTB) by affecting tight junctions (TJ)-associated proteins zonula occluden-1 (ZO-1), occludin and caludin-5. In a rat brain glioma model, we found that the mRNA and protein expression levels of ZO-1, occludin and claudin-5 were decreased by LFU irradiation and PA infusion. LFU-induced and PA-induced decrease of ZO-1, occludin and claudin-5 was further decreased after combining LFU irradiation with PA infusion. Immunohistochemistry assay showed that the decreased expression of ZO-1, occludin and claudin-5 was the most obvious in the tumor capillaries. Meanwhile, Evans blue assay showed that the permeability of BTB was increased, and transmission electron microscopy (TEM) indicated that TJ was opened. This led to the conclusion that LFU irradiation and PA infusion together can open the BTB by paracellular pathway. Significantly down-regulated expression levels of ZO-1, occludin and claudin-5 might be one of the molecular mechanisms of combining LFU and PA enhancing the permeability of BTB. © 2010 Springer Science+Business Media, LLC.


PubMed | Shenyang Seventh Peoples Hospital, Shenyang University, Shenyang First Peoples Hospital and Shenyang Medical College
Type: | Journal: Molecular neurobiology | Year: 2016

The majority of Alzheimers disease (AD) patients have a late onset, and chronic neuroinflammation, characterized by glial activation and secretion of pro-inflammatory cytokines and chemokines, plays a role in the pathogenesis of AD. The chemokine CCL11 has been shown to be a causative factor of cognitive decline in the process of aging, but little is known whether it is involved in the pathogenesis of AD. In the present study, we showed that CCR3, the receptor for CCL11, was expressed by hippocampal neurons and treatment of primary hippocampal neuronal cultures (14days in vitro) with CCL11 resulted in activation of cyclin-dependent kinase 5 and glycogen synthase kinase-3, associated with elevated tau phosphorylation at multiple sites. CCL11 treatment also induced the production of A and dendritic spine loss in the hippocampal neuronal cultures. All these effects were blocked by the CCR3 specific antagonist, GW766994. An age-dependent increase in CCL11, predominantly expressed by the activated microglia, was observed in the cerebrospinal fluid of both APP/PS1 double transgenic mice and wild-type (WT) littermates, with a markedly higher level in APP/PS1 double transgenic mice than that in WT littermates. Deletion of CCR3 in APP/PS1 double transgenic mice significantly reduced the phosphorylation of CDK5 and GSK3, tau hyperphosphorylation, A deposition, microgliosis, astrogliosis, synaptic loss, and spatial learning and memory deficits. Thus, the age-related increase in CCL11 may be a risk factor of AD, and antagonizing CCR3 may bring therapeutic benefits to AD.


Zhang X.,Shenyang First Peoples Hospital | Hu W.,Liaoning Medical University | Feng F.,Liaoning University of Traditional Chinese Medicine | Xu J.,Shenyang First Peoples Hospital | Wu F.,Shenyang First Peoples Hospital
Molecular Medicine Reports | Year: 2016

Myocardial infarction is a serious health threat. Apelin is an endogenous ligand of angiotensin II receptor-like 1 (APJ) and the apelin/APJ system is associated with various types of heart disease. However, whether apelin protects against myocardial infarction-induced myocardial fibrosis remains unclear. The present study aimed to investigate the function of apelin-13 during myocardial infarction-induced myocardial fibrosis, and to determine the mechanism underlying the effects of apelin-13. Apelin-13 was demonstrated to improve left ventricular function and results of hematoxylin and eosin staining, Masson's trichrome staining and western blotting showed that apelin-13 attenuated myocardial fibrosis. Further mechanistic investigation was performed by enzyme-linked immunosorbent assay, western blotting and electrophoretic mobility shift assay. The results demonstrated that apelin-13 inhibited the activation of nuclear factor (NF)-κB signaling in vitro and in vivo. To the best of our knowledge, the present study was the first to demonstrate that apelin-13 may attenuate myocardial infarction-induced myocardial fibrosis, and that this protective function may be mediated by inhibition of NF-κB signaling. The present study suggests a theoretical basis for the effects of apelin-13 and provides insight into the potential clinical application of apelin-13.


PubMed | Liaoning University of Traditional Chinese Medicine, Liaoning Medical University and Shenyang First Peoples Hospital
Type: Journal Article | Journal: Molecular medicine reports | Year: 2016

Myocardial infarction is a serious health threat. Apelin is an endogenous ligand of angiotensinII receptor-like1 (APJ) and the apelin/APJ system is associated with various types of heart disease. However, whether apelin protects against myocardial infarctioninduced myocardial fibrosis remains unclear. The present study aimed to investigate the function of apelin13 during myocardial infarctioninduced myocardial fibrosis, and to determine the mechanism underlying the effects of apelin13. Apelin13 was demonstrated to improve left ventricular function and results of hematoxylin and eosin staining, Massons trichrome staining and western blotting showed that apelin13attenuated myocardial fibrosis. Further mechanistic investigation was performed by enzymelinked immunosorbent assay, western blotting and electrophoretic mobility shift assay. The results demonstrated that apelin13inhibited the activation of nuclear factor (NF)B signaling invitro and invivo. To the best of our knowledge, the present study was the first to demonstrate that apelin13 may attenuate myocardial infarctioninduced myocardial fibrosis, and that this protective function may be mediated by inhibition of NFB signaling. The present study suggests a theoretical basis for the effects of apelin13 and provides insight into the potential clinical application of apelin-13.


PubMed | Shenyang First Peoples Hospital, Liaoning Medical University and Chinese People's Liberation Army
Type: Journal Article | Journal: Molecular medicine reports | Year: 2015

Bone marrow stromal cells (BMSCs), derived from the mesoderm, have been applied in the repair and reconstruction of injured tissues. The present study was conducted to explore the effects of BMSCs on cell viability of tumor necrosis factor- (TNF-)-stimulated PC12 cells. PC12 cells were co-cultured with BMSCs under TNF- treatment, with normal PC12 cells as controls. Results from an MTT assay indicated that BMSCs significantly increased cell growth and proliferation of TNF--treated PC12 cells (survival rates were 56.71 and 76.86% for the positive control (PC) and co-culture group, respectively). Furthermore, Annexin V/propidium iodide staining and flow cytometric analysis demonstrated that TNF- increased PC12-cell apoptosis from 3.49 to 40.74% in the negative control and PC group, and the apoptotic rate was significantly reduced upon co-culture with BMSCs to 16.97%. In addition, data from reverse transcription-quantitative polymerase chain reaction and western blot analyses illustrated that TNF--induced upregulation in TNF receptor (TNFR)-1 (TNFR1) and caspase-8 expression in PC12 cells were partially reversed by co-culture with BMSCs. In conclusion, the present study suggested that BMSCs protect PC12 cells against stimulation with TNF-, which is partially mediated through the TNFR/caspase signaling pathway. The results of the present study also suggested a therapeutic use of BMSCs in clinical neurodegenerative diseases.


PubMed | University of Melbourne, Shenyang First Peoples Hospital and St Vincents Hospital
Type: Evaluation Studies | Journal: Neuroscience bulletin | Year: 2015

The aim of this prospective blinded study was to evaluate an automated algorithm for spike-and-wave discharge (SWD) detection applied to EEGs from genetic absence epilepsy rats from Strasbourg (GAERS). Five GAERS underwent four sessions of 20-min EEG recording. Each EEG was manually analyzed for SWDs longer than one second by two investigators and automatically using an algorithm developed in MATLAB. The sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated for the manual (reference) versus the automatic (test) methods. The results showed that the algorithm had specificity, sensitivity, PPV and NPV >94%, comparable to published methods that are based on analyzing EEG changes in the frequency domain. This provides a good alternative as a method designed to mimic human manual marking in the time domain.


Hao D.,Liaoning Medical University | Zhang J.,Shenyang First Peoples Hospital
World Chinese Journal of Digestology | Year: 2011

AIM: To observe the effect of body position on respiratory mechanics in patients during laparoscopic surgery. METHODS: Reserve trendelenburg position was adopted in 20 patients undergoing laparoscopic gastrectomy, while conventional trendelenburg position was adopted in 20 patients undergoing laparoscopic enterectomy. All patients were subjected to general anaesthesia, and controlled ventilation was selected. The compliance of the lungs (Cpat) and airway pressure (Paw) were monitored with the Drager primus anesthesia machine. PaCO2 and PaO2 were monitored with the Siemens Rapidlab1265 Blood Gas Analyzer. Measurements were divided into five distinct phases: 5 minutes after the induction of anesthesia (T1); 5 minutes after pneumoperitoneum (T2); 5 minutes after position change (T3); 5 minutes after adjusting ventilation parameters (T4); and 5 minutes after peritoneal deflation (T5). Respiratory mechanics were analyzed using SPSS15.0 statistics software. RESULTS: PaCO2 and Paw at T2 in the conventional trendelenburg group were significantly higher than those in the reserve trendelenburg group (both P < 0.05). PaO2 and Cpat at T2 and T3 in the conventional trendelenburg group were significantly lower than those in the reserve trendelenburg group (all P < 0.01). CONCLUSION: Body position can affect respiratory parameters during laparoscopic surgery.

Loading Shenyang First Peoples Hospital collaborators
Loading Shenyang First Peoples Hospital collaborators