First Peoples Hospital of Shenyang

Shenyang, China

First Peoples Hospital of Shenyang

Shenyang, China

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Zhou H.C.,Dalian Medical University | Liu J.,Dalian Medical University | Ren L.Y.,Dalian Medical University | Ren L.Y.,Friendship Hospital of Dalian | And 6 more authors.
Chinese Medical Journal | Year: 2014

Background The mechanisms underlying diabetic encephalopathy are largely unknown, and no effective treatments are available. Catalpol has received much attention due to its numerous biological effects, especially in neuroprotective studies. The aim of this study was to investigate the effects of catalpol on cognitive functions in diabetic rats and the underlying mechanisms. Methods A rat model of diabetes was established by streptozotocin injection, followed by intraperitoneal infusion of catalpol after 10 weeks. Two weeks later, the Morris water maze was used to test the spatial learning performance. Nissl staining was performed to evaluate the morphological changes in the hippocampus. Expression of protein kinase Cγ (PKCγ) and caveolin-1 (Cav-1) in the hippocampus were assessed by reverse transcription PCR and Western blotting. Activities of anti-oxidative enzymes such as glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) and levels of malonaldehyde (MDA) were measured using commercial kits. Results Significant hippocampal neuronal injury was observed in rats with streptozotocin-induced diabetes. Moreover, cognitive dysfunction was associated with markedly increased oxidative stress in the brain. Catalpol treatment significantly attenuated cognitive deficits, neuronal damage, and oxidative stress in the brain of diabetic rats. Biochemical analyses showed that catalpol reversed the down-regulation of PKCγ and Cav-1 expression in the diabetic rats. Conclusions Spatial memory in diabetic rats is associated with the expression of PKCγ and Cav-1. Catalpol treatment markedly attenuated oxidative stress, reversed the alteration of PKCγ, Cav-1 and spatial memory deficits.


Zhang F.-Y.,Shenyang University | Zhang F.-Y.,Shenyang Medical College | Zhang F.-Y.,First Peoples Hospital of Shenyang | Xue Y.-X.,Shenyang Medical College | And 7 more authors.
Cellular Physiology and Biochemistry | Year: 2014

Background: This study was performed to explore the mechanism underlying tinnitus by investigating the changes in the synaptic ribbons and RIBEYE expression in cochlear inner hair cells in salicylate-induced tinnitus. Methods: C57BL/6J mice were injected with salicylate (350 mg/kg) for 10 days and grouped. Behavioral procedures were performed to assess whether the animals experienced tinnitus. The specific presynaptic RIBEYE protein and non-specific postsynaptic glutamate receptor 2&3 protein in basilar membrane samples were examined by immunofluorescent labeling. RT-PCR and Western blot assays were used to examine RIBEYE expression. Serial sections were used to build three-dimensional models using 3ds MAX software to evaluate the changes in the synaptic ribbons. Results: The administration of salicylate increased false positives in the behavioral procedure from 3 d to 10 d. The membrane profiles of inner hair cells in all mice were intact. The number of synaptic ribbons in the salicylate group increased on the 7th d and decreased on the 9th and 10th d. mRNA and protein expression of RIBEYE were initially up-regulated and later down-regulated by injecting salicylate for 10 consecutive days. Conclusion: This change in the ribbon synapses of cochlear inner hair cells in salicylate-induced mice might serve as a compensatory mechanism in the early stages of ototoxicity and contribute to tinnitus later. The alteration of RIBEYE expression could be responsible for the changes in the morphology of ribbon synapses and for salicylate-induced tinnitus. © 2014 S. Karger AG, Basel.


Lin R.P.,First Peoples Hospital Of Shenyang | Yao C.Y.,Shenyang University | Ren D.X.,First Peoples Hospital Of Shenyang
Genetics and Molecular Research | Year: 2015

Several previous studies indicated that genetic polymorphisms in inflammatory factor genes were associated with glioma risk. However, the relationship between the prostaglandin-endoperoxide synthase 2 (PTGS2) genetic polymorphism and glioma remains unclear in the Chinese population. We selected 199 histologically confirmed adult glioma patients and 199 cancer-free controls for the present study and analyzed the distribution of the PTGS2 genotypes and haplotypes. We found that the CC+CT genotype of rs5275 was common in the control group but not in the glioma group (P = 0.033). In addition, we found that the frequency of the C allele was higher in the control group than in the glioma group (P = 0.014). For rs6681231, although we found no significant difference between the 2 groups in genotype distribution, we found that the frequency of the C allele was lower in glioma patients than in control subjects (P = 0.044). We found no significant difference between these 2 groups in the rs689466 genotype and allele distributions. Haplotype analysis suggested that the frequency of the C-A-C haplotype was significantly lower in glioma patients than in control subjects [P = 0.028, odds ratio (OR) = 0.628, 95% confidence interval (CI) = 0.413-0.955]. However, the frequency of the T-A-G haplotype was higher in glioma patients than in control subjects (P = 0.036, OR = 1.418, 95%CI = 1.022-1.967). Therefore, polymorphisms in the PTGS2 gene may be associated with glioma susceptibility in the Chinese population. © FUNPEC-RP.


Xu J.-H.,First Peoples Hospital Of Shenyang | Li X.-F.,Transfusion Medicine Institute | Li X.-F.,Key Laboratory of Blood Safety Research of Liaoning | Li X.-F.,Key Laboratory of Blood Safety Research of Shenyang
Chinese Journal of Tissue Engineering Research | Year: 2015

BACKGROUND: Hematopoietic stem cell transplantation is an important means for clinical cure of hematologic malignancies, congenital hereditary diseases and autoimmune diseases. Although ABO-incompatibility has no effects on the survival of transplanted hematopoietic stem cells, the transfusion strategy to ABO-incompatible grafts in allogeneic hematopoietic stem cell transplantation is worth studying. OBJECTIVE: To explore the antigen-antibody changes during blood conversion after ABO-incompatible hematopoietic stem cell transplantation as well as transfusion strategies. METHODS: Blood grouping, antibody detection, antibody titer determination, cross-match test were employed for antigen-antibody monitoring during blood conversion and pre-transfusion compatibility detection in 24 cases undergoing ABO-incompatible allogeneic hematopoietic stem cell transplantation. Another 30 cases undergoing ABO-compatible allogeneic hematopoietic stem cell transplantation were enrolled as controls to select the appropriate blood. RESULTS AND CONCLUSION: All of the 24 ABO-incompatible patients developed the hematopoietic reconstitution after transplantation, but both major and major-minor ABO incompatibility were different from ABO compatibility in the time of erythrocytic recovery (P < 0.05). According to the changes of ABO antigen and antibody during the blood conversion, the patients of major ABO incompatibility were selected the red blood cells of their own type, the patients of minor ABO incompatibility were selected the red blood cells of the blood group from patients to donors gradually, and the patients of major-minor ABO incompatibility were selected the red blood cells from O-type blood to donor’s type gradually. None of the 24 recipients presented hemolytic reaction during transplantation and after transfusion. Therefore, the transfusion strategy to ABO-incompatible grafts in allogeneic hematopoietic stem cell transplantation is dynamically varied according to the changes of patient’s ABO antigen and antibody, and evaluating the recovery of erythropoietic system can guide blood component selection, avoid hemolytic transfusion reaction, and insure the safety of hematopoietic stem cell transplantation. © 2015 Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Chen Z.,China Medical University at Heping | Chen Z.,First Peoples Hospital of Shenyang | Yu M.,China Medical University at Heping | Zhang Y.,China Medical University at Heping | And 3 more authors.
MicroTAS 2015 - 19th International Conference on Miniaturized Systems for Chemistry and Life Sciences | Year: 2015

We established a gastric cancer subline with highly metastatic potential by a novel, efficient microfluidic system. The system consisted of two parts: a microfluidic device with an opened channel for cell culture and selected subpopulation collection, and a Petri-dish-based liquid supply equipment providing a stable concentration gradient for long-time cell migration driving using a single pump. Human gastric cancer cell line SGC-7901 was used for subline screening. The established subline named SGC-7901/B2 revealed a highly metastatic potential by in vitro and in vivo assays. This simple, efficient, easily controlled device provided a new way to investigate tumor invasion and metastasis. © 15CBMS-0001.


PubMed | First Peoples Hospital of Shenyang, Liaoning Medical University and Liaoning Provincial Blood Center
Type: Journal Article | Journal: Neural regeneration research | Year: 2014

This study aimed to investigate the neural differentiation of human umbilical cord mesenchymal stem cells (hUCMSCs) under the induction of injured neural cells. After in vitro isolation and culture, passage 5 hUCMSCs were used for experimentation. hUCMSCs were co-cultured with normal or A1-40-injured PC12 cells, PC12 cell supernatant or PC12 cell lysate in a Transwell co-culture system. Western blot analysis and flow cytometry results showed that choline acetyltransferase and microtubule-associated protein 2, a specific marker for neural cells, were expressed in hUCMSCs under various culture conditions, and highest expression was observed in the hUCMSCs co-cultured with injured PC12 cells. Choline acetyltransferase and microtubule-associated protein 2 were not expressed in hUCMSCs cultured alone (no treatment). Cell Counting Kit-8 assay results showed that hUCMSCs under co-culture conditions promoted the proliferation of injured PC12 cells. These findings suggest that the microenvironment during neural tissue injury can effectively induce neural cell differentiation of hUCMSCs. These differentiated hUCMSCs likely accelerate the repair of injured neural cells.

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