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Design and Implementation of Secure Subnet Inside of Data Sensitive Network  [PDF]
Haiwei Xue, Yunliang Zhang, Zhien Guo, Yiqi Dai
Journal of Software Engineering and Applications (JSEA) , 2013, DOI: 10.4236/jsea.2013.63B012
Abstract: Sensitive data leak can cause significant loss for some organizations, especially for technology intensive companies and country security departments. Traditional mandatory access control (MAC) can only control whether the user can access the sensitive data or not, and cannot prevent the user to leak or spread the data. So even designed impeccable access control policies, we still cannot prevent inside leak. A nature solution is using physical isolation to prevent sensitive data from being leaked outside network; however inside the physical isolated network, data still can be spread from one subnet to another. We present Secure Subnet System, a BLP model base security system that can provide more strong access control, which is called mandatory action control. In our system after a user read sensitive data, system will dynamically change security policies to prevent the user to leak these data or spread the data outside to another subnet. We use a state machine model to describe our system, and use secure transfer equations to dynamically calculate the system policies for each new state. Our model can be proved to be secure by formal methods. We implemented a demon of our system. In this paper we also show the design details of the demon and evaluate the demon both from security and performance. The evaluation results show that the output of the security tests case are under expected; and the performance test case show that, for the 64KB IO chunk size, IO read loss can be improved to 6.6%, IO write loss can be improved to 1.2% after optimization.
The Neuroprotective Effect of Picroside II and Its Best Therapeutic Dose and Time Window in Cerebral Ischemic Injury in Rats  [PDF]
Li Zhao, Xiaodan Li, Yunliang Guo, Cuicui Chang, Fangfang Pang
Journal of Behavioral and Brain Science (JBBS) , 2013, DOI: 10.4236/jbbs.2013.35039
Abstract: Objective: To study the neuroprotective effect of picrosede II and explore the best therapeutic dose and time window according to orthogonal design in cerebral ischemic injury in rats. Methods: The forebrain ischemia rat models were established by bilateral common carotid artery occlusion (BCCAO) method. The successful models were randomly grouped according to orthogonal experimental design and treated by injecting picroside II intraperitoneally at different ischemic time with different doses. The contents of neuron-specific enolase (NSE), neuroglial marker protein S100B and myelin basic protein (MBP) in serum and brain tissue were determined by enzyme linked immunosorbent assay (ELISA) to evaluate the therapeutic effect of picroside II in cerebral ischemic injury. Results: The best therapeutic time window and dose of picroside II in cerebral ischemic injury may be 1) ischemia 1.5 h with 20 mg/kg and ischemia 1.5 h with 10 mg/kg body weight according to the content of NSE in serum and brain tissue respectively, 2) ischemia 1.5 h with 20 mg/kg according to the content of S100B in both serum and brain tissue, and 3) ischemia 1.5 h with 20 mg/kg and ischemia 1.5 h with 10 mg/kg according to the content of MBP in serum and brain tissue respectively. Conclusion: Based on the principle of the minimization of therapeutic drug dose and maximization of therapeutic time window, the optimal composition of the therapeutic dose and time window of picroside II in treating cerebral ischemic injury should be achieved by injecting picroside II intraperitoneally with 10-20 mg/kg body weight at ischemia 1.5 h in cerebral ischemic injury in rats.
The anti-inflammatory effect of picroside II and the optimizing of therapeutic dose and time window in cerebral ischemic injury in rats  [PDF]
Li Zhao, Xiaodan Li, Tingting Wang, Yunliang Guo, Fangfang Pang, Cuicui Chang
Modern Research in Inflammation (MRI) , 2013, DOI: 10.4236/mri.2013.23006
Abstract:

The aim is to optimize the anti-inflammatory effect and the therapeutic dose and time window of picrosede II by orthogonal test in cerebral ischemic injury in rats. The forebrain ischemia models were established by bilateral common carotid artery occlusion (BCCAO) methods in 30 Wistar rats. The successful models were randomly divided into sixteen groups according to orthogonal experimental design and treated by injecting picroside II intraperitoneally at different ischemic time with different dose. The concentrations of aquaporins 4 (AQP4), matrix metalloproteinases9 (MMP9) and cyclooxygenase 2 (COX2) in serum and brain tissue were determined by enzyme linked immunosorbent assay to evaluate the therapeutic effect of picroside II in cerebral ischemic injury. The best therapeutic time window and dose of picroside II in cerebral ischemic injury were 1) ischemia 2.0 h with 20 mg/kg and 1.5 h with 20 mg/kg body weight according to the concentration of AQP4 in serum and brain tissue; 2) ischemia 1.5 h with 20 mg/kg and ischemia 2.0 h with 20 mg/kg according to the concentrations of MMP9 in serum and brain tissue; and 3) ischemia 1.5 h with 10 mg/kg and ischemia 1.5 h with 20 mg/kg according to the concentrations of COX2 in serum and brain tissue respectively. According to the principle of the lowest therapeutic dose with the longest time window, the optimized therapeutic dose and time window were injecting picroside II intraperitoneally with 10 - 20 mg/kg body weight at ischemia 1.5 - 2.0 h in cerebral ischemic injury.

Effects of Carpio Decoction on the Structure of Kidney in Rats with Adriamycin-Induced Nephrosis  [PDF]
Huaying Ning, Hui Wu, Xiaojian Tian, Yunliang Guo, Wei Shen, Xin Wang, Zhou Zhen
Food and Nutrition Sciences (FNS) , 2013, DOI: 10.4236/fns.2013.47A015
Abstract: The aim of this study was to observe the effects of Cyprinus carpio decoction on the expression of aquaporins in rats with adriamycin-induced nephropathy and to explore the therapeutic mechanism on nephrotic edema. Total of 50 Wistar rats were randomly divided into normal group, model group, fosinopril group, Cyprinus carpio decoction treated with high dose group and low dose group consisting of 10 rats respectively. Nephropathy models were established by injecting adriamycin through tail vein and treated with Cyprinus carpio decoction. Urinary protein excretions in 12 h, serum albumin, total serum protein, serum sodium and potassium were measured by biochemical assay. The pathological changes and the expression of AQP1, AQP2, AQP3 inrat kidneys were respectively detected by HE stain and immunohistochemiscal assay. The results indicated: 1) The urinary protein excretion in 12 h (proteinuria) increased significantly along the time longed modeling, while no significant increasing in Cyprinus carpio decoction treated group (F = 5.23 - 41.89, P < 0.05); 2) The serum albumin and total protein in model group were significantly lower than that in normal group, but that in Cyprinus carpio decoction treated group were higher than that in model group (F = 13.12 - 15.48, P < 0.05). The serum sodium and potassium in model group were higher than those in normal group, while that in Cyprinus carpio decoction treated group were higher than that in model group (F = 3.42 - 3.96, P < 0.05); 3) Renal glomerular capillaries congestive of group M rats were expansion. Glomerular mesangial cells and the basement membrane were diffuse hyperplasia, inflammatory cell infiltration. Glomerular mesangial cells and the basement membrane of Cyprinus carpio decoction with interventing groups reduced proliferation, less inflammatory cell infiltration; 4) In model group, the expressions of AQP1-3 in the renal tubule and collecting duct cells increased significantly than those in normal group, and those in Cyprinus carpio decoction treated group decreased than those in model group (F = 3.97 - 6.19, P < 0.05). It is suggested that Cyprinus carpio decoction could reduced the urinary protein excretion and alleviate pathological lesion and edema with adriamycin-induced nephropathy by decreasing the expressions of AQPs in kidneys.
Anti-inflammation effects of picroside 2 in cerebral ischemic injury rats
Yunliang Guo, Xinying Xu, Qin Li, Zhen Li, Fang Du
Behavioral and Brain Functions , 2010, DOI: 10.1186/1744-9081-6-43
Abstract: The middle cerebral artery occlusion reperfusion models were established with intraluminal thread methods in 90 adult healthy female Wistar rats. Picroside 2 and salvianic acid A sodium were respectively injected from tail vein at the dosage of 10 mg/kg for treatment. The neurobehavioral function was evaluated with Bederson's test and the cerebral infarction volume was observed with tetrazolium chloride (TTC) staining. The apoptotic cells were counted by in situ terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL) assay. The immunohistochemistry stain was used to determine the expressions of toll-like receptor 4 (TLR4), nuclear transcription factor κB (NFκB) and tumor necrosis factor α (TNFα). The concentrations of TLR4, NFκB and TNFα in brain tissue were determined by enzyme linked immunosorbent assay (ELISA).After cerebral ischemic reperfusion, the rats showed neurobehavioral function deficit and cerebral infarction in the ischemic hemisphere. The number of apoptotic cells, the expressions and the concentrations in brain tissue of TLR4, NFκB and TNFα in ischemia control group increased significantly than those in the sham operative group (P < 0.01). Compared with the ischemia control group, the neurobehavioral scores, the infarction volumes, the apoptotic cells, the expressions and concentrations in brain tissue of TLR4, NFκB and TNFα were obviously decreased both in the picroside 2 and salvianic acid A sodium groups (P < 0.01). There was no statistical difference between the two treatment groups in above indexes (P > 0.05).Picroside 2 could down-regulate the expressions of TLR4, NFκB and TNFα to inhibit apoptosis and inflammation induced by cerebral ischemic reperfusion injury and improve the neurobehavioral function of rats.Excitatory amino acid toxicity, oxidative stress, intracellular calcium overload, as well as inflammation and apoptosis, are involved in the pathological process after cerebral ischem
Hypoglycemic Effect of Laminaria japonica Polysaccharide in a Type 2 Diabetes Mellitus Mouse Model
Xiaodan Li,Zhuqin Yu,Shaohua Long,Yunliang Guo,Delin Duan
ISRN Endocrinology , 2012, DOI: 10.5402/2012/507462
Abstract: The aim is to investigate the hypoglycemic effect of Laminaria japonica polysaccharides (LJPS) on type 2 diabetes mellitus (T2DM) mice model. 60 healthy male mice have been used in the experiment. T2DM animal mode was prepared by high fatty forage feeding and intraperitoneal injection with alloxan. Diabetic mice were orally supplied with LJPS. Then their blood was collected for various biomedical measurements of fasting blood glucose (FBG), serum insulin, and amylin. Treatment with LJPS significantly reduced fasting blood glucose ( ) and increased the levels of insulin and amylin in serum ( ). Overall, the study presented that LJPS can reverse several components of T2DM. Therefore, LJPS may become a new oral candidate medicine for the treatment of diabetes. 1. Introduction Type 2 diabetes mellitus (T2DM) is a chronic, progressive metabolic disease that involves multiple factors such as age, life style, genetic factor, obesity and viral infection [1–5]. The pathogenesis of T2DM includes insulin resistance (IR), glucotoxicity, lipotoxicity, oxidative stress, genetic deficiency and inflammatory reaction among which, IR is crucially important occupying the central position in this metabolic syndrome [6–9]. The “common soil hypothesis” theory [10] considers IR a common pathogenic factor for coronary heart disease, diabetes, and hypertension. Amylin secreted from the pancreatic islets into the blood circulation contributes to glucose metabolism control in physiological condition [11]. But, long-term hyperglycemia stimulated to induce the production of amylin that can inhibit insulin releasing, also inhibit insulin-stimulated glucose transport in skeletal muscle and the glucose metabolism of liver cell. The turbulence of excretion of amylin induces insulin resistance, interfering with fat metabolism [12]. The current therapies of type 2 DM include increasing secretion of islet cells, improving insulin sensitivity to peripheral tissue, reducing glucose absorption in the gastrointestinal tract and decreasing serum lipid and increasing insulin level. However, drug susceptibility declines with long-term use and toxic side effects are accompanied by increased dosage. Therefore, new and much more effective medical therapies must be developed to improve the treatment and protection of the patients with T2DM. Inhibitors of glucagon and amylin analogues may avoid the above shortcomings to some degree [13]. A traditional Chinese medicine, named Kelp, was used in the present study as an anti-T2DM drug. The main effective components of this kelp are Laminaria japonica
Evodiamine Inhibits the Proliferation of BGC-823 and SGC-7901 Cells by Inducing Cell Cycle Arrest and Apoptosis in Gastric Cancer  [PDF]
Hanni Zhang, Yunliang Guo, Keli Ge, Yanan Wang
Open Access Library Journal (OALib Journal) , 2019, DOI: 10.4236/oalib.1105217
Abstract:
Gastric cancer represents a major cause of cancer-related death worldwide. Although various tactics and anti-tumor drugs have been used to improve curative effects, five-year survival rate of lung cancer patients remains poor. Evodiamine, a sophora alkaloid, has been demonstrated to exert antitumor effects on many types of cancer. However, the molecular mechanism of evodiamine against gastric cancer has not been clearly elucidated. In this study, we investigated the anti-tumor activity and the underlying mechanisms of EVO on gastric cancer cells, and found that it significantly inhibited the proliferation of BGC-823 and SGC-7901 cells by inducing cell cycle arrest at G2/M phase and cell apoptosis in a dose- and time-dependent manner. Its molecular mechanism may be that it reduces the expression of cell cycle- promoting protein Cdc25C and promotes the expression of cell cycle inhibitor p53, as well as prompts the activity of caspases pathways, such as the expression level of cleaved caspase-3 and cleaved caspase-8; cleaved caspase-9 and cleaved PARP-1 are up-regulated, treated with EVO (10 μM) at different points in time (0, 3, 6, 9, 12, 24 h). Collectively, our data demonstrated that EVO was a potential anti-tumor agent against gastric cancer.
Anti-Tumor Effect and Mechanism of Parthenolide in Gastric Cancer Cellline BGC-823  [PDF]
Wenhao Zhu, Hanni Zhang, Yunliang Guo, Keli Ge, Yonghong Zhou
Open Access Library Journal (OALib Journal) , 2019, DOI: 10.4236/oalib.1105271
Abstract:
Objective: To study the anti-tumor effect and mechanism of parthenolide in gastric cancer cell BGC-823. Methods: The cck8 assay was used to detect the changes of BGC-823 cells viability after treatment with different con-centrations of parthenolide at different time points. The proliferation ability of BGC-823 cells was detected by clone formation assay. And the cell cycle and apoptosis were measured by flow cytometry. Meanwhile, to detect the different in intracellular ROS production levels, the fluorescence assay was used. And with the help of western blotting, cell cycle- and apoptosis-related protein expression can be detected. Results: Parthenolide could inhibit the viability of BGC-823 cells in a dose- and time-dependent manner (P < 0.01). In BGC-823 cells exposed to parthenolide, the apoptosis rate was found significantly increased (P < 0.01), and the protein expression of cleaved-caspase3, cleaved-caspase8, and cleaved-caspase9 significantly increased (P < 0.01); the cell cycle was arrested at G1phase (P < 0.01); the protein levels of CyclinD1 and CyclinE1 decreased (P < 0.01), and the expression of P53 and P21 protein increased (P < 0.01); massive intracellular ROS generation was found (P < 0.01). Furthermore, the nuclear protein levels of c-Myc, E2F1, and NF-κB and the protein level of phosphorylated STAT3 decreased in BGC-823 cells exposed to parthenolide (P < 0.01). Conclusion: Parthenolide may inhibit the proliferation of BGC-823 cells and induce G1-phase cell cycle arrest and apoptosis via inhibiting STAT3-c-Myc-E2F1 axis.
Bone Morphogenetic Protein-7 Ameliorates Cerebral Ischemia and Reperfusion Injury via Inhibiting Oxidative Stress and Neuronal Apoptosis
Haitao Pei,Dongming Cao,Zhuangli Guo,Guofang Liu,Yunliang Guo,Chenglong Lu
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms141223441
Abstract: Previous studies have indicated that bone morphogenetic protein-7 (BMP-7) is neuroprotective against cerebral ischemia/reperfusion (IR) injury. The present study was undertaken to determine the molecular mechanisms involved in this effect. Adult male Wistar rats were subjected to 2 h of transient middle cerebral artery occlusion (MCAO), followed by 24 h of reperfusion. BMP-7 (10 ?4 g/kg) or vehicle was infused into rats at the onset of reperfusion via the tail vein. Neurological deficits, infarct volume, histopathological changes, oxidative stress-related biochemical parameters, neuronal apoptosis, and apoptosis-related proteins were assessed. BMP-7 significantly improved neurological and histological deficits, reduced the infarct volume, and decreased apoptotic cells after cerebral ischemia. BMP-7 also markedly enhanced the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and reduced the level of malondialdehyde (MDA) in IR rats. In addition, Western blot analysis indicated that BMP-7 prevented cytochrome c release, inhibited activation of caspase-3, caspase-9 and caspase-8. Our data suggested that BMP-7 has protective effects against cerebral IR injury in rats, and the neuroprotective effects may be attributed to attenuating oxidative stress and inhibiting neuronal apoptosis.
Effects of transplanted GDNF gene modified marrow stromal cells on focal cerebral ischemia in rats
Yunliang Wang
Frontiers in Integrative Neuroscience , 2011, DOI: 10.3389/fnint.2011.00089
Abstract: Objective: To evaluate the therapeutic effect of transplanted glial cell derived neurotrophic factor (GDNF) modified marrow stromal cells (MSCs) on an experimental ischemic brain injury based on the behavioral, morphological, and immunohistochemical observations. Methods: The MSCs from four-week newborn rats were cultured in vitro. The cerebral ischemia and reperfusion model was established in adult Sprague–Dawley (SD) rats by using the suture method. Three days after model establishment, the animals were injected with prepared MSCs via their caudal veins. The animals were then divided into a sham-operation group, ischemia group, MSCs transplantation group, or GDNF+MSCs transplantation group and were scored for their neurobehavioral manifestations at 3, 14, and 28 days after the transplantation was performed. At this time, the survival condition of intracerebral transplanted cells was measured by laser confocal microscopy while the effect of transplantation on the Generic Digital Beam Former (GDNF) expression in the ischemic brain tissue was evaluated. Results: The MSCs cells transfected with GDNF gene were characterized by green fluorescence. Three days after the transplantation, the animals that underwent the cell transplantation showed significantly better behavioral data than the controls. Fourteen days after transplantation, the animals transplanted with GDNF gene modified MSCs were better than those transplanted with common MSCs. As compared with common MSCs transplantation, GDNF+MSCs transplantation was significantly more effective in reducing apoptotic cell volume and enhancing Bcl-2 expression, which was favorable for the ischemic brain injury. Conclusions: Transplanted GDNF modified MSCs can improve the nervous function and have a protective effect on the ischemic brain injury through reducing apoptotic cell volume and enhancing the expression of anti-apoptotic gene Bcl-2.
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