Objective To introduce and analyze the current user security authentication system in the campus network and point out the secure problems and hidden dangers of the correspondence entities in the campus network. Methods The authentication technologies and protocols in the TCP/IP network model were compared. It was proposed that the campus network security authentication solution should include access control in data link layer, connection control in network layer and unified authentication in application layer. Results The solution could improve the campus network authentication security rank. Conclusion The security and reliability of the network system are enhanced.

Dioxin,one of the persistent organic pollutants,persistently exists in the environment and does serious harm to the ecological environment as well as to the human body because of its reproductive toxicity,carcinogenicity,immune toxicity,skin toxicity and toxicity to other systems and organs.This paper reviewed the toxicities of dioxins to the human body,especially to the endocrine and immune systems.

Calcium Channel Blockers ; pharmacology ; therapeutic use ; Cerebral Infarction ; drug therapy ; Coronary Disease ; drug therapy ; Humans ; Pyrazines ; pharmacology ; therapeutic use ; Vasodilator Agents ; pharmacology ; therapeutic use

Chromatography, Reverse-Phase ; methods ; Humans ; Sorbic Acid ; analogs & derivatives ; analysis ; Urinalysis ; methods

Aim To study and compare the pharmaco-kinetic parameters of roxithromycin under normoxic and hypoxic rats. Methods A highly effective and rapid ultra-performance liquid chromatography with tandem mass spectrometry ( UPLC-MS/MS) method with posi-tive electrospray ionization source was successfully de-veloped and validated for quantification of roxithromy-cin in rat plasma. Sprague-Dawley rats were randomly divided into the hypoxia and normoxic groups. Each rat obtained a single dose of roxithromycin with 10 mg · kg-1 via intragastric administration. The pharmacoki-netic parameter comparison between normoxic and hy-poxic groups was calculated by SPSS software using in-dependent sample t test method. Results The main pharmacokinetic parameters of roxithromycin between the normoxic and hypoxic rats were:the AUC(0-t) 7 576 and 3 761 μg·h·L-1 , MRT(0-t) 5. 6 and 7. 7 h, T1/2 3. 4 h and 3. 9 h, CL 1. 5 and 3. 0 L · h-1 · kg-2 , tmax3. 1 and 3. 4 h, Cmax 1 116 and 372 μg·L-1 , re-spectively. The levels of Cmax and AUC of roxithromy-cin in hypoxic rats were statistically lower than those in normoxic rats. Conclusion The exposure level of rox-ithromycin in hypoxic rats markedly decreased. Our re-sults may provide an important experimental basis to adjust the dosage for roxithromycin in hypoxic clinical practice.

OBJECTIVETo evaluate the protective effects of punicosides on alcohol induced acute liver injury in mice and its possible mechanisms as well.

METHODThe 60 mice were randomly divided into normal control, model group, three dose groups of punicosides with low, medium and high, then there is silibinin group. Three dose groups of punicosides and silibinin were given in advance by gavage for 4 weeks, then the mouse model of alcoholic acute liver injury was established. The serum levels of ALT, AST and TG were determined, and the mice were killed to calculate somatic index of liver, thymus as well as spleen. MDA, SOD, GSH-Px and GSH-ST were detected in the liver homogenate. Histopathological changes of the liver were observed by HE staining. The expression of MCP-1 and NF-kappaB in the liver tissues were detected by immunohistochemistry.

RESULTMid and high dose of punicosides reduced the liver index in mice significantly, improved liver steatosis, decreased the level of ALT, AST and TG in serum and the content of MDA in liver homogenate, furthermore the two dose groups increased the activity of SOD, GSH-Px and GSH-ST, inhibited the expression of MCP-1 and NF-kappaB in liver tissue.

CONCLUSIONPunicosides can protect the acute liver damage induced by alcohol.

Alcohols ; adverse effects ; Animals ; Chemical and Drug Induced Liver Injury ; blood ; drug therapy ; metabolism ; pathology ; Chemokine CCL2 ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Female ; Gene Expression Regulation ; drug effects ; Liver ; drug effects ; enzymology ; pathology ; Male ; Malondialdehyde ; metabolism ; Mice ; NF-kappa B ; metabolism

OBJECTIVEThe purpose of the present study was to investigate the in vitro effects of baicalin on induction of apoptosis in human prostate cancer cell line DU145.

METHODHuman prostate cancer cell line DU145 was treated with different concentration of baicalin in vitro. The apoptosis rate was determined by FACS analysis, cell cycle distribution was detected by flow cytometry, morphological changes and protein analysis were determined by means of electron microscope techniqueand immunohistochemical techniquerespectively.

RESULT50micromol x L(-1) and 125 micromol x L(-1) of baicalin dose-dependently induced apoptosis and inhibited the proliferation of prostate cancer cell DU145 in a dose and time-dependent manner. DNA flow cytometric analysis indicated that baicalin induced a arrest in G1 phase, showing a typical apoptosis peak. Electron microscopy detected a characteristic appearance of the apoptotic cells morphology. Immunohistochemical analysis revealed that induction of apoptosis by ways of inhibition of the bcl-2, loss of the Bax, and upregulation of Fas.

CONCLUSIONThe results indicate that baicalin may induce apoptosis and inhibit proliferation of prostate cancer cells, and has direct anti-tumor effects on human prostate cancer cells.

Antineoplastic Agents, Phytogenic ; pharmacology ; Apoptosis ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Dose-Response Relationship, Drug ; Flavonoids ; isolation & purification ; pharmacology ; G1 Phase ; Humans ; Male ; Plants, Medicinal ; chemistry ; Prostatic Neoplasms ; metabolism ; pathology ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Scutellaria ; chemistry ; bcl-2-Associated X Protein ; fas Receptor ; metabolism

UNLABELLEDOBJECTIVE To study the in vitro effect and mechanism of Ginkgo biloba Extract 50 (GBE50) for inhibiting beta-amyloid (Abeta)-induced oxidative stress in rats' hippocampal neurons.

METHODSThe primary hippocampal neurons were cultured in vitro and divided into 4 groups, i. e. the normal control group (Ctrl), the Abeta group, the propanediol control group (PDO), and the six GBE50 concentrations groups (5, 10, 25, 50, 100, and 200 microg/mL). Excepted the Ctrl group, neurons were induced to oxidative stress by 20 gmolLAbeta25-35. The MTT and fluorescent probes labeling were used to observe the effect of GBE50 with different concentrations on the cell viability and the generation of intracellular reactive oxygen species (ROS) in neurons. Furthermore, Western blot was used to detect the cytoplasmic/total cytochrome C (Cyto C) ratio and total intracytoplasmal Cyto C, and the effect of the expression of oxidative stress-related protein Cyto C and activated Caspase-3 in three GBE50 concentrations groups (25, 50, and 100 microg/mL).

RESULTSCompared with the Ctrl group, the cell vitality was obviously lowered and intracellular ROS generation significantly increased after induction of 20 micromol/L Abeta25-35 (both P < 0.05). Compared with the Abeta group, the cell vitality was evidently improved after treated with different GBE50 doses. Except for 10 microg/mL, the cell vitality could be obviously elevated along with increased drug concentrations (P < 0.05). Meanwhile, the intracellular ROS generation decreased significantly in each GBE50 dose groups (P < 0.05). Abeta could increase the cytoplasmic/total Cyto C ratio and enhance the activated Caspase-3 expression significantly (P < 0.05). Compared with the Abeta group, among the three concentrations of GBE50, the Cyto C ratio was obviously lowered in the 100 microg/mL GBE50 group (P < 0.05), and the expression of activated Caspase-3 significantly decreased in 50 microg/mL and 100 microg/mL GBE50 groups (P < 0.05).

CONCLUSIONS20 micromol/L Abeta25-35 could induce the generation of intracellular ROS in hippocampal neurons. GBE50 could inhibit Abeta induced intracellular oxidative stress of neurons through lowering the cytoplasmic/total Cyto C ratio and inhibiting the activation of apoptosis protein Caspase-3 expression.

Amyloid beta-Peptides ; toxicity ; Animals ; Cells, Cultured ; Cytochromes c ; metabolism ; Hippocampus ; metabolism ; Neurons ; drug effects ; metabolism ; Oxidative Stress ; drug effects ; Peptide Fragments ; toxicity ; Plant Extracts ; pharmacology ; Rats ; Rats, Sprague-Dawley

To evaluate the properties of solidifying volatile oil with graphene oxide, clove oil and zedoary turmeric oil were solidified by graphene oxide. The amount of graphene oxide was optimized with the eugenol yield and curcumol yield as criteria. Curing powder was characterized by differential scanning calorimetry (DSC) and scanning electron microscopy (SEM). The effects of graphene oxide on dissolution in vitro and thermal stability of active components were studied. The optimum solidification ratio of graphene oxide to volatile oil was 1:1. Dissolution rate of active components had rare influence while their thermal stability improved after volatile oil was solidified. Solidifying herbal volatile oil with graphene oxide deserves further study.
Calorimetry, Differential Scanning ; Clove Oil ; chemistry ; Curcuma ; chemistry ; Eugenol ; Graphite ; chemistry ; Microscopy, Electron, Scanning ; Oils, Volatile ; chemistry ; Oxides ; chemistry ; Plant Extracts ; chemistry ; Powders ; Sesquiterpenes

Objective There is little research focusing on the expression and function of bradykinin 1 receptor ( B1R ) and bradykinin 2 receptor ( B2R) after cerebral ischemia/reperfusion on the basis of diabetes .The aim of this study was to compare the ex-pression difference and function change of B 1R and B2R in non-dia-betic and diabetic rats . Methods The cerebral ischemia/reperfu-sion model was established on 41 non-diabetic and type 2 diabetic rats, the weight and the biochemical index were measured on these two types of rats .8 non-diabetic rats and 8 diabetic rats were respec-
tively assigned to two groups according to random number tables:control group and I/R 24 h group, 4 in each group.Real-time PCR was performed to observe the expressions of two receptors at 24 h after reperfusion .Then, 33 non-diabetic rats and 33 diabetic rats were randomly divided into 4 groups respectively, including sham group (n=6), saline group (n=9), B1R antagonist group (n=9) and B2R antagonist group (n=9).At 24 hours after cerebral I/R, neurological deficiency was evaluated by neurological severity scores ( NSS);infarct volume was observed by TTC staining;cell apoptosis was determined by TUNEL staining;neuron degeneration was de-tected by Fluoro-Jade C staining. Results Glucoses of diabetics at 3, 7, 14 d after model establishment [(23.45 ±5.01), (23.71 ±4.87), (22.72 ±4.11) mmol/L] were obviously elevated compared with non-diabetics [(5.77 ±0.75), (6.05 ±0.69), (7.15 ±1.09) mmol/L];blood cholesterin [(4.59 ±3.43) mmol/L] and insulin [(67.26 ±12.02) pmol/L] at 14 d after model establishment were evidently incresaed in comparison to those in non-diabetics [(1.58 ±0.37) mmol/L, (25.34 ±4.88) pmol/L] (P<0.05), while no significant difference was found in the blood triglyceride of diabetics between them (P>0.05).Compared with non-diabetics, diabetics suffered from more apparent up-regulation of B1R mRNA (P<0.01) but relatively less B2R mRNA (P<0.05) at 24 h after I/R.NSS score, infarction volume, damaged and apoptotic cells in B2R antagonis-treated non-diabetic rats at 24 h after I/R conspicuously decreased compared with saline-treated non-daibetic rats.Those indicators in B1R antagonis-treated diabeics were strikingly lessened compared with saline-treated daibetics . Conclusion I/R induced distinct up-regulation of B2R mRNA in non-diabetics and inhibiton of B 2R effectively ameliorated the infarct volume and cell injury after I/R in non-diabetics; I/R induced more notable up-regulation of B1R mRNA in diabetics and B1R antagonist exerted neuroprotective effects instead of B 2R antagonist af-ter I/R in diabetics.