Due to the development of economy,the mature of technology,and the improvement of institution,the under-treatment and over-treatment of percutaneous coronary intervention (PCI) gradually tends to be balanced in our country.However,these two phenomena still exist in some regions,even in the same hospital.Under the background of the medical conjoined in the new medical reform,it should play its positive role through strengthening the guidanceof medical ethics and the abiding the principle of optimization,in order to apply PCI scientifically and rationally,benefit patients more,and improve the medical quality.

To evaluate the cost-effectiveness of two cephosporin antibiotics in the treatment of lung RRinfections. Method: The cost and effectiveness of two therapy regimens in treatme nt of lung infections were compared by cost-effectiveness analysis. Result: Ceftriaxone was a cost-effective antibiotic compared with su lperazon (cefaperazone sulbactam) to treat lung infections. Conclusio n: The analysis result showed that pharmacoeconomics was avery impor tant for rational use of drug and decrease of medical care cost.

Objective To investigate the effects of ursolic acid (UA) on oxidative stress and apoptosis in focal cerebral ischemia reperfusion in rats. Methods One hundred and twenty SD rats were randomly divided into 6 groups:sham operation group, model group, and groups of 20, 40, 80 120 mg/kg UA, with 20 rats in each group. A model of focal cerebral ischemic reperfusion was induced using the intraluminal thread method. Drugs were administrated immediately via tail vein injection when the suture was inserted. At 6h later, the total antioxidative capacity (T-AOC), malondialdehyde (MDA) level, and the activity of creatine kinase (CK), lactate dehydrogenase (LDH) in the serum, and the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) in the ischemic cortex were measured. Apoptosis in the ischemic cortex was detected by TUNEL staining. Results Compared with the model group, the activity of CK (301.2 ± 86.8 U/L, 258.5 ± 58.4 U/L, 228.7 ± 49.2 U/L vs. 352.6 ± 88.1 U/L), LDH (327.5 ± 87.1 U/L, 288.6 ± 69.5 U/L, 243.7 ± 74.9 U/L vs. 395.4 ± 98.6 U/L) in the serum in the groups of 40, 80 120 mg/kg UA were significantly decreased (P<0.05 or P<0.01), MDA (5.5 ± 1.4 mmol/L, 4.8 ± 1.1 mmol/L, 4.4 ± 1.3 mmol/L vs. 7.8 ± 2.0 mmol/L) and T-AOC (9.4 ± 2.2 U/L, 10.5 ± 2.9 U/L, 11.8 ± 3.1 U/L vs. 8.0 ± 2.1 U/L) were significantly increased (P<0.05 or P<0.01); the activity of SOD (10.1 ± 2.7 U/mg, 11.6 ± 2.5 U/mg vs. 6.9 ± 2.6 U/mg),GSH-Px (12.9 ± 2.9 U/mg, 14.2 ± 3.2 U/mg vs. 9.5 ± 2.3 U/mg), CAT (3.3 ± 1.3 U/mg, 3.9 ± 1.2 U/mg vs. 2.3 ± 0.9 U/mg) in the ischemic cortex in the groups of 80 120 mg/kg UA were significantly increased (P<0.05 or P<0.01). TUNEL staining showed that apoptosis in the ischemic cortex in all the UA groups were significantly decreased compared with the model group. Conclusion UA could effectively enhance the activity of antioxidant enzymes and free radical scavenging capacity, ameliorate oxidative stress and inhibit apoptosis in focal cerebral ischemia reperfusion in rats.

Objective To investigate the expression of nucleotide-binding oligomerization domain 2(NOD2),an intracelluar pathogen pattern recognition receptor,and Toll like receptor(TLR) 2,4 in human vascular smooth muscle cells(VSMC),and its effect on production of proinflammatory cytokines in VSMC.Methods Human coronary artery smooth muscle cells were in vitro stimulated with NOD2 agonist Muramyl dipeptide(MDP),TLR2 agonist Pam3CSK4(PAM3)and TLR4 agonist lipopolysaccharides(LPS) alone or MDP in cocultured with either PAM3 or LPS.The mRNA expression of NOD2 and fibroblast growth factor-2(FGF-2) were measured by real time RT-PCR.The concentration in the culture supernatants of interleukin-8(IL-8) and tumor necrosis factor-?(TNF-?) was determined by ELISA.VSMC proliferation was analyzed by the MTT assay.Results MDP up-regulate the expression of NOD2 mRNA in VSMC in a time-dependent manner(0 h:0.028?0.001;3 h:0.045?0.002;6 h:0.053?0.002;24 h:0.162?0.013).It up-regulate the expression of FGF-2 mRNA(MDP 9.3?0.4 vs control 7.4?0.2;P

AIM: Nucleotide binding oligomerization domain receptor 1 (NOD1) is a recently identified intracellular pathogen pattern recognition receptor of innate immunity. This study was designed to explore the role of NOD1-mediated innate immune signal pathway in the activation of vascular smooth muscle cells (VSMCs), and investigate the effect of peptidoglycan (PGN) on the activation and expression of NOD1 in human VSMCs. METHODS: The experiment was performed in the central laboratory of the Second Affiliated Hospital of Dalian Medical University from June 2006 to March 2007.①Subject: Human coronary artery VSMCs were purchased from Cambrex company.② Methods: Human coronary artery VSMCs were cultured in vitro, and stimulated with NOD1 agonist PGN (10 mg/L) for 0, 3, 6 and 24 hours. ③ Evaluation: The mRNA expression of NOD1 in VSMCs was measured by real time quantitative reverse transcription-polymerase chain reaction. The concentration in the culture supernatants of interleukin-8 (IL-8) and tumor necrosis factor-? (TNF-?) was determined by enzyme linked immunosorbent assay. RESULTS: ①Human VSMCs constitutively expressed a low level of NOD1 at resting condition. Upon PGN stimulation, the expression of NOD1 mRNA was up-regulated in VSMCs, from 0.164?0.005 to 0.231?0.027 (P

We have made an investigation on medica1 college students' thinking about the teaching of human parasitology,and put forward a preliminary tentative plan and suggestion to the teaching goal,teaching content,method and so on to human parasitology teaching.

NODs are cytosolic proteins that contain a nucleotide-binding oligomerization domain(NOD).These intracellular proteins are a class of pattern recognition receptors with unique functions in the innate and the acquired immune systems.NOD like receptors,including NOD1 and NOD2,are associated with host responses to intracellular invasion by bacteria or the intracellular presence of specific bacterial products.Activation of NOD like receptors initiates proinflammatory signalling via NF-?B activation,which is necessary for clearance of infecting pathogens from the host.Several different mutations in the genes encoding NOD1 and NOD2 are associated with susceptibility to inflammatory disorders.

Objective To investigate the protective effects of ursolic acid (UA) on global cerebral ischemic-reperfusion injury in rats.MethodsThe experimental rats were divided into the sham operation group, the model group, the UA low, medium and high dose groups, 20 in each group. Except the rats in the sham operation group, the rats in other groups were dealed by four arteries occlusion to made global cerebral ischemia-reperfusion model. The rats in the UA low, medium, high dose groups were given UA as 40, 80, 120 mg/kg immediately after the occlusion line was inserted; the rats in the sham operation group and the model group were given equal-volume saline. And 6 hours later, the recovery time of righting reflex and electrical activity of brain were recorded, water content of the brain were evaluated, and the activity of LDH, MDA, SOD, CAT in brain tissue were determined; the inflammatory cytokines content of TNF-α, IL-1β, IL-6 were determined by ELISA. Results Compared with the model group, the recovery time of righting reflex (20.6 ± 7.2 min, 18.2 ± 6.9 min vs. 27.3 ± 8.8 min) and electrical activity of brain (16.2 ± 5.8 min, 14.9 ± 5.6 min vs.24.1 ± 7.2 min) of the UA medium and high dose groups were shortened (P<0.05 orP<0.01); the water content were significantly decreased (79.0% ± 0.7%, 78.6% ± 0.5%vs. 80.7% ± 0.9%;P<0.05 orP<0.01); the activity of SOD (158.5 ± 8.4 U/mg, 165.4 ± 9.0 U/mgvs. 143.0 ± 7.1 U/mg), CAT (3.3 ± 1.4 U/mg, 3.9 ± 1.5 U/mgvs. 2.4 ± 0.9 U/mg) in brain tissue of the UA medium and the high dose groups were significantly improved; the content of LDH (16.0 ± 2.6 mmol/g, 18.4 ± 2.8 mmol/gvs. 12.4 ± 1.9 mmol/g) were significantly increased; the content of MDA (18.6 ± 2.8μmol/g, 17.2 ± 2.4μmol/gvs. 24.9 ± 3.4μmol/g), TNF-α (45.8 ± 6.3 nmol/L, 40.1 ± 5.6 nmol/Lvs. 56.3 ± 7.2 nmol/L), IL-6 (187.2 ± 18.5 nmol/L, 136.8 ± 15.7 nmol/Lvs. 238.4 ± 22.9 nmol/L) were significantly decreased, and the content of IL-1β in UA 120 mg/kg treated group was significantly decreased (713.6 ± 56.3 nmol/L vs. 915.7 ± 70.5 nmol/L;P<0.05 orP<0.01).Conclusion UA can effectively promote righting reflex and EEG recovery, reduce brain water content, which perhaps related with its pharmacological effects of enhanceing the activity of antioxidant enzymes, lower oxidative stress, and inhibit inflammation.

Aged ; Carcinoma, Squamous Cell ; pathology ; Female ; Humans ; Laryngeal Neoplasms ; pathology ; Male ; Postoperative Period

Objective To investigate the protective effect and the mechanisms of triptolide on antibody-mediated rejection (AMR) in kidney transplantation.Method A rat model of AMR in kidney transplantation was constructed by sensitizing major histocompability complex (MHC) completely incompatible species of rats via blood transfusion before kidney transplantation.The protective effect of Triptolide on the renal function and pathologic injury was studied in this rat model.The levels of donor specific antibodies were measured by flow cytometry.C4d expression and macrophage infiltration were examined by immunohistochemistry and immunofluorescence.Result Triptolide could improve the function of transplanted kidney significantly (P＜0.05) and alleviate the pathologic injury.Triptolide can also reduce the levels of IgM,IgG2b and IgG2c in the serum of the recipient rats and inhibit the macrophage infiltration as well (P＜0.05).Conclusion Triptolide plays protective and therapeutic roles in AMR of kidney transplantation,which may be contributed to the inhibition of the production of donor specific antibody and the macrophage infiltration.