As the integration of human parasitology and medical microbiology curriculum, pathogen biology, although constructed and developed about 20-years, didn't realize the true integration of the two disciplines. Beyond that, it was also faced with numerous difficulties such severe compression of human par-asitology class, lack of teaching materials to achieve the true meaning of integration, difficulty to cultivate teachers and so on. The organ-system based learning (OBL) curriculum model may provide new strategies for the dilemma, to be resolved through the following channels: Rearranging the curriculum and teaching materials based on the classification of pathogenic organism parasitic or invasive organs; Corresponding training in microbiology and parasitology teaching by teachers continuous realization, while highlighting the professional teaching level of highly qualified teachers in both courses.

Objective To assess the cardiovascular events after percutaneous transluminal coronary intervention (PCI) and the influence of fluvastatin on inflammation factors and prognosis of PCI patients.Methods One hundred and eighty-seven patients whose coronary stenosis ≥ 70% diagnosed through coronarography and underwent PCI from Jun.2005 to Feb.2008 were recruited in the current study.These patients were divided into two groups,the control group (n =91) was treated regularly and the treat group (n =96) was treated with additionally fluvastatin(40 mg/d).Fasting venous blood was obtained before and after medicine treatment,12,24 hours and two weeks after PCI.IL-18,IL-6 and TNF-α were measured through ELISA.Results Before medicine treatment,there were no difference of IL-18 ,IL-6 and TNF-α between the two groups( P ＞ 0.05 ).After medicine treatment,IL-18,TNF-α and IL-6 decreased significantly compared to those before treatment in both groups ( P ＜ 0.05 ),and these measurements decreased more in the treatment group ( P ＜ 0.01 ).At the 12th hours after PCI,IL-18,TNF-αand IL-6 in the control group increased to (423.5 ± 298.7 ),( 316.1 ± 72.6 ) and (42.3 ± 10.1 ) ng/L,respectively,and arrived the peak at the 24th hour,which were significantly higher than those before medicine treatment( P ＜ 0.01 ).In the treatment group,these measurements at the 12th and 24th hour after PCI were slightly higher than those before medicine treatment without significant difference ( P ＞ 0.05 ).After 12 hours ofPCI,IL- 18,TNF -αand IL-6were (276.5 ± 189.4 ),( 175.3 ± 51.9) and ( 10.1 ± 8.1 ) ng/L,which were significantly lower than those in the control group(P ＜ 0.01 ).Two weeks after PCI,IL-18,TNF-α and IL-6 in the treatment group were (137.0 ±34.2),(35.1 ± 21.6) and ( 8.7 ± 3.2 ) ng/L,which were significantly lower than before medicine treatment ( P ＜0.01 ).Conclusions PCI may aggravate the inflammation response of coronary artery.Statins may alleviate the inflammation response.IL-18,TNF-α and IL-6 are sensitive indices of early inflammation response after PCI,their changes might have prediction value for adverse cardiovascular events.Therefore these indices might be used as a target in the statins treatment in the primary prevention,as well as the evaluation of the effectiveness of PCI,statins and joint PCI and statins.

Objective To investigate the phenotypes and genotypes of a hereditary protein C(PC) deficiency pedigree.Methods Imrnunoassay(ELISA)was used for PC antigen and PS antigen; Immunoturbidimetry assay was used for measuring AT antigen;Chromogenic substrate assay was used for measuring the activity of PC,PS and AT in Sysmex 1500 automatic Blood Coagulation Analyzer.Polymerase chain reaction(PCR)for amplification of the fragment of each exon and side sequences of PC gene in 10 members of the 3 generations;Direct DNA sequencing was used to examine the mutation site.Results Among 10 members of the 3 generation pedigree,8 of them had a PC:Ag level of 1.06-1.92 mg/L(normal references 3.00-6.00 rag/L),the activity of PC was between 41% and 67%(normal references 70%- 140%),which was significantly lower than the normal references while the levels of PS:Ag,PS:A,AT:Ag and AT:A were all within normal range.DNA sequencing analysis showed that there was a G to T mutation in exon IX of the PC gene at 12 918 position in 8 members.This mutation resulted in the substitution of terminator TGA for TGG which encoding tryptophan at 372 amino acid.There was a polymorphism in 2 405C/ T,2 418A/G,2 583A/T in the promotor area.Conclusions This pedigree is a type I hereditary protein C deficiency.There is a G12 918T mutation in exon IX of PC gene.This mutation is reported for the first time and there is a polymorphism in 2 405C/T,2 418A/G,2 583A/T in the promotor area.

Objective To investigate clinically and in laboratory a genealogical tree with hemoglobin H disease Combining Hemoglobin Q-Thailand and Hemoglobin E Disease.Methods Genealogical laboratory studies were carried out with the following methods:hemoglobin electrophoresis, various biochemical determinations,and DNA analysis.Results Father's genotype of ?-THAL:??/?~Q ?~(4.2); genotype of ?-THAL:?E/N;phenotype:minor ?-THAL carrier combining Hb Q and Hb E multiple heterozygote;mother' s genotype of ct-THAL:--~(SEA)/??;genotype of ?-THAL:?n/?n.According to comprehensive analysis,mother's phenotype:minor ?-THAL,complex minor ?-THAL carrier combining Hb F ? Initial sign of ?-THAL genotype:--~(SEA)/?~Q ?~(4.2);phenotype:deletion type Hb H genotype disease;?- THAL genotype:?E/?E;phenotype:? E homozygote.According to comprehensive analysis:deletion type Hb H combining HbE multiple heterozygote.Youger brother's ?-THAL genotype:--~(SEA)/?~Q ?~(4.2);?-THAL genotype:?n/?n;phenotype:deletion type Hb H disease.Both mother and her youngest son have G6PD deficiency.Conclusions Guangdong Province is an area with high morbidity of ?-THAL and ?-THAL,Hb E and Hb Q as well as G6PD deficiency.There may be some correlation between Hb E and Fib Q in term's of the high morbidity of regional Hb,but the two types of Hb combining Hb H disease are rare in China and the world in point of nonhomologous chromosome.Attention should be paid to the problems of double heterozygote of ?-THAL complex ?-THAL,and THAL complex G6PD deficiency.Data from the study have enriched the scientific information of molecular genetics of erythroeyte thalassemia and of molecular pathology with important significance in genetics guidance and clinical treatment for patients.

A reliable UPLC-MS method was developed for the simultaneous determination of 4 chemicals (Sudan Ⅰ, tetrabromobisphenol A, tris ( 1, 3-dichloroisopropyl ) phosphate and tris ( chlorisopropyl ) Phosphate) in children products. The samples were ultrasonic extracted with acetonitrile, and then the four chemicals were separated on a C18 column in 3 min. Results showed that the limit of quantification of the method was between 5 and 500μg/kg. The calibration curves were linear within 2-3 orders of magnitude with typical correlation coefficient above 0 . 9995 . The recoveries ranged from 83 . 7% to 97 . 8% with three addition levels. The sensitivity, recovery and selectivity of the method could fully meet the requirements of practical work.

Objective To investigate the expression of water channel aquapoin-4 (AQP4) and its relationship to brain edema formation after status epilepticus (SE) in rats. Methods Fifty-four Sprague-Dawley rats (weighing 250～300 g) were randomly divided into 9 groups (n=6 in each group): the control group and the post-SE 6, 12, 24, 48, 72, 96, 120, 168 h groups. SE models were established with Lithium-pilocarpine. Immunohistochemistry and semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) were used to assess AQP4 protein and mRNA expression following SE. Results AQP4 expression significantly increased at 24 h, reached to a peak level at 48 h, lasted for 3 d and then began to decline, but still existed at day 7 (P＜0.05 vs control group). The time-dependent change displayed an obvious positive correlation with the process of brain edema after SE (r=0.73, P＜0.05).Conclusion The time-related change of AQP4 expression after SE has a positive correlation with brain edema, indicating that AQP4 may play an important role in the formation of brain edema following SE.

OBJECTIVETo study survivin expression in human hepatoma cells and the effects of survivin siRNA on the malignant phenotypes of human hepatocellular cell line HCCLM6.

METHODSFour hepatocellular carcinoma (HCC) cell lines were used. Semi-quantitative RT-PCR and Western blot were used to measure and compare their survivin expressions. The siRNA expression vector pshRNA-survivin targeting the mRNA of survivin and vector pGPU6/GFP/Neo-NC (as a control) were constructed, and then transfected into HCCLM6 cells. FQ-PCR was used to quantify the mRNA levels of survivin. The malignant phenotypes of transfected HCCLM6 cells, including invasive activities and adhesive capabilities, were analyzed.

RESULTSSurvivin expression gradually increased with the increase of the invasion and metastasis behaviors of the four HCC cell lines (P<0.05). The expression of survivin was highest in cell line HCCLM6. Survivin mRNA level was decreased by 93.500%+/-3.117% after the pshRNA-survivin transfection. The cell adhesion rates significantly decreased in the cells transfected with pshRNA-survivin (cell adhesion rates were 11.403%+/-1.256% vs 32.545%+/-1.367%, t=20.732, P<0.01). The migrating number of HCCLM6 cells (13.5+/-0.9) transfected with pshRNA-survivin was also significantly decreased (t=14.5, P<0.01) as compared with the control group (32.6+/-1.4).

CONCLUSIONThe expression of survivin in HCC might have a close relationship to their invasion and metastasis properties. Sequence-specific shRNA can significantly reduce the survivin expression in the HCCLM6 cell line. Suppression of survivin expression in HCCLM6 cells transfected with pshRNA-survivin can reduce their invasive and adhesive capabilities.

Cell Line, Tumor ; Humans ; Inhibitor of Apoptosis Proteins ; Liver Neoplasms ; genetics ; pathology ; Microtubule-Associated Proteins ; genetics ; RNA, Small Interfering

OBJECTIVETo establish a mouse model of abdominal aorta stenosis and analyze the alterations in the arterial wall response to high and low shear stress.

METHODSTwenty mouse were randomized equally into 4 groups, including 3 test groups (1, 7 and 14 day groups) with surgically induced stenosis of the abdominal aorta, and a sham-operated group without stenosis. The hemodynamics and the internal diameter of the blood vessel were measured by color Doppler flow imaging. The wall shear stress was calculated by Poiseiulle hydrodynamics formula (τ(m)=η×4×V(m)/D). Pathological examination and immunohistochemistry were performed to observe the arterial morphological changes and the endothelial vascular cell adhesion molecule-1 (VCAM-1) expression. The intimal-media thickness of the aorta was measured and endothelial VCAM-1 expression analyzed quantitatively.

RESULTSRegions of low and high flow shear stress were created upstream from the stenosis and within the stenosis, respectively. Compared with the sham-operated group, the mice with aorta stenosis showed gradually increased vascular intimal-media thickness and VCAM-1 expression intensity in the upstream aorta, but not within the regions of the stenosis.

CONCLUSIONVascular remodeling may occur shortly after exposure to low shear stress, which plays a significant role in initiation and progression of the pathological process of atherosclerosis mediated by VCAM-1, whereas high shear stress may exert an anti-atherosclerotic effect.

Animals ; Aorta, Abdominal ; metabolism ; pathology ; physiopathology ; Aortic Valve Stenosis ; physiopathology ; Atherosclerosis ; physiopathology ; Constriction ; Hemodynamics ; Male ; Mice ; Shear Strength ; physiology ; Stress, Mechanical ; Vascular Cell Adhesion Molecule-1 ; metabolism

AIMTo investigate the dynamic changes of Egr-1 expression in the lungs of acute pulmonary embolism of rats by infusion of autoblood thrombs.

METHODSThe model of pulmonary embolism by infusion of autoblood thrombs in the pulmonary artery of rats was established and the mean pulmonary arterial pressure was continuously monitored by computer, and the results were evaluated by lung perfusion scan and pathological changes. Expression of Egr-1 proteinum and mRNA were measured by immunohistochemistry and reverse transcription polymerase chain reaction.

RESULTSThe mPAP of rats was increased significantly after infusion of autoblood thrombs at the half hour, and reached high level at the second hour, then remained the high level to four hours compared with group control at the same time point (P < 0.01). ECT image was showed significantly filling defect after infusion of autoblood thrombs at the first hour. The infused thromb was witnessed by hematoxylin and eosin stain. In the tracheal epithelium cells, alveolar epithelium cells and vascular smooth muscle cells of embolism rats, Egr-1 protein expression was increased significantly after embolization at the second hour compared with group control at the same time point (P<0.01), and was decreased slowly at the fourth hour. Egr-1 mRNA expression was showed the similar changes.

CONCLUSIONExpression of Egr-1 was low level in group control, but increased significantly after infusion of autoblood thromb at the second hour in the specificity of cells, suggesting that Egr-1 expression might be an important link of pathological changes in the acute pulmonary embolism.

Animals ; Early Growth Response Protein 1 ; genetics ; metabolism ; Gene Expression ; Lung ; metabolism ; Male ; Pulmonary Embolism ; genetics ; metabolism ; pathology ; RNA, Messenger ; genetics ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo investigate the diversify of the nuclear pathway of c-Jun NH2-terminal kinases (JNK) during transient brain ischemia/reperfusion injury in hippocampal neuron apoptosis in spontaneously hypertensive rats (SHR) and to test whether the neuroprotection of curcumine on transient brain ischemia/reperfusion injury in SHR is related to the nuclear pathway of JNK.

METHODSMale Wistar-Kyoto (WKY) rats and SHR were randomly divided into five groups (n = 6): WKY sham group (W-Sham), WKY ischemia/reperfusion group (W-I/ R), SHR sham group (S-Sham), SHR ischemia/reperfusion group (S-I/R) and SHR curcumine (a chinese traditional medicine)100 mg/kg treatment group (S-Cur), which were sacrificed at 2 h, 6 h, 24 h, 3 d and 7 d after reperfusion. Global brain ischemic model was established by 4-VO method. The TdT-mediated dUTP nick end labeling (TUNEL) method was used to detect the neuron apoptosis in hippocampal CA1 region. The immunohistochemical method was applied to investigate the expressions of c-jun and c-fos in hippocampal CA1 region.

RESULTSThe expressions of apoptosis and c-jun and c-fos in CA1 region in S-Sham group, W-I/R group and S-I/R group were more than those in W-Sham group (P < 0.05), were significantly increased in S-I/R group than those in W-I/R group (P < 0.05), and were significantly decreased in S-Cur group than those in S-I/R group (P < 0.05).

CONCLUSIONNeuronal apoptosis and the expressions of c-jun and c-fos are more in SHR hippocampal. Global brain ischemia/reperfusion injury induces more expressions of apoptosis in hippocampal neuron in SHR, and the more expressions of c-jun and c-fos may participate in that process. The neuroprotection of curcumine in SHR is related to c-jun and c-fos.

Animals ; Apoptosis ; drug effects ; Brain Ischemia ; metabolism ; pathology ; CA1 Region, Hippocampal ; drug effects ; metabolism ; Curcumin ; pharmacology ; JNK Mitogen-Activated Protein Kinases ; metabolism ; Male ; Neurons ; drug effects ; metabolism ; Proto-Oncogene Proteins c-fos ; metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Reperfusion Injury ; metabolism ; pathology