Adult ; Anaphylaxis ; etiology ; Female ; Humans ; Male ; Semen ; immunology

Objective To screen and identify protein interacted with enterovirus 71 (EV71)3A protein by means of T7-phage display system.Methods The prokaryotic expression vector of 3A protein was constructed for expressing and purifying 3A pro-tein.With 3A protein as the target protein,the T7-phage display system was adopted to screen the human hepatocyte cDNA library. The screened products were performed the DNA sequence analysis and the homologous research.Results 3A protein was expressed and purified,after 4 rounds of biopanning,37 positive clones were selected.The inserted fragments were amplified by PCR using specific T7 primer.The products were sequenced,2 proteins were identified to interact with 3A protein by homologous analysis. Conclusion Trough the T7 phage display system,two proteins interacted with 3A are obtained.The possible function of 3A protein can be speculated by researching the function of these two proteins,which lays the foundation for the further studying the pathogen-ic mechanism of EV71.

Objective To explore the animal model making method for diarrhea-predominant irritable bowel syndrome (IBS-D) caused by the disharmony of liver and spleen in TCM.Methods In order to define the period of the animal model making,the 32 neonatal rats were divided into 3 days group,6 days group,9 days group and control group.In order to determine the weight of the experimental rats,the 48 rats with different weight were divided into lower weight model group,lower weight control group,medium weight model group,medium weight control group,higher weight model group and higher weight control group.In order to decide the method of causing diarrhea,the 32 rats were divided into lactose enriched diet group,restraint stress group,lactose enriched diet plus restraint stress group,and a control group.The body weight and diarrhea rate of all groups were compared respectively.After the method of model making was decided,the 16 rats were divided into a model group and a control group,and 5-hydroxytryptamin (5-HT),lactate dehydrogenase (LDH) and aquaporin 4 (AQP4) of the two groups were compared for model-proving.Results Based on the results step by step,the best method was decided:the period of the animal model making was 6 days,rats with higher body weight should be subjects,and the lactose enriched diet combining with restraint stress should be used to induce diarrhea.Model-proving test:compared with the control group,5-HT and LDH decreased (P

Child ; Cough ; chemically induced ; Disinfectants ; adverse effects ; Humans ; Irritants ; adverse effects ; Male

Objective: This study was undertaken to access the impact of hyperthermic chemotherapy (HTCT) on human gastric cancer cells in vitro. Methods: Six human gastric cancer cell lines (AGS, MKN45, SGC7901, NCI-N87, SNU-1 and SNU-16) and gastric cancer cells originated from clinical patients were used in this study. Treatment conditions were categorized into 4 modes: normothermic control (NT, 37°C), hyperthermia (HT, 43°C), normothermic chemotherapy (NTCT) and HTCT. The cells were treated with different concentrations of cis-diammine dichloroplatinum (CDDP, 0 to 32 mg/L) in combination with hyperthermia for 2 h. MTT assay was adopted to evaluate cell proliferation and cytotoxicity after HTCT. Preliminary morphological changes were observed under light microscope (LM) while ultrastructure changes and the definite cell death type were determined by transmission electron microscopy (TEM) and fluorescent microscopy (FM). The quantitative ratio of apoptosis and necrosis was determined by Annexin V-FITC and PI double staining using flow cytometry (FCM). Results: According to MTT assay and LM observation, there was a synergistic effect between hyperthermia and chemotherapy in inhibiting proliferation of the different types of gastric cancer cells. Hyperthermia enhanced the sensitivity of gastric cancer cells to CDDP chemotherapy. The concentration of CDDP required for inhibiting cell proliferation and inducing cell death was much lower in HTCT group than that of NTCT group. TEM and FCM examination showed that HTCT induced both apoptosis and necrosis of AGS and SNU-1 cells and apoptosis was the major type of cell death. Conclusion: There exists significant synergistic effect between hyperthermia and chemotherapy in inhibiting the proliferation of gastric cancer cells. Hyperthermia enhances the sensitivity of gastric cancer cells to chemotherapy. HTCT induces two patterns of cell death, apoptosis and necrosis, in gastric cancer cells. Apoptosis was the major type of cell death.

One of the major responsibilities for medical students is to save lives and to popularize emergency medical treatment knowledge for the masses of society.Based on research analysis,systemic training of cardiopulmonary resuscitation program including lectures,simulation education and social practice were performed for medical students.After practice activities,these students could proficiently apply the basic knowledge and skills of cardiopulmonary resuscitation in practical work and spread what they have learned to the public.Furthermore the program could improve students' abilities in social practice and team spirit and it is of great social significance.

Objective To investigate the effects of soluble CD40 ligand combined with LY294002,a specific inhibitor of phosphatidylinositol 3-kinase,on proliferation and invasion of gastric cancer cells (AGS ) and its potential mechanisms. Methods The effect of gradient concentration of sCD40L and its combination with LY294002 on cellular proliferation was determined using MTT assay. The ability of cellular invasion and migration was evaluated by wound healing and Transwell invasion assay. The protein expression of PI3K, p-Akt and vascular endothelia growth factor (VEGF) was tested by Western blotting. Results The inhibitory effect of cellular proliferation in sCD40L, LY294002 and sCD40L + LY294002 groups was 70. 1%, 65. 7% and 41. 3%, respectively, with significant difference (P<0. 05). And wound healing was also delayed in cells treated with sCD40L plus LY294002 when compared with those treated with sCD40L or LY294002. These results indicated that the inhibitory effect of cellular proliferation, migration and invasion was enhanced when cells were treated with sCD40L plus LY294002. The protein expression of PI3K,p-Akt and VEGF increased in cells treated with sCD40L, but reduced drastically in cells treated with sCD40L plus LY294002. Conclusion Inhibiting PI3K/Akt signaling pathway may enhance the inhibitory effect of proliferation, migration and invasion by sCD40L on AGS cells, which provide a new way for biochemical therapy of gastric cancer.

It is usually a challenge to repair the abdominal wall defect to general surgeons. With developing of materials science, the use of mesh provides a novel method of primary closure of abdominal wall defects in this set-ting. Recently , biological mesh has been reported to reconstruct abdominal wall successfully. This review is to in-troduce the recent status and progress on its biological characteristics,animal experiments and clinical Study.

High mobility group box chromosomal protein (HMGB1), an abundant eukaryotic nonhistone chromosomal protein, is previously known as a nuclear DNA-binding protein that stabilizes the structure and function of chromatin, regulates gene transcription. Recent studies identify that extracellular HMGB1 as a late mediator of endotoxemia and sepsis.HMGB1 is released by activated macrophages,induces the release of other proinflammatory mediators,and mediates lethality when overexpressed. It may also be a key signal for eliciting immune responses to cellular injury and death.Moreover,the late kinetics of HMGB1,in compared with other proinflammatory cytokines such as TNF and IL-1,suggest that targeting HMGB1 may provide a wide and clinically accessible therapeutic window.Three independent strategies to inhibit HMGB1 release and action are now available:anti-HMGB1 antibodies,A box,and ethyl pyruvate. This review covers the general features of HMGB1 and progress in research on its newly role as a cytokine participating in the development of sepsis.

Objective To study the mutations of Pseudomonas aeruginosa oprD gene in Imipenem-resistant clinical isolates. Methods Random amplified polymorphic DNA typing(RAPD) was carried out to analyse the homology in 10 Imipenem-resistant clinical isolates. Pseudomonas aeruginosa oprD gene in 10 Imipenem-resistant clinical isolates were amplified by polymerase chain reaction and sequenced. Results Ten Imipenem-resistant clinical isolates were divided into four different clones which can not produce metallo ?-lactamase. As compared with sequence X63152, oprD gene of Pseudomonas aeruginosa varied greatly. The aberration rates exceed 50%. There were multiple point mutations within 276～387 bp coding region of 30, 11, 9, 20, 31 strains. Due to the mutations of 308 bp G→C and 344 bp C→A, threonine and diaminocaproic acid were replaced by serine and threonine respectively. The DNA deletion of 393～412 bp in oprD gene contributes to the frame shift mutation in the following nucleotide sequence. The deletion of 264～273 bp in the coding region of oprD gene in 13 and 21 clone strains leads to frame shift mutations forming terminal codon TAA(319～321 bp).Base substitutions and multiple point mutations were obvious in the coding regions of 1 and 22 clone strains. Their aberration rates were 54.03% and 74.89% respectively. Conclusions The mutations of Pseudomonas aeruginosa oprD gene in Imipenem-resistant clinical isolates are various.