Objective The purpose of this study was to determine if recombinant ?-defensin-2 can prevent the lung from being injured by pseudomonas aeruginosa infection. Methods Ten male SD rats ( class SPF) weighing 250-300 g were randomly divided into 2 groups ( n = 5 each) : I defensin group and II control group. The animals were anesthetized with intraperitoneal thiopental 10 mg? kg-1 and intubated. 50 ? l of 5 ? 107 PFU? ml-1 adenovirus with or without ?-defensin-2 gene was instilled into the trachea via tracheal tube. 48 h later 200 ? l of 6? 108 CFU?ml-1 pseudomonas aeruginosa ATCC27853 was instilled into the trachea in both groups. All the rats were killed after 24 h and the lungs were removed for (1) histologic examination, (2) determination of ICAM-1 expression in the lung and (3) broncho-alveolar lavage. The number of WBC and pseudomonas aeruginosa in broncho-alveolar lavage fluid (BALF) was counted. Results The number of WBC and pseudomonas aeruginosa in BALF was significantly less in defensin group than in control group. The degree of instologic damage and the expression of ICAM-1 in lung tissue were significantly decreased in the defensin group as compared with control group. Conclusion Recombinant ?-defensin-2 can kill pseudomonas aeruginosa in vivo and modulate the expression of ICAM-1. It can protect the lung against injury induced by pseudomonas aeruginosa infection.

"3+2" educational model was performed in our clinical medical college as a reformation based on traditional "4+1" model.After 5 years teaching practice,it obtained some good results as we prospected,however,there still exists some problems.This article analyzes the problems around the aspect of the teachers,the students,the teaching administration and arrangements,and proposes the corresponded measure to improve it.

A growing number of children and adolescents are being diagnosed as Chiari malformation type Ⅰ (CM-Ⅰ) for behavioral disorders,developmental delay,seizures,or abnormal orpharyngeal function.The aim of this study was to compare the clinical characteristics,imaging findings and surgical outcomes of CM-Ⅰ in pediatric and adult patients.Between January 2014 and June 2017,84 patients with CM-Ⅰ underwent surgical treatment in our department.We divided the patients into two groups:pediatric group (n=1 1,age ＜18 years)and adult group (n=73,age ≥18 years).Data on clinical characteristics,imaging findings,surgical outcomes,and prognosis were retrospectively reviewed and compared between these two groups.For clinical presentation,scoliosis (36.4％) and developmental delay (36.4％) were more common in pediatric patients,whereas,sensory disturbance (58.9％) and motor weakness (41.1％) were more common in adult patients.Imaging findings showed that the incidence of hydrocephalus and craniovertebral junctional abnormalities was significantly higher in pediatric group than in adult group (P＜0.05).Compared to adult group,pediatric group showed a better improvement or resolution of syrinx and tonsillar herniation after surgical treatments (P＜0.05).The total Chicago Chiari Outcome Scale (CCOS) score in pediatric patients at the last follow-up was significantly higher than that in adult patients (P=0.002).In conclusion,the clinical characteristics and imaging findings appeared to be different in pediatric and adult patients with CM-Ⅰ.The surgical outcomes of pediatric patients were shown to be significantly better than those of adult patients.

OBJECTIVETo assess the long-term clinical effectiveness of Chinese herbal medicines for benefiting qi and activating blood circulation (CHMBQABC) plus routine Western medical intervention in treating unstable angina (UA) patients of qi deficiency blood stasis syndrome (QDBSS) after percutaneous coronary intervention (PCI) based on Markov model.

METHODSA Markov model was established based on prognosis and sequelae of UA patients after PCI treated by CHMBQABC plus routine Western medical intervention or by routine Western medical intervention. According to the transition probabilities of 40 Markov cycles and quality-adjusted life years (QALYs) averagely gained, we assessed the therapeutic advantage of CHMBQABC plus routine Western medical intervention.

RESULTSBy the prediction of Markov model for 20 years, the transition probabilities of revascularization, non-fatal myocardial infarction, non-fatal stroke, and all-cause death in the CHMBQABC plus routine Western medical intervention group was 56.65%, 6.53%, 5.16%, and 31.66%, respectively, and the QALYs averagely gained was 12.95; while the transition probabilities of revascularization, non-fatal myocardial infarction, non-fatal stroke, and all-cause death in the Western medical intervention group was 55.31%, 6.87%, 5.25%, and 32.57%, respectively, and the QALYs averagely gained was 12.84. Compared with the Western medical intervention group, the QALYs averagely gained was 0.11 in the CHMBQABC plus routine Western medical intervention group.

CONCLUSIONBased on predicted results of the Markov model, CHMBQABC plus routine Western medical intervention got better efficacy in treating UA patients after PCI, indicating CHMBQABC plus routine Western medical intervention could improve the long-term clinical effectiveness for UA patients of QDBSS after PCI.

Aged ; Angina, Unstable ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Male ; Markov Chains ; Middle Aged ; Models, Theoretical ; Phytotherapy ; Treatment Outcome

Objective To identify differently expressed genes and pathways between Kashin-Beck disease (KBD) cartilage and healthy cartilage,and to explore the mechanism of articular cartilage lesions of KBD.Methods Cartilage specimens were collected from 9 patients with KBD and 9 healthy controls.Total RNA was extracted from cartilage specimens,and transcribed into cDNA.KBD and control groups were labeled by Cy3 and Cy5,respectively.Agilent genome-wide microarray was applied to compare the expression profile of KBD cartilage and healthy cartilage.The microarray data was analyzed by single gene and pathway expression analysis to identify differently expressed genes and pathways between KBD and healthy controls.Results ①Tweenty nine genes were significantly up-regulated in KBD group (averaged ratio =6.68 + 1.98,P ＜ 0.05),mainly involved in apoptosis,metabolism,extracellular matrix,cytoskeleton and cell movement.Additionally,extracellular matrix-related FBLN1 gene was down-regulated in KBD group(ratio =0.14 + 0.06,P ＜ 0.05).②Five apoptosis and 6 hypoxia-related pathways presented higher expression levels in KBD compared to healthy controls(all P＜ 0.05).Conclusions We find significant expression differences of apoptosis and hypoxia-related genes and pathways between KBD cartilages and healthy cartilages,suggesting that hypoxia might contribute to chondrocytes apoptosis of KBD.Further studies may be needed to investigate the relationship between hypoxia and articular cartilage lesions of KBD.

Objective To compare the expression profile of mycotoxin-related environmental response genes (MERGs) in the articular cartilage of patients with Kashin-Beck disease (KBD) and healthy controls,and explore the relationship between MERG and KBD.Methods Articular cartilage specimens were collected from 9 healthy human subjects and 9 adult KBD patients.Agilent microarray was used to evaluate the expression levels of MERG in cartilage specimens,and the expression ratios of MERG between KBD and healthy controls were calculated.GSEA software was used to calculate the NES scores and P values of gene ontology(GO).Results ①T-2 toxin,deoxynivalenol,zearalenone,aflatoxin B1,fumonisin B1 and ochratoxin A related 15 MERGs presented expression differences between KBD and healthy controls(ratios ＞ 2.0 or ＜ 0.5).Thirteen MERGs were up-regulated in KBD,including BAX,BCL2,COL5A2,FER1L3,GSTT2,IGFBP2,IGFBP4,PDE8B,SOCS3,THBS1,TMSL8,VGLL3 and TUBB2A (ratio ＞ 2.0).Two MERGs,POSTN and FABP4,were down-regulated in KBD (ratio ＜ 0.5).The 15 MERGs were involved in various biological processes; such as collage synthesis,apoptosis,metabolism,growth & development and so on.②Mycotoxin related 4 apoptosis GOs and 5 growth & development related GOs were up-regulated in KBD compared to healthy controls(NES ＞ 0),including ANTI_APOPTOSIS,REGULATION_OF_PROGRAMMED_CELL_DEATH,APOPTOSIS_GO,REGULATION_OF_APOPTOSIS,ORGAN_MORPHOGENESIS,ANATOMICAL_STRUCTURE_DEVELOPMENT,ORGAN_DEVELOPMENT,SYSTEM_DEVELOPMENT and REGULATION OF DEVELOPMENTAL_PROCESS (NES ＞ 0 and P ＜ 0.05).Conclusions There are multiple mycotoxins related environmental response genes presenting significant expression difference between KBD cartilage and normal cartilage.Mycotoxin can affect the expression of MERGs in KBD articular cartilage,which might lead to dysfunction of chondrocytes,and articular cartilage lesions.

Panax quinquefolium L., also named American ginseng, is a valuable tonic medicine. Because of its main active ingredient ginsenoside's extensive biological effects, researches on the Panax quinquefolius saponin have important clinical and scientific value. Its basic components, bioactivities, cardiovascular effects and mechanisms will be covered in this paper.
Animals ; Cardiovascular System ; drug effects ; Humans ; Saponins ; pharmacology

Objective To investigate the mechanism of endotoxin tolerance (ETT) through observing the expression of OX40 in liver tissues of ETT rats.Methods SD male rats were randomly divided into three groups:normal group (n=6),acute liver failure (ALF) group (n=24) and ETT group (n=24).Lipopolysacharide (LPS) 0.1 mg/kg (ETT groups) or 0.9 ％NaC1 (ALF groups) was administered by five consecutive intraperitoneal injections at 24 h intervals,and at the sixth day,all animals were treated with intraperitoneal injections of D-galactosamine (D-GalN) 800 mg/kg and LPS 8 μg/rat.Blood and liver tissue were collected at 6,12,24 and 48 hours after the injection of D-GalN/LPS.The gene expression of OX40 in the liver was measured by reverse transcription-polymerase chain reaction (RT-PCR).The protein expression of OX40 was estimated by Western blot.The tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels were determined by enzyme-linked immunosorbent assay (ELISA).The data analysis was performed by one-way ANOVA,lease significant difference (LSD) and Dunnett's T3 test.Results The expressions of TNF α and IL-6 were both significantly lower in ETT group compared to ALF group,but still higher than that of control group.The gene expressions of OX40 peaked at 12 hours and decreased gradually in ALF group.The gene expressions of OX40 were significantly lower in ETT group compared to ALF group (6 h:F=5.027,24 h:F=5.539,48 h:F=5.011,all P＜0.05; 12 h:F=36.688; P＜0.01),but still higher than that of normal group.The tendency of OX40 protein expression in ALF group was peaked at 12 hours and decreased at 24 hours.In ETT group,the expression of OX40 was lower,and the difference between ETT group and ALF group had statistical significance (6 h:F=8.658,P＜0.05; 12 h:F=34.611,24 h:F=28.176,48 h:F=16.747; all P＜0.01).Conclusions The level of OX40 is increased in ALF group,while the expressions of OX40,TNF-α and IL-6 are lower in ETT group,which suggested that OX40 may play an important role in the process of ETT.

Objective To study the effect of endotoxin tolerance (ETT) on chemokine receptor 7 (CXCR7) in the liver tissue of rats with acute liver failure (ALF).Methods SD male rats were randomly divided into three groups:normal group,ALF group and ETT group.The rats in the ETT group and ALF group were injected with lipopolysacharide (LPS) 0.1 mg/kg or saline respectively,one time / day for 5 days.At 24 hours after the 5th-day injection,all rats were injected with D-GalN 800 mg/kg and LPS 8μg/rat.Blood sample and liver tissue were collected on 2,6,12,24 and 48 hours after injection.The gene expressions of CXCR7 in the liver were measured by RT-PCR,and the protein expressions of CXCR7 were determined by Western Blot.The data analysis was performed by LSD,Dunnett's t test.Results The histological damage in the liver tissue was significantly mider in ETT group compared to ALF group.The gene expressions of CXCR7 were significantly milder in ETT group compared to ALF group (2 h:F =29.222,6 h:F=166.892,12 h:F=38.975,24h:F=34.603,48 h:F=18.929,allP＜0.01),but still severer than that of normal group.The CXCR7 protein expression in ALF group and ETT group peaked at 24 hours,but the expression of CXCR7 in ETT group was lower compared with that in in ALF group (2h:F=11.155,6 h:F=42.553,12h:F=17.082,all P＜0.01; 24 h:F=7.242,P＜0.05).Conclusions During the process of endotoxin tolerance,LPS pretreatment and D-GalN can decrease the liver injury,down-regulate the expressions of CXCR7mRNA and CXCR7.This suggests that CXCR7 may play an important role in the ETT.

AIM: To establish a arsenic trioxide (As 2O 3 )-resistant leukemic cell line to explore the mechanism of resistance to As 2O 3, and the relationship between the resistant cell line and the multidrug resistance was also investigated. METHODS: The arsenic trioxide (As 2O 3 )-resistant leukemic cell line was established by exposing the cells to the increasing concentration of As 2O 3. MTT assay was used to detect the cytotoxicity. Cell cycle was detected by PI assay. Flow Cytometry was used to detect the P-glycoprotein on the surface of the cells, the intracellular concentration of DNR, and the immuetype of the cells. RESULTS: The cell doublings time and the cell cycle of the arsenic trioxide (As 2O 3 )-resistant leukemic cell line, K562/AS2, is similar to that of K562. The relative resistant fold of K562/AS2 to As 2O 3, DNR, VP16 and Ara-C was 7.4, 2.9, 3.8 and 1.1, respectively. The relative resistant fold of multidrug resistant cell line, K562/ A02, to As 2O 3, DNR, VP16 and Ara-C was 0.8?94?2.5 and 0.9, respectively. The fluorescence of the P-glycoprotein on the surface or of the DNR inside the cells detected was not significantly different between the K562 and the K562/AS2 cell lines. CONCLUSIONS: A cell line, K562/AS2, resistant to clinical achieving level (2 ?mol/L) of As 2O 3 has been established. The relative resistant fold of K562/ AS2 to As 2O 3 is about 7.4 fold to the parent K562 line sensitive to As 2O 3. Partial resistance of K562/AS2 to DNR and VP16 is observed , the mechanism of which is unrelated to the P-gp, the expression product of multidrug resistance gene 1 (mdr1).