Objective To investigate the expression of macrophage migration inhibition factor (MIF) in pulmonary tissues of the smokers with and without chronic obstructive pulmonary disease (COPD).Methods The subjects were assigned into three groups:non-smokers without COPD (control group,n =12),smokers without COPD (smoker group,n =13) and smokers with COPD (COPD group,n =16).The specimens were obtained from lung tissues as far away from cancer focus as possible (＞ 5cm).Real-time quantitative PCR and immunohistochemistry were used to investigate the expression and distribution of MIF in pulmonary tissues.The relationship between the severity of airflow obstruction and the differential expressions of MIF in lung tissues of the smokers with or without COPD was analyzed.Results (1) MIF mRNA expression in COPD group (4.87 ± 1.79) was higher than that in the smoker group (2.16 ±0.72;P＜0.01),which was higher than that in the control group (1.09 ±0.48;P ＜0.01).(2)Immunohistochemistry analysis showed that MIF protein expression in lung tissues of the COPD group (0.277±0.025) was higher than that in the smokers group (0.199 ±0.034;P ＜0.01),which was significantly higher than that in control group (0.130 ±0.021 ;P ＜0.01).(3) Correlation analysis of MIF mRNA expression in the lung tissues and pulmonary function parameters of forced expired volume in one second (FEV1) percentage of predicted (FEV1 pred) and ratio of FEV1 to forced vital capacity (FEV1/FVC) suggested that MIF mRNA expression in the lung tissues was negatively related with FEV1 pred (r=-0.578,P ＜ 0.01) and FEV1/FVC (r =-0.607,P ＜ 0.01).Conclusions MIF expression significantly increases in the smokers with COPD,and MIF level in the lung is positively correlated with airflow limitation.The results suggest that MIF may play an important role in the pathogenesis of smokinginduced COPD.

AIM: To investigate the role of nuclear factor kappa B (NF-?B) inhibitor in the responsiveness of isolated pulmonary artery rings to protein kinase C (PKC) in rats with hypoxia-induced pulmonary hypertension. METHODS: The pulmonary artery rings removed endothelium were prepared from model rats with hypoxia-induced pulmonary hypertension and control rats. The effects of PKC activator PMA (0.5 ?mol/L) time-response cures and NF-?B inhibitor PDTC (0- 1 000 ?mol/L) concentration-response cures on pulmonary artery rings were observed. The responsiveness of each ring was tested by applying a maximally effective concentration of phenylephrine (10 ?mol/L). Data were calculated as relative ratio by the maximally responseness ( P_0 ) setting at 100%,and the relative responseness tensions to PMA and PDTC were derived by dividing by the counts in P_0. t_ 1/2 and T show the time achieving half-maximal response and lasting maxima response to 0.5 ?mol/L PMA,respectively. RESULTS: mPAP and RV/(LV+S) in hypoxia group were greater than those in control group ( P

AIM: To investigate DNA damage and cell stress (heat shock protein 70 expression) in human bronchi smooth muscle cells by cigarette smoke extract (CSE) in vitro. METHODS: 30 mL smog was dissolved in 1 mL culture medium as stock solution of CSE. Human bronchi smooth muscle cells were cultured 3 hours with 1∶16, 1∶10, 1∶8, 1∶6 and 1∶4 of CSE. The DNA damage and HSP70 expression were determined by single cell gel assay (comet assay) and Western blot, respectively. RESULTS: Associated with rising CSE concentration, DNA damage aggravated. Compared with the untreated group, except 1∶16 of CSE, the level of DNA damage was significantly different (P

In order to investigate whether polymorphism in gene for heat shock protein 70 (HSP70) has any bearing on individual susceptibility to the development of chronic obstructive pulmonary disease (COPD), the geotypes of 88 patients with COPD and 87 healthy smoking control subjects were tested by polymerase chain reaction followed by restriction fragment polymorphism analysis for HSP70 gene. In COPD group, HSP70-1 genotype A/A, A/B and B/B was 59.1%, 35.2% and 5.7%, HSP70-2 genotype A/A, A/B and B/B was 26.1%, 54.6% and 19.3%, and HSP70-hom genotype A/A, A/B and B/B was 70.4%, 27.3% and 2.3% respectively. In the control group, it was 60.9%, 27.5% and 3.5%, 20.7%, 56.3% and 23.0%, and 54.0%, 42.5% and 3.5%, respectively. The frequency of polymorphic genetypes showed no difference between the COPD group and the control group (P>0.05). It was suggested that geneic polymorphism in HSP70 is not associated with development of COPD in Han nationality of China.
China/ethnology ; Ethnic Groups ; Genetic Predisposition to Disease/*genetics ; HSP70 Heat-Shock Proteins/*genetics ; *Polymorphism, Restriction Fragment Length ; Pulmonary Disease, Chronic Obstructive/*genetics ; Smoking

To investigate the effect of cigarette smoke extract (CSE) on the role of protein kinase C (PKC) in the proliferation of passively sensitized human airway smooth muscle cells (HASMCs). After synchronization of cultured HASMCs, they were divided into a group A and Group B. The group A was treated with normal human serum and served as controls and the group B was treated with the serum of asthma patients. The group A was further divided into group of A1, A2 and A3 and the group B was sub-divided into the group of B1, B2, B3, B4 and B5. No other agents were added to the group A1 and B1. The cells of group A2 and B2 were stimulated with 5% CSE for 24 h. HASMCs from group A3 and B3 were treated with PKC agonist PMA (10 nmol/L) and CSE (5%) for 24 h. PKC inhibitor Ro-31-8220 (5 micromol/L) was added to the HASMCs of group B4 for 24 h. The cells from group B5 were stimulated with Ro-31-8220 (5 micromol/L) and CSE (5 %) for 24 h. The proliferation of HASMCs isolated from group A and B was examined by cell cycle analysis, MTT colorimetric assay and 3H-TdR incorporation test. The expression of PKC-a in each group was observed by Western blotting and RT-PCR, respectively. The results showed that the percentage of S phase, absorbance (A) value, the rate of 3H-TdR incorporation, the ratios of A value of PKC-alpha mRNA and the A value of PKC-alpha protein in HASMCs from group B1, B2 and B3 were significantly increased compared to those of group A1, A2 and A3 correspondingly and respectively (P< 0.01). The proliferation of HASMCs of group A2 and B2 stimulated with CSE and group A3 and B3 stimulated with CSE and PMA were also significantly enhanced when group A1, A2 and A3 and group B1, B2 and B3 compared to each other (P<0.05, P<0.01, respectively). The percentage of S phase, absorbency (A) value, 3H-TdR incorporation rate, the ratios of A value of PKC-alpha mRNA and the A value of PKC-alpha protein in HASMCs from group B4 treated with Ro-31-8220 and group B5 treated with CSE and Ro-31-8220 were significantly decreased as compared to those of group B1 and B2 correspondingly and respectively (P<0.05, P<0.01). It was concluded that CSE can enhance the passively sensitized HASMC proliferation and the expression of PKC alpha. PKC and its alpha subtype may contribute to this process. Our results suggest cigarette may play an important role in ASMCs proliferation of asthma through PKC signal pathway.
Asthma/*blood ; Bronchi/cytology ; Bronchi/metabolism ; Cell Cycle/drug effects ; Cell Proliferation ; Cells, Cultured ; Culture Media ; Myocytes, Smooth Muscle/*cytology ; Myocytes, Smooth Muscle/enzymology ; Protein Kinase C/biosynthesis ; Protein Kinase C/*physiology ; Serum ; Signal Transduction ; Tobacco/adverse effects ; Tobacco Smoke Pollution/*adverse effects

As the research work went further and more detailed, a variety of new treatments compete to come out.However, it remains unclear that how the antigen works to distinguish cancer cells and normal cells.Neoantigen, which is located in the tumor cell surface of a specific antigen, its presence makes human immunotherapy into new areas which may make personalized treatment possible in the near future.Emerging data suggest that the identification of such newantigens is a major factor in clinical immunotherapy.They can form a biomarker in cancer immunotherapy to provide targets for a variety of therapeutic approaches to attack, which allows T cells to selectively enhance the immune response against this class of antigens.

American medical colleges attach great importance to the humanistic education.The rich humanities curriculum is fully integrated into the teaching practice thus the mutual penetration of medicine and the humanities is achieved.They have specific and detailed examination evaluation system and the teaching method was more practical and participatory.By contrast,nost of the medical colleges in our country neglect the humanities construction and the cultivation of medical students' humanistic spirit.The coverage of the humanities curriculum is relatively narrow and the faculty is insufficient.We should promote the development of humanistic cducation,attach importance to the construction of medical humanities,set up appropriate curriculum system,increase the investment in faculty and reform the teaching method and examination method.

Objective To assess the correlation of serum 25-hydroxyvitamin D (25-OHD) levels with vitamin D-binding protein (the group-specific component,GC) gene polymorphism in chronic obstructive pulmonary disease (COPD).Methods In a cross-sectional case-control study,250participants,including 116 COPD patients with smoking history and 134 healthy smokers,were investigated.A questionnaire about smoking history,vitamin D intake and comorbidities was collected.General pulmonary function was done by routine.Serum 25-OHD levels were detected by ELISA.The genetic variants (rs4588and rs7041) were genotyped by real time fluorescence polymerase chain reaction (RT-PCR) with TaqMan probe technology.Results The COPD patients had lower serum vitamin D level than the smoker subjects (36.58 nmol/L vs 43.80 nmol/L,P ＜0.001).In the COPD patients,vitamin D level was 39.43 nmol/L in those with percentage of predicted forced expiratory volume in 1 second (FEV1 ％ pred) greater than or equal to 80％.In other groups with FEV1 ％ pred 50％-80％,30％-50％ and lower than 30％,vitamin D levels were 35.32 nmol/L,32.21 nmol/L,26.25 nmol/L respectively (P ＜ 0.01).Moreover,there was a significant relevance of 25-OHD levels with FEV1 ％ pred in both COPD patients and healthy smokers (r2 =1.911; P ＜0.000 1).The mean 25-OHD concentration had a negative correlation with Global Initiative for Obstructive Lung Disease (GOLD) stages.Homozygous carriers of vitamin D-binding protein gene rs7041 T allele were independently related to 25-OHD levels and susceptibility of COPD (P ＜ 0.01 ; OR =2.140,95％ CI 1.157-3.959,P =0.015 respectively).Conclusions Patients with COPD are at high risk of vitamin D deficiency and the severity of COPD is inversely correlated with vitamin D levels.Furthermore,homozygous carrier of rs7041 T allele influences 25-OHD serum levels and is related to susceptibility of COPD,which may be a potential candidate gene for screening COPD.

Objective To explore the effects of Sodium Nitroprusside(SNP) on apoptosis of airway smooth muscle cells(ASMCs) of asthmatic rats in vitro.Methods Ten Wister rats were selected to make the models of asthma.The effect of SNP on the survival rate of asthmatic rat airway smooth muscle cells was detected by MTT method.The apoptosis of cells was detected by TUNEL method and flow cytometry.Results Comparing with asthma group,the survival rate of ASMCs was decreased significantly in SNP plus asthma group by MTT method(P

AIM: To study the effect of cigarette smoke medium(CSM) on the gene expression and activity of gelatinases from alveolar macrophages(AMs) in the rat,and then to explore their role in the pathogenesis of chronic obstructive pulmonary disease(COPD).METHODS: AMs were obtained from BALF of the rats that had smoked for 12 weeks.CSM was produced following the method of Wirtz and colleagues,and the cultured AMs were respectively stimulated for 24 h by 0%,1%,3%,5%,10%, 15% CSM.The mRNA levels of MMP-9 and MMP-2 were detected by semi-quantitative RT-PCR,and the enzyme activity was measured by Zymography.RESULTS: When the concentration of CSM was below 5%,the expression and activity of MMP-9 and MMP-2 signficantly increased with the concentration of CSM in a dose-depended manner(P