Objective To evaluate the effectiveness and prospect of innovative interactive follow-up mode for rehabilitation ofpostopera-tive breast cancer patietns in new medical environment. Methods The novel patient-centered medical care was promoted,and Pink Ribbon Clubs was established in different regions. Meanwhile,the patients’ self-support groups were formed, and a specialist for out-patients follow-up of outpatients by telephone or on the internet was arranged to provide psychological assessment,with timely and effective response. All data concerning to the follow-up were recorded and the patients were required to complete the relevant questionnaires. Results Compared with the same period in 2013,the follow-up rate was significantly increased to 80. 25%,and the patients showed higher satisfaction. The incidence of lymphedema in the patients was significantly reduced from 13% in 2013 to 7%. The quality of life was significantly improved and self-rat-ing score on depression was decreased from (51. 90 ± 8. 55) to (35. 81 ± 6. 21). Conclusion The kind of“Trinity” interactive mode is an effective follow-up mode with the clinical benefit in patients’ rehabilitation of physical and mental health,which is worthy of further applica-tion.

OBJECTIVETo study the metastasis-associated molecules differentially expressed in highly and poorly metastatic sublines and the mechanism of metastasis in lung giant cell carcinoma.

METHODSHighly and poorly metastatic sublines (PLA801D and PLA801C)were used as metastasis model. Cell motility and invasion assay in vitro were first compared between the two sublines. Then, gelatin zymography analysis was used to determine the MMP-2 and MMP-9 activity. The protein expression level of secreted MMP-2, MMP-9, TIMP-1, TIMP-2 and intracellular expression level of p53, p16, PCNA, CD44(V6) isomeride, E-cadherin, CK18, nm23-H1 as well as the mRNA expression level of MMP-2, MMP-9, TIMP-1, TIMP-2, VEGF were compared through Western blot. Semi-quantitative RT-PCR analysis was used to determine the intracellular mRNA expression of MMP-2, MMP-9, TIMP-1, TIMP-2 and VEGF.

RESULTSThe in vitro cell invasion potential of highly metastatic subline PLA801D was significantly higher than that of poorly metastatic subline PLA801C by about 4 folds, while the cell motility potential was similar. The secreted MMP-2 activity was notably higher in PLA801D, which was initiated by the higher expression of MMP-2 at protein and mRNA level. In addition, the expression level of p53, PCNA, CK18 protein and VEGF mRNA were significantly higher, while the expression level of p16, E-cadherin and nm23-H1 protein were significantly lower in PLA801D. Some molecules such as MMP-9, TIMP-1, TIMP-2, CD44(V6) isomeride, which had been reported to be associated with tumor metastasis, were not observed to change significantly between the two sublines.

CONCLUSIONThere are significant differences in metastatic potential and phenotypes between highly and poorly metastatic sublines of lung giant cell carcinoma. Some differentially expressed molecules might be playing roles in promoting or inhibiting metastasis of lung giant cell carcinoma, which may be useful to elucidate the mechanism of metastasis.

Carcinoma, Giant Cell ; metabolism ; pathology ; Cell Line, Tumor ; Humans ; Interleukin-8 ; genetics ; Lung Neoplasms ; metabolism ; pathology ; Matrix Metalloproteinase 2 ; genetics ; metabolism ; Matrix Metalloproteinase 9 ; genetics ; metabolism ; Neoplasm Invasiveness ; Neoplasm Metastasis ; RNA, Messenger ; analysis ; Tissue Inhibitor of Metalloproteinase-1 ; analysis ; Vascular Endothelial Growth Factor A ; genetics

Objective To assess the efficacy of two antibiotic prophylactic regimens in a prospective randomized trial in 1 year for patients undergoing insertion of catheters,and to provide the evidence for uniform consensus existing on the timing,route,and choice of antibiotic.Methods During a period of 12 months,78 patients,who consecutively entered the peritoneal dialysis programme,[45 women and 33 men,mean age (48.2?15.7)years] were included.The prophylactic regimens were a single dose of ceftriaxone (1.0 g) given intravenously 30 minutes before surgery (Group A) and given cefazolin (0.25 g/L) i.p.in the each dialysis bag for 3 days postoperatively (Group B).All operations were performed in one room.The wound was observed every day,and body temperature,Count of white blood corpuscle and type,dialysate were examined every day. Results In Group A and B,none of the patients showed peritonitis or wound infection during the post-operative period (within 10 days).One of 39 patients(2.5%) in the group A,and 2 of 39 patients (5.1%) in the group B had exit site infection (P＞0.05).Conclusions There is no significant difference in the incidence of peritonitis and wound infection between two groups. Prophylactic preoperative single-dose antibiotics intravenously do as well as antibiotics given intraperitoneally for peritoneal dialysis catheter insertion,but is much more convenient.

Objective To investigate the characteristics of infecting pathogens,their changes and antimicrobial susceptibilities on CAPD related peritonitis in our peritoneal dialysis(PD) center in the past 15 years.Methods Two hundred and six CAPD related peritonitis episodes in 145 patients from 2000 to 2005 were analyzed and compared with 109 episodes from 1991 to 2000.The causative pathogens,their antimicrobial susceptibilities and outcomes on CAPD related peritonitis from the two periods were retrospectively reviewed and compared.Results Culture negative rate decreased from 60.6% in 1990 s to 47.6% in the last five years (P=0.031 ).Among culture positive peritonitis episodes,the incidence of gram positive bacteria (GPB) peritonitis increased from 25.6% to 39.8% (P=0.059).This was mainly due to a significant increase in coagulase-neagative staphylococcus peritonitis,which significantly increased from 4.7% to 26.9% (P=0.01).Gram negative bacteria (GNB) peritonitis decreased slightly (44.2% vs 34.3%,P=0.322).The incidence of Klebsiella pneumoniae peritonitis significantly decreased (14.0% vs 3.7%,P=0.023),while Pseudomonas aeruginosa and Escherichis coli peritonitis rates slightly increased (4.7% vs 9.3%,P = 0.338;7% vs 18.7%,P=0.072).The decrease of fungal peritonitis rate was not significant (30.2% vs 17.6%,P= 0.123).The comparison of clinical outcomes showed an improvement of total recovery rate from 68.8% in 1990 s to 73.9% for 2000-2005 (P=0.09).The catheter removal rate decreased from 19.2% to 14.3% (P=0.238),and the mortality from 10.1% to 5.4% (P=0.118).In both periods,fungal peritonitis had the poorest results,which all the patients either withdrew from PD or died.Conclusions Compared with that in 1990 s,the culture positive rate for CAPD related peritonitis in 2000-2005 has been greatly improved.Coagulase-negative staphylococcus is the most common causative pathogen.The mortality and catheter removal rate have been markedly reduced in the last five years.Fungal peritonitis is the most important reason for patients' dropout.

OBJECTIVETo study the function of IL-18 in promoting metastasis of lung cancer.

METHODSThe differential expression of IL-18 protein or mRNA level between highly and poorly metastatic sublines of human lung giant cell carcinoma metastatic model was detected by Western blot, semi-quantitative RT-PCR and northern blot analysis. The poorly metastatic PLA801C subline or highly metastatic PLA801D subline was transfected with constructed IL-18 sense or IL-18 antisense expressed plasmid by lipofectamine stable transfection technique. The metastasis-related effect mediated by IL-18, the metastatic phenotype differences, cell motility and cell invasion potential in vitro determined by MICS system and the expression level of metastasis-associated biomarkers detected by Western blot analysis, were compared between IL-18 stably transfectants and mock control, i.e. between PLA801C/IL-18(S) and PLA801C/pcDNA3.1, or between PLA801D/IL-18(As) and PLA801D/pcDNA3.

RESULTSIL-18 was only present in highly metastatic PLA801D subline at either protein or mRNA level, which implied that IL-18 might play a role in promoting metastasis of lung cancer. After IL-18 sense expressed plasmid was transfected into poorly metastatic PLA801C subline, IL-18 fused protein with myc tag detected by Western blot analysis using either IL-18 or myc tag monoclonal antibody. In addition, cell motility ability in vitro was significantly increased about 3 times and E-cadherin protein was significantly down-regulated at about 50% in PLA801C/IL-18(S) transfectants compared with mock control. While IL-18 expressed plasmid was transfected into highly metastatic PLA801D subline, IL-18 protein and mRNA were simultaneously decreased by 30%. In addition, cell invasion ability in vitro was significantly decreased at about 75% and E-cadherin protein was significantly up-regulated in PLA801D/IL-18(As) transfectants compared with mock control.

CONCLUSIONIL-18 might play a role in enhancing tumor metastasis of lung cancer by down-regulating E-cadherin protein expression.

Cadherins ; metabolism ; Carcinoma, Giant Cell ; metabolism ; secondary ; Cell Line, Tumor ; Cell Movement ; DNA, Antisense ; genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Interleukin-18 ; biosynthesis ; genetics ; Lung Neoplasms ; metabolism ; pathology ; Neoplasm Invasiveness ; Neoplasm Metastasis ; genetics ; Plasmids ; RNA, Messenger ; biosynthesis ; genetics ; Transfection

Objective： The current study was designed to investigate the relationship between cyclin A expression in non-small cell lung carcinoma (NSCLC) and the proliferative activity and the prognosis. Methods： Cyclin A expression in 60 non-small cell lung carcinoma specimens was detected by immunohistochemical method. DNA content was measured by flow cytometry. Results： Twenty-nine cases (48.3％ ) showed cyclin A expression. The median S-phase fraction of the cyclin A-positive 14.4± 3.9％ was higher than that of the cyclin A-negative 9.4± 3.5％ . The overall survival was significantly lower in patients with cyclin A expression than in those without cyclin A expression. Conclusion： Cyclin A expression contributed to the high proliferative activity in non-small cell lung carcinoma cells. Cyclin A might be a prognostic marker of non-small cell lung carcinoma.

Objective To investigate the effect from different pore sizes of co culture inserts on the permeability of biomacromolecules through polyethylene terephthalate (PET) membrane so as to solve the key technology problem in mechanobiology experiment on vascular cells. Methods Inserts with 0.4 μm and 1.0 μm pores on the PET membrane were studied using flow chamber system. Low shear stress was subjected to the co-cultured system of endothelial cell (EC)/vascular smooth muscle cell (VSMC) and the concentration of platelet-derived growth factor BB (PDGF-BB) was detected by ELISA. Under the static condition, vascular cells were cultured on the plate (with no cell on PET membrane), on the outer side of PET membrane, and on the both sides of PET membrane, respectively. Then the recombinants PDGF-BB (rPDGF-BB) were added on the different sides of PET membrane. Western blotting was used to detect the change in expressions of p-ERK1/2, p-Akt and Lamin after cells were stimulated by rPGDF BB. Results After low shear stress subjection for 12 h, the concentration of PDGF-BB in the medium from VSMC side was significantly higher than that from EC-side. rPDGF-BB passed through 0.4 μm and 1.0 μm pores on the PET membrane and modulated expressions of p-ERK1/2, p-Akt and Lamin A in cells cultured on the opposite side of PET membrane and cells cultured on the plate separately. When cells were cultured on the both sides of PET membrane, rPDGF-BB only stimulated cells cultured on the same side of 0.4 μm pores on PET membrane, but had no specific effect on cells cultured on the opposite side. Conclusions PET membrane with both 0.4 μm and 1.0 μm pores was permeable to PDGF-BB, and cells cultured on the membrane could affect the permeability. The efficiency of PDGF BB passing through 0.4 μm pores was significantly repressed with cells cultured on the both sides, which was more similar to that in vivo.

BACKGROUNDThioredoxin is one of the most important redox regulating proteins. Although thioredoxin has been shown to protect cells against different kinds of oxidative stress, the role of thioredoxin in myocardial ischemia and reperfusion injury has not been fully understood. This study was conducted to explore the protective role of human thioredoxin on myocardial ischemia and reperfusion injury and its potential mechanisms.

METHODSPurified human thioredoxin was injected into adult Wistar rats, which were subjected to 30 minutes of myocardial ischemia followed by 2 or 24 hours of reperfusion. We detected 1) the infarct size; 2) the level of malondisldehyde (MDA) in serum; 3) the expression of caspase-9, and cytochrome c in/out of mitochondria by Western blotting; 4) apoptosis by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) assay and caspase-3 and its protein by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting; 5) the expression of bcl-2 and bax in cardium by immunohistochemical (IHC) assay.

RESULTSHuman thioredoxin reduced myocardial ischemia/reperfusion injury as evidenced by significant decrease of myocardial infarct size (P < 0.01), notable reduction of myocyte apoptosis (P < 0.01), lower systemic oxidative stress level (P < 0.01) after reperfusion for 2 hours, and few inflammatory cell infiltration after reperfusion for 24 hours in rats. Furthermore, treatment with human thioredoxin significantly reduced the release of mitochondrial cytochrome C (P < 0.05), and inhibited the activity of caspase-9 (P < 0.05) and caspase-3 (P < 0.01 in mRNA and P < 0.05 at protein level). Meanwhile, human thioredoxin markedly increased bcl-2 expression (P < 0.05).

CONCLUSIONSThese results strongly suggest that human thioredoxin has cardioprotective effects on myocardial ischemia/reperfusion and its anti-apoptotic role may be mediated by modulating bcl-2 and the mitochondria-dependent apoptotic signaling pathway.

Animals ; Apoptosis ; drug effects ; Caspase 3 ; genetics ; Humans ; Mitochondria, Heart ; drug effects ; physiology ; Mitochondrial Membrane Transport Proteins ; drug effects ; Myocardial Reperfusion Injury ; prevention & control ; Oxidative Stress ; Rats ; Rats, Wistar ; Thioredoxins ; pharmacology

OBJECTIVETo investigate the role of TGF-beta(1)/MAPK signaling pathways in the expression of type I collagen and activity of MMP-2, 9 in human lung fibroblasts.

METHODSHuman lung fibroblasts cell line (HLF-02) was cultured and and then stimulated with 10 ng/ml TGF-beta(1) for different time; SB203580 or PD98059 was added into culture medium to block p38 or ERK kinase pathway before incubated with TGF-beta(1); the expression of type I collagen was detected by Western blotting and RT-PCR; zymogram analysis was used to analyze the activity of MMP-2 and MMP-9.

RESULTS(1) In the process of stimulation by TGF-beta(1), the type I collagen mRNA level of 24 h, 48 h and 72 h group was: 1.33 +/- 0.07, 2.46 +/- 0.09 and 2.39 +/- 0.08 respectively; and the type I collagen protein level of 24 h, 48 h and 72 h group was: 114.89 +/- 8.95, 208.16 +/- 6.75 and 211.46 +/- 8.05 respectively; and the activity of MMP-2 of 24 h, 48 h and 72 h group was: 190.33 +/- 5.86, 214.33 +/- 8.39 and 212.67 +/- 11.59 respectively. (2) SB203580 significantly inhibited the TGF-beta(1)-induced expression of type I collagen mRNA, protein and MMP-2 activity (inhibition ratio: 51%, 24% and 20%); (3) PD98059 also significantly attenuated the TGF-beta(1)-induced expression of type I collagen mRNA, protein and MMP-2 activity (inhibition ratio: 42%, 13% and 16%).

CONCLUSIONTGF-beta(1) is capable of inducing the expression of type I collagen mRNA and protein and up-regulating MMP-2 activity in HLF-02 cells. p38 and ERK kinase signaling pathways play important role in regulation and control for this process.

Blotting, Western ; Cell Line ; Collagen Type I ; biosynthesis ; genetics ; Extracellular Signal-Regulated MAP Kinases ; antagonists & inhibitors ; physiology ; Fibroblasts ; drug effects ; metabolism ; Flavonoids ; pharmacology ; Humans ; Imidazoles ; pharmacology ; Lung ; cytology ; Matrix Metalloproteinase 2 ; metabolism ; Matrix Metalloproteinase 9 ; metabolism ; Pyridines ; pharmacology ; RNA, Messenger ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; physiology ; Transforming Growth Factor beta1 ; pharmacology ; p38 Mitogen-Activated Protein Kinases ; antagonists & inhibitors ; physiology

BACKGROUNDClinical observations have shown that the complex fractionated atrial electrogram (CFAE) associates with ganglionated plexus activity in the cardiac autonomic nervous system. This study aimed to investigate the impact of CFAE ablation on vagal modulation to atria and vulnerability to develop atrial fibrillation (AF).

METHODSTen adult mongrel dogs were involved. Cervical sympathovagal trunks were decentralized and sympathetic effects were blocked. CFAE was color tagged on the atrial 3-dimensional image and ablated during AF induced by S1S2 programmed stimulation plus sympathovagal trunk stimulation. Atrial effective refractory period (ERP) and vulnerability window (VW) of AF were measured on baseline and at vagal stimulation at 4 atrium sites. Serial tissue sections from ablative and control specimens received hematoxylin and eosin staining for microscopic examination.

RESULTSMost CFAE areas were localized at the right superior pulmonary quadrant, distal coronary sinus (CS(d)) quadrant, and proximal coronary sinus (CS(p)) quadrant (21.74%, separately). Sinus rhythm cycle length (SCL) shortening did not decrease significantly after ablation at the sites, including right atrial appendage, left atrial appendage, CS(d), and CS(p) (P > 0.05). ERP shortening during vagal stimulation significantly decreased after ablation (P < 0.01); the VW to vagal stimulation significantly decreased after ablation (P < 0.05). The architecture of individual ganglia altered after ablation.

CONCLUSIONSCFAE has an autonomic basis in dogs. The decreased SCL and ERP shortening to vagal stimulation after CFAE ablation demonstrate that CFAE ablation attenuates vagal modulation to the atria, thereby suppressing AF mediated by enhanced vagal activity. CFAE ablation could suppress AF mediated by enhanced vagal activity.

Animals ; Atrial Fibrillation ; therapy ; Autonomic Nervous System ; Catheter Ablation ; methods ; Dogs ; Electrophysiologic Techniques, Cardiac ; methods ; Electrophysiology ; Female ; Male