Objective To investigate the expression and biological significance of cytosolic phospholipase A2(cPLA2)in lung cancer and to provide a theoretical basis for understanding the molecular mechanism of the lung cancer carcinogenesis and development.MethodsTheexpression of cPLA2 at mRNA level in tumor and tumor-adjacent tissue was detected byRT-PCR.The immunohistochemical SP method was used to evaluate the expression of cPLA2 protein in the corresponding tissues.ResultsThe quantitive expression levels of cPLA2 mRNA in tumor and tumor-adjacent tissue were0.82±0.10 and 0.08± 0.01,respectively.The mRNA level of cPLA2 significantly increased (P =0.001) in lung tumor when compared with those in the tumor-adjacent tissue. By immunohistochemistry, the positive rate of cPLA2 protein expression in lung tumor tissue was 76.7 ％(46/60),while no expression was detected in tumor-adjacent tissue.The positive rate of cPLA2 protein expression in lung cancer was correlated with clinicopathological parameters including histological type,histological grade,lymph node metastasis and TNM staging(x2 was 7.565,9.161,4.424,5.416,respectively,and all P ＜0.05),but not correlated with the size of tumor (x2 =0.366,P ＞ 0.05).ConclusionThe expression of cPLA2 in lung cancer may play an important role in the process of carcinogenesis,and may provide a clinical basis for the early diagnosis and targeted therapy for lung cancer.

ObjectiveTo explore the expression and biological significance of microsomal prostaglan din E synthase-1 ( mPGES-1 ) and cyclooxyenase-2 (COX-2) in lung cancer.MethodsThe expressions of mPGES-1 and COX-2 mRNA in cancerous tissue and tumor-adjacent tissue were detected by RT-PCR,while the immunohistochemical S-P method was used to evaluate the expression of mPGES-1 and COX-2 proteins in the corresponding tissues.ResultsThe mRNA level of COX-2 and mPGES-1 significantly increased( P ＜0.05) in lung cancer group as compared with those in the tumor-adjacent tissue.The positive expression rate of mPGES-1 in cancerous tissue and tumoradjacent tissue were 66.7％ (40/60) and 10.0％ (6/60) respectively.The positive expression rate of COX-2 protein in cancerous tissue and tumor-adjacent tissue were 73.3％ (44/60)and 13.3％ (8/60),respectively.The positive expression rate of COX-2 was significantly higher in lung cancer than m tumor-adjacent tissue( x =21.99,P ＜ 0.01 ).The positive expression rate of mPGES-1 and COX-2 protein in lung cancer was independent of size of tumor and histological type(P ＞0.05 ),but correlated with histological grade,lymph node metastasis and TNM staging.(P ＜0.05 ).ConclusionIt suggested that the expression of mPGES-1 and COX-2 in lung cancer may play an important role in the process of carcinogenesis,and may provide a clinical basis for the early diagnosis and targeted therapy of lung cancer.

Most colorectal cancers develop from adenomas. Environmental factors play an important role in the development and progression of adenoma. Recently,epidemiologic investigations on lifestyle change including diet and exercise and drug intervention studies have proved the relationship between environmental factors and colorectal cancer. Screening,polypectomy and surveillance via colonoscopy are the main measures of colorectal cancer prevention. However, the efficacy is unsatisfactory. Therefore,attention should be paid to studies on colorectal cancer prophylaxis via intervention on environmental factors. Emphasis should be put on various aspects of environmental intervention in clinical practice,and prophylaxis strategies should be generated individually in accordance with the local condition and situation.

Objective: To detect the expression of focal adhesion kinase (FAK) and vascular endothelial growth factor (VEGF) in human rectal carcinoma, to study their correlation in invasion and metastasis. Methods: The expression of FAK and VEGF in 86 specimens resected from patients with rectal carcinoma and 30 non-rectal carcinoma specimens, was investigated by immunohistochemical SABC method respectively. Results: the positive rate of FAK, VEGF was 80 % and 59% respectively in rectal carcinoma. However, non-rectal carcinoma was 10% and 13 % respectively. The diference was significant (P

Objective To study the tissue pathology and the expression of related factors during renal tubular-interstitial fibrosis in aristolochic acid (AA) nephropathy in rat. Methods 46 male Wistar rats were randomly divided into 2 groups. The test group consisted of 26 rats which were gavaged with the extract of Caulis Aristolochiae Manshuriensis (CAM) (AA 20mg?kg -1 ?d -1 ); the control group consisted of 20 rats which were given with equal volume of potable water. At the end of 4th, 8th, 12th week, the kidneys of each rat were separately harvested. The HE, PAS and Masson staining were used to analyze the degree of tubular damage and interstitial fibrosis, and immunohistochemical method was applied to assess the protein expression of proliferating cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF), transforming growth factor-?_1 (TGF-?_1) in the renal specimens. The mRNA expression of VEGF, endothelin-1 (ET-1), bone morphogenetic protein-7 (BMP-7) in renal tissue were determined by RT-PCR respectively. Results A severe renal tubular-interstitial damage and an early fibrosis were observed at the end of 12th week, and the interstitial fibrotic area was 31.36%. The protein expression of PCNA was increased at 4th week, but down-regulated after 8th week; the expression of TGF-?_1 and VEGF was increased at 4th week, while TGF-?_1 was maintatined on a high level with passage of time, but VEGF decreased gradually. The mRNA expression of VEGF and ET-1 increased notably at 4th week, slightly decreased after 8th week, but maintained at a high level. The BMP-7 declined slowly with the progression of pathological changes, reaching its lowest level at 12th week. Conclusion The mechanism of the rapid progression of fibrosis in AAN might be the renal result of severe impairment of regeneration of epithelial cells, lowering of expression of factors of promoting repair and inhibiting fibrosis, while the expression of factors of promoting fibrosis was maintained at a highlevel.

OBJECTIVE: To investigate the pathogenic mechanism of aristolochic acid nephropathy (AAN) by observing the renal tubular injury and the change of the expression of bone morphogenetic protein-7 (BMP-7) mRNA in renal tissue of rats induced by aristolochic acid (AA), an active constituent in Caulis Aristolochiae Manshuriensis (CAM). METHODS: Forty-six male Wistar rats were randomly divided into normal control group (n=20) and AA-treated group (n=26). Rats in AA-treated group were intragastrically administered with AA 20 mg/(kg.d), and rats in control group were treated with equal volume of potable water. At the end of the 4th, 8th and 12th week of administration, the 24 h-urine was collected by metabolic cage for detecting the activity of N-acetyl-beta-D-glucosaminidase (NAG) and the blood samples were obtained from abdominal aorta for detecting serum creatinine (SCr). Pathological change and the degree of injury of the kidneys were observed by microscopy. The expression of proliferative cell nuclear antigen (PCNA) was detected by immunohistochemical method, and mRNA expression of bone morphogenetic protein-7 (BMP-7) in the renal tissue was detected by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Compared with the normal control group, the activity of NAG and the ratio of SCr vs body weight were markedly increased in rats of the AA-treated group after treatment (P<0.05 and P<0.01). Pathological section of renal tissue showed that most renal tubules had cloudy swelling, and vacuolar degenerating in tubular epithelial cells, with brush border dropping off, and parts of tubular basement membrane were exposed. The degrees of injuries were aggravated depending on treating time. The tubulointerstitial injury (TI) parameter in rats of AA-treated group was higher than that of the normal control group. The positive expression of PCNA was observed in the damaged tubular cells. The proliferation index of PCNA was significantly increased after 4- and 8-week treatment (P<0.01), but was decreased after 12-week treatment (P<0.05). The mRNA expression of BMP-7 was markedly decreased in the AA-treated group compared with the normal control group after 4-week treatment (P<0.05), and decreased with the extension of treatment time. CONCLUSION: AA can induce injury of the renal tubules, impair the cell regeneration, and inhibit the expression of BMP-7 mRNA in renal tissue. This may be one of the pathogenic mechanisms of AAN.

Objective To systematically review the efficacy and safety of photodynamic therapy (PDT) and intravitreal vascular endothelial growth factor (VEGF) inhibitors in the treatment of polypoidal choroidal vasculopathy (PCV),and to investigate the primary treatment tentatively.Methods A systematic search of Pubmed,Embase,the Cochrane Library and the Wanfang Data was performed to identify all comparative studies that compared the outcomes of PDT alone,intravitreal VEGF inhibitors alone and combined intravitreal VEGF inhibitors and photodynamic therapy.Outcomes of interest included the regression and recurrence rate of polypoidal lesions,best corrected visual acuity (BCVA),central retinal thickness (CRT),therapeutic times,and the occurrence rate of adverse events.2 randomized controlled trials (RCT) and 19 non-RTCs were identified.According to treatment methods,the data extracted was classified to 3 groups,analyzed with odds ratio (OR),weighted mean difference (WMD) and 95％confidence interval (95％CI).Results Meta-analysis suggests that the regression rate of polypoidal lesions (OR=0.34,0.07;95％CI=0.13-0.88,0.02-0.36) and BCVA (WMD=0.25,0.11;95％CI=0.14-0.36,0.01-0.21) in combined therapy group were significantly better than those in PDT group and intravitreal VEGF inhibitors group (P＜0.05).The recurrence rate of polypoidal lesions in PDT group was significantly lower than intravitreal VEGF inhibitors group (OR=0.35,95％CI=0.16-0.74,P=0.006).BCVA (P=0.025) and the occurrence rate of adverse events (OR=60.36,95％CI=6.04-603.50,P=0.000 5) in intravitreal VEGF inhibitors group were significant better than PDT group.Conclusions Combined treatment appeared to be superior to PDT alone or intravitreal VEGF inhibitors alone.Combined treatment takes priority over all others in the primary treatment of PCV.

Objective To investigate the effects of aristolochic acid on renal function and tissues morphology in rats.Methods Forty-six male Wistar rats were divided into the normal control group(n=20) and the tested group (n=26) at random.The tested group was treated with the extract of Caulis Aristolochiae Manshuriensis(CAM) (aristolochic acid 20 mg?kg-1?d-1) by gastric gavage,the control group with the same volume of potable water.The body weight of rats was meausured weekly.At the end of 4th,8th,12th weeks,the 24-hour-urine were collected,and blood samples were taken from abdominal artery for detection of indexes of renal function.The pathological changes of renal tissues were also observed.Results The body weight increased slowly and urine volume increased in tested group.The urine albumin level and N-acetyl-?-glucosaminidase (NAG) excretion increased significantly,and the ratio of serum creatinin and body weight increased progressively,indicating that renal function has been impaired.The renal pathological changes under light microscope were as follows:degeneration and necrosis of renal tubule in the early stage and serious tubular structure disorders of focal atrophy and interstitial inchoate fibrosis in the late stage.The changes of ultrastructure of renal tissues under the electronic microscope were as follows:obvious organelle impairment and nucleus variation,interstitial inchoate fibrosis occurring at the 8th week and fibrosis rate arriving 31.36 %at the 12th week.Conclusion Aristolochic acid in CAM has renal toxicity,which is shown as remarkably renal pathological changes,tubular-interstitial injury,interstitial inchoate fibrosis,and cell nuclear variation.

Aim To investigate the role of peripheral benzodiazepine receptor in rat cardiac mitochondrial permeability transition.Methods The isolated rat cardiac mitochondria were incubated with different doses(50,100,200 ?mol?L-1) of PBR antagonist 1-(2-chlorophenyl-N-methyl-1-methylpropyl)-3-isoquinolinecarboxamide (PK 11195). In additional group(CsA group), 5 ?mol?L-1 cyclosporine A (CsA), an inhibitor of MPT was added 5 minutes before the addition of 100 ?mol?L-1 PK 11195. Negative control group(Con group) was given none treatment. Positive control group(Ca2+ group) was given 150 ?mol?L-1 CaCl2. The absorbanceat 520 nm(Abs 520 nm) was monitored with a split-beam spectrophotometer at 30℃ for 10 min. The mitochondrial ultrastructure was assessed by transmission electron microscopy. Mitochondrial cytochrome C release was demonstrated by Western Blotting.Results PK11195 triggered large-amplitude mitochondrial swelling in a dose dependent manner(vs Con group,P