Objective To investigate the expression and clinical significance of CDx2 and hepatocyte antigen(Hep) in gastric carcinoma.Methods The expression of CDx2 and Hep in 9 cases of nomal gastric mucosa,15 cases of small intestinal mucosa,8 cases of colon mucosa,15 cases of intestinal metaplasia of the stomach and 130 cases of gastric carcinoma were detected with immuohistochemical EnVisionTM Systems measures.Results The positive rates of CDx2 expressed in the nomal gastric mucosa were 0,small intestinal mucosa 80%(12/15),colon mucosa 87.5%(7/8),intestinal metaplasia of the stomach 86.7%(13/15),gastric carcinoma 37.7%(49/130);The positive rate of Hep was 11.1%(1/9),86.7%(13/15),12.5%(1/8),100%(15/15),55.4%(72/130) respectively.There was much higher positive expression of CDx2 in intestinal-type carcinoma than in diffuse-type gastric carcinoma(P

I uptake of thyroid and color Doppler flow imaging (CDFI) of superior thyroid artery (STA) were performed in 20 patients with Graves′ disease (GD) and 19 patients with other causes of hyperthyroidism. Maximum velocity and diameter of STA in patients with GD were much higher than those in non-GD group. CDFI of STA seems to be a useful tool in differential diagnosis of hyperthyoidism.

~(131)I uptake by thyroid were assayed in 64 patients with Graves′ disease (GD) and 69 patients with non-GD hyperthyroidism. GD group had higher rate of ~(131)I uptake than non-GD group at 2, 6 and 24 h, and there was no overlap between the two groups at these 3 time points.~(131)I uptake at 2 and 6 h could differentiate GD fromlow ~(131)I uptakehyperthyroidism.

AIM: To study the role of carbon monoxide (CO) in the mechanism of cholecystokinin-octapeptide (CCK-8) for attenuation of acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: Fifty-six adult male rats were randomly divided into seven groups: control group, LPS group, LPS+ZnPP (a specific inhibitor of HO-1) group, LPS+Hemin (Hm, CO donor) group, CCK-8+LPS group, CCK-8+LPS+ZnPP group and CCK-8 group (n=8 for each). Bronchoalveolar lavage was performed 2 h, 6 h and 12 h respectively after treatments. The numbers of polymorphonuclear leukocytes (PMN) in bronchoalveolar lavage fluid (BALF) was detected. The mortality of rats and the structure of lung tissues were observed. MDA and CO contents in lung tissues were also measured. RESULTS: The mortalities of rats were both zero 2 h and 6 h after agent administration. The mortality of rats was higher than control group 12 h after LPS administration. The mortality of rats in LPS+Hm and CCK-8+LPS group were lower than that in LPS group, and its in LPS+ZnPP and CCK-8+LPS+ZnPP group were lower than that in LPS and CCK-8+LPS group, respectively. Lung injury was observed in LPS group. At the same time the number of PMN, MDA and CO content were higher than those in control group. The degree of lung injury, PMN numbers and MDA content were lower, while CO content in LPS+Hm and CCK-8+LPS group were higher than those in LPS group. However, the degree of lung injury, PMN number and MDA content were higher, CO content were lower in LPS+ZnPP and CCK-8+LPS+ZnPP group than those in LPS and CCK-8+LPS group, respectively. CONCLUSION: CCK-8 attenuates the LPS-induced acute lunginjury by means of anti-oxidation and inhibition of PMN aggregation, which are both mediated by CO.

AIM:To study the role of heme oxygenase (HO)-1 in the mechanism of cholecystokinin-octapeptide (CCK-8) for attenuation of acute lung injury (ALI) induced by lipopolysaccharide (LPS). METHODS: Adult male rats were randomly divided into five groups: control group, LPS group, CCK-8+LPS group, LPS+ Hm (hemin, HO-1 donor) group and LPS+ZnPP (zinc protoporphyrin, specific inhibitor of HO-1) group. PMN number in bronchoalveolar lavage fluid (BALF), the structure of the lung, MDA content, HO-1 activity, the expressions of HO-1 mRNA and protein in the lung were detected respectively. RESULTS: The lung injury in LPS group was observed, at the same time the numbers of PMN, the content of MDA, the activity and the expression of HO-1 were all higher than those in control group (all P

Objective To investigate the clinical efficacy of intravitreal injection of Lucentis combined with pan retinal photocoagulation and trabeculectomy for neovascular glaucoma(NVG). Methods Seventeen eyes of 15 patients with NVG were treated by 0.5 mg Lucentis intravitreal injection first. Trabeculectomy was performed 7 days later and Pan retinal photocoagulation 2 weeks later. Iris,anterior chamber angle neovascularization,intraocu?lar pressure ,and visual acuity were observed in the following 6 months. Results Iris and anterior chamber angle neovascularization were completely regressed 7 days after the injection in 17 eyes. Six months after photocoagulation, 6 eyes had different degrees of improvement in visual acuity,10 eyes no change in visual acuity and 1 eye decreased from anterior index to immediate manual. There was significant difference in pre?treatment IOP and postoperative IOP( t = 12.75 ,10.26 ,9.73 ,10.77 ,P < 0.01 ). No serious complications were observed after intravitreal injec?tion and trabeculectomy. Conclusions Intravitreal injection of Lucentis could significantly accelerate the regres?sion of iris and anterior chamber angle neovascularization ,which could improve the successful rate of trabeculecto?my and pan retinal photocoagulation. Intravitreal injection of Lucentis combined with trabeculectomy and panretinal photocoagulation is safe and effective for NVG.

AIM: To detect the changes of inducible nitric oxide synthase (iNOS) expression in kidney following ischemia-reperfusion(I-R)of hindlimbs and to elucidate their significance. METHODS: I-R was established using the occlusion of the femoral arteries for 4 h and re-opening for 2-24 h in rats. The expression of iNOS mRNA,and iNOS protein and the nitrotyrosine (NT),a marker of peroxynitrite (ONOO -),in renal tissue were detected with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical technique,respectively. The superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents in renal tissue were spectraphotometrically measured. The observation of pathologic changes of renal tissue was made following the inhibition of iNOS by aminoguanidine (AG). RESULTS: Compared with control group,the relative expression level of iNOS mRNA significantly increased in I-R group. There were more iNOS and more NT positive product in the epithelial cells of renal proximal convoluted tubules and thick segments of Henle′ loops in I-R group than control group. The contents of MDA markedly increased,while the activity of SOD significantly decreased in I-R group,compared to those in the control groups. The pathologic changes of kidney became milder in I-R group following the inhibition of iNOS by AG. CONCLUSION: The expression of iNOS mRNA and protein in renal tissue were significantly upregulated,excess induction of NO contributed to the kidney injury during the I-R of hindlimbs.

AIM: To detect the changes of heme oxygenase-1 (HO-1) expression in kidney following ischemia-reperfusion of hindlimbs and to elucidate their significance. METHODS: Health SD rats were randomly divided into normal (N), sham (S), 4h ischemia without reperfusion (I), 4 h ischemia-2, 6, 12, 18 or 24 h reperfusion (I-R) groups and I-R18h+zinc protoporphyrin (ZnPP) group. I-R was established using the occlusion for 4 h and re-opening for 2-24 h of the femoral arteries. In I-R 18 h+ZnPP group, ZnPP (5 ?mol?kg~(-1) body weight) was intravenously injected 6 h and 12 h after reperfusion, respectively. The expression of HO-1 mRNA in kidney was detected with reverse transcription-polymerase chain reaction (RT-PCR). The expression and location of HO-1 protein were detected with immunohistochemical technique. The observation of pathologic changes of kidney was made following the inhibition of HO-1 by ZnPP. RESULTS: The relative expression level of HO-1 mRNA significantly increased in I-R group, compared to those in the control groups, It was maximal in I-R 18 h group, and thereafter expression level of HO-1 mRNA decreased, however significant expression was still detected in I-R 24 h group (P

AIM:To study the effect of ONOO- on the airway epithelial injury. METHODS: The mitochondrial respiration, the amount of lactate dedydrogenase (LDH) release into the cell culture medium, the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG), and the cellular apoptosis were examined after exposure of cultured rat tracheal epithelial (RTE) cells to ONOO-. RESULTS: Exposure of RTE cells to 0.25, 0.5 and 1 mmol/L ONOO- caused a dose-dependent suppression of the mitochondrial respiration . ONOO- also caused a dose-dependent increase in the percentage of LDH release. Exposure of RTE cells to ONOO- resulted in an increased generation of 8-OHdG in a dose-dependent manner. ONOO- caused an increase in apoptotic percentage in RTE cells in a time-dependent manner at different concentrations. CONCLUSION: ONOO- could cause necrosis and apoptosis in cultured RTE cells. Low concentration of ONOO- caused apoptosis in a time-dependent manner. Whereas exposure to high concentration of ONOO- resulted in cell necrosis, ONOO- caused a dose-dependent increase in the percentage of LDH release. Suppression of mitochondrial respiration and oxidative DNA damage by ONOO- may be the major cause of cellular injury induced by ONOO-.

AIM: To investigate the role of hydrogen sulfide (H_2S) in the cholecystokinin octapeptide (CCK-8) attenuating lipopolysaccharide (LPS)-induced lung injury. METHODS: A rat model of lung injury induced by intravenous injection of LPS was developed. Male Wistar rats were divided into normal control group, LPS group, LPS+CCK-8 group and CCK-8 group. Six hours after LPS injection, partial pressure of oxygen in the arterial blood (PaO_2), H_2S content and cystathionine-γ-lyase (CSE) activity in lung tissue were detected. The mRNA expression of CSE in lung tissue was determined by RT-PCR;the structure of lung tissues was observed under optical microscope. RESULTS: Compared to normal control rats, the LPS-treated rats had significantly decreased PaO_2 level, increased index of quantitative assessment (IQA) score, while H_2S content, CSE activity and the mRNA expression of CSE in lung tissue were significantly increased (all P<0.05). Administration of CCK-8 into LPS-treated rats increased the PaO_2 level and alleviated the degree of lung injury (measured by IQA score). In addition, CCK-8 decreased H_2S content, CSE activity, and the mRNA expression of CSE (all P<0.05). No significant difference of the above-mentioned parameters between CCK-8 group and normal control group was observed. CONCLUSION: CCK-8 reduces LPS-induced lung injury through inhibiting the generation of endogenous H_2S.