Objective To investigate the effects of submucosal resection by guidance under esophageal endoscopic ultrasound. Methods 79 cases ofsuspected upper gastrointestinal submucosal tumors were found by endoscopic ultrasonography,transesophageal endoscopic ultra-sound showed lesions under muscularis mucosa,after informed consent,they were underwent endoscopic mucosal resection. Pathological diag-nose of the lesions were found out after resection. Results Compared with pathological results showed that endoscopic ultrasound accurately determine tumor location in the hierarchy;through endoscopic mucosal resection to remove all lesions,5 patients were found bleeding postop-erative,6 patients were found esophageal stricture,the prognosis was good after treatment. Conclusion Endoscopic ultrasonography can accu-rately determine submucosal myoma,it can be used to guide resection of submucosal myoma.

AIM: To investigate the primary culture method for coronary artery smooth muscle cells (CASMCs), and to establish the endoplasmic reticulum stress ( ERS) model in CASMCs of SD rats.METHODS:CASMCs were cultured by tissue explant method .The morphological characteristics were observed under optical micro-scope.The marker proteins of CASMCs , including α-SMA and SM-MHC, were identified by immunofluorescence tech-nique.The protein expression levels of BiP and CHOP , the marker molecules of ERS, were determined by Western blot . RESULTS:The spindle-shaped CASMCs climbed out from the edge of coronary artery tissues after 6 d, and formed the typical hill and valleygrowth pattern of CASMCs at 9~10 d.The result of immunofluorescence technique showed that α-SMA and SM-MHC were positively expressed .The results of Western blot showed that the protein expression of BiP and CHOP in TG ( 1 and 2 μmol/L ) treatment groups was increased compared with control group .Compared with control group, the protein expression of BiP and CHOP was significantly increased after 1 μmol/L TG treatment for 24 and 48 h. CONCLUSION:CASMCs can be successfully cultured by tissue explant method .ERS model of CASMCs was established by 1 μmol/L TG treatment for 24 h.

OBJECTIVETo investigate the clinical manifestations, complications and treatment of medicament-like dermatitis due to trichloroethylene (TCE), so as to provide basis for studying its etiology and mechanism.

METHODSFifty patients with dermatitis due to TCE from 1997 to 2000 were analysed retrospectively.

RESULTSThe occurrence of the dermatitis was not parallel to TCE exposure levels, without significant dose-effect relationship. This disease could be caused by both inhalation and skin exposure. The latency period of TCE dermatitis ranged from 5 to 66 days, and the average was 31.5 d (Medium). The major clinical manifestations included skin lesions, fever, superficial lymph node swelling and liver dysfunction. Infection was the major complication. Glucocorticoid was effective for treatment of this disease.

CONCLUSIONThe clinical manifestations due to TCE exposure were similar to dermatitis medicamentosa. The major clinical types of TCE dermatitis included exfoliative dermatitis and erythema multiforme. The dermatitis is considered to be mediated by delayed-type (IV) hypersensitivity. The key factors to treat this disease successfully included the use of glucocorticoid in time with sufficient dose and full course, professional skin care, active treatment to protect the liver and to avoid infection.

Adolescent ; Adult ; Allergens ; adverse effects ; Dermatitis, Exfoliative ; diagnosis ; etiology ; therapy ; Drug Eruptions ; diagnosis ; etiology ; therapy ; Female ; Humans ; Male ; Occupational Exposure ; adverse effects ; Retrospective Studies ; Trichloroethylene ; adverse effects

BACKGROUND AND OBJECTIVEAdenovirus vectors were widely used in gene therapy for tumors. We used adenovirus vector to transfer small interfering RNA (siRNA) against vascular epithelium growth factor A (VEGF-A) molecules to mouse lung adenoma LA795 cells and used low dose of chemotherapeutic drugs to further elevate the infection efficiency of adenovirus vector in and therapeutic effect of RNAi on tumor cells.

METHODSLA795 cells were infected by Ad/EGFP and treated with different dosages of gemcitabin, epirubicin, cisplatin, or 5-fluorouracil (5-FU). Cells were observed under fluorescence microscope continuously using green fluorescent protein (GFP) as the reporter gene. The percentage of GFP-positive cells and fluorescent intensity were tested by flow cytometry to determine optimum concentrations of drugs. Ad/siVEGF-A containing VEGF-A siRNA was constructed. Real-time PCR and ELISA were applied to measure the expression level of VEGF-A after LA795 cells were infected by Ad/siVEGF-A and treated with 5-FU. The combination of Ad/siVEGF-A and 5-FU was also applied in treating subcutaneous tumor in mice.

RESULTSLow dose of 5-FU elevated the Ad/EGFP infection in LA795 cells significantly, and also enhanced the effect of Ad/siVEGF-A in down-regulating VEGF-A mRNA and protein levels in tumor cells. When used in tumor in vivo, the combination strategy repressed tumor growth effectively.

CONCLUSIONLow dose of 5-FU can enhance the capability of adenovirus infecting tumor cells and promote the efficiency of gene therapy by adenovirus.

Adenocarcinoma ; metabolism ; pathology ; Adenoviridae ; genetics ; Animals ; Antimetabolites, Antineoplastic ; administration & dosage ; pharmacology ; Cell Line, Tumor ; Cell Proliferation ; Fluorouracil ; administration & dosage ; pharmacology ; Genetic Therapy ; Genetic Vectors ; Lung Neoplasms ; metabolism ; pathology ; Mice ; RNA Interference ; RNA, Messenger ; metabolism ; RNA, Small Interfering ; genetics ; Transfection ; Vascular Endothelial Growth Factor A ; biosynthesis ; genetics ; physiology

AIM:To investigate whether the association of connexin 43 ( Cx43 ) and L-type calcium channel involved in the pathogenesis of atrial fibrillation ( AF) .METHODS:The biochemical assays and whole-cell patch-clamp technique were used to study the expression of Cx43 in human atrial tissue.The co-localization of Cx43 and L-type calcium channel, and the regulation of L-type calcium current in atrial myocytes were investigated.RESULTS:The expression of Cx43 at mRNA and protein levels was decreased in human atrial tissues of AF patients.In cultured atrium-derived myocytes ( HL-1 cells) , knockdown of Cx43 significantly inhibited the mRNA expression of L-type calcium channelα1c subunit, as well as L-type calcium current.Co-localization of Cx43 with L-type calcium channel α1c subunit in mouse atrial myocytes was observed.CONCLUSION:The decrease in Cx43 is involved in the pathogenesis of AF, probably through reducing the L-type calcium current in atrial myoctyes by co-localization with L-type calcium channel, thus representing the potential pathogenesis in atrial fibrillation.

AIM:Increasing evidence indicates that inflammation contributes to the initiation and perpetuation of atrial fibrillation ( AF) .Al-though tumor necrosis factor ( TNF)-αlevels are increased in patients with AF , the role of TNF-αin the pathogenesis of AF remains unclear.Recent research has revealed that T-type Ca2+currents ( ICa,T ) play an important role in the pathogenesis of AF .METH-ODS:In this study , we used the whole-cell voltage-clamp technique and biochemical assays to explore the role of TNF-αin the regula-tion of ICa,T in atrial myocytes.RESULTS:We found that compared with sinus rhythm (SR) controls, T-type calcium channel (TCC) subunit mRNA levels were decreased , while TNF-αexpression levels were increased , in human atrial tissue from patients with AF .In murine atrial myocyte HL-1 cells, after cultured for 24 h, 12.5, 25 and 50 μg/L TNF-αsignificantly reduced the protein expression levels of the TCC α1G subunit in a concentration-dependent manner .The peak current was reduced by the application of 12.5 or 25μg/L TNF-αin a concentration-dependent manner [from ( -15.08 ±1.11) pA/pF in controls to ( -11.89 ±0.83) pA/pF and (-8.54 ±1.55) pA/pF in 12.5 and 25 μg/L TNF-αgroups, respectively].TNF-αapplication also inhibited voltage-dependent inactivation of ICa,T shifted the inactivation curve to the left .CONCLUSION:These results suggest that TNF-αis involved in the path-ogenesis of AF, probably via decreasing ICa,T function in atrium-derived myocytes through impaired channel function and down -regula-tion of channel protein expression .This pathway thus represents a potential pathogenic mechanism in AF .

AIMTo investigate the relationship between low androgen level and ultrastructure of vascular endothelium.

METHODSForty-eight male Sprague-Dawley rats were randomly divided into four groups: group A, normal rats with sham castration; group B, castrated rats; group C, castrated rats given testosterone (T) undecanoate; and group D, intact rats treated with 5alpha-reductase inhibitor. After 10 weeks of treatment or castration, rats in different groups were killed and serum T, free T (FT) and dihydrotestosterone (DHT) were measured. The aortic endothelia were scanned under electron microcopy and the Vascular Endothelium Structure Score (VESS) was computed.

RESULTSSerum T and FT concentrations of rats in group B were significantly lower than those of the other three groups (P < 0.01); DHT concentrations of group D rats were significantly decreased (P < 0.01) when compared with those of groups A and C. Rats in groups B and D rats (with low androgen levels) had obvious damage to their endothelial surfaces, which appeared crimpled, rough, adhesive and ruptured, and had high destruction of VESS.

CONCLUSIONThese results suggest that low concentrations of T and DHT are associated with ultrastructural damage of the aortic endothelia in male rats.

5-alpha Reductase Inhibitors ; Animals ; Aorta ; drug effects ; ultrastructure ; Dihydrotestosterone ; blood ; Endothelium, Vascular ; drug effects ; ultrastructure ; Enzyme Inhibitors ; pharmacology ; Male ; Orchiectomy ; Rats ; Rats, Sprague-Dawley ; Testosterone ; blood ; pharmacology

OBJECTIVETo establish a new staging system based on analysis of several presently used clinical staging systems for carcinoma of nasal cavity.

METHODSThe data of 122 patients treated from 1985 to 1997 in the cancer center of Sun Yat-sen University were analyzed, and a new clinical staging system was established using computer optimizing and screening combined with the clinical results. The survival analysis was performed by Kaplan-Meier estimates, and the multivariate analysis was achieved by Cox proportional hazard model.

RESULTSThe flaws in the presently used clinical staging systems proposed by Zhuang, Qiu, Department of Head and Neck of Cancer Center of Sun Yat-sen University and University of Florida and the AJCC'2002, were as follows: insufficient consideration of the modern tomography resulting in indefinite location of the tumor in clinical practice, the uneven distribution of patients in different stages, being unable to separate survival curves of different stages, and not containing of all necessary clinical staging information in some staging systems. However, based on our new staging system, the cases distributed in T1, T2, T3 and T4 was 16, 32, 42 and 32, and the 5-year survival rate was 78.8%, 64.6%, 49.9% and 30.0%, respectively. The cases distributed in stage I, II, III and IV was 16, 26, 45 and 35, and the 5-year survival rate was 78.8%, 68.4%, 51.3% and 29.0%, respectively. The overall 5-year survival rate was 61.6%.

CONCLUSIONCompared to the presently used clinical staging systems, the new staging system may have more advantages in various parameters for the clinical staging in the carcinoma of nasal cavity, and may be worth to be widely and clinical used.

Adenocarcinoma ; mortality ; pathology ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; Carcinoma, Squamous Cell ; mortality ; pathology ; Female ; Humans ; Male ; Middle Aged ; Nasal Cavity ; Neoplasm Staging ; standards ; Nose Neoplasms ; mortality ; pathology ; Proportional Hazards Models ; Reference Standards ; Survival Analysis

Aim To study whether there was arterial heterogeneity and association with L-type calcium channel (LCC) in different parts of arteries in re-sponse to certain vasoconstrictor. Methods The aor-ta, renal arteries and coronary arteries were dissected from rats. Arterial ring contractions induced by pheny-lephrine (Phe), 5-hydroxyl tryptamine (5-HT) or U46619 in concentration-dependent manner were meas-ured using the Multi Myograph system and the response to nifedipne was observed. Results (1) Phe had no obvious effect on the tension of coronary artery,but in-duced concentration-dependent vasoconstriction in aor-ta and renal artery,and pEC50of aorta was significantly higher than that of renal artery (P<0.05). The inhi-bition rate of nifedipine on the aortic contractile re-sponses was significantly higher than that of renal arter-y (P<0.05). (2) The contraction induced by 5-HT on aorta was not obvious, but was significant on renal artery and coronary artery. The inhibitory rate of nife-dipine on coronary artery vasoconstriction was signifi-cantly higher than that of renal artery (P <0.05). (3) U46619 could induce aorta,renal artery and coro-nary artery concentration- dependent contraction, but the Emaxof them were both higher than that of renal ar-tery (P<0.05). And the pEC50of aorta was the lar-gest (P<0.05). Nifedipine significantly inhibited the contraction of aorta, renal artery and coronary artery induced by U46619 with the greatest inhibitory rate on the coronary artery vasoconstriction and minimal inhibi-tion on aortic vasoconstriction. Conclusions The re-sponse to certain vasoconstrictor is different among aor-ta, renal artery and coronary artery in rats, and the contraction mediated by L-type calcium channel is also different.

AIM:To investigate the possible mechanism of coronary artery contraction induced by 5-hydroxytryptamine(5-HT).METHODS:Isolated coronary artery rings were obtained from male Wistar rats,and the vas-cular tension meter was used to determine the tension of the coronary artery rings.The effects of inhibitors of different sig-naling pathway on vascular contraction tension induced by 5-HT were observed.RESULTS:Firstly,we found that 5-HT2A receptor antagonist sarpogrelate(1 μmol/L)completely eliminated the coronary artery contraction induced by 5-HT.Phos-pholipase Cβ(PLCβ)inhibitor U73122(10 μmol/L and 50 μmol/L), Rho-related protein kinase inhibitor Y-27632(3 μmol/L and 10 μmol/L)and protein kinase C δ subunit(PKCδ)inhibitor rottlerin(3 μmol/L and 10 μmol/L)signifi-cantly inhibited the contraction of coronary artery ring caused by 5-HT(P<0.05).In addition, compared with the un-treated group,vascular contraction tension induced by 5-HT was also decreased significantly by L-type calcium channel (Cav1.2)blocker nifedipine(1 μmol/L), store-operated Ca2+entry(SOCE)inhibitor SKF96365(10 μmol/L and 30 μmol/L)and 2-aminoethoxydiphenyl borate(2-APB,50 μmol/L and 100 μmol/L)(P<0.05).At the same time,5-HT also induced vasoconstriction after treated with nifedipine(1 μmol/L)Kerbs-Henseleit(K-H)liquid without calcium (P<0.05).CONCLUSION:5-HT activates 5-HT2Areceptor induced coronary artery contraction,possibly related to the PKC/Rho kinase signaling pathway and calcium regulation.