Twelve specimens of genital warts were excised from 12 patients and divided into three parts. One part was untreated, the second and the third part were treated with CO_2 laser and microwave respectively. HPV DNA was amplified and detected in 100% of untreated specimens (HPV16 and HPV11 in six patients each), in 83% and 50% of specimens treated with CO_2 laser and microwave respectively. There was a significant difference in the detection rates between untreated and microwave treated specimens (X~2=4.18, P

Objective To investigate the inhibitory effects of traditional Chinese medicine (TCM) on hypermelanosis and provide experimental evidence for treating skin pigmentary disorders. Methods Five TCMs with strong inhibitory effects on tyrosinase activity were tested. The changes of the number and morphology of melanocytes induced by UVB were observed in the experimental hypermelanosis model (brownish guinea pig). Results Decreased melanocytes and melanin granules were found with the treatment of Poria cocos, Polyporus umbellatus, Cornus officinalis Sieb. et Zucc., Atractylodes macrocephala Koidz., Astoagalus complanatus R. Br. ex Bge. Conclusion There are inhibitory effects on hypermelanosis induced by UVB with the treatment of Poria cocs, Polyporus umbellatus, Cornus officinalis Sieb.et Zucc., Atractylodes macrocephala Koidz., Astoagalus complanatus R. Br.ex Bge.

Hepatocellular carcinoma (HCC)is a disease with high incidence and mortality and has become a serious threat to human health. So far,none of the available markers can be used alone for early diagnosis of HCC.Recently identified serum markers with potential clinical value for early diagnosis of HCC are summarized,and their diagnostic sensitivity and specificity,as well as their applications in assessment of progression of the disease,are reviewed.It is suggested that alpha -fetoprotein should be used in combination with other serum markers to achieve accurate diagnosis of HCC at early stages.

砄bjective:To observe streptococcus sanguis (S.s) and Actinomycetes viscosus (A.v) in oral plaque biofilm formation.Methods:20 ml of saliva obtained from a health adult was centrifuged at 4 ℃ and 10 000 r/min for 10 min.The supernatant was disinfected in 60 ℃ water bath for 30 min.Glass coverslips in the size of 24 mm?24 mm were immersed into the saliva supernatant for 2 h to obtain biofilm.100 ?l of S.s ATCC 34 and A.v ATCC 19246 mixture cultured in TSB at the density of 10 5～6 CFU/ml was added into 20 ml of TSB,and then,the coverslips with biofilm were put into the mixture.The biofilm and bacteria were observed by scanning confocal laser microscopy at various times.Resuts:The biofilm reached the thickness of 15.4 ?m in 8 h and the clumps of the bacteria were mostly in the midle layer of the biofilm.The biofilm increased to 34.3 ?m in 16 h and became tassle like in 48 h.Conclusion: S.s and A.v may play some roles in the oral biofilm formation.

Objective: To develop a new antimicrobial sensitivity test model for oral products in vitro. Methods: An artificial biofilm mouth model for antimicrobial sensitivity test was established by modified LKB chromatography chamber. Using sodium fluoride and tea polyphenol as antimicrobial agents and Streptococcus mutans as target, various methodologies on the sensitivity tests were compared. Results: Agar diffusion, agar dilution and broth macro-dilution were more sensitive than modeling biofilms method. The modeling biofilm assay resulted in MIC values of fluoride or tea polyphenol against S. mutans 32 and 12 times higher respectively than the MIC values generated by broth macro-dilution method. Conclusion :The biofilm artificial mouth model may simulate the environment for oral products test.

Objective To investigate the ultrastructural characteristics of amelanotic melanocytes (AMMCs). Methods Individual hair follicles from normal human scalp were digested with collagenase type V, then washed in phosphate buffer saline. Hair-follicle cell suspensions were prepared by trypsin and cultured in a medium suitable for melanocyte growth. The keratinocytes were removed by differential trypsinization. Geneticin (100?g/mL) was used to eliminate contaminating fibroblasts. After 3 passages the cells were trypsinized, washed in phosphate buffer saline, and finally processed for transmission electron microscopy. Results Under transmission electron microscope, the cultured cells were round or oval-shaped with a single large nucleus and double-layered karyotheca. Abundant euchromosome but sparse heterochromosome was observed within the nucleus. There were various organelles in the cytoplasm, including mitochondria, rough endoplasmic reticulum (RER), ribosomes and abundant melanosomes of nearly uniform size. The electronic density granules distributed in a concentric pattern in most of the melanosomes. Colgi complexes were inconspicuous in the cells. Conclusions Compared to epidermal melanocytes, AMMCs from human hair follicles have different ultrastructural characteristics which implies their functional immaturity. AMMCs may serve as the depot for mature melanocytes.

OBJECTIVE: To explore the antitumor activities of kushen (Sophora flavescens) flavonoids (KS-Fs) in vivo and in vitro. METHODS: Cell proliferation was assayed by using methyl thiazolyl tetrazolium (MTT) method. H22 hepatocellular carcinoma and S180 sarcoma were induced in ICR mice. Lewis lung carcinoma was induced in C57BL/6 mice. H460 and Eca-109 tumor were induced in Balb/c nude mice by injecting 5x10(5) or 5x10(6) tumor cells in the right flank, respectively. RESULTS: KS-Fs could inhibit the growth of a variety of human tumor cell lines (A549, SPC-A-1, NCI-H460, etc.) in vitro. The antitumor efficacies were confirmed in the mice models of H22, S180 and Lewis lung tumors and the nude mice models of human H460 and Eca-109 xenografted tumors. The oral or intravenous maximum tolerated dose of KS-Fs was more than 2.8 g/kg or 750 mg/kg respectively, far more than the oral medial lethal dose of kushen alkaloids (< or = 1.18 g/kg). No adverse reactions were observed. CONCLUSION: These results suggest that KS-Fs or kurarinone may be developed as a novel antitumor agent.

Objective To investigate the role of inducible nitric oxide synthase (iNOS) in reduction of myocardial ischemia-reperfusion (I/R) injury by sufentanil preconditioning in rats. Methods Thirty adult male SD rats, weighing 250-330 g, were randomly divided into 5 groups ( n =6 each): sham operation group (group S),I/R group, sufentanil preconditioning group (group SF), sufentanil preconditioning + a specific inhibitor of iNOS S-methyl thiourea (SMT) group (group SF+ SMT) and S-methyl thiourea group (group SMT). In I/R,SF,SF+SMT and SMT groups, myocardial I/R was produced by occlusion of left anterior descending coronary artery for 30 min followed by 120 min reperfusion. Group SF received 30 min infusion of sufentanil 120 μg/kg via caudal vein 24 h before ischemia. Group SF + SMT received infusion of sufentanil 120 μg/kg via caudal vein 24 h before ischemia and then SMT 10 mg/kg was injected 10 min before ischemia. In group SMT, SMT 10 mg/kg was injected 10min before ischemia. MAP and HR were recorded at 30 min before ischemia, at 30 min of ischemia and at the end of reperfusion. The rate-pressure product (RPP) was calculated. Arterial blood samples were obtained immediately at the end of reperfusion to determine the plasma concentration of NO. Then the animals were sacrificed and myo cardial tissues were obtained to determine the area at risk (AAR), infarct size (IS) and iNOS expression. IS/AAR was calculated. Results Compared with group S, MAP and RPP were significantly decreased, while IS/AAR was significantly increased at 120 min of reperfusion in the other four groups, and MAP and RPP were significantly decreased at 30 min of ischemia in I/R and SMT groups ( P ＜ 0.05). Compared with group I/R, no significant change was found in HR, MAP and RPP in SF, SF + SMT and SMT groups, and in IS/AAR and plasma NO concentrations in SF + SMT and SMT groups ( P ＞ 0.05), but IS/AAR was significantly decreased, and the plasma NO concentration and iNOS expression were significantly increased in group SF ( P ＜ 0. 05). Conclusion iNOS is involved in reduction of myocardial I/R injury by sufentanil preconditioning in rats.

Objective To evaluate the effect of remffentanil postconditioning on myocardial ischemiareperfusion (I/R) injury in patients undergoing open heart surgery under CPB.Methods Thirty patients (ASA grade Ⅱ or Ⅲ, NYHA class Ⅰ or Ⅱ ) of both sexes aged 18-45 yr undergoing repair: of ventricular septal defect and/or atrial septal defect under CPB were randomly divided into 2 groups ( n = 15 each): control group (group C)and remifentanil postconditioning group (group R). Anesthesia was induced with midazolam, sufcntanil, propofol and rocuronium. The patients received 5 min infusion of remifentanil at 4 μg · kg- 1 · min - 1 8 min before aortic unclamping in group R, while the patients received equal volume of normal saline in group C. Blood samples were obtained from the right internal jugular vein for determination of plasma concentrations of cardiac troponin-I (cTnI)and MDA and activities of CK-MB and SOD before induction of anesthesia (baseline) and at4, 8, 24 and48 h after aortic unclamping. Results The plasma concentrations of cTnI and MDA and activity of CK-MB were significantly lower, while the plasma SOD activity was significantly higher at 4 and 8 h after aortic unclmping, and the plasma concentration of MDA was significantly lower at 24 h after aortic unclamping in group R than in group C ( P ＜ 0.05 ). Conclusion Remifentanil postconditioning can attenuate myocardial I/R injury in patients undergoing open heart surgery under CPB through inhibiting lipid peroxidation.

Objective To evaluate the effect of emulsified isoflurane preconditioning on myocardial iachemia-reperfusion (I/R) injury in rabbits.Methods Thixty-two male New Zealand white rabbits weighing 2.5-3.0 kg were randomly divided into 4 groups(n=8 each):group Ⅰ I/R;group Ⅱ isoflurane preconditioning (group Ⅰ);group Ⅲ emulsified isoflurane preconditioning (group EI) and group Ⅳ intralipid (group INT).Myocardial I/R was induced by 30 min occlusion of left anterior descending branch of coronary artery followed by 180 min of reperfusion.After 30 min of post-preparation equilibration.the animal inhaled 3%isoflurane for 30 min followed by 15 min washout in group Ⅰ(group Ⅱ);8% emulsified isoflurane 8-10 ml was injected iv at 1 ml/s followed by continuous infusion at 6-8 ml·kg-1·h-1,maintaining end-tidal isoflurane concentration at 1.28% for 30 min in group EI (groupⅢ);30% intralipid 9 ml was injected iv at 1 ml/s fullowed by continuous infusion at 7 ml·kg-1·h-1 for 30 min in group INT (group IV).HR and BP were monitored and recorded at 30 min of post-preparatory equilibration(T0),before ischemia(T1),at the beginning of ischemia(T2),at 30 min ofischemia(T3),60,120 and 180 min of reperfnsion(T4,5,6).HR-SP product (RPP) was calculated.Infarct size (IS) was determined by TIC staining.Blood samples were taken from carotid artery at T6 for determination of serum CK and LDH activities and IL-6 and IL-10 concentrations.Results HR,MAP and RPP were decreasing during T2-6, but there was no significant difference in HR, MAP and RPP among the 4 groups.The infarct size was signigicantly smaller, serum CK and LDH activities and IL-6 concentration were significantly lower while serum IL-10 concentration was significantly higher in group I and EI than in group I/R and INT.Conclusion Emulsified isoflurane preconditioning can attenuate myocardial I/R injury by inhibiting inflammatory response.