Objective Antimicrobial peptides are the focus of recent research in oral microbiology .This study aimed to eval-uate the activity of a novel antimicrobial peptide pm 11 against oral microorganisms and its action mechanisms . Methods We ana-lyzed the effect of pm11 on oral microorganisms and determined its antimicrobial activity in the saliva environment by measuring its min -imal inhibitory concentration (MIC), minimal bactericide concentration (MBC), and bactericidal kinetics.We observed its bacteri-cidal activity on the biofilms of streptococcus mutans by confocal laser scanning microscopy (CLSM) and the structural changes in the bacterial membrane by scanning electron microscopy (SEM). Results The antimicrobial activity of pm11 varied greatly against dif-ferent oral microorganisms , with its MIC values ranging from 2 μg/mL to 256 μg/mL and its MBC values from 2 μg/mL to >256μg/mL.The bactericidal kinetics showed a decreasing survival rate of bacteria with the lengthening of the intervention time .The inhib-itory-zone diameters exhibited no significant indifference between the water solution and the sterile saliva solution .CLSM revealed an increased number of dead bacteria in the pm 11-treated biofilms , while SEM manifested obvious changes in the shape of the bacteria membrane treated with pm11. Conclusion Our findings suggest that pm11 has a broad spectrum of antimicrobial activities on oral mi-croorganisms and a potential value of clinical application .

Objectives To study the expression patterns of steroid receptor coactivators (SRC) and steroid-induced stromal cell-derived factor-1 (SDF-1) in endometriosis,and to explore the roles of SRC in the steroid-induced SDF-1 expression endometriosis.Methods From May 2010 to October 2012,16 endometriosis cases at stages Ⅲ or Ⅳ according to the revised American Society for Reproductive Medicine classification undergoing surgery in the First Affiliated Hospital to Nanjing Medical University were enrolled in this study.Their ectopic endometrium were from ovarian endometriomata which were identified pathologically with 9 cases at proliferative phase and 7 cases at secretory phase.The normal endometrium were acquired from the healthy women with normal menstrual cycle (n =10,proliferative phase =5,secretory phase =5).The mnRNA levels of SRC and SDF-1α during the menstrual cycle were detected by quantitative real-time polymerase chain reaction.Ectopic endometrium stromal cells were purified and cultured in medium containing 17β-estradiol (10-8mol/L) or 17β-estradiol (10-8 mol/L) + progesterone (10-6 mol/L).At 24,48,72 and 96 hours,the supernatants were collected to measure SDF-1α expression by ELISA.Ectopic endometrium stromal cells were transfected respectively with siRNA of SRC-1 and SRC-2 using lipofectamine.Two days after transfection,17β-estradiol (10-8 moL/L) or 17β-estradiol (10-8 mol/L) + progesterone (10-6 mol/L) were added into the media.On the third day after the steroid hormones treatment,the media were collected to quantify SDF-1α expression with ELISA.Results (1) Cyclical changes: the SRC-1,SRC-2 and SDF-1 α showed marked cyclic differences in normal endometrium (P ＜ 0.05).In proliferative phase and secretory phase,the SRC-1,SRC-2 and SDF-1 α were 5.6 ± 1.2,3.8 ± 1.1,2.7 ± 0.5 and 2.6 ± 1.0,2.1 ± 1.0,1.6-± 0.5,respectively.There was no periodic variation in the expression of SRC-1,SRC-2 and SDF-1α in ectopic endometrium throughout the menstrual cycle.(2) Steroid-induced SDF-1α expression in ectopic endometrium stromal cells: the 17β-estradiol-induced SDF-1α expression was (1 803 ± 196),(2 272 ± 261) and (2 162 ± 258) ng/L at 48,72 and 96 hours.At the same time points,the SDF-1α expression induced by 17β-estradiol and progesterone was (1 307 ± 150),(1 518 ± 301) and (1 550 ± 144) ng/L,respectively.There was significant difference between two groups (P ＜0.05).(3) The effects of SRC silencing on steroid hormones-induced SDF-1 α expression in ectopic endometrium stromal cells: the expression of 17β-estradiol-induced SDF-1α at 72 hours was significantly decreased from (2 313 ± 357) ng/L to (1 155 ± 244) ng/L after the silencing of SRC-1 (P ＜ 0.05).After the silencing of SRC-2,the 17β-estradiol-induced SDF-1 α at 72 hours was (1 958 ±324) ng/L.There was no significant difference compared with the before the silencing (P ＞ 0.05).The expression of SDF-1 α at 72 hours induced by 17β-estradiol + progesterone was (1 534 ± 449) ng/L and (2 051 ± 380) ng/L respectively before and after the silencing of SRC-2 and showed the significant difference (P ＜ 0.05).Conclusion During the expression of SDF-1 α regulated by steroids in ectopic endometrium cells,SRC-1 is the major coactivator of 17β-estradiol and SRC-2 is the major coactivator of progesterone.

0.05),and NK cells function(CD56),humoral immunologic function(IgG,IgM,IgA)were significantly elevated after TP-5 administration for 3 months(Pa

Abatacept ; Case-Control Studies ; Chromosomes, Human, Pair 2 ; Diabetes, Gestational ; genetics ; Exons ; Female ; Genetic Predisposition to Disease ; Glucokinase ; genetics ; Humans ; Immunoconjugates ; genetics ; Mutation ; Pregnancy ; Promoter Regions, Genetic

Antineoplastic Agents ; administration & dosage ; therapeutic use ; Child ; Female ; Humans ; Injections, Intralesional ; Interferon-alpha ; administration & dosage ; therapeutic use ; Male ; Neoplasms ; drug therapy ; Recombinant Proteins ; Treatment Outcome

Objective To observe the effects of iodine excess on thyroid morphology,the expression of thyroid peroxidase and sodium iodide symporter mRNA and to explore their mechanisms.Methods One-month SD rats were divided into three groups:control iodine(CI),high iodine Ⅰ(HI Ⅰ)and high iodineⅡ(HI Ⅱ)and were fed with water containing iodine in different concentrations by adding K103(5,5000,10 000μg/L)respectively.Rats were sacrificed after being fed for six months.The morphology of thyroid was investigated under light microscopy and electron microscopy,the serum thyroid hormones and ratio of TPO/β-actin and NIS/β-actin were measured by radio-immunoassay and RT-PCR method.Results The major changes were increased follicles with colloid accumulation in HI groups.The levels of serum thyroid hormones TT3 and TT4 were decreased gradually from CI[(75.68±13.99,1.45±0.49)nmol/L]to HI Ⅰ[(73.82±16.48,1.34±0.31)nmol/L]and HIⅡ groups[(70.65±11.43,1.15±0.39)nmol/L],but there were no significant differences among three groups(F=O.371,l.163,P＞0.05).The TPO and NIS mRNA expressions in HI Ⅰ(1.28±0.10,0.56±O.17)and HI Ⅱ(1.14±0.04,0.39±0.06)were significantly lower(F=30.863,62.62.675,P＜O.05)than those of control group(1.39±0.08,0.71±0.13).Conclusions Chronic iodine excess leads to definite histological changes in rat thyroid,and inhibits the expressions of TPO and NIS mRNA as well as thyroid hormone synthesis,which in turn acts as a protective mechanism against iodine excess.

It is an important task to lab of clinical microbiology to surveille multi-drag or pan-drug resistant strains,such as penicillin-or macrolide-resistant Streptococcus pneumoniae,methicillin-resistant Staphylococcus aureus(MRSA),3rd generation cephalosporin-or quinolone-resistant Enterobacteriaceae, carbapenem-resistant Pseudomonas aeruginosa or Acinetobacter baumannii,and so on.We must understand characteristics of these resistant strains to guide doctors' empirical therapy of infective diseases.

Objective:To express and purify the TRIM5? chimaera[TRIM5? H(R328-332)] protein and to explore the interaction between the TRIM5? H(R328-332)and HIV-1gag. Methods:The plasmid pET28aTRIM5? H(R328-332) was transformed to E.coli BL21 (DE3) strain ,and the expression of TRIM5? H(R328-332) protein was induced by IPTG,purified with Ni2+ chromatography.The expression and purification of TRIM5? H(R328-332) were analyzed by SDS-PAGE and Western blot,and the interaction between TRIM5? H(R328-332) and HIV-1gag was detected by co-immunoprecipitation,His pull-down and ELISA. Results:The recombinant plasmid pET28aTRIM5? H(R328-332) was successfully expressed in E.coli. The results showed that the purified full length TRIM5? H(R328-332) interacted with HIV-1gag protein. Conclusion:The human TRIM5? chimaera was expressed successfully in vitro,and the study demonstrates that the human TRIM5? chimaera interacts with HIV-1 gag in vitro.

Objective To study the method of internal boundary parameters identification of middle ear.Method The numerical model is created using CT technology.Based on Matlab tools,the neural network for identifying internal boundary is proposed.Result The uniform pressure of 105 dB is applied at the outside of the tympanic membrane,and the harmonic analysis is calculated on the model to take the training samples.The internal condition parameters are identified using the good neural network.Conclusions The investiga-tion shows that the inverse method reveals a fast convergence and a high degree of accuracy.

Objective To study the method of internal boundary parameters identification of middle ear.Method The numerical model is created using CT technology.Based on Matlab tools,the neural network for identifying internal boundary is proposed.Result The uniform pressure of 105 dB is applied at the outside of the tympanic membrane,and the harmonic analysis is calculated on the model to take the training samples.The internal condition parameters are identified using the good neural network.Conclusions The investiga-tion shows that the inverse method reveals a fast convergence and a high degree of accuracy.