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 .

Objective Streptococcus sanguis is a possible candidate bacterium for the caries replacement therapy, which has no advantages in the acidic environment.The aim of the study was to construct acid-resistant strains of Streptococcus sanguis, determine its acid tolerance, and explore the mechanism of its antagonism against Sterptococcus mutans.Methods By gradually reducing the pH value of the medium, we constructed acid-resistant strains of Streptococcus sanguis, observed their growth and measured their acid tolerance according to their survival rate against lethal pH.We evaluated the competitive relationship between Streptococcus sanguis and Streptococcus mutans by plate experiment and detected the changes of related acid resistance genes by real-time quantitative PCR.Results The growth of Streptococcus sanguis and its acid-resistant strains were limited by the pH value, and that of Streptococcus sanguis was better in either acidic or normal environment.The lethal pH value of Streptococcus sanguis was 3.6, that of its acid-resistant strains was 2.3, and the survival rate of the acid-resistant strains was 66.59% in the pH 3.6 environment.In comparison, the lethal pH value of Streptococcus mutans was 2.5, that of its acid-resistant strains was 2.1, and the survival rate of the acid-resistant strains was 2.55% in the pH 2.5 environment.In the presence of chloramphenicol, the acid-resistant strains could not survive in the original lethal pH.In the sub-lethal pH environment, the expressions of the acid resistance-related genes Groel and Dnak in the acid-resistant strains were significantly up-regulated as compared with those in the original Streptococcus sanguis (P<0.05).Conclusion Streptococcus sanguis has an acid adaptability and can enhance acid resistance in the sub-lethal pH environment.Acid-resistant Streptococcus sanguis in the replacement therapy may provide some new ideas for the treatment of dental caries.

Objective To evaluate the role of Src tyrosine kinase in damage to alveolar epithelial cells caused by mechanical stretch.Methods MLE-12 cells cultured in vitro were randomly divided into 3 groups using a random number table:mechanical stretch group (group S),dimethyl sulfoxide control group (group D),and Src tyrosine kinase inhibitor PP2 group (group P).In D and P groups,dimethyl sulfoxide 30 μl/ml and PP2 100 μmol/L were added to the culture medium,respectively,and the cells were then cultured for 30 min.The cells underwent mechanical stretch for 8 h with frequency of0.5 Hz and amplitude of 20％ in the three groups.At 0,2,4 and 8 h of mechanical stretch,MLE-12 cells in 3 wells of each group were collected for determination of cell apoptosis with flow cytometry and expression of occludin using Western blot.The apoptosis rate was calculated.Results Compared with S group,no significant changes were found in the apoptosis rate and expression of occludin at each time point in group D,and the apoptosis rate was significantly decreased,and the expression of occludin was up-regulated at 2,4 and 8 h of mechanical stretch in group P.Conclusion The activation of Src tyrosine kinase is involved in damage to alveolar epithelial cells caused by mechanical stretch.

Objective To investigate the effects of angelica solution on chronic hypoxic pulmonary hypertension in rats.Methods Thirty SD rats were randomized into normoxic group,hypoxic group and angelica solution-protected group.The model of rat chronic hypoxic pulmonary hypertension was made by method of isobaric hypoxia.Angelica solution were injected before hypoxia,while the other two groups were injected normal saline.After 28d of hypoxia,pulmonary artery pressure were measured.Expressions of proliferating cell nuclear antigen (PCNA) and inducible nitric oxide synthase (iNOS) in pulmonary artery were detected by immunohistochemical staining.The index of wall thickness of rat pulmonary arteriole-percentage of the wall area in the total vascular area(wA%) were measured by a computerized image analyzer.Results The mean pulmonary artery pressure (mPAP) of normoxic group,hypoxic group and angelica solution-protected group were10.50±1.90,35.36±9.11,18.32±2.30 (mm Hg);wA% of the three groups were 52.71±5.16,82.38±8.43,64.58±9.54 (%),mPAP and wA% were significantly higher in the hypoxic group than those in the normoxic group (P<0.01) and angelica solution-protected group (P<0.01).PCNA expression of normoxic group,hypoxic group and angelica solution-protected group were 3.15±1.10,24.50±5.72,12.67±3.46 (%).The PCNA expression in the pulmonary artery was significantly higher in the hypoxic group than those in the normoxic group (P<0.01) and in the angelica solution-protected group (P<0.01).iNOS expression of normoxic group,hypoxic group and angelica solution-protected group were 2.13±1.01,17.33±3.53,37.50±7.04 (%).iNOS expression in the pulmonary artery was higher in the hypoxic group than those in normoxic group (P<0.01),and angelica significantly increased iNOS expression in comparison with the normoxic and hypoxic groups (P<0.01).Conclusion Angelica solution alleviates chronically hypoxia induced pulmonary hypertension in rats by inhibiting the espression of PCNA in pulmonary artery and up-regulating the expression of iNOS.

Objective To evaluate the effect of recombinant human annexin A5 on the expression of phosphorylated protein kinase C alpha (p-PKCα) and p120-catenin during endotoxin-induced damage to cardiomyocytes.Methods H9c2 cells cultured in vitro were randomly divided into 3 groups (n=18 each) using a random number table:control group (group C),endotoxin group (group L),and recombinant human annexin A5 group (group A).Recombinant human annexin A5 (final concentration 5 ng/ml) was added,and the cells were incubated for 2 h in group A,and then lipopolysaccharide (final concentration 1 μg/ml) was added,and the cells were incubated for 4 h in L and A groups.At 4 h of incubation,cell apoptosis was detected using the cell apoptosis detection kit,the intercellular space was measured using the confocal microscopy,and the expression of p-PKCα and p120-catenin was determined by Western blot.The apoptosis rate was calculated.Results Compared with group C,the apoptosis rate was significantly increased,the intercellular space was significantly widened,the expression of p120-catenin was significantly down-regulated,and the expression of p-PKCα was significantly up-regulated in group L (P＜0.05).Compared with group L,the apoptosis rate and intercellular space were significantly decreased,the expression of p120-catenin was significantly up-regulated,and the expression of p-PKCα was significantly down-regulated in group A (P＜0.05).Conclusion Recombinant human annexin A5 can inhibit phosphorylation of PKCα and up-regulate the expression of p120-catenin,thus attenuating endotoxin-induced damage to cardiomyocytes.

Objective To investigate the effect of the Shaofu zhuyu decoction on the changes of the body writhing behavior,inflammatory reaction and COX-2 expression of the rats with the primary dysmenorrhea. Methods Fifty SD female rats were randomly divided into blank control group,model control group,high,middle and low dose of Shaofu zhuyu decoction groups,10 in each group.Dysmenorrhea rat model was established by treating with estradiol benzoate and oxytocin.Effect of Shaofu zhuyu decoction of different doses on writhing behavior,changes of endometritis cells and COX-2 expression in uterine smooth muscle of dysmenorrhea rats were observed. Results In the model control group,latency of the body writhing behavior was shortened and the total score was high,many inflammatory cells (especially for neutrophils) infiltrated in endometrium and uterine smooth muscle,immunohistochemistry showed that brown granules were found in the cytoplasm of smooth muscle cells of uterus,and COX-2 expression was positive in uterine smooth muscle cells.As compared with the model control group,writhing latency increased,total score decreased in both the high and middle dose of Shaofu zhuyu decoction groups,and infiltration of a small number of inflammatory cells was seen in the endometrium and smooth muscle(P<0.01);COX-2 expression was decreased (P<0.01) especially for the high dose of Shaofu zhuyu decoction group.As compared with the model control group,the latency of the low dose of Shaofu zhuyu decoction group was significantly increased,and the total score was decreased(P<0.01),but there was no significant difference in inflammatory cell infiltration and COX-2 expression (P>0.05). Conclusion A potential mechanism by which Shaofu zhuyu decotion treats primary dysmenorrhea may be related with alleviating pain,inhibiting inflammatory responses,and down-regulating expression of COX-2.

Objective: To explore the association between digital devices usage and body weight overestimation in children and adolescents aged 7-18, in order to provide a scientific basis for body weight overestimation prevention in children and adolescents. Methods: Based on the data of the Research Special Project for Public Welfare Industry of Health using stratified cluster sampling method in 2012, a tatal of 40 073 children and adolescents from 7 provinces with complete information were chosen. Ordinal multivariable Logistic regression model estimated the association between digital devices usage and body weight overestimation. Results: A total of 4 276(11.8%) students with overestimation of body weight were detected, who spent >300 min/d time in digital devices(5.12%) than others (3.84%)( χ 2=19.14, P <0.01). Univariate analysis showed that students with time spent on digital devices >300 min/d had a higher risk in overestimation of body weight ( OR=1.36,95%CI=1.18-1.57,P <0.01) compared with students who spent on digital devices≤120 min/d. There was still a significant association after confounder adjustment ( OR=1.28, 95%CI= 1.10-1.48,P <0.05). Stratified analysis showed that the association between digital devices usage and overestimation of body weight were only observed in girls, 11-18 years old and non single child( P <0.05). Conclusion The time usage of digital devices is associated with overestimation of body weight in children and adolescents. It may helpful for children and adolescents to prevent overestimation of body weight by reducing time spent on digital devices.

The hospital introduced a multi-department synergy in management of the rational use of carbapenems. Specifically,the medical affairs department conducts training and appraisal of doctors along with a monthly checkup of medical records. The pharmaceutical affairs division conducts prior prescriptions checkup and follow-up comment. The clinical microbiology laboratory and the hospital-acquired infection management department monitors and releases such infection and bacterial resistance information of the whole hospital in real time. The results showed increased prescriptions of imipenem and cilastatin sodium, and decreased prescriptions of biapenem for injection. Drug resistance analysis showed that carbapenem resistant strains increased by 28%,but the total number of patients reduced by 10% and total number of patients with multidrug resistance remained unchanged. It is proposed to further antimicrobial stewardship in the hospital to achieve rational drug use and curb bacterial resistance.

ObjectiveTo explore the mechanism of Dihuang Yinzi （DHYZ）in improving astrocyte injury in the brain and regulating energy metabolism and autophagy disorder in Alzheimer's disease （AD） model mice. MethodForty male APP/PS1 transgenic mice aged four months were randomly divided into a model group and a model + DHYZ group （2.5 g·kg^-1）， with 20 mice in each group. Forty C57BL/6J mice with the same background and same age were randomly divided into a control group and a control + DHYZ group （2.5 g·kg^-1）， with 20 mice in each group. The mice in the control group and the model group were administered with an equal volume of sterilized normal saline by gavage， once a day for 150 days. Novel object recognition test and step-down test were performed to evaluate the learning and memory ability of mice. The expression of glial fibrillary acidic protein （GFAP） in astrocytes was detected by immunofluorescence and Western blot. High-performance liquid chromatography （HPLC） was used to detect adenosine triphosphate （ATP）， adenosine diphosphate （ADP）， and adenosine monophosphate （AMP） in brain tissues of mice， and the data obtained were used to calculate energy charge （EC） levels. The phosphorylation levels of liver kinase B1 （LKB1）， adenosine 5′-monophosphate （AMP）-activated protein kinase （AMPK）， UNC-51-like kinase 1 （ULK1）， and mammalian target of rapamycin （mTOR） and the expression levels of autophagy-related proteins Beclin-1， microtuble-associated protein 1 light chain 3 （LC3）-Ⅱ/LC3-Ⅰ， and p62 in mouse brain were measured by Western blot. ResultCompared with the control group， the model group showed decreased novel object recognition index， shortened retention latency， increased error times in the step-down test， up-regulated protein expression of GFAP， decreased content of ATP， ADP， and EC in brain tissues， elevated AMP ， increased levels of p-AMPK， p-LKB1， and p-mTOR， and protein expression of p62 ， and down-regulated p-ULK1 level and protein expression of Beclin-1 and LC3-Ⅱ/LC3-Ⅰ（P<0.01）， while the above experimental indexes were not significantly different in the control + DHYZ group. Compared with the model group， the model + DHYZ group showed increased novel object recognition index（P<0.05）， prolonged retention latency（P<0.01）， decreased error times（P<0.01） in the step-down test， reduced protein expression of GFAP（P<0.05）， increased content of ATP， ADP， and EC in brain tissues （P<0.05， P<0.01）， decreased AMP content（P<0.05）， reduced p-AMPK， p-LKB1， and p-mTOR levels and protein expression of p62， and up-regulated p-ULK1 level and protein expression of Beclin-1 and LC3-Ⅱ/LC3-Ⅰ（P<0.01）. ConclusionBy protecting astrocytes， DHYZ can improve energy metabolism and autophagy disorder in AD mice to improve the learning and memory ability of model mice.

ObjectiveTo investigate the mechanism of Dihuang Yinzi in improving astrocyte injury and protecting synaptic structure and function in the brain of Alzheimer's disease （AD） mice. MethodForty male APP/PS1 transgenic mice aged four months were randomly divided into a model group and a model + Dihuang Yinzi （0.25 g·kg^-1） group， with 20 mice in each group. Forty C57BL/6J mice with the same background and same age were randomly divided into a control group and a control + Dihuang Yinzi （0.25 g·kg^-1） group， with 20 mice in each group. The mice in the control + Dihuang Yinzi group and the model + Dihuang Yinzi group were administered with Dihuang Yinzi by gavage， and those in the control group and the model group received an equal volume of sterilized normal saline， once a day for 150 days. The learning and memory ability of mice was tested by the light-dark box test and Y-maze spontaneous alternation test. The content of glutamate （Glu） and glutamine （Gln） was measured by liquid chromatography-tandem mass spectrometry （LC-MS）. Long-term potentiation （LTP） assay was used to detect synaptic plasticity in brain tissues. The protein expression levels of excitatory amino acid transporter 2 （EAAT2）， postsynaptic density protein95 （PSD95）， and synaptophysin （SYN） in brain tissues were measured by Western blot. Immunofluorescence was used to assess the localization and expression of EAAT2. Colorimetry was performed to detect Na⁺-K⁺ ATPase activity in mouse brain tissues. ResultAs compared with the control group， the model group showed shortened residence latency （P<0.01）， increased number of errors （P<0.01） in the light-dark box test， reduced spontaneous alternation behaviors （P<0.01）， no significant difference in the total number of arm entries in the Y-maze spontaneous alternation test， down-regulated expression of EAAT2， PSD95， and SYN （P<0.01）， blunted activity of Na⁺-K⁺ ATPase （P<0.01）， up-regulated Glu level （P<0.01）， down-regulated Gln level （P<0.01）， and reduced relative population spike （PS） amplitude and the slope of excitatory postsynaptic potential （EPSP） （P<0.05， P<0.01）， while the above experimental indexes were not significantly different in the control + Dihuang Yinzi group. Compared with the model group， the model + Dihuang Yinzi group displayed prolonged residence latency （P<0.05）， decreased number of errors （P<0.01） in the light-dark box test， increased spontaneous alternation behaviors （P<0.01）， no significant difference in the total number of arm entries in the Y-maze spontaneous alternation test， up-regulated expression of EAAT2， PSD95， and SYN （P<0.01）， potentiated activity of Na⁺-K⁺ ATPase （P<0.01）， reduced Glu level （P<0.01）， up-regulated Gln level （P<0.01）， and increased PS amplitude and EPSP slope （P<0.01）. ConclusionDihuang Yinzi can improve cognitive dysfunction in AD mice by protecting astrocytes， increasing Glu uptake to reduce its abnormal accumulation， and protecting synaptic structure and function.