Caries is one of the most common chronic progressive oral diseases. TCM medicinal herbs have many advantages compared with traditional dental drugs for caries (such as fluoride). In recent years, cariogenic TCM medicinal herbs have attracted the attention of many domestic and foreign scholars. Caries is not caused by a single factor. The development of caries is closely related to bacterial biofilms that are formed by streptococcus mutans, streptococcus sanguis, actinomyces inside, actinomyces and lactobacillus. Therefore, this article took a brief overview of TCM medicinal herbs and their active ingredients that inhibit the bacterial biofilms.

Objective:To study the effects of 3 extracts from Chinese gall on the growth and metabolism of 6 kinds of oral bacteria.Methods:Through a series of extraction and purification,3 active monomer,gallnut extract gallic acid,methyl gallate and gallic acid ethyl ester were selected.Streptococcus mutansUA159(UA159),Actinomyces viscosus (Av),Porphyromonas gingivalis (Pg),Enterococcus faecalis (Ef),Fusobacterium nucleatum(Fn) and Candida albicans (Ca) were treated by the extracts respectively,The growth and metabolism of the becteria were studied by liguid dilution method.Results:The MIC(mg/ml) of Gallic acid anainst the bacteria was 2.5-5,methyl gallate 2.0-4.0 and gallic acid ethyl ester 1.25-2.5.The extracts at 1 mg/ml could inhibit the growth,acid production and extracellular polysaccharides of the 6 oral pathogens.And ethyl gallate showed the strongest effects.Conclusion:Gallic acid and methyl gallate and ethyl gallate at low concentration may inhibit the growth,acid metabolism and glucose metabolism of oral bacteria.

Objective To observe the impact of modified Liangge powder (MLP) on platelet activation markers and the release of proinflammatory cytokine in mice by stimulation of lipopolysaccharide (LPS). Methods 112 male mice were randomly divided into control group, model group and MLP low, middle and high dose treatment groups. The sepsis model was reproduced by injection of LPS 10 mg/kg into a mouse tail vein. In the control group, normal saline 10 mg/kg was injected into the tail vein of mouse. The MLP low, middle, and high dose groups received 0.94, 1.89, 2.84 g/mL MLP 0.02 mL/g by gavage respectively for 3 days, while the control group and model group received equal amount of normal saline by gavage for 3 days. After modeling for 24 hours and 72 hours, 8 mice in each of the three different dose MLP groups and model group were killed and their blood was taken. In the control group, after modeling for 24 hours, 8 mice were killed and their blood was taken. Platelet (PLT) was counted by blood cell analyzer, plasma interleukin-10 (IL-10), high mobility group protein B1 (HMGB1) and platelet factor 4 (PF4) were detected by enzyme-linked immunosorbent assay (ELISA). In each group after modeling for 72 hours, another 8 mice were taken, and laser scanning confocal microscopy was used to measure the platelet cytosolic Ca2+ concentration. Results Compared with the control group, the level of PLT at 24 hours(×109/L: 347.70±115.10 vs. 1 013.10±136.60) was decreased, and the levels of IL-10 (μg/L: 356.86±34.72 vs. 39.50±23.45), HMGB1 (mg/L: 16.24±4.49 vs. 10.75±1.91), PF4 (μg/L: 5.43±0.61 vs. 1.33±0.40) and Ca2+ (nmoL/L: 8.60±0.52 vs. 1.05±0.33) were elevated in model group. Compared with the model group, the levels of PLT in the MLP high, middle and low dose groups were all significantly elevated; the increase in PLT in middle dose group after modeling for 72 hours was the most remarkable (×109/L:952.13±104.02 vs. 771.50±129.30, P < 0.05); the levels of IL-10, HMGB1, PF4, Ca2+ in MLP low, middle, high dose groups were significantly decreased. The most obvious degree of decrease in level of the following indexes were as follows:IL-10 in MLP high dose group at 72 hours after modeling (μg/L:110.17±29.12 vs. 441.50±30.72), HMGB1 in MLP high dose group after modeling for 24 hours (mg/L: 10.33±3.52 vs. 16.24±4.49), PF4 in MLP middle dose group after modeling for 24 hours (μg/L:2.08±0.92 vs. 5.43±0.61) and Ca2+ in MLP high dose group (nmoL/L:2.97±0.96 vs. 8.60±0.52, all P<0.05). Conclusion MLP may possibly down-regulate the inflammatory cytokines release induced by LPS to inhibit the activation of platelet Ca2+, in turn prevent the activation of platelet and improve thrombocytopenia caused by LPS.

Objective To comparatively study the characteristics of 3 kinds of culture substrates of human odontogenic induced pluripotent stem cells(iPSCs).Methods The human odontogenic iPSCs were cultured by 3 kinds of substrates:mouse embryonic fibroblasts(MEF),matrigel and recombinant human vitronectin(VTN-N).The iPSCs growth situation was compared among three groups.Results The preparation time of these 3 kinds of substrates was 14,3,1 hlespectively,and,the difference was statistically significant (P＜0.05).The iPSCs reprogramming time was (30± 1.6),(26 ± 2.1),(27 ± 1.4) d,lespectively,wht that in the MEF group significantly higer than in other two groups (P＜0.05).The reprogramming efficiencies were 0.3 ％ ± 0.03 ％,0.56 ％ ± 0.08 ％,0.7 ％ ± 0.02 ％ respectively (P＜ 0.05).Three kinds of substrate could better support iPSCs growth and make them to maintain un-differentiation status.Conclusion with no heterologous animal components,and the adrantaga of simple pleparation,oonfrollable standard and shorter gramming time is easy to prepare,the standard is controllable and the reprogramming time is shorter,which is an ideal substrate for supporting iPSCs growth.

Objective To compare the growth characteristics,proliferation and osteo/odontogenic differentiation capability of stem cells from human dental pulp (dental pulp stem cells,DPSCs) and apical papilla (stem cells from apical papilla,SCAP) in vitro.Methods Human dental pulp and apical papilla tissues were separated from impacted third molars of young healthy donors at the age of root development and digested by collagenase type Ⅰ and dispase type Ⅱ to derive primitive DPSCs and SCAP.Cells were then induced for osteo/odontongenic differentiation by medium containing β-glycerophosphate,dexamethasone and KH2PO4.Flow cytometry was utilized to test the expression of specific markers of stem cells,including CD24,CD34,CD45,CD90,CD105,CD146,STRO-1 and OCT-4.AR-S was used to display the mineralization structure and RT-PCR was applied to analyze the expression of bone sialoprotein (BSP),osteocalcin (OCN) and dentine sialophosphoprotein (DSPP).Results Both DPSCs and SCAP were positive for CD90,CD105,CD146,STRO-1 and OCT-4,in percentages varying according to cell type,without expression of CD34 or CD45.Only SCAP expressed CD24 positively.Both cells formed organized mineralization structure after 2 weeks of induction in time-dependent manner,with more mineralization by SCAP and expressed differentiation markers,including BSP,OCN and DSPP.Conclusion Human DPSCs and SCAP possess the characteristics of MSCs and could be differentiated into odontonblast-like cells in vitro.Both cells are approachable stem cell sources for dental tissue engineering.

ObjectiveTo evaluate the effects of Esmolo on the hemodynamic and tissue oxygenation of the patients with septic shock and tachycardia.MethodsSeventy four septic shock patients with tachycardia were enrolled and randomized into Esmolo-treated group and control group after early goal-directed therapy (EGDT).The patients in Esmolo group were given intravenous Esmlol to decrease the heart rate to below 110 beats per minute.Hemodynamic data and tissue oxygenation parameters,such as Heart rate (HR),Mean Artery Pressure ( MAP),Central Venous Pressure ( CVP),Cardiae Index ( CI),Stroke Volume Index ( SVI),Systemic Vascular Resistance Index (SVRI),Lactate,Centrol Venous Oxygen Saturation (SCVO2 ) were recorded before and 2,3,4 hours after the Esmolol treatment.Results Heart rate of Esmolol group was reduced at all time points after treatment,The difference of that from the control group was significant ( H R: [ 108 ± 16 ] beats/min vs.[ 132 ± 18 ] beats/min,[ 101 ± 14] beats/min vs.[ 135 ± 19 ] beats/min,[ 106 ± 21 ] beats/rin vs.[ 129 ± 14]beats/min,all P ＜ 0.01 ).Compared to the control group,Stroke Volume Index of Esmolol group was significantly increased at each time point ( SVI: [32 ± 12] ml/m2 vs.[22 ±8] ml/m2,[34 ± 14] ml/m2 vs.[21 ±6] ml/m2,[37 ± 10] ml/m2vs.[23 ±9] ml/m2,all P ＜0.05).Lactate of Esmolol group was significantly decreased at the end of the 3rd,4th hour of Esmolol treatment ( lactate: [ 1.6 ± 1.1 ] mmol/L vs.[ 2.7 ± 1.2 ]mmol/L,[ 1.3 ± 0.9 ] mmol/Lvs.[ 2.8 ± 1.4 ] mmol/L,both P ＜ 0.01.There were no significant differences in MAP,CI,SVRI,SCVO2 between the two groups at each time point ( all P ＞ 0.05 ).Conclusion Esmolol can reduce heart rate significantly,improve cardiac work and tissue perfusion in septic shock patients with tachycardia.It is a feasible and safe treatment for this kind of patients.

Objective:To treat the chronic non-atrophic gastritis patients induced by Helicobacter pylori with Qingweizhitong Weiwan combined with standard triple therapy,and to detect the differential expression of related immflammation genes with PCR array,and to clarify its mechanism.Methods: Ten patients with chronic non-atrophic gastritis complicated with Helicobacter pylori infection were used as treatment group and 10 health people were used as health control group. The patients in treatment group were treated with Qingweizhitong Weiwan combined with standard triple therapy for 14 d. The blood samples of the subjects in treatment group and health control group were collected before and after treatment,and QIAGEN human antibacterial response PCR array was performed to test the total RNA inperipheral blood and to analyze the differential expressions of 84 inflammation-related genes.Results:The differential expressions of 20 inflammation-related genes were found.Compared with health control group,the expression levels of 20 genes in treatment group before treatment were up-regulated (Fold-change>2);after treatment,the expression levels of 20 genes were down-regulated,and 11 of them were similar to the level in health control group (Fold-change< 2).More specifically,part of 20 genes was related to NLRP3 inflammasome.Compared with health control group,the gene expression levels of CASP1,IL1B,NLRP3,and PYCARD in treatment group before treatment were up-regulated (P <0.05).Compared with before treatment,the expression levels of CASP1,IL1B,NLRP3,and PYCARD in treatment group after treatment were down-regulated (P <0.05).Conclusion:The mechanism of Qingweizhitong Weiwan combined with standard triple therapy in the treatment of chronic non-atrophic gastritis patients induced by Helicobacter pylori may be related to inhibiting the expressions of NLRP3 inflammasome-related genes and interfering the antimicrobial innate immune response.

Objective To determine the safety and the therapeutic efficacy of autolagous nonmyeloablative hematopoietic stem cell transplantation (AHST) in newly-onset type 1 diabetes mellitus patients. Methods Fifteen patients with type 1 diabetes mellitus were enrolled. Hematopoietic stem cells were mobilized with cyclophosphamide and granulocyte colony-stimulating factor and then collected from peripheral blood by leukapheresis and cryopreserved. The cells were injected intravenously after conditioning with cyclophosphamide and rabbit antithymocyte globulin. Serum levels of HbA1c, C-peptide levels, and anti-glutamic acid decarboxylase antibody (GAD-Ab)titers were measured before and after AHST. Meanwhile, adverse event was recorded.Results The average age of 18 patients (6 males and 12 females)was ( 18.8±4.4 )years, the mean follow-up was ( 414± 150 ) days. 67 % ( 12/18 ) patients became insulin free, the earliest one happened at 2 weeks after AHST, and the latest one at 6 months. 4 cases resumed insulin use because of influenza and other reasons resulting in the rise of blood glucose level. Currently, 8 patients (44.4%) were completely free of insulin therapy, and the remaining cases reduced the insulin dosage by 67.3% ±22.4%. 18 cases had lowered GAD-Ab level, the negative rate was 33.3% (6/18 ). Fasting and postprandial 2 h C-peptide levels increased significantly after A HST. Area under the curve for C-peptide ( AUCC ) increased much more markedly, and it could be maintained for 1 year. Duringtransplantation,all patients had varying degrees of gastrointestinal reactions, hair loss, fever, bone marrow suppression, and other side effects. 5 patients received blood component transfusion. No damage or other severe adverse events of heart, liver, kidney, and other organs were observed. Most side effects gradually disappeared after 2-4 weeks. The recovery of neutropenia was the slowest. Conclusion Autologous hematopoietic stem cell transplantation for treatment of newly-onset type 1 diabetes with residual islet function showed a certain effect and high safety. The widened use of this new technique should be cautious until the therapeutic mechanism has been further studied.

Objective To evaluate the role of sirtuin 3 ( SIRT3)∕forkhead box O3α ( FOXO3α) signaling pathway in dexmedetomidine-induced reduction of hepatic ischemia-reperfusion ( I∕R) injury in mice. Methods Forty clean-grade C57BL∕6 mice of both sexes, aged 2 weeks, weighing 6-8 g, were di-vided into 4 groups (n＝10 each) using a random number table method: sham operation group (group S), hepatic I∕R group ( group I∕R), dexmedetomidine group ( group D) and SIRT3 inhibitor 3-TYP plus dexmedetomidine group (group T+D). Portal vein and hepatic artery supplying left and middle lobes of the liver and biliary tract were clamped resulting in ischemia of 70% of the liver in anesthetized rats. Normal sa-line 0. 25 ml was intraperitoneally injected at 1 h before establishing model, and 30 min later dexmedetomi-dine 50 μg∕kg (diluted to 0. 25 ml in normal saline) was intraperitoneally injected in group D. In group T+D, 3-TYP 5 mg∕kg (diluted to 0. 25 ml in normal saline) was intraperitoneally injected at 1 h before estab-lishing model, and 30 min later dexmedetomidine 50 μg∕kg (diluted to 0. 25 ml in normal saline) was in-traperitoneally injected. Mice were selected at 6 h after reperfusion, blood samples were obtained through eyeball, and the mice were then sacrificed and kidneys were removed for determination of the serum concen-trations of creatinine (Cr) and blood urea nitrogen (BUN), cell apoptosis (by TUNEL), malondialdehyde (MDA) content (using thiobarbituric acid method), superoxide dismutase (SOD) activity (by xanthine oxidase method), and acetylation of FOXO3α in renal tissues (by using immunoprecipitation) and for ex-amination of the pathologic changes. The damage to renal tubules was scored. Apoptosis index ( AI) was calculated. Results Compared with group S, the renal tubular damage score and AI were significantly in-creased, serum concentrations of Cr and BUN were increased, the content of MDA was increased, the ac-tivity of SOD was decreased, and the acetylation of FOXO3α was decreased in I∕R, D and T+D groups ( P＜0. 05). Compared with group I∕R, the renal tubular damage score and AI were significantly decreased, serum concentrations of Cr and BUN were decreased, the content of MDA was decreased, the activity of SOD was increased, and the acetylation of FOXO3α was decreased in group D (P＜0. 05), and no signifi-cant change was found in the parameters mentioned above in group T+D (P＞0. 05). Compared with group D, the renal tubular damage score and AI were significantly increased, serum concentrations of Cr and BUN were increased, the content of MDA was increased, the activity of SOD was decreased, and the acetylation of FOXO3α was decreased in group T+D ( P＜0. 05). Conclusion Activation of SIRT3∕FOXO3α signaling pathway is involved in dexmedetomidine-induced reduction of hepatic I∕R injury in mice.

There is an increasing histological clinical evidence that both hepatic fibrosis and some degree of cirrhosis reversal can improve prognosis. Hepatic fibrosis involves a variety of cells and steps, and its reversal mechanism is also very complex, mainly including the reduction of hepatocyte necrosis and regeneration, the apoptosis and inactivation of activated hepatic stellate cells, and the reversal of hepatic sinusoidal endothelial cells and microvessels, restorative hepatic macrophages polarization and cell-to-cell interactions. Furthermore, the biochemical basis for reversal of hepatic fibrosis is decreased expression of matrix metalloproteinase inhibitors, up-regulation of matrix metalloproteinase activity, and increased degradation of extracellular matrix. However, at present, there are few studies on the clinicopathological mechanism of liver fibrosis reversal, and the key target groups of different etiologies with different degrees are still unclear, and the corresponding translational application research is lacking. Therefore, an in-depth and systematic understanding of the characteristics and mechanisms of hepatic fibrosis reversal can not only enrich the understanding of the natural history of hepatic fibrosis and cirrhosis, but also provide reference for the development and clinical application of anti-hepatic fibrotic drugs.