Bioinspired catechol chemistry for dentin remineralization: A new approach for the treatment of dentin hypersensitivity

ObjectiveDentin remineralization is of considerable clinical interest for dentin hypersensitivity and developing biomimetic analogs that can regulate hydroxyapatite (HAp) nucleation and growth remains a challenge. This study aimed to evaluate in vitro the potential for dentin remineralization using the following biomimetic in situ prepared poly(catechols): poly(dopamine), poly(DOPA), poly(caffeic acid) and a synthesized DOPA-peptide possessing collagen and calcium-binding domains (DOPA-Ahx-(Gly)₃-(Glu)₅).MethodsDentin samples were immersed in a freshly prepared phosphate-buffered saline (PBS) containing the respective catechol and laccase. After the reaction, they were immersed in calcium and phosphate remineralization solution, which was changed every day for 10 days. Samples of intact and demineralized dentin were used as control groups and kept in deionized water under the same experimental conditions. The remineralized dentin was characterized by scanning electron microscopy (SEM), Micro-energy dispersion X-ray fluorescence spectroscopy (μEDX) and X-ray diffraction (XRD).ResultsThe application of different poly(catechols) and DOPA-peptide promoted crystal nucleation and the formation of HAp, which partially covered both the dentin surface and dentinal tubules walls.SignificanceBy mimicking the role of charged non-collagenous proteins in vivo, polymers consisting of catechol groups showed the ability to modify demineralized dentin surface properties, promoting mineral formation. The use of poly(catechols) may be encouraged for the development of a therapeutic technique for dentin hypersensitivity.     

3种脱敏剂治疗支托窝牙本质敏感症的临床观察

目的 观察比较3种脱敏剂对(牙合)支托窝牙本质敏感治疗的效果.方法 选择201颗(牙合)支托窝牙本质敏感的天然牙,随机使用氟钾酚醛树脂(FK)、不含氟钾酚醛树脂(FR)和Gluma脱敏剂进行脱敏,每组67颗,使用视觉模拟评分法(visual analog scale,VAS)记录其敏感度,比较连续脱敏5天后即刻、1m、2m和3m的脱敏效果以及有效率的差异.结果 3组患者脱敏治疗后,2m时FK组脱敏有效率高于Gluma组,3m时FK组脱敏有效率高于FR组,其余各组不同时间点组间脱敏有效率及VAS值差异无统计学意义(P＞0.05).FR组3m脱敏有效率低于脱敏后即刻、1m、2m,Gluma组3m脱敏有效率低于脱敏后即刻、1m,其余组间脱敏有效率差异无统计学意义.结论 氟钾酚醛树脂脱敏剂和不含氟钾酚醛树脂脱敏剂用于(牙合)支托窝脱敏效果优于Gluma;氟钾酚醛树脂脱敏剂持久性更好.     

2种自制牙本质粘接剂的微拉伸粘接强度和耐久性能的实验研究

目的 测试自行研制的自酸蚀及全酸蚀粘接剂的微拉伸粘接强度和耐久性能,并与市售的进口同类产品进行对比.方法 选用正畸拔除前磨牙60颗,随机分成4组,每组分循环前、后各2个亚组,各15个试件,分别为自制的自酸蚀粘接剂(44组)和全酸蚀粘接剂(45组),Easy one(EO组)和Single Bond2(SB组).测试各组冷热循环前后的微拉伸粘接强度变化,并进行统计分析,体视显微镜观察断裂模式.结果 冷热循环前,各组微拉伸粘接强度从大到小分别为SB组(35.05±3.01)Mpa＞44组(27.76±1.44)Mpa＞ 45组(27.65±1.67)Mpa＞EO组(26.03±2.15)Mpa,45组和SB组之间及44组和EO组之间微拉伸粘接强度的差异有统计学意义(P＜0.05).冷热循环后,各组从大到小为SB组＞44组＞EO组＞45组,45组和SB组之间及44组和EO组之间微拉伸粘接强度的差异有统计学意义(P＜0.05).同一粘接剂冷热循环前后相比,粘接强度均呈下降趋势(P＜0.05);试件的断裂面类型以混合型断裂为主.结论 自制牙本质粘接剂和市售的进口同类产品相比,自酸蚀粘接剂粘接强度高且耐久性能好,全酸蚀粘接剂则与之相反.冷热循环后各组粘接剂的微拉伸粘接强度均有下降.     

低频超声在大脑中动脉狭窄急性脑梗死治疗中的应用价值

目的分析低频超声治疗在大脑中动脉狭窄引起急性脑梗死患者中的应用效果及临床价值。方法将我院2017年8月—2019年1月收治的50例发病1~3天的大脑中动脉狭窄引起的急性脑梗死患者作为研究对象,按照抽签法将其分为常规组和试验组,各25例。常规组接受常规的治疗方法。试验组在常规组基础上给予低频超声治疗。对比两组治疗后效果。结果:治疗前,两组的大脑中动脉收缩期血流速度相比无差异(P>0.05),治疗后,试验组的大脑中动脉收缩期血流速度低于常规组(P<0.05),治疗前2组超敏C反应蛋白对比无差异(P>0.05),治疗后试验组超敏C反应蛋白较对照组下降(P<0.05)。结论低频超声治疗可以明显改善患者大脑中动脉的狭窄情况,改善脑梗死预后。     

不同温度新型大气压冷等离子体处理对牙本质粘接强度的影响

目的:研究不同温度条件下新型大气压冷等离子体(radio-frequency atmospheric-pressure glow discharge,RF-APGD)处理对牙本质粘接强度的影响。方法:(1)收集新鲜拔除的、无龋坏的、完整的第三磨牙52颗,采用精密低速切割机制备平行于牙合中层牙本质薄片,每颗离体牙制备1片 [(900±100) μm]。将52个中层牙本质薄片随机分为对照组和实验组,其中对照组4片,无处理;实验组48片,按新型RF-APGD等离子体不同处理温度(4 ℃、10 ℃、20 ℃、30 ℃)平均分为4组,每大组12片。每大组按照不同处理时间(10 s,20 s,30 s)平均分为3个小组,每小组4片。采用扫描电镜观察脱矿牙本质表面形貌。(2)收集20颗完整第三磨牙随机分为对照组和4个实验组,每组4颗。对照组,无处理;4 ℃、10 ℃、20 ℃和 30 ℃ 4个实验组,每组采用新型RF-APGD等离子体处理20 s。实验组及对照组采用低速水冷精密切割机垂直于牙长轴去除牙合面牙釉质,暴露中层牙本质;采用32%磷酸酸蚀剂对牙本质表面进行酸蚀;采用牙本质粘接剂和树脂进行牙本质-树脂粘接,采用万能力学机进行牙本质-树脂粘接试件即刻微拉伸强度测定,观察不同温度新型RF-APGD等离子体处理对牙本质-树脂即刻粘接性能的影响。结果:(1)扫描电镜观察脱矿牙本质表面形貌显示,30 ℃和20 ℃新型 RF-APGD 等离子体处理组,脱矿牙本质胶原纤维表面经新型RF-APGD等离子体处理10 s即会出现微结构的破坏;10 ℃新型RF-APGD等离子体处理脱矿牙本质表面 20 s,即会出现牙本质胶原纤维之间间隙变小、表面结构坍塌等现象;4 ℃新型RF-APGD等离子体处理10 s、20 s及30 s,脱矿牙本质表面胶原纤维网状结构均能维持蓬松结构。(2)牙本质-树脂即刻微拉伸强度结果显示,对照组为(47.4±0.5) MPa,4 ℃、10 ℃、20 ℃和30 ℃新型RF-APGD等离子体处理组分别为(57.8±0.7) MPa、(51.9±0.7) MPa、(29.7±1.0) MPa和(22.2±1.5) MPa,其中4 ℃新型RF-APGD等离子体处理组所获得的微拉伸强度最高,与其他各组相比,差异具有统计学意义(P<0.05), 4 ℃和10 ℃新型RF-APGD等离子体处理组和对照组相比,牙本质-树脂微拉伸粘接强度分别提高了21.9%和9.5%。结论:4 ℃新型RF-APGD等离子体对脱矿牙本质胶原纤维的处理,较更高温度的新型RF-APGD等离子体更有利于提高牙本质-树脂的即刻粘接性能。     

根面龋牙本质中厌氧菌的培养分离及鉴定

目的对组成根面龋的致龋菌进行培养、分离和鉴定.方法选择25例患者的32颗根面龋患牙,收集龋损根面牙本质标本,于牛心脑浸液血琼脂中37℃厌氧培养5d,并进行分离鉴定.结果32例中分离出厌氧菌10个属,共125株.链球菌、放线菌和韦荣氏菌的检出率较高,占所有检出菌株的59.2%.结论根面龋菌丛的优势菌为链球菌、放线菌和韦荣氏菌.     

The Arabidopsis ZED1 pseudokinase is required for ZAR1-mediated immunity induced by the Pseudomonas syringae type III effector HopZ1a

Plant and animal pathogenic bacteria can suppress host immunity by injecting type III secreted effector (T3SE) proteins into host cells. However, T3SEs can also elicit host immunity if the host has evolved a means to recognize the presence or activity of specific T3SEs. The diverse YopJ/HopZ/AvrRxv T3SE superfamily, which is found in both animal and plant pathogens, provides examples of T3SEs playing this dual role. The T3SE HopZ1a is an acetyltransferase carried by the phytopathogen Pseudomonas syringae that elicits effector-triggered immunity (ETI) when recognized in Arabidopsis thaliana by the nucleotide-binding leucine-rich repeat (NB-LRR) protein ZAR1. However, recognition of HopZ1a does not require any known ETI-related genes. Using a forward genetics approach, we identify a unique ETI-associated gene that is essential for ZAR1-mediated immunity. The hopZ-ETI-deficient1 (zed1) mutant is specifically impaired in the recognition of HopZ1a, but not the recognition of other unrelated T3SEs or in pattern recognition receptor (PRR)-triggered immunity. ZED1 directly interacts with both HopZ1a and ZAR1 and is acetylated on threonines 125 and 177 by HopZ1a. ZED1 is a nonfunctional kinase that forms part of small genomic cluster of kinases in Arabidopsis. We hypothesize that ZED1 acts as a decoy to lure HopZ1a to the ZAR1–resistance complex, resulting in ETI activation.The plant immune system can be divided into two major branches that share commonalities with animal innate immunity. Pattern recognition receptor (PRR)-triggered immunity (PTI) is activated by the recognition of conserved microbial molecules called microbe-associated molecular patterns (MAMPs) by extracellular PRRs (1), similar to the recognition of MAMPs by animal Toll-like receptors (2). Effector-triggered immunity (ETI) is activated by the recognition of pathogen-derived effector proteins by intracellular NB-LRR proteins that share structural features with animal nucleotide-binding domain, leucine-rich repeat containing (NLR) proteins (3). The ETI response overlaps significantly with PTI but is accelerated, amplified, and often accompanied by the hypersensitive cell death response (HR; refs. 4 and 5). Recognition of effector proteins can occur directly where the effector protein binds directly to the NB-LRR protein, or indirectly, in which case both the effector and NB-LRR proteins bind to a common host protein. In the latter case, ETI is initiated by the NB-LRR protein in response to an effector-induced modification to the host protein (6). In some cases, the host protein monitored by the NB-LRR may represent a true virulence target of the effector protein, whereas in other cases, this protein may be a nonfunctional decoy of the true virulence target maintained by the host for the purposes of pathogen surveillance (7).The continual arms race between host and pathogen has directed the coevolution of host innate immunity with bacterial virulence strategies. The type III secretion system (T3SS) is a predominant virulence mechanism used by many Gram-negative bacterial pathogens to cause disease in eukaryotic hosts (8). The T3SS delivers type III secreted effector (T3SE) proteins into host cells where they can promote the infection process by suppressing host immunity and/or participating in the pathogen life cycle.The YopJ/HopZ/AvrRxv T3SE superfamily is evolutionary diverse and found in both animal and plant pathogens (9, 10). Yersinia pestis YopJ, the archetypal member of this superfamily, acetylates serine or threonine residues in the activation loops of members of the mitogen-activated protein kinase kinase (MAPKK) and MAP kinase kinase kinase superfamilies, thereby suppressing innate immunity (11–15). In the plant pathogen Pseudomonas syringae, the HopZ1 subfamily is represented by three closely related alleles, HopZ1a, HopZ1b, and HopZ1c, that diversified under pressure from the host immune system (10). The most phylogenetically basal representative of this subfamily, HopZ1a, is recognized in Arabidopsis by the ZAR1 NB-LRR protein (16, 17) as well as by unidentified proteins in rice, Nicotiana benthamiana, sesame, and soybean (10). Like YopJ, HopZ1a is an acetyltransferase and can promote pathogen growth in Arabidopsis plants lacking the ZAR1 NB-LRR protein. The virulence and immune-eliciting functions of HopZ1a both require the cysteine residue in the acetyltransferase catalytic triad (16, 17). It is likely that ZAR1 evolved to recognize an ancestral virulence activity of HopZ1a; however, the molecular relationship between virulence and immunity-eliciting functions remain to be established (17, 18).Here, we describe a forward genetic screen designed to characterize the genetic requirements of ZAR1-mediated immunity by identifying Arabidopsis mutant plants that lacked a HopZ1a-induced HR response. We named these mutants hopZ-ETI deficient (zed) and mapped zed1 to At3g57750 by Illumina-based next-generation sequencing. Different zed1 point mutants identified from our mutant screen or a tDNA insertion line in At3g57750 all lack recognition of HopZ1a. PTI and basal defenses are unaffected in zed1; however, zed1 exhibits a loss of HopZ1a-mediated ETI. We show that ZED1 interacts directly with HopZ1a, as well as the N-terminal coiled-coil (CC) domain of ZAR1. ZED1 is an uncharacterized pseudokinase and is acetylated on threonines 125 and 177 by HopZ1a. We hypothesize that ZAR1 is activated in response to ZED1 acetylation by HopZ1a and speculate that ZED1 may be a decoy of the true HopZ1a virulence target because HopZ1a retains its virulence function in zed1 Arabidopsis plants.     

Pulpal space pressure and temperature changes from Nd:YAG laser irradiation of dentin

Objectives. To investigate pulpal space pressure and temperature after application of Nd:YAG laser, and high-speed diamond bur on dentin surface.

Methods. One and 3 W Nd:YAG laser and high-speed diamond bur were used to remove dentine from twenty extracted premolars. The pulp chambers were monitored for pressure and temperature changes with a pressure transducer and thermocouple, respectively.

Results. Regardless of the remaining dentin thickness (RDT), laser irradiation and high-speed diamond bur use generated an increase in pulpal space pressure and temperature (ANOVA and Fisher's LSD tests, P<0.001). Pressure and temperature increased with an increase in laser power. Three-Watt laser irradiation caused greater changes than 1 W (1.75 kPa and 1.31 °C, 0.53 kPa and 0.34 °C, respectively). Both pulpal space pressure (P<0.001) and temperature (P<0.005) increased as the RDT decreased.

Conclusions. Laser irradiation and the use of a high-speed diamond bur generated an increase in pulpal space pressure and temperature. Pulpal space pressure and temperature increased with an increase in energy density of laser and a decrease in RDT.     

dNCPs、TGF-β1及联合应用对人牙髓成纤维细胞增殖、ALP及矿化的影响

目的 :观察牙本质非胶原蛋白 (dentinnon collageproteins ;dNCPs)、转化生长因子 (transforminggrowthfactor ;TGF β1)及联合应用对人牙髓成纤维细胞生物学特性的影响。 方法 :利用混合酶消化法成功培养了人牙髓成纤维细胞 ,角蛋白及波形丝蛋白鉴定其来源。在细胞中分别加入牙本质粉、dNCPs、TGF β1及其复合物 ,通过MTT、ALPase和Von Kossa染色检测其作用。 结果 :dNCPs和TGF β1可显著增加细胞的增殖及ALPase分泌 ,细胞可聚集成团形成矿化结节。 结论 :dNCPs和TGF β1可改变人牙髓成纤维细胞的生物学活性 ,但两者间无相互促进作用。