Altered oral microbiota composition associated with recurrent aphthous stomatitis in young females

Oral microbiota has been implicated in pathogenesis of recurrent aphthous stomatitis (RAS), which is a common mucosal disorder with unclear etiology. This study has explored the association between oral microbiota disorder and RAS in high-risk young female population.Forty-five young females were enrolled, including 24 RAS patients and 21 healthy individuals. Oral microbiome was analyzed by Illumina Miseq sequencing.Oral microbiota associated with RAS was characterized by the lower alpha-diversity indices (Chao1 and ACE). Several infectious pathogens increased in RAS, such as genera Actinobacillus, Haemophilus, Prevotella and Vibrio. The PICRUSt analysis indicated that the oral microbiota might be related with the up-regulation of genes involving infectious and neurodegenerative diseases, environmental adaptation, the down-regulation of genes involving basal metabolism, such as carbohydrate, energy, and amino acid metabolism.This study indicated that oral microbiota may play a significant role in RAS development.     

Single-dose live-attenuated vesicular stomatitis virus-based vaccine protects African green monkeys from Nipah virus disease

Nipah virus is a zoonotic paramyxovirus that causes severe respiratory and/or encephalitic disease in humans, often resulting in death. It is transmitted from pteropus fruit bats, which serve as the natural reservoir of the virus, and outbreaks occur on an almost annual basis in Bangladesh or India. Outbreaks are small and sporadic, and several cases of human-to-human transmission have been documented as an important feature of the epidemiology of Nipah virus disease. There are no approved countermeasures to combat infection and medical intervention is supportive. We recently generated a recombinant replication-competent vesicular stomatitis virus-based vaccine that encodes a Nipah virus glycoprotein as an antigen and is highly efficacious in the hamster model of Nipah virus disease. Herein, we show that this vaccine protects African green monkeys, a well-characterized model of Nipah virus disease, from disease one month after a single intramuscular administration of the vaccine. Vaccination resulted in a rapid and strong virus-specific immune response which inhibited virus shedding and replication. This vaccine platform provides a rapid means to afford protection from Nipah virus in an outbreak situation.     

Assessment of a novel recombinant vesicular stomatitis virus with triple mutations in its matrix protein as a vaccine for pigs

Vesicular stomatitis virus (VSV) causes a serious vesicular disease responsible for economic losses in the livestock industry. Currently, there are no suitable vaccines to prevent VSV infection. Although the structural matrix (M) protein of VSV has been shown to be a virulence factor in rodent models, its role in the pathogenicity of VSV infection in livestock species is unknown. We hypothesized that VSV with mutations in the M protein represents a novel live attenuated vaccine candidate. To test this, we introduced mutations into VSV M protein using reverse genetics and assessed their attenuation both in vitro and in pigs, an important natural host of VSV. A recombinant VSV with a triple amino acid mutation in M protein (VSV_MT) demonstrated a significantly reduced ability to inhibit the type I interferon (IFN) signaling pathway and to shutoff host gene expression compared to WT-VSV and a mutant virus with a single amino acid deletion (VSV_ΔM51). Inoculation of pigs with VSV_MT induced no apparent vesicular lesions but stimulated virus-neutralizing antibodies and animals were protected against virulent VSV challenge infection. These data demonstrate that the M protein is an important virulence factor for VSV in swine and VSV_MT represents a novel vaccine candidate for VSV infections in pigs.     

连花清瘟颗粒联合利巴韦林和康复新液治疗疱疹性口腔炎的疗效观察

目的：观察连花清瘟颗粒联合利巴韦林和康复新液治疗疱疹性口腔炎的临床疗效。方法选择2012年1~10月份在医院儿科门诊进行诊治的疱疹性口腔炎的患儿80例,完全随机平分为治疗组和对照组各40例,2组除给予维生素 C 和维生素 B2等支持、对症治疗以外,均给予利巴韦林注射液静脉滴注10~15mg·kg _1·d _1,分2次给药和口服康复新液,＜3岁患儿每次5ml,＞3岁患儿每次10ml,均3次∕ d,治疗组患儿在此治疗基础上加用连花清瘟颗粒口服（石家庄以岭药业股份有限公司,6g∕袋）,≤3岁3g∕次,3次∕ d;＞3岁 6g∕次,3次∕ d,均治疗5d。结果治疗组总有效率为97,5％明显高于对照组的87,5％（p ＜0,01）,治疗组热退时间,口腔炎疱疹溃疡愈合时间为（1,4±0,7）d、（2,9±0,6）d 比较对照组的（3,2±1,2）d、（3,7 ± 0,9）d 明显缩短,差异有统计学意义（p ＜0,01）。结论连花清瘟颗粒联合利巴韦林和康复新液治疗疱疹性口腔炎,能迅速缓解临床症状,疗效确切,值得临床推广和应用。     

过敏性疾病在口腔中表现的研究进展

过敏性疾病是常见的全身疾病,可发生于口腔、皮肤、消化道、呼吸道等全身各系统器官。表现在口腔的过敏性疾病通常发生在摄入某些药物、食物或者接触过敏原后,可能局限于口腔,也可能作为整个病程的首发症状。过敏性疾病在口腔主要表现为药物过敏性口炎、接触过敏性口炎、血管神经性水肿、多形红斑及口腔过敏综合征等,病损形式多样,可无特异性,如充血、水肿、红斑、水疱、糜烂或者溃疡等。熟悉过敏性疾病在口腔中的不同表现,对于其诊治有重要意义。     

Chronic ulcerative stomatitis: A comprehensive review and proposal for diagnostic criteria

Chronic ulcerative stomatitis (CUS) is an immune‐mediated disorder characterized by oral erosions and ulcers usually refractory to conventional treatments. The disease often involves middle‐aged and older women with painful lesions sometimes resembling those of erosive oral lichen planus (OLP). The most affected sites are the buccal mucosa, the gingiva and the tongue, but the skin is involved in 22.5% of cases. Histopathologic features in CUS are non‐specific and indistinguishable from those of OLP, with the exception of the presence of a mixed infiltrate composed of lymphocytes and plasma cells. Direct immunofluorescence (DIF) analysis reveals the presence of stratified epithelium‐specific antinuclear antibodies (SES‐ANA) in the lower third of the epithelium. The IgG antibodies detected on DIF are directed against the ?Np63α isoform of p63 expressed in the nuclei of the epithelial basal cells. A distinguishing feature of CUS is the low response to conventional corticosteroid therapy and the good outcome with hydroxychloroquine at the dosage of 200 mg/day or higher dosages. This paper presents a comprehensive review of CUS and is accompanied by a new case report (the 73rd case) and a proposal for updated diagnostic criteria.     

水泡口炎病毒在人前列腺癌模型的溶瘤效应

目的 探讨利用水泡口炎病毒(VSV)作为一种新型药物治疗前列腺癌的可能性.方法 (1)确定VSV-绿色荧光蛋白(GFP)在不同时段对癌细胞的细胞毒性作用;(2)利用DU145细胞在裸鼠建立动物肿瘤模型,荷瘤动物经注射不同剂量的VSV-GFP(1×106、1×107 PFU/100μ1)后,观察不同时间点肿瘤的变化及治疗效果,并确定瘤体内病毒的复制水平、肿瘤大小变化及动物生存期的相关性.结果 VSV-GFP能选择性地杀伤前列腺癌细胞,在转染倍数(MOI) =0.1时,DU145细胞死亡率＞85％,与之比较,RWPE-1细胞死亡率＜20％,而RPMI 1640对照组细胞死亡率＜5％.体内实验中,移植瘤体内不同时间点(12、24、48 h)病毒复制滴度分别为2.36×107 PFU/g、3.82×107 PFU/g、4.38×107 PFU/g,1×107 PFU剂量组,1×106 PFU剂量组,RPMI 1640对照组在治疗48 d后,移植瘤平均体积分别为(1470.54±480.67)、(903.40±3245.50)、(408.54±224.40)mm3,3组比较差异有统计学意义(P＜0.05),与注射不含病毒RPMI 1640对照组比较,肿瘤明显缩小,动物生存期延长.结论 溶瘤病毒VSV-GFP在DU145为模型的体内、外实验中具有较好的治疗效果.     

臭氧水对水泡性口炎病毒灭活效果的检测

经检测，在２０～２６℃室温下，浓度为５０±１ｍｇ／Ｌ的臭氧水溶液，作用３０ｓ，可灭活悬液中水泡性口炎病毒；用其冲洗、作用１ｍｉｎ，可灭活干燥于玻璃片上的水泡性口炎病毒。     

Antibiofilm and Protein-Repellent Polymethylmethacrylate Denture Base Acrylic Resin for Treatment of Denture Stomatitis

Candida albicans (C. albicans) biofilm is a common etiological factor in denture stomatitis. The purpose of this study was to investigate the effects of incorporating 2-methacryloyloxyethyl phosphorylcholine (MPC) as a protein repellent into a new high-impact denture acrylic (HIPA) resin on the surface roughness, solution pH, and C. albicans biofilm adhesion to the denture base. The new acrylic denture resin base was formulated by mixing MPC into HIPA resin at mass fractions of 1.5%, 3%, and 4.5%. Surface roughness was measured using a Mitutoyo surface roughness tester. C. albicans biofilm growth and viability were assessed via colony forming unit counts. The pH of the biofilm growth medium was measured using a digital pH meter. Adding MPC to the HIPA resin at percentages of 1.5% and 3% increased the roughness values significantly (p < 0.05), while adding 4.5% MPC resulted in no difference in roughness values to that of the control group (p > 0.05). All experimental groups demonstrated neutral pH values (pH ≅ 7) and were not significantly different from each other (p > 0.05). Incorporating 2-methacryloyloxyethyl phosphorylcholine at 4.5% resulted in a significant (≅1 log) colony-forming unit reduction compared with the control group with 0% MPC (p < 0.05). A fungal-retarding denture acrylic resin was developed through the incorporation of MPC for its protein-repelling properties. This newly developed denture acrylic material has the potential to prevent oral microbial infections, such as denture stomatitis.     

Molecular determinants of susceptibility to oncolytic vesicular stomatitis virus in pancreatic adenocarcinoma

Background

M protein mutant vesicular stomatitis virus (M51R-VSV) has oncolytic properties against many cancers. However, some cancer cells are resistant to M51R-VSV. Herein, we evaluate the molecular determinants of vesicular stomatitis virus (VSV) resistance in pancreatic adenocarcinoma cells.

Methods

Cell viability and the effect of β-interferon (IFN) were analyzed using 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium assay. Gene expression was evaluated via microarray analysis. Cell infectability was measured by flow cytometry. Xenografts were established in athymic nude mice and treated with intratumoral M51R-VSV.

Results

Four of five pancreatic cancer cell lines were sensitive to M51R-VSV, whereas Panc 03.27 cells remained resistant (81 ± 3% viability 72 h after single-cycle infection). Comparing sensitive MiaPaCa2 cells with resistant Panc 03.27 cells, significant differences in gene expression were found relating to IFN signaling (P = 2 × 10⁻⁵), viral entry (P = 3 × 10⁻⁴), and endocytosis (P = 7 × 10⁻⁴). MiaPaCa2 cells permitted high levels of VSV infection, whereas Panc 03.27 cells were capable of resisting VSV cell entry even at high multiplicities of infection. Extrinsic β-IFN overcame apparent defects in IFN-mediated pathways in MiaPaCa2 cells conferring VSV resistance. In contrast, β-IFN decreased cell viability in Panc 3.27 cells, suggesting intact antiviral mechanisms. VSV-treated xenografts exhibited reduced tumor growth relative to controls in both MiaPaCa2 (1423 ± 345% versus 164 ± 136%; P < 0.001) and Panc 3.27 (979 ± 153% versus 50 ± 56%; P = 0.002) tumors. Significant lymphocytic infiltration was seen in M51R-VSV–treated Panc 03.27 xenografts.

Conclusions

Inhibition of VSV endocytosis and intact IFN-mediated defenses are responsible for M51R-VSV resistance in pancreatic adenocarcinoma cells. M51R-VSV treatment appears to induce antitumor cellular immunity in vivo, which may expand its clinical efficacy.