Machine learning models can predict subsequent publication of North American Spine Society (NASS) annual general meeting abstracts.

BACKGROUND CONTEXT: Academic meetings serve as an opportunity to present and discuss novel ideas. Previous studies have identified factors predictive of publication without generating predictive models. Machine learning (ML) presents a novel tool capable of generating these models. As such, the objective of this study was to use ML models to predict subsequent publication of abstracts presented at a major surgical conference. STUDY DESIGN/SETTING: Database study. METHODS: All abstracts from the North American Spine Society (NASS) annual general meetings (AGM) from 2013-2015 were reviewed. The following information was extracted: number of authors, institution, location, conference category, subject category, study type, data collection methodology, human subject research, and FDA approval. Abstracts were then searched on the PubMed, Google Scholar, and Scopus databases for publication. ML models were trained to predict whether the abstract would be published or not. Quality of models was determined by using the area under the receiver operator curve (AUC). The top ten most important factors were extracted from the most successful model during testing. RESULTS: A total of 1119 abstracts were presented, with 553 (49%) abstracts published. During training, the model with the highest AUC and accuracy metrics was the partial least squares (AUC of 0.77±0.05, accuracy of 75.5%±4.7%). During testing, the model with the highest AUC and accuracy was the random forest (AUC of 0.69, accuracy of 67%). The top ten features for the random forest model were (descending order): number of authors, year, conference category, subject category, human subjects research, continent, and data collection methodology. CONCLUSIONS: This was the first study attempting to use ML to predict the publication of complete articles after abstract presentation at a major academic conference. Future studies should incorporate deep learning frameworks, cognitive/results-based variables and aim to apply this methodology to larger conferences across other fields of medicine to improve the quality of works presented.

Induction of Antimicrobial Protein S100A15 Expression by Oral Microbial Pathogens Is Toll-like Receptors-Dependent Activation of c-Jun-N-Terminal Kinase (JNK), p38, and NF-κB Pathways.

The antimicrobial protein S100A15 belongs to the S100 family, which is differentially expressed in a variety of normal and pathological tissues. Although the function of S100A15 protein has been discussed in several studies, its induction and regulation in oral mucosa, so far, are largely unknown. In this study, we demonstrate that S100A15 is induced by the stimulation of oral mucosa with gram- or gram+ bacterial pathogens, as well as with the purified membrane components, namely lipopolysaccharides (LPS) and lipoteichoic acid (LTA). The stimulation of the human gingival fibroblast (GF) and the human mouth epidermal carcinoma (KB) cell lines with either gram- or gram+ bacterial pathogens or their purified membrane components (LPS and LTA) results in the activation of NF-κB, apoptosis-regulating kinase1 (ASK1), and MAP kinase signaling pathways including, c-Jun N-terminal kinase (JNK) and p38 together with their physiological substrates AP-1 and ATF-2, respectively. Inhibition of S100A15 by antibodies-mediated Toll-like receptor 4 (TLR4) or Toll-like receptor 2 (TLR2) neutralization reveals the induction of S100A15 protein by LPS/gram- bacterial pathogens to be TLR4- dependent mechanism, whereas induction by LTA/gram+ bacterial pathogens to be TLR2- dependent mechanism. Pre-treatment of GF and KB cells with JNK (SP600125), p38 (SB-203580), or NF-κB (Bay11-7082) specific inhibitors further demonstrates the importance of JNK, p38 and NF-κB pathways in the regulation of gram-/gram+ bacterial pathogen-induced S100A15 expression. Our data provide evidence that S100A15 is induced in cancer and non-cancer oral mucosa-derived cell lines by gram-/gram+ bacterial pathogens and provide insight into the molecular mechanisms by which gram- and gram+ bacterial pathogens induce S100A15 expression in the oral mucosa.

Psychobiological Factors in Global Health and Public Health.

Psychobiological research is a systems approach that aims to integrate the biological, psychological and social systems that may influence health or pathology, particularly in chronic diseases and physical and/or psychiatric disorders. In this approach, we can expect to be able to deduce a 'biological signature' associated with particular symptom clusters. Similarly, psychosocial factors such as life events, health attitudes and behaviours, social support, psychological well-being, spirituality and personality are to be considered in terms of their influence on individual vulnerability to disease. At the psychophysiological level, it is important to understand, for example, the pathways that link the effects of chronic stress, social support and health, through the neuroendocrine and autonomic mechanisms that determine stress responses. At the macroscopic level, the role of individual socio-demographic variables such as personality, treatment modalities and health promotion through psycho-educational interventions needs to be explored.

Tumor necrosis factor-α triggers opposing signals in head and neck squamous cell carcinoma and induces apoptosis via mitochondrial- and non-mitochondrial-dependent pathways.

Head and neck squamous cell carcinoma (HNSCC) remains one of the most common malignancies worldwide. Although the treatment outcomes of HNSCC have improved in recent years, the prognosis of patients with advanced-stage disease remains poor. Current treatment strategies for HNSCC include surgery as a primary therapy, while radio-, chemo-, and biotherapeutics can be applied as second-line therapy. Although tumor necrosis factor-α (TNF-α) is a potent tumor suppressor cytokine, the stimulation of opposing signals impairs its clinical utility as an anticancer agent. The aim of this study was to elucidate the mechanisms regulating TNF-α­induced opposing signals and their biological consequences in HNSCC cell lines. We determined the molecular mechanisms of TNF-α-induced opposing signals in HNSCC cells. Our in vitro analysis indicated that one of these signals triggers apoptosis, while the other induces both apoptosis and cell survival. The TNF-α-induced survival of HNSCC cells is mediated by the TNF receptor-associated factor 2 (TRAF2)/nuclear factor (NF)-κB-dependent pathway, while TNF-α-induced apoptosis is mediated by mitochondrial and non-mitochondrial-dependent mechanisms through FADD-caspase-8-caspase-3 and ASK-JNK-p53-Noxa pathways. The localization of Noxa protein to both the mitochondria and endoplasmic reticulum (ER) was found to cause mitochondrial dysregulation and ER stress, respectively. Using inhibitory experiments, we demonstrated that the FADD­caspase-8­caspase-3 pathway, together with mitochondrial dysregulation and ER stress-dependent pathways, are essential for the modulation of apoptosis, and the NF-κB pathway is essential for the modulation of anti-apoptotic effects/cell survival during the exposure of HNSCC cells to TNF-α. Our data provide insight into the mechanisms of TNF-α-induced opposing signals in HNSCC cells and may further help in the development of novel therapeutic approaches with which to minimize the systemic toxicity of TNF-α.

Effect of different remaining dentin thickness and long term water storage on dentin bond strength.

The purpose of this study was to investigate the effect of remaining dentin thickness (RDT) and long term water storage on dentin bond strength in-vitro. Twenty-seven third molars were randomly divided into 3 groups: Clearfil Bond SE ONE (SE1, Kuraray Noritake Dental, Okayama, Japan), G-Bond plus (GB, GC, Tokyo, Japan) and Clearfil Mega Bond (MB, Kuraray Noritake Dental). Bonded specimens were stored in water at 37ºC for 24 h. The teeth were then sectioned perpendicular to the adhesive interface to produce beams. RDT of each beam was measured digital calliper. Microtensile bond strength testing was carried out at a crosshead speed of 1 mm/min after 24 h and 1 year water storage. Thicker RDT produced higher bond strengths with one/two-step self-etch materials tested except for the group of 24 h MB. Nevertheless water storage time and RDT affected µTBS in all materials used.

Effect of topical fluoride application on enamel after in-office bleaching, as evaluated using a novel hardness tester and a transverse microradiography method.

This study evaluated the effect of topical fluoride application on enamel hardness after in-office bleaching. Twelve human incisors were cut along the long axis, resulting in 24 halves used in four treatment groups (n = 6 in each group): (i) untreated group (C); (ii) in-office bleaching material (B); (iii) treatment with surface reaction-type prereacted glass-ionomer varnish after in-office bleaching (B+PRG); and (iv) treatment with acidulated phosphate fluoride solution after bleaching (B+F). All specimens were subjected to pH-cycling for 4 wk. Knoop hardness was measured using a Cariotester. The decalcification of enamel was assessed quantitatively by measuring the integrated mineral loss (ΔIML). Games-Howell analysis was used to assess statistical significance of between-group differences. The Knoop hardness decreased significantly after bleaching for all groups. In treatment groups B+PRG and B+F, the Knoop hardness returned to the original unbleached values after the first pH cycle and did not change afterwards. In treatment groups C and B there was a gradual decrease in the Knoop hardness until the fourth pH cycle. The integrated mineral loss, ΔIML, was significantly higher in treatment group B+F after 2 wk than in the other treatment groups. After 4 wk, the ΔIML in treatment group B was significantly higher than in treatment group B+PRG. The application of fluoride-containing materials after bleaching results in recuperation of hardness to levels similar to those of unbleached enamel.

Effect of air-blowing duration on the bond strength of current one-step adhesives to dentin.

OBJECTIVES: To evaluate the influence of different air-blowing durations on the micro-tensile bond strength (µTBS) of five current one-step adhesive systems to dentin. METHODS: One hundred and five caries-free human molars and five current one-step adhesive systems were used: ABU (All Bond Universal, Bisco, Inc.), CUB (CLEARFIL™ Universal Bond, Kuraray), GPB (G-Premio BOND, GC), OBA (OptiBond All-in-one, Kerr) and SBU (Scotchbond Universal, 3M ESPE). The adhesives were applied to 600 SiC paper-flat dentin surfaces according to each manufacturer's instructions and were air-dried with standard, oil-free air pressure of 0.25MPa for either 0s, 5s, 15s or 30s before light-curing. Bond strength to dentin was determined by using µTBS test after 24h of water storage. The fracture pattern on the dentin surface was analyzed by SEM. The resin-dentin interface of untested specimens was visualized by panoramic SEM image. Data from µTBS were analyzed using two-way ANOVA (adhesive vs. air-blowing time), and Games-Howell (a=0.05). RESULTS: Two-way ANOVA revealed a significant effect of materials (p=0.000) and air-blowing time (p=0.000) on bond strength to dentin. The interaction between factors was also significantly different (p=0.000). Maximum bond strength for each system were recorded, OBA/15s (76.34±19.15MPa), SBU/15s (75.18±12.83MPa), CUB/15s (68.23±16.36MPa), GPB/30s (55.82±12.99MPa) and ABU/15s (44.75±8.95MPa). The maximum bond strength of OBA and SUB were significantly higher than that of GPB and ABU (p<0.05). SIGNIFICANCE: The bond strength of the current one-step adhesive systems is material-dependent (p=0.000), and was influenced by air-blowing duration (p=0.000). For the current one-step adhesive systems, higher bond strengths could be achieved with prolonged air-blowing duration between 15-30s.

Hepatitis C virus-associated pruritus: Etiopathogenesis and therapeutic strategies.

In addition to its contributing role in the development of chronic liver diseases, chronic hepatitis C virus (HCV) infection is associated with extrahepatic manifestations, particularly, cutaneous-based disorders including those with pruritus as a symptom. Pruritus is frequently associated with the development of chronic liver diseases such as cholestasis and chronic viral infection, and the accumulation of bile acids in patients' sera and tissues as a consequence of liver damage is considered the main cause of pruritus. In addition to their role in dietary lipid absorption, bile acids can trigger the activation of specific receptors, such as the G protein-coupled bile acid receptor (GPBA/ TGR5). These types of receptors are known to play a crucial role in the modulation of the systemic actions of bile acids. TGR5 expression in primary sensory neurons triggers the activation of the transient receptor potential vanilloid 1 (TRPV1) leading to the induction of pruritus by an unknown mechanism. Although the pathologic phenomenon of pruritus is common, there is no uniformly effective therapy available. Understanding the mechanisms regulating the occurrence of pruritus together with the conduction of large-scale clinical and evidence-based studies, may help to create a standard treatment protocol. This review focuses on the etiopathogenesis and treatment strategies of pruritus associated with chronic HCV infection.

Interferon gamma-induced apoptosis of head and neck squamous cell carcinoma is connected to indoleamine-2,3-dioxygenase via mitochondrial and ER stress-associated pathways.

BACKGROUND: Tumor response to immunotherapy is the consequence of a concerted crosstalk between cytokines and effector cells. Interferon gamma (IFNγ) is one of the common cytokines coordinating tumor immune response and the associated biological consequences. Although the role of IFNγ in the modulation of tumor immunity has been widely documented, the mechanisms regulating IFNγ-induced cell death, during the course of immune therapy, is not described in detail. RESULTS: IFNγ triggered apoptosis of CLS-354 and RPMI 2650 cells, enhanced the protein expression and activation of indoleamine 2,3-dioxygenase (IDO), and suppressed the basal expression of heme oxygenase-1(HO-1). Interestingly, IFNγ induced the loss of mitochondrial membrane potential (Δψm) and increased accumulation of reactive oxygen species (ROS). The cytokine also induced the activation of Janus kinase (JAK)/Signal Transducer and Activator of Transcription (STAT)1, apoptosis signal-regulating kinase 1 (ASK1), p38, c-jun-N-terminal kinase (JNK) and NF-κB pathways and the transcription factors STAT1, interferon regulatory factor 1 (IRF1), AP-1, ATF-2, NF-κB and p53, and expression of Noxa protein. Furthermore, IFNγ was found to trigger endoplasmic reticulum (ER) stress as evidenced by the cleavage of caspase-4 and activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and inositol-requiring-1α (IRE1α) pathways. Using specific inhibitors, we identified a potential role for IDO as apoptotic mediator in the regulation of IFNγ-induced apoptosis of head and neck squamous cell carcinoma (HNSCC) cells via Noxa-mediated mitochondrial dysregulation and ER stress. CONCLUSION: In addition to the elucidation of the role of IDO in the modulation of apoptosis, our study provides new insights into the molecular mechanisms of IFNγ-induced apoptosis of HNSCC cells during the course of immune therapy.

Imiquimod-induced apoptosis of melanoma cells is mediated by ER stress-dependent Noxa induction and enhanced by NF-κB inhibition.

Melanoma is characterized by dysregulated intracellular signalling pathways including an impairment of the cell death machinery, ultimately resulting in melanoma resistance, survival and progression. This explains the tumour's extraordinary resistance to the standard treatment. Imiquimod is a topical immune response modifier (imidazoquinoline) with both antiviral and antitumour activities. The mechanism by which imiquimod triggers the apoptosis of melanoma cells has now been carefully elucidated. Imiquimod-induced apoptosis is associated with the activation of apoptosis signalling regulating kinase1/c-Jun-N-terminal kinase/p38 pathways and the induction of endoplasmic stress characterized by the activation of the protein kinase RNA-like endoplasmic reticulum kinase signalling pathway, increase in intracellular Ca(2+) release, degradation of calpain and subsequent cleavage of caspase-4. Moreover, imiquimod triggers the activation of NF-κB and the expression of the inhibitor of apoptosis proteins (IAPs) such as, X-linked IAP (XIAP) together with the accumulation of reactive oxygen species (ROS). Also, imiquimod triggers mitochondrial dysregulation characterized by the loss of mitochondrial membrane potential (Δψm), the increase in cytochrome c release, and cleavage of caspase-9, caspase-3 and poly(ADP-ribose) polymerase (PARP). Inhibitors of specific pathways, permit the elucidation of possible mechanisms of imiquimod-induced apoptosis. They demonstrate that inhibition of NF-kB by the inhibitor of nuclear factor kappa-B kinase (IKK) inhibitor Bay 11-782 or knockdown of XIAP induces melanoma apoptosis in cells exposed to imiquimod. These findings support the use of either IKK inhibitors or IAP antagonists as adjuvant therapies to improve the effectiveness topical imiquimod in the treatment of melanoma.

Endoplasmic reticulum stress-mediated pathways to both apoptosis and autophagy: Significance for melanoma treatment.

Melanoma is the most aggressive form of skin cancer. Disrupted intracellular signaling pathways are responsible for melanoma's extraordinary resistance to current chemotherapeutic modalities. The pathophysiologic basis for resistance to both chemo- and radiation therapy is rooted in altered genetic and epigenetic mechanisms that, in turn, result in the impairing of cell death machinery and/or excessive activation of cell growth and survival-dependent pathways. Although most current melanoma therapies target mitochondrial dysregulation, there is increasing evidence that endoplasmic reticulum (ER) stress-associated pathways play a role in the potentiation, initiation and maintenance of cell death machinery and autophagy. This review focuses on the reliability of ER-associated pathways as therapeutic targets for melanoma treatment.

Hepatitis C virus-mediated angiogenesis: molecular mechanisms and therapeutic strategies.

Angiogenesis is an essential process for organ growth and repair. Thus, an imbalance in this process can lead to several diseases including malignancy. Angiogenesis is a critical step in vascular remodeling, tissue damage and wound healing besides being required for invasive tumor growth and metastasis. Because angiogenesis sets an important point in the control of tumor progression, its inhibition is considered a valuable therapeutic approach for tumor treatment. Chronic liver disease including hepatitis C virus (HCV) infection is one of the main cause for the development of hepatic angiogenesis and thereby plays a critical role in the modulation of hepatic angiogenesis that finally leads to hepatocellular carcinoma progression and invasion. Thus, understanding of the molecular mechanisms of HCV-mediated hepatic angiogenesis will help design a therapeutic protocol for the intervention of HCV-mediated angiogenesis and subsequently its outcome. In this review, we will focus on the molecular mechanisms of HCV-mediated hepatic angiogenesis and the related signaling pathways that can be target for current and under development therapeutic approaches.

Identification and analysis of CD133(+) melanoma stem-like cells conferring resistance to taxol: An insight into the mechanisms of their resistance and response.

The presence and the involvement of cancer stem-like cells (CSCs) in tumor initiation and progression, and chemo-resistance are documented. Herein, we functionally analyzed melanoma stem-like cells (MSC)/CD133(+) cells on their resistance and response to taxol-induced apoptosis. Besides being taxol resistant, the CD133(+) cells demonstrated a growth advantage over the CD133(-) subpopulation. Taxol induced apoptosis on CD133(-) cells, but not on CD133(+) cells. In the CD133(-) subpopulation, the exposure to taxol induced the activation of apoptosis signal-regulating kinase1 (ASK1)/c-jun-N-terminal kinase (JNK), p38, extracellular signal regulated kinase (ERK) pathways and Bax expression, while in CD133(+) cells taxol was able only to enhance the activity of the ERK pathway. In CD133(+) cells, the direct gene transfer of Bax overcame the acquired resistance to taxol. Taken together, our data provide an insight into the mechanistic cascade of melanoma resistance to taxol and suggest Bax gene transfer as a complementary approach to chemotherapy.

Vinblastine-induced apoptosis of melanoma cells is mediated by Ras homologous A protein (Rho A) via mitochondrial and non-mitochondrial-dependent mechanisms.

Despite the availability of melanoma treatment at the primary site, the recurrence of local melanoma can metastasize to any distant organ. Currently, the available therapies for the treatment of metastatic melanoma are of limited benefit. Thus, the functional analysis of conventional therapies may help to improve their efficiency in the treatment of metastatic melanoma. In the present study, the exposure of melanoma cells to vinblastine was found to trigger apoptosis as evidenced by the loss of mitochondrial membrane potential, the release of both cytochrome c and apoptosis inducing factor, activation of caspase-9 and 3, and cleavage of Poly (ADP-ribose)-Polymerase. Also, vinblastine enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, c-jun-N-terminal kinase, p38, inhibitor of kappaBα (IκBα) kinase, and inositol requiring enzyme 1α. In addition, vinblastine induces the DNA-binding activities of the transcription factor NF-κB, HSF1, AP-1, and ATF-2, together with the expression of HSP70 and Bax proteins. Moreover, inhibitory experiments addressed a central role for Rho A in the regulation of vinblastine-induced apoptosis of melanoma cells via mitochondrial and non-mitochondrial-dependent mechanisms. In conclusion, the present study addresses for the first time a central role for Rho A in the modulation of vinblastine-induced apoptosis of melanoma cells and thereby provides an insight into the molecular action of vinblastine in melanoma treatment.

Bonding performance of a newly developed step-less all-in-one system on dentin.

The purpose of this study was to evaluate the short-term µTBS (Micro-tensile bond strength) and microscopic (SEM and TEM) observation of four recent adhesives. One adhesive was an experimental step-less 1-step system (LLB-2, Tokuyama Dental), which is an all-in-one system without the light-curing step in the application process. The other two were self-adhering light-cured flowable composite resin systems FLD (Fusio Liquid Dentin, Pentron Clinical Technologies) and VF (Vertise Flow Dental Restorative Materials, Kerr Corporation), which combine all the bonding steps together. A 2-step self-etching system MG (Clearfil MegaBond, Kuarary Medical) was employed as the control group in this study. The µTBS of MG was the highest (79.0 MPa) followed by that of LLB-2 (63.1 MPa), FLD (23.6 MPa), and VF (13.1 MPa). The microscopic observations showed that MG and LLB-2 had an approximately 20 µm and 5 µm adhesive layer respectively, without bubble or gap-formation at the resin-dentin interface, which were found in FLD and VF.

Crosstalk between apoptosis and autophagy: molecular mechanisms and therapeutic strategies in cancer.

Both apoptosis and autophagy are highly conserved processes that besides their role in the maintenance of the organismal and cellular homeostasis serve as a main target of tumor therapeutics. Although their important roles in the modulation of tumor therapeutic strategies have been widely reported, the molecular actions of both apoptosis and autophagy are counteracted by cancer protective mechanisms. While apoptosis is a tightly regulated process that is implicated in the removal of damaged or unwanted cells, autophagy is a cellular catabolic pathway that is involved in lysosomal degradation and recycling of proteins and organelles, and thereby is considered an important survival/protective mechanism for cancer cells in response to metabolic stress or chemotherapy. Although the relationship between autophagy and cell death is very complicated and has not been characterized in detail, the molecular mechanisms that control this relationship are considered to be a relevant target for the development of a therapeutic strategy for tumor treatment. In this review, we focus on the molecular mechanisms of apoptosis, autophagy, and those of the crosstalk between apoptosis and autophagy in order to provide insight into the molecular mechanisms that may be essential for the balance between cell survival and death as well as their role as targets for the development of novel therapeutic approaches.

Bortezomib/proteasome inhibitor triggers both apoptosis and autophagy-dependent pathways in melanoma cells.

Generally, both endoplasmic reticulum (ER) stress and mitochondrial dysregulation are a potential therapeutic target of anticancer agents including bortezomib. The treatment of melanoma cells with bortezomib was found to induce apoptosis together with the upregulation of Noxa, Mcl-1, and HSP70 proteins, and the cleavage of LC3 and autophagic formation. Also, bortezomib induced ER-stress as evidenced by the increase of intracellular Ca(2+) release. In addition, bortezomib enhanced the phosphorylation of inositol-requiring transmembrane kinase and endonuclease 1α (IRE1α), apoptosis signal-regulating kinase 1 (ASK1), c-jun-N-terminal kinase (JNK) and p38, and the activation of the transcription factors AP-1, ATF-2, Ets-1, and HSF1. Bortezomib-induced mitochondrial dysregulation was associated with the accumulation of reactive oxygen species (ROS), the release of both apoptosis inducing factor (AIF) and cytochrome c, the activation of caspase-9 and caspase-3, and cleavage of Poly (ADP-ribose) polymerase (PARP). The pretreatment of melanoma cells with the inhibitor of caspase-3 (Ac-DEVD-CHO) was found to block bortezomib-induced apoptosis that subsequently led to the increase of autophagic formation. In contrast, the inhibition of ASK1 abrogated bortezomib-induced autophagic formation and increased apoptosis induction. Furthermore, the inhibition of JNK, of HSP70 also increased apoptosis induction without influence of bortezomib-induced autophagic formation. Based on the inhibitory experiments, the treatment with bortezomib triggers the activation of both ER-stress-associated pathways, namely IRE1α-ASK1-p38-ATF-2/ets-1-Mcl-1, and IRE1α-ASK1-JNK-AP-1/HSF1-HSP70 as well as mitochondrial dysregulation-associated pathways, namely ROS-ASK1-JNK-AP-1/HSF1-HS70, and AIF-caspase-3-PARP and Cyt.c, and caspase-9-caspase-3-PARP. Taken together, our data demonstrates for the first time the molecular mechanisms, whereby bortezomib triggers both apoptosis and autophagic formation in melanoma cells.

The effect of air-blowing duration on all-in-one systems.

The purpose of this study was to evaluate the effect of air-blowing duration on the bonding performance of all-in-one systems using the same pressure (0.25 MPa). Three all-in-one systems were: EB (Easy Bond, 3M ESPE, USA), BB (BeautiBond, Shofu Inc., Japan) and GBp (G-Bond plus, GC Corporation, Japan). After adhesive application, the 3 systems were air-blown thereafter using 7 different durations (5 s, 10 s, 15 s, 20 s, 25 s, 30 s and 35 s). Bond strengths to dentin were determined using µTBS test after 24 h water storage. In addition, evaluation of both the resin-dentin interface and the fractured surface on the dentin side were performed by SEM. The maximum µTBS for each system, BB (40.4±14.8 MPa), EB (79.8±16.5 MPa), and GBp (47.3±17.6 MPa), were recorded with 15 s, 15 s and 25 s air-blowing duration respectively. Under the same air-pressure, the air-blowing duration could affect evaporation and the thickness of the adhesive layer, which contributed to the different bond strengths.

Involvement of toll-like receptors in autoimmune sialoadenitis of the non-obese diabetic mouse.

The aim of this study was to characterize the expression of Toll-like receptors (TLRs) during the development of sialoadenitis in the non-obese diabetic mouse. Submandibular glands were dissected from non-obese diabetic mice at 4, 8, 10, 12, and 16 weeks of age. The mRNA expression levels of TLR1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 12, 13, MyD88, and TRIF was quantified using real-time reverse transcription polymerase chain reaction. The mRNA expression levels in 4-week-old non-obese diabetic mice were used as controls. The expression levels of TLR1, 2, 4, and 9 were significantly higher at 8, 10, 12, and 16 weeks than the levels in the controls. The expression level of TLR3 was significantly higher at 16 weeks than in the controls. A group of mice were given drinking water containing 4.75% chloroquine starting at 4 weeks. Chloroquine caused a significant decrease in the expression of TLR1, 2, 3, 4, and 9 at 16 weeks compared with control mice who did not receive chloroquine. The areas of lymphocyte infiltration seen on serial sections of submandibular glands in the mice receiving chloroquine were significantly smaller than the areas of infiltration in control glands. Increased expression of Toll-like receptors may be involved in the development and/or progression of sialoadenitis in the non-obese diabetic mouse. Toll-like receptors may be a therapeutic target for autoimmune sialoadenitis.