The effect of the KTP laser on smear layer and temperature change: an in vitro study

Abstract

The purpose of this study was to evaluate the effects of potassium-titanyl-phosphate (KTP) laser irradiation on smear layer removal and temperature changes of the root surfaces. Two hundred four extracted single-root human premolars were included. The canals were instrumented and divided into two main groups: group A (smear layer examination n:119) and group B (temperature change examination n:85). Each group was divided into subgroups (n:17) according to the different five laser power settings: A1, B1: 1 W–5.33 J/cm²; A2, B2: 1.5 W–7.52 J/cm²; A3, B3: 2 W–10.3 J/cm²; A4, B4: 3 W–15.5 J/cm², A5, B5: 4 W–20.1 J/cm2, A6: positive control no laser irradiation-irrigated 2 mL for 2 min 2.5% NaOCl + 2 mL distilled water and A7: negative control groups no laser irradiation irrigated 2 mL for 2 min 17% EDTA + 2 mL for 2 min 2.5% NaOCl + 2 mL distilled water. The temperature elevations were measured with an infrared thermographic camera and smear layer examined by scanning electron microscope. According to Kruskal-Wallis and Tukey's tests, in all groups the highest smear scores were in the apical third. In all areas, there were statistically significant differences between negative control group (17% EDTA) and all other groups (p < 0.05). The highest smear scores were determined in 1 W KTP laser and positive control (2.5% NaOCl) groups. Statistically, in all thirds, the differences the 3 W and 4 W KTP laser groups between each other and all other groups were significant (p < 0.05). After the end of the use of the laser, increase in temperature values in all groups were found to be below 10 °C in 20 s.

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Scrotal calcinosis: two case reports

Scrotal calcinosis is a rare and benign condition. It usually gives rise to few symptoms, and the impact is mainly functional and aesthetic. It is considered part of dystrophic calcinosis cutis. Surgical manag...

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Downregulation of BDH2 modulates iron homeostasis and promotes DNA demethylation in CD4+ T cells of systemic lupus erythematosus

Publication date: Available online 4 November 2017
Source:Clinical Immunology
Author(s): Ming Zhao, Meng-ying Li, Xiao-fei Gao, Su-jie Jia, Ke-qin Gao, Yin Zhou, Hui-hui Zhang, Yi Huang, Jing Wang, Hai-jing Wu, Qian-jin Lu
DNA hypomethylation plays an important role in the pathogenesis of systemic lupus erythematosus (SLE). Here we investigated whether 3-hydroxy butyrate dehydrogenase 2 (BDH2), a modulator of intracellular iron homeostasis, was involved in regulating DNA hypomethylation and hyper-hydroxymethylation in lupus CD4⁺ T cells. Our results showed that BDH2 expression was decreased, intracellular iron was increased, global DNA hydroxymethylation level was elevated, while methylation level was reduced in lupus CD4⁺ T cells compared with healthy controls. The decreased BDH2 contributed to DNA hyper-hydroxymethylation and hypomethylation via increasing intracellular iron in CD4⁺ T cells, which led to overexpression of immune related genes. Moreover, we showed that BDH2 was the target gene of miR-21. miR-21 promoted DNA demethylation in CD4⁺ T cells through inhibiting BDH2 expression. Our data demonstrated that the dysregulation of iron homeostasis in CD4⁺ T cells induced by BDH2 deficiency contributes to DNA demethylation and self-reactive T cells in SLE.



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Natural killer cells play an essential role in resolution of antigen-induced inflammation in mice

Publication date: January 2018
Source:Molecular Immunology, Volume 93
Author(s): Osk U.U. Anuforo, Stefania P. Bjarnarson, Hulda S. Jonasdottir, Martin Giera, Ingibjorg Hardardottir, Jona Freysdottir
This study examined whether NK cells are important for resolution of antigen-induced inflammation. C57BL/6 mice were immunized twice with methylated BSA (mBSA) and inflammation induced by intraperitoneal injection of mBSA. Mice were injected intravenously with anti-asialo GM1 (αASGM1) or a control antibody 24h prior to peritonitis induction and peritoneal exudate collected at different time points. Expression of surface molecules and apoptosis on peritoneal cells was determined by flow cytometry and concentration of chemokines, cytokines, soluble cytokine receptors and lipid mediators by ELISA and LC–MS/MS. Apoptosis in parathymic lymph nodes and spleens was determined by TUNEL staining. Mice administered αASGM1 had lower peritoneal NK cell numbers and a higher number of peritoneal neutrophils 12h after induction of inflammation than control mice. The number of neutrophils was still high in the αASGM1 treated mice when their number had returned to baseline levels in the control mice, 48h after induction of inflammation. Peritoneal concentrations of the neutrophil regulators G-CSF and IL-12p40 were higher at 12h in the αASGM1 treated mice than in the control mice, whereas concentrations of lipid mediators implicated in resolution of inflammation, i.e. LXA4 and PGE2, were lower. Reduced apoptosis was detected in peritoneal neutrophils as well as in draining lymph nodes and spleens from the αASGM1 treated mice compared with that in the control mice. In addition, αASGM1 treated mice had lower number of peritoneal NK cells expressing NKp46 and NKG2D, receptors implicated in NK cell-induced neutrophil apoptosis. Furthermore, αASGM1 treatment completely blocked the increase in CD27⁺ NK cells that occurred in control mice following induction of inflammation, but CD27⁺ NK cells have been suggested to have a regulatory role. These results indicate a crucial role for NK cells in resolution of antigen-induced inflammation and suggest their importance in tempering neutrophil recruitment and maintaining neutrophil apoptosis.



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Traitement du lupus érythémateux par le bélimumab en pratique courante : étude rétrospective de 15 malades

Publication date: Available online 4 November 2017
Source:Annales de Dermatologie et de Vénéréologie
Author(s): E. Garval, J.-L. Pennaforte, R. Jaussaud, A. Servettaz, P. Bernard, Z. Reguiai
IntroductionLe bélimumab (anticorps monoclonal anti-BLyS) a été récemment commercialisé dans le traitement du lupus érythémateux (LE) systémique. Le but de cette étude était d'en décrire l'efficacité, la tolérance, l'impact sur les paramètres sérologiques du LE et le rôle d'épargne des traitements de fond en pratique courante.Malades et méthodesCette étude rétrospective menée au CHU de Reims incluait tous les malades atteints de LE traités par bélimumab entre 2012 et 2016. L'efficacité du traitement était évaluée sur l'évolution clinique, la normalisation des concentrations d'anticorps anti-DNA et de complément, et l'épargne des autres traitements du LE.RésultatsUne réponse thérapeutique était obtenue chez 9 des 15 malades inclus (60 %), à type de rémission partielle pour 8 d'entre eux. La concentration médiane d'anti-DNA était de 50UI/mL (4 à 50) et celle de C3 sérique de 0,82g/L (0,36 à 1,23) à l'instauration du bélimumab, versus respectivement 25,5UI/mL (2 à 50) et 0,89g/L (0,34 à 1,22) à la date des dernières nouvelles (DDN), sans modification significative (respectivement p=0,12 et p=0,45). La posologie médiane de prednisone à l'instauration du bélimumab passait de 9,5mg/j (0 à 18) à 6mg/j (0 à 20) à la DDN. Huit malades (53 %) ont présenté des effets secondaires, toujours minimes.ConclusionLe bélimumab a eu chez 15 malades une efficacité modérée et une faible toxicité ; il a permis une épargne cortisonique modérée, en vue de limiter les effets secondaires de la corticothérapie au long cours.BackgroundBelimumab (an anti-BLyS monoclonal antibody) was recently approved for the treatment of systemic lupus erythematosus (SLE). The aim of the study was to describe efficacy and safety of the drug as well as its impact on serologic parameters and the role of long-term systemic sparing of treatment in clinical practice in LE.Patients and methodsWe conducted a retrospective study at Reims University Hospital between 2012 and 2016 including consecutive patients with LE treated with belimumab. Efficacy was evaluated in terms of clinical progression, and normalisation of laboratory factors (anti-DNA antibody and C3 serum levels) and sparing of associated long-term systemic therapies for LE.ResultsAmong the 15 patients included, a therapeutic response was obtained in 9 patients (60%), with partial remission in 8 of 9 cases. The median titre of anti-DNA antibody was 50IU/mL (range: 4–50) and the median C3 level was 0.82g/L (range: 0.36–1.23) before initiation of belimumab, vs. 25.5IU/mL (range: 2–50) and 0.89g/L (range: 0.34–1.22) at the last evaluation, respectively, without significant modification (P=0.12 and P=0.45). The median dose of prednisone at the time of the first belimumab infusion was reduced from 9.5mg/day (range: 0–18) to 6mg/day (range: 0–20) at the last clinical evaluation. Eight patients (53%) experienced adverse events, and these were very slight or moderate in all cases.ConclusionBelimumab appears to be an effective and well-tolerated treatment for moderately severe systemic LE, allowing sparing of maintenance corticosteroid therapy in order to decrease its frequent adverse events.



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Human plasma C3 is essential for the development of memory B, but not T, lymphocytes

Publication date: Available online 4 November 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Anaïs Jiménez-Reinoso, Ana V. Marin, Marta Subias, Alberto López-Lera, Elena Román-Ortiz, Kathryn Payne, Cindy S. Ma, Giuseppina Arbore, Martin Kolev, Simon J. Freeley, Claudia Kemper, Stuart G. Tangye, Edgar Fernández-Malavé, Santiago Rodríguez de Córdoba, Margarita López-Trascasa, José R. Regueiro

Teaser

Primary or secondary plasma C3 deficiency due to mutations in C3 or in complement Factor I impairs memory B, but not T, cell differentiation, but does not preclude intracellular C3 fragment expression in lymphocytes.


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TRIM21 negatively regulates intestinal mucosal inflammation through inhibiting Th1/Th17 cell differentiation in inflammatory bowel diseases

Publication date: Available online 4 November 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Guangxi Zhou, Wei Wu, Lin Yu, Tianming Yu, Wenjing Yang, Ping Wang, Xiaoping Zhang, Yingzi Cong, Zhanju Liu
BackgroundTripartite motif-containing (TRIM)21 has been implicated in pathogenesis of several types of autoimmune diseases.ObjectiveWe sought to elucidate expression of TRIM21 in patients with inflammatory bowel disease (IBD) and its role in regulating intestinal mucosal inflammation.MethodsTRIM21 expression was analyzed in inflamed mucosa of IBD patients by qRT-PCR and immunohistochemistry. Peripheral blood CD4⁺ T cells were transfected with lentivirus-expressing-TRIM21 (LV-TRIM21) or LV-sh-TRIM21, and cytokine expression was determined by qRT-PCR and ELISA. TRIM21^−/− mice were generated, and trinitrobenzene sulphonic acid (TNBS)- and CD45RB^highCD4⁺ T cell-induced colitis models were established to determine its role in the induction of intestinal inflammation.ResultsTRIM21 was predominantly expressed in CD4⁺ T cells and markedly decreased in inflamed mucosa of IBD patients compared with healthy controls. Ectopic expression of TRIM21 inhibited IBD CD4⁺ T cells to differentiate into T helper (Th)1 and Th17 cells, whereas downregulation of TRIM21 had opposite effects. TRIM21^−/− mice developed more severe colitis following administration of TNBS compared with wild-type mice, characterized by increased expression of IFN-γ, TNF-α, and IL-17A in the colon. TRIM21^−/− CD45RB^highCD4⁺ T cells reconstituted into Rag-1^−/− mice induced more severe colitis than wild-type controls. Mechanistically, IRF3 was identified as a functional downstream target of TRIM21, in that silencing of IRF3 suppressed TRIM21^−/−CD4⁺ T cell differentiation into Th1 and Th17 cells.ConclusionsTRIM21 plays a protective role in mucosal inflammation through inhibiting Th1 and Th17 cell differentiation. Thus, TRIM21 may serve as a potential therapeutic target for treatment of IBD.

Teaser

●TRIM21 is decreased in inflamed mucosa of patients with active IBD and plays a protective role in mucosal inflammation through inhibiting Th1 and Th17 cell differentiation. TRIM21 may serve as a potential therapeutic target for treatment of IBD.


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