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Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked recessive disorder and is the most common enzyme deficiency worldwide. Although this disease is rare in Korea, its prevalence may increase due to an increase of multicultural families. Patients with this deficiency are prone to hemolytic anemia provoked by specific drugs commonly used or prescribed in pediatric dentistry. It is necessary for pediatric dentists to have accurate knowledge of a patient's medical history and to consult with a pediatric hematologist to avoid oxidative stress that can lead to hemolysis. The most effective treatment is prevention of exposure to factors that may trigger anemia. Appropriate education regarding risk factors is essential for patients diagnosed with this disease. This case report aimed to discuss the drugs and dental management methods that should be cautious in children with G6PD deficiency.

The objectives of this study were to evaluate the performance of the BD Phoenix™ M50 system with two antimicrobial susceptibility testing (AST) panels against clinical isolates in South Korea and the accuracy of determining carbapenem and colistin susceptibility compared with reference methods. A total of 825 nonduplicated clinical isolates were included in this study. Bacterial identification was performed using Bruker Biotyper and 16S rDNA sequencing. Antimicrobial susceptibilities were tested by disk diffusion, broth microdilution, and agar dilution methods. AST with the Phoenix system was performed following the manufacturer's instructions. The categorical agreement (CA), very major error (VME), major error (ME), and minor error (mE) rates were calculated for each antibiotic. CA rates between the results of the Phoenix system and reference methods were more than 90% for most antibiotics except for ciprofloxacin in enterococci (82.7%, 163/197) and cefepime in Acinetobacter species (88.9%, 88/99). VME and ME rates were less than 3% for all the antibiotics tested in this study. Minimum inhibitory concentration (MIC) values for carbapenem and colistin determined by the Phoenix system were highly correlated with those of dilution methods, exhibiting 99.2% (384/387), 96.7% (374/387), and 98.5% (129/131) of the agreement rate within onefold dilution difference for imipenem, meropenem, and colistin, respectively. The BD Phoenix M50™ system showed reliable performance for AST in clinical microbiology laboratories and for detecting carbapenem and colistin resistance in Gram-negative clinical isolates.

AIM To investigate the role of autophagy in MTA-induced odontoblastic differentiation of human dental pulp cells (HDPCs). METHODOLOGY In MTA-treated HDPCs, odontoblastic differentiation was assessed based on expression levels of dentine sialophosphoprotein (DSPP) and dentine matrix protein 1 (DMP1), alkaline phosphatase activity (ALP) activity by ALP staining and the formation of mineralized nodule by Alizarin red S staining. Expression of microtubule-associated protein 1A/1B-light chain3 (LC3), adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) signalling molecules and autophagy-related genes was analysed by Western blot analysis and Acridine orange staining was used to detect autophagic lysosome. For in vivo experiments, tooth cavity preparation models on rat molars were established and the expression of proteins-related odontogenesis and autophagy markers was observed by Immunohistochemistry and Western blot analysis. Kruskal-Wallis with Dunn's multiple comparison was used for statistical analysis. RESULTS Mineral trioxide aggregate (MTA) promoted odontoblastic differentiation of HDPCs, accompanied by autophagy induction, including formation of autophagic lysosome and cleavage of LC3 to LC3II (P

본 연구의 목적은 산부식 시간과 접착제 적용에 따른 유구치 치면열구전색제의 미세인장 결합강도를 평가하여 비교하는 것이다. 40개의 발거된 건전한 하악 유구치를 선정하여 산부식을 시행하지 않은 군과 산부식을 각각 15, 30, 60초 시행한 군으로 분류하였다. 이를 다시 접착제를 적용하지 않은 군과 적용한 군으로 나...

교내에서 학생들의 치과적 외상은 흔하며 일반교사들보다 보건교사들이 외상의 일차적인 처치를 담당한다. 본 연구는 광주, 전남지역의 초, 중, 고등학교 보건교사들을 대상으로 어린이들의 치아외상시의 대처 방법에 대한 지식수준을 조사하고, 치과 응급처치에 대한 교육을 시행한 후 그 효과가 어느 정도인지를 알아보고...

Ligands of the B7 family provide both positive and negative costimulatory signals to the CD28 family of receptors on T lymphocytes, the balance of which determines the immune response. B7-H3 is a member of the B7 family whose function in T-cell activation has been the subject of some controversy: in autoimmunity and tumor immunity, it has been described as both costimulatory and coinhibitory, while in transplantation, B7-H3 signaling is thought to contribute to graft rejection. However, we now demonstrate results to the contrary. Signaling through a putative B7-H3 receptor prolonged allograft survival in a fully MHC-mismatched cardiac model and promoted a shift toward a Th2 milieu; conversely, B7-H3 blockade, achieved by use of a blocking antibody, resulted in accelerated rejection, an effect associated with enhanced IFN-γ production. Finally, graft prolongation achieved by CTLA4 Ig was shortened both by B7-H3 blockade and the absence of recipient B7-H3. These findings suggest a coinhibitory role for B7-H3. However, experience with other CD28/B7 family members suggests that immune redundancy plays a crucial role in determining the functions of various pathways. Given the abundance of conflicting data, it is plausible that, under differing conditions, B7-H3 may have both positive and negative costimulatory functions.

Type 1 diabetes (T1D) remains a major health problem worldwide, with a steadily rising incidence yet no cure. Phosphoinositide 3-kinase-γ (PI3Kγ), a member of a family of lipid kinases expressed primarily in leukocytes, has been the subject of substantial research for its role in inflammatory diseases. However, the role of PI3Kγ inhibition in suppressing autoimmune T1D remains to be explored. We tested the role of the PI3Kγ inhibitor AS605240 in preventing and reversing diabetes in NOD mice and assessed the mechanisms by which this inhibition abrogates T1D. Our data indicate that the PI3Kγ pathway is highly activated in T1D. In NOD mice, we found upregulated expression of phosphorylated Akt (PAkt) in splenocytes. Notably, T regulatory cells (Tregs) showed significantly lower expression of PAkt compared with effector T cells. Inhibition of the PI3Kγ pathway by AS605240 efficiently suppressed effector T cells and induced Treg expansion through the cAMP response element-binding pathway. AS605240 effectively prevented and reversed autoimmune diabetes in NOD mice and suppressed T-cell activation and the production of inflammatory cytokines by autoreactive T cells in vitro and in vivo. These studies demonstrate the key role of the PI3Kγ pathway in determining the balance of Tregs and autoreactive cells regulating autoimmune diabetes.

B7 ligands deliver both costimulatory and coinhibitory signals to the CD28 family of receptors on T lymphocytes, the balance between which determines the ultimate immune response. Although B7-H4, a recently discovered member of the B7 family, is known to negatively regulate T cell immunity in autoimmunity and cancer, its role in solid organ allograft rejection and tolerance has not been established. Targeting the B7-H4 molecule by a blocking antibody or use of B7-H4(-/-) mice as recipients of fully MHC-mismatched cardiac allografts did not affect graft survival. However, B7-H4 blockade resulted in accelerated allograft rejection in CD28-deficient recipients. B7-1/B7-2-double-deficient recipients are truly independent of CD28/CTLA-4:B7 signals and usually accept MHC-mismatched heart allografts. Blockade of B7-H4 in these mice also precipitated rejection, demonstrating regulatory function of this molecule independent of an intact CD28/CTLA-4:B7 costimulatory pathway. Accelerated allograft rejection was always accompanied by increased frequencies of alloreactive IFN-γ-, IL-4- and Granzyme B-producing splenocytes. Finally, intact recipient, but not donor, B7-H4 is essential for prolongation of allograft survival by blocking CD28/CTLA4:B7 pathway using CTLA4-Ig. These data are the first to provide evidence of the regulatory effects of B7-H4 in alloimmune responses in a murine model of solid organ transplantation.

OBJECTIVE A number of clinical trials are underway to test whether mesenchymal stem cells (MSCs) are effective in treating various diseases, including type 1 diabetes. Although this cell therapy holds great promise, the optimal source of MSCs has yet to be determined with respect to major histocompatibility complex matching. Here, we examine this question by testing the ability of congenic MSCs, obtained from the NOR mouse strain, to reverse recent-onset type 1 diabetes in NOD mice, as well as determine the immunomodulatory effects of NOR MSCs in vivo. RESEARCH DESIGN AND METHODS NOR MSCs were evaluated with regard to their in vitro immunomodulatory function in the context of autoreactive T-cell proliferation and dendritic cell (DC) generation. The in vivo effect of NOR MSC therapy on reversal of recent-onset hyperglycemia and on immunogenic cell subsets in NOD mice was also examined. RESULTS NOR MSCs were shown to suppress diabetogenic T-cell proliferation via PD-L1 and to suppress generation of myeloid/inflammatory DCs predominantly through an IL-6-dependent mechanism. NOR MSC treatment of experimental type 1 diabetes resulted in long-term reversal of hyperglycemia, and therapy was shown to alter diabetogenic cytokine profile, to diminish T-cell effector frequency in the pancreatic lymph nodes, to alter antigen-presenting cell frequencies, and to augment the frequency of the plasmacytoid subset of DCs. CONCLUSIONS These studies demonstrate the inimitable benefit of congenic MSC therapy in reversing experimental type 1 diabetes. These data should benefit future clinical trials using MSCs as treatment for type 1 diabetes.

In order to establish the bleaching process for cotton fabrics under the neutral condition, cotton fabrics were bleached by hydrogen peroxide with urea. It was revealed that hydrogen peroxide bleaching with urea showed the higher whiteness of bleached fabrics than that without urea at more than 70 degrees Celsius. Tensile strength did not decrease after bleaching. Some radicals were observed by ESR measurement when urea was added into hydrogen peroxide aqueous solution. The effects of urea on hydrogen peroxide bleaching seems to be caused by active oxygen ; hydroxyl radical, perhydroxyl radical and superoxide anion radical as well as perhydroxyl anion. The residual hydrogen peroxide concentrations in bleaching baths were measured. When urea is added to the bleaching baths, the decomposition of hydrogen peroxide is accelerated even in the neutral bath.

In order to establish the bleaching method for cotton fabrics under the neutral or acid condition, the cotton fabrics were pretreated by iron(II) sulfate before subsequent hydrogen peroxide bleaching. The white index and tensile strength at break for yarns from bleached fabrics were measured and considered concerning the pretreated condition by iron(II) sulfate. It was revealed that the high white index attained, by contraries, tensile strength for yarns decreased ca. 20% by processing. However, an addition of a small amount of sodium hydroxide into bleaching bath enabled to depress a decrease of tensile strength for yarns. In addition, it was observed by ESR measurement that an amount of radicals increased when a small amount of NaOH was added into hydrogen peroxide solution in the presence of iron (II) sulfate.

The proinflammatory cytokine IL-6 plays an important role in controlling T-cell differentiation, especially the development of Th17 and regulatory T cells. To determine the function of IL-6 in regulating allograft rejection and tolerance, BALB/c cardiac grafts were transplanted into wild-type or IL-6-deficient C57BL/6 mice. We observed that production of IL-6 and IFN-γ was upregulated during allograft rejection in untreated wild-type mice. In IL-6-deficient mice, IFN-γ production was greater than that observed in wild-type controls, suggesting that IL-6 production affects Th1/Th2 balance during allograft rejection. CD28-B7 blockade by CTLA4-Ig inhibited IFN-γ production in C57BL/6 recipients, but had no effect on the production of IL-6. Although wild-type C57BL/6 recipients treated with CTLA4-Ig rejected fully MHC-mismatched BALB/c heart transplants, treatment of IL-6-deficient mice with CTLA4-Ig resulted in graft acceptance. Allograft acceptance appeared to result from the combined effect of costimulatory molecule blockade and IL-6-deficiency, which limited the differentiation of effector cells and promoted the migration of regulatory T cells into the grafts. These data suggest that the blockade of IL-6, or its signaling pathway, when combined with strategies that inhibit Th1 responses, has a synergistic effect on the promotion of allograft acceptance. Thus, targeting the effects of IL-6 production may represent an important part of costimulation blockade-based strategies to promote allograft acceptance and tolerance.

Ischemic reperfusion injury (IRI) enhances allograft immunogenicity, worsens transplantation outcome, and is the primary cause of activation of the recipient innate immune response, resulting in subsequent amplification of the alloimmune adaptive response. Here, we aimed at demonstrating that the link between innate injury and alloimmunity occurs predominantly through activation of allograft-derived dendritic cells (ADDC). Perfusion of MCI-186, a free radical scavenger, into donor cardiac allografts prior to transplantation resulted in prolongation of complete MHC-mismatched allograft survival in the absence of immunosuppression (MST of 8 vs. 26 days). This prolongation was associated with a reduction in trafficking of ADDC to recipient lymphoid tissue as well as a reduction in T cell priming. Depleting ADDC with diphtheria toxin (using DTR-GFP-DC mice as donors) 24 h prior to transplant resulted in abrogation of the prolongation observed with MCI-186 treatment, demonstrating that the beneficial effect of MCI-186 is mediated by ADDC. This donor-specific anti-ischemic regimen was also shown to reduce chronic rejection, which represents the primary obstacle to long-term allograft acceptance. These data for the first time establish a basis for donor anti-ischemic strategies, which in the ever-expanding marginal donor pools, can be instituted to promote engraftment.

Clinical trials using mesenchymal stem cells (MSCs) have been initiated worldwide. An improved understanding of the mechanisms by which allogeneic MSCs evade host immune responses is paramount to regulating their survival after administration. This study has focused on the novel role of serine protease inhibitor (SPI) in the escape of MSCs from host immunosurveillance through the inhibition of granzyme B (GrB). Our data indicate bone marrow–derived murine MSCs express SPI6 constitutively. MSCs from mice deficient for SPI6 (SPI6−/−) exhibited a 4-fold higher death rate by primed allogeneic cytotoxic T cells than did wild-type MSCs. A GrB inhibitor rescued SPI6−/− MSCs from cytotoxic T-cell killing. Transduction of wild-type MSCs with MigR1-SPI6 also protected MSCs from cytotoxic T cell–mediated death in vitro. In addition, SPI6−/− MSCs displayed a shorter lifespan than wild-type MSCs when injected into an allogeneic host. We conclude that SPI6 protects MSCs from GrB-mediated killing and plays a pivotal role in their survival in vivo. Our data could serve as a basis for future SPI-based strategies to regulate the survival and function of MSCs after administration and to enhance the efficacy of MSC-based therapy for diseases.