Comparison of the Effects of Two Whitening Toothpastes on Microhardness of the Enamel and a Microhybride Composite Resin: An in Vitro Study

Introduction: Whitening toothpastes which have been accepted in populations may affect properties of enamel and restorative materials. The aim of this study was to compare the microhardness of human enamel and Z250 microhybrid composite resin after brushing with two whitening toothpastes.Materials and Methods: In this experimental study of enamel specimens, forty five freshly extracted human incisors were prepared and divided into three groups of control enamel (ClE), Crest enamel (CtE) and Aquafresh enamel (AfE). For composite resin specimens, forty five cylindrical-shaped specimens of light-cured Z250 composite were prepared and divided into three groups of control composite (ClC), Crest composite (CtC) and Aquafresh composite (AfC). The control groups were brushed without toothpaste. Crest and Aquafresh group specimens were brushed with Crest and Aquafresh whitening toothpastes, respectively. Vickers microhardness test wasperformed for all groups. Data were analyzed by One-way ANOVA and Tukey tests.Results: Microhardness values of ClE, CtE, AfE, ClC, CtC and AfC groups were 332.99 ± 26.59, 313.99 ± 20.56, 323.57 ± 27.96, 137.1 ± 3.16, 122.95 ± 3.27 and 130.36 ± 4.8, respectively. One-way ANOVA showed no significant differences among three enamel groups but there was significant difference among composite groups(p<0.01).Conclusion: Crest and Aquafresh whitening toothpastes did not affect enamel hardness but reduced the microhardness value of Z-250 composite resin. However, Crest whitening toothpaste decreased the microhardness more than Aquafresh

Point Mutations on Mitochondrial DNA in Iranian Patients with Friedreich’s Ataxia

ObjectiveMitochondrial DNA (mtDNA) is considered a candidate modifier factor for neuro-degenerative disorders. The most common type of ataxia is Friedreich's ataxia (FA). The aim of this study was to investigate different parts of mtDNA in 20 Iranian FA patients and 80 age-matched controls by polymerase chain reaction (PCR) and automated DNA sequencing methods to find any probable point mutations involved in the pathogenesis of FA.Materials and MethodsWe identified 13 nucleotide substitutions including A3505G, T3335C, G3421A, G8251A, A8563G, A8563G, G8584A, T8614C, T8598C, C8684T, A8701G, G8994A and A9024G.ResultsTwelve of 13 nucleotide substitutions had already been reported as polymorphism. One of the nucleotide substitutions (A9024G) had not been reported before. The A9024G nucleotide substitution does not change its amino acid. The controls were also investigated for this polymorphism which was found in two of them (2.5%).ConclusionNone of the mutations found in this study can affect the clinical manifestations of FA. This survey also provides evidence that the mtDNA A9024G allele is a new nonpathogenic polymorphism. We suggest follow-up studies for this polymorphism in different populations.

Investigation on mitochondrial tRNALeu/Lys, NDI and ATPase 6/8 in Iranian multiple sclerosis patients

As with chromosomal DNA, the mitochondrial DNA (mtDNA) can contain mutations that are highly pathogenic .In fact, many diseases of the central nervous system are known to be caused by mutations in mtDNA. Dysfunction of the mitochondrial Respiratory Chain (RC) has been shown in patients with neurological disease including Alzheimer's disease (AD), Parkinson's disease (PD) and Multiple sclerosis (MS). MS is a demyelinating disease of central nervous system characterized by morphological hallmarks of inflammation, demyelination and axonal loss. Considering this importance, we decided to investigate several highly mutative parts of mtDNA for point mutations as MT-LTI (tRNALeucine1(UUA/G)), MT-NDI (NADH Dehydrogenase subunit 1), MT-COII (Cytochrome c oxidase subunit II), MT-TK (tRNALysine), MT-ATP8 (ATP synthase subunit F0 8) and MT-ATP6 (ATP synthase subunit F0 6) in 20 Iranian MS patients and 80 age-matched control subjects by PCR and automated DNA sequencing to evaluate any probable point mutations. Our results revealed that 15 (75) out of 20 MS patients had point mutations. Some of point mutations were newly found in this study. This study suggested that point mutation occurred in mtDNA might be involved in pathogenesis of MS. © 2007 Springer Science+Business Media, LLC

The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/ IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal–regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells did not signal to IL-31 in spite of IL-31R expression. GC B cells expressed predominantly the inhibitory short IL-31RA isoform, whereas FL cells expressed predominantly the long signaling isoform. Moreover, GC B cells lacked expression of other IL-31RA isoforms potentially involved in the signaling pathway. IL-31 protein expression was significantly higher in surface membrane than in cytosol of both FL and GC B cells. IL-31 was detected in plasma membrane microvesicles from both cell types but not released in soluble form in culture supernatants. IL-31 and IL-31RA expression was higher in lymph nodes from FL patients with grade IIIa compared with grade I/II, suggesting a paracrine and/or autocrine role of IL-31/IL-31RA complex in tumor progression through microvesicle shedding

A mechanistic target of rapamycin complex 1/2 (mTORC1)/V-Akt murine thymoma viral oncogene homolog 1 (AKT1)/cathepsin H axis controls filaggrin expression and processing in skin, a novel mechanism for skin barrier disruption in patients with atopic dermatitis

Background Filaggrin, which is encoded by the filaggrin gene (FLG), is an important component of the skin's barrier to the external environment, and genetic defects in FLG strongly associate with atopic dermatitis (AD). However, not all patients with AD have FLG mutations. Objective We hypothesized that these patients might possess other defects in filaggrin expression and processing contributing to barrier disruption and AD, and therefore we present novel therapeutic targets for this disease. Results We describe the relationship between the mechanistic target of rapamycin complex 1/2 protein subunit regulatory associated protein of the MTOR complex 1 (RAPTOR), the serine/threonine kinase V-Akt murine thymoma viral oncogene homolog 1 (AKT1), and the protease cathepsin H (CTSH), for which we establish a role in filaggrin expression and processing. Increased RAPTOR levels correlated with decreased filaggrin expression in patients with AD. In keratinocyte cell cultures RAPTOR upregulation or AKT1 short hairpin RNA knockdown reduced expression of the protease CTSH. Skin of CTSH-deficient mice and CTSH short hairpin RNA knockdown keratinocytes showed reduced filaggrin processing, and the mouse had both impaired skin barrier function and a mild proinflammatory phenotype. Conclusion Our findings highlight a novel and potentially treatable signaling axis controlling filaggrin expression and processing that is defective in patients with AD