ABSTRACT
The pathogenesis of systemic lupus erythematosus [SLE] is influenced by both genetic factors and epigenetic modifications; the latter is a result of exposure to various environmental factors. Epigenetic modifications affect gene expression and alter cellular functions without modifying the genomic sequences. CpG-DNA methylation, histone modifications, and miRNAs are the main epigenetic factors of gene regulation. In SLE, global and genespecific DNA methylation changes have been demonstrated to occur in CD4+ T-cells. Moreover, histone acetylation and deacetylation inhibitors reverse the expression of multiple genes involved in SLE, indicating histone modification in SLE. Autoreactive T-cells and B-cells have been shown to alter the patterns of epigenetic changes in SLE patients. Understanding the molecular mechanisms involved in the pathogenesis of SLE is critical for the introduction of effective, target-directed and tolerated therapies. In this review, we summarize the recent findings that highlight the importance of epigenetic modifications and their mechanisms in SLE
ABSTRACT
The use of low level laser to reduce pain, inflammation and edema, to promote wound, deeper tissues and nerves healing, and to prevent tissue damage has been known for almost forty years since the invention of lasers. This review will cover some of the proposed cellular mechanisms responsible for the effect of visible light on mammalian cells, including cytochrome c oxidase [with absorption peaks in the Near Infrared [NIR]]. Mitochondria are thought to be a likely site for the initial effects of light, leading to increased ATP production, modulation of reactive oxygen species, and induction of transcription factors. These effects in turn lead to increased cell proliferation and migration [particularly by fibroblasts]
ABSTRACT
There are several problems associated to the management of patients with phenylketonuria [PKU]. Social status could be one of the affecting factors on dietary adherence in these patients. The aim of this study was to evaluate family social status and dietary adherence of PKU patients in Iranian population. In a cross-sectional study, we studied 105 Iranian PKU patients [born 1984 to 2010], treated and followed at Mofid Children's Hospital, Tehran. Social status was defined by number of children in family, number of affected children in family, maternal and paternal education, marital and employment status of the parents. Age at diagnosis and duration of treatment were also recorded. Mean plasma phenylalanine level was considered as a sign of dietary adherence in PKU patients and was calculated considering the phenylalanine measurements throughout at least one year. Mean plasma phenylalanine concentration was 5.9 +/- 3.6 mg/dl in patients <12 years old and 13.1 +/- 3.9 mg/dl in patients >12 years old. Blood phenylalanine concentrations in 47.6% of patients were in normal age-related reference range. There was a significant association between divorced and unemployed parents, and higher levels of blood phenylalanine concentration [P=0.02 and P=0.03 respectively]. There was a significant positive correlation between number of affected children in the family [r=0.43, P<0.001], age at diagnosis [r=0.2, P=0.03], treatment duration [r=0.7, P=<0.001] and blood phenylalanine concentrations. There was no significant relation between parental education, family size and dietary adherence. Social status affects dietary adherence to some extent. We suggest exploring care-givers dietary knowledge as the next step to improve dietary compliance in these patients
ABSTRACT
Systemic Lupus Erythematosus is a chronic autoimmune disorder that almost involves all of tissues and organs in body. The etiology of Lupus is mostly unknown. It seems that both genetic and environmental factores contribute in the disease development. Numerous genes have been suggested as candidate gene for Systemic Lupus Erythematosus, for example, the genes for apoptosis and genes for production of immune system. Linkage analysis is used to identify susceptibility genes for inherited diseases like Lupus. For this reason, the candidate genes and their polymorphism are evaluated in various populations. If finding can be repeated in an independent set of samples, the polymorphism causing genetic association with a candidate gene may identify the actual disease-causing gene. Linkage studies use a set of markers and different studies for the coinheritance of genetic markers with the disease phenotype in families lead us to the significant conclusions: role of genetics in the development of SLE, disease association on a population basis, and once the power of the genetic analyses is correlated with the differences in the disease symptoms in different populations, we may have the ability to identify particular individuals as belonging to a specific subgroup with a predictable disease course. Finally understanding the genetics of SLE also should lead to more specific therapeutic interventions