Family, Peers and School Programs and the Influence on Juvenile Marijuana Use

Drug use has is a common form of deviance among adolescents. This paper focuses on the different ways that social institutions try to positively or negatively influence juveniles from becoming involved in drug use. I will provide evidence on school programs and give conclusions on the helpfulness of them. I will also write about the parent-child relationship and whether or not this is a main influence of substance abuse. Finally, the peer group will be analyzed to determine how much of an effect they might have. These three factors will be explored throughout the content of this literature review. By showing the effects of how family, peers and school programs influence drug and alcohol use, one will have a better understanding of why adolescents might or might not turn to these illegal activities. For the purpose of this paper, the main drug I will be focusing on will be marijuana. My research question asks what the different ways that family, peers and school programs influence drug use such as marijuana among adolescents. Through research of scholarly journal articles, I hypothesize that I will find both negative and positive effects that all three groups will have on drug use by a young person

MicroRNA-30 mediates anti-inflammatory effects of shear stress and KLF2 via repression of angiopoietin 2

MicroRNAs are endogenously expressed small noncoding RNAs that regulate gene expression. Laminar blood flow induces atheroprotective gene expression in endothelial cells (ECs) in part by upregulating the transcription factor KLF2. Here, we identified KLF2- and flow-responsive miRs that affect gene expression in ECs. Bioinformatic assessment of mRNA expression patterns identified the miR-30-5p seed sequence to be highly enriched in mRNAs that are downregulated by KLF2. Indeed, KLF2 overexpression and shear stress stimulation in vitro and in vivo increased the expression of miR-30-5p family members. Furthermore, we identified angiopoietin 2 (Ang2) as a target of miR-30. MiR-30 overexpression reduces Ang2 levels, whereas miR-30 inhibition by LNA-antimiRs induces Ang2 expression. Consistently, miR-30 reduced basal and TNF-a-induced expression of the inflammatory cell-cell adhesion molecules E-selectin, ICAM1 and VCAM1, which was rescued by stimulation with exogenous Ang2. In summary, KLF2 and shear stress increase the expression of the miR-30-5p family which acts in an antiinflammatory manner in ECs by impairing the expression of Ang2 and inflammatory cell-cell adhesion molecules. The upregulation of miR-30-5p family members may contribute to the atheroprotective effects of shear stress