Finding Common Ground: Abortion, Television, And The Changing American Culture

As Oscar Wilde once said, life imitates art far more than art imitates life , but there is a reciprocal relationship between the two. The more society talks about an issue, the more we are going to see that issue present in television, which then spurs even more discussion on that topic. Today, we use the media to understand what is important and popular in our society. Conversely, the media uses society to capture polarizing topics, such as abortion, to attract viewers. Media critics often argue that television has too large of an impact on developing societies perspectives. However, the viewpoint could be the opposite. I am making the argument that as societies understandings and viewpoints on abortion have evolved over the past decades with changing regulations, laws, and attitudes, the portrayal of abortion in the media has reflected that development. With studies done to find that three in ten women will have an abortion by age 45, we see how prevalent abortion is in our society, with about 21% of pregnancies ending in abortion1. By showing how the media\u27s portrayal of abortion has reflected the transformation of societies views, we can see how the media and society have created a symbiotic relationship and how television mimics our reality. The media reflects societies current thoughts, and when portrayed equally this generates a greater understanding and discussion for both views on the issue. By knowing this relationship, we can use media as a way to produce healthy dialogue and explanations on certain topics that are currently significant to society

BRAFV600E induces reversible mitotic arrest in human melanocytes via microrna-mediated suppression of AURKB.

Benign melanocytic nevi frequently emerge when an acquired BRAFV600E mutation triggers unchecked proliferation and subsequent arrest in melanocytes. Recent observations have challenged the role of oncogene-induced senescence in melanocytic nevus formation, necessitating investigations into alternative mechanisms for the establishment and maintenance of proliferation arrest in nevi. We compared the transcriptomes of melanocytes from healthy human skin, nevi, and melanomas arising from nevi and identified a set of microRNAs as highly expressed nevus-enriched transcripts. Two of these microRNAs-MIR211-5p and MIR328-3p-induced mitotic failure, genome duplication, and proliferation arrest in human melanocytes through convergent targeting of AURKB. We demonstrate that BRAFV600E induces a similar proliferation arrest in primary human melanocytes that is both reversible and conditional. Specifically, BRAFV600E expression stimulates either arrest or proliferation depending on the differentiation state of the melanocyte. We report genome duplication in human melanocytic nevi, reciprocal expression of AURKB and microRNAs in nevi and melanomas, and rescue of arrested human nevus cells with AURKB expression. Taken together, our data describe an alternative molecular mechanism for melanocytic nevus formation that is congruent with both experimental and clinical observations

Exome sequencing of 20,979 individuals with epilepsy reveals shared and distinct ultra-rare genetic risk across disorder subtypes

Identifying genetic risk factors for highly heterogeneous disorders such as epilepsy remains challenging. Here we present, to our knowledge, the largest whole-exome sequencing study of epilepsy to date, with more than 54,000 human exomes, comprising 20,979 deeply phenotyped patients from multiple genetic ancestry groups with diverse epilepsy subtypes and 33,444 controls, to investigate rare variants that confer disease risk. These analyses implicate seven individual genes, three gene sets and four copy number variants at exome-wide significance. Genes encoding ion channels show strong association with multiple epilepsy subtypes, including epileptic encephalopathies and generalized and focal epilepsies, whereas most other gene discoveries are subtype specific, highlighting distinct genetic contributions to different epilepsies. Combining results from rare single-nucleotide/short insertion and deletion variants, copy number variants and common variants, we offer an expanded view of the genetic architecture of epilepsy, with growing evidence of convergence among different genetic risk loci on the same genes. Top candidate genes are enriched for roles in synaptic transmission and neuronal excitability, particularly postnatally and in the neocortex. We also identify shared rare variant risk between epilepsy and other neurodevelopmental disorders. Our data can be accessed via an interactive browser, hopefully facilitating diagnostic efforts and accelerating the development of follow-up studies