Dissociative Identity Disorder: Etiology, Media, and Stigma

Dissociative Identity Disorder (DID) is often portrayed incorrectly in the media, causing the public to know little about the disorder other than the stigmatizing information from the media. Because of this, individuals with the disorder often face more stigmatizing behaviors than the normal amount of stigma those with mental disorders often face. The newest revision of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) contributes the etiology of the disorder to underlying trauma, however many psychologists consider a sociocognitive or fantasy model. Current research provides more support for the trauma/posttraumatic model of the disorder and further supports the harm the media is causing

Genomic, transcriptomic, and protein landscape profile of CFTR and cystic fibrosis

Cystic Fibrosis (CF) is caused most often by removal of amino acid 508 (Phe508del, deltaF508) within CFTR, yet dozens of additional CFTR variants are known to give rise to CF and many variants in the genome are known to contribute to CF pathology. To address CFTR coding variants, we developed a sequence-to-structure-to-dynamic matrix for all amino acids of CFTR using 233 vertebrate species, CFTR structure within a lipid membrane, and 20 ns of molecular dynamic simulation to assess known variants from the CFTR1, CFTR2, ClinVar, TOPmed, gnomAD, and COSMIC databases. Surprisingly, we identify 18 variants of uncertain significance within CFTR from diverse populations that are heritable and a likely cause of CF that have been understudied due to nonexistence in Caucasian populations. In addition, 15 sites within the genome are known to modulate CF pathology, where we have identified one genome region (chr11:34754985-34836401) that contributes to CF through modulation of expression of a noncoding RNA in epithelial cells. These 15 sites are just the beginning of understanding comodifiers of CF, where utilization of eQTLs suggests many additional genomics of CFTR expressing cells that can be influenced by genomic background of CFTR variants. This work highlights that many additional insights of CF genetics are needed, particularly as pharmaceutical interventions increase in the coming years