Screenings to Decrease Pediatric Suicide

This project aimed to examine the current practice related to mental health and depression screenings in pediatric patients. The benefits of implementing screening in schools in identifying depression and suicide risks sooner were also considered. This project focused on the correlation between earlier mental health screening and identification of these mental health disorders earlier in the life of pediatric patients and suicide rates. Current, published literature notes mental health screening in the pediatric population in schools is an effective method to facilitate monitoring and early intervention in detecting a mental illness. Schools implementing mental health screenings can result in increased outreach, help the youth in need, and mobilize school and community efforts to promote student mental health while reducing barriers to their learning. Lastly, it was identified schools represent a primary service delivery setting for children who do receive treatment, with estimates indicating up to 80% who receive mental health services do so at school. It is recommended for quarterly universal depression and suicide screening for all students in public schools should be implemented. It is also recommended for more research be done on the effects of the implementation of early pediatric depression screening on reducing suicide rates

Home Visitation to Prevent and Reduce Postpartum Depression

Postpartum depression (PPD) occurs in 13-19% of women worldwide, and is a stigmatized medical condition affecting maternal and infantile long term outcomes. The purpose of this evidence-based practice project was to determine if women at high risk for PPD are affected by home visitation programs from discharge up to three years postpartum. CINHAL Ultimate, Google Scholar, and Medline databases were used. Current evidence supports the use of home-visitation programs for postpartum women to decrease the prevalence and the symptoms of PPD by allowing nurses access into homes to provide early intervention for PPD. In addition to providing care for prevention and treatment of PPD, nurses are able to educate mothers on proper infant care and provide additional resources for potential needs (car seats, formula, food stamps, etc.). Screening for PPD at least four times from 28 weeks prenatal up to 12 weeks postpartum is optimal for identifying and treating high risk women. The benefits of home visitation programs should be discussed during prenatal and postnatal appointments. In conclusion, home-visitation programs and frequent screenings should become the standard of care for prevention and treatment of postpartum depression. Future research should include how to generate use of home based visitation programs and feasibility of developing these programs as the standard of care for PPD. Keywords: postpartum depression, infant outcomes, maternal outcomes, home healthcare, postpartum treatment, EDPS screening

Ovarian carcinoma CDK12 mutations misregulate expression of DNA repair genes via deficient formation and function of the Cdk12/CycK complex

The Cdk12/CycK complex promotes expression of a subset of RNA polymerase II genes, including those of the DNA damage response. CDK12 is among only nine genes with recurrent somatic mutations in high-grade serous ovarian carcinoma. However, the influence of thesemutations on the Cdk12/CycK complex and their link to cancerogenesis remain ill-defined. Here, we show that most mutations prevent formation of the Cdk12/CycK complex, rendering the kinase inactive. By examining the mutations within the Cdk12/CycK structure, we find that they likely provoke structural rearrangements detrimental to Cdk12 activation. Our mRNA expression analysis of the patient samples containing the CDK12 mutations reveals coordinated downregulation of genes critical to the homologous recombination DNA repair pathway. Moreover, we establish that the Cdk12/CycK complex occupies these genes and promotes phosphorylation of RNA polymerase II at Ser2. Accordingly, we demonstrate that the mutant Cdk12 proteins fail to stimulate the faithful DNA double strand break repair via homologous recombination. Together, we provide the molecular basis of how mutated CDK12 ceases to function in ovarian carcinoma. We propose that CDK12 is a tumor suppressor of which the loss-of-function mutations may elicit defects in multiple DNA repair pathways, leading to genomic instability underlying the genesis of the cancer.Peer reviewe