Getting that Sinking Feeling: Analysis and Impacts of Sea Level Rise on Three National Parks along the East Coast, USA

Due to global climate change, sea level rise (SLR) has become a threat for future generations, but the extent of this danger is unknown. To help understand the possible effects of SLR on the east coast of the United States, we studied three national parks: Acadia National Park (ACAD), Assateague Island National Seashore (ASIS) and Everglades National Park (EVER). We predicted that ACAD would be less affected by SLR than ASIS and EVER due to the construction of its beach profile. By measuring the beach profile, we found that Sand Beach in ACAD was reflective with an average slope of 3.2 cm/m while South Ocean Beach in ASIS had an intermediate morphology with an average slope of 1.57 cm/m. The Snake Bight Channel beach in EVER was dissipative and had no slope. Using historical Landsat imagery from 1984 to 2016, we estimated that ACAD’s water area increased by 1.61%, that ASIS’s water area increased by 2.47%, and that the EVER’s water area decreased by 0.22% between 1992 and 2011. Using RCP scenarios from the latest IPCC report, we estimated future inundation levels in each park along with the percent change between the best and worst-case scenarios. Under the RCP8.5 scenario, ACAD had 1.36 km2 of inundation, ASIS had 37.11 km2, and EVER had 366.47 km2. ACAD had the highest percent change between the worst and best RCP scenario at 15.70%. ASIS had a slightly smaller percent change at 14.25% and EVER had even less at 10.42%. This study suggests that continued SLR will cause national parks billions of dollars in property damage and the loss of their inherent ecological value

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Break the News to Mother / words by Chas K. Harris

Cover: photo of a mortally wounded soldier with three of his comrades; Publisher: Chas K. Harris (New York)https://egrove.olemiss.edu/sharris_a/1035/thumbnail.jp

Disruption of the nascent polypeptide-associated complex leads to reduced polyglutamine aggregation and toxicity

The nascent polypeptide-associate complex (NAC) is a heterodimeric chaperone complex that binds near the ribosome exit tunnel and is the first point of chaperone contact for newly synthesized proteins. Deletion of the NAC induces embryonic lethality in many multi-cellular organisms. Previous work has shown that the deletion of the NAC rescues cells from prion-induced cytotoxicity. This counterintuitive result led us to hypothesize that NAC disruption would improve viability in cells expressing human misfolding proteins. Here, we show that NAC disruption improves viability in cells expressing expanded polyglutamine and also leads to delayed and reduced aggregation of expanded polyglutamine and changes in polyglutamine aggregate morphology. Moreover, we show that NAC disruption leads to changes in de novo yeast prion induction. These results indicate that the NAC plays a critical role in aggregate organization as a potential therapeutic target in neurodegenerative disorders

“I Wouldn’t Want to Be a Gender Expert:” Gender Experts in Peace Mediation

Peace mediation is a professional practice that is increasingly reliant on thematic technical experts, including gender experts. The strategy of including gender expertise in peace mediation reflects the Women, Peace and Security agenda and the call to include dedicated gender expertise in all peacemaking efforts. Based on interviews with peace mediation practitioners, the article analyzes the role of gender experts in peace mediation. We argue that there is a tension between the art of mediation and the art of gender expertise that reflects the gendered power dynamics of peace mediation. We conclude that the strategy of appointing gender experts to peace mediation teams will not “dismantle the master’s house.” However, we acknowledge that without a gender expert very little will be accomplished on this issue. For peace mediation to address the gendered foundations of conflict we argue for the development of an alternate feminist peace mediation practice

Boolean analysis identifies CD38 as a biomarker of aggressive localized prostate cancer.

The introduction of serum Prostate Specific Antigen (PSA) testing nearly 30 years ago has been associated with a significant shift towards localized disease and decreased deaths due to prostate cancer. Recognition that PSA testing has caused over diagnosis and over treatment of prostate cancer has generated considerable controversy over its value, and has spurred efforts to identify prognostic biomarkers to distinguish patients who need treatment from those that can be observed. Recent studies show that cancer is heterogeneous and forms a hierarchy of tumor cell populations. We developed a method of identifying prostate cancer differentiation states related to androgen signaling using Boolean logic. Using gene expression data, we identified two markers, CD38 and ARG2, that group prostate cancer into three differentiation states. Cancers with CD38-, ARG2- expression patterns, corresponding to an undifferentiated state, had significantly lower 10-year recurrence-free survival compared to the most differentiated group (CD38+ARG2+). We carried out immunohistochemical (IHC) staining for these two markers in a single institution (Stanford; n = 234) and multi-institution (Canary; n = 1326) cohorts. IHC staining for CD38 and ARG2 in the Stanford cohort demonstrated that combined expression of CD38 and ARG2 was prognostic. In the Canary cohort, low CD38 protein expression by IHC was significantly associated with recurrence-free survival (RFS), seminal vesicle invasion (SVI), extra-capsular extension (ECE) in univariable analysis. In multivariable analysis, ARG2 and CD38 IHC staining results were not independently associated with RFS, overall survival, or disease-specific survival after adjusting for other factors including SVI, ECE, Gleason score, pre-operative PSA, and surgical margins

Disease-associated mutations within the yeast DNAJB6 homolog Sis1 slow conformer-specific substrate processing and can be corrected by the modulation of nucleotide exchange factors

Molecular chaperones, or heat shock proteins (HSPs), protect against the toxic misfolding and aggregation of proteins. As such, mutations or deficiencies within the chaperone network can lead to disease. Dominant mutations within DNAJB6 (Hsp40)-an Hsp70 co-chaperone-lead to a protein aggregation-linked myopathy termed Limb-Girdle Muscular Dystrophy Type D1 (LGMDD1). Here, we used the yeast prion model client in conjunction with in vitro chaperone activity assays to gain mechanistic insights into the molecular basis of LGMDD1. Here, we show how mutations analogous to those found in LGMDD1 affect Sis1 (a functional homolog of human DNAJB6) function by altering the structure of client protein aggregates, interfering with the Hsp70 ATPase cycle, dimerization and substrate processing; poisoning the function of wild-type protein. These results uncover the mechanisms through which LGMDD1-associated mutations alter chaperone activity, and provide insights relevant to potential therapeutic interventions

Common genetic risk of major depression and nicotine dependence: The contribution of antisocial traits in a United States veteran male twin cohort

Many studies that found associations between depression and nicotine dependence have ignored possible shared genetic influences associated with antisocial traits. The present study examined the contribution of genetic and environmental effects associated with conduct disorder (CD) and antisocial personality disorder (ASPD) to the comorbidity of major depression (MD) and nicotine dependence (ND). A telephone diagnostic interview, the Diagnostic Interview Schedule-III-R, was administered to eligible twins from the Vietnam Era Twin (VET) Registry in 1992. Multivariate genetic models were fitted to 3360 middle-aged and predominantly white twin pairs (1868 monozygotic, 1492 dizygotic pairs) of which both members completed the pertinent diagnostic interview sections. Genetic influences on CD accounted for 100%, 68%, and 50% of the total genetic variance in risk for ASPD, MD and ND, respectively. After controlling for genetic influences on CD, the partial genetic correlation between MD and ND was no longer statistically significant. Nonshared environmental contributions to the comorbidity among these disorders were not significant. This study not only demonstrates that the comorbidity between ND and MD is influenced by common genetic risk factors, but also further suggests that the common genetic risk factors overlapped with those for antisocial traits such as CD and ASPD in men