Sexual harassment in academia is endemic driven by gender-based inequalities and sustained through organizational tolerance, and its impact extends beyond the primary victim(s). Applying principles of emergency management provides a framework for institutions to balance their obligations to the primary victim(s) while also acknowledging the need to restore the well-being and culture of secondary victims.
Nausea and vomiting (NVP) affect most pregnant women. At the severe end of the clinical spectrum, hyperemesis gravidarum (HG) can be life-threatening. The condition is fraught with misconceptions that have slowed progress and left women undertreated. Herein, recent scientific advances are presented that dispel common myths associated with HG related to maternal/offspring outcomes, etiology, and evolution. There is now strong evidence that (i) HG is associated with poor outcomes, (ii) a common cause of NVP and HG has been identified, and (iii) NVP is likely a protective evolutionary mechanism that occurs throughout the animal kingdom but is no longer necessary for human survival. Therefore, it is encouraging that we are finally on the cusp of testing treatments that may put an end to unnecessary suffering.
The enzyme dimethylarginine dimethylaminohydrolase (DDAH) 1 metabolizes asymmetric dimethylarginine (ADMA), a critical endogenous cardiovascular risk factor. In the past two decades, there has been significant controversy about whether DDAH2, the other DDAH isoform, is also able to directly metabolize ADMA. There has been evidence that DDAH2 regulates several critical processes involved in cardiovascular and immune homeostasis. However, the molecular mechanisms underpinning these effects are unclear. In this opinion, we discuss the previous and current knowledge of ADMA metabolism by DDAH in light of a recent consortium study, which convincingly demonstrated that DDAH2 is not capable of metabolizing ADMA, unlike DDAH1. Thus, further research in this field is needed to uncover the molecular mechanisms of DDAH2 and its role in various disorders.
The zebrafish has become an outstanding model for studying organ development and tissue regeneration, which is prominently leveraged for studies of pancreatic development, insulin-producing β-cells, and diabetes. Although studied for more than two decades, many aspects remain elusive and it has only recently been possible to investigate these due to technical advances in transcriptomics, chemical-genetics, genome editing, drug screening, and in vivo imaging. Here, we review recent findings on zebrafish pancreas development, β-cell regeneration, and how zebrafish can be used to provide novel insights into gene functions, disease mechanisms, and therapeutic targets in diabetes, inspiring further use of zebrafish for the development of novel therapies for diabetes.
Amphiphysin-2 is a ubiquitously expressed protein also known as bridging integrator 1 (BIN1), playing a critical role in membrane remodeling, trafficking, and cytoskeleton dynamics in a wide range of tissues. Mutations in the gene encoding BIN1 cause centronuclear myopathies (CNM), and recent evidence has implicated BIN1 in heart failure, underlining its crucial role in both skeletal and cardiac muscle. Furthermore, altered expression of BIN1 is linked to an increased risk of late-onset Alzheimer's disease and several types of cancer, including breast, colon, prostate, and lung cancers. Recently, the first proof-of-concept for potential therapeutic strategies modulating BIN1 were obtained for muscle diseases. In this review article, we discuss the similarities and differences in BIN1's functions in cardiac and skeletal muscle, along with its associated diseases and potential therapies.
MORF4 (mortality factor on chromosome 4)-related gene 15 (MRG15) is a chromodomain protein that exists in various multiprotein complexes involved in transcription, DNA repair, and development. Here we summarize the recent advances involving MRG15 in modulating liver metabolism, both through its chromatin-binding capability and independently of it, highlighting MRG15 as a potential therapeutic target for liver metabolic diseases.