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PURPOSE OF REVIEW This review highlights recent progress in applying genome editing to the study and treatment of cardiovascular disease (CVD). RECENT FINDINGS Recent work has shown that genome editing can be used to determine the pathogenicity of variants of unknown significance in patient-derived induced pluripotent stem cells. These cells can also be used to test therapeutic genome editing approaches in a personalized manner. Somatic genome editing holds great promise for the treatment of CVD, and important proof of concept experiments have already been performed in animal models. Here we briefly review recent progress in patient-derived cells, as well as the development of somatic genome-editing therapies for CVD, with a particular focus on liver and heart. SUMMARY Translating this technology into the clinic will require precise editing enzymes, efficient delivery systems, and mitigation of off-target events and immune responses. Further development of these technologies will improve diagnostics and enable permanent correction of some of the most severe forms of CVD.PURPOSE OF REVIEW Neurocritical care has matured as a field and there is now a growing body of literature on the subject of quality improvement in neurocritically ill patients. This review will highlight major recent contributions in this field and discuss future directions. RECENT FINDINGS Articles published in the past 18 months have evaluated neurocritical care unit staffing, structure, and disease-specific protocols including subarachnoid hemorrhage and severe traumatic brain injury management. An assessment of current quality improvement practices in neurocritical care was also conducted. A neurocritical care-specific metric bundle is being proposed. SUMMARY The quality improvement movement is gaining momentum in neurocritical care with evaluation of general medical and surgical critical care quality improvement approaches in this specific patient population. Future work should focus on improving systems of neurocritical care delivery through iterative evaluation of structure, staffing, minimizing unnecessary variation, and evaluation of neurocritical care-specific metrics.Algae are photosynthetic organisms that drive aquatic ecosystems, e.g. fuelling food webs or forming harmful blooms. The discovery of viruses that infect eukaryotic algae has raised many questions about their influence on aquatic primary production and their role in algal ecology and evolution. Although the full extent of algal virus diversity is still being discovered, this review summarizes current knowledge of this topic. Where possible, formal taxonomic classifications are referenced from the International Committee on Taxonomy of Viruses (ICTV); since the pace of virus discovery has far surpassed the rate of formal classification, however, numerous unclassified viruses are discussed along with their classified relatives. In total, we recognized 61 distinct algal virus taxa with highly variable morphologies that include dsDNA, ssDNA, dsRNA, and ssRNA genomes ranging from approximately 4.4 to 560 kb, with virion sizes from approximately 20 to 210nm in diameter. These viruses infect a broad range of algae and, although there are a few exceptions, they are generally lytic and highly species or strain specific. Dedicated research efforts have led to the appreciation of algal viruses as diverse, dynamic, and ecologically important members of the biosphere, and future investigations will continue to reveal the full extent of their diversity and impact.Understanding the sequence of events leading to cancer relies in large part upon identifying the tumour cell of origin. Glioblastoma is the most malignant brain cancer but the early stages of disease progression remain elusive. Neural lineages have been implicated as cells of origin, as have glia. Interestingly, high levels of the neural stem cell regulator TLX correlate with poor patient prognosis. Here we show that high levels of the Drosophila TLX homologue, Tailless, initiate tumourigenesis by reverting intermediate neural progenitors to a stem cell state. Strikingly, we could block tumour formation completely by re-expressing Asense (homologue of human ASCL1), which we show is a direct target of Tailless. Our results predict that expression of TLX and ASCL1 should be mutually exclusive in glioblastoma, which was verified in single-cell RNA-seq of human glioblastoma samples. Counteracting high TLX is a potential therapeutic strategy for suppressing tumours originating from intermediate progenitor cells. SGLT inhibitor © 2020, Hakes and Brand.The rates of opioid overdose in the United States quadrupled between 1999 and 2017, reaching a staggering 130 deaths per day. This health epidemic demands innovative solutions that require uncovering the key brain areas and cell types mediating the cause of overdose- opioid-induced respiratory depression. Here, we identify two primary changes to murine breathing after administering opioids. These changes implicate the brainstem's breathing circuitry which we confirm by locally eliminating the µ-Opioid receptor. We find the critical brain site is the preBötzinger Complex, where the breathing rhythm originates, and use genetic tools to reveal that just 70-140 neurons in this region are responsible for its sensitivity to opioids. Future characterization of these neurons may lead to novel therapies that prevent respiratory depression while sparing analgesia. plain-language-summary Opioids such as morphine or fentanyl are powerful substances used to relieve pain in medical settings. However, taken in too high a dosponsible for breathing becoming depressed under the influence of opioids. The region with the most critical impact also happens to be where the breathing rhythms originate. There, a small group of 50 to 140 neurons were used by opioids to depress breathing. Crucially, these cells were not necessary for the drugs’ ability to relieve pain. Overall, the work by Bachmutsky et al. highlights a group of neurons whose role in creating breathing rhythms deserves further attention. It also opens the possibility that targeting these neurons would help to create safer painkillers. © 2020, Bachmutsky et al.
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