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Vitamin D supplements may reduce the risk of major cardiovascular events such as heart attacks among people aged over 60, finds a clinical trial published by The BMJ.

The researchers stress that the absolute risk difference was small, but say this is the largest trial of its kind to date, and further evaluation is warranted, particularly in people taking statins or other cardiovascular disease drugs.

Cardiovascular disease (CVD) is a general term for conditions affecting the heart or blood vessels and is one of the main causes of death globally. CVD events such as heart attacks and strokes are set to increase as populations continue to age and chronic diseases become more common.

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A breathtaking scientific revolution is taking place – biotechnology has been progressing at stunning speed, giving us the tools to eventually gain control over biology. On the one hand solving the deadliest diseases while also creating viruses more dangerous than nuclear bombs, able to devastate humanity.

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Computers are built around logic: performing mathematical operations using circuits. Logic is built around things such as Adders—not the snake; the basic circuit that adds together two numbers. This is as true of today’s microprocessors as all those going back to the very beginning of computing history. You could go back to an abacus and find that, at some fundamental level, it does the same thing as your shiny gaming PC. It’s just much, much less capable.

Nowadays, processors can do a lot of mathematical calculations using any number of complex circuits in a single clock. And a lot more than just add two numbers together, too. But to get to your shiny new gaming CPU, there has been a process of iterating on the classical computers that came before, going back centuries.

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AG mednet’s abraham gutman on harnessing AI in medical imaging.

Abraham gutman speaks at national cancer institute medical imaging workshop.

Scientists discovered Fanzor proteins, which work like CRISPR but are smaller and more easily delivered into cells, and used them to edit human DNA.

Human natural killer (NK) cells are cytotoxic effector cells that are increasingly harnessed in cancer immunotherapy. NKG2A/CD94 is an inhibitory receptor on NK cells that has established regulatory functions in the direct interaction with target cells when engaged with its ligand, the non-classical HLA class I molecule HLA-E. Here, we confirmed NKG2A as a checkpoint molecule in primary human NK cells and identified a novel role for NKG2A in maintaining NK cell expansion capacity by dampening both proliferative activity and excessive activation-induced cell death. Maintenance of NK cell expansion capacity might contribute to the preferential accumulation of human NKG2A+ NK cells after hematopoietic cell transplantation and enrichment of functionally impaired NK cells in human cancers. Functional silencing of NKG2A for cancer immunotherapy is highly attractive but will need to consider that this might also lead to a reduced survival by driving activation-induced cell death in targeted NK cells.

Reversal of fetal hemoglobin (HbF) silencing can ameliorate the effects of sickle cell anemia. Despite available gene therapy and stem cell transplantation modalities, the majority of affected patients worldwide will not have access to these in the near future. Thus, there is a need for safe and effective small-molecule therapeutics. We report here that stable occupancy of a major HbF silencing complex containing BCL11A, MBD2a–NURD, and PRMT5 and exclusion of the transcriptional activator NF-Y at the γ-globin gene promoter require specific features of MBD2a. These results provide a unified model for the relationships between the previously reported HbF silencers MBD2–NuRD, BCL11A, DNA methylation, and PRMT5 that may facilitate development of therapeutic agents to reverse HbF silencing.

During human development, there is a switch in the erythroid compartment at birth that results in silencing of expression of fetal hemoglobin (HbF). Reversal of this silencing has been shown to be effective in overcoming the pathophysiologic defect in sickle cell anemia. Among the many transcription factors and epigenetic effectors that are known to mediate HbF silencing, two of the most potent are BCL11A and MBD2–NuRD. In this report, we present direct evidence that MBD2–NuRD occupies the γ-globin gene promoter in adult erythroid cells and positions a nucleosome there that results in a closed chromatin conformation that prevents binding of the transcriptional activator, NF-Y. We show that the specific isoform, MBD2a, is required for the formation and stable occupancy of this repressor complex that includes BCL11A, MBD2a–NuRD, and the arginine methyltransferase, PRMT5. The methyl cytosine binding preference and the arginine-rich (GR) domain of MBD2a are required for high affinity binding to methylated γ-globin gene proximal promoter DNA sequences. Mutation of the methyl cytosine–binding domain (MBD) of MBD2 results in a variable but consistent loss of γ-globin gene silencing, in support of the importance of promoter methylation. The GR domain of MBD2a is also required for recruitment of PRMT5, which in turn results in placement of the repressive chromatin mark H3K8me2s at the promoter. These findings support a unified model that integrates the respective roles of BCL11A, MBD2a–NuRD, PRMT5, and DNA methylation in HbF silencing.

Better communication between surgeons and engineers, better fit, and faster design iteration are among the benefits of using virtual patients for implant R&D.