Neutrophil Extracellular Traps (NETs) and Hypercoagulability in Plasma Cell Dyscrasias—Is This Phenomenon Worthy of Exploration?

Plasma cell dyscrasias (PCDs) are neoplastic diseases derived from plasma cells. Patients suffering from PCDs are at high risk of hypercoagulability and thrombosis. These conditions are associated with disease-related factors, patient-related factors, or the use of immunomodulatory drugs. As PCDs belong to neoplastic diseases, some other factors related to the cancer-associated hypercoagulability state in the course of PCDs are also considered. One of the weakest issues studied in PCDs is the procoagulant activity of neutrophil extracellular traps (NETs). NETs are web-like structures released from neutrophils in response to different stimuli. These structures are made of deoxyribonucleic acid (DNA) and bactericidal proteins, such as histones, myeloperoxidase, neutrophil elastase, and over 300 other proteins, which are primarily stored in neutrophil granules. NETs immobilize, inactivate the pathogens, and expose them to specialized cells of immune response. Despite their pivotal role in innate immunity, they contribute to the development and exacerbation of autoimmune diseases, trigger inflammatory response, or even facilitate the formation of cancer metastases. NETs were also found to induce activity of coagulation and are considered one of the most important factors inducing thrombosis. Here, we summarize how PCDs influence the release of NETs, and hypothesize whether NETs contribute to hypercoagulability in PCDs patients.

Neuronal Activity-Induced BRG1 Phosphorylation Regulates Enhancer Activation

SUMMARYNeuronal activity-induced enhancers drive the gene induction in response to stimulation. Here, we demonstrate that BRG1, the core subunit of SWI/SNF-like BAF ATP-dependent chromatin remodeling complexes, regulates neuronal activity-induced enhancers. Upon stimulation, BRG1 is recruited to enhancers in an H3K27Ac-dependent manner. BRG1 regulates enhancer basal activities and inducibility by affecting cohesin binding, enhancer-promoter looping, RNA polymerase II recruitment, and enhancer RNA expression. Furthermore, we identified a serine phosphorylation site in BRG1 that is induced by neuronal activities and is sensitive to CaMKII inhibition. BRG1 phosphorylation affects its interaction with several transcription co-factors, possibly modulating BRG1 mediated transcription outcomes. Using mice with knock-in mutations, we showed that non-phosphorylatable BRG1 fails to efficiently induce activity-dependent genes, whereas phosphomimic BRG1 increases the enhancer activities and inducibility. These mutant mice displayed anxiety-like phenotypes and altered responses to stress. Therefore, our data reveal a mechanism connecting neuronal signaling to enhancer activities through BRG1 phosphorylation.

Where Does Time Go When You Blink?

Retinal input is frequently lost because of eye blinks, yet humans rarely notice these gaps in visual input. Although previous studies focused on the perceptual and neural correlates of diminished awareness to blinks, the impact of these correlates on the perceived time of concurrent events is unknown. Here, we investigated whether the subjective sense of time is altered by spontaneous blinks. We found that participants ( N = 22) significantly underestimated the duration of a visual stimulus when a spontaneous blink occurred during stimulus presentation and that this underestimation was correlated with the blink duration of individual participants. Importantly, the effect was not present when durations of an auditory stimulus were judged ( N = 23). The results point to a link between spontaneous blinks, previously demonstrated to induce activity suppression in the visual cortex, and a compression of subjective time. They suggest that ongoing encoding within modality-specific sensory cortices, independent of conscious awareness, informs the subjective sense of time.

Magnetism and activity of planet hosting stars

The magnetic activity levels of planet host stars may differ from that of stars not known to host planets in several ways. Hot Jupiters may induce activity in their hosts through magnetic interactions, or through tidal interactions by affecting their host's rotation or convection. Measurements of photospheric, chromospheric, or coronal activity might then be abnormally high or low compared to control stars that do not host hot Jupiters, or might be modulated at the planet's orbital period. Such detections are complicated by the small amplitude of the expected signal, by the fact that the signals may be transient, and by the difficulty of constructing control samples due to exoplanet detection biases and the uncertainty of field star ages. We review these issues, and discuss avenues for future progress in the field.