Catálogo de publicaciones - revistas

<jats:p>Vaccines, AI, and sexually transmitted infections among first topics</jats:p>

<jats:p>Poor sleep disproportionately undermines the health of communities of color. Researchers want to figure out why—and find solutions</jats:p>

<jats:p>Common human experience is that a long period without sleep is unsustainable, and it is also detrimental to health and behavior. The powerful and primal urge to sleep after sleep deprivation is intense and seems inescapable. The longer we stay awake, the more we feel the need to sleep, and however much we resist, we will inevitably succumb. Although it is obvious what benefits derive from other common and strong physiological drives, such as hunger, sex, and thirst, it is less obvious what drives us to sleep and what benefits accrue. Understanding the biochemical or circuit basis for the sleep drive could enable the benefits of sleep to be artificially stimulated with a new generation of sedative drugs.</jats:p>

<jats:p>Sleep is crucial for healthy cognition, including memory. The two main phases of sleep, REM (rapid eye movement) and non-REM sleep, are associated with characteristic electrophysiological patterns that are recorded using surface and intracranial electrodes. These patterns include sharp-wave ripples, cortical slow oscillations, delta waves, and spindles during non-REM sleep and theta oscillations during REM sleep. They reflect the precisely timed activity of underlying neural circuits. Here, we review how these electrical signatures have been guiding our understanding of the circuits and processes sustaining memory consolidation during sleep, focusing on hippocampal theta oscillations and sharp-wave ripples and how they coordinate with cortical patterns. Finally, we highlight how these brain patterns could also sustain sleep-dependent homeostatic processes and evoke several potential future directions for research on the memory function of sleep.</jats:p>

<jats:p>Sleep is essential for brain function in a surprisingly diverse set of ways. In the short term, lack of sleep leads to impaired memory and attention; in the longer term, it produces neurological dysfunction or even death. I discuss recent advances in understanding how sleep maintains the physiological health of the brain through interconnected systems of neuronal activity and fluid flow. The neural dynamics that appear during sleep are intrinsically coupled to its consequences for blood flow, cerebrospinal fluid dynamics, and waste clearance. Recognizing these linked causes and consequences of sleep has shed new light on why sleep is important for such disparate aspects of brain function.</jats:p>

<jats:p>Sleep is entwined across many physiologic processes in the brain and periphery, thereby exerting tremendous influence on our well-being. Yet sleep exists in a social-environmental context. Contextualizing sleep health with respect to its determinants—from individual- to societal-level factors—would enable neuroscientists to more effectively translate sleep health into clinical practice. Key challenges and opportunities pertain to (i) recognizing and exploring sleep’s functional roles, (ii) clarifying causal mechanisms in relation to key outcomes, (iii) developing richer model systems, (iv) linking models to known contextual factors, and (v) leveraging advances in multisensory technology. Meeting these challenges and opportunities would help transcend disciplinary boundaries such that social-environmental considerations related to sleep would become an ever-greater presence in the clinic.</jats:p>

<jats:p> Highlights from the <jats:italic>Science</jats:italic> family of journals </jats:p>

<jats:p>Editors’ selections from the current scientific literature</jats:p>

<jats:title>Distinct mechanisms to block transporters</jats:title> <jats:p> Transmembrane ATP-binding cassette (ABC) transporters are crucial cellular machines that move molecules small and large across membranes. In Gram-negative bacteria, outer membrane biogenesis is aided by an ABC transporter called MsbA, which flips lipopolysaccharide from the inner face of the cell membrane to the periplasmic face. Thélot <jats:italic>et al</jats:italic> . determined structures of two first-generation inhibitors bound to MsbA, TBT1 and G247, and found that they have distinct binding modes. Unlike most inhibitors, TBT1 triggers unproductive ATPase activity and induces a conformation similar to substrate bound. These structures will provide valuable information for the design of potential antimicrobial drugs. The authors have already identified a new lead compound from virtual screening based on the TBT1-induced conformation. —MAF </jats:p>