Architectures could support quantum-chemistry simulations
NVIDIA CEO Jensen Huang says his daily success comes from a simple habit, starting each morning by completing his highest priority task first. Speaking at the California Institute of Technology graduation ceremony, he explained that this approach gives him a sense of achievement early in the day and frees up time to focus on others.
What if we stopped managing disease…and started eliminating it entirely?
Horner’s syndrome (HS) occurs when there is interruption of the oculosympathetic pathway (OSP). This article reviews the anatomy of the OSP and clinical findings associated with lesions located at various positions along this pathway. The imaging findings of lesions associated with HS at various levels of the OSP, classified as preganglionic HS (first-and second-order neuron HS) or postganglionic HS (third-order neuron HS), are demonstrated.
‘Practices that reduce perceived threat – mindfulness, social support, time in nature, deliberate recovery periods – are not indulgences. They are forms of energetic repair.’
The energy systems in our brains are implicated in how clearly we think, how resilient we feel, and how well we adapt to uncertainty. Understanding them can help us better care for our bodies as we age.
In this sharp and insightful essay, Hannah Critchlow takes you through the many ways in which our brains generate and use energy, and offers some helpful recommendations for looking after your brain health. Read or listen now.
In an era preoccupied with cognitive enhancement and artificial minds, it is worth remembering that intelligence depends on sustaining delicate energetic equilibria. To care for our bodies, our relationships and our environment is, in a literal sense, to care for the energy that makes thought possible.
The evolutionary merger that gave rise to mitochondria offers a final lesson. Complexity and intelligence did not emerge from domination but from partnership. Within us, ancient bacteria still labour – not as servants but as collaborators. Every thought we have, every spark of imagination, is powered by this quiet cooperation at the cellular level. Intelligence, in any form, is a partnership with energy itself.
One takeaway is that a brain fit for the 21st century may be one that understands – and respects – its bioenergetic foundations.
Online now:(Cell Metabolism 36, 2402–2418.e1–e10; November 5, 2024)
Online now: (Cell Metabolism 36, 2402–2418.e1–e10; November 5, 2024)
In the originally published article, due to figure preparation mistakes, there were errors in Figures 2, 3, and S9. Specifically, the line legends in Figure 2J were accidentally lost during the creation of the figure using AI software, the marker positions for the β-actin bands in Figure 3J were incorrectly labeled, the H&E staining image of the wild-type mouse DOX+17-OH PREG treatment group in Figure S9A was erroneously pasted during figure compilation, and the IHC staining image of the liver ischemia-reperfusion treatment group in Figure S9I was flipped during copying. We apologize for these oversights that occurred during the many revisions.
Because certain western bands were not clear, we corrected Figures 2C and 3G with full-membrane original data. In addition, CD36 appears to be over 100 kDa in Figure S10S, whereas it is consistently between 70 and 100 kDa in all other figures. We have previously encountered similar problems with certain proteins with a little difference in molecular weight, and we have solved this issue by using other lysis buffers. Therefore, we used another lysis buffer (epizyme CAT: PC201) to examine whether there is a consistent phenotype of CD36 between 70 and 100 kDa. As expected, we detected a significant decrease of CD36 located within 70–100 kDa upon IR, Dox, and MCDD treatment, which was consistent with our published data of CD36 above 100 kDa. Because the major CD36 band should appear at approximately 88 kDa based on numerous studies, we have removed the original data from Figure S10S and presented the corrected bands in Figure S10U to avoid confusion.
The authors discovered that training mice to exhibit a placebo effect with one type of pain produces marked relief of several different types of pain, including pain caused by injury.
To establish that the native opioid peptides actually drive pain relief, similar to opioid painkillers such as morphine, the researchers employed a light-activated drug developed in Banghart’s lab called PhNX, for photoactivatable naloxone. Naloxone, also known as Narcan, is the medicine used to reverse opioid overdoses by blocking opioid receptors. Using light, they were able to precisely control the site and timing of opioid signaling interference. Using PhNX, the scienists found that both morphine-induced pain relief and placebo pain relief rely on opioid signaling in the vlPAG brain region.
Co-first author: “We essentially trained a mouse brain to create its own broad-spectrum painkillers on demand, precisely where they are needed to treat pain, without the off-target effects of opioid-based painkillers.”
“These results increase the translational relevance of rodent placebo models to clinical contexts, in which patients’ prior experiences with drugs and treatment settings can generalize to broader expectations of improvement,” the researchers conclude in their paper. ScienceMission sciencenewshighlights.
Placebo effects, in which patients experience relief without therapeutic treatment, increasingly have been considered as potentially powerful clinical treatments for ailments such as depression and pain. Yet the neurological mechanisms underlying such processes are not fully understood.
Now, a multi-institutional team has pinpointed the brain circuitry responsible for placebo pain relief. Their findings, reported in the journal Neuron, describe brain regions that support placebo effects and identify sites where endogenous opioid neuropeptides (commonly referred to as endorphins) provide signals that are critical for placebo pain relief.