Research Roundup: Global methane emissions at all-time high, neuronal pathway prevents relapse, possible drug target to help fight infectious diseases

Research Roundup: Global methane emissions at all-time high, neuronal pathway prevents relapse, possible drug target to help fight infectious diseases

Our roundup this week highlights research that found global methane emissions have reached an all-time high, with the planet absorbing nearly 600 million tons of methane emissions in 2017. (Photo: Unsplash) Each week, The Daily’s Science & Tech section produces a roundup of the most exciting and influential research happening on campus or otherwise related to Stanford. Here’s our digest for the week of July 12 – July 18.

Global methane emissions reach an all-time high

The global methane emissions have reached an all-time high, despite carbon dioxide emissions temporarily dropping due to the coronavirus pandemic, a study published on July 14 in “Earth System Science Data” and “Environmental Research Letters” found.

“We still haven’t turned the corner on methane,” earth system science professor Rob Jackson told Stanford News. “Emissions from cattle and other ruminants are almost as large as those from the fossil fuel industry for methane. People joke about burping cows without realizing how big the source really is.”

The team analyzed emissions from 2017, the most recent year from which complete global methane data is available, and found that the atmosphere absorbed almost 600 million tons of methane. Methane traps heat more powerfully than carbon dioxide.

The findings suggest agriculture made up two-thirds of methane emissions between 2000 to 2017, with fossil fuel making up the final third.

“We’ll need to eat less meat and reduce emissions associated with cattle and rice farming and replace oil and natural gas in our cars and homes,” Jackson told Stanford News. “I’m optimistic that, in the next five years, we’ll make real progress in that area.”

Neuronal pathway prevents drug relapse in mice

Disrupting a neuronal pathway that causes opiate-associated memories in mice prevents drug relapse and has the potential to treat opioid addiction in patients, a study published on July 16 in “Neuron” found.

“The most difficult part of treating addiction is to prevent relapse, especially for opioids,” biology associate professor Xiaoke Chen told Stanford News. “To prevent relapse, we really need to deal with the withdrawal.”

The findings suggest when the researchers silenced the paraventricular thalamus in morphine-dependent mice, the mice no longer preferentially chose morphine over the drug-free saline solution. Through disrupting this neural pathway, researchers found that the animals had no memory of the effects of the drug. Paraventricular thalamus is a brain region that connects many different brain areas associated with drug addiction.

“Drugs as a stimulus can drive a very robust behavior,” Chen told Stanford News. “I want to understand the mechanism underlying that behavior and hope that this knowledge can help address the devastating opioid epidemic in the U.S.”

Molecular signal, a possible drug target, allows virus-infected cells to evade immune system

Blocking CD47, a molecular signal, in virus-infected cells allows the immune system to target infected cells, a study published on June 23 in “mBio” found. Decreasing CD47 may help the body fight infectious disease, serving as a potential drug target.

Cancer cells also increase their CD47 signaling to evade immune system attack.

“We wondered whether the mechanism activated by all cancer cells to avoid being destroyed could also be used by persistent infections, so that the microbes can hide inside cells to evade immune cells,” pathology stem cell and developmental biology professor Irving Weissman M.D. ’65 told Stanford Medicine News. “Amazingly, we found that to be true, and blocking the CD47 signal helped the body get rid of more infected cells.”

The findings suggest mice and humans cells infected by pathogens show increased expression of the CD47 molecular signal. Additionally, the team found that mice without the gene for CD47 were more resistant to tuberculosis-causing bacteria than control mice.

Infected cells with SARS-CoV-2 — the virus that causes COVID-19 — also produce increased CD47 signaling, so treatments that block CD47 production could potentially be used in coronavirus patients.

“It’s probably important for the innate immune system to have a balance of activating and suppressing forces, but we showed that if we play with that balance a little bit, we can clear some pathogens faster,” Michal Tal, an instructor at the Institute for Stem Cell Biology and Regenerative Medicine, told Stanford Medicine News. “In some cases, it might be better to ease up on this particular immunological brake by blocking CD47.”

Contact Derek Chen at derekc8 ‘at’ stanford.edu.

Read more at www.stanforddaily.com

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