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Monday, September 11, 2023

Half in new poll expect AI-related misinformation to affect 2024 election outcome

A little more than half of Americans believe that misinformation spread by artificial intelligence (AI) will impact the outcome of the 2024 presidential election.

A new Axios-Morning Consult AI poll found that 53 percent of respondents said misinformation spread by AI would impact who wins the upcoming presidential election, with frequent watchers of Fox, CNN and MSNBC sharing that view.

Those who voted for former President Trump in 2020 were twice as likely to say AI will decrease their trust in the election results than those who voted for President Biden. Of those who say AI misinformation will impact the election, 47 percent voted for Trump in 2020 and 27 percent voted for Biden.

Regarding election advertising that utilizes AI, which is already changing the 2024 election, 35 percent of respondents said AI will decrease their trust in election advertising. Of that group, 42 percent were Trump voters and 33 percent were Biden voters.

The latest results highlight the doubt about election integrity in the first presidential election following the Jan. 6, 2021, attack on the Capitol. However, the distrust in AI crosses party lines, with no presidential candidate having “a lot” of trust from their own party to oversee AI.

The poll found that 35 percent of Democrats had “a lot” of trust in Biden to oversee AI regulation. For Republicans, 40 percent of those who voted for Trump had “a lot” of trust in his handling of AI.

Overall, 1 in 3 adults said they are “very concerned” about AI development. The poll also found that 34 percent of respondents said humans are smarter than AI, compared to 22 percent who said AI is smarter.

However, nearly two-thirds said humans will definitely or probably reach a point where we will lose control of AI. Of that group, 54 percent said we will reach that point within five years, while 90 percent said it will be reached within the next 25 years.

The poll was conducted Aug. 10-13 among a sample of 2,203 U.S. adults and has a margin of error of plus or minus 2 percentage points.

https://thehill.com/policy/technology/4197625-half-in-new-poll-expect-ai-related-misinformation-to-affect-2024-election-outcome/

Threads blocks COVID-related searches amid spiking cases

 Threads, a new text-based social media platform created by industry giant Meta, is now blocking terms related to COVID-19 and vaccines on its search engines. 

The Washington Post reported Monday that the social media platform rolled out its revamped search engine last week, only for users to be met with a blank screen and a pop-up linking to the Centers for Disease Control and Prevention’s (CDC) website when they type terms related to “covid” or “long covid”. 

Words such as “sex,” “nude,” “gore,” “porn,” “coronavirus,” “vaccines” and “vaccination” are also blocked on the social media platform’s search engine, according to the Post. 

In a statement, Meta told The Hill that Threads’s new search engine “temporarily doesn’t provide results” for words that may include “sensitive content.” 

“We just began rolling out keyword search for Threads to additional countries last week. The search functionality temporarily doesn’t provide results for keywords that may show potentially sensitive content,” a Meta spokesperson said in its statement. 

“People will be able to search for keywords such as ‘COVID’ in future updates once we are confident in the quality of the results.”

Meta’s decision comes as COVID-19 has been rising in the United States; hospitalizations from the virus increased to 16 percent last week and has been steadily rising since July, according to data from the CDC.

Public health care workers have criticized Meta’s decision to block COVID-related searches, including World Health Network Outreach Director Julia Doubleday, who said that social media is vital to patients who are searching for more information about their recent illness diagnosis. 

“Long COVID patients have died of organ failure, infections, cardiac events and more, and social media is one place they can share information. Cutting off communication between suffering and disabled patients is cruel in the extreme,” Doubleday said. “It’s indefensible.”

https://thehill.com/policy/technology/4198601-threads-blocks-covid-related-searches-amid-spiking-cases/

'White House prepares for sharp rise in poverty rate'

 The White House is preparing for a sharp rise in the U.S. poverty rate following the end of pandemic-era child tax credit (CTC) expansion.

President Biden and Democrats fought unsuccessfully last year to extend an expanded version of the CTC that started during the depths of the pandemic and temporarily lifted millions of children out of poverty.

The Census Bureau is set to release Tuesday its annual report on poverty, income, and health insurance. The new poverty data will be a hit for Biden, whose reelection campaign could hinge on how Americans feel about the economy.

The Council of Economic Advisers (CEA) said in a blog post Friday that it expects a “sharp rise” in the Supplemental Poverty Measure, which measures income and benefits plus government programs such as tax refunds and food stamps.

To “understand why this is likely to happen in 2022, it is crucial to remember what happened in 2021,” the CEA argued.

A Democratic-controlled Congress passed the beefed-up CTC in 2021, boosting the credit eligible parents could receive to $3,000 per child over the age of 6 and $3,600 per child under the age of 6. 

The enhanced CTC alone lifted almost 3 million children out of poverty in 2021 and cut the child poverty rate by more than 40 percent in 2021, the CEA wrote.

The expansion expired in December 2021, and Democrats have not been able to strike a deal with Republicans to bring it back since.

Sen. Michael Bennet (D-Colo.), who has championed expanding the program, said that the census data will show that Congress should have not allowed the expanded credit to expire.

“When we expanded the Child Tax Credit, we demonstrated that we don’t have to accept one of the highest childhood poverty rates in the industrialized world as a permanent feature of our democracy. Tomorrow’s data will show we never should have let it expire, and I’m committed to doing everything I can to restore it,” he told The Hill in a statement.

The CEA argued Friday that the increase in poverty is likely to persist absent congressional action to restore the enhanced child tax credit.

Zach Moller, director of the economic program at the center-left think tank Third Way, said Democrats will uphold this report as a good reason to continue the child tax credit expansion because it’s proof that government intervention is necessary.

“The government can absolutely fight childhood poverty, it just costs money to do it,” he said. “Those policies that the Biden administration and the Congress were able to implement in the American Rescue Plan act were temporary, so the improvement in child poverty is temporary.”

Cutting child poverty for the long term has been a goal for Biden since he took office.

The expanded CTC was a centerpiece of Biden’s American Rescue Plan, the 2021 economic relief bill passed after Democrats took control of the White House and Congress. 

Biden and fellow Democrats are eager to tout the benefits of the president’s economic plan, dubbed “Bidenomics,” with the 2024 election roughly a year away. 

Republicans have blamed Biden for the surge in inflation that began shortly after he took office, though price growth sped up across the world in the wake of the pandemic.

Biden, meanwhile, has recently stepped up attacks on former President Trump about the economy while hoping to highlight the rapid recovery and the historically strong job market of his own presidency.

Biden and Democratic lawmakers have also touted trillions of dollars allocated for improving infrastructure, bringing down drug prices, expanding manufacturing and cracking down on tax evasion by the wealthy and corporations.

But messaging about the economy hasn’t been easy for the Biden administration; Bidenomics is a major talking point for the administration on the campaign trail but has yet to really take off with Americans.

A recent RealClearPolitics polling average shows just 38 percent of those surveyed approve of Biden’s handling of the economy, compared with 58.4 percent who disapprove.

Biden has been hit with dismal polling numbers overall lately. A CNN poll released last week found that 46 percent of registered voters said any Republican presidential nominee would be better than Biden in next year’s election and found his overall approval rating at a 39 percent.

Moller argued that Biden’s focus on creating jobs, especially for low-income Americans, could bring him closer to his goal of cutting child poverty because of provisions in his top legislative achievements — the Inflation Reduction Act, the infrastructure bill, and the CHIPs and Science Act.

“All that manufacturing is going to be incredibly helpful for folks with out there that don’t have a college degree. And so that is another way of trying to tackle childhood poverty, by making sure that parents have a good-paying job,” Moller said.

In its blog post, the CEA noted that the Congressional Budget Office projected in 2021 that it would take until the end of 2025 for the jobless rate to fall under 4 percent. The unemployment rate was 3.8 percent as of August, not far from its 3.5 percent rate before the pandemic.

Inflation is steadily improving, a success that the president touts often. But the CEA expects Tuesday’s census data to show inflation-adjusted income falling in 2022.

The agency blamed “elevated pandemic inflation” and “factors such as the Russian invasion of Ukraine and avian bird flu” for the 2022 data, and the Biden administration will likely argue that the data is in the rear-view because of the improvements in inflation in 2023.

https://thehill.com/policy/healthcare/4198264-white-house-prepares-for-sharp-rise-in-poverty-rate/

Specialized T cells in the brain slow progression of Alzheimer's disease

 As many as 5.8 million Americans are currently living with Alzheimer's disease, a neurodegenerative condition associated with progressive cognitive decline, including loss of memory capabilities . Protein aggregates, composed of beta-amyloid or other proteins, form in the brains of individuals with Alzheimer's. These beta-amyloid plaques appear to be a significant contributor to the disease. St. Jude Children's Research Hospital scientists uncovered a subset of immune cells that appears to slow this beta-amyloid plaque accumulation and the key proteins involved in the process. The findings were published today in Nature Immunology.

"People typically think of the immune system as being involved in defense from bacterial or viral infection, though there is growing interest in the role of the immune system in neurodegenerative diseases," said co-first author Jordy Saravia, Ph.D., St. Jude Department of Immunology. "We uncovered an important immune cell communication axis that is protective in an Alzheimer's disease model."

Microglia are immune cells in the brain responsible for clearing beta-amyloid plaques. As Alzheimer's disease progresses, microglia can lose their capacity to remove these plaques and instead produce inflammatory mediators that may accelerate beta-amyloid plaque progression. The St. Jude team found that accumulating another subtype of immune cells, called CD8+ T cells, is essential to slow this process by interacting with microglia. This interaction, in turn, was important to limit beta-amyloid burden and preserve memory capabilities in a mouse model of the disease.

"Our paper is the first to demonstrate that a subpopulation of CD8+ T cells can be protective in a mouse model of Alzheimer's disease," said co-first author Wei Su, Ph.D., St. Jude Department of Immunology. "Moving forward, we may be able to extend this work to find an effective intervention for neurodegenerative diseases."

Immune cells' opposing roles in Alzheimer's disease

Previous research has established complex roles for T cells and other immune system cells in Alzheimer's disease. In particular, research groups using other experimental systems have suggested that certain T cells with inflammatory functions worsen the disease. However, the St. Jude scientists showed that CD8+ T cells with suppressive features accumulate in the brains of both mouse models and patients with Alzheimer's disease, highlighting that T cells play a complex role in this disease.

"We showed that CD8+ T cells can play a protective role against Alzheimer's disease pathogenesis, although there is also evidence for a contributing role," said corresponding author Hongbo Chi, Ph.D., St. Jude Department of Immunology. "Our results demonstrate the need to better understand these complex neuro-immune interactions to improve outcomes for this neurodegenerative disease."

To understand how T cells were delaying symptom progression in their Alzheimer's disease model, the St. Jude group searched for the most abundant molecular interaction between CD8+ T cells and the microglia. They found a protein on the surface of CD8+ T cells, CXCR6, interacts with the protein CXCL16 expressed by microglia.

A molecular handshake slows Alzheimer's disease

The two surface proteins, CXCR6 and CXCL16, essentially performed a handshake between the two cells, communicating in both directions. Just like the firmness of a human handshake can convey information, so can the interaction of these two proteins on the outside of their respective cells.

"We found CD8+ T cells use CXCR6 to interact with CXCL16 from microglia," Chi said. "Moreover, CD8+ T-cell accumulation, localization and function in the brain are regulated by CXCR6."

The scientists determined how the handshake occurs and delays the onset of Alzheimer's disease-related pathologies. The CD8+ T cells first move next to the microglia, which are localized next to the beta-amyloid plaques. Then, the CD8+ T cells use the handshake to signal to the microglia to stop causing uncontrolled inflammation, which, in turn, slows plaque growth and symptoms in the mouse models.

When the scientists deleted the gene for the CD8+ T cell's protein CXCR6, the mice developed worse Alzheimer's disease-related symptoms. This effect was partially because the CD8+ T cells without CXCR6 failed to accumulate in the brain near the microglia or plaque site. These cells also did not acquire the appropriate suppressive function. Thus, disrupting the CD8+ T cell's ability to perform the handshake prevented its protective effect against Alzheimer's disease symptoms.

"We have two major findings," Chi said. "One is the crucial role of CD8+ T cells in maintaining homeostasis of the brain, thereby providing a protective role in Alzheimer's disease." Homeostasis is the process of keeping a system in a relatively stable state. In this case, the CD8+ T cells attempt to limit the disruption caused by microglia dysfunction and Alzheimer's disease-related plaques.

"The other major finding is identifying the central importance of the T cell protein CXCR6 for CD8+ T-cell accumulation and function in the brain," Chi continued. "We really need to characterize these kinds of neuro-immune interactions better. Only by understanding this basic biology can we advance the field and find new treatments."

Journal Reference:

  1. Wei Su, Jordy Saravia, Isabel Risch, Sherri Rankin, Cliff Guy, Nicole M. Chapman, Hao Shi, Yu Sun, Anil KC, Wei Li, Hongling Huang, Seon Ah Lim, Haoran Hu, Yan Wang, Danting Liu, Yun Jiao, Ping-Chung Chen, Hadeer Soliman, Koon-Kiu Yan, Jonathan Zhang, Peter Vogel, Xueyan Liu, Geidy E. Serrano, Thomas G. Beach, Jiyang Yu, Junmin Peng, Hongbo Chi. CXCR6 orchestrates brain CD8+ T cell residency and limits mouse Alzheimer’s disease pathologyNature Immunology, 2023; DOI: 10.1038/s41590-023-01604-z

Structure of red blood cell transporter may pave way for new drugs

Researchers at the Icahn School of Medicine at Mount Sinai have identified the structure of a special transporter found in red blood cells and how it interacts with drugs. Details on the findings, which were reported in the September 7 issue of Nature Structural & Molecular Biology, could lead to the development of more targeted medicines.

The research team, led by Daniel Wacker, PhD, Bin Zhang, PhD, and Avner Schlessinger, PhD, found that this transporter facilitates the movement of a substance called bicarbonate, which certain drugs can inhibit. They discovered how these drugs block the transporter and devised novel compounds capable of achieving the same effect.

"Our findings provide a detailed understanding of how bicarbonate transporters work, and the newly identified tool compounds open doors to studying conditions involving red blood cells, including hemolytic anemias," says Dr. Wacker, corresponding author and an Assistant Professor of Pharmacological Sciences, Neuroscience, and Genetic and Genomic Sciences at Icahn Mount Sinai.

Previously, human bicarbonate transporters were poorly understood, despite being involved in many aspects of human physiology, including regulating pH that involves keeping the level of acidity within a specific range.

Using cryo-electron microscopy, the team identified high-resolution structures revealing bicarbonate and inhibitor binding, and their impact on the transport mechanism. With these insights, the researchers used computer simulations to analyze millions of compounds that could interact with the substrate binding site.

Their experiments pinpointed a group of innovative chemical inhibitors specifically designed for anion exchanger 1, a protein that is crucial for maintaining the proper function of the blood and red blood cells.

"Our study also demonstrates the potential for developing new inhibitors with medical potential for other solute carrier (SLC) proteins, a protein family gaining importance in drug development," says co-author Dr. Zhang, the Willard T.C Johnson Research Professor of Neurogenetics and Director of the Mount Sinai Center for Transformative Disease Modeling at Icahn Mount Sinai.

Next, the researchers plan to expand their studies to other SLC proteins involved in a variety of disorders including neurodegenerative diseases, psychiatric maladies, and cancer.

"This study effectively paves the way to using atomic-level insights toward the rapid development of promising drug-like molecules for SLC proteins," says co-author Dr. Schlessinger, Associate Professor of Pharmacological Sciences and Associate Director of the Mount Sinai Center for Therapeutics Discovery at Icahn Mount Sinai.

The paper is titled "Substrate binding and inhibition of the anion exchanger 1 transporter."

Additional co-authors, all with Icahn Mount Sinai except where indicated, areMichael J. Capper, PhD; Shifan Yang, PhD; Alexander C. Stone; Sezen Vatansever, MD, PhD (Amgen); Gregory Zilberg, PhD Candidate; Yamuna Kalyani Mathiharan, PhD; Raul Habib, (University of California, Berkeley);

Keino Hutchinson, PhD; Yihan Zhao, PhD Candidate; Mihaly Mezei, PhD; and Roman Osman, PhD.

The project was supported by National Institutes of Health grants R35GM133504, R01GM108911, U01AG046170, RF1AG057440, R01AG068030, R01DK073681, R01DK067555, R01DK061659, T32GM062754, T32DA053558, as well as a Sloan Research Fellowship in Neuroscience, an Edward Mallinckrodt, Jr. Foundation Grant, and a McKnight Foundation Scholars Award.

Journal Reference:

  1. Michael J. Capper, Shifan Yang, Alexander C. Stone, Sezen Vatansever, Gregory Zilberg, Yamuna Kalyani Mathiharan, Raul Habib, Keino Hutchinson, Yihan Zhao, Avner Schlessinger, Mihaly Mezei, Roman Osman, Bin Zhang, Daniel Wacker. Substrate binding and inhibition of the anion exchanger 1 transporterNature Structural & Molecular Biology, 2023; DOI: 10.1038/s41594-023-01085-6

UPS says Teamsters deal will raise costs by 3.3%

 United Parcel Service Inc. (UPS) on Monday said it expects costs related to its deal with the Teamsters union to increase at a rate of 3.3% over the contract's five-year lifespan. Chief Financial Officer Brian Newman, in a presentation, said that compound annual growth rate figure accounted for all contract provisions -- like stronger wages and benefits -- that affect operating costs, but that it did not include any impacts from productivity improvements over that time. But he said that UPS "retains flexibility to implement technology to further drive productivity inside our buildings," with more opportunity to automate. The contract is effective from Aug. 1 of this year to July 31, 2028, UPS said.

https://www.morningstar.com/news/marketwatch/20230911857/ups-says-teamsters-deal-will-raise-costs-by-33

How Paxlovid resistance emerges in persistent infections

 Paxlovid is still a highly effective treatment for most people infected with SARS-CoV-2 and the drug prevents many hospitalizations and deaths from COVID.

But for millions of immunocompromised people whose infections may persist for months, the antiviral drug can lose its effectiveness as the virus mutates. Although patients may initially experience a decrease in , as these mutations arise, the virus can return unimpeded by the drug, bringing the risk of disease and even death.

A study that reveals how the virus mutates to escape Paxlovid could now help chemists design better drugs that are more difficult for SARS-CoV-2 to sidestep. The study, led by researchers at Columbia University and several universities in China, was published Sept. 11 in Nature.

"This type of approach helped to improve HIV drugs, and we think it's a good way to improve antivirals against SARS-CoV-2," says Sho Iketani, Ph.D., assistant professor of medical sciences at Columbia University's Vagelos College of Physicians and Surgeons and Aaron Diamond AIDS Research Center, who co-led the research with David D. Ho, MD, the Clyde '56 and Helen Wu Professor of Medicine, professor of microbiology & immunology, and director of the Aaron Diamond AIDS Research Center, and Haitao Yang, Ph.D., of ShanghaiTech University.

"Right now, patients only have three  options, nirmatrelvir (the  in Paxlovid), remdesivir, and molnupiravir. More choice is always better."

Escape mutations in SARS-CoV-2

In the study, Iketani and colleagues looked at how mutations allow the virus to evade nirmatrelvir. Images of the drug when bound to its viral target, Mpro, revealed that mutations in the binding pocket have the greatest effect and prevent the drug from binding.

The same mutations also allowed the coronavirus to escape another Mpro inhibitor, Japan's ensitrelvir, but to a lesser degree, providing clues to how Mpro inhibitors could be improved.

Paxlovid-resistant viruses with these  have been found in some  and others with persistent infections.

"The good news is that it seems that the virus suffers a pretty big fitness penalty when it develops resistance, so I don't think we'll see resistant variants spread widely if it must balance this loss," Iketani says.

Paxlovid-resistant variants of SARS-CoV-2 are also unlikely to develop outside of the immunocompromised population. "Because otherwise healthy individuals taking Paxlovid will rapidly clear the virus, the opportunity for the virus to mutate to evade the drug in the general population is low," Iketani says.

More information: Duan, Y. et al, Molecular mechanisms of SARS-CoV-2 resistance to nirmatrelvir. Nature (2023). DOI: 10.1038/s41586-023-06609-0 www.nature.com/articles/s41586-023-06609-0


https://medicalxpress.com/news/2023-09-paxlovid-resistance-emerges-persistent-infections.html