Education Department says 60 universities under investigation for antisemitism

 The Department of Education’s Office of Civil Rights (OCR) is investigating 60 universities for antisemitism, according to letters sent on Monday. 

The department said the 60 institutions are receiving warnings due to allegedly not complying with Title IX obligations to protect Jewish students.  

“The Department is deeply disappointed that Jewish students studying on elite U.S. campuses continue to fear for their safety amid the relentless antisemitic eruptions that have severely disrupted campus life for more than a year. University leaders must do better,” said Education Secretary Linda McMahon.  

“U.S. colleges and universities benefit from enormous public investments funded by U.S. taxpayers. That support is a privilege and it is contingent on scrupulous adherence to federal antidiscrimination laws,” she added. 

The list includes Ivy League schools such as Harvard University and smaller schools such as Middlebury College. 

The letters come after the federal government cut off $400 million in funding to Columbia University over alleged inaction in handling antisemitism complaints and OCR announced prioritization in addressing the backlog of antisemitism allegations at schools with its office.  

The action also comes days after U.S. Immigration and Customs Enforcement arrested a Columbia University graduate student with a green card who led pro-Palestinian protests. 

The escalation in investigations and threats has had some effect on schools.  

Harvard University said Monday it was implementing a hiring freeze due to uncertainties around federal policy and funding concerns, and the University of California, Los Angeles announced it is starting a new initiative to combat antisemitism on campus.  

https://thehill.com/homenews/education/5186555-department-of-education-antisemitism-investigation/

Transport sec rescinds Biden memos prioritizing infrastructure resilience to climate change

 Transportation Secretary Sean Duffy rescinded memos from the Biden administration prioritizing infrastructure resilience to climate change, according to a Monday press release.

According to the press release from the department, the announcement about the rescinding came from Duffy on Monday. The department said the memos “displaced the long-standing authorities granted to States by law, added meritless and costly burdens related to greenhouse gas emissions and equity initiatives.”

The Trump Transportation Department also put forth a memo of its own dated last Friday in which it called the memos “controversial” and asked for their rescinding.

Webpages for the memos on the Federal Highway Administration’s (FWHA) website are both currently displaying “Page Not Found.” 

According to a Government Accountability Office report from 2022, one of the memos from 2021 had aims including pushing for states to “invest in projects that upgrade the condition of streets, highways and bridges and make them safe for all users” and “modernizing” those same pieces of infrastructure to make the transport network “more sustainable and resilient to a changing climate.”

An archived version of the other memo, which is from 2023, also states that the FWHA would carry on with focusing on “infrastructure that is less vulnerable and more resilient to a changing climate.” The 2021 memo was also superseded by the 2023 memo.

Duffy said in the release that his department “is getting back to basics — building critical infrastructure projects that move people and move commerce safely.” 

“The previous administration flouted Congress in an attempt to push a radical social and environmental agenda on the American people,” he continued. “This was an act of federal overreach. It stops now.”

https://thehill.com/homenews/state-watch/5186694-transportation-secretary-rescinds-biden-memos-prioritizing-infrastructure-resilience-to-climate-change/

Gut bacterium restores bile acid balance to heal intestinal injuries, potential ulcerative colitis treatment

 The human gut is home to trillions of bacteria that play vital roles in digestion, immunity, and overall health. When this microbial balance is disturbed, it can contribute to the development of chronic diseases like ulcerative colitis (UC), an inflammatory condition of the large intestine. For some patients, current treatments offer limited relief or carry significant risks, including immune suppression. Researchers are now exploring alternative ways to restore gut health, focusing on the microbiome's ability to heal the intestinal lining.

One of the hallmarks of UC is a deficiency in certain bile acids, molecules that help digest fats and regulate gut health. These molecules aren't just produced by the liver—they are further processed by gut bacteria into forms that support intestinal healing. UC patients often show lower levels of these microbial bile acids, suggesting that their restoration could promote recovery.

The research teams led by Kristina Schoonjans and Rizlan Bernier-Latmani at EPFL, have identified Clostridium scindens, a bacterium that converts primary bile acids into 7α-dehydroxylated bile acids, as a key player in gut healing. Their study, published in the journal EMBO Molecular Medicine, shows that supplementing the gut with this bacterium could improve recovery from colonic injury, offering a new potential therapy for UC and related disorders.

The researchers tested their hypothesis in mice with colitis, a disease model that mimics UC. They introduced Clostridium scindens into some mice while leaving others untreated. The team then monitored the animals' recovery by measuring weight loss, colon inflammation, and markers of intestinal healing.

Mice that received Clostridium scindens recovered more quickly, showing reduced inflammation and enhanced regeneration of the gut lining. The researchers found that these effects were dependent on TGR5, a receptor that responds to 7α-dehydroxylated bile acids, which stimulates the proliferation and differentiation of intestinal stem cells. When they tested the therapy in mice lacking this receptor, the benefits disappeared, confirming that bile acid metabolism is essential for healing.

To further validate their findings, they analyzed patient data to determine whether similar mechanisms were at play in humans. They found that in UC patients, the lower levels of 7α-dehydroxylated bile acids strongly correlated with impaired intestinal cell renewal. This reinforces the link between bile acid metabolism and intestinal healing.

"Our findings highlight the potential of microbiome-targeted strategies to modulate bile acid metabolism and promote gut healing," says Antoine Jalil, the first author of the study.

Unlike conventional treatments that focus on suppressing inflammation, this approach targets the underlying issue: the impaired ability of the gut to heal itself. By restoring natural bile acid balance through beneficial bacteria, this strategy could provide an alternative and more sustainable treatment option for UC patients. While further research is needed to explore its clinical applications, the findings highlight the therapeutic potential of microbiome-based interventions.

More information: Antoine Jalil et al, Bile acid 7α-dehydroxylating bacteria accelerate injury-induced mucosal healing in the colon, EMBO Molecular Medicine (2025). DOI: 10.1038/s44321-025-00202-w

https://medicalxpress.com/news/2025-03-gut-bacterium-bile-acid-intestinal.html

Natural defense mechanism may help slow down tumor cell metastasis

 Researchers at Karolinska Institutet, led by Dr. Helin Norberg and Dr. Erik Norberg, have identified a previously unknown mechanism that affects the ability of cancer cells to spread in the body. The study, published in EMBO Molecular Medicine, shows that a process called chaperone-mediated autophagy (CMA) may function as a natural defense mechanism against metastases.

Cancer remains one of the most common and deadliest diseases worldwide. Cancer cells can spread through the bloodstream and begin growing in other organs; these are known as metastases and represent a frequent and severe complication that often determines the seriousness of a tumor disease. Blocking cancer cells' ability to spread is a crucial strategy, yet there are currently few effective treatments for cancer metastasis.

Unexpected findings

Dr. Helin Norberg has long studied CMA, a process in which cells break down specific proteins, while Dr. Erik Norberg's research has long had a central focus on cancer metabolism. By removing the gene LAMP2A, which controls CMA, they discovered that cancer cells without a functioning CMA changed their metabolism and grew faster and formed more metastases.

"This was an unexpected finding. Previously, CMA was believed to stimulate cancer growth, but our results suggest the opposite," says Dr. Helin Norberg.

To confirm their discovery, the researchers analyzed patient samples from lung cancer patients with brain metastases. The results showed that the metastases had significantly lower levels of LAMP2A compared to the primary tumors. Similar patterns were observed in metastases from 19 different organs.

Tumor spread and autophagy

Cancer cells can alter their identity through epithelial-mesenchymal transition (EMT), a process that enhances their ability to spread. The researchers demonstrated that several proteins involved in EMT are broken down via CMA, indicating that CMA functions as a natural tumor-suppressing mechanism.

"A deeper understanding of metastasis-driving proteins can help us comprehend how cancer cells spread and develop new treatment strategies," says Dr. Erik Norberg.

The current goal is to identify ways to activate CMA in order to prevent or eliminate metastases. The researchers are already well advanced in this field and hope that their discovery will pave the way for new treatment methods to combat cancer spread.

Many types of cancer lead to metastases, and today, one in three cancer patients already has metastases at the time of diagnosis. Gaining deeper insight into how metastasis-driving proteins can be eliminated in cancer cells could improve our understanding of the underlying causes of cancer cell spread.

"Our hope is that the new knowledge we have contributed will be utilized to develop effective treatments to prevent or eliminate metastases. This requires the activation of CMA—a research focus that we are fully committed to and have already made significant progress in," says Dr. Erik Norberg.

"This study is an excellent example of strong collaboration between clinicians and preclinical researchers from four different departments at Karolinska Institutet," he adds.

More information: Xun Zhou et al, Chaperone-mediated autophagy regulates the metastatic state of mesenchymal tumors, EMBO Molecular Medicine (2025). DOI: 10.1038/s44321-025-00210-w

https://medicalxpress.com/news/2025-03-natural-defense-mechanism-tumor-cell.html

Compound in common herbs inspires potential anti-inflammatory drug for Alzheimer's

 The herb rosemary has long been linked with memory. "There's rosemary, that's for remembrance," says Ophelia in Shakespeare's "Hamlet." So it is fitting that researchers would study a compound found in rosemary and sage—carnosic acid—for its impact on Alzheimer's disease. In the disease, which is the leading cause of dementia and the sixth-leading cause of death in the US, inflammation is one component that often leads to cognitive decline.

Carnosic acid is an antioxidant and anti-inflammatory compound that works by activating enzymes that make up the body's natural defense system. While pure carnosic acid is too unstable to be used as a drug, scientists at Scripps Research have now synthesized a stable form, diAcCA. This compound is fully converted to carnosic acid in the gut before being absorbed into the bloodstream.

The research, published in Antioxidants, showed that when diAcCA was used to treat mouse models of Alzheimer's disease, it achieved therapeutic doses of carnosic acid in the brain and led to enhanced memory and synaptic density, or more synapses (representing the connections between nerve cells), in the brain. Because the decline of neuronal synapses is also closely correlated to dementia in Alzheimer's disease, this approach could counteract the progression of cognitive decline.

Analysis of tissue samples showed the drug also markedly decreased inflammation in the brain. This unique drug is activated by the very inflammation that it then combats and thus is only active in areas of the brain undergoing inflammatory damage. This selectivity limits the potential side effects of carnosic acid, which is on the US Food and Drug Administration's "generally regarded as safe" (GRAS) list, easing the way for clinical trials.

"By combating inflammation and oxidative stress with this diAcCA compound, we actually increased the number of synapses in the brain," says senior author and professor Stuart Lipton, MD, Ph.D., the Step Family Foundation Endowed Chair at Scripps Research and a clinical neurologist in La Jolla, California. "We also took down other misfolded or aggregated proteins such as phosphorylated-tau and amyloid-β, which are thought to trigger Alzheimer's disease and serve as biomarkers of the disease process."

Lipton's group had previously determined that carnosic acid crosses the blood-brain barrier and activates the Nrf2 transcriptional pathway, which turns on antioxidant and anti-inflammatory genes. But the compound oxidizes easily, making it unsuitable as a drug because of its short shelf-life.

In this new study, Lipton and co-author Phil Baran, Ph.D., the Dr. Richard A. Lerner Endowed Chair in the Department of Chemistry at Scripps Research, synthesized a range of carnosic acid derivatives and selected diAcCA as the best candidate because of its stability, bioavailability, and other drug-like properties. Lipton's group then treated mouse models with the compound over the course of three months. The group examined the mice by testing their spatial learning and memory in behavioral tests and then analyzing brain tissue under the microscope.

"We did multiple different tests of memory, and they were all improved with the drug," Lipton says. "And it didn't just slow down the decline; it improved virtually back to normal." Analysis of tissues also showed increased neuronal synaptic density and decreased formation of phosphorylated-tau aggregates and amyloid-β plaques.

The mice tolerated diAcCA well. In toxicity studies, the compound even soothed baseline inflammation in the esophagus and stomach as it was converted to carnosic acid.

The group also found that the mice took up about 20% more carnosic acid after ingesting diAcCA than they did after taking plain carnosic acid. Because most carnosic acid oxidizes while being stored or upon ingestion, "diAcCA produces more carnosic acid in the blood than if you took carnosic acid itself," Lipton explains.

Lipton sees a potential for diAcCA to work in tandem with Alzheimer's treatments currently on the market. Not only could the drug work on its own by combating inflammation, but "it could make existing amyloid antibody treatments work better by taking away or limiting their side effects," such as a form of brain swelling or bleeding known as ARIA-E and ARIA-H, he says.

Lipton hopes diAcCA can be fast-tracked through clinical trials because of its safety profile. He thinks it could also be explored as a treatment for other disorders marked by inflammation, such as type 2 diabetes, heart disease, and other forms of neurodegeneration such as Parkinson's disease.

In addition to Lipton and Baran, authors of the study include Piu Banerjee, Yubo Wang, Lauren N. Carnevale, Parth Patel, Charlene K Raspur, Nancy Tran, Xu Zhang, and Amanda J. Roberts of Scripps Research and Ravi Natarajan of Socrates Biosciences.

More information: Piu Banerjee et al, diAcCA, a Pro-Drug for Carnosic Acid That Activates the Nrf2 Transcriptional Pathway, Shows Efficacy in the 5xFAD Transgenic Mouse Model of Alzheimer's Disease, Antioxidants (2025). DOI: 10.3390/antiox14030293

https://medicalxpress.com/news/2025-03-compound-common-herbs-potential-anti.html

US FDA to hold off action on weight-loss drug copies pending court ruling

 The U.S. Food and Drug Administration said on Monday it will not take action against compounding pharmacies making copies of Novo Nordisk's (NOVOb.CO) , opens new tab weight-loss drug Wegovy until a federal court delivers its ruling in a lawsuit against the agency.

https://www.reuters.com/business/healthcare-pharmaceuticals/us-fda-hold-off-action-weight-loss-drug-copies-pending-court-ruling-2025-03-10/

Trump administration aims to cancel oil reserve sales, support small nuclear power

 U.S. Energy Secretary Chris Wright said on Monday he was planning to work with Congress on cancelling previously mandated sales from the Strategic Petroleum Reserve as one way to address low stockpiles.

Congress has mandated some 100 million barrels in sales from the reserve, the world's largest emergency stockpile of crude oil, with a 7 million barrel sale set for fiscal year 2026-2027, and further sales through 2031.

"Anything with Congress is more difficult, you know, and that takes time, but absolutely," Wright told Reuters in an interview at the CERAWeek conference.

It would take five to seven years and $20 billion to refill the reserve, Wright said. U.S. President Donald Trump's predecessor Joe Biden sold nearly 300 million barrels from the SPR, including its largest sale ever after Russia invaded Ukraine in 2022.

Due to ongoing maintenance issues, refilling the reserve takes more time than selling from it, Wright said. The Energy Department said on Friday that Wright would not ask Congress for $20 billion for purchases all in one go, and that working with lawmakers to buy oil could take years.

Wright also wants to boost U.S. exports of liquefied natural gas. Trump talked up a proposed $44 billion Alaska LNG project in his address to Congress last week.

Trump has said Japan, South Korea and other countries want to partner with the United States in a "gigantic" natural gas pipeline in Alaska, claiming they would invest "trillions of dollars each." The Alaska LNG project needs an 800-mile pipeline to bring gas from Alaska's north to send it to customers in Asia and no final investment decisions have yet been made.

Wright said all options for supporting the project are on the table including a potential loan guarantee from his department's Loan Programs Office, or LPO.

"The administration will look at every way we can to get a large infrastructure project like that built," Wright said, adding that included diplomacy and a potential loan guarantee, which would help the project get financing at a lower rate than offered by banks.

U.S. Senators Lisa Murkowski and Dan Sullivan secured a provision in a 2021 infrastructure law for Alaska LNG to be eligible for federal loan guarantee of roughly $30 billion that is indexed to inflation.

If the Trump administration uses the LPO for Alaska LNG, it would mark a policy change from his first term as president when he did not significantly tap the LPO. Biden frequently used the LPO and signed legislation to swell its financial aid to hundreds of billions of dollars.

Wright also downplayed regional opposition to new natural gas pipelines in regions like the U.S. Northeast, saying he did not expect it to get in the way of building new projects.

"Everyone wants lower energy prices. Everyone in New York, everyone in New England," he said.

Trump, on his first day in office, signed an emergency energy declaration intended to expand federal powers to push through big projects like generators, pipelines, and transmission to meet rising power demand.

Wright, who stepped down from the board of small modular reactor company Oklo when he was confirmed as energy secretary, said the administration was also likely to give the emerging nuclear technology both financial and regulatory support, but did not detail how.

Small modular reactors are seen as a potential partial solution to meeting soaring power demand from data centers, but there are no commercial plants yet

https://www.yahoo.com/news/trump-administration-aims-cancel-oil-190744430.html