'Study finds key factors to boost school readiness in low birth weight kids'

 School readiness is central to child well-being and is predictive of not only academic, but also long-term economic and health outcomes according to the American Academy of Pediatrics (AAP). However, new research reveals a concerning gap in school readiness for children with low birth weight, with only one-third of these children being on track for school readiness — lower than reported for the general pediatric population.

A new Boston Medical Center (BMC) study identifies five key protective factors that can support children, especially those with low birth weight, in reaching developmental milestones and being prepared for school. Neighborhood amenities, better parental mental health, emotional support networks, regular reading or bedtime routines, and limiting screen time to one hour or less each day are all associated with improved school readiness, according to findings published recently in Academic Pediatrics.

Using data from the 2016–2019 National Survey of Children's Health, the BMC research team, led by Gen Guyol, MD, MAT, explored developmentally sound and emotionally supportive early life experiences that can improve school readiness.

"Our findings underscore the critical role that family routines and parental supports play in shaping early child development. By fostering predictability, such as through consistent household routines and spending dedicated time together, parents can create an environment that supports their child's readiness for school," says Dr. Guyol, a health services researcher in neonatology at BMC.

The study highlights the importance of emotional support for not only children, but also parents and caregivers. Having someone to turn to for guidance and reassurance can be a vital resource for families as they navigate the complexities of raising a young child. Dr. Guyol, who is also an assistant professor in pediatrics at Boston University Chobanian & Avedisian School of Medicine, adds, "It's essential to recognize that the support of parents and caregivers is a protective factor. When parents feel supported, they are better equipped to create an environment that promotes positive developmental outcomes for their children."

'This research contributes to a growing body of evidence that emphasizes the importance of early, accessible interventions and supportive environments in fostering school readiness, particularly for vulnerable populations like children with low birth weight.'

"Investing in school readiness has far-reaching effects that extend well beyond the classroom. By supporting parents and creating environments that foster early development, we are not only helping children thrive in school but also setting the foundation for lifelong success and well-being," says Dr. Guyol.

More information: Genevieve G. Guyol et al, Child, Parent, and Contextual Correlates of School Readiness Among Children with Low Birth Weight, Academic Pediatrics (2025). DOI: 10.1016/j.acap.2025.102808

https://medicalxpress.com/news/2025-03-key-factors-boost-school-readiness.html

Experimental drug found to more than double survival time for glioblastoma patients

 A drug developed at The University of Texas Health Science Center at San Antonio (UT Health San Antonio) has been shown to extend survival for patients with glioblastoma, the most common primary brain tumor in adults.

Results of a trial led by the university revealed that a unique investigational drug formulation called Rhenium Obisbemeda (186RNL) more than doubled median survival and progression-free time, compared with standard median survival and progression rates, and with no dose-limiting toxic effects.

"As a disease with a pattern of recurrence, resistance to chemotherapies and difficulty to treat, glioblastoma has needed durable treatments that can directly target the tumor while sparing healthy tissue," said Andrew J. Brenner, MD, Ph.D., professor and chair of neuro-oncology research with Mays Cancer Center at UT Health San Antonio.

"This trial provides hope, with a second phase under way and planned for completion by the end of this year."

Brenner, who is also a clinical investigator for the Institute for Drug Development at UT Health San Antonio and co-leader of its Experimental and Development Therapeutics Program, is lead author of the trial's study, titled, "Convection Enhanced Delivery of Rhenium (186Re) Obisbemeda (186RNL) in Recurrent Glioma: a multicenter, single arm, phase 1 clinical trial." It is published in the journal Nature Communications.

Other authors are also with Mays Cancer Center, as well as UT Southwestern Medical Center of Dallas, Case Western Reserve University, University of Texas MD Anderson Cancer Center and trial sponsor Plus Therapeutics Inc. (Nasdaq: PSTV), a clinical-stage pharmaceutical company receiving a license to the trial technology to investigate the treatment of central nervous system cancers.

Brenner said that the median overall survival time for patients with glioblastoma after standard treatment fails with surgery, radiation and chemotherapy is only about eight months. More than 90% of patients have a recurrence of the disease at its original location.

Rhenium Obisbemeda enables very high levels of a specific activity of rhenium-186 (186Re), a beta-emitting radioisotope, to be delivered by tiny liposomes, referring to artificial vesicles or sacs having at least one lipid bilayer. The researchers used a custom molecule known as BMEDA to chelate or attach 186Re and transport it into the interior of a liposome where it is irreversibly trapped.

In this trial, known as the Phase I ReSPECT-GBM trial, scientists set out to determine the maximum tolerated dose of the drug, as well as safety, overall response rate, disease progression-free survival and overall survival.

After failing one to three therapies, 21 patients who were enrolled in the study between March 5, 2015, and April 22, 2021, were treated with the drug administered directly to the tumors using neuronavigation and convection catheters.

The researchers observed a significant improvement in survival compared with historical controls, especially in patients with the highest absorbed doses, with a median survival and progression-free time of 17 months and six months, respectively, for doses greater than 100 gray (Gy), referring to units of radiation.

Importantly, they did not observe any dose-limiting toxic effects, with most adverse effects deemed unrelated to the study treatment.

"The combination of a novel nanoliposome radiotherapeutic delivered by convection-enhanced delivery, facilitated by neuronavigational tools, catheter design and imaging solutions, can successfully and safely provide high absorbed radiation doses to tumors with minimal toxicity and potential survival benefit," Brenner concluded.

More information: Andrew J. Brenner, et al. Convection Enhanced Delivery of Rhenium (186Re) Obisbemeda (186RNL) in Recurrent Glioma: a multicenter, single arm, phase 1 clinical trial, Nature Communications (2025). DOI: 10.1038/s41467-025-57263-1

https://medicalxpress.com/news/2025-03-experimental-drug-survival-glioblastoma-patients.html

Calcium channel inhibition promotes cardiac regeneration, offering hope for heart failure treatment

 Researchers report a discovery in cardiac regeneration that offers new hope for the treatment of ischemic heart failure. Published in npj Regenerative Medicine, the study reveals a novel approach to promoting cardiomyocyte proliferation. The researchers are from the Michael E. DeBakey Department of Surgery at Baylor College of Medicine, the QIMR Berghofer Medical Research Institute in Brisbane, Australia, and collaborating institutions.

"When the heart cannot replace injured cardiomyocytes with healthy ones, it becomes progressively weaker, a condition leading to heart failure. In this study, we investigated a new way to stimulate cardiomyocyte proliferation to help the heart heal," said co-corresponding author Dr. Riham Abouleisa, assistant professor in the Division of Cardiothoracic Surgery at Baylor.

Previous studies showed that calcium plays an important role in cardiomyocyte proliferation. In the current study, Abouleisa and her colleagues explored how modulating calcium influx in cardiomyocytes would affect their proliferation.

"We found that preventing calcium influx in cardiomyocytes enhances the expression of genes involved in cell proliferation," Abouleisa said. "We prevented calcium influx by inhibiting L-Type Calcium Channel (LTCC), a protein that regulates calcium in these cells. Our findings suggest that LTCC could be a target for developing new therapies to induce cardiomyocyte proliferation and regeneration."

The study demonstrates that both pharmacological and genetic inhibition of LTCC can induce cardiomyocyte replication and that this occurs by modulating the activity of calcineurin, a known regulator of cardiomyocyte proliferation. This innovative approach showed promising results both in human cardiac slices grown in the lab and in live animals.

Drug screen targeting proteins involved in CM Ca2+ cycling revealed that inhibition of LTCC enhances CM cell cycle activity in hCOs. Credit: npj Regenerative Medicine (2025). DOI: 10.1038/s41536-025-00389-z

"Abouleisa's multi-continent collaborations led to a discovery that can revolutionize the use of current medicines that regulate calcium entry to the cells, such as Nifedipine, in heart failure patients," said Dr. Tamer Mohamed, co-author and director of Baylor College of Medicine's Laboratory for Cardiac Regeneration.

Co-author Dr. Todd K. Rosengart, chair and professor of the Michael E. DeBakey Department of Surgery, emphasized that, "The premise of regenerating heart tissue, which once seemed like an impossible dream, is getting closer almost daily. The work of Dr. Abouleisa and the Baylor cardiac regeneration team represents a major step toward human trials that I believe are in the not-too-distant future."

Abouleisa and her colleagues' research highlights the importance of targeting calcium signaling pathways to unlock the regenerative potential of the heart and opens new avenues for developing cardiac regenerative therapies, potentially transforming the treatment landscape for patients suffering from heart failure.

Other contributors to this work include Lynn A C Devilée, Abou Bakr M Salama, Jessica M Miller, Janice D Reid, Qinghui Ou, Nourhan M Baraka, Kamal Abou Farraj, Madiha Jamal, Yibing Nong, Douglas Andres, Jonathan Satin and James E Hudson.

More information: Lynn A. C. Devilée et al, Pharmacological or genetic inhibition of LTCC promotes cardiomyocyte proliferation through inhibition of calcineurin activity, npj Regenerative Medicine (2025). DOI: 10.1038/s41536-025-00389-z

https://medicalxpress.com/news/2025-03-calcium-channel-inhibition-cardiac-regeneration.html

Ammonia buildup kills liver cells but can be prevented using existing drug

 High levels of ammonia kill liver cells by damaging the mitochondria that power the cells. But this can be prevented using an existing drug due to start clinical trials, finds a new study in mice led by researchers from UCL.

The study, published in Science Advances, is the first to observe that the buildup of ammonia (hyperammonemia) can harm liver cells, and the first to describe how this damage occurs in mouse models that are clinically relevant for humans.

Hyperammonemia is known to cause brain dysfunction in those with liver disease, but a lack of effective treatments for the condition has meant the prognosis for patients is often poor.

Professor Rajiv Jalan, senior author of the study from the UCL Institute for Liver & Digestive Health, said, "Ammonia is a toxin that is usually cleared from the body via the urea cycle, which takes place in the liver. We know that liver disease patients accumulate ammonia and that this can lead to problems, including in the brain. But until now we didn't understand exactly how this occurred.

"In this study we've demonstrated that ammonia kills liver cells by damaging the mitochondria, which—apart from their role in clearing ammonia from the body—also act as the powerhouse of cells. It's a vicious cycle where the more the mitochondria are damaged, the more ammonia builds up, which snowballs into complete system breakdown."

Of the 100 million people in the world with cirrhosis (scarring of the liver), about three million are hospitalized with an episode of confusion or coma that is associated with elevated ammonia levels in blood and brain tissues, with 10–15% of these expected to die within three months of the episode.

In promising news for these patients, the research demonstrated that an existing drug, called YAQ-005 (previously known as TAK-242), can halt damage to the mitochondria in liver cells, allowing them to do their job of converting ammonia into urea so that it can be excreted as urine (a process called the urea cycle).

YAQ-005, which has been patented by UCL Business (UCLB), the commercialization company for UCL, and licensed to UCL spinout company Yaqrit, is currently in a phase II clinical trial for acute-on-chronic liver failure, a condition related to cirrhosis.

The authors believe that the drug may also be effective for children with urea-cycle disorders and other genetic diseases that lead to increased levels of ammonia by causing mitochondrial dysfunction (hepatic mitochondriopathies).

In the study, the researchers observed that in two mouse models, elevated levels of ammonia caused an increase in two proteins, called RIPK1 and RIPK3, which leads to mitochondrial damage and a dangerous form of cell death that not only harms the liver but also other organs, including the immune system.

There was also increased activity in the TLR4 signaling pathway, which alerts the immune system when pathogens are detected and is known to induce the production of RIPK1 proteins.

Increases in RIPK1 and RIPK3 corresponded to increased liver scarring and liver cell death, proving that ammonia directly causes liver injury for the first time.

The team then administered two drugs, RIPA-56 to block the RIPK1 pathway and YAQ-005 to prevent the activation of the TLR4 pathway, which led to significant reduction in liver injury and cell death in the mice.

Dr. Annarein Kerbert, first author of the study from UCL Institute for Liver & Digestive Health and Leiden University Medical Centre, said, "Targeted drugs to prevent chronic liver disease progression currently do not exist. In this study, we have shown the potential of the drug YAQ-005 in protecting the liver from the toxic effects of hyperammonemia. We therefore believe that this could be a potential novel therapy for disease progression in cirrhosis. Our aim is to investigate this further in proof-of-concept clinical studies."

A phase II clinical trial for YAQ-005 is due to begin recruiting patients with liver failure in mid-2025, which will provide the first proof of concept for this treatment in human patients.

Troels Jordansen, CEO of Yaqrit, added, "We are looking forward to advancing this innovative drug, licensed from UCL, into phase II trials in acute-on-chronic liver failure. This is a complicated life-threatening condition and there is an urgent need for new approaches."

More information: Annarein Kerbert et al, Hyperammonemia induces programmed liver cell death, Science Advances (2025). DOI: 10.1126/sciadv.ado1648. www.science.org/doi/10.1126/sciadv.ado1648

https://medicalxpress.com/news/2025-03-ammonia-buildup-liver-cells-drug.html

Consumer Credit Jumps More Than Expected In January, Back Over $5 Trillion

 We have repeatedly warned that with their savings - and especially "emergency covid savings" - gone or nearly gone, Biden admin's residual savings data manipulation notwithstanding...

... US consumers had no choice but to max out their credit cards in order to "extend and pretend" their moment of purchasing greatness, or as we called it three months ago, their last hurrah (see In "Last Hurrah", Credit Card Debt Explodes Higher Despite Record High APRs As Savings Rate Craters), a hurrah that would last very briefly as it was only a matter of months if not weeks before said cards were denied.

One month later, that's exactly what happened, when to our surprise, revolving credit cratered at the fastest pace since the covid crash, contracting a whopping $13 billion, an event which for a country that lives on debt - literally - is unheard of outside of a recession.

Commenting on the plunge, we said that "we don't know what sparked this sudden reversal in the favorite American pastime - i.e., to buy stuff one can't afford and hope to pay it back some time in the future for a modest 29.95% APR - but we know what didn't: falling rates... because they didn't." We then proceeded to show that the average interest rate on credit card balances were at the second highest on record ever though the Fed had already cut rates by 100 bps.

And while it would have been normal, if not expected, for credit card balances to continue declining with savings rates near record lows and with credit card rates at record highs, trust the US economy to do precisely the opposite of what is logical and according to the latest just released consumer credit data, US consumers exited 2024 with a bang after Consumer credit soared by a record $40.8 billion in December, a complete reversal of the November drop, and a month that sticks out like a sore thumb in the history of consumer credit as shown below.

And while one would expect that the record December surge in credit would quickly reverse at the start of the year amid the ongoing drawdown in savings - and the lack of holiday spending - the US consumer has a habit of doing just the opposite of what is expected, and according to the latest NY Fed data, in January consumer credit surged again, rising by $18.084 billion (from a downward revised $37.1 billion vs $40.8 billion previously), and the third highest monthly increase since June 2023...

... which sent the total back over $5 trillion.

Taking a closer look at the number, revolving credit - i.e., credit card debt - increased by $9 billion or roughly half of the near record $21 billion surge in December.

Non-revolving debt (i.e. student and auto loans) rose almost by the same amount, up $9.1 billion and also down from the $16.2 billion the previous month.

Looking at the composition of nonrevolving credit, the Fed reported that in Q4 student loans rose by $4.2 billion, well below the $31.8 billion increase in Q3, though still enough to push the total amount to a new record high of $1.777 trillion, while auto loans posted a more modest $2.1 billion increase to $1.569 trillion.

To be sure, while a drop in consumer credit could have been explained with the fact that credit card APRs were at all time highs (currently 23% up almost 10% from a decade again), the fact that APRs remained just shy of a record high - half a year into the Fed's easing cycle - certainly does not explain why US consumers scrambled to max out their credit cards both at the end of 2024 and at the start of 2025, just as their savings accounts hit the lowest level in years.

And as we warned last month, "while the recent surge in credit card usage may explain the burst in spending to end the year, there is only so far that an economy can be pushed with maxed out credit cards", something which the market is finally starting to realize today.

https://www.zerohedge.com/markets/consumer-credit-jumps-more-expected-january-back-over-5-trillion

Hims & Hers bought a skincare startup for $190 million 4 years ago. Today it shut it down

 

• Hims & Hers is shutting down the dermatology business it acquired in 2021, BI has learned.

• It said it's closing the skincare site Apostrophe to centralize its teledermatology offerings.

• Hims & Hers' stock has seesawed wildly this year as its weight-loss business faces new pressures.

Hims & Hers is shutting down the dermatology business it acquired four years ago, Business Insider has learned.

On Friday, the telehealth company discontinued Apostrophe, the direct-to-consumer skincare startup that it bought in 2021 for $190 million.

According to a message on Apostrophe's website, all subscriptions will be canceled as of Friday and customers will lose access to their provider teams and patient accounts after 30 days. The message suggested visiting Hims & Hers to pursue further skincare treatment.

"After careful consideration, we are discontinuing Apostrophe to simplify our dermatology products and operations into one seamless experience for our customers and our continued focus to provide customers with access to the most effective care," Hims & Hers said in a statement to BI.

The company said it eliminated some roles as part of the decision but didn't specify how many people were affected. Some Apostrophe employees will be moved into new roles across Hims & Hers' business lines, the company said.

Hims & Hers already offered dermatology services before buying Apostrophe and has continued to provide them after the acquisition. The company, which offers various services through its online platform, including treatments for hair loss, erectile dysfunction, and mental health, said shuttering Apostrophe would help it centralize its skincare offerings for customers.

The company said the shutdown wasn't related to the coming changes to its weight-loss business or the pressures on its stock, which fell by 27% last month after the Food and Drug Administration declared an end to the shortage of semaglutide, the active ingredient in Ozempic and Wegovy, two blockbuster drugs used for weight loss.

Hims & Hers has bet big on prescribing compounded versions of these drugs, including by buying its own compounding pharmacy in September. The FDA has allowed pharmacies to make compounded versions of semaglutide since 2022 to broaden patient access to the drugs.

But with the shortage now over, the company will no longer be able to make copycat versions of the shots.

The company's chief financial officer, Yemi Okupe, confirmed after Hims & Hers' fourth-quarter earnings that the company planned to remove all commercially available doses of semaglutide from its platform.

The company had a strong 2024, buoyed by the growth of its weight-loss business. Its revenue jumped 69% to $1.48 billion, with its GLP-1 offering bringing in $225 million.

The company said it still expected its weight-loss business to bring in $725 million in revenue in 2025, excluding commercially available doses of semaglutide. Hims & Hers is set to continue offering weight-loss pills and personalized weight-loss support, including nutrition plans and coaching. Outside of weight-loss care, the company saw its subscriber count grow about 40% last year.

The stock is up more than 40% since the beginning of the year, peaking in mid-February after Hims & Hers ran a controversial commercial about its weight-loss platform during the Super Bowl and announced the next week that it had bought Trybe Labs, a company that offers at-home lab testing.

https://www.aol.com/hims-hers-just-shut-down-202449968.html

ActBlue, the Democrat party’s fundraising engine, is in deep trouble

 

By Andrea Widburg

Right before the 2024 election, the House Administration Committee found evidence indicating that foreign donations from countries hostile to America may have been laundered straight into Democrat campaigns through ActBlue, the Democrats’ primary fundraising engine. That information came out during a Democrat administration. With Republicans in charge now in D.C., the investigation into ActBlue’s activities is being turned up a notch. That may explain why ActBlue is in complete disarray, with top executives fleeing the organization.

According to Wikipedia, which is probably accurate on this, ActBlue, which was founded in 2004, “is a major part of the Democratic Party’s fundraising infrastructure.” In the 20 years from 2004 to 2024, it raised $13.7 billion for Democrat causes and candidates. Indeed, most Democrat politicians and organizations used ActBlue as their clearinghouse for credit card donations.

Image by Grok.

By 2023, though, Republicans were raising questions about ActBlue’s practices. For one thing, for a long time, donors weren’t required to provide the little three-digit (or, in the case of Amex, four-digit) code that hides on their credit cards. The code is an important way to ensure that the person donating actually possesses the card, rather than the card number having come from information gained via electronic theft. (ActBlue eventually changed that policy.)

Another problem, alluded to in the opening paragraph, was the allegation that Act Blue’s security measures were so lax that the identities of legitimate, individual ActBlue donors were being used to launder illegal foreign money into Democrat party politics:

The Republican-led House Administration Committee has found evidence that illegal donations from China, Russia, Iran and Venezuela may have been laundered to Democratic campaigns through the party’s online fundraising juggernaut ActBlue.

Administration Committee Chairman Bryan Steil (R-Wis.) wrote to ActBlue CEO Regina Wallace-Jones on Monday “to demand information on ActBlue’s donor verification policies,” which are allegedly letting US adversaries use unwitting straw donors to make political contributions.

“Our investigation has indicated that these [foreign] actors may be exploiting existing U.S. [sic] donors by making straw donations without the individuals’ or your platform’s knowledge,” Steil wrote. 

“This failure to verify donor identity may have allowed foreign actors to fraudulently participate in the political process.”

It’s against that background that the New York Times reported yesterday that ActBlue is, as my mom would have said, in deep doo-doo:

ActBlue, the online fund-raising organization that powers Democratic candidates, has plunged into turmoil, with at least seven senior officials resigning late last month and a remaining lawyer suggesting he faced internal retaliation.

The departures from ActBlue, which helps raise money for Democrats running for office at all levels of government, come as the group is under investigation by congressional Republicans. They have advanced legislation that some Democrats warn could be used to debilitate what is the party’s leading fund-raising operation.

The exodus has set off deep concerns about ActBlue’s future. Last week, two unions representing the group’s workers sent a blistering letter to ActBlue’s board of directors that listed the seven officials who had left. The letter described an “alarming pattern” of departures that was “eroding our confidence in the stability of the organization.”

The reason behind the mass exodus is a mystery, as none of the people jumping ship would agree to be interviewed. Perhaps they didn’t want to say anything that can be used or misused against them later. In any event, when a company suddenly starts hemorrhaging high-level people, one can only assume that damaging news will follow.

I think it’s becoming pretty clear that, while there are certainly Democrat voters (e.g., all of my high school classmates from my long-ago youth in San Francisco), the Democrat party that’s been winning elections and controlling policy for the past many years may well be an illusion. I’ve long suspected that many of the votes have more than a whiff of the graveyard about them.

And now, with the DOGE revelations about how Democrat people and organizations were using taxpayer money as their personal slush funds—and the news that many of the organizations instantly collapsed when the money flow stopped—it seems to me that the Democrat party is effectively over. It was held together by corruption and, with the corruption exposed, it’s just melting away.

https://www.americanthinker.com/blog/2025/03/actblue_the_democrat_party_s_fundraising_engine_is_in_deep_trouble.html