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The federal agency claims the company’s practices amount to antitrust activity, a new salvo in the government’s scrutiny of health care consolidation that has led to higher prices.After vowing to tackle consolidation in the health care industry, the Federal Trade Commission filed an antitrust lawsuit on Thursday that challenged the growing practice of private-equity firms backing companies that amass medical practices and dominate local markets.The suit targeted a large doctors’ group that operates anesthesia practices in several states, claiming the group and the private equity firm advising and financing it were consolidating doctors’ groups in Texas so they could raise prices and increase their profits.The agency brought the civil lawsuit in federal court against U.S. Anesthesia Partners and Welsh, Carson, Anderson & Stowe, a private-equity firm in New York.“These tactics enabled USAP and Welsh Carson to raise prices for anesthesia services — raking in tens of millions of extra dollars for these executives at the expense of Texas patients and businesses,” said Lina M. Kahn, the chair of the F.T.C., in a statement. “The F.T.C. will continue to scrutinize and challenge serial acquisitions, roll-ups and other stealth consolidation schemes that unlawfully undermine fair competition and harm the American public.”The case is significant because it focuses on a business strategy that has become increasingly common in health care. Private equity firms have been helping companies to buy more doctors’ practices in various medical specialties, and those purchases have allowed them to control a large share of certain local markets.The suit is also unusual because it was also brought against the private equity investor, which now owns a minority stake in U.S. Anesthesia Partners, and not just the company.A recent study from researchers at the Petris Center at the University of California, Berkeley, and the Washington Center for Equitable Growth, a progressive think tank in Washington, found that private equity-funded consolidation had led to price increases in gastroenterology, dermatology and other medical specialties.The F.T.C. has said it considers this type of health care merger to be an enforcement priority, a sign that this case may be the first of several scrutinizing the growth of private equity in the industry. The firms have argued that their businesses do not violate federal antitrust law.The suit argues that Welsh Carson and U.S. Anesthesia Partners have expanded their reach across Texas with an explicit goal of using market share to raise prices its doctors and nurses would be paid by insurers.Brian Regan, the head of Welsh Carson’s health care group who sat on the board of U.S. Anesthesia Partners, was quoted in the lawsuit as telling lenders who were financing a key deal that the firm planned to “build a platform with national scale by consolidating practices with high market share in a few key markets” and to improve “negotiating leverage” with insurers.After learning of the strategy, an executive in a practice the firm bought in Austin, Texas, responded, “Awesome! Cha-ching,” according to the suit.The suit also accused U.S. Anesthesia Partners of conspiring with another large anesthesia company to stay out of its markets in Texas. The name of that company was redacted from the legal filing.Two of the largest acquisitions in U.S. Anesthesia Partners’ history were previously reviewed and approved by the F.T.C.Welsh Carson and U.S. Anesthesia Partners disputed the F.T.C.’s claims and said they would fight the lawsuit.“The F.T.C.’s civil complaint is based on flawed legal theories and a lack of medical understanding about anesthesia, our patient-oriented business model and our level of care for patients in Texas,” said Dr. Derek Schoppa, a Texas physician and board member of U.S. Anesthesia Partners, in a statement.The company said its commercial prices in Texas had only “increased modestly over the years,” remaining “essentially” flat after being adjusted for inflation.Amy Stevens, a spokeswoman for Welsh Carson, said the private equity firm was “disappointed” by the suit. “Unfortunately, this is consistent with the series of recent lawsuits that the F.T.C. has filed using litigation to pursue radical policy theories,” she said in a statement. “We are confident we will prevail.”Fiona Scott Morton, a professor of economics at Yale and the former chief economist for the Justice Department’s antitrust division, said the case highlighted how many small mergers could have the same effect as a large one.“If each individual transaction is small but there’s lots of them, you end up with a cumulative effect,” she said. “It’s important not to get caught up in evaluating one transaction at a time and missing the forest for the trees.”

While millions of people have undergone LASIK eye surgery since it became commercially available in 1989, patients sometimes develop cataracts later in life and require new corrective lenses to be implanted in their eyes. With an increasing number of intraocular lens options becoming available, scientists have developed computational simulations to help patients and surgeons see the best options.
In a study in the Journal of Cataracts & Refractive Surgery, researchers from the University of Rochester created computational eye models that included the corneas of post-LASIK surgery patients and studied how standard intraocular lenses and lenses designed to increase depth of focus performed in operated eyes. Susana Marcos, the David R. Williams Director of the Center for Visual Science and the Nicholas George Professor of Optics and of Ophthalmology at Rochester, says the computational models that use anatomical information of the patient’s eye provide surgeons with important guidance on the expected optical quality post-operatively.
“Currently the only pre-operative data used to select the lens is essentially the length and curvature of the cornea,” says Marcos, a coauthor of the study. “This new technology allows us to reconstruct the eye in three dimensions, providing us the entire topography of the cornea and crystalline lens, where the intraocular lens is implanted. When you have all this three-dimensional information, you’re in a much better position to select the lens that will produce the best image at the retinal plane.”
The future of optical coherence tomography
Marcos and her collaborators from the Center for Visual Science, as well as Rochester’s Flaum Eye Institute and Goergen Institute for Data Science, are conducting a larger study to quantify in three dimensions the eye images using the optical coherence tomography quantification tools they’ve developed to find broader trends. They are using machine-learning algorithms to find relationships between pre- and post-operation data, providing parameters that can inform the best outcomes.
Additionally, they have developed technology that can help patients see for themselves what different lens options will look like.
“What we see is not strictly the image that is project on the retina,” says Marcos. “There is all the visual processing and perception that comes in. When surgeons are planning the surgery, it is very difficult for them to convey to the patients how they are going to see. A computational, personalized eye model tells which lens is the best fit for the patient’s eye anatomy, but patients want to see for themselves.”
With an optical bench, the researchers use technology originally developed for astronomy, such as adaptive optics mirrors and spatial light modulators, to manipulate the optics of the eye as an intraocular lens would. The approach allows Marcos and her collaborators to perform fundamental experiments and collaborate with industry partners to test new products. Marcos also helped develop a commercial headset version of the instrumentation called SimVis Gekko that allows patients to see the world around them as if they had had the surgery.
In addition to studying techniques to help treat cataracts, the researchers are applying their methods to study other major eye conditions, including presbyopia and myopia.

A gene sequencing method called ribosome profiling has expanded our understanding of the human genome by identifying previously unknown protein coding regions.
Also known as Ribo-seq, this method allows researchers to get a high-resolution snapshot of protein production in cells.
Ribo-seq has the potential to advance cancer research, but many of the discoveries enabled by Ribo-seq provide an untraditional view of where and how protein production might happen.
As such, scientists must first verify these regions code for proteins.
A tool for cancer research
“Ribo-seq has garnered major interest for use in studying protein production in cancer cells to identify a specific abnormal proteins as targets for immunotherapy or other treatment approaches,” said John Prensner, M.D., Ph.D. a pediatric neuro-oncologist at the University of Michigan Health C.S. Mott Children’s Hospital and researcher with the Michigan Medicine Chad Carr Pediatric Brain Tumor Center.
Immunotherapy treatment activates the patient’s own immune system to destroy cancer cells. It lacks the toxic side effects of chemotherapy like nausea, vomiting and hair loss, making it a highly desirable treatment for patients that qualify.

Artemisinin-based combination therapies (ACTs) are the globally-accepted first-line treatments for malaria — a mosquito-borne disease caused by the Plasmodium falciparum parasite that annually kills around 600,000 people, mostly children. Yet resistance to ACTs by P. falciparum has emerged in recent years in Africa, threatening their effectiveness.
To slow this resistance and reduce treatment failures, an international research team led by Penn State investigated various drug policy interventions in Rwanda, where artemisinin resistance was first reported in 2020. Among other strategies, the team found that next-generation interventions such as triple ACTs (TACTs) — which combine an artemisinin derivative with two partner drugs or which use a sequential course of one ACT formulation, followed by a different ACT formulation — resulted in treatment failure counts that were at least 81% lower. Their results were published today (Sept. 21) in Nature Medicine.
“The malaria drug-resistance situation in Rwanda is urgent,” said Robert Zupko assistant research professor of biology, Penn State. “If we let things continue as is, artemisinin-resistant genotypes will begin to dominate by the end of this decade. Of the two dozen interventions we evaluated, we found that TACTs — a treatment yet to be approved to treat malaria but undergoing clinical evaluations — was projected to minimize both treatment failures and drug resistance.”
Dr. Aline Uwimana, head of case management at the Rwanda Biomedical Center and a senior author on the study, cautioned that waiting for optimal therapies may not be the best approach as resistance could soon be widespread.
“Of the available and approved approaches that we evaluated for this study, there were several options using multiple first-line therapies, or MFT, that we could begin to put into place next year,” Uwimama said. “This is likely the most feasible choice in the near term.”
Under an MFT strategy, multiple therapies are deployed at once and different patients get treated with different drugs.
According to Maciej Boni, professor of biology, Penn State, the current situation in Rwanda is a repeat or “three-peat” of past malaria drug failures. Since the 1940s, multiple antimalarial drugs have been deployed worldwide, but the eventual development of drug resistance in the malaria parasite forced the withdrawal of all of them. In the 1990s, new artemisinin drugs were trialed and found to be effective, and by 2005 they were recommended worldwide, he said. The following year, Rwanda adopted the ACT artemether-lumefantrine (AL) as its first-line therapy for malaria, but by 2020, a mutation, known as ‘pfkelch13 R561H’, was shown to have emerged over the previous decade; the R561H mutation is associated with delayed clearance of the parasite in the presence of AL.

Tumor vaccines can help the body fight cancer. These vaccines alert the patient’s immune system to proteins that are carrying cancer-typical alterations. Physicians and cancer researchers from Heidelberg and Mannheim have now treated adult patients with advanced midline gliomas, difficult-to-treat brain tumors, with a peptide vaccine for the first time. The vaccine mimicked a mutational change in a histone protein typical of this type of cancer. The vaccine proved to be safe and induced the desired immune responses directed against the brain tumor.
Crucial for the success of cancer vaccinations are protein structures by which the immune cells can recognize the cancer — and which are not present (or only to a small extent) on healthy cells. Mutations in the tumor genome often lead to protein structures that are altered in a way typical of cancer.
Diffuse midline gliomas are among the most aggressive brain tumors. They usually occur in children and young adults near the brain stem and are therefore difficult to access surgically. Chemotherapy or radiation therapy also have limited effectiveness. In this type of cancer, mutations characteristically occur in the gene encoding histone H3 (H3K27M), a packaging protein of DNA. The mutation gives rise to a novel protein structure — a so-called neoepitope — that can be recognized as foreign by the patient’s immune system.
“Such mutations, which occur in identical form in many patients, are rare in cancer. They literally lend themselves to the development of tumor vaccines because they occur in all cancer cells, since the mutated histone is causative for the development of midline gliomas. This means that vaccination against the mutated protein gets to the root of the problem,” explains Michael Platten, Director of the Department of Neurology at the University Medical Center Mannheim and Head of Department at the German Cancer Research Center (DKFZ).
The researchers led by Katharina Sahm and Michael Platten synthetically reconstructed the section of the histone H3 protein with the characteristic mutation. Using this peptide, they were able to curb the growth of H3K27M-mutated tumors in a mouse model. Encouraged by the results, the team decided to test the mutation-specific vaccine produced at the University of Tübingen in patients in a phase I-trial*, which is still ongoing.
In parallel, the physicians, together with colleagues from Munich, Berlin, Bonn and Münster, treated eight adult patients with the peptide vaccine in time-limited individual curative trials. These patients, who could not be enrolled in the trial protocol, suffered from diffuse midline gliomas with H3K27M mutation that progressed after standard therapy. Some of the affected individuals received therapy with immune checkpoint inhibitors in addition to tumor vaccination.
No serious side effects were observed in any of the vaccinated patients. Five of the eight treated patients developed specific immune responses against the mutant protein, which were dominated by CD4 T-helper cells. In one of the patients who had shown a strong immune response, the tumor regressed completely and she remained tumor-free for 31 months.

After a traumatic experience, most people recover without incident, but some people — between 2% and 10%- develop posttraumatic stress disorder (PTSD), a mental health condition that can cause debilitating symptoms of anxiety due to emotional dysregulation. PTSD symptoms are present in up to 40% of trauma survivors in the acute aftermath of trauma, but full-blown PTSD develops in only a small subset of cases. Early identification of those at risk is critical for both early treatment and possible prevention.
A new study led by Israel Liberzon, MD, at Texas A&M University, aimed to do just that. The study appears in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, published by Elsevier.
Researchers have long understood that PTSD involves altered brain processing in areas associated with emotion processing and modulation, including the amygdala, insula, and prefrontal cortex. But, it has remained unclear when the PTSD-associated differences arise. In this work, the researchers collected brain scans from 104 survivors of trauma — usually a car accident — at 1, 6, and 14 months after the accident. By looking at brain activity so soon after the trauma, the researchers hoped to identify predictors of who would be more at risk or resilient to developing chronic PTSD.
Dr. Liberzon said of the findings, “In this largest-to-date, prospective study of early post-trauma survivors, greater activation in right inferior frontal gyrus, a region linked to cognitive control and emotional reappraisal, predicts better recovery from early PTSD symptoms. These findings highlight the key roles of cortical/cognitive regions in regulation of fear and in PTSD development.”
Importantly, the researchers saw changes in the patients’ brain activity change over time, reflecting an ongoing, perhaps pathological process.
Cameron Carter, MD, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, said of the study, “These findings highlight the key role that the prefrontal cortex may play in conferring resilience to the harmful effects of trauma, through its function representing contextual information and regulating emotional responses.”
Dr. Liberzon added, “Understanding brain circuits linked to the progression of PTSD from an acute to a chronic condition is critical for understanding its pathophysiology, and eventually for the development of mechanism-informed treatment. The results might also help clinicians to start identifying and treating early trauma survivors at greater risk of developing chronic PTSD a year after the traumatic event.”

A Ludwig Cancer Research study has shown that combining adoptive T cell therapy (ACT) with an innovative, personalized cancer vaccine under development at the Lausanne Branch of the Ludwig Institute for Cancer Research can benefit patients with late-stage, drug-resistant ovarian cancer.
Researchers led by Ludwig Lausanne’s Sara Bobisse, Alexandre Harari, Lana Kandalaft and Director George Coukos analyzed responses to the combination therapy of 18 patients with advanced ovarian cancer who had previously participated in a clinical trial evaluating a therapeutic regimen that incorporated the personalized cancer vaccine. In the current study — which, like the previous one, was done in partnership with researchers at the University of Pennsylvania — patients received an infusion of their own vaccine-primed, circulating immune cells (specifically, T cells), followed by multiple periodic doses of their personalized vaccines.
The researchers report today in Nature Cancer that combining the personalized cancer vaccine with ACT yielded control of the disease within three months in 12 of 17 patients. The treatment was also found to be safe and relatively well tolerated.
“This treatment could not eliminate tumors, but it did provide considerable benefit to many of the patients, who had all undergone extensive treatment prior to enrolling in the trial and were in the late stages of the disease,” said Kandalaft.
Though not a double-blind, placebo-controlled trial, the study’s findings suggest the benefits of the combination therapy were significant: the median overall survival time of patients who completed the regimen was 14.2 months, compared to a median historical survival of six months or less for comparable patients receiving fourth- and fifth-line chemotherapy.
“It was also exciting to be able to suggest, through sophisticated immunologic analysis, the mechanisms underlying treatment efficacy,” said Harari.
Ovarian cancer, like many other malignancies, has so far proved largely resistant to immunotherapies, most of which harness killer T cells, which destroy sick and infected cells. Ovarian cancer cells do, however, express neoantigens, which are randomly mutated proteins that can activate anti-tumor T cell responses. Multiple approaches are today being developed at Ludwig Lausanne and elsewhere to target neoantigens for cancer immunotherapy. The personalized dendritic cell vaccine, developed over the past dozen years under the leadership of Kandalaft and Coukos, is one of them.

In the new study, researchers developed a process to systematically identify areas of agreement and disagreement among three individual state-of-the-art air-quality datasets: satellite observations, a simulation developed at Northwestern and sensors from Microsoft Research’s Project Eclipse.
Although one or two datasets identified multiple areas as NO2 hotspots, all three datasets consistently flagged Chicago’s West Side as having elevated NO2 pollution. The West Side also has more Black, Hispanic and Latinx residents compared to the rest of the city, highlighting the disproportionate pollution and health burdens shouldered by these communities.
The study was published today in Environmental Research Letters.
“The three tools that we explored sometimes identified different areas of elevated pollution from one another,” said Northwestern’s Anastasia Montgomery, who led the study. “That doesn’t necessarily mean the tools are not working. It could be that they are looking at different things. However, in areas where we found agreement between the datasets, we have greater confidence that NO2 pollution is significantly high. The three different tools we used all pointed to the West Side as an area where pollution is significantly elevated relative to the Chicago average.”
“High spatial resolution air quality data has the potential to reveal inequitable exposure to pollution by identifying localized hotspots,” said Northwestern’s Daniel Horton, the study’s senior author. “Using this science-backed evidence, residents can advocate for change, and government officials can develop more targeted policies. By combining and improving tools to identify these hotspots, we can ensure that mitigation efforts serve the most affected communities.”
Horton is an assistant professor of Earth and planetary sciences at Northwestern’s Weinberg College of Arts and Sciences, where he leads the Climate Change Research Group. Montgomery recently completed her Ph.D. as a member of Horton’s research group.
To conduct the study, the researchers compared how each dataset quantified NO2. A byproduct of fossil-fuel combustion engines, NO2 is incredibly harmful to human health. Chronic exposure to these fumes can lead to bronchitis, pneumonia, asthma and even premature death. And under certain conditions, when NO2 interacts with sunlight, it can also produce ground-level ozone, which is linked to childhood asthma and other respiratory health issues.

To make a gene-editing tool more precise and easier to control, Rice University engineers split it into two pieces that only come back together when a third small molecule is added.
Researchers in the lab of chemical and biomolecular engineer Xue Sherry Gao created a CRISPR-based gene editor designed to target adenine ⎯ one of the four main DNA building blocks ⎯ that remains inactive when disassembled but kicks into gear once the binding molecule is added.
Compared to the intact original, the split editor is more precise and stays active for a narrower window of time, which is important for avoiding off-target edits. Moreover, the activating small molecule used to bind the two pieces of the tool together is already being used as an anticancer and immunosuppressive drug.
According to a study published in Nature Communications, the tool developed by Gao and collaborators performed well both in human cell cultures and in living mice, where it accurately edited a single base pair on a target gene. Given that single base-pair mutations ⎯ also known as point mutations ⎯ are responsible for thousands of diseases, the split editor could have broad therapeutic applications.
“This tool has the potential to correct nearly half of the disease-causing point mutations in our genome,” said Hongzhi Zeng, the lead author of the study and a graduate student in the Gao lab. “However, current adenine base editors are in a constant ‘on’ state, which could lead to unwanted genome changes alongside the desired correction in the host genome.
“Our team set out to create a much improved version that can be turned on or off as needed, providing an unparalleled level of safety and accuracy.”
To install an ‘on/off’ switch, the researchers broke the adenine base editor into two separate proteins that remain inactive until sirolimus (previously known as rapamycin) is added ⎯ a molecule discovered in 1972 in soil bacteria on Easter Island that is approved by the U.S. Food and Drug Administration for use in cancer therapies and other medical procedures.

Researchers have shown in a mouse model and lab cultures that a compound derived from hops reduces the abundance of a gut bacterium associated with metabolic syndrome.
The findings, published today in the journal Microbiome, are important because an estimated 35 percent of the U.S. adult population suffers from the syndrome, a common and serious condition linked with cognitive dysfunction and dementia as well as being a major risk factor for cardiovascular disease and type 2 diabetes.
A diet high in saturated fat results in chronic low-grade inflammation in the body that in turn leads to the development of metabolic syndrome.
Patients are considered to have metabolic syndrome if they have at least two of the following: abdominal obesity, high blood pressure, high blood sugar, low levels of “good” cholesterol, and high levels of triglycerides.
OSU researchers for years have been studying the potential health benefits of xanthohumol, a chemical found in hops, and its derivatives including tetrahydroxanthohumol. The latter is commonly abbreviated to TXN, the former to XN.
XN is a polyphenol, a type of abundant organic compound existing in plants and used for millennia by practitioners of traditional medicine. XN is one of the flavonoids, natural products found in fruits, vegetables, grains, bark, roots, stems, flowers, tea and wine that are well known for their positive effects on health.
In the most recent study, Andrey Morgun of the OSU College of Pharmacy, Natalia Shulzhenko of the Carlson College of Veterinary Medicine and Adrian Gombart of the Linus Pauling Institute and College of Science demonstrated that TXN can combat metabolic syndrome by reducing the population of Oscillibacter species within the gut microbiome.