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Her research advanced understanding of the brain and the origins of language — signed and spoken — and shed light on how humans communicate and socialize.Ursula Bellugi, a pioneer in the study of the biological foundations of language who was among the first to demonstrate that sign language was just as complex, abstract and systematic as spoken language, died on Sunday in San Diego. She was 91. Her death, at an assisted living facility, was confirmed by her son Rob Klima.Dr. Bellugi was a leading researcher at the Salk Institute for Biological Studies in San Diego for nearly five decades and, for much of that time, was director of its laboratory for cognitive neuroscience. She made significant contributions in three main areas: the development of language in children; the linguistic structure and neurological basis of American Sign Language; and the social behavior and language abilities of people with a rare genetic disorder, Williams syndrome.“She leaves an indelible legacy of shedding light on how humans communicate and socialize with each other,” Rusty Gage, president of the Salk Institute, said in a statement.Dr. Bellugi’s work, much of it done in collaboration with her husband, Edward S. Klima, advanced understanding of the brain and the origins of language, both signed and spoken.American Sign Language was first described as a true language in 1960 by William C. Stokoe Jr., a professor at Gallaudet University, the world’s only liberal arts university devoted to deaf people. But he was ridiculed and attacked for that claim.Dr. Bellugi and Dr. Klima, who died in 2008, demonstrated conclusively that the world’s signed languages — of which there are more than 100 — were actual languages in their own right, not just translations of spoken languages.Dr. Bellugi, who focused on American Sign Language, established that these linguistic systems were passed down, in all their complexity, from one generation of deaf people to the next. For that reason, the scientific community regards her as the founder of the neurobiology of American Sign Language.The couple’s work led to a major discovery at the Salk lab: that the left hemisphere of the brain has an innate predisposition for language, whether spoken or signed. That finding gave scientists fresh insight into how the brain learns, interprets and forgets language.“This was a critical discovery for deaf people, as it verified that our language is treated equally by the brain — just as we must be treated equally by society,” Roberta J. Cordano, the president of Gallaudet, said in a statement.Until then, sign languages were regarded disparagingly either as crude pantomime, with no rules, or as broken English, and deaf children were discouraged from learning to sign. The couple’s work contributed to a wider acceptance of A.S.L. as a language of instruction and helped empower deaf people as the Deaf Pride movement developed in the 1980s.Dr. Bellugi with the celebrated deaf actress Marlee Matlin in 2009.Family photoAnother subject that Dr. Bellugi and her husband studied was Williams syndrome. She sought to understand how the disorder, in which a set of about 20 genes is missing from one copy of a chromosome, changed the brain and ultimately shaped behavior.Her body of work, the Salk Institute said in a profile of Dr. Bellugi, “helped paint a picture of the biology humans use to interact with the world around us.”Ursula Herzberger was born on Feb. 21, 1931, in Jena, in central Germany, a center of science and technology. With Hitler on the rise, her family fled Germany in 1934 and eventually settled in Rochester, N.Y. There, her father, Max Herzberger, a mathematician and physicist, became head of Eastman Kodak’s optical research laboratories, a job arranged for him by Albert Einstein, his friend and former teacher in Berlin.Mr. Herzberger went on to develop a special lens that resolved the color distortion in glass. Ursula’s mother, Edith (Kaufmann) Herzberger, was an artist.Ursula attended Antioch College in Ohio, where she majored in psychology and graduated in 1952. She married Piero Bellugi, an Italian composer and conductor, in 1953; they had two sons before divorcing in 1959.Interested in psychology and language, she moved to Cambridge, Mass., where she became a research assistant to Roger Brown, an eminent psychologist at Harvard and the Massachusetts Institute of Technology, who was studying how young children acquire language. Soon she was studying at Harvard, where she earned a doctor of education degree in 1967 while raising her sons as a single mother. She also took courses at M.I.T., where one of her teachers was Dr. Klima.When they married, she changed her name legally to Bellugi-Klima but continued to use Bellugi professionally. They moved west when he began teaching at the University of California, San Diego. She started in 1968 at the Salk Institute, a 10-minute walk from her husband’s campus, where she also taught. She later taught at San Diego State University.At the time, San Diego was a hotbed of linguistic research, revolving largely around Dr. Bellugi and Dr. Klima, as well as colleagues who had come from Harvard and M.I.T. She attracted a parade of research assistants and made a point of hiring many who were deaf.Over the years, Dr. Bellugi received multiple awards. She was elected to the National Academy of Sciences in 2007. She retired from Salk in 2017 at 86.She co-wrote hundreds of papers and several books, some of them with her husband. Their best-known book was “The Signs of Language” (1979), written with 10 associates. It was the first comprehensive study of the grammar and psychology of signed languages and was hailed by the Association of American Publishers as the year’s “most outstanding book in the behavioral sciences.”In addition to her son Rob, Dr. Bellugi is survived by her sister, Ruth Rosenberg; her brother, Hans Herzberger; four grandchildren; and five great-grandchildren. Another son, David Bellugi, died in 2017.

Federal funding for biomedical research has a “ripple effect” of stimulating new studies even beyond the original purposes of a grant and may provide unexpected benefits, a new study suggests.
Researchers used a unique dataset to get a never-before-seen view of how science funding is spent and the results it produces.
The findings, published today (April 22, 2022) in the journal Science Advances, showed that funding of research by the National Institutes of Health mostly goes to hiring people who work on the projects funded by grants.
But these people — which includes staff and trainees like graduate students — go on to do more than just work on the grants for which they were hired, said Enrico Berkes, co-author of the study and postdoctoral researcher in economics at The Ohio State University.
“We see a great increase in productivity in publications directly linked to a grant but also in new studies that go beyond it,” Berkes said. “There is this ripple effect where people supported by the grant also produce other quality work.”
And the biomedical researchers who are the focus of this study produced more clinical research as the result of receiving more funding — studies directly related to patient care and health, said study co-author Bruce Weinberg, professor of economics at Ohio State.

A UCLA-led team of researchers studying the effect of the monoclonal antibody Leronlimab on long COVID-19 may have found a surprising clue to the baffling syndrome, one that contradicts their initial hypothesis. An abnormally suppressed immune system may be to blame, not a persistently hyperactive one as they had suspected.
The study, which was funded by Leronlimab maker CytoDyn Inc. and conducted by researchers either employed by or serving as consultants to the company, will be published online April 22 in the peer reviewed journal Clinical Infectious Diseases.
“While this was a small pilot study, it does suggest that some people with long COVID may actually have under-active immune systems after recovering from COVID-19, which means that boosting immunity in those individuals could be a treatment,” said senior author Dr. Otto Yang, a professor of medicine, division of infectious diseases, and of microbiology, immunology and molecular genetics at the David Geffen School of Medicine at UCLA.
COVID-19 is known to be caused by hyperactive immune responses against SARS-CoV-2 resulting in damage to lungs and other organs, and sometimes what is known as a “cytokine storm” that overwhelms the individual, which could lead to severe illness and death.
In a subset of persons who recover from the initial illness, various symptoms persist, such as fatigue, mental haziness, and shortness of breath, which can be debilitating and last for months. This is generally classified as long COVID, although symptoms vary widely and this syndrome is probably not a single disease entity. Limited understanding of its causes, however, makes finding ways to treat the condition particularly difficult.
Many scientists have suggested that persistence of immune hyperactivity after COVID-19 is a major contributor. Working under this theory, the researchers conducted a small exploratory trial of Leronlimab — an antibody that attaches to an immune receptor called CCR5 that is involved in inflammation — on 55 people with the syndrome.
Participants were randomly assigned to receive weekly injections of the antibody or a saline placebo for eight weeks, over which time they tracked any changes in 24 symptoms associated with long COVID, which also included loss of smell and taste, muscle and joint pain, and brain fog.
The researchers originally thought that blocking CCR5 with the antibody would dampen the activity of an overactive immune system after COVID-19 infection.
“But we found just the opposite,” Yang said. “Patients who improved were those who started with low CCR5 on their T cells, suggesting their immune system was less active than normal, and levels of CCR5 actually increased in people who improved. This leads to the new hypothesis that long COVID in some persons is related to the immune system being suppressed and not hyperactive, and that while blocking its activity, the antibody can stabilize CCR5 expression on the cell surface leading to upregulation of other immune receptors or functions.”
The findings, the researchers write, “suggests a complex role for CCR5 in balancing inflammatory and anti-inflammatory effects, e.g. through T regulatory cells,” although the results need to be confirmed in a larger, more definitive study.
Study co-authors are Norman Gaylis of Arthritis & Rheumatic Disease Specialties in Aventura, Florida; Angela Ritter of the Center for Advanced Research & Education in Gainesville, Georgia; Scott Kelly, Nader Pourhassan, and Christopher Recknor of CytoDyn Inc. in Vancouver, Washington; and Meenakshi Tiwary, Jonah Sacha, and Scott Hansen of Oregon Health & Science University.
Sacha, Hansen, and Yang are paid consultants for CytoDyn. Gaylis is on CytoDyn’s scientific board with stock options.

Over the past 15 years, public health authorities have downgraded recommendations for the prostate-specific antigen (PSA) test as a screening tool to reduce the overdiagnosis and overtreatment of men with low-grade prostate cancer. Now, researchers from Weill Cornell Medicine have found that while these efforts have been effective, the incidence of higher-grade disease and metastasis at diagnosis have risen. The research was published March 22 in the Journal of the National Cancer Institute.
“To our knowledge, this is the first study to demonstrate nationally that low-grade prostate cancer is no longer the most commonly diagnosed type of prostate cancer,” said senior author Dr. Jim Hu, the Ronald P. Lynch Professor of Urologic Oncology at Weill Cornell Medicine and director of the LeFrak Center for Robotic Surgery at NewYork-Presbyterian/Weill Cornell Medical Center. “One of the weaknesses of PSA/prostate cancer screening was that it led to over-detection of indolent cancers that would not harm men, subjecting them to anxiety and future testing.”
In 2012, the U.S. Preventative Services Task Force (USPSTF) recommended against screening all men with the PSA test, concluding that the benefits of the test, which measures levels of a protein often overproduced in prostate cancer cells, did not outweigh the risks. Then in 2018, the USPSTF issued a revision to include shared decision making for the PSA test for men aged 55 to 69 years, reflecting emerging evidence of longer-term benefits and widespread adoption of active surveillance after detection of low-risk disease.
For their study, Dr. Hu and colleagues identified more than 438,000 men with newly diagnosed prostate cancer between 2010 and 2018 using a nationally representative database. They examined trends in the incidence of prostate cancer by disease risk using several measures. One measure was the Gleason Grade, a pathology score based on the microscopic appearance of the prostate cells, determined at biopsy and after radical prostatectomy, a procedure in which the entire prostate is surgically removed. Additional measures were PSA level and presence of metastasis at diagnosis. They also investigated whether increasing rates of obesity or the advent of newer diagnostic tools such as pre-biopsy magnetic resonance imaging (MRI) and biomarkers might explain incidence trends.
The analysis revealed a significant decrease in the incidence of the lowest-risk prostate cancer, Gleason Grade 1 (GG1), falling from 52 to 26 cases per 100,000 men across all age groups. Further, the proportion of GG1 found on pathology in men who had a radical prostatectomy decreased from 32 to 10 percent. However, metastases rates at diagnosis increased from 3.0 percent to 5.2 percent over the same period. Halting PSA testing appeared to be the primary driver of these trends.
“The fact that only 10 percent of radical prostatectomy specimens demonstrate low-grade prostate cancer indicates that even when low grade cancer is diagnosed, it is being treated much less frequently, said Dr. Hu. “This demonstrates that there has been acceptance of active surveillance, also known as monitoring with curative intent, among doctors and patients nationally.”
“It is encouraging to see that urologists in the United States have moved away from overutilization of radical therapies for the management of low-risk prostate cancer,” added first author Dr. Leonardo Borregales.
Public health authorities should consider implementing risk-stratified screening, such as MRI or biomarkers, continuing to minimize overdiagnosis and avoid biopsy in men with low-risk prostate cancer while addressing the rising trends of high-grade and metastatic prostate cancer, the authors concluded.
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For more than two decades, University of Alabama at Birmingham researcher Susan Bellis, Ph.D., has studied how the addition of sialic acid to various proteins increases cancer resistance and oncogenicity.
One of the enzymes that transfers sialic acid to target glycoproteins is ST6Gal-I, and it has attracted increased attention in the cancer field in recent years. ST6Gal-I is upregulated in breast cancer, gliomas, pancreatic cancer, prostate cancer and ovarian cancer, and it plays a key role in tumor progression and metastasis.
Metastasis is the spread of a tumor to other parts of the body, through the migration of tumor cells. Cells move themselves through cell adhesion mechanics — integrins at the cell membrane can attach themselves to a surface, acting as tiny anchors. The cell’s cytoskeleton then pushes the front of the cell forward to establish new anchors, and the now-rear anchors let go. Such cell mobility is vital in embryogenesis, development and wound healing. However, in cancer, cell migration can be deadly.
UAB researcher Alexa Mattheyses, Ph.D., is able to study cell adhesion mechanics directly, using DNA tension-gauge tether probes displaying an integrin ligand and attached to a coverslip surface. When a cell binds to the tension probe and exerts force, the DNA duplex separates, generating a fluorescent signal whose changes are monitored by sophisticated fluorescence microscopy. Two years ago, the Mattheyses lab showed that activation of the epidermal growth factor receptor, or EGFR, by its ligand — epidermal growth factor, or EGF — modulated integrin forces and attenuated the mechanical threshold for integrin tension and formation of focal adhesions. Focal adhesions are the mechanical linkages, the anchors, to the extracellular matrix outside the cell. They are also the place where mechanical force and regulatory signals are transmitted. A cell-surface receptor like EGFR transfers a signal from its external ligand to the interior of the cell.
The Mattheyses and Bellis labs collaborated to expand their EGFR work by looking at the effect of adding sialic acid to EGFR on cell mechanics. In a study published in the Journal of Biological Chemistry that included tests of three types of human cancer cells, they report that ST6Gal-I-mediated sialylation of the EGFR modulates cell mechanics and enhances invasion by the cancer cells.
“Given the widespread impact of sialylation and the prognostic value of ST6Gal-I expression, an improved understanding of how ST6Gal-I-mediated sialylation alters cell mechanics may open the door to a new range of cancer therapeutics,” Mattheyses said. “Our results help bridge the mechanistic gap in the field, while demonstrating the potential value in oncogenic mechanosignaling as a therapeutic target.”
“Clinically, increased glycoprotein sialylation has been associated with carcinogenesis, and ST6Gal-I promotes vital cancer hallmarks such as self-renewal, invasiveness, proliferative potential and resistance to cell death,” Mattheyses said. “While mechanical changes in cells and tissues also contribute to malignancy and metastasis, the underlying mechanisms by which these changes promote cancer have remained understudied.”

While cancer is a genetic disease, the genetic component is just one piece of the puzzle — and researchers need to consider environmental and metabolic factors as well, according to a research review by a leading expert at the University of Alberta.
Nearly all the theories about the causes of cancer that have emerged over the past several centuries can be sorted into three larger groups, said David Wishart, professor in the departments of biological sciences and computing science. The first is cancer as a genetic disease, focusing on the genome, or the set of genetic instructions that you are born with. The second is cancer as an environmental disease, focusing on the exposome, which includes everything your body is exposed to throughout your life. The third is cancer as a metabolic disease, focusing on the metabolome, all the chemical byproducts of the process of metabolism.
The metabolic perspective hasn’t had much research until now, but it’s gaining the interest of more scientists, who are beginning to understand the metabolome’s role in cancer.
The genome, exposome and metabolome operate together in a feedback loop as cancer develops and spreads.
According to the data, heritable cancers account for just five to 10 per cent of all cancers, Wishart said. The other 90 to 95 per cent are initiated by factors in the exposome, which in turn trigger genetic mutations.
“That’s an important thing to consider, because it says that cancer isn’t inevitable.”
The metabolome is critical to the process, as those genetically mutated cancer cells are sustained by the cancer-specific metabolome.

A promo for an upcoming Fox show describes a testosterone “calamity” among American men, along with an unlikely treatment.Are you a man worried about your testosterone levels? Hoping to give them a boost? Tucker Carlson, the Fox News host, has a solution.A promotional video for a new installment in a video series by Mr. Carlson describes a “total collapse of testosterone levels in American men,” positing an explanation for what he and many conservatives see as a creeping loss of masculinity in today’s society.Chock-full of oiled, shirtless men performing vaguely masculine tasks, like turning over giant tires and throwing a javelin, the video has already been widely remarked upon on social media for its bizarre erotic imagery.But one shot in particular stands out: a naked man atop a rock pile, limbs outflung, exposing his genitals to the red light issuing from what appears to be a waist-high air purifier. Something very like the theme from “2001: A Space Odyssey” plays in the background.This is the treatment proposed by Mr. Carlson’s “documentary”: Revive your underperforming testicles with red light, in particular a device made by a little known company called Joovv.A leading endocrinologist says — no surprise — the whole thing is ridiculous, and not just because of the man receiving light therapy atop a pile of stone slabs in the dead of night.First, there is precious little evidence that testosterone “levels are declining by roughly 10 percent per decade, completely changing the way people are at the most fundamental level,” as Mr. Carlson has said.Studies examining changes in testosterone over time are challenging for several reasons, including difficulties in recruiting large populations of normal subjects, daily circadian changes in testosterone, and differences in testing methods over time, noted Dr. John Amory, an expert on male reproductive health at the University of Washington.Mr. Carlson and Fox News did not respond to requests for comment.Tied to the anxiety over testosterone is another hotly disputed assertion: that sperm counts have been declining among men in the Western world for decades. Huge numbers of studies have been done, and there is no scientific consensus on the scope of the problem or whether it exists at all.So what’s all this about bathing one’s testicles in red light?Scott Nelson, co-founder of Joovv, said in an email, “The published data around light therapy and testosterone production is pretty light, but the limited evidence is fairly compelling.” He provided a link to a study on the Joovv website, apparently unpublished, reporting that red light worked best to boost testosterone in four men who were also on a ketogenic diet.Dr. Amory was not impressed. “Obviously, doing two interventions — red light and diet — at once in a non-randomized, non-blinded, underpowered study with unclear methods isn’t of much use to understanding cause and effect,” he said. “Biological plausibility here is also very weak.”The bottom line, for readers anxious about the decline of American virility: “In the absence of any evidence of benefit from clinical trials, I wouldn’t currently recommend this as a treatment for testosterone or symptoms of low testosterone,” Dr. Amory said.“It’s notable that there is a long history of pseudoscientific treatments for low testosterone that have not proven to be useful over time,” he added.

Pancreatic cancer has a significantly poor prognosis; therefore, the development of effective treatments is an unmet clinical need. The major drawback in this field was the lack of useful model animals, which delayed the establishment of markers for early diagnosis and therapeutic options. The research group established an effective carcinogenesis method with wild-type rats by selectively introducing oncogenes into the pancreas, using the pancreas-targeted hydrodynamic gene delivery method that has been developed by the group.
The research group of Professor Kamimura in Niigata University have established a novel pancreatic carcinogenesis model in wild-type rats utilizing the pancreas-targeted selective hydrodynamic gene delivery method developed by their research group.
“The gene human pancreatic cancer-related gene transfer of the KRASG12D efficiently developed the pancreatic cancer,” says Prof. Kamimura. KRASG12D-induced pancreatic intraepithelial neoplasia lesions showed malignant transformation in the main pancreatic duct at four weeks and developed acinar-to-ductal metaplasia, which led to pancreatic ductal adenocarcinoma within five weeks and the gene combination of KRASG12D and YAP enhanced these effects.
In addition, the combination of oncogenes revealed the metastatic tumors in the liver, lymph nodes, etc., and invasive growth to the surrounding organ and tissues, mimicking the clinical course of human pancreatic cancer. The pancreas-targeted hydrodynamic gene delivery showed its efficacy in developing novel animal models and is promising methods for the organ specific gene therapy. Prof. Kamimura concluded that this pancreatic cancer model will speed up pancreatic cancer research for novel treatments and biomarkers for early diagnosis.
Glossary
1. Hydrodynamic gene delivery method
This method introduces a gene from a blood vessel of a target organ using physical force (water pressure) to express the target protein in the organ cells. Authors have reported the usefulness of this method for gene therapy for the liver cirrhosis etc., and developed organ-selective gene transfer methods such as for the liver and pancreas. and verified the procedure in large animals for clinical application (Kamimura K, et al. Mol Ther, 2009; Kamimura K, et al. Mol Ther, 2010; Yokoo T & Kamimura K, et al. Gene Ther, 2013; Kamimura K, et al. Mol Ther Nucleic Acids, 2013; Abe H & Kamimura K, et al. Mol Ther Nucleic Acids, 2016; Kobayashi Y & Kamimura K, et al. Mol Ther Nucleic Acids, 2016; Ogawa K & Kamimura K, et al. Mol Ther Nucleic Acids, 2017)
2. KRAS gene
A member of the ras family of oncogenes, which transmits cell proliferation signals to the cell nucleus and promotes cell proliferation. Mutations in this gene (e.g. KRASG12D) play an important role in promoting carcinogenesis.
3. YAP gene
The YAP (yes-associated protein) gene is one oncogene that functions in various human cancers. Involved in cell proliferation as a transcription factor, the YAP is also reported to be inhibited by the Hippo signaling pathway, which enables controlling organ size and suppressing tumors.
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High blood pressure, or hypertension, is a very common condition that can arise from physical activity, stress, or certain disorders. Unfortunately, persistent hypertension can cause long-lasting changes in the structure of vascular smooth muscle cells (the cells making up the walls of blood vessels) through a process called “vascular remodeling.” If left unchecked, this restructuring can stiffen arterials walls, which lose their ability to adjust their size appropriately. This, in turn, leads to arteriosclerosis and increases the risk of cerebrovascular disease.
Why and how hypertension triggers vascular remodeling is not entirely clear. Scientists have shown that macrophages, a type of white blood cells that kill foreign bodies, are involved in the transformation. Specifically, the macrophages accumulate within blood vessel walls from outside the vessels and cause chronic inflammation. However, the underlying mechanism that orchestrates this process remains unknown.
Against this backdrop, researchers from Japan and Canada, in a new study, recently investigated a mechanism known as “excitation-transcription (E-T) coupling” in vascular smooth muscle cells. By unveiling the mysteries behind the E-T coupling in these cells through experiments spanning single cells to whole organisms, they successfully linked the E-T coupling mechanism with vascular remodeling. The study, published in the Proceedings of the National Academy of Sciences (PNAS),was led by Junior Associate Professor Yoshiaki Suzuki, Hisao Yamamura and Yuji Imaizumi from Nagoya City University, Japan, and Gerald W. Zamponi and Wayne R. Giles from University of Calgary, Canada.
Various types of cells are known to undergo E-T coupling. In neurons, for example, an excitation in the form of calcium ions (Ca2+) entering the cell through calcium channels activates certain transcription factors and enzymes. These, in turn, trigger the transcription of various genes. Meanwhile, although E-T coupling also occurs in vascular smooth muscle cells after an influx of Ca2+ under high pressure, not much was known about how it happens, what genes are triggered, and the role it plays in our bodies.
The researchers sought to answer these questions by focusing on caveolae, small structures resembling depressions widely present on the cell’s membrane. Through detailed experiments in individual cells, cell cultures, and live mice, the team found that a specific protein complex found in caveolae is a key player in E-T coupling in vascular smooth muscle cells.
They proved that this complex, referred to as Cav1.2/CaMKK2/CaMK1a, is formed within caveolae and both CaMKK2 and CaMK1a are directly activated by Ca2+ entering through Cav1.2 when subjected to certain stimuli, such as high pressure. Moreover, they showed that this complex activates a signaling pathway that phosphorylates a transcription factor called CREB, which ultimately leads to an increased transcription of multiple genes.
By taking a detailed look at the genes promoted by E-T coupling and observing their effects when blocked or amplified, the researchers made some important discoveries. Firstly, some of these genes were related to chemotaxis, the phenomenon by which cells movement is triggered and directed by chemical stimuli. This helped explain the accumulation of macrophages in blood vessel walls from outside the vessels.
Additionally, these genes promoted the remodeling of the “medial” layer of arteries, where vascular smooth muscle cells reside and control blood flow through contraction and expansion. “Taken together, our results explain how E-T coupling caused by high pressure in vascular smooth muscle cells can modulate macrophage migration and subsequent inflammation, altering the vascular structure,” explains Dr. Suzuki.
The findings of this study have important implications regarding anti-hypertension drugs. For one, they explain why medications like nicardipine, a classic calcium channel blocker, prevents vascular remodeling and the progression of arteriosclerosis. This not only fills an important knowledge gap in medicine but also presents several potential drug targets for treating or preventing vascular remodeling, such as the constituents of the Cav1.2/CaMKK2/CaMK1a complex.
“About 40 million people suffer from hypertension in Japan alone, and are at high risk of stroke, end-stage renal failure, and vascular dementia,” says Dr. Suzuki, “Understanding the mechanisms behind arteriosclerosis is, therefore, very important for reducing the incidence, progression, and recurrence of cerebrovascular diseases and extend healthy life expectancy.”

Micropollutants in water often are hormones that accumulate in the environment and may have negative impacts on humans and animals. Researchers of Karlsruhe Institute of Technology (KIT) and Leibniz Institute of Surface Engineering (IOM) in Leipzig have now developed a process for the photocatalytic degradation of these pollutants when they flow through polymer membranes. It is presented in Nature Nanotechnology. Irradiation with light triggers a chemical reaction, as a result of which steroid hormones are degraded on the membranes coated with titanium dioxide.
Wherever people are living, hormones used in e.g. contraceptives or agriculture enter the wastewater. Steroid hormones, such as sex hormones and corticosteroids, may accumulate in the environment and adversely affect humans and animals, as they impair behavioral development and fertility. Sex hormones, for instance, may cause male fish to develop female sexual characteristics. It is therefore important to remove hormones, together with other micropollutants, from the wastewater before they enter the natural water cycle again, from which drinking water is extracted. “Supplying people with clean drinking water presently is one of the most important challenges worldwide,” says Professor Andrea Iris Schäfer, Head of KIT’s Institute for Advanced Membrane Technology (IAMT). “Micropollutants represent a big threat for our future, as they impair our fertility and brain function.”
Inspired by Solar Cell Technology
For years, Schäfer has studied water processing by nanofiltration. For this purpose, she uses polymer membranes with nanometer-sized pores. However, nanofiltration requires high pressure and, hence, much energy. Moreover, micropollutants may accumulate in the polymer membrane materials and gradually enter the filtered water. Even if the pollutants are separated completely, a flow of concentrated pollutants may develop and require further treatment.
Inspired by solar cell technology, the field of work of Professor Bryce S. Richards from KIT, Schäfer had the idea to coat polymer membranes with titanium dioxide and to design photocatalytic membranes. Photocatalytically active titanium dioxide nanoparticles are applied to microfiltration membranes, whose pores are somewhat larger than in nanofiltration. Irradiation with light then triggers a chemical reaction, as a result of which steroid hormones are degraded on the membranes. Together with her team at IAMT and colleagues from the Leibniz Institute of Surface Engineering (IOM), Leipzig, Schäfer has now realized her idea and presented the new technology in Nature Nanotechnology.
Catalyst for Water
“We have developed a catalyst for water,” Schäfer summarizes her work. Using the photocatalytic polymer membranes, steroid hormones were removed in the continuous flow mode down to the analytical detection limit of 4 ng/l. In fact, the concentrations measured were very close to 1 ng/l, the limit given in the new Drinking Water Guideline of the WHO. The researchers are now optimizing their technology by reducing the time needed and energy consumed. Moreover, their focus lies on using natural light. In particular, their research is aimed at degrading other pollutants by photocatalysis, such as industrial chemicals like perfluoro-alkylated and polyfluorinated substances (PFAS) or pesticides, such as glyphosate. Another goal is to upscale the technology.
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