Publisher Health

Of the many contemporary conveniences often taken for granted in developed countries, modern sanitation may be among the most important. A new study suggests that wastewater infrastructure may provide societal benefits far beyond the dramatic improvements in community hygiene.
The research highlights a technique known as Wastewater-based Epidemiology (WBE), in which samples of municipal wastewater can be used as a diagnostic tool to explore a surprisingly broad range of community-wide health indices.
In research published in the peer-reviewed, high-impact journal Environment International, Rolf Halden and Sangeet Adhikari, describe how WBE can be used to help achieve a number of ambitious objectives outlined in the United Nations Sustainable Development Goals.
The study, the largest and most comprehensive assessment of wastewater infrastructure around the world to date, examines wastewater treatment facilities in 129 countries, serving over a third of the world’s population. It is also the first study to propose and evaluate the feasibility of using WBE to measure progress toward achieving several UN sustainability objectives.
The WBE technique can be used to assess factors influencing community-wide health, from the consumption of local diets, alcohol, illicit drugs and tobacco to exposure to hazardous chemicals, pharmaceuticals, personal care products, viruses, and antibiotic-resistant microbes.
In addition to infectious disease monitoring, new disease biomarkers detectable in wastewater are being developed, enabling researchers to mine samples for evidence of afflictions including diabetes, heart disease and cancer. The study emphasizes the dire need for the expansion of wastewater services to large swaths of the globe where such resources are still lacking.

Researchers at Columbia University Mailman School of Public Health and colleagues evaluated whether dietary fiber intake was associated with a decrease in inflammation in older adults and if fiber was inversely related to cardiovascular disease. The results showed that total fiber, and more specifically cereal fiber but not fruit or vegetable fiber, was consistently associated with lower inflammation and lower CVD incidence. Until now there had been limited data on the link between fiber and inflammation among older adults, who have higher levels of inflammation compared with younger adults. The study findings are published in JAMA Network Open.
The research includes data from a large and well-characterized prospective cohort of elderly individuals, with detailed data on dietary intake, inflammation, and incidence of CVD. The research confirmed previously observed associations between dietary fiber and CVD and extended those investigations to include the source of the fiber, the relationship of fiber with multiple inflammatory markers, and to test whether inflammation mediated the relationship between dietary fiber and CVD.
Of the 4125 adults enrolled in the Cardiovascular Health Study from 1989 to 1990 participants received a food frequency questionnaire that was administered to those without prevalent CVD at enrollment and then were followed up visits for development CVD (stroke, myocardial infarction, and atherosclerotic cardiovascular death) through June 2015. Blood samples were assessed for markers of inflammation.
“Higher intakes of dietary fiber is associated with lower CVD risk. A common hypothesis has been that higher fiber intakes reduce inflammation, subsequently leading to lower CVD risk” said Rupak Shivakoti, PhD, assistant professor of epidemiology at Columbia Mailman School. ‘With findings from this study, we are now learning that one particular type of dietary fiber — cereal fiber — but not fruit or vegetable fiber was associated with lower inflammation. With findings from this study we now are learning that cereal fiber has the potential to reduce inflammation and will need to be tested in future interventional studies.”
Although there are data to suggest that fiber in general might have anti-inflammatory effects by improving gut function, modifying diet and satiety (eg, reduced fat and total energy intake), and improving lipid and glucose profile metabolism, why cereal fiber but not vegetable or fruit fiber is associated with lower inflammation is not clear and warrants further investigation, noted Shivakoti. Further, he notes that it is not clear whether cereal fiber per se or other nutrients in foods rich in cereal fiber are driving the observed relationships.
“Additionally, we learned that inflammation had only a modest role in mediating the observed inverse association between cereal fiber and CVD,” observed Shivakoti. “This suggests that factors other than inflammation may play a larger role in the cereal fiber-associated reduction in CVD and will need to be tested in future interventions of specific populations.
Co-authors are from Columbia University Mailman School of Public Health; University of Washington; Brigham and Women’s Hospital; Harvard Medical School; Boston Veterans Healthcare; Larner College of Medicine at the University of Vermont; San Francisco Veterans Affairs Health Care System; University of California-San Francisco; Kaiser Permanente Washington Health Research Institute; New York Academy of Medicine; Beth Israel Deaconess Medical Center; and Harvard Chan School of Public Health,
The research was supported by the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, and the Eunice Kennedy Shriver National Institute of Child Health and Human Development.
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Materials provided by Columbia University’s Mailman School of Public Health. Note: Content may be edited for style and length.

The number of potential therapeutic targets on the surfaces of human proteins is much greater than previously thought, according to the findings of a new study in the journal Nature.
A ground-breaking new technique developed by researchers at the Centre for Genomic Regulation (CRG) in Barcelona has revealed the existence of a multitude of previously secret doors that control protein function and which could, in theory, be targeted to dramatically change the course of conditions as varied as dementia, cancer and infectious diseases.
The method, in which tens of thousands of experiments are performed at the same time, has been used to chart the first ever map of these elusive targets, also known as allosteric sites, in two of the most common human proteins, revealing they are abundant and identifiable.
The approach could be a game changer for drug discovery, leading to safer, smarter and more effective medicines. It enables research labs around the world to find and exploit vulnerabilities in any protein — including those previously thought ‘undruggable’.
“Not only are these potential therapeutic sites abundant, there is evidence they can be manipulated in many different ways. Rather than simply switching them on or off, we could modulate their activity like a thermostat. From an engineering perspective, that’s striking gold because it gives us plenty of space to design ‘smart drugs’ that target the bad and spare the good,” explains André Faure, postdoctoral researcher at the CRG and co-first author of the paper.
Proteins play a central role in all living organisms and carry out vital functions such as providing structure, speeding up reactions, acting as messengers or fighting disease. They are made of amino acids, folding into countless different shapes in three-dimensional space. The shape of a protein is crucial for its function, with just one mistake in an amino acid sequence resulting in potentially devastating consequences for human health.

Researchers have identified the complete series of 10 factors that regulate the development of brain cell types in the visual system of fruit flies — including in what order these neurons develop. The findings, published in Nature, open new avenues of research to understand how brain development evolved in different animals and hold clues for regenerative medicine.
The human brain is composed of 80 billion neurons. These nerve cells differ in their form, function, and connectivity with other neurons to form neural networks. This complexity allows the brain to perform its many functions, from controlling speech and vision to storing memories and generating emotions.
While scientists have identified many types of neurons, how this complexity arises during the brain’s development is a central question for developmental neurobiology and regenerative medicine.
“Knowing how the human brain develops could allow us in the future to repeat these developmental processes in the lab to generate specific types of neurons in a Petri dish — and potentially transplant them in patients — or to trigger neuronal stem cells in living organisms to generate and replace missing neurons,” said Claude Desplan, Silver Professor of Biology at NYU and the study’s senior author.
Because studying the human brain is an incredibly complex endeavor, researchers rely on model organisms, such as mice and flies, to explore the intricate mechanisms involved in the brain’s processes. In both vertebrates, like mice and humans, and invertebrates, like flies, different types of neurons are generated sequentially as the brain develops, with specific types of neurons being generated first and other types being generated later from the same progenitor stem cell.
The mechanism by which neural stem cells produce different neurons over time is called temporal patterning. By expressing different molecules — termed temporal transcription factors, or tTFs — that regulate the expression of specific genes in each window of time, neural stem cells produce different neurons.

An international team of researchers has created a series of brain charts spanning our entire lifespan — from a 15 week old fetus to 100 year old adult — that show how our brains expand rapidly in early life and slowly shrink as we age.
The charts are the result of a research project spanning six continents and bringing together possibly the largest ever MRI datasets ever aggregated — almost 125,000 brain scans from over a 100 different studies. Although not currently intended for clinical use, the team hopes the charts will become a routine clinical tool similar to how standardised paediatric growth charts are used.
Growth charts have been a cornerstone of paediatric healthcare for over 200 years and are used ubiquitously in clinics to help monitor the growth and development of children in comparison to their peers. A typical growth chart might plot age on the horizontal axis versus height on the vertical axis, but rather than being a single line, it will show a range that reflects the natural variability in height, weight or head circumference.
There are no analogous reference charts for measuring age-related changes in the human brain. The lack of tools for standardised assessment of brain development and aging is particularly relevant to the study of psychiatric disorders, where the differences between conditions and the heterogeneity within them demands instruments that can say something meaningful about a single individual in the way clinical reference charts can, and to conditions such as Alzheimer’s disease that cause degeneration of brain tissue and cognitive decline.
Today’s study, published in Nature, is a major step towards filling this gap. Unlike paediatric growth charts, BrainChart — published on the open access site brainchart.io — covers the whole lifespan, from development in the womb through to old age, and aims to create a common language to describe the variability in brain development and maturation.
The incredible growing and shrinking brain
The brain charts have allowed the researchers to confirm — and in some cases, show for the first time — developmental milestones that have previously only been hypothesised, such as at what age the brain’s major tissue classes reach peak volume and when do specific regions of the brain reach maturity.

The largest ever genetic study of schizophrenia has identified large numbers of specific genes that could play important roles in the psychiatric disorder.
A group of hundreds of researchers across 45 countries analysed DNA from 76,755 people with schizophrenia and 243,649 without it to better understand the genes and biological processes underpinning the condition.
The Psychiatric Genomics Consortium study, led by scientists at Cardiff University, found a much larger number of genetic links to schizophrenia than ever before, in 287 different regions of the genome, the human body’s DNA blueprint.
Furthermore, they showed that genetic risk for schizophrenia is seen in genes concentrated in brain cells called neurons, but not in any other tissue or cell type, suggesting it is the biological role of these cells that is crucial in schizophrenia.
The research team say this global study sheds the strongest light yet on the genetic basis of schizophrenia. It is published today in the journal Nature.
“Previous research has shown associations between schizophrenia and many anonymous DNA sequences, but rarely has it been possible to link the findings to specific genes,” said co-lead author Professor Michael O’Donovan, from the Division of Psychological Medicine and Clinical Neurosciences at Cardiff University.

Most antibiotics are double-edged swords. Besides killing the pathogen they are prescribed for, they also decimate beneficial bacteria and change the composition of the gut microbiome. As a result, patients become more prone to reinfection, and drug-resistant strains are more likely to emerge.
The answer to this problem might be narrow-spectrum antibiotics that kill only one or a few species of bacteria, minimizing the risk of collateral damage. In a recent study, Rockefeller scientists took a close look at one such antibiotic, fidaxomicin, used to treat Clostridium difficile, or C. diff, one of the most common healthcare associated infections. The researchers demonstrated at a molecular level how fidaxomicin selectively targets C. diff while sparing the innocent bacterial bystanders.
The findings, detailed in Nature, might help scientists in the race to develop new narrow-spectrum antibiotics against other pathogens.
“I want people, scientists, and doctors to think differently about antibiotics,” says Elizabeth Campbell, a research associate professor at Rockefeller. “Since our microbiome is crucial to health, narrow-spectrum approaches have an important part to play in how we treat bacterial infections in the future.”
Enigmatically selective
C. diff is a toxin-producing bacterium that can inflame the colon and cause severe diarrhea. It infects about half a million people in the United States, mostly in a hospital setting, and about one in 11 of those over age 65 who die within a month.

Most immunocompromised people with a blood cancer called multiple myeloma benefited from a third dose of COVID-19 vaccines, a promising sign after it was shown that two doses tended to not be sufficient for them. However, some people with multiple myeloma still remained vulnerable and may need a fourth dose or antibody treatments as restrictions lift and new variants emerge, according to a fast-tracked study in Cancer Cell.
“This study is the first to comprehensively capture the immune effect of the third dose of the COVID-19 vaccine in patients with plasma cell disorders and blood cancers like multiple myeloma,” said one of the study’s lead authors, Samir Parekh, MD, Director of Translational Research in Multiple Myeloma at The Tisch Cancer Institute at Mount Sinai and Professor of Medicine (Hematology and Medical Oncology), and Oncological Sciences, at the Icahn School of Medicine at Mount Sinai. “It provides guidance to myeloma patients, who are at risk for severe infection because they may be immunocompromised due to the disease itself and the cancer treatment.”
Mount Sinai’s previous research had shown that breakthrough infections occurred in multiple myeloma patients due to poor or no response to the normal regimen of COVID-19 vaccines, the majority of which were the two-dose mRNA vaccines. These vulnerable patients’ lack of complete protection led to antibody testing and a third vaccine in hopes that this would increase the immune response. This study was important in understanding whether vulnerable patients were adequately protected by the third dose or needed to continue to follow strict social distancing and masking or seek additional vaccines or treatments when available.
In this latest study, blood samples were collected from 476 patients with plasma cell disorders over a period of 15 months and were compared to samples collected from healthy, vaccinated health care workers. The findings showed that the third dose significantly increased the level of antibodies in patients with and without prior COVID-19 infection but levels of COVID-19-fighting antibodies in multiple myeloma patients remained below those observed in healthy people.
Just more than a quarter of the multiple myeloma patients had no detectable antibodies after the standard two doses of the vaccine, but in these patients, 88 percent developed antibodies after a third dose. The third dose also resulted in a significant increase of other immune cells such as T cells and B cells, which also help neutralize COVID-19.
After the third dose, neutralization of the wild-type virus increased in multiple myeloma patients in patients who had minimal or no response to the standard two doses. However, neutralizing titers against the Omicron variant was still lower in myeloma patients as compared to healthy controls. Therefore, a subset of patients may still remain vulnerable to SARS-CoV-2 infection.
“Our findings underscore the need for continued monitoring of immune responses and further research around measures such as additional vaccine doses or passive immunization for individual multiple myeloma patients who may remain vulnerable after third-dose vaccination, especially as COVID-19 restrictions are being lifted worldwide and new waves of viral variants are emerging,” said the study’s other lead author, Viviana A. Simon, MD, PhD, Professor of Microbiology, Infectious Diseases, and Pathology, Molecular and Cell Based Medicine at the Icahn School of Medicine at Mount Sinai.
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Materials provided by The Mount Sinai Hospital / Mount Sinai School of Medicine. Note: Content may be edited for style and length.

Licorice is more than a candy people either love or hate — it may play a role in preventing or treating certain types of cancer, according to researchers at the University of Illinois Chicago.
Gnanasekar Munirathinam and his research team are studying substances derived from the licorice plant Glycyrrhiza glabra to determine if they could be used to prevent or stop the growth of prostate cancer. Munirathinam is an associate professor in the department of biomedical sciences at the College of Medicine Rockford.
A research review into molecular insights of a licorice-derived substance called glycyrrhizin for preventing or treating cancer conducted by Dr. Munirathinam and student researchers suggests further research could lead to specific agents for clinical use.
The journal Pharmacological Research recently published the study titled “Oncopreventive and oncotherapeutic potential of licorice triterpenoid compound glycyrrhizin and its derivatives: Molecular insights.”
“When we look at the research out there and our own data, it appears that glycyrrhizin and its derivative glycyrrhetinic acid have great potential as anti-inflammatory and anti-cancer agents,” Munirathinam said. “More research is needed into exactly how these could best be used to develop therapies, but this appears to be a promising area of cancer research.”
Should everyone go out and eat a bunch of licorice? Probably not, because it may affect blood pressure, interact with certain medications, and cause serious adverse effects, including death, when used excessively. An occasional sweet treat of licorice candy or tea may be better options until more studies can show how to best harness the plant’s benefits.
“Very few clinical trials in humans have been conducted,” Munirathinam said. “We hope our research on prostate cancer cells advances the science to the point where therapies can be translated to help prevent or even cure prostate and other types of cancer.”
College of Medicine Rockford students Rifika Jain, Mohamed Ali Hussein, Preksha Shahagadkar, Shannon Pierce and Chad Martens are co-authors of the review, which was partly supported by the National Institutes of Health (R0CA227218) and Brovember Inc.
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Materials provided by University of Illinois Chicago. Original written by Carrie Foust. Note: Content may be edited for style and length.

Machines can beat the world’s best chess player, but they cannot handle a chess piece as well as an infant. This lack of robot dexterity is partly because artificial grippers lack the fine tactile sense of the human fingertip, which is used to guide our hands as we pick up and handle objects.
Two papers published in the Journal of the Royal Society Interface give the first in-depth comparison of an artificial fingertip with neural recordings of the human sense of touch. The research was led by Professor of Robotics & AI (Artificial Intelligence), Nathan Lepora, from the University of Bristol’s Department of Engineering Maths and based at the Bristol Robotics Laboratory.
“Our work helps uncover how the complex internal structure of human skin creates our human sense of touch. This is an exciting development in the field of soft robotics — being able to 3D-print tactile skin could create robots that are more dexterous or significantly improve the performance of prosthetic hands by giving them an in-built sense of touch,” said Professor Lepora.
Professor Lepora and colleagues created the sense of touch in the artificial fingertip using a 3D-printed mesh of pin-like papillae on the underside of the compliant skin, which mimic the dermal papillae found between the outer epidermal and inner dermal layers of human tactile skin. The papillae are made on advanced 3D-printers that can mix soft and hard materials to create complicated structures like those found in biology.
“We found our 3D-printed tactile fingertip can produce artificial nerve signals that look like recordings from real, tactile neurons. Human tactile nerves transmit signals from various nerve endings called mechanoreceptors, which can signal the pressure and shape of a contact. Classic work by Phillips and Johnson in 1981 first plotted electrical recordings from these nerves to study ‘tactile spatial resolution’ using a set of standard ridged shapes used by psychologists. In our work, we tested our 3D-printed artificial fingertip as it ‘felt’ those same ridged shapes and discovered a startlingly close match to the neural data,” said Professor Lepora
“For me, the most exciting moment was when we looked at our artificial nerve recordings from the 3D-printed fingertip and they looked like the real recordings from over 40 years ago! Those recordings are very complex with hills and dips over edges and ridges, and we saw the same pattern in our artificial tactile data,” said Professor Lepora.
While the research found a remarkably close match between the artificial fingertip and human nerve signals, it was not as sensitive to fine detail. Professor Lepora suspects this is because the 3D-printed skin is thicker than real skin and his team is now exploring how to 3D-print structures on the microscopic scale of human skin.
“Our aim is to make artificial skin as good — or even better — than real skin,” said Professor Lepora.
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Materials provided by University of Bristol. Note: Content may be edited for style and length.