Walking With a Partner is Great But Might Slow You Down (Psychology)

If you walk with your spouse or partner on a regular basis, you might want to speed up. Or tell them to.

A new study by Purdue University nursinghealth and kinesiology, and human development and family studies researchers shows that couples often decreased their speed when walking together. Speed further decreased if they were holding hands.

The study looked at walking times and gait speeds of 141 individuals from 72 couples. The participants ranged from age 25-79 and were in numerous settings, including clear or obstacle-filled pathways, walking together, walking together holding hands and walking individually.

“In our study, we focused on couples because partners in committed relationships often provide essential support to promote one another’s healthy lifestyle behaviors, including exercise,” says Melissa Franks, associate professor of human development and family studies.

Libby Richards, associate professor of nursing, says, “We were hoping that there would not be a reduction in speed where partners walked together. We hoped that slower partners would speed up to match the faster partner, but that was not the case. However, it’s important to note that any physical activity or walking – regardless of speed – is better than none.”

Richards says it is common for people to walk or exercise with a spouse, partner or friend, as it increases one’s likelihood to be active, especially as Americans are encouraged to meet a goal of 150 minutes of moderate activity every week.

“If someone substantially slows down when they are walking with someone else, that could negate some of the health benefits recognized if they walked alone at a faster pace,” Richards says.

Shirley Rietdyk, professor of health and kinesiology who specializes in biomechanics, says there are many reasons to measure gait speed.

“Gait speed is important to measure because it is related to overall health. Typical gait speed is predictive of fall risk, functional ability, disability recovery and mortality,” Rietdyk says.

“Common exercise interventions, including strength, coordination and multimodal training, are all effective in increasing gait speed. These interventions can also delay the onset of slower gait speed and help slow the loss of gait speed. No one type of training is better than the other, so do the activity you are most likely to stick with.”

While walking is one of the easiest activities, people tend to walk slower as they get older and may have to find other fitness routines to stay active.

“Older adults who are more active tend to maintain their gait speed,” Rietdyk says. “In other words, slower gait speed is not an inevitable aspect of aging. Older adults who walk slower tend to have poorer health and lower functional status.”

The article appeared in a recent edition of Gait & Posture.

HyeYoung Cho, a recent Ph.D. graduate of Purdue’s Department of Health and Kinesiology; Anna Forster, a Ph.D. student in Purdue’s School of Nursing; and Sharon Christ, associate professor of human development and family studies, were on the research team, all from Purdue’s College of Health and Human Sciences. All research team members are members of Purdue’s Center on Aging and the Life Course. The Purdue Center for Families and the American Nurses Foundation funded the study.

Featured image: A new study from researchers at Purdue University’s College of Health and Human Sciences explores the benefits of walking with a partner for exercise – only if each person goes at the faster pace. (Markus Distelrath/Pixabay)


Reference: HyeYoung Cho, Anna Forster, Sharon L. Christ, Melissa M. Franks, Elizabeth A. Richards, Shirley Rietdyk, Changes to gait speed when romantic partners walk together: Effect of age and obstructed pathway, Gait & Posture, Volume 85, 2021, Pages 285-289, ISSN 0966-6362, https://doi.org/10.1016/j.gaitpost.2021.02.017. (https://www.sciencedirect.com/science/article/pii/S0966636221000552)


Provided by Purdue University


About Purdue University

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COVID-19 Patients Can Be Categorized Into Three Groups (Medicine)

Phenotypes I, II and III show distinct characteristics and show adverse, normal and favorable clinical outcomes respectively

In a new study, researchers identify three clinical COVID-19 phenotypes, reflecting patient populations with different comorbidities, complications and clinical outcomes. The three phenotypes are described in a paper published this week in the open-access journal PLOS ONE 1st authors Elizabeth Lusczek and Nicholas Ingraham of University of Minnesota Medical School, US, and colleagues.

COVID-19 has infected more than 18 million people and led to more than 700,000 deaths around the world. Emergency department presentation varies widely, suggesting that distinct clinical phenotypes exist and, importantly, that these distinct phenotypic presentations may respond differently to treatment.

In the new study, researchers analyzed electronic health records (EHRs) from 14 hospitals in the midwestern United States and from 60 primary care clinics in the state of Minnesota. Data were available for 7,538 patients with PCR-confirmed COVID-19 between March 7 and August 25, 2020; 1,022 of these patients required hospital admission and were included in the study. Data on each patient included comorbidities, medications, lab values, clinic visits, hospital admission information, and patient demographics.

Most patients included in the study (613 patients, or 60 percent) presented with what the researchers dubbed “phenotype II.” 236 patients (23.1 percent) presented with “phenotype I,” or the “Adverse phenotype,” which was associated with the worst clinical outcomes; these patients had the highest level of hematologic, renal and cardiac comorbidities (all p<0.001) and were more likely to be non-White and non-English speaking. 173 patients (16.9 percent) presented with “phenotype III,” or the “Favorable phenotype,” which was associated with the best clinical outcomes; surprisingly, despite having the lowest complication rate and mortality, patients in this group had the highest rate of respiratory comorbidities (p=0.002) as well as a 10 percent greater risk of hospital readmission compared to the other phenotypes. Overall, phenotypes I and II were associated with 7.30-fold (95% CI 3.11-17.17, p<0.001) and 2.57-fold (95% CI 1.10-6.00, p=0.03) increases in hazard of death relative to phenotype III.

The authors conclude that phenotype-specific medical care could improve COVID-19 outcomes, and suggest that future research is needed to determine the utility of these findings in clinical practice.

The authors add: “Patients do not suffer from COVID-19 in a uniform matter. By identifying similarly affected groups, we not only improve our understanding of the disease process, but this enables us to precisely target future interventions to the highest risk patients.”

Funding: 1. NIH National Heart, Lung, and Blood Institute T32HL07741 (NEI) 2. This research was supported by the Agency for Healthcare Research and Quality (AHRQ) and Patient-Centered Outcomes Research Institute (PCORI), grant K12HS026379 (CJT) and the National Institutes of Health’s National Center for Advancing Translational Sciences, grant UL1TR002494. 3. NIH National Heart, Lung, and Blood Institute T32HL129956 (JP, LS) The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Featured image: Clinical outcomes by phenotype. Chord diagram illustrates the prevalence of clinical outcomes (% observed) for the three clinical phenotypes. Abbreviations: ICU (intensive care unit); Vent (mechanical ventilation); Readmit (readmission to hospital or ICU); ECMO (extracorporeal membrane oxygenation). Lusczek et al, 2021, PLOS ONE (CC-BY 4.0, https://creativecommons.org/licenses/by/4.0/)


Reference: Lusczek ER, Ingraham NE, Karam BS, Proper J, Siegel L, Helgeson ES, et al. (2021) Characterizing COVID-19 clinical phenotypes and associated comorbidities and complication profiles. PLoS ONE 16(3): e0248956. https://doi.org/10.1371/journal.pone.0248956


Provided by PLoS

Study Identifies Possible COVID-19 Drugs — Including Several That Are FDA-approved (Medicine)

Promising candidates include widely used transplant-rejection drug cyclosporine

A team led by scientists in the Perelman School of Medicine at the University of Pennsylvania has identified nine potential new COVID-19 treatments, including three that are already approved by the Food and Drug Administration (FDA) for treating other diseases.

The team, whose findings were published in Cell Reports, screened thousands of existing drugs and drug-like molecules for their ability to inhibit the replication of the COVID-19-causing coronavirus, SARS-CoV-2. In contrast to many prior studies, the screens tested the molecules for anti-coronaviral activity in a variety of cell types, including human airway-lining cells that are similar to the ones principally affected in COVID-19.

Of the nine drugs found to reduce SARS-CoV-2 replication in respiratory cells, three already have FDA approval: the transplant-rejection drug cyclosporine, the cancer drug dacomitinib, and the antibiotic salinomycin. These could be rapidly tested in human volunteers and COVID-19 patients.

The experiments also shed light on key processes the coronavirus uses to infect different cells and found that the antiviral drug remdesivir, which has an FDA Emergency Use Authorization for treating COVID-19, does appear to work against the virus in cell-culture tests on respiratory cells, whereas hydroxychloroquine does not.

“Our discoveries here suggest new avenues for therapeutic interventions against COVID-19, and also underscore the importance of testing candidate drugs in respiratory cells,” said co-senior author Sara Cherry, PhD, a professor of Pathology and Laboratory Medicine and scientific director of the High-Throughput Screening (HTS) Core at Penn Medicine.

Study collaborators included co-senior authors David Schultz, PhD, technical director of the HTS Core, and Holly Ramage, PhD, assistant professor of microbiology & immunology at Thomas Jefferson University.

Although great progress has been made in the development of vaccines and treatments for the SARS-CoV-2 coronavirus, there is still much room for improvement. In the United States, the only antiviral COVID-19 treatments that have received FDA Emergency Use Authorization — remdesivir and several anti-SARS-CoV-2 antibody preparations — are expensive and far from 100 percent effective.

For their screening project, Cherry and colleagues assembled a library of 3,059 compounds, including about 1,000 FDA-approved drugs and more than 2,000 drug-like molecules that have shown activity against defined biological targets. They then tested all of these for their ability to significantly inhibit SARS-CoV-2 replication in infected cells, without causing much toxicity.

Initially, they performed antiviral screens using cell types they could grow easily in the lab and infect with SARS-CoV-2, namely African Green Monkey kidney cells, and a cell line derived from human liver cells. With these screens, they identified and validated several compounds that worked in the monkey kidney cells, and 23 that worked in the human liver cells. Hydroxychloroquine, which is used as a malaria drug, and remdesivir, were effective in both cell types.

Since SARS-CoV-2 is mainly a respiratory virus and is thought to initiate infections via airway-lining cells, the researchers sought a respiratory cell type that they could infect experimentally with the virus. They eventually identified a suitable cell line, Calu-3, that is derived from human airway-lining cells. They used these respiratory-derived cells to test the antiviral compounds identified through the human liver cell screen, and found that only nine had activity in the new cells. The nine did not include hydroxychloroquine. (Remdesivir worked in the Calu-3 cells but was not included in the list because it is already in use against COVID-19.)

By identifying different sets of drugs that work in different cell types, the researchers also shed light on the mechanisms SARS-CoV-2 uses to gain entry to cells. The findings suggest that in kidney and liver cells, the virus uses a mechanism that can be disrupted, for example, by hydroxychloroquine; yet the virus appears to use a different mechanism in respiratory cells, thus explaining hydroxychloroquine’s lack of success in those cells — and in COVID-19 clinical trials.

The nine antivirals active in respiratory cells did include salinomycin, a veterinary antibiotic that is also being investigated as an anticancer drug; the kinase enzyme inhibitor dacomitinib, an anticancer drug; bemcentinib, another kinase inhibitor now being tested against cancers; the antihistamine drug ebastine; and cyclosporine, an immune suppressing drug commonly used to prevent the immune rejection of transplanted organs.

The study highlights cyclosporine as particularly promising, as it appears to works against SARS-CoV-2 in respiratory and non-respiratory cells, and via two distinct mechanisms: inhibiting cell enzymes called cyclophilins, which the coronavirus hijacks to support itself, and suppressing the potentially lethal inflammation of severe COVID-19.

“There may be important benefits to the use of cyclosporine in hospitalized COVID-19 patients, and ongoing clinical trials at Penn and elsewhere are testing that hypothesis,” Cherry said.

The research was supported by funding from the National Institutes of Health (5R01AI140539, 1R01AI1502461, R01AI152362), the Mark Foundation, the Dean’s Innovation Fund, the Laddie and Linda Montague Foundation, the Burroughs Wellcome Fund, Mercatus, and the Bill and Melinda Gates Foundation.

Featured image: Graphical abstract by Dittmar et al.


Reference: Mark Dittmar, Jae Seung Lee, Kanupriya Whig, Elisha Segrist, Minghua Li, Brinda Kamalia, Lauren Castellana, Kasirajan Ayyanathan, Fabian L. Cardenas-Diaz, Edward E. Morrisey, Rachel Truitt, Wenli Yang, Kellie Jurado, Kirandeep Samby, Holly Ramage, David C. Schultz, Sara Cherry, Drug repurposing screens reveal cell-type-specific entry pathways and FDA-approved drugs active against SARS-Cov-2, Cell Reports, 2021, 108959, ISSN 2211-1247, https://doi.org/10.1016/j.celrep.2021.108959. (https://www.sciencedirect.com/science/article/pii/S2211124721002734)


Provided by University of Pennsylvania School of Medicine

Unusual Mechanism in Rare Mutation Associated With Alzheimer’s Uncovered (Neuroscience)

A novel mechanism has been identified that might explain why a rare mutation is associated with familial Alzheimer’s disease in a new study by investigators at the University of Chicago. The paper, published on April 2 in the Journal of Experimental Medicine, characterizes a mutation located in a genetic region that was not previously thought be pathogenic, upending assumptions about what kinds of mutations can be associated with Alzheimer’s Disease.

Alzheimer’s, a neurodegenerative disease that currently affects more than 6 million Americans, has been characterized by the accumulation of A? peptides into plaques in the spaces between neurons in the brain. These A? peptides are generated when a larger precursor protein, APP, is cleaved into smaller fragments as APP transits through different cellular compartments.

Most mutations that have previously been associated with Alzheimer’s lie either within or just next to a region of the APP gene that codes for the eventual A? peptide fragment. However, while the mutation studied by the research team is located in the APP gene, itis quite far from the area where previously characterized mutations are found. The mutation, S198P, was first found in two patients affected by Alzheimer’s, and raised eyebrows due to its distance from known disease-associate mutations.

“This mutation, which is not in the region of APP that codes for the A? fragment, was so interesting because it was so far away from where all the other mutations are normally located,” said senior author Sangram Sisodia, PhD, the Thomas Reynolds Sr. Family Professor of Neurosciences at UChicago, “Thus it was not clear how this mutation might be contributing to the pathology of the disease.”

The investigators, led by Xulun Zhang, Ph.D., a Research Professional in the Sisodia lab, examined how S198P could affect A? peptide production by studying both cultured cells and mice. They found that the presence of the S198P mutation resulted in both cultured cells and mice having elevated levels of A? peptides. To further understand why S198P caused elevated A? levels, the authors looked at different steps of the APP-to-A? production pipeline.

Using cultured cells, the authors found that S198P causes APP to fold more quickly, allowing A? peptides to be produced from mature APP more quickly than from APP that did not contain the S198P mutation. “The rapid folding enhances the egress of APP through the cellular compartments where A? is made, allowing faster production of the A? peptide” said Sisodia. Mice harboring S198P also had more plaques causes by A? accumulation, reinforcing the likelihood that the mutation does indeed contribute to disease.

However, like with many other mutations, the presence of S198P is not a guarantee that Alzheimer’s will develop. “This variant is only partially penetrant,” said Sisodia, meaning that not every person with S198P will go on to develop Alzheimer’s. Similar to mutations in the breast cancer genes BRCA1/2, S198P influences only the probability that an affected person will develop Alzheimer’s.

“Geneticists would argue that this is not a pathogenic mutation because you can find this mutation in unaffected people, but this is a complex disease and studying these rare variants uncovers new biology,” said Sisodia.

The fact that S198P is located so far away from previously characterized mutations underscores that there is much to still be understood about Alzheimer’s. “A lot of mutations that have been described for the past 20 years have been dismissed because they don’t look like they follow the normal rules. We need to pay attention to these rare variants because they open up new areas of investigation to completely decipher this disease,” said Sisodia.

Though effective treatments for Alzheimer’s still remain in development, Sisodia believes his group’s findings argue for a renewed focus on A? peptides. “Failures in clinical trials have led some people to think that maybe A? has nothing to do with this disease, but these results clearly support a role for A? in disease pathogenesis. I hope this revives people’s notions about the importance of A? in Alzheimer’s.”

The identification of S198P’s mechanism has led Sisodia to plan to go back to other overlooked mutations and investigate them as well. “There are all these other rare variants that were seemingly benign according to other people, but we know from clinical studies that they too drive Alzheimer’s pathology and clinical phenotypes,” said Sisodia. “We figured out S198P, great! Now let’s move on to all these other variants!”

The study, “An APP ectodomain mutation outside of the Aβ domain promotes Aβ production in vitro and deposition in vivo,” was supported by the Cure Alzheimer’s Fund and the JPB Foundation. Additonal authors include Can Zhang, Dmitry Prokopenko, Yingxia Liang, Sherri Y. Zhen, and Rudolph E Tanzi of Massachusetts General Hospital, and Ian Weigle, Weinong Han, and Manish Aryal of the University of Chicago.


Reference: Xulun Zhang, Can Martin Zhang, Dmitry Prokopenko, Yingxia Liang, Sherri Y. Zhen, Ian Q. Weigle, Weinong Han, Manish Aryal, Rudolph E. Tanzi, Sangram S. Sisodia; An APP ectodomain mutation outside of the Aβ domain promotes Aβ production in vitro and deposition in vivo. J Exp Med 7 June 2021; 218 (6): e20210313. doi: https://doi.org/10.1084/jem.20210313


Provided by University of Chicago Medical Center

Experimental Therapy For Parasitic Heart Disease May Also Help Stop COVID-19 (Medicine)

By blocking human enzyme cathepsin L, chemical inhibitor K777 reduces coronavirus’ ability to infect cell lines; clinical trials are underway

James McKerrow, MD, PhD, dean of the Skaggs School of Pharmacy and Pharmaceutical Sciences at University of California San Diego, has long studied neglected tropical diseases — chronic and disabling parasitic infections that primarily affect poor and underserved communities in developing nations. They’re called “neglected” because there is little financial incentive for pharmaceutical companies to develop therapies for them.

One of these neglected diseases is Chagas disease, the leading cause of heart failure in Latin America, which is spread by “kissing bugs” carrying the parasite Trypanosoma cruzi. These parasites produce an enzyme called cruzain that helps them replicate and evade the human immune system. McKerrow’s research team looks for inhibitors of cruzain — small molecules that might form the basis for new anti-parasitic medicines. One particularly effective cruzain inhibitor is called K777.

Then, in the spring of 2020, the COVID-19 pandemic began to sweep through the United States. Researchers quickly reported that SARS-CoV-2, the coronavirus that causes COVID-19, can’t dock on and infect human cells unless a human enzyme called cathepsin L cleaves the virus’ spike protein.

And it just so happens that cathepsin L looks and acts a lot like cruzain.

In a study published March 31, 2021 by ACS Chemical Biology, McKerrow and team show that low concentrations of K777 inhibit cathepsin L can reduce SARS-CoV-2’s ability to infect four host cell lines, without harming the cells.

“Since K777 inhibits a human enzyme, not the virus itself, it’s our hope that it’s less likely the virus will evolve resistance against it,” said McKerrow, co-senior author of the study with Thomas Meek, PhD, of Texas A&M University.

K777 wasn’t equally effective in all cell lines. That’s likely because not all cell lines produced the same amount of cathepsin L or the same amount of ACE2, the host cell receptor that the virus’ spike protein uses to latch onto cells after it’s cleaved by cathepsin L. The inhibitor was best at preventing SARS-CoV-2 infection in the cells that produced the most cathepsin L and ACE2.

The cell lines tested were derived from African green monkey kidney epithelium, human cervical epithelium and two types of human lung epithelium. While an important research tool, cell lines such as these are not necessarily representative of patients. They are easy to grow and manipulate in research laboratories because they are cancer cells, but that also means their molecular features likely differ from the average person’s healthy lung or cervical cells.

“We were surprised at just how effective K777 is in blocking viral infection in the lab,” McKerrow said. “Yet under usual circumstances it would be impractical and unlikely that we ourselves would be able to move the compound so quickly into clinical trials. We’re fortunate that an ‘entrepreneur-in-residence’ program here at UC San Diego has helped bridge that gap.”

Selva Therapeutics, a privately held biotechnology company, has licensed K777 from UC San Diego. In parallel with this study, the company has also found that the experimental therapeutic prevented lung damage in COVID-19 animal models and was well-tolerated by people who participated in a Phase I clinical trial to assess safety. Selva is planning a Phase IIa clinical trial in non-hospitalized COVID-19 patients for late 2021.

Many people with COVID-19 experience mild disease and can recover at home with supportive care to help relieve their symptoms. Currently, severe cases of COVID-19 may be treated with the antiviral drug remdesivir, approved by the U.S. Food and Drug Administration (FDA) for use in hospitalized patients, or a medication that has received emergency use authorization from the FDA, such as monoclonal antibodies. Worldwide, more than 124 million people have been diagnosed with COVID-19 and 2.72 million have died from the infection.

Co-authors of the study include: Drake M. Mellott, Bala C. Chenna, Demetrios H. Kostomiris, Jiyun Zhu, Zane W. Taylor, Klaudia I. Kocurek, Ardala Katzfuss, Linfeng Li, Frank M. Raushel, Texas A&M University; Chien-Te Tseng, Aleksandra Drelich, Jason Hsu, Vivian Tat, University of Texas; Pavla Fajtová, UC San Diego and Academy of Sciences of the Czech Republic; Miriam A. Giardini, Danielle Skinner, Ken Hirata, Michael C. Yoon, Sungjun Beck, Aaron F. Carlin, Alex E. Clark, Laura Beretta, Vivian Hook, Anthony J. O’Donoghue, Jair Lage de Siqueira-Neto, UC San Diego; Daniel Maneval, Felix Frueh, Selva Therapeutics; Brett L. Hurst, and Hong Wang, Utah State University.

Disclosure: James McKerrow is an advisor to and holds stock shares in Selva Therapeutics, Inc.

Featured image: Creative rendition of SARS-CoV-2 particles (not to scale). © National Institute of Allergy and Infectious Diseases, NIH


Reference: Drake Mellott, “A Clinical-Stage Cysteine Protease Inhibitor blocks SARS-CoV-2 Infection of Human and Monkey Cells”, ACS Chem. Biol., 2021. https://pubs.acs.org/doi/10.1021/acschembio.0c00875 https://doi.org/10.1021/acschembio.0c00875


Provided by University of California – San Diego

Understanding COVID-19 Vaccine Side Effects, Why Second Dose Could Feel Worse (Medicine)

All vaccines could cause some degree of reaction, and the same is true for COVID-19 vaccines. Post-vaccine symptoms are typically mild and resolve quickly without the need to use any medication.

Common COVID-19 vaccine side effects include:

  • Redness or soreness at injection site.
  • Muscle aches.
  • Fatigue.
  • Headache.
  • Fever or chills.

For some people, the second dose in a COVID-19 vaccine series is causing a stronger reaction and more side effects than the initial dose. The same was true during clinical trials.

Watch: Dr. Melanie Swift explains possible COVID-19 vaccine side effects.

Journalists: Broadcast-quality sound bites with Dr. Swift are available in the downloads at the end of the post. Please courtesy: “Melanie Swift, M.D./COVID-19 Vaccine Allocation and Distribution/Mayo Clinic.”

In this Q&A, Dr. Melanie Swift, co-chair of the COVID-19 Vaccine Allocation and Distribution Work Group at Mayo Clinic, explains why vaccine side effects happen and what is known about symptoms following COVID-19 vaccination:

Why do people experience side effects from COVID-19 vaccines?

When we get vaccinated for COVID-19, we often experience some side effects. The reason that we get side effects is that our immune system is revving up and reacting. When you get sick, the same thing happens. Actually, a lot of the symptoms from illnesses that we get, like influenza and COVID-19, are actually not caused by the direct action of the virus, but rather by our immune system. Our bodies react, and that gives us these general symptoms like fever, achiness and headache.

Why are some people more likely to experience side effects after the second dose of a COVID-19 vaccine?

When you take two doses of a COVID-19 vaccine, the first dose is the first time for your body to see the spike protein that the COVID-19 vaccines produce, and your body begins to develop an immune response. But that happens slowly. Then when you come back with a second dose, your body is ready to attack it. Your body is primed by that first dose of vaccine. The second vaccine dose goes into your body, starts to make that spike protein, and your antibodies jump on it and rev up your immune system response. It’s kind of like they’ve studied for the test. And it’s acing the test.

How long could symptoms or side effects of COVID-19 vaccination last?

The vaccine side effects that we’ve seen in these large phase three trials resolve within about 72 hours of taking a COVID-19 vaccine. At most, those side effects can last up to a week. We really have not seen long-term side effects from COVID-19 vaccines beyond that, and that makes sense when you look at other vaccines. And we have a lot of experience with different vaccines. Long-term side effects are just basically unheard of in the vaccine world.

So with two months of follow-up data in people undergoing those clinical trials, and now even longer follow-up from the trials and our experience giving vaccines to the public, we really are not seeing any trend toward any long-term side effects.

Featured image: A Mayo Clinic employee, a white woman wearing a mask, sitting in a chair, receiving a covid-19 vaccine © Mayo Clinic


Provided by Mayo Clinic

Unprecedented Accuracy: Theoretical Physicists at PRISMA+ Cluster of Excellence Calculate the Radius of the Proton (Physics)

New calculations favor a smaller value for the size of the proton, helping to resolve the proton radius puzzle

Calculations based on fundamental theories of particle physics could help solve the so-called proton radius puzzle. Now, for the first time, a team of theoretical physicists at Johannes Gutenberg University Mainz (JGU) around Prof. Hartmut Wittig have succeeded in making their calculations accurate enough to provide a clue: The latest findings point towards a smaller proton radius.

All known atomic nuclei consist of protons and neutrons, yet many of the characteristics of these ubiquitous nucleons remain to be understood. Specifically, despite several years of effort, scientists have been unable to pin down the radius of the proton. In 2010, the result of a new proton radius measurement technique involving laser spectroscopy of muonic hydrogen caused a stir – in this ‘special’ kind of hydrogen, the electron in the shell of the atom was replaced by its heavier relative, the muon, which is a much more sensitive probe for the proton’s size. The experimentalists came up with a significantly smaller value than that found following corresponding measurements of ‘normal’ hydrogen, as well as the traditional method of determining the proton radius using electron-proton scattering. The big question that physicists have been asking ever since is whether this deviation could be evidence for ‘new physics’ beyond the Standard Model or ‘simply’ reflects systematic uncertainties inherent to the different measuring methods.

Theoretical calculations play an important role in shedding light on the situation and deciding on the relevance of the various results. A group of physicists at the PRISMA+ Cluster of Excellence is currently focusing on the so-called ‘electromagnetic form factors’. “These have to be determined using just the underlying theory of quantum chromodynamics (QCD),” explains Prof. Hartmut Wittig. “This means that we compute these quantities without including experimental data in our calculations.” Electromagnetic form factors describe the spatial distribution of electrical charge and magnetization within the proton. Their measurement also forms the basis for the experimental determination of the proton radius in electron-proton scattering experiments. They therefore represent an important piece of the proton radius puzzle.

Describing the interplay of forces within the atomic nucleus

Quantum chromodynamics is concerned with the interplay of forces within the nucleus. The strong interaction binds the quarks, the elementary building blocks of matter, to form protons and neutrons, and is mediated by gluons which act as exchange particles. In order to be able to treat these processes mathematically, the scientists at Mainz draw on what is called lattice field theory. In this case, as if in a crystal, the quarks are distributed over the points of a discrete space-time lattice. Special simulation methods can then be used to calculate the properties of the nucleons using supercomputers.

“Recently there have been many efforts to determine the size of the proton using lattice calculations but to date the outcomes have not been accurate enough to identify which is likely to be more reliable; the result of muonic hydrogen measurement or the result obtained from electron proton scattering,” points out Hartmut Wittig. “Now, for the first time, we have calculated the electromagnetic form factors so precisely that we are able to contribute to the proton radius debate.”

Once the form factors have been computed, the proton radius can be derived. The result is a further indication that the proton is probably smaller than what was thought before and represents the first time such evidence has been obtained using a method independent of the previous measurements. However, the physicists still cannot rule out the larger value entirely. “The margin for error in our calculations is small enough to enable us to favor the smaller radius, but still too big to allow us to completely eliminate the larger value,” concludes Hartmut Wittig. “At the same time, we already have ideas as to how we can increase the accuracy of our calculations even further.”

Featured image: Supercomputers such as the high-performance computer MOGON II at JGU have been used to calculate the radius of the proton. Photo: Stefan F. Sämmer


Publication
D. Djukanovic et al., Isovector electromagnetic form factors of the nucleon from lattice QCD and the proton radius puzzle, arXiv:2102.07460 (hep-lat)


Provided by Johannes Guntenberg Mainz

Scientists Develop High-performance Lithium-ion Battery-supercapacitor Hybrid Devices (Chemistry)

Battery-supercapacitor hybrid devices (BSHDs), which combine battery-type and capacitor-type electrodes in one cell, can fulfill the dual demands for high energy and power densities.

However, the performance of current BSHDs is restricted by the electrolyte-consuming mechanism and imbalance of charge-storage capacity and electrode kinetics between the two types of electrodes.

Recently, a research team led by Prof. WU Zhongshuai from the Dalian Institute of Chemical Physics (DICP) of the Chinese Academy of Sciences developed new BSHDs based on two matched faradaic electrodes with a rocking-chair mechanism analogous to lithium-ion batteries.

The study was published in Energy & Environmental Science on March 17.

The scientists developed these new BSHDs with a rocking-chair mechanism analogous to lithium-ion batteries by employing an intercalation pseudocapacitive T-Nb2O5 anode and a battery-type nickel-rich layered oxide (LiNi0.815Co0.15Al0.035O2) cathode with comparable faradaic capacities.

For electrode kinetics matching, they constructed a porous nanoflower structure and a three-dimensional interconnected conductive network formed by one-dimensional carbon nanotubes, two-dimensional electrochemically exfoliated graphene sheets, and conductive polymer binder for the anode and cathode, respectively. This facilitated BSHDs’ charge transfer processes.

By virtue of doubly matched capacities and kinetics, the assembled BSHDs achieved superior performance to previously reported rocking-chair BSHDs and other counterparts with unmatched electrodes.

“This work could inspire cell configuration design and electrode structure optimization for high-energy and high-power electrochemical energy storage,” said Prof. WU.

Featured image: Schematic illustration of the charge storage mechanisms for rocking-chair T-Nb2O5-NF//NCA-3D BSHD (Image by SU Feng) 


Reference

A high-performance rocking-chair lithium-ion battery-supercapacitor hybrid device boosted by doubly matched capacity and kinetics of the faradaic electrodes


Provided by Chinese Academy of Sciences

Excellent Overall Water Splitting Performance Unveiled with Core-shell Alloy Nano-catalyst (Chemistry)

With the development of proton exchange membrane water electrolyzers (PEMWEs), hydrogen production by electrolysis of water under acidic conditions is considered to be the most promising way to efficiently convert sustainable hydrogen energy.

Electrocatalytic water splitting contains the oxygen evolution reaction (OER) at the anode and the hydrogen evolution reaction (HER) at the cathode. Compared with the outstanding HER performance realized by Pt-based catalysts at low overpotentials, the sluggish OER kinetics and the rapid deactivation of OER catalysts in acidic electrolytes limit the wide commercialization of PEMWEs.

In a study published in J. Am. Chem. Soc., the research group led by Prof. CAO Rong and Prof. CAO Minna from Fujian Institute of Research on the Structure of Matter (FJIRSM) of the Chinese Academy of Sciences, reported an Au@AuIr2 core-shell alloy nanocatalyst with partial oxidation surface, which exhibited excellent overall water splitting performance in acidic media.

Ir-based nanomaterials have been widely studied owing to effective OER performance under acidic electrolytes. To make the scarcely stored precious metals cost-effective, the researchers have to improve atomic utilization rate without sacrificing performance in order to meet commercial demand.

The researchers used a one-pot reaction to synthesize AuIr core-shell nanoparticles with HAuCl43H2O and IrClxH2O being the precursors, and oleylamine being both the solvent and the reducing agent.

At low temperature, Au, with a higher redox potential, is reduced prior to Ir and then forms as a core. As the temperature increased, Ir atoms were deposited on the surface of Au to form a Au-Ir alloy surface by atomic diffusion. When the reaction time was prolonged to 3 h, all the nanoparticles (NPs) evolved into uniform core-shell structure NPs with Au core and AuIr2 alloy shell (Au@AuIr2).

Through powder X-ray diffraction (PXRD), the researchers confirmed two components with lattice constants of a = 4.078(5) Å and 3.889(4) Å in Au@AuIr2, which can be assigned as Au and AuIr alloy. By means of high-angle annular dark-field scanning transmission electron microscopy (HAADF-STEM), high-resolution transmission electron microscopy (HRTEM), energy dispersive X-ray spectroscopy (EDS) and energy dispersive X-ray (EDX) line scan, they confirmed the core-shell alloy structure.

There is a gradient of declining Au distribution from core to shell, with Au core and AuIr2 alloy shell. The local atomic and electronic structures of Au@AuIr2 were characterized by X-ray photoelectron spectroscopy (XPS) and (X-ray absorption fine structure spectroscopy) AFS. The results suggest that amorphous IrOx in the surface of Au@AuIr2 NPs, and the partially oxidized surface was mainly from the interaction between Au and Ir.

Au@AuIr2 showed excellent catalytic activity under acidic conditions, and displayed 4.6 (5.6) times higher intrinsic (mass) activity toward OER than a commercial Ir catalyst. It presented HER catalytic properties comparable to those of commercial Pt/C. Significantly, when Au@AuIr2 was used as both the anode and cathode catalyst, the overall water splitting cell achieved 10 mA/cm2 with a low cell voltage of 1.55 V and maintained this activity for more than 40 h, which greatly outperformed the commercial couples (Ir/C||Pt/C, 1.63 V, activity decreased within minutes).

Density Functional theory (DFT) calculations demonstrated that the partially oxidized Au@AuIr2 core-shell alloy nanoparticles achieve a better balance for intermediates binding and thus exhibit a better OER performance. Theoretical calculations coupled with X-ray-based structural analyses suggest that partially oxidized surfaces originating from the electronic interaction between Au and Ir provide a balance for different intermediates binding and realize significantly enhanced OER performance.

This study realizes the regulation of the nanostructure and electronic structure of core-shell alloy at the atomic scale, which is helpful to understand the structure-activity relationship between the structure and properties of catalysts, and provides an idea for material design. The rational design of the surface oxidation and material composition can enable a suitable balance for intermediates binding, which not only improves the activity and stability of the catalyst to a greater extent, but also greatly improves the utilization efficiency of precious metal catalyst.

Featured image: Core-shell alloy nano-catalyst composed of Au core and AuIr2 alloy shell (Au@AuIr2) with partially oxidized surfaces enhanced water splitting performance in acidic media (Image by Prof. CAO’s group) 


Reference

Significantly Enhanced Overall Water Splitting Performance by Partial Oxidation of Ir through Au Modification in Core–Shell Alloy Structure


Provided by Chinese Academy of Sciences