The printable polymer enables sand structures with intricate geometries and exceptional strength — and is also water soluble.

The study, published in Nature Communications, demonstrates a 3D-printed sand bridge that at 6.5 centimeters can hold 300 times its own weight, a feat analogous to 12 Empire State Buildings sitting on the Brooklyn Bridge.

The binder jet printing process is cheaper and faster than other 3D-printing methods used by industry and makes it possible to create 3D structures from a variety of powdered materials, offering advantages in cost and scalability. The concept stems from inkjet printing, but instead of using ink, the printer head jets out a liquid polymer to bind a powdered material, such as sand, building up a 3D design layer by layer. The binding polymer is what gives the printed sand its strength.

The team used polymer expertise to tailor a polyethyleneimine, or PEI, binder that doubled the strength of sand parts compared with conventional binders.

Parts printed via binder jetting are initially porous when removed from the print bed. They can be strengthened by infiltrating the design with an additional super-glue material called cyanoacrylate that fills in the gaps. This second step provided an eight-fold strength increase on top of the first step, making a polymer sand composite stronger than any other and any known building materials, including masonry.

“Few polymers are suited to serve as a binder for this application. We were looking for specific properties, such as solubility, that would give us the best result. Our key finding was in the unique molecular structure of our PEI binder that makes it reactive with cyanoacrylate to achieve exceptional strength,” said ORNL’s Tomonori Saito, a lead researcher on the project.

Parts formed with conventional binders are made denser with infiltrate materials, such as super glue, but none have reached close to the performance of the PEI binder. The PEI binder’s impressive strength stems from the way the polymer reacts to bond with cyanoacrylate during curing.

One potential application for the super-strength sand is to advance tooling for composites manufacturing.

Silica sand is a cheap, readily available material that has been gaining interest in automotive and aerospace sectors for creating composite parts. Lightweight materials, such as carbon fiber or fiberglass, are wrapped around 3D-printed sand cores, or “tools,” and cured with heat. Silica sand is attractive for tooling because it does not change dimensions when heated and because it offers a unique advantage in washable tooling. In composite applications, using a water-soluble binder to form sand tools is significant because it enables a simple washout step with tap water to remove the sand, leaving a hollow composite form.

“To ensure accuracy in tooling parts, you need a material that does not change shape during the process, which is why silica sand has been promising. The challenge has been to overcome structural weakness in sand parts,” said Dustin Gilmer, a University of Tennessee Bredesen Center student and the study’s lead author.

Current sand casting molds and cores have limited industrial use because commercial methods, such as washout tooling, apply heat and pressure that can cause sand parts to break or fail on the first try. Stronger sand parts are needed to support manufacturing at a large scale and enable rapid part production.

“Our high-strength polymer sand composite elevates the complexity of parts that can be made with binder jetting methods, enabling more intricate geometries, and widens applications for manufacturing, tooling, and construction,” said Gilmer.

The novel binder won a 2019 R&D 100 Award and has been licensed by industry partner ExOne for research.

The journal article is published as “Additive manufacturing of strong silica sand structures enabled by polyethyleneimine binder.”

Coronavirus disease (COVID-19) is a multifaceted infectious disease. While, at the start of the global pandemic, it was assumed that COVID-19 was primarily a disease of the lungs, it is now known that several functional systems in the human body are affected following infection with the pathogen SARS-CoV-2. One of these functional systems is blood clotting. COVID-19 patients have an increased risk of thromboses and embolisms, such as strokes, pulmonary or myocardial infarctions, and even deep vein thromboses. The use of drugs that inhibit blood clotting has been part of the treatment guidelines for COVID-19 since July 2020. “These complications during hospitalisation have a direct impact on the well-being of patients and increased the risk of dying from COVID-19,” reports David Pereyra from MedUni Vienna’s Department of General Surgery, who is first author of the publication. The underlying coagulopathy is still not fully understood.

COVID-19 triggers unique clotting problems

“The coagulopathy observed in COVID-19 patients is novel and differs in many respects from previously known coagulation problems,” says Alice Assinger, group leader at the Institute of Vascular Biology and Thrombosis Research at the Medical University of Vienna and last author of the publication, “COVID-19-associated coagulopathy displays characteristics that, although partially comparable with other coagulation diseases, cannot be fully explained by them.” Alice Assinger’s group therefore started to look for an explanation for this sub-condition of COVID-19 in the spring of 2020, in an early phase of the pandemic.

In a multi-centre analysis of COVID-19 patients in Vienna, Linz and Innsbruck, the group observed that COVID-19-associated coagulopathy occurs almost exclusively in patients requiring intensive care or in patients who die as a result of COVID-19. Although anticoagulant drugs improve the survival of COVID-19 patients, they show no effect on immunological processes related to blood coagulation (immunothrombosis).

Low-molecular-weight heparin curtails duration of infection

The analyses showed, however, that the period of active SARS-CoV-2 infection is curtailed in patients treated with low-molecular-weight heparin, the most commonly used anticoagulant. “In patients who receive this drug, infection time is an average of four days shorter than in patients who are not treated with low-molecular-weight heparin. We were surprised to see that low-molecular-weight heparin may have a direct effect on coronavirus and its infectivity,” said David Pereyra. Experimental data show that heparin can inhibit the ability of SARS-CoV-2 to bind to cells, thereby preventing them from being infected.

These observations were made in the context of a close collaboration between the three hospitals involved — the Favoriten Hospital in Vienna, the Innsbruck Regional Hospital Innsbruck and the Johannes Kepler University Hospital in Linz — as well as through the active exchange between basic researchers and clinicians,” says Alice Assinger, underscoring the relevance of good cooperation during the COVID-19 pandemic for a better understanding of the disease and its treatment.

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Materials provided by Medical University of Vienna. Note: Content may be edited for style and length.

The study finds that 90% of current COVID patients’ rooms had detectable coronavirus on at least one surface, and that the virus was still detectable days later on certain surfaces, especially TV remote controls and nurse call buttons.

In all, 28% of the more than 2,000 samples taken from inside and near the rooms of 104 COVID patients turned up positive for coronavirus RNA. The researchers did not test to see if the viruses on the swabs were capable of causing an infection but it can help identify surfaces that need cleaning and inform infection prevention policies.

Reassuringly, the study also finds that the virus was rare or not detectable on surfaces outside the COVID patients’ rooms — probably reflecting the aggressive infection prevention protocols in COVID units. The study was conducted by University of Michigan researchers in four Michigan nursing homes between October 2020 and January 2021 when the state had a prolonged surge of cases.

“These data show that coronavirus is ubiquitous and persistent in the rooms of nursing home residents with COVID-19, and highlight the ongoing importance of rigorous cleaning and protection of staff and visitors,” said Lona Mody, M.D., M.Sc., the study’s first author and leader of nursing home infection prevention research at Michigan Medicine’s Department of Internal Medicine, Division of Geriatric and Palliative Medicine as well as VA Ann Arbor Healthcare System.

She worked with Emily Martin, Ph.D., of the U-M School of Public Health, and members of their teams and the staff of the four nursing homes to conduct the study.

One-third of the people in the United States who have died from COVID-19 have been nursing home residents, mainly in the early months of the pandemic.

Now, despite high rates of vaccination among nursing home residents, and growing vaccination among nursing home staff, the risk to unvaccinated patients, staff and visitors, and the risk of breakthrough cases among chronically ill, recently hospitalized and frail elderly residents, is still significant.

All of the patients had been diagnosed with COVID in the past two weeks and were staying in dedicated COVID units to keep them away from other nursing home residents. Nearly one in four had been in the hospital in the past month.

More than half of the patients had dementia, and most needed extensive help with bathing, dressing and eating. Half of the patients were short-stay residents of the nursing home, and by February nearly a third of the sample had gone home.

The more independently the patients could move or function, the higher the chance that surfaces such as bed and TV remote controls, nurse call buttons, windowsills and doorknobs had persistent coronavirus present. Very few positive swabs turned up in the sitting areas, nurses’ stations and elevator buttons nearest the COVID units.

The study was funded by the National Institute on Aging (3P30AG024824-16S1AG041780, AG050685, AG024824).

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Materials provided by Michigan Medicine – University of Michigan. Original written by Kara Gavin. Note: Content may be edited for style and length.

Now, researchers from the University of Copenhagen have come a significant step closer, as they have found an important difference between naturally acquired immunity and immunity following vaccination.

“The antibodies which the body produces when you have been infected with malaria look different from those produced by the body when you have been vaccinated. And that probably means that our immune system has a more efficient response when we have been naturally infected than when we are vaccinated against malaria,” says Lars Hviid, Professor at the Department of Immunology and Microbiology.

“Natural killer cells”

The immune system can trigger various mechanisms in order to defend the body. The usual defence against infections with parasites, viruses and bacteria consists of so-called macrophages.

“When we are exposed to an attack from the outside, the immune system can produce antibodies that attach to the foreign body that needs to be fought. They are then recognised by some small cells called macrophages, which are attracted to the antibody and eat the bacterium or virus. This is basically how immunity to most infectious diseases works,” explains Lars Hviid.

But, now, researchers have discovered that immunity to malaria seems to work differently. Here, the body’s immune system uses some other types of cells to fight an infection with the malaria parasite.

“We have found that the antibodies look different, depending on whether you have been vaccinated or infected. And that means that the body launches some other defence mechanism as, instead, it uses what we call natural killer cells,” says Lars Hviid.

More in common with cancer

Natural killer cells are usually known to researchers as one of the body’s best weapons to fight cancer cells. But, now, it seems that the defence against malaria has features in common with the immune system against cancer.

“In popular terms, you could say that the immune system has a more tailored defence against malaria than against other typical infections. Maybe we have evolved in this way because it is such a contagious and deadly disease — that is difficult to guess,” says Lars Hviid.

The researchers made the findings by comparing blood samples from Ghanaian people who had been infected with malaria with blood samples from people who participated in Phase 1 clinical trials of an experimental malaria vaccine.

He explains that the new knowledge may be used to develop new and improved malaria vaccines.

“Our study points to a new strategy for developing even better malaria vaccines in the future. Because, now, we know how the body mobilises the defence with natural killer cells, and we can imitate that with vaccines,” he says.

He looks forward to being able to test — together with other researchers — whether a future malaria vaccine will be able to utilise natural killer cells instead of the macrophages that the current vaccines use.