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Visualizing cement hydration on a molecular level

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Imaging technique could enable new pathways for reducing concrete’s hefty carbon footprint, as well as for 3-D printing of concrete.

Credit: Image courtesy of Franz-Josef Ulm, Admir Masic, Hyun-Chae Chad Loh, et al

The concrete world that surrounds us owes its shape and durability to chemical reactions that start when ordinary Portland cement is mixed with water. Now, MIT scientists have demonstrated a way to watch these reactions under real-world conditions, an advance that may help researchers find ways to make concrete more sustainable.

The study is a “Brothers Lumière moment for concrete science,” says co-author Franz-Josef Ulm, professor of civil and environmental engineering and faculty director of the MIT Concrete Sustainability Hub, referring to the two brothers who ushered in the era of projected films. Likewise, Ulm says, the MIT team has provided a glimpse of early-stage cement hydration that is like cinema in Technicolor compared to the black and white photos of earlier research.

Cement in concrete contributes about 8 percent of the world’s total carbon dioxide emissions, rivaling the emissions produced by most individual countries. With a better understanding of cement chemistry, scientists could potentially “alter production or change ingredients so that concrete has less of an impact on emissions, or add ingredients that are capable of actively absorbing carbon dioxide,” says Admir Masic, associate professor of civil and environmental engineering.

Next-generation technologies like 3D printing of concrete could also benefit from the study’s new imaging technique, which shows how cement hydrates and hardens in place, says Masic Lab graduate student Hyun-Chae Chad Loh, who also works as a materials scientist with the company Black Buffalo 3D Corporation.
Loh is the first author of the study published in ACS Langmuir, joining Ulm, Masic, and postdoc Hee-Jeong Rachel Kim.

Cement from the start

Loh and colleagues used a technique called Raman microspectroscopy to get a closer look at the specific and dynamic chemical reactions taking place when water and cement mix. Raman spectroscopy creates images by shining a high-intensity laser light on material and measuring the intensities and wavelengths of the light as it is scattered by the molecules that make up the material.

Different molecules and molecular bonds have their own unique scattering “fingerprints,” so the technique can be used to create chemical images of molecular structures and dynamic chemical reactions inside a material. Raman spectroscopy is often used to characterize biological and archaeological materials, as Masic has done in previous studies of nacre and other biomineralized materials and ancient Roman concretes.

Using Raman microspectroscopy, the MIT scientists observed a sample of ordinary Portland cement placed underwater without disturbing it or artificially stopping the hydration process, mimicking the real-world conditions of concrete use. In general, one of the hydration products, called portlandite, starts as a disordered phase, percolates throughout the material, and then crystallizes, the research team concluded.

Before this, “scientists could only study cement hydration with average bulk properties or with a snapshot of one point in time,” says Loh, “but this allowed us to observe all the changes almost continuously and improved the resolution of our image in space and time.”

For instance, calcium-silicate-hydrate, or C-S-H, is the main binding ingredient in cement that holds concrete together, “but it’s very difficult to detect because of its amorphous nature,” Loh explains. “Seeing its structure, distribution, and how it developed during the curing process was something that was amazing to watch.”

Building better

Ulm says the work will guide researchers as they experiment with new additives and other methods to reduce concrete’s greenhouse gas emissions: “Rather than ‘fishing in the dark,’” we are now able to rationalize through this new approach how reactions occur or do not occur, and intervene chemically.”

The team will use Raman spectroscopy as they spend the summer testing how well different cementitious materials capture carbon dioxide, Masic says. “Tracking this up to now has been almost impossible, but now we have the opportunity to follow carbonation in cementitious materials that helps us understand where the carbon dioxide goes, which phases are formed, and how to change them in order to potentially use concrete as a carbon sink.”

The imaging is also critical for Loh’s work with 3D concrete printing, which depends on extruding concrete layers in a precisely measured and coordinated process, during which the liquid slurry turns into solid concrete.

“Knowing when the concrete is going to set is the most critical question that everyone is trying to understand” in the industry, he says. “We do a lot of trial and error to optimize a design. But monitoring the underlying chemistry in space and time is critical, and this science-enabled innovation will impact the concrete printing capabilities of the construction industry.”

This work was partially supported by the scholarship program of the Kwanjeong Educational Foundation.

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Written by Becky Ham, MIT News correspondent
Paper: “Time-space-resolved chemical deconvolution of cementitious colloidal systems using Raman spectroscopy”
https://pubs.acs.org/doi/10.1021/acs.langmuir.1c00609

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Source: https://bioengineer.org/visualizing-cement-hydration-on-a-molecular-level/

Bioengineer

Genetic cause of neurodevelopmental disorder discovered

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Transport system of essential materials in brain cells disrupted in certain genetic developmental disorders.

Credit: Dr. Riazuddin

University of Maryland School of Medicine (UMSOM) researchers identified a new gene that may be linked to certain neurodevelopmental disorders and intellectual disabilities. The researchers believe that finding genes involved in certain types of developmental disorders, provide an important first step in determining the cause of these disorders and ultimately in developing potential therapies for treating them. The paper was recently published in the American Journal of Human Genetics.

About 3 percent of the world’s population has intellectual disability. Up to half the cases are due to genetics, however, because many thousands of genes contribute to brain development, it has been difficult to identify the specific cause for each patient.

Once the researchers identified the gene, they worked with collaborators to give clinical diagnoses to 10 other families around the world, who had relatives with this condition. The researchers also used zebrafish to show the gene’s role in development and survival, demonstrating its importance in helping the brain’s neurons function properly.

“Our goal is to find as many of these genes required for brain function and take this knowledge back to patients and families to provide a clinically relevant genetic diagnosis,” says Saima Riazuddin, PhD, MPH, MBA, Professor of Otorhinolaryngology-Head & Neck Surgery and Biochemistry & Molecular Biology at UMSOM.

Dr. Riazuddin and her team collaborate regularly with several scientists in Pakistan studying a group of 350 families geographically isolated, which as a result has led to inbreeding resulting in genetic disorders such as neurodevelopmental disorder and intellectual disability.

The team focused on one particular family with two brothers and an uncle with symptoms of intellectual disability, delayed speech and other developmental milestones and epilepsy. Other members of the family with similar symptoms had since passed in childhood or early adulthood. Dr. Riazuddin and her team identified the gene AP1G1 as the culprit.

Then through collaboration with 27 other institutions, her team was able to identify ten other families with the variations in the same gene that led to growth retardation and intellectual disability. These families lived in Italy, Germany, the Netherlands, Poland, and the United States.

To determine the gene’s role in development, the researchers engineered zebrafish without Ap1g1. These zebrafish embryos all began to die off by the fourth day. When the researchers added back mutated versions of the genes, like those found in the families with neurodevelopment disorder and intellectual disability, they observed a spectrum of symptoms with some zebrafish embryos dying off, some with major structural defects, and others with only minor tail deformities.

The gene AP1G1 contains the blueprints to make the protein Adaptor Protein 1 gamma 1 (AP1γ1). This protein is one of five pieces that makes up the Adaptor Protein Complex, which builds transport vesicles to move materials around cells.

“Think of these transport vesicles as little vehicles like trucks that have to load, transport, and unload their cargo around the cells (e.g. neurons) to provide the necessary supplies for the cell to function,” says Dr. Riazuddin.

Dr. Riazuddin’s team made normal and mutant versions of AP1G1 which they put in mammalian cells with cargo molecules labeled in red. The cells with the mutant versions of AP1G1 had vesicles that were delayed in delivering their cargo or did not make their deliveries at all.

“Improving clinical diagnosis of these developmental disorders may eventually provide new targets for therapies, in order to one day be able to treat these conditions allowing more people to live independently,” says E. Albert Reece, MD, PhD, MBA, Executive Vice President for Medical Affairs, UM Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor and Dean, University of Maryland School of Medicine.

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This studied was funded by National Institute of Neurological Disorders and Stroke (R01NS107428), the EU FP7 Large-Scale Integrating Project Genetic and Epigenetic Networks in Cognitive Dysfunction (241995), Higher Education Commission of Pakistan (NRPU project 10700), and a Fondazione del Monte grant (ID ROL: FDM/4021).

The researchers have no conflicts of interest to declare.

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Source: https://bioengineer.org/genetic-cause-of-neurodevelopmental-disorder-discovered/

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Pathogenic bacteria rendered almost harmless

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By identifying one of the mechanisms regulating the virulence of Pseudomonas aeruginosa, a UNIGE team is proposing a new strategy to combat this bacterium, which is resistant to many common antibiotics

Pseudomonas aeruginosa is an opportunistic pathogenic bacterium present in many ecological niches, such as plant roots, stagnant water or even the pipes of our homes. Naturally very versatile, it can cause acute and chronic infections that are potentially fatal for people with weakened immune systems. The presence of P. aeruginosa in clinical settings, where it can colonise respirators and catheters, is a serious threat. In addition, its adaptability and resistance to many antibiotics make infections by P. aeruginosa increasingly difficult to treat. There is therefore an urgent need to develop new antibacterials. Scientists from the University of Geneva (UNIGE), Switzerland, have identified a previously unknown regulator of gene expression in this bacterium, the absence of which significantly reduces the infectious power of P. aeruginosa and its dangerous nature. These results, to be published in the journal Nucleic Acid Research, could constitute an innovative target in the fight against this pathogen.

RNA helicases perform essential regulatory functions by binding and unwinding various RNA molecules to perform their functions. RNA helicases are present in the genomes of almost all known living organisms, including bacteria, yeast, plants, and humans; however, they have acquired specific properties depending on the organism in which they are found. “Pseudomonas aeruginosa has an RNA helicase whose function was unknown, but which was found in other pathogens”, explains Martina Valentini, a researcher leading this research in the Department of Microbiology and Molecular Medicine at UNIGE Faculty of Medicine, and holder of an SNSF “Ambizione» grant. “We wanted to understand what its role was, in particular in relation to the pathogenesis of the bacteria and their environmental adaptation.”

A severely reduced virulence

To do this, the Geneva team combined biochemical and molecular genetic approaches to determine the function of this protein. “In the absence of this RNA helicase, P. aeruginosa multiplies normally in vitro, both in a liquid medium and on a semi-solid medium at 37°C”, reports Stéphane Hausmann, a researcher associate in the Department of Microbiology and Molecular Medicine at UNIGE Faculty of Medicine and first author of this study. “To determine whether the infection capacity of the bacteria was affected, we had to observe it in vivo in a living organism.”

The scientists then continued their research using Galleria mellonella larvae, a model insect for studying host-pathogen interactions. Indeed, the innate immune system of insects has important similarities with that of mammals. Moreover, these larvae can live at temperatures between 5°C and 45°C, which makes it possible to study bacterial growth at different temperatures, including that of the human body. Three groups of larvae were observed; the first, after injection of a saline solution, saw 100% of its population survive. In the presence of a normal strain of P. aeruginosa, less than 20% survived at 20 hours after infection. In contrast, when P. aeruginosa no longer possessed the RNA helicase gene, over 90% of the larvae remained alive. “The modified bacteria became almost harmless, while remaining very much alive,” says Stéphane Hausmann.

Inhibiting without killing

The results of this work show that this regulator affects the production of several virulence factors in the bacteria. “In fact, this protein controls the degradation of numerous messenger RNAs coding for virulence factors”, summarises Martina Valentini. “From an antimicrobial drug strategy point of view, switching off the pathogen’s virulence factors rather than trying to eliminate the pathogen completely, means allowing the host immune system to naturally neutralise the bacterium and potentially reduces the risk for the development of resistance. Indeed, if we try to kill the bacteria at all costs, the bacteria will adapt to survive, which favours the appearance of resistant strains.”

The Geneva team is currently continuing its work by screening a series of known drug molecules in order to determine whether any of them have the capacity to selectively block this protein, and to study in detail the inhibition mechanisms on which the development of an effective therapeutic strategy could be based.

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Source: https://bioengineer.org/pathogenic-bacteria-rendered-almost-harmless/

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Novel interactions between proteins that help in recovering from brain injury

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Neuroinflammatory response-induced proteases impede the recovery process from brain injury; novel interactions between proteins (hevin and calcyon) help in the recovery of neurons in a mature brain

Patients with brain injury (caused by stroke or trauma) primarily rely on rehabilitation therapy for recovery, as there are no other known effective treatment methods. The rate of recovery from brain injury observed in adults is significantly slower (or the recovery is impossible) than that observed in young children. The consensus among researchers is that the number of excess neural stem cells capable of restoring brain functions is lower in a mature brain than that in the brain of young children.

A Korean research team reported a novel mechanism to describe the brain injury recovery process. The researchers reported that when the animal model experiment was conducted, the time taken to recover from a brain injury could be controlled by regulating the proteins. The Korea Institute of Science and Technology (KIST) has released an announcement that a team led by Dr. Eun Mi Hwang of the Brain Science Institute, KIST collaborated with another team led by Prof. Kyoungho Suk of the School of Medicine, Kyungpook National University and reported the presence of a novel interaction between proteins (hevin-calcyon); this interaction plays a critical role in the brain injury recovery process in adults. The researchers also revealed that this interaction plays an important role in the early stages of recovery.

The researchers working at KIST identified the calcyon protein as a novel interaction partner of hevin, a protein secreted by the glial cells present in the brain. They also reported that the interaction between the proteins played a critical role in the recovery process of neuronal cells present in an injured adult brain. As neurons are cells that directly influence brain activity, it is believed that brain diseases can be cured when they are recovered and/or treated.

*Glial cells : Cells that support the tissues of the central nervous system, provide nutrients to neurons inside the brain and spinal cord, and create a chemical environment suitable for the activities of neurons

The results from the experiments revealed that an increase in the number of hevin-calcyon interactions in the brain could promote synaptic contacts and reorganization, which could help in the early recovery of the impaired brain. The hevin-calcyon interaction and the expression of these proteins were confirmed by studying healthy brain tissues. It was also observed that the number of interactions in patients suffering from the condition of traumatic brain injury was significantly reduced.

Researchers at the Kyungpook National University studied the recovery process of brain injury by studying the hevin and calcyon interaction using a brain injury animal model. They reported that the neuroinflammatory response-induced proteases formed in the early stages of brain injury resulted in the fragmentation of hevin. This also impeded the generation of the hevin and calcyon interaction. Experiments were conducted using an animal model of brain injury. It was observed that the recovery time could be reduced to approximately 2 to 3 weeks (from 4 weeks) if an inflammatory response inhibitor was administered directly to the injured region of the brain. The rate of recovery could be further slowed by administering an additional inflammatory protein.

The joint research team reported that the absence of the hevin-calcyon interaction in the early stages (a critical period in the recovery process of brain injury) of the recovery process might negatively impact the effective recovery process. The reported result is the outcome of the five years of persistent efforts by the team led by Dr. Eun Mi Hwang of KIST (this team identified the novel interaction between proteins), team led by Dr. Hoon Ryu of KIST (this team investigated human traumatic brain injury), and team led by Prof. Kyoungho Suk of the Kyungpook National University (this team studied the properties of inflammation using various animal models). Each team contributed to the findings based on their area of expertise.

Dr. Eun Mi Hwang of KIST said, “The hevin-calcyon interaction can potentially help in treating brain diseases as brain injury and neurodegenerative diseases can result in the generation of inflammatory responses.” She also added, “The findings can potentially help in the development of procedures for treating refractory brain diseases caused by impaired synaptogenic activity.”

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This research was conducted as a part of the Core Technology Development Project in Neuroscience funded by the National Research Foundation of Korea and supported by the Ministry of Science and ICT (MSIT). The results were published in the latest issue of “Cell Death & Differentiation” (IF: 10.717, top 6.229% in JCR), an international academic journal.

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Source: https://bioengineer.org/novel-interactions-between-proteins-that-help-in-recovering-from-brain-injury/

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New study uncovers details behind the body’s response to stress

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Findings could lead to new treatments for post-traumatic stress disorder and other conditions

Study Highlights

  • New research reveals how key proteins interact to regulate the body’s response to stress
  • Targeting these proteins may help treat or prevent stress-related psychiatric disorders

The biological mechanisms behind stress-related psychiatric conditions, including major depressive disorder and post-traumatic stress disorder (PTSD), are poorly understood.

New research now details the interplay between proteins involved in controlling the body’s stress response and points to potential therapeutic targets when this response goes awry. The study, which was conducted by an international team led by investigators at McLean Hospital, appears in the journal Cell Reports.

“A dysregulated stress response of the body can be damaging for the brain and promote susceptibility to mood and anxiety disorders,” said lead author Jakob Hartmann, PhD. Hartmann is an assistant neuroscientist in the Neurobiology of Fear Laboratory at McLean and an instructor in psychiatry at Harvard Medical School.

“A key brain region involved in the regulation of the stress response is the hippocampus,” said Hartmann. “The idea for this study occurred to us when we noticed interesting distinctions in hippocampal localization of three important stress-regulating proteins.”

The researchers’ experiments in non-human tissue and postmortem brain tissue revealed how these proteins–the glucocorticoid receptor (GR), the mineralocorticoid receptor (MR), and the FK506-binding protein 51 (FKBP5)–interact with each other.

Specifically, MRs, rather than GRs, control the production of FKBP5 under normal conditions. FKBP5 decreases GRs’ sensitivity to binding stress hormones during stressful situations. FKBP5 appears to fine-tune the stress response by acting as a mediator of the MR:GR balance in the hippocampus.

“Our findings suggest that therapeutic targeting of GR, MR, and FKBP5 may be complementary in manipulating central and peripheral regulation of stress,” said senior author Kerry J. Ressler, MD, PhD. Ressler is the chief scientific officer at McLean Hospital, chief of McLean’s Division of Depression and Anxiety Disorders, and a professor in psychiatry at Harvard Medical School.

“Moreover, our data further underline the important but largely unappreciated role of MR signaling in stress-related psychiatric disorders,” added Ressler. “The findings of this study will open new directions for future research.”

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ABOUT McLEAN HOSPITAL:

McLean Hospital has a continuous commitment to put people first in patient care, innovation and discovery, and shared knowledge related to mental health. It is consistently named the #1 freestanding psychiatric hospital in the United States by U.S. News & World Report. McLean Hospital is the largest psychiatric affiliate of Harvard Medical School and a member of Mass General Brigham. To stay up to date on McLean, follow us on Facebook, YouTube, and LinkedIn.

https://www.mcleanhospital.org/news/new-study-uncovers-details-behind-bodys-response-stress

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Source: https://bioengineer.org/new-study-uncovers-details-behind-the-bodys-response-to-stress/

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