For the very first time, a study led by Julian Chen and his group in Arizona State University's School of Molecular Sciences and the Biodesign Institute's Center for the Mechanism of Evolution, has discovered an unprecedented pathway producing telomerase RNA from a protein-coding messenger RNA (mRNA).
The central dogma of molecular biology specifies the order in which genetic information is transferred from DNA to make proteins. Messenger RNA molecules carry the genetic information from the DNA in the nucleus of the cell to the cytoplasm where the proteins are made. Messenger RNA acts as the messenger to build proteins.
"Actually, there are many RNAs (ribonucleic acids) that are not used to make proteins," explained Chen. "About 70 percent of the human genome is used to make noncoding RNAs that don't code for protein sequences but have other uses."
Telomerase RNA is one of the noncoding RNAs that assembles along with telomerase proteins to form the enzyme telomerase. Telomerase is crucial for cellular immortality in cancer and stem cells. In this study, Chen's group shows that a fungal telomerase RNA is processed from a protein-coding mRNA, instead of being synthesized independently.
"Our finding from this paper is paradigm-shifting. Most RNA molecules are synthesized independently and here we uncovered a dual function mRNA that can be used to produce a protein or to make a noncoding telomerase RNA, which is really unique," said Chen. "We will need to do a lot more research to understand the underlying mechanism of such an unusual RNA biogenesis pathway."
Antibiotics are standard treatments for fighting dangerous bacterial infections. Yet the number of bacteria developing a resistance to antibiotics is increasing. Researchers from Texas A&M University and the University of São Paulo are overcoming this resistance with light.
The researchers tailored antimicrobial photodynamic therapy (aPDT)—a chemical reaction triggered by visible light—for use on antibiotic-resistant bacteria strains. Results showed the treatment weakened bacteria to where low doses of current antibiotics could effectively eliminate them.
"Using aPDT in combination with antibiotics creates a synergy of interaction working together for a solution," said Vladislav Yakovlev, University Professor in the Department of Biomedical Engineering at Texas A&M and co-director of the project. "It's a step in the right direction against resistant bacteria."
The research results were published in Proceedings of the National Academy of Sciences (PNAS).
Medical optical imaging using the world's first 'ultrasound-induced tissue transparency' technology https://phys.org/news/2022-10-medical-o ... duced.html
by DGIST (Daegu Gyeongbuk Institute of Science and Technology)
A joint research team from DGIST led by Professors Jin Ho Chang and Jae Youn Hwang of the Department of Electrical Engineering and Computer Science has developed the world's first laser scanning microscopy technology that enables deeper and more detailed observation of biological tissues using gas bubbles that are temporarily produced by ultrasound.
Optical imaging and therapeutic technologies are widely utilized in life science research and clinical practice. However, due to the occurrence of optical scattering in the tissue, the light transmission is low. Consequently, there exists an inherent limitation in the image acquisition and treatment of deep tissue. This significantly hinders the expansion of the application field.
To overcome this, in 2017, Professor Jin Ho Chang's team envisioned that it would be possible to use micrometer-sized gas bubbles that are normally observed when tissues are exposed to high-intensity ultrasound. They developed a technology based on the fact that gas bubbles temporarily created by ultrasonic waves cause optical scattering in the same direction as the propagation of incident light, thus increasing the penetration depth of light.
Furthermore, the joint research team of Professors Jin Ho Chang and Jae Youn Hwang focused on expanding the application of optical imaging technology using ultrasound-induced gas bubbles. A confocal fluorescence microscope is a device that selectively detects fluorescence signals generated at the focal plane of light and provides high-resolution, high-contrast images of microstructures such as cancer cells. It is the most widely used device in life science research owing to its high performance. However, the focus of the light is blurred at depths exceeding 100 µm owing to the scattering of light that occurs inside the tissue, which significantly limits the application and effectiveness of confocal fluorescence microscopy.
To increase the maximum imaging depth of optical imaging modalities, such as confocal fluorescence microscopy, photons constituting the irradiated light must not have a phenomenon in which their propagation direction is distorted by light scattering in tissues. However, the previously developed method based on gas bubbles sparsely created by ultrasound was not a solution.
Researchers have identified a promising strategy for development of broad-spectrum antiviral therapies that centers around promoting a strong immune response capable of stopping a number of viruses in their infectious tracks.
Experiments in cell cultures and mice showed that blocking the function of a specific enzyme present in all cells triggers a powerful innate immune response, the body's first line of defense against any foreign invader. When challenged by several types of viruses in the study, this response dramatically lowered replication of viral particles and protected mouse lungs from damage.
There are still several avenues to explore, but the scientists say the finding could help change the approach to developing antiviral medications.
"Typically, in antiviral development, the saying is, 'one bug, one drug,'" said Jianrong Li, co-senior author of the study and a professor of virology in The Ohio State University Department of Veterinary Biosciences and Infectious Diseases Institute.
"A drug that can stimulate the immune system to have broad antiviral activities would be very attractive—one drug against multiple bugs would be an ideal situation."
The study is published in the journal Proceedings of the National Academy of Sciences.
This discovery was enabled in part by a technique the researchers used to map the precise location of an RNA modification they were studying, and to see which enzyme made the modification. The mapping led them to determine that this enzyme's work happens not in viruses, but in mammal hosts that viruses want to infect.
In a study published Thursday in the journal PLOS One, biochemist Patrick Griffin, Ph.D., and colleague Mi Ra Chang, Ph.D., describe a specific protein that manages activities within chondrocytes, a critical cell type that maintains healthy cartilage in joints.
As people age and stress their joints, their chondrocytes begin to fail. The UF Scripps team found that activating a specific protein in these cells called RORβ (beta) could restore multiple factors needed for smooth joints to healthier levels, helping to control inflammation. Activating RORβ could thus present a useful new strategy to prevent or delay development of the degenerative joint disease osteoarthritis, said Griffin, a professor of molecular medicine and scientific director of UF Scripps Biomedical Research.
"People need an osteoarthritis medication that addresses the root cause of cartilage damage and depletion as there currently are no disease-modifying drugs for what is the No. 1 cause of disability in the United States," Griffin said. "While our work is in the early stages, our study suggests that the nuclear receptor RORβ could present a novel therapeutic target to protect cartilage damage and perhaps turn on cartilage regeneration."
For around 40 years, scientists all over the world have been unsuccessfully trying to find a cure for HIV, but now a team of researchers from Aarhus University and Aarhus University Hospital have apparently found an important element in the equation.
So says Dr. Ole Schmeltz Søgaard, Professor of Translational Viral Research at Aarhus University, who is the senior author of an innovative study that has just been published in the journal Nature Medicine.
"This study is one of the first to be carried out on human beings in which we have demonstrated a way to strengthen the body's own ability to fight HIV—even when today's standard treatment is paused. We thus regard the study as an important step in the direction of a cure," he says.
The study was conducted in close collaboration with researchers from the UK, U.S., Spain and Canada.
The high level of reactive oxygen species (ROS) in the rheumatoid arthritis (RA) microenvironment and its persistent inflammatory nature can promote damage to joints, bones, and the synovium. Strategies that integrate effective RA microenvironment regulation with imaging-based monitoring could lead to improvements in the diagnosis and treatment of RA.
A joint research team from the Shenzhen Institute of Advanced Technology of the Chinese Academy of Sciences and the University of Texas at Austin has proposed a new strategy that can achieve targeted treatment of rheumatoid arthritis.
The researchers integrated small interfering RNAs (siRNAsT/I) and Prussian blue nanoparticles (PBNPs) to silence the expression of the proinflammatory cytokines TNF-α/IL-6 and scavenge the ROS associated with the RA microenvironment.
The study was published in PNAS on Oct. 18.
To enhance the in vitro and in vivo biological stability, biocompatibility, and targeting capability of the siRNAsT/I and PBNPs, the researchers prepared macrophage membrane vesicles (MMVs) to construct biomimetic nanoparticles, M@P-siRNAsT/I.
Significant time is needed to determine the drug susceptibility profile of a bacterial infection. Now, researchers from Nara Institute of Science and Technology and collaborating partners have published reports on a technology that will dramatically speed up this otherwise slow process and possibly help save lives.
The CDC states that antibiotic-resistant infections are responsible for killing over a million people worldwide every year. Central to managing resistant infections is quickly identifying an appropriate treatment to which the infective bacteria are susceptible. "Oftentimes susceptibility results are needed much faster than conventional tests can deliver them," says Yaxiaer Yalikun, senior author. "To address this, we developed a technology that can meet this need."
The group's work is based on impedance cytometry which measures the dielectric properties of individual cells with high throughput—more than a thousand cells per minute. Because the electrical readout of a bacterium corresponds to its physical response to an antibiotic, one has a straightforward means of determining whether the antibiotic works against the bacteria.
Conventional impedance cytometry involves analyzing the test (antibiotic treated) and reference (untreated) particles in one sample followed by calibrating the impedance of the two particles—both steps require technical specialists to carry out extensive post-processing, which was a major limitation the group was determined to overcome.
In a study published in ACS Sensors, the group develops a novel impedance cytometry method that simultaneously analyzes the test and reference particles in separate channels, creating easily analyzable separate datasets. This cytometry had nanoscale sensitivity, allowing for detection of even minute physical changes in bacterial cells.
A team of researchers from Japan studying the processes of hair follicle growth and hair pigmentation has successfully generated hair follicles in cultures. Their in vitro hair follicle model adds to the understanding of hair follicle development which could contribute to development of useful applications in treating hair loss disorders, animal testing, and drug screenings.
Their findings were published in Science Advances on October 21.
As an embryo develops, interactions occur between the outer layer of skin called the epidermal layer and the connective tissue called mesenchyme. These interactions work kind of like a messenger system to trigger hair follicle morphogenesis. Morphogenesis is the process in an organism where cells are organized into tissues and organs.
During the last several decades, scientists have explored the crucial mechanisms related to hair follicle development using animal models. Because fully understanding these mechanisms for hair follicle development remains challenging, hair follicle morphogenesis has not been successfully reproduced in a laboratory culture dish.
New research from Children's Medical Center Research Institute at UT Southwestern (CRI) found that different skeletal stem cell (SSC) populations contribute to repair of different kinds of bone injuries.
In the study, published in Cell Stem Cell, researchers identified distinct cell markers that allowed them to track SSCs in the bone marrow inside of bones versus SSCs in the periosteum on the outer surface of bones. They found that while bone marrow SSCs are responsible for the ongoing production of bone cells in normal bones and the repair of certain bone injuries, periosteal SSCs are primarily responsible for fracture repair.
SSCs must generate new bone cells throughout life to maintain and repair the skeleton. The skeleton is unusual in that it has multiple kinds of stem cells that reside in different regions of bone, including within the bone marrow and in the periosteum. After bone injuries, like fractures, SSCs in the bone marrow and periosteum begin to proliferate but make very different contributions to bone repair.
Researchers in the Morrison lab found that bone marrow SSCs repair smaller, stabilized bone injuries and are responsible for new bone growth under normal conditions during adulthood. In contrast, periosteal SSCs are primarily responsible for the repair of larger, unstabilized injuries like fractures. Surprisingly, researchers also found that periosteal SSCs regenerate not only bone but also cells within the bone marrow at the fracture site, giving rise to new bone marrow SSCs.
Two new studies from Washington University School of Medicine in St. Louis support development of a broadly applicable treatment for neurodegenerative diseases that targets a molecule that serves as the central executioner in the death of axons, the wiring of the nervous system.
Blocking this molecular executioner prevents axon loss, which has been implicated in many neurodegenerative diseases, from peripheral neuropathies to Parkinson's disease, and glaucoma to amyotrophic lateral sclerosis (ALS).
The new studies, both published Oct. 26 in the Journal of Clinical Investigation, reveal surprising details about how the molecule—called SARM1—triggers axon death that underlies the development of neurodegenerative diseases. The research also points to new therapeutic approaches for diseases defined by axon loss.
"We desperately need treatments for neurodegenerative diseases," said co-senior author Jeffrey Milbrandt, MD, Ph.D., the James S. McDonnell Professor and head of the Department of Genetics. "With the evidence of SARM1's central role in these diseases, we're very interested in finding ways to block this molecule—whether with small molecule inhibitors or gene therapy techniques. Our latest research suggests we also may be able to interfere with its ability to drive damaging neuroinflammation. We're hopeful this work will lead to effective new therapies across a range of neurodegenerative and neuroinflammatory diseases."
Scientists analyzing the effects of an organic compound on drug resistance bacteria have discovered how it can inhibit and kill a germ that causes serious illness or in some cases death.
Pseudomonas aeruginosa is a type of bacteria, often found in hospital patients, which can lead to infections in the blood, lungs (pneumonia), or other parts of the body after surgery.
Hydroquinine, an organic compound found in the bark of some trees, was recently found to have bacterial killing activity against the germ and several other clinically important bacteria, including Staphylococcus aureus, Escherichia coli, and Klebsiella pneumoniae.
The team behind the discovery, from the University of Portsmouth and Naresuan and Pibulsongkram Rajabhat Universities in Thailand, have now explored the molecular responses of Pseudomonas aeruginosa strains to hydroquinine. They did this by looking at which genes were switched on and which were switched off in response to the drug.
The new study, published in Antibiotics, revealed hydroquinine significantly alters the expression levels of virulence factors Pseudomonas aeruginosa. It also suggests the compound interferes with the assembly and movement of the bacteria.
Research by Royal College of Surgeons in Ireland (RCSI) University of Medicine and Health Sciences has discovered a new role for the blood clotting protein known as von Willebrand Factor (VWF), which could lead to the development of new treatments for patients with inflammatory and blood clotting disorders.
Published in Nature Communications, the research finds that VWF plays an important role in regulating immune responses at sites of blood vessel injury. This means that the protein has a newly discovered role in repairing damaged blood vessels in addition to its role in blood clotting.
Deficiency in VWF is called "von Willebrand Disease" and occurs in about 1 in 1,000 people in Ireland. People with this condition have increased risk of serious heavy bleeding. In contrast, people with high levels of the protein in their blood are at risk of developing serious blood clots. For example, very high VWF levels have been implicated in the unusual blood clots seen in the lungs of patients with severe COVID-19.
This research shows, for the first time, that VWF not only regulates blood clotting at the site of damage but also triggers local immune responses. Understanding this new biological role for VWF in regulating inflammatory responses may offer the opportunity to develop entirely new treatment options for patients with inflammatory and blood clotting disorders, such as von Willebrand Disease, deep vein thrombosis and myocardial infarction.
Lead author of the research Professor James O'Donnell, Director of the Irish Centre for Vascular Biology at RCSI School of Pharmacy and Biomolecular Sciences, said, "For more than 50 years, it has been known that von Willebrand factor plays a key role in preventing bleeding by acting as a glue at the site of injury. This research now helps us to further understand the role that VWF plays in linking blood coagulation and inflammation and thereby paves the way for the development of new treatments."
The first time I remember hearing the words “biology’s century,” it was a sales pitch.
I was standing by the Long Island Sound in Sachem’s Head, Conn., in the shadow of an 11-foot-tall granite Stonehenge replica built by Jonathan Rothberg, a biotech entrepreneur, as he talked up his newest gadget, a tabletop DNA sequencer. It was 2010.
Near his monument to the ancient past, Rothberg was conjuring a vision of the future, one based on harnessing the power of biology and technology to transform the world. The phrase he uttered wasn’t new, having been in circulation since the Human Genome Project in the 1990s, and I’d been covering biotech for a decade. But that was the moment the phrase sunk in. I added it to my Twitter bio, where it has remained.
Over the next decade, I’d see even more amazing things. Genetically altered white blood cells that can cure cancer. A gene therapy that gave sight to blind children. Pills that wrench decades of life from a cancer death sentence or ease the breathing of patients with cystic fibrosis. And, of course, not one but several effective Covid-19 vaccines created only a year into a once-in-a-century pandemic.
Here’s what “biology’s century” means to me: In the same way the 20th century belonged to physics, the 21st is biological. But while physics in the 20th century brought airplanes, personal computers, and posters of Albert Einstein, it also meant the atom bomb and a complete transformation of the social order.
And remember my friend, future events such as these will affect you in the future
Lab-grown red blood cells transfused into patient in world-first clinical trial
Laboratory-grown red blood cells have been transfused into a person in a world-first clinical trial.
If proved safe and effective, manufactured blood cells could revolutionise treatments for people with blood disorders such as sickle cell and rare blood types.
It can be hard to find well-matched donated blood for many with these disorders - and lab-grown red blood cells would mean people who require regular transfusions could need fewer in the future.
Ashley Toye, director of the NIHR Blood and Transplant Unit in red cell products, said: "This challenging and exciting trial is a huge stepping stone for manufacturing blood from stem cells.
"This is the first-time lab-grown blood from an allogeneic donor has been transfused and we are excited to see how well the cells perform at the end of the clinical trial."
Life extension tech, synth blood that can be infused with anything like nanotech, and so much more. Would be cool someday to reconstruct someone as needed as in Mass Effect or even Deus Ex. I think even Star Citizen has that as well or any of the space games on here which is one heck of a job put in to an even more marvelous concept.
An unusual type of antibody that even at miniscule levels neutralizes the Zika virus and renders the virus infection undetectable in preclinical models has been identified by a team led by Weill Cornell Medicine, New York-Presbyterian and National Institutes of Health (NIH) investigators.
Because Zika can cause birth defects when passed from a pregnant person to their fetus, this discovery could lead to the development of therapies to protect babies from the potentially devastating effects of this disease.
In research published Nov. 18 in Cell, the investigators isolated an ultrapotent immunoglobulin M (IgM) antibody—a five-armed immune protein that latches onto the virus— using blood cells taken from pregnant people infected with Zika. In experiments with mice, they determined that the antibody not only protected the animals from otherwise lethal infections, but also suppressed the virus to the point that it could not be detected in their blood.
Zika is currently circulating at low levels in many tropical countries, but that will inevitably change, according to co-senior author Dr. Sallie Permar, the Nancy C. Paduano Professor in Pediatrics and chair of pediatrics at Weill Cornell Medicine and pediatrician-in-chief at New York-Presbyterian/Weill Cornell Medical Center and New York-Presbyterian Komansky Children's Hospital. Dr. Mattia Bonsignori, chief of the Translational Immunobiology Unit of the Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases (NIAID), part of NIH, is a co-senior author.
A team of researchers at Duke University has developed a vaccine against uropathogenic E. coli (UPEC), the type of bacteria that cause urinary tract infections (UTIs) in humans. In their paper published in the journal Science Advances, the group describes how they made their vaccine and its performance when tested in mice and rabbits.
Urinary tract infections are most common in women and can produce extreme pain during urination—they can also lead to other complications that, if not treated, can be fatal. Such infections are generally treated with antibiotics. Unfortunately, some women develop chronic infections, which means they experience UTIs several times a year.
In such circumstances, it becomes problematic to continue to prescribe antibiotics because they kill all the bacteria in the gut, which tends to cause other intestinal problems. In this new effort, the researchers have taken a new approach to dealing with UTIs, avoiding antibiotics in general and instead creating a pill that targets only the bacteria behind the infection.
Scientists have been trying for many years to create a vaccine for UTIs, but have failed, mainly due to problems with getting a medication to penetrate the cellular mucosa that coats the walls of the mouth, throat and urinary tract. To overcome this problem, the researchers tried a variety of approaches that involved manipulating drugs that were able to penetrate cellular mucosa.
With the help of an AI, researchers at Chalmers University of Technology, Sweden, have succeeded in designing synthetic DNA that controls the cells' protein production. The technology can contribute to the development and production of vaccines, drugs for severe diseases, as well as alternative food proteins much faster and at significantly lower costs than today.
How genes are expressed is a process that is fundamental to the functionality of cells in all living organisms. Simply put, the genetic code in DNA is transcribed to the molecule messenger RNA (mRNA), which tells the cell's factory which protein to produce and in which quantities.
Researchers have put a lot of effort into trying to control gene expression because, among other things, it can contribute to the development of protein-based drugs. A recent example is the mRNA vaccine against COVID-19, which instructed the body's cells to produce the same protein found on the surface of the coronavirus.
The body's immune system could then learn to form antibodies against the virus. Likewise, it is possible to teach the body's immune system to defeat cancer cells or other complex diseases if one understands the genetic code behind the production of specific proteins.
Most of today's new drugs are protein-based, but the techniques for producing them are both expensive and slow, because it is difficult to control how the DNA is expressed. Last year, a research group at Chalmers, led by Aleksej Zelezniak, Associate Professor of Systems Biology, took an important step in understanding and controlling how much of a protein is made from a certain DNA sequence.
