Its powers may not rival Wolverine's, but a regenerative implant engineered by researchers at the University of Nebraska Medical Center and University of Nebraska–Lincoln could help repair bone-deep damage following physical trauma, surgery or osteoporosis.
The team has developed a biodegradable, nanofiber-based implant, or scaffold, whose design could better regenerate bone by effectively guiding the migration of recuperative cells to the injury site. When implanted in rats with bone defects, the cylindrical scaffold promoted the regeneration of bone that was denser, more voluminous and more like the surrounding tissue than that achieved by many other state-of-the-art designs.
The implant spurred regeneration even without the aid of externally sourced stem cells or so-called growth factors, which help promote healing but can also introduce regulatory complications and side effects that range from inflammation to unchecked tissue formation.
An innovative strategy that analyzes a region of the genome offers the possibility of early diagnosis of schizophrenia, reports a team led by researchers at Baylor College of Medicine. The strategy applied a machine learning algorithm called SPLS-DA to analyze specific regions of the human genome called CoRSIVs, hoping to reveal epigenetic markers for the condition.
In DNA from blood samples, the team identified epigenetic markers, a profile of methyl chemical groups in the DNA, that differ between people diagnosed with schizophrenia and people without the disease and developed a model that would assess an individual's probability of having the condition. Testing the model on an independent dataset revealed that it can identify schizophrenia patients with 80% accuracy. The study appears in the journal Translational Psychiatry.
Researchers at the University of Massachusetts Amherst recently unveiled their discovery of a new process for making RNA. The resulting RNA is purer, more copious and likely to be more cost-effective than any previous process could manage. This new technique removes the largest stumbling block on the path to next-generation RNA therapeutic drugs.
If DNA is the blueprint that tells the cells in our bodies what proteins to make and for what purposes, RNA is the messenger that carries DNA's instruction to the actual protein-making machinery within each cell. Most of the time this process works flawlessly, but when it doesn't, when the body can't make a protein it needs, as in the case of a disease like cystic fibrosis, serious illness can result.
One method for treating such protein deficiencies is with therapeutics that replace the missing proteins. But researchers have long known that it's more effective when the body can make the protein it needs itself. This is the goal of an emerging field of medicine—RNA therapeutics. The problem is, the current methods of producing lab-made RNA can't deliver RNA that is pure enough, in enough quantities in a way that's cost-effective. "We need lots of RNA," says Elvan Cavaç, lead author of the paper that was recently published in the Journal of Biological Chemistry, MBA student at UMass Amherst, and a recent Ph.D. graduate in chemistry, also from UMass. "We've developed a novel process for producing pure RNA, and since the process can reuse its ingredients, yielding anywhere between three and ten times more RNA than the conventional methods, it also saves time and cost."
Bacterial infections relating to medical implants place a huge burden on healthcare and cause great suffering to patients worldwide. Now, researchers at Chalmers University of Technology, Sweden, have developed a new method to prevent such infections, by covering a graphene-based material with bactericidal molecules.
"Through our research, we have succeeded in binding water-insoluble antibacterial molecules to the graphene, and having the molecules release in a controlled, continuous manner from the material," says Santosh Pandit, researcher at the Department of Biology and Biological Engineering at Chalmers, and first author of the study which was recently published in Scientific Reports.
"This is an essential requirement for the method to work. The way in which we bind the active molecules to the graphene is also very simple, and could be easily integrated into industrial processes."
Researchers have found a way to reduce organ rejection following a transplant by using a special polymer to coat blood vessels on the organ to be transplanted.
The polymer, developed by UBC medicine professor Dr. Jayachandran Kizhakkedathu and his team at the Centre for Blood Research and Life Sciences Institute, substantially diminished rejection of transplants in mice when tested by collaborators at SFU and Northwestern University.
"We're hopeful that this breakthrough will one day improve quality of life for transplant patients and improve the lifespan of transplanted organs," said Dr. Kizhakkedathu.
Researchers from the group of Hans Clevers (Hubrecht Institute) corrected mutations that cause cystic fibrosis in cultured human stem cells. In collaboration with the UMC Utrecht and Oncode Institute, they used a technique called prime editing to replace the 'faulty' piece of DNA with a healthy piece. The study, published in Life Science Alliance on August 9, shows that prime editing is safer than the conventional CRISPR/Cas9 technique. "We have for the first time demonstrated that this technique really works and can be safely applied in human stem cells to correct cystic fibrosis."
Cystic fibrosis (CF) is one of the most prevalent genetic diseases worldwide and has grave consequences for the patient. The mucus in the lungs, throat and intestines is sticky and thick, which causes blockages in organs. Although treatments are available to dilute the mucus and prevent inflammations, CF is not yet curable. However, a new study from the group of Hans Clevers (Hubrecht Institute) in collaboration with the UMC Utrecht and Oncode Institute offers new hope.
Endometriosis is a painful, chronic condition in which tissue from the uterus inappropriately grows outside the uterus. Current treatments are limited and include surgery and hormone therapy, which can involve unwanted side effects. New research conducted by Baylor College of Medicine, the University of Oxford, the University of Wisconsin-Madison and Bayer AG, offers new insight into how to treat this debilitating disease.
The researchers performed genetic analyses of humans and rhesus macaques to identify a specific gene, NPSR1, that increases risk of suffering from endometriosis. The results reveal a potential new nonhormonal drug target that may lead to improved therapy. Their results are published in Science Translational Medicine.
The Oxford team, led by corresponding author Dr. Krina T. Zondervan, had previously found a genetic linkage to endometriosis on chromosome 7p13-15 by analyzing DNA from families containing at least three women diagnosed with endometriosis. The Baylor team, led by senior author Dr. Jeffrey Rogers, verified this genetic linkage in the DNA of rhesus monkeys with spontaneous endometriosis at the Wisconsin National Primate Research Center at the University of Wisconsin-Madison. This validation justified further research through in-depth sequencing analysis of the endometriosis families at Oxford, which narrowed down the genetic cause to rare variants in the NPSR1 gene. Most of the women carrying these rare variants had stage III/IV disease. The Baylor researchers similarly sequenced rhesus monkeys and again showed suggestive evidence also in this species. Finally, an Oxford study of more than 11,000 women, including patients with endometriosis and healthy women, identified a specific common variant in the NPSR1 gene also associated with stage III/IV endometriosis.
Researchers at the Institute of Molecular Biology (IMB) and Johannes Gutenberg University Mainz (JGU) have developed a method to engineer new functionalities into cells. The results were published today in the journal Cell in the article "Dual film-like organelles enable spatial separation of orthogonal eukaryotic translation."
Numerous processes occur inside living cells, from DNA replication and repair to protein synthesis and recycling. In order to organize this plethora of reactions, they must be separated in three-dimensional space. One way eukaryotic cells do this is by extruding a piece of membrane to form a membrane-enclosed space—an organelle—in which specific functions can take place. Alternatively, the cell can also segregate molecules into distinct areas (so-called membraneless organelles) through phase separation, a phenomenon similar to the separation of vinegar and oil in a salad dressing. Such membraneless organelles have advantages: As they are not separated from the rest of the cell by a membrane barrier, large molecules can get in and out more easily. Membrane-enclosed organelles therefore operate like separate "rooms" in a cell, while membraneless organelles operate like different corners of the same room.
Neuroinflammation is the key driver of the spread of pathologically misfolded proteins in the brain and causes cognitive impairment in patients with Alzheimer's disease, researchers from the University of Pittsburgh School of Medicine reveal in a paper published today in Nature Medicine.
For the first time ever, the researchers showed in living patients that neuroinflammation—or activation of the brain's resident immune cells, called microglial cells—is not merely a consequence of disease progression; rather, it is a key upstream mechanism that is indispensable for disease development.
"As a young resident neurologist in my home country of Brazil, I noticed that many patients with Alzheimer's disease are left neglected and without access to appropriate care," said lead author Tharick Pascoal, M.D., Ph.D., assistant professor of psychiatry and neurology at Pitt. "Our research suggests that combination therapy aimed to reduce amyloid plaque formation and limit neuroinflammation might be more effective than addressing each pathology individually."
High blood pressure is the world's leading killer but poor rates of blood pressure control remain common. A new strategy where patients are started on a pill containing four medicines, each at a quarter of their usual doses, has been shown to be much more effective in getting blood pressure under control, compared to the common practice of monotherapy, where treatment commences with just one drug.
This first large-scale, randomized controlled clinical trial of starting this novel combination blood pressure medication brought blood pressure under control in 80 percent of participants in 12 weeks, compared to 60 percent in the control group who nonetheless had access to the best patient care.
Traditionally doctors have started with one drug and then follow up to consider adding or changing treatment—but this strategy is often not successful in practice and blood pressure control rates have remained stubbornly low for decades.
Researchers at CÚRAM, the SFI Research Centre for Medical Devices based at NUI Galway, have shown how the simple act of walking can power an implantable stimulator device to speed up treatment of musculoskeletal diseases.
The results of have been published in the prestigious journal Advanced Materials.
The research establishes the engineering foundations for a new range of stimulator devices that enable control of musculoskeletal tissue regeneration to treat tendon damage and disease and sports injuries, without the use of drugs or external stimulation.
Lead researcher on the study, CÚRAM Investigator Dr. Manus Biggs, said, "One of the most exciting parts of our study is that these implantable devices may be tailored to individual patients or disorders and may show promise in accelerating the repair of sport-related tendon injuries, particularly in athletes."
The study investigated whether electrical therapy, coupled with exercise, would show promise in treating tendon disease or ruptures. It showed that tendon cell function and repair can be controlled through electrical stimulation from an implantable device which is powered by body movement.
Chronic back pain affects upwards of 15 million adults in the US, racking up billions in healthcare costs and lost work days. Degeneration of the discs that cushion and support vertebrae, a common occurrence of aging, is a major contributor to low back pain. Although a widespread condition, few treatments are available. Now Jefferson's Makarand Risbud, Ph.D., James J. Maguire Jr. Professor of Spine Research in orthopedic surgery, division director of orthopedic research and co-director of the cell biology and regenerative medicine graduate program, and colleagues have shown that treating mice with a drug cocktail that removes aging cells reduces disc degeneration. The findings, reported in Nature Communications on September 3rd, show how a novel approach to preventing age-related disc degeneration may pave the way for treating chronic back pain.
Scientists from Nanyang Technological University, Singapore (NTU Singapore), in collaboration with clinicians at Tan Tock Seng Hospital (TTSH) in Singapore have developed a novel method that uses artificial intelligence (AI) to screen for glaucoma, a group of eye diseases that can cause vision loss and blindness through damage to the optic nerve at the back of the eye.
The AI-enabled method uses algorithms to differentiate optic nerves with glaucoma from those that are normal by analyzing stereo fundus images—multi-angle 2D images of the retina that are combined to form a 3D image.
When tested on stereo fundus images from TTSH patients undergoing expert examination, the AI method yielded an accuracy of 97 percent in diagnosing glaucoma.
Glaucoma is often called "the silent thief of sight" as it is usually asymptomatic until latter stages, when prognosis is poor. It is the principal cause of irreversible blindness worldwide and, in tandem with the rapid growth of the aging population, is expected to affect 111.8 million people globally by 2040, up from 76 million in 2020.
More than 3 million people in America have dental implants, used to replace a tooth lost to decay, gum disease, or injury. Implants represent a leap of progress over dentures or bridges, fitting much more securely and designed to last 20 years or more.
But often implants fall short of that expectation, instead needing replacement in five to 10 years due to local inflammation or gum disease, necessitating a repeat of a costly and invasive procedure for patients.
"We wanted to address this issue, and so we came up with an innovative new implant," says Geelsu Hwang, an assistant professor in the University of Pennsylvania School of Dental Medicine, who has a background in engineering that he brings to his research on oral health issues.
DNA is the instruction manual for every living organism, guiding the development and functioning of all biological processes. In essence, it is a molecule with a double helix structure with each unit of a helix containing what are known as "DNA bases."
Maintenance of DNA is extremely important for smooth operation of all bodily functions. DNA may be damaged by cellular metabolism byproducts, such as reactive oxygen species, and ionizing radiation (UV and gamma rays). In such a scenario, a set of enzymes (proteins that act as catalysts for biochemical reactions) are activated to repair the damage. The sequence of processes undertaken by the enzymes to fix DNA damage is known as "base excision repair" (BER).
BER is mainly carried out by the exonuclease III (ExoIII) and polymerase I (Pol I) enzymes. Despite the importance of the functions of these enzymes, the mechanism underlying their coordination has not been elucidated in previous studies.
Now, scientists led by Dr. Gwangrog Lee from the Gwangju Institute of Science and Technology (GIST) in Korea have utilized the latest technology in single molecule detection to study enzymatic interactions and observe the mechanism of BER, filling the gap in our understanding of this coordination mechanism.
A new study by researchers at University of Illinois Chicago suggests that when the protein optineurin, or OPTN, is present in cells it restricts the spread of HSV-1, the herpes simplex virus type 1.
In a "first of its kind" study, researchers also found a potential direct connection between neurodegenerative diseases, such as Alzheimer's disease, amyotrophic lateral sclerosis (ALS), glaucoma, and the herpesvirus, said Dr. Deepak Shukla, the Marion H. Schenk Esq. Professor in Ophthalmology for Research of the Aging Eye, and vice chair for research at UIC.
The research paper, "OPTN is a host intrinsic restriction factor against neuroinvasive HSV-1 infection," led by Shukla, was published recently in the journal Nature Communications.
Researchers sought to discover why HSV-1 can become fatal for individuals who are immunocompromised but not for healthy individuals. Herpesviruses naturally infect the central nervous system and can result in degenerative brain and eye disorders, as well as encephalitis. However, in most individuals, the virus is suppressed during a primary infection before it can significantly damage the central nervous system
A team of researchers affiliated with a host of institutions in China has developed an injectable hydrogel for use in repairing damaged cartilage. In their paper published in the journal Science Advances, the group describes how they made their hydrogel, how it can be applied and how well it worked when tested on mice and pigs.
Repair of torn or eroded cartilage has improved dramatically in recent years as scientists have learned to grow chondrocytes (cells that grow into cartilage) and to use them to encourage growth of new cartilage. They are typically grown on structures in patches which are then applied to the area in need of repair. One major drawback to such treatment, however, is the need to cut through the skin and lay open the area to be treated. Such treatment can lead to a painful recovery over several months. In this new effort, the researchers have developed a type of hydrogel that can be used for the same type of treatment without the need for surgery.
