There are plenty of great scientific research stories out this week. Here’s a look at just a few of them.
New Type of Cell Only Found in Human Brains
An international team of researchers identified a brain cell in humans that doesn’t exist in mice. They published their research in the journal Nature Neuroscience. The cells are one of 10 GABAergic interneuron subtypes and are called rosehip neurons. “This particular type of cell had properties that had never actually been described in another species,” Ed Lein, one of the study’s authors and a researcher at the Allen Institute for Brain Science in Seattle, told National Public Radio.
Although it is believed that certain types of neurons are unique to humans, they have all eventually been identified in other mammals. It’s possible these new cell types will be as well. The researchers speculate that if the cells are unique to humans, it might help explain why some treatments for brain disorders sometimes work in mice, but not in humans. It may also support new understanding of brain disorders such as autism, schizophrenia or Alzheimer’s disease.
The researchers don’t know exactly what rosehip cells do. They seem to be involved in controlling information flow to specific brain areas.
Stunted Telomeres Found in People with Cardiomyopathy
Telomeres are the structures found at the end of DNA. Think of them like those little plastic things, called aglets, found at the end of shoelaces that keep the laces from unraveling. Telomeres grow shorter as cells divide, which is linked to aging. Researchers at Stanford University found that patients with cardiomyopathy, a form of heart disease, have abnormally short telomeres in the heart muscles responsible for contraction. They published their research in the Proceedings of the National Academy of Sciences.
A similar finding was identified in patients with Duchenne muscular dystrophy (DMD), a muscle-wasting disease. “The shortening of telomeres in cardiomyocytes appears to be a reliable hallmark of cardiac failures that arise due to genetic defects, and it’s very specific to cells that require the missing contractile proteins such as dystrophin, troponin T or myosin heavy chain, among others,” said Helen Blau, professor of microbiology and immunology and member of the Stanford Cardiovascular Institute, in a statement.
It’s still unknown if the shortened telomeres directly affect the cardiomyoctyes’ function or are caused by heart failure. It does provide another avenue of investigation and research. Blau stated, “Now we can study this phenomenon in the lab in real time and start to ask questions about cause and effect. We’d love to know, for example, how this shortening might impact the DNA damage response, mitochondrial dysfunction and cell-death pathways. It opens up a whole new line of investigation.”
A New Way to Fight Herpesviruses
A team of researchers led by Leo Weinberger, the William and Ute Bowes Distinguished Professor and director of the Gladstone-UCSF Center for Cell Circuitry, identified the mechanism by which the human cytomegalovirus is able to bypass the body’s immune system. They published their work in the journal PNAS.
Normally, a virus enters a cell and the cell blocks the viral DNA, preventing it from intercalating into the DNA. Cytomegalovirus takes a slightly different approach to work around this, carrying its viral DNA into the cell with proteins called PP71. Once in the cell, the cytomegalovirus releases the proteins, which then allow the viral DNA to replicate.
“The way the virus operates is pretty cool, but it also presents a problem we couldn’t solve,” stated Noam Vardi, a postdoctoral scholar in Weinberger’s laboratory and first author of the study. “The PP71 proteins are needed for the virus to replicate. But they actually die after a few hours, while it takes days to create new virus. So how can the virus successfully multiply even after these proteins are gone?”
PP71, it turns out, activates another protein called IE1, which takes over after PP71 dies. Cytomegalovirus is a leading cause of birth defects and transplant failures. This research could provide scientists with a new therapeutic target for cytomegalovirus and other herpesviruses, such as Epstein-Barr, which causes mononucleosis, and herpes simplex virus 1 and 2 that produce cold sores and genital herpes.
Using Stem Cells in Live Transplants
Researchers from the Medical Research Council (MRC) Centre for Regenerative Medicine at the University of Edinburgh were able to transform stem cells into 3D human liver tissue. The research was published in the journal Archives of Toxicology.
The team took human embryonic stem cells and stimulated them to become pluripotent stem cells, which are adult cells that have been induced to turn back into stem cells, and then stimulated them to develop the characteristics of liver cells, called hepatocytes. Over the course of a year, these cells grew into small spheres in a Petri dish. “This is the first time anyone has kept stem cell-derived liver tissue alive for more than a year in the lab,” stated David Hay, who led the research. “Keeping the cells alive and stable as liver cells for a long time is a very difficult step, but crucial if we hope to use this technology in people.”
Hay and his team took the next step, which was to load the liver cells onto 3D scaffolds built of a biodegradable polyester, polycaprolactone, and implanted them under the skin of mice. Blood vessels grew on the scaffolds and the mice had human liver proteins circulating in their blood, which meant the tissue had been successfully integrated into the animals’ circulatory systems. The scaffolds weren’t rejected by their immune systems.
Regenerating Nerve Fibers from Spinal Cord Injury
Researchers at the Ecole Polytechnique Federale de Lausanne (EPFL) in Switzerland and University of California, Los Angeles (UCLA) developed a three-step process for regenerating electro-physiologically active nerve fibers across complete spinal cord lesions in rodents. The research was published in the journal Nature.
“Our aim was to replicate, in adults, the conditions that encourage the growth of nerve fibers during development,” stated senior author Gregoire Courtine of EPFL. “We have understood the combinations of biological mechanisms that are necessary to enable severed nerve fiber regrowth across complete spinal cord injuries in adult mammals.”
The process involved delivering a sequence of growth factors, proteins or hormones, which resulted in reactivating the axons’ genetic programming for growth, develop a permissive environment for them to grow, and a “chemical slope that marks the path along which axons are encouraged to regrow.” And regrow they did. This is a long way from being applied to humans, but it is an intriguing start.
How Jupiter was Born
Although completely and happily unrelated to the life sciences and biopharma, researchers at the University of Zurich have figured out how the planet Jupiter was formed. The scientists collected data from meteorites that indicated that Jupiter’s growth had been delayed for two million years, but until now they weren’t really sure why.
Jupiter is 300 times the mass of the Earth and has an equator diameter of approximately 143,000 kilometers. “We could show that Jupiter grew in different, distinct phases,” stated Julia Venturini, a postdoctoral scholar at the University of Zurich.
“Especially interesting is that it is not the same kind of bodies that bring mass and energy,” stated Yann Alibert, Science Officer of PlanetS and first author of the paper.
In the first million years of “life,” Jupiter’s embryo gathered small, centimeter-sized pebbles and built up its core. The next two million years were a slower accretion of larger, kilometer-sized rocks dubbed planetesimals. They slammed into the growing planet with a huge amount of energy, which released heat. “During the first stage, the pebbles brought the mass,” Alibert states. “In the second phase, the planetesimals also added a bit of mass, but what is more important, they brought energy.”
And after three million years, the planet grew to a body about 50 times Earth’s mass. A third phase began that caused the accumulation of gas that led to the current gas giant.
The work was published in Nature Astronomy.
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