Health Equity

Traditional heart surgery, which involves opening the chest by cutting through the breastbone, comes with a high risk of complications and a long recovery time. Newer, minimally invasive procedures avoid a lot of that risk and can get people back on their feet more quickly.

But a new Medical Center study suggests that Black patients have less access to the safer procedures compared to white patients.

The study, led by Laurent Glance, a professor of anesthesiology and perioperative medicine, appears in JAMA Network Open.

Glance and his colleagues found that non-Hispanic Black patients were 35 percent less likely to undergo minimally invasive mitral valve surgery and 62 percent more likely to have serious complications or to die compared to non-Hispanic white patients. Hispanic patients were 26 percent more likely to have major complications or die compared to white patients, but unlike Black patients, were not less likely to get minimally invasive surgery.

The findings were based on an analysis of data from the Society of Thoracic Surgeons National Adult Cardiac Surgery Database. Nearly 104,000 patients across 1,085 hospitals who underwent mitral valve surgery between 2014 and 2019 were included in the analysis.

The authors note several patterns in the data that may offer reasons for the inequity: Black patients were more likely to have Medicaid than commercial insurance, seek treatment at under-resourced hospitals, and be treated by less experienced surgeons.

Based on the findings, the authors argue in favor of several reforms: increasing access to commercial insurance; lowering the age of eligibility or creating a buy-in model for Medicare; eliminating federal incentives that unintentionally impose financial penalties on hospitals that serve the greatest number of vulnerable patients; and regionalizing care, which enables high-risk patients to be referred to centers where they receive expert, specialist care.

—Susanne Pallo ’15M (PhD)

Energy Efficiency

Perovskites—a family of materials nicknamed for their crystalline structure—have been identified as a much less expensive, equally efficient replacement for silicon in solar cells. Now, a study led by optics professor of Chunlei Guo suggests that perovskites may be far more efficient silicon replacements.

The key, Guo reports in Nature Photonics, is taking a physics-based approach that relies on unique properties of metals. In a solar cell, photons from sunlight interact with and excite electrons, causing the electrons to leave their atomic cores and generate an electrical current. But the electrons can also recombine with their atomic cores. Researchers typically synthesize perovskites in a wet lab, and then apply the material as a film on a glass substrate.

But by introducing substrates made instead of either a layer of metal or of alternating layers of metal and dielectric material, Guo and his coauthors found they could increase the efficiency of light conversion by 250 percent.

“A piece of metal can do just as much work as complex chemical engineering in a wet lab,” says Guo, adding that the new research may be particularly useful for future solar energy harvesting.

—Bob Marcotte

Neuroscience

Researchers have described in the journal Science a previously unknown component of brain anatomy. Maiken Nedergaard, codirector of the Center for Translational Neuromedicine, and a colleague at the University of Copenhagen, where Nedergaard also has an appointment, describe a membrane that acts as a protective barrier and a platform from which immune cells monitor the brain for infection and inflammation.

According to Nedergaard, the membrane—called SLYM, for subarachnoidal lymphatic-like membrane—“segregates and helps control the flow of cerebrospinal fluid (CSF) in and around the brain.” In doing so, it “provides us much greater appreciation of the sophisticated role that CSF plays not only in transporting and removing waste from the brain, but also in supporting its immune defenses.”

Nedergaard and her colleagues have transfomed the understanding of the fundamental mechanics of the human brain by detailing many critical functions of previously overlooked cells as well as the brain’s unique process of waste removal, which the lab named the glymphatic system.

Just a few cells in thickness, the membrane acts as a tight barrier, allowing only very small molecules to pass through. It also seems to separate “clean” and “dirty” cerebrospinal fluid. The second observation hints at the likely role played by the membrane in the glymphatic system, which the researchers suggest will led to a more precise understanding of the system.

—Mark Michaud

Medicine & Health

The most common cause of hearing loss stems from damage to cochlear hair cells, the primary cells to detect sound waves. People who have repeated exposure to loud noises—military personnel, construction workers, and many musicians and frequent concertgoers, for example—are most at risk for such hearing loss.

Because cochlear hair cells can’t regenerate, the most common cause of hearing loss is also progressive. But not in birds and fish, whose hair cells can regenerate.

Researchers at the Del Monte Institute for Neuroscience are getting closer to identifying the mechanisms that may promote such regeneration in mammals, as explained in research published in Frontiers in Cellular Neuroscience.

Previous research conducted in the lab of Patricia White, a professor of neuroscience and otolaryngology, showed that the expression of a gene called ERBB2 was able to activate the growth of new hair cells in mammals. The new research, led by Dorota Piekna-Przybylaka, a staff scientist in White’s lab, shows the mechanism for that activation.

The researchers found that in adult mice, the gene initiates the expression of multiple proteins, including one that activates a receptor known to be present in cochlear-supporting cells. The increase in cellular response promoted mitosis in the supporting cells, a key event for regeneration.

“This discovery has made it clear that regeneration is not only restricted to the early stages of development,” says Piekna-Przybylaka. “We believe we can use these findings to drive regeneration in adults.”

—Kelsie Smith Hayduk

RNA Biology

Researchers at the Center for RNA Biology have discovered a new way to suppress mutations that lead to a wide range of genetic disorders.

A study in the journal Molecular Cell describes a strategy that co-opts a normal RNA modification process within cells to transform disease genes into normal genes that produce healthy proteins. The findings may ultimately help researchers alter the course of devastating disorders such as cystic fibrosis, muscular dystrophy, and many forms of cancer.

Around 15 percent of mutations that lead to genetic diseases are called nonsense mutations. Aptly named, nonsense mutations occur when an mRNA molecule contains an early “stop” signal. When the mRNA takes genetic instructions from DNA to create a protein, the early stop sign orders the cell to stop reading the instructions partway through the process. The result is the creation of an incomplete protein that can lead to disease.

A team led by Yi-Tao Yu, Dean’s Professor of Biochemistry and Biophysics, designed an artificial guide RNA—a piece of RNA that can modify other types of RNA. Guide RNAs are a natural mechanism that cells use all the time, but Yu’s team designed one that targets mRNA molecules containing early stop signals by rendering the signals invisible. As a result, cells can read the genetic instructions all the way through and create full-length, functional proteins.

The team also discovered that the artificial guide RNA suppressed another mechanism in the cell known as nonsense-mediated mRNA decay, a process that eliminates mRNAs with early stop signals so that no protein is produced. Curbing it offered a second way for the artificial guide RNA to ensure that a significant amount of mRNA was present in the cell, and that the genetic instructions carried by the targeted mRNAs were read completely.

—Emily Boynton