MIT Research News' Journal

Wireless communication breaks through water-air barrier

MIT researchers have taken a step toward solving a longstanding challenge with wireless communication: direct data transmission between underwater and airborne devices.

Today, underwater sensors cannot share data with those on land, as both use different wireless signals that only work in their respective mediums. Radio signals that travel through air die very rapidly in water. Acoustic signals, or sonar, sent by underwater devices mostly reflect off the surface without ever breaking through. This causes inefficiencies and other issues for a variety of applications, such as ocean exploration and submarine-to-plane communication.

In a paper being presented at this week’s SIGCOMM conference, MIT Media Lab researchers have designed a system that tackles this problem in a novel way. An underwater transmitter directs a sonar signal to the water’s surface, causing tiny vibrations that correspond to the 1s and 0s transmitted. Above the surface, a highly sensitive receiver reads these minute disturbances and decodes the sonar signal.

“Trying to cross the air-water boundary with wireless signals has been an obstacle. Our idea is to transform the obstacle itself into a medium through which to communicate,” says Fadel Adib, an assistant professor in the Media Lab, who is leading this research. He co-authored the paper with his graduate student Francesco Tonolini.

The system, called “translational acoustic-RF communication” (TARF), is still in its early stages, Adib says. But it represents a “milestone,” he says, that could open new capabilities in water-air communications. Using the system, military submarines, for instance, wouldn’t need to surface to communicate with airplanes, compromising their location. And underwater drones that monitor marine life wouldn’t need to constantly resurface from deep dives to send data to researchers.

Another promising application is aiding searches for planes that go missing underwater. “Acoustic transmitting beacons can be implemented in, say, a plane’s black box,” Adib says. “If it transmits a signal every once in a while, you’d be able to use the system to pick up that signal.”

Decoding vibrations

Today’s technological workarounds to this wireless communication issue suffer from various drawbacks. Buoys, for instance, have been designed to pick up sonar waves, process the data, and shoot radio signals to airborne receivers. But these can drift away and get lost. Many are also required to cover large areas, making them impracticable for, say, submarine-to-surface communications.

TARF includes an underwater acoustic transmitter that sends sonar signals using a standard acoustic speaker. The signals travel as pressure waves of different frequencies corresponding to different data bits. For example, when the transmitter wants to send a 0, it can transmit a wave traveling at 100 hertz; for a 1, it can transmit a 200-hertz wave. When the signal hits the surface, it causes tiny ripples in the water, only a few micrometers in height, corresponding to those frequencies.

To achieve high data rates, the system transmits multiple frequencies at the same time, building on a modulation scheme used in wireless communication, called orthogonal frequency-division multiplexing. This lets the researchers transmit hundreds of bits at once.

Positioned in the air above the transmitter is a new type of extremely-high-frequency radar that processes signals in the millimeter wave spectrum of wireless transmission, between 30 and 300 gigahertz. (That’s the band where the upcoming high-frequency 5G wireless network will operate.)

The radar, which looks like a pair of cones, transmits a radio signal that reflects off the vibrating surface and rebounds back to the radar. Due to the way the signal collides with the surface vibrations, the signal returns with a slightly modulated angle that corresponds exactly to the data bit sent by the sonar signal. A vibration on the water surface representing a 0 bit, for instance, will cause the reflected signal’s angle to vibrate at 100 hertz.

“The radar reflection is going to vary a little bit whenever you have any form of displacement like on the surface of the water,” Adib says. “By picking up these tiny angle changes, we can pick up these variations that correspond to the sonar signal.”

Listening to “the whisper”

A key challenge was helping the radar detect the water surface. To do so, the researchers employed a technology that detects reflections in an environment and organizes them by distance and power. As water has the most powerful reflection in the new system’s environment, the radar knows the distance to the surface. Once that’s established, it zooms in on the vibrations at that distance, ignoring all other nearby disturbances.

The next major challenge was capturing micrometer waves surrounded by much larger, natural waves. The smallest ocean ripples on calm days, called capillary waves, are only about 2 centimeters tall, but that’s 100,000 times larger than the vibrations. Rougher seas can create waves 1 million times larger. “This interferes with the tiny acoustic vibrations at the water surface,” Adib says. “It’s as if someone’s screaming and you’re trying to hear someone whispering at the same time.”

To solve this, the researchers developed sophisticated signal-processing algorithms. Natural waves occur at about 1 or 2 hertz — or, a wave or two moving over the signal area every second. The sonar vibrations of 100 to 200 hertz, however, are a hundred times faster. Because of this frequency differential, the algorithm zeroes in on the fast-moving waves while ignoring the slower ones.

Testing the waters

The researchers took TARF through 500 test runs in a water tank and in two different swimming pools on MIT’s campus.

In the tank, the radar was placed at ranges from 20 centimeters to 40 centimeters above the surface, and the sonar transmitter was placed from 5 centimeters to 70 centimeters below the surface. In the pools, the radar was positioned about 30 centimeters above surface, while the transmitter was immersed about 3.5 meters below. In these experiments, the researchers also had swimmers creating waves that rose to about 16 centimeters.

In both settings, TARF was able to accurately decode various data — such as the sentence, “Hello! from underwater” — at hundreds of bits per second, similar to standard data rates for underwater communications. “Even while there were swimmers swimming around and causing disturbances and water currents, we were able to decode these signals quickly and accurately,” Adib says.

In waves higher than 16 centimeters, however, the system isn’t able to decode signals. The next steps are, among other things, refining the system to work in rougher waters. “It can deal with calm days and deal with certain water disturbances. But [to make it practical] we need this to work on all days and all weathers,” Adib says.

The researchers also hope that their system could eventually enable an airborne drone or plane flying across a water’s surface to constantly pick up and decode the sonar signals as it zooms by.

The research was supported, in part, by the National Science Foundation.

Study: Cellular changes lead to chronic allergic inflammation in the sinus

Chronic rhinosinusitis is distinct from your average case of seasonal allergies. It causes the sinuses to become inflamed and swollen for months to years at a time, leading to difficulty breathing and other symptoms that make patients feel miserable. In some people, this condition also produces tissue outgrowths known as nasal polyps, which, when severe enough, have to be removed surgically.

By performing a genome-wide analysis of thousands of single cells from human patients, MIT and Brigham and Women’s Hospital researchers have created the first global cellular map of a human barrier tissue during inflammation. Analysis of this data led them to propose a novel mechanism that may explain what sustains chronic rhinosinusitis.

Their findings also offer an explanation for why some rhinosinusitis patients develop nasal polyps, which arise from epithelial cells that line the respiratory tract. Furthermore, their study may have broader implications for how researchers think about and treat other chronic inflammatory diseases of barrier tissues, such as asthma, eczema, and inflammatory bowel disease.

“We saw major gene-expression differences in subsets of epithelial cells which had been previously obscured in bulk tissue analyses,” says Alex K. Shalek, the Pfizer-Laubach Career Development Assistant Professor of Chemistry, a core member of MIT’s Institute for Medical Engineering and Science (IMES), and an extramural member of the Koch Institute for Integrative Cancer Research, as well as an associate member of the Ragon and Broad Institutes.

“When you look across the entire transcriptome, comparing cells from patients with different disease statuses over thousands of genes, you can start to understand the relationships between them and discover which transcriptional programs have supplanted the usual ones,” Shalek says.

The lead authors of the paper, which appears in the Aug. 22 issue of Nature, are Jose Ordovas-Montanes, an IMES postdoc fellow supported by the Damon Runyon Cancer Research Foundation, and Daniel Dwyer, a research fellow at Brigham and Women’s Hospital. Shalek and Nora Barrett, an assistant professor of medicine at Brigham and Women’s, are the paper’s senior authors.

Clinical single-cell RNA sequencing

Last year, Shalek and his colleagues developed a new portable technology that enables rapid sequencing of the RNA contents of several thousand single cells in parallel from tiny clinical samples. This technology, known as Seq-Well, allows researchers to see what transcriptional programs are turned on inside individual cells, giving them insight into the identities and functions of those cells.

In their latest study, the MIT and Brigham and Women’s researchers applied this technology to cells from the upper respiratory tract of patients suffering from chronic rhinosinusitis, with the hypothesis that distinct gene-expression patterns within epithelial cells might reveal why some patients develop nasal polyps while others do not.

This analysis revealed striking differences in the genes expressed in basal epithelial cells (a type of tissue stem cell) from patients with and without nasal polyps. In nonpolyp patients and in healthy people, these cells normally form a flat base layer of tissue that coats the inside of the nasal passages. In patients with polyps, these cells begin to pile up and form thicker layers instead of differentiating into epithelial cell subsets needed for host defense.

This type of gross tissue abnormality has been observed through histology for decades, but the new study revealed that basal cells from patients with polyps had turned on a specific program of gene expression that explains their blunted differentiation trajectory. This program appears to be sustained directly by IL-4 and IL-13, immune response cytokines known to drive allergic inflammation when overproduced at pathologic levels.

The researchers found that these basal cells also retain a “memory” of their exposure to IL-4 and IL-13: When they removed basal cells from nonpolyps and polyps, grew them in equivalent conditions for a month, and then exposed them to IL-4 and IL-13, they found that unstimulated cells from patients with polyps already expressed many of the genes that were induced in those without polyps. Among the IL-4 and IL-13 responsive memory signatures were genes from a cell signaling pathway known as Wnt, which controls cell differentiation.

Immunologists have long known that B cells and T cells can store memory of an allergen that they have been exposed to, which partly explains why the immune system may overreact the next time the same allergen is encountered. However, the new finding suggests that basal cells also contribute a great deal to this memory.

Since basal cells are stem cells that generate the other cells found in the respiratory epithelium, this memory may influence their subsequent patterns of gene expression and ability to generate mature specialized epithelial cells. The team noted a substantial impact on the balance of cell types within the epithelium in patients with severe disease, leading to a population of cells with diminished diversity.

“Once you know that IL-4 and IL-13 act on stem cells, it changes the way in which you have to think about intervening, versus if they acted on differentiated cells, because you have to erase that memory in order to bring the system back to homeostasis,” Shalek says. “Otherwise you’re not actually dealing with a root cause of the problem.”

The findings show the importance of looking beyond immune cells for factors that influence chronic allergies, says Shruti Naik, an assistant professor of pathology, medicine, and dermatology at New York University School of Medicine.

“They examined the tissue as a whole rather than biasing the study toward one cell type or another, and what they found is that other components of the tissue are irreversibly impacted by inflammation,” says Naik, who was not involved in the research.

Blocking cytokines in humans

The findings suggested that ongoing efforts to block the effects of IL-4 and IL-13 might be a good way to try to treat chronic rhinosinusitis, a hypothesis that the researchers validated using an antibody that blocks a common receptor for these two cytokines. This antibody has been approved to treat eczema and is undergoing further testing for other uses. The researchers analyzed the gene expression of basal cells taken from one of the patients with polyps before and after he had been treated with this antibody. They found that most, but not all, of the genes that had been stimulated by IL-4 and IL-13 had returned to normal expression levels.

“It suggests that blockade of IL-4 and IL-13 can help to restore basal cells and secretory cells towards a healthier state,” Ordovas-Montanes says. “However, there’s still some residual genetic signature left. So now the question will be, how do you intelligently target that remainder?”

The researchers now plan to further detail the molecular mechanisms of how basal cells store inflammatory memory, which could help them to discover additional drug targets. They are also studying inflammatory diseases that affect other parts of the body, such as inflammatory bowel disease, where inflammation often leads to polyps that can become cancerous. Investigating whether stem cells in the gut might also remember immunological events, sustain disease, and play a role in tumor formation, will be key to designing early interventions for inflammation-induced cancers.

The research was funded by the Searle Scholars Program, the Beckman Young Investigator Program, the Pew-Stewart Scholars Program, Sloan Fellowship Program, the Steven and Judy Kaye Young Innovators program, the Damon Runyon Cancer Research Foundation, the Bill and Melinda Gates Foundation, and the National Institutes of Health.