Isegoria

Native to Africa, watermelons have been grown throughout the continent since ancient times — despite the fact that watermelons were not sweet until much, much later:

In southwest Libya, 5,000-year-old seeds were excavated, and watermelon remnants from 1500 B.C. have been discovered in the foundational deposits beneath walls of a Sudanese temple. Archeologists have also found seeds and paintings of various species of watermelon in ancient Egyptian tombs dating back from as long as 4,000 years ago. These species include wild watermelons, as well as the oblong predecessors of the “dessert” watermelon.

But if not a flavorful fruit, what were these watermelons good for? According to the work of Harry S. Paris, a horticulturalist at the Agricultural Research Organization in Israel, ancient Egyptians likely harvested the round fruit for its water. Wild, or “spontaneous” plants, Paris writes, can be sources of clean water during the long, dry season, and can provide food for livestock and animals.

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Living travelers, too, needed reliable water sources to sustain them. According to Paris, it’s likely that travelers took watermelons with them as a kind of nature-made canteen. Along with trade, he writes, the watermelon’s role as a portable fresh water supply helped the fruit find its way into new regions.

Once the Greeks got a hold of the pepo (as they called it) around 400 B.C., they, too, put it to use. While some varieties were eaten (and others had to be boiled, fried, or simply avoided), the watermelon made a splash in the medical world. Pliny the Elder found pepones to be incredibly refreshing, and, according to one translation, “also laxative.” The first-century physician Dioscorides also noted that the pepon was cooling, wet, and diuretic.

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But by the first few centuries A.D., posits Paris, the watermelon had likely sweetened up. Writings in Hebrew from the end of the second century, as well as sixth-century Latin texts, group the watermelon with other sweet fruits, including pomegranates, figs, and grapes.

Harvard Medical School graduate and lecturer Dr. Stephanie Taylor and colleagues studied 370 patients in one unit of a hospital to try to isolate the factors associated with patient infections:

They tested and retested 8 million data points controlling for every variable they could think of to explain the likelihood of infection. Was it hand hygiene, fragility of the patients, or room cleaning procedures? Taylor thought it might have something to do with the number of visitors to the patient’s room.

While all those factors had modest influence, one factor stood out above them all, and it shocked the research team. The one factor most associated with infection was (drum roll): dry air. At low relative humidity, indoor air was strongly associated with higher infection rates. “When we dry the air out, droplets and skin flakes carrying viruses and bacteria are launched into the air, traveling far and over long periods of time. The microbes that survive this launching tend to be the ones that cause healthcare-associated infections,” said Taylor. “Even worse, in addition to this increased exposure to infectious particles, the dry air also harms our natural immune barriers which protect us from infections.”

Since that study was published, there is now more research in peer-reviewed literature observing a link between dry air and viral infections, such as the flu, colds and measles, as well as many bacterial infections, and the National Institutes of Health (NIH) is funding more research. Taylor finds one of the most interesting studies from a team at the Mayo Clinic, which humidified half of the classrooms in a preschool and left the other half alone over three months during the winter. Influenza-related absenteeism in the humidified classrooms was two-thirds lower than in the standard classrooms—a dramatic difference. Taylor says this study is important because its design included a control group: the half of classrooms without humidity-related intervention.

Scientists attribute the influence of dry air to a new understanding about the behavior of airborne particles, or “infectious aerosol transmissions.” They used to assume the microbes in desiccated droplets were dead, but advances in the past several years changed that thinking. “With new genetic analysis tools, we are finding out that most of the microbes are not dead at all. They are simply dormant while waiting for a source of rehydration,” Taylor explained. “Humans are an ideal source of hydration, since we are basically 60% water. When a tiny infectious particle lands on or in a patient, the pathogen rehydrates and begins the infectious cycle all over again.”

This isn’t exactly news though.

To pay attention, the brain uses filters, not a spotlight:

For a long time, because attention seemed so intricately tied up with consciousness and other complex functions, scientists assumed that it was first and foremost a cortical phenomenon. A major departure from that line of thinking came in 1984, when Francis Crick, known for his work on the structure of DNA, proposed that the attentional searchlight was controlled by a region deep in the brain called the thalamus, parts of which receive input from sensory domains and feed information to the cortex. He developed a theory in which the sensory thalamus acted not just as a relay station, but also as a gatekeeper — not just a bridge, but a sieve — staunching some of the flow of data to establish a certain level of focus.

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[Michael Halassa, a neuroscientist at the McGovern Institute for Brain Research at the Massachusetts Institute of Technology] was drawn to a thin layer of inhibitory neurons called the thalamic reticular nucleus (TRN), which wraps around the rest of the thalamus like a shell. By the time Halassa was a postdoctoral researcher, he had already found a coarse level of gating in that brain area: The TRN seemed to let sensory inputs through when an animal was awake and attentive to something in its environment, but it suppressed them when the animal was asleep.

In 2015, Halassa and his colleagues discovered another, finer level of gating that further implicated the TRN as part of Crick’s long-sought circuit — this time involving how animals select what to focus on when their attention is divided among different senses. In the study, the researchers used mice trained to run as directed by flashing lights and sweeping audio tones. They then simultaneously presented the animals with conflicting commands from the lights and tones, but also cued them about which signal to disregard. The mice’s responses showed how effectively they were focusing their attention. Throughout the task, the researchers used well-established techniques to shut off activity in various brain regions to see what interfered with the animals’ performance.

As expected, the prefrontal cortex, which issues high-level commands to other parts of the brain, was crucial. But the team also observed that if a trial required the mice to attend to vision, turning on neurons in the visual TRN interfered with their performance. And when those neurons were silenced, the mice had more difficulty paying attention to sound. In effect, the network was turning the knobs on inhibitory processes, not excitatory ones, with the TRN inhibiting information that the prefrontal cortex deemed distracting. If the mouse needed to prioritize auditory information, the prefrontal cortex told the visual TRN to increase its activity to suppress the visual thalamus — stripping away irrelevant visual data.

The attentional searchlight metaphor was backward: The brain wasn’t brightening the light on stimuli of interest; it was lowering the lights on everything else.

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With tasks similar to those they’d used in 2015, the team probed the functional effects of various brain regions on one another, as well as the neuronal connections between them. The full circuit, they found, goes from the prefrontal cortex to a much deeper structure called the basal ganglia (often associated with motor control and a host of other functions), then to the TRN and the thalamus, before finally going back up to higher cortical regions. So, for instance, as visual information passes from the eye to the visual thalamus, it can get intercepted almost immediately if it’s not relevant to the given task. The basal ganglia can step in and activate the visual TRN to screen out the extraneous stimuli, in keeping with the prefrontal cortex’s directive.

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Halassa’s findings indicate that the brain casts extraneous perceptions aside earlier than expected. “What’s interesting,” said Ian Fiebelkorn, a cognitive neuroscientist at Princeton University, is that “filtering is starting at that very first step, before the information even reaches the visual cortex.”

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According to his findings, the focus of the attentional spotlight seems to get relatively weaker about four times per second, presumably to prevent animals from staying overly focused on a single location or stimulus in their environment. That very brief suppression of what’s important gives other, peripheral stimuli an indirect boost, creating an opportunity for the brain to shift its attention to something else if necessary. “The brain seems to be wired to be periodically distractible,” he said.

University of Maryland School of Medicine (UMSOM) researchers have found a two-way link between traumatic brain injury (TBI) and intestinal changes:

Researchers have known for years that TBI has significant effects on the gastrointestinal tract, but until now, scientists have not recognized that brain trauma can make the colon more permeable, potentially allowing allow harmful microbes to migrate from the intestine to other areas of the body, causing infection.. People are 12 times more likely to die from blood poisoning after TBI, which is often caused by bacteria, and 2.5 times more likely to die of a digestive system problem, compared with those without such injury.

In this study, the researchers examined mice that received an experimental TBI. They found that the intestinal wall of the colon became more permeable after trauma, changes that were sustained over the following month.

It is not clear how TBI causes these gut changes. A key factor in the process may be enteric glial cells (EGCs), a class of cells that exist in the gut. These cells are similar to brain astroglial cells, and both types of glial cells are activated after TBI. After TBI, such activation is associated with brain inflammation that contributes to delayed tissue damage in the brain. Researchers don’t know whether activation of ECGs after TBI contributes to intestinal injury or is instead an attempt to compensate for the injury.

The researchers also focused on the two-way nature of the process: how gut dysfunction may worsen brain inflammation and tissue loss after TBI. They infected the mice with Citrobacter rodentium, a species of bacteria that is the rodent equivalent of E. coli, which infects humans. In mice with a TBI who were infected with this the bacteria, brain inflammation worsened. Furthermore, in the hippocampus, a key region for memory, the mice who had TBI and were then infected lost more neurons than animals without infection.