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Scientists Use the Tweaked Genes of a Virus to Halt Vision Loss

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What if you could tweak the genes of a virus to turn its ability to invade cells into a delivery system for eyesight therapy? That’s what researchers at Johns Hopkins School of Medicine say they’ve done by modifying an adenovirus, a type of virus that can infect tissue linings. The cutting edge gene therapy was developed to help those who suffer vision loss from a particular eye disorder—wet age-related macular degeneration (AMD).

Approximately 1.6 million Americans have AMD, the number one cause of vision loss. The disease is characterized by the growth of abnormal blood vessels that leak retinal fluid into the eye and destroy the macula, an area near the retina important for high acuity vision. This gene therapy both reduces fluid buildup and improves vision loss in humans, according to study results published in The Lancet.

The best current treatment for the disease requires injections of antibodies into the retina to suppress vascular endothelial growth factor (VEGF), a protein that is responsible for the growth of blood vessels—which in turn cause leaking fluid. But the problem is that patients must obtain these injections at four- to six-week intervals, or else the disease symptoms return and worsen over time. Peter Campochiaro, a professor of ophthalmology and neuroscience at Johns Hopkins Medicine's Wilmer Eye Institute and one of the authors of the study, explains that during this treatment, if a patient takes too long to get their next injection, the abnormal blood vessel net grows larger and recruits other cells. “That scarring causes permanent decrease in vision,” he tells Mental Floss. So over time, it’s common even for patients in treatment to “end up with less vision.”

His team has been working to make a form of injections that last longer, so patients don’t have to come in as frequently. For phase one of this trial, Campochiaro’s team recruited 19 participants to participate in a 52-week study. He was looking for people “who don’t have great visual potential, but have evidence of the disease process that you can measure in effect,” he says.

Since viruses are naturally good at getting into cells and depositing their genetic material, the researchers decided to modify a virus to deposit a gene that codes for a protein called sFLT01. sFLT01 blocks the factor that causes the abnormal vessels and fluid production. When the modified virus is injected into the eye, “the viral vector enters cells and deposits the gene, and the gene begins to produce the [sFLT01] protein,” he says. The protein binds to VEGF, preventing it from causing vessel growth and subsequent fluid leakage.

The 19 participants were divided into five different groups and given increasing doses of the viral vector. After determining there was no toxicity at the dose-limit of the first three groups, they proceeded to increase the dosage to its highest level.

Of the 11 participants with symptoms judged to be reversible, six showed “a substantial reduction in the fluid,” and four of those six saw “a pretty dramatic effect.” Those patients had big pockets of fluid in their retinas decrease, Campochiaro says. Better yet, the treatment lasted throughout the yearlong study, though the protein numbers peaked at 26 weeks, and then declined slightly (although not enough to reactivate disease symptoms).

In assessing why five patients saw no reduction in fluid, the scientists discovered those patients had pre-existing antibodies to the virus. They theorize that in these patients, the immune system may have killed the viral vector before it could deposit the genes, though they will have to do more research to prove this. This could be a problem in using this particular virus—a carrier virus called AAV2—since some 60 percent of patients tend to have these antibodies.

A possible solution might be to give resistant patients a surgical injection instead. During this procedure, scientists could take out the vitreous—a gel-like substance that gives your eye its round shape—and inject the vector surgically under the retina instead. While patients might prefer not to have surgery, “our data suggests that it doesn’t matter if there’s pre-existing antibodies [with this method],” he says.

Alternately, other viral vectors have proven to be more effective than AAV2, including a variation on the virus, AAV8, which provides better infections of the virus into the cell. Even more promising, the researchers recently finished a four-year study on a lentiviral vector (a totally different group of viruses) “that take [the genes] into the nucleus of the cell and inserts the gene right into the chromosomes,” Campochiaro explains.

His next steps will be to retest the treatment with a longer study period to identify just how long-lasting the effects are, as well as to test higher doses of the viral vector.

But right now, he is just excited that the gene therapy works. “We injected this gene, the gene is producing a protein, and you can measure that protein in the eye over time,” he says.

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Department Of Classics, University Of Cincinnati
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Stones, Bones, and Wrecks
Ancient Poop Contains First Evidence of Parasites Described by Hippocrates
Department Of Classics, University Of Cincinnati
Department Of Classics, University Of Cincinnati

The long-held mystery of Hippocrates and the parasitic worms has finally been solved, and it’s all thanks to a few samples of ancient poop.

Researchers don’t know much about the parasites that plagued the Greeks thousands of years ago, and what they do know is largely from the Hippocratic Corpus, the medical texts that the father of medicine and his students put together between the 4th and 3rd centuries BCE. Modern historians have spent years trying to figure out which diseases and parasites Hippocrates and his followers were referring to in their writing, relying solely on their descriptions to guess at what ailments the ancient Greeks might have suffered from. Now, they finally have concrete evidence of the existence of some of the intestinal worms Hippocrates mentioned, Helmins strongyle and Ascaris.

As part of a study in the Journal of Archaeological Science: Reports, an international group of researchers analyzed the ancient remains of feces in 25 prehistoric burials on the Greek island of Kea to determine what parasites the people were carrying when they died. Using microscopes, they looked at the soil (formed by the decomposed poop) found on the pelvic bones of skeletons dating back to the Neolithic, Bronze, and Roman periods.

A roundworm egg under the microscope
A roundworm egg
Elsevier

Around 16 percent of the burials they studied contained evidence of parasites. In these ancient fecal samples, they found the eggs of two different parasitic species. In the soil taken from the skeletons dating back to the Neolithic period, they found whipworm eggs, and in the soil taken from the Bronze Age skeletons, roundworm.

With this information, researchers deduced that what Hippocrates called the Helmins strongyle worm was probably what modern doctors would call roundworm. The Ascaris worm probably referred to two different parasites, they conclude, known today as pinworm (which was not found in this analysis) and whipworm (pictured below).

Whipworm under a microscope
A whipworm egg
Elsevier

Though historians already hypothesized that Hippocrates's patients on Kea had roundworm, the Ascaris finding comes as a particular surprise. Previous research based solely on Hippocrates’s writing rather than physical evidence suggested that what he called Ascaris was probably a pinworm, and another worm he mentioned, Helmins plateia, was probably a tapeworm. But the current research didn’t turn up any evidence of either of those two worms. Instead of pinworm eggs, the researchers found whipworm, another worm that’s similarly small and round. (Pinworms may very well have existed in ancient Greece, the researchers caution, since evidence of their fragile eggs could easily have been lost to time.) The soil analysis has already changed what we know about the intestinal woes of the ancient Greeks of Kea.

More importantly, this study provides the earliest evidence of ancient Greece’s parasitic worm population, proving yet again that ancient poop is one of the world’s most important scientific resources.

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Arctic Temperatures are Rising So Fast, They're Confusing the Hell Out of Computers
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This past year was a brutal one for northern Alaska, which saw temperatures that soared above what was normal month after month. But you wouldn't know that by looking at the numbers from the weather station at Utqiaġvik, Alaska. That's because the recent heat was so unusual for the area that computers marked the data as incorrect and failed to report it for the entirety of 2017, leaving a hole in the records of the Climate Monitoring group at the National Centers for Environmental Information (NCEI), according to the Huffington Post.

The weather station in the northernmost tip of Alaska has been measuring temperatures for nearly a century. A computer system there is programed to recognize if the data has been influenced by artificial forces: Perhaps one of the instruments isn't working correctly, or something is making the immediate area unnaturally hot or cold. In these cases, the computer edits out the anomalies so they don't affect the rest of the data.

But climate change has complicated this failsafe. Temperatures have been so abnormally high that the Utqiaġvik station erroneously removed all its data for 2017 and part of 2016. A look at the region's weather history explains why the computers might have sensed a mistake: The average yearly temperature for the era between 2000 and 2017 has gone up by 1.9°F from that of the era between 1979 and 1999. Break it down by month and the numbers are even more alarming: The average temperature increase is 7.8°F for October, 6.9°F for November, and 4.7°F for December.

"In the context of a changing climate, the Arctic is changing more rapidly than the rest of the planet," Deke Arndt, chief of NOAA's Climate Monitoring Branch, wrote for climate.gov. The higher temperatures rise, the faster Arctic sea ice melts. Arctic sea ice acts as a mirror that reflects the Sun's rays back into space, and without that barrier, the sea absorbs more heat from the Sun and speeds up the warming process. “Utqiaġvik, as one of a precious few fairly long-term observing sites in the American Arctic, is often referenced as an embodiment of rapid Arctic change,” Arndt wrote.

As temperatures continue to grow faster than computers are used to, scientists will have to adjust their algorithms in response. The team at NCEI plans to have the Utqiaġvik station ready to record our changing climate once again within the next few months.

[h/t Huffington Post]

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