An 83-year-old woman operated on last summer was the first person to receive an entire 3D-printed jaw transplant, her Belgian doctors announced Monday. The woman’s own lower jaw was riddled with infection, and given her age, and the fact that reconstructive surgery would have been a long and painful process, her doctors decided to have a new jaw specially manufactured for her. The replacement jaw is made out of titanium, assembled in thousands of layers by a 3D printer. It took 4 hours of surgery to get the jaw in place, but that’s just a fifth of how long a reconstructive surgery session would have been. She will receive follow-up surgery later this month to have permanent dentures attached to the jaw.
The new jaw is about 30% heavier than her old jaw was, but the doctors say she’ll get used to it. Someday, though, patients may be able to get replacement bones printed in more bone-like material: scientists are working on getting 3D printers to accept calcium-based substances as ink.
Image courtesy of LayerWise
What’s the News: When prions or amyloids make the news, it’s usually because they cause mad cow disease or Alzheimer’s—prions, after all, cause any proteins they touch to become as misfolded as they are, and amyloids, which are large clumps of wadded-together proteins, can jam the workings of cells.
But a new study in Cell suggests that a prion-like protein that forms amyloids has a normal, vital function in the brain. Far from being a memory destroyer, this protein, called CPEB, is necessary for long-term memory in fruit flies.
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About three months ago, otherwise healthy girls at a high school in LeRoy, NY, started stuttering, jerking, and making odd noises, among other symptoms similar to Tourette’s syndrome, a neurological disorder. The number of people affected has grown now to more than a dozen, though a more specific count is difficult to nail down, and seems to include one boy and one 36-year-old woman in addition to the teenage girls.
What could be causing these symptoms? Health officials have inspected the girls’ school and found no environmental contaminants. A variety of other causes, including the Gardasil vaccine and strep throat, have been investigated as causes of the uncontrollable tics (neither of those panned out, as in each case only some of the girls had had the shots or been sick). The pattern of cases doesn’t suggest an infectious cause. The current best guess comes from a pediatric neurologist who has examined eight of the girls and has given a diagnosis of conversion disorder, which is defined as the development of tics, paralysis, or a variety of other neurology-related symptoms as a result of stress. (more…)
What’s the News: If you’ve ever been told been that a massage is good for “releasing toxins”—or to sound more scientific, “lactic acid”—from your muscles, then you’ve been told wrong. Turns out muscle cells do like a good massage, but it has nothing to do with lactic acid.
In the first study on the cellular effects of massage post-exercise, researchers found that massage bolsters chemical signals reducing inflammation and promoting repair of muscle cells.
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A protein tangle in an Alzheimer’s-afflicted neuron
Exactly how Alzheimer’s disease proliferates through the brain, overtaking one region after another, has eluded scientists. As the disease progresses, tau—a malformed protein that forms snarls and tangles inside neurons—shows up in more and more brain areas. Researchers have wondered whether tau, and the disease, are working their way out from a single area of origin or mounting numerous, distinct attacks on vulnerable parts of the brain. Two new studies in mice provide strong support for the first idea: Tau seems to pass from affected cells to their neighbors, spreading much the same way a virus or bacteria infection would.
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What’s the News: The bacterial hordes that call your mouth home—and yes, even if you brush rigorously, you’ve got ‘em—are generally a pretty benign bunch. Mostly they just mooch around, snagging tastes of whatever you’re eating, but Streptococcus mutans, the bad boy that causes cavities, releases tooth-corroding acid whenever you eat sugar. Even mouthwash that kills everything it touches can’t save you from the ravages of S. mutans in the long term; it just grows back, along with the rest of your bacteria.
Scientists who study the mouth microbiome, however, think that a mouthwash that kills S. mutans and leaves the rest of the bacteria to take over S. mutans‘s real estate could spell the end of cavities. In a small clinical study last year, one team found that one application of the mouthwash knocked down S. mutans levels, and that harmless bacteria grew back in its place. If the mouthwash pans out, it could join the ranks of an emerging new type of treatment: better living through hacking the microbiome.
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Chemotherapy is poison that happens to kill cancer cells faster than it kills healthy cells; that it wreaks havoc on the bodies of patients is unsurprising. But chemo may also affect their unborn children. According to a new study in PNAS, the offspring of mice treated with chemotherapy have higher rates of mutation, even though the offspring themselves were never exposed to the drugs.
The results suggest that these mutations arise from genome destabilization caused by exposure to chemo, rather than just mutated sperm from the treated father. Male mice in the study were exposed to one of three common anticancer drugs—cyclophosphamide, mitomycin C, or procarbazine—and then allowed to mate with untreated females. After sequencing a small piece of DNA from the offspring, the researchers found that mice with treated fathers had mutation rates up to twice that of mice with untreated fathers. Notably, these mutations were present in DNA inherited from both the treated father and untreated mother.
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Vultures eating a gazelle.
By now, you’re probably familiar with the Body Farm at University of Tennessee. It’s one of the places where bodies donated to science go to rot while being closely observed by appreciative forensic scientists, and we say that with the greatest respect: if not for the brave few who gave their mortal remains to be studied, we would have a much harder time telling when and how people found in fields, woods, and other unusual locales died. Now, scientists working at another Body Farm-like facility, Texas State University’s Forensic Anthropology Research Facility, have performed a fascinating study to see exactly what happens when a human body is eaten by vultures.
Their findings imply that vultures can take much longer—37 days instead of 24 hours—to find a body than the carcass of a pig left in the wilderness, which is what previous studies in the Texas facility have used. On the other hand, vultures can also pick clean, or skeletonize, a body much faster than we’d thought: it took just 5 hours instead of the expected 24. The scientists also tracked where the vultures spread the body parts that they didn’t consume, as they kept visiting the body over the following five months, which will be useful in figuring out how far away a body might be if a bone or other part is found by itself in future forensic investigations.
[via New Scientist]
Image courtesy of appenz / flickr
Family reunion time!
Digging around in your DNA is getting cheaper and easier all the time. For only $207, you can now subscribe to 23andMe’s genotyping service, for instance, which gives you information about your genetic background, potential disease susceptibilities, and other traits. And as the numbers of people in such companies’ databases climb into the hundreds of thousands, it has become possible for software to connect customers who share so much DNA, they may well be relatives. For adoptees who don’t have access to their adoption records and are curious about biological family, there’s never been a better time to go searching. The New York Times follows the story of one 42-year-old woman who, after learning she was adopted, finds her third cousin through a DNA service, and details the relationship that they form as she deals with the revelation that she is not, after all, the daughter of her adoptive parents.
About five weeks after shipping off two tiny vials of her cells from a swab of her cheek, Mrs. Vaughan received an e-mail informing her that her bloodlines extended to France, Romania and West Africa. She was also given the names and e-mail addresses of a dozen distant cousins. This month, she drove 208 miles from her hometown here to Evansville, Ind., to meet her third cousin, the first relative to respond to her e-mails. Mrs. Vaughan is black and her cousin is white, and they have yet to find their common ancestor. But Mrs. Vaughan says that does not matter.
“Somebody is related to me in this world,” she said. “Somebody out there has my blood. I can look at her and say, ‘This is my family.’ ”
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Shiga toxin is nasty stuff. If you are infected with a Shiga-producing bacterium, like Shigella dysenteriae or some E. coli strains, there is no clear treatment: if you are given antibiotics, your infected cells will explode, spraying the toxin all over neighboring cells and exacerbating your symptoms. Each year, 150 million people are infected with Shiga-producing bacteria, which cause dysentery and food poisoning, and a million of those die. The lack of effective treatment for such Shiga toxicosis infections is one of the main reasons this year’s outbreak of E. coli poisoning in Europe was so deadly, with more than 3,700 people infected and 45 dead. But now scientists studying how the toxin makes its way around the cell have discovered that treating mice with the metal element manganese makes them resistant to Shiga poisoning. Since manganese’s chemistry is already well understood and it’s readily available, the possibility of using it as a treatment is exciting.
Here’s how manganese blocks Shiga’s spread, according to the group’s experiments in cultured human cells:
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A recent column by Dr. Pauline Chen at the New York Times explores a surprising oversight in modern healthcare: Doctors don’t really have a clue how to predict how long a patient will live. In the absence of a widely accepted, systematic method of prognosis, they’re kind of making it up—an informed guess, with the benefit of education and experience, but a guess nonetheless.
Prognosis was once a diligently studied, widely practiced part of a physician’s job, Chen writes. But as treatments improved, and keeping patients alive longer became ever more possible, the unpleasant but necessary skill of predicting when patients might die fell by the wayside. A recent study, she reports, revealed just how much:
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Artist’s rendering of a mitochondrian, the energy-producing
cellular structure affected by ARSACS
Scientists have pinpointed the cause of a rare, fatal neurodegenerative disorder called ARSACS, or autosomal recessive spastic ataxia of Charlevoix-Saguenay. The disease is due to defects in neuron’s mitochondria, the bit of biological machinery that generates energy for the cell—a structure known to be affected in Parkinson’s, Alzheimer’s, and other neurological diseases, as well.
ARSACS was first observed in the descendants of a small group of 17th century French settlers who made their homes near the Charlevoix and Saguenay rivers in what is now Quebec, and has since been seen worldwide. But its incidence remains unusually high in that particular French Canadian community, with 1 in 1,500 to 2,000 people developing ARSACS and 1 in 23 people unaffected genetic carriers of the disease.
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When tuberculosis kills lung tissue, it can produce gaping
holes like in the lung on the right.
For a long time, tuberculosis was a gruesome and incurable disease. Antibiotics changed that, but over the last century, as the drugs have been incorrectly used, the tuberculosis bacterium has been developing resistance to them. Multi-drug resistant tuberculosis, which requires a cocktail of many drugs to treat it, has become common. Now Indian doctors have reported in a medical journal that a strain that is resistant to all known drugs for tuberculosis has appeared in Mumbai. Twelve patients so far have been diagnosed with the strain, and it’s likely that they are just the tip of the iceberg in terms of those infected.
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How a living material of cheese fungi sandwiched between plastic sheets works.
The crusty rind of cheeses like Camembert provide more than texture: they are miniature fortress walls, made of fungus, that protect the cheese’s creamy insides from bacterial invasions. Now, taking inspiration from this delicious snack, chemical engineers at ETH Zurich in Switzerland have shown that such a fungus can be enclosed in porous plastic and will digest spills, with implications for creating antibacterial surfaces from living material.
The team sandwiched a layer of Penicillium roqueforti—from, you guessed it, Roquefort cheese—between a plastic base and a top sheet of plastic with nanoscale pores that allowed gas and liquids to move through, but did not allow the fungus to spread. Then, they mimicked a kitchen spill by pouring sugary broth on the surface and watched as, over the course of two weeks, the captive fungus gradually consumed the entire spill, leaving the surface clean. As shown in the figure above, the fungi can go dormant when there is no food around, so if one had a countertop of such a material, you wouldn’t need to keep spilling sugar on it to keep the fungi happy. (more…)
Roku and Hex from OHSU News on Vimeo.
Researchers have announced the birth of three unusual, though healthy, baby monkeys. They are the first non-mouse chimeras—creatures made up of cells from multiple other parents—to be created by science.
Making chimeric mice is a time-consuming but fairly routine part of biology these days: embryos are injected with modified cultured stem cells containing the traits the researchers desire (like glowing in the dark). Those embryos grow up into mice who have some glow-in-the-dark cells and some normal cells, called chimeras. These chimeras are useful because if any of them have glow-in-the-dark sperm or eggs, they can be bred with each other to produce babies who are 100% glow-in-the-dark.
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