Blocking Inflammation May Lead To Chronic Pain

Using anti-inflammatory drugs and steroids to relieve pain could increase the chances of developing chronic pain, according to researchers from McGill University and colleagues in Italy. Neuroscience News reports: Their research puts into question conventional practices used to alleviate pain. Normal recovery from a painful injury involves inflammation and blocking that inflammation with drugs could lead to harder-to-treat pain. […] In the study published in Science Translational Medicine, the researchers examined the mechanisms of pain in both humans and mice. They found that neutrophils — a type of white blood cell that helps the body fight infection — play a key role in resolving pain. Experimentally blocking neutrophils in mice prolonged the pain up to ten times the normal duration. Treating the pain with anti-inflammatory drugs and steroids like dexamethasone and diclofenac also produced the same result, although they were effective against pain early on.

These findings are also supported by a separate analysis of 500,000 people in the United Kingdom that showed that those taking anti-inflammatory drugs to treat their pain were more likely to have pain two to ten years later, an effect not seen in people taking acetaminophen or anti-depressants. “Our findings suggest it may be time to reconsider the way we treat acute pain. Luckily pain can be killed in other ways that don’t involve interfering with inflammation,” says Massimo Allegri, a Physician at the Policlinico of Monza Hospital in Italy and Ensemble Hospitalier de la Cote in Switzerland.

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Scientists Try Injecting Tumor-Fighting Viruses Coated in Magnets Made By Soil Bacteria

To attack tumors, the Guardian reports, “scientists are developing magnetically guided microscopic projectiles that can be injected into patients’ blood.”

The project — led by researchers at Sheffield University — builds on progress in two key medical fields. The first involves viruses that specifically attack tumours…. After infection with an oncolytic virus, a cancer cell will burst open and die. The US Food and Drug Administration has already approved the use of T-Vec, a modified herpes simplex virus that infects and kills tumour cells and is now being used to treat people with certain types of melanoma, a skin cancer.
Unfortunately, the viruses soon get attacked by the body’s immune system. So the scientists want to coat the viruses with magnetic particles, so that magnets (outside a patient’s body) can quickly guide those viruses where they’re needed.

And to accomplish this they’re using a soil bacteria which is known to make magnets to align with Earth’s own magnetic field. “The essence of this approach is straightforward,” one of the project’s leaders explains to the Guardian. “We are using bugs as drugs…. we have found bacteria do a better job of manufacturing them than we could.”
Having developed the technology, the Sheffield team is now working to ensure they can manufacture sufficient supplies so that clinical trials on humans can begin soon. To date, trials have focused on animal models. “These early tests have been very encouraging and we now need to take the next steps to bring this technique to a state where it can be administered to humans — hopefully in a few years’ time.”

Thanks to Slashdot reader Falconhell for sharing the article!

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MS Symptoms May Have Been ‘Reversed’ In Immunotherapy Breakthrough

A new immunotherapy that targets cells infected with Epstein-Barr Virus (EBV) has halted the progression of multiple sclerosis (MS) in a small trial. Perhaps even more incredibly, in some patients, it is possible that symptoms of MS were actually reversed, though this was not fully identified in the most recent presentation of results (PDF). IFLScience reports: [S]ignificant evidence has linked infection of EBV and the eventual development of MS. […] Attempting to “transform treatment of Multiple Sclerosis,” Atara Biotherapeutics has developed an allogeneic T-cell therapy called ATA188. The concept is simple — when cells are infected with EBV, they express small proteins called antigens on the cell surface, and the immunotherapy contains immune cells that target and destroy them.

In a trial of 24 patients who received the therapy, 20 saw improvements or stability in their symptoms and no fatal or serious adverse effects were reported. Early brain scans suggest that some damaged nerve cells may have been “repaired” by the therapy in a process called remyelination, which could mean a reversal of damage caused by MS in the nervous system, but this has not yet been confirmed. While the results are extremely promising, it is an early Phase 1 trial with a small sample size and no placebo or control group, so it is unclear whether the results are significant at this stage. However, it is unlikely that this repair would occur naturally, suggesting the therapy is having a beneficial effect on some level.

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Researchers Create Bacteria That Could Protect Your Gut From Antibiotics

In a new study published in the journal Nature Biomedical Engineering, researchers from Harvard and MIT detail work they’ve done on a “living cellular therapeutic device” that promises to protect humans from the harmful side effects antibiotics can have on our guts. Engadget reports: Per Science Daily, they modified a strain of bacteria that is frequently used in cheese production to deliver an enzyme that can break down beta-lactam antibiotics. Many of the most commonly prescribed antibiotics in the US, including penicillin, fall under that family. Using gene editing, they further modified how their bacterium synthesizes the enzyme to prevent it from transferring that capability to other bacteria. The result is a treatment that reduces the harmful effects of antibiotics while still allowing those drugs to do their work.

In a study involving mice, the researchers found their bacteria “significantly” reduced the damage ampicillin did to the test subject’s gut microbes and allowed those communities to recover fully after just three days. By contrast, in mice that only received the antibiotic, the researchers saw a much greater loss of microbial diversity. “We are now focusing on getting these living therapies to patients and are finalizing the design of an effective, short, and inexpensive clinical trial,” said Andres Cubillos-Ruiz, the lead author of the study.

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Psilocybin Frees Up Depressed Brain, Study Shows

Psilocybin, a drug found in magic mushrooms, appears to free up the brains of people with severe depression in a way that other antidepressants do not, a study has found. The BBC reports: The results, based on brain scans of 60 people, mean the drug could treat depression in a unique way, the researchers say. Patients with depression are warned not to take psilocybin on their own. A synthetic form of the drug is tested on people in trials under strict medical conditions, with psychological support from experts provided before, during and after it is taken.

With depression, the brain can get stuck in a rut and locked into a particular negative way of thinking, he said. But when given psilocybin, people’s brains opened up and became “more flexible and fluid” up to three weeks later. This could be seen in increased connections between regions of the brain when patients were scanned. These patients were more likely to experience an improvement in mood months later. Similar changes were not seen in the brains of people treated with a standard antidepressant.

The results, published in Nature Medicine, are taken from two studies. In the first, everyone received psilocybin; and in the second — a randomized controlled trial – some were given the drug while others were given a different antidepressant. All participants also received talking therapies with registered mental health professionals. Brain scans were taken before, and then one day or three weeks after taking the therapy.

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CDC Coding Error Led To Overcount of 72,000 COVID-19 Deaths

Last week, after reporting from the Guardian on mortality rates among children, the CDC corrected a “coding logic error” that had inadvertently added more than 72,000 Covid deaths of all ages to the data tracker, one of the most publicly accessible sources for Covid data. The Guardian reports: The agency briefly noted the change in a footnote, although the note did not explain how the error occurred or how long it was in effect. A total of 72,277 deaths in all age groups reported across 26 states were removed from the tracker “because CDC’s algorithm was accidentally counting deaths that were not Covid-19-related,” Jasmine Reed, a spokesperson for the agency, told the Guardian. The problem stemmed from two questions the CDC asks of states and jurisdictions when they report fatalities, according to a source familiar with the issue.

One data field asks if a person died “from illness/complications of illness,” and the field next to this asks for the date of death. When the answer is yes, then the date of death should be provided. But a problem apparently arose if a respondent included the date of death in this field even when the answer was “no” or “unknown.” The CDC’s system assumed that if a date was provided, then the “no” or “unknown” answer was an error, and the system switched the answer to “yes.” This resulted in an overcount of deaths due to Covid in the demographic breakdown, and the error, once discovered, was corrected last week. The CDC did not answer a question on how long the coding error was in effect.

“Working with near real-time data in an emergency is critical to guide decision-making, but may also mean we often have incomplete information when data are first reported,” said Reed. The death counts in the data tracker are “real-time and subject to change,” Reed noted, while numbers from the National Center for Health Statistics, a center within the CDC, are “the most complete source of death data,” despite lags in reporting, because the process includes a review of death certificates.

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Scientists Say They Can Read Nearly the Whole Genome of an IVF-Created Embryo

sciencehabit shares a report from A California company says it can decipher almost all the DNA code of a days-old embryo created through in vitro fertilization (IVF) — a challenging feat because of the tiny volume of genetic material available for analysis. The advance depends on fully sequencing both parents’ DNA and “reconstructing” an embryo’s genome with the help of those data. And the company suggests it could make it possible to forecast risk for common diseases that develop decades down the line. Currently, such genetic risk prediction is being tested in adults, and sometimes offered clinically. The idea of applying it to IVF embryos has generated intense scientific and ethical controversy. But that hasn’t stopped the technology from galloping ahead.
Predicting a person’s chance of a specific illness by blending this genetic variability into what’s called a “polygenic risk score” remains under study in adults, in part because our understanding of how gene variants come together to drive or protect against disease remains a work in progress. In embryos it’s even harder to prove a risk score’s accuracy, researchers say. The new work on polygenic risk scores for IVF embryos is “exploratory research,” says Premal Shah, CEO of MyOme, the company reporting the results. Today in Nature Medicine, the MyOme team, led by company co-founders and scientists Matthew Rabinowitz and Akash Kumar, along with colleagues elsewhere, describe creating such scores by first sequencing the genomes of 10 pairs of parents who had already undergone IVF and had babies. The researchers then used data collected during the IVF process: The couples’ embryos, 110 in all, had undergone limited genetic testing at that time, a sort of spot sequencing of cells, called microarray measurements. Such analysis can test for an abnormal number of chromosomes, certain genetic diseases, and rearrangements of large chunks of DNA, and it has become an increasingly common part of IVF treatment in the United States. By combining these patchy embryo data with the more complete parental genome sequences, and applying statistical and population genomics techniques, the researchers could account for the gene shuffling that occurs during reproduction and calculate which chromosomes each parent had passed down to each embryo. In this way, they could predict much of that embryo’s DNA.

The researchers had a handy way to see whether their reconstruction was accurate: Check the couples’ babies. They collected cheek swab samples from the babies and sequenced their full genome, just as they’d done with the parents. They then compared that “true sequence” with the reconstructed genome for the embryo from which the child originated. The comparison revealed, essentially, a match: For a 3-day-old embryo, at least 96% of the reconstructed genome aligned with the inherited gene variants in the corresponding baby; for a 5-day-old embryo, it was at least 98%. (Because much of the human genome is the same across all people, the researchers focused on the DNA variability that made the parents, and their babies, unique.) Once they had reconstructed embryo genomes in hand, the researchers turned to published data from large genomic studies of adults with or without common chronic diseases and the polygenic risk score models that were derived from that information. Then, MyOme applied those models to the embryos, crunching polygenic risk scores for 12 diseases, including breast cancer, coronary artery disease, and type 2 diabetes. The team also experimented with combining the reconstructed embryo sequence of single genes, such as BRCA1 and BRCA2, that are known to dramatically raise risk of certain diseases, with an embryo’s polygenic risk scores for that condition — in this case, breast cancer.

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