News
'VGH is a changemaker’: Hematology and Transfusion Medicine team wins People First Award of Merit
“They are our hospital's unsung heroes," says anesthesiologist Dr. Jacqueline Trudeau. “When the sickest of patients come through our doors, they silently, efficiently, and seemingly effortlessly provide blood products and test results… Without them, our patients would perish."
The team recently helped implement a groundbreaking new system for a laboratory test used to assess bleeding and clotting in very ill patients. The project was challenging: traditionally the test is performed at the bedside of patients in the operating or emergency rooms, but clinicians wanted to provide access across all critical care areas of the hospital.
“This required the lab to implement the test in a way that is not traditionally done," explains Dr. Trudeau, noting no other hospitals in Canada have achieved the same unique implementation of the test. “We felt that this was the only way to optimally improve care for all of these patient populations."
The change equaled disruption and new ways of doing things, but the team took it in stride.
“It was the opportunity to do something new, although no easy solutions were available," adds Dr. Trudeau. “The team worked together to solve difficult, new problems; they stayed late often; they tolerated additional stress, and took on this extra work with excitement for the challenge."
And all their hard-work paid off: clinicians at VGH can now see the test in real-time as it is being handled in the lab, something that has made a meaningful difference – and improved outcomes –for patients.
Theranos: Scandal hit blood-testing firm to shut
Scandal-hit US blood-testing start-up Theranos is to formally dissolve, the firm's chief executive David Taylor has told shareholders in an email. Mr. Taylor said Theranos had run "out of time" to secure further investment or secure a buyer for its assets.
Theranos founder Elizabeth Holmes and former president Ramesh Balwani are facing criminal charges of wire fraud. Prosecutors say they engaged in a multi-million dollar scheme to defraud investors, doctors and patients.
Mr. Taylor, who also serves as general counsel to the firm, said that Theranos had engaged the services of investment bank Jeffries to try to "maximise the value of the company" for shareholders. In the email obtained by the Wall Street Journal, he said the investment bank had "reached out" to over 80 potential buyers, but to no avail. "Unfortunately, none of those leads has materialized into a transaction. We are now out of time," he wrote.
Mr Taylor said the firm had breached the terms of its loan agreement with investor Fortress Investment Group, meaning the firm was now entitled to sell or take ownership of Theranos' intellectual property and assets.
There's A New Antibiotic In Town, And We Can Create It In The Lab
Bacteria are shifty little things. We isolate antibiotics to kill them, and they evolve to dodge the attack. This is called antibiotic resistance, and it’s gotten so bad the United Nations (UN) actually declared it a crisis back in September 2016.
Now, a team of Chinese researchers think they’ve found a new weapon against antibiotic resistance: a fungal compound called albomycin δ2 that we can actually recreate in the lab.
They published their study Tuesday in the journal Nature Communications.
We knew from previous research that albomycins had antimicrobial properties, but it wasn’t until this research team dug into the fungal compounds that they learned that one specific compound, albomycin δ2, was especially adept at killing bacteria. It even outperformed a number of established antibiotics, including penicillin, when tested against the notoriously difficult to treat methicillin-resistant Staphylococcus aureus (MRSA).
Most antibiotics we use today are natural substances, and they often have complex chemical structures. That means that, most of the time, it’s really hard to reproduce them in the lab, which means they take longer to develop in large quantities. However, the researchers figured out a way we could synthesize albomycin δ2, which grants us the ability to evaluate it far more extensively than if we were relying on naturally produced samples.
Microbiology
Global spread of three multidrug-resistant lineages of Staphylococcus epidermidis
Staphylococcus epidermidis is a conspicuous member of the human microbiome, widely present on healthy skin. Here we show that S. epidermidis has also evolved to become a formidable nosocomial pathogen.
Using genomics, we reveal that three multidrug-resistant, hospital-adapted lineages of S. epidermidis (two ST2 and one ST23) have emerged in recent decades and spread globally. These lineages are resistant to rifampicin through acquisition of specific rpoB mutations that have become fixed in the populations.
Analysis of isolates from 96 institutions in 24 countries identified dual D471E and I527M RpoB substitutions to be the most common cause of rifampicin resistance in S. epidermidis, accounting for 86.6% of mutations. Furthermore, we reveal that the D471E and I527M combination occurs almost exclusively in isolates from the ST2 and ST23 lineages. By breaching lineage-specific DNA methylation restriction modification barriers and then performing site-specific mutagenesis, we show that these rpoB mutations not only confer rifampicin resistance, but also reduce susceptibility to the last-line glycopeptide antibiotics, vancomycin and teicoplanin.
Our study has uncovered the previously unrecognized international spread of a near pan-drug-resistant opportunistic pathogen, identifiable by a rifampicin-resistant phenotype. It is possible that hospital practices, such as antibiotic monotherapy utilizing rifampicin-impregnated medical devices, have driven the evolution of this organism, once trivialized as a contaminant, towards potentially incurable infections.
8,000 new antibiotic combinations are surprisingly effective, UCLA biologists report
Scientists have traditionally believed that combining more than two drugs to fight harmful bacteria would yield diminishing returns. The prevailing theory is that the incremental benefits of combining three or more drugs would be too small to matter, or that the interactions among the drugs would cause their benefits to cancel one another out.
Now, a team of UCLA biologists has discovered thousands of four- and five-drug combinations of antibiotics that are more effective at killing harmful bacteria than the prevailing views suggested. Their findings, reported today in the journal npj Systems Biology and Applications, could be a major step toward protecting public health at a time when pathogens and common infections are increasingly becoming resistant to antibiotics.
"There is a tradition of using just one drug, maybe two," said Pamela Yeh, one of the study's senior authors and a UCLA assistant professor of ecology and evolutionary biology. "We're offering an alternative that looks very promising. We shouldn't limit ourselves to just single drugs or two-drug combinations in our medical toolbox. We expect several of these combinations, or more, will work much better than existing antibiotics."
Working with eight antibiotics, the researchers analyzed how every possible four- and five-drug combination, including many with varying dosages -- a total of 18,278 combinations in all -- worked against E. coli. They expected that some of the combinations would be very effective at killing the bacteria, but they were startled by how many potent combinations they discovered.
For every combination they tested, the researchers first predicted how effective they thought it would be in stopping the growth of E. coli. Among the four-drug combinations, there were 1,676 groupings that performed better than they expected. Among the five-drug combinations, 6,443 groupings were more effective than expected.
Molecular Genetics
Researchers find a way to mimic clinical trials using genetics
Health researchers are wielding a new tool they hope will let them determine the true causes of chronic disease. And it comes through a surprise route: genetics. Researchers say that by employing innate genetic differences between people—an inborn susceptibility to alcohol, say, or to higher cholesterol levels in the arteries—they can now mimic, at much less effort and expense, the kinds of large trials that would be necessary to determine if an HDL-lowering medicine is really beneficial. The new technique, called Mendelian randomization, is already being used by drug companies to make billion-dollar decisions about which drugs to pursue.
Here’s how it works, using HDL as the example. At the moment of conception, some of us inherit specific variants of genes that boost our HDL levels. If HDL really protects against heart disease, then people with more of these HDL-raising variants should have lower rates of heart disease and live longer than those who get other variations. If so, it suggests that elevating HDL through drugs or diet is an excellent idea. Before randomly assigning people to different HDL-raising drugs or diets in huge, costly studies, the equally random lottery that determines which gene variants we inherit can be used to gauge whether such trials would be worth the risk and investment.
“We’ve all been recruited into an experiment, without knowing it, at conception,” says George Davey Smith, an epidemiologist at the University of Bristol in the UK, who has championed the new method as an invaluable tool for untangling causality and correlation throughout medical research.
The method is already settling long-standing and critical questions about heart disease—among other things, putting to rest 40 years of uncertainty about HDL. In 2012, a large international collaboration reported that despite the impressive correlation between HDL and heart disease, those of us born with genes that naturally raise our HDL cholesterol have no fewer heart attacks than people without those genes. In short, though HDL is inversely correlated with heart disease, it plays no causal role. And that’s why the drugs failed. They went after a target that turned out to be just a bystander.
Read more about this topic by clicking on the article title above.
Research
Medical students study tampons as possible screening test for cancer
There is no screening test for ovarian cancer. Three FIU medical students would like to change that. They are hoping to save lives by collecting used tampons.
The idea began to germinate when Jessica Seigel, Leah Cohen and Lauren Dittman, who are in their fourth year at Herbert Wertheim College of Medicine, were awarded scholarships by Hearing the Ovarian Cancer Whisper, an organization that supports victims of ovarian cancer and funds education and research of the deadliest of gynecologic cancers. The award allowed them to shadow a gynecologic oncologist.
"During the experience I was shocked to learn how late ovarian cancer patients presented, and most with incurable disease, " says Cohen, who with her classmates Seigel and Dittman, is conducting a pilot study they hope will lead to development of a screening test. The research is funded by the HERA Foundation.
"Our study is trying to determine whether DNA collected from tampons can be used in the detection of ovarian cancer," says Dittman.
The students have collected tampons from 30 women who have tested positive for the BRCA1 mutation. The idea is that cells shed by the fallopian tubes, where ovarian cancer originates, travel down the reproductive tract to the vagina and may be collected in the tampons. DNA extracted from the tampon samples can then be sequenced and analyzed for mutations in the tumor suppressor gene known as TP53 which is a commonly mutated gene in people with cancer.
Dr. Sheldon Cherry— professor of obstetrics and gynecology, and a mentor to the young women since their first year in medical school—suggested the study, based on an earlier tampon study of women who had already developed ovarian cancer and presented a TP53 mutation.
"I thought, 'why don't we try to see if we can find this same mutation in seemingly healthy at-risk women before they show clinical signs of cancer,'" says Cherry.
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