Blood lab technician Elissa Mays claimed she was acting in the interest of efficiency when she asked a roomful of patients if any of them “were there for drug testing.” That question got her fired for violating the hyper-secretive federal Health Insurance Portability and Accountability Act, better known as HIPAA. It also thwarts the Pittsburgh woman’s bid to get unemployment compensation, a Commonwealth Court panel ruled Thursday.
Mays’ September 2017 firing came 17 years into her employment with the Laboratory Corporation of America. Judge Anne E. Covey concluded in the state court’s opinion that Mays’ drug testing question constituted willful misconduct that bars her from getting jobless aid.
HIPAA bars medical professionals from disclosing health information regarding patients. Mays was fired after a patient in the waiting room lodged a complaint about her drug testing question, Covey noted.
She wrote that Mays claimed because the lab had only one restroom available for administering drug tests she “sought to decrease waiting times for the 13 patients who had already signed in by asking them the nature of their business and then directing them to the appropriate room.”
Although Mays argued before the court that she never asked a specific patient whether they were there for drug testing, Covey found that Mays had admitted to a supervisor that she had violated HIPAA. Mays had been warned, repeatedly, that she would be fired for breaching that law, the judge noted. Mays herself testified she was “aware of the HIPAA laws and the sensitivity surrounding them,” Covey wrote.
Researchers at the University of Coimbra in Portugal may have found a simple new way to help predict which people with depression will later go on to develop bipolar disorder: a blood test for uric acid. [The] scientists observed that people hospitalized with major depressive disorder who also happened to have higher levels of uric acid in their blood were more likely to be diagnosed with bipolar disorder in the next eight to eleven years.
A remarkable 48% of people (53 out of 111) with high uric acid levels went on to develop bipolar disorder, whereas only 1.4% of people (two out of 139) with low uric acid levels went on to develop bipolar disorder. This observation suggests that if you have depression, and your uric acid levels are too high, you are 34 times more likely to go on to develop bipolar disorder in the coming years than if your uric acid levels are low.
In men, uric acid levels higher than 5.35 mg/dL (or 318 micromoles/liter) were associated with increased risk for bipolar disorder. In women, uric acid levels higher than 4 mg/dL (or 357 micromoles/liter) were associated with increased risk for bipolar disorder. Interestingly, these higher levels are considered to be in the “normal” range simply because they are well below the levels typically associated with gout (people with gout tend to have uric acid levels above 6.8 mg/dL).
Jesse Karmazin, the 34-year-old founder of the startup Ambrosia, had a pitch journalists couldn’t resist: For a fee, he could help his clients combat aging and its related ills with infusions of blood plasma from the young. Teen donors, vampiric undertones, a serious-sounding study, an $8,000-per-person price tag. One hundred and four people paid to receive plasma from 16- to 25-year-old donors as part of Ambrosia’s participant-funded study, Karmazin told HuffPost.
[Despite] declaring the study a success and announcing plans this week to accept new clients, Karmazin never showed any proof that the transfusions actually helped people. He said he got the idea for young plasma transfusions from several studies in which young and old mice were surgically conjoined in order to examine the effects of mixing their blood. Scientists have questioned Karmazin’s interpretation of the data.
To launch his study, Karmazin needed plasma, the liquid part of blood, from young people. He needed a lot of it — Karmazin would have required at least 80 gallons of young plasma, hundreds of donations’ worth. But he faced a hitch: Blood banks don’t typically separate out blood plasma by age and sell it for rejuvenation purposes.
Eventually, Karmazin said, he found two blood banks to provide the company with “excess” young plasma that he could use for his study. Karmazin refused to say which ones they were. Read this article the hear the full history behind this so-called miracle treatment and why blood banks refused to participate.
California State Athletic Commission (CSAC) executive officer Andy Foster told MMA Fighting that, after reviewing multiple statements from scientists and experts, there was something that stood out above all the rest, swaying his choice to allow Jones to fight Alexander Gustafsson in the main event of UFC 232 on [Dec 29th] in Inglewood, Calif.
It was a single line from a letter written by Dr. Daniel Eichner, the director at Sports Medicine Research and Testing Laboratory (SMRTL), the World Anti-Doping Agency (WADA)-accredited lab in Salt Lake City. That line read: “There is no evidence that DHCMT has been re-administered,” per the document obtained from the commission.
Eichner, whose lab analyzed Jones’ tests, wrote that the “most likely” cause of the long-term metabolite of the steroid Turinabol (4-chloro-18-nor-17β-hydroxymethyl,17α-methyl-5α-androst-13-en-3α-ol (M3)) still being in Jones’ system was due to “residual levels from a previous exposure.” The low levels of the M3 metabolite were “not indicative of further exposure,” he wrote. So, Foster gave the go-ahead last weekend.
There are still many questions, some of which cannot be answered by published, peer-reviewed science. How could a steroid metabolite remain in Jones’ system for 17 months or longer? Does that steroid metabolite — as small as it may be — have any performance-enhancing benefits? And even if it doesn’t, should someone still be allowed to compete with something like that in their system? Come read the science behind this in the article!
To uncover the chemical architecture governing the timing of DNA replication, molecular biologist David Gilbert and his team turned to the emerging technology known as CRISPR to snip away at mouse chromosomes in order to work out which factors made a difference.
Gilbert used it to target a variety of structures within the DNA architecture of mouse embryonic stem cells, switching them around or cutting them out completely. Initial focus was on the binding sites for a protein called CCCTC-binding factor (CTCF). This protein helps regulate the whole transcription process, making its landing zone a natural place to look for locations that govern DNA's more spatiotemporal operations.
Yet tinkering with these had little effect on the actual timing of replication processes. Something else had to be at work. Finding this virtual needle in a haystack would require more than a little luck, though. It came in the form of a high resolution 3D analysis of the contact sites the DNA was making with itself. In what was a little like a close up of the hands of a skilled magician at work, the team were able to work out which 'fingertips' were in action.
Specifically, they identified several key locations outside of CTFC-associated boundaries. Breaking them caused chaos – replication timing was thrown, the DNA architecture itself was weakened, and transcription was missed. "Removing these elements shifted the segment's replication time from the very beginning to the very end of the process," says Gilbert.
Northwestern Medicine scientists have discovered two successful therapies that slowed the progression of pediatric leukemia in mice, according to three studies published over the last two years in the journal Cell, and the final paper published Dec. 20 in Genes & Development.
For the past 25 years, Ali Shilatifard, the Robert Francis Furchgott Professor of Biochemistry and Molecular Genetics and Pediatrics [and his] laboratory has been studying the molecular function of MLL, a key protein responsible for leukemia, within its complex known as COMPASS (Complex Proteins Associated with Set1). Most recently, it was demonstrated that COMPASS components are one of the most frequently identified mutations in cancer. The next step of this work will be to bring the drug to a clinical trial setting, which Shilatifard said he hopes will happen in the next three to five years. Earlier work from Shilatifard’s laboratory published in Cell in 2018 identified compounds that could slow cancer growth by interrupting a gene transcription process known as “Super Elongation Complex” (SEC). It was the first compound in its class to do this.
This MLL stabilization process discovered in the most recent paper could potentially work in cancers with solid tumors, such as breast or prostate cancer, said first author Zibo Zhao, a postdoctoral research fellow in Shilatifard’s lab. “This opens up a new therapeutic approach not only for leukemia, which is so important for the many children who are diagnosed with this terrible cancer, but also for other types of cancers that plague the population,” Zhao said.