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Bachman–Turner Overdrive Drummer Robbie Bachman Dead at 69 – Rolling Stone
Robbie Bachman, the drummer for Bachman–Turner Overdrive who powered the band’s biggest hits including “You Ain’t Seen Nothing Yet” and “Takin’ Care of Business,” has died.He was 69.
Randy Bachman, the drummer’s brother and bandmate,
confirmed the news on Twitter Thursday night.“Another sad departure,” he wrote.“The pounding beat behind BTO, my little brother Robbie has joined Mum, Dad & brother Gary on the other side.Maybe Jeff Beck needs a drummer! He was an integral cog in our rock ‘n’ roll machine and we rocked the world together.” Further details surrounding Robbie’s death have not yet been revealed.
Robbie and Randy began playing music together as kids while growing up in Winnipeg, Canada.Eventually, guitarist Randy asked Robbie to become the drummer for his band Brave Belt, which he had formed with musician Chad Allan, Randy Bachman’s former bandmate in the Guess Who.Together, the band recorded two albums released in the early Seventies before eventually adding middle brother Tim Bachman on rhythm guitar and bassist C.
Fred Turner, and changing their name to Bachman–Turner Overdrive.
While their first self-titled album as Bachman–Turner Overdrive in 1973 wasn’t a huge hit upon release – though it did boast the gem “
Hold Back the Water,” featuring a rare co-writing credit for Robbie – they quickly found their real success with their second album later that same year.The LP, Bachman-Turner Overdrive II, featured their most famous song, “Takin’ Care of Business,” as well as the hit “Let It Ride.” Not Fragile followed in 1974, and with it another hit, “You Ain’t Seen Nothing Yet.”
The group continued to make music throughout the mid-Seventies, releasing a handful of albums, before Randy Bachman exited the band in 1977 following the release of Freeways, leaving Robbie as the lone Bachman still in the Overdrive.
BTO briefly disbanded in 1979, but by 1983, the band reunited with Randy and Tim Bachman returning, though without Robbie; BTO’s 1984 self-titled semi-reunion album is the lone album by the band to not feature Robbie on drums.
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However, Robbie would later rejoin Bachman-Turner Overdrive in 1988, and when Randy once again left the band in 1991, Robbie continued on with “BTO” – the band’s legally agreed upon name when Randy wasn’t involved – through 2005.When Randy revived Bachman-Turner Overdrive in 2009, it was once again without his younger brother.
In 2014, Bachman–Turner Overdrive were inducted into the Canadian Music Hall of Fame.
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Chemicals accumulated in the vagina may contribute to spontaneous preterm birth – News-Medical.Net
Chemicals that accumulate in the vagina, potentially originating from personal care products, may contribute to spontaneous preterm birth, according to a new study by researchers at Columbia University Vagelos College of Physicians and Surgeons.
The study of 232 pregnant women found that a handful of non-biological chemicals previously found in cosmetics and hygiene products are strongly associated with preterm birth.
Our findings suggest that we need to look more closely at whether common environmental exposures are in fact causing preterm births and, if so, where these exposures are coming from.The good news is that if these chemicals are to blame, it may be possible to limit these potentially harmful exposures.”
Tal Korem, PhD, study co-leader, assistant professor in the Program for Mathematical Genomics and the Departments of Systems Biology and Obstetrics and Gynecology at Columbia University
The study was published January 12 in Nature Microbiology.
Preterm birth, childbirth before 37 weeks of pregnancy, is the number one cause of neonatal death and can lead to a variety of lifelong health issues.Two-thirds of preterm births occur spontaneously, but despite extensive research, there are no methods for predicting or preventing spontaneous preterm birth.
Several studies have suggested that imbalances in the vaginal microbiome play a role in preterm birth and other problems during pregnancy.However, researchers have not been able to reproducibly link specific populations of microorganisms with adverse pregnancy outcomes.
The research team, co-led by Korem and Maayan Levy, PhD, of the University of Pennsylvania, decided to take a more expansive view of the vaginal microenvironment by looking at its metabolome.The metabolome is the complete set of small molecules found in a particular biological niche, including metabolites produced by local cells and microorganisms and molecules that come from external sources.
“The metabolome can be seen as a functional readout of the ecosystem as a whole,” Korem says.“Microbiome profiling can tell us who the microbes are; metabolomics gets us close to understanding what the microbes are doing.”
In the current study, the researchers measured over 700 different metabolites in the second-trimester metabolome of 232 pregnant women, including 80 pregnancies that ended prematurely.
The study found multiple metabolites that were significantly higher in women who had delivered early than in those who delivered at full term.
“Several of these metabolites are chemicals that are not produced by humans or microbes-;what we call xenobiotics,” says Korem.
“These include diethanolamine, ethyl-beta glucoside, tartrate, and ethylenediaminetetraacetic acid.While we did not identify the source of these xenobiotics in our participants, all could be found in cosmetics and hygiene products.”
Algorithm predicts preterm birth
Using machine learning models, the team also developed an algorithm based on metabolite levels that can predict preterm birth with good accuracy, potentially paving the way for early diagnostics.
Though the predictions were more accurate than models based on microbiome data and maternal characteristics (such as age, BMI, race, preterm birth history, and prior births), the new model still needs improvement and further validation before it could be used in the clinic.
Despite the current limitations, Korem says, “our results demonstrate that vaginal metabolites have the potential to predict, months in advance, which women are likely to deliver early.”
Kindschuh, W.F., et al.
(2023) Preterm birth is associated with xenobiotics and predicted by the vaginal metabolome.Nature Microbiology.
doi.org/10.1038/s41564-022-01293-8.
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Madagascar mouse lemur retroviruses are diverse and surprisingly similar to ones found in polar bears or domestic sheep – EurekAlert
Madagascar is home to a unique biodiversity with a large number of endemic species, among those many lemur species, including the mouse lemurs.This diversity is also found in their retroviruses, a team led by scientists from the Leibniz Institute of Zoo and Wildlife Research (Leibniz-IZW) and the University of Stirling reports in the journal “Virus Evolution”.
They analysed the mouse lemur genome and identified viruses of two classes that represent ancient infections of the mouse lemur germline.The viruses now behave similarly to lemur genes and are thus called endogenous retroviruses (ERVs).It was surprising that some of the identified retroviruses are closely related to viruses found in other, very different mammals such as polar bears or domestic sheep.This suggests an intriguing and complex pattern of host switching of retroviruses, much more complex than previously thought.
For their analysis, the team collected blood samples from four species of Malagasy mouse lemurs and screened them using high throughput sequencing.The scientists identified two gamma and three beta retrovirus sequences in the lemurs’ genomes, representing ancient infections of the mouse lemur germlines.Since then, the virus DNA has been incorporated in the host genomes and the viruses are no longer active or infectious.“We were surprised to find that one of the two identified gamma retroviruses was related to an ERV described in polar bears”, states Dr Sharon Kessler, a German Academic Exchange Service (DAAD) supported scientist and Assistant Professor at the University of Stirling.
The polar bear virus is young from an evolutionary point of view whereas the lemur virus is old.“How these related viruses infected such geographically separated species is unclear”, Kessler says.
There were further surprises among the beta retroviruses.
A virulent retrovirus that infects domestic sheep called Jaagsiekte sheep retrovirus (JSRV), which also forms ERVs in domestic sheep, is thought to be a virus confined to domestic sheep, goats and their relatives – the first cloned sheep “Dolly” had to be euthanised after a JSRV infection and subsequent illness.The mouse lemurs have a closely related JSRV-like virus in their genome.
“This suggests that JSRV-like viruses have been more widespread among mammals and are considerably older than previously thought.Why they only show up in such disparate species and in such a punctuated way is curious”, says Prof Alex Greenwood, head of the Leibniz-IZW Department of Wildlife Diseases, where the sample screening was conducted.Similarly, the team also identified a virus in the mouse lemurs related to retroviruses found in squirrel monkeys, vampire bats and marsupials.
“This group of viruses is becoming more interesting over time as more and more examples of similar viruses are being found in many places including very young ones that may still have currently infectious exogenous counterparts in nature”, says Greenwood.
Much of the mouse lemur retroviral diversity observed is associated with non-primate viruses, suggesting a complex pattern of viral host switching around the time the ancestors of lemurs colonized Madagascar.Further studies of viral diversity will help to clarify the complex history of retroviral transmission among mammals.
Dr Kessler and Prof Greenwood collaborated with Prof Solofonirina Rasoloharijaona of the University of Mahajanga, (Madagascar), Prof Ute Radespiel of the University of Veterinary Medicine Hannover, Foundation, (Germany) and Dr Kyriakos Tsangaras of the University of Nicosia (Cyprus) in this scientific investigation that was also made possible with funding from the American Association of Physical Anthropologists.
Retroviruses are viruses that replicate by incorporating their genetic material into the genome of a host cell.If the infected cell is a germ cell, the retrovirus can subsequently be passed on as an “endogenous” retrovirus and spread throughout a population as part of the host genome.Repeated infections have resulted in endogenous retroviruses being ubiquitous in mammalian genomes, sometimes making up significant portions of the host genome.However, most retrovirus integrations are very old and already degraded and therefore inactive – their initial impact on host health reduced by millions of years of evolution.
Journal
Virus Evolution
Article Title
Long-term host-pathogen evolution of endogenous beta- and gammaretroviruses in mouse lemurs with little evidence of recent retroviral introgression
Article Publication Date
14-Dec-2022
Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.
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Machine learning tools help unravel why human accelerated regions evolved so quickly – News-Medical.Net
Humans and chimpanzees differ in only one percent of their DNA.Human accelerated regions (HARs) are parts of the genome with an unexpected amount of these differences.HARs were stable in mammals for millennia but quickly changed in early humans.
Scientists have long wondered why these bits of DNA changed so much, and how the variations set humans apart from other primates.
Now, researchers at Gladstone Institutes have analyzed thousands of human and chimpanzee HARs and discovered that many of the changes that accumulated during human evolution had opposing effects from each other.
This helps answer a longstanding question about why HARs evolved so quickly after being frozen for millions of years.An initial variation in a HAR might have turned up its activity too much, and then it needed to be turned down.”
Katie Pollard, PhD, director of the Gladstone Institute of Data Science and Biotechnology and lead author of the new study
The findings, she says, have implications for understanding human evolution.
In addition-;because she and her team discovered that many HARs play roles in brain development-;the study suggests that variations in human HARs could predispose people to psychiatric disease.
“These results required cutting-edge machine learning tools to integrate dozens of novel datasets generated by our team, providing a new lens to examine the evolution of HAR variants,” says Sean Whalen, PhD, first author of the study and senior staff research scientist in Pollard’s lab.
Enabled by machine learning
Pollard discovered HARs in 2006 when comparing the human and chimpanzee genomes.While these stretches of DNA are nearly identical among all humans, they differ between humans and other mammals.Pollard’s lab went on to show that the vast majority of HARs are not genes, but enhancers-; regulatory regions of the genome that control the activity of genes.
More recently, Pollard’s group wanted to study how human HARs differ from chimpanzee HARs in their enhancer function.In the past, this would have required testing HARs one at a time in mice, using a system that stains tissues when a HAR is active.
Instead, Whalen input hundreds of known human brain enhancers, and hundreds of other non-enhancer sequences, into a computer program so that it could identify patterns that predicted whether any given stretch of DNA was an enhancer.
Then he used the model to predict that a third of HARs control brain development.
“Basically, the computer was able to learn the signatures of brain enhancers,” says Whalen.
Knowing that each HAR has multiple differences between humans and chimpanzees, Pollard and her team questioned how individual variants in a HAR impacted its enhancer strength.For instance, if eight nucleotides of DNA differed between a chimpanzee and human HAR, did all eight have the same effect, either making the enhancer stronger or weaker?
“We’ve wondered for a long time if all the variants in HARs were required for it to function differently in humans, or if some changes were just hitchhiking along for the ride with more important ones,” says Pollard, who is also chief of the division of bioinformatics in the Department of Epidemiology and Biostatistics at UC San Francisco (UCSF), as well as a Chan Zuckerberg Biohub investigator.
To test this, Whalen applied a second machine learning model, which was originally designed to determine if DNA differences from person to person affect enhancer activity.The computer predicted that 43 percent of HARs contain two or more variants with large opposing effects: some variants in a given HAR made it a stronger enhancer, while other changes made the HAR a weaker enhancer.
This result surprised the team, who had expected that all changes would push the enhancer in the same direction, or that some “hitchhiker” changes would have no impact on the enhancer at all.
Measuring HAR strength
To validate this compelling prediction, Pollard collaborated with the laboratories of Nadav Ahituv, PhD, and Alex Pollen, PhD, at UCSF.The researchers fused each HAR to a small DNA barcode.Each time a HAR was active, enhancing the expression of a gene, the barcode was transcribed into a piece of RNA.Then, the researchers used RNA sequencing technology to analyze how much of that barcode was present in any cell-;indicating how active the HAR had been in that cell.
“This method is much more quantitative because we have exact barcode counts instead of microscopy images,” says Ahituv.“It’s also much higher throughput; we can look at hundreds of HARs in a single experiment.”
When the group carried out their lab experiments on over 700 HARs in precursors to human and chimpanzee brain cells, the data mimicked what the machine learning algorithms had predicted.
“We might not have discovered human HAR variants with opposing effects at all if the machine learning model hadn’t produced these startling predictions,” said Pollard.
Implications for understanding psychiatric disease
The idea that HAR variants played tug-of-war over enhancer levels fits in well with a theory that has already been proposed about human evolution: that the advanced cognition in our species is also what has given us psychiatric diseases.
“What this kind of pattern indicates is something called compensatory evolution,” says Pollard.“A large change was made in an enhancer, but maybe it was too much and led to harmful side effects, so the change was tuned back down over time-;that’s why we see opposing effects.”
If initial changes to HARs led to increased cognition, perhaps subsequent compensatory changes helped tune back down the risk of psychiatric diseases, Pollard speculates.
Her data, she adds, can’t directly prove or disprove that idea.But in the future, a better understanding of how HARs contribute to psychiatric disease could not only shed light on evolution, but on new treatments for these diseases.
“We can never wind the clock back and know exactly what happened in evolution,” says Pollard.“But we can use all these scientific techniques to simulate what might have happened and identify which DNA changes are most likely to explain unique aspects of the human brain, including its propensity for psychiatric disease.”
Whalen, S., et al.(2023) Machine learning dissection of Human Accelerated Regions in primate neurodevelopment.Neuron.
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