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Microplastics discovered in human and dog testes

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Microplastics discovered in human and dog testes

Researchers have located one more anatomical organ where microplastics — of all shapes and constituents — are found: human testes.

And although they can’t say for sure, they suspect the presence of these jagged bits and strands of polymers such as polyethylene, polyvinyl chloride and polystyrene could be — in part — behind a global trend in diminishing sperm quality and quantity.

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In 2022, a team of researchers published a paper showing that global sperm counts fell about 1.2% per year between 1973 and 2018. From the year 2000, that rate accelerated to more than 2.6% per year.

“What I think will grab people’s attention with this study is the fact that plastic is in the testicles and potentially contributing to disarray in the function of the testicles,” said Leonardo Trasande, a pediatrician and public policy expert at New York University’s Grossman School of Medicine and Wagner School of Public Service.

“What should have gotten people excited all along is the fact that we’ve known that the invisible chemicals — the phthalates, the bisphenols and the PFAS that are used in plastic materials — are already known to be problems,” he said. “And so if this is what it takes to get people’s attention, I’m a bit sad. Because we already had enough evidence that plastics were bad for testicular function.”

Others, including Philip Landrigan, director of the Program for Global Public Health and the Common Good at Boston College, said the study was “consistent with a whole series of papers that have come out now in the last few years” showing these particles in a variety of organs, including the heart, liver, lungs and brain.

“It’s no surprise that microplastics are in the testes. The plastic is ubiquitous in today’s world, the stuff breaks down, and the smaller the particle, the more easily it can move into and throughout the human body,” he said.

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Xiaozhong Yu, a professor of environmental health at the University of New Mexico — and an author on this latest research — said he’d been researching the effects of different chemicals on sperm production for years, and it was only recently that a colleague suggested he look for microplastics in testes.

“I said, ‘Are you joking?’,” he said, recalling the conversation, explaining he was pretty certain he wouldn’t find microplastics in tests because — like the brain — these sperm-generating factories are insulated by a protective barrier.

Nevertheless, they gave it a go.

They started by trying it out in dog testes. They were able to acquire 47 from neutering clinics. (The pet owners all provided permission.)

They found microplastics in small dogs, big dogs, young dogs and old dogs. The plastic bits were in every dog testis they examined. The number ranged from 2.36 micrograms per gram to 485.77 micrograms per gram. The average was 122.63 micrograms per gram, and 12 polymers were identified. The most abundant were polyethylene — the material found in plastic packaging, films and bottles — and polyvinyl chloride — a material found in most household water pipes.

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He said he immediately went back to investigate their quality control. Maybe the testes had become contaminated at some point during the procedure or testing?

He and his team were able to rule that out, although Landrigan noted that contamination was still possible — unless everything, from procurement to analysis had been done in a “clean” room devoid of all plastic.

Yu and his team then decided to look at human samples. In the end, they were able to examine 23 testes from men ages 16 to 88. The tissue was acquired from males who had died in accidents and whose testes had been preserved post-autopsy. He said all samples were from men who had died in 2016 — made available following a seven-year storage requirement, after which time such samples are usually discarded.

Once again, they found microplastics in every sample they examined, and as with the dog testes, there was wide variation — from 161.22 micrograms per gram to 695.94 micrograms per gram, with an average of 328.44 micrograms per gram — nearly three times greater than what they found in dogs.

The microplastics in human testes were also composed of a variety of polymers, with polyethylene being the most common, followed by ABS (acrylonitrile, butadiene and styrene monomers — which is used to make a variety of products, including toys, automotive parts, medical equipment and consumer electronics), N66 (a kind of nylon), polyvinyl chloride and others.

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The researchers also noted a correlation between the concentrations of PVC and polyethylene and testes weight: The higher the concentration, the lower the weight.

“Generally, a decreased testis weight is indicative of reduced spermatogenesis,” wrote the authors in the paper.

Yu said the difference in humans and dogs between polymer types — with dogs showing higher concentrations of PVC than men — likely has to do with lifestyle differences. He said consumer trends show a general aversion to eating or drinking out of bottles and foodware made from PVC, which contains bisphenol A — an additive that has been associated with health and developmental harm.

However, he began looking at dog toys, and noticed many of them are made from this kind of plastic.

“People are choosing to avoid it,” he said. But the market hasn’t budged in the same way for dogs.

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Asked what the major route of exposure was for dogs and people, he said “microplastics are everywhere — in the air, in the drinking water, in the food, in our clothes. We don’t exactly know what is the most probable route. But they are everywhere.”

He also noticed variation within the groups. Dog testes acquired from public veterinary clinics showed higher levels of microplastics than those from private clinics, “potentially reflecting the influence of socioeconomic differences on the living environments and lifestyles of dogs.”

The researchers were also not able to find a correlation between age and microplastic concentration — a finding that surprised them. (Although men over the age of 55 had the least amount).

“The absence of a distinct age-dependent accumulation of microplastics in human testes may be due to unique physiological and biological processes of spermatogenesis,” they wrote, noting the continual renewal and release of sperm, which could “help mitigate the buildup of microplastics over time.”

That hypothesis, they noted, was supported by the presence of microplastics in human seminal fluid.

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“The reality is that the petrochemical industry has gotten a pass all these years,” said Trasande, the NYU professor. “We know that plastics come from the petrochemical industry … and it’s no secret that we have paid as a society by letting the petrochemical industry pollute us. Now we’re paying the consequences. And if we don’t reverse course fairly quickly, we will have an even bigger problems before us because plastic consumption is growing, not slowing down.”

Landrigan agreed and noted that nations were currently in negotiations to sign a treaty that would curb the use of plastic and cap production.

“Plastic production is increasing exponentially,” he said noting that it’s increased more than 200-fold since the 1950s. He said plastic production is on a trajectory to double by 2040 and triple by 2060. There have been a total of about 8 billion tons of plastic produced since 1950, he said, and about 6 billion tons is “floating around us, most of it in the form of microplastics.”

He said the anatomical location of this latest microplastic discovery may hit close to home for lawmakers, who until this time, have not been too concerned.

He said he’d had to testify in the Senate several years ago about endocrine disruptors, and mentioned that sperm quantity was reduced in men who’d been exposed.

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“Two senators sat back and unconsciously crossed their legs,” he said. “The body language was amazing.”

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Column: The abortion pill is safe. Is your uterus?

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Column: The abortion pill is safe. Is your uterus?

Huge sigh of relief.

In a ruling that I happily admit surprised me, the Supreme Court on Thursday affirmed the obvious: Women should have the right to safe medication abortions.

But ladies, our uteri are not safe yet.

For now, in a unanimous decision, the justices have tossed a case that would have prevented the drug mifepristone from being used by women seeking to end pregnancies.

So mify, as the drug is commonly called, is safe. But this is far from the end of the MAGA war on women.

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Let’s be clear on this: The ruling wasn’t actually about the drug. It was about the folks who brought the suit, a bunch of doctors who really didn’t have much of a reason to keep millions of women from accessing care other than they didn’t like the care those women wanted.

That’s not actually a reason to sue, even by Samuel Alito and Clarence Thomas standards.

So this ruling is about “standing” and the fact that these docs didn’t have it. Already, antiabortion activists are lining up other cases with defendants whose legal footing is much more solid.

And the Supreme Court is hardly the only front in this war for women’s rights. Here’s three other ways the far-right wants to control female bodies:

First, “fetal personhood” has bubbled up as a scary push by the religious right.

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Alito hinted at this concept in the Dobbs ruling, which knocked out Roe vs. Wade, when he referred to an embryo as an “unborn human being.”

In Alabama, we saw this take greater life recently when state Supreme Court judges ruled that embryos created during in vitro fertilization should be considered protected human life (though the state Legislature for now has protected the procedure).

And this week, the Southern Baptist Conference, which speaks for more than 10 million Protestant Americans, announced it would now opposes IVF on those embryos-are-life grounds.

If courts do recognize the idea of fetal personhood, it would pave the way for abortion to be considered not just illegal, but murder. It would also give a state the right to police pregnant women in any way it deems necessary to protect the “unborn child.”

We are already seeing some states attempting to prosecute women for abortions under strict new abortion laws and dozens of states (such as Kansas) either have outright legal language broadly giving fetuses rights or language that edges right up to it. We are closer to this than you think.

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The second front on the war on women is contraception.

Though it seems insane and inane to most of us to forbid women from taking the pill or an emergency medication in the immediate aftermath of intercourse to prevent pregnancy, some folks do want to ban it as a form of abortion.

There is a logic to it. If all abortion is illegal, then anything affecting the embryo after conception is off limits.

Finally, there’s former President Trump.

I’ve written before about the Comstock Act, an obscure and angry old law that many speculated the Supreme Court justices might dredge up in this mifepristone case.

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That law (which is on the books, but not enforced) theoretically makes it illegal to mail anything that could be used in an abortion — so not just the medication. Hard-liners could argue that anything shipped to an abortion clinic to help it operate could be verboten, even latex gloves.

MAGA types are already floating the frightening notion that if Trump were elected, he could simply bypass courts and Congress and order his Department of Justice to enforce the Comstock Act — ending abortion access without technically ending abortion access.

This week, Trump send a recorded message to the Danbury Institute, an ultraconservative organization that has advocated for abortion to be prosecuted as homicide and called it “child sacrifice.”

He didn’t mention abortion, but there’s this:

“These are gonna be your years, because you’re gonna make a comeback like just about no other group,” he said. “I know what’s happening, I know where you’re coming from and where you’re going, and I’ll be with you side by side.”

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So while Thursday’s ruling is a welcome win in the fight to keep women equal, it’s a victorious battle.

The war continues.

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You can help name L.A.’s newest dinosaur fossil. Just don't call it Dino McDinoface

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You can help name L.A.’s newest dinosaur fossil. Just don't call it Dino McDinoface

Sage? Esme? Gnatalie?

The Los Angeles County Natural History Museum is seeking the public’s help in naming a 70-foot-long sauropod skeleton unearthed by the museum’s paleontologists.

The dinosaur will be the focal point of the NHM Commons, a $75-million welcome center currently under construction on the southwest end of the museum in Exposition Park.

Slated to open this fall, the Commons will offer gardens, an outdoor plaza, a 400-seat theater and a glass-walled welcome center that can be toured without a ticket.

Its centerpiece is the sauropod, whose late Jurassic remains were found in southeast Utah and collected by museum paleontologists between 2007 and 2019. The long-necked, long-tailed dinosaur appears to be part of a new species, similar to the Diplodocus, which will be scientifically named in the future.

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Currently under construction at the museum, the skeleton is made up of about 350 fossils from six animals whose bones washed into a river after death some 150 million years ago and commingled.

How to vote

Online poll is open to name Natural History Museum dinosaur fossil

The voting is open until Thursday, June 20. You can choose from five names.

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Thanks to celadonite minerals that replaced organic matter during the fossilization process, the fossils are a striking emerald green, unique to this specimen.

Museum staff have long referred to the dinosaur internally as “Gnatalie,” a reference to the relentless gnats that plagued the dig site during the excavation. As its debut approaches, it’s time to turn the dinosaur over to the public.

“We want the people of Los Angeles to feel that this completely unique green giant is theirs, because it is,” said Lori Bettison-Varga, president and director of the Natural History Museums of Los Angeles County. “It’s not every day you build a more than 75-foot-long green dinosaur skeleton.”

In an online poll that runs through June 20, voters can choose from one of five names selected by museum staff:

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  • Gnatalie: A nod to the original quarry, and the scientists, students and community members who participated in the excavation (and endured the bugs).
  • Sage: An iconic green L.A. native plant that is also grown in NHM’s Nature Gardens.
  • Verdi: A derivative of the Latin word for green whose variations appear in multiple languages.
  • Esme: Short for “Esmeralda,” the Spanish word for “emerald.”
  • Olive: Olive trees are green, like the dinosaur, and a symbol of peace in many cultures.

The NHM Commons, depicted in a rendering, is set to open this fall in Exposition Park.

(Frederick Fisher and Partners, Studio-MLA, Studio Joseph / NHMLAC)

By limiting voting to a few pre-approved choices, the museum seeks to avoid the pitfalls of previous naming campaigns that have allowed more latitude for the public’s creativity. Few have forgotten a U.K. government agency’s 2016 online poll to name a $287-million polar research vessel, which yielded a landslide vote for the name “Boaty McBoatFace.”

Despite voters’ overwhelming preference for Boaty over dignified, pre-approved suggestions like “Shackleton” and “Endeavour,” the U.K.’s Natural Environment Research Council ultimately overrode the will of the people and christened its ship the R.R.S. Sir David Attenborough, after the beloved British television host and natural historian. (In a concession to the popular vote, the NERC agreed to grant the McBoatFace moniker to one of the ship’s three autonomous submarines.)

The winning name will be announced on June 25.

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Antibiotics wreak havoc on the gut. Can we kill the bad bugs and spare the good ones?

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Antibiotics wreak havoc on the gut. Can we kill the bad bugs and spare the good ones?

Inside every human is a thriving zoo of bacteria, fungi, viruses and other microscopic organisms collectively known as the microbiome. Trillions of microbes live in the digestive tract alone, a menagerie estimated to contain more than 1,000 species.

This ecosystem of tiny stuff affects our health in ways science is only beginning to understand, facilitating digestion, metabolism, the immune response and more. But when serious infection sets in, the most powerful antibiotics take a merciless approach, wiping out colonies of beneficial bacteria in the digestive tract and often prompting secondary health problems.

“Increasingly, researchers are recognizing the benefits of protecting the human gut microbiome, particularly because its integrity and diversity is linked to metabolic influences on mental health and physical health conditions,” said Dr. Oladele A. Ogunseitan, a professor of population health and disease prevention at UC Irvine.

Drug-resistant bugs are evolving faster than new medicines are being developed, rendering the current arsenal of medicines increasingly ineffective. But the more we understand about the microbiome, the clearer it is that we need antibiotics that are discerning in their targets.

With that goal in mind, a chemistry team at the University of Illinois Urbana-Champaign is experimenting with a compound that attempts to address both problems. The antibiotic, lolamicin, both successfully vanquished several drug-resistant pathogens in mice while sparing the animals’ microbiome. The results were published in the journal Nature.

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“Only recently has it been recognized that killing these [beneficial] bacteria is having many deleterious effects on patients,” said Paul J. Hergenrother, a chemistry professor at the University of Illinois Urbana-Champaign who co-led the study. “We have been interested for some time in finding antibiotics that would be effective without killing the good bacteria.”

The team set out to create an antibiotic that would both preserve the gut microbiome while targeting gram-negative bacteria, a particularly hardy category of superbugs. Encased in both an inner and outer membrane that antibiotics struggle to cross, gram-negative bacteria are resistant to most currently available therapies. They are responsible for the majority of the estimated 35,000 deaths in the U.S. each year from drug-resistant infections, according to the U.S. Centers for Disease Control and Prevention.

Worldwide, antimicrobial resistance kills an estimated 1.27 million people directly every year and contributes to the deaths of millions more.

Not all gram-negative bugs make us sick. Bacteria populations in the average human gut are roughly split between gram-negative and gram-positive types, said Kristen Munoz, a former doctoral student at the University of Illinois who co-led the study.

Broad spectrum antibiotics can’t tell which bugs to spare, she said. As a result, anything strong enough to treat a bad infection “is going to wipe out a good amount of your gut microbiome,” she said, even though they “aren’t doing anything wrong.”

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The team focused its search for a new drug on compounds that suppress the Lol system, which shuttles lipoproteins between the inner and outer membranes in gram-negative bacteria.

The Lol system’s genetic code looks different in harmful bacteria than it does in beneficial ones, which suggested to researchers that medicines that targeted the Lol system would be able to distinguish good bugs from bad ones.

The team designed multiple versions of these Lol-inhibiting compounds. When tested against 130 drug-resistant strains of Escherichia coli, Klebsiella pneumoniae and Enterobacter cloacae, one in particular proved especially potent.

They tested this antibiotic, which they named lolamicin, on mice that had been infected with drug-resistant strains of septicemia or pneumonia. All of the mice with septicemia survived after receiving lolamicin, as did 70% of the mice with pneumonia.

To measure the effect on gut bacteria, the researchers gave healthy mice either lolamicin, a placebo or one of two common antibiotics, amoxicillin and clindamycin. After collecting baseline stool samples, they sampled the animals’ poop seven, 10 and 31 days after treatment.

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Mice treated with amoxicillin or clindamycin had lower beneficial bacteria counts and less diversity of gut bacteria. In contrast, the guts of lolamicin-treated mice appeared largely the same.

“It was exciting to see that lolamicin did not really cause any changes in the microbiome, whereas the other clinically used antibiotics did,” Munoz said.

A disrupted microbiome can have immediate consequences for people battling infection. When beneficial microbes are decimated, dangerous bugs have fewer competitors and secondary infections can take hold.

Clostridium difficile is a notorious opportunistic pathogen, so the researchers did an experiment where they exposed mice treated with lolamicin, amoxicillin or clindamycin to C. difficile. The mice who took standard antibiotics were soon crawling with C. difficile. The lolamicin mice showed little to no infection.

The lab hopes to one day take lolamicin or a version of it to clinical trials, Hergenrother said. (Munoz received her doctorate last year and now works as a scientific analyst in Los Angeles.) Yet these are still early days for the drug. While the concept of a discerning antibiotic is a welcome development, it must clear significant barriers before it could make a difference for patients.

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“Distinguishing a quote-unquote ‘bad bug’ from a quote-unquote ‘good bug’ is not always as straightforward as it may seem,” said Dr. Sean Spencer, a Stanford University gastroenterologist and physician scientist who was not involved with the research.

Some beneficial bugs in the gut bear a striking genetic resemblance to harmful pathogens, he said. Others are benign in some contexts and dangerous in others: “In a critically ill individual, a good bug can do bad things.”

Years can pass between a new antibiotic’s proof of concept and its entry to the market, and the vast majority never make it to the end of that pipeline. It’s also not clear how easily or how quickly bacteria will develop resistance, which is perhaps the most formidable obstacle that lolamicin or any new antibiotic faces.

“One of the biggest problems is that bacteria are so smart. You can tackle one particular protein system or protein target in bacteria, but they will quickly find a resistance mechanism,” Munoz said. “They just have so many inherent mechanisms to overcome antibiotics.”

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