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.

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.

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.

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.

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.”

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

The war continues.

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.

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.

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:

• 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.

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.

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.

“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.”

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.

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.

“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.”