#Lymph Node Sampling

[phagodyke]

worked an hour extra bc they have no respect for my half day but I knew they were gonna do that so whatever..... at least I'm omw home now

[jenthebug]

Had an ultrasound (abdominal, for my wound) today which sounded kinda inconclusive.

Also had a CT scan of my chest, abdomen, and pelvis for my oncologist. That one found a lymph node that has doubled in size, and I’m trying not to freak out. Tissue sampling (biopsy) is suggested.

Can I freak out a little?

I know they don’t joke around so I can’t email the radiologist all like “say sike right now.”

What I don’t know is what, besides more cancer, would cause a lymph node to double in size. Or if there’s a medication that I can take that doesn’t give me brain fog.

I’m doing SO GOOD at work right now.

Brain fog would fuck that all up. I just got my brain back and am doing well and somewhat enjoying myself, which tells me that I’ll have a blast when I get the hang of things.

We’ll see what oncology says.

[a-high-femme]

hi, folks. I always feel weird putting disclaimers like this on my blog, but I wanted to give you guys a heads up.

I'm still chronically online, but I can feel myself pulling away from DMs a little bit, and I'm assuming that that's going to be a trend for at least the next week. the past month has been hell and my social battery is always the first thing that's compromised when I'm dealing with prolonged stress; please don't take it personally if I'm slow to respond. scrolling and reblogging and responding to asks on here is a significant way that I distract myself when I'm stressed, and doing these things takes a LOT less effort for my brain than holding a full conversation, especially with people I have less-established rapports with. it isn't reflective of how I feel about any particular mutuals— it's just reflective of how at-capacity (honestly, beyond capacity) my brain is right now.

tI;dr: just because I'm active/online doesn't mean I'm going to be responding to my DMs consistently or swiftly. I generally try my best to keep up with them, but that's not a realistic expectation to hold myself to right now. it isn't personal.

for those keeping up with the saga of my cat's health (the resorptive lesions on her teeth which likely caused the inflamed lymph node two weeks ago), most of her bloodwork panel came back today and the clinic just called with results. I'll describe the results under the break (along with a full summary of what's been going on/details of her treatment going forward).

Lettie had to go to the vet on 5/16 for a big lump on her throat; they originally thought it was an abscess, but when they went to drain it it became clear that it was a severely swollen lymph node. they drained the area, sampled the fluid, and took a small tissue sample and sent it off for a biopsy. while she was under sedation, they also discovered some resorptive lesions* below the gumline on a couple of her teeth; they scraped away the excess inflamed gum, but they gave me a heads-up that it would have to be dealt with sooner rather that later, since it would reoccur without extraction. luckily, her annual appointment (which I scheduled months ago) was this past Saturday on 5/31, the day after her two-week recovery period from her 5/16 visit ended, so her teeth were the first thing I mentioned to them.

her biopsy results from the lymph node sample came back negative for cancerous cells, but it was inconclusive as to what caused the infection in the first place. at her annual this past weekend, they ran a full panel of bloodwork for two reasons: 1.) to try to rule out some major possibilities for why a young cat could be having these dental issues this early in her life (primarily they were worried about FIV/FeLV) and 2.) to get bloodwork on file ahead of her emergency dental extractions, which are scheduled for this Wednesday (6/4).

Lettie's chemistry is altogether pretty normal— she has a mildly elevated liver-related value, but that could be from her recent infections, so they'll be retesting a few weeks after her upcoming surgery. FIV/FeLV both came back negative, her thyroid results are normal, and her white and red blood cells counts are both normal. her coronavirus results are still pending, but if the corona comes back negative and the follow-up testing on her liver value comes back normal (later this summer, after the infections clear), that means this issue is ✨genetic✨ and it's likely that her dental issues will reoccur long-term. translation: it's almost certain that eventually she'll need more teeth extracted.

these results are a bit of a mixed bag. let me state the obvious: I'm SO fucking relieved that she doesn't have FIV/FeLV. I hate seeing my cat sick and I was worried about the possibility of it being a big scary disease. but the thing about those big scary diseases is that, even though they aren't curable, they are treatable/ manageable. since this is likely a progressive, genetic dental issue, she could end up losing more/all of her teeth as she gets older, and the best thing I can do for her is to just brush her teeth, keep an eye on her gumline, and reach out to her care team when she shows signs of lesions again, which... just thinking about it makes me want to cry.

on Wednesday morning I'll be dropping her off at her vet's office; she'll get x-rays and they'll determine how many teeth need to come out. right now they know for sure that she needs 1-2 teeth extracted, but it's possible that there are more teeth with lesions beneath the gum line that they can't see without the x-rays. she'll be sedated, they'll extract the compromised teeth, I'll get her back by the end of the day, and we'll restart the two-week countdown for getting her out of a cone; her sutures from 5/16 are almost fully dissolved, but she'll have new stitches after the dental extractions, so back into the soft donut-patterned cone she goes. she weirdly doesn't like wet food, so I suspect that it's going to be a struggle to get her to eat for a few days. I will be a wreck.

I'm currently trying to breathe through it and remind myself that her genetic issues are completely out of my control, and the only thing I can control is giving her the best and most timely care that I can get her, which is what l'm doing. she doesn't get as much time as we do, and I just want her life to be as good and easy as it can be for her. ✨this shit sucks.✨

* her teeth are essentially eating themselves, and the surrounding gum is trying to fill in the holes in her teeth, which inflames the area and makes her very uncomfortable. long-term, extractions should relieve a lot of pain and discomfort for her once they heal up and the initial pain of the stitches goes away.

here is a Lettie photo for those of you who made it to the end of this very long post:

[mariacallous]

When David Fajgenbaum was a twenty-five-year-old medical student, at the University of Pennsylvania, he started to feel so tired that he could barely stand. Fajgenbaum, a former college quarterback, could still bench-press three hundred and seventy-five pounds; he was known for doing pullups on a tree near his workplace. But now he was desperately ill. The lymph nodes in his groin and neck swelled. Small red dots—blood moles—emerged on his chest, and he woke up soaked in sweat. One day, at the hospital where he was doing his rotation, he stumbled down the hall into the emergency room, and doctors told him that his liver, bone marrow, and kidneys were failing. Fluid had leaked out of his blood vessels, into his abdomen and around his heart; bleeding in his retina temporarily blinded him in his left eye. Fajgenbaum was admitted to the I.C.U. and given enormous doses of steroids to try to quell runaway inflammation. It took him a month to recover enough to leave the hospital.

Fajgenbaum remembers asking a doctor what had caused his strange illness. “We don’t know,” the doctor said. “But let’s just hope it doesn’t come back.” When it did, a month later, he was diagnosed with a form of Castleman disease—a rare, often fatal condition that straddles the line between cancer and autoimmune disorder. There were few studies of the disease and no approved treatments. Doctors started Fajgenbaum on an aggressive chemotherapy regimen, but his condition deteriorated so much that a priest delivered last rites. Miraculously, and mysteriously, the illness receded. And yet it kept coming back.

Fajgenbaum scoured his medical records and the available scientific literature. He requested a series of tests. Eventually, he noticed something curious. A few months before one of his hospitalizations, the number of activated T cells in his blood had started to rise, and so did the amount of a protein called VEGF, which promotes the growth of blood vessels. Fajgenbaum performed experiments on his own blood samples and lymph nodes that identified a link between the two processes—a signalling cascade known as mTOR—and convinced his doctors to give him a potent suppressor of the pathway called sirolimus. The drug had been on the market for more than a decade; it was often given to transplant patients to stop their immune systems from attacking a new organ. After Fajgenbaum started the medication, months passed without a relapse, then years. When I spoke with him, a few weeks ago, his disease had been in remission for more than a decade.

Fajgenbaum told his story in a 2019 memoir, “Chasing My Cure: A Doctor’s Race to Turn Hope Into Action.” He focussed on a central irony: the medication that saved his life already existed, and nobody had thought to give it to him. “There is a systemic problem,” he told me. “There are all these drugs available, sitting in your local pharmacy, but they aren’t being used to treat all the conditions they could.” But in the years since the book came out—and, more specifically, since the rise of powerful A.I. models—Fajgenbaum has started to find solutions for that problem. He co-founded a nonprofit called Every Cure, which trained an A.I. model on what he described as “the world’s knowledge of every disease, gene, protein, and molecule, as well as the interactions between them.” The algorithm began to propose previously unknown applications for known treatments.

Talking to Fajgenbaum, I thought about how I’d often been in the uniquely discouraging position that his doctors were once in, with little to offer someone for a perplexing or intractable condition. Doctors have long prescribed off-label medications, usually through trial and error or in clinical trials, but now A.I. appears poised to supercharge the practice. Earlier models needed examples of effective drugs to learn, so they were unlikely to identify promising candidates unless treatments already existed. But more advanced models can conduct what’s called “zero-shot inference,” nominating drug candidates for conditions without any known treatments. “We’re at an inflection point,” Marinka Zitnik, a computer scientist at Harvard and a member of Every Cure’s advisory board, told me. “I think we’ve entered a new era.”

More than eighteen thousand diseases afflict humans, by Every Cure’s count, including upward of nine thousand that don’t have a single approved treatment. Meanwhile, there are thousands of medications on the market. The tally of conceivable drug-disease combinations numbers in the tens of millions. Some combinations obviously won’t work—penicillin won’t treat cancer—but many others could save lives if only we had a way to identify them. Of course, few patients can conduct the sort of rigorous self-study that Fajgenbaum did, and pharmaceutical companies have little incentive to find novel uses for old drugs, which bring in little money. “Who’s going to invest in uncovering all the potential matches?” Fajgenbaum said. “And how do you rank and prioritize all the possibilities?”

Every Cure’s A.I. platform, dubbed the MATRIX, is trained on what are known as “knowledge graphs”—networks of data representing the relationships between genes, proteins, drugs, and diseases. Knowledge graphs pull their information from the scientific literature and from curated medical sources: biobanks with health data from millions of people, for example, or repositories of chemicals and their safety profiles. The power of these networks has grown considerably over the past decade, allowing models such as Every Cure’s to generate a ranked list of the likelihood that a medication will treat a disease, on a scale from zero to one. Fajgenbaum’s team then undertakes a lengthy review process to determine which drug-disease pairs warrant further study or promotion. “At this stage, it’s less that the A.I. is outsmarting us humans and more that it’s really good at highlighting things that we’ve already discovered,” Fajgenbaum said. “Often, we just aren’t making the connections. Scientists might write something up in a journal somewhere, but then there’s no one to take it forward.”

A common heart drug called propranolol might be useful for treating angiosarcoma, an aggressive form of cancer. (The medication inhibits a receptor that’s expressed in such tumors.) A Botox injection between the eyebrows could theoretically reduce the symptoms of depression. (Perhaps making it harder to frown could disrupt physical feedback loops that reinforce negative emotions.) Several studies suggest that giving folinic acid, a kind of vitamin, to certain autistic children could enhance their verbal abilities. A recent randomized trial in India found that injecting high doses of lidocaine around breast tumors at the time of surgery significantly improved survival rates for women with breast cancer. Some of these pairings may not work, but it wouldn’t take many successes to justify the effort. “Lidocaine is one of the most inexpensive substances in all of medicine,” Fajgenbaum said. “With breast-cancer surgery, it’s already going to be injected at the site of the incision. We’re not even talking about bringing a new substance into the surgery. We’re just talking about injecting the same substance at a higher volume!”

Last year, Fajgenbaum received an e-mail from a woman named Tara Theobald, whom he’d met at a conference for Castleman disease. Her boyfriend, Joseph Coates, had initially been diagnosed with the condition, but was later found to have a rare blood disorder called POEMS syndrome. Coates was now entering a terminal stage: his heart and kidneys were failing, and fluid had to be drained from his belly several times a week. He was too sick to undergo a stem-cell transplant, which could save his life. Every Cure doesn’t usually offer treatment recommendations for individual cases, but this time Fajgenbaum used the organization’s A.I. platform to recommend a combination of drugs normally used to treat a blood cancer: a steroid called dexamethasone; a chemotherapy called cyclophosphamide; an immunotherapy called carfilzomib. “It was a Hail Mary, last-ditch effort,” Fajgenbaum told me. The doctor treating Coates thought that the regimen sounded “a little bit crazy.” But, with little to lose, they gave it a try—and within days Coates started to improve. A few months later, he’d recovered sufficiently to receive a stem-cell transplant. He is now in remission.

Stories like this have earned Fajgenbaum a reputation as a miracle worker. Each week, he receives hundreds of inquiries from patients and families asking whether he can conjure a treatment to help them. He is in touch with as many as he can be, but “we’re not naïve enough to think that one hundred per cent of these matches will be successful,” he said. “Plus, a one-off approach is not how we can help the most people.” Fajgenbaum and his team manually sift through around a thousand drug-disease combinations per month. Is there a plausible biological mechanism by which a medication can treat a disease? How many patients would benefit, and how much would they benefit? What are the chances of being able to prove that a medicine created for one condition works for another? Drug development is a bit like foraging in an unfamiliar forest; some fruits will nourish you and others might poison you. Drug repurposing is more like wandering around an overgrown orchard. Every candidate has already been vetted for safety; A.I. can identify low-hanging fruit, and then humans can decide whether the pairing is ripe for picking.

Every Cure classifies high-scoring drugs into one of four buckets: frontier explorers, clinical gems, unsung heroes, and known entities. A frontier explorer does well in the model and has a strong biological rationale, but there’s little research supporting its use for the target condition. A clinical gem has some evidence, for example in cells or animals, but requires more study in people. Unsung heroes have proved themselves—they’re just not being used. And known entities are already widely repurposed in clinical practice. Fajgenbaum’s goal is to move as many drugs up the ladder as possible, whether by prompting investigations of little-studied treatments or by helping proven pairings become more broadly adopted. To do so, the nonprofit has secured more than a hundred million dollars in awards from the TED Audacious Project and the federal government’s Advanced Research Projects Agency for Health, or ARPA-H.

A few weeks ago, I sat in on a meeting at which Every Cure employees discussed the drug-disease pairs that the MATRIX had deemed worthwhile. Much of the medical team sat around a conference table in Boston with Fajgenbaum; members of the tech team Zoomed in from London. A physician named Elliott Sharp, with neat brown hair and red-rimmed glasses, presented a summary of Rosai-Dorfman disease, or R.D.D., a rare and little-understood condition that can lead to enlarged lymph nodes and serious skin problems, such as nodules and ulcerations. A doctor named Luke Chen, in Canada, had used a cancer drug called lenalidomide to treat some of his patients with the disease, Sharp said, and had suggested it to Every Cure. The medication scored highly in the A.I. model—in the top 0.3 per cent of all drug-disease matches—and ranked twenty-third on the A.I.’s list of possible treatments for R.D.D. “Pretty much everything above it is a chemotherapy, steroid, or a known treatment,” Sharp told the group. There seemed to be a clear biological mechanism by which it could work—it suppressed an inflammatory molecule that was thought to play a critical role in the disease—and by 2026 the medication would fall in price and be more widely available. Sharp pulled up an A.I.-generated graphic that displayed linkages between the drug and the disease; it looked like a jumble of yarn and multicolored Christmas ornaments, each labelled with a word such as “papule,” “prednisone,” or “erythema.”

“It seems promising,” Matt Goddeeris, a cell biologist and former biotech researcher, who serves as the vice-president of discovery at Every Cure, said. “Looks like the N.C.C.N.”—National Comprehensive Cancer Network—“guidelines have it as a late-line option. The question is: Should it actually be higher? And do we think this is a clinical gem or an unsung hero?” For the former, Every Cure might conduct or facilitate a trial; for the latter, the organization would focus on outreach and advocacy. The group decided to advance lenalidomide for a “deep dive”: the medical team would spend weeks or months researching and, if needed, consult a scientific advisory committee about whether the organization should invest in further research or advocacy.

Every Cure’s A.I. also provides an assessment of a disease’s level of unmet need—though this assessment depends in part on the subjective values that the programmers have encoded. A condition such as R.D.D. can be debilitating and has few effective treatments; on the other hand, it generally isn’t lethal, and only about a hundred cases are diagnosed in the U.S. each year. Fajgenbaum said that the algorithm prioritizes how much an individual suffers from a disease, and whether any treatments exist, in addition to population-wide metrics such as the total number of people who suffer and die from it. R.D.D. had a score of 21.5 out of twenty-eight, placing it in the top one-third of conditions. (“David should get a tattoo of ‘No disease is too rare,’ ” one of his colleagues wrote in the Zoom chat.)

The group turned to the next potential pairing: a common immunosuppressant that had been flagged as a possible therapy for Alzheimer’s disease. “This was very, very high in MATRIX,” Nick Fragola, a research fellow at Every Cure, said. “And, in a vacuum, the mechanism makes sense.” But, Fragola went on, the few existing studies haven’t demonstrated results, and a small trial found that the drug didn’t easily enter the brain. “That’s probably a deal-breaker,” he said. “When you look at the molecule, it definitely doesn’t scream ‘brain penetrant,’ ” someone wrote in the Zoom chat. This time, the group decided to table the drug.

In early 2020, a biotech company called BenevolentAI used its knowledge graph to identify baricitinib, a rheumatoid-arthritis drug, as a potential treatment for COVID-19. The medication worked, and was formally approved for use in seriously ill COVID patients. Five years later, baricitinib remains one of the only medications that’s successfully been repurposed on a large scale as a result of A.I. “Finding medicines that work is tremendously difficult,” Derek Lowe, a longtime drug researcher and a blogger for Science, said. “Whenever someone says, ‘Ta-da, we’ve solved it!,’ I just make sure to keep my hand on my wallet.” Companies that make such claims sound like they’re selling snake oil. Lowe told me that he’s a “short-term pessimist but a long-term optimist” when it comes to using machine-learning tools to repurpose medicines. In his view, the approach may be most useful in treating certain rare diseases, for which “the standard of care is just to sit back and shake your head. Anything is going to be an improvement.” A.I.’s utility for tackling common and widely researched conditions is less certain. “A lot of what the models are doing has already been done by humans,” he said.

Next year, Fajgenbaum plans to publicly release scores for the tens of millions of drug-disease pairs that Every Cure’s A.I. platform has examined. For virtually any disease, researchers, doctors, and patients will be able to visit a website and see much of what his team saw—a prospect that, to me, sounded both empowering and overwhelming. The database is sure to offer useful ideas, but it could also generate floods of inquiries from patients and families about untested remedies. During the pandemic, the antiparasitic drug ivermectin gained traction as a possible COVID treatment because there were mechanistic reasons to think the drug might work. Studies repeatedly showed that it didn’t, but ivermectin remains a cause célèbre in certain circles—and, for some people, doctors’ unwillingness to prescribe it suggests that the medical establishment can’t be trusted. “I applaud the transparency,” Eric Topol, the director of the Scripps Translational Research Institute, told me when I described Every Cure’s plans. “But I’m also concerned that this could lead to wild-goose chases.”

Around the turn of the twenty-first century, a theoretical biologist named Stuart Kauffman introduced the concept of the “adjacent possible.” Single-celled organisms don’t suddenly evolve into fish and then primates; instead, a cell might evolve into a slightly more complex cell, and then perhaps into a multicellular organism, and that organism might gradually evolve new ways of using its biological machinery. Kauffman argued that natural selection is fundamentally a process of repurposing. Useful adaptations increase the complexity of a system; they expand the set of novel and nearby states available to an organism and its descendants. Dinosaur scales might evolve, step by step, into jury-rigged flight feathers; fish fins might eventually become mammalian limbs. “Anything can be used for more than one thing,” he has said.

Kauffman’s theory has since been adapted to explain innovation of all kinds, from the printing press to the iPhone. “The adjacent possible is a kind of shadow future, hovering on the edges of the present state of things,” the author Steven Johnson writes in his book, “Where Good Ideas Come From.” “Each new combination ushers new combinations into the adjacent possible.” Johnson likens the adjacent possible to a house that continually expands as you stroll through it. Walk through a door and another room materializes. This is one theory of scientific advancement. “Keep opening new doors,” Johnson writes, “and eventually you’ll have built a palace.” In this metaphor, drug repurposing may be less about building and more about discovering secret hallways and hidden doors. The room we are looking for might already exist out there, but the palace of biomedicine is so sprawling that simply assembling a blueprint—let alone exploring the whole structure—would be a superhuman task. Human intelligence built this place; artificial intelligence will help us navigate it.

[anonymolly]

hi, folks. I always feel weird putting disclaimers like this on my blog, but I wanted to give you guys a heads up.

I’m still chronically online, but I can feel myself pulling away from DMs a little bit, and I’m assuming that that’s going to be a trend for at least the next week. the past month has been hell and my social battery is always the first thing that’s compromised when I’m dealing with ongoing stress; please don’t take it personally if I’m slow to respond. scrolling and reblogging and responding to asks on here is a significant way that I distract myself when I’m stressed, and doing these things takes a LOT less effort for my brain than holding a full conversation, especially with people I have less-established rapports with. it isn’t reflective of how I feel about any particular mutuals— it’s just reflective of how at-capacity (honestly, beyond capacity) my brain is right now.

tl;dr: just because I’m active/online doesn’t mean I’m going to be responding to my DMs consistently or swiftly. I generally try my best to keep up with them, but that’s not a realistic expectation to hold myself to right now. it isn’t personal.

for those keeping up with the saga of my cat’s health (the resorptive lesions on her teeth which likely caused the inflamed lymph node two weeks ago), most of her bloodwork panel came back today and the clinic just called with results. I’ll describe the results under the break (along with a full summary of what’s been going on/details of her treatment going forward).

Lettie had to go to the vet on 5/16 for a big lump on her throat; they originally thought it was an abscess, but when they went to drain it it became clear that it was a severely swollen lymph node. they drained the area, sampled the fluid, and took a small tissue sample and sent it off for a biopsy. while she was under sedation, they also discovered some resorptive lesions* below the gumline on a couple of her teeth; they scraped away the excess inflamed gum, but they gave me a heads-up that it would have to be dealt with sooner rather that later, since it would reoccur without extraction. luckily, her annual appointment (which I scheduled months ago) was this past Saturday on 5/31, the day after her two-week recovery period from her 5/16 visit ended, so her teeth were the first thing I mentioned to them.

her biopsy results from the lymph node sample came back negative for cancerous cells, but it was inconclusive as to what caused the infection in the first place. at her annual this past weekend, they ran a full panel of bloodwork for two reasons: 1.) to try to rule out some major possibilities for why a young cat could be having these dental issues this early in her life (primarily they were worried about FIV/FeLV) and 2.) to get bloodwork on file ahead of her emergency dental extractions, which are scheduled for this Wednesday (6/4).

Lettie’s chemistry is altogether pretty normal— she has a mildly elevated liver-related value, but that could be from her recent infections, so they’ll be retesting a few weeks after her upcoming surgery. FIV/FeLV both came back negative, her thyroid results are normal, and her white and red blood cells counts are both normal.

her coronavirus results are still pending, but if the corona comes back negative and the follow-up testing on her liver value comes back normal (later this summer, after the infections clear), that means this issue is ✨genetic✨ and it’s likely that her dental issues will reoccur long-term. translation: it’s almost certain that eventually she’ll need more teeth extracted.

these results are a bit of a mixed bag. let me state the obvious: I’m SO fucking relieved that she doesn’t have FIV/FeLV. I hate seeing my cat sick and I was worried about the possibility of it being a big scary disease. but the thing about those big scary diseases is that, even though they aren’t curable, they are treatable/manageable. since this is likely a progressive, genetic dental issue, she could end up losing more/all of her teeth as she gets older, and the best thing I can do for her is to just brush her teeth, keep an eye on her gumline, and reach out to her care team when she shows signs of lesions again, which… just thinking about it makes me want to cry.

on Wednesday morning I’ll be dropping her off at her vet’s office; she’ll get x-rays and they’ll determine how many teeth need to come out. right now they know for sure that she needs 1-2 teeth extracted, but it’s possible that there are more teeth with lesions beneath the gum line that they can’t see without the x-rays. she’ll be sedated, they’ll extract the compromised teeth, I’ll get her back by the end of the day, and we’ll restart the two-week countdown for getting her out of a cone; her sutures from 5/16 are almost fully dissolved, but she’ll have new stitches after the dental extractions, so back into the soft donut-patterned cone she goes. she weirdly doesn’t like wet food, so I suspect that it’s going to be a struggle to get her to eat for a few days.

I’m currently trying to breathe through it and remind myself that her genetic issues are completely out of my control, and the only thing I can control is giving her the best and most timely care that I can get her, which is what I’m doing. she doesn’t get as much time as we do, and I just want her life to be as good and easy as it can be for her. ✨ this shit sucks. ✨

*her teeth are essentially eating themselves, and the surrounding gum is trying to fill in the holes in her teeth, which inflames the area and makes her very uncomfortable. long-term, extractions should relieve a lot of pain and discomfort for her once they heal up and the initial pain of the stitches goes away.

[dearcervus]

I'm not even sure what all I said in my ask last night but here's my best attempt at rewriting it.

It seems like when I'm having medical anxiety my interest in medical play increases. I can't stop thinking about the procedure I had earlier this week but in a scene context.

The procedure was to take out samples of my lymph node to check for infection or cancer. The feeling of the large needle entering my numbed neck was so odd that now I'm almost craving it. I think it's partially so stuck in my mind because it was my neck. Such a vulnerable place to have people working on.

Over the years I've generally gotten used to needles for blood draw purposes but I don't seem to be over my fear of them when used for other things. When I saw the large needle that was going to be used I tensed in fear but I think that would feel so good in a scene. Just that slight fear but having trust in the doctor.

(Health update in case anyone is curious: the results of the procedure came back inconclusive so I have to go in and have them fully remove one of my enlarged lymph nodes to test it. For that operation I'll have to be put under with general anesthesia which always feels really weird to me lol)

-🦊

Responding to this by copying your ask since it won’t let me respond to the actual thing 🖤

That makes a lot of sense honestly, a lot of people interested in medical play seem to have a decent amount of experience with medical procedures or even medical trauma. Needles can certainly be scary even if you trust the person holding them, but that’s why they’re so interesting. That rush of fear and the vulnerability of it all can be so fun. 🖤

I’m glad everything went well and I wish you luck with your surgery, I’m sure everything will be just fine 🖤

[drhouseasks]

are you willing to talk about the plague (i’m not a doctor i’m just really interested in the plague and it’s different manifestations)

When you say “the plague,” try not to sound like you learned everything you know from Monty Python and the Holy Grail. There are three versions of this bacterial nightmare: bubonic, septicemic, and pneumonic — all courtesy of Yersinia pestis, or Y. pestis if you want to look clever while you die.

It’s zoonotic. That means animals give it to you, you give it back, and everyone ends up on my table so I can roll my eyes at your bad life choices.

Bubonic is the medieval classic. The Black Death’s signature track. You get swollen, pus-dripping lymph nodes called buboes. You’ll also enjoy a high fever, chills, headaches, pain in your arms, legs, abdomen. Basically, you’ll wish you were dead before you actually are. Usually it’s fleas hitching a ride on rats. Or your cat decides to eat Ratatouille for lunch and brings the fourteenth century into your kitchen. Ironically, its the easiest to treat

Septicemic skips the lumps. It goes straight for your bloodstream. Fever, chills, weakness, severe abdominal pain, shock, and then your skin turns black and necrotic because your blood vessels decide to peace out. If you’re aiming for “extra in a zombie movie,” this is your plague.

Pneumonic is the attention seeker. It hits your lungs, so not only are you dying, you’re turning everyone around you into collateral damage. Fever, headache, weakness, and a cough that sprays bloody, bacteria-laced mist like you’re auditioning for Contagion 2.

How do we diagnose this mess? We stick a needle in you. Swollen nodes? Fine-needle aspiration. Septicemic? Blood cultures. Pneumonic? Sputum samples. Basically, if you can ooze it, we can test it.

How do we treat it? Antibiotics.

Ciprofloxacin.

Levofloxacin.

Moxifloxacin.

Doxycycline.

Gentamicin.

Streptomycin.

Chloramphenicol.

Trimethoprim-sulfamethoxazole.

Get them fast — untreated plague is a medieval horror show for a reason.

How do we prevent it? Try not living in a rat motel. Control fleas on pets, don’t cuddle dead rodents, don’t let your cat be a rodent sushi chef, and maybe don’t breathe in someone else’s bloody cough. And if you’ve been exposed? Post-exposure prophylactic antibiotics — same menu: Doxycycline or Ciprofloxacin.

OOC: DO NOT TAKE THIS AS MEDICAL ADVICE, I AM A TEENAGE BOY WHO IS STILL IN HIGH SCHOOL AND GOT THE INFORMATION FROM THE CLEVELAND CLINIC WEBSITE

[covid-safer-hotties]

Also preserved in our archive (Daily updates!)

As part of the COVID-19 International Research Team, researchers at the Johns Hopkins Kimmel Cancer Center, Children's Hospital of Philadelphia, the University of Pittsburgh and Weill Cornell Medicine discovered a novel cause of cytokine storm -; the extreme inflammatory response associated with increased risk of death in COVID-19 infection.

Their findings were reported Nov. 27 in the online issue of Proceedings of the National Academy of Sciences.

In an intensive genomic search for causes of cytokine storm, the research team used autopsy samples obtained from 40 patients who died from COVID-19. They performed genome analysis on samples taken from multiple sites, including the lung, heart, liver, kidney, lymph nodes in the chest that initially filter the virus, and the nasal cavity where the virus enters the body.

They zeroed in on some 50 upregulated immune genes in the samples obtained from nasal swabs and followed through in the genomics for the autopsy tissues.

Stephen Baylin, M.D., Virginia and D.K. Ludwig Professor for Cancer Research and co-senior author, and first author Michael Topper, Ph.D., Evelyn Grollman Glick Scholar and instructor in oncology, were

familiar with many of the genes as part of the inflammasome, a protein signaling network they helped define that is activated to rid the body of virus or bacteria-infected cells.

"Some of the same genes involved in overactivation of the inflammasome appear to be key immune gene regulators of the hyperinflammatory process that leads to a new view of how these subsequently activate the "cytokine storm syndrome" and severely damage multiple tissues, says Topper.

The genes should turn on and off, Baylin explains, but when they stay on, it results in cytokine storm, the very severe inflammation that can be lethal to patients with COVID.

Essentially, immune genes in the nasal cavity, where the virus enters, send signals downstream through a system called renin-angiotensin-aldosterone system (RAAS) to initiate cytokine storm.

RAAS, a hormone system that normally turns on and off to help regulate blood pressure, body fluids and electrolytes, is the spark that pushes the immune response into overdrive, the researchers found, compromising the infection-fighting function of lymph nodes and causing severe damage to the lungs, kidneys, heart, liver and other organs.

The researchers also believe their findings may have implications for long COVID, a chronic condition following COVID-19 infection that is characterized by a wide range of symptoms, including fever, fatigue, coughing, chest pain, heart palpitations, headaches, joint and muscle pain, gastrointestinal issues and more. This is a focus of ongoing research, Topper and Baylin say.

In addition to Baylin and Topper, other researchers participating in the investigation are co-first author Joseph W. Guarnieri and co-corresponding authors with Baylin: Afshin Behesti (leader of COVIRT) and Douglas C. Wallace, Simon Pollett, Deanne Taylor, Eve Syrkin Wurtele, Robert E. Schwartz, Christopher E. Mason, Jeffrey A. Haltom, Amy Chadburn, Henry Cope, Justin Frere, Julia An, Alain Borczuk, Saloni Sinha, JangKeun Kim, Jiwoon Park, Daniel Butler, Cem Meydan, Jonathan Foox, Yaron Bram, Stephanie A. Richard, Nusrat J. Epsi, Brian Agan, Josh G. Chenoweth, Mark P. Simons, David Tribble, Timothy Burgess, Clifton Dalgard, Mark T. Heise, Nathaniel J. Moorman, Victoria K. Baxter, Emily A. Madden, Sharon A. Taft-Benz, Elizabeth J. Anderson, Wes A. Sanders, Rebekah J. Dickmander, Katherine Beigel, Gabrielle A. Widjaja, Kevin A. Janssen, Timothy Lie, Deborah G. Murdock, Alessia Angelin, Yentli E. Soto Albrecht, Arnold Z. Olali, Zimu Cen, Joseph Dybas, Waldemar Priebe, Mark R. Emmett, Sonja M. Best, Maya Kelsey Johnson, Nidia S. Trovao, Kevin B. Clark, Victoria Zaksas, Robert Meller, Peter Grabham, Jonathan C. Schisler, and Pedro M. Moraes-Vieira.

This researach was supported by the Division of Intramural Research, NIAID, NIH grant to Sonja Best, and DOD W81XWH-21-1-0128 grant awarded to Douglas Wallace, the Bill & Melinda Gates Foundation Grant INV-046722 awarded to Douglas Wallace, Adelson Medical Research Foundation, Hodson Scholar Foundation, Glick scholar awards and Samuel Waxman Research Foundation awarded to Stephen Baylin from the Defense Health Program (HU00012020067 and HU00012120103), the National Institute of Allergy and Infectious Disease (HU00011920111), and the USU RESPONSE award (HU00012020070).

Source: Johns Hopkins Medicine

Journal reference: Topper, M. J., et al. (2024). Lethal COVID-19 associates with RAAS-induced inflammation for multiple organ damage including mediastinal lymph nodes. Proceedings of the National Academy of Sciences. doi.org/10.1073/pnas.2401968121.

Study link: www.pnas.org/doi/10.1073/pnas.2401968121

[so-long-soldier-writes]

drabble #7 - kissing disease

kai parker x reader

summary: despite the deal he had made with her several weeks ago, kai needs his sister for her medical opinion, again.

tags: doctor / hospital, sickness, small mention of blood, caught / confession

word count: 1,023

a/n: here is a short lil drabble-ish piece i wrote as i'm trying to get back in the swing of things. i went to a tvd con, and then got a cold 😭 so i'm a little out of it. but, i did produce this, so here it is!

A series of knocks disturb the couple and their guest from their conversation. It’s bad enough to have one uninvited guest, and now there’s another at the door. Even worse, when Ric answers, it’s the person he and his girlfriend want to see least in the world. 

Kai Parker, visibly ill, is hunched over his entryway. One hand is gripping the doorframe, while the other is raised to knock again, but drops when Ric opens it. 

“Oh no-” the older man starts.

“Wait, wait, wait-”

Upon hearing the direct ‘no’ from Ric, Jo joins his side. At the sight of her twin brother, though, she’s immediately pissed. “No. We had a deal. I give you my magic and you never speak to me again.”

“I know-”

“So why the hell would you think it’s okay to come here?”

“I need your help.”

“You’re insane! If you think I’m going to help you, after all you’ve ever done to me, you’re insane.”

“I know, and I know we had a deal. But, look, I’m really sick, I don’t know why. It’s not a magical problem this time, because I’ve tried to heal it with magic and it’s not working. I don’t know if I did the right spell, or if there’s something blocking it, I don’t know. All I ask is that you just look. Just, try to see me as a patient, just for today. Please?”

“You will not manipulate me like that. I won’t let you.”

“I’m not trying to, I promise.”

By now, Damon’s joined the doorway. “Oh, it’s you,” he says bluntly. “Why are you here?”

“I’m sick. I came to see my sister because she’s a doctor, not because I wanted to hurt her. Please, Josette.”

The girl sighs. “Fine. But if you try anything, I will kill you.”

“Promise I won’t.”

Ten minutes later, she has Kai sitting on a patient bed in Whitmore hospital. The three had decided it would be easier to do there, so they made the quick drive over to the medical center. Luckily, it’s after busy hours, so they’re able to work without interruption. 

At first, Jo asks all the typical questions and runs all the standard tests. She rules out that it’s definitely not a magical issue, and that it seems to be a virus of some sort. She just can’t seem to narrow it down to which one, though. 

“It’s not strep; that test came up negative. Could you repeat your symptoms to me?”

Kai rolls his eyes, but answers, “throat has been sore for a couple days, my, like, lymph nodes are swollen, up here on my neck,” he points to the area, “I’m really tired, skin is kinda hot, and I’ve had a headache.”

“Right. So this is kind of a Hail Mary, but I’m gonna do it anyway. I need a sample of your blood. Just a finger-prick.” She holds out a little test, then a needle, and takes his hand. “Try not to flinch,” she says, before remembering to whom she’s talking. Jo then almost flinches herself when she realizes it’s her brother’s hand she’s grasping. 

Kai doesn’t budge when she pricks his finger. In fact, he just yawns, like he’s bored. It disturbs her. 

“Just give it a couple minutes.”

Jo leaves to find the other two while the test takes the time it needs. In a couple minutes, though, she returns, both men on her tail. She reads the test, then scoffs. 

“What is it?” Ric asks before anyone else can.

“It’s positive.”

“For what?”

“Mono.”

“What?!” The man asks a third time. 

“What’s that mean?” Damon questions, too.

“Mononucleosis. Epstein-Barr. Whatever you want to call it. The Kissing Disease.” She looks at Kai, who says nothing. “Spread through saliva. Either you got it from kissing someone, or sharing drinks, silverware, or something like that. So what’s it from?”

“No way,” Damon interrupts, “there’s no way someone was kissing him, that’s got to be a false positive.”

“It’s the only one of all my tests to come out positive.”

“Alright, fine,” Kai says, “of all the ways I expected to be caught, this was not one of them.”

The two men seem to get angry at this. At nearly the same time, they bark, “who was the poor girl?”

“Hey, she was a willing participant!”

“Who was it, Kai?”

“Really pretty. Sweet voice. Likes the bad boys, but she seems so innocent, you wouldn’t know unless she told you. Friend of yours, Damon. You had her babysit me one day, and then things just kind of… took off!”

“No.” Damon denies, not wanting it to be true. 

“Oh, yes.”

“She wouldn’t be caught with the likes of you. Y/N is too good for that.”

“Oh, but she wasn’t caught… until, well, she apparently gave me mono.”

“But that was months ago I had her watch you.”

“And it was months ago since we started hanging out. And then hanging turned to kissing, which I started, because she’s way too shy to give in the first time, but once she does, she’s just… crazyyyy cute about it. Always stealing kisses when I’m not expecting it. Guess it makes sense how this could’ve happened.”

“You’re lying. Y/N would never.” Ric agrees with his best friend. 

“I swear to you I am not.”

“I’ve got an easy way to figure this out. Hold on one second.” Damon puts a finger up while dialing a number on his phone. After a few rings, it picks up. “Y/N?”

“Yeah, hi. What’s up?”

“Not much. Was just wondering if you’re up for a drink later, at the grill?”

“Mm, I’m not actually feeling too great today. Raincheck for another time?”

“Oh, really? That sucks.”

“Yeah, I think it’s just a typical common cold.” You clear your throat rather loudly. “Sorry.”

“Hey, no worries. Feel better okay?”

“I’ll try,” you chuckle, “see you later?”

“Let me know when you’re better. Bye.”

“Will do. Bye.”

Damon looks at Alaric, then Jo, and all three, horrified, stare down at Kai together.

The little troublemaker manages to smirk. “Still think I’m lying?” 

[theotherstephencobert]

March 20, 2025 - "Life is what happens to you while you're busy making other plans..."

I have a confession to make. A major life event started about two months ago for me. I held off on posting it on social media because it seems as if a lot of misfortune has occurred in my life over the past few years and I didn't want my blog to come across as a replay of the Linda Ronstadt song "Poor Poor Pitiful Me". But it's been going on long enough that it clearly isn't any false diagnosis. And I'll be frank: prayers, positive energy and well-wishes would be appreciated at this time.

You may remember about four years ago I was making jokes about how I had gotten my sh## together, sending a sample to Madison, WI, where Exact Sciences Laboratories, the makers of Cologuard, were located. When I did that in 2020 the results came back negative and I breathed a sigh of relief. Well, they recommend re-testing every 4-5 years, so near the end of 2024 I sent them another sample, well wrapped and sealed. This time the results came back "Abnormal", so my doctor made an appointment for me to get a colonostomy.

On the morning of February 6 I arrived at Kansas Gastroenterology on the far east side of town. The examination took maybe an hour and I was knocked out throug all of it. I was hoping this was going to be one of those "false positives" the commercials for Cologuard admit can hapen, but it was not to be. The doctors found eight polyps in my colon. Seven were pre-cancerous, and one had progressed to cancer. More concerning, the examination found a growth "about the size of a peach" in my cecum (the pouch that connects my small intestine to my colon). The doctors sent a tissue sample to their lab for analysis, and the results came back the next week that there were cancer cells in the tumor.

This is very, very early stage cancer - the doctor described it as "superficial" - but it is cancer and needs to be treated now. The month of February was a plethora of doctor visits of all sorts: blood work, CT scans, discussing my options. A CT scan of my chest revealed a lymph node that one doctor thought was a little suspicious, so on March 14 I had a biopsy done at Wesley Hospital. I got the news back on March 19 that the results were negative: there was no cancer found. I suppose this is something I had better get used to - now that it's established that I have or had cancer, we have to watch and make sure it doesn't gestate or metastasize.

Almost 20 years ago, my daughter Tandra discovered she had Stage 4 cancer that her doctors believed started as colon cancer or ovarian caner. She was only 27 at the time, and by the time it was discovered it had progressed too far for any treatment to save her. I have no doubt that the whole point of me taking care of this now is so the cancer doesn't progress to the point that it's life threatening.

The actual surgery to remove the tumor is scheduled for Monday, March 31, quite early in the morning (I have to report to Wesley Hospital at 5:30 am). Prayers and positive energy for me between now and then will be very much appreciated.

[fullyunsourced]

The most radiation absorbed by a human in history (who survived?)

More medical stuff this post, sorry! Albert Stevens is a person who received the highest sustained dose of radiation over his lifetime out of any known human. And how that happened? Horrible, tragic medical malpractice.

We're once again back in the wild times of the early Atomic Age. Plutonium is brand-new and while we have a lot of data for the short term, we don't have a clue what it does to the human body over time. Some experiments were performed on animals, and it was decided in 1945 that it was time for human experiments. The project was run by Dr. Joseph Gilbert Hamilton, a member of the Manhattan Project who already had experience in radioactivity testing on humans, including himself.

Stevens was a house painter who checked into the hospital where Hamilton worked. Stevens was diagnosed with terminal stomach cancer, and considered doomed to die from it. To Hamilton and his group of researchers, this made him a terrific subject for a plutonium injection, and Stevens received nearly 1 microgram total of plutonium without his knowledge, many times the lethal dose.

When specimens for radiation impact studies were taken from Stevens, they were explained as being part of the cancer treatment. During the biopsies, it was found that a "huge, ulcerating, carcinomatous mass that had grown into his spleen and liver... Half of the left lobe of the liver, the entire spleen, most of the ninth rib, lymph nodes, part of the pancreas, and a portion of the omentum... were taken out."

Here's the catch: Stevens likely never had cancer. Instead, it was just a misdiagnosed gastric ulcer. The biopsies of the samples removed for research showed no signs of cancer. Stevens was sent home and was struggling financially to pay the colossal medical bills from him cancer treatment, and the Manhattan Project paid him for his samples, under the pretext that his "remarkable recovery" from cancer was worth studying.

Stevens was never told he did not have cancer, nor was his family. His son always reported to doctors that there was a history of cancer in the family due to his father's treatment. Over the course of his lifetime (he would die in 1966 at 79 of heart disease) Stevens received about 10 times the lethal dose of radiation over 20 years. His remains were sent to Argonne National Laboratory for study and never returned to his family for burial.

After an investigative journalist found Stevens's classified story in 1993, she uncovered at least 18 people who had been experimented on in this way. Dr. Hamilton had died of leukemia in 1957, likely as a result of his own exposure to radiation.

[transgenderer]

Human and rodent placentation is hemochorial, the fetomaternal interaction between the two blood circulations involving direct physical interaction between maternal blood and the chorionic trophoblasts.

The mechanism by which cells are exchanged across the placental barrier is unclear. Possible explanations include deportation of trophoblasts, microtraumatic rupture of the placental blood channels or that specific cell types are capable of adhesion to the trophoblasts of the walls of the fetal blood channels and migration through the placental barrier created by the trophoblasts. Intervillous thrombi containing mixed maternal and fetal cells occur in the fetal placenta/labyrinth.44,45 Histological defects in the continuity of the trophoblasts lining the vasculature of the placenta are also reported.46,47 Together these observations suggest the possibility that fetomaternal hemorrhage within the fetal placenta/labyrinth may allow exchange of cells between the fetal and maternal circulation. Microtraumatic dislodgment of trophoblasts from the trophoblast-lined blood channels through which the maternal blood passes may also explain why trophoblasts appear in maternal circulation. The microtraumatic hypothesis of cell exchange does not appear consistent with the hypothesis that fetomaternal microchimerism may be of adaptive value to the fetus but fits well with the hypothesis that fetomaternal microchimerism is an epiphenomenon of pregnancy with potential pathological consequences.

An alternative hypothesis is that cells cross the placental barrier by mechanisms akin to the active adhesion and transmigration that occurs across high endothelial venule (HEV) endothelium in peripheral lymph nodes and at the blood-brain barrier (BBB).48 Intriguingly, in the mouse at least some of the fetal cells that enter the mother are also capable of crossing the blood brain barrier into the brain.35,49

Fetomaternal microchimerism appears to occur with great frequency following human pregnancy. It has been suggested that fetomaternal traffic occurs in all pregancies.14 Moreover fetal cells are reported to persist in the mother for decades. Male cells have been found in maternal blood even decades after pregnancy,7,77 including in one case in which the women was last pregnant with a male child 27 years earlier.7 Fetal cells also may persist for even longer after engrafting maternal bone marrow14 and perhaps other organs. By engrafting into niches such as the bone marrow, fetal cells may also be able to proliferate and reinfiltrate blood or other tissues later. There is strong evidence that fetal cells with the characteristics of mesenchymal cells do engraft the bone marrow. Male DNA was detected in 48% of CD34-enriched apheresis products from nonpregnant female marrow donors.1 Male cells were also detected in all bone marrow samples from women who had previously been pregnant with males, including one woman who was last pregnant with a son 51 years earlier.14

The absence of Y chromosome markers in samples from women who had never born sons in some studies14 strongly supports the argument that the male cells observed originate from the fetus. However, it is important to note that there are crucial caveats in the use of the Y chromosome alone as a marker for fetomaternal microchimerism that may have led to over estimation of the incidence and persistence of fetomaternal microchimerism in humans. Male cells have been found in the blood of women without sons.78,79 Male cells may occur in the blood of as many as 8–10% of healthy women without sons and no known history of abortion.79 It has been speculated that the male cells arise from unrecognized spontaneous abortions, vanished male twins, an older brother transferred by the maternal circulation, or sexual intercourse. However, a history of unrecognized spontaneous abortions or sexual intercourse cannot explain all cases of the presence of male cells in females as another study detected the presence of the Y chromosome in normal liver from seven of eleven female fetuses and five of six female children.80 Such microchimerism may be best explained, by fetofetal transfer from an undetected vanishing male twin or maternofetal transfer of male cells harbored by the mother. Estimates of the frequency of vanishing twins range from 3.7–100% of pregnancies81 however not all twins share connected placenta vasculature, especially at the early stages of development at which many twins disappear. Maternofetal transfer to the mother may also have occurred if the mother's mother had a history of blood transfusion, transplantation or previous pregnancy with a male fetus. It is difficult to estimate how frequently male cells in females could arise as a result of fetofetal or maternofetal transfer. Although one might expect such events to be rare, the incidence may be high enough to have biased estimates of the incidence of fetomaternal microchimerism in humans. While the possibility that the Y chromosome could also enter the mother via microchimerism as a consequence of previous blood transfusion or transplantation has been considered in most studies, the possibility that male cells detected in the mother may have arrived via fetofetal or maternofetal transfer to the mother in utero has not be systematically excluded. Conclusive proof of fetomaternal microchimerism in humans would require the use of other paternal markers that differentiate between the father of the fetus and the father of the mother. One scenario might be to investigate cases where the mother and the mother's father share a genetic mutation or polymorphism not carried by the father of the fetus. In such cases, evidence of genetic markers derived from the father of the fetus in the mother could provide more conclusive evidence of fetomaternal microchimerism in humans. If the genetic mutation or polymorphism caused disease the presence of fetal cells in the diseased tissue could also offer evidence of the potential of fetomaternal tissue repair.

[swede1952]

Good morning, friends. 🌹🥀💐

2 May 2025

A couple of days ago, my wife noticed that Ben's lymph nodes beneath his jaw were swollen. I took him to the veterinarian yesterday and, unfortunately, didn’t receive good news. There’s no definitive diagnosis yet—the vet sent samples to a pathologist, and I should hear something today. Ben is 16, and I fear the inevitable may be approaching. Still, he remains his calm, steady self. I think of him as a gentle giant, despite his small size. It takes a lot to ruffle him, except for my other dog, Charlie, who—every so often—manages to find that one nerve to step on. The dynamic at home is what I cherish most, and I struggle with the thought of change.

"A dog will teach you unconditional love. If you can have that in your life, things won’t be too bad." — Robert Wagner

[fortunesque]

Jay's ultrasound

We have potentially good news from oncology, today! Preliminary findings of the ultrasound don't show spread. They will be examined closer, and we will have the results in 1-2 days. He had a suspicious-looking lymph node, of which a sample is being examined. We will also have those results in 1-2 days.

They can do scar revision surgery, and removal of the suspicious lymph node. He is also a candidate for the vaccine.

It's tentatively good news. The downside is that the vaccine is expensive. I'm going to discuss with his adoption group and see if it is feasible to do.

[earthenorgan]

Once I Dated an Oncologist

…who could tell me everything there was to know about my body. From the white lines on my stomach (melanoma? No, just stretch marks) to the fizzing of my blood in response to his touch, as if disturbed, leaving a shimmering trail from his bed to his door (hereditary, passed down most often from mother to son, though sometimes from mother to daughter).

Once I dated an oncologist who held back my hair when I heaved into the toilet at night, terrified by visions of something floating beneath the glassy surface of the water like the last olive at the bottom of the jar, though most times when I opened my eyes there was nothing there.

Once I dated an oncologist who lived in an apartment where he kept no knives. I let him catch me while I was searching, lead me to the couch where I laid with my arms tucked up against my bare stomach.

Once I dated an oncologist who showed me the scan of a patient who had a sarcoma of the sacrum. In the thin sheet of plastic I thought I saw a bundle of figs hanging from a tree, so heavy in their ripeness they bent the body to their shape. She has a daughter your age. He let me keep a copy of the scan and I taped to my wall, drew lines in red pen from the mass leading outward, one for the heart, liver, lungs. Roots of connection. The patient died next month. 

Once I dated an oncologist who worked long, late hours. I would stay up in his apartment counting time on the clock above the kitchen window, a plate with an orange in front of me ready to be peeled, arranged, shared. Sometimes sun would cut me awake before he did. He would stumble in, kiss my head, peel the orange and split it even though he kept his nails short. You could survive a tumor of this size growing in your frontal lobe for a year. After that, I didn’t want to eat my half anymore, its neat sections like the bisected brain of an infant in my sleepless palm.

Once I dated an oncologist who told me that life begets life. I wanted to know what causes cancer. He said, what causes babies?

Once I dated an oncologist who stole my sleeping pills and swapped them for sugar tablets—I found him drooling on the couch. Once I dated an oncologist who tongued words like psychosomatic and placebo into my aching mouth. Once I dated an oncologist who hated the neurologist I used to date (once I dated a neurologist who diagnosed me with Anton Syndrome, but I swear I can see just fine). Once I dated an oncologist who tried to show me there was nothing wrong with my body, squeezing my lymph nodes, tracing my veins, rolling off me wordlessly when I went still as a corpse.

A week before he left me, the oncologist I once dated got fed up and wrote me a referral for the clinic across the street. The physician laid me on the bed and listened with her stethoscope to the hot thrum of my heart. I wondered if I should ask to see a cardiologist, preferably one with strong hands. But then she sent me to the bathroom for a urine sample, laid me in a white tube while the scanner moved above me like the hand of heaven, and discharged me an hour later with a single sheet of paper telling me not to take ibuprofen for a day, that my heart was unremarkable, liver unremarkable, uterus unremarkable except for a trace of something that is now gone.