I recently finished the second cycle of the clinical trial I’m participating in. I’ll have a bone marrow biopsy on Tuesday and about a week later the results will be the first indication of how well I’m responding to the treatment, which will probably guide future treatment. I’ve mostly tolerated it well—at times feeling crappy, and I seem to have some very slight neuropathy issues recently in my finger tips and toes, but mostly feeling pretty well. (Though lots of blood transfusions recently too.)
Besides that I’ve been working on more curved crease origami, along with trying to model it in 3D.
In mathematics, a developable surface is a surface that can be flattened out into a plane. Since origami starts with a flat sheet of paper, and paper doesn’t squash or stretch, the results of origami must too be a developable surface. Ruled surfaces are surfaces that can be constructed with straight lines. The hyperbolic paraboloid (also called a hypar) is a ruled surface, but not developable. The cylinder (without end caps) is both developable and ruled.
Folding concentric circles into a piece of paper seems to be both a developable surface (or at least a close approximation of one), and an approximation of a hypar. It makes me wonder if there is some kind of limit or something we could move towards, maybe as the distance between the concentric circular creases goes towards zero.
This is the second piece I’ve made with vinyl, it is very similar to the first but with the width of each concentric strip about 30% smaller. In the first one I put a sheet of aluminum foil between the two self adhesive vinyl layers, this time I tried a sheet of plastic. I’ve also been considering trying fabric and cheesecloth. I have three more sets of scored vinyl waiting to be assembled (stuck together probably with a layer of something between them) and folded. Two are variations of nested circles (not completely concentric), and one is two spirals—one forming all peaks and the other forming all troughs.
I suspect that the creases should each lie on the intersection of a hypar and a sphere. I’ve been working on making 3D models of it recently, and can tell it isn’t quite right yet, but believe it is getting close.
My next attempt will be entirely programmatically I think, inside blender with python.
I’m writing this because it’s a lot of nuance to tell everyone individually. To summarize, a few weeks ago my blood counts started to drop so they did a biopsy last Tuesday and today I got the results: it looks like I still have some leukemia cells. There are a variety of possible treatments they’re looking at (they choose depending on the details of what is happening). The rest of this is a more detailed explanation of those points.
(Also the original title of this post was “less than ideal news” until I realized I used that same title last year when I relapsed. So this post is more blunt instead.)
My appointments were cut back to monthly in mid-August. The September appointment went fine, but in the first week of October my counts had declined, and my doctor was concerned. So the next week they did a bone marrow biopsy, and today he told me the preliminary results, which is that I have myelodyplastic syndrome, which is a fancy way of saying that my body isn’t producing blood cells in the right amounts, which is probably because there are still leukemia cells floating around. (MDS and leukemia are not identical, I think there are a variety of causes of MDS, but since I had leukemia a year ago that’s the obvious conclusion. Sometimes MDS become leukemia later. Also, I already knew about MDS a little because I know Carl Sagan had it. Turns out he died of pneumonia, but I think it was probably as a complication. Huh, he had three bone marrow transplants from his sister. The two things I have going that he didn’t are, I’m almost 30 years younger than he was, and there has been an extra 20 years of learning in the medical community. In spite of those, we still haven’t gotten that good at this.)
As a little review, the cells in our bone marrow produce our blood, red blood cells that carry oxygen, white blood cells that fight infection, and all sorts of other stuff, like platelets, which form clots when we’re bleeding. Leukemia is the result of one of those bone marrow cells dividing out of control, instead of maturing into an adult blood cell. The immature cells are called blasts, and I think typically you don’t really see any blast cells in the “peripheral blood” (the blood in your veins). To diagnose leukemia they do a bone marrow biopsy, they use a needle to get a sample of my bone marrow (from the bones in my lower back, which are easy to get to, cause I’m boney), and then they count up the blast cells.
A leukemia diagnoses is when 20% or more of the cells in the bone marrow sample are blasts (normally they expect 5% or less to be blast cells). My biopsy last week had about 6% blasts, so it’s not exactly considered a relapse, and that’s why it’s considered MDS. (When I was diagnosed last year it was 100% blasts, and at that point they were circulating through my peripheral blood too, so a hematologist that I still have never met knew when he saw it that I had leukemia, and he called me and told me I needed to go to a big hospital right away. After the first chemotherapy I still had 5% blasts, which is why they did a second “induction” chemotherapy.)
So what will we do about it?
To start we’ll try and induce some graft-vs-host-disease. Since the transplant last November, the main concern (besides the leukemia coming back), was that the new donor cells I received could attack me as if I were a foreign invader (this is what HLA typing is for; my donor was a half match). So until today I’ve been taking some immunosuppressant drugs, which slow down the white blood cells and make them less likely to attack me. The upside is that sometimes they see a graft-vs-tumor effect, where the new donor cells attack any remaining leukemia cells as invaders. That’s the plan right now.
Next week we’ll see if that’s helping, and they’ll probably do another biopsy in a few weeks. There are a lot of other options, but which we pursue might depend on how things go in the near future. There are some new drugs that might help, some new chemotherapy drugs, and some that might help induce graft-vs-host (and hopefully also graft-vs-tumor). Another possibility is that they might collect some adult T cells from my donor (a cousin on my dad’s side). It’d be a small amount, because they can be quite dangerous to me, and once they put them in they can’t take them back out.
That’s pretty much all we discussed.
I mentioned how the results were preliminary, the other part is called cytogenetic analysis, which involves sequencing the genome (probably just part of it), in the leukemia cells, to see which mutations they might have. Some mutations are known to be vulnerable to certain drugs, so if any such mutations are identified they will likely dictate how we respond. They cytogenetics should be complete sometime over the next week or so.
Short digression, I’m watching a David Attenborough BBC show about predators, and the first episode just ended with cheetahs, following a mother with four cubs, and they mentioned that 90% of cheetah cubs don’t survive to their second birthday.
The original cytogenetic analysis from last year found an inversion on chromosome three, which is associated with a poor prognosis, and not long ago I read on quora how leukemias are among the fastest cancers, which is both good and bad. Good because chemotherapy drugs are specifically chemicals that interfere with cell division (since that’s what cancers are), and by dividing so rapidly they’re more vulnerable to chemicals that are really good at killing young cells. The downside is that because they divide so rapidly, they also develop resistance quickly. When I relapsed last summer they used a different chemotherapy drug, because whatever cells survived the previous treatments were most likely to have some mutation that made them resistant to the previous chemotherapy drugs.
That’s pretty much all I have to say about my health situation.
The second episode of that show (I think it’s called Hunt?), I think he just said polar bears are only successful in 1 out of every 20 hunts. A failure rate of 95%!
So in light of this (my health), I’m focusing my work and time on things I enjoy, and which I think are achievable. Which has meant more curved-crease origami, and less programming. (Because a lot of my programming projects I’m unsure will ever pan out.) Spending time with friends. I should probably order a bunch of 3D models printed.
Okay, now a polar bear is climbing around an incredibly steep cliffs, eating bird eggs & hatchlings. First I was really worried for the bear, he’s so high up, and it’s ridiculously steep and crumbly. But then I’m watching him just slowly eating every egg and bird he can get near, and the birds are helplessly squawking at him, inches away as he eats their babies. I think there is something I find comforting about being reminded of how nature works. No matter how much time I have left, it’s really unlikely I’ll be eaten alive, or starve to death, which is what most animals deal with every day for their entire lives.
I’ve always loved nature programs. Though even as a little kid I remember feeling really bad seeing animals get caught. I’m not sure when it occurred to me that the animals chasing them had to eat too.