Sunday, October 21, 2018

Nasty flaw in Minnesota mail ballot process

There’s a nasty flaw in Minnesota’s vote by mail process.

When you apply for a mail ballot you are asked to provider either a SSN last 4 or License number or State ID number.

When you complete the ballot you are asked to provider either a SSN last 4 or License number or State ID number.

The two numbers have to match or the ballot will be rejected.

Hope you remember if you used your MN License number or your SSN Last 4 on the ballot application.

I tried testing for the identifier I used by querying my absentee ballot status, but it found the same status regardless of which identifier I used.

Saturday, October 20, 2018

Attack of the Clones - New disease mechanism identified

First came CHIP - Clonal hematopoiesis of indeterminate potential (Jan 2018)

… a bizarre accumulation of mutated stem cells in bone marrow increases a person’s risk of dying within a decade, usually from a heart attack or stroke, by 40 or 50 percent. They named the condition with medical jargon: clonal hematopoiesis of indeterminate potential…

… Up to 20 percent of people in their 60s have it, and perhaps 50 percent of those in their 80s …

… large numbers of study participants had blood cells with mutations linked to leukemia — but they did not have the cancer. Instead, they had just one or two of the cluster of mutations…

… [mutations], especially those linked to leukemia, seem to give stem cells a new ability to accumulate in the marrow. The result is a sort of survival of the fittest, or fastest growing, stem cells in the marrow…

… researchers described a 115-year-old woman. Nearly her entire supply of white blood cells was generated by mutated stem cells in her bone marrow.

At the first she had developed just two mutated stem cells. But over time their progeny came to dominate her bone marrow. She lived about as long as a human can, nonetheless, and died of a tumor.

… Mutated blood cells began proliferating in the mice, and they developed rapidly growing plaques that were burning with inflammation.

“For decades people have worked on inflammation as a cause of atherosclerosis,” Dr. Ebert said. “But it was not clear what initiated the inflammation.”

Now there is a possible explanation — and, Dr. Ebert said, it raises the possibility that CHIP may be involved in other inflammatory diseases, like arthritis.

That was mindboggling. An entirely new mechanism of disease! It’s easy to speculate on relationships to unexplained disorders like osteoarthritis.

This week the clones are everywhere …

Researchers Explore a Cancer Paradox Oct 2018

… a large portion of the cells in healthy people carry far more mutations than expected, including some mutations thought to be the prime drivers of cancer…

… rogue cells spread out across the esophagus, forming colonies of mutant cells, known as clones. Although these clones aren’t cancer, they do exhibit one of cancer’s hallmarks: rapid growth.

These mutant clones colonize more than half of your esophagus by middle age” …

… By examining the mutations, the researchers were able to rule out external causes for them, like tobacco smoke or alcohol. Instead, the mutations seem to have arisen through ordinary aging. As the cells divided over and over again, their DNA sometimes was damaged. In other words, the rise of these mutations may just be an intrinsic part of getting older…

It’s been a long time since we’ve had an entirely new class of pathophysiology. We may be entering a new and exciting era of medical research with near term clinical implications. Nobel prizes have been awarded for less.

We still need a way to explore and resurface old blog posts

Six years ago I wrote about browsing the blog blacklist and the need to resurface content from old blog postings. Today, even in the supposed twilight of blogs [1], I was again reminded how much we need a tool for excavation of old posts. I can think of at least one way do it (standard metadata for blog history, random selection of past posts based on internal and external inbound links) but there are probably several.

Maybe something for a future blog renaissance to tackle. Or if Feedbin is looking for a new feature set …

- fn -

[1] On the one hand I accept that RSS and blogs are vanishing, on the other my Feedbin stream is a rich and engrossing as ever, covering hundreds of sources.

Why is the hamstring connected to the paraspinal muscles?

The hamstrings (biceps fermoris, semitendonosis, semimembranosus, some include adductor magnus) flex the knee and extend the hip. The erector spinae and latissimus dorsi flex, extend and rotate the spine [1].

These muscles don’t directly connect with one another. They are innervated by different nerve roots. As far as we know [2] they only connect in the brain.

So it’s curious to observe the connection between the minor back strains I get [3] and my hamstrings. I normally have a good hamstring stretch for my age, but even a minor erector spinae strain will immediately tighten the ipsilateral (same side) hamstring. Improving the back strain is likewise intimately related to stretching the hamstring.

I presume it’s some kind of injury reflex, but I can’t figure out why it’s adaptive.

[1] Kudos to my all-time favorite medical app, Visible Body’s Human Anatomy Atlas.app, for helping me visualize these areas. It takes a while to learn this powerful app, but it’s worth the time.
[2] Decades after we thought we understood anatomy we keep learning new things. So who knows :-)?
[3] There’s a personal history here. I have been mildly surprised how little this history interests other people — including people with disabling back pain. The back strains I get now are more annoying than painful; they are usually related to heavy weights and intense exercise.

Saturday, October 13, 2018

Bostromism rediscovered

While recently rereading Banks’ marvelous book The Algebraist I decide I ought to write a post about “The Truth”, which is basically Bostrom’s simulation hypothesis made theology.

An initial topic search lead me to a 2013 pinboard post, where I learned I’d started to write that post 5 years ago - in 2013. I didn’t finish then, because at that time a topic search uncovered a post from 5 years before that. In 2008, 10 years ago now.

My 2008 post includes an excerpt from The Algebraist — it’s worth a read. Banks begins with the consensus response to the simulation hypothesis — “a difference that made no difference wasn’t a difference to be much bothered about, and one might as well get on with (what appeared to be) life.”  I’m not sure the hypothesis is totally irrelevant though; it is one answer to the Fermi Paradox.

Now I’m looking forward to doing this again in 2023.

PS. deGrasse in 2016.

PPS. I’ve been lately thinking about the other odd aspects of Oldness. Such as realizing I’m supposed to be the sober and silent sage in meetings whose primary duty is to do introductions and conclude with expressions of appreciation. Most unfairly, for someone who never missed a nap during meetings and classes, I’m not allowed to fall asleep any more.