If you have symptoms that can be ascribed to no known disease, you probably aren’t sick.
It’s a useful principle to remember. I’ve had a few false alarms too.
If you have symptoms that can be ascribed to no known disease, you probably aren’t sick.
It’s a useful principle to remember. I’ve had a few false alarms too.
There are relatively few innovators and many people who like to copy and make incremental advances, but I didn’t quite realize how out-of-hand it was getting in social bookmarking until I looked into actually adding those buttons (via the Add to Any widget) to one of my sites. It looks nice and innocuous at first, but click on the down arrow in the popup menu and see just how many sites are listed, all serving the same function.
I’m a member of several groups on polymathy and on harnessing talent in multiple areas (it’s something I’m interested in myself, after all). One of the more interesting things I’ve noticed is that when asked about their MBTI types:
1. Everyone knows them already.
2. Almost everyone is an INTJ. Next common is INTP, then ENTP.
3. Most historical polymaths are thought to be INFJs. (What happened to cause the shift? Did thinking types suddenly become more in-tune with their artistic sides recently, or was there something cultural to it?)
How much faith one can put in MBTI types is questionable, but it does support my hypothesis that nonlinear intuitive thought, not straight logic, is required to see the connections between disciplines.
Choose writing.
The presence of good writing guarantees nothing, but its lack is a fatal blow to any idea you may ever come up with. Ideas possess an inherent, objective worth – but you must demonstrate it to others before they will recognize it.
From penicillin to global warming, ideas require two people to flourish: one to generate the idea and another to popularize it. Very seldom are these functions performed by the same person. In fact, it’s common for a great deal of time to elapse between generation and popularization.
Lots of treatments work very well in mice but fail to show benefits in human trials. They’re false positives, and they get lots of people excited over treatments that never end up working in humans.
(Why do they work so well in mice, I wonder? Is it because so much of our research uses them? I wonder, if we were willing to completely throw morals out the window, could we get those sorts of results in humans by experimenting on them directly? Not that I’m advocating this.)
I just realized something blindingly obvious: there are false negatives too. But how are these handled? Treatments that don’t work in mice never make it to human trials, even though they may work in humans. Without doing human trials on treatments that failed to work in mice, we can’t evaluate a false negative rate, but it could potentially be high. Certainly it’s nonzero in any case.
This is another example of snap judgments shooting down ideas, but this is far less clear-cut than most criticism because failing to analyze the treatment prior to human trials can endanger people’s health.
I think that what we need are better computer models.
Apparently the recent work I’ve done for my dissertation is patentable and the team wishes to apply for one. On the one hand, I disagree with the very concept of patenting an algorithm; on the other, this is a huge addition to a CV which would very definitely put me ahead of others when I seek a research position.
Maybe I can get the patent then license it freely?
I don’t know if it’s coincidence or what, but these two pieces are built around the same theme.
Unless the specificity of an anticancer drug approaches 100%, anything that kills off cancer cells is going to kill off some normal ones as well. This means side effects, often quite nasty.
But what if, instead of killing off cancerous cells, we just shut down their invasive potential?
I’ve been reading up on what differentiates noninvasive cancer cells – carcinoma in situ – against invasive cells. The literature on this has been surprisingly sparse, so either I’m not looking for the right things (quite possible), or this is a very understudied approach. The papers I’ve read have identified a few gene loci and a protein called Twist, but that is as far as I can take my search, lacking the resources to experimentally pursue such lines of study.
My point is this: carcinoma in situ is harmless except in its ability to become invasive cancer. Most of the proteins that seem to cause aberrant behavior in cancer cells seem those that are present during embryonic development (which makes sense in a way, since embryonic development is high-rate controlled, regulated division, whereas carcinogenesis is high-rate uncontrolled, unregulated division), but these proteins are all but absent in adults.
So rather than attempting to kill off the cancer cells, why not attempt to remove their ability to invade (and thus metastasize, destroy tissue, and cause other problems)? Even if the treatment were nonspecific, side effects should be far milder than the “killer” drugs, since normal cells are not known to depend on the function of the identified proteins. And unlike drugs that kill cells, there is little selective pressure against the treatment.
I see so many solutions to this problem. How I wish I could take part…
Zeus’ thunderbolts are made on Hephaestus’ forge -> cumulonimboids, which frequently have anvil-shaped peaks, herald thunderstorms.
“Charis” is the root of “charisma” and “charity”.
The Latin term for God, “deus”, probably came from “Zeus”.