This is a pretty big deal. Vision has proved to be one of the more difficult areas to treat and affects a huge number of people. As developers, we’re also more likely to have eye issues. Laser treatments have not been very helpful for macular degeneration and side effects are common and can be just as damaging, so ophthalmologists have stopped doing them except to halt the most aggressive cases.
I think we should fund more research like this, as well as technological solutions.
There have been several studies linking myopia and other eye issues to close work, digital eye strain, dry eyes, etc. I leave it to you to find them on your own via google.
Well, NIH posts some supporting evidence here (https://nei.nih.gov/health/errors/myopia), but they seem pretty constrained to people within a critical opthalmic development window.
> I leave it to you to find them on your own via google.
Considering you made the assertion, is it really a stretch to do the heavy lifting yourself? For all you know, the person who asked for your specific insight ("What leads you to believe this?") tried and failed to find anything within the software engineering realm which could account for an increase in eye issues.
The closest I could find among the links you provided are:
> People who do an excessive amount of near-vision work may experience a false or "pseudo" myopia. Their blurred distance vision is caused by overuse of the eyes' focusing mechanism. After long periods of near work, their eyes are unable to refocus to see clearly in the distance. Clear distance vision usually returns after resting the eyes. However, constant visual stress may lead to a permanent reduction in distance vision over time.
But no studies are referenced. I'm unable to find anything specifically, and I'm the second person asking you. It'd be neat to know what you read which specifically substantiated the long-term effects of near-space work on the eyes.
Muscle strain is caused by keeping a static load on a muscle for a while without enough breaks to relax and recover.
Both focusing and convergence of the eyes require muscle contraction, and can lead to eye strain.
Moving work a bit further from the eyes and lower in the field of vision will reduce the amount of muscle contraction needed. Periodically focusing on more distant objects will help relax those muscles. For people working at a computer workstation, it is usually possible to arrange the computer display 3+ feet away from the eyes, and in the bottom half of the field of view. Periodically looking away from the display while thinking and remembering to get up and stretch/walk around every once in a while can make a big difference for anyone experiencing eye strain.
It's not considered best practice in science or on HN to make claims and then essentially say, now go strengthen my argument for me.
I don't think it should be some draconian rule, but if it's not obvious to the general audience where to quickly get an authoritative source the burden generally falls to the claimant.
An alternative possibility is that spending most of your time in childhood indoors reading and using computers leads to myopia and later a career in computers. That makes more sense to me because by the time you are adult and have a job, your myopia probably isn't just developing.
3 blind mice. 3 blind mice. We went to school and studied real hard. We got some grants and worked even more. We did some research and spliced their genes now 2 blind mice, 2 blind mice.
But its the way they're doing the rescue that matters. AAV delivering a green opsin gene into ganglion cells which normally _would_not_have_ expressed or used that gene. Its supposed to be the cone photoreceptor cells that use that gene. So this isn't just replacing a knocked our gene, its a true 'hack', utilising other cells that are easier to target.
This are not normal mice that gone blind. These are special mice that have one of they gene broken. (The same gene in all the mice in the experiment.) So it is "easy" to fix their problem by giving them a new working copy of the defective gene.
It's a nice result, but now the interesting question is if this can be generalized to people that doesn't have that a more diverse type of problems.
I'd like to provide you with some more background because you are conflating this research with a different type of study and incorrectly interpreting its impact.
For background, I have inherited retinal disease in my family, am the founder of a gene therapy company that is working on genetic blindness, and have met John Flannery a few times.
This is not a simple 1) knockout gene in mouse, 2) put same gene back in study, like has been done many times before.
The model system here, the rd1 mouse, is not a "knockout mouse" per se. It is a strain of visually impaired lab mouse that was identified in the 1920s before knockout mouse technology was available. These mice have mutations in the PDE6B gene (due to a virus insertion) and the Gpr179 gene (which was identified much later).
Rd1 mice have severe early onset blindness caused by the death of cells that allow normal eyes to perceive light - photoreceptors. In these mice, the rod photoreceptors die first, then the cone photoreceptors follow, and this all happens pretty quickly.
In this study, researchers are introducing a different gene (green cone opsin) into second-order cells that do not normally perceive light (retinal ganglion cells or bipolar cells). This approach gives retinal ganglion cells/bipolar cells the new ability to perceive light. Importantly, these cells survive in patients that are blind because of photoreceptor death, so this approach can be generalized.
Scientists have been trying this for a while and there have been a number of limitations due to the performance of the introduced genes (opsins). There are clinical trials planned and ongoing in optogenetics, but those include things like light filters/amplifiers, and also often some form of implant.
It is not yet clear the quality / resolution of vision that people could regain. A very good outcome with the technology described would be providing monochrome vision of useful resolution to patients who currently cannot perceive light at all.
There are likely many subtleties I haven't considered or don't know about. Nevertheless, this is significant progress with an approach that is in theory applicable to very advanced cases of over 270 genetic diseases that cause blindness.
No, this is correct. They've identified 2 known corrupted 'files', and by restoring them from 'backup' they were able to restore functionality. What is cool/notable is that the restore method worked on a running device, and they didn't even need to 'reboot' for the fix to take effect.
Following the same analogy, could we say that researches knew what exact file was missing and happened to have that same file at hand?
In other words, making this applicable to blind humans with different kinds of blindness would be a whole different story?
Yes. They removed the file, then put it back. The study is about proving the insertion vector works for whatever treatment needs to be done in the future, not about being able to cure blindness.
I think we should fund more research like this, as well as technological solutions.