I had been told by a couple of my eye doctors that I had a bad eye, and this was a big no-no for me.
“No eye drops for the rest of your life, no prescription, no no no”, I had read.
But I didn’t have a problem.
Instead, I was told that my eyes were very sensitive to the light, and that the problem was the light in the room.
So I had to spend hours in my bedroom, adjusting the curtains and adjusting my eye-mask, before the doctor would admit that I wasn’t having any problems.
I was given a number of treatments and procedures and all of them failed to work.
So what happened?
And what does this mean for me?
It means I’m going to need a lot more medication than I thought I would, and a lot of the drugs are very expensive.
But there are treatments I can try that will make things better.
In my case, the problem wasn’t that I was seeing a lot.
Rather, it was that my pupils were contracting because of a problem with my eye, which is called retinopathy.
In retinitis pigmentosa, a pigmentous tumour in the outer layer of the retina, the eye is made up of layers.
It has a lens on top, and the retina contains the nerve cells that are responsible for vision.
When the light is too strong, the nerve cell cells that normally send signals to the retina to make it see are unable to do their job, and when the light falls on the retina the light can actually damage the nerve and cause damage to the eye itself.
What is retinoblastoma?
The retina is where the light that comes in from the sun is absorbed by the cells in the retina.
The light then travels through the inner layer of retina to reach the inner lining of the eyeball, where the cells that make up the retina absorb the light and make the image.
In this way, we have three layers of the eye, each of which is made of cells that produce the light signals that make our eyes work.
If we lose sight in one of the layers, we can be blind.
But in the other two layers, our vision is unaffected, so we can still see.
It’s this process of light coming in and getting absorbed by cells in each layer that causes retinopathies.
This is because retinocytes, or light-sensitive cells, that make the retina are sensitive to light.
They can be stimulated to make the light glow, or if they don’t respond, they can die off.
The retinosis of my eyes is caused by retinoblasts, or cells that can make the cells on the outer surface of the inner retina glow.
But these cells are not making the light to make my eyes glow, they are making it to send out signals to make me see.
They have to have a light signal that is capable of making me see, and so, retinoids are made from these light-producing cells.
A retinoid drug called tetracycline is one of these light signals.
The drug tetracecline, which was invented by German scientist Albert Pohl in 1939, has been used since the 1960s to treat retinopathic conditions.
The drug is designed to stimulate the light-receptor cells that the outer retina is made from.
Tetracycleline has been shown to improve the sensitivity of the outer retinas to light by up to 60%.
It has also been shown that tetraccline reduces the amount of retinal degeneration that occurs in the eye and can improve vision for people who have retinotopic diseases such as retinomatosis.
I was lucky, though, because I had the right treatment.
This medication is known as an antagonist.
It works by blocking the activity of a gene that causes the cells to die off in the inner retinas.
If you have retinal diseases that make you blind, then you have an abnormally low amount of light-sensing cells in your eye, so you don’t get the light signal your eyes are sensitive for.
Tetracycal drugs that block the gene responsible for retinal light-signaling, or the genes that are expressed by the outer cells, also prevent the outer cell death.
So if you have a retinal disease, tetracline will stop the retinal cells from dying and it will also stop the outer-cell death that occurs during retinotic disease.
There are a lot less drugs available to treat these eye conditions than there are drugs that treat retinal tumours.
In the early 2000s, a few drugs were introduced, but only one of them, an antibody called mirolimus, has worked.
Other drugs have failed to help.
So now I am going to have to try all the drugs I can get my hands on