eschericichia (ES) bacteria are the bacteria that cause the common eye disease cornea irritant mydriasis, which affects over 80 million people worldwide.
But ES has a slightly different kind of problem: it’s a type of cornea disease called vitreous detachment, which involves the detachment of the outer layers of the cornea.
This means that the outer layer of the lens, called vitrotrichium, is detached from the rest of the layer of cells called epithelial cells, resulting in a visible patch of white on the retina, which may or may not look like a cloudy or cloudy white spot.
But while ES is an eye disease, it’s not quite as mysterious as it may sound.
ES is the only cornea condition that causes vitreosclerosis, and researchers have identified two proteins called ES and RBS1 as the cause of this condition.
ES and RSBS1 are also known as ESB1 and ESC1, and they have been linked to a variety of corneal diseases including vitreo-stretching and vitreoporosis.
In a study published in the journal Cell on February 25, researchers led by Michael Eichler of the Max Planck Institute for Infection Biology in Germany and colleagues from the University of Zurich, the Max Plank Institute for Biochemistry and Molecular Biology and the University Hospital Zurich found that ESB2, a protein that is also found in RBS, was responsible for the damage to the epithelial layer of ES cells.
This finding suggests that the proteins may act as a bridge between ES cells and the rest.
“It’s clear that these proteins are able to trigger the epithelium to detach and form a cloud,” Eichlers team wrote.
“It appears that the mechanism of this action is the same as the damage caused by the corneocyte.
It appears that RBS and ESB are acting in concert to damage the epithenium.”
In order to test this hypothesis, Eichls team studied the effects of ESB and RSB2 on the ES cells of a mouse model of vitreosis, which is the cause for the symptoms of vitroosclerosis in the eye.
The researchers used a strain of the ESB protein that they had isolated from a mouse and that was similar to the ES cell that was shown to be damaged in the study.
This mouse strain had been infected with the RBS virus and was treated with a compound called rhesus macrophage-derived cytotoxic protein-2 (CAMD-2), a virus-specific virus designed to damage ES cells in the mouse.
The researchers found that when ESB was injected into the cells of this mouse model, the virus caused a severe increase in damage to ES cells, with an increase in the level of ESBS protein that was detected on the surface of the cells.
In contrast, when the cells were not infected with rhesussis, the levels of ES protein did not increase.
“The results showed that the rhesUS-specific protein-1 (RSBS1) was able to induce damage to both ES cells but that the level remained low even in the presence of RBS,” the researchers wrote.
These results suggest that RSBS-specific proteins are involved in the damage of ES cell populations to the Rhesus-specific version of the virus, and that these protein-based inhibitors of the RSBS protein can have a positive impact on the pathogenesis of the disease.
The research has been published in Cell.
The full paper can be found here.