Diabetes leads to retinopathy

Loss of vascular cells in the retina of the eye, loss of barrier function in vessels, edema, and a cascade of inflammatory events lead to blindness. The eye generates a dihydroxy metabolite from polyunsaturated fatty acids that initiates pericyte loss and breakdown of the endothelial barrier function in the eye, the scientists said. This leads to vascular edema and ultimately to a proliferation of new blood vessels and loss of vision.

The small molecule which initiates this process is a diol of a long chain poly unsaturated fatty acid produced by sEH, the researchers said. The enzyme converts an anti-inflammatory epoxy fatty acid into the pro inflammatory and in this case, toxic diol. The research team demonstrated this process and the cellular mechanism involved in diabetic mice and in transgenic mice that over-produce the sEH enzyme.

They were able to block the process by inhibiting the sEH enzyme. The expression of the sEH enzyme also increased with severity of diabetic retinopathy in human patients.The expression of the soluble epoxide hydrolase gene was shown to increase in the retinas of human patients with the severity of the disease with non-proliferative diabetic retinopathy. Diabetic eye disease can affect many parts of the eye, including the retina, macula, lens and the optic nerve.

Diabetic retinopathy is the most common diabetic eye disease and a leading cause of adult blindness. Chronically high blood sugar from diabetes damages the tiny blood vessels in the retina, leading to diabetic retinopathy, according to the National Eye Institute (NEI) of the National Institutes of Health. The blood vessels can leak fluid or hemorrhage and distorting vision. The sEH enzyme generates a toxic metabolite, but when the enzyme is inhibited, eye disease is prevented.

Inhibiting the soluble epoxide hydrolase preserves fatty acid epoxides which reduce the late or proliferative stages of diabetic retinopathy and macular degeneration. Research team used the same soluble epoxide hydrolase inhibitors to block production of a pro inflammatory mediator that initiates the early stages of vascular permeability and inflammation of the retina. They discovered that 19,20-dihydroxydocosapentaenoic acid, a product of soluble epoxide hydrolase (sEH) activity, as a key regulator of pericyte loss and endothelial barrier breakdown has brought to light a previously unknown mechanism of action in the induction of diabetic retinopathy.

 Inhibition of sEH blocks formation of this degenerative lipid metabolite thereby halting disease progression, which is of vital interest for the potential management of this blinding disease.The diol of the fatty acid linoleate produced by the soluble epoxide hydrolase was highly toxic to cells leading to vascular permeability and sepsis. These epoxy fatty acid chemical mediators control blood pressure, fibrosis, immunity, tissue growth, pain and inflammation.
         haleplushearty.blogspot.com

Digital scan of the eyes reveals health condition

In terms of diagnostic imaging, the eye is a unique part of the human body. Using optical coherence tomography OCT technology, 40,000 scans are produced within 1.2 seconds, with a total volume of 65 million voxels.  Voxel is a contraction of "volume" and "element" and refers to a grid point in a three-dimensional grid and overall to a huge volume of information about a patient's retina.

The OCT data are analysed using automated algorithms generated on the basis of Artificial Intelligence. A digital image of the retina provides enormous amount of data, offering information about a person's entire personal and medical Life Data, not only about existing or potential diseases, but also about lifestyle.

The retina shows how old a person is, their gender, smoking habits, blood pressure and whether they have diabetes, or at least an increased risk of developing it. Diabetes and high blood-pressure are very common conditions and in many patients, result in long-term retinal damage, incorporating these new technologies into clinical care will give accurate picture of patients general health for customised treatments.
          haleplushearty.blogspot.com

Deep sleep for visual learning

When we see something, our retinas transmit that image to the thalamus in the brain, where neurons send very basic visual information to the visual cortex to be processed. When the brain is awake, neurons in the thalamus and cortex fire steadily to transmit visual information between them. However, in slow-wave sleep, those neurons will burst and then pause rhythmically and in synchrony.

There is also communication in the opposite direction between the visual cortex and thalassemia forming a loop of communication between the two structures. After presenting mice with a new type of visual experience and then allowing those mice to sleep, neurons in the cortex fired more when seeing that stimuli again. But the lab also showed the brain needs sleep in order to make cortical changes. If mice were sleep deprived after the experience, no changes in the cortex occurred.

If you disrupt communication from the cortex to the thalamus during slow-wave sleep, it will completely disrupt that slow-wave rhythm and the plasticity in the visual cortex. The researchers turned off neurons in the visual cortex that complete the loop, sending information back to the thalamus, while the mice were naturally asleep or awake.

While this did not wake the sleeping mice, it did keep them from having coordinated rhythms of activity between the two structures during slow-wave sleep. If cortex-to-thalamus communication is disrupted in any other behavioral state such as wakefulness, there is no effect on sleep-dependent plasticity of the visual cortex.

But if these oscillatory patterns during slow-wave sleep, you see a deficit, you need these big waves of activity occurring in order to have that benefit of sleep. Researchers made recordings in both a part of the thalamus called the lateral geniculate nucleus, which processes visual information, and the visual cortex of mice.

They tracked the activity of these populations of neurons while presenting the mice with patterns of visual stimulation for hours of subsequent sleep. During visual experience, they discovered immediate changes in the neurons in the thalamus, but nothing going on in the visual cortex. These waves during subsequent sleep are apparently able to transfer information from the thalamus to the cortex, and that information reflects what that animal has just been looking at.
            haleplushearty.blogspot.com