Corneal Repair: A Clear Vision!

Damage to the surface of the cornea causes pain and loss of vision, but regenerative therapies are providing a clearer, brighter future.

If the eyes are the window to the soul, then it is the cornea that lets the light enter.

For more than 200 years, physicians have been preoccupied with keeping this dome-shaped, transparent surface in front of the iris and pupil clear. German surgeon Franz Reisinger was the first to attempt a corneal transplant in animals in 1818. And in 1838, US ophthalmologist Richard Kissam tried to replace the opaque cornea of a young patient with the healthy cornea of a pig, but the procedure failed when the transplant was rejected. The first successful transplant in humans was in 1905, but outcomes remained poor until the mid-twentieth century, when developments in infection control, anaesthesiology, surgical techniques and immunology vastly improved the success rate of corneal transplantation. In the twenty-first century, advances in cell-culture techniques and bioengineering have opened the door to regenerative treatments for people with damage to one or both corneas.

Unclouded vision requires a clear cornea. Its epithelial surface constantly renews itself to maintain an unblemished, uniformly refractive surface. Cells that are shed from the surface are replaced by new ones that emanate from a small population of stem cells located at the edge, or limbus, of the cornea.

If the stem cells at the limbus are damaged, the renewal process is interrupted. The complete or partial loss of these stem cells — limbal stem-cell deficiency (LSCD) — allows the opaque conjunctiva to grow over the cornea. This can lead to intense pain and, in the most-severe cases, blindness.

Let there be sight -David Holmes

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Source: Nature

Association Between Genetic Variation And Influenza Severity.

It is estimated that in the USA influenza -related deaths in recent years have ranged from 12,000 to 56,000. Factors like age, obesity, pregnancy and such chronic health conditions as asthma, chronic lung disease and heart disease are associated with an elevated risk of complications and death.

However, there are no proven genetic markers of influenza risk with an established mechanism of action. Interferon Induced Transmembrane Protein 3 (IFITM3) is an anti-viral protein that helps to block influenza infection of lung cells and to promote survival of the killer T cells that help clear the infection in the airways.

Image: A scanning electron micrograph of a CD8+ T cell engaging a virus.

(Photo courtesy of Dennis Kunkel).

A group of scientists collaborating with those at St. Jude Children's Research Hospital (Memphis, TN, USA) searched for other possible IFITM3 variants that correlated with gene expression, levels of the IFITM3 proteins and were common in influenza patients in the USA. The search led to an IFITM3 variant known as rs34481144. They checked 86 children and adults in Memphis with confirmed influenza infections and found two-thirds of patients with the most severe symptoms carried at least one copy of the newly identified high-risk IFITM3 variant. The high-risk variant was found in just 32% of patients with milder symptoms.

The team also found an association between the newly identified high-risk variant and severe and fatal influenza infections in 265 critically ill pediatric patients hospitalized in one of 31 intensive care units nationwide. The patients did not have health problems that put them at high risk for severe influenza. Of the 17 patients in this group who died from the infection, 14 carried at least one copy of the newly identified high-risk variant. Further study revealed how binding differed between the high-risk and protective variants. Those differences led to lower levels of the IFITM3 protein in individuals with two copies of the high-risk gene variant compared to other patients. The Memphis influenza patients also had fewer of the killer T cells in their upper airways. The study identifies a new regulator of IFITM3 expression that associates with CD8+ T cell levels in the airways and a spectrum of clinical outcomes.

Paul Thomas, PhD, an immunologist and corresponding author of the study, said, “A genetic marker of influenza risk could make a life-saving difference, particularly during severe influenza outbreaks, by helping prioritize high-risk patients for vaccination, drug therapy and other interventions. These results raise hopes that this newly identified IFITM3 variant might provide such a marker.” The study was published on July 17, 2017, in the journal Nature Medicine.

Source: labmedica