For most women, a tiny pimple on the face is enough to ruin their day. Or week. Even the slightest imperfection that may have a 1% chance of getting noticed by others will freak them out. For these women, Melasma is their darkest nightmare. It’s a pretty common issue, a result of exposure to sun, that causes brown patches on the face. Permanent patches, I should add.

If you’re suffering from Melasma, the road to “recovery” usually looks like this.

  1. You hope that it’ll fade away.
  2. Your friend suggests you try apple cider vinegar and lemon juice treatment.
  3. Slightly disappointed.
  4. You visit a dermatologist who’ll prescribe a bleaching cream (hydroquinone or similar).
  5. Full-on disappointment.
  6. You Google the hell out of the topic.
  7. Overwhelm.
  8. Concealers and makeup becomes your best friend.

At this point, no one can convince you there is a treatment for getting rid of melasma. Trying more and more treatment only runs the risk of making the condition worse. So what would you do?

Platelet-Rich Plasma For Melasma

What about Platelet-Rich Plasma For Melasma?

According to recent Turkish and Malaysian studies, Platelet-Rich Plasma is showing great promise for melasma. The one good thing about PRP for Melasma is the fact that PRP won’t make the condition worse unlike IPL, fraxel or other treatments. So that’s one of the treatment you can confidently try without worry. It’s like getting a natural facial treatment that has a whole lot of potential benefits even if it didn’t help cure melasma.

PRP injections work by supplying growth factors to reduce the pigmentation. And being an independant treatment with no downtime, it can be done in conjunction with conventional treatments for melasma to add and enhance the effects. There are more than 30 bioactive substances in Platelet-Rich Plasma that has separate roles like increasing skin volume and adding new blood vessels to name a few.

Platelet-Rich Plasma with Microneedling

This is the most common combination for Platelet-Rich Plasma therapy. Here’s a video of Dr. Michael Somenek performing PRP injection on a patient of his immediately after microneedling. The combination is known to have produced results for a lot of varieties of skin pigmentation issues that it’d not be wise for anyone to ignore it for melasma, especially when creams and peels didn’t help. More important is PRP’s ability to stimulate collagen production in the area so it tightens the pores and makes your skin glowing.

Why Platelet-Rich Plasma?

PRP is primarily a healing vehicle. It needs to be injected into the membrane below the skin. The way it works is by supplying the underlying skin membrane with collagen and tenascin stimulated by the transforming growth factors in PRP. These growth factors also promote formation of new blood vessels that in some cases results in disappearance of spider veins.

The released growth factors (mainly platelet derived growth factor (PDGF), epidermal growth factor (EGF), vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF) and transforming growth factor-beta (TGF-ß)) can stimulate proliferation of fibroblast and epidermal cell, and collagen synthesis. In addition, the transforming growth factor-beta (TGF-ß) has been proven to inhibit melanogenesis — or reverse skin pigmentation — the exact opposite effect of exposure to UV-B radiation.

Typically, patients see excellent results with 2-3 PRP injections in the first 3 months. And clinical studies have shown that it will maintain after 6 months.

However, Melasma is known to recur even after successful treatments. So you must take precautions against it by using sunscreen with broad-spectrum protection and an SPF of 30 or higher. And avoid skin care products that are harsh as they can exacerbate melasma.

 

insulin-producing pancreatic beta cells

A new discovery by researchers on how to activate lab-grown beta cells to mature into functioning cells that produce and release insulin in response to glucose take a significant step toward a cell therapy treatment for diabetes.

Difficulties in manipulating beta cells derived from human stem cells to mature beyond the precursor stage into fully functioning insulin releasers has been an on-going challenge for researchers..

However, researchers from the Salk Institute for Biological Studies and a team of researchers  have achieved this goal with lab-grown beta cells by activating a protein called estrogen-related receptor γ (ERRγ). Their study findings were recently published in the journal Cell Metabolism.

Self-renewing capacity of human pluripotent stem cells (hPSCs)

Ronald Evans, senior author of the study, titled, “ERRγ Is required for the Metabolic Maturation of Therapeutically Functional Glucose-Responsive β Cells,”insulin-producing says the self-renewing capacity of human pluripotent stem cells (hPSCs) and their ability to differentiate into most cell types—from neurons to skin cells, to muscles cells and insulin-producing pancreatic beta cells—has inspired many research teams to find ways to make glucose-responsive beta cells in the lab.

Evans and his research team discovered the answer to the insulin-releasing cell conundrum, and summed it up thusly:

“In a dish, with this one switch, it’s possible to produce a functional human beta cell that’s responding almost as well as the natural thing.”

Evans, a molecular biologist at the Salk Institute, says that to create the different types of cells in the lab, researchers coax the pluripotent stem cells (hPSCs) down the various branching paths that fetal cells normally travel in order to differentiate into the various cell types. However, he explains there are many developmental points in this process, and in the case of lab-grown pancreatic beta cells, research kept getting stuck at an early stage.

Adult beta cells have more ERRγ protein for a very energy-intensive process

In order to determine what might trigger the next step in getting the cells to mature, the researchers compared transcriptomes of adult and fetal beta cells. The transcriptome contains, among other things, the full catalog of molecules that switch genes on and off in the genome, which led them to discover that the nuclear receptor protein ERRγ was more abundant in adult beta cells. The team was already familiar with the protein’s role in muscle cells and had studied its ability to enhance endurance running.

Evans says that in muscles, protein promotes greater growth of mitochondria—the power generators inside cells that accelerate the burning of sugars and fats to make energy.

“It was a little bit of a surprise to see that beta cells produce a high level of this regulator,” Evans says. “But beta cells have to release massive amounts of insulin quickly to control sugar levels. It’s a very energy-intensive process.”

The research team then decided to run some tests to look more closely at what role ERRγ might play in insulin-producing beta cells.

A new era in creating  functional, insulin-producing beta cells

insulin-producingAfter they genetically engineering a deficiency of ERRy in mice, the researchers found the animals’ beta cells did not produce insulin in response to spikes in blood sugar.

Next they tried to get beta cells made from hPSCs to produce more ERRγ, and it worked! The cells in culture began to respond to glucose and release insulin.

Finally, the team transplanted the lab-grown insulin-producing beta cells into diabetic mice and found that from day one, the cells produced insulin in response to glucose spikes in the animals’ blood.

Evans and the research team were justifiably excited by the results. It appears that just switching on the ERRγ protein is sufficient to get the lab-grown beta cells to mature and produce insulin in response to glucose – both in cultures and in live animals.

Speculating on the implications of their findings, Evans suggests that when a fetus is developing, because it gets a steady supply of glucose from the mother, it does not need to produce insulin to regulate its blood sugar, so the switch is inactive. But, when the baby is born and takes its first breath and takes in oxygen, this activates the switch.

Previous lab attempts to produce beta cells got stuck at the fetal stage. The Salk Institute researchers discovered how to take it to the adult stage, using the same protein that is switched on in nature.

“I believe this work transitions us to a new era in creating functional beta cells at will,” Evans says.

He and his research team now plan to examine how the switch might work in more complex models of diabetes treatments.

The Salk Institute study proceeds another study Medical News Today in which researchers generated mini-stomachs that produce insulin when transplanted into mice.

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