Apr 22, 2017

Becky, Barbie's friend who uses a wheelchair, was discontinued.

Last year, Mattel announced that it was giving Barbie a makeover — introducing new body shapes, skin tones and even flat feet to make the iconic doll look more realistic. “Barbie reflects the world girls see around them,” Mattel president and COO Richard Dickson said.
Here's why. Studio 360 April 09, 2017 · 10:30 AM EDT Writer Julia FranzPlayer utilities
This story is based on a radio interview. Listen to the full interview.
Mattel made a similar statement in 1997 when it introduced “Share-a-Smile Becky,” a Barbie friend who used a wheelchair — but that time, the toymaker’s efforts didn’t go quite as planned.
With her shiny pink wheelchair and tiny backpack, Becky was an instant hit. As many as 6,000 dolls were sold in the first two weeks, and disability advocates praised Mattel for bringing visibility and representation to wheelchair users.
But the warm, fuzzy feeling didn’t last. Kids and collectors soon discovered that Becky’s wheelchair didn’t fit through the doors of the Barbie Dreamhouse — that pink-swathed epicenter of Barbie’s social world. The chair couldn’t squeeze inside the house’s elevator, either.
At the time, Mattel responded to the controversy by saying that the company was “looking at the accessibility of all Barbie accessories.” But as producer Renee Gross reports, that’s not the end of Becky’s lesson about disability and inclusivity. 
Recently, Gross brought a “Share-a-Smile Becky” doll and a brand-new Barbie Dreamhouse to Monique Kulick, an accessibility advocate based in Ann Arbor, Michigan. As it turns out, Becky’s wheelchair still doesn’t fit in the Dream House elevator, 20 years later.
“There's absolutely no way,” Kulick says. “It won't even fit with her legs sticking out. So pretty much in this house, Becky could go to the kitchen.”
And even then, she says, there would still be problems. “If this were Becky's house, her kitchen would have a clear space under the sink so she could roll directly up to it. Dishwashers are normally for an accessible kitchen and universal. They're raised, so that that bottom rack, you don't have to bend down so far for the bottom rack.”
The bottom line? Mattel never changed the house, Gross says. “But what did change was Becky.”
She explains that "Share a Smile Becky" became "Becky, I'm the School Photographer," then "Sign Language 'I Love You' Becky" and then "Paralympic Becky."
Finally, Becky disappeared from shelves altogether — but not before Mattel reportedly considered making her wheelchair smaller, so she could fit through the doors of Barbie’s house.
“A lot of the talk about why Becky doesn't exist anymore in any iteration is that it was too complicated to redesign Barbie world to fit Becky,” says Karin Hitselberger, who has blogged about the Becky dolls she had as a child. “So, they just got rid of her.”
For Hitselberger, who has cerebral palsy and uses a wheelchair, Becky’s story “speaks volumes to the way we think about disability.”
“A lot of the ways we think about disabilities, we talk about ‘fixing disability,’ instead of focusing on ‘fixing society,’” she says.
Kulick agrees. “Oh my god, that’s a huge thing — a huge thing,” she says.
This article is based on a story that aired on PRI's Studio 360 with Kurt Andersen. 

Post Polio Litaff, Association A.C _APPLAC Mexico

Curbing Damage New small molecule treatments could reduce damage due to diabetic eye disease

A team led by Harvard Medical School researchers at Massachusetts Eye and Ear has identified a new therapeutic target for abnormal blood vessel growth in the retina, a hallmark of advanced diabetic eye diseases such as diabetic retinopathy.
According to a report published online in Diabetes on April 11, the transcription factor RUNX1 was found in abnormal retinal blood vessels, and by inhibiting RUNX1 with a small molecule drug, the researchers achieved a 50 percent reduction of retinopathy in preclinical models. These findings pave the way for new therapies that address diabetic retinopathy and other conditions involving abnormal vessel growth within the retina, known as retinal neovascularization.
“We’re hopeful that we may have an opportunity to change the treatment paradigm for these conditions.” —Leo Kim
“Current treatments to control retinal neovascularization require injecting very large proteins, including antibodies, into the eyes of patients, as often as once a month. Our study opens the door for new modalities of treatment based on small molecules that could cross biological barriers on their own. Such a treatment could be self-administered by patients and eliminate the need for intravitreal injections,” said co-corresponding author Joseph Arboleda-Velasquez, HMS assistant professor of ophthalmology and assistant scientist at Schepens Eye Research Institute of Mass. Eye and Ear.
Neovascularization is a feature of various health conditions, including diabetic retinopathy, wet age-related macular degeneration, retinopathy of prematurity and cancer. In the case of diabetic retinopathy—the most common diabetic eye disease and a leading cause of blindness in American adults—blood vessels in the retina (the structure in the back of the eye that senses and perceives light) become damaged and leak fluid. Accumulation of fluid into the retina can lead to swelling at the center of the retina and growth of pathological blood vessels on its surface. As diabetes-related damage progresses, these vessels can leak, rupture or cause retinal detachment leading to impaired vision. 
In the Diabetes report, the authors studied tissue from patients with proliferative diabetic retinopathy. They identified the presence of RUNX1 in the diseased blood vessels but not in the normal blood vessels. Next, they used a small molecule drug originally developed as a cancer therapy to inhibit the activity of RUNX1 in the eye, which led to a significant reduction of abnormal blood vessels.
Current strategies for treating abnormal blood vessel growth in the retina for proliferative diabetic retinopathy include laser treatments or eye injections targeting a growth factor, VEGF. While these therapies have been remarkably successful in saving vision in many patients, they can, in rare instances, trigger complications such as retinal hemorrhages, detachments or retinal atrophy.
The study authors are hopeful that inhibiting RUNX1 may present a more targeted opportunity for managing the retinopathy of certain eye conditions—perhaps earlier in the disease process, before the abnormal blood vessels develop. Future studies will test whether the drug can be delivered through topical eye drops rather than by injection and further explore the relationship between RUNX1 and VEGF, as these factors seemingly both play a role in angiogenesis.
“We’re hopeful that we may have an opportunity to change the treatment paradigm for these conditions,” said co-corresponding author Leo Kim, HMS assistant professor of ophthalmology and a retina surgeon at Mass. Eye and Ear. “Instead of treating patients after these abnormal blood vessels form in the eye, we may be able to give patients eye drops or systemic medications that prevent their development in the first place.”
Adapted from a Mass. Eye and Ear news release.
This study was supported by the National Institutes of Health (grants R01EY005318, R00EY021624, UH2NS100121-01, R21EY027061, K12EY16335 and P30EY003790). Additional support was provided by an American Diabetes Association Innovation award, the Massachusetts Lions Eye Research Fund, the E. Matilda Ziegler Foundation for the Blind, the Karl Kirchgessne

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