I am enjoying Lupita’s shine. But not without my reservations. And these reservations of course have nothing to do with Lupita herself, but everything to do with the way in which white supremacy maintains itself by utilizing tokens to give the appearance of fairness and equity.

Is Hollywood really challenging racist beauty standards? Or any beauty standards at all? Or is it maintaining the status quo and welcoming Lupita in as an anomaly?

Any dark-skinned girl knows that just because an individual may find us physically or sexually attractive doesn’t mean that they are anti-colorist or anti-racist. That’s why comments like “you’re pretty for a dark-skinned girl” are so common. An individual dark-skinned Black girl can always be recognized as beautiful. But it must be done so by positing her as an exception.

I believe there is no difference for a white-dominated magazine or Hollywood in general.

And I cannot trust a magazine or industry predicated on anti-Blackness 364 days out of the year to suddenly fundamentally change their behavior now that Lupita has been named as the world’s most beautiful woman.

I will be a believer when I am able to pick up a magazine that has racial and ethnic diversity without looking directly for Essence or Jet. I’ll be a believer when I start to see dark-skinned women cast in movie roles where they are neither evil and unwanted or the victims of vicious sexist and racist violence.

I know that I must remain vigilant so that honors such as this do not make me too comfortable.

So I celebrate this. But I also demand more.

talesofthestarshipregeneration:

….
…
…
…….
The fuck?!?!? 
Are these people fucking serious?
Its fucking whiteout on that cover!

And I am not here for what they did with the Black lady. UGH UGH UGH 

talesofthestarshipregeneration:

….

…….

The fuck?!?!? 

Are these people fucking serious?

Its fucking whiteout on that cover!

And I am not here for what they did with the Black lady. UGH UGH UGH 

neurosciencestuff:

Loss of Memory in Alzheimer’s Mice Models Reversed through Gene Therapy
Alzheimer’s disease is the first cause of dementia and affects some 400,000 people in Spain alone. However, no effective cure has yet been found. One of the reasons for this is the lack of knowledge on the cellular mechanisms which cause alterations in nerve transmissions and the loss of memory in the initial stages of the disease.
Researchers from the Institute of Neuroscience at the Universitat Autònoma de Barcelona have discovered the cellular mechanism involved in memory consolidation and were able to develop a gene therapy which reverses the loss of memory in mice models with initial stages of Alzheimer’s disease. The therapy consists in injecting into the hippocampus - a region of the brain essential to memory processing - a gene which causes the production of a protein blocked in patients with Alzheimer’s, the “Crtc1” (CREB regulated transcription coactivator-1). The protein restored through gene therapy gives way to the signals needed to activate the genes involved in long-term memory consolidation.
To identify this protein, researchers compared gene expression in the hippocampus of healthy control mice with that of transgenic mice which had developed the disease. Through DNA microchips, they identified the genes (“transcriptome”) and the proteins (“proteome”) which expressed themselves in each of the mice in different phases of the disease. Researchers observed that the set of genes involved in memory consolidation coincided with the genes regulating Crtc1, a protein which also controls genes related to the metabolism of glucose and to cancer. The alteration of this group of genes could cause memory loss in the initial stages of Alzheimer’s disease.
In persons with the disease, the formation of amyloid plaque aggregates, a process known to cause the onset of Alzheimer’s disease, prevents the Crtc1 protein from functioning correctly. “When the Crtc1 protein is altered, the genes responsible for the synapsis or connections between neurons in the hippocampus cannot be activated and the individual cannot perform memory tasks correctly”, explains Carlos Saura, researcher of the UAB Institute of Neuroscience and head of the research. According to Saura, “this study opens up new perspectives on therapeutic prevention and treatment of Alzheimer’s disease, given that we have demonstrated that a gene therapy which activates the Crtc1 protein is effective in preventing the loss of memory in lab mice”.
The research, published today as a featured article in The Journal of Neuroscience, the official journal of the US Society of Neuroscience, paves the way for a new therapeutic approach to the disease. One of the main challenges in finding a treatment for the disease in the future is the research and development of pharmacological therapies capable of activating the Crtc1 protein, with the aim of preventing, slowing down or reverting cognitive alterations in patients.

neurosciencestuff:

Loss of Memory in Alzheimer’s Mice Models Reversed through Gene Therapy

Alzheimer’s disease is the first cause of dementia and affects some 400,000 people in Spain alone. However, no effective cure has yet been found. One of the reasons for this is the lack of knowledge on the cellular mechanisms which cause alterations in nerve transmissions and the loss of memory in the initial stages of the disease.

Researchers from the Institute of Neuroscience at the Universitat Autònoma de Barcelona have discovered the cellular mechanism involved in memory consolidation and were able to develop a gene therapy which reverses the loss of memory in mice models with initial stages of Alzheimer’s disease. The therapy consists in injecting into the hippocampus - a region of the brain essential to memory processing - a gene which causes the production of a protein blocked in patients with Alzheimer’s, the “Crtc1” (CREB regulated transcription coactivator-1). The protein restored through gene therapy gives way to the signals needed to activate the genes involved in long-term memory consolidation.

To identify this protein, researchers compared gene expression in the hippocampus of healthy control mice with that of transgenic mice which had developed the disease. Through DNA microchips, they identified the genes (“transcriptome”) and the proteins (“proteome”) which expressed themselves in each of the mice in different phases of the disease. Researchers observed that the set of genes involved in memory consolidation coincided with the genes regulating Crtc1, a protein which also controls genes related to the metabolism of glucose and to cancer. The alteration of this group of genes could cause memory loss in the initial stages of Alzheimer’s disease.

In persons with the disease, the formation of amyloid plaque aggregates, a process known to cause the onset of Alzheimer’s disease, prevents the Crtc1 protein from functioning correctly. “When the Crtc1 protein is altered, the genes responsible for the synapsis or connections between neurons in the hippocampus cannot be activated and the individual cannot perform memory tasks correctly”, explains Carlos Saura, researcher of the UAB Institute of Neuroscience and head of the research. According to Saura, “this study opens up new perspectives on therapeutic prevention and treatment of Alzheimer’s disease, given that we have demonstrated that a gene therapy which activates the Crtc1 protein is effective in preventing the loss of memory in lab mice”.

The research, published today as a featured article in The Journal of Neuroscience, the official journal of the US Society of Neuroscience, paves the way for a new therapeutic approach to the disease. One of the main challenges in finding a treatment for the disease in the future is the research and development of pharmacological therapies capable of activating the Crtc1 protein, with the aim of preventing, slowing down or reverting cognitive alterations in patients.

Goodbye, Net Neutrality; Hello, Net Discrimination

newyorker:

image

Tim Wu on a new rule that violates Obama’s promise of net neutrality: http://nyr.kr/1jU2AQ2

“It threatens to make the Internet just like everything else in American society: unequal in a way that deeply threatens our long-term prosperity.”

Above: Obama at Coe College, in 2007. Photograph by David Lienemann/AP.

dynastylnoire:

alivesoul:

23-year-old fashion student Taj Patterson, a gay black male, was walking home in Ft. Greene, Brooklyn
He was mistaken for a car vandal and beaten senselessly by five hasidic jews who were a part of some neighborhood watch group. He has lost the vision in his right eye.
No one called police.
His alleged attackers Pinchas Braver, 19; Mayer Herskovic, 21; Joseph Fried, 25; Aharon Hollander, 28; and Abraham Winkler, 39 were indicted today on bevy of felony charges including gang assault.
I am hoping this brother gets justice.

BOOOOOOOOOOOOOOOOOOOOOOOOOOOOST

dynastylnoire:

alivesoul:

23-year-old fashion student Taj Patterson, a gay black male, was walking home in Ft. Greene, Brooklyn

He was mistaken for a car vandal and beaten senselessly by five hasidic jews who were a part of some neighborhood watch group. He has lost the vision in his right eye.

No one called police.

His alleged attackers Pinchas Braver, 19; Mayer Herskovic, 21; Joseph Fried, 25; Aharon Hollander, 28; and Abraham Winkler, 39 were indicted today on bevy of felony charges including gang assault.

I am hoping this brother gets justice.

BOOOOOOOOOOOOOOOOOOOOOOOOOOOOST