Honestly I don’t understand how people don’t get this aro/ace thing.
-It’s an orientation
-It’s discriminated against by straight people (and everyone else tbh…)
-It’s faced systematic oppression (I mean it was categorized as a mental disorder until… 2013 I believe was when DSM-V came out? Plus lots of other things although I’m too lazy to look up sources atm)
-People who have this orientation suffer under heteronormativity
-Much like any other orientation that isn’t straight it requires constant coming out and dealing with backlash
-There’s more but I’m tired
But somehow we’re evil parasites invading the LGBT+ community. I literally just saw a person saying they wished allies would “reclaim the A”. The LGBT+ community would rather have straight people than aro/ace people? What the fuck. Also, as a queer aro/ace spec person can I just say that NO, het aro/aces are not any more evil than otherwise LGBT+ aro/aces.
Please stop gatekeeping and bullying and making death threats. The LGBT+ community is supposed to be a community for those oppressed and discriminated against because of their romantic/sexual orientations and/or their gender. We fit under that category. We’re a part of the community, like it or not.
So I’ve been having a really frustrating argument with an anti-vaxxer on Twitter tonight, and one of the super frustrating (but also transparent, once you know it’s coming, and it’s always coming) things that anti-vaxxers do is this particular variety of goalpost-moving where, once you assert the evidence that [mercury, aluminum, whatever] doesn’t cause autism, they’ll be like “but other thing! causes other brain injury! devastating effects on the nervous system!”
And, yeah, dude, it sure does.
But that stuff isn’t autism. B12 deficiency causes varieties of neurological deterioration that can closely mimic dementia or severe depression. Folate deficiency causes spina bifida. Mercury poisoning causes, well, mercury poisoning, but we know what mercury poisoning looks like, and it isn’t autism.
None of those things are autism. Those are different neurological disabilities, and we pretty much know what causes them, and the fact that those things do cause neurological disability does not mean they cause autism, because everything isn’t autism.
I can’t believe I have to say this, but apparently I do. Not all neurological disabilities are autism. Autism comprises a pretty distinctive set of features, and not only have many of those features been described incredibly consistently since something like autism was first specifically identified, but autistic people across the spectrum report certain incredibly similar experiences even when our superficial presentations look almost nothing alike.
And it’s super frustrating when anti-vaxxers do this, and yes, it proves they don’t really know the first fracking thing about autism, not that you will ever convince them of that.
But you know what? There’s a reason why this works so well, and I absolutely hold partially culpable every doctor, every therapist, and every fucking mouse researcher who has catastrophized autism as a condition only of the worst kinds of deficits or extreme or unsocial behavior, or conflated autism with any and all inability, or sidelined autistic people’s own reports of sensorimotor, language, and processing differences in favor of pet theories.
Part of the reason why this shit is so convincing to scared parents is because actual professionals use remarkably similar language about autism.
The quacks are just managing to say more effectively to certain parents your real child was damaged, and it’s not your fault, it was the evil government/vaccine manufacturers.
But it has absolutely been the real doctors and researchers and ABA therapists, not the utter quacks, who set the stage for this to work, and who still are. And I have had it.
note: if you have any questions please feel free to leave a message in my ask! sorry for the time skips, there’s more than usual. enjoy.
You couldn’t help but think about every one of Taehyung’s moves. You could remember that conversation forever; the grass dewy from rain droplets and the golden sunset that made his profile glow. His eyes stared off towards the horizon, slowly drifting away as he continued to explain his life dreams. Staring into his flawless visual, and wished you could sit there for the rest of your life. You fell into a trance, not responding to his question. He turned and saw your stare, and was immediately filled with satisfaction. You could even imagine his boxy smile, almost every detail of his face.
The Party Tour has come to an end, each show to seem to have its own special quality. I’m so proud to be a fan of someone who puts his all in his work and pleases his fans. As I stated earlier, here are my fave looks from the tour. What are yours?
1. Juun J Hooded Oversized Coat with Bape Combat Boots
2. Vintage Jeff Hamilton Mickey Mouse Jacket (do your research, Jeff is the GOAT)
3. Custom Black Pyramid Flight Suit/Jumpsuit/Romper
Expression of combinations of three different fluorescent proteins in a mouse brain produced ten different colored neurons. Individual neurons in a mouse brain appear in different colors in a fluorescence microscope. This “Brainbow” method enables many distinct cells within a brain circuit to be viewed at one time.
WHAT IS IT? The hippocampus is found deep in the brains of many mammals, including humans. It’s named for its seahorse shape (in Greek, hippokampos literally means “horse sea monster”).
WHY IS IT IMPORTANT? It helps us form memories and navigate space. It contains special cells called “place cells” that create a mental map of our environment. The hippocampus is also one of the first structures to suffer in patients with Alzheimer’s disease, which is characterized by memory loss. The number of patients with Alzheimer’s is predicted to triple by 2050.
WHERE DO WE GO FROM HERE? Scientists at Harvard Medical School were recently able to re-create Alzheimer’s disease from human cells in a culture dish. This will “revolutionize drug discovery in terms of speed, costs and [disease relevance],” according to a senior co-author on the study.
Image by Chris Henstridge/MTA-KOKI/Nikon Small World.
I’m coming up on the end of my reporting cycle for professional credits, which means a bunch of data entry, and a tired me drinking lots of tea and hiding my hair under my new favourite knitted scarf. On the plus side, I made a felted mouse for my friend who just earned his PhD.
Every user moves the mouse in a unique way. If you can observe those movements in enough pages the user visits outside of Tor, you can create a unique fingerprint for that user. Then you can identify him inside of Tor, based on how he or she uses the mouse.
Lily is an African Soft Furred Rat, also known as a multimammate mouse. I have researched them and several months ago, I sought one out for Bengal. I have seen both ASF pet breeders and feeder breeders keep them with fancy. Females apparently make great companions for males, as they act like a female mouse, but cannot get pregnant as they are not the same species.
I was not able to find any breeders, so I have up on it. But a few weeks ago, Lisa called me from Virginia and said she had bought me a female ASF. There was only one left in the store and Lisa got her!
She is extremely soft, as the name implies. However, she is not at all tame and very skittish. She is very very slowly coming around. These guys seem to act more like gerbils than mice. She will happily throw herself out of my hand when she is scared, which a mouse will almost never do.
She does however, LOVE Bengal, and he loves her! I cannot believe how well they get along. I had wanted a friend for Bengal since before I got Dallas neutered. But nearing the age of two, I couldn’t bear to put him through it. So we have the next best solution. Lily seems much happier than being a feeder too.
How Huntington’s Disease Protein Could Cause Death of Neurons
Scientists at the University of Pittsburgh School of Medicine have identified for the first time a key molecular mechanism by which the abnormal protein found in Huntington’s disease can cause brain cell death. The results of these studies, published today in Nature Neuroscience, could one day lead to ways to prevent the progressive neurological deterioration that characterizes the condition.
Huntington’s disease patients inherit from a parent a gene that contains too many repeats of a certain DNA sequence, which results in the production of an abnormal form of a protein called huntingtin (HTT), explained senior investigator Robert Friedlander, M.D., UPMC Professor of Neurosurgery and Neurobiology and chair, Department of Neurological Surgery, Pitt School of Medicine. But until now, studies have not suggested how HTT could cause disease.
“This study connects the dots for the first time and shows how huntingtin can cause problems for the mitochondria that lead to the death of neurons,” Dr. Friedlander said. “If we can disrupt the pathway, we may be able to identify new treatments for this devastating disease.”
Examination of brain tissue samples from both mice and human patients affected by Huntington’s disease showed that mutant HTT collects in the mitochondria, which are the energy suppliers of the cell. Using several biochemical approaches in follow-up mouse studies, the research team identified the mitochondrial proteins that bind to mutant HTT, noting its particular affinity for TIM23, a protein complex that transports other proteins from the rest of the cell into the mitochondria.
Further investigation revealed that mutant HTT inhibited TIM23’s ability to transport proteins across the mitochondrial membrane, slowing metabolic activity and ultimately triggering cell-suicide pathways. The team also found that mutant HTT-induced mitochondrial dysfunction occurred more often near the synapses, or junctions, of neurons, likely impairing the neuron’s ability to communicate or signal its neighbors.
To verify the findings, the researchers showed that producing more TIM23 could overcome the protein transport deficiency and prevent cell death.
“We learned also that these events occur very early in the disease process, not as the result of some other mutant HTT-induced changes,” Dr. Friedlander said. “This means that if we can find ways to intervene at this point, we may be able to prevent neurological damage.”
The team’s next steps include identifying exact binding sites and agents that can influence the interactions of HTT and TIM23.