(via chiisana-ai)


lil-jawn:

Home Alone (1990, Comedy) Two burglars attempt to murder an abandoned 8-year-old child

(via tyleroakley)


ohnewty:

(via redlimez)


zainazahira:

kanyetaughtyou:

rosiesays:

Oppression is cooking being “women’s work,” while the overwhelming majority of top restaurant chefs are male.

Oppression is fashion being a “silly girl thing,” while the top earning designers and CEOs in fashion are male.

Oppression is reducing women to consumers profiting a male system, even in fields that we supposedly dominate.

!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Wow

(via catqueenbia)


sixpenceee:

sixpenceee:

perfect pictures for an imperfect world

im glad this is exploding. it’s one of the most powerful things on my blog. make it known worldwide guys. 

(via got7-bang10)


assortedtrolls:

lohgan:

This sums up my life pretty well

assortedtrolls:

lohgan:

This sums up my life pretty well

Error

(via got7-bang10)


On Asian “accents”

traumachu:

It started when I was in kindergarten, and I was so proud I did not have to go to Bingo class, unlike my friends, because I could speak good English -

although I had no idea what a yellow dog that could spell had anything to do with Chinese. 

(I figure out now that it was probably called Bilingual class)

I am lucky. I speak the fluent, accentless English of newscasters, the dialect spoken by the children of immigrants, that we learned not from our parents but rather from watching Sesame Street and other things on tv.

Last year, a white facebook friend of mine posted, “In order to celebrate Chinese New Year, me talk rike chinese man arr day.” 

And then told me that she was “sorry I was offended” and “she didn’t mean anything by it” when I (nicely, sweetly) told her that that shit was not okay. She said that she saw it the same as doing an accent, like Irish. Or British. Or Italian. (for bonus points, she even said that she has lots of Asian co-workers and friends, and LOVES Asian people, and so is not a racist.)

And when one of my white friends gets drunk, he thinks his “Asian accent” is hilarious.

And I was told by a coworker about the time my Asian coworker mispronounced “Barroway” as “Bwawwoway” and how hilarious it was.

Here’s the thing - can you guess how many Asian people I know who actually say

me rikey

me from _____

me so solly

(or, if you like, the fetishized versions: me so horny, me love you long time)

if you said ZERO, then ding ding ding! Congratulations, you have working brain cells.

No, my misguided fb friend, the “Asian accent” is not an actual imitation of an accent, comparable to your bad British/Irish/Italian - but rather a mockery of Asian people and their supposed inability to speak English. It is the perpetuation of the image of Asian people as perpetual foreigners in America.

Like that time when my family was at an Italian restaurant, and we were speaking to my father in Cantonese, and a drunken white lady said very loudly, “GOD when you come to this country at least learn the language!”

Or when my father was pulled over for speeding, and although he said “what’s the problem, officer?” the first thing the state trooper said was, “Do you speak English?”

Your fake “Asian accents” are not harmless and silly, because at the root of the joke, it says - you, you are stupid. You cannot speak English. You are Other. You do not belong.

my parents have been in this country for 30 years. They have been American citizens for 30 years.

And they are very self-conscious of their imperfect English, afraid that it makes them look ignorant, knowing that it marks them as immigrants. That, after 30 years, you can still be told (in not so many words) that you do not belong.

The Cultural Revolution started in China when my father was 13. He was pulled out of school and, later, sent to work in the fields. (He escaped to Hong Kong when he was 18, but that is another story for another time.)

When my father came to this country, he had a middle school education and did not speak a lick of English. He worked as a busboy at a Chinese restaurant, the evening shift that ran until 3 or 4 in the morning, and went to school during the day.

It took my father ten years to earn his bachelor’s degree. He is now an engineer.

Is this not your “American Dream?”

When my mother came to this country, she spoke very little English. She got a job as an entry level clerk. Over the years she earned one promotion after another. She is now management at a large federal agency, and manages funds for the whole state.

Is this not your “American Dream?”

And my father didn’t understand why his coworkers said, “flied lice, flied lice!” to him over and over and laughed.

And my father is still afraid to speak in a professional setting, even when he has ideas. 

And my mother still checks and double checks her professional e-mails with me, for fear of mockery from the same people she manages.

And people don’t understand why I can’t take a harmless joke. Why I don’t think that shit is funny.

No, I don’t “rikey.” 

No, I won’t “love you long time.”

And no, I’m not sorry.

So, please, kindly - FUCK OFF.

(via moriarty)


onlyalittlelion:

motherfuckingriverrun:

game of thrones will really surprise people next season when in the ninth episode they kill off actual viewers

image

(via cryingmanlytears)


stunningpicture:

They call him Bagel Jesus. He takes the old bagels from work and distributes them to the hungry on the street. GGG right here!

stunningpicture:

They call him Bagel Jesus. He takes the old bagels from work and distributes them to the hungry on the street. GGG right here!

(via kelkat9)


fredslastjoke:

Doctor Who Fest: day #3

↳ seasons [insp. x]

(via dryadalis)


lomonette:

sweatyscrotum:

I’m not like other girls!XD

image

I only have guy friends. I mean all girls do is start drama.image

Oh my god, i hate sluts! image

Other girls my age like to drink and party but i like to stay inside and read or watch netflix! I’m so weird. image

All the girls in my school care about is makeup and shopping and all i care about is FOOD and VIDEO GAMES. lol sometimes i think i was born a guy.image

This is everything.

(via dryadalis)


neurosciencestuff:

Compound protects brain cells after traumatic brain injury
A new class of compounds has now been shown to protect brain cells from the type of damage caused by blast-mediated traumatic brain injury (TBI). Mice that were treated with these compounds 24-36 hours after experiencing TBI from a blast injury were protected from the harmful effects of TBI, including problems with learning, memory, and movement.
Traumatic brain injury caused by blast injury has emerged as a common health problem among U.S. servicemen and women, with an estimated 10 to 20 percent of the more than 2 million U.S. soldiers deployed in Iraq or Afghanistan having experienced TBI. The condition is associated with many neurological complications, including cognitive and motor decline, as well as acquisition of psychiatric symptoms like anxiety and depression, and brain tissue abnormalities that resemble Alzheimer’s disease.
"The lack of neuroprotective treatments for traumatic brain injury is a serious problem in our society," says Andrew Pieper, senior study author and associate professor of psychiatry, neurology, and radiation oncology at the University of Iowa Carver College of Medicine. “Everyone involved in this work is motivated to find a way to offer hope for patients, which today include both military personnel and civilians, by establishing a basis for a new treatment to combat the deleterious neuropsychiatric outcomes after blast injury.”
It is known that TBI, as well as certain neurodegenerative diseases, damages axons—the tendril-like fibers that sprout from brains cells (neurons) and form the connections called synapses. In TBI, axon damage is followed by death of the neuron. The new study, published Sept. 11 in the journal Cell Reports, shows that a group of compounds, called the P7C3 series, blocks axon damage and preserves normal brain function following TBI.
Pieper led the team of scientists that discovered the P7C3 compound several years ago at UT Southwestern Medical Center. Subsequent studies showed that the root compound and its active analogs protect newborn neurons from cell death and also protect mature neurons in animal models of neurodegenerative diseases, including Parkinson’s disease and amyotrophic lateral sclerosis (ALS).
The researchers have also previously shown efficacy of P7C3 molecules in brain injury due to concussion, and plan to investigate whether these compounds might be applicable in stroke as well, given that there appear to be common factors mediating neuronal cell death in these conditions.
By tweaking the structure of the original P7C3 compound, Pieper and his colleagues Joseph Ready and Steven McKnight, at UT Southwestern Medical Center, have further improved its potency and drug-like properties. In the latest study, Pieper’s team at the UI Carver College of Medicine, including co-first authors graduate student Terry Yin, senior technician Jeremy Britt, and graduate student Hector De Jesus-Cortes, tested the neuroprotective effects of the newest version, (-)-P7C3-S243, which can be given orally, in mice with blast-induced TBI.
In the study, blast-induced TBI caused learning, memory, and movement problems in the mice, which resemble the problems experienced by people affected by TBI. The researchers found that (-)-P7C3-S243 prevented acute memory and learning impairment caused by TBI. The compound also prevented TBI-associated balance and coordination problems in mice exposed to blast-injury. By examining the brain tissue at a cellular level, the team also found that the protection afforded to brain functions after injury was matched by preservation of normal neuronal axon structure and synaptic neurotransmission.
Importantly, the compound still produced its protective effects even when treatment was delayed until 24 to 36 hours after the blast injury.
"Seeing protection even when the compound was given this long after injury was important because it represents a liberal window of time within which almost all patients would be expected to be able to access treatment after injury," Pieper says.
The team also found that learning, memory, and coordination problems caused by the TBI persisted in untreated mice at least eight months after the single injury occurred, suggesting that the compound actually prevented these problems rather simply speeding up a normal recovery process.
In a separate study led by Pieper’s colleagues McKnight and Ready at UT Southwestern, and also published on Sept. 11 in the journal Cell, the team has identified the biological mechanism by which P7C3 compounds act in the brain. The compounds activate the molecular pathway that preserves neuronal levels of an energy molecule known as nicotinamide adenine dinucleotide (NAD).
"Based on the well-established role of NAD in axonal degeneration, the ability of (-)-P7C3-S243 to protect mice after blast-mediated traumatic brain injury is likely related to preservation of NAD levels," Pieper explains. "Now that we understand the mechanism of action of the P7C3 class of compounds, we can see why they should have therapeutic utility in an unusually broad spectrum of neurodegenerative conditions, without impeding any of a number of other normal forms of cell death.
"Our ultimate goal is to facilitate development of a new class of neuroprotective drugs with wide applicability to treating patients with TBI and other currently untreatable forms of neurodegeneration," he adds.

neurosciencestuff:

Compound protects brain cells after traumatic brain injury

A new class of compounds has now been shown to protect brain cells from the type of damage caused by blast-mediated traumatic brain injury (TBI). Mice that were treated with these compounds 24-36 hours after experiencing TBI from a blast injury were protected from the harmful effects of TBI, including problems with learning, memory, and movement.

Traumatic brain injury caused by blast injury has emerged as a common health problem among U.S. servicemen and women, with an estimated 10 to 20 percent of the more than 2 million U.S. soldiers deployed in Iraq or Afghanistan having experienced TBI. The condition is associated with many neurological complications, including cognitive and motor decline, as well as acquisition of psychiatric symptoms like anxiety and depression, and brain tissue abnormalities that resemble Alzheimer’s disease.

"The lack of neuroprotective treatments for traumatic brain injury is a serious problem in our society," says Andrew Pieper, senior study author and associate professor of psychiatry, neurology, and radiation oncology at the University of Iowa Carver College of Medicine. “Everyone involved in this work is motivated to find a way to offer hope for patients, which today include both military personnel and civilians, by establishing a basis for a new treatment to combat the deleterious neuropsychiatric outcomes after blast injury.”

It is known that TBI, as well as certain neurodegenerative diseases, damages axons—the tendril-like fibers that sprout from brains cells (neurons) and form the connections called synapses. In TBI, axon damage is followed by death of the neuron. The new study, published Sept. 11 in the journal Cell Reports, shows that a group of compounds, called the P7C3 series, blocks axon damage and preserves normal brain function following TBI.

Pieper led the team of scientists that discovered the P7C3 compound several years ago at UT Southwestern Medical Center. Subsequent studies showed that the root compound and its active analogs protect newborn neurons from cell death and also protect mature neurons in animal models of neurodegenerative diseases, including Parkinson’s disease and amyotrophic lateral sclerosis (ALS).

The researchers have also previously shown efficacy of P7C3 molecules in brain injury due to concussion, and plan to investigate whether these compounds might be applicable in stroke as well, given that there appear to be common factors mediating neuronal cell death in these conditions.

By tweaking the structure of the original P7C3 compound, Pieper and his colleagues Joseph Ready and Steven McKnight, at UT Southwestern Medical Center, have further improved its potency and drug-like properties. In the latest study, Pieper’s team at the UI Carver College of Medicine, including co-first authors graduate student Terry Yin, senior technician Jeremy Britt, and graduate student Hector De Jesus-Cortes, tested the neuroprotective effects of the newest version, (-)-P7C3-S243, which can be given orally, in mice with blast-induced TBI.

In the study, blast-induced TBI caused learning, memory, and movement problems in the mice, which resemble the problems experienced by people affected by TBI. The researchers found that (-)-P7C3-S243 prevented acute memory and learning impairment caused by TBI. The compound also prevented TBI-associated balance and coordination problems in mice exposed to blast-injury. By examining the brain tissue at a cellular level, the team also found that the protection afforded to brain functions after injury was matched by preservation of normal neuronal axon structure and synaptic neurotransmission.

Importantly, the compound still produced its protective effects even when treatment was delayed until 24 to 36 hours after the blast injury.

"Seeing protection even when the compound was given this long after injury was important because it represents a liberal window of time within which almost all patients would be expected to be able to access treatment after injury," Pieper says.

The team also found that learning, memory, and coordination problems caused by the TBI persisted in untreated mice at least eight months after the single injury occurred, suggesting that the compound actually prevented these problems rather simply speeding up a normal recovery process.

In a separate study led by Pieper’s colleagues McKnight and Ready at UT Southwestern, and also published on Sept. 11 in the journal Cell, the team has identified the biological mechanism by which P7C3 compounds act in the brain. The compounds activate the molecular pathway that preserves neuronal levels of an energy molecule known as nicotinamide adenine dinucleotide (NAD).

"Based on the well-established role of NAD in axonal degeneration, the ability of (-)-P7C3-S243 to protect mice after blast-mediated traumatic brain injury is likely related to preservation of NAD levels," Pieper explains. "Now that we understand the mechanism of action of the P7C3 class of compounds, we can see why they should have therapeutic utility in an unusually broad spectrum of neurodegenerative conditions, without impeding any of a number of other normal forms of cell death.

"Our ultimate goal is to facilitate development of a new class of neuroprotective drugs with wide applicability to treating patients with TBI and other currently untreatable forms of neurodegeneration," he adds.

(via dryadalis)


YA Book: wHite yoUng girl!!!1!
YA Book: sHe is difFERenT!!!!!1!!@
YA Book: speciAL pOWer!!!-!!
YA Book: cute boY love HeR!!!
YA Book: bUTttttt
YA Book: anOTher boy alsO??? love heR?!?!??!!!
YA Book: HOw will sHe cHOOse!!?!?!?!?1!! aNd save wORld?????!?!!

nintendo6664:

death—420:

artist-refs:

nevver:

Undo the Damage of Sitting

(Technically, this isn’t about saving your hands… but if you draw, you’re probably doing a lot of sitting, so…)

image

image

image

(via redlimez)