whatsdifferentincanada:

Metric vs. Imperial

whatsdifferentincanada:

Metric vs. Imperial

mapsontheweb:

Syraq
Everyone Who Wants To Destroy ISIS Needs To Know One Hard Truth: 

Given the momentum that ISIS has built over the past two years in Syria and Iraq, it will be very difficult to dislodge them from the region. To actually do it will require a full-scale war.

mapsontheweb:

Syraq

Everyone Who Wants To Destroy ISIS Needs To Know One Hard Truth:

Given the momentum that ISIS has built over the past two years in Syria and Iraq, it will be very difficult to dislodge them from the region. To actually do it will require a full-scale war.

wtfevolution:

"Hey, evolution, you seem like you’re feeling better. That’s a pretty red bug you’re making there.”
"Oh, thanks. It’s a flatid leaf bug."
"I like the shape. And that’s a lovely shade of red."
"I picked it myself."
"That’s a weird fuzzy branch it’s crawling on, though, huh?"
"What? No. Those are the babies."
"I’m sorry?"
"Babies. Dozens of creepy, squirmy, waxy, fringy babies.”
"… you are so weird.”
Source: Flickr / christophandre / licensed under CC BY-NC-ND 2.0 (exposure adjusted from original)

wtfevolution:

"Hey, evolution, you seem like you’re feeling better. That’s a pretty red bug you’re making there.”

"Oh, thanks. It’s a flatid leaf bug."

"I like the shape. And that’s a lovely shade of red."

"I picked it myself."

"That’s a weird fuzzy branch it’s crawling on, though, huh?"

"What? No. Those are the babies."

"I’m sorry?"

"Babies. Dozens of creepy, squirmy, waxy, fringy babies.”

"… you are so weird.”

Source: Flickr / christophandre / licensed under CC BY-NC-ND 2.0 (exposure adjusted from original)

DNA methylation involved in Alzheimer's disease

neurosciencestuff:

A new study led by researchers at Brigham and Women’s Hospital (BWH) and Rush University Medical Center, reveals how early changes in brain DNA methylation are involved in Alzheimer’s disease. DNA methylation is a biochemical alteration of the building blocks of DNA and is one of the markers that…

(Source: eurekalert.org)

Epigenetic breakthrough bolsters understanding of Alzheimer’s disease

neurosciencestuff:

A team led by researchers at the University of Exeter Medical School and King’s College London has uncovered some of the strongest evidence yet that epigenetic changes in the brain play a role in Alzheimer’s disease.

image

Epigenetic changes affect the expression or activity of genes without…

(Source: exeter.ac.uk)

(via mydrunkkitchen)

thatcurlyhurdgirl:

I will reblog this everyday

(Source: milestellers, via ketocami)

thequeenandthephoenix:

kiichu:

shawtyimmaonlytellyouthisonce:

so i went on the american apparel site today

looking at the socks

and

image

image

image

image

image

image

for reference

here’s one of the pictures for men’s socks

image

seriously i’m not one to complain about sexism much but i just looked on this site and??

headwear

image

what

image

THE FUCK IS THIS???

image

????????

also BAGS AND WALLEtS???

male:

image

female:

image

????????????????????? I DON’T FUCKING GET IT????

"gendered marketing doesn’t exist!! shut up femenazi"

(via ketocami)

neurosciencestuff:

Researchers develop strategy to combat genetic ALS, FTD
A team of researchers at Mayo Clinic and The Scripps Research Institute in Florida have developed a new therapeutic strategy to combat the most common genetic risk factor for the neurodegenerative disorders amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) and frontotemporal dementia (FTD). In the Aug. 14 issue of Neuron, they also report discovery of a potential biomarker to track disease progression and the efficacy of therapies.
The scientists developed a small-molecule drug compound to prevent abnormal cellular processes caused by a mutation in the C9ORF72 gene. The findings come on the heels of previous discoveries by Mayo investigators that the C9ORF72 mutation produces an unusual repetitive genetic sequence that causes the buildup of abnormal RNA in brain cells and spinal cord.
While toxic protein clumps have long been implicated in neurodegeneration, this new strategy takes aim at abnormal RNA, which forms before toxic proteins in C9ORF72-related disorders (c9FTD/ALS). “Our study shows that toxic RNA produced in people with the c9FTD/ALS mutation is indeed a viable drug target,” says the study’s co-senior investigator, Leonard Petrucelli, Ph.D., a molecular neuroscientist at Mayo Clinic in Florida.
The compound, which was tested in cell culture models of c9FTD/ALS, bound to and blocked RNA’s ability to interact with other key proteins, thereby preventing the formation of toxic RNA clumps and “c9RAN proteins” that results from a process called repeat-associated non-ATG (RAN) translation.
The researchers also discovered that c9RAN proteins produced by the abnormal RNA can be measured in the spinal fluid of ALS patients. They are now evaluating whether these proteins are also present in spinal fluid of patients diagnosed with FTD. Although ALS primarily affects motor neurons leading to impaired mobility, speech, swallowing, and respiratory function and FTD affects brain regions that support higher cognitive function, some patients have symptoms of both disorders.
“Development of a readily accessible biomarker for the c9FTD/ALS mutation may aid not only diagnosis of these disorders and allow for tracking disease course in patients, but it could provide a more direct way to evaluate the response to experimental treatments,” says co-author Kevin Boylan, M.D., medical director of the Mayo Jacksonville ALS Center, the only ALS Certified Center of Excellence in Florida.
For example, a decrease in the levels of c9RAN proteins in response to treatment would suggest that a drug is having a desired effect. “The potential of this biomarker discovery is very exciting — even if we are in early days of development of such a test,” he says.
Since ALS is usually fatal two to five years after diagnosis and there is currently no effective treatment for FTD, these landmark findings offer the possibility of both improved diagnosis and treatment for up to 40 percent of all patients with familial (inherited) ALS and up to 25 percent of patients with familial FTD, says Dr. Boylan.
“One of the most exciting aspects of these studies has, in my opinion, been the seamless collaboration of our Florida biosciences institutes — Scripps and Mayo. Our collective biological and chemical expertise made this research possible,” says the other co-senior investigator, Mathew Disney, Ph.D., a professor of chemistry at Scripps Florida.
Dr. Disney and his group studied the structure of the RNA that resulted from the C9ORF72 mutation, and then designed the lead small-molecules. The Mayo team developed the patient-derived cell models to test the compounds in. Both teams then worked together to show that the lead agent’s mode of action was targeting the toxic RNA.

neurosciencestuff:

Researchers develop strategy to combat genetic ALS, FTD

A team of researchers at Mayo Clinic and The Scripps Research Institute in Florida have developed a new therapeutic strategy to combat the most common genetic risk factor for the neurodegenerative disorders amyotrophic lateral sclerosis (ALS or Lou Gehrig’s disease) and frontotemporal dementia (FTD). In the Aug. 14 issue of Neuron, they also report discovery of a potential biomarker to track disease progression and the efficacy of therapies.

The scientists developed a small-molecule drug compound to prevent abnormal cellular processes caused by a mutation in the C9ORF72 gene. The findings come on the heels of previous discoveries by Mayo investigators that the C9ORF72 mutation produces an unusual repetitive genetic sequence that causes the buildup of abnormal RNA in brain cells and spinal cord.

While toxic protein clumps have long been implicated in neurodegeneration, this new strategy takes aim at abnormal RNA, which forms before toxic proteins in C9ORF72-related disorders (c9FTD/ALS). “Our study shows that toxic RNA produced in people with the c9FTD/ALS mutation is indeed a viable drug target,” says the study’s co-senior investigator, Leonard Petrucelli, Ph.D., a molecular neuroscientist at Mayo Clinic in Florida.

The compound, which was tested in cell culture models of c9FTD/ALS, bound to and blocked RNA’s ability to interact with other key proteins, thereby preventing the formation of toxic RNA clumps and “c9RAN proteins” that results from a process called repeat-associated non-ATG (RAN) translation.

The researchers also discovered that c9RAN proteins produced by the abnormal RNA can be measured in the spinal fluid of ALS patients. They are now evaluating whether these proteins are also present in spinal fluid of patients diagnosed with FTD. Although ALS primarily affects motor neurons leading to impaired mobility, speech, swallowing, and respiratory function and FTD affects brain regions that support higher cognitive function, some patients have symptoms of both disorders.

“Development of a readily accessible biomarker for the c9FTD/ALS mutation may aid not only diagnosis of these disorders and allow for tracking disease course in patients, but it could provide a more direct way to evaluate the response to experimental treatments,” says co-author Kevin Boylan, M.D., medical director of the Mayo Jacksonville ALS Center, the only ALS Certified Center of Excellence in Florida.

For example, a decrease in the levels of c9RAN proteins in response to treatment would suggest that a drug is having a desired effect. “The potential of this biomarker discovery is very exciting — even if we are in early days of development of such a test,” he says.

Since ALS is usually fatal two to five years after diagnosis and there is currently no effective treatment for FTD, these landmark findings offer the possibility of both improved diagnosis and treatment for up to 40 percent of all patients with familial (inherited) ALS and up to 25 percent of patients with familial FTD, says Dr. Boylan.

“One of the most exciting aspects of these studies has, in my opinion, been the seamless collaboration of our Florida biosciences institutes — Scripps and Mayo. Our collective biological and chemical expertise made this research possible,” says the other co-senior investigator, Mathew Disney, Ph.D., a professor of chemistry at Scripps Florida.

Dr. Disney and his group studied the structure of the RNA that resulted from the C9ORF72 mutation, and then designed the lead small-molecules. The Mayo team developed the patient-derived cell models to test the compounds in. Both teams then worked together to show that the lead agent’s mode of action was targeting the toxic RNA.

A little bit nerdy, occasionally geeky, mildly funny, endeavouring to be kind, but slipping into sarcasm.