(Source: radiofort, via tiny-little-dot)

ucsdhealthsciences:

Breaking Bad MitochondriaMechanism helps explain persistence of hepatitis C virus
Researchers at the University of California, San Diego School of Medicine have identified a mechanism that explains why people with the hepatitis C virus get liver disease and why the virus is able to persist in the body for so long.
The hard-to-kill pathogen, which infects an estimated 200 million people worldwide, attacks the liver cells’ energy centers – the mitochondria – dismantling the cell’s innate ability to fight infection. It does this by altering cells mitochondrial dynamics.
The study, published in today’s issue of the Proceedings of the National Academy of Sciences, suggests that mitochondrial operations could be a therapeutic target against hepatitis C, the leading cause of liver transplants and a major cause of liver cancer in the U.S.
“Our study tells us the story of how the hepatitis C virus causes liver disease,” said Aleem Siddiqui, PhD, professor of medicine and senior author. “The virus damages mitochondria in liver cells. Cells recognize the damage and respond to it by recruiting proteins that tell the mitochondria to eliminate the damaged area, but the repair process ends up helping the virus.”
Mitochondria are organelles in a cell that convert energy from food (glucose) into a form of energy that can be used by cells called adenosine triphosphate.
Specifically, the researchers discovered that the virus stimulates the production of a protein (Drp 1) that induces viral-damaged mitochondria to undergo asymmetric fragmentation. This fragmentation (fission) results in the formation of one healthy mitochondrion and one damaged or bad mitochondrion, the latter of which is quickly broken down (catabolized) and dissolved in the cell’s cytoplasm.
More here
Pictured: Mitochondria in hepatitis C-infected cells (bottom row) are self-destructing. The self-annihilation process explains the persistance and virulence of the virus in human liver cells.

ucsdhealthsciences:

Breaking Bad Mitochondria
Mechanism helps explain persistence of hepatitis C virus

Researchers at the University of California, San Diego School of Medicine have identified a mechanism that explains why people with the hepatitis C virus get liver disease and why the virus is able to persist in the body for so long.

The hard-to-kill pathogen, which infects an estimated 200 million people worldwide, attacks the liver cells’ energy centers – the mitochondria – dismantling the cell’s innate ability to fight infection. It does this by altering cells mitochondrial dynamics.

The study, published in today’s issue of the Proceedings of the National Academy of Sciences, suggests that mitochondrial operations could be a therapeutic target against hepatitis C, the leading cause of liver transplants and a major cause of liver cancer in the U.S.

“Our study tells us the story of how the hepatitis C virus causes liver disease,” said Aleem Siddiqui, PhD, professor of medicine and senior author. “The virus damages mitochondria in liver cells. Cells recognize the damage and respond to it by recruiting proteins that tell the mitochondria to eliminate the damaged area, but the repair process ends up helping the virus.”

Mitochondria are organelles in a cell that convert energy from food (glucose) into a form of energy that can be used by cells called adenosine triphosphate.

Specifically, the researchers discovered that the virus stimulates the production of a protein (Drp 1) that induces viral-damaged mitochondria to undergo asymmetric fragmentation. This fragmentation (fission) results in the formation of one healthy mitochondrion and one damaged or bad mitochondrion, the latter of which is quickly broken down (catabolized) and dissolved in the cell’s cytoplasm.

More here

Pictured: Mitochondria in hepatitis C-infected cells (bottom row) are self-destructing. The self-annihilation process explains the persistance and virulence of the virus in human liver cells.

(via currentsinbiology)

passionatedancing:

Rudolf Nureyev and Margot Fonteyn

(via yoiness)

this is what my nightmares are made of

(Source: sweetestpotatoes, via liamdryden)

nevver:
“Nothing is funnier than unhappiness.” ― Samuel Beckett

nevver:

“Nothing is funnier than unhappiness.” ― Samuel Beckett

(via yoiness)

our-lady-of-perpetual-misandry:

celestia:

once i had a dream that my cat was working at mcdonalds w/ me and she had a lil uniform and she kept getting fur in the fries and everyone was yelling at me and saying “ur cat sucks on fries” and i was like “shes just a cat give her a break!” and i woke up crying

attn: abbey

aseaofquotes:

Jean-Paul Sartre, Nausea

aseaofquotes:

Jean-Paul Sartre, Nausea

(via cutthroatchorus)

tiny-little-dot:

falseloki:

shootingstarsafterdark:

ChaosLife - Homo Hint

With comments too great not to include. You should check the heck out of that webcomic series either way 8D

Don’t forget, being Genderqueer I had Gerry the Genderqueer giraffe visit me!

gerry’s sweet but daaaamn i had to crane my neck.

(via lacigreen)

currentsinbiology:

A lengthy but informative article…
What the Tamiflu saga tells us about drug trials and big pharma (The Guardian)
Today we found out that Tamiflu doesn’t work so well after all. Roche, the drug company behind it, withheld vital information on its clinical trials for half a decade, but the Cochrane Collaboration, a global not-for-profit organisation of 14,000 academics, finally obtained all the information. Putting the evidence together, it has found that Tamiflu has little or no impact on complications of flu infection, such as pneumonia.
That is a scandal because the UK government spent £0.5bn stockpiling this drug in the hope that it would help prevent serious side-effects from flu infection. But the bigger scandal is that Roche broke no law by withholding vital information on how well its drug works. In fact, the methods and results of clinical trials on the drugs we use today are still routinely and legally being withheld from doctors, researchers and patients. It is simple bad luck for Roche that Tamiflu became, arbitrarily, the poster child for the missing-data story…
…. So does Tamiflu work? From the Cochrane analysis – fully public – Tamiflu does not reduce the number of hospitalisations. There wasn’t enough data to see if it reduces the number of deaths. It does reduce the number of self-reported, unverified cases of pneumonia, but when you look at the five trials with a detailed diagnostic form for pneumonia, there is no significant benefit. It might help prevent flu symptoms, but not asymptomatic spread, and the evidence here is mixed. It will take a few hours off the duration of your flu symptoms. But all this comes at a significant cost of side-effects. Since percentages are hard to visualise, we can make those numbers more tangible by taking the figures from the Cochrane review, and applying them. For example, if a million people take Tamiflu in a pandemic, 45,000 will experience vomiting, 31,000 will experience headache and 11,000 will have psychiatric side-effects. Remember, though, that those figures all assume we are only giving Tamiflu to a million people: if things kick off, we have stockpiled enough for 80% of the population. That’s quite a lot of vomit.
Star anise provides the principal component of Tamiflu. Photograph: Adrian Bradshaw/EPA

currentsinbiology:

A lengthy but informative article…

What the Tamiflu saga tells us about drug trials and big pharma (The Guardian)

Today we found out that Tamiflu doesn’t work so well after all. Roche, the drug company behind it, withheld vital information on its clinical trials for half a decade, but the Cochrane Collaboration, a global not-for-profit organisation of 14,000 academics, finally obtained all the information. Putting the evidence together, it has found that Tamiflu has little or no impact on complications of flu infection, such as pneumonia.

That is a scandal because the UK government spent £0.5bn stockpiling this drug in the hope that it would help prevent serious side-effects from flu infection. But the bigger scandal is that Roche broke no law by withholding vital information on how well its drug works. In fact, the methods and results of clinical trials on the drugs we use today are still routinely and legally being withheld from doctors, researchers and patients. It is simple bad luck for Roche that Tamiflu became, arbitrarily, the poster child for the missing-data story…

…. So does Tamiflu work? From the Cochrane analysis – fully public – Tamiflu does not reduce the number of hospitalisations. There wasn’t enough data to see if it reduces the number of deaths. It does reduce the number of self-reported, unverified cases of pneumonia, but when you look at the five trials with a detailed diagnostic form for pneumonia, there is no significant benefit. It might help prevent flu symptoms, but not asymptomatic spread, and the evidence here is mixed. It will take a few hours off the duration of your flu symptoms. But all this comes at a significant cost of side-effects. Since percentages are hard to visualise, we can make those numbers more tangible by taking the figures from the Cochrane review, and applying them. For example, if a million people take Tamiflu in a pandemic, 45,000 will experience vomiting, 31,000 will experience headache and 11,000 will have psychiatric side-effects. Remember, though, that those figures all assume we are only giving Tamiflu to a million people: if things kick off, we have stockpiled enough for 80% of the population. That’s quite a lot of vomit.

Star anise provides the principal component of Tamiflu. Photograph: Adrian Bradshaw/EPA