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Home country: USA
Current location: Georgia
Member since: Tue Feb 10, 2004, 01:08 PM
Number of posts: 43,390

About Me

Environmental Scientist

Journal Archives

Sunday's Pearls Before Swine Toon

Sunday's Non Sequitur Toon- New Invention

Weekend Toon Roundup 2: The Rest








Weekend Toon Roundup 1 Virus or Dung Beetle?

Trump calling Hillary Clinton a bigot is the tactic of a 5-year-old

By David Horsey
Donald Trump has said many crazy things, some quite entertaining, many wildly fantastical and incendiary. Now he may have outdone himself with his charge that Hillary Clinton is a bigot.

Even people who oppose Clinton and loathe her political views — maybe even those who believe that she is corrupt and think she should be “locked up” — would have a hard time agreeing that she is a bigot. Perhaps Trump does not know what the word actually means. Given his record and the company he keeps, he should.

Back in the early 1970s, around the same time a young Clinton was going undercover in Alabama to expose discrimination against black children in segregated academies, a young Trump and his father were sued by the Nixon Justice Department for blatant discrimination against blacks in Trump-owned rental housing. In a CNN interview Thursday, Trump misrepresented the nature of that suit and how it was settled. He claimed that the resolution of the case proved there had been no wrongdoing. The record, however, shows that the Trumps were required to take remedial actions and were later sued again when they failed to follow through.

Trump bends reality to put himself in a better light on a near daily basis, so it is no surprise when he revises his own history. His charge that Clinton is a bigot is yet another attempt to twist facts after being stung by allegations that he is empowering real bigots.


Friday TOON Roundup 3 - The Rest









Friday TOON Roundup 2 - Blood Suckers

Friday TOON Roundup 1 - Mr Flip Flop

How do antidepressants trigger fear and anxiety?

More than 100 million people worldwide take selective serotonin reuptake inhibitors (SSRIs), such as Prozac and Zoloft, to treat depression, anxiety and related conditions, but these drugs have a common and mysterious side effect: they can worsen anxiety in the first few weeks of use, which leads many patients to stop treatment. Scientists at the University of North Carolina (UNC) School of Medicine have mapped out a serotonin-driven anxiety circuit that may explain this side effect and lead to treatments to eliminate it.

“The hope is that we’ll be able to identify a drug that inhibits this circuit and that people could take for just the first few weeks of SSRI use to get over that hump,” said senior investigator Thomas L. Kash, PhD, the John Andrews Distinguished Professor of Alcohol Studies in the UNC School of Medicine’s department of pharmacology. “More generally, this finding gives us a deeper understanding of the brain networks that drive anxiety and fear behavior in mammals.”

The new study, published in Nature, counters the popular view of serotonin as a neurotransmitter that promotes only good feelings. SSRIs, which are taken by about one in 10 people in the United States and about one in four women in their 40s and 50s, are thought to improve mood by boosting serotonin activity in the brain. There are brain circuits through which serotonin does seem to improve mood, and some studies have linked depression to abnormally low levels of serotonin. But the short-lived promotion of anxiety in many patients on SSRIs – even suicidal thinking, particularly in younger people – has long hinted that serotonin can have negative effects on mood, depending on the precise brain circuit where it acts.


Scientists have finally figured out how cancer spreads through the bloodstream


In what could be a major step forward in our understanding of how cancer moves around the body, researchers have observed the spread of cancer cells from the initial tumour to the bloodstream.

The findings suggest that secondary growths called metastases 'punch' their way through the walls of small blood vessels by targeting a molecule known as Death Receptor 6 (no, really, that's what it's called). This then sets off a self-destruct process in the blood vessels, allowing the cancer to spread.

According to the team from Goethe University Frankfurt and the Max Planck Institute in Germany, disabling Death Receptor 6 (DR6) may effectively block the spread of cancerous cells - so long as there aren't alternative ways for the cancer to access the bloodstream.

"This mechanism could be a promising starting point for treatments to prevent the formation of metastases," said lead researcher Stefan Offermanns.

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