Science and logic



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Reblogged from brains-and-bodies
brains-and-bodies:

From Daily Anatomy



"This is where the sperms get produced: Cross section of a human testis tubule filled with sperm." (assuming they mean the seminiferous tubules?


Scanning electron micrograph, magnification x363.By Richard Kessel

http://www.visualsunlimited.com/image/I0000ab2NgqXhXOQ
http://en.wikipedia.org/wiki/Seminiferous_tubule

brains-and-bodies:

From Daily Anatomy

"This is where the sperms get produced: Cross section of a human testis tubule filled with sperm." (assuming they mean the seminiferous tubules?

Scanning electron micrograph, magnification x363.
By Richard Kessel

(via afro-dominicano)

Reblogged from sixpenceee

yosuke-rolling-in-a-trash-can:

rainamermaid:

memewhore:

sean3116:

sixpenceee:

As someone who wants to study the human consciousness I found this very interesting.

Scott Routley was a “vegetable”. A car accident seriously injured both sides of his brain, and for 12 years, he was completely unresponsive.

Unable to speak or track people with his eyes, it seemed that Routley was unaware of his surroundings, and doctors assumed he was lost in limbo. They were wrong.

In 2012, Professor Adrian Owen decided to run tests on comatose patients like Scott Routley. Curious if some “vegetables” were actually conscious, Owen put Routley in an fMRI and told him to imagine walking through his home. Suddenly, the brain scan showed activity. Routley not only heard Owen, he was responding.

Next, the two worked out a code. Owen asked a series of “yes or no” questions, and if the answer was “yes,” Routley thought about walking around his house. If the answer was “no,” Routley thought about playing tennis.

These different actions showed activity different parts of the brain. Owen started off with easy questions like, “Is the sky blue?” However, they changed medical science when Owen asked, “Are you in pain?” and Routley answered, “No.” It was the first time a comatose patient with serious brain damage had let doctors know about his condition.

While Scott Routley is still trapped in his body, he finally has a way to reach out to the people around him. This finding has huge implications.

SOURCE

HOLY STEAMING SHITFUCKS

WHY IS EVERYONE NOT LOSING THEIR SHIT ABOUT THIS

What a fucking nightmare, just kill me.

I know a girl who was hit by a drunk driver and in that state for a year. When she woke up the first thing she did was tell off the doctor who tried to convince her mom to pull the plug. She heard *everything* while being called brain dead.

OH MY FUCK

(via they-chose-family)

Reblogged from jarabacek
i-made-my-choice-a-long-time-ago:

songofages:

bobeestinger:

muchymozzarella:

thefingerfuckingfemalefury:

^ TRUTH
Seriously, whenever I use a flip phone the first thing I always think of is Star Trek :D

NO 
THIS SHIT AIN’T RIGHT
STAR TREK DIDN’T PREDICT THE FUTURE FOOL
IT CREATED THE FUTURE
IT INSPIRED THE FUTURE
THE REASON THESE THINGS EXIST IS BECAUSE STAR TREK MADE PEOPLE WANT THEM TO HAPPEN
STAR TREK IS THE FUTURE

Dont forget about automatic doors

People are currently trying to make tricorders  as well. So far it can monitor heart functions.

oh an hyposprays are in the works, too

i-made-my-choice-a-long-time-ago:

songofages:

bobeestinger:

muchymozzarella:

thefingerfuckingfemalefury:

^ TRUTH

Seriously, whenever I use a flip phone the first thing I always think of is Star Trek :D

NO 

THIS SHIT AIN’T RIGHT

STAR TREK DIDN’T PREDICT THE FUTURE FOOL

IT CREATED THE FUTURE

IT INSPIRED THE FUTURE

THE REASON THESE THINGS EXIST IS BECAUSE STAR TREK MADE PEOPLE WANT THEM TO HAPPEN

STAR TREK IS THE FUTURE

Dont forget about automatic doors

People are currently trying to make tricorders  as well. So far it can monitor heart functions.

oh an hyposprays are in the works, too

(Source: jarabacek, via emomlaren)

Reblogged from meredithalden

kyunomahou:

whatfulllipsyouhave:

meredithalden:

a public service announcement

I still don’t understand why none of my art teachers ever told us this.

THANK YOU!

(via illuminanze)

Reblogged from wildcat2030
wildcat2030:

Evolution’s Random Paths Lead to One Place - A massive statistical study suggests that the final evolutionary outcome — fitness — is predictable. - In his fourth-floor lab at Harvard University, Michael Desai has created hundreds of identical worlds in order to watch evolution at work. Each of his meticulously controlled environments is home to a separate strain of baker’s yeast. Every 12 hours, Desai’s robot assistants pluck out the fastest-growing yeast in each world — selecting the fittest to live on — and discard the rest. Desai then monitors the strains as they evolve over the course of 500 generations. His experiment, which other scientists say is unprecedented in scale, seeks to gain insight into a question that has long bedeviled biologists: If we could start the world over again, would life evolve the same way? Many biologists argue that it would not, that chance mutations early in the evolutionary journey of a species will profoundly influence its fate. “If you replay the tape of life, you might have one initial mutation that takes you in a totally different direction,” Desai said, paraphrasing an idea first put forth by the biologist Stephen Jay Gould in the 1980s. Desai’s yeast cells call this belief into question. According to results published in Science in June, all of Desai’s yeast varieties arrived at roughly the same evolutionary endpoint (as measured by their ability to grow under specific lab conditions) regardless of which precise genetic path each strain took. It’s as if 100 New York City taxis agreed to take separate highways in a race to the Pacific Ocean, and 50 hours later they all converged at the Santa Monica pier. The findings also suggest a disconnect between evolution at the genetic level and at the level of the whole organism. Genetic mutations occur mostly at random, yet the sum of these aimless changes somehow creates a predictable pattern. The distinction could prove valuable, as much genetics research has focused on the impact of mutations in individual genes. For example, researchers often ask how a single mutation might affect a microbe’s tolerance for toxins, or a human’s risk for a disease. But if Desai’s findings hold true in other organisms, they could suggest that it’s equally important to examine how large numbers of individual genetic changes work in concert over time. “There’s a kind of tension in evolutionary biology between thinking about individual genes and the potential for evolution to change the whole organism,” said Michael Travisano, a biologist at the University of Minnesota. “All of biology has been focused on the importance of individual genes for the last 30 years, but the big take-home message of this study is that’s not necessarily important.” (via Yeast Study Suggests Genetics Are Random but Evolution Is Not | Simons Foundation)

wildcat2030:

Evolution’s Random Paths Lead to One Place
-
A massive statistical study suggests that the final evolutionary outcome — fitness — is predictable.
-
In his fourth-floor lab at Harvard University, Michael Desai has created hundreds of identical worlds in order to watch evolution at work. Each of his meticulously controlled environments is home to a separate strain of baker’s yeast. Every 12 hours, Desai’s robot assistants pluck out the fastest-growing yeast in each world — selecting the fittest to live on — and discard the rest. Desai then monitors the strains as they evolve over the course of 500 generations. His experiment, which other scientists say is unprecedented in scale, seeks to gain insight into a question that has long bedeviled biologists: If we could start the world over again, would life evolve the same way? Many biologists argue that it would not, that chance mutations early in the evolutionary journey of a species will profoundly influence its fate. “If you replay the tape of life, you might have one initial mutation that takes you in a totally different direction,” Desai said, paraphrasing an idea first put forth by the biologist Stephen Jay Gould in the 1980s. Desai’s yeast cells call this belief into question. According to results published in Science in June, all of Desai’s yeast varieties arrived at roughly the same evolutionary endpoint (as measured by their ability to grow under specific lab conditions) regardless of which precise genetic path each strain took. It’s as if 100 New York City taxis agreed to take separate highways in a race to the Pacific Ocean, and 50 hours later they all converged at the Santa Monica pier. The findings also suggest a disconnect between evolution at the genetic level and at the level of the whole organism. Genetic mutations occur mostly at random, yet the sum of these aimless changes somehow creates a predictable pattern. The distinction could prove valuable, as much genetics research has focused on the impact of mutations in individual genes. For example, researchers often ask how a single mutation might affect a microbe’s tolerance for toxins, or a human’s risk for a disease. But if Desai’s findings hold true in other organisms, they could suggest that it’s equally important to examine how large numbers of individual genetic changes work in concert over time. “There’s a kind of tension in evolutionary biology between thinking about individual genes and the potential for evolution to change the whole organism,” said Michael Travisano, a biologist at the University of Minnesota. “All of biology has been focused on the importance of individual genes for the last 30 years, but the big take-home message of this study is that’s not necessarily important.” (via Yeast Study Suggests Genetics Are Random but Evolution Is Not | Simons Foundation)

(via scinerds)

Reblogged from natskep
Reblogged from whats-out-there
The fossil record implies trial and error, the inability to anticipate the future - features inconsistent with a Great Designer. Carl Sagan, Cosmos (via whats-out-there)

(via eclecticdreamweaver)

Humans with autism often show a reduced frequency of social interactions and an increased tendency to engage in repetitive solitary behaviors. Autism has also been linked to dysfunction of the amygdala, a brain structure involved in processing emotions. Now Caltech researchers have discovered antagonistic neuron populations in the mouse amygdala that control whether the animal engages in social behaviors or asocial repetitive self-grooming. This discovery may have implications for understanding neural circuit dysfunctions that underlie autism in humans.  This discovery, which is like a “seesaw circuit,” was led by postdoctoral scholar Weizhe Hong in the laboratory of David J. Anderson, the Seymour Benzer Professor of Biology at Caltech and an investigator with the Howard Hughes Medical Institute. The work was published online on September 11 in the journal Cell.  “We know that there is some hierarchy of behaviors, and they interact with each other because the animal can’t exhibit both social and asocial behaviors at the same time. In this study, we wanted to figure out how the brain does that,” Anderson says.  Anderson and his colleagues discovered two intermingled but distinct populations of neurons in the amygdala, a part of the brain that is involved in innate social behaviors. One population promotes social behaviors, such as mating, fighting, or social grooming, while the other population controls repetitive self-grooming — an asocial behavior.  Interestingly, these two populations are distinguished according to the most fundamental subdivision of neuron subtypes in the brain: the “social neurons” are inhibitory neurons (which release the neurotransmitter GABA, or gamma-aminobutyric acid), while the “self-grooming neurons” are excitatory neurons (which release the neurotransmitter glutamate, an amino acid).  To study the relationship between these two cell types and their associated behaviors, the researchers used a technique called optogenetics. In optogenetics, neurons are genetically altered so that they express light-sensitive proteins from microbial organisms. Then, by shining a light on these modified neurons via a tiny fiber optic cable inserted into the brain, researchers can control the activity of the cells as well as their associated behaviors.  Using this optogenetic approach, Anderson’s team was able to selectively switch on the neurons associated with social behaviors and those linked with asocial behaviors.  With the social neurons, the behavior that was elicited depended upon the intensity of the light signal. That is, when high-intensity light was used, the mice became aggressive in the presence of an intruder mouse. When lower-intensity light was used, the mice no longer attacked, although they were still socially engaged with the intruder — either initiating mating behavior or attempting to engage in social grooming.  When the neurons associated with asocial behavior were turned on, the mouse began self-grooming behaviors such as paw licking and face grooming while completely ignoring all intruders. The self-grooming behavior was repetitive and lasted for minutes even after the light was turned off.  The researchers could also use the light-activated neurons to stop the mice from engaging in particular behaviors. For example, if a lone mouse began spontaneously self-grooming, the researchers could halt this behavior through the optogenetic activation of the social neurons. Once the light was turned off and the activation stopped, the mouse would return to its self-grooming behavior.  Surprisingly, these two groups of neurons appear to interfere with each other’s function: the activation of social neurons inhibits self-grooming behavior, while the activation of self-grooming neurons inhibits social behavior. Thus these two groups of neurons seem to function like a seesaw, one that controls whether mice interact with others or instead focus on themselves. It was completely unexpected that the two groups of neurons could be distinguished by whether they were excitatory or inhibitory. “If there was ever an experiment that ‘carves nature at its joints,’” says Anderson, “this is it.”  This seesaw circuit, Anderson and his colleagues say, may have some relevance to human behavioral disorders such as autism.  “In autism,” Anderson says, “there is a decrease in social interactions, and there is often an increase in repetitive, sometimes asocial or self-oriented, behaviors” — a phenomenon known as perseveration. “Here, by stimulating a particular set of neurons, we are both inhibiting social interactions and promoting these perseverative, persistent behaviors.”  Studies from other laboratories have shown that disruptions in genes implicated in autism show a similar decrease in social interaction and increase in repetitive self-grooming behavior in mice, Anderson says. However, the current study helps to provide a needed link between gene activity, brain activity, and social behaviors, “and if you don’t understand the circuitry, you are never going to understand how the gene mutation affects the behavior.” Going forward, he says, such a complete understanding will be necessary for the development of future therapies.  But could this concept ever actually be used to modify a human behavior?  “All of this is very far away, but if you found the right population of neurons, it might be possible to override the genetic component of a behavioral disorder like autism, by just changing the activity of the circuits — tipping the balance of the see-saw in the other direction,” he says.  Story Source:  The above story is based on materials provided by California Institute of Technology. The original article was written by Jessica Stoller-Conrad. Note: Materials may be edited for content and length.  Journal Reference:      Weizhe Hong, Dong-Wook Kim, David J. Anderson. Antagonistic Control of Social versus Repetitive Self-Grooming Behaviors by Separable Amygdala Neuronal Subsets. Cell, 2014; 158 (6): 1348 DOI: 10.1016/j.cell.2014.07.049

Humans with autism often show a reduced frequency of social interactions and an increased tendency to engage in repetitive solitary behaviors. Autism has also been linked to dysfunction of the amygdala, a brain structure involved in processing emotions. Now Caltech researchers have discovered antagonistic neuron populations in the mouse amygdala that control whether the animal engages in social behaviors or asocial repetitive self-grooming. This discovery may have implications for understanding neural circuit dysfunctions that underlie autism in humans. This discovery, which is like a “seesaw circuit,” was led by postdoctoral scholar Weizhe Hong in the laboratory of David J. Anderson, the Seymour Benzer Professor of Biology at Caltech and an investigator with the Howard Hughes Medical Institute. The work was published online on September 11 in the journal Cell. “We know that there is some hierarchy of behaviors, and they interact with each other because the animal can’t exhibit both social and asocial behaviors at the same time. In this study, we wanted to figure out how the brain does that,” Anderson says. Anderson and his colleagues discovered two intermingled but distinct populations of neurons in the amygdala, a part of the brain that is involved in innate social behaviors. One population promotes social behaviors, such as mating, fighting, or social grooming, while the other population controls repetitive self-grooming — an asocial behavior. Interestingly, these two populations are distinguished according to the most fundamental subdivision of neuron subtypes in the brain: the “social neurons” are inhibitory neurons (which release the neurotransmitter GABA, or gamma-aminobutyric acid), while the “self-grooming neurons” are excitatory neurons (which release the neurotransmitter glutamate, an amino acid). To study the relationship between these two cell types and their associated behaviors, the researchers used a technique called optogenetics. In optogenetics, neurons are genetically altered so that they express light-sensitive proteins from microbial organisms. Then, by shining a light on these modified neurons via a tiny fiber optic cable inserted into the brain, researchers can control the activity of the cells as well as their associated behaviors. Using this optogenetic approach, Anderson’s team was able to selectively switch on the neurons associated with social behaviors and those linked with asocial behaviors. With the social neurons, the behavior that was elicited depended upon the intensity of the light signal. That is, when high-intensity light was used, the mice became aggressive in the presence of an intruder mouse. When lower-intensity light was used, the mice no longer attacked, although they were still socially engaged with the intruder — either initiating mating behavior or attempting to engage in social grooming. When the neurons associated with asocial behavior were turned on, the mouse began self-grooming behaviors such as paw licking and face grooming while completely ignoring all intruders. The self-grooming behavior was repetitive and lasted for minutes even after the light was turned off. The researchers could also use the light-activated neurons to stop the mice from engaging in particular behaviors. For example, if a lone mouse began spontaneously self-grooming, the researchers could halt this behavior through the optogenetic activation of the social neurons. Once the light was turned off and the activation stopped, the mouse would return to its self-grooming behavior. Surprisingly, these two groups of neurons appear to interfere with each other’s function: the activation of social neurons inhibits self-grooming behavior, while the activation of self-grooming neurons inhibits social behavior. Thus these two groups of neurons seem to function like a seesaw, one that controls whether mice interact with others or instead focus on themselves. It was completely unexpected that the two groups of neurons could be distinguished by whether they were excitatory or inhibitory. “If there was ever an experiment that ‘carves nature at its joints,’” says Anderson, “this is it.” This seesaw circuit, Anderson and his colleagues say, may have some relevance to human behavioral disorders such as autism. “In autism,” Anderson says, “there is a decrease in social interactions, and there is often an increase in repetitive, sometimes asocial or self-oriented, behaviors” — a phenomenon known as perseveration. “Here, by stimulating a particular set of neurons, we are both inhibiting social interactions and promoting these perseverative, persistent behaviors.” Studies from other laboratories have shown that disruptions in genes implicated in autism show a similar decrease in social interaction and increase in repetitive self-grooming behavior in mice, Anderson says. However, the current study helps to provide a needed link between gene activity, brain activity, and social behaviors, “and if you don’t understand the circuitry, you are never going to understand how the gene mutation affects the behavior.” Going forward, he says, such a complete understanding will be necessary for the development of future therapies. But could this concept ever actually be used to modify a human behavior? “All of this is very far away, but if you found the right population of neurons, it might be possible to override the genetic component of a behavioral disorder like autism, by just changing the activity of the circuits — tipping the balance of the see-saw in the other direction,” he says. Story Source: The above story is based on materials provided by California Institute of Technology. The original article was written by Jessica Stoller-Conrad. Note: Materials may be edited for content and length. Journal Reference: Weizhe Hong, Dong-Wook Kim, David J. Anderson. Antagonistic Control of Social versus Repetitive Self-Grooming Behaviors by Separable Amygdala Neuronal Subsets. Cell, 2014; 158 (6): 1348 DOI: 10.1016/j.cell.2014.07.049