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Brain upgrade
#1
Telepathic superhumans with ability to read anyone’s mind could be real by 2038

Deni

http://www.news.com.au/technology/science/human-body/telepathic-superhumans-with-ability-to-read-anyones-mind-could-be-real-by-2038/news-story/8375c45de524ea855ab017742326320f

A LEADING surgeon claims within the next two decades, chips could be implanted in our brains which would give us the ability to read each other’s minds.
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#2
...
An aggressive clown with a brain implant that allows such a possibility,
does not have the guarantee that the person he is probing,
will be totally ignorant of the intrusion.
Also, this would be someone in close proximity commiting the act.
It would be well known to the public if the technology began to be used.
Then people would be more aware of expecting such possibilities,'
and strike back,
with 
Reefer reverse videodrome intent Reefer  -- for instance ... if I knew there was an intrusion:
"to read my mind"
I could focus intent and send the thoughts I want them to see,
and they would lose interest fast,
in further nefarious mind probing.

Good luck with the side effects of the implants as well.

...
Reply
#3
Hmm  ok ... but imagine that    Hmm2

You are directly connected to the internet and you can access THM directly ... like all the content of the THM is in Your brain...

How about that ?

Doh
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#4
[Image: cQQC7op.jpg]
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#5
It’s not my fault, my brain implant made me do it

April 3, 2018 6.44am EDT

[Image: file-20180329-189810-cbug78.jpg?ixlib=rb...6&fit=clip]
Probes that can transmit electricity inside the skull raise questions about personal autonomy and responsibility. Hellerhoff, CC BY-SA

Mr. B loves Johnny Cash, except when he doesn’t. Mr. X has watched his doctors morph into Italian chefs right before his eyes.


The link between the two? Both Mr. B and Mr. X received deep brain stimulation (DBS), a procedure involving an implant that sends electric impulses to specific targets in the brain to alter neural activity. While brain implants aim to treat neural dysfunction, cases like these demonstrate that they may influence an individual’s perception of the world and behavior in undesired ways.



Mr. B received DBS as treatment for his severe obsessive compulsive disorder. He’d never been a music lover until, under DBS, he developed a distinct and entirely new music preference for Johnny Cash. When the device was turned off, the preference disappeared.



Mr. X, an epilepsy patient, received DBS as part of an investigation to locate the origin of his seizures. During DBS, he hallucinated that doctors became chefs with aprons before the stimulation ended and the scene faded.


In both of these real-world cases, DBS clearly triggered the changed perception. And that introduces a host of thorny questions. As neurotechnologies like this become more common, the behaviors of people with DBS and other kinds of brain implants might challenge current societal views on responsibility.


Lawyers, philosophers and ethicists have labored to define the conditions under which individuals are to be judged legally and morally responsible for their actions. The brain is generally regarded as the center of control, rational thinking and emotion – it orchestrates people’s actions and behaviors. As such, the brain is key to agency, autonomy and responsibility.


Where does responsibility lie if a person acts under the influence of their brain implant? As a neuroethicist and a legal expert, we suggest that society should start grappling with these questions now, before they must be decided in a court of law.


Who’s to blame if something goes wrong?

[Image: file-20180329-189824-17tsjlv.jpg?ixlib=r...7&fit=clip]
An uncontrollable urge to aim right for them? Fabio Venni, CC BY-SA 


Imagine that Ms. Q was driving one day and had a sudden urge to swerve into a crowded bus stop. As a result, she ended up injuring several people and damaging the bus stop. During their investigation, police found that Ms. Q had a brain implant to treat her Parkinson’s disease. This implant malfunctioned at the time the urge occurred. Furthermore, Ms. Q claims that the bus stop was not there when she acted on the impulse to swerve.


As brain stimulating technology advances, a hypothetical case like Ms. Q’s raises questions about moral and legal responsibility. Is Ms. Q solely responsible for her actions? Can we attribute any blame to the device? What about to the engineers who designed it or the manufacturer? The neurosurgeon who implanted it or the neurologist who programmed the device parameters?


Historically, moral and legal responsibility have largely focused on the autonomous individual – that is, someone with the capacity to deliberate or act on the basis of one’s own desires and plans, free of distorting external forces.


However, with modern technological advances, many hands may be involved in the operation of these brain implants, including artificial intelligence programs directly influencing the brain.


This external influence raises questions about the degree to which someone with an implant can control their actions and behaviors. If brain implants influence someone’s decisions and behaviors, do they undermine the person’s autonomy? If autonomy is undermined, can we attribute responsibility to the individual?


Society needs to discuss what happens when science and technology start challenging those long-held assumptions.


So many shades of gray


There are different legal distinctions concerning responsibility, such as causal responsibility and liability responsibility.
Using this distinction, one may say that the implant is causally responsible, but that Ms. Q still has liability for her actions. One might be tempted to split the liability in this way because Ms. Q still acted on the urge – especially if she knew the risk of brain implant side effects. Perhaps Ms. Q still bears all primary responsibility but the influence of the implant should mitigate some of her punishment.


These are important gradations to reckon with, because the way we as a society divide liability may force patients to choose between potential criminal liability and treating a debilitating brain condition.


[Image: file-20180329-189830-pslzsp.jpg?ixlib=rb...4&fit=clip]
Would the surgeon bear some responsibility? Or the device manufacturer? Allurimd (talk), CC BY-SA 


Questions also arise about product liability for companies, professional responsibility issues for researchers and technology developers, and medical malpractice for the health professionals who placed and programmed the device. Even if multiple actors share responsibility, the question regarding how to distribute responsibility among multiple actors still remains.


Adding an additional layer is the potential for malicious interference of these implants by criminals. Newer implants may have wireless connectivity. Hackers could attack such implants to use Ms. Q for their own (possibly nefarious) purposes, posing more challenges to questions of responsibility.


Insulin pumps and implantable cardiac defibrillators have already been hacked in real life. While there have not been any reports of malicious interference with brain implants, their increasing adoption brings greater opportunity for tech-savvy individuals to potentially use the technology for evil.


Considering the impact brain implants can have on moral and legal notions of responsibility, it’s time to discuss whether and when brain interventions should excuse people. New technologies often require some modification or extension of existing legal mechanisms. For example, assisted reproductive technologies have required society to redefine what it means to be a “parent.”


It’s possible that soon we will start hearing in courtrooms: “It’s not my fault. My brain implant made me do it.”

Authors:
  1. [Image: image-20180131-157488-r2upih.jpg] Laura Y. Cabrera
    Assistant Professor of Neuroethics, Michigan State University
  2. [Image: image-20180131-157470-1w0qekf.jpg] Jennifer Carter-Johnson
    Associate Professor of Law, Michigan State University

Sources: https://theconversation.com/its-not-my-f...o-it-91040


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Me Hmm2 

Depends if it helps me Split_spawn   I already have 2nd pacemaker


Bob... Ninja Assimilated
"The Light" - Jefferson Starship-Windows of Heaven Album
I'm an Earthling with a Martian Soul wanting to go Home.   
You have to turn your own lightbulb on. ©stevo25 & rhw007
Reply
#6
During choir practice I had a sudden urge
to sail a paper airplane off the choir loft.

The head nun paddled me in the office over the intercom
as a school wide warning.

I suppose a predictive behavior monitor chip
could eliminate thought criminality
much like noise cancelling headphones,
with more severe penalties
involving paralyzing muscular functions.

Which reminds me...

I heard that alibaba is involved in a thought control program
to completely monitor all people in Hangzhou(?),
rendering individual subject implants obsolete,
presumably through immediately applied negative reinforcement
techniques delivered through electrical stimulus.
Reply
#7
I've tried using TEMs pads using electrical stimulus to alter this 2nd pacemaker.  I do NOT have the courage to place electrodes directly atop it; thus SURELY to 'maybe' short-circuit the thing COMPLETELY .

Each check up of the thing I try to have them set the lower limit to 50 h/b/m and max up to 130 h/b/m.

They usually refuse the upper limit; though I believe the last one DID allow to lower it to 50 h/b/m; they would NOT do the 20 h/b/m I had NATURALLY before I HAD a pacemaker put in.

I would prefer to have a machine I could alter it myself. $$$ way too much.

Bob... Ninja Assimilated
"The Light" - Jefferson Starship-Windows of Heaven Album
I'm an Earthling with a Martian Soul wanting to go Home.   
You have to turn your own lightbulb on. ©stevo25 & rhw007
Reply
#8
New Brain Maps With Unmatched Detail May Change Neuroscience



[/url]Monique Brouillette
Contributing Writer
April 4, 2018

[Image: NeuralPathsArt_2880x1620-2880x1620.jpg]
Olena Shmahalo/Quanta Magazine

Sitting at the desk in his lower-campus office at Cold Spring Harbor Laboratory, the neuroscientist [url=https://www.cshl.edu/research/faculty-staff/anthony-zador/]Tony Zador
turned his computer monitor toward me to show off a complicated matrix-style graph. Imagine something that looks like a spreadsheet but instead of numbers it’s filled with colors of varying hues and gradations. Casually, he said: “When I tell people I figured out the connectivity of tens of thousands of neurons and show them this, they just go ‘huh?’ But when I show this to people …” He clicked a button onscreen and a transparent 3-D model of the brain popped up, spinning on its axis, filled with nodes and lines too numerous to count. “They go ‘What the _____!’”

What Zador showed me was a map of 50,000 neurons in the cerebral cortex of a mouse. It indicated where the cell bodies of every neuron sat and where they sent their long axon branches. A neural map of this size and detail has never been made before. Forgoing the traditional method of brain mapping that involves marking neurons with fluorescence, Zador had taken an unusual approach that drew on the long tradition of molecular biology research at Cold Spring Harbor, on Long Island. He used bits of genomic information to imbue a unique RNA sequence or “bar code” into each individual neuron. He then dissected the brain into cubes like a sheet cake and fed the pieces into a DNA sequencer. The result: a 3-D rendering of 50,000 neurons in the mouse cortex (with as many more to be added soon) mapped with single cell resolution.

This work, Zador’s magnum opus, is still being refined for publication. But in a paper recently published by Nature, he and his colleagues showed that the technique, called MAPseq (Multiplexed Analysis of Projections by Sequencing), can be used to find new cell types and projection patterns never before observed. The paper also demonstrated that this new high-throughput mapping method is strongly competitive in accuracy with the fluorescent technique, which is the current gold standard but works best with small numbers of neurons.

[Image: tonyzador.jpg]
Tony Zador, a neurophysiologist at Cold Spring Harbor Laboratory, realized that genome sequencing techniques could scale up to tame the astronomical numbers of neurons and interconnections in the brain.

jeansweep/Quanta Magazine

The project was born from Zador’s frustration during his “day job” as a neurophysiologist, as he wryly referred to it. He studies auditory decision-making in rodents: how their brain hears sounds, processes the audio information and determines a behavioral output or action. Electrophysiological recordings and the other traditional tools for addressing such questions left the mathematically inclined scientist unsatisfied. The problem, according to Zador, is that we don’t understand enough about the circuitry of the neurons, which is the reason he pursues his “second job” creating tools for imaging the brain.

The current state of the art for brain mapping is embodied by the Allen Brain Atlas, which was compiled from work in many laboratories over several years at a cost upward of $25 million. The Allen Atlas is what’s known as a bulk connectivity atlas because it traces known subpopulations of neurons and their projections as groups. It has been highly useful for researchers, but it cannot distinguish subtle differences within the groups or neuron subpopulations.
If we ever want to know how a mouse hears a high-pitched trill, processes that the sound means a refreshing drink reward is available and lays down new memories to recall the treat later, we will need to start with a map or wiring diagram for the brain. In Zador’s view, lack of knowledge about that kind of neural circuitry is partly to blame for why more progress has not been made in the treatment of psychiatric disorders, and why artificial intelligence is still not all that intelligent.

Justus Kebschull, a Stanford University neuroscientist, an author of the new Nature paper and a former graduate student in Zador’s lab, remarked that doing neuroscience without knowing about the circuitry is like “trying to understand how a computer works by looking at it from the outside, sticking an electrode in and probing what we can find. … Without ever knowing the hard drive is connected to the processor and the USB pod provides input to the whole system, it’s difficult to understand what’s happening.”


Inspiration for MAPseq struck Zador when he learned of another brain mapping technique called Brainbow. Hailing from the lab of Jeff Lichtman at Harvard University, this method was remarkable in that it genetically labeled up to 200 individual neurons simultaneously using different combinations of fluorescent dyes. The results were a tantalizing, multicolored tableau of neon-colored neurons that displayed, in detail, the complex intermingling of axons and neuron cell bodies. The groundbreaking work gave hope that mapping the connectome—the complete plan of neural connections in the brain—was soon to be a reality. Unfortunately, a limitation of the technique in practice is that through a microscope, experimenters could resolve only about five to 10 distinct colors, which was not enough to penetrate the tangle of neurons in the cortex and map many neurons at once.

That’s when the light bulb went on in Zador’s head. He realized that the challenge of the connectome’s huge complexity might be tamed if researchers could harness the increasing speed and dwindling costs of high-throughput genomic sequencing techniques. “It’s what mathematicians call reducing it to a previously solved problem,” he explained.





MAPseq, researchers inject an animal with genetically modified viruses that carry a variety of known RNA sequences, or “bar codes.” For a week or more, the viruses multiply inside the animal, filling each neuron with some distinctive combination of those bar codes. When the researchers then cut the brain into sections, the RNA bar codes can help them track individual neurons from slide to slide.

Zador’s insight led to the new Nature paper, in which his lab and a team at University College London led by the neuroscientist Thomas Mrsic-Flogel used MAPseq to trace the projections of almost 600 neurons in the mouse visual system. (Editor’s note: Zador and Mrsic-Flogel both receive funding from the Simons Foundation, which publishes Quanta.)

Six hundred neurons is a modest start compared with the tens of millions in the brain of a mouse. But it was ample for the specific purpose the researchers had in mind: They were looking to discern whether there is a structure to the brain’s wiring pattern that might be informative about its function. A currently popular theory is that in the visual cortex, an individual neuron gathers a specific bit of information from the eye—about the edge of an object in the field of view, or a type of movement or spatial orientation, for example. The neuron then sends a signal to a single corresponding area in the brain that specializes in processing that type of information.


[video=liveleak]https://media.wired.com/clips/5ac7ca8fadec2c7358430614/original/pass/inline-clip.mp4[/video]


To test this theory, the team first mapped a handful of neurons in mice in the traditional way by inserting a genetically encoded fluorescent dye into the individual cells. Then, with a microscope, they traced how the cells stretched from the primary visual cortex (the brain area that receives input from the eyes) to their endpoints elsewhere in the brain. They found that the neurons’ axons branched out and sent information to many areas simultaneously, overturning the one-to-one mapping theory.

Next, they asked if there were any patterns to these projections. They used MAPseq to trace the projections of 591 neurons as they branched out and innervated multiple targets. What the team observed was that the distribution of axons was structured: Some neurons always sent axons to areas A, B and C but never to D and E, for example.





These results suggest the visual system contains a dizzying level of cross-connectivity and that the pattern of those connections is more complicated than a one-to-one mapping. “Higher visual areas don’t just get information that is specifically tailored to them,” Kebschull said. Instead, they share many of the same inputs, “so their computations might be tied to each other.”

Nevertheless, the fact that certain cells do project to specific areas also means that within the visual cortex there are specialized cells that have not yet been identified. Kebschull said this map is like a blueprint that will enable later researchers to understand what these cells are doing. “MAPseq allows you to map out the hardware. … Once we know the hardware we can start to look at the software, or how the computations happen,” he said.

MAPseq’s competitive edge in speed and cost for such investigations is considerable: According to Zador, the technique should be able to scale up to handle 100,000 neurons within a week or two for only $10,000 — far faster than traditional mapping would be, at a fraction of the cost.

Such advantages will make it more feasible to map and compare the neural pathways of large numbers of brains. Studies of conditions such as schizophrenia and autism that are thought to arise from differences in brain wiring have often frustrated researchers because the available tools don’t capture enough details of the neural interconnections. It’s conceivable that researchers will be able to map mouse models of these conditions and compare them with more typical brains, sparking new rounds of research. “A lot of psychiatric disorders are caused by problems at the circuit level,” said Hongkui Zeng, executive director of the structured science division at the Allen Institute for Brain Science. “Connectivity information will tell you where to look.”

High-throughput mapping also allows scientists to gather lots of neurological data and look for patterns that reflect general principles of how the brain works. “What Tony is doing is looking at the brain in an unbiased way,” said Sreekanth Chalasani, a molecular neurobiologist at the Salk Institute. “Just as the human genome map has provided a scaffolding to test hypotheses and look for patterns in [gene] sequence and function, Tony’s method could do the same” for brain architecture.

The detailed map of the human genome didn’t immediately explain all the mysteries of how biology works, but it did provide a biomolecular parts list and open the way for a flood of transformative research. Similarly, in its present state of development, MAPseq cannot provide any information about the function or location of the cells it is tagging or show which cells are talking to one another. Yet Zador plans to add this functionality soon. He is also collaborating with scientists studying various parts the brain, such as the neural circuits that underlie fear conditioning.


“I think there are insights to be derived from connectivity. But just like genomes themselves aren’t interesting, it’s what they enable that is transformative. And that’s why I’m excited,” Zador said. “I’m hopeful it’s going to provide the scaffolding for the next generation of work in the field.”

Original story reprinted with permission from Quanta Magazine, an editorially independent publication of the Simons Foundation whose mission is to enhance public understanding of science by covering research developments and trends in mathematics and the physical and life sciences.


Sources: https://www.wired.com/story/new-brain-maps-with-unmatched-detail-may-change-neuroscience/
Orig source: https://www.quantamagazine.org/new-brain...-20180404/

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Note there are animations that are .mp4 videos that show the 3-D views

Also here is 45 min YouTube with Scientists:  https://www.youtube.com/watch?v=OMGBSGiKoes

Bob... Ninja Assimilated
"The Light" - Jefferson Starship-Windows of Heaven Album
I'm an Earthling with a Martian Soul wanting to go Home.   
You have to turn your own lightbulb on. ©stevo25 & rhw007
Reply
#9
Recall:

"It makes sense in retrospect," Walsh says. "The genes that put our brains together during development must have been the genes that evolution tweaked to make our brains bigger." RE: Brain upgrade

Quote:The result: a 3-D rendering of 50,000 neurons in the mouse cortex (with as many more to be added soon) mapped with single cell resolution.

This work, Zador’s magnum opus, is still being refined for publication.



In the post below Itz evident the Magnum Opus Mouse Model couldn't ferret this out. Arrow





Nibble   Old school brain upgrade. 


Mutant ferrets Doh offer clues to human brain size
April 11, 2018, Howard Hughes Medical Institute

[Image: mutantferret.jpg]
Ferrets have an outer brain layer that is large and folded -- similar to that of humans. A new genetically engineered ferret has a smaller brain (right 3-D rendering) than a normal ferret (left) and may offer clues about brain development …more

A genetically engineered ferret could help reveal how humans got their big brains.

By inactivating a gene linked to abnormally small brain size in humans, researchers have created the first ferret with a neurological mutation. Although the original impetus of the work was to study human brain disease and development, says Howard Hughes Medical Institute (HHMI) Investigator Christopher Walsh, the results also shed light on how the human brain expanded during the course of evolution.
"I'm trained as a neurologist, and study kids with developmental brain diseases," says Walsh, of Boston Children's Hospital. "I never thought I'd be peering into the evolutionary history of humankind."
He and colleagues, along with Byoung-Il Bae's lab at Yale University, report the work April 11, 2018, in the journal Nature.
Usually, the outer layer of the human brain, called the cerebral cortex, is large and highly folded. But things can go wrong when the embryonic brain is being built, resulting in a much smaller cortex. This occurs in microcephaly, a condition where babies have significantly smaller heads and brains than normal. Microcephaly can have a genetic root, and has also been linked to recent outbreaks of the Zika virus.
Researchers have identified genes that play a role in the condition, some of which are essential for cerebral cortex growth during embryonic development. Mutations in a gene called ASPM, for example, reduce the size of a human brain by up to 50 percent, making it about the same size as a chimpanzee's brain.
[Image: 2-mutantferret.jpg]
In a ferret's developing brain, stem cells (green) send long fibers (green threads) throughout the cortex. These fibers shepherd new neurons to the right place -- and ultimately help the cortex form its folded structure. Credit: Walsh Lab/HHMI/Boston Children's Hospital
Scientists have studied microcephaly in mice to better understand the condition in humans, but learning about human disorders from mice can be tricky. A mouse brain is a thousand times smaller than a human brain, and lacks several kinds of brain cells that are abundant in humans. Inactivating Aspm in mice shrinks their brains by only about 10 percent. It's such a subtle defect that these animals, called Aspm knockout mice, provide limited insight into human cortical development, says Walsh, who leads the Allen Discovery Center at Boston Children's Hospital and Harvard Medical School.
This prompted Bae and Walsh's team to genetically inactivate, or "knock out," Aspm in a mammal with a larger, more convoluted cortex, more like that of humans. Ferrets fit that bill because they are a large-brained mammal that breeds quickly and easily, Walsh says. "On the face of it, ferrets may seem a funny choice, but they have been an important model for brain development for thirty years."

Still, scientists haven't done much research on ferret genetics. The whole idea of an Aspm knockout ferret was considered new - and a little risky. In 2013 Walsh pitched his project to HHMI and got the budget boost he needed to make it happen. His team's Aspm knockout ferret is only the second knockout ferret ever created. One of the study's coauthors, John Engelhardt of the University of Iowa, made the first nearly 10 years ago to study cystic fibrosis.
Walsh, Bae, and their colleagues discovered that their ferrets model human microcephaly much more accurately than do mice. The ferrets displayed severely shrunken brains, with up to 40 percent reduced brain weight. And, as in humans with the condition, cortical thickness and cell organization were preserved.
What's more, the ferrets reveal a possible mechanism for how human brains have grown over evolutionary time. Over the last seven million years, human brain size has tripled. Most of this expansion has occurred within the cerebral cortex.
Indeed, in the mutant ferrets, researchers traced the cerebral cortex deficits to a type of stem cell called outer radial glial cells (ORGs). ORGs are created by stem cells capable of making all sorts of different cells in the cortex. Walsh's team found that Aspm regulates the timing of the transition between these stem cells and ORGs. This affects the ratio of ORGs to other types of cells. Thus, tweaking Aspm can actually dial up or down the number of nerve cells in the brain, Walsh says, without having to change many genes all at once.
[Image: 1-mutantferret.jpg]
In the mutant ferret, neural progenitor cells form abnormal clumps (in box) and differentiate earlier in the developing brain compared with the normal ferret. Credit: M. Johnson et al./Nature 2018
That's a clue that the gene could have played a role in the evolution of the human brain. "Nature had to solve the problem of changing the size of the human brain without having to reengineer the whole thing," Bae says.
Aspm codes for a protein that is part of a cellular complex called the centriole. Walsh and colleagues found that knocking out this gene disturbs the centriole's organization and function, suggesting an underlying biochemical mechanism for the brain deficits seen in the ferrets.

In humans, a few genes associated with centriole proteins, including ASPM, have undergone recent evolutionary changes. These genes might even be important for distinguishing humans from Neanderthals and our closest living relatives, chimpanzees, Walsh says.

Overall, he says, the study demonstrates the advantages of using ferrets to study some human neurological disorders. It also points to new mechanisms at work in the brain development of individuals and in species like humans over evolutionary time.
"It makes sense in retrospect," Walsh says. "The genes that put our brains together during development must have been the genes that evolution tweaked to make our brains bigger."

 Explore further: Folding of the cerebral cortex—identification of important neurons
More information: Aspm knockout ferret reveals an evolutionary mechanism governing cerebral cortical size, Nature (2018). nature.com/articles/doi:10.1038/s41586-018-0035-0

Journal reference: Nature [Image: img-dot.gif] [Image: img-dot.gif]
Provided by: Howard Hughes Medical Institute


https://medicalxpress.com/news/2018-04-m...brain.html
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