Lithium Flower

[wakinglithiumflower-blog]

Knowing somebody isn't part of your life anymore is hard, but the harder part is coming to realize that there's no one who can ever fully replace that person.

Unknown author

[wakinglithiumflower-blog]

It's crazy how you can go months or years without talking to someone but they still cross your mind everyday.

Unknown author

[wakinglithiumflower-blog]

Missing someone is not about how long it has been since you have seen them or the amount of time since you have talked.. it is about that very moment when you are doing something and wishing they were there with you.

Unknown author

[wakinglithiumflower-blog]

The saddest thing about burning a bridge is realizing that you can never get back to the beautiful place it used to take you.

Unknown author

[wakinglithiumflower-blog]

It's all in the details. The way someone stops smiling the moment you aren't looking. How their answers become shorter, their laughter a little bit more forced for every time. You'll sometimes catch them with a distant look in their eyes, as if they're staring into the big nothingsness that surrounds them. Completely gone. Lost. Alone. You might find that they start distancing themselves from you, making excuses, feeding you with their little covering lies. "I'm just tired," they'll say. They'll laugh it off, every single time. You should pay attention to how they start covering up their bodies, hiding every inch of their skin, hating every inch of their skin. They won't take your compliments, if so, you'll only get a simple 'thank you' and they will take it all for lies. Self hate could easily be mistaken for self irony - altough they say it with a smile on their face, keep your eyes open for the empty look that follows. Pay attention. Never look away. Because they are nearly impossible to spot, unless you're one of them.

unknown author

[wakinglithiumflower-blog]

Some people have reached such high levels of depression they simply lose interest in talking to people. The symptoms usually start with the person slowly becoming more and more silent in real life, and if he really lets his depression run amok, he will eventually lose interest in talking online as well. It reaches a point where the person starts losing his online friends one by one. Month after month. Here and there, slowly disappearing off of peoples friends lists. Eventually, the person becomes a ghost. Slowly and quietly forgotten by society, left on the sidelines. The person has no motivation to socialize. He only wishes to exist in perfect stoic silence. Never to share his problems, joys, wishes, sorrows, regrets or experiences with a friend or acquaintance, because he does not see a reason to. He understands that most people only wish for you to cease talking so they could begin. Whilst others only wish to listen for the sake of listening. Never really connecting with what you say. He understands that it's pointless to argue online or in real life, because it never changes anything, and instead - only further entrenches both sides. He understands that he will live a quiet, subtle life. He understands that he will probably die alone on a rainy saturday afternoon. He never feels anxiety or anger. Lust or hatred. Happiness or love. He just feels an addictive kind of emptiness. The kind that calls you back home to wallow in self-pity whenever you are outside.

anonymous author

[wakinglithiumflower-blog]

It’s sad when people you know become people you knew. When you can walk right past someone like they were never a big part of your life. How you used to be able to talk for hours and how now, you can barely even look at them.

unknown author

[wakinglithiumflower-blog]

You met someone. You two get close. It's all great for a while. Then someone stops trying. Talk less. Awkward conversations. The drifting. No communication whatsoever. Memories start to fade. Then that person you know becomes that person you KNEW. That's how it usually goes, right? Sad isn't it.

anonymous author

[wakinglithiumflower-blog]

Do you ever see a picture of someone that you used to be so close to and you just remember every thing you did together and all the things you said you would do together, all the late night conversations or phone calls and remember all the good things and bad things both of you have been trough together but then you remember that they're now just a memory and they're not in your life anymore?

anonymous author

[did-you-know]

If a catastrophe caused the Internet to crash, there are 7 people in the world who have keycards that can reboot the system when all 7 keys are used together. Source

[rasec-wizzlbang-blog]

It’s getting to the point where technology is indistinguishable from magic. “Oh, no, the MASSIVE INTANGIBLE LIBRARY OF INFORMATION which allows humans all over the planet to communicate and share information has ceased functioning! Call upon the seven sages whom hold the artifacts which will repair it!”

[puppetshell]

Dude its even better than that, they have to journey to a certain location in america to combine their codes into the Master Code which can revive the internet.

[ewtgdgwgysdhgh-deactivated20150]

did fucking hideo kojima design this system

[wakinglithiumflower-blog]

Complete fucking bullshit.

There is no key to restart the internet. This whole thing is about a system called DNSSEC which can be used to help users gain assurance that the remote DNS server they are seeking to communicate with has been independently verified and is genuine. The Keys only ‘restart’ the very small proportion of internet sites using DNSSEC. The rest of the Internet would continue to work normally.

[neurosciencestuff]

(Image caption: Estimated structure of the nucleosomal DNA loops, which are temporarily formed during transcription of chromatin containing intact DNA by RNA polymerase II (Pol II). In the presence of a single-strand DNA break, the loop structure likely changes, preventing rotation of the RNA polymerase along the DNA helix (orange arrow). Credit: Nadezhda S. Gerasimova et al.)

Novel DNA repair mechanism brings new horizons

The DNA molecule is chemically unstable giving rise to DNA lesions of different nature. That is why DNA damage detection, signaling and repair, collectively known as the DNA damage response, are needed.

A group of researchers, lead by Vasily M. Studitsky, professor at the Lomonosov Moscow State University, discovered a new mechanism of DNA repair, which opens up new perspectives for the treatment and prevention of neurodegenerative diseases. The article describing their discovery is published in AAAS’ first open access online-only journal Science Advances.

“In higher organisms DNA is bound with proteins in complexes called the nucleosome. Every ~200 base pairs are organized in nucleosomes, consisting of eight histone proteins, which, like the thread on the bobbin, wound double helix of DNA, which is coiled into two supercoiled loops. Part of the surface of the DNA helix is hidden, because it interacts with histones. Our entire genome is packed this way, except for the areas, from which the information is being currently read”, – says Vasily M. Studitsky , who is the leading researcher and the head of the Laboratory of Regulation of Transcription and Replication at the Biological Faculty of the Lomonosov Moscow State University.

The dense packing allows DNA molecule with a length of about two meters to fit into a microscopic cell nucleus, but it makes significant surfaces of the DNA inaccessible for the repair enzymes – the proteins that manage the “repair” of damaged DNA regions. The damage of the DNA, if not repaired, leads to accumulation of mutations, cell death, and to the development of various diseases, including neurodegenerative, e.g. Alzheimer’s disease.

A group of researchers, lead by Vasily M. Studitsky, studied the mechanism of detection of single-stranded DNA breaks at which the connection is lost between nucleotides on one strand in the places where the DNA is associated with histones.

Scientists know quite a lot about the mechanism of the repair. It is known that for the synthesis of a protein, information written in the genetic code, which could be imagined as the manual for its assembly where triples of nucleotides match certain amino acids, should be taken out of the nucleus into the cytoplasm of the cell.

Thin and long strand of the DNA is packed in the nucleus and can tear at the exit to the outside. Moreover, it cannot be sacrificed as the cell’s nuclear DNA is only present in two copies. Therefore, when it is necessary to synthesize specific protein, small region of DNA is unwound, the two strands are disconnected, and the information on the protein structure with one of the DNA strands is written in form of RNA, single-stranded molecule. The mRNA molecule, which serves as the template for making a protein, is synthesized by the principle of complementarity: each nucleotide pair corresponds to another one.

During the transcription of information (its rewriting into RNA) the RNA polymerase enzyme “rides” on the DNA chain, and stops when it finds the break. Like a proofreader of a text, RNA polymerase after it is stalled, triggers a cascade of reactions, resulting in the repair enzymes fixing the damaged area. At the same time, the RNA polymerase cannot detect discontinuities present in the other DNA strand.

“We have shown, not yet in the cell, but in vitro, that the repair of breaks in the other DNA chain, which is "hidden” in the nucleosome, is still possible. According to our hypothesis, it occurs due to the formation of special small DNA loops in the nucleosome, although normally DNA wounds around the histone “spool” very tightly", – says Vasily M. Studitsky, – “The loops form when the DNA is coiled back on nucleosome together with polymerase. RNA polymerase can "crawl” along the DNA loops nearly as well as on histone-free DNA regions, but when it stops near locations of the DNA breaks, it “panics”, triggering the cascade of reactions to start DNA “repairs”.

During the experiment, special sites, where single-stranded breaks can be introduced by adding specific enzymes in a test tube, were inserted into the DNA. Then a single nucleosome transcribed by a single RNA molecule was studied. In this model system, which was developed in 2002 by the same group of scientists, histones were assembled on the molecule with an accuracy within one nucleotide. Having specially introduced breaks at precise locations on the DNA, the researchers examined the impact of breaks on the progression of the RNA polymerase. It turned out that only in nucleosomes, rather than in the histone-free DNA, the enzyme stopped, when the break was present in the other DNA strand. Wherein it did not stop before the break, but immediately after it. It was difficult enough to understand the mechanism that allows it to notice the damage at the “back” of RNA polymerase, as if it had “eyes on the back of the head”, although, obviously, it does not have neither one nor the other.

The analysis of breaks in different positions allowed to hypothesize that stalling of RNA polymerase is caused by the formation of the loop, which blocks movement of the enzyme. The findings open up a new direction for the work on the subject of DNA repair.

Previously the role of chromatin considered passive as scientists thought the DNA repair is possible only on histone-free DNA. However, professorr Vasily M. Studitsky and his colleagues found that the thread can be repaired without complete unwinding of DNA “coils”. The highly conserved histones play an important role in this process as changes in their structure are rejected by natural selection. Moreover, the high level of protein conservation just assumes its active participation in many processes.

Furthermore, the models proposed by the scientists first time ever explains the role of the so-called topological locks, which are formed during the passage of any enzyme along the DNA when it meets a nucleosome.

“In terms of applied science discovery of a new mechanism of reparation promises new prospective methods of prevention and treatment of diseases. We have shown that the formation of loops, which stop the polymerase, depends on its contacts with histones. If you make them more robust, it will increase the efficiency of the formation of loops and the probability of repair, which in turn will reduce the risk of disease. If these contacts are destabilized, then by using special methods of drug delivery you can program the death of the affected cells”, – Vasily Studitsky concluded, adding that the process of development and testing of such drugs, of course, requires considerable time.

[roachswallower]

i need an app like tinder just to find people to smoke wit

[roachswallower]

i’m patenting this shit and calling it “buds”

[roachswallower]

fellow weedheads, who will kickstart this

[crimewave420]

“Ahh yes brothere let us meet up and toke together mayhaps you can point me in the direction of your ‘plug’ as they put it roflmao”

[wakinglithiumflower-blog]

http://uk.businessinsider.com/high-there-is-tinder-for-pot-smokers-2015-2?r=US

[themedicalstate]

Recalling happier memories can reverse depression

MIT neuroscientists have shown that they can cure the symptoms of depression in mice by artificially reactivating happy memories that were formed before the onset of depression.

The findings, described in the June 18 issue of Nature, offer a possible explanation for the success of psychotherapies in which depression patients are encouraged to recall pleasant experiences. They also suggest new ways to treat depression by manipulating the brain cells where memories are stored. The researchers believe this kind of targeted approach could have fewer side effects than most existing antidepressant drugs, which bathe the entire brain.

“Once you identify specific sites in the memory circuit which are not functioning well, or whose boosting will bring a beneficial consequence, there is a possibility of inventing new medical technology where the improvement will be targeted to the specific part of the circuit, rather than administering a drug and letting that drug function everywhere in the brain,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, director of the RIKEN-MIT Center for Neural Circuit Genetics at MIT’s Picower Institute for Learning and Memory, and senior author of the paper.

Although this type of intervention is not yet possible in humans, “This type of analysis gives information as to where to target specific disorders,” Tonegawa adds.

Graduate student Steve Ramirez is the paper’s lead author.

Memory control

In 2012, Tonegawa, former MIT postdoc Xu Liu, Ramirez, and colleagues first reported that they could label and reactivate clusters of brain cells that store specific memories, which they called engrams. More recently, they showed that they could plant false memories, and that they could switch the emotional associations of a particular memory from positive to negative, and vice versa.

In their new study, the researchers sought to discover if their ability to reactivate existing memories could be exploited to treat depression.

To do this, the researchers first exposed mice to a pleasurable experience. In this case, all of the mice were male and the pleasurable experience consisted of spending time with female mice. During this time, cells in the hippocampus that encode the memory engram were labeled with a light-sensitive protein that activates the neuron in response to blue light.

After the positive memory was formed, the researchers induced depression-like symptoms in the mice by exposing them to chronic stress. These mice show symptoms that mimic those of human sufferers of depression, such as giving up easily when faced with a difficult situation and failing to take pleasure in activities that are normally enjoyable.

However, when the mice were placed in situations designed to test for those symptoms, the researchers found that they could dramatically improve the symptoms by reactivating the neurons that stored the memory of a past enjoyable experience. Those mice began to behave just like mice that had never been depressed — but only for as long as the pleasant memory stayed activated.

In another set of experiments, the researchers found that they could achieve a longer-lasting improvement by reactivating the positive memory cells for 15 minutes, twice a day, for five days, before the mice underwent the tests for depressive behavior. This time, the memories were not reactivated during the test, but the mice behaved just like mice that had never been depressed.

The researchers found that the repeated memory activation provoked formation of new brain cells in a part of the hippocampus called the dentate gyrus. This did not happen during the brief activations during the behavioral tests; instead, depressive behavior was overcome by activation of a circuit connecting engram cells located in the hippocampus, amygdala, and nucleus accumbens.

“Harnessing the brain’s power”

Interestingly, the researchers found that allowing the mice to engage in pleasurable experiences after becoming depressed did not improve their symptoms nearly as much as reactivating an old memory.

“People who suffer from depression have those positive experiences in the brain, but the brain pieces necessary to recall them are broken. What we’re doing, in mice, is bypassing that circuitry and forcing it to be jump-started,” Ramirez says. “We’re harnessing the brain’s power from within itself and forcing the activation of that positive memory, whereas if you give a natural positive memory to the person or the animal, the depression that they have prevents them from finding that experience rewarding.”

The study suggests a possible scientific explanation for why psychotherapy works for some depressed patients, Tonegawa says. “In some way this depression state suppresses the ability to recall positive experiences, and what the psychiatrist is doing is trying to override that and help them to recall those memories,” he says.

That link between the neural circuit manipulations in mice and therapies now used in humans makes the findings particularly exciting, says Tom Insel, director of the National Institute of Mental Health.

“This is a big step toward helping to understand not only the underlying circuits for a really serious illness like depression, but also the circuits that underlie treatment,” says Insel, who was not involved in the research.

The findings also offer possible new approaches to developing new types of depression treatments, the researchers say. If scientists could develop a noninvasive way to stimulate specific brain circuits, they might be able to achieve the same effects seen in this study using optogenetics. One way to accomplish this could be a more targeted form of deep-brain stimulation, which requires implantation of a brain pacemaker that sends electrical impulses to specific parts of the brain. Deep-brain stimulation is sometimes used to treat Parkinson’s disease, depression, and obsessive-compulsive disorder, among other diseases.

“The problem is that deep-brain stimulation is crude and activates a large chunk of the brain,” Ramirez says. “You could imagine in the future that if you could target deep-brain stimulation not to patches of brain but to specific sets of cells that we think are holding onto a positive memory, then it offers a new therapeutic avenue.”

Source

[angelophile]

Currently sat on my desk, after being removed from its home in Big Ben. With special permission from The Elders of the Internet.

[wakinglithiumflower-blog]

Is Dvorak what you use, then? I'm also thinking about Colemak, which is s'posed to be easier to learn... (not gonna be starting typing drills any time soon, obviously)

I use Neo because it's optimized for german but still works good enough with english. Colemak is suposed to be slightly better than Dvorak but I never bothered learning it because it doesn't seem to work that well with german.

[explodingbat-deactivated2017072]

fluffy-critter replied to your post:Owww

What kind of keyboard and mouse do you use? Also how’s your chair and desk set up?

Just got a left-handed Razer gaming mouse (has programmable thumb buttons, trying to preserve remaining index finger). Keyboard is just a generic supermarket one...

[wakinglithiumflower-blog]

Here is something every programmer should have:

It does a great job preventing wrist problems.

You should also consider spending a bit more for an ergonomic keyboard and/or changing your keyboard layout to dvorak.

[neurosciencestuff]

Meditation Can Reduce Chronic Neck Pain

Meditation might be an effective treatment for reducing chronic neck pain, according to research reported in The Journal of Pain.

Chronic neck pain can lead to serious comorbidities like depression. Patients with chronic neck pain frequently experience distress. Meditation has been increasingly used as a supportive treatment for individuals with chronic pain.  

Previous research has shown that chronic pain is associated with distress and that meditation has stress relieving benefits. German researchers compared the effects of meditation on pain, perceived stress and psychological well being. They hypothesized that an eight-week meditation program will decrease pain more effectively than a standardized exercise program and that pain relief will coincide with stress reduction.

For the study, 89 patients with chronic neck pain who showed increased perceived stress were randomized into meditation and exercise program groups. Outcomes were assessed at baseline and after eight weeks.    

Results showed that meditation training significantly reduced pain when compared to the exercise group and pain-related “bothersomeness” decreased more in the meditation group as well. No significant differences between meditation and exercise were found for pain during movement, pain disability, psychological scores and quality of life, which is consistent with the known benefits of exercise on pain-related outcomes. The authors concluded that meditation has unique benefits for producing pain relief and for pain coping.