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Medicine of hemp

15 May 2018

The usual way of creating a medicine is to find a biological target and to search for / select / design an active selective molecule, looking through hundreds and thousands of options. But there is another approach - to take a substance or a group of substances (say from an extract of a plant) and with perseverance to look for him for some activity. The approach is somewhat strange, and often doomed to failure. But we must admit that it, in some places, works ...

The company GW Pharmaceuticals, founded in 1998 by two British doctors Geoffrey Guy and Brian Whittle (hence the name), chose this approach and focused exclusively on extracts from cannabis, in order to withdraw products from this plant to the pharmaceutical market. They received permission from the British authorities to cultivate certain strains of cannabis for scientific research and began fruitful cooperation with Dutch pioneers of marijuana research HortaPharm.

The first success came in 2010. The product GW Pharma-Nabiximols (trade name Sativex), as a spray, has successfully passed clinical trials to alleviate a number of symptoms of multiple sclerosis and has been approved in the UK as well as in several other countries. Nabiximols, in fact, is a mixture of products of marijuana extracts: tetrahydrocannabinol (tetrahydrocannabinol, THC) and cannabidiol (cannabidiol, CBD) in an approximate ratio of 1: 1. In fact, according to the real effectiveness of Nabiximols, there are still many questions and doubts. The latest statistics says that for a number of symptoms the drug is "probably effective" - which, in general, is on the verge of ... The drug did not enter the US market, incidentally, there is evidence that in the US clinical trials were stopped in 2007.

However, it seems that in the coming months another GW Pharma drug, Epidolex, will be released to the US market, which is essentially pure cannabidiol (CBD), derived from marijuana. The drug showed significant effectiveness in cases of epilepsy (with a regular admission, the number of seizures is halved) and with the Drava and Lennox-Gastaut syndromes in children. The mechanism of action of Epidolex is unknown, which, incidentally, did not prevent him from obtaining a "fast track" status from the FDA. Just last week, an advisory committee with the FDA recommended approval of the drug, and such recommendations, as a rule, are not rejected by the regulator. With this news, the company's shares soared by 10%.

In development, GW Pharmaceuticals has a number of cannabinoids isolated from marijuana that are being tested for the treatment of epilepsy, schizophrenia and a number of oncological diseases ...


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Sleep - one day from the life of the brain

10 May 2018

What happens in our head when we wake up, open our eyes and realize ourselves here and now? And when breakfast, walk with a dog and then go to work? What processes are activated in our brain, when we, tired, return home, where an unresolved problem awaits us?

A piercing sound fills your skull. The misty veil that isolates you from the outside world evaporates as the signal becomes more and more intrusive. Fumbling in the dark source of noise, you finally restore the silence. But the devil's device has already done its job: you are awake. However, you are not yet immersed in the surrounding reality. The eyes are still closed, you feel the images slowly rise in consciousness ...

Neuroscientists have long known that unconsciousness of sleep has gradations. In fact, the previous night, you have passed about five cycles of sleep, repeatedly approaching the surface and deepest levels. During the first five or ten minutes, when reality is just beginning to "float away" from you, you were still relatively vigilant. If someone tried to wake you up, you might even say that you are in no way sleeping. This is the first stage, the beginning of the cycle and the beginning of your immersion in the unconscious.

Sometimes during this period you experience strange and extremely bright sensations, as if you fall or hear someone say your name. Sometimes the body seems to pierce a cramp - this phenomenon is known as the "myoclonic reflex": the muscles involuntarily contract, seemingly completely without a cause. During the first stage, if you had electrodes attached to your head, an electroencephalogram (EEG) would record a characteristic pattern of small and fast brain waves (theta waves).

Then, as you relax, over the next twenty minutes, the brain begins to generate additional complex electrical wave signatures (eight to fifteen cycles per second). This is the second stage. Then the body temperature decreases, the pulse slows down. It is at this point that you go from a shallow sleep to a deep one - this is the third stage. The profile of brain waves on the EEG slows down even more, the frequency ranges from two to four cycles per second. When these "delta waves" slow down even more, forming from half to two cycles per second, you enter the deepest, fourth phase of sleep. After about thirty minutes, the brain returns to the third phase, and then to the second. What for?

Undoubtedly, it would be simpler if unconsciousness remained simply a stable state. One possible reason is that a deep, almost comatose state can be fraught with for a long time: the world is full of dangers, one must be on the alert. In addition, the duration of the phases of sleep changes during the night: perhaps the brain adjusts to their needs. In the middle of the night, the fourth phase ends almost completely, and the fifth phase following it becomes dominant and lasts almost an hour.

The fifth phase is also called the "fast sleep" phase (REM), because your eyes actively move under closed eyelids. Meanwhile, the depth and frequency of breathing increases, the EEG reveals a profile of fast irregular waves, indicative of increased mental activity, comparable to activity during wakefulness. Dreams (which will be discussed in more detail later) are seen in this phase, although not throughout its entire length. Despite intense mental activity during this phase, your muscles, on the other hand, are the most relaxed, there is a sleepy paralysis: "fast sleep" is also known as a "paradoxical dream", because you seem to be conscious but immobilized. Just remember the situations that usually arise in nightmares when you try to escape from danger, but strangely find yourself immovable. This phase is repeated four to five times during the night.

But how is sleep monitoring controlled? It has long been known that the regulation of these cycles is based on the isolation of specific chemical transmitters, neurotransmitters. Acting as intermediaries between two neurons, these substances by diffusion move from one cell membrane (presynaptic) to another (postsynaptic) through a narrow slit - synapse: they run in the postsynaptic neuron pathway, causing "excitation" or "inhibition". In the language of neurobiology, inhibition is simply a reduction in the likelihood that a neuron will be able to generate an action potential (electrical impulse). Excitation is, on the contrary, an increase in probability. This vital electrical impulse lasts approximately one thousandth of a second (approximately 1 millisecond) and is a universal sign that the brain cell is active and signals this to the next cell. The excited neuron will generate volleys of action potentials at high speed, while the one that is "stalled" can be completely silent.

Transmitters controlling sleep, wakefulness and dreams are close in molecular structure to dopamine, noradrenaline, histamine and serotonin, together with the fourth, acetylcholine, a slightly more distant "relative", the most well-known and well-studied neurotransmitters. But the peculiarities of their distribution and localization are really of great interest: they can more than just make a connection between two neurons through a synaptic cleft, but instead they work on the principle of garden sprayers. Of course, there must be reasons for that. Each member of this chemical family plays a key role in controlling sleep and wakefulness. The levels of norepinephrine and its chemical precursor dopamine, as well as serotonin and histamine are highest during wakefulness, but decrease significantly during normal sleep and are practically absent in the fifth phase. Meanwhile, acetylcholine still "works". So what are these transmitters responsible for? It turns out that these molecules lead a double life and can act in a completely alternative role - as modulators.

The modulator does not cause immediate inhibition or excitation: instead, it affects how the brain cell reacts to the input signal for some time interval in the future. To better understand how this happens, imagine this situation: you work in the office, and today there was a rumor about raising wages. By itself, the rumor will not force employees, say, to pick up the phone of a silent phone. However, when a standard signal is received - a phone call, the employee will answer it faster and more willingly. The modulator works in the same way as this rumor: in itself it does not cause an effect, but strengthens the subsequent event. Theory and practice show that the classification of neurotransmitters as uniquely inhibitory or excitatory would be erroneous. It all depends on the time and the specific area of the brain in which they work.

So, for a certain period of time, the effects of the incoming stimulus (another transmitter) will differ in the presence of the modulator, up to the point that the effect of the stimulus can be completely leveled. Thus, the huge value of modulation lies in changing the time frame for signal transmission processes in the brain. Such fine regulation would never have been possible with a simple signal transmission. While you were sleeping and now when you are lying awake, the levels of these ubiquitous modulators rise and fall at different times, supporting different stages of sleep, placing large populations of brain cells more active or quiet. Therefore, it is very likely that modulators make an important contribution to the formation of consciousness and unconsciousness, as well as to the regulation of the transition between them. But we just found out that sinking into and out of sleep is a gradual process. This indicates that the modulators do not act as a key switch. Rather, they work as a kind of dimmer control ...


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What the brain loves and does not like

07 May 2018

The brain likes:

1. Specific purpose. As soon as you formulate for yourself a specific goal, the task - then miracles will begin. There will be funds, opportunities and time for its implementation.

And if you, having put the main goal, will be able to break it into components, and calmly, gradually, constantly, step by step will fulfill them - no problem before you will not stand.

2. Positive emotions. Emotions are short-term subjective reactions of a person to the surrounding world (joy, anger, shame, etc.). Feelings - a stable emotional attitude towards other people, phenomena. Feelings are connected with consciousness and can develop and improve.

Emotions are exciting - increasing the life of a person, and depressing - that is, overwhelming life processes. Positive emotions induce a person to act. They arise with satisfaction. Begin to search for simple joys of life - and stimulation begins in the brain - the release into the body of large doses of endorphins, pleasure hormones, and therefore, the satisfaction, and therefore the positive emotions that excite and increase your vital activity and allow you to quietly flow to thought processes, give rise to a good mood and positive mood for peace. It is natural for a person to seek joy - this is not a named instinct of self-preservation.

3. Movement and fresh air. In the fresh air, blood is more actively saturated with oxygen, faster carries oxygen and nutrition to the brain cells, oxidation and metabolism processes are increased, so is the energy we need, new biochemical compounds are born. The brain makes us move to save ourselves and us, of course. To give pleasure to think, create, solve complex problems, have memories.

There is no movement of fresh air, blood is sour-brains are "sour".

4. Simple food in moderation. Simple food is easier to get, cook, and digest. The brain says (if you want to hear it): my friend, 50% of the energy received by the body is spent on vision, 40% on digestion and disinfection of food toxins, and only 10% remains on movement, the work of mental and nervous systems, fighting billions microbes. If all the time to eat, when we think?

It is useful to eat soups - they improve digestion, metabolism, quickly fill the stomach, which gives a feeling of satiety with less food.

5. Sleep, rest. The brain, like the entire human body, needs rest. With physical activity, rest is a mental exercise, with intellectual exercise, from moral fatigue, a change of places.

A full rest is a dream. Sleep - the most mysterious state of man, without sleep a person can not live, although sleep is called "a small death."

In a dream, consciousness is disconnected, but the person continues to think, his thinking changes and obeys other laws. This is due to the fact that in the dream the subconscious enters the foreground. The brain analyzes what happened over the past day, structured it in a new way and gives the most likely outcome. This result may have been predicted for a long time, but the consciousness did not accept it, it was forced into the subconscious and extracted from there in a dream.

It is assumed that the brain at night can be given the installation: make a prediction, decision, output, output, for just a pleasant dream. Unnecessary impressions, obsession, are washed off by the night protective wave of the brain. People who constantly see prophetic dreams are likely good analysts.

6. Addictive. The brain can not immediately adapt to dramatically altered foreign circumstances: new living conditions, new work, study, place of residence, company, food, new people. In any activity, enter gradually, calmly, getting used to it. Every day doing the maximum possible, you will achieve the impossible. The habit of learning, working is developed gradually and constantly. Sudden understanding and insight always involves knowledge, perhaps not always fully realized.

Often parents, teachers, bosses, loved ones (and sometimes we ourselves), not understanding the whole complexity of addiction, require from us (and we from others) an instant result. This does not happen. It is best not to start, calm down, say good-naturedly to yourself or others - not all at once, "wait, kids, give only a period, you will be a squirrel, there will be a whistle." And slowly start moving, accelerating as you get used to it.

The brain itself creates stereotypes (habits, skills, conditioned reflexes). Stereotyped thinking essentially helps to live - there is no need to solve the standard problems anew. Every day, doing the same actions, we turn them into a habit, skill skill, conditioned reflex. Not including the brain to salivate at the sight of the lemon, close the front door, the tap, wash the dishes, shudder from the harsh car beep, click the cross when you need to close the program window.

Instinct and a little life experience make us from childhood create stereotypes of friends, enemies, lovers. This helps in the "sea of men" still someone to choose, to build their team and then stop, releasing time and energy for other life goals. Stereotypes help you communicate with other people, get on with your parents, educate your children.

7. Freedom. Let and limited by the instinct of self-preservation and social rules, useful primarily to ourselves. Freedom is independence from fears and stereotypes. Of course, we need stereotypes in the form of unconditioned and conditioned reflexes - we will not be burned, the second time to shove hands into the fire - it hurts! But if circumstances demand, show your contempt for pain and death - burn your right hand, like the Roman "military" Muzio Scevola. And do not be afraid to think in your own way and in a new way; defend their way of thinking, their lives, their appearance, their loved ones. And do not blame the whole world for not understanding and not recognizing you "all that extraordinary." And let others not be like you, have your own way of thinking, look at life.

8. Creativity - the ability of the brain, using and relying on the old, create a new, different, unlike. Creativity is the favorite work of the brain, which brings us together with God, making us gods. Creativity in the form of science studies, describes, explains the surrounding world and man, puts forward ideas, finds ways and means of translating them into life, looks into the future and is ready to change it for the better.

Creativity in the form of art, combining labor and emotions, reflects reality with artistic images. Art unites people: the writer, sharing his life, feelings, describing other people, shows that we are not alone in our experiences. The artist offers to see how the surrounding, we ourselves can be beautiful or ugly. The musician with the sounds of his heart forces the tuning fork to respond to our soul.

Art awakens our imagination, enriches our inner world, helps us see the world in a different light. Art creates ideals.

9. Division, sitting, communication, embrace. Life is a constant division of cells, a constant metabolism and distribution of information. The work of nerve cells in the brain of neurons is "love." They constantly "embrace", touching each other with dendrites (processes, "hands"), constantly transmit energy (nerve impulses) information about everything (biochemical compounds). Harmfully not to share, you can not demand, it is confusing. You have to be friends with your head, you have to be friends with people.

It is the essence of the brain - it constantly needs to receive information and give it away.

The brain does not like

1.Fearing. Oppressive, overwhelming life processes emotion. When we feel fear, the instinct of self-preservation, the brain zones, the groups of nerve cells, can not enter into thinking activity. A person is deprived of creative thought.

We are constantly worried about food, about loved ones, about pain (illness, treason, death), about life (war, tsunami, fool-boss, revolution, dollar rate, meeting with terminator) - i.e. we are in a state of stress. How to deal with this:
Pain and death must be despised.
Difficulties, if not avoided, should be tempered. In overcoming difficulties, you lose something, but you definitely get something.
Educate yourself in courage, pride and fortitude.
We must admit to ourselves that problems and troubles are inevitable companions of human life. They are not the first and not the last, which will have to be solved.
Believe in yourself and in your bright future, you are a problem, not it is you!

Fear is dangerous for mental health and for life. But one adaptive form of fear is necessary for us - caution!

2. Strong emotions of any kind. Strong emotions sharply inhibit the mental ability of the brain. Great joy and great grief can for a time deprive the ability to think. A prolonged such condition leads to a painful helplessness of the brain.

Girls, this is for you. When you "hysterize" (too emotional), your brain turns off. This made it possible to say "Women are fools!" But it has already been proved that the female and male brains are equally capable of education, social adaptation, and politics.

Different hormones affect neurology - men often have dyslexia, schizophrenia, autism. And representatives of the fair sex suffer from anxiety, depression, eating disorders. So do not impose this condition on your men - it literally makes them fools.

In men, logical thinking, not including the areas of the brain responsible for emotions, men fairly calmly solve the problem. In women, on the contrary, the catalytic thinking, i.e. they solve the problem through the prism of conflicting emotions. This is their physiology, they can not do otherwise. Guys, did you get it too? There is a way out: help them calm down: "chmoki-chmoki", "keep the ice cream", "let's warm the seagulls", "so calm down you! I'll solve your problem, let's go, take a walk, think about it, "etc. etc. The main idea: "I love you, but the problem will be solved when you calm down." And you will be surprised how a woman can handle everything perfectly.

The mechanism of emotions is first understanding (situations, phenomena), then emotions. And do we always understand the situation correctly, the other person, if in the three pines we are wandering, we do not really understand ourselves. First it's worth to calmly understand, and only then to "emotionally".

3. Darkness, loneliness. Such conditions include the instinct of self-preservation. Usual sources of the brain tone decrease and the "dark forces" of negative emotions walk freely through the unprotected brain (in the dark the enemy lurks, man is a herd creature, to him alone is dangerous and scary).

Loneliness is a severe mental condition associated with negative emotions and discomfort. But loneliness will have a beneficial effect on a person if taken as voluntary solitude. The lack of communication can not be a disaster, if a person has contact with someone, understanding. Perhaps in this world you are only a person, but for someone you are the whole world.

Throw away unnecessary stereotypes, give any of your states the right names, support you, soothing, carrying the energy you need.

4. Stereotypes. The brain creates stereotypes, but also "misses" them. The brain struggles with stereotypes for self-preservation "I want to think!" The brain reacts to every change in the external and internal environment.

There are people who, having spent some time developing basic life or professional skills (ideally all of them get in childhood and adolescence), bring them to automaticity, can implement them, allowing the brain at this time to solve more complex or creative tasks (cook - culinary, driver - ac, draftsman - artist, engineer - inventor, layout designer - designer)

Stereotypes destroy our relationships with people: with friends, with colleagues, with children, parents, beloved, when they behave contrary to our stereotypes. Do not be afraid to give up old ideas about people. Create new stereotypes taking into account new data ("do not persist in stupidity!"). Let people change, be different. And calmly and firmly do not let others impose on you stereotypes about you, if you do not need it.

Never be afraid of anything, with you is your treasure, your most reliable friend is your brain!

Take care of your treasure, study it, remember, the brain has reserves - but it's reserves. You can make the brain work in extreme mode, but the adaptive capabilities will be exhausted. This also explains the overly early and intensive development of children and their subsequent problems with adaptation in society.


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Recommendations for parents to correct the behavior of hyperactive children (ADHD)

24 Apr 2018

1. Define an acceptable behavior framework. The child should clearly understand what is possible and what is not allowed. The sequence is also important. If today the child can not be at night chocolate, then tomorrow can not be, and in the following days, too.

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2. It should be remembered that the actions of a hyperactive child are not always intentional.

3. Do not go to extremes: you should not allow excessive permissiveness, but you should not demand fulfillment of excessive tasks.

4. Strictly demand the implementation of rules that relate to the child's health and safety. Only do not overdo it if there are too many rules, the hyperactive child will not be able to remember them.

5. If you are persistent in meeting the requirements, do it in a neutral tone, with the same words, with restraint, calmly, automatically. Try not to say more than 10 words.

6. Reinforce oral requirements with a visual example of how to do it right.

7. It is not necessary to demand from the child simultaneous execution of accuracy, attentiveness and perseverance.

8. Do not insist on mandatory apology for misconduct.

9. Respond to the child's wrong behavior in an unexpected way: repeat the child's actions, photograph it, joke, leave one (only not in a dark place).

10. Stick to the daily routine. Meals, walks, games and other activities should take place on the same schedule. A hyperactive child can not be removed from fulfilling the usual requirements for other children, he must be able to cope with them.
11. Do not let the child take on a new job until he completes the first.

12. In advance, tell the child the time frame for his playing activity and set the alarm. When the timer expires, and not the parent, the aggressiveness of the child is lower.

13. Do not allow your child to stay behind a computer and television for a long time, especially if he is watching programs of aggressive and negative content.

14. Try to provide the child with long walks in the open air every day.

15. For physical hyperactivity, physical activities such as boxing and wrestling are not welcome.

16. It is more effective to persuade a child through bodily encouragement: praise the child by hugging him.

17. Punishments should be less than rewards.

18. Encourage the child also for what he already knows well, with the help of a smile or a touch.

19. Encouragement can be to provide opportunities to do what the child is interested in.

20. Remember that blame acts on hyperactive children more than other children.

21. Do not resort to assault. If there is a need for punishment, then for the hyperactive child, the cessation of his violent activity, forced isolation and house arrest will be punished.

22. As a measure of punishment, there can be a ban: watching TV, playing games on the computer, making phone calls.

23. After the punishment, have a conversation with the child. He must realize and remember why he was punished and what kind of behavior is not encouraged.

24. The child should have his own household duties, like the rest of the family members. For example, to clean the bed, arrange toys, lay out clothes in their places. Important! Parents should not fulfill these duties for the child.

25. Make sure that the child sleeps sufficiently. Nedosyp leads to further weakening of attention and self-control. By the evening the child can become completely uncontrollable.


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Tips for parents of a non-talking child

23 Apr 2018

1. Speak more with the child, voicing all the actions (feeding, dressing, bathing), commenting on the environment, not fearing the repetition of the same words, pronounce them clearly, patiently, kindly.

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2. Develop understanding of speech, using simple instructions such as "Give me a pen", "Where's the leg?" Lean on what the child is available.

3. Repeat the already mastered. Repeat the simplified versions in the speech along with the full words: the car - the bi-bi, the doll - la-la, fell-bah.

4. Sing to the child before going to bed. It is better not to change the repertoire often.

5. Desire to imitate an adult. This is possible when the emotional interest and availability of words that the child utters during joint games are combined (Hide-and-seek, Steam Engine-To-To). You can be surprised at what you saw: "Wow!"

6. The first words pronounced on an emotional background can be interjections: oh, oh, uh. The child is only allowed to repeat the vowels: o, a, y.

7. More often tell, read the first children's fairy tales, poems.

8. Encourage wording as you speak. Do not overload your child with television, video or audio.

9. When reading, shorten the text to understandable phrases. Do not say when the child is behind him. Be irritated, do not be shy about what your child does not say. Do not show unnecessary anxiety: everyone has their own terms, their problems. Without waiting for the child to speak. Begin to teach him to distinguish objects by size (large - small); to correlate colors, form (give the same);
number (one - many).

10. Massage the fingers and hands of the child. Give some meds: Cortexin, Cerebrolysin, Cogitum.


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Challenges for logopedic work with speechless children

20 Apr 2018

Recently, specialists are increasingly confronted with speechless children, i.e. with children who do not have speech. They have a complex organic disorder, which greatly complicates the logopedic work with them. For a full-fledged development of speech, it is necessary: innate linguistic ability, primarily preserved intellect, stimuli from the external environment, motivation for speech, the usefulness of the conductive pathways between the individual analyzers for which information is transmitted. In the brain there are speech zones: the posterior parts of the lower frontal gyrus; temporal gyrus; lower parietal region; as well as a zone located at the junction of the parietal, temporal and occipital regions of the left, dominant hemisphere by speech.

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Who can be called a non-talkative, speechless child?

A group of no-speech children is not homogeneous. It includes children with motor and sensory alalia, with a temporary delay in speech development, early childhood autism, intellectual insufficiency, infantile cerebral palsy, and hearing impairment. However, for all these children, there is a lack of motivation for speech activity, a lack of basic ideas about the meanings of objects and phenomena of the surrounding reality, an inadequacy of communicative, regulating, planning speech functions, a lack of sensorimotor level of speech activity.

Thus, at the initial stages of working with non-speaking children, its goals and tasks will be similar, regardless of etiopathogenesis and mechanisms of speech disturbance. At the present stage of the development of special education, it is urgent to develop educational programs and pedagogical technologies that ensure the comprehensive development of children with developmental disabilities.

The main goals of speech therapy with non-speaking children at the initial stages are: development of speech initiative, creation of motivation for speech activity simultaneously with enrichment of internal and external vocabulary; the formation of a child's ability to create an internal plan, a program of utterance (at first - primitive).

Logopedic work with non-speaking children provides a corrective effect, both on speech activity and on non-verbal psychic processes, on the emotional and personal development of the child.

The main tasks of corrective work with non-speaking children at the initial stage:

1. Stimulation of speech and mental activity.

2. Development of emotional communication with an adult. Expression of the teacher at each stage of the exercise with a no-speech child contributes to the development of imitation and emotionally adjusts children to speech and speech production.

3. Improving the ability to imitate the actions (echopraxia) of an adult, peers and speech imitation - echolalia.

4.Development and correction of psycho-physiological basis of speech activity: different types of perception, physiological and speech breathing, articulatory skills.

5. Formation of motivational and motivational level of speech activity.

6. Formation of internal and external lexicon (nominative, predicative, and attributive), providing minimal communication.

7. Formation of the initial skills of grammatical (morphological and syntactic) structuring of the speech message.

8. Prevention of secondary speech disorders.

The implementation of the tasks of speech therapy with non-speech children occurs in the process of using the following means:

- Games and exercises that activate all higher mental functions;

-Games and exercises regulating the muscle tone of children, allowing to correct the behavior of children, to affect the emotional-personal sphere;

-self-independent game activity;

-Igra, forming the structure of speech activity at all levels (from motivational-incentive to executive);

-Specifically organized correctional-developing environment;

-Organized family education of children.

Thus, a speech from a non-speaking child can only be triggered by using both all analyzer systems and the targeted impact of parents and professionals.


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What is the difference between a speech therapist and a Defectologist?

19 Apr 2018

The defectologist can begin work with children of one-year-old age, and the speech therapist starts to study with kids from three years old. Speech therapist corrects and develops speech, puts sounds and pronunciation, while the defectologist is engaged in the lag in the development of the child, caused by various disorders, and helps the kid to know the world.

Cortexin for speech development

So, for example, the speech therapist will not teach the child color, he will pronounce their names, striving for correct pronunciation, while the defectologist's task is to familiarize the baby with the flowers and learn the name of each of them. That is, in fact, a defectologist is a broad-profile specialist, while a speech therapist is only responsible for correcting speech disorders.

1.Defectologist works with problem and sick children, the speech therapist deals exclusively with healthy children.

2.Defektolog starts to study with one-year-olds, the speech therapist begins to work with children when they reach three years.

3.Defectologist - a specialist in a wide profile, speech therapist - a narrow-profile specialist.


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Problem of defective sound-pronunciation

18 Apr 2018

The problem of defective sound reproduction is also relevant in adulthood.

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Is it possible to correct the violation of sound reproduction in an adult? Of course!
But there are some conditions: to make the correct sound come into independent speech (automated), it is necessary to have a very great desire, and therefore motivation. Because in adulthood, the interactions between the articulatory zone of the cerebral cortex and the muscles of the articulation organs are already extremely strong (in contrast to preschool children, in which such connections, as they master the sounds of their native language, are just beginning to form). The sound setting in adults occurs, as a rule, faster than in children, but an adult will need more (in comparison with the child) the number of independent classes to fix the correct pronunciation and huge self-control at a long stage. With a positive attitude and some persistence, the new sound is automated and you will be self-sufficient, as all familiar will pay attention to your updated, clear pronunciation. Believe me, the efforts are worth it!

Another problem that an adult may face is a voice disturbance. Such violations can be organic or functional, arise rapidly (as a result of stress, disease, surgical intervention) or increase gradually. With this problem (especially with a sharp loss of voice), in no case should you delay the visit to the otolaryngologist, but against the background of the prescribed treatment, to the phoniatrist and the speech therapist. Here (as in the case of aphasia) the most important role is played by the time factor of contacting a specialist. In the future, the speech therapist will teach you how to perform the necessary vocal and breathing exercises to restore and strengthen the voice.

In adulthood, stammering is less likely to occur, most often in the remission stage it passes from childhood or adolescence. An adult can alleviate his condition by significantly reducing or completely eliminating the stumbling in speech under the guidance of a speech therapist. But since stuttering requires an integrated approach, it must be understood that along with the speech therapist needs to receive the support of a neurologist who will pick up a mild nerve-supporting treatment, and perhaps (with a pronounced stutter), recommend an additional examination. Often a good result is obtained if the psychologist also works in parallel with the patient.

Speech restoration in patients with aphasia is one of the most difficult areas of speech therapy with adults. Aphasia is amenable to logopedic correction, although the results depend not only on the qualification of the specialist, but also most significantly on the severity of the lesion of the speech centers of the cerebral cortex and the time to call on the speech therapist (extremely preferably the first six months or a year), as well as the patient's personal qualities and desire for lessons. However, with timely access to a specialist, there is the possibility of a significant restoration of speech functions. Speech therapist will conduct a survey and make a plan of work based on the causes of aphasia, since the methods of speech therapy correction for various forms of aphasia have their own peculiarities in each specific case. I assure you, at home, relatives and relatives will be able to deal with aphasias according to the tasks of the speech therapist, achieving good results in restoring speech.


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The Mysterious World of Neuropeptides

17 Apr 2018

Hormones are the most famous regulators of processes in the body. Their functions and chemical structure have been studied quite well, which makes it possible to create medications on their basis and successfully carry out, for example, substitution therapy. On the second place in the illumination are located neurotransmitters. These compounds preferentially link the nerve cells to each other, thereby activating or inhibiting various regions and processes. Influence on neurotransmitters is somewhat more complicated, but many drugs have been developed that affect metabolism, ejection, reverse capture, etc., hence the neurotransmitter system is adjustable.

Human peptides

At this stage in the development of medicine and pharmacology, the neuropeptides are least studied and controlled. Nevertheless, they take an active part in almost all processes in the body, regulate the most important behavioral and adaptive reactions, control circadian rhythms, food and sexual behavior, affect hormones and neurotransmitters. It is impossible to ignore this topic, as well as to collect all the data on it. According to the results of the studies, the data does not always coincide, sometimes they are directly opposite, which makes the description of neuropeptides difficult, due to the lack of a single classification, there is still much confusion. Thus, information on neuropeptides is not systematized enough, nevertheless this material is the most complete in Russian and includes a significant number of compounds not listed in other reviews.

Neuropeptides (NP) - biologically active compounds that participate in the regulation of metabolism, maintenance of homeostasis, affect immune processes, play an important role in the mechanisms of memory, learning, sleep, etc. The NP is characterized by a relatively short sequence of a chain consisting of amino acid residues, as a rule, it is 5-52 elements.

NPs are formed as a result of sequential hydrolytic decomposition of the precursor peptide, for example, several substances can form from the same initial molecule, which at each stage may have biological activity different from the initial and final products. The NP precursors are synthesized in the body of the cell by translating the gene encoding the peptide, then the proteases point split the long molecule into shorter chains that can later undergo transformation or remain unchanged. If it is a neuron, then the NP is transported to the presynaptic terminal, from which it is released into the synaptic cleft. Some neuropeptides are able to perform the functions of mediators, carrying out a direct transmission of the nerve impulse, others change the metabolism of the cell, acting as a neuromodulator. NP can transmit the signal not only to close distances, the receptors to some of them are at a sufficient distance from the site of synthesis, which makes it possible to compare them with hormones. The functions of many NPs duplicate each other, nevertheless everyone has a unique spectrum of activity. This feature allows you to more accurately transmit the signal and regulate the interaction of different parts of the body, coordinate a complex system of continuously occurring processes that somehow affect each other and require constant corrections. The vast majority of neuropeptides affect the "slow" metabotropic receptors associated with G-proteins. In addition, NP can change the activity of each other and some hormones (more often inhibit or activate their synthesis), which leads to the launch of cascade reactions.

Many neuropeptides are synthesized to a greater or lesser degree in various organs and tissues, and only some of them are strictly specific for certain zones. Distribution of NP in the body is not uniform, there are places that are most characteristic for each substance, but in small amounts they are determined in virtually all tissues. In the neural tissue, NPs are present in unmyelinated C-type fibers and small A-delta-type myelinated fibers. In the spinal cord, NPs are synthesized by the cells of the dorsal horns of the ganglia, then transported along the axons to the nerve endings, where they can act as neurotransmitters. In synaptic terminals, NPs are able to act together with non-protein neurotransmitters. A neuropeptide may be colocalized with one or more mediators, which leads to some enhancement or modification of the action. If their selection coincides in time, then the effect depends on both of them, but they can also be separated separately, which leads to the realization of the biological effect of each of them separately from each other.

At present, there is no complete and comprehensive classification of NPs. Attempts were made to develop it on the basis of the chemical structure, functions or place of synthesis. However, many NPs are able to perform several functions depending on the location, similar in structure of the compound - responsible for different processes, and various substances of origin being agonists. NP found in any tissues were not always specific to them and were later found in other organs. In addition, at the moment, new compounds are opening, which can not be attributed to any of the existing groups, since their functions are not fully understood. The classification of NPs by families can be regarded as the most complete and functional, since it takes into account the greatest number of features of these substances.

Classification of Neuropeptides:

  • Hypothalamic liberins and statins
  • Opioid peptides
  • Melanocortins
  • Vasopressin-tocine
  • Pancreatic peptides
  • Glucagon secretions
  • Cholecystokinin
  • Tachykinins
  • Motilin
  • Neurotensins
  • Bombesins
  • Kininy
  • Angiotensins
  • Peptides encoded by a gene similar to the calcitonin gene
  • Atriopeptides
  • Endozepines
  • Galanin
  • Endothelins

Hypothalamic liberins and statins
Tyroliberin, corticoliberin, lyuliberin, somatoliberin, somatostatin, melanostatin. The first family includes neuropeptides synthesized by the hypothalamus. They were combined into one group according to the topological feature and had mainly the function of stimulation (liberins) or inhibition (statins) of the synthesis of pituitary hormones. According to the chemical structure, the hypothalamic neuropeptides differ considerably from each other and have different precursors. In addition to influencing the structures remote from the site of synthesis, the NPs of this group can influence neighboring neurons, depressing or vice versa stimulating each other's formation. As they studied, representatives of the first family were found in other organs and tissues and found the ability to influence the emotional state, food and sexual behavior, the regulation of the sleep-wake cycle, the provision and launch of stress-protective mechanisms, the stimulation of immune processes, neurogenesis and many others.

Opioid peptides
The family of opioid peptides is characteristic of the majority of representatives of the amino acid sequence Tyr-Gly-Gly-Phe. Accordingly, OP works on opioid receptors, mainly μ (MOP), δ (DOP), and κ (KOP), associated with G-proteins. Due to the ability to bind to the listed receptors, OPs have a naloxone-inhibiting, morphine-like analgesic and sedative effect. EP have a variety of biological effects. With regard to the impact on behavior, they have the ability to influence aggression, motivation for satisfaction, sexual attraction, food saturation, stressor adaptive processes, drug dependence, sedation, modulation of pain sensitivity, etc. In addition, they participate in neurodegenerative processes, damage to brain tissue due to trauma and ischemia.

Opioid peptides (OP) are widely distributed in the central and peripheral nervous systems, GIT, serum, are produced not only by neurons, but also by cells of the endocrine and immune systems. Most opioid peptides are formed from common protein progenitors - proopiomelanocortin (α-MSH, γ-MSH, β-MSH, ACTH, β-endorphin, α-endorphin, γ-endorphin, β-lipoprotein (β-LPH), γ-LPH , CLIP), prodinorphine (dinorphin A, dinorphin B, α-neoendorfin, β-neoendorfin, dinorphin-32, leimorfin), preproenkephalin (leu-enkephalin, meth-enkephalin, amidorfin, adrenorphine, peptide B, peptide E, peptide F), prepro- nociceptin, preproorpharin (nociceptin (orfanin FQ)), prepro-NPFF (NP FF, NP AF, NP SF), and others.

Enkephalins are short peptide chains, from 5 amino acid residues. Typical members of the family are leu-enkephalin and met-enkephalin, named for the fifth amino acid, respectively leucine and methionine. In addition, the group includes DTLET and DAMGO. They act mainly on the δ-opioid receptors. Both neuropeptides have a pronounced morphine-like analgesic, sedative effect. They take part in the formation of behavioral reactions. Their participation in many neurodegenerative pathologies is proved.

Endorphins α and β are products of hydrolysis of POMC and contain 16 and 31 amino acid residues, respectively. They participate in the motivation of alcoholic behavior, nociceptive reactions, stress response, regulation of circadian rhythms. Β-endorphin is less specific to receptors and can activate to a greater or lesser extent all three of the number of opioids.

Dinorphins are formed during the conversion of prodinorphine and contain in their structure a sequence of leu-enkephalin. The most important action is the central and peripheral nociceptive process. The group includes dinorfin A and dinorfin B (rimorphin), containing respectively 17 and 13 amino acid residues. In addition, α-, β-neoendorfin is formed. All of them activate mainly κ-opioid receptors. Their selectivity is due to the presence of arginine and lysine at the C-terminus. If the precursor proteolysis does not take place completely, a so-called "big" dinorphine is formed, which includes dinorphine A and B, and has the same properties, but is more selective for BCD.

Dermorphin and deltorphin-specific agonists of the μ- and δ-opioid receptors, respectively, consisting of 7 amino acid residues. They participate in reducing the threshold of epileptic readiness, have a pronounced analgesic effect, stimulate the release of β-endorphin. They differ in the presence of the D-amino acid in the second position, which makes them more resistant to enzymatic hydrolysis.

Hemorphins are products of proteolytic decomposition of hemoglobin, have an affinity for μ-opioid receptors. Participate in the analgesic reaction and the development of euphoria after exercise.

Endomorphin-1 and -2 are tetrapeptides, show the greatest specificity for the μ-opioid receptors from the family. Have a pronounced and long analgesic effect.

Nocystatin contains 17 amino acid residues in its composition. Reduces pain sensitivity. Studies are under way to create on its basis analgesic agents that are not addictive and morphine-like addiction.

Β-Casamorphin consists of 7 amino acid residues and is formed by the hydrolysis of casein. It is able to activate μ-opioid receptors, stimulate the immune system and increase food intake.

Leumorfin (leimorfin) is formed from the precursor of preprodinorphin. Have sufficient affinity for opioid receptors and for biological action is comparable with other OP.

Adrenorphine is synthesized mainly in the adrenal glands. Has the ability to influence nociceptive processes, as well as other peptides of the family.

A group of peptides with anti-opioid activity enhance the pain response, increase anxiety, stimulate the release of ACTH and corticosterone, inhibit morphine-induced effects. Prevent the formation of dependence on alcohol and morphine, affect the development of withdrawal syndrome in animals with morphine dependence.

Presented are:

Neuropeptides AF and SF consist of 18 and 11 amino acid residues, respectively. The neuropeptide FA consists of 8 amino acid residues. Receptors to it are located mainly in the spinal and supraspinal zones containing a large number of endogenous opioids.

Nociceptin (Orphanin FQ) - consists of 17 amino acid residues and has a structure similar to that of opioid peptides. The receptors for nociceptin are similar to opioid receptors, linked to adenylate cyclase. When these receptors are activated, potassium channels are activated and calcium is inhibited. Nociceptin and its receptors are most widely represented in the cortex, olfactory nuclei, amygdala, hippocampal formation and dorsal horns of the spinal cord. Takes part in the processes of memory, learning, stressful reactions. In experimental models showed the ability to reduce anxiety. Activation of the nociceptin receptors leads to analgesia, but it interferes with the action of opioids.

Melanocortins
Adrenocorticotropin (ACTH) is a hormone synthesized in the anterior pituitary gland, the main function of which is stimulation of adrenal corticosteroid production. It is proved that he is able to synthesize and other parts of the brain, and in addition to the hormonal function to act as a neurotransmitter, to participate in the regulation of higher cortical functions such as memory, attention, training.

A-β-γ-melanotropins (melanocyte-stimulating hormones) are formed from proopiomelanocortin. Synthesis occurs most intensively in the median lobe of the pituitary gland. The receptors for MSH are associated with G-proteins and are divided into 2 types: MCHR1 and MCHR2. The expression of Type 1 receptors is highest in the cortex, hippocampus, amygdala and nucleus accumbent, suggesting that these neuropeptides are involved in the development of pathologies such as mood disorders and schizophrenia. This is confirmed by the introduction of antagonists to this type of receptor, which caused anxiolytic and antidepressant effects. A-MSH stimulates the formation of pigment in the skin, participates in mental processes - memory and learning, sleep, aggression, modulates inflammation in the brain, blocks the synthesis of gliosis of tumor necrosis factor. Γ-MSG has a lesser effect on the pigment metabolism, but enhances the steroidogenic function of ACTH. All MSG are able to participate in the regulation of gastrointestinal function, immune processes, cell growth and mitosis, and eating behavior.

Vasopressin-tocine
Vasopressin and oxytocin are produced in the hypothalamus, along the axons enter the posterior lobe of the pituitary gland, from which they are released into the blood. They have a strong effect on the formation of behavioral reactions, such as affection, sexual, parental behavior. Under stress, they participate in the creation of protective mechanisms. In addition, they can influence blood pressure, reduce smooth muscle, metabolism.

Mesotocin, isotocin, vasotocin is composed of 10 amino acid residues, having a common initial sequence of 6 amino acids. Synthesize mainly in the posterior lobe of the pituitary gland together with oxytocin and vasopressin and are similar to them for biological effects, but less active.

Predecessors - preprovazopressin-neurofizin II (vasopressin, neurofizin II), preproxitocin-neurofizin I (oxytocin, neurofizin I).

Pancreatic peptides
The neuropeptide Y consists of 36 amino acid residues. Distributed in the brain (hypothalamic and cortical regions, hippocampus, thalamus) and peripheral nervous system, postganglionic sympathetic fibers, adrenal glands, megakaryocytes and platelets. There is evidence of a change in the distribution of NP in the neuronal population of the prefrontal cortex in ontogenesis in pathological disorders. Oppressing the selection of the transmitter from the nerve endings. The effect is manifested by hypotension, hypothermia and respiratory depression, secretion of water and electrolytes in the intestine, regulation of circadian rhythms and motivational behavior. Is able to participate in the regulation of eating behavior, so, with its chronic introduction into the central nervous system, the body weight increased. During the period of food intake decrease, the amount of neuropeptide Y in arched and paraventricular nuclei increased. With the breakdown of the neuropeptide Y, the resulting substances can act as its agonists and antagonists, which is determined by their chemical structure.

The tyrosine tyrosine peptide (PYY) has a similar structure to the neuropeptide Y and differs from it with the additional amino acid residue -Tyr. By function, they are just as similar and competing for binding to the same receptors.

Pancreatic polypeptide (PPY) is synthesized by PP-cells of the islets of Langerhans pancreas. It has 36 amino acid residues. By the mechanism of action it is a cholecystokinin antagonist, suppresses the secretory activity of pancreatic cells and stimulates the production of gastric juice, delaying food in the stomach.

The precursors are prepro-NPY (NPY), prepro-PPY (PPY), prepro-PYY (PYY).

Glucagon secretions
Glitsentinya is an intermediate product of the formation of glucagon from preproglucagon. Until the end of its properties are not studied, it is assumed that the spectrum of its activity is similar to that of glucagon.

Glucagon (GRP) contains 27 amino acid residues. The largest amounts are contained in the gastrointestinal tract and brain, secreted by some tumors, where it stimulates mitosis, has a trophic effect on normal and neoplastic cells, including autocrine stimulation of small cell lung cancer proliferation. Participates in the regulation of glucose metabolism, with an increase in its level stimulates the synthesis of insulin and inhibits eating behavior. In the central nervous system improves the processes of memory formation, takes part in the body's response to stress. It takes care of the regulation of sleep-wake cycles, body temperature, appetite and satiety. Modulates the activity of macrophages. Regulates the secretion of pancreatic and hydrochloric acid enzymes in the stomach, stimulates the contraction of smooth muscles and the release of certain intestinal hormones, including gastrin.

VIP (vasoactive intestinal peptide) consists of 28 amino acid residues. Widely represented in the central nervous system, especially in the cerebral cortex, where it participates in the formation of behavioral reactions, has a positive effect on the processes of learning and memory, sexual behavior. Can act as a mediator in serotonergic and cholinergic systems. On the periphery causes the expansion of the bronchi, vessels (including cerebral).

Secretin contains 27 amino acid residues. It is mainly produced by brain structures, adrenals and intestines. Most strongly, its effect is manifested in the cells of the gastrointestinal tract, where it leads to relaxation of smooth muscles and increased secretion of hormones by the pancreas.

Gastrin is mainly produced by G-cells of the stomach and pancreas. A "large" gastrin is formed, which consists of 34 amino acid residues, gastrin-17 and gastrin 14, which contain respectively 17 and 14 amino acids. On the functions performed they are similar, since all contain the same active center. Increase the secretion of hydrochloric acid, pepsin, bicarbonates, secretin, cholecystokinin, somatostatin and some other peptides involved in digestion. Stops the emptying of the stomach. It leads to the expansion of the stomach vessels by increasing the production of prostaglandin E. Participates in the regulation of eating behavior, reducing the motivation for food search.

Predecessors - preprogastrin (gastrin), preproglycagon (glycinthin, glucagon), preprosecretin (secretin), prepro-VIP (VIP).

Cholecystokinin
Cholecystokinin contains 33 amino acid residues. Influencing the structure of the central nervous system affects the emotional state, leads to the activation of behavior aimed at obtaining food, has an antidepressant effect. It is of great importance in the regulation of the functions of the gastrointestinal tract - it stimulates secretion in the pancreas, motility of the gallbladder and intestines. In the decay of cholecystokinin, products that have their own action are formed. Some of them can reduce the effects of morphine and enkephalins with respect to pain sensitivity. Preecessor is preprocholecystocinin.

Tachykinins
This group includes NPs that have a β-preprotachykinin precursor and contain the-Gly-Leu-Met sequence at the C-terminus. Biological effects are mediated by exposure to receptors associated with G-protein. Tahikinins can also act as neurotransmitters and are widely represented in various tissues of the body. The main physiological effects are the regulation of the tone of the smooth muscles of the intestine, bronchi, participate in behavioral reactions, nociceptive processes, inflammatory processes.

The substance contains in its composition 11 amino acid residues. It was opened in 1931. and is the most studied of the family. It is synthesized mainly in the central nervous system - the amygdala, the septum, the hippocampus, the hypothalamus and the gray matter in the brain water pipeline, which are involved in the formation of anxiety and depression. Occurs in the posterior horns of the spinal cord is a neuromodulator in primary afferent fibers and unmyelinated C-type fibers. It has a wide spectrum of physiological effects - it can influence the blood pressure level, capillary permeability, smooth muscle contraction, possesses secretory action, participates in the control of secretion of prolactin and digestive hormones. The synthesis of substance P is enhanced by dopamine: thus, it was revealed that when dopanergic fibers are damaged, mRNA expression is reduced, which corresponds not only to the formation of substance P, but also to enkephalins and dinorphine. Participates in the transmission of a pain signal. The ability of substance P to influence training, sleep, resistance to stress is studied.

Neurokinins (A, B and K) are similar in their effects to substance P, but have a different specificity for the receptors. They change the excitability of nerve cells, have the ability to exert an anti-inflammatory effect - their effect leads to vasodilation and increase in their permeability, the release of prostaglandin E2, cytokines and amines by mast cells and leukocytes. In addition to these physiological effects, they participate in the transmission of a nerve impulse.

Cassinin consists of 12 amino acid residues. Takes part in lowering blood pressure, stimulating contraction of smooth muscles. There is evidence that cassinin has anticonvulsant activity.

Motilin
In its composition contains 22 amino acid residues. It is produced mainly in the gastrointestinal tract, where it affects mainly the motor function - it strengthens the tone of the lower sphincter-esophagus, stimulates the emptying of the stomach and the motility of the large intestine. Stimulates the production of insulin and somatostatin by the pancreas. In the central nervous system, the highest concentration is found in the hippocampus. The effect of motilin on mental functions has not been studied enough, it is assumed that it affects food behavior.

The predecessor is prepromotilin.

Neurotensins
Neurotensin is found mainly in the hypothalamus, mesocorticolimbic and nigrostriatic zones, ventral cover, septum, cingulate gyrus, small intestinal mucosa. The peptide has a strong hypotensive effect, leads to a reduction in smooth muscle, reduces body temperature, increases the glucose and glucagon content, can bind to mast cell receptors. Neurotensin has in some sense a hormonal action - in the pituitary gland enhances the secretion of LH and FSH. There are data on its ability to influence sexual behavior, the development of stress reactions and nociceptive processes. It is established that dysfunction in the neurotensin system occurs in mental illnesses, in particular schizophrenia. It is assumed that the effect on its metabolism can have an effect in psychotic states, without causing at the same time an increase in weight and cataleptic manifestations. However, clinically significant evidence for this was not obtained. Associated with dopaminergic, serotonergic, GABAergic, glutamatergic and cholinergic systems.

Neuromedins N and U (NMN, NMU) are secreted in the cells of the central nervous system and gastrointestinal tract. Receptors to them are located in neurons, cells of the small intestine, pancreas, stomach, lymphocytes, monocytes, muscle fibers of the uterus. Exposure to NMU leads to a decrease in body weight by reducing appetite. In the regulation of immune processes increases inflammation, activating the mast cells. NMN can act as a neurotransmitter.

Xenopsy is involved in the regulation of smooth muscle tone.

The precursor is propreneurotensin.

Bombesins
Bombesin consists of 14 amino acid residues. It is a powerful activator of the hypothalamic-pituitary-adrenal axis, participates in the regulation of the body's stress reaction, affects the memorization processes. In addition, it regulates the consumption of ethanol. Physiological effects consist in vasoconstriction, decrease in body temperature, regulation of secretory processes in the gastrointestinal tract, takes part in autocrine stimulation of cell proliferation and growth of small lung cancer cells.

Gastrin-releasing peptide (GRP) consists of 27 amino acid residues. It is common in the brain tissue, intestines, lungs, immune system, and others. Its main functions can be called regulation of sleep-wake cycles, thermoregulation, effects on appetite and satiety, modulation of macrophage activity, increased secretion of enzymes by the pancreas, hydrochloric acid in the stomach , a reduction in smooth muscles, the release of gastrin in the intestine, and participation in the regulation of respiration at the level of the brainstem. GRP stimulates the mitotic activity of cells, including small cell lung cancer.

Litorin has many properties of the family, in particular, the ability to regulate body temperature.

Kinines
Kinins have a wide spectrum of activity and are a link in the regulation of vascular tone, blood coagulation and fibrinolysis. They are synthesized in most tissues, including the CNS.

Bradykinin consists of 9 amino acid residues. Its effect leads to relaxation of the smooth muscles of the walls of the vessels, bronchi, uterus, intestine. It takes part in the regulation of hemostasis, electrolyte balance, permeability of capillaries, local inflammatory reactions and pain sensitivity. The muscle fibers outside the vessels act in the opposite way, leading to their constriction, which is important in the development of inflammation and pain intensification.

Kallidin consists of 10 amino acid residues and differs from bradykinin by the presence of a lysine residue at the beginning of the chain. By physiological effects similar to bradykinin.

The predecessor is the kininogen.

Angiotensins
Angiotensins I, II, III are synthesized in the central nervous system and other tissues and organs. The most studied functions of these peptides are the regulation of the state of the cardiovascular system, water-salt metabolism, and blood pressure. Angiotensins are products of sequential hydrolytic cleavage from the terminal portion of several amino acids. Thus, angiotensin II is formed from angiotensin II and further with a shortening of the chain. The most powerful of the group is angiotensin II, which is formed under the influence of renin and PDA. It plays a role in the formation of mechanisms of arterial hypertension. It is part of the renin-angiotensin-aldosterone system. It is associated with the adrenergic system and tachykinins by the mechanism of action. It has been proven that angiotensins participate in learning processes, memory formation, motivation, internal reinforcement, pain sensitivity and control of emotions.

The precursor is the preprotein angiotensinogen.

Peptides encoded by a gene similar to the calcitonin gene
Calcitonin (contrinsular hormone) consists of 32 amino acid residues. It is produced mainly by C-cells of the thyroid gland. Calcitonin-like immunoreactivity is found in the pituitary gland, cerebrospinal fluid, lungs, thymus, intestine, liver, bladder. In the brain, the highest content of calcitonin is found in the zone surrounding the posterior part of the hypothalamus, mid elevation and pituitary gland. He takes an active part in the regulation of the water-salt balance. Reduces the content of calcium and phosphorus in the blood plasma, which leads to a change in the metabolism and activity of cell membranes. Has analgesic and anorectic effect, leads to vasodilation, hypotension, hyperglycemia, stimulates gluconeogenesis and glycogenolysis.

Calcitonin-gene-related peptide (CGRP) consists of 37 amino acid residues. In fairly large amounts, it occurs in the central and peripheral nervous, cardiovascular, genitourinary, GIT and C-cells of the thyroid gland. Has the ability to influence blood pressure, depending on the attendant factors leads to hypo- or hypertension, is a strong vasodilator, causes tachycardia, is involved in maintaining the tone of the coronary vessels and modulating the pain sensitivity, affects food behavior and cerebral circulation.

The precursor is prepro-CALC (calcitonin).

Endozepines
The peptide inhibitor of diazepam binding (DBI) consists of a large number of amino acids. Biological activity has both DBI itself and its fragments - endozepin-6 and octadecaneuropeptide (6 and 18 amino acid residues in its composition, respectively). These peptides are in large numbers in the central nervous system and are ligands of benzodiazepine receptors. By structure - strong antagonists GABA, which determines their biological effects. The level of endozapines increases in brain tissue under stress and aging. It has been proved that these peptides play a role in the formation of reactions to stress and the development of anxiety states - when intragastric administration has an anxiogenic and proconflicogenic effect, the search for their antagonists can lead to the creation of a new type of anti-anxiety drugs.

The predecessor is BDI in isoforms 1, 2, 3.

Galanin
Galanin consists of 29 amino acid residues. Receptors to it are located in the hippocampus, hypothalamus, amygdala, preoptic zone, supraoptic, arcuate nucleus. Receptors are divided into 3 types and they are all associated with G-protein. In experiments it was shown that when exposed to galanin receptors, anxiolytic and antidepressant effects can be obtained. When combined with other substances, it can exert the most diverse influence - when colocalized with acetylcholine takes part in mnestic processes, the role in the development of Alzheimer's disease, with noradrenaline - the formation of social status, with vasopressin and oxytocin in supraoptic and paraventricular nuclei acquires the ability to influence osmoregulation. Formed in the hypothalamus stimulates the secretion of LH and takes part in the regulation of the feedback of the HGH axis. It is able to inhibit the secretion of glutamate and the electrical activity of the arcuate nucleus.

The predecessor is pre-progalanin.

Endothelins
Endothelin I, II, III are synthesized predominantly in the vascular endothelium, their expression is present in the neural tissue. They are powerful vasoconstrictors. Together with other peptides and hormones play an important role in the regulation of the endothelium, the development of renal ischemia, hypertension, bronchial asthma, heart failure and cerebral vascular pathologies. The main active peptide of the group is endothelin I. Endothelins have different precursors expressed by different genes.

In addition to the neuropeptides represented in this classification, there are a large number of compounds not included in it. To date, several hundred NPs have been opened, which for various reasons can not be attributed to existing groups. Here are some of them.

Orexins
Orexins belong to the group of hypothalamic peptides and include orexin A and orexin B, consisting of 33 and 28 amino acid residues, respectively. Both peptides interact with the OXR1 and OXR2 receptors. Neurons secreting orexins are contained in the perifornical zone of the lateral hypothalamic field. Despite the fact that there are not many of them, these neurons strongly branch, having connections with various parts of the brain, such as paraventricular, dorsomedial arcuate nucleus of the hypothalamus, blue spot, posterior hypothalamic field, spinal cord. Orexins control food intake, participate in the regulation of circadian rhythms and the development of stress reactions, sexual behavior. Their concentration in the hypothalamus increases with fasting, but intracerebral administration causes only a brief increase in appetite without a noticeable effect on the total amount of food consumed. Narcolepsy and catalepsy are associated with the absence of orexin, as they can inhibit both phases of sleep and prolong the period of wakefulness. Orexins increase the activity of the sympathetic nervous system and maintain muscle tone, which is important with increasing physical activity and maintaining it at a high level. In addition, they can positively influence the secretion of HGH-axis hormones. It is assumed that orexins can play a role in the development of diseases such as Huntington's chorea, Parkinson's disease, obstructive sleep apnea syndrome, type II diabetes.

Leptin
Leptin consists of 35 amino acid residues. The predecessor is preproleptin. It is synthesized mainly in adipocytes and only in small amounts in other organs and tissues, including such parts of the brain as the cortex, hippocampus, cerebellum, basal ganglia, trunk. The greatest number of receptors for leptin in the brain is concentrated in the ventrobasal and ventromedial hypothalamus. With the accumulation of white adipose tissue in the body, the content of leptin increases and, accordingly, when fasting decreases. The peptide plays an important role in food behavior and energy metabolism - it reduces the need for food, suppresses appetite and speeds up the metabolic processes at the periphery. Directly or indirectly regulates the synthesis of hormones that affect food behavior, reducing the synthesis of oryxigenic and increasing anorexigenic. There is evidence that leptin may act as a neuroprotective agent, a neuroplastic factor. Leptin inhibits the development of excitotoxicity of glutamate and limits the damage caused by oxidative stress. In the hippocampus, under the influence of the hippocampus, the formation of free radicals is suppressed. In dopaminergic neurons it is able to stabilize mitochondrial membranes and to limit the phenomena of oxidative stress due to expression of uncoupling proteins of UCP2. Limits apoptosis in cells. Has an anticonvulsant effect. Affects memory processes, contributing to the consolidation of short-term and long-term. It is suggested that a reduction in leptin levels may be positively associated with the development of Alzheimer's disease, because it limits amyloidogenesis, by inhibiting β-secretase and activating α-secretase, and also participates in τ-phosphorylation processes, reducing the formation of abnormal τ-protein, facilitating elimination β-amyloid. It is suggested that it may be important in the development of Huntington's chorea and Parkinson's disease. In addition, it regulates blood pressure and vascular tone.

DSIP (delta-sleep-inducing peptide)
DSIP (delta-sleep-inducing peptide) consists of 9 amino acid residues. Until now, the gene, its coding, predecessor and specific receptors with the genes encoding them has not been identified. DSIP is found in the neurons of Brock's diagonal ligament, the ventral septum, the anterior hypothalamus, in the areas with gonadotropin-releasing hormone-reactivity, melanin concentrating hormone, thyroid-stimulating hormone, peptides of the secretory cells of the gastrointestinal tract, melanocorticotropes of the intermediate lobe of the pituitary gland, brainstem, pituitary and epiphysis; has specific differences in localization. Often, DSIP is colocalized with catecholamines in the chromafin granules of the adrenal medulla. With intraperitoneal administration of its rats, an increase in the content of norepinephrine and serotonin in the cerebral cortex and an increase in adrenaline without a change in the concentration of dopamine have been established, due to which it can exert a inhibitory effect on the central nervous system. There are data on stimulation of GABA production and prophylaxis. DSIP blocks the stimulating effect of glutamate by reducing the sensitivity of the "fast" ionotropic NMDA receptors of the glutamatergic system of the brain and the subsequent reduction of glutamate stress-induced excitotoxicity. Has a membrane-stabilizing effect on neuronal, erythrocyte and leukocyte membranes. Increases the activity of c-Fos gene expression, which is a marker of neuronal activity, of various parts of the limbic system, playing a trigger role in the development of emotional reactions to stress and forming their neurotransmitter integration, which leads to activation of somatovegetative manifestations. It has an anti-stress action and helps to create a state of "pre-adaptation".

The involvement of DSIP in the regulation of sleep-wake cycles is controversial, different authors provide various data, from the ability to suppress to stimulation of sleep phases. Has antiepileptic and anticonvulsant activity. The peptide can participate in analgesic processes by enhancing the binding of met-enkephalin to the OP. Enhances the release of melatonin by cleaving the remainder of tryptophan from the terminal portion of the molecule. It affects the decrease in MAO activity, inhibition of corticoliberin synthesis, stimulation of the synthesis of somatotropin, somatostatin and lylyberyrin. Determines naloxone-dependent analgesia. It is able to reduce the level of lipids and cholesterol, the cholesterol coefficient of atherogenicity. DSIP is able to prevent oxidative modification of proteins during physiological aging. Has hyperglycemic activity, which may be due to an increase in the concentration of catecholamines, which reduce the release of insulin against the background of increased production of glucagon.

PACAP (a peptide that activates pituitary adenylate cyclase)
PACAP (a peptide that activates pituitary adenylate cyclase) contains 38 amino acid residues. The structure and functions are similar to VIP. PACAP is widely distributed in brain structures and peripheral organs, including the endocrine system. The greatest number of neurons containing a peptide is found in the hypothalamus, in particular in the supraoptic and paraventricular nuclei synthesizing vasopressin and oxytocin. The peptide stimulates their production by activation of cAMP. Can act in the hypothalamus as a neurotransmitter and neuromodulator in the regulation of hormone secretion. Modulates vasopressin and oxytocin in the regulation of blood pressure and osmosis of cells, takes part in modulating the function of the cerebellum with physical activity. It is suggested that PACAP is involved in regulating the rhythm of melatonin production in the pituitary and, accordingly, affects circadian rhythms. Participates in the regulation of food behavior, having an anorexigenic effect by activating cAMP in supraoptic and paraventricular nuclei. It is important in ontogenesis, inhibiting the programmed apoptosis in the developing brain, stimulating the growth of neurites, decreasing the number of mitotically dividing cells and promoting the differentiation of neuroblasts, has a neuroprotective effect in neurotoxicity caused by an increased concentration of glutamate. Consequently, in the developing brain, PACAP acts as a neurotrophic factor, and in the developed brain as a neuroprotective agent. By activating the pituitary adenylate cyclase, the peptide stimulates the release of hormones.

BINP (neurotrophic peptide from the damaged brain)
BINP consists of 13 amino acid residues. It protects brain cells from excitotoxicity of glutamate, promotes survival of cholinergic neurons of the septum and dopaminergic neurons of mesencephalon in the primary culture of the neonatal brain.

It is difficult to overestimate the role of neuropeptides. Their study over time could open prospects for the creation of drugs and artificial regulators of the body's processes. Now a lot of research is being done and attempts are being made to create preparations based on them, but the matter is complicated by the insufficient study of all the properties of neuropeptides and their interaction with other systems. As an example of such studies, the following table can be cited.

Examples of the results of II and III phases of clinical trials of ligandine neuropeptide receptors in mental disorders.


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One of the main causes of developing demension

16 Apr 2018

Scientists have confirmed that traumatic brain damage is associated with an increased risk of dementia. In addition, the maximum risk increases in patients with multiple traumatic brain injuries, they emphasize.

The study analyzed data for almost 2.8 million patients, 132,000 (4.7%) of which had at least one traumatic brain injury in 1977-2013, and 126.7 thousand ( 4,5%) was diagnosed with dementia during 1999-2013. After adjusting for socio-demographic factors and co-morbidities, including neurological and psychiatric factors, the researchers found that, compared with persons who did not have traumatic brain damage, the risk of developing dementia was 24% higher in patients who underwent similar injuries. In patients with five or more traumatic brain damage, the risk increased more than threefold. Moreover, even a single case of light traumatic brain damage increased the likelihood of developing dementia by 17%.
However, the authors of the study from the Medical School of Washington University noted earlier that the absolute risk of developing dementia under the age of 50 remained relatively low. More efforts are needed to prevent traumatic brain damage and identify strategies to reduce the risk of subsequent dementia.


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