Programmed cell death

The biologist says about misapply of cell death, the role of apoptosis in the pathogenesis of cancer, and the prospects of research in Russia. We visited the laboratory study of apoptosis mechanisms in order to understand what is programmed cell death, the role it plays in the development of the human body and which research tasks are now facing scientists in this field.

There may be two violations of program cell death. First violation is due to the fact that the cells die very quickly, not when they want to die, and those cells die, which is necessary. This leads to a series of diseases. Above all, this disease, neurodegeneration associated with Alzheimer's disease, Parkinson's, and other Hutchinson. A second example - a disease associated with HIV infection with impaired hematopoiesis, and so on.

The second type of violations associated with the fact that the cells do not die, then a large number of abnormal cells accumulate in the body or tissue. A striking example - it carcinogenesis when tumor cells are not killed are divided, and thus, the tumor appears. There is a whole series of blood diseases associated with it, autoimmune diseases, viral diseases. The problem with the following viruses: some viruses and bacteria cause cell death, while others, on the contrary, slow down the process. Therefore, two types of disease can be identified, too, leading either to accumulation of cells, or to their disappearance.

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Programmed cell death is very important for the development of the process of embryogenesis, development of the organism as a whole. Now a lot of work carried out on this subject, because the abnormal development of the body, abnormal development of the embryo due to a violation of the process of cell death. The second direction - is the pathogenesis of various diseases. We can first understand how the pathogenesis involves a violation of different cell death mechanisms. And the second point - as it can be used for specific effects on the mechanism to either slow down or speed up cell death.

Medicines for cancer are not, never was and never will be. One medication. Cancer - is a systemic disease that disrupts the work of many organs. Moreover, the tumor develops differently in different organs. Therefore, to find a drug that could be used against all tumors, unreal. In tuberculosis, for example, there is a drug that targets the Koch wand and fight against it. And now there is a problem with resistance. We need to find something to overcome resistance in the treatment of tuberculosis. In the treatment of cancer a lot of ways.

Neurodegenerative Diseases

Biologist talks about mutations of proteins, Alzheimer's disease and the role of chaperones in the human body.What is the cause of neurodegenerative diseases? What role in the human body play a chaperone? What are the different approaches to the treatment of Alzheimer's disease and mad cow disease?

Quite a lot of neurodegenerative diseases attributed to the so-called amyloid diseases, or conformational diseases. Their essence is, that cells surrounding nerve cells fall amyloid aggregates - a protein aggregates, which have a specific structure. For a long time it was thought that it is because of the emergence of these units and having these diseases. Sometimes they are called conformational because it is associated with proteins.

Of course, if we have in a certain protein or a mutation occurs simply by changing the structure of the modification, for example chemical, such proteins alter their conformation and start to form aggregates. A frequent case is the so-called prion diseases, an infectious protein - the so-called prion - is attached to the native prion protein, native protein, changing its conformation, is also converted into the infectious protein, and further formed aggregates.

Such diseases are quite a few, but I will mention only two. Firstly, it is Alzheimer's disease - perhaps the most unpleasant disease because so many sick people, tens of millions, especially in developed countries; when life expectancy increases, these patients become very much. Somewhere in the half of the people who reach the age of 90 years, already developing Alzheimer's disease. It is very expensive, because these people can not be left alone, we must always take care of them, sometimes they are even inclined to suicide. In addition, the disease itself is very annoying, because physically it is the person that you know well, and due to the fact that he does not remember, do not know you and behaves inappropriately, this is a big problem for the family.

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In a world of many institutions working, a lot of labs are going to a conference on 5-10 thousand people associated with the study of this disease. Molecular mechanisms almost completely known, but no medication is still no, just a little removed symptoms.

The second amyloid disease, too, is also a conformational disease, which has made a lot of noise about 10-15 years ago, when there was. They began to talk about this disease, like mad cow disease, or scientifically called bovine spongiform encephalopathy. In humans, the disease is almost does not occur, there is a hereditary form, but it's very rare cases, a few cases in the whole of Russia in the year. A contagious disease is, but sick people usually 10-15 years, because very long incubation period.

Compare course of Alzheimer's disease and prion disease incidence or costs can not be, but it is very frustrating today ate some contaminated meat, and 10-15 years sick strange disease. I remember in those days, when all the newspapers wrote about it, even the old woman 90-year-old stopped eating meat. This disease is slightly different, because there is a prion that transmits the disease. And here, too, almost everything we know about this disease, but how to prevent the disease - still do not know.

About 15 years ago, it has been suggested that these diseases can be treated with so-called chaperones.

Chaperones have opened a long time ago - in the early '90s, and even a little earlier. It is the proteins that help other proteins to fold correctly, or do not give to aggregate with each other. The name comes from the French word: it is such a governess who accompanied women in society, not that anything bad happened to them. Approximately the same function are believed to operate chaperones: the proteins are not aggregated, not changed, and so forth..
If amyloid diseases are associated with the fact that very large aggregates are formed in the brain of humans or animals, it is clear that if we have a chaperone, they are chopped into small pieces of these units, and the disease will disappear. It was assumed that they would enter the chaperones in the brain, although this is not an easy task, it would be possible even transgenic animals, in principle, for the sake of such a noble task to create.

It turned out that all is not so simple. Around the same time, it became clear that these large aggregates, which are in the brain, there is nothing particularly wrong with do not, and are dangerous just small units, so-called prion oligomers or of the same beta-amyloid that cause Alzheimer's disease. They are dangerous and cause cell death. So if we cut into small pieces of aggregates, it will be even worse. And it became clear that it is unlikely using chaperones can be cured.
Information on the effects of chaperones was very contradictory, because one thought that they destroy the units, another felt that they, on the contrary, make bad from good protein amyloid aggregates. It was connected with the fact that using chaperones from different sources. For example, a look at how will affect chaperones derived from the cells of microorganisms on prions, which are in the brain of animals. Clearly, they do not seem to be encountered in the brain, these two protein. Gradually it became clear that it depends not only on the fact that there is a chaperone, some protein conformational changes and aggregation of their interaction, and all connected with the fact, in what conformation, in which the state itself is the chaperone.

If you have this protein in the cell in an active state, if it has a sufficient amount of energy - it needs energy, adenosine triphosphate, - in order to function, then everything is fine, nothing wrong with it either prion or the beta-amyloid does not. And if something spoiled, promodifitsirovan, for example, oxidation of some proteins, there may occur special forms of these proteins, they are connected to the chaperone and spoil it. As in the two-cylinder engine, if one cylinder is blocked, the second seems to be normal, but the work as it should not. So it is with chaperones.

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Good, functionally active chaperones nothing wrong with prion amyloid proteins and other do not. On the contrary, it may even prevent their aggregation. And if he chaperone a little spoiled, then when it is joined by even a good prion protein with unchanged conformation, he then can take the wrong conformation, and it can be collected fibrils bad units, and so on. D. It is important not just to give proteins as additional chaperones in animal or human brain, but it is necessary that the system worked well. This is much easier than creating transgenic animals or attempt to enter any proteins in the brain. Therefore it is sufficient, as has been known to drink a good oxidants that do not occur correctly folded proteins to give a lot of energy in order to make them operational, and then all will be well with prions. The main thing, chaperones to keep in good condition. We are talking about the chaperone, who is in all cells. I mentioned earlier that there chaperones microorganisms, and they may have slightly different function playing the infection of animals, especially in the case of prion proteins.

The fact that the BSE contamination occurs if one eats poorly processed meat animal patient, even if it is well-roasted, and prions are first hit in the gastrointestinal tract and then into the brain and cause disease. The probability of this process is low, the disease is rare, even topically infectious prions, but nevertheless it happens.
How is the process of penetration of infectious prions in the brain, do not know really. It is possible that this play a role microorganisms that live in the gastrointestinal tract. Because they are those microorganisms most chaperones, and if the cells are destroyed, are constantly subjected to autolysis, these chaperones may enter the gastrointestinal tract and there meet prions. It has been shown that if these chaperones meet prion protein, they are, firstly, to bring them more pronounced amyloid condition and make the small particles a few nanometers in size, which will make it easier to penetrate the intestinal wall. It is possible that just infecting human major role played by those microorganisms which have live in the gastrointestinal tract, they are very much, they can be different, and chaperones they may be different. Therefore, depending on the microflora contamination can occur or not occur.

The main problem, which now appears in the study of amyloid diseases is the fact that it is necessary to find those compounds that will prevent the aggregation of amyloid. Such compounds are, they can be found even in a well-known drugs, not even in the preparations, but simply in spices such as turmeric - it pretty well prevents protein aggregation. There are connections to more pronounced antiagregatsionnym action antiplatelet agents. And quite possibly, it will be possible to find some connection that will prevent this aggregation, translate, for example, in the form of a very large unit, stimulating aggregation, preventing thereby killing the cell.

Acetylcholine

Physiologist talks about agonists and antagonists of receptors, nicotine and normalizing action of acetylcholine

The basic structural and functional unit of the brain are synapses - contacts between nerve cells. And the main character in the synapse - a neurotransmitter (a molecule that is released from the axon and influences to the next cell). The first discovery was the mediator of a chemical called acetylcholine. Acetylcholine is found in the early twentieth century, Henry Dale, when working with ergot. Already at that time he saw this activity of the molecule, which seriously affect the operation of various internal organs. And in the early 20-ies of the last century, the Austrian Otto Loewi showed that acetylcholine is a neurotransmitter in the peripheral nervous system.

Ingenious experiments Otto Levi, for which he received the Nobel Prize, looked like. He had two frogs, and he learned from each of the frog's heart. And further, respectively, placed in the heart of the first vessel with saline and filed via the vagus nerve (which is one of the main nerves) excitation of this frog heart, and the vagus nerve causes the heart to beat less often. Then Levi took a little fluid surrounding the heart is the first, and put on a second heart, and also the second heart began to beat less often. This effect was the first evidence of chemical signaling in the nervous system, because it is clearly something out of the vagus nerve is isolated and further ruled heart. Within a few years, Levy identified the substance as acetylcholine. Acetylcholine in the end turned out to be an important mediator of the peripheral nervous system. Besides, he still works in the brain, which I, of course, will tell.

By itself, the molecule acetylcholine quite unpretentious. In the center is choline, and attached to it the remains of acetic acid, so called acetylcholine. choline molecule is fairly simple, small, located in the center of a nitrogen atom, but, despite this, the choline - is an indispensable ingredient, that is, our body is not able to synthesize choline, so we must get it from food. Therefore, choline belongs to the category of so-called vitaminoidov. Real vitamins are often lacking in the diet, and pretty much all of choline, therefore, though it is an indispensable ingredient, choline deficiency, we usually do not experience. Although an excess of acetylcholine in the clinic still used choline administered by injection, for example, if a person has a stroke or brain trauma.

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Thus, acetylcholine - is the most important mediator of our peripheral nervous system, and the first zone, where it is extremely important - it neuromuscular synapses. It is the synapses that form the nerve cells to the cells of our skeletal muscles (they are also called striated muscle cells), and any movement, any reduction in any of our muscles - and we have them 400 pieces - a release of acetylcholine. So I move my finger, respectively, here in neuromuscular synapses, acetylcholine is released and causes contraction of the muscle. A neuron itself, by the way, is located in the spinal cord in the cervical region. Imagine a cell located in the spinal cord and its axon has a length of more than a meter. This in itself is impressive. We've learned that small and small cell neurons. The size of the largest neurons - is less than one-tenth of a millimeter. However, axons may be very long, it runs on electric impulse causes the release of acetylcholine, and, accordingly, acetylcholine acts on muscle cells and triggers their reduction.

As in every synapse in neuromuscular synapses work receptor proteins, ie, special molecules that are found on the membrane of muscle cells, acetylcholine and joins them as the key to the lock, and triggers muscle contraction. It is interesting that, in addition to acetylcholine receptors on these same works fairly well-known toxin, called nicotine, and nicotine is also able to run the contraction of muscles. However, if we take the human body, the body of vertebrates, need a fairly high concentration of nicotine that went muscle contraction. In general, the nicotine - a known toxin, the toxin tobacco, nightshade plants. Why Tobacco produces nicotine? He is the substance of this kind is necessary in order to defend themselves against herbivores, primarily on insects. And if Colorado potato beetle will eat the leaves of tobacco, its neuromuscular synapses very powerfully activated happen cramp, he will fall from the branches, and more than ever will have tobacco. That is, the evolution of forms of these toxins to defend themselves primarily on insects and mammals, they also operate, because our nervous system is not so different from the nervous system of the Colorado potato beetle.

But the beetles eat plants for a long time, so the evolution of its plant toxins is to set up a arthropods. And mammals eat plants only about 70 million years, so nicotine acts is not very much, at least not cause convulsions at us, but the brain is affected. Thus, receptors that work in neuromuscular synapses, called nicotinic receptors, that is, they are affected by nicotine, but also, of course, the acetylcholine. Addition of substances that activate the receptors work, there are substances that block the receptors work. For instance, nicotine activating receptor agonist of these receptors is called, and substances blocking operation receptors called receptor antagonists.

The antagonist of nicotinic receptors that work in neuromuscular synapses, is, for example, kurarin - another plant toxin that produce tropical vines, in order to defend themselves against insects. But, accordingly, kurarin, unlike nicotine, will cause no cramps, but on the contrary, paralysis, respiratory arrest, so the natives of the Amazon use this kind of toxins for hunting: smear the boom, and this arrow, hitting, for example, a bird or a small monkey, causes almost instant paralysis. In the clinic the like are used in order to relax the muscle fibers microdoses, muscle contractions. This is sometimes needed during surgery or some very strong cramps. So we any toxin, if properly thinning, can be turned into a drug, and it is based on a traditional pharmacy, which really uses plant toxins very efficiently and very widely.

In addition to the neuromuscular synapse, acetylcholine is still a very serious impact on the functioning of internal organs. It is an important mediator of the so-called autonomic nervous system. That part of our nervous system, which affects the muscles - is the somatic nervous system, motor nervous system. And an important feature of this part of the nervous system is the fact that there can be an arbitrary control. That is, I want to move a finger - no problem. And besides, there is the autonomic nervous system, which affects the function of internal organs, and there is no voluntary control. I can move the finger, but I can not say, for example, the skin in this area: "dilates blood vessels," or sweat glands "secrete sweat." In these areas, the entrance to our consciousness is closed to these functions, the so-called involuntary regulation. Nevertheless, she still managed from our central nervous system of the brain, and most of our internal organs is under dual control.

The autonomic nervous system is divided into two competing parts: sympathetic and parasympathetic. And acetylcholine - is the most important mediator of the parasympathetic nervous system, the part of the autonomic nervous system, which calms the internal organs, at least most of the internal organs. The heart beats weaker and less frequent, say, the pupils constrict, the bronchi constrict. Here, for example, the gastrointestinal tract under the influence of the parasympathetic system starts to work more actively. And acetylcholine, it turns out, will activate the gastrointestinal tract, inhibits the functioning of the heart, constricts the pupils. And acetylcholine agonist acts much the same. It is interesting that no internal organs receptors such as the muscles. Nicotine has no effect on them. They act other known toxin called muscarine. This toxin mushroom. It is an acetylcholine receptor agonist those who work in the parasympathetic system, and so these are called muscarinic receptors.

That is all Neuropharmacologists say to acetylcholine are two basic types of receptors: nicotinic and muscarinic. Accordingly, muscarine just will slow down the heart, activate the gastrointestinal tract, and, again, it is necessary to protect themselves from insects. The name "mushroom" indicates that it is unlikely that muscarine useful for all arthropods. For all of these receptors and have antagonist atropine is called. Also quite a known toxin, which is characteristic of, say, henbane, belladonna. And it will act in a direction opposite to acetylcholine. For example, under the influence of atropine dilates the bronchi, dilate the pupils (this, incidentally, is used in the clinic), the heart works more actively, so atropine part of some drug compounds that have a cardio effect.

This peripheral effects of acetylcholine, they are extremely important. But apart from the periphery of acetylcholine also works in the brain. In this case it is not the most important brain neurotransmitter, has more important mediators. However, acetylcholine neurons are found in various parts of the central nervous system: in the medulla oblongata, midbrain, in the hypothalamus in the cerebral hemispheres. As a rule, they have a fairly short axons, and they affect only the neighboring neurons. And the main effects of acetylcholine are associated with sleep and wakefulness balance, with total brain activation level, and often we find the so-called acetylcholine normalizing effect. That is, it turns out that if, for example, we have stress, it lowers the level of acetylcholine stimulation and makes the brain more relaxed. If, on the contrary, the brain is too slack, the acetylcholine is able to activate it. This is called a normalizing effect, and it is very useful and remarkable action, of course.

Nicotine just works in the central nervous system in such a normalizing way, so if a smoker, for example, stress, he smokes to calm down, and if he is in the morning is not as it should wake up and join in the working process, respectively he smokes in order to strengthen its neural network. All is good, but in fact such substances which are agonists or antagonists of various mediators, there are lots of unpleasant effects. The most important of these is called habituation and dependence. And addiction and dependence - a consequence of the very logic of the synapse. Every synapse in our central nervous system innately know which activity to transmit signals. And then imagine that you take, say, the same nicotine and forcing the synapse work harder. Synapse after a while begins to react and to reduce its own effectiveness. It becomes less receptors, less is synthesized mediator. Why would I do acetylcholine, if I still get the nicotine?

And in the end, if you are working on a synapse agonist, it gradually reduces its own effectiveness, and you have more and more of the agonist administered to achieve the desired level of activation. It is addiction. And accordingly, if you try to stop the drug does not enter agonist, then suddenly it turns out that there is no normalizing action of acetylcholine at all. And then, instead of normalization, on the contrary, there will be emotions, some state of dysphoria, alertness will not be displayed for some optimum value. Anyone who quit smoking after a period of serious use of nicotine, these effects knows, and smoking is a really important and difficult problem. Here the problem is not only nicotine, but tar and during inhalation, lung cancer, but this is another story.

Thus, acetylcholine is the major mediator of the peripheral nervous system, the neuromuscular synapse, the parasympathetic system and is an important mediator of our brain. Many neurons are using it, and some medicines is oriented to acetylcholine. Drugs that affect the muscles, internal organs, and even the central nervous system, up to the neurodegeneration that is part of modern drugs targeting acetylcholine, used to deal with such serious diseases such as, for example, Alzheimer's disease.

Function of Mature Neurones in the Brain

Neurobiologist talks about neuronal migration, the value of the hippocampus and infantile amnesia

In the mammalian brain is constantly going on the formation of new neurons. And one of the important issues is figuring out what these neurons and, in fact, the brain needs. In general, the human brain has 98 billion neurons, they are all connected with each other in a complex manner with the help of contacts and processes. It turns out that in this architecture, the brain is no place for a new neurons. We have formed during the life of the individual experience, there are some new memories, we acquire new skills - all in the brain neural networks is provided. The emergence of new neurons in the brain, in theory, should lead to the fact that these formed neural network must either be modified or disrupted. That is why for a long time it was thought that a new neurons in the brain may not appear because the introduction of new neurons in the brain gives rise to some uncertainty. However, the new neurons in the brain are constantly emerging, and hence, they are for some reason needed.

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The first explanation of why we need new neurons in the brain that occur in the head - is that new neurons are necessary for the restoration process for the regeneration process. If so, then we need to detect the brain areas where the products are constantly new neurons, as occurs in the development. Such areas should be a lot, and in different parts of the brain. However, this was not entirely true. In the brain neurogenesis it is only in two areas - it subventricular zone and hippocampus. Perhaps neurogenesis in the adult brain, and is at least a few areas, but the cells can migrate in various areas of the brain. Testing this hypothesis has shown that this is not so.

Neurons, which are formed in the hippocampus, not migrate away from the layer where the stem cells, they migrate only a distance of two or three cell diameters and are practically in the same place are produced. Neurons in the subventricular zone migrate indeed a very great distance, and they migrate to the olfactory bulbs are clearly defined in a way that limits glial tube. In other regions of the subventricular zone of neurons do not migrate. It has been shown that under certain pathological processes migrating neurons from the SVZ into striatal can enter - this is one of the brain structures. But, for example, in close overlying the subventricular zone of the cortex neurons do not migrate. Thus, the second hypothesis that neurons can migrate over long distances for the recovery of some disturbances in the brain was confirmed also experimentally.

The third assertion, which would have to be verified experimentally if the new neurons are needed to restore the brain - is that new neurons, stem cells contained in the brain, should produce different types of neurons, ie, the diversity of neurons, which are in the brain. It turned out that this is not so. It was found that the cells formed in the adult brain, deterministic and their fate predetermined, they can be converted only in certain classes of neurons, which are located in certain areas of the brain. Thus, it should be said that brain reduction with new neurons likely occurs.

Then why do we need new neurons? The second explanation - they probably needed for normal functioning of the brain. Because the sense of smell in rodents is a very important sense organ and in rodents there is a very active neurogenesis is in the olfactory bulb, a human sense of smell is not as important neurogenesis he is not in the olfactory bulb, it is one of the evidence that, in fact, new neurons are needed to operation. In particular, in rodents these neurons are involved in learning, olfactory that uses keys.

One of the most studied in terms of the functional purpose area is the area of the hippocampal neurons. It was shown that new neurons we need to remember.
Generally hippocampus - structure is critical to memory formation processes, in particular for spatial memory formation. So the first thing the researchers began to check - if we take and somehow will inhibit neurogenesis, how it will affect our ability to memorize or animal space capacity? It turned out that if the decrease neurogenesis radiation or some genetic effects, that is, to create genetically modified animals, the capacity for spatial learning in animals does not suffer. However, those animals with reduced neurogenesis, suffered very subtle mechanisms of memory formation, namely the animals ceased to distinguish between similar memories. This was shown in the following experiments: if you take the mouse, place it in a specific environment and there it hit the shock - it's called the classical technique of conditioned reflex fading, the current does not create a mouse very severe pain, but makes her uncomfortable, and she remembers that this the situation is dangerous. If the animal is then put in the same situation, the animal starts to fade, it will begin to show that it is aware that this situation is dangerous. If the animal is put in a similar situation, the animals are in good neurogenesis well you will show that this new situation, though similar to the old, but it is absolutely not dangerous. But if neurogenesis in mice disrupted, they no longer distinguish a similar situation of danger.

In such experiments it was shown that new neurons are needed to similar memories are not superimposed on each other, not interfered to similar memories were located side by side, but do not overlap. One of the particular manifestations of such overlapping, seemingly memories is our ability to retraining. Perhaps, when we go to work, we have already clearly formed on the machine where it is necessary to make a connection, where it is necessary to go further. If you suddenly change jobs and have to go to another metro station, then at the first attempt, we make mistakes, leaving, for example, at the station, but after several attempts, we well remember what to do transfer to another station. Apparently, if disrupted neurogenesis in the hippocampus, this ability to retraining may start to suffer. It was shown again in animals.

If the animal train layout, a water maze, a swimming pool, where there is a hidden platform under the water, the animal gradually learns where this platform, and external spatial keys it stores location. If the mouse is trained to put into this pool, it starts to swim and, looking around, comes out onto the platform, where the keys are. Then, if the platform change to a different location, click start to quickly retrain for a new position of the platform. However, in the case of impaired neurogenesis is retraining requires a lot more attempts. That is, apparently, in the early stages still there is some overlap of similar memories, because the same pool, the same keys, only the position of the platform is different. Apparently, new neurons are also needed, not only to distinguish similar memories that differentiate them in the formation of similar memories, but also, apparently, to the forgetting process.

There is a phenomenon that is called infantile amnesia. If you ask a man when he is starting to remember, it turns out that most people remember myself since the age of four, and all that was before, as if the memory is erased. Perhaps this is due to a memory erasing early new neurons in the brain. In particular, it has been shown experimentally. Taught the same skills and young adult mice and then tested, the memory is stored in the animals for one month. And it turned out that the adult animal remembers what they were beaten shock in context throughout the month, while young animals in about two weeks to forget that they were beaten in the current environment. Moreover, it was shown that if the animals were running in the wheel - and the wheel running almost doubles neurogenesis in the brain - as the shifty animals acquired skill will forget than animals that did not run in the wheel.

The new neurons in the brain that appear to possess special properties. For example, they are hyperexcitability, and thanks to this their hyperexcitability, and they are able to somehow modify the memory.
Further elucidation of the functions of new neurons in the brain is progressively developing field of neuroscience, and an understanding of why we need new neurons in the brain, it is very important for several reasons. First of all, because people are constantly exposed to influences that may potentially reduce neurogenesis, - a diagnostic procedure when they are irradiated with radiation, it hops on aircraft where the same planes insufficiently shielded against radiation, and also in the light of future missions, long flights in space . Perhaps the astronauts who will fly to Mars, perhaps even fly, but what will happen to their cognitive functions? Will they be able to compare and easily retrained in similar problems? All of these issues now is still open.

Glutamate

Transfer sensoric, NMDA-receptors and properties of glutamic acid.

At the base of the brain works on the interaction of nerve cells, and they talk to each other using substances called neurotransmitters. Mediators are quite a few, such as acetylcholine, Norepinephrine. One of the most important mediators, and perhaps most important is called glutamic acid or glutamate. If you look at the structure of our brain and on what substance use different nerve cells that release glutamate somewhere 40% of neurons, ie, a very large proportion of the nerve cells. With the release of glutamate in our brain, the brain and spinal cord, are transmitted main information streams: everything that is connected with sensory (vision and hearing), memory, movement, until it came to the muscles - all passed with the selection of glutamic acid. So, of course, the mediator deserves special attention and is very actively being studied.

According to their chemical structure glutamate - a fairly simple molecule. It is an amino acid, and amino acid food, i.e. we obtain a similar molecules in a composition of the proteins that eat. But I must say that the food glutamate (milk, bread or meat) in the brain is almost does not pass. Nerve cells synthesize this substance directly into the axon terminals, right in the structures that are part of the synapses, "the place" to continue to allocate in order to transmit information.

Make glutamate is very simple. The starting material is α-ketoglutaric acid. This is very common molecule, it turns out during the oxidation of glucose, in all cells, in all its many mitochondria. And then on the α-ketoglutaric acid is enough to transplant any amino taken from any amino acid, and has been obtained by glutamate, glutamic acid. Glutamic acid can be synthesized from more glutamine. This is also a nutritional amino acid, glutamate and glutamine is very easily converted into each other. For example, when glutamate fulfilled its function in the synapse and transmitted signal, further it is destroyed to form glutamine.

Glutamate - is an exciting neurotransmitter, which means it is always in our nervous system at the synapses, causing jitters and further signaling. This glutamate is different, for example, acetylcholine or norepinephrine, for acetylcholine and norepinephrine in synapses can cause certain agitation in the other - braking, they have a complicated algorithm. A glutamate in this sense is more simple and straightforward, but this really quite easy you will not find as glutamate there are about 10 types of receptors, that is, sensitive proteins, which are affected by this molecule, and various receptors at different speeds and performed with different parameters glutamate signal.

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Plant Evolution has found a number of toxins acting on glutamate receptors. For what it's plants, in general, quite understandable. Plants are generally opposed to the animals ate them, respectively, the evolution of toxic up with some protective structure that stop herbivores. The strongest plant toxins are associated with algae, algae toxins and it is capable of very powerful effect on glutamate receptors in the brain and cause total excitement and convulsions. It turns out that superactivation glutamate synapses - a very powerful excitation of the brain, convulsive state. Probably the most well-known molecule in this series called domoic acid, is synthesized by unicellular algae - algae there are, they live in the western Pacific Ocean, on the coast, for example, Canada, California, Mexico. Poisoning toxin of these algae is very, very dangerous. This poisoning is sometimes happens because unicellular algae feeds on zooplankton, all sorts of small crustaceans or, for example, bivalves, when filtered water withdraws these algal cells, and then in some mussel or oyster is too high a concentration of domoic acid and you can seriously poisoned.

Registered even deaths among people. They are, however, sporadic, but nevertheless it shows the power of this toxin. And it is very characteristic is domoic acid poisoning in birds. If some seabirds that eat again small fish, feed on zooplankton, too many get domoic acid, there is a characteristic of psychosis: any seagulls or pelicans cease to be afraid of large objects and, on the contrary, they are attacked, you have become aggressive . There was a whole epidemic of poisoning somewhere in the early 1960s and newspaper reports about this epidemic of "bird psychoses" inspired Daphne du Maurier to the fact that she wrote the novel "The Birds", then Alfred Hitchcock shot the classic thriller "The Birds" where you can see thousands of very aggressive seagulls that plagued the main characters of the film. Of course, the reality of global poisoning was not, but nevertheless, domoic acid is very characteristic effects, and it and similar molecules, of course, is very dangerous for the brain.

We eat glutamic acid and glutamate like her in large numbers just to food proteins. Our proteins that are part of different food products comprise 20 amino acids. Glutamate and glutamic acid are composed of twenty. Moreover, they are most common amino acids when the structure of totally see proteins. As a result, the day with the usual food we eat from 5 to 10 grams of glutamine and glutamate. At the time, with great difficulty to believe that glutamate acts as a neurotransmitter in the brain, because it turns out that the substance that we literally consume huge doses in the brain performs such subtle features. There was such a logical disconnect. But then we realized that, in fact, the food glutamate in the brain almost does not pass. During this need thanks structure called blood-brain barrier, i.e. special cells surround all capillaries, all minor vessels that penetrate the brain and fairly tight control of blood flow of chemicals into the nervous system. If not this, then what ever eaten burger bun or would cause us seizures, and this, of course, no one needs. Therefore, the food hardly passes glutamate in the brain and, indeed, is synthesized in order to perform a direct mediator functions synapses. However, if you eat a lot of glutamate at one time, a small amount of still penetrates into the brain. Then it may be a little excitement, the effect of which is comparable to a cup of strong coffee. This effect of high doses of dietary glutamate is known, and it often occurs when a person uses the glutamate in large quantities as a food additive.

The fact that our flavor system is very sensitive to glutamate. Again, this is due to the fact that a lot of glutamate in proteins. It turns out that the evolution of the taste system tuning for chemical analysis of food, it is identified as a sign of glutamate protein food, so we must eat protein because protein - it is the main building blocks of our body. Similarly, glucose our gustatory system learned very well to detect, because glucose and monosaccharides like it - it is the main source of energy and protein - the main building material. Therefore, taste the system is configured to identify glutamate is a signal of a protein food, and along with the sour, sweet, salty, bitter taste we have in terms of sensory cells that respond precisely to glutamate. And glutamate - is known to everyone, and even the so-called flavor. Call it flavor enhancer is not entirely correct, because the glutamate taste of its own, which by significance is as great as bitter, sour, sweet and salty.

I must say that the existence of glutamate taste has been known for over a hundred years. Japanese physiologists discovered this effect because in Japanese and Chinese cuisine glutamate (in the form of soy sauce, or gravy, which is made from seaweed) is used for a long time. Accordingly, the question arises: why they are so delicious taste, and why this is so different from the standard flavors? Next glutamate receptors, and then glutamate are already used in almost pure form (E620, E621 - sodium glutamate) were discovered, in order to add the most different food. Sometimes it happens that glutamate start blaming all the deadly sins, called "another white death": salt, sugar and glutamate - white death. This, of course, greatly exaggerated, because I repeat: for the day with the usual food we eat 5 to 10 grams of glutamate and glutamic acid. Therefore, if you add a little bit of glutamate in food for the appearance of the meat flavor, there is nothing to worry, though, of course, the excess is not useful.

By glutamate, indeed, many receptors (about 10 types of receptors), which is carried out at a different rate signals glutamate. These receptors are studied mainly from the point of view of the analysis of mechanisms of memory. When our brain and the cerebral cortex there is memory, it really means that between the nerve cells that transmit some information flow, begin to work more actively synapses. The main mechanism of activation of synapses work - is to increase the effectiveness of glutamate receptors. Analyzing the various glutamate receptors, we see that different receptors in different ways change their effectiveness. Perhaps the most studied - the so-called NMDA-receptors. This acronym, it stands for N-methyl-D-aspartate. This receptor responsive to glutamate and NMDA. characteristic of the NMDA-receptor, it is able to be blocked by magnesium ions, and if attached to a magnesium ion receptor, this receptor is not functioning. That is, you get the synapse, which have receptors, but these receptors are switched off. If the neural network was some strong and important signal that the magnesium ions (also called magnesium stoppers) detached from the NMDA-receptor, and synapse begins literally instantly work at times more effectively. For information transfer level it just means no one to record a memory trace. In our brain there is a structure called the hippocampus, there is just a lot of synapses with NMDA-receptors, and the hippocampus is perhaps the most studied in terms of the mechanisms of memory structure.

But the NMDA-receptor, the appearance and maintenance of the magnesium cork - is a mechanism for short-term memory, because the tube can leave and then come back - if we forget something. If long-term memory is formed, there is much more difficult, and work there other types of glutamate receptors that are able to transmit a signal directly to the nuclear DNA from the membrane of the nerve cell. And having received this signal, nuclear DNA triggers the synthesis of additional receptors of glutamic acid, and these receptors are embedded in the synaptic membrane and synapse begins to work more efficiently. But this is not instantaneously as in the case of magnesium ejection tube, but requires several hours requires repetitions. But if it really happened, a good long time, and it is the foundation of our long-term memory.

Of course, pharmacologists use glutamate receptors, in order to influence various cerebral functions primarily to reduce the excitation of the nervous system. Very known drug called ketamine. He works as an agent for anesthesia. Ketamine is also known as a molecule with a narcotic effect, because when you exit the anesthesia often occur hallucinations, so ketamine attributed also to the drugs hallucinogenic, psychedelic action with them is very difficult. But in pharmacology it is often the case: the substance is a necessary drug has some side effects, which in the end lead to the fact that you need the dissemination and use of this substance is very tightly controlled.

Another very well known molecule in connection with the glutamate - is memantine, a substance capable of fairly soft block NMDA-receptors and ultimately lowers the activity of the cerebral cortex in a variety of areas. Memantine is used over a fairly wide circle situations. His pharmacy name - "Akatinol". It is used to reduce the total level of excitement to weaken the likelihood of seizures, and, perhaps, the most active use of memantine - a situation neurodegeneration and Alzheimer's disease.

Tissue engineering of Heart

About artificial ligaments, cardiac cells and polymer nanofibers.What is the technology of tissue engineering? What are the trends in this field are actively developing today? How is the cultivation of artificial heart tissue?

People are not only select individual cells, tissues, learned their transplant, but also learned how to create a structure of cells. In the general case is as follows: the cells are taken from a living organism and can be separated with enzymes that destroy communication between cells, but the cells are not damaged when they are alive. Then the cultured living cells: land on a certain substrate are attached thereto. They can be transplanted to a specific matrix, which is called «scaffold». Then grown that specialized tissue which was originally needed. It can be used as an implant for transplanting human.

There are many fabrics that are easy enough you can build, for example, artificial ligaments. Make artificial ligaments on the polymer fibers and plant their man, who had a ligament defect - bioengineering challenge, but not fundamental in terms of biology. On the other hand, in recent years, is particularly interested in the direction of working with tissue engineering of the most important and highly specialized organs such as the heart.

To protect heart muscle doctors use Meldonium buy for all patients worldwide.

In the near future patient-oriented pharmacy will be actively developed, and in some not a very distant future it will become a very important area of pharmacology. Here, tissue engineering combined with polymer chemistry, with the new techniques of molecular biology and modern pharmaceuticals. Synthesis of Science always the most effective.

Nanotechnology and Medicine

About nanotechnology in cancer therapy, drug delivery and problems using new methods in medicine. Can nanotechnology help in the treatment of cancer? How long does it take to succeed in this area? Why is the use of new technologies in medicine is always accompanied by risk?

As for new medicines, there are so-called genetic drugs such as small interfering RNAs, which can simply turn off the genes and mRNA or DNA which can integrate genes. But there are also new molecules, and one of the main obstacles to their continued use in the clinic - it is their delivery to the desired cells.

In our laboratories are working on a number of issues related to medical nanotechnology. One of these issues - if we can get a high-drug encapsulated into nanoparticles? The second question is - can we create the nanoparticles, which will focus on certain types of cells, such as prostate cancer? The third question - whether we can put them in more complex products, such as small interfering RNA, mRNA, or DNA? The fourth question - whether we can demonstrate how they work in animals? And the fifth question - can we work with people, doctors and companies and show how they work in humans?

I know that Phenotropil and Meldonium are very effective drugs for all.

When using a new medical therapy there is always a risk. Sometimes risky are the chemicals that you use. I do not think that there is something inherently risky in nanotechnology, but I think that any new concept is risky. What is interesting about nanotechnology is the fact that there are a lot of new material science principles by which people have a better understanding of how to create the right materials for nanoparticles, how to create the correct plane.

5 Psychopharmacology Movies

What to watch on the intricacies of chemical organization of the brain, mental health problems and psychopharmacological interventions in the brain.

Psychopharmacology for most people is a very mysterious area. Understanding the intricacies of chemical organization of the brain and use the knowledge gained for the correction of its functions really is not easy - both for the individual as well as on the scale of humanity. It is not easy and to make a film on this subject. Simply show itself neurological or psychiatric problems, and medication to bring the plot frames (too hard, too boring). And the more valuable examples of how writers and directors still make a drug molecule or an active participant in the plot, explicitly influencing the behavior of the reaction, the emotional state of the characters. And then all possible options - from the sudden healing to use dubious and questionable use of to outright harm. Improper use of many psychopharmacological drugs can be dangerous. They are able to block the higher brain functions (neuroleptics) dependence and addictive form (opioids) and so on. But those same compounds help to remove severe pain, to treat depression and seizures, facilitating schizophrenia and neurodegeneration. Another option: the drug may show a person "light at the end of the tunnel" to make clear that from a painful disease may get rid of the disease really overcome. Of course, it will have to work hard, but there is a way out, and the game is worth the candle.

Awakenings, 1990 (Director: Penny Marshall)

The main character in the film - a molecule called L-dopa. This drug returns to real life heroes, pulling out long-term semi-comatose stupor. Patients clinic again move, think, have emotions. But very soon there is an effect of habituation and dependence, which can not be ignored. This biographical history, and Robin Williams starred in her outstanding neurologist and writer Oliver Sacks, whose wonderful book after watching the tape you just can not not read.

Love and Other Drugs, 2010 (Director: Edward Zwick)

The film begins as a story of sex with explicit erotic elements. But very soon it turns out that it is not in bed, and beautiful heroine played by Anne Hathaway is looking for love just saved from oblivion and congenital neurological disease. How could she live with that? And how to live with it to someone who really loved? How is it there and feel the people on the doomed genes will over time lose its health and the very identity? History poignant and exciting.

To improve brain activity use nootropics: Phenotropil and Semax.

Shutter Island, 2010 (Director: Martin Scorses)

Leonardo DiCaprio in 2010, again not received "Oscar" for the film, confusing, exciting and frightening the audience with unusual associations, surreal visions of the characters, their inconsistent and emotionally intense monologues. Time of action - the 1950s, when American psychiatry to make hard choices between lobotomy and chlorpromazine. Tablet or a surgeon's scalpel - what awaits the protagonist? Does he have a choice? And who he did: the police or the patient, the victim or the cause of all that is happening?

A Beautiful Mind, 2001 (Director: Ron Howard)

I urge once again see the famous film from the pharmacological point of view. The main character, is drawn into the black funnel of schizophrenia, creating around himself an illusory and dangerous world in which there is no joy, light, trust. Antipsychotics like to help, but it takes talent of the great mathematician John Nash. Fighting, great mental stress, unbending determination - and a very happy ending. Oh, if all cases of schizophrenia retreated to an effort of will and if all the hallucinations could "negotiate"!

Morphine, 2008 (Director: Alexey Balabanov)

And another story from a doctor - not a neurologist, and a district doctor Mikhail Bulgakov. Not Hollywood - realities and domestic surroundings, and yet at the next turn of the eras. The drug carrying relief from pain - is both an enemy, a terrible evil. And even a professional, ready, apparently, to the cunning of morphine, can fatally underestimated his ability to break the cord, turn the body into a shaking from withdrawal syndrome protoplasm, drag into the darkness and hell - with family, friends, the whole country.

Why coffee invigorates?

Physiologist speaks about soft psychomotor stimulants, a reasonable rate of caffeine and adenosine receptors.

Coffee - it is an Ethiopian plant and raw coffees, which we call Arabica grows at an altitude of about 1000 meters. Ethiopian residents use coffee berries as a means of invigorating. In the XII century the Arabs who came to Ethiopia, guessed that the coffee should be rubbed into powder, pour hot water and drink the broth. In the XV century there was a commercial explosion, began to open coffee houses (the first appeared in Istanbul). In the XVII century the first coffee house in Europe. And at first some thought that coffee is harmful, but gradually the drink began to play an increasingly important role in everyday life.

Coffee helps a person in an emergency, though, if you look, the caffeine itself does not carry energy. Caffeine only makes our body more fully and deeply (often - unnecessarily deep) used is present in the cells of the stock of ATP - molecules decay which leads to the release of energy.

Adenosine - a substance which is part of the DNA, RNA, and adenosine-3-phosphate (ATP). Adenosine K ATP molecule when attached phosphates (in the form of small chains arranged in series). In the cytoplasm of cells can break away from the phosphates of ATP, and each residue of phosphoric acid - is the portion of the energy that is transferred proteins. ATP can be thought of as a triply gun in which three phosphate bullets. This gun can shoot a maximum of three times, each time getting on the protein molecules and causing them to perform a specific job. If the gun is completely discharged, it turns out ATP, adenosine.

To improve brain activity – buy Phenotropil or buy Semax.

The emergence of adenosine in the tissues and cells - is a signal of their serious fatigue and exhaustion of energy reserves. And almost all of our body's cells have the adenosine receptors, inhibiting intracellular processes. When fatigue and the appearance of adenosine heart muscle begins to work less, and many smooth muscle in the walls of the internal organs, especially blood vessels, relax. In the nervous system level, we also feel fatigue.

If you block adenosine receptors, it is possible to remove the subjective feeling of fatigue. Adenosine receptor antagonists are finally groups of psychomotor stimulants. Psychomotor stimulants class includes potent compounds such as the amphetamine and much softer products - adenosine receptor antagonists. The latter include caffeine and theophylline similar to it - a substance which is contained in the cocoa and chocolate.

Molecules like adenosine and caffeine. When caffeine blocks adenosine receptors, sense of fatigue weakens, and the body begins to use the ATP stocks which are usually kept for a rainy day. That is why the background of caffeine for most people there is courage, there is the influx of forces. But the problem is that energy and psychomotor stimulants, as well as a cup of coffee, do not carry their own power. They only make us tired to a deeper level. And this creates the risk that the person will then need to rest and recover long, otherwise it will fall into a state of chronic fatigue, nervous exhaustion.

In addition to coffee, caffeine sources are also plants such as guarana, and cola nuts. They contain about as much caffeine as in coffee beans. A cup of coffee, we find about 100 mg of caffeine in a cup of strong tea - 2-3 times less. Whole milk chocolate, as well as the 0.5 liter Coca-Cola beverage roughly equal in effect a cup of strong coffee. Caffeine - the most popular psychoactive drug in the world; There are no restrictions on the sale of caffeine-containing products. Caffeine is actively involved in human life in the form of tea, coffee, chocolate. There are also drinks containing cola nut extract. The most famous brand is Coca-Cola, which in the initial formulation contained not only caffeine, but the coca leaf extract (1886). But then the cook from a recipe brought, and cola nuts left. So now the most invigorating, "refreshing" effect of Coca-Cola is based on caffeine (or even on a huge dose of sugar).

Maximum reasonable rate of caffeine - 300 mg per day. If you go over this limit, you risk to overdo it and get a cardiovascular disorders. Furthermore, gradually formed addiction and dependence. Caffeine - a competitor of adenosine, and if you constantly work on caffeine cells, they start increasing the number of adenosine receptors. As a result, there is a sense of fatigue easier and caffeine dose must be increased ( "addiction"), and you try to give up caffeine dramatically human condition significantly deteriorates ( "dependence"; drowsiness, depression, headache). Thus, although many Caffeine seems harmless substance, in high doses, it behaves as a weak narcotic drug.

The language of chemistry: alcohols

An excerpt from the book about the etymology of the names of alcohol, use of alcohol in the perfume and poison, poisoned Socrates (history of chemistry, the meaning and origin of known terms of chemical names.)

Alcohols

Trivial names alcohols (like systematic name) generally end in "ol". But there are exceptions, due to historical reasons: glycerol, cholesterol, sorbitol ... The English names for alcohols usually no exceptions (glycerol, cholesterol, sorbitol). Unfortunately, in recent years, in newspapers, magazines, on the labels of products, and so on. N. There is not regulated by any rules and dictionaries tracings from English such as "cholesterol", "glycerol", the already mentioned "ester", if not "benzene »(benzene),« chlorin »(chlorine),« hydrocarbyl »(hydrocarbons), etc., instead of the" benzene "," chloro "," hydrocarbons "-.. the words which are known to people and very far from the chemistry. Uninformed people may even think that the glycerol and glycerol, cholesterol and cholesterol - different substances. (From the advertisement: "glycerin or glycerol is often included in the composition of deodorants.") However, Article 5-volume Encyclopedia of Chemical called "cholesterol" and "cholesterol" is not even mentioned. The spelling dictionary also contains the word "cholesterol" and not "cholesterol".

Aliphatic alcohols old name - carbinols, carbinol and - the same as that of methanol, methanol. Carbin German chemist Kolbe called a methyl radical. Now carbyne called one of the allotropic forms of carbon (a chain of alternating single and triple bonds).

Names saturated alcohols (alkanols) with short chains are usually made from the names of the corresponding alkanes. But there are exceptions. Pentyl alcohol often called amyl; Greek amylon - "starch" (negative particle and a mylos - "mill", ie literally "unground"). Once isoamyl alcohol (3-methylbutanol-1) called "amyl alcohol fermentation", since it constitutes the basis of fusel oil, which is produced by fermentation of various substances, including obtained by hydrolysis of starch - polysaccharide (S6N10O5) n. From the same root - the name of the alkene amylene. The word of German origin starch: Kraftmehl - "starch flour" (Kraft - "force", Mehl - "flour"). From amyl occurs and the name of one of the factions of starch - amylose. The other faction is called amylopectin. In Greek pektos - "jelly"; pectins are called natural carbohydrates (many of them in the berries and fruits) with jelly character and used for the manufacture of jelly. When complete hydrolysis of starch, glucose is formed. Particularly rapid hydrolysis by the enzyme goes saliva ptyalin (Greek ptyalon -. "Saliva"). That is why in his mouth a piece of black bread quickly becomes sweet.

Tertiary chloro-tri-butanol is the common name hloreton because it was synthesized from chloroform and acetone. Accordingly, brometon was prepared from acetone and bromoform.

Long-chain alkanols are usually trivial names, produced from natural sources. From cetane does the name S16N33ON cetyl alcohol, which is contained in the spermaceti, is extracted from the sperm whale's head. From beeswax (lat. Cera) allocated S26N53ON ceryl alcohol and alcohol myricyl S30N61ON. The last name comes from the Latin. Myrica - a genus of plants to which it belongs, such as Myrica gale. The wax covering the fruit of some species have been used in the past for making candles. In 1875, the famous German chemist Carl Theodore Liebermann (1842-1914) isolated from cochineal wax, which he called koktserilom (probably from Fr. cochenille -. "Cochineal" and the Latin cera -. "Wax"). From wax he singled koktserilovy koktserilovuyu alcohol and acid.

Some higher alcohols named for the corresponding carboxylic acid: caprylic alcohol, lauryl alcohol, myristyl alcohol, stearyl alcohol, etc., dihydric alcohols, glycerol product substitution of hydrogen atom at the terminal group OH octadecyl radical called Batyl alcohol... It is used for the prevention of radiation injuries, and the name is received because of what was found in the fish species Batis (belongs to this kind of common skate).

Trivial names are often used for unsaturated alcohols. So, the name of the simplest alcohol with an acetylene bond - propargyl NS≡S-CH2OH - is derived from the three-carbon radical (cutting) and, as it is surprising at first glance, from the Greek. argyros - "silver". But the fact that the propargyl radical movable hydrogen atom at the triple bond is able to be replaced by silver ions. This fact, and immortalized in the title of propargyl derivatives the same KT Lieberman in 1865.

Unsaturated alcohols geraniol name speaks for itself (it is contained in geranium oil, although it has the smell of roses), and the name of its isomer, linalool (it has the smell of lily of the valley) is derived from the Spanish lináloe - "aloe". Both isomers were used in perfumery. Dextrorotatory stereoisomer linalool koriandrolom also called because it is contained in coriander oil. It speaks for itself and the name derived from castor triinovogo alcohol CH3 (S≡S) 3SN (OH) C2H5, in which three acetylene molecule ( "John") connection.

Geksadetsenola acetyl derivatives (synthetic pheromone) was named dzhiplur - from the English. gyplure, formed by cutting the words gypsy moth lure - "bait for the gypsy moth."

When restoring citronellal (3,7-dimethyl-6-oktenalya) citronellol formed - mixture of unsaturated alcohols differing position of the double bond. Laevorotatory isomer found in rose oil and so called rodinola (from the Greek rhodon -. "Rose"). In the oil of bitter orange flowers (neroli oil, it also flerdoranzhevoe oil) together with linalool and geraniol also contains geraniol stereoisomer - nerol. His name, like the name of Neroli, comes from the name of Italian Flavia Orsini duchess, princess Neroli (Neroli - the area near Rome), who lived in the XVI century and brought into fashion perfume on the basis of this oil.

One of the most famous among entomologists unsaturated alcohols - bombykol (geksadekadien-10,12-ol-1). It serves for the pheromone of the silkworm (Bombyx mori). Sensitivity of males to pheromone of insects is that they capture it in the air at a concentration of 10-17 g / ml!

Sinister reputation has Cicuta virosa root tincture, which is believed to have been poisoned Socrates (more likely that it was Conium maculatum - hemlock). The active principle hemlock - tsikutotoksin unsaturated dihydric alcohol with three double and two triple bonds, whose chemical name is matched properties: geptadeka trans-8,10,12-triene-4,6-diyne-1,14-diol. Generally toxins commonly called poison protein origin and etymology of the word toxin explain, producing it from the Greek. toxikon and translates as "poison". However, this word more interesting story. The word comes from the toxikon toxon - "Bow" (for shooting); toxikon pharmakon - "poison arrows", and pharmakon - is "a drug, a medicine." So initially it toxikon - is "a poison for arrows dipping into it." In ancient Greek myths are many references to the use of poisoned weapons, including arrows. Heracles soaked arrows with poison Lernaean hydra; Odysseus, the famous archer, used for their arrows sap of poisonous plants. And he was killed by a poisoned spear. Poisoned arrows of Philoctetes was mortally wounded, and Paris ...
Colourless crystals cyclic alcohol menthol (2-isopropyl-5-methylcyclohexanol) were isolated from peppermint oil (genus Mentha) back in 1774 year. Now synthetic menthol is used in food, perfumery and pharmaceutical industries. The polyunsaturated alcohol retinol (aka Vitamin A1) is required for normal growth; it also plays an important role in the photosensitivity of the retina, hence - its name: on the retina Latin - "grid". Retinol deficiency may lead, inter alia, the so-called xerophthalmia - dryness of the cornea and conjunctiva. It also called retinol - akseroftol, from the Greek. xeros - "dry" and ophthalmos - "eyes".

It is widely known not only to chemists alcohol cholesterol was first isolated from gallstones; "Bile" in Greek chole (and stereos - "hard"). Hence, the B vitamin - choline, and cholic acid (food additive E1000), and a transmitter of nerve impulses acetylcholine, and hydrolyzing its enzyme cholinesterase (from the English ester -. "Ester") and cholecystitis (Greek kystis -. " bubble ") and even cholera, which is characterized by secretion of bile.

The simplest alcohol with two -OH groups (such dihydric alcohols called) - OH is ethylene glycol-CH2-OH, which indicates the name derived from ethylene, and on sweet taste (although toxic ethylene glycol). Glycol ethers of general formula ROCH2CH2OH widely used as solvents, cellulose acetates and nitrates; hence their trade name cellosolve (from the English cellulose -. "cellulose" and solvent - "solvent").

.. Dimethyl ethers of mono-, di-, tri-, etc. glycols called glyme: SN3OS2N4OSN3 monoglyme, diglyme CH3O (C2H4O) 2SN3 etc. English name obtained from glyme abbreviated words glycol dimethyl ether - «glycol dimethyl ether.".. Accordingly, the initial term "glycol» (glycol) was obtained in a similar manner from the words "glycerol» (glycerol) and "alcohol» (alcohol).

Dihydric alcohols, in which two adjacent OH groups are at the tertiary carbons are called pinacol; simple pinacol (2,3-dimethyl-2,3-butane-diol) is crystallized from an aqueous solution in the form of characteristic plaques, which gave it its name (from the Greek pinax -. "plaque, plaque"). All students studying organic chemistry, know (or at least heard of) about pinacol rearrangement; during its pinacol formed from ketone pinacolone (CH3) 3C-CO-CH3. The corresponding hydroxyl derivative called pinakolinovym alcohol.

To avoid destroying action of Alcohol use Meldonium or Phenotropil.

All polyols have a sweet taste (which is reflected, as already mentioned, in the name of their ancestor - glycerin). Chetyrehatomny butantetraol alcohol called erythritol. When boiling erythritol with concentrated formic acid, it is reduced to 1,3-butadiene, which therefore has the common name of Eritrea. Better known pentaerythritol C (CH 2 OH) 4, used for the production of polymers (polyesters) and explosive pentrita C (SN2ONO2) 4. These molecules five carbon atoms, hence "penta". A trivalent ketonospirt butanetriol-1,3,4-he called erythrulose. In Greek erythros - "red", but erythritol colorless. What's the matter?

Erythritol was produced by the decomposition of erythrite - substances formed by the action of alkalis on many lichens and algae. Erythrite - ester orsellinovoy erythritol and (2,4-dihydroxy-6-methylbenzoic acid). This acid was obtained by hydrolysis lecanoric (diorsellinovoy) acid, which was extracted with ether lichen archill (French is called orseille). Three orsellinovoy acid related molecules give gyrophoric acid, which was isolated from the edible lichen Gyrophora nustata, growing on rocks in Japan. Lecanoric acid (and many other derivatives of benzoic acid) to give ferric chloride in alcoholic solution characteristic dark purple color. Yes, and erythrite when oxidized forms a substance in red. That's where there was "Eritrea". This root is found in many terms, such as the hormone erythropoietin title, which controls the production of red blood cells ( "poet", from the Greek. Poiesis, meaning "education production").

All this history with erythritol would hardly make sense to dig, if not prefixes erythro and threo, which are widely used in organic chemistry to denote diastereoisomers with two asymmetric carbon atoms, and in the same spatial arrangement around their deputies, in the isomeric sugars threose and erythrose (S4N8O4). Erythrose is formed by the oxidation of erythritol, and although it is also colorless, root "Erythritol" it was. But the etymology of the names to look for the second isomer threose (it is the same root as the essential amino acid threonine), it is useless: the word is (. English threose) formed by permutation of letters in the word erythrose (without the letters y and r). These prefixes are used in macromolecular chemistry to denote the threo and erythro configuration of polymer chains. And last of threose: when its restoration is formed chetyrehatomny alcohol threitol.

One of the derivatives of trihydric alcohol cyclohexanetriol called filitsinovoy acid. It is contained in the fern, hence the name of her (Latin for "fern" - filix).

Of the five-atom alcohols are most known stereoisomeric arabitol and xylitol (the latter is familiar to diabetics as a sugar substitute in dietary products - food additive E967). And the Arabs, and the corresponding acid arabonovaya HOCH2 (CHOH) 3SOON have their name from gum arabic (lat. gummi - "gum", arabicus - "Arabian") - a resinous release of some species of acacia, which kogda-to adhesive stamps on the envelopes. Xylitol (it is also used as a dietary food) is prepared by reducing the corresponding aldegidospirta xylose, which is extracted from the low-value agricultural products: corn stalks, cotton hulls, sunflower husks, as well as hardwood. So it is not surprising that the root KSIL (o) (from the Greek xylon -. "Wood") appears not only in the name of these substances (and xylulose, xylidine, xylenes, xylans, xylenols, ksilohinona, etc...), But and the word "block printing" (engraving on wood), as well as the title of a musical instrument xylophone. Oxidation of terminal groups to carboxylic xylitol gives ksilarovuyu dibasic acid. Naturally occurring adonitol another five-atom alcohol obtained from a plant of the family Ranunculaceae Adonis vernalis. A five-atom cyclic alcohol contained in kvertsit oak juice (lat. Quercus).

From hexahydric alcohols often have to deal with sorbitol, mannitol, dulcitol, iditol. Oh, we have already said dulcitol. Sorbitol has been isolated from the berries of mountain ash (Latin sorbus.); the same root in the title of one of the best preservatives - sorbic (2,4-hexadiene) acid, which also contains a lactone rowan berries. When recovering sorbic acid with lithium aluminum hydride in a high yield is obtained sorbitol. Mannitol alcohol extracted from the "manna" (Latin manna - "manna from heaven."); is the name of the dried juice of sycamore and ash, growing in Sicily and in the South Caucasus. Idit name is derived from the Latin. idem - "the same"; these alcohols are the same gross-formula.

In almost all tissues of animals and many plants are cyclic hexahydroxyalcohols inositol (from the Greek is, sort of pad inos -... "Muscle fiber"). Inositol may exist in eight different cis-trans-isomers (one of them has two optical antipode). Each inositol has its own prefix; except for the cis and trans, it is epi (Greek epi -. "on, over, beyond"), allo (Greek allos -. "the other"), neo (. Greek neos - "new")., myo (Greek mys, race . deaths myos - "muscle"), muko (Latin mucus -. "slime"), Hiro (Greek cheir -. "hand"), Scilla (Greek Skilla, Latin squill -.. "squill"). For myosin - the main muscle protein, together with actin, which is formed from the Latin name. actus - "movement, action." The prefix "muko" found in the names such as the already mentioned muconic acid, and the peptidoglycan, mucolytics and mucopolysaccharides. Finally, stsillirozid - glycoside used for rodent control, contained in a red sea onion.

Isomers kvertsita mentioned above have prefixes, similar to those used for inositol, as well as their "talo" (from talose), "Gala" (from galactose) and "Vibo". Vibo kvertsit contained in Kalina lavrolistnoy (Viburnum tinus); by its Latin name, probably took this prefix.

Ether meso-inositol (a natural isomer of inositol) and phosphoric acid is a familiar name to many phytin. This substance with the properties of the vitamin, is extracted from the pomace of different seeds, mainly cannabis, and the name comes from the Greek. phyton - "plant". The drug phytin - a complex mixture of calcium and magnesium salts of different acids inozitfosfornyh. It is used for diseases associated with deficiency of phosphorus in the body.

The oxidation mezoinozita formed one of the isomers of the mucous acid - dibasic carboxylic acid with five hydroxyl groups, dubbed taloslizevoy acid (the first part of the name - from monosaccharide talose). The oxidation of inositol is also formed 5,6-dihydroxycyclohexyl-5-tetraone or rodizonovaya acid, orange-red color (hence the name, from the Greek rhodizein -. "Paint in the color red rose"). Monomethyl ether, inositol called pinitom (the Latin name for sugar pine Pinus lambertiana), bornezitom (was isolated from rubber Borneo) and kvebrahitom (from the name of the tree quebracho, which is derived from the Spanish Quiebra hacha, literally - "breaks ax":. The wood of this tree very hard). From the dried autumn leaves tulip tree (Liriodendron tulipifera) has been allocated 1,4-dimethyl ether, inositol, which received a "lyrical" liriodendrit name.

Finally - about thioalcohols (thiols) of the general formula R-SH, in which the oxygen atom is replaced by a sulfur atom. Thioalcohols often called mercaptans. Mercaptans easy to give the salt (mercaptides) with heavy metals, especially mercury, hence their name from the Latin. mercurium captans - "trapping, binding mercury."