Bioono - Medical & Health

Epilepsy is a neurological disorder characterized by recurrent seizures. It affects more than 65 million people worldwide and is one of the most common neurological disorders. Treatment for epilepsy has traditionally included anticonvulsant drugs, neurosurgery, and lifestyle changes. Recently, peptides have been used as an alternative form of treatment for patients with epilepsy.

Causes of epilepsy

Epilepsy can be caused by a variety of factors, including genetics, head trauma, infections, and diseases. Genetic factors may also play a role in causing epilepsy; it is believed that up to 70% of cases of the disease are associated with a genetic predisposition or family history. Head injuries and other physical injuries can lead to brain damage, which increases the risk of developing epilepsy later in life. Infections such as meningitis and encephalitis can also cause epileptic seizures in susceptible people. In addition, certain medical conditions, such as Alzheimer's disease, stroke, or brain tumors, can increase your risk of developing this disorder.

Treatment of epilepsy with peptides

Peptides are short chain amino acids that act as neurotransmitters in the brain and have been shown to be useful in the treatment of some forms of epilepsy.
Peptide therapy involves administering these peptides by intravenous infusion, intranasal spray, or inhalation therapy, which helps reduce seizure activity by modulating neurotransmitter levels in the brain. Various types of peptides used to treat epilepsy include gamma-aminobutyric acid (gaba), glutamate receptor antagonists (gra) and opioid receptor agonists (ora).

How Peptide Therapy Is Prescribed and Its Benefits for Treating Patients with Epilepsy The use of peptide therapy has proven beneficial for some patients with epilepsy who do not respond well to traditional therapies such as anticonvulsants or surgery.

One promising area of research in the field of epilepsy prevention is the use of the sleep-inducing delta peptide (DSIP), a peptide bioregulator that plays a key role in regulating sleep patterns and modulating the immune system.

Peptide therapy is usually given on a case-by-case basis based on the specific needs of the patient and their medical history; it is important that any potential risks associated with this type of treatment be discussed with a healthcare professional prior to starting any kind of regimen that includes peptides. In addition to reducing seizure activity, peptide therapy may also reduce the level of anxiety experienced by people suffering from this disorder due to its calming effect on neurotransmitters in the nervous system.

Research and study of peptide therapy in patients with epilepsy
Several clinical studies have been conducted on the use of peptides to treat patients with refractory (drug-resistant) epilepsy who do not respond well to conventional therapies; these studies have shown promising results when it comes to reducing the frequency of seizures without any of the serious side effects, such as drowsiness or sedation, that usually occur with anticonvulsant drugs.

Research has shown that DSIP can help reduce the severity and frequency of seizures in people with epilepsy. In one study, researchers found that DSIP reduced the number of seizures in rats with induced epilepsy by more than 60%.

DSIP works by stimulating the production of neurotransmitters and regulating the activity of certain brain cells, which can help prevent seizures from occurring. In addition, DSIP has been shown to be neuroprotective, helping to keep neurons healthy and prevent brain damage.

One of the delta sleep peptide preparations is DELLIN, which can be a valuable addition to a comprehensive treatment plan that includes medication, therapy and lifestyle changes.

Dellin (DSIP) is a promising tool for the prevention and treatment of epilepsy. By helping regulate sleep patterns and modulate the immune system, DSIP may help reduce the severity and frequency of seizures, and may even have a neuroprotective effect on the brain. For anyone living with epilepsy, it's important to explore all available treatment options and work with your doctor to develop a comprehensive treatment plan.

In conclusion, peptides offer promising alternatives in the treatment of refractory cases where other common treatments may no longer be effective. While much more research needs to be done before they become accepted treatments, they appear to be reasonably safe at current doses when carefully monitored by qualified medical professionals.

Ultimately, it all depends on the individual needs of each patient, whether they should try this type of therapy along with other, more well-known treatments.

Bioregulator DELLIN - is produced in the form of ampoules with odorless lyophilized powder. It is highly soluble in water. The ampoule contains 0.3 mg of the delta-sleep-inducing peptide DSIP and the rest is a specially selected mixture of glycine, turine, L-carnosine and pantel (an extract from reindeer antlers).

COMPLETE SOLUTION FOR YOUR NEUROLOGICAL PROBLEMS

Indications for the use of the DELLIN supplement:

In pediatric neurology and psychiatry:

Complex therapy of infantile cerebral palsy (ICP);

Complex therapy of autism syndromes;

Complex therapy of epilepsy

Benign childhood epilepsy with EEG peaks in the central temporal region

Pediatric epilepsy with paroxysmal EEG activity in the occipital region

Focal seizures of epilepsy without change of consciousness

Simple partial seizures progressing to secondary generalized seizures

Myoclonic epilepsy in early childhood neonatal seizures

Childhood epileptic absences (pycnolepsy)

Epilepsy with grand mal seizures

Complex therapy of organic brain lesions;

Traumatic brain injury (TBI), both in the acute period and at the stage of rehabilitation;

Syndrome of delayed neuropsychic development of a child (ZNPR), moreover, regardless of etiology;

Psycho-speech delay (PRS), as well as speech disorders associated with functional changes in the central nervous system (takhilalia, bradilalia, stuttering);

Active rehabilitation after surgical neurosurgical measures (brain cyst excision, stenting in case of hydrocephalus, removal of a hematoma or brain tumor, etc.);

Emotional and behavioral disorders, in childhood and adolescence, states of motor and sensory disinhibition, as well as CNS hyperexcitability syndromes;

Signs of a violation of social adaptation, against the background of a change in the environment of stay (area, team, environment);

Tiki;

Phobias.

In general neurology and psychiatry:
Complex therapy of acute cerebrovascular accident (ACC) - according to the ischemic and hemorrhagic type (both in the acute period and at the stage of early and late rehabilitation);

Transient cerebral ischemic attacks;

Diencephalic disorders and autonomic crises of various etiologies;

Vestibulo-ataxic syndromes;

Traumatic brain injury (TBI), both in the acute period and at the stage of early and late rehabilitation;

Complex therapy of epilepsy
Localized epilepsy (focal)

Symptomatic epilepsy

Epileptic syndromes with complex partial seizures

Generalized idiopathic epilepsy

Epileptic syndromes - Kozhevnikov's syndrome, seizures associated with the use of alcohol, the use of drugs, hormonal changes, sleep deprivation, exposure to stress factors.

Unspecified seizures of epilepsy

Small seizures of epilepsy (petitmal)

Grand mal seizures (grandmal)

Neurodegenerative diseases (NDD), including Alzheimer's disease and multiple sclerosis;

Rehabilitation after transferred encephalitis and meningo-encephalitis;

Diabetic and toxic polyneuropathy;

Correction of astheno-neurotic syndrome, including chronic fatigue syndrome;

Therapy of unipolar depressions (resistant depression, minor depression, atypical depression, postnatal depression, recurrent depression, dysthymia, cyclothymia, vital depressions without psychotic disorders);

Sleep disturbances (impaired falling asleep and maintaining sleep - insomnia, disorders in the form of increased drowsiness - hypersomnia, violation of the cyclical sleep and wakefulness - dyssomnia, obstructive sleep apnea syndrome);

Eliminates dependence on long-term sleeping pills;

Dementia (including vascular dementia and senile dementia);

Anxiety disorders and Phobias;

Correction of mental disorders and behavioral disorders associated with the use of psychoactive substances;

Rehabilitation of patients after surgical, compression effects on the brain;

Rehabilitation after tissue hypothermia, or as a result of chronic brain hypoxia (for example, a decrease in the perfusion capacity of blood vessels against the background of atherosclerotic changes).

In drug practice:
Relief of withdrawal symptoms and prevention of delirious conditions;

Prevention of primary pathological attraction to alcohol or narcotic products;

Restoration of genetically determined sensitivity of op**te receptors.

Courses for children under 14:

A course for children from 1 to 3 years old - 1 ampoule daily, in the morning, for 5-10 days, if necessary, repeat the course after a 10-15 day pause;
A course for children from 3 to 6 years old - 1 ampoule daily, in the morning, for 10-15 days, if necessary, repeat the course after a 10-15 day break;
A course for children from 6 to 14 years old - 1 ampoule daily, in the first half of the day, for 10-20 days the daily dose is 2 ampoules, and then 1 ampoule per day), after a 15-day pause, repeat the course of taking 1 ampoule daily for 10-15 days.

ETALON cell or why are we getting old?

The question “Why are we getting old” worries humanity throughout its existence. Several times a year new “youth pills” appear on the market - goji berries, acai and blueberries; probiotics, resveratrol, coenzyme Q10, turmeric ... At the same time, scientists involved in aging and genetics say that “our body can repair itself and, contrary to popular belief, aging is treatable” - for example, David Sinclair ), a genetics specialist from Harvard.

As you know, on the packaging with food additives you can write anything you want - manufacturers do not have to confirm their promises with research, however, there are additives that have undergone clinical trials and the effect of which is confirmed by scientific facts. It will be about Etalon cell - telomerase activator.

TELOMERIC THEORY OF AGING:
In 1938, American scientists Barbara McClintock, Herman Meller came to the conclusion that the ends of linear chromosomes are protected by telomeres.
In 1965, the American biologist Leonard Hayflick found that most cells can divide no more than 50-60 times. After this, aging begins.
In 1971, the Soviet scientist Aleksey Olovnikov put forward a hypothesis about the protection of telomeric DNA using a special enzyme - telomerase.
In the 80s, Elizabeth Blackburn, Carol Grader and Jack Shostak experimentally proved the validity of these assumptions and discovered the telomerase enzyme, which can form new telomeres. For these studies, they were awarded the Nobel Prize in 2009.

That is, the lifespan of a cell depends on the length of the telomeres. After 50-55 divisions, the cells either die, or fall into suspended animation, or degenerate. In the nucleus of each cell are chromosomes with genetic information. At the end of each chromosome there are special “protective” formations - telomeres, which become shorter with each cell division.

The ETALON cell preparation is based on a molecule that can activate telomerase. Clinical trials have confirmed that taking ETALON cell helps build telomeres, prolonging cell life. More importantly, studies have confirmed that the duration of a healthy cell life is increasing.

AT 40 YEARS OF LIFE ONLY BEGINS?

The point of taking the ETALON cell telomerase activator is not just to rejuvenate the body and not to prolong life (although studies on mice showed that they do not live for 43, but 86 weeks when using ETALON cell, such studies have not yet been accumulated in humans), but to improve the quality of life after 40 years.

Why do we take 40 years as a reference point?

In the past, women died before menopause, and men did not survive to heart attacks. Now, when life expectancy reaches 80 years, we have a choice - to live these extra 40 years cheerfully and in good health or to live them with illnesses.

After 40 years, women begin to have menopause, endocrine changes, disorders in the reproductive system, vision deteriorates, diseases of the cardiovascular system appear - these diseases are also based on shortening telomeres.

What factors affect telomere length? Of course, this is ecology, stress, smoking and other factors of a healthy or unhealthy lifestyle (especially relevant for those who live in megacities).

It is interesting that moderate sports loads lead to an increased level of telomerase, and excessive loads lead to a decrease in telomeres, which is probably why athletes of “high achievements” often look older than their age. Proper nutrition and healthy sleep lead to an increase in telomeres. Omega-3, vitamin D (I hope you take these affordable supplements?) Also lead to an increase in telomeres but indirectly, while the telomerase activator - ETALON cell leads directly.

Viral and infectious diseases shorten our telomeres. What is there - depression and just a bad mood also “work” against our beautiful telomeres (an extra reason to reconsider our morale and slowly learn to enjoy life).

In people leading a healthy lifestyle, telomeres are either equal to the norm or higher than the norm, but they are still declining.

It is important to know that female s*x hormones activate telomerase, while male hormones, on the contrary, inhibit telomerase. From this point of view, men age earlier, while we are protected from age-related problems before menopause ...

As you know, to feel the direct effect of ETALON cell is not easy. The analogy with makeup products comes to my mind. I was always skeptical of reviews in the style of “woke up and did not recognize my reflection in the mirror, wrinkles were smoothed out, bruises under my eyes resolved” - the authors of such tales are cunning or just lying. The same thing with telomeres - we cannot touch the effects of telomere extension with our hands. Meanwhile, there is a blood test for the length of telomeres (can be done in Odessa, Kiev), which allows you to determine the biological age of a person (I just really want to do it!).

That is, Etalon cell is a biologically active drug whose effect can be measured. Ukrainian distributors of ETALON cell are planning clinical trials that will take 4-5 years and claim that the first thing a person feels taking a telomerase activator is improving the immune system. When taking a telomerase activator, we allow the cells of the immune system not to die faster, but continue to divide, slowing down their aging, staying in a young phenotype. This means that people get sick less - is this one of the main factors to improve the quality of life?

I hope you found it interesting to read about new research into anti-aging supplements.

Are you ready to spend “serious” money on such a drug with proven effectiveness, or is it difficult for you to imagine how, by prolonging the life of telomeres, you can improve the quality of your life?

PREVENTAVIR is a powerful set for against-hand protection
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PREVENTAVIR, completed a specialist study at the University of the Department of Psychology, Kentucky, USA.

The critical data received from previous research projects has allowed us to make sure that glucans are high-active adjuvants:
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There was an increase of 30-40 % compared to the test model without adding an addition.
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The immunostimuliruûŝaâ activity of the test model for moral immunity was confirmed.
There has been an increase of 30-40 times the development of the anti-2-40 times as compared to the standard reaction.
200-300 % increase in 200-300 % compared to the control.
A small increase in the products of own cell products by 5-10 % has been confirmed.
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arvi and GRIPP, viral infection of the upper breath, bronchi and lungs (Bronze, pneumonia), ENT pathological, vaginal infection and infection of the wet system for the prevention of infection.
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During the period of seasonal disease of arvi and INFLUENZA, for the prevention of infection and disease

Sostav: Grifolin acid, Triterpenes, Crystalline amino acid, Bifidobacterium longum, Streptococcus thermophilus, smesʹ Lactobacillus (acidophilus, bulgaricus, rhamnosus, fermenti, helveticus, paracasei)

Always happy to answer all your questions 🤗

More info:
https://bioono.com/preventavir-antiviral-immunostimulant/

COVID-19 – WE Have Questions ?

Over the past months, we have been told a lot about the COVID-19 pandemic and the SARS-CoV-2 virus that causes it. Also in the information space "flies" a lot of different rumors and alternative information - truthful and not.We learn a lot all the time - but is it really so?

The number of scientific articles on the SARS-CoV-2 virus is increasing and increasing, however, there are still many dark areas regarding its origin.

Let’s take into account only the official statements and see how everything will look from different angles. So. What animal species did this virus spread to humans?To us, some genetic scientists answered and showed evidence that the greatest likelihood of such a transmission is the path from the bat to people.

Other genetic scientists claim that the intermediate transmission occurred through palm civet or through lizards, or through ... another species of wild animal. All versions are good - the main thing is that the transmission path remains within the boundaries of the ANIMAL-HUMAN model.

Okay. If we take this model as a basis, then the possibility of spreading and transmitting the virus to humans through the market with wild animals (close contact or eating) is also understandable.Then another question, why in the Chinese province of Hubei, and not somewhere else?

Why didn’t this happen in another place where these animals also exist and the conditions for the possible spread of the NATURAL MUTING virus? From official data: in December 2019, 27 people from the first 41 hospitalized people (approximately 66% of people) were in a market located in the center of Wuhan in Hubei province, where wild animals are sold. However, they cannot provide us with medical data on the so-called primary patient (patient No. 0).

And to the real patient. Perhaps this state of affairs will become clear if this fact is taken into account: according to the initial study of the material, from the very first detected case of a human disease with the SARS-CoV-2 virus, with further elaboration of the movements, it will become clear that the patient of the Wuhan hospital with the “FIRST IDENTIFIED CASE "generally NEVER visited this market!

Moreover, an assessment of molecular dating based on the genomic sequences of SARS-CoV-2 indicates their rather STRANGE origin (part of the genome has a strange non-natural character - at least it is difficult to imagine the natural possibility of such a mutation), and in the period October-November 2019 year.This raises further questions about the reality of the link between the COVID-19 pandemic and wildlife.

Genomic data:

After laboratory samples were provided, the SARS-CoV-2 virus genome was sequenced. Comparative genomic analysis showed that SARS-CoV-2 belongs to the group of beta-coronaviruses and that it is very close to SARS-CoV, responsible for the epidemic of athepatic pneumonia that appeared in November 2002 in the Chinese province of Guangdong, after which it spread to 29 countries .

Then, as indeed now, it was argued that the source of transmission of the virus to humans was bats of the genus Rhinolophus (potentially indicating a possible pathway for mutating the virus in several species of cave bats). Bats are known to have been the reservoir of this virus.

However, a palm civet (Paguma larvata) could become a similar reservoir. Moreover, by sequential coincidence, palm civet could well serve as an intermediate host (at least in the first cases of human diseases). There are many beta coronaviruses. Some of them may be in people. But the interesting thing is that so far only 3 of them behave differently when in contact with a person.

They differ in the genome and mutational manifestations and even suggest an unnatural origin. Moreover, if we talk about SARS-CoV (2003-2004), then it was directly stated that the “clone” of this virus was isolated in several laboratories. Today it is said and confirmed that the SARS-CoV and SARS-CoV-2 viruses in the genome sequences are very similar to each other. Their identity, according to various experts, is about 96%.

The question arises:

If SARS-CoV could be artificial (at least with a repeated small outbreak of the SARS epidemic) and it is very similar to the current SARS-CoV-2, then what do we have today?
Let's go back to the natural carriers of coronaviruses. For example, it was discovered that another RaTG13 virus isolated from a bat was described as very similar to SARS-CoV-2. Consequently, animals of different species can be carriers of several very similar deadly viruses, while they only remain reservoir.

How should this be understood and evaluated? In this case, a reservoir is one or several species of animals that are not very sensitive to a particular virus or not very sensitive to a group of viruses that are in them. In vivo, they somehow do not have any symptoms of the disease. Nevertheless, these same viruses in mutagenic manifestations in other organisms become quite dangerous and ultimately even fatal. Not the effect of the virus on a living organism (the host cell) is explained by one very important parameter - the efficiency of their immune system, which allows you to fight the excessive spread of the virus.

Recombination mechanism:

On February 7, 2020, as a result of research, scientists from China, with the assistance of Australian colleagues, discovered a virus very similar to SARS-CoV-2. However, a subsequent review study showed that the genome of a coronavirus isolated from Malaysian pangolin (Manis javanica) is similar to SARS-Cov-2, with only 90% genomic consistency. This is less than genomic consistency with the virus from the bat. This seems to indicate that the virus isolated from the lizard is not responsible for the COVID-19 epidemic, which is currently raging.

But...
96% of the similarities between bat coronaviruses and today's human coronavirus are in the entire genome. If we take specifically its S segment (the S gene encodes a protein located on the surface of the viral envelope and is responsible for the attachment of the virus to the host cell), then in this segment the similarity of bat and human coronaviruses will be 76.8%. However, coronavirus isolated from pangolin in a specific region of protein S is 99% similar to the same segment of human coronavirus. It also more closely matches the 74 amino acids involved in the binding domain of the ACE2 receptor (angiotensin-converting enzyme 2), which allows the virus to pe*****te human cells and infect them.This means that coronavirus isolated from pangolin is more able to pe*****te human cells, but is less identical to SARS-Cov-2 virus, while coronavirus isolated from bat is more identical to SARS-Cov-2 virus, but less able to pe*****te the cell person. There is such a paradoxical situation at first glance.
But this is only at first glance.

More detailed genomic comparisons in specific parts (segments) show that the SARS-Cov-2 virus is the result of recombination between two different viruses. Moreover, one area (replicative pattern) is close to the bat virus, and the other is closer to the pangolin virus. In other words, it is a chimera between two pre-existing viruses. The meaning of a chimera is usually used in a figurative sense, to mean something unreasonable or unrealizable. However, in the case of Novel Coronavirus (2019-nCoV) / COVID-19, it turned out to be POSSIBLE! It is also very important to understand that recombination leads to a new virus that is potentially capable of infecting a new host species. However, for such a recombination to occur under natural conditions, it is necessary that two, diverging viruses, SIMULTANEOUSly infect the host cell at the same time period in the same organism. It is VERY, VERY and VERY hard to believe in a natural mutation. However, in the laboratory, in an artificial way, this is completely possible!

So, the following two questions remain without an affirmative answer:In what organism did this “NATURAL” recombination take place? And, first of all, under what conditions did this "NATURAL" recombination take place, given that the bat and pangolin in natural nature have NOT MET EVER? To date, the “OFFICIAL” version of the primary source of the SARS-CoV-2 pandemic is that bats were the source.But in order for the virus to be transmitted from a bat to humans, an intermediate animal is necessary - this is a well-known fact. Moreover, in previous coronovirus epidemics (SARS-CoV and MERS-CoV), such intermediate animals were at least designated.
With the latest COVID-19 pandemic, a transitional animal species in which the SARS-CoV-2 virus would mutate to the “human” variant has not been found !!!

Officially answer like this: Since the market in Wuhan, which is associated with the outbreak of a new coronavirus infection, has been eliminated, the search for an intermediate animal carrier of the coronavirus is not possible.

A distinctive feature of the new SARS-CoV-2 coronavirus is its ability to rapidly spread. This also distinguishes him from the two previous pandemiological “brethren” (SARS-CoV and MERS). However, unlike them, it is not so dangerous, since it has a lower mortality rate (about 9.6%, for SARS-CoV, about 36%, for MERS, and so far about 5.4%, for COVID-19 (SARS-CoV-2 ) respectively).

For reference:

The most transmitted virus between people is measles virus. One person can infect measles in the next 11-18 people. SARS-CoV-2 can be transmitted to 3-4 people.
How can COVID-19 Disease really occur?

Asymptomatic, mild, or bed-like form of the disease will be in 81.5% of peopleHospitalization will require about 13.8% of peopleIntensive care will be needed 4.7% Moreover, the disease mostly affects the oldest age-old category of people - more than 83% of sick people requiring medical intervention or intensive care are people aged 60+.
Where and how can a SARS coronavirus enter a host cell?The ACE2 gene encodes an angiotensin converting enzyme-2, which has been proven to be a receptor for both SARS-coronavirus (SARS-CoV) and human respiratory coronavirus NL63. Studies and analyzes show that ACE2 can be the host receptor for the new 2019-nCoV / SARS-CoV-2 coronavirus.

Although, based on official statements, a systematic analysis of coded-region variants in ACE2 and eQTL variants did not reveal direct, genetically confirmed evidence for the existence of ACE2 mutants that are resistant to the binding of coronavirus S-protein in different populations, in reality it is observed that, in populations of East Asia, AFs, Novel Coronavirus (2019-nCoV) / SARS-CoV-2 / COVID-19 in eQTL variants was much higher, and was associated with higher expression of ACE2 in tissues. This indicates that, in different populations under similar conditions, 2019-nCoV / SARS-CoV-2 has a different susceptibility and / or reaction. In certain parts of the SARS-CoV-2 viral genome, "natural oddities" of NOT NATURAL origin were observed. For example, in segments nsp3, nsp12, Orf8b, Orf9. By the way, these same "natural oddities" were observed in the last phase of the SARS epidemic in 2004.

QUESTIONS? QUESTIONS? QUESTIONS?

FOR REFERENCE:
Description of the action of viral genes and proteins, as well as cellular responses to their actionExplanation of the description: First, the nomenclature of the gene is given (the number of amino acid residues is indicated in parentheses), the gene product and / or its characteristics are described below, as well as the possible effect of this gene on the host cell response.

1. Orf1a / b. Not described

2.nsp1 (180). Expression promotes the degradation of endogenous host mRNA, which can inhibit host protein synthesis and prevent the accumulation of endogenous IFN-β mRNA. It induces the expression of CCL5, CXCL10 (IP10) and CCL3 in human lung epithelial cells by activation of NF-κB, and also enhances the degradation of cellular RNA, which can promote SARS-CoV replication or block immune responses.

3.nsp2 (638). Removal weakens the growth of the virus and subsequent RNA synthesis.

4.nsp3 (1922). Papain-like protease 2 provides proteolytic processing of viral polyprotein at 3 sites and takes part in the synthesis of the subgenomic RNA segment. Another action is via ADP-ribose-1-phosphatase (ADP-ribose 1-phosphatase), which dephosphorylates Appr-1 ‴ -p (a by-product of tRNA cell splicing), to ADP-ribose. The putative catalytic triad (Cys1651-His1812-Asp1826) and the zinc binding site have deubiquitinating activity; this unexpected activity in addition to its papain-like protease offers a new viral. a strategy for modulating the mechanism of ubiquitination of host cells.

5.nsp4 (500). Not described.

6.nsp5 (306). 3C-like protease, provides proteolytic processing of replicative polyprotein at 11 specific sites with the formation of key functional enzymes, such as replicase and helicase. In SARS-CoV, growth arrest and apoptosis using caspase-3 and caspase-9 activity were demonstrated in 3CLpro-expressing human promonocyte cells with increased activation of the nuclear factor κB-dependent reporter.

7.nsp6 (290). Not described.

8.nsp7 (83). Nuclear magnetic resonance research has discovered potential sites for protein interactions. So far, only a three-dimensional structure has been described.

9. nsp8 (198). The putative RNA-dependent RNA polymerase is the crystal structure of the nsp7-nsp8 hexadecamera and has a central channel with positive electrostatic properties and sizes favorable for nucleic acid binding. This is probably another unique RNA-dependent RNA polymerase of the large genome.

10.nsp9 (113). The three-dimensional crystal structure of a dimer that binds viral RNA and interacts with nsp8.

11. nsp10 (139). A crystalline structure that has the function of nucleic acid binding in a larger complex of RNA-binding proteins for transcription and replication of viral genes. Specifically interacts with the NADH 4L subunit and cytochrome oxidase II with depolarization of the inner mitochondrial membrane of a transfected human lung fibroblast. It has a pronounced cytopathic effect.

12. nsp11 (13). Not described.

13. nsp12 (932). RNA-dependent RNA polymerase replicates and transcribes to produce RNA, the bipolar dimension of the gene with the subgene.

14. nsp13 (601). Helicase (dNT phase and RNA 5'-triphosphatase activity).

15. nsp14 (527). 3 '→ 5'-exoribonuclease. Its unusual 3 ′ → 5′-exoribonuclease activity complements the endoribonuclease activity in the replication of the giant RNA genome.

16. nsp15 (346). Uridylate-specific RNA endonuclease that is critically involved in the coronavirus replication cycle.

17. nsp16 (298). Alleged 2'-O-ribose methyltransferase (2'-O-ribose methyltransferase).

18. Orf2 (1.255). Spike protein. It binds to the ACE2 host cell receptor and other coreceptors, mediates the pe*******on of the virus into host cells as a type 1 viral fusion protein. However, endosome acidification is required for effective S-mediated viral pe*******on. For fusion, protease activation and proteolytic cleavage by abundantly expressing factor Xa is required to bind to the membranes of the virus and infected cells (S1 and S2). T cells (after IL-2 activation) respond to transfected ACE2, which can form a bond with an expressing viral spike followed by a significant accumulation of protein S in the endoplasmic reticulum, which can modulate virus replication, thereby increasing acute pulmonary failure.

19. Orf3a (274). Forms an ion channel sensitive to potassium, contributing to budding and subsequent isolation of the virus. Overexpression of Orf3a in the cell line can cause apoptosis. Its expression in lung epithelial cells A549 increases the level of mRNA and the intracellular and secreted levels of all three subunits - alpha, beta and gamma, as well as fibrinogen. With overexpression of Orf3a, an increase in the production of inflammatory chemokines is also observed (in large quantities, they are activated by SARS-CoV infection).

20. Orf3b (154). It is mainly localized in the nucleolus of various transfected cells. Orf3b inhibits IFN-β expression in signal synthesis and transmission. With the expression of Orf3b, cells can undergo simultaneous necrosis and apoptosis within 6 hours after transfection, but this action can occur at later times.

21. Orf4 (76). The shell protein, which in flat lipid bilayers creates ion channels that become more permeable to monovalent cations, compared with the permeability of monovalent anions. Presumably involved in the nucleation and release of the virus. Over time, it induces apoptosis in transfected Jurkat T cells, especially in the absence of growth factors.

22. Orf5 (221). Membrane surface protein responsible for viral assembly and budding. M-protein induces apoptosis in cells, which can be suppressed by caspase inhibitors.
23. Orf6 (63). A membrane protein that accelerates the replication and virulence of recombinant murine coronavirus. Inhibits synthesis and IFN signaling. Inhibits nuclear translocation, but not phosphorylation of STAT1. Orf6 is localized in the endoplasmic reticulum / Golgi membrane of infected cells, binds and disrupts the formation of a nuclear import complex, linking karyopherin alpha 2 and karyopherin beta 1 to the membrane. This retention of the complex leads to the loss of STAT1 transport to the nucleus, despite the induced viral RNA IFN signaling. Thus, Orf6 blocks the expression of STAT1-activated genes, which are necessary for establishing the antiviral state.

24. Orf7a (122). A unique type I transmembrane protein that participates in the assembly of the virus by interacting with M and E (necessary for the formation of virus-like particles when co-expressed with S and N). Expression of Orf7a induces apoptosis via a caspase-3-dependent pathway in cell lines originating from different organs, but especially in the lungs, kidneys and liver.

25. Orf7b (44). Not described.

26. Orf8a (39). Orf8a was localized in the mitochondria, and its overexpression led to an increase in the mitochondrial transmembrane potential, production of reactive oxygen species, caspase-3 activity, and cell apoptosis. Orf8a enhances virus replication and induces apoptosis via the mitochondrial dependent pathway.

27. Orf8b (84). May modulate virus replication.

28. Orf9 (422). Nucleocapsid protein. Binding and packaging of viral RNA in the assembly of the virion, N-antagonized IFN by inhibiting the synthesis of IFN-β. It can cause pneumonia by activating COX-2 gene expression by binding directly to the promoter, leading to inflammation through numerous COX-2 signaling cascades. It leads to induced reorganization of actin in cells lacking growth factors.

29. Orf9b (98). The crystal structure of Orf9b can participate in attachment to the membrane and associate with intracellular vesicles, which indicates that Orf9b plays one of the roles in the assembly of the virion.

Mortality from Covid19 has not yet affected the statistics on total annual mortality in Europe.
In recent years, official statistics for 24 European countries show that not only the overall mortality rate does not increase, but, for now, is actually much lower than the latest average annual and intermediate indicators.

The statistics are compiled by the European Monitoring of Excess Mortality for Public Health Action (EuroMOMO - European Mortality Monitoring Agency). The data presented resulted from an international partnership of institutions from 24 European countries. The purpose of this data collection is declared to be to promote public health emergency preparedness.

This project tracks “excess mortality,” that is, the number of officially registered deaths compared to average mortality. Each country is disaggregated by age demography.

As we see at the 12th week of 2020 (March 19-25) in the vast majority of European countries there is no excess mortality. This means that mortality is at the expected level.

The one obvious exception is Italy. But note that mortality is classified as "high" (High 5; 7), but not "very high" (Very high> 7), as, for example, it was in Europe in previous years.

So today, in Europe, Italy is the country most affected by the coronavirus pandemic. Events in Italy give rise to harsh quarantine conditions, not only in Italy but also in other European countries. The main reason for this is high mortality and the rapid spread of the virus.
However, for comparison, let's look at the same mortality map, only in previous years (please note this is the statistics of the same agency)

In 2019, in a global sense, Europe was much worse.
France has a "very high" mortality rate (Very high> 7)
In Spain and Portugal, mortality is classified as "high" (High 5; 7) - at the same level as today in Italy
In several other countries, mortality is classified as “above average”
Nevertheless, in 2019 there was no quarantine and no blocking of movement.

DO YOU HAVE QUESTIONS?

It was the height of the huge flu season 2017-2018. As you can see, Europe then also suffered rather badly in terms of "excess mortality."
However, in 2018 there was nothing similar in terms of blocking movement. And no one declared a global epidemic.

ARE ANY QUESTIONS?
According to the results of “excess mortality”, the 2nd week of 2017 was probably even worse than the situation now, because almost the entire western part of Europe and especially the Mediterranean countries had a huge surge in “excess mortality”

And in 2017, the flu virus or “excess mortality” as a result of “something”, otherwise, did not lead to the announcement of an epidemic or the closure of borders
The question naturally arises:
Or maybe "excess mortality" is just a NORMAL PHENOMENON for this period of the year?
For example, in its current form, so far, the indicators of "excess mortality" in 2020 are lower than the indicators of "excess mortality" in 2017.

Then the question is:

IF THERE WAS NO QUARANTINE AND FREEDOM OF MOVEMENT IN THE FIRST MONTHS OF 2017, NOT IN 2018, NOT IN 2019 - SO WHY DO WE ALL HAVE IT TODAY?