Who is a virus?
Humanity fights DNA and viruses
Immortalization and carcinogenesis of cells
Immortalization and carcinogenesis of cells
It is important to recognize that some viruses that infect multicellular organisms can "immortalize" or "cancerize" infected cells.
Such viruses are called "tumor viruses" or "cancer viruses".
There are various mechanisms by which viruses "immortalize" or "cancerize" the host cells they infect. It is the "cell cycle" that is essential for the growth of any organism that accurately replicates large amounts of DNA and distributes it into genetically identical daughter cells.
The "cell cycle" consists of two preparatory periods for cell division: the intercellular phase: the G1 phase: the preparatory phase for DNA synthesis→ the S: synthesis phase: the DNA synthesis phase→ the G2 phase: the preparatory phase for mitotic phases, and the mitotic phase: M phase. The "cell cycle" begins with the G1 phase.
In the G1 stage, replication occurs in the next S phase, so it is dangerous if the DNA is damaged, so checkpoints are set up to check for DNA damage.
In the event of DNA damage, the work is done to buy time to repair the DNA. If the damage is severe and the DNA cannot be cured, the p53 gene has the function of controlling DNA repair, cell growth arrest, apoptosis, and other cell proliferation cycle suppression in each cell, so when the cell becomes cancerous, "apoptosis: cell death" occurs.
When this gene malfunctions, cancer is thought to occur. The G1 phase has "checkpoints" and is an important place to determine the fate of cells.
Cells in the G1 phase have four routes: they move on to S and go around the cell cycle one more time, they stay in G1 and wait until the conditions are right, they rest for a while after progressing to G0, and they stop dividing and finally differentiate as seen in neurons and muscle cells.
The G0 phase is still alive and well in the cell cycle regulatory system. It is separated from the cell cycle once and rests, but can be divided if necessary. Hepatocytes are in the G0 stage and can proliferate when hepatocytes are injured.
In the S phase, cells that have passed the "checkpoint" of the G1 phase are replicated. The S phase is the replication phase, which doubles the DNA.
In the G2 phase, we can prepare for the next phase of the division, the M phase. If there is a problem with DNA replication in the S phase, a checkpoint will also work here to prevent DNA from separating incompletely.
In the M phase, cell division takes place.
When DNA "cell cycle arrest" or "cell cycle progression" caused by host cells resisting infection by cancer viruses, "production of gene products that suppress apoptosis", which is a planned "programmed cell death" by active gene expression in vital activities, "activates cell proliferation", and in retroviruses, when incorporating viral genes into the genome of the host cell, It is also known to cause host cells to become cancerous by damaging tumor suppressor genes.
~From a research group led by Professor Hiroshi Kimura and Associate Professor Yoshitaka Sato of the Department of Virology, Nagoya University Graduate School of Medicine, Tokai National University Organization and joint research with Professor Hitoshi Kiyoi and graduate student Ken Saai of the Department of Hematology and Oncology, Professor Shinya Toyokuni of the Department of Bioreaction Pathology, Professor Yusuke Okuno of the Department of Virology, Nagoya City University, and Professor Takayuki Murata of the Department of Virology, Fujita Health University~
Epstein-Barr Virus: EB Virus is a virus that is about 50 It is an oncogenic herpes virus that causes tumors in humans that was discovered many years ago.
It is infected in more than 90% of adults, but shows few symptoms and hides mainly in B cells in the body. In some cases, it can cause "blood cancer lymphoma" such as "Burkitt lymphoma", "diffuse Bimansei large B-cell lymphoma", and "post-transplant lymphoproplasia".
EB Virus 70 It has these genes, and these viral genes work skillfully in infected cells to take over the host cell and convert it into a cell state that is convenient for the virus. The genes of the EB virus are numerous, and the function of many genes is not yet fully understood.
In the case of diffuse Bimansei large B-cell lymphoma, it is known that the prognosis is worse in patients with EB virus in tumor cells and cases without EB virus, and it is generally considered that EB virus-related lymphoma is less effective against anticancer drugs. We focused on the gene BNRF1 and clarified its function. The BNRF1 gene of the EB virus, which causes malignant lymphoma, suppresses cell death in infected cells and enables stable growth
The "stable cell proliferation" induced by BNRF1 involves mitochondrial protein: IFI27. EB virus-infected cells in the absence of BNRF1 and IFI27 have a significantly reduced tumorigenic capacity, and the formation of EBVIRUS-associated tumors requires efficient energy production.
Such viruses are called "tumor viruses" or "cancer viruses".
There are various mechanisms by which viruses "immortalize" or "cancerize" the host cells they infect. It is the "cell cycle" that is essential for the growth of any organism that accurately replicates large amounts of DNA and distributes it into genetically identical daughter cells.
The "cell cycle" consists of two preparatory periods for cell division: the intercellular phase: the G1 phase: the preparatory phase for DNA synthesis→ the S: synthesis phase: the DNA synthesis phase→ the G2 phase: the preparatory phase for mitotic phases, and the mitotic phase: M phase. The "cell cycle" begins with the G1 phase.
In the G1 stage, replication occurs in the next S phase, so it is dangerous if the DNA is damaged, so checkpoints are set up to check for DNA damage.
In the event of DNA damage, the work is done to buy time to repair the DNA. If the damage is severe and the DNA cannot be cured, the p53 gene has the function of controlling DNA repair, cell growth arrest, apoptosis, and other cell proliferation cycle suppression in each cell, so when the cell becomes cancerous, "apoptosis: cell death" occurs.
When this gene malfunctions, cancer is thought to occur. The G1 phase has "checkpoints" and is an important place to determine the fate of cells.
Cells in the G1 phase have four routes: they move on to S and go around the cell cycle one more time, they stay in G1 and wait until the conditions are right, they rest for a while after progressing to G0, and they stop dividing and finally differentiate as seen in neurons and muscle cells.
The G0 phase is still alive and well in the cell cycle regulatory system. It is separated from the cell cycle once and rests, but can be divided if necessary. Hepatocytes are in the G0 stage and can proliferate when hepatocytes are injured.
In the S phase, cells that have passed the "checkpoint" of the G1 phase are replicated. The S phase is the replication phase, which doubles the DNA.
In the G2 phase, we can prepare for the next phase of the division, the M phase. If there is a problem with DNA replication in the S phase, a checkpoint will also work here to prevent DNA from separating incompletely.
In the M phase, cell division takes place.
When DNA "cell cycle arrest" or "cell cycle progression" caused by host cells resisting infection by cancer viruses, "production of gene products that suppress apoptosis", which is a planned "programmed cell death" by active gene expression in vital activities, "activates cell proliferation", and in retroviruses, when incorporating viral genes into the genome of the host cell, It is also known to cause host cells to become cancerous by damaging tumor suppressor genes.
~From a research group led by Professor Hiroshi Kimura and Associate Professor Yoshitaka Sato of the Department of Virology, Nagoya University Graduate School of Medicine, Tokai National University Organization and joint research with Professor Hitoshi Kiyoi and graduate student Ken Saai of the Department of Hematology and Oncology, Professor Shinya Toyokuni of the Department of Bioreaction Pathology, Professor Yusuke Okuno of the Department of Virology, Nagoya City University, and Professor Takayuki Murata of the Department of Virology, Fujita Health University~
Epstein-Barr Virus: EB Virus is a virus that is about 50 It is an oncogenic herpes virus that causes tumors in humans that was discovered many years ago.
It is infected in more than 90% of adults, but shows few symptoms and hides mainly in B cells in the body. In some cases, it can cause "blood cancer lymphoma" such as "Burkitt lymphoma", "diffuse Bimansei large B-cell lymphoma", and "post-transplant lymphoproplasia".
EB Virus 70 It has these genes, and these viral genes work skillfully in infected cells to take over the host cell and convert it into a cell state that is convenient for the virus. The genes of the EB virus are numerous, and the function of many genes is not yet fully understood.
In the case of diffuse Bimansei large B-cell lymphoma, it is known that the prognosis is worse in patients with EB virus in tumor cells and cases without EB virus, and it is generally considered that EB virus-related lymphoma is less effective against anticancer drugs. We focused on the gene BNRF1 and clarified its function. The BNRF1 gene of the EB virus, which causes malignant lymphoma, suppresses cell death in infected cells and enables stable growth
The "stable cell proliferation" induced by BNRF1 involves mitochondrial protein: IFI27. EB virus-infected cells in the absence of BNRF1 and IFI27 have a significantly reduced tumorigenic capacity, and the formation of EBVIRUS-associated tumors requires efficient energy production.
Impact at the individual level
Viral infections cause various diseases, not only at the cellular level, but also at the individual level of multicellular organisms.
Collectively, these diseases are called "viral infections."
Influenza, smallpox, measles, rubella, acquired immunodeficiency syndrome(ＡＩＤＳ)Diseases such as the new coronavirus infection belong to viral infections, and the pathogenic viruses of these infections often cause pandemics, which are human→-to-human outbreaks, and have a history of causing many casualties to humanity.
In addition, when a viral infection occurs in animals, an immune response called an antigen-antibody reaction is triggered in response to it, and against the virus particles themselves in the blood and mucus, a neutralizing antibody against the virus called "humoral immunity" acts to prevent infection.
Antibodies are ineffective against viruses in cells after infection, but cytotoxic T cells and NK cells called "cell-mediated immunity" prevent the spread of infection by killing infected cells.
The immune response is also produced by vaccines that artificially confer immunity against certain viral infections.
Some viruses, including those that cause AIDS and viral hepatitis, have also been found to evade these immune responses and cause chronic infections.
However, HTVL-1, which is common in tropical countries, latently lives in T lymphocytes, which are a type of white blood cell. The "human T-lymphotropic virus" incorporates its genetic information into the DNA of lymphocytes, which causes leukemia.
Unlike Helicobacter pylori and hepatitis C virus, once infected with "HTVL-1", there is unfortunately no treatment that eliminates the virus, but not all people will get leukemia even if infected with the virus, and the probability of developing leukemia in people infected with "HTVL-1" is about 5%.
However, it has also been announced that people infected with this "HTVL-1" have a long life. If you don't suffer from leukemia, you can live a long life.
There are areas where there are many virus carriers in Kyushu and Okinawa in the southwestern part of the Japan, on the Japan Sea side of the Chugoku region along the coastline, on the Pacific side of Shikoku, on the Kii Peninsula, in Hokkaido and Tohoku, and there are certainly mysterious viruses that are more common on remote islands but few in inland areas.
Among the symptoms in a viral infection, there are also abnormalities in the body due to the viral infection itself. However, as in the case of tissue injury caused by fever or apoptosis of infected cells, the expression of the body's defense mechanism against the immune response itself changes the physiology of a healthy body and even damages the body's homeostasis.
This immune response often manifests itself as a symptom of the disease, and may lead to autoimmune diseases.
Humans, as humans, are at the tail end of biological evolution, and it is called a "host shift" that changes hosts and hosts, but it is also called "host jumping" to switch hosts and hosts to distantly related species from other animals, and it is thought that many viruses have become pathogens for humans.
These viruses are often harmless in natural hosts, but hosts infected with attenuated viruses behave for a long time and have more opportunities for infection, so it is predicted that "adaptive evolution of viruses" will occur.
In other words, in general, the virus is attenuated in the long run. However, in the short term, it can become more toxic. The virus cannot be taken lightly on the grounds of long-term attenuation.
In the case of the new coronavirus infection, I was informed of cases of onset that did not recover even with the ECMO device. It should not be an excessive strong immunity called immune runaway.
Collectively, these diseases are called "viral infections."
Influenza, smallpox, measles, rubella, acquired immunodeficiency syndrome(ＡＩＤＳ)Diseases such as the new coronavirus infection belong to viral infections, and the pathogenic viruses of these infections often cause pandemics, which are human→-to-human outbreaks, and have a history of causing many casualties to humanity.
In addition, when a viral infection occurs in animals, an immune response called an antigen-antibody reaction is triggered in response to it, and against the virus particles themselves in the blood and mucus, a neutralizing antibody against the virus called "humoral immunity" acts to prevent infection.
Antibodies are ineffective against viruses in cells after infection, but cytotoxic T cells and NK cells called "cell-mediated immunity" prevent the spread of infection by killing infected cells.
The immune response is also produced by vaccines that artificially confer immunity against certain viral infections.
Some viruses, including those that cause AIDS and viral hepatitis, have also been found to evade these immune responses and cause chronic infections.
However, HTVL-1, which is common in tropical countries, latently lives in T lymphocytes, which are a type of white blood cell. The "human T-lymphotropic virus" incorporates its genetic information into the DNA of lymphocytes, which causes leukemia.
Unlike Helicobacter pylori and hepatitis C virus, once infected with "HTVL-1", there is unfortunately no treatment that eliminates the virus, but not all people will get leukemia even if infected with the virus, and the probability of developing leukemia in people infected with "HTVL-1" is about 5%.
However, it has also been announced that people infected with this "HTVL-1" have a long life. If you don't suffer from leukemia, you can live a long life.
There are areas where there are many virus carriers in Kyushu and Okinawa in the southwestern part of the Japan, on the Japan Sea side of the Chugoku region along the coastline, on the Pacific side of Shikoku, on the Kii Peninsula, in Hokkaido and Tohoku, and there are certainly mysterious viruses that are more common on remote islands but few in inland areas.
Among the symptoms in a viral infection, there are also abnormalities in the body due to the viral infection itself. However, as in the case of tissue injury caused by fever or apoptosis of infected cells, the expression of the body's defense mechanism against the immune response itself changes the physiology of a healthy body and even damages the body's homeostasis.
This immune response often manifests itself as a symptom of the disease, and may lead to autoimmune diseases.
Humans, as humans, are at the tail end of biological evolution, and it is called a "host shift" that changes hosts and hosts, but it is also called "host jumping" to switch hosts and hosts to distantly related species from other animals, and it is thought that many viruses have become pathogens for humans.
These viruses are often harmless in natural hosts, but hosts infected with attenuated viruses behave for a long time and have more opportunities for infection, so it is predicted that "adaptive evolution of viruses" will occur.
In other words, in general, the virus is attenuated in the long run. However, in the short term, it can become more toxic. The virus cannot be taken lightly on the grounds of long-term attenuation.
In the case of the new coronavirus infection, I was informed of cases of onset that did not recover even with the ECMO device. It should not be an excessive strong immunity called immune runaway.
To vaccinate or not to vaccinate?
Urban legends were also included in this discussion, and "awareness of the physical circumstances of potential host recipients" was not discussed.
"The prevalence of excessive vaccination fear among people who are psychologically worried and concerned", "Development of vaccination denial arguments based on the desire to support self-affirmation of strong immunity holders", "Manifestation of self-judgment and opposition to vaccination accidents by strong immunity holders", "Ignorant subjective claims of TV commentators on infection terminology", "Lack of explanation on the vaccination side", "Discrepancy between the explanation efforts of the Ministry of Health, Labour and Welfare and the efforts of the public to understand" was in the background.
Novel coronavirus infection: It has been reported that single nucleotide polymorphisms (SNPs) in the region where many genes such as chromosome 3 SLC6A20, LZTFL1, FYCO1, CXCR6, XCR1, CCR1, CCR1, CCR3, and CCR9 are involved in the genetic factors of people involved in the severity of COVID-19 are associated with severe disease.
Single nucleotide polymorphisms: It has been shown that having a risk type of SNP increases the risk of severe disease by about 2 times.
In a report in Nature by Dr. Pääbo and his colleagues, it was announced that the risk factor for COVID-19 severity on chromosome 3 was actually inherited from Neanderthals.
Homo sapiens and Neanderthals, who became extinct about 40,000 years ago, are said to have diverged from a common ancestor about 550,000 years ago.
Therefore, two possibilities were considered regarding the "core haplotypes" associated with the severity of COVID-19. It is "inherited from a common ancestor of Homo sapiens and Neanderthals" or "originated in Neanderthals, which was then inherited by Homo sapiens".
As a result of the analysis, it was concluded that it was very likely that it originated in Neanderthals and was inherited by Homo sapiens due to the characteristics of this "core haplotype", and that it was inherited from Neanderthals to Homo sapiens as a result of hybridization between Neanderthals and Homo sapiens.
People of South Asian descent have a high frequency of "core haplotypes" associated with the severity of COVID-19, especially in more than 60% of Bangladeshis.
On the other hand, less than 20% of people of European descent have this "core haplotype", while few people of African and East Asian descent have it. The paper statistically shows that such a large difference in frequency is not something that usually happens. And this suggests that it may have been "influenced by natural selection" in the past.
The genome inherited from Neanderthals to Homo sapiens is related to the immune response, and it is said that it may have affected the survival of Homo sapiens. In particular, around Bangladesh, it has been reported that the genome inherited from Neanderthals was preserved by "positive natural selection".
Dr. Pääbo and his colleagues speculate that people with this 'core haplotype' may have been resistant to certain pathogens other than the new coronavirus. On the other hand, in the immediate vicinity of East Asia, most people do not have this "core haplotype". In the past, people with this "core haplotype" in East Asia were less resistant to coronaviruses and certain other pathogens, and "negative natural selection" may have reduced their frequency, he said.
Humans have evolved with diseases, especially viral infections. And right now, we are in the midst of the new coronavirus and various viral infections.
"The prevalence of excessive vaccination fear among people who are psychologically worried and concerned", "Development of vaccination denial arguments based on the desire to support self-affirmation of strong immunity holders", "Manifestation of self-judgment and opposition to vaccination accidents by strong immunity holders", "Ignorant subjective claims of TV commentators on infection terminology", "Lack of explanation on the vaccination side", "Discrepancy between the explanation efforts of the Ministry of Health, Labour and Welfare and the efforts of the public to understand" was in the background.
Novel coronavirus infection: It has been reported that single nucleotide polymorphisms (SNPs) in the region where many genes such as chromosome 3 SLC6A20, LZTFL1, FYCO1, CXCR6, XCR1, CCR1, CCR1, CCR3, and CCR9 are involved in the genetic factors of people involved in the severity of COVID-19 are associated with severe disease.
Single nucleotide polymorphisms: It has been shown that having a risk type of SNP increases the risk of severe disease by about 2 times.
In a report in Nature by Dr. Pääbo and his colleagues, it was announced that the risk factor for COVID-19 severity on chromosome 3 was actually inherited from Neanderthals.
Homo sapiens and Neanderthals, who became extinct about 40,000 years ago, are said to have diverged from a common ancestor about 550,000 years ago.
Therefore, two possibilities were considered regarding the "core haplotypes" associated with the severity of COVID-19. It is "inherited from a common ancestor of Homo sapiens and Neanderthals" or "originated in Neanderthals, which was then inherited by Homo sapiens".
As a result of the analysis, it was concluded that it was very likely that it originated in Neanderthals and was inherited by Homo sapiens due to the characteristics of this "core haplotype", and that it was inherited from Neanderthals to Homo sapiens as a result of hybridization between Neanderthals and Homo sapiens.
People of South Asian descent have a high frequency of "core haplotypes" associated with the severity of COVID-19, especially in more than 60% of Bangladeshis.
On the other hand, less than 20% of people of European descent have this "core haplotype", while few people of African and East Asian descent have it. The paper statistically shows that such a large difference in frequency is not something that usually happens. And this suggests that it may have been "influenced by natural selection" in the past.
The genome inherited from Neanderthals to Homo sapiens is related to the immune response, and it is said that it may have affected the survival of Homo sapiens. In particular, around Bangladesh, it has been reported that the genome inherited from Neanderthals was preserved by "positive natural selection".
Dr. Pääbo and his colleagues speculate that people with this 'core haplotype' may have been resistant to certain pathogens other than the new coronavirus. On the other hand, in the immediate vicinity of East Asia, most people do not have this "core haplotype". In the past, people with this "core haplotype" in East Asia were less resistant to coronaviruses and certain other pathogens, and "negative natural selection" may have reduced their frequency, he said.
Humans have evolved with diseases, especially viral infections. And right now, we are in the midst of the new coronavirus and various viral infections.
Virus discovery
Only males of wild birds such as sandpipers have long beaks, long legs, and large and long wings that are popular with females. This is because the beak and legs are long so that viruses and bacteria from the ground, such as mud, do not get attached to the torso.
The reason why migratory birds migrate to cold regions is not only to secure food, but also to avoid infection from viruses and bacterial bacteria.
Swallows also have only one male with large wings and a long tail, which is why they are suitable for continental migration due to their high flying ability and long-distance flight ability. In order to avoid severe cold regions and hot hot areas, we move to a suitable temperature area for the bird.
If you trace the origin of all "influenza A", you will inevitably end up with waterfowl. The influenza A virus, which infects humans, does not show pathogenicity because waterfowl multiply only in the intestinal tract even if they are infected.
However, it infects chickens, quails, and turkeys from waterfowl and human poultry, and develops a very high pathogenicity as it repeatedly mutates within the poultry population.
This type of avian influenza is called "highly pathogenic avian influenza (HPAI)" and is a threat to the poultry industry around the world, and every year we see in the news that employees in protective suits dig large holes in the nurseries and incinerate them with lime.
This is because livestock → waterfowl→poultry, mutated mutant "highly pathogenic avian influenza (HPAI)" does not infect humans. If → mutation occurs that infects humans, there will be deaths on a global scale.
The reason why migratory birds migrate to cold regions is not only to secure food, but also to avoid infection from viruses and bacterial bacteria.
Swallows also have only one male with large wings and a long tail, which is why they are suitable for continental migration due to their high flying ability and long-distance flight ability. In order to avoid severe cold regions and hot hot areas, we move to a suitable temperature area for the bird.
If you trace the origin of all "influenza A", you will inevitably end up with waterfowl. The influenza A virus, which infects humans, does not show pathogenicity because waterfowl multiply only in the intestinal tract even if they are infected.
However, it infects chickens, quails, and turkeys from waterfowl and human poultry, and develops a very high pathogenicity as it repeatedly mutates within the poultry population.
This type of avian influenza is called "highly pathogenic avian influenza (HPAI)" and is a threat to the poultry industry around the world, and every year we see in the news that employees in protective suits dig large holes in the nurseries and incinerate them with lime.
This is because livestock → waterfowl→poultry, mutated mutant "highly pathogenic avian influenza (HPAI)" does not infect humans. If → mutation occurs that infects humans, there will be deaths on a global scale.
ミトコンドリアは太古には恐ろしいウイルスだった
Mitochondria are important cells that serve as a source of energy for humans and are the cornerstone of immunity.
However, this mitochondria was a virus that drove humanity to extinction.
The species that were successfully incorporated into the human body became the ancestors of today's humans.
It is said that the upright posture and bipedal walking of humans were successful in the uptake of mitochondria, which produce a large amount of energy.
The history of human beings is the history of infection by antigens such as viruses and bacterial bacteria, and the formation of antibodies, absorption, and intake of "another enhanced life form."
However, this mitochondria was a virus that drove humanity to extinction.
The species that were successfully incorporated into the human body became the ancestors of today's humans.
It is said that the upright posture and bipedal walking of humans were successful in the uptake of mitochondria, which produce a large amount of energy.
The history of human beings is the history of infection by antigens such as viruses and bacterial bacteria, and the formation of antibodies, absorption, and intake of "another enhanced life form."
遺伝子脆弱性と覚醒させるストレス
ミトコンドリア
生命の起源である４０億年前という太古の地球では、「原核生物」から樹形上に「光合成細菌」が分派して「真正細菌」と「αプロテオ細菌」「藍色細菌：シアノバクテリア」となり、「真核生物」と「αプロテオ細菌」「藍色細菌」が「ミトコンドリア：トリバノゾーマ」となりました。「ミトコンドリア」とは「糸ミトス」と「顆粒コンドリオン」というギリシャ語から「糸粒体」とも呼ばれます。「ミトコンドリア」が登場するまでは「酸素」は生物には「毒」でしかありませんでした。「酸素」を利用して「ブドウ糖」を「二酸化炭素」と「水」に分解し、「ブドウ糖」に蓄えられた「化学エネルギー」を「ＡＴＰ(Adenosine Tri Phosphate)通貨」に変換できる能力が備わりました。これにより、人間や動物が元気に生きていけるようになりました。
２００１年９月１１日、いわゆる９．１１のアメリカで起こった同時多発テロ事件では、「ミトコンドリア」は母方からしか遺伝しないことと、１つの細胞に数百から数千存在し、複数のＤＮＡ情報が得られることから、２，９７７人から半数の身元が判明しました。人間の細胞は約３７兆個あり、１つの細胞に数百から数千存在するために約１２京個あります。
「ミトコンドリア」は、「酸素」を使って「ネルギー」となる「ＡＴＰ通貨」を作りますが、その時に電子が滞ると発生する「活性酸素フリーラジカル」を攻撃します。この「活性酸素」こそ、「老化」が人間の天敵で、「ガン」や「生活習慣病」や「指定難病」や「糖尿病」、「ウイルス・細菌・カビ(白癬菌・カンジダ等)・原虫感染症」の原因です。「ミトコンドリア病」といわれることもあります。
「ミトコンドリア」は「量」と「質」が大切です。「量」「質」は「バランスのよい食事」と「適度な運動」により「ＡＴＰ通貨」を増やすことです。「自然免疫パトロール」「自律神経バランス」「ホルモン分泌バランス」は、大切なバリアです。
「ミトコンドリア」には、「アポトーシス(自死)」「マイトファジー(活性酸素による損傷部位分捨)」「オートファジー(損傷リソゾーム・ゴルジ体分捨)」によって「ガン化」を事前に予防しています。
「還元型コエンザイムＱ１０」や「ビタミンＢ１」や「ミドリムシ」もトレンドになった時期もありました。
「栄養」という必要の研究を「ＫＩＢＯＯ 希望」は追求しています。
２００１年９月１１日、いわゆる９．１１のアメリカで起こった同時多発テロ事件では、「ミトコンドリア」は母方からしか遺伝しないことと、１つの細胞に数百から数千存在し、複数のＤＮＡ情報が得られることから、２，９７７人から半数の身元が判明しました。人間の細胞は約３７兆個あり、１つの細胞に数百から数千存在するために約１２京個あります。
「ミトコンドリア」は、「酸素」を使って「ネルギー」となる「ＡＴＰ通貨」を作りますが、その時に電子が滞ると発生する「活性酸素フリーラジカル」を攻撃します。この「活性酸素」こそ、「老化」が人間の天敵で、「ガン」や「生活習慣病」や「指定難病」や「糖尿病」、「ウイルス・細菌・カビ(白癬菌・カンジダ等)・原虫感染症」の原因です。「ミトコンドリア病」といわれることもあります。
「ミトコンドリア」は「量」と「質」が大切です。「量」「質」は「バランスのよい食事」と「適度な運動」により「ＡＴＰ通貨」を増やすことです。「自然免疫パトロール」「自律神経バランス」「ホルモン分泌バランス」は、大切なバリアです。
「ミトコンドリア」には、「アポトーシス(自死)」「マイトファジー(活性酸素による損傷部位分捨)」「オートファジー(損傷リソゾーム・ゴルジ体分捨)」によって「ガン化」を事前に予防しています。
「還元型コエンザイムＱ１０」や「ビタミンＢ１」や「ミドリムシ」もトレンドになった時期もありました。
「栄養」という必要の研究を「ＫＩＢＯＯ 希望」は追求しています。
ホルモンvs神経伝達物質
「ホルモン」と「神経伝達物質」は、動物が作り出す２種類の化学シグナル伝達物質です。これらは、生物の行動や態度に関与しています。
「ホルモン」は、タンパク質・脂質・コレステロールをベースとした分子のいずれかになります。「神経伝達物質」はタンパク質です。
「ホルモン」は、タンパク質・脂質・コレステロールをベースとした分子のいずれかになります。「神経伝達物質」はタンパク質です。
ホルモン
「ホルモン」は「内分泌腺」で産生され、血流に放出されて、その起源から少し離れたところに作用対象を見つけるのに対し、「神経伝達物質」は、刺激を受けたシ「ナプス前神経細胞の端末」によってシナプスの隙間に放出されて、隣接するシナプス後神経細胞に神経信号を伝達することが、「ホルモン」と「神経伝達物質」の主な違いです。
「ホルモン」は生きた細胞の産物で、血液や樹液などの液体を循環し、その発生源から離れた場所にある細胞の活動に対して、特定の、通常は刺激的な効果をもたらすことから、「ホルモン」は「化学的メッセンジャー」という「コミュニケーション・ヘルパー」として、体内の異なる部位から発生して、他の部位へ「化学的シグナル」を送ります。
「ホルモン」は、「ポリペプチド」「アミン」「テルペノイド」「ステロイド」「フェノール化合物」で、接触により、「細胞や組織の成長」「発達」「性的発達の開始と維持」「食物代謝」「体温」「気分」などに影響を与えます。
「ホルモン」は非常に強力な分子で、少数のホルモンが身体に大きな影響作用を与え、作用した後、破壊されて、再利用はできません。
「下垂体」「松果体」「膵臓」「肝臓」「胸腺」「甲状腺」「副腎」「卵巣」「精巣」などの内分泌腺から直接血流に放出された後は、目的の組織や臓器が見つかるまで体内を循環します。
「自律神経」と「ホルモン」が常に連動しながら、互いに協力し合って体内環境を整えます。
「ホルモン」は、「ポリペプチド」「アミン」「テルペノイド」「ステロイド」または「フェノール化合物」です。
出血などによって血圧が急に低下した状態では、「自律神経系のルート」が、「大動脈弓」「頸動脈洞」「腎臓」にある受容器により、血圧の低下情報がキャッチされて「延髄の血管運動中枢」に伝わり、「血管運動中枢」は「交感神経」に働きかけて心臓の収縮力を高め、心拍数を上げるように指令を出し、手足などの末梢血管を収縮させる指令を出します。生命維持に欠かせない「脳」「心臓」など器官に、優先的に血液が送られるようになります。「交感神経」の働きはそれだけでなく、「副腎髄質」に「ノルアドレナリン」や「アドレナリン」を分泌させ、細動脈を収縮させます。このようなメカニズムで血管の収縮を促し、血圧を上昇させるのですが、これはあくまでも一時的な緊急処置に過ぎません。
次に、「内分泌系」の血圧の低下をキャッチする受容器の１つに「腎臓」があります。「腎臓」に情報が伝わると、「腎臓」の「輸入細動脈にある傍糸球体細胞」から、「レニン」という酵素活性のあるホルモンが分泌されます。「レニン」は「腎臓の遠位尿細管」での「ナトリウム再吸収」を促し、それによって同時に「水分の再吸収」が促され、「血液量が増加」します。血液量が増えるということは、血管壁にかかる圧力（血圧）が上がるということですから、これによって血流の維持が可能になるのです
「男性ホルモン」と「女性ホルモン」を合わせて「性ホルモン」といい、性差を生みますが、分泌量は性別によって大きく異なりますが、男性にも女性ホルモンが少量分泌され、女性にも男性ホルモンが少量分泌されています。
「女性ホルモン」には「エストロゲン(卵胞ホルモン)」と「プロゲステロン(黄体ホルモン)」があり、どちらも卵巣から分泌されます。「エストロゲン」は、「乳腺の発達」や「皮下脂肪の沈着」など、女性の「二次性徴促進ホルモン」です。「プロゲステロン」は、「受精卵着床」や「妊娠維持」に関与するホルモンです。「女性ホルモン」が「男性ホルモン」と大きく異なるのは、分泌量が周期的に変化することです。
「男性ホルモン」は、「精巣」から分泌される「テストステロン」があります。ひげや変声など男性の「二次性徴」を促し、「精子形成」にも関与します。
「ホルモン」は生きた細胞の産物で、血液や樹液などの液体を循環し、その発生源から離れた場所にある細胞の活動に対して、特定の、通常は刺激的な効果をもたらすことから、「ホルモン」は「化学的メッセンジャー」という「コミュニケーション・ヘルパー」として、体内の異なる部位から発生して、他の部位へ「化学的シグナル」を送ります。
「ホルモン」は、「ポリペプチド」「アミン」「テルペノイド」「ステロイド」「フェノール化合物」で、接触により、「細胞や組織の成長」「発達」「性的発達の開始と維持」「食物代謝」「体温」「気分」などに影響を与えます。
「ホルモン」は非常に強力な分子で、少数のホルモンが身体に大きな影響作用を与え、作用した後、破壊されて、再利用はできません。
「下垂体」「松果体」「膵臓」「肝臓」「胸腺」「甲状腺」「副腎」「卵巣」「精巣」などの内分泌腺から直接血流に放出された後は、目的の組織や臓器が見つかるまで体内を循環します。
「自律神経」と「ホルモン」が常に連動しながら、互いに協力し合って体内環境を整えます。
「ホルモン」は、「ポリペプチド」「アミン」「テルペノイド」「ステロイド」または「フェノール化合物」です。
出血などによって血圧が急に低下した状態では、「自律神経系のルート」が、「大動脈弓」「頸動脈洞」「腎臓」にある受容器により、血圧の低下情報がキャッチされて「延髄の血管運動中枢」に伝わり、「血管運動中枢」は「交感神経」に働きかけて心臓の収縮力を高め、心拍数を上げるように指令を出し、手足などの末梢血管を収縮させる指令を出します。生命維持に欠かせない「脳」「心臓」など器官に、優先的に血液が送られるようになります。「交感神経」の働きはそれだけでなく、「副腎髄質」に「ノルアドレナリン」や「アドレナリン」を分泌させ、細動脈を収縮させます。このようなメカニズムで血管の収縮を促し、血圧を上昇させるのですが、これはあくまでも一時的な緊急処置に過ぎません。
次に、「内分泌系」の血圧の低下をキャッチする受容器の１つに「腎臓」があります。「腎臓」に情報が伝わると、「腎臓」の「輸入細動脈にある傍糸球体細胞」から、「レニン」という酵素活性のあるホルモンが分泌されます。「レニン」は「腎臓の遠位尿細管」での「ナトリウム再吸収」を促し、それによって同時に「水分の再吸収」が促され、「血液量が増加」します。血液量が増えるということは、血管壁にかかる圧力（血圧）が上がるということですから、これによって血流の維持が可能になるのです
「男性ホルモン」と「女性ホルモン」を合わせて「性ホルモン」といい、性差を生みますが、分泌量は性別によって大きく異なりますが、男性にも女性ホルモンが少量分泌され、女性にも男性ホルモンが少量分泌されています。
「女性ホルモン」には「エストロゲン(卵胞ホルモン)」と「プロゲステロン(黄体ホルモン)」があり、どちらも卵巣から分泌されます。「エストロゲン」は、「乳腺の発達」や「皮下脂肪の沈着」など、女性の「二次性徴促進ホルモン」です。「プロゲステロン」は、「受精卵着床」や「妊娠維持」に関与するホルモンです。「女性ホルモン」が「男性ホルモン」と大きく異なるのは、分泌量が周期的に変化することです。
「男性ホルモン」は、「精巣」から分泌される「テストステロン」があります。ひげや変声など男性の「二次性徴」を促し、「精子形成」にも関与します。
神経伝達物質
「神経伝達物質」は、シナプスを介してニューロンから標的細胞へ信号を伝達する化学物質です。神経細胞によっては、１種類の「神経伝達物質」しか生成しないものもあります。シナプスに複数の神経伝達物質が同時に存在することで、神経細胞は同時に複数の影響を及ぼすことができます。
「神経伝達物質」は、「シナプス前細胞の末端に存在するシナプス小胞」に貯蔵されて、「シナプス前細胞」が「神経インパルス：神経衝撃」によって刺激されると、「神経伝達物質」が「軸索末端」から「シナプス」に放出されるというシステムです。放出された「神経伝達物質」は「シナプス」を横切って拡散し、「シナプス後神経細胞上の特定の受容体」に結合します。
「神経伝達物質」は、その機能により「興奮性神経伝達物質」と「抑制性神経伝達物質」に分類され、「興奮性神経伝達物質」は、膜を通過するイオンの流れを増加させ、シナプス後神経細胞が活動電位を発生させることを可能にし、「抑制性神経伝達物質」は、膜を通過するイオンの流れを減少させ、シナプス後神経細胞が活動電位を発生させるのを禁止します。「シナプス後神経細胞」の「発火」、「興奮性機能」と「抑制性機能」の総合的な作用によって決定されます。
「神経伝達物質」には、「アセチルコリン」「生体アンミン」「アミノ酸」など、いくつかのクラスがあります。「アセチルコリン」、「アセチル」と「コリン」から生成され、「神経筋接合部」に作用し、「アセチルコリン放出神経細胞」は「中枢神経系」にも存在します。放出された「アセチルコリン」は、「シナプス後神経細胞の受容体」と結合し、「受容体」から「アセチルコリン」を分解するために、「アセチルコリンエステラーゼ」という酵素が必要となります。
「生物起源アミン：生体アミン」とは、「ドパミン」「エピネフリン」「ノルエピネフリン(ＮＥ)」などの「カテコールアミン」と、「セロトニン」「ヒスタミン」どの「インドールアミン」のことです。「カテコールアミン」と「インドールアミン」は脳内で発生し、情動行動に関与し、「体内時計の調節」にも役立ちます。「ドパミン」「ヒスタミン」「ＮＥ」は、受容体の種類によって興奮性にも抑制性にもなります。
「アミノ酸」の「神経伝達物質」には、「グルタミン酸」と「γ-アミノ酪酸(ＧＡＢＡ)があります。脳内の「グルタミン酸」は興奮作用を促し、「ＧＡＢＡ」は抑制作用を促します。
「神経ペプチド」はアミノ酸の紐で、「エンドルフィン」や「サブスタンスＰ」などは「痛み」のシグナルを媒介します。「神経伝達物質」は、「タンパク質」「アミノ酸」または「気体」です。
「神経伝達物質」は、「シナプス前細胞の末端に存在するシナプス小胞」に貯蔵されて、「シナプス前細胞」が「神経インパルス：神経衝撃」によって刺激されると、「神経伝達物質」が「軸索末端」から「シナプス」に放出されるというシステムです。放出された「神経伝達物質」は「シナプス」を横切って拡散し、「シナプス後神経細胞上の特定の受容体」に結合します。
「神経伝達物質」は、その機能により「興奮性神経伝達物質」と「抑制性神経伝達物質」に分類され、「興奮性神経伝達物質」は、膜を通過するイオンの流れを増加させ、シナプス後神経細胞が活動電位を発生させることを可能にし、「抑制性神経伝達物質」は、膜を通過するイオンの流れを減少させ、シナプス後神経細胞が活動電位を発生させるのを禁止します。「シナプス後神経細胞」の「発火」、「興奮性機能」と「抑制性機能」の総合的な作用によって決定されます。
「神経伝達物質」には、「アセチルコリン」「生体アンミン」「アミノ酸」など、いくつかのクラスがあります。「アセチルコリン」、「アセチル」と「コリン」から生成され、「神経筋接合部」に作用し、「アセチルコリン放出神経細胞」は「中枢神経系」にも存在します。放出された「アセチルコリン」は、「シナプス後神経細胞の受容体」と結合し、「受容体」から「アセチルコリン」を分解するために、「アセチルコリンエステラーゼ」という酵素が必要となります。
「生物起源アミン：生体アミン」とは、「ドパミン」「エピネフリン」「ノルエピネフリン(ＮＥ)」などの「カテコールアミン」と、「セロトニン」「ヒスタミン」どの「インドールアミン」のことです。「カテコールアミン」と「インドールアミン」は脳内で発生し、情動行動に関与し、「体内時計の調節」にも役立ちます。「ドパミン」「ヒスタミン」「ＮＥ」は、受容体の種類によって興奮性にも抑制性にもなります。
「アミノ酸」の「神経伝達物質」には、「グルタミン酸」と「γ-アミノ酪酸(ＧＡＢＡ)があります。脳内の「グルタミン酸」は興奮作用を促し、「ＧＡＢＡ」は抑制作用を促します。
「神経ペプチド」はアミノ酸の紐で、「エンドルフィン」や「サブスタンスＰ」などは「痛み」のシグナルを媒介します。「神経伝達物質」は、「タンパク質」「アミノ酸」または「気体」です。
幸せホルモン
「ホルモン」とは、血中に排出されて全身に送られる分泌物。ホルモンとして有名なアドレナリンは、血管を通って各器官に作用し、心拍数を上げる、瞳孔を開く、膀胱を広げるといったさまざまな身体反応を引き起こします。
「神経伝達物質」という分泌物もあり、「ホルモン」とは違い細胞から細胞へ送られます。
多くの表記では、"幸せホルモン"として扱っている「セロトニン」「エンドルフィン」「ドパミン」は、「神経伝達物質」です。“幸せホルモン”は、文字通りの「ホルモン」だけでなく、「神経伝達物質」との複合呼称です。
「ドーパミン」という一般名は、専門的には「ドパミン」と言われます。
「ドパミン」は、さまざまな機能に重要な役割を果たす脳内の神経伝達物質です。それは喜び、報酬、そしてモチベーションに関連しているので、しばしば「心地よい神経伝達物質」と呼ばれます。
「ドパミン」は、気分や感情を調節し、動きや協調を制御するのに役立ちます。それは脳の報酬システムに関与しており、喜び、学習、強化に関連する行動に影響を与えます。「ドパミンレベルの不均衡」は、「パーキンソン病」や「統合失調症」などの状態に関連しています。モチベーション、集中力、そして日常の活動で喜びを体験するために重要です。
「パーキンソン病」では「脳内ドパミン」が不足することで手足の震えや筋肉のこわばりなどが起こります。「脳内ドパミン」は「ドパミン受容体」を刺激することで「パーキンソン病」の症状などを改善する作用があります。「ドパミン」と同じ様に「ドパミン受容体」を刺激することができれば「パーキンソン病」の症状の改善が期待できます。「脳内ドパミン受容体（主にＤ２受容体）」を刺激する作用により、不足している「ドパミン」の作用を補うことで、「パーキンソン病」の症状を改善します。
「ドパミン」は「乳汁分泌ホルモン(プロラクチン)や成長ホルモンの分泌を抑える作用」ももっています。そのためドパミンと類似した作用をもつ薬剤の中には、「乳汁漏出症」や「末端肥大症（先端巨大症）」などに使用する薬剤もあります。
「神経伝達物質」という分泌物もあり、「ホルモン」とは違い細胞から細胞へ送られます。
多くの表記では、"幸せホルモン"として扱っている「セロトニン」「エンドルフィン」「ドパミン」は、「神経伝達物質」です。“幸せホルモン”は、文字通りの「ホルモン」だけでなく、「神経伝達物質」との複合呼称です。
「ドーパミン」という一般名は、専門的には「ドパミン」と言われます。
「ドパミン」は、さまざまな機能に重要な役割を果たす脳内の神経伝達物質です。それは喜び、報酬、そしてモチベーションに関連しているので、しばしば「心地よい神経伝達物質」と呼ばれます。
「ドパミン」は、気分や感情を調節し、動きや協調を制御するのに役立ちます。それは脳の報酬システムに関与しており、喜び、学習、強化に関連する行動に影響を与えます。「ドパミンレベルの不均衡」は、「パーキンソン病」や「統合失調症」などの状態に関連しています。モチベーション、集中力、そして日常の活動で喜びを体験するために重要です。
「パーキンソン病」では「脳内ドパミン」が不足することで手足の震えや筋肉のこわばりなどが起こります。「脳内ドパミン」は「ドパミン受容体」を刺激することで「パーキンソン病」の症状などを改善する作用があります。「ドパミン」と同じ様に「ドパミン受容体」を刺激することができれば「パーキンソン病」の症状の改善が期待できます。「脳内ドパミン受容体（主にＤ２受容体）」を刺激する作用により、不足している「ドパミン」の作用を補うことで、「パーキンソン病」の症状を改善します。
「ドパミン」は「乳汁分泌ホルモン(プロラクチン)や成長ホルモンの分泌を抑える作用」ももっています。そのためドパミンと類似した作用をもつ薬剤の中には、「乳汁漏出症」や「末端肥大症（先端巨大症）」などに使用する薬剤もあります。
「イジメＩＪＩＭＥ」とペシミスト
脳内の「ドパミンレベルの不均衡」への課題の認識は、「遺伝子脆弱性」と「覚醒させるストレス」の研究です。
「統合失調症」も「発達障害性」と「パーソナリティー障害性」を背景に持っている学生が、「イジメ」というストレスとの遭遇から発症しますが、「遺伝子脆弱性の覚醒」とも考えられます。
「ツナミＴＵＮＡＭＩ」と同様に、「ＫＩＢＯＯ 希望」では、「イジメＩＪＩＭＥ」と表記しています。「ＫＩＢＯＯ 希望」から発信し、世界共通用語となることでしょう。
「イジメＩＪＩＭＥ」は、被害者の一生を崩壊させます。
「イジメＩＪＩＭＥ」は、「ペシミスト(Pessimist：悲観主義者)」へ人間を変化させます。「幻覚」や「妄想」や「感情低下」や「意欲喪失」という「ドパミンレベルの不均衡」を発症させます。
誰もが出社したくない朝の駅やバス停で、心の均衡の揺れを、ネガティブ方向に向けて、やる気を台無しにさせる心無い一言を放射します。
「ペシミスト」の「イジメＩＪＩＭＥ」は、次々と伝染します。反撃に出ずに「笑って涙をこらえた人」だけが、「抑うつ症」から「脳内ホルモン分泌障害」へと墜落していきます。
「ペシミスト」はすべての取り組みへ中途半端となりますから、屁理屈で自己正当化の弁論を展開します。他人の夢への挑戦に対しては、現実論と称した否定説を展開します。「オプティミスト(Optimist：楽観主義者)だけがなぜ成功するのか」という議論には、「イジメＩＪＩＭＥ」の体験の有無と体験への解釈の違いがあるからです。
「ペシミスト」の「自己肯定感の低さ」と「厭世的悲観思考」には、「イジメＩＪＩＭＥ」への「心的解決性」が関与しています。「卑屈感生成」は「イジメＩＪＩＭＥ」への対応の「勇気の無さ」が関係します。
「統合失調症」も「発達障害性」と「パーソナリティー障害性」を背景に持っている学生が、「イジメ」というストレスとの遭遇から発症しますが、「遺伝子脆弱性の覚醒」とも考えられます。
「ツナミＴＵＮＡＭＩ」と同様に、「ＫＩＢＯＯ 希望」では、「イジメＩＪＩＭＥ」と表記しています。「ＫＩＢＯＯ 希望」から発信し、世界共通用語となることでしょう。
「イジメＩＪＩＭＥ」は、被害者の一生を崩壊させます。
「イジメＩＪＩＭＥ」は、「ペシミスト(Pessimist：悲観主義者)」へ人間を変化させます。「幻覚」や「妄想」や「感情低下」や「意欲喪失」という「ドパミンレベルの不均衡」を発症させます。
誰もが出社したくない朝の駅やバス停で、心の均衡の揺れを、ネガティブ方向に向けて、やる気を台無しにさせる心無い一言を放射します。
「ペシミスト」の「イジメＩＪＩＭＥ」は、次々と伝染します。反撃に出ずに「笑って涙をこらえた人」だけが、「抑うつ症」から「脳内ホルモン分泌障害」へと墜落していきます。
「ペシミスト」はすべての取り組みへ中途半端となりますから、屁理屈で自己正当化の弁論を展開します。他人の夢への挑戦に対しては、現実論と称した否定説を展開します。「オプティミスト(Optimist：楽観主義者)だけがなぜ成功するのか」という議論には、「イジメＩＪＩＭＥ」の体験の有無と体験への解釈の違いがあるからです。
「ペシミスト」の「自己肯定感の低さ」と「厭世的悲観思考」には、「イジメＩＪＩＭＥ」への「心的解決性」が関与しています。「卑屈感生成」は「イジメＩＪＩＭＥ」への対応の「勇気の無さ」が関係します。
弱気はダメ！ 弱気は損気！
「問題解決能力」とは、「問題や課題があることに気づき、その問題の解決策を考え実行し、解決することができる能力」のことを指します。問題とは、「困った事柄」「厄介な事件」「解決すべき事柄」を指します。
「天才とは問題解決に最短距離の通路を選択する人」と言われます。「オプティミスト(Optimist：楽観主義者)」だけがなぜ成功するのか？ではなく、「オプティミスト」しか「イジメＩＪＩＭＥ」の社会に適応できないのです。
「問題解決をする能力が低い人の特徴」は、「問題点を見つけることが苦手」「論理的に考えることができない」「問題をネガティブに捉えてしまう」という３点です。
「オプティミスト」だけが、「困った事柄」「厄介な事件」「解決すべき事柄」へのチャレンジをします。
つまり、当方の屋号である「ＫＩＢＯＯ 希望」の有る無ししだいなのです。
「問題解撤能力(ＰＳＳ：Problem-Solving Skills)」は、自分を「天才」だと信じ込めるほどの「自惚れウヌボレ」が無ければ、逆境に遭遇するとあたふためいてしまいます。
自身にストレスが過剰に積載しないように、アイデアによって逆境から脱出しなければなりません。
「思考の脆弱性」は、脳の神経伝達物質の分泌のコントロール力の消失に陥りやすいからです。
「母源病という母という病」や「父源病という父という病」も、必ず自分に影響をしています。
しかし、「ポジティブ思考の活性」こそが、一番の妙薬となります。
「蜂力飽和」が起きることで、「感情の安定」が得られることを祈念いたしながら生産しております。
「天才とは問題解決に最短距離の通路を選択する人」と言われます。「オプティミスト(Optimist：楽観主義者)」だけがなぜ成功するのか？ではなく、「オプティミスト」しか「イジメＩＪＩＭＥ」の社会に適応できないのです。
「問題解決をする能力が低い人の特徴」は、「問題点を見つけることが苦手」「論理的に考えることができない」「問題をネガティブに捉えてしまう」という３点です。
「オプティミスト」だけが、「困った事柄」「厄介な事件」「解決すべき事柄」へのチャレンジをします。
つまり、当方の屋号である「ＫＩＢＯＯ 希望」の有る無ししだいなのです。
「問題解撤能力(ＰＳＳ：Problem-Solving Skills)」は、自分を「天才」だと信じ込めるほどの「自惚れウヌボレ」が無ければ、逆境に遭遇するとあたふためいてしまいます。
自身にストレスが過剰に積載しないように、アイデアによって逆境から脱出しなければなりません。
「思考の脆弱性」は、脳の神経伝達物質の分泌のコントロール力の消失に陥りやすいからです。
「母源病という母という病」や「父源病という父という病」も、必ず自分に影響をしています。
しかし、「ポジティブ思考の活性」こそが、一番の妙薬となります。
「蜂力飽和」が起きることで、「感情の安定」が得られることを祈念いたしながら生産しております。
Microscope Finds Virus
Leeuwenhoek in the Netherlands in 1674
The history of microbiology begins with the discovery of bacteria through microscopic observation.
Louis Pasteur of France in 1860
Robert Koch of Germany in 1876
The ideas they discovered and proposed are the basis of our current research. "Infectious diseases are caused by pathogenic bacteria" and "All infectious diseases are caused by bacteria, except for parasites," began to be recognized.
Dmitry Ivanovsky of Russia, 1892
We found that the pathogen of tobacco mosaic disease does not lose its infectivity when it passes through a bacterial filter (at that time it was unglazed clay). We reported that its existence is smaller than that of bacteria and cannot be observed with an optical microscope.
1898: Friedrich Loeffler and Paul Frosch in Germany, Martinus Bejerink and Ivanovsky in the Netherlands
With the discovery of pathogens and phages, the existence of viruses was generally understood. Subsequently, the physicochemical properties were gradually elucidated, and it was thought that viruses were made of proteins.
Wendell Stanley, United States, 1935
He was awarded the Nobel Prize in Chemistry in 1946.
The tobacco mosaic virus was successfully crystallized, which made the virus visible for the first time with an electron microscope. His discovery showed that this crystal has the ability to infect, and the existence of an organism that can crystallize like a chemical shocked the biological and scientific community.
Hershey and Chase, 1952
It becomes clear that DNA plays a role in genes in bacteriophages. We have shown that the genes of living organisms are DNA.
Subsequent research has led to the discovery of genomic analysis and new viruses.
The history of microbiology begins with the discovery of bacteria through microscopic observation.
Louis Pasteur of France in 1860
Robert Koch of Germany in 1876
The ideas they discovered and proposed are the basis of our current research. "Infectious diseases are caused by pathogenic bacteria" and "All infectious diseases are caused by bacteria, except for parasites," began to be recognized.
Dmitry Ivanovsky of Russia, 1892
We found that the pathogen of tobacco mosaic disease does not lose its infectivity when it passes through a bacterial filter (at that time it was unglazed clay). We reported that its existence is smaller than that of bacteria and cannot be observed with an optical microscope.
1898: Friedrich Loeffler and Paul Frosch in Germany, Martinus Bejerink and Ivanovsky in the Netherlands
With the discovery of pathogens and phages, the existence of viruses was generally understood. Subsequently, the physicochemical properties were gradually elucidated, and it was thought that viruses were made of proteins.
Wendell Stanley, United States, 1935
He was awarded the Nobel Prize in Chemistry in 1946.
The tobacco mosaic virus was successfully crystallized, which made the virus visible for the first time with an electron microscope. His discovery showed that this crystal has the ability to infect, and the existence of an organism that can crystallize like a chemical shocked the biological and scientific community.
Hershey and Chase, 1952
It becomes clear that DNA plays a role in genes in bacteriophages. We have shown that the genes of living organisms are DNA.
Subsequent research has led to the discovery of genomic analysis and new viruses.
Structure of the virus
・ "Viral nucleic acid" that has either DNA or RNA, which carries genetic information
・ "Protein shell" that envelops and protects viral nucleic acids
Viral particles "virions" in full form
・Capsid is a protein shell that takes in internal viral nucleic acids
The structure of "virus particles" and "protein shells" is "nucleocapsid"
"Viral nucleic acids" are either DNA or RNA, but they can be double-stranded or single-stranded, respectively. "Viral nucleic acids" act as "replicators" that create the same thing as themselves. It has the genetic information that makes it possible to make proteins, and it causes mutations, gene recombination, and gene recombination. "Viral nucleic acids" are responsible for the infectivity of viruses, and are called "infectious nucleic acids" that are infected by nucleic acids alone, and child viral particles that are identical to the parent virus particles are produced.
・ "Protein shell" that envelops and protects viral nucleic acids
Viral particles "virions" in full form
・Capsid is a protein shell that takes in internal viral nucleic acids
The structure of "virus particles" and "protein shells" is "nucleocapsid"
"Viral nucleic acids" are either DNA or RNA, but they can be double-stranded or single-stranded, respectively. "Viral nucleic acids" act as "replicators" that create the same thing as themselves. It has the genetic information that makes it possible to make proteins, and it causes mutations, gene recombination, and gene recombination. "Viral nucleic acids" are responsible for the infectivity of viruses, and are called "infectious nucleic acids" that are infected by nucleic acids alone, and child viral particles that are identical to the parent virus particles are produced.
Characteristics and definition of viruses
inanimate
inanimate
Viruses are about 20~30 nm to 250 nm in diameter, and cannot be observed with an optical microscope, but can only be observed with an electron microscope.
Viruses are basically made up of nucleic acids and proteins, and they do not have the ability to multiply outside the cell.
Viruses are basically made up of nucleic acids and proteins, and they do not have the ability to multiply outside the cell.
Obligate intracellular organisms
When it spreads itself into living cells, it can replicate a large number of viral particles that are identical to its own based on genetic information.
Basic Structure of Viruses
The basic structure of viruses is the viral nucleic acid at the center of the particle(DNA or RNA)and particles made up of a protein shell called a capsid, which is a protein shell that envelops and protects it.
The lipid bilayer and proteins in the outer shell are called envelopes, and some have spike proteins.
The lipid bilayer and proteins in the outer shell are called envelopes, and some have spike proteins.
Viral nucleic acid replication
It is only when it infects the cells of other organisms that viral nucleic acids can replicate.
Viral nucleic acid replication requires the procurement of materials and the production of energy, but since it does not have the necessary enzyme genetic information, it has no choice but to replicate itself using the protein synthesis mechanism, metabolism, and energy of the host cell.
In addition to enzymes that replicate their own genes, which are often very different from those of the host, enzymes that adsorb and invade the host cell, or escape the host's immune system, are coded.
Some viruses contain proteins inside the capsid that are different from the capsid proteins along with the nucleic acid, but the combination of this protein and the viral nucleic acid is called the "core", and this protein is called the "core protein".
Viruses cannot multiply on their own, but can only multiply when they infect the cells of other organisms. This property is called obligate intracellular parasitism.
Viral nucleic acid replication requires the procurement of materials and the production of energy, but since it does not have the necessary enzyme genetic information, it has no choice but to replicate itself using the protein synthesis mechanism, metabolism, and energy of the host cell.
In addition to enzymes that replicate their own genes, which are often very different from those of the host, enzymes that adsorb and invade the host cell, or escape the host's immune system, are coded.
Some viruses contain proteins inside the capsid that are different from the capsid proteins along with the nucleic acid, but the combination of this protein and the viral nucleic acid is called the "core", and this protein is called the "core protein".
Viruses cannot multiply on their own, but can only multiply when they infect the cells of other organisms. This property is called obligate intracellular parasitism.
Viral multiplication
1Adsorption on the cell surface
2Intracellular penetration
3Synthesis of parts → deshelling
4Assembling Parts
5Release from infected cells
1From 5 this step is done in the mechanism.
The first step in viral infection is adsorption on the surface of its cells. When a virus comes into contact with a host cell, proteins on the surface of the virus target and adsorb to any molecule exposed on the surface of the host cell.
The target molecule on the cell side at this time is called a receptor receptor for the virus, and whether or not the virus infects depends on whether the cell has a receptor against the virus.
Typical viral receptors include sialic acid glycans in airway epithelial cells against influenza viruses and CD4 molecules on the surface of helper T cells against human immunodeficiency viruses.
Virus particles adsorbed on the cell surface then invade the inside of the cell, which is the actual place of proliferation. The mechanism of invasion varies depending on the virus, and a typical one is that the endocytosis mechanism of the cell itself is taken into the cell as an endosomal vesicle and then escapes from there into the cytoplasm. It is an intrusive system found in many viruses that do not have an envelope, as well as influenza viruses.
The adsorbed viral envelope fuses with the cell membrane of the cell, and the nucleocapsids inside the particles are pumped into the cytoplasm. This is found in many enveloped viruses. It is found in bacteriophages such as T phages, and viral nucleic acids are actively injected into the cytoplasm through the caudal duct from adsorbed virus particles.
Even though it is an injection, the transfer of genes after the tail of the viral particle penetrates the bacterial cell wall does not occur unless the bacterial cell is alive, so it is sucked in by the action of the bacterial cell itself. When a virus invades a cell, the capsid is degraded and viral nucleic acids are released from the inside. This process is called shedding.
The period between the time the shelling occurs and the reconstitution of the particles means that there are no virions, which are full infectious virus particles, and this period is called the Dark Period, or the Eclipse Phase, which is analogous to a solar or lunar eclipse.
Viral nucleic acids released by shelling are replicated in large quantities to create the next generation of daughter viruses, and at the same time, a large amount of virus-specific proteins such as capsomers are synthesized through mRNA. The synthesis of viruses is a terrifying system in which nucleic acids and proteins, which are its components, are mass-produced separately and then assembled.
Since viral nucleic acids differ in many ways from the nucleic acids of host cells, their replication cannot be covered by the host's enzymes alone, so enzymes involved in transcription and replication, such as DNA polymerases and RNA polymerases, which are unique to each virus, are used.
It has been found that genetic information can also be transmitted from RNA to DNA, and retroviruses with reverse transcriptase also use the host's DNA replication mechanism by incorporating their own genes into the host's DNA.
Protein synthesis may require a virus's own enzyme to create the mRNA that encodes the protein, but the translation of the mRNA into the protein is done using the host cell's protein synthesis system, such as ribosomes.
As a collection of components and the release of viral particles, separately mass-produced viral nucleic acids and proteins assemble in cells.
Ultimately, the mechanism by which capsomers envelop viral nucleic acids and nucleocapsids are formed varies from virus to virus, and viruses that assemble in cells are either germinated from the cell or released by the death of infected cells.
At this time, a part of the virus with an envelope acquires a part of the host's cell membrane that was covered at the time of emergence as an envelope.
I am astonished by the struggle to repeat "migration" by infection so that I do not die before the host dies.
Viruses that are not living organisms have the guts to connect genetic information with their hands.
2Intracellular penetration
3Synthesis of parts → deshelling
4Assembling Parts
5Release from infected cells
1From 5 this step is done in the mechanism.
The first step in viral infection is adsorption on the surface of its cells. When a virus comes into contact with a host cell, proteins on the surface of the virus target and adsorb to any molecule exposed on the surface of the host cell.
The target molecule on the cell side at this time is called a receptor receptor for the virus, and whether or not the virus infects depends on whether the cell has a receptor against the virus.
Typical viral receptors include sialic acid glycans in airway epithelial cells against influenza viruses and CD4 molecules on the surface of helper T cells against human immunodeficiency viruses.
Virus particles adsorbed on the cell surface then invade the inside of the cell, which is the actual place of proliferation. The mechanism of invasion varies depending on the virus, and a typical one is that the endocytosis mechanism of the cell itself is taken into the cell as an endosomal vesicle and then escapes from there into the cytoplasm. It is an intrusive system found in many viruses that do not have an envelope, as well as influenza viruses.
The adsorbed viral envelope fuses with the cell membrane of the cell, and the nucleocapsids inside the particles are pumped into the cytoplasm. This is found in many enveloped viruses. It is found in bacteriophages such as T phages, and viral nucleic acids are actively injected into the cytoplasm through the caudal duct from adsorbed virus particles.
Even though it is an injection, the transfer of genes after the tail of the viral particle penetrates the bacterial cell wall does not occur unless the bacterial cell is alive, so it is sucked in by the action of the bacterial cell itself. When a virus invades a cell, the capsid is degraded and viral nucleic acids are released from the inside. This process is called shedding.
The period between the time the shelling occurs and the reconstitution of the particles means that there are no virions, which are full infectious virus particles, and this period is called the Dark Period, or the Eclipse Phase, which is analogous to a solar or lunar eclipse.
Viral nucleic acids released by shelling are replicated in large quantities to create the next generation of daughter viruses, and at the same time, a large amount of virus-specific proteins such as capsomers are synthesized through mRNA. The synthesis of viruses is a terrifying system in which nucleic acids and proteins, which are its components, are mass-produced separately and then assembled.
Since viral nucleic acids differ in many ways from the nucleic acids of host cells, their replication cannot be covered by the host's enzymes alone, so enzymes involved in transcription and replication, such as DNA polymerases and RNA polymerases, which are unique to each virus, are used.
It has been found that genetic information can also be transmitted from RNA to DNA, and retroviruses with reverse transcriptase also use the host's DNA replication mechanism by incorporating their own genes into the host's DNA.
Protein synthesis may require a virus's own enzyme to create the mRNA that encodes the protein, but the translation of the mRNA into the protein is done using the host cell's protein synthesis system, such as ribosomes.
As a collection of components and the release of viral particles, separately mass-produced viral nucleic acids and proteins assemble in cells.
Ultimately, the mechanism by which capsomers envelop viral nucleic acids and nucleocapsids are formed varies from virus to virus, and viruses that assemble in cells are either germinated from the cell or released by the death of infected cells.
At this time, a part of the virus with an envelope acquires a part of the host's cell membrane that was covered at the time of emergence as an envelope.
I am astonished by the struggle to repeat "migration" by infection so that I do not die before the host dies.
Viruses that are not living organisms have the guts to connect genetic information with their hands.
Cytopathic effects
Effects on the host
Infection by viruses affects the host organism in a variety of ways at the cellular and individual levels. In many cases, viruses act as pathogens and cause significant damage to the host, but there are also known cases where viruses act as carriers of foreign genes, such as some phages and retroviruses, which favors the survival of the host.
Effects at the cellular level
When a virus is infected and multiplies, the energy and nutrients such as amino acids that the host cell originally produced and used for itself are taken away for the replication of the virus's particles, so to speak, it becomes "hijacked by the virus".
Host cells, on the other hand, try to resist by suppressing the synthesis of proteins and genes as a whole.
On the other hand, viruses try to control the physiology of host cells by using various viral gene products to replicate themselves more efficiently.
In addition, the large amount of protein synthesis of the virus at one time is physiologically stressful for cells. When the finished particles are released, they can also destroy the cell membrane and cell wall of the host.
Various physiological and morphological changes appear in the individual follicles infected with the virus, but this is the most important parting road for the end of the virus, and at the end of the road, it is a great fear of humans.
Of these phenomena, those that exhibit particularly morphological changes are called cytogenic degeneration effects.
Some viruses exhibit morphologically distinctive cytogenic effects on specific host cells.
Typical cytogenic effects include the accumulation of abnormal substances formed in cells and those that do not have an active function, that is, the formation of inclusions.
In neurodegenerative diseases such as amyotrophic lateral sclerosis and Parkinson's disease, inclusions composed of disease-specific proteins are found. It is becoming clear that it is closely related to the pathophysiology of each disease.
Due to various physiological changes, cells infected with the virus eventually suffer one of two fates: cell death, immortality, or cancer.
・Cell death
Invariable or cancerous
Viruses take the fate of one of two paths.
Will immunity prevail and end the war, or will immunity lose and the host will be invaded?
Rather than discussing the effectiveness of mitochondrial quality and quantity intake, please understand that it will be faster to acquire new immunity by building and embodying another power advocated by KIBOO.
Host cells, on the other hand, try to resist by suppressing the synthesis of proteins and genes as a whole.
On the other hand, viruses try to control the physiology of host cells by using various viral gene products to replicate themselves more efficiently.
In addition, the large amount of protein synthesis of the virus at one time is physiologically stressful for cells. When the finished particles are released, they can also destroy the cell membrane and cell wall of the host.
Various physiological and morphological changes appear in the individual follicles infected with the virus, but this is the most important parting road for the end of the virus, and at the end of the road, it is a great fear of humans.
Of these phenomena, those that exhibit particularly morphological changes are called cytogenic degeneration effects.
Some viruses exhibit morphologically distinctive cytogenic effects on specific host cells.
Typical cytogenic effects include the accumulation of abnormal substances formed in cells and those that do not have an active function, that is, the formation of inclusions.
In neurodegenerative diseases such as amyotrophic lateral sclerosis and Parkinson's disease, inclusions composed of disease-specific proteins are found. It is becoming clear that it is closely related to the pathophysiology of each disease.
Due to various physiological changes, cells infected with the virus eventually suffer one of two fates: cell death, immortality, or cancer.
・Cell death
Invariable or cancerous
Viruses take the fate of one of two paths.
Will immunity prevail and end the war, or will immunity lose and the host will be invaded?
Rather than discussing the effectiveness of mitochondrial quality and quantity intake, please understand that it will be faster to acquire new immunity by building and embodying another power advocated by KIBOO.
Cell death due to viral infection
When a virus multiplies in large numbers in a cell, the host cell often dies as a result of disruption of the cell's natural physiology and destruction of the cell membrane and cell wall.
This also corresponds to the lytic phenomenon caused by phage infection. In cells of multicellular organisms, apoptosis is also known to occur by stopping the cell cycle during viral infection and activating cytotoxic T cells through antigen-presenting molecules such as MHC class I. It is thought that the virus is prevented from spreading to surrounding cells by killing itself, but virus therapy that artificially administers the virus to cancer cells and infects them and destroys them has been implemented and researched.
Some viruses have persistent infections in which a large number of viruses are produced in a short period of time and do not immediately kill the host, but rather produce a small amount of virus continuously over a long period of time to reduce the damage to the host. Persistent infection is established when the rate at which host cells proliferate is balanced by the rate at which cells die due to viral replication.
This includes lymegenization by temperate phages.
Among persistent infections, latent infection is a condition in which virus replication is particularly slow and almost no particle replication occurs.
This also corresponds to the lytic phenomenon caused by phage infection. In cells of multicellular organisms, apoptosis is also known to occur by stopping the cell cycle during viral infection and activating cytotoxic T cells through antigen-presenting molecules such as MHC class I. It is thought that the virus is prevented from spreading to surrounding cells by killing itself, but virus therapy that artificially administers the virus to cancer cells and infects them and destroys them has been implemented and researched.
Some viruses have persistent infections in which a large number of viruses are produced in a short period of time and do not immediately kill the host, but rather produce a small amount of virus continuously over a long period of time to reduce the damage to the host. Persistent infection is established when the rate at which host cells proliferate is balanced by the rate at which cells die due to viral replication.
This includes lymegenization by temperate phages.
Among persistent infections, latent infection is a condition in which virus replication is particularly slow and almost no particle replication occurs.
Number of viral infections that must be reported
As for the classification and notification and reporting obligations under the Infectious Diseases Act, the Infectious Diseases Act classifies infectious diseases into Category 1~5 according to the characteristics of infectious diseases, and the obligation to report and reporting is set.
If you know the names of infectious diseases that are subject to the obligation to be notified and reported, you can see how the Ministry of Health, Labour and Welfare has a sense of crisis about infectious diseases.
If you know the names of infectious diseases that are subject to the obligation to be notified and reported, you can see how the Ministry of Health, Labour and Welfare has a sense of crisis about infectious diseases.
1.Infectious diseases
Ebola hemorrhagic fever, Crimean-Congo hemorrhagic fever, smallpox, South American hemorrhagic fever, plague, Marburg disease, Lassa fever
Main measures and measures: Notification immediately after diagnosis
Main measures and measures: Notification immediately after diagnosis
2.Infectious diseases
Acute gray myelitis, tuberculosis, diphtheria, severe acute respiratory syndrome (limited to those whose pathogen is the genus SARS coronavirus), avian influenza (H5N1)
Main measures and measures: Notification immediately after diagnosis
Main measures and measures: Notification immediately after diagnosis
3.Infectious diseases
Cholera, bacterial dysentery, enterohemorrhagic Escherichia coli infection (O157), typhoid fever, paratyphoid fever
Main measures and measures: Notification immediately after diagnosis
Main measures and measures: Notification immediately after diagnosis
4.Infectious diseases
Hepatitis E, Hepatitis A, Yellow fever, Q fever, Rabies, anthrax, Avian influenza (except avian influenza (H5N1)), botulism, malaria, tularemia, West Nile fever, echinococcosis, Parrot disease, Omsk hemorrhagic fever, Relapsing fever, Catsanul forest disease, Coccidioidomycosis, Monkeypox, Nephrosymptomatic hemorrhagic fever, Western equine encephalitis, Tick-borne encephalitis, Chikungunya fever, Tsutsuga worm disease, Dengue fever, Eastern equine encephalitis, Nipah virus infection, Japan spotted fever, Japan encephalitis, Hantavirus pulmonary syndrome, B virus disease, Rhinopox, Brucellosis, Venezuelan equine encephalitis, Hendra virus infection, Typhus, Lyme disease, Lyssa virus infection, Rift Valley fever, Rhinoid pox, Legionnaires' disease, Leptospirosis, Rocky Mountain spotted fever, Zika fever
Main measures and measures: Notification immediately after diagnosis
Main measures and measures: Notification immediately after diagnosis
5.Infectious diseases
Viral hepatitis (except hepatitis E and hepatitis A), cryptosporidiosis, acquired immunodeficiency syndrome (AIDS), syphilis, measles, amoebic dysentery, acute encephalitis (excluding West Nile encephalitis, western equine encephalitis, tick-borne encephalitis, eastern equine encephalitis, Japan encephalitis, Venezuelan equine encephalitis and Rift Valley fever), Creutzfeldt-Jakob disease, fulminant hemolytic streptococcal infection, giardiasis, Meningococcal meningitis, Congenital rubella syndrome, Tetanus, Vancomycin-resistant Staphylococcus aureus infection, Vancomycin-resistant enterococcal infection, Rubella
Main measures and measures: Notification within 7 days (all cases) (Measles and rubella should be reported as soon as possible)
RS virus infection, pharyngeal conjunctival fever, group A hemolytic streptococcal pharyngitis, infectious gastroenteritis
chickenpox, hand, foot and mouth disease, infectious erythropod, sudden rash, whooping cough, herpangina, mumps
Main measures and measures: The following Monday (notification by pediatric fixed-point medical institutions)
Influenza (excluding infectious diseases such as avian influenza and new influenza)
Main measures and measures: Next Monday (notification by influenza fixed-point medical institutions and core fixed-point medical institutions)
Acute hemorrhagic conjunctivitis, epidemic keratoconjunctivitis
Main measures and measures: Next Monday (notification by ophthalmology fixed-point medical institutions)
Genital Chlamydia Infection, Genital Herpes Virus Infection, Condyloma Warts and Gonococcal Infection
Main measures and measures: The first day of the following month (notification by a fixed-point medical institution for sexually transmitted diseases)
Chlamydial pneumonia (except parrot disease), bacterial meningitis, mycoplasma pneumonia, aseptic meningitis
Main measures and measures: Next Monday (notification by the core fixed-point medical institution)
Methicillin-resistant Staphylococcus aureus infection, Penicillin-resistant Streptococcal pneumoniae infection, Medrug-resistant Acinetobacter infection, drug-resistant Pseudomonas aeruginosa infection
Main measures and measures: The first day of the following month (core fixed point)
Main measures and measures: Notification within 7 days (all cases) (Measles and rubella should be reported as soon as possible)
RS virus infection, pharyngeal conjunctival fever, group A hemolytic streptococcal pharyngitis, infectious gastroenteritis
chickenpox, hand, foot and mouth disease, infectious erythropod, sudden rash, whooping cough, herpangina, mumps
Main measures and measures: The following Monday (notification by pediatric fixed-point medical institutions)
Influenza (excluding infectious diseases such as avian influenza and new influenza)
Main measures and measures: Next Monday (notification by influenza fixed-point medical institutions and core fixed-point medical institutions)
Acute hemorrhagic conjunctivitis, epidemic keratoconjunctivitis
Main measures and measures: Next Monday (notification by ophthalmology fixed-point medical institutions)
Genital Chlamydia Infection, Genital Herpes Virus Infection, Condyloma Warts and Gonococcal Infection
Main measures and measures: The first day of the following month (notification by a fixed-point medical institution for sexually transmitted diseases)
Chlamydial pneumonia (except parrot disease), bacterial meningitis, mycoplasma pneumonia, aseptic meningitis
Main measures and measures: Next Monday (notification by the core fixed-point medical institution)
Methicillin-resistant Staphylococcus aureus infection, Penicillin-resistant Streptococcal pneumoniae infection, Medrug-resistant Acinetobacter infection, drug-resistant Pseudomonas aeruginosa infection
Main measures and measures: The first day of the following month (core fixed point)
You will be surprised at how many viral infections are required to be notified.
Humanity is fighting a virus.
Even "warts" on the feet and hands, the cause of viral warts is a type of virus called "human papillomavirus". "Human papillomavirus" is a virus that infects human skin and exists anywhere in the world where humans are. Viral warts occur when the "human papillomavirus" infects human skin.
If the skin is in a healthy state, it is unlikely to be invaded by the virus, but the "human papillomavirus" invades through a small wound on the skin.
In order to reduce the occurrence of viral warts, it is important not to leave even small cuts and abrasions unattended, but to disinfect them immediately.
"Acquired Immunodeficiency Syndrome" or "AIDS"(AIDS)At the end of the day, "AIDS virus infection" spreads to the whole body and dies.
Humanity is fighting a virus.
Even "warts" on the feet and hands, the cause of viral warts is a type of virus called "human papillomavirus". "Human papillomavirus" is a virus that infects human skin and exists anywhere in the world where humans are. Viral warts occur when the "human papillomavirus" infects human skin.
If the skin is in a healthy state, it is unlikely to be invaded by the virus, but the "human papillomavirus" invades through a small wound on the skin.
In order to reduce the occurrence of viral warts, it is important not to leave even small cuts and abrasions unattended, but to disinfect them immediately.
"Acquired Immunodeficiency Syndrome" or "AIDS"(AIDS)At the end of the day, "AIDS virus infection" spreads to the whole body and dies.
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