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      "memo": "Accumulate free upvotes on your posts every 6 hours! All you need to do is vote our witness account -> se-witness as one of your 30 witness votes. ->  See actual rewards not just 0.001 every day. https://steemlogin.com/sign/account-witness-vote?witness=se-witness&approve=1"
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      "parent_permlink": "medical",
      "author": "dandymee",
      "permlink": "antibiotic-resistance-a-threat-to-human-existence-the-causes-mechanisms-and-possible-solutions",
      "title": "Antibiotic Resistance: A Threat to Human Existence- (The Causes, Mechanisms and Possible Solutions)",
      "body": "According to [medical experts](www.cdc.gov/drugresistance/threat-report-2013/index.html), over 2 million people in the United States become ill every  year with antibiotic resistant infections, and an estimated 23,000 people die in the process.\n\nhttps://images.pexels.com/photos/159211/headache-pain-pills-medication-159211.jpeg?h=350&auto=compress&cs=tinysrgb\n\n[Image Source: Pixabay]( https://images.pexels.com/photos/159211/headache-pain-pills-medication-159211.jpeg?h=350&auto=compress&cs=tinysrgb)\n\nThe discovery and sales of antimicrobial drugs, was a milestone achievement in modern medicine. Antibiotics grew to become the most important medical inventions, and have been of great use in the management of most complex medical conditions, including cancer treatment, organ transplantation and many surgical procedures. Sadly however, over the years, some microorganisms have developed mechanisms of resisting the effects of these antibiotics.  This increased resistance comes mostly as a result of the over-exposure of microorganisms to antibiotics. The more a microorganism comes in contact with an antibiotic; it starts to develop different mechanisms of resistance against the effect of such antibiotics. \n\n![Steem divide.png](https://steemitimages.com/DQmNqCJdULZdfqjtJ4yb9kME1ZUFsZAQk7ptJNmQ5AoVX17/Steem%20divide.png)\n### To understand the problem of antibiotic resistance better, it is necessary to point out some relevant concepts. \nFirstly, microorganisms can develop resistance to antibiotics naturally by staying in the same environment with the antibiotic-producing molecules inside the body. Just as stated by Darwinian evolution, this is a form of natural adaptation technique termed intrinsically developed resistance. \n\n>Intrinsically developed resistance is not the center of focus when talking about the problem of multi-drug resistance. Rather, the main culprit of antibiotic resistance in clinical medicine is the development of acquired resistance towards an antibiotic molecule which a bacterial population was formerly susceptible to. \nIn this article, we will look at some of the molecular mechanism of antibiotic resistance. \n\n#  Mechanisms of Antibiotic Resistance\n\nhttps://images.pexels.com/photos/33355/capsule-pill-health-medicine.jpg?w=940&h=650&auto=compress&cs=tinysrgb\n\n[Source](https://images.pexels.com/photos/33355/capsule-pill-health-medicine.jpg?w=940&h=650&auto=compress&cs=tinysrgb)\nOver years of evolution and constant antibiotic attacks, microorganisms have developed sophisticated mechanisms of resisting the action of the antibiotics. A singular microorganism can use one or more of these techniques in evading the effect of any antibiotic. The resistance mechanisms include:\n\n# Mechanism One: Modification of the Antibiotic Molecule \nThis is the mechanism in which bacterial organisms produce some enzymes that can deactivate the antibiotics by either totally destroying the drug, or attaching some chemical moieties to it, such that it is unable to bind to its target site. Micro organisms do this by two main methods:\n\n## 1. By Chemical Alteration of the Antibiotic Molecule\nThis mechanism applies mostly to antibiotics that exert their effects by inhibiting bacterial protein synthesis at molecular levels. The microorganisms produce enzymes that cause the following:\n\n*\tAcetylation of drugs like chloramphenecol, aminoglycosides and lincosamines\n*\tPhosphorylation of chloramphenecol and aminoglycosides\n*\tAdenylation of lincosamines and aminoglycosides\n\nNo matter which of these mechanisms a bacteria uses, it reduces the affinity of the antibiotic for its target. \n## 2. Destruction of Antibiotic Molecule\nSome micro organisms inactivate antibiotics by the action of ß-lactamarase. ß-lactamarase destroys the ß-lactam ring, which is the active component of penicillin and other ß-lactam-based antibiotics.\n# Mechanism Two: By Decreasing the Penetration and Increasing the Efflux of Antibiotics\nIn this mechanism, microorganisms alter the permeability level of their cytoplasmic membrane to hinder antibiotic molecules from penetrating their cells. Alternatively, microorganisms can produce efflux pumps on their cell membrane, which massively pump out antibiotics from the cells. \n![Steem divide 2.jpg](https://steemitimages.com/DQmNp4BfgZXQ18Hzm6VJQHmncfSV9t6rTZcEchW5GibnRGk/Steem%20divide%202.jpg)\n\n# How Human Activities Increase Antibiotic Resistance\nOver exposure to antibiotics may be as a result of self-medication and misuse of antibiotics by sick persons and health workers who administer antibiotics to patients without adequate testing. Also, when farmers treat cows and other livestock with antibiotics, consumption of such meat transfers the antibiotics to humans. With time, the microorganisms in the body will develop resistance to such antibiotics.\n\nhttps://cdn.pixabay.com/photo/2017/05/18/17/33/pocket-2324214_960_720.jpg\n[Each time you abuse drugs, you contribute to your own problem]( https://cdn.pixabay.com/photo/2017/05/18/17/33/pocket-2324214_960_720.jpg)\n\nThese antibiotic-resistance superbugs have become a massive threat to human existence, and doctors are now skeptical about treating patients with new drugs, as there is a big possibility that the superbugs will develop resistance for the new drugs as well.\n\n# Recommendations to Fight Antibiotic Resistance\n\nThe fight against antibiotic resistance is everyone’s responsibility. Experts have come up with the suggestions to help tackle the issues.![SOS.jpg](https://steemitimages.com/DQmaHBHqLBmS33viR3v15ztuvw3wwTeGZept5LnsPLaRbzB/SOS.jpg)\n\n[Image Source: Pixabay]( https://cdn.pixabay.com/photo/2013/04/24/10/34/sos-106826_960_720.jpg)\n\n•\tHealth workers should not administer any antibiotics on patients unless if determined by antibiotic sensitivity test.\n•\tWhen antibiotics are prescribed for sick persons, they should take the full dosage to ensure that the antibiotic kills the pathogens completely. This is because taking half dosage only suppresses the pathogens and allows them to evolve into resistant superbugs.\n•\tLivestock farmers are advised to seek the services of a veterinary doctor when administering antibiotics on their animals. \n\nGovernments and research institutes also need to invest more time and resources into developing stronger antibiotics that’ll help curb this global crisis. While all this is going on, we must all team up to create awareness and sensitize people on the causes of this menace, because if we don’t rise and fight now, antibiotic resistant infections may one day wipe all of us out of the surface of the earth. \n\nReferences\n[Mechanisms of Antibiotic Resistance](www.ncbi.nlm.nih.gov/pmc/articles/PMC4888801/)\n[Resistance Mechanism](https://www.reactgroup.org/toolbox/understand/antibiotic-resistance/)\n [Antibiotic resistant superbugs](https://www.nytimes.com/2017/02/27/health/who-bacteria-pathogens-antibiotic-resistant-superbugs.html?_r=0)\n[Antibiotic Resistance: Drug conditions](http://www.rxlist.com/antibiotic_resistance-page3/drugs-condition.htm)\n[The epidemic of antibiotic resistant infections](https://academic.oup.com/cid/article/46/2/155/452327/The-Epidemic-of-Antibiotic-Resistant-Infections-A)\n[Drug Resistance Threat Report](www.cdc.gov/drugresistance/threat-report-2013/index.html)\nImage sources (All images are collected from free sources)\n[A](https://images.pexels.com/photos/159211/headache-pain-pills-medication-159211.jpeg?h=350&auto=compress&cs=tinysrgb)\n[B](https://images.pexels.com/photos/33355/capsule-pill-health-medicine.jpg?w=940&h=650&auto=compress&cs=tinysrgb)\n[C]( https://cdn.pixabay.com/photo/2017/05/18/17/33/pocket-2324214_960_720.jpg)\n[D]( https://pixabay.com/en/sos-disease-bless-you-chemistry-106826/)\n\nFor more interesting articles, please upvote, resteem and follow  @dandymee\n![Steemstem.gif](https://steemitimages.com/DQmf73yPMua6pUfHX4QJ3zgkffnddNTS1QscKovcFzbqBoW/Steemstem.gif)",
      "json_metadata": "{\"tags\":[\"medical\",\"clinical\",\"health\",\"content\",\"medicine\"],\"users\":[\"dandymee\"],\"image\":[\"https://images.pexels.com/photos/159211/headache-pain-pills-medication-159211.jpeg?h=350&auto=compress&cs=tinysrgb\",\"https://steemitimages.com/DQmNqCJdULZdfqjtJ4yb9kME1ZUFsZAQk7ptJNmQ5AoVX17/Steem%20divide.png\",\"https://images.pexels.com/photos/33355/capsule-pill-health-medicine.jpg?w=940&h=650&auto=compress&cs=tinysrgb\",\"https://steemitimages.com/DQmNp4BfgZXQ18Hzm6VJQHmncfSV9t6rTZcEchW5GibnRGk/Steem%20divide%202.jpg\",\"https://cdn.pixabay.com/photo/2017/05/18/17/33/pocket-2324214_960_720.jpg\",\"https://steemitimages.com/DQmaHBHqLBmS33viR3v15ztuvw3wwTeGZept5LnsPLaRbzB/SOS.jpg\",\"https://steemitimages.com/DQmf73yPMua6pUfHX4QJ3zgkffnddNTS1QscKovcFzbqBoW/Steemstem.gif\"],\"links\":[\"www.cdc.gov/drugresistance/threat-report-2013/index.html\",\"https://images.pexels.com/photos/159211/headache-pain-pills-medication-159211.jpeg?h=350&auto=compress&cs=tinysrgb\",\"https://images.pexels.com/photos/33355/capsule-pill-health-medicine.jpg?w=940&h=650&auto=compress&cs=tinysrgb\",\"https://cdn.pixabay.com/photo/2017/05/18/17/33/pocket-2324214_960_720.jpg\",\"https://cdn.pixabay.com/photo/2013/04/24/10/34/sos-106826_960_720.jpg\",\"www.ncbi.nlm.nih.gov/pmc/articles/PMC4888801/\",\"https://www.reactgroup.org/toolbox/understand/antibiotic-resistance/\",\"https://www.nytimes.com/2017/02/27/health/who-bacteria-pathogens-antibiotic-resistant-superbugs.html?_r=0\",\"http://www.rxlist.com/antibiotic_resistance-page3/drugs-condition.htm\",\"https://academic.oup.com/cid/article/46/2/155/452327/The-Epidemic-of-Antibiotic-Resistant-Infections-A\",\"https://pixabay.com/en/sos-disease-bless-you-chemistry-106826/\"],\"app\":\"steemit/0.2\",\"format\":\"markdown\"}"
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      "parent_permlink": "medical",
      "author": "dandymee",
      "permlink": "4e6may-viral-hemorrhagic-fevers-killer-diseases-that-turn-humans-into-biological-weapons",
      "title": "Viral Hemorrhagic Fevers: Killer Diseases that turn humans into Biological Weapons",
      "body": "#### <center>Introduction</center>\n___\n\n<div class=\"pull-right\">\n<center> <img src=\"https://steemitimages.com/DQmdSpADcgxUvvus1U4yqxDogTMnhkeqMyqLTVxkj29idRs/mask-469217_640.jpg\">\n<sub>  The Ebola Outbreak was a nightmare to mankind (License: Public Domain]: <a href=\"https://pixabay.com/en/mask-gas-male-man-boy-young-469217/\"> \nPixabay </a></sub> </center> \n</div>\n\n\nBetween the years 2013 and 2015, Africa suffered the biggest outbreak of Ebola virus disease ever recorded in history. The disease spread through West Africa, affecting countries like Guinea, Sierra Leone, Liberia, Senegal, Mali and Nigeria, infecting more than 28,000 people, and leaving at least 11,000 dead.\n\nEbola virus, just like Zika virus, Lassa Fever, etc, is one of the group of diseases called Hemorrhagic Fevers, which are very contagious and can spread like wildfire in any geographical area. \n\n\nViral Hemorrhagic Fevers are different groups of animal and human diseases caused by four families of RNA viruses namely Filoviridae, Flaviviridae, Bunyaviridae and Arenaviridae. All hemorrhagic fevers manifest with symptoms such as fever and bleeding disorders, but the most severe ones like Ebola, Lassa fever and Marburg virus cause lethal bleeding, loss of organ coordination and death.\n\nTo better understand the different kinds of Hemorrhagic Fevers, we'll discuss them according to their causative organisms. \n\n<br>\n#### Causes of Hemorrhagic Fevers \n<br>\n\nHemorrhagic Fevers are caused by four groups of zoonotic RNA viruses. (Zoonotic viruses are viruses which naturally live in animal hosts). They include\n\n* Arenaviridae (Arena viruses) \n\nThis family of viruses live mainly in different species of rodents. The viral particles are spherical in shape with a very tiny diameter of 110 to 130 nanometers enclosed in a lipid membrane. \n\nThe viral particle is made completely of only RNA, and although their replication system is yet to be totally understood, it has been established that their new virion particles are formed by budding through the surface of their host cells. Examples of arenaviruses are Junin virus, Machupo virus Lassa virus which causes Lassa fever. \n\n* Filoviridae (Filoviruses) \n\nFiloviruses are pleomorphic in nature (They can exist in different shapes). Some have long (up to 14,000 nanometers) branched filaments of circular, “U” or “6” shape enclosed in a lipid membrane. The virion particles contain a single molecule of single-stranded negative-sense RNA. Just like arenaviruses, their replication system is not fully understood yet, but they replicate by budding out of the surface of the host cells. \nOnly two Filoviruses have been identified so far: Ebola virus and Marburg virus. \n\n* Bunyaviridae (Bunyaviruses) \n\n They're also single-stranded negative sense RNA viruses enveloped in a lipid membrane. They're found in arthropods (ticks, mosquitoes and sandfly) and rodents. Examples include Hantavirus and Crimea-Congo hemorrhagic fevers virus. \n\n* Flaviviridae (Flaviviruses) \n\nThe yellow fever virus belongs to this family. Flaviviruses have diameters of about 40 to 60 nm. They're positive-sense single stranded RNA viruses of  spherical and icosahedral geometry, enveloped in a lipid membrane. They cause diseases such as hepatitis encephalitis and a birth defect called microcephaly. \n\nHaving established a background, now let's talk about two of the most endemic Hemorrhagic Fevers that has affected Africa in recent times: Ebola virus fever  and Lassa virus fever. \n\n<br>\n#### Ebola Virus Disease \n<br>\n\nEbola fever is a viral haemorrhagic disease which affects humans and other primates. It is caused by the Ebola virus, and its symptoms include high grade fever, muscular pain, severe bleeding, sore throat, headache and diarrhea, most of which begin to manifest from 2 days to 3 weeks of contracting the disease.\n\n\n Other complications include low blood pressure due to excessive loss of fluids, decrease in kidney and liver function and life threatening internal and external bleeding. Ebola fever has a high mortality rate, Ebola virus is spread by direct contact with the body fluids of people who already have the disease, or by touching or eating infected animals like bats and monkeys. \n\n<br>\n#### Structure of Ebola Virus\n<br>\n\n<div class=\"pull-left\">\n<center> <img src=\"https://steemitimages.com/DQmPtKJSVNCQ5ZBdFMzXFRMXcv88JwhoFGVwoAdjZoADj2n/Ebola_virus_em.png\">\n<sub>  The Ebola Virus (License: Public Domain]: <a href=\"https://commons.m.wikimedia.org/wiki/File:Ebola_virus_em.png\"> \nWikicommons </a></sub> </center> \n</div>\n\n\nThe Ebola virus belongs to the filoviridae family.  There are five strains of Ebola virus (Zaire, Bundibugyo, Sudan, Reston and Tai forest), but amongst them all, Ebola Zaire strain is most virulent.\n\n\n Structurally, the Ebola virus  looks like a thread of approximately 970 nm length and 80 nm diameter. It mostly exists in  long filamentous and cylindrical body, and can sometimes come in a “U” shape, circular shape or “6” shape. Ebola virus has viral glycoprotein spikes of 7-10 nm projecting from its outer viral envelope (which is derived from the host cell membrane). \n\nThe viral envelope contains the nucleocapsid  which consists of a single stranded RNA genome wound around the nucleoprotein (np), polymerase complex protein (VP30), minor nucleoprotein (VP30) and L protein. \n\n<br>\n#### Mechanism of infection of Ebola Virus \n<br>\n\n\n<div class=\"pull-right\">\n<center> <img src=\"https://steemitimages.com/DQmZYkA1ipg2ymgufZbXo33StzvSyeuSV6EpDms8a8YWiwW/EbolaCycle.png\">\n<sub>  Mode of Transmission of The Ebola Virus (License: Public Domain]: <a href=\"https://commons.m.wikimedia.org/wiki/File:EbolaCycle.png#mw-jump-to-license\"> \nWikicommons </a></sub> </center> \n</div>\n\nThe mechanism of infection of Ebola virus is poorly understood, but it is well known that the virus penetrates the human body through abrasions, mucosal surface, injuries on the skin or directly through the skin surface when an uninfected person comes in contact with the body fluids of an infected human or animal. \n\nEbola virus thus invade the cells using mechanisms such as  macropinocytosis and receptor mediated endocytosis mediated by through the glycoprotein. The virus is delivered into the acidic endosome of the cell, where the viral envelope is uncoated to release the genomic RNA into the cytoplasm. \n\nThe most interesting thing about the Ebola virus is that it has a way of totally evading the immune system, such that it can go ahead and wreck  havoc while the body immune system would still  be busy trying to find out what the problem is. \n\nAs soon as the Ebola virus makes its way into the body, it targets the cells of the immune system. It's first targets are the dendritic cells. The dendritic cells can be described as the signaling cells of the immune system. They normally show signals of an invading infection and cause the activation of T-lymphocytes which destroy infected cell before the pathogen can replicate further. \n\nOnce the Ebola virus successfully destroys the dendritic cells, they would no longer be able to present signals for the activation of T-cells, and antibodies will not be formed to combat the infection. The virus therefore takes advantage of the defective immune system to replicate rapidly using the host's cells. \n\nOnce a person is infected by this disease, he/she becomes a walking biological weapon because it takes only a single contact with a healthy person to place that person on the same “death row”. \n\n<br>\n#### Symptoms of Ebola Virus\n<br>\n\nBleeding from the nose, gastrointestinal tract, guns and other internal and external surfaces. \nAnuria (Inability to form urine) \nImpaired blood clotting \nBloody vomit, reddening eyes\nMultiple organ dysfunction which results in death. \n\n<br>\n#### Treatment and Prevention \n<br>\n\nTill date, there has been no established cure for Ebola fever. It has over 90% mortality rate, and the only way to prevent it is by avoiding contact with body fluids and corpse of people or animals infected with the disease. \n\n<br>\n#### Lassa Fever \n<br>\n\nLassa fever is a fatal haemorrhagic fever caused by the Lassa virus. The Lassa virus belongs to the Arenaviridae family of viruses, and its main host is the rodent Mastomys natalensis (aka multimammate mouse). It was first reported in Nigeria,West Africa in 1969.\n\nLassa fever is not as contagious as Ebola virus fever as it is not normally passed from person to person, instead, Humans typically get infected by the disease through  the urine or feces of mastomys rats. In rare cases, health workers might get infected through direct contact with the blood and body fluids of infected patients. \n\n<br>\n#### Structure of Lassa Virus\n<br>\n\n\n<div class=\"pull-left\">\n<center> <img src=\"https://steemitimages.com/DQmT8qpNGPo7a7yH3mBfGMvVaKiLsUg87p2GRzuRmhHVhaz/689px-Lassa_virus_virions_TEM_8699_lores.jpg\">\n<sub>  The Lassa Virus Structure (License: Public Domain]: <a href=\"https://commons.m.wikimedia.org/wiki/File:Lassa_virus_virions_TEM_8699_lores.jpg\"> \nWikicommons </a></sub> </center> \n</div>\n\n\nThe Lassa virus is pleomorphic in nature. This entails that It can exist in round, oval or any other shape. It has a diameter of 110 to 131 nm and it has an outer envelope which contains two single stranded RNA segments, the small S-segment and the large L-segment. \n\n\nThe L-segment encodes the viral RNA polymerase and zinc binding protein, while the S-segment encodes the precursor of the surface glycoprotein and structural protein-nucleoprotein. The surface glycoprotein precursor is then glycolytically cleaved to form the envelope glycoproteins GP1 and GP2, which facilitate the entry of the virus by binding to alpha dystroglycan receptors on the host cells.\n\n<br>\nMechanism of Infection of Lassa Fever \n<br>\n\nLassa virus enters the host cells through cell surface receptors, alpha dystroglycan. Some amino acids present on the GP1 protein on the surface of the virus aide high affinity binding of the virus to alpha dystroglycan. Lassa virus suppresses the immune system and replicates very quickly in the body. \n\n<br>\n## Symptoms of Lassa Fever \n<br>\n\nSome symptoms of Lassa Fever include;    \n* High grade fever\n* Depression\n* Mucosal bleeding\n* Facial edema\n* Internal bleeding \n* Weakness \n* Convulsion\n\n<br>\n#### Treatment of Lassa fever\n<br>\n\nCurrently, there has been no confirmed vaccine used for treating Lassa fever, but a drug called Ribavirin has been proven effective when administered within six days of exposure to the virus. \n\n<br>\n#### Conclusion \n<br>\n\nAmongst other hemorrhagic fevers, Ebola fever and Lassa fever have caused major concerns in sub Saharan Africa. Because these diseases do not have any sure cure, it is better to prevent exposure and spread of the disease. It is recommended that we report all cases of severe fever to health-care providers and avoid contact with body fluids of infected persons. \n\nPeople mostly at the risk of infection are those living in rural areas where one can easily get in contact with wild animals which may be vectors of the disease, so we are strongly advised against eating Bush meat especially those sold by the roadside, and to cook all meat properly before eating. Also, maintaining a clean and healthy environment can reduce the risk of invasion of rats which may spread Lassa virus. \n___\n#### <center>References</center>\n___\n\n<sup>\n[Arenaviridae](https://www.cdc.gov/vhf/virus-families/arenaviridae.html). Retrieved on May 7th, 2018.\n[Filoviridae](https://www.cdc.gov/vhf/virus-families/filoviridae.html). Retrieved on May 7th, 2018.\n[MOI of the Ebola virus](https://microbewiki.kenyon.edu/index.php/Infection_Mechanism_of_Genus_Ebolavirus). Retrieved on May 8th, 2018.\n[Lassa Fever](https://www.medicinenet.com/lassa_fever/article.htm#WHAT_IS_THE_HISTORY_OF_LASSA_FEVER). Retrieved on May 9th, 2018. </sup>",
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      "parent_permlink": "medical",
      "author": "dandymee",
      "permlink": "on-understanding-albinism-debunking-the-myths-and-the-possibility-of-having-a-cure",
      "title": "On Understanding Albinism, Debunking the Myths, and the  Possibility of Having a Cure",
      "body": "#### <center>Introduction</center>\n\nThis post was inspired by the news I read, that [a popular Nigerian Nollywood actor is set to divorce his wife for giving birth to an albino baby](https://www.yabaleftonline.ng/mike-ezuruonye-set/).\n\n<div class=\"pull-right\"><center><img src=\"https://cdn.steemitimages.com/DQmaQcv9HAjPDePamh4ooL225aUsewaurmRkDChRAB3NaTD/400px-Albino_woman_in_canoe,_Benin.jpg\"/><br/><em><a href=\"https://commons.m.wikimedia.org/wiki/File:Albino_woman_in_canoe,_Benin.jpg\"><sup>(License:CC BY-SA 3.0 by  Ferdinand Reus. Wikimedia Commons]</sup></a></em></center></div>\n\n\nOn reading this headline, any learned fellow would see it as a ridiculous thing, but the saddening truth is that in Africa and many other parts of the world, a large number of people still do not understand the concept behind albinism. In this article, I will try to shade light on the disorder called albinism from a biochemical perspective. \n\n<br>\n#### Definition of Albinism\n<br>\nAlbinism is a congenital (hereditary) autosomal disorder characterized by the complete absence or a deficiency in the production of melanin pigment.  This disorder is not peculiar to humans; it is obtainable in all vertebrates.  \n<br>\n\n#### To fully understand this disorder, we need to briefly talk about Melanin\n<br>\nThe main culprit,  Melanin, is a generic name given to some pigments found in the skin,  eyes and hair of vertebrates. Basically, melanin exists in three variants namely:\n<br>\n\nEumelanin: This is the most popularly kind of melanin which and is largely responsible for black and brown color of the skin and hair. In the hair, black eumelanin would cause the production of black hair, brown eumelanin would cause production of blonde hair, while a mixture of brown eumelanin mixed with red phemelanin causes the production of strawberry blonde hair. \n\n<div class=\"pull-center\"><center><img src=\"https://cdn.steemitimages.com/DQmX4Y36aVTnkUpo1iqbCRYetJWePDYpxSAHKDbXcmnpKin/woman-2917736_1280.jpg\"/><br/><em><a href=\"https://pixabay.com/en/woman-face-portrait-red-hair-hair-2917736/\"><sup>(Licenses:Public Domain. Pixabay]</sup></a></em></center></div>\n\n<br>\n Pheomelanin: Pheomelanin is mainly responsible for red, pink and other colors. It is more concentrated in areas like the nipples, lips and the genital organs.\n\nNeuromelanin: The function of neuromelanin is yet to be extensively studied, and the main thing known about it is that it is found in the brain.\n\nMelanin gives the skin its color, and protects us from the UV radiation of the sun. It actively absorbs the light from the sun and darkens the skin, thereby protecting it from UV radiation damage. \n<br>\n### Production of Melanin\n<br>\nMelanin is produced from the catabolism of the aromatic amino acid, tyrosine.  It is produced in specialized cells called melanocytes, which are densely packed in the dermis and epidermis of the skin, the uvea (iris-containing part of the eyes), inner ear, hair follicles and around the leptomeninges of the brain and spinal cord. \n<br>\nThe enzyme tyrosinase is chiefly  in charge of the melanin biosynthesis pathway. The synthesis of melanin starts in the liver where phenylalanine hydroxylase converts phenylalanine to tyrosine. \nNext, tyronsine is then transported to the pigment granules (melanosomes) of the melanocytes where tyrosinase oxidizes L-tyrosine to dihydrophenylalanine (DOPA).  Tyrosinase then converts DOPA to DOPAquinone, from which two varients of melanin, the pheomelanins (red and yellow polymers) and the eumelanins (black and brown polymers) can be obtained. \n\n<br>\n> The production of pheomelanin requires glutathione or cysteine which converts DOPAquinone to cysteinyl DOPA, from which pheomelanin is made. \n\n> To produce eumelanine,  DOPAquinone is sponteanously converted to LeocoDOPAchrome and DOPAchrome respectively, from where it goes through several other reactions to result in eumelanine.\n<br>\n####  So What Causes Albinism?\n<br>\nAlbinism is primarily caused by defect or complete absence of tyrosinase, which is the rate-limiting enzyme in the production of melanin. Generally, it is caused by a genetic mutation which either affects the melanin-producing proteins, the melanin receptor cells or the cells involved in packaging and distributing melanin, and it is inherited as a recessive allele. \n<br>\n#### Types of Albinism\n<br>\nThere are two  types of albinism- oculocutaneous albinism and ocular albinism. Oculocutaneous albinism affects the skin, eyes and hair, whereas ocular albinism only affects the eyes, while skin and hair coloring remains normal. \n<br>\n#### How Does Albinism Affect the Eyes? \n\n<div class=\"pull-left\"><center><img src=\"https://cdn.steemitimages.com/DQmbw78959BDoZXibg7UaiSXpWhNyKKmF91CLzQdLFSPDxU/Red_(albino)_eye.png\"/><br/><em><a href=\"https://commons.m.wikimedia.org/wiki/File:Red_(albino)_eye.png\"><sup>(License: CC BY-SA 3.0 by Karen Grønskov, Jakob Ek, and Karen Brondum-Nielsen Wikimedia Commons]</sup></a></em></center></div>\n\n\nAs we have established, both types of albinism will affect sight. It reduces the pigmentation of the iris and the retinal pigment epithelial cells, which is located between the choroid and retina. This lack of pigmentation causes the vessels of the retina to assume an abnormal shape, while the vessels of the choroid becomes more visible. \nUltimately, this abnormality causes light sensitivity because there is no or not enough pigments to absorb light. \n<br>\nAlso, albinos have an underdeveloped fovea. Fovea is the part of the eye mainly responsible for clarity of vision. \nApart from light sensitivity, underdevelopment of the fovea is the primary cause of impaired vision in albinos. Depending on the level of underdevelopment of the fovea, sight defect may be either mild or severe. \n\n<br>\nAlbinism also causes a misrouting of visual signal in the pathway that connects the eyes to the brain. This obstructs the movement of nerve impulse from the retina to the brain, thereby further affecting vision acuity. \n<br>\n\n<br>\nAlbinos also have defective eye conditions called Nystagmus and Strabismus. Nystagmus causes involuntary side-to-side, circular or up-to-down movement of the eyes, while strabismus is a condition where the eye muscles do not work in sync with each other. In this condition,  it is difficult to direct both of the eyes  at the object simultaneously. \n\n>These two conditions strain the eyes of the albino, and causes them to squint tilt their head in an unusual manner before they can get a fairly good view of their surroundings. \n\n<br>\n### Can Two Non-Albino Parents Have an Albino Baby?\n<br>\nThis is where many persons get it twisted. It is true that albinism is an inherited disorder, but it is also true that it can be inherited from two non-albino parents. I will try to explain this in the most simplistic manner. \n\nTwo different genes called the OCA2 gene and the TYR (Tyrosinase) genes are important in pigmentation. Remember that genes are stored in strands of DNA called chromosomes. Each person has two of these chromosomes (OCA2 and TYR), one of each is inherited from either parents.\n<br>\nA mutation (alteration) in any of these genes is what causes albinism, and for one to be an albino,   the two copies of chromosomes, inherited from both parents must be mutated. If one has one mutated copy and one normal copy, the person wouldn’t be an albino. Instead, they will be carriers of the albino gene. Carriers of albinism have normal skin pigmentation, and may not have albino children unless if their partners are also carriers of the albinism gene, and the two mutated genes get “mixed up” in their child.\n<br>\nThere is however a little complication in the inheritance pattern of ocular albinism. It is an X-linked disorder, which means that the mutated gene is carried on the X-chromosomes. This implies that, considering that males have only one X-chromosomes, a single copy of the mutated gene is enough to cause ocular albinism. In females however, because they have two X-chromosomes, a single mutated copy of the gene is not enough to cause the disorder.  \n\n#### What all of these mean is that two perfectly non-albino parents can have an albino baby. \n<br>\n#### Treatment and Management \n<br>\nFor now, there is no known cure for albinism. However, the following can be done to manage the condition.\n<br>\nProper diagnosis can identify refractive errors, so they can be treated to increase vision acuity.\nWearing of absorptive sunglasses helps reduce light sensitivity and eye strain. \nPatients can be given contact lenses with colored components at the regions overlapping the iris. These lenses reduces light sensitivity by blocking the entry of light into the iris.  They also reduce refractive error.\n<br>\nSurgical operations can be done to correct ocular misalignment in very severe cases of strabismus and nystagmus. \n<br>\nHaving established these, it is necessary to state that on-going studies using animal models promises a possible solution via gene therapy, in which abnormal genes can be replaced with normal ones. These studies have however not been evaluated in human subjects.\n<br>\n#### Dispelling some myths about albinism\n<br>\nSome myths you may have heard about albinos are mostly false.\nFor starters, albinism is not contagious. You cannot contract it from interacting with albinos. It can only be passed from parents to children if both parents are carriers of albinism gene. Also, albinos can have non-albino children, as long as their partners do not also have (or transfer) the albinism gene to the offspring.\n\nAlbinism is not a curse or punishment, so do not believe any religious myth that says such and suggests the use of albinos for any religious ritual. \n \n\n<br>\n#### <center>Conclusion</center>\n \nIn conclusion, I want to state that albinos are normal people. They have normal brain function, and are not less intelligent than people with proper pigmentation. Two non albino parents can have an albino baby, and it doesn’t mean that the woman cheated. \n\n\n<br>\n\nReferences \n[1.](https://health.howstuffworks.com/skin-care/problems/medical/albinism1.htm) \n\n[2.](http://www.skinwhiteningscience.com/melanin_synthesis_pathways.html) \n\n[3.](https://bjo.bmj.com/content/82/2/189) \n\n[4.](https://health.howstuffworks.com/skin-care/problems/medical/albinism.htm)\n\n[5.](https://www.healthline.com/health/albinism#treatment) \n\n[6.](https://www.aboutkidshealth.ca/Article?contentid=877&language=English) \n\n[7.](http://www.visionaware.org/info/your-eye-condition/guide-to-eye-conditions/albinism-6165/125)\n\n[8.](https://ghr.nlm.nih.gov/condition/oculocutaneous-albinism#Inheritance) \n\n[9.](http://www.visionaware.org/info/your-eye-condition/guide-to-eye-conditions/12#N)",
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      "author": "dandymee",
      "permlink": "what-gives-cockroaches-the-ability-to-survive-without-their-heads-and-why-can-t-humans-do-the-same",
      "title": "What gives cockroaches the ability to survive without their heads, and why can't humans do the same?",
      "body": "### <center>Introduction</center>\n\nDecapitation (cutting of the head) is easily  the most gruesome way anyone could be killed, but unlike humans and other animals, cutting a cockroach's head isn't a sure way of killing  it. In fact, even if you crush its head to fine powder, this creepy flying insect can still stay alive for a few days.  \n\n<div class=\"pull-centre\"><center><img src=\"https://steemitimages.com/DQmPQz2aAoAeB1zU4WaXczks8oGyniwuUZxVEEid21fxzF2/cockroach-15093_640.jpg\"/><br/><em><a href=\"https://pixabay.com/en/cockroach-animals-nature-dead-15093/\"><sup>Image of a cockroach(License: Public Domain]</sup></a></em></center></div>\n\n<br>\n\nApart from its body, the decapitated head can also survive in isolation for a few days as long a predator doesn't eat or crush it. This is why scientists have been able to perform several studies using the body and head of decapitated cockroaches.\n\n\nSo, the million dollar questions are: how is this possible, especially considering the fact that the brain, which coordinates all life processes, including blood flow, is located in the head? Well, in this article, I will explain the simple complexities that make it possible for these flying insects to survive decapitation. \n\n To help us understand how cockroaches pull off this stunt, I will compare their survival chances with that of humans in the same condition. Let's go: \n\n<br>\n#### Cockroaches would not suffer severe bleeding like humans would \n<br>\n\nWhen a sharp object cuts into human flesh, the person bleeds profusely, and if the bleeding is not stopped on time, the person may die. In a more severe situation, if a human’s head is chopped off, there would be severe bleeding and decrease in blood pressure such that the supply of oxygen to most organs of the body would cease, and the person bleeds to death. \n\n<div class=\"pull-right\"><center><img src=\"https://steemitimages.com/DQmfXfay6hi12CAG9USkQmFzrbYicZor11FPYBgY6AbHxZB/lungs-39980_640.png\"/><br/><em><a href=\"https://pixabay.com/en/lungs-organ-biology-respiratory-39980/\"><sup>Model of the human lungs (License: Public Domain]</sup></a></em></center></div>\n\nIn humans, blood is transported through a network of blood vessels which pump oxygenated blood from the heart to the body tissues through arteries and, deoxygenated blood from the body tissues through veins to the lungs where it is bathed in blood and sent back to the heart for redistribution.\n  \n<br>\n\nThis system of blood circulation termed “closed circulation” requires a considerable amount of blood pressure (typically within 120/80-140/90 mm Hg) to pump the blood round the body in an enclosed space. \n\n\n### Circulatory system in Cockroaches \n\n<br>\nBlood circulation in cockroaches doesn’t require much pressure like the one in humans. They have an *open circulatory system*, which doesn’t require all the arteries  \n\nIn cockroaches, the fluid which performs the function of blood is called hemolymph. In the open circulatory system, hemolymph is confined inside vessels only for a little period of time, after which the rest of the circulation takes place inside their body cavity (hemocoel).\n<br>\nUnlike humans, cockroaches do not need much amount of hemolymph to survive. In fact, the body cavity is reduced to minimize the amount of hemolymph in the general circulation. \nAlso, when you cut off the head of cockroach, their neck seals off almost immediately just by clotting. Hence there is no uncontrollable bleeding (or loss of hemolyph as the case may be). \n<br>\n #### Unlike Humans, in Cockroaches, Oxygen is not distributed by the circulatory system.\n<br>\nAlso, unlike in humans and other higher animals where the circulatory system is responsible for the transportation of oxygen to body tissues and removal of carbon dioxide, in cockroaches, hemolymph is not an oxygen-carrying pigment. Gaseous exchange in cockroaches takes place in the tracheal system, and hemolymph plays absolutely no role in it.\n<br>\n#### Unlike humans, the respiratory system of cockroaches is not controlled by organs in the head \n<br>\nHumans breathe through their nostrils and mouth, and the whole respiration process is controlled by the brain. This makes the head one of the most important organs critical for human survival. However, in cockroaches (and a few other lower animals), the case is different\n<br>\n### Respiration in Cockroaches\n<br>\nJust like every other organism respiration is very critical to the survival of cockroaches. Unlike humans that have lungs, cockroaches breath through the means of spiracles. \n\n<div class=\"pull-left\"><center><img src=\"https://steemitimages.com/DQmWYUDE1uJJXC373MGN13FYAXoG2osEWn2XeprREc9veNu/DytiscusSpiracles.png\"/><br/><em><a href=\"https://cs.m.wikipedia.org/wiki/Soubor:DytiscusSpiracles.png\"><sup>Cockroaches Breath through spiracles. Wikicommons,License: Author- Miall, L. C BY-SA CC 3.0</sup></a></em></center></div>\n\n\n\nCockroaches have ten pairs of spiracles on the lateral side of their body. The first and largest pair are located on their mesothorax, the second pair on their metathorax, while the remaining eight pairs are attached to their abdominal segments. \nThe thoracic spiracles open into a segmental trachea, while the abdominal spiracles open in the segmental  trachea through the atrium. The trachea branches and reaches out to all cells of the cockroach’s body to perform the crucial function of gaseous exchange. \n<br>\nThe spiracles in cockroaches are controlled by the central nervous system. Respiration can occur solely on the body surface with the involvement of the brain (unlike in humans where the brain is in control of the respiratory process). \n\nBecause of the spiracles, even when the cockroach is decapitated, respiration can still continue smoothly in both the body and the lonely head, hence the insect can continue to live for a few more days or even weeks until it eventually dies of starvation. \n<br>\nAnother important point we must note is that  cockroaches have numerous nerve tissue agglomerations  (ganglia) scattered within the body segments which are capable of initiating and completing the basic functions of the nervous system without the brain. \n<br>\n### Conclusion\n<br>\nDecapitation of cockroach may seem like such a ruthless way of killing them, but scientists have found that they can indeed survive longer than you expect even in their “headlessness.”\nSo many variations between the human body system and that of the cockroach makes it possible for the insects to withstand this macabre which kills humans instantly.  \nWhen their head is cut off, cockroaches are able to withstand loss of body fluid by sealing of the neck through clotting. Also, they can perform basic respiratory and nervous functions. \n_____\n#### <center>References</center>\n____\n<sup>[Cockroach can live without their heads: Fact or Fiction](https://www.scientificamerican.com/article/fact-or-fiction-cockroach-can-live-without-head/) | [Process of respiration on Cockroaches](www.notesonzoology.com/cockroaches/process-of-respiration-in-cockroaches-invertebrates/1989) | [Difference between Closed and open circulatory system](https://sciencing.com/difference-closed-open-circulatory-system-6594843.html) | [Open and closed circulatory system](http://www2.gsu.edu/~bioasx/closeopen.html)</sup>\n\n\n<br>\n\nThanks for reading. Please kindly upvote, resteem and follow me @dandymee",
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      "memo": "Hi @dandymee. Would you like to earn solid (115k SP) upvote on your latest post from @project.hope? Check out our recent post for more details. And hopefully you will find this publication worth your time and attention. We're explaining our community economy \"business model\", hoping that more people will join our efforts in the future. // LINk: https://steemit.com/hive-175254/@project.hope/project-hope-economy-explained-2021"
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      "permlink": "an-a-b-c-explanation-of-the-nervos-network-after-reading-this-you-must-hop-in",
      "title": "An A-B-C Explanation of the Nervos Network- After Reading this, you Must Hop In!",
      "body": "@@ -3808,21 +3808,22 @@\n  allows \n-e\n+E\n ther\n+e\n um holde\n@@ -4287,20 +4287,16 @@\n ardano. \n-This\n  At the \n@@ -4361,16 +4361,19 @@\n be able \n+to \n transact\n@@ -4421,53 +4421,12 @@\n rom \n-being able to transact assets interchangeably\n+that\n , th\n@@ -4469,26 +4469,8 @@\n ers \n-will also be able \n to c\n@@ -4480,16 +4480,17 @@\n te token\n+s\n  using t\n",
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      "title": "An A-B-C Explanation of the Nervos Network- After Reading this, you Must Hop In!",
      "body": "@@ -4173,16 +4173,620 @@\n twork. %0A\n+---%0ARecently also, the IOHK and Nervos teams collaborated to build a unifying bridge between Nervos and Cardano. This At the completion of this bridge, users on both blockchains will be able transact assets between both blockchains. Apart from being able to transact assets interchangeably, this bridge will also enable Nervos users will also be able to create token using the Cardano native asset standard, and port same into the Nervos blockchain. This bridge will ultimately enable enhanced interoperability between both blockchains, and create more possibilities for both Cardano and Nervos users. %0A%0A\n %0A### Sus\n",
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      "permlink": "an-a-b-c-explanation-of-the-nervos-network-after-reading-this-you-must-hop-in",
      "title": "An A-B-C Explanation of the Nervos Network- After Reading this, you Must Hop In!",
      "body": "The Nervos Network has been around since 2018, working to provide a universal ecosystem where different networks can enjoy unhinged interaction and interoperability. As the name implies, the Nervos Network is designed to become the nervous system of the blockchain, but many people still do not know enough about the network, and it’s taken the CKB token. \n\n\n![nervos ...png](https://cdn.steemitimages.com/DQmdeEPjJyr25PMvxkwhwXp3CZmWdTV3LDCgzthzFdatH9b/nervos%20...png)\n\n\nHowever, a few months ago, Nacho of the Nervos Africa team had a chat with Binance Nigeria, where he gave some remarkable insights about the Nervos project, and I’m here to share the scoop with you. \n\n## The Challenge of Unlimited Supply, and how CBK Plans to Stay Bullish and Valuable  \n---\n\nNaturally, the price of any item that has an unlimited supply will be lower than items with a limited supply. This is because scarcity drives prices upwards. It’s a basic economic principle, but it is not the case with the CKB token despite its unlimited supply. This is because CKB is designed with an issuance schedule that helps prevent devaluation, thereby protecting its long-term holders.  \n\n_Let me explain how this works_\n\n\n>•CKB is currently undergoing a primary issuance stage—just like Bitcoin—which will end in due time. \n\n>•\tAt the end of the primary issuance stage, miners will still be able to mine and get paid via secondary issuance. \n\n_So what’s the difference? And how will they get paid during the secondary issuance?_\n\n>•\tPayment in the secondary issuance is made by making users pay for a space to store data on the CBK blockchain. This means that for users to store data on the CBK blockchain, they have to pay for their own space. It will cost 1CKB to buy 1byte of space on the CKB blockchain. Hence, the more space each user needs, the more CKB they have to buy. This also implies that as more users adopt the CKB space, increased demand will increase the value of CKB. \n\n>•\tUsers can also place their CBK tokens in the Nervos DAO to protect them from any inflationary effects. \n\n---\n\n## Why Should You Choose Nervos Over Other Cross-chain Projects?\n---\nWhile there are many other cross-chain solutions out there, most of them are limited in functionality and do not fully support interoperability. Those other solutions allow developers to build apps with their tools and interoperate with other apps within their networks. But they neglect the other large chunk of the blockchain ecosystem that wasn’t built inside their network, isolating and preventing them from benefiting from their offerings. \n\nNow, this is where Nervos comes in! Nervos aims to provide a universal network—just like the internet— that’ll interconnect all universal and cross-chain applications such that users can interact effectively within the Nervos blockchain and other blockchains globally. \n\n![network-4025614_1920-1-1-1600x1000.jpg](https://cdn.steemitimages.com/DQmcBx8jKbcbZexEqy14zoETeHF8afvwV4bcZFqqk5aQARE/network-4025614_1920-1-1-1600x1000.jpg)\nApart from creating a solution where developers can build apps on the Nervos blockchain, the goal is to also allow them to port the apps they already built elsewhere, into the Nervos ecosystem. From there, they can interact and interoperate seamlessly with other apps and data within and outside the system. \n\n---\n### The Nervos Strategy of Achieving this plan\n---\nTo achieve its pipedream, the Nervos network has introduced the “Universal Passport Force Bridge.” The force bridge is a chain link that connects Etherum to Nervos. Unlike other etherum bridges that require users to complete several steps before they can move their assets around, the Universal Passport Force Bridge only needs your ERC-20 contract address. Just paste it, and voila! The job is done. \n\nThe bridge also allows etherum holders to buy CKB directly using their ETH instead of going through the tedious task of locking their assets before placing an order. \nThis force bridge will also incorporate other crypto assets in the nearest future, and within a bit of time, Nervos will reach the ultimate goal of universal interoperability of all crypto assets via the Nervos network. \n\n### Sustainability and Adoption Plan\n---\nThe Nervos team is doing a lot of work to increase the adoption of CKB and the Nervos network. They have launched a 30 million dollars ecosystem fund to accelerate this project. Also, over 1.5 million grans have been awarded to developers to strengthen the works on development and operability. \nThere’s also the CKLabs which was launched for the massive building of apps on Nervos. On the other hand, local organizers are working hard at the grassroots level, canvassing for adoption, educating people on what the future holds, and igniting enthusiasm. \nThe truth is, the future is bright, and within a few years, Nervos Network will achieve its ultimate goal of becoming the nervous system of the crypto world. This is your best opportunity to hop on the train. Don’t miss it! \n\nFind out more on [the Nervos website](http://nervos.com) or join their [Telegram Channel](http://t.me/NervosAfrica).",
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