Activity code 1 General Concepts about Epoxy Polymers

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Crack Initiation - an overview

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Myths of Conquest, Part Seven: Death by Disease Alone

This is the seventh of what I hope will be a several part series of the myths of European conquest in the Americas. Check out the previous myths of conquest here…
This post will examine the multiple factors responsible for Native American population decline in the years following contact. I often rail against the “death by disease alone” myth of conquest. Though I’m fascinated by the subject, I intentionally tried to keep this post below 2,000 words to not exhaust your patience. If you would like more in-depth analysis check out the “More Information” section for some of my longer posts on the topic, and feel free to ask further questions. As always, if you see any errors, let me know so I can fix them and learn from my mistakes. Scholars of the Americas, feel free to add information from your areas of research.
Here we go…
The Myth: Universal > 95% Mortality from Introduced Infectious Organisms
The dominant narrative of Native American population decline after contact cites introduced infectious diseases as the chief mechanism of widowing the Americas of its original inhabitants. Per the myth, Native Americans throughout the New World died at unprecedented, catastrophic, apocalyptic levels, victims of invisible assailants they neither understood nor were evolutionarily prepared to combat. In the worst versions of the narrative, immunological naïveté is folded into the larger metaphor of Native Americans as inexperienced, genetically weaker, and helpless to defend themselves against the oncoming tide of colonialism. Disease, a scythe cutting a path ahead of colonial encounters, conveniently explains the absence of Native Americans from the narrative of post-contact history and obscures the history of rebellion, revolt, conflict, peace and negotiation that followed on the heels of colonial encounters.
The Reality: A Toxic Cocktail Poured Out Over Centuries
Previous myths of conquest posts highlighted the persistence of dynamic Native American communities who allied with Cortés against Tenochtitlan, defeated the majority of entradas into North America, served as translators throughout the New World, violently resisted conquest for centuries, and actively negotiated an autonomous existence in the mission system. With a firm foundation on this abundant evidence of life we now turn to the narrative of death. The reality of excess mortality after contact requires an examination the complete colonial cocktail leading to population decline, as well as the ecological factors that allowed for the initiation and propagation of epidemics. Demographic decline occurred due to a variety of factors striking over the course of centuries, not just by disease alone.
Mexican Demographic Trends Inappropriately Generalized
The 90-95% figure that dominates the popular discourse has its foundation in the study of mortality in conquest-period Mexico. Several terrible epidemics struck the population of greater Mexico (estimated at ~22 million at contact) in quick succession. Roughly 8 million died in the 1520 smallpox epidemic, followed closely by the 1545 and 1576 cocoliztli epidemics where ~12-15 million and ~2 million perished, respectively (Acuna-Soto et al., 2002). After these epidemics and other demographic insults, the population in Mexico hit its nadir (lowest point) by 1600 before slowly beginning to recover.
Though the data from Mexico represents a great work of historic demography, the mortality figures from one specific place and time have been uncritically applied across the New World. Two key factors are commonly omitted when transferring the 90-95% mortality seen in Mexico to the greater Americas: (1) the 90-95% figure represents all excess mortality after contact (including the impact of warfare, famine, slavery, etc. with disease totals), and (2) disease mortality in Mexico was highest in densely populated urban centers where epidemics spread by rapidly among a population directly exposed to large numbers of Spanish colonists. Very few locations in the Americas mimic these ecological conditions, making the application of demographic patterns witnessed in one specific location inappropriate for generalization to the entire New World.
Interaction of Host, Pathogen, and Environment
As hinted earlier, any examination of disease epidemiology after contact must incorporate a larger ecological perspective. Epidemics require the proper conditions for the host, the pathogen, and the environment to spread widely. Too often the narrative of “death by disease alone” fails to examine the greater context that facilitated the spread of epidemics. Infectious agents are treated as an inevitable miasma spreading ahead of contact. As the case study on the U.S. Southeast showed, the ecological context underscores how pathogens spread in conjunction with the repercussions of conquest. In the Florida missions, early disease outbreaks failed to travel beyond the immediate mission environs due to contested buffer zones between rival polities. Only after English slaving raids changed the social environment, erased these protective buffer zones, and destabilized the region did the first verifiable smallpox pandemic sweep the greater U.S. Southeast.
When attacks by slavers disrupted normal life, hunting and harvesting outside the village defenses became deadly exercises. Nutritional stress led to famine as food stores were depleted and enemies burned growing crops. Displaced nations attempted to carve new territory inland, escalating violence as the shatterzone of English colonial enterprises spread across the region. The slave trade united the Southeast in a commercial enterprise involving the long-range travel of human hosts, crowded susceptible hosts into dense palisaded villages, and weakened host immunity through the stresses of societal upheaval, famine, and warfare (Kelton). All of these factors were needed to propagate a smallpox epidemic across the Southeast, and all of these factors led to increase mortality once the epidemic arrived.
The myth of catastrophic disease spread often cites an incredibly high case fatality rate (number of people infected who die of that disease) for introduced pathogens in the Americas. We hear that an infectious organism like smallpox, which historically has an overall fatality rate of 30%, killed 95% of infected Native Americans. Taken without reference to the greater ecological situation, and assuming the validity of colonial mortality rates (a large assumption), the myth arises of an immunologically weaker Indian population unable to respond to novel pathogens.
Examining the greater context reveals how the cocktail of colonial stressors often stacked the deck against host immune defense before epidemics arrived. Plains Winter Counts recount disease mortality consistently increased in the year following nutritional stress (Sundstrom), and this link was understood by European colonists who routinely burned growing crops and food stores when invading Native American lands, trusting disease and depopulation would soon follow (Calloway). Mortality increased in populations under nutritional stress, geographically displaced due to warfare and slaving raids, and adapting to the breakdown of traditional social support systems caused by excess conquest-period mortality. Context highlights why many Native Americans, like modern refugee populations facing similar concurrent physiological stress, had a decreased capacity to respond to infection, and therefore higher mortality to periodic epidemics.
Post Hoc Ergo Propter Hoc
Traditionally, the discussion of epidemic disease after contact contains an element of a post hoc fallacy. Archaeologists uncover evidence of population dispersal in the protohistoric and assume disease led to the abandonment of the site. Historians read de Soto’s retelling of the Plague of Cofitachequi and assumed the population perished from introduced infectious disease. This assumption rests on the flawed notion that the New World was a disease-free paradise, that site abandonment can only be attributed to disease, and the belief that observed epidemics arose solely from introduced pathogens.
A full discussion of the New World disease load before contact is beyond the scope of this post, but populations in the Americas were subject to a wide variety of intestinal parasites, Chagas, pinta, bejel, tick-borne pathogens like Lyme disease and Rocky Mountain Spotted Fever, syphilis, TB, and zoonotic pathogens. Those infectious organisms didn’t stop infecting Native Americans after European arrival. Changes in host ecology associated with conquest could alter the transmission cycle of native infectious organisms, and transform a benign, or at least contained, infectious organism into one capable of causing massive mortality. Researchers propose the devastating cocoliztli epidemics, which killed millions in 1545 and 1576 in Mexico, were the work of a native viral hemorrhagic pathogen similar to our modern Hantavirus rather than an introduced infection. The authors hypothesize that extended drought altered the interaction of the mouse host with human populations and, combined with other shocks of conquest, allowed for the virus to jump to humans. The story of cocoliztli encourages us to at least entertain that notion that epidemics after contact could occur from pathogens indigenous to the New World, and not solely from introduced infectious organisms.
Wrapping Up
One consequence of the dominance of “disease and acculturation models” of the postcontact period has been a lack of scholarly attention paid to the subjects of conflict, violence, and resistance between colonists and Native peoples through extended periods of time. (Wilcox, p. 17)
The “death by disease alone” myth ignores the myriad of factors influencing the demography of Native American populations after contact. Introduced infectious disease mortality was awful. However, I intentionally placed the disease myth later in the series, after discussing abundant evidence of persisting Native American communities, to place epidemics in the larger context of vibrant populations adapting, resisting, accommodating, and negotiating in the post-contact environment. Southeastern populations responded to the shocks of conquest by coalescing into powerful confederacies. Violent resistance to conquest continued throughout the Americas, and periodic waves of disease could not diminish the vitality of mission inhabitants across the northern border of New Spain. Epidemics were not an automatic cultural death sentence.
Humans are demographically capable of rebounding from high mortality events, like epidemics, provided other sources of excess mortality are limited. In the mid-twentieth century when the Aché of Paraguay moved to the missions ~38% of the population died from respiratory diseases alone. However, the Aché rallied quickly and are now a growing population. The key factor for population survival after high mortality events is limiting other demographic shocks, like violent incursions from outsiders, providing sufficient food resources, and the territory needed for forage and hunt to supplement food intake.
When the colonial cocktail arrived in full force demographic recovery became challenging. Warfare and slaving raids added to excess mortality, while simultaneously displacing populations from their stable food supply, and forcing refugees into crowded settlements where disease can spread among weakened hosts. Later reservations restricted access to foraged foods and exacerbated resource scarcity where disease could follow quickly on the heels of famine. The greater cocktail of colonial insults, not just the pathogens themselves, decreased population size and prevented rapid recovery during the conquest.
By far the greatest sin of the “death by disease alone” myth is the emphasis it places on a terminal narrative that contextualizes the story of Native Americans in terms of eventual defeat and disappearance. Disease provides the easy answer to Amerindian population decline, and discourages further investigation into the rich, abundant evidence of persisting native communities who continued to shape the history of the Americas.
More myths of conquest to come. Stay tuned.
More Information
Acuna-Soto et al., (2002) “Megadrought and Megadeath in 16th Century Mexico”
Beck Chiefdoms, Collapse, and Coalescence in the Early American South
Calloway One Vast Winter Count: The Native American West before Lewis and Clark
Etheridge & Shuckhall, editors Mapping the Mississippian Shatter Zone: The Colonial Indian Slave Trade and Regional Instability in the American South
Kelton Epidemics and Enslavement: Biological Catastrophe in the Native Southeast 1492-1715
Panich & Schneider, editors Indigenous Landscapes and Spanish Missions: New Perspectives from Archaeology and Ethnohistory
Sundstrom (1997) “Smallpox Used Them Up: References to Epidemic Disease in Northern Plains Winter Counts, 1714-1920.”
Wilcox The Pueblo Revolt and the Mythology of Conquest: An Indigenous Archaeology of Contact
Reddit Posts of Interest
400-Rabbits and I tag team a discussion of cocoliztli and matlazahuatl epidemics in Mexico
Evidence of Epidemics in the Americas before European Contact
Guns, Germs, and Steel – Chapter 11: Lethal Gift of Livestock
Slavery, Smallpox, and Virgins: the U.S. Southeast as a case study against the “virgin soil” narrative of Native American disease mortality
Timing Disease Arrival on the North American Great Plains
submitted by anthropology_nerd to badhistory

so i decided i wanted to figure this whole corona virus thing out guys

So i did some research...

initial analysis of what becomes SARS-CoV-2
inventing the term "covid-19" and using the terminology "disease"
(no medical research refers to covid-19 or as a "disease", only as SARS-CoV-2 virus and viral infection)
SARS-COVID-(1) = 2003 virus pandemic in China
SARS-COVID-2 **COVID 19*\* = 2020 virus global pandemic
MERS-COVID-1 = MIddle east virus pandemic 2012
(Initially called simply novel coronavirus or nCoV, it was first reported in 2012 after genome sequencing of a virus isolated from sputum samples from a person who fell ill in a 2012 outbreak of a new flu-like respiratory illness.)
  1. 229E (alpha coronavirus)
  2. NL63 (alpha coronavirus)
  3. OC43 (beta coronavirus)
  4. HKU1 (beta coronavirus)
*Corona viruses that cause "cold" or respiratory illness, 7 CoVs are well known to cause respiratory illness ; coronaviruses = common cold
"People around the world commonly get infected with human coronaviruses 229E, NL63, OC43, and HKU1."
(there is no proven mechanism for asymptomatic transmission, only contagious with symptoms, zero documented and proven asymptomatic transmission cases for SARS-CoV-1 or 2 ) 2020
"One previous study reported an asymptomatic 10-year-old boy with COVID-19 infection, but he had abnormalities on chest CT.6 If the findings in this report of presumed transmission by an asymptomatic carrier are replicated, the prevention of COVID-19 infection would prove challenging. The mechanism by which asymptomatic carriers could acquire and transmit the coronavirus that causes COVID-19 requires further study."
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2916580/#r26 2010
"All coronaviruses are associated with high coinfection rates..."
“Samples representing monoinfections were frequently (26/184 [14.1%]) from subjects in intensive care and/or high-dependency units, with presentations that included severe lower respiratory tract disease and pyrexia, and case reports have associated all coronaviruses with high morbidity and/or fatal outcomes’”
(exact scenario for SARS-COVID-1 or 2, but actually another corona virus) 2006
"These findings underscore the virulence of human CoV-OC43 in elderly populations and confirm that cross-reactivity to antibody against nucleocapsid proteins from these viruses must be considered when
interpreting serological tests for SARS-CoV."
(there are a variety of corona viruses similar to SARS-COVID-2) 2010
" Four human coronaviruses (human coronavirus 229E [HCoV-229E], HCoV-HKU1, HCoV-NL63, and HCoV-OC43) are associated with a range of respiratory symptoms, including high-morbidity outcomes such as pneumonia and bronchiolitis "
(antibody tests are not 100% accurate, maybe over 10% false positive for other antibody)
https://www.ncbi.nlm.nih.gov/pubmed/15583332 2004
https://www.ncbi.nlm.nih.gov/pubmed/15897988 2005
"Three of the 21 and 1 of the 7 convalescent-phase serum samples from persons with increases in antibodies against HCoV-OC43 and HCoV-229E, respectively, tested positive by the recombinant SARS-CoV nucleocapsid protein-based ELISA. None of these samples were found to contain a specific antibody in the recombinant SARS-CoV spike polypeptide-based Western blot assay."
"Cross-reactivity between antibodies to different human coronaviruses (HCoVs) has not been systematically studied. " <---- false positives for SARS-CoV-2
**(precedent for bat meme)** 2013
"However, the source of SARS virus remains a myth.” A recent report denied the role of civets in transmitting SARS virus and argued that bat is the real culprit. According to Dr. He, however, this is not a new story: early in 2005, some scientists had made the same conclusion. However, up to now there has been no final conclusion. "
developing advanced techniques for corona virus splicing as a result of SARS 2014
"The potential risk to public health posed by SARS-CoV and other CoVs, and the lack of specific antiviral agents and vaccines, have triggered a global effort to study this family of viruses at the molecular level in order to develop effective strategies to prevent and control CoV infections. Molecular genetic analysis of the structure and function of RNA virus genomes has been profoundly advanced by the availability of full-length cDNA clones. In the case of CoV, the huge genome size and the instability of specific CoV cDNA sequences in bacterial systems hindered the development of infectious cDNA clones until recently. A tremendous amount of creativity in the CoV field resulted in the development of four independent and unique reverse genetic systems that overcame these problems. These reverse genetic systems have been established using non-traditional approaches, which are based on the use of targeted recombination, BACs, in vitro ligation of CoV cDNA fragments, and vaccinia virus as a vector for the propagation of CoV genomic cDNAs. The availability of CoV full-length infectious clones and recombinant viruses expressing reporter genes constitute important tools for the study of CoV replication and transcription mechanisms, virus-host interaction and pathogenesis, and also for the rapid and rational development and testing of genetically defined vaccines. In addition to full-length cDNA clones, the generation of CoV replicons has greatly facilitated the functional analysis of viral replication and transcription, as well as the analysis of antiviral drugs without the need of manipulating infectious viruses."
collecting corona viruses from bats 2018
Initial clinical findings of SARS-CoV-2 2020
“2019-nCoV caused clusters of fatal pneumonia with clinical presentation greatly resembling SARS-CoV.”
No vaccines for CoVs 2009
“Finally, no effective treatments exist for any coronavirus infections, including SARS140; vaccines, even for animal coronaviruses, are not effective; and live attenuated vaccines are prone to recombination with circulating coronaviruses. One future goal will be to translate new information about the structure and function of coronavirus proteins into specific anti-virus therapies. Also, development of live, attenuated, safe vaccines that do not recombine in the wild is another goal, made more feasible as more is learned about basic coronavirus biology. Over the past few years, the development of new technologies has simplified the identification of novel coronaviruses; the next major goals will be to understand viral pathogenesis and to design effective coronavirus vaccines and therapies.”
SARS-CoV-2 Less infectious but highly similar to previous SARS MERS 2020
So, in the beginning " The initial working case definitions for suspected NCIP were based on the SARS and Middle East respiratory syndrome (MERS) case definitions, as recommended by the World Health Organization (WHO) in 2003 and 2012 " with a consideration for a connection to the seafood market, until January 18th when they began performing tests
"We estimated an R0 of approximately 2.2, meaning that on average each patient has been spreading infection to 2.2 other people. In general, an epidemic will increase as long as R0 is greater than 1, and control measures aim to reduce the reproductive number to less than 1. The R0 of SARS was estimated to be around 3" (its less infectious than SARS-CoV-1 so thats a difference)
"Although infections in health care workers have been detected, the proportion has not been as high as during the SARS and MERS outbreaks."
"Super-spreading events have not yet been identified for NCIP, but they could become a feature as the epidemic progresses."
The precedent of SARS-CoV-1 characteristics have driven and guided the research of SARS-CoV-2 since it was discovered, it may have been a hint that one is called SARS-CoV-1 and the other is called SARS-CoV-2, this is because after the discovery of the nCoV2019 they classified it as being in the subgenera Sarbecovirus due to genetic similarity to SAR-CoV(1), thus SAR-CoV-2
initial studies demonstrated "2019-nCoV caused clusters of fatal pneumonia with clinical presentation greatly resembling SARS-CoV."
"It appears that 2019-nCoV uses the same cellular receptor as SARS-CoV (human
angiotensin-converting enzyme 2 [hACE2]),3 so transmission is expected only after signs of lower respiratory tract disease develop. SARS-CoV mutated over the 2002–2004 epidemic to better bind to its cellular receptor and to optimize replication in human cells, enhancing virulence.7 Adaptation readily occurs because coronaviruses have error-prone RNA-dependent RNA polymerases, making mutations and recombination events frequent. By contrast, MERS-CoV has not mutated substantially to enhance human infectivity since it was detected in 2012."
{based on the shared characteristics of SARS-CoV 1&2 (hACE2 receptor transmission) SARS-CoV-2 doesn't begin transmission until you get symptoms which is of course logical as the viral load is highest after onset of symptoms}
"Together, these observations suggest that the affinity of S protein for ACE2 is an important determinant in the overall rate of viral replication and in the severity of disease. If so, adaptations within the S protein that are critical for high‐affinity association with human ACE2 may have contributed to the unusual severity of SARS."
{hACE2 receptor strong determinant for overall rate of viral replication and in the severity of disease}
"In addition, we found bat SARSr-CoV strains with different S proteins that can all use the receptor of SARS-CoV in humans (ACE2) for cell entry, suggesting diverse SARSr-CoVs capable of direct transmission to humans are circulating in bats in this cave. Our current study therefore offers a clearer picture on the evolutionary origin of SARS-CoV and highlights the risk of future emergence of SARS-like diseases."
{from 2017, eerily predictive}
"Currently, there was no evidence of air-borne transmission. Viral RNAs could be found in nasal discharge, sputum, and sometimes blood or feces.1,9,10,13,15 But whether oral-fecal transmission can happen has not yet been confirmed. Once people are infected by the 2019-nCoV, it is believed that, like SARS, there is no infectivity until the onset of symptoms.15 However, one report describes infection from an asymptomatic contact but the investigation was not solid.10 The infectious doses for 2019-nCoV is not clear, but a high viral load of up to 108 copies/mL in patient’s sputum has been reported.10 The viral load increases initially and still can be detected 12 days after onset of symptoms.9 Therefore, the infectivity of patients with 2019-nCoV may last for about 2 weeks. However, whether infectious viral particles from patients do exist at the later stage requires validation."
“there is great concern about the negative impact of a false positive laboratory test, and the World Health Organization has recommended protocols for the laboratory diagnosis of SARS in the post outbreak period (WHO, 2003b), which includes the use of two different RT-PCR assays. The assay described here provides an alternative test that can be helpful in that regard. Furthermore, because our assay detects several coronaviruses, it is quite feasible to use RNA from a coronavirus other than SARS-HCoV as a positive control. In fact, our laboratory now uses as positive control RNA transcribed from the cloned amplicon of the IBV; IBV has never been implicated in human infections. The use of IBV as a positive control removes a potential source of PCR contamination by SARS-HCoV genetic material in the laboratory.”
"Symptoms of COVID-19 are non-specific and the disease presentation can range from no symptoms (asymptomatic) to severe pneumonia and death." (there is no actual definition of COVID-19, only the presence of SARS-CoV-2)
"A4. Vital Records Criteria for Reporting A person whose death certificate lists COVID-19 disease or SARS-CoV-2 as a cause of death or a significant condition contributing to death.
A5. Other Criteria for Reporting Autopsy findings consistent with pneumonia or acute respiratory distress syndrome without an identifiable cause." ( if it looks like you died from pneumonia or ARDS then you satisfy requirements for being COVID 19 death)
"A5. Case Classifications
• Meets confirmatory laboratory evidence.
• Meets clinical criteria AND epidemiologic evidence with no confirmatory laboratory testing performed for COVID-19.
• Meets presumptive laboratory evidence AND either clinical criteria OR epidemiologic evidence.
• Meets vital records criteria with no confirmatory laboratory testing performed for COVID19."
"X. Data sharing/release and print criteria
CSTE recommends the following case statuses* be included in the ‘case’ count released outside of the public health agency:

Turns out its a big friggin conspiracy yall
submitted by snowyz42 to conspiracy