steering the world’s public in the wrong direction and blaming everything on nature

https://pubmed.ncbi.nlm.nih.gov/20216934/ Nano Res . 2008;1(3):203-212. doi: 10.1007/s12274-008-8021-8. Nano-Graphene Oxide for Cellular Imaging and Drug Delivery Xiaoming Sun  1 , Zhuang Liu, Kevin Welsher, Joshua Tucker Robinson, Andrew Goodwin, Sasa Zaric, Hongjie Dai PMID: 20216934 PMCID: PMC2834318 DOI: 10.1007/s12274-008-8021-8 Abstract Two-dimensional graphene offers interesting electronic, thermal, and mechanical properties that are currently being explored for advanced electronics, membranes, and composites. Here we synthesize and explore the biological applications of nano-graphene oxide (NGO), i.e., single-layer graphene oxide sheets down to a few nanometers in lateral width. We develop functionalization chemistry in order to impart solubility and compatibility of NGO in biological environments. We obtain size separated pegylated NGO sheets that are soluble in buffers and serum without agglomeration. The NGO sheets are found to be photoluminescent in the visible and infrared regions. The intrinsic photoluminescence (PL) of NGO is used for live cell imaging in the near-infrared (NIR) with little background. We found that simple physisorption via pi-stacking can be used for loading doxorubicin, a widely used cancer drug onto NGO functionalized with antibody for selective killing of cancer cells in vitro. Owing to its small size, intrinsic optical properties, large specific surface area, low cost, and useful non-covalent interactions with aromatic drug molecules, NGO is a promising new material for biological and medical ap covid … [Read More...] …………………………..  J Transl Med. 2004; 2: 3. Published online 2004 Jan 20. doi: 10.1186/1479-5876-2-3 PMCID: PMC340389 PMID: 14733617 The site of origin of the 1918 influenza pandemic and its public health implications John M Barry1 Author information Article notes Copyright and License information Disclaimer The 1918–1919 influenza pandemic killed more people than any other outbreak of disease in human history. The lowest estimate of the death toll is 21 million, while recent scholarship estimates from 50 to 100 million dead. World population was then only 28% what is today, and most deaths occurred in a sixteen week period, from mid-September to mid-December of 1918. It has never been clear, however, where this pandemic began. Since influenza is an endemic disease, not simply an epidemic one, it is impossible to answer this question with absolute certainty. Nonetheless, in seven years of work on a history of the pandemic, this author conducted an extensive survey of contemporary medical and lay literature searching for epidemiological evidence – the only evidence available. That review suggests that the most likely site of origin was Haskell County, Kansas, an isolated and sparsely populated county in the southwest corner of the state, in January 1918 [1]. If this hypothesis is correct, it has public policy implications. But before presenting the evidence for Haskell County it is useful to review other hypotheses of the site of origin. Some medical historians and epidemiologists have theorized that the 1918 pandemic began in Asia, citing a lethal outbreak of pulmonary disease in China as the forerunner of the pandemic. Others have speculated the virus was spread by Chinese or Vietnamese laborers either crossing the United States or working in France. More recently, British scientist J.S. Oxford has hypothesized that the 1918 pandemic originated in a British Army post in France, where a disease British physicians called "purulent bronchitis" erupted in 1916. Autopsy reports of soldiers killed by this outbreak – today we would classify the cause of death as ARDS – bear a striking resemblance to those killed by influenza in 1918 [2]. But these alternative hypotheses have problems. After the 1918–1919 pandemic, many investigators searched for the source of the disease. The American Medical Association sponsored what is generally considered the best of several comprehensive international studies of the pandemic conducted by Dr. Edwin Jordan, editor of The Journal of Infectious Disease. He spent years reviewing evidence from all over the world; the AMA published his work in 1927. Since several influenza pandemics in preceding centuries were already well-known and had come from the orient, Jordan first considered Asia as the source. But he found no evidence. Influenza did surface in early 1918 in China, but the outbreaks were minor, did not spread, and contemporary Chinese scientists, trained by Rockefeller Institute for Medical Research (now Rockefeller University) investigators, stated they believed these outbreaks were endemic disease unrelated to the pandemic [3]. Jordan also looked at the lethal pulmonary disease cited by some historians as influenza, but this was diagnosed by contemporary scientists as pneumonic plague. By 1918 the plague bacillus could be easily and conclusively identified in the laboratory [3]. So after tracing all known outbreaks of respiratory disease in China, Jordan concluded that none of them "could be reasonably regarded as the true forerunner" of the pandemic [3]. Jordan also considered Oxford's theory that the "purulent bronchitis" in British Army camps in 1916 and 1917 was the source. He rejected it for several reasons. The disease had flared up, true, but had not spread rapidly or widely outside the affected bases; instead, it seemed to disappear [3]. As we now know a mutation in an existing influenza virus can account for a virulent flare-up. In the summer of 2002, for example, an influenza epidemic erupted in parts of Madagascar with an extremely high mortality and morbidity; in some towns it sickened an outright majority – in one instance sixty-seven percent – of the population. But the virus causing this epidemic was an H3N2 virus that normally caused mild disease. In fact, the epidemic affected only thirteen of 111 health districts in Madagascar before fading away [4]. Something similar may have happened in the British base. Jordan considered other possible origins of the pandemic in early 1918 in France and India. He concluded that it was highly unlikely that the pandemic began in any of them [3]. That left the United States. Jordan looked at a series of spring outbreaks there. The evidence seemed far stronger. One could see influenza jumping from Army camp to camp, then into cities, and traveling with troops to Europe. His conclusion: the United States was the site of origin. A later equally comprehensive, multi-volume British study of the pandemic agreed with Jordan. It too found no evidence for the influenza's origin in the Orient, it too rejected the 1916 outbreak among British troops, and it too concluded, "The disease was probably carried from the United States to Europe [5]." Australian Nobel laureate MacFarlane Burnet spent most of his scientific career working on influenza and studied the pandemic closely. He too concluded that the evidence was "strongly suggestive" that the disease started in the United States and spread with "the arrival of American troops in France [6]." Before dismissing the conclusions of these contemporary investigators who lived through and studied the pandemic, one must remember how good many of them were. They were very good indeed. The Rockefeller Institute, whose investigators were intimately involved in the problem, alone included extraordinary people. By 1912 its head Simon Flexner – his brother wrote the "Flexner report" that revolutionized American medical education – used immune serum to bring the mortality rate for meningococcal meningitis down from over 80% to 18%; by contrast, in the 1990s at Massachusetts General Hospital a study found a 25% mortality rate for bacterial meningitis. Peyton Rous won the Nobel Prize in 1966 for work he did at the institute in 1911; he was that far ahead of the scientific consensus. By 1918 Oswald Avery and others at Rockefeller Institute had already produced both an effective curative serum and a vaccine for the most common pneumococcal pneumonias. At least partly because of the pandemic, Avery would spend the rest of his career studying pneumonia. That work led directly to his discovery of the "transforming principle" – his discovery that DNA carries the genetic code. The observations of investigators of this quality cannot be dismissed lightly. Jordan was of this quality. More evidence against Oxford's hypothesis comes from Dr. Jeffrey Taubenberger, well-known for his work extracting samples of the 1918 virus from preserved tissue and sequencing its genome. He initially believed, based on statistical analysis of the rate of mutation of the virus that it existed for two or three years prior to the pandemic. But further work convinced him that the virus emerged only a few months prior to the pandemic (personal communication with the author from J Taubenberger, June 5th 2003). So if the contemporary observers were correct, if American troops carried the virus to Europe, where in the United States did it begin? Both contemporary epidemiological studies and lay histories of the pandemic have identified the first known outbreak of epidemic influenza as occurring at Camp Funston, now Ft. Riley, in Kansas. But there was one place where a previously unknown – and remarkable – epidemic of influenza occurred. Haskell County, Kansas, lay three hundred miles to the west of Funston. There the smell of manure meant civilization. People raised grains, poultry, cattle, and hogs. Sod-houses were so common that even one of the county's few post offices was located in a dug-out sod home. In 1918 the population was just 1,720, spread over 578 square miles. But primitive and raw as life could be there, science had penetrated the county in the form of Dr. Loring Miner. Enamored of ancient Greece – he periodically reread the classics in Greek – he epitomized William Welch's comment that "the results [of medical education] were better than the system." His son was also a doctor, trained in fully scientific ways, serving in the Navy in Boston. In late January and early February 1918 Miner was suddenly faced with an epidemic of influenza, but an influenza unlike any he had ever seen before. Soon dozens of his patients – the strongest, the healthiest, the most robust people in the county – were being struck down as suddenly as if they had been shot. Then one patient progressed to pneumonia. Then another. And they began to die. The local paper Santa Fe Monitor, apparently worried about hurting morale in wartime, initially said little about the deaths but on inside pages in February reported, "Mrs. Eva Van Alstine is sick with pneumonia. Her little son Roy is now able to get up... Ralph Lindeman is still quite sick... Goldie Wolgehagen is working at the Beeman store during her sister Eva's sickness... Homer Moody has been reported quite sick... Mertin, the young son of Ernest Elliot, is sick with pneumonia... Pete Hesser's children are recovering nicely... Ralph McConnell has been quite sick this week (Santa Fe Monitor, February 14th, 1918)." The epidemic got worse. Then, as abruptly as it came, it disappeared. Men and women returned to work. Children returned to school. And the war regained its hold on people's thoughts. The disease did not, however, slip from Miner's thoughts. Influenza was neither a reportable disease, nor a disease that any state or federal public health agency tracked. Yet Miner considered this incarnation of the disease so dangerous that he warned national public health officials about it. Public Health Reports (now Morbidity and Mortality Weekly Report), a weekly journal produced by the U.S. Public Health Service to alert health officials to outbreaks of communicable diseases throughout the world, published his warning. In the first six months of 1918, this would be the only reference in that journal to influenza anywhere in the world. Historians and epidemiologists have previously ignored Haskell most likely because his report was not published until April and it referred to deaths on March 30, after influenza outbreaks elsewhere. In actuality, by then the county was free of influenza. Haskell County, Kansas, is the first recorded instance anywhere in the world of an outbreak of influenza so unusual that a physician warned public health officials. It remains the first recorded instance suggesting that a new virus was adapting, violently, to man. If the virus did not originate in Haskell, there is no good explanation for how it arrived there. There were no other known outbreaks anywhere in the United States from which someone could have carried the disease to Haskell, and no suggestions of influenza outbreaks in either newspapers or reflected in vital statistics anywhere else in the region. And unlike the 1916 outbreak in France, one can trace with perfect definiteness the route of the virus from Haskell to the outside world. All Army personnel from the county reported to Funston for training. Friends and family visited them at Funston. Soldiers came home on leave, then returned to Funston. The Monitor reported in late February, "Most everybody over the country is having lagrippe or pneumonia (Santa Fe Monitor, February 21st 1918)." It also noted, "Dean Nilson surprised his friends by arriving at home from Camp Funston on a five days furlough. Dean looks like soldier life agrees with him." He soon returned to the camp. Ernest Elliot left to visit his brother at Funston as his child fell ill. On February 28, John Bottom left for Funston. "We predict John will make an ideal soldier," said the paper (Santa Fe Monitor February 28th, 1918). These men, and probably others unnamed by the paper, were exposed to influenza and would have arrived in Funston between February 26 and March 2. On March 4 the first soldier at the camp reported ill with influenza at sick call. The camp held an average of 56,222 troops. Within three weeks more than eleven hundred others were sick enough to require hospitalization, and thousands more – the precise number was not recorded – needed treatment at infirmaries scattered around the base. Whether or not the Haskell virus did spread across the world, the timing of the Funston explosion strongly suggests that the influenza outbreak there did come from Haskell. Meanwhile Funston fed a constant stream of men to other American locations and to Europe, men whose business was killing. They would be more proficient at it than they knew. Soldiers moved uninterrupted between Funston and the outside world, especially to other Army bases and France. On March 18, Camps Forrest and Greenleaf in Georgia saw their first cases of influenza and by the end of April twenty-four of the thirty-six main Army camps suffered an influenza epidemic [3]. Thirty of the fifty largest cities in the country also had an April spike in excess mortality from influenza and pneumonia [7]. Although this spring wave was generally mild – the killing second wave struck in the fall – there were still some disturbing findings. A subsequent Army study said, "At this time the fulminating pneumonia, with wet hemorrhagic lungs, fatal in from 24 to 48 hours, was first observed [8]." (Pathology reports suggest what we now call ARDS.) The first recorded autopsy in Chicago of an influenza victim was conducted in early April. The pathologist noted, "The lungs were full of hemorrhages." He found this unusual enough to ask the then-editor of The Journal of Infectious Diseases "to look over it as a new disease" [3]. By then, influenza was erupting in France, first at Brest, the single largest port of disembarkation for American troops. By then, as MacFarlane Burnet later said, "It is convenient to follow the story of influenza at this period mainly in regard to the army experiences in America and Europe [6]." The fact that the 1918 pandemic likely began in the United States matters because it tells investigators where to look for a new virus. They must look everywhere. In recent years the World Health Organization and local public health authorities have intervened several times when new influenza viruses have infected man. These interventions have prevented the viruses from adapting to man and igniting a new pandemic. But only 83 countries in the world – less than half – participate in WHO's surveillance system (WHO's flunet website http://rhone.b3e.jussieu.fr/flunet/www/docs.html). While some monitoring occurs even in those countries not formally affiliated with WHO's surveillance system, it is hardly adequate. If the virus did cross into man in a sparsely populated region of Kansas, and not in a densely populated region of Asia, then such an animal-to-man cross-over can happen anywhere. And unless WHO gets more resources and political leaders move aggressively on the diplomatic front then a new pandemic really is all too inevitable. reference: Jordan E. Epidemic influenza. First. Chicago: AMA; 1927. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC340389/ ……………….. Let me comment on the above. It is quite plausible; the 1918 swine influenza has long been studied because samples get preserved. As to idolizing Rockefeller Institute, that is not my cup of tea, nor is the added WHO advertisement at the end. Kansas rings a bell for me 2 ways: the just-prior to US Civil War “bleeding Kansas “ scenario about 60 years before the early 1918 outbreak is one item; the other is the cattle roundups to the stockyards at Kansas where cattle were/are loaded on trains for the slaughterhouses of Chicago and often exported by refigerated shipping to Europe. Karmas are involved with mankind certainly. It seems very unlikely to me that East Coast labs would start an influenza in the rural Haskell town that had its own hogs, but whether or not said labs played a role in 1918 would go far past this little contribution above which I think is a bit too simplistic. I do think that Rockefeller (like Gates or WHO or Skull and Bones Order or Fauci) has whitewashers for sure and rather have to go that way, let’s not be naive. -r.; more on Kansas follows: …though Union control of Kansas was never seriously threatened. Bleeding Kansas demonstrated that armed conflict over slavery was unavoidable. Its severity made national headlines, which suggested to the American people that the sectional disputes were unlikely to be resolved without bloodshed, and it therefore acted as a preface to the American Civil War.[6] As abolitionism became increasingly popular in the United States and tensions between its supporters and detractors grew, the U.S. Congress maintained a tenuous balance of political power between Northern and Southern representatives. At the same time, the increasing emigration of Americans to the country's western frontier and the desire to build a transcontinental railroad that would connect the eastern states with California urged incorporation of the western territories into the Union….In May 1854, the Kansas–Nebraska Act created from Indian lands the new territories of Kansas and Nebraska for settlement by U.S. citizens. The Act was proposed by Senator Stephen A. Douglas of Illinois as a way to appease Southern representatives in Congress who had resisted earlier proposals to admit states from the Nebraska Territory because of the Missouri Compromise of 1820, which had explicitly forbidden the practice of slavery in all U.S. territory north of 36°30' latitude and west of the Mississippi River, except in the state of Missouri…. On November 21, 1855, the so-called Wakarusa War began in Douglas County when a pro-slavery settler, Franklin Coleman, shot and killed a Free-Stater, Charles W. Dow, with whom Coleman had long been engaged in a feud that was unrelated to local or national politics. Dow was the first American settler to be murdered in the Kansas Territory. The decision by Douglas County Sheriff Samuel J. Jones to arrest another Free-Stater rather than Coleman and the prisoner's subsequent rescue by a Free-State posse erupted into a conflict that pitted, for the first time, armed pro-slavery settlers against anti-slavery settlers…. following the commencement of the American Civil War in 1861, additional guerrilla violence erupted on the border between Kansas and Missouri and would sporadically continue until the end of the war. https://en.wikipedia.org/wiki/Bleeding_Kansas#cite_note-Etcheson_1-7 ……………………………… One new historical development that has been evolving over a few years and now brought into focus because of COVID-19, is the so-called “Spanish Flu” of 1918. Recurring reports and documentation are emerging to tell us that this ‘Greatest Pandemic in History’ was not [1] “Spanish” [2], not “the flu” and, not a natural occurrence [3] but the result of human tinkering with vaccines. There surely is much more to emerge, but the accumulating evidence to date is too compelling to dismiss. In simple terms, the emerging evidence supports postulations that the 1918 pandemic was caused by a misguided – and very experimental – Rockefeller Institute meningitis vaccination program which was initiated at Fort Riley by the US military and spread to the world from there. This essay will attempt to briefly document the evidence that is available so far. There will, of course, be many objections to the content of this essay not only from the ideologues and trolls but from those in high places with vital body organs requiring protection. First, there was never any justification for associating the 1918 pandemic with Spain. The pathogen did not originate in Spain nor was Spain the hardest hit. The most commonly-accepted “official story” as related by our MSM is that all countries but Spain had initiated severe censorship (due to the war) and thus the facts of the pandemic freely circulated only in the Spanish media, and so it was “natural” to refer to this as the Spanish Flu. From this reasoning, since we all know the US has at least 125% freedom of speech and minus the same degree of censorship, we should rename COVID-19 “The American curse”. (This may yet happen, for other more valid reasons). In any case the documented evidence is increasingly voluminous – and increasingly solid – that this outbreak originated at Fort Riley, Kansas, in the US Conspiracy theorists and historical revisionists cannot change this now. The 1918 pandemic was quite possibly the worst the world had seen, certainly for centuries. It infected about 500 million people and killed at least 50 million worldwide. The current “official narrative” (again) is that it was caused by “an H1N1 virus that originated in birds” (which is not a ‘flu’ in any case), and its only tenuous connection with the US was that it was “first identified in the US in military personnel” in the spring of 1918. These claims appear to be false. In a 2008 report the US NIH admitted that most of the deaths were not from ‘the flu’ nor from any bird virus but from bacterial pneumonia [1]. The details of the studies corroborate this extensively, in which even Dr. Anthony Fauci says, “We agree completely that bacterial pneumonia played a major role in the mortality of the 1918 pandemic.” [2][3][4][5]. In fact, it is now stated that the reason modern medical technology was never able to identify the “killer influenza strain” from this pandemic was that influenza was not the killer. It might be obvious to us today because we know that influenza attacks the young, old and immunocompromised. While the “Spanish Flu” attacked healthy people in their prime – which is what bacterial pneumonia does. Again the official narrative tells us that, due to troop movements because of the war, the pathogen was spread worldwide. But the current emerging thesis is that troop movements might have been irrelevant because the Rockefellers, in their combined haste and hubris, “sent their experimental anti-meningococcal serum to England, France, Belgium, Italy and many other countries. Helping spread the epidemic worldwide.” It certainly appears to be the prime suspect, and we can understand the reluctance of today’s WHO and CDC to reveal this to the popular press. As Dr. Kevin Barry wrote: It would be much more difficult to maintain the marketing mantra of “vaccines save lives” if a vaccine experiment originating in the United States . . . caused the deaths of 50-100 million people. (and) “The American Rockefeller Institute for Medical Research and its experimental bacterial meningococcal vaccine may have killed 50-100 million people in 1918-19” is a far less effective sales slogan. [6] According to the 2008 National Institute of Health paper, bacterial pneumonia was the killer in a minimum of 92.7% of the 1918-19 autopsies reviewed. It is likely higher than 92.7%. The researchers looked at more than 9,000 autopsies, and “there were no negative (bacterial) lung culture results.” “… In the 68 higher-quality autopsy series in which the possibility of unreported negative cultures could be excluded, 92.7% of autopsy lung cultures were positive for ≥1 bacterium. In one study of approximately 9,000 subjects who were followed from the clinical presentation with influenza to resolution or autopsy, researchers obtained, with sterile technique, cultures of either pneumococci or streptococci from 164 of 167 lung tissue samples. “There were 89 pure cultures of pneumococci; 19 cultures from which only streptococci were recovered; 34 that yielded mixtures of pneumococci and/or streptococci; 22 that yielded a mixture of pneumococci, streptococci, and other organisms (prominently pneumococci and non-hemolytic streptococci); and 3 that yielded non-hemolytic streptococci alone. There were no negative lung culture results.” [2] Pneumococci or streptococci were found in “164 of (the) 167 lung tissue samples” autopsied. That is 98.2%. Bacteria was the killer [6]. “The 1918 and 1919 volumes of the Journal of the American Medicine Association include many articles on the cause, prevention, and treatment of influenza. Again and again, investigators wonder at the spotty presence of B. influenzae in the ill, note its presence in healthy individuals, and observe it in other infections such as measles, scarlet fever, diphtheria, and varicella (chickenpox). In one article the authors write, “There seems to be no justification for the belief that the epidemic was due to the influenza bacillus, which is probably a secondary invader and bears about the same relation to the influenza cases as to respiratory infections of a different sort” (Lord 1919). [7] This appears to be where the story begins Following an outbreak of epidemic meningitis at Camp Funston, Kansas, in October and November 1917, a series of antimeningitis vaccinations was undertaken on volunteer subjects from the camp. [8] At that time vaccinations (and perhaps much of medical science generally) were in their infancy, with very much unknown. In particular, Dr. Gates himself [8] notes that prior to this time, “meningococcus vaccines have not been extensively employed for prophylactic immunization, and only a few references are to be found in the literature that relates vaccination experiences.” He further relates that the few referenced cases experienced “very severe” reactions to the vaccines – which were entirely experimental. In this case the Rockefeller Institute, which seems to be where the experiments in opening this special compartment of Pandora’s Box originated, contrived an experimental vaccine and were understandably anxious to “see what happens”. It was apparently a rather crude anti-bacterial vaccine that was made in horses. I haven’t the medical competence to comment on the equine portion, but others more knowledgeable have suggested this might not have been the best method. One enormous advantage of the war to Rockefeller was that the US Army ballooned from little more than 250,000 to 6,000,000 men, with the “Rockefeller Institute for Medical Research” now having an enormous pool of human guinea pigs to conduct vaccine experiments. In a 26-page paper published in July of 1918 by Dr. Fredrick L. Gates, M. D., First Lieutenant, Medical Corps, U. S. Army, writing from the Base Hospital, Fort Riley, Kansas, and The Rockefeller Institute for Medical Research, New York, Dr. Gates outlines the procedure. [8] For the determination of dosage and the study of reactions and antibody formation, six groups of about 50 men each were chosen from the various companies in the regiment. Successive groups received increasing doses of vaccine in a series of three injections at 4 to 10 day intervals. The determination of the dosage of vaccine for subsequent groups followed from the reports of the reactions produced by the given doses. It was considered important to increase the doses gradually in order to locate closely the zone of mild reactions and to avoid unexpectedly severe results. The occurrence of an occasional reaction of greater severity even with the smaller doses, and increasing local tenderness after the injection of the larger doses of vaccine led to the choice of relatively lower doses for the general series throughout the camp rather than the attempt to push the dosage up to the limit of endurance. Later experience fully justified this decision. The preliminary series of vaccinations, therefore, served to establish the method of injection, the proper dosage for extended vaccination, the reactions which might be expected to follow the chosen doses, and the production of immune bodies in the serum of vaccinated men. On the basis of these findings the vaccine was offered to the camp at large. “Heretofore meningococcus vaccines have not been extensively employed for prophylactic immunization, and only a few references are to be found in the literature that relate vaccination experiences.” Those few references listed apparently experienced severe reactions, all of which indicates this was truly an experiment intruding on ground not before traveled. The results were not long in coming “… Fourteen of the largest training camps had reported influenza outbreaks in March, April, or May, and some of the infected troops carried the virus with them aboard ships to France … As soldiers in the trenches became sick, the military evacuated them from the front lines and replaced them with healthy men. This process continuously brought the virus into contact with new hosts – young, healthy soldiers in which it could adapt, reproduce, and become extremely virulent without the danger of burning out. … Before any travel ban could be imposed, a contingent of replacement troops departed Camp Devens (outside of Boston) for Camp Upton, Long Island, the Army’s debarkation point for France, and took influenza with them. Medical officers at Upton said it arrived “abruptly” on September 13, 1918, with 38 hospital admissions, followed by 86 the next day, and 193 the next. Hospital admissions peaked on October 4 with 483, and within 40 days, Camp Upton sent 6,131 men to the hospital for influenza. Some developed pneumonia so quickly that physicians diagnosed it simply by observing the patient rather than listening to the lungs…” [9] I would say here that all indications are that this event was accidental. There may well have been hubris and ‘god-like’ imaginings at the Rockefeller Institute, but I am not in a position to make such accusations. From everything I have seen in researching this subject and, while I cannot speak for Rockefeller, the US military appears to have approached this with sincerity, good intentions, and high hopes of staving off meningitis infections in their troops. I have referenced above the paper by Dr. Gates that was written in 1918, and have studied it repeatedly. From those readings, I recognize no hint of deception or cover-up, no recklessness, no disdain for the lives of the soldiers, and no attempt (as we see with vaccines today) to minimize or discard the dangers of adverse reactions. The entire tone of his paper is one of an intelligent and educated medical officer sincerely documenting the situation of a dangerous pathogen and his efforts to eliminate it. He is careful in his statements, he documents the care in administering minor and increasing doses of the vaccine and monitoring their effects at every stage. From everything I have learned, I could find no fault with the US military in this ‘experiment’, except perhaps the fact that it was an experiment. The faults, disdain, cover-ups, and deception came later. My reading of the aftermath is that both the Rockefeller Institute and the US military (after conducting their thousands of autopsies) fully realized what had happened and, in humanly-understandable terms in the face of the calamity they had inadvertently unleashed, decided the most prudent course was to bury the truth rather than face the recriminations of an already war-weary world. Let’s not forget this pandemic killed more people than did the war itself, by a very large margin. In that situation, what would you do? Can you see the headlines in the NYT and London Times, reading “Whoops!”. I believe that this pandemic became the ‘flu’ and ‘Spanish’ because it disguised both the origin and the pathogen itself, steering the world’s public in the wrong direction and blaming everything on nature. But perhaps after more than 100 years, it is time for the US to show a bit of courage and integrity and tell the truth. There is after all a first time for everything. Additional References – Deaths from Bacterial Pneumonia during 1918–19 Influenza Pandemic. John F. Brundage* and G. Dennis Shanks†. Author affiliations: *Armed Forces Health Surveillance Center, Silver Spring, Maryland, USA; †Australian Army Malaria Institute, Enoggera, Queensland, Australia. https://wwwnc.cdc.gov/eid/article/14/8/07-1313_article – PDF of Fort Riley Study [1918] https://news.fiar.me/2021/01/did-rockefeller-created-the-spanish-flu-pandemic-of-1918-ii/ ……………………