Pandemic Watch, our "best of" the news

[Jenny Lake]

World Death Toll updated June 24 from swine flu:
Mexico -115
U.S.- 87
all other countries combined - 36
Grand Total according to the WHO --238 swine flu deaths

Swine Flu deaths reported from the following countries (excludes US and Mex):
Argentina -7
Australia -2
Canada -15
Chile - 4
Colombia - 2
Costa Rica -1
Dom. Republic -2
Guatemala -1
Philippines -1
UK (Scotland) -1

[veritasvincit]

Jenny,  I'd be interested to know the breakdown of these numbers by age and health and how the mortality rate of this flu differentiates from other any other flu worldwide within the same time frame?

Jenny wrote:
World Death Toll updated June 24 from swine flu:
Mexico -115
U.S.- 87
all other countries combined - 36
Grand Total according to the WHO --238 swine flu deaths

Swine Flu deaths reported from the following countries (excludes US and Mex):
Argentina -7
Australia -2
Canada -15
Chile - 4
Colombia - 2
Costa Rica -1
Dom. Republic -2
Guatemala -1
Philippines -1
UK (Scotland) -1

[CrackSmokeRepublican]

Alan Hall Inverview on the SocioEconomics of Epidemics.

He has an interesting perspective.  Basically, people worrying about their personal economy globally will make them susceptible to infections.


http://www.howestreet.com/audio/alanhall_24062009.mp3

http://www.howestreet.com/audio/0906_RadioInterview.pdf

[Jenny Lake]

SOURCE MATERIAL from the first commercially designated Influenza vaccine experiments:


http://jci.org/articles/view/101633
 
"Protective Effect of Vaccination Against Induced Influenza A"
by Drs. Thomas Francis Jr., Jonas E. Salk, Harold E. Pearson, Philip N. Brown
 
--experiment sponsored by the U.S. Army's Commission on Influenza and "also aided by a grant from the International Health Division of the Rockefeller Foundation."
published July, 1945  (Journal of Clinical Investigation archives, www.jci.org)

This experiment was conducted from December 1942 to May 1943 on 102 male residents of the Ypsilanti, Michigan State Hospital, all from the same ward who worked maintenace day-jobs at the institution and ate, slept, and spent 'day room' activities together. Most of the men were between 30 and 54 years of age.
 
On Dec. 21, 1942, alternate residents of the ward were injected with an experimental flu A & B vaccine made by Sharp and Dohme containing viruses, formalin (formaldehyde) and phenyl mercuric nitrate. The others were injected with a solution of salts, formalin and "preservative" (the same mercuric nitrate? --not specified).
 
On April 21, with 45 individuals who rec'd vaccination and 57 who had rec'd "control material", 17 subjects of the 45 vaccinated were re-vaccinated with the same lot and 21 of the 57 "controls" were given the real initial vaccine. Two weeks later the entire group was exposed to inhaled influenza virus of the 'Baum strain' type A. On the day before virus exposure everyone got a check-up and presumably x-rays ('roentgenograms').
 
In addition to being challenged by x-rays and injections, the inhalation virus used in inducing the flu was procured from an acutely ill patient from a 1940 epidemic that had been attenuated by being "passed through 9 ferrets and 10 series of mice before egg inoculation with viral material used from the third egg passage."
 
The experimenters created this study "for the purpose of determining the value of subcutaneous vaccination with a vaccine of inactivated influenza viruses, Type A and B, against the epidemic form of influenza. The anticipated outbreak of this disease did not occur but the opportunity to test the resistance of certain of the vaccinated individuals to induced infection presented itself...The present report is intended to present the details of the evidence for the protective effect of vaccination against induced influenza A..." [ emphasis mine ]. The results of the 'effectiveness' sought were measured in 'febrile' and antibody response.
 
Quotes:
(p.539)
"since antibody response of human subjects to vaccination varies widely, studies of the antigenic activity of vaccines must be done in large groups of individuals"
 
(p.542)
"vaccinated subjects do not represent a uniform group with regard to vaccination experience, the data do not permit a conclusive statement regarding the relationship between antibody level and resistance."
 
(p.542)
"The fact that antibody rises can occur in the absence of any clinical evidence of infection has been repeatedly noted with the natural disease and with induced infection, but the present data emphasize again that clinical infection does not always evoke measurable changes in concentration of serum antibody."
 
(p.545)
"serological response in a group of individuals previously exposed to inhalation of attenuated active virus has been employed as index of infection...if serological findings, rather than clinical observation are used as index of infection, the evidence is immediately weighted in favor of the vaccinated...As a result of this study of the effectiveness of vaccination against experimentally induced influenza A, it has become apparent that laboratory criteria of infection alone are not sufficient to determine the effectiveness of vaccination..."
 
"Clinical signs of infection with influenza virus may occur with or without serological evidence; the latter set of circumstances is most commonly noted in vaccinated individuals with high antibody titers. Similarly, serological evidence of infection may be obtained with or without obvious clinical signs."
 
(p.540)
"reinoculation of a group of adults who probably have had multiple experiences with influenza viruses did not seem to have a 'booster effect'."
 
(p.538)
"White blood cell counts taken on days following inoculation tended to be lower in comparison with the pre-inoculation level. This trend was not uniform..."
 
(p.545)
..."The reason why there was a relatively large number of persons who responded with febrile reactions in the group vaccinated four-and-one-half months previously cannot be fully explained. It could represent the results of a failure to develop immunity following vaccination or...a decrease of an immunity which originally was developed in response to inoculation..."

[Jenny Lake]

Spanish Flu and Early 20th-Century Expansion of a Coronary Heart Disease–Prone Subpopulation
Maria Inês Reinert Azambuja, MD, PhD
Department of Social Medicine, School of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, RS, 90035-003 – Brazil

S. Ward Casscells, MD, Section Editor and Mohammad Madjid, MD, Section Editor

According to Stephen Jay Gould, "we have a strong preference for seeing trends as entities moving somewhere." However, trends may instead be the product of relative expansions and contractions of different subpopulations constituting the system. Variation in attributes of coronary heart disease cases during the decline in coronary heart disease mortality suggests a change in the primary source-subpopulation of cases over time. It is proposed that an early 20th-century expansion of a coronary heart disease–prone subpopulation, characterized by high serum-cholesterol phenotype and high case-fatality—which contributed to most of the coronary heart disease cases and deaths during the 1960s—may have been a late result of the 1918 influenza pandemic. The same unusual immune response to infection that in 1918 killed preferentially men, whites, and those born from 1880 to 1900 (20–40 years old) may have "primed" survivors of those birth cohorts to late coronary heart disease mortality. Ecologic evidence in favor of a birth cohort and geographic association between both epidemics is presented. Cross-reactive auto-immune response upon reinfection could explain the excess coronary heart disease deaths reported during influenza epidemics from the late 1920s onward. Mimicry between the viral hemagglutinin and the apolipoprotein B or the low-density lipoprotein receptor could be the link between infection and hypercholesterolemia. The extinction of those birth cohorts would result in a relative increase in cases coming from a 2nd subpopulation, which was characterized by insulin resistance and chronic expression of low-grade inflammation markers and was comparatively less vulnerable to die acutely from coronary heart disease.

found at
http://www.pubmedcentral.nih.gov/articl ... d=15061621

[Jenny Lake]

Here's a few words on vaccine-induced infections, especially from FLU vaccines ---note the rate of adverse reactions given as from 5 to 35 percent of patients!! http://ndt.oxfordjournals.org/cgi/reprint/21/2/530.pdf

Adverse reactions to influenza vaccines varies and non-specific systemic side effects have been reported to occur in 5-35% of vaccinated patients [1,2]. Specific adverse reactions to influenza vaccines have also been reported in the past and these include neurological disorders such as Gullian-Barre, peripheral neuropathy and demyelinating disease [3,4]. Muscle syndromes such as myalgias, myositis, and rhabdomyolysis are recognised to not infrequently complicate viral infections, the most common associations being with influenza A and B, cytomegalovirus, adenovirus, Coxsackie virus, Herpes virus and Epstein-Barr virus [5].

rhabdomyolysis "is the rapid breakdown of skeletal muscle tissue...acute, fulminant, potentially fatal..."

[CrackSmokeRepublican]

Here's another one:

Tamiflu-Resistant Swine Flu Virus Found in Hong Kong (Update2)
Share | Email | Print | A A A

By Nipa Piboontanasawat and Jason Gale

July 3 (Bloomberg) -- Tamiflu-resistant swine flu was found in a teenager who hadn't taken Roche Holding AG's best-selling antiviral medicine, Hong Kong's health department said.

The city's Public Health Laboratory Services Branch identified the drug-evading variant during routine surveillance of flu specimens, the department said in a statement today.

This marks the first known case of Tamiflu resistance in a swine flu patient not treated with the drug, which has been stockpiled by governments worldwide to fight pandemic influenza. The specimen was collected from a 16-year-old girl who flew from San Francisco and was intercepted by officials at Hong Kong International Airport on June 11, according to the statement.

"Picking it up in a patient who was not treated is a cause for concern," Malik Peiris, professor of microbiology at Hong Kong University, said in an interview. "One case doesn't change the world, but if we are seeing more and more cases in patients who are not treated, then I think it would be more serious."

The patient, who was admitted to Queen Mary Hospital for isolation, tested positive for the new H1N1 flu strain and opted not to take Tamiflu, Hong Kong's health department said. She had mild symptoms and was discharged upon recovery on June 18.

Denmark, Japan

Basel, Switzerland-based Roche said on June 29 that a swine flu patient treated with Tamiflu in Denmark showed resistance to the drug for the first time. Japan's health ministry reported a case of resistance yesterday in a woman from Osaka who had taken a 10-day course.

Studies have shown that Tamiflu-resistant bugs develop in 0.4 percent to 4 percent of adults and children treated for seasonal influenza, Claudia Schmitt, a spokeswoman at Roche, said by phone from Basel today.

It's likely the few reported cases of drug-resistant swine flu emerged independently, Hong Kong University's Peiris said.

"The key point is whether the strains will become dominant and then we will have a problem," he said. "At this moment, I don't think there is cause for alarm. There is certainly cause for heightened surveillance."

The new H1N1 pandemic virus and a seasonal H1N1 variant are more likely to develop resistance to Tamiflu than other common flu strains, Peiris said. About 95 percent of the H1N1 seasonal flu viruses circulating around the world evade the Roche pill, according to a March 21 World Health Organizationreport.

Glaxo's Relenza

No widespread resistance to GlaxoSmithKline Plc's flu drug Relenza has been reported in seasonal flu, and there have been no reports of resistance in swine flu.

"Constant, random mutation is the survival mechanism of the microbial world," WHO Director-General Margaret Chan said in an address to a meeting on the flu pandemic in Cancun, Mexico, yesterday. "Like all influenza viruses, H1N1 has the advantage of surprise on its side."

Tamiflu and Relenza, an inhaled powder, reduce the severity and the duration of flu symptoms by 24 to 30 hours if treatment is started within the first two days of illness, according to the companies.

Both drugs work by blocking a protein on the surface of influenza particles called neuraminidase, which allows the virus to spread from infected cells to other cells in the body.

Scientists say mutant H1N1 viruses have evolved to evade Tamiflu through a single mutation in the neuraminidase that prevents the medicine from clinging to the viral protein, enabling the pathogen to spread.

The case in Hong Kong indicates that the mutant virus is capable of being transmitted among people, said Jennifer McKimm- Breschkin, a virologist at the Commonwealth Science and Industrial Research Organization in Melbourne.

"It's very disturbing that, fresh into the human population, this one appears now to be able to retain fitness despite having the mutation and to be able to spread," she said in a telephone interview today.

To contact the reporters on this story: Nipa Piboontanasawat in Hong Kong at j.gale@bloomberg.net.
Last Updated: July 3, 2009 07:46 EDT

http://www.bloomberg.com/apps/news?pid= ... GPdD61pf30

[Jenny Lake]

Early abundant medical literature exists about the causes and consequences of infection from online journals such as the Journal of Experimental Medicine (JEM)., though unable to detect and differentiate viruses, infectious bacteria were well studied such as strep, staph, the 'coli' intestinal bacteria, etc.
 
 
 http://jem.rupress.org/cgi/reprint/1/3/559
"A Statistical and Experimental Study of Terminal Infections"
Simon Flexner
 
 
"...certain bacteria appear with such uniformity within certain organs that these must be regarded as presenting better opportunities for their growth than do others. Examples are afforded by the colon bacillus which is so commonly found in the kidneys and the lungs..."
 
"The intestine, as will appear from these statements, is regarded as the portal of entry, not only of many of the bacteria found in the inflamed peritonaeum, but also of some of those present in the pleura, upon the heart valves, and within the organs. This conclusion is based in part upon the behavior of those species which are known to be derived from the intestine, namely the colon group of bacilli. It has been found that these bacteria wander through the intestinal walls with great regularity where lesions of the intestinal mucosa exist. The lesions present here need not for this purpose be considerable, as localized areas of hyperemia and small hemorrhages often suffice to open a way for their escape; in grave lesions such as necroses, ulcerations and tumors, the colon bacilli are found almost without exception in some of the distant viscera..."
 
"The occurrence of the colon bacilli in the organs is frequently unassociated with any lesion...in a few cases, however, they were present so generally in the body and in such large numbers that they could not be disregarded, and in rare instances they were found in association with definite lesions in such a manner as to leave no doubt of their pathogenic character..."
 
"On the other hand, the frequent occurrence of the colon bacillus in combination with pyogenic cocci is a matter of considerable importance...The majority of cases of acute pericarditis and endocarditis are found at the autopsy to be associated with pneumonia, either lobar or lobular."
 
 
From the JEM published in Sept. 1897
http://jem.rupress.org/cgi/content/abstract/2/5/549
 
"...there can be no doubt that the bacillus coli communis at times possesses pathogenic properties, and that by artificial methods of treatment it may often be brought from a condition of benignity to one of virulence."

[Jenny Lake]

On July 3 the WHO designated a global death toll from swine flu at 382. Total cases reported as 89, 921
This does not include additional deaths reported on July 2 in Argentina. The WHO gives 26 deaths in Argentina. Other reports state 43, or 17 additional.
http://www.who.int/csr/don/2009_07_03/en/index.html

On the same day, the British government was announcing its discouragement of "swine flu parties" hoping to dissuade UK mums from exposing their children to the flu at the convenient summer school vacation.
http://news.yahoo.com/s/time/20090703/h ... 9190840700

Dr. Joseph Mercola posted a video from Barbara Loe Fisher from the National Vaccine Information Center
http://articles.mercola.com/sites/artic ... -Soon.aspx

[Jenny Lake]

The US Army tells its flu history:
written by Dr.Thomas Francis Jr. who was developing flu vaccines with his colleagues, all with officer rank and under the "public-private" partnership of the military and civilian sector. Francis was a dean at the University of Michigan School of Public Health which had been newly created in 1941 by a one million dollar grant, split equally, from the Rockefeller Foundation and the W.K. Kellogg Foundtion. Out of 8 major beneficiaries of public funds provided by the army for medical research during WWII, U Michigan was approx. the third largest recipient. Yale was no.1.

The "Influenza Commission" evolved into the Army Epidemiological Board (AEB) and it's major subdivision was called the Commission on Epidemiological Survey. The Epidemiological Survey was the biowarfare branch later installed as the executive administration of Fort Detrick. The AEB changed to reflect the spectrum of the US military service and became the AFEB --the Armed Forces Epidemiological Board-- carrying on its work after the war.

They want you to know that the retrospective correlation between influenza outbreaks and Army manuevers is happenstance and not directly causal.
http://history.amedd.army.mil/booksdocs ... luenza.htm

This history appears to be written in the early post-WWII, Francis' last citations given stem from his own work published in July 1945. Despite a historical flu time-table in conflict with the 'pattern' set forth in this history (large 30 year cycle of major pandemic), the crafted cycle of flu remains as the standard reference. Quoting from the website above:

Influenza after 1918 had reverted to its normal behavior of recurrent epidemics at intervals of a few years, varying in distribution and severity but commonly mild. This increased the tendency to conclude that interpandemic influenza was a different disease and that influenza was in fact a clinical syndrome rather than a disease entity

[Jenny Lake]

The following is an address given by Dr. George K. Hirst (military rank on the AFEB and alumnus of Rockefeller), eminent flu researcher, in October of 1961.
This speech was presented at the University of Glasgow and published in the British Medical Journal May 26, 1962.
"Development of Virology as an Independent Science"
http://www.pubmedcentral.nih.gov/pagere ... id=1958569
 
All [brackets] are mine, selectively condensed below:
 
The opening page (p.1431) gives some history about virus research and discovery of the very first virus, Tobacco Mosaic Virus (TMV) by a Russian in 1892.
 

"The discovery of the infectivity of TMV nucleic acid was followed almost immediately by similar demonstrations with animal viruses and, later, with bacterial agents. This has affirmed the importance of the nucleic acid core as the repository of all the essential information for replication of the total virus. It is also apparent from TMV work that one of the main functions of the [viral] coat is to preserve the core in the extracellular state, and this is probably one of its functions for all viruses. Whether or not all virus coats play the same part in regard to attachment is not entirely clear as yet.
 
The interest in plant viruses continues from the academic standpoint and has extended now so that one phase of TMV work involves the general problem of protein synthesis. The induction of mutants in TMV with nitrous acid was rapidly followed by similar demonstrations with poliomyelitis and Newcastle disease virus, as well as with phage. The academic approach to plant virology has been most fruitful...It requires a very large amount of virus to infect a plant and the reasons for this...are poorly understood.
 
Now let us consider the development of...veterinary and medical virology...[T]he attention of investigators was focused on viruses as agents of disease. The pressure...was for the isolation of new agents...and for efforts to cure or prevent diseases...Relatively little emphasis was placed on the virus particle itself or on virus infection at a cellular level....The discovery of the high susceptibility of ferrets to influenza by a natural route created a wide but transient interest in unusual animals as potential hosts for stubborn viruses. The next step was the widespread use of the chick embryo...the next step, the use of animal cells cultivated in vitro was by far the most important advance...actually the techniques of tissue culture are quite old [and] this source of host material might well have been developed much earlier if virologists had not been so preoccupied with models of the clinical disease.
 
In general, the discovery of new agents was followed by a fairly regular pattern of development: adaptation of the virus to new and convenient hosts, hopefully accompanied by high levels of virus production...clinical diagnostic tests, application of such tests...and finally, the study of disease prevention, which usually took several forms --vaccination with killed virus, vaccination with live but attenuated virus and environmental or vector control....there seemed to be adequate reason for satisfaction with this emphasis because the application of rather empirical methods to public health problems has actually worked very well. Smallpox, urban yellow fever, and poliomyelitis are all good examples of diseases brought under control by these methods.
 
Bacteriophage
 
We turn our attention now to...the discovery of bacterial viruses or bacteriophage. This was due to a British bacteriologist, Twort, who in 1915 described a disease of staphylococci. This paper...passed unnoticed and Twort did not further pursue the matter, possibly because it was wartime. The same reaction was independently discovered by a Canadian, d'Herelle, who was looking for a synergistic action between a virus and a bacterium in dysentery infections...summarized in a book published in 1921 and entitled "Bacteriophage: Its Role in Immunity". At this time the arguments raged over whether bacteriophage was an organism or whether it was something pre-formed in the cell...He had, however, an overwhelming conviction that bacteriophages were powerful therapeutic agents and a large part of his and the general effort in phage research between 1920 and 1930 was spent testing phages against all sorts of diseases...even by this time, very few investigators had made bacteriophage the subject of their life work.
 
A turning point came in 1936 when [Max] Delbruck and [Salvador] Luria, in a joint effort, initiated some phage studies...on what proved to be a rapidly expanding front. The scientists who participated...were physicists, biochemists, cytologists, microbiologists, electron microscopists, and others....The success of this joint effort was immediate...and the approach was so powerful that the disorganized effort in this field was swept away. Before long the influence of phage work extended beyond virology to biology in general, and today is one of the greatest importance as a tool in the study of replication...We left animal virology on the threshold of a new era.
 
Methodology
 
Prior to 1952 the methods of quantitating the infectivity of animal viruses were really very rough, depending by and large on the death or survival of whole animals that had been given widely varying amounts of virus...[A]dvance was made possible by the recent introduction of tissue-culture techniques into virology....It provided a ready and precise way of obtaining pure line clones...[and] the possibility of studying the events of infection at a cellular level devoid of all the complications arising from using a whole animal. Formerly...after inoculation the investigator has little control and no knowledge of what goes on in the animal determining death or survival...IN the new way, the antigen and antibody react in the test-tube...and the assay becomes relatively straightforward and uncomplicated.
 
Phenomenology
 
...The penetration of viruses into cells appears to be one of the most varied functions among the virus groups. The plant cell requires injury, apparently of a special sort, for infection to take place. For bacteriophage to breach the tough bacterial wall a complicated and specialized injection apparatus has developed, the existence of which has given rise to misgivings about the relationship of bacterial to animal viruses...where the problem of animal-virus penetration has been considered at all, some form of phagocytosis or pinocytosis has been proposed...However,recent experiments with poliovirus have suggested that some weakening of the coat may take place outside the cell. Clearly, experiments should be designed to determine the fate of the capsomers with animal-virus penetration.
 
[A] number of experiments with animal viruses in which the occurrence of an eclipse phase was studied...were fairly conclusive with some viruses...[an] assumption that reproduction can proceed from a stripped virus core...with naked viral ribonucleic acid (RNA). Maturation by assembly seems to be a hallmark of virus reproduction...[giving] rise to a phenomenon called "phenotypic mixing", where particles are made up of parts arising from different [virus] parents. This non-specificity of assembly was also discovered with influenza viruses, but the interpretation of the results as being due to phenotypic mixing came directly from phage work.
 
Genetic recombination of viruses in mixedly infected cells provides still another example of a phenomenon worked out with bacteriophage which stimulated similar though necessarily much more restricted research with influenza and vaccinia....In some other areas, such as the changes in cell metabolism brought about by infection, the results with mammalian cells are quite different from those found with infected bacteria...This is not surprising...
 
Latent Infections
 
Perhaps the most important effects of phage research on general virology may occur in the future, and this may be in the area of latent infections....An invading virus becoming an integral part of the host cell genome, a latent virus replicating synchronously with the cell itself, and an invading virus altering the host cell phenotype were all fascinating and unexpected findings which provide a concept of parasite and host as evolutionary partners. The results suggest the possibility of a viral origin of at least a part of the host genome...and at the moment the mechanism of their maintaining a latent condition is completely unknown....
 
Burnet suggested in 1931, on the basis of some experiments in lysogeny, that the lysogenic virus might be an integral part of the host genome, and while this surmise was essentially correct, it required 20 years and the development of bacterial and viral genetics to prove it.
 
Before finishing, I should like to briefly present some work being carried on currently in my laboratory with the collaboration of Dr. Robert W. Simpson...it has not been developed very far and , at the present time, permits no far-reaching conclusions. For the genetic analysis of a species, genetic interaction between two members of the species is required. It was surprising to hear just a short time after the birth of bacterial genetics, that genetic recombination takes place between two phage particles invading the same cell.Shortly thereafter Burnet described influenza recombination. Phage genetics turned bacterial virology into one of the central sciences of modern biology while the influenza story which we are to follow has slowed to an almost imperceptible pace.
 
The basic experiment, which is due to Burnet and his collaborators, consists of crossing two related but antigenically different influenza A strains by putting both into either mouse brain or the allantoic sac [egg] and examining the viral progeny. These two strains may be considered to have M and W as antigenic markers. The W strain was virulent for mice by the intracerebral route while the M strain was not. After mixed infection it was possible to sort out four virus types from the progeny, the two parent viruses and two recombinant types, avirulent W and virulent M....there is no doubt that these results were due to recombination of genetic material between influenza viruses. The main defect of this [experimental] approach was that it could not be made really quantitative, and quantitation has always been an essential part of genetics. After a few years this work was dropped and there have been virtually no publications in this field for the past four or five years.
 
At about this time we began looking for an RNA virus which could be handled quantitatively and was suitable for recombination studies. Newcastle disease virus seemed like a good possibility [but failed]...Poliovirus, which also lends itself well to quantitative work was tried...but progress has been slow. Influenza, as mentioned above, gives readily demonstrable recombination even in crude systems but it has been very difficult to develop quantitative methods...[It] seemed unfortunate that most strains of influenza A either do not kill the cells in monolayers in such a way that plaques can be detected or else the efficiency of plaque formation is so low as to make the technique virtually unusable.
 
Most strains of influenza are rather pneumotropic in the mouse, but a mutant of the original human influenza strain (WS) was isolated many years ago which has the capacity of multiplying in the endothelial cells of the mouse, and as a consequence, it can multiply in the brain where it is lethal. This strain (WSN), inaccurately described as being neurotropic, also produces excellent sharply outlined plaques on chick embryo monolayers and does so with a very high efficiency. As noted before, influenza strains in general either produce poor plaques at low efficiency on this medium or fail to produce plaques at all.
 
[The experiment] method is carried out as follows: The so-called neurotropic plaque-forming strain (WSN --or a recombinant derivative of it) is irradiated by ultra-violet light until very little survives [intact] and it is then used to 'infect' suspended chick fibroblasts along with another active non-plaque-forming (or weak plaque-forming) strain. These cells, which have received at least one of each type of particle are then plated as infective centers on fibroblast monolayers and overlaid with agar. If the suspended cells are infected with either of these two types of virus singly, no plaques will be formed and the controls are therefore negative. After combined infection however, a number of clearly outlined plaques appear. These plaques are readily transmissible in series, and the virus in them is plentiful and plates with high efficiency. In the case of some crosses the new plaques are caused by viruses of the same serotype as the non-plaque-forming parent.
 
Similar experiments have been carried out using a number of influenza A strains, and have been successful in isolating plaque-forming recombinants from a wide variety of them, including old laboratory strains isolated from epidemics in the early 'thirties as well as obtained from Asian influenza [1957]. The actual frequency of recombination is not known and is difficult to determine from this type of approach. All that can be said is that the rate varies enormously with different crosses.... Strains that were very dissimilar antigenically, such as types A and B, gave no recombination.
 
A cross was carried out between a Melbourne strain (isolated in 1934 and converted to a plaque formation by recombination) and the prototype of A2 or Asian influenza (isolated in Japan in 1957). These two strains are quite disparate in a number of respects although both are influenza A....a very high rate of recombination was found....[M]ore surprisingly...these appeared to assort independently...for at least two passages these new characters proved to be stable. From the preliminary results we feel that it may be possible to analyze the genetic system of the influenza A viruses in a systematic manner along classical lines. If so, it will be the first time that a genetic system based solely on inheritence through RNA has been so examined...
this may be only a step in the direction of analyzing other animal viruses which we are not prepared to work with at the present time.....

[Jenny Lake]

From Wikipedia, the free encyclopedia

Salvador Edward Luria
Born August 13, 1912 (1912-08-13)
Turin, Italy
Died February 6, 1991 aged 78 (1991-02-07)
Lexington, Massachusetts
 
 
Salvador Edward Luria (August 13, 1912 – February 6, 1991) was an Italian-born American microbiologist and a Nobel laureate (Nobel Prize in Physiology or Medicine) for his pioneering work with Max Delbrück and Alfred Hershey on phages in molecular biology.
 Biography
Luria was born Salvatore Luria in Turin, Italy to an influential Italian Jewish family. He attended the medical school at the University of Turin studying with Giuseppe Levi. There, he met two other future Nobel laureates: Rita Levi-Montalcini and Renato Dulbecco. He graduated from the University of Turin in 1935. From 1936 to 1937, Luria served his required time in the Italian army as a medical officer. He then took classes in radiology at the University of Rome. Here, he was introduced to Max Delbrück's theories on the gene as a molecule and began to formulate methods for testing genetic theory with the bacteriophages, viruses that infect bacteria.

In 1938, he received a fellowship to study in the United States, where he intended to work with Delbrück. Soon after Luria received the award Benito Mussolini's fascist regime banned Jews from academic research fellowships. Without funding sources for work in the U.S. or Italy, Luria left his home country for Paris, France in 1938. As the Nazi German armies invaded France in 1940, Luria fled on bicycle to Marseilles where he received an immigration visa to the United States.

Phage research
Luria arrived in New York City on September 12, 1940 and soon changed his first and middle names. With the help of physicist Enrico Fermi, whom he knew from his time at the University of Rome, Luria received a Rockefeller Foundation fellowship at Columbia University. He soon met Delbrück and Hershey, and they collaborated on experiments at Cold Spring Harbor Laboratory and in Delbrück's lab at Vanderbilt University.

His famous experiment with Delbrück in 1943, known as the Luria-Delbrück experiment, demonstrated statistically that inheritance in bacteria must follow Darwinian rather than Lamarckian principles and that mutant bacteria occurring randomly can still bestow viral resistance without the virus being present. The idea that natural selection affects bacteria has profound consequences, for example, it explains how bacteria develop antibiotic resistance.

From 1943 to 1950, he worked at Indiana University. His first graduate student was James D. Watson, who went on to discover the structure of DNA with Francis Crick. In January 1947, Luria became a naturalized citizen of the United States.

In 1950, Luria moved to the University of Illinois at Urbana-Champaign. While investigating how a culture of E. coli was able to stop the production of phages, Luria discovered that specific bacterial strains produce enzymes that cut DNA at certain sequences. These enzymes became known as restriction enzymes and developed into one of the main molecular tools in molecular biology.

Later work
In 1959, he became chair of Microbiology at the Massachusetts Institute of Technology (MIT). At MIT, he switched his research focus from phages to cell membranes and bacteriocins.[1] While on sabbatical in 1963 to study at the Institut Pasteur in Paris, he found that bacteriocins impair the function of cell membranes. Returning to MIT, his lab discovered that bacteriocins achieve this impairment by forming holes in the cell membrane, allowing ions to flow through and destroy the electrochemical gradient of cells. In 1972, he became chair of The Center for Cancer Research at MIT. The department he established included future Nobel Prize winners David Baltimore, Susumu Tonegawa, Phillip Allen Sharp and H. Robert Horvitz.

In addition to the Nobel Prize, Luria received a number of awards and recognitions. He was named a member of the National Academy of Sciences in 1960. From 1968 to 1969, he served as president of the American Society for Microbiology. In 1969, he was awarded the Louisa Gross Horwitz Prize from Columbia University together with Max Delbruck co-winner of 1969 Nobel Prize in Physiology or Medicine. He received the National Book Award in 1974 for his popular science book Life: the Unfinished Experiment. He also received National Medal of Science in 1991.

Throughout his career, Luria was an outspoken political advocate. He joined with Linus Pauling in 1957 to protest the nuclear weapon testing. Luria was an opponent of the Vietnam War and a supporter of organized labor. In the 1970s, he was involved in debates over genetic engineering, advocating a compromise position of moderate oversight and regulation rather than the extremes of a complete ban or full scientific freedom. Due to his political involvement, he was blacklisted from receiving funding from the National Institutes of Health for a short time in 1969.

He died in Lexington, Massachusetts of a heart attack.

Fields Molecular biology
Institutions Columbia University
Indiana University
University of Illinois at Urbana-Champaign
Massachusetts Institute of Technology
Alma mater Università degli Studi di Torino
Doctoral students James D. Watson
Notable awards Nobel Prize in Physiology or Medicine

[Jenny Lake]

Max Delbrück
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Max Delbrück


Delbrück in the early 1940s.
Born September 4, 1906(1906-09-04)
Berlin, German Empire
Died March 9, 1981 (aged 74)
 
Fields Biophysicist
Notable awards Nobel laureate
Max Ludwig Henning Delbrück (September 4, 1906 – March 9, 1981) was a German-American biophysicist and Nobel laureate.

Biography
Delbrück was born in Berlin, German Empire. His father was Hans Delbrück, a professor of history at the University of Berlin, and his mother was the granddaughter of Justus von Liebig.

Delbrück studied astrophysics, shifting towards theoretical physics, at the University of Göttingen. After receiving his Ph.D. in 1930, he traveled through England, Denmark, and Switzerland. He met Wolfgang Pauli and Niels Bohr, who got him interested in biology.

Delbrück went back to Berlin in 1932 as an assistant to Lise Meitner, who was collaborating with Otto Hahn on the results of irradiating uranium with neutrons. During this period he wrote a few papers, one of which turned out to be an important contribution on the scattering of gamma rays by a Coulomb field due to polarization of the vacuum produced by that field (1933). His conclusion proved to be theoretically sound but inapplicable to the case in point, but 20 years later Hans Bethe confirmed the phenomenon and named it "Delbrück scattering".[1]

In 1937, he moved to the United States to pursue his interests in biology, taking up research in the Biology Division at Caltech on genetics of the fruit fly Drosophila melanogaster. While at Caltech Delbrück became acquainted with bacteria and their viruses (bacteriophage or 'phage'). In 1939, he co-authored a paper called The Growth of Bacteriophage with E.L. Ellis in which they demonstrated that viruses reproduce in "one step", rather than exponentially as cellular organisms do.

In 1941, he married Mary Bruce, with whom he had four children. Delbrück's brother Justus Delbrück, a lawyer, his sister Emmi Bonhoeffer and his brother-in-law Klaus Bonhoeffer (brother of the theologian, Dietrich Bonhoeffer) were in the German Resistance against the Nazi Regime. Klaus and Dietrich Bonhoeffer were executed in the last days of Hitler's Germany.

 
Plaque in Buttrick Hall, Vanderbilt University to commemorate the centenary of the birth of Max Delbrück, September 4, 2006Delbrück remained in the US during World War II, teaching physics at Vanderbilt University in Nashville while pursuing his genetic research. In 1942, he and Salvador Luria of Indiana University demonstrated that bacterial resistance to virus infection is caused by random mutation and not adaptive change. This research, known as the Luria-Delbrück experiment, was also significant for its use of mathematics to make quantitative predictions for the results to be expected from alternative models. For that work, they were awarded the Nobel Prize in Physiology or Medicine in 1969, sharing it with Alfred Hershey.[2] In the same year together with Salvador Luria he was awarded the Louisa Gross Horwitz Prize from Columbia University.

In 1947, Delbrück returned to Caltech as a professor of biology where he remained until 1977.

From the 1950s on, Delbrück applied biophysical methods to problems in sensory physiology rather than genetics. He also set up the institute for molecular genetics at the University of Cologne.

Delbrück was one of the most influential people in the movement of physical scientists into biology during the 20th century. Delbrück's thinking about the physical basis of life stimulated Erwin Schrödinger to write the highly influential book, What Is Life?[3]. Schrödinger's book was an important influence on Francis Crick, James D. Watson and Maurice Wilkins who won a Nobel prize for the discovery of the DNA double helix[4]. During the 1940s Delbrück developed a course in bacteriophage genetics at the Cold Spring Harbor Laboratory to encourage interest in the field. Delbrück's efforts to promote the "Phage Group" (exploring genetics by way of the viruses that infect bacteria) was important in the early development of molecular biology. On 26-27 August 2007, what would have been his 100th birthday celebration, Cold Spring Harbor Laboratory hosted a meeting of Delbrück's family members and friends to reminisce about the life and work of Delbrück.[5]

[Jenny Lake]

Looking for the toxic 'sensitizer' for the Spanish Flu, I stumbled into a can of worms about nitrogen poisoning and added it to the perspective of "Spanish Flu on the Comeback" as an overlooked cause of influenza.
 
There's alot of veterinary literature on nitrate toxicosis that looks exactly like the horrific version of 1918 flu and is/was a major hazard to livestock, especially cows and pigs. Bacteria in the rumen of these animals converts 'nitrate' (concentated in their feed) to nitrite and hence nitric oxide.
 
Dr. Stefan Lanka has this to say about nitric oxide (http://www.whale.to/a/lanka_h.html) which in very low concentrations controls blood pressure:
"It has to be detoxified by the body immediately because in higher concentrations it acts agressively destroying everything. That's why the macrophages of the immune system release nitric oxide in high quantities in inflammation reactions; to destroy and digest the bacterial cells. So if you take up nitrites...it means you start the self-destroying process in your own body, especially in the lungs. You're destroying your lung tissue, and fungal infections are growing on this dead organic matter....
The first cells to suffer oxygen deficiency are the lining of the epithelium, the smallest vessels, where nitrites are transformed into nitric oxide-- this is the definition of KS, kaposi sarcoma, when the lining of the smallest vessels develops cancerous form, growing bigger and multiplying...."
 
The Merck Veterinary Manual
http://www.merckvetmanual.com/mvm/index ... 212300.htm
among other resources on the subject offers description of the disease process in animals, basically a conversion by bacteria of nitrates to nitrites which is ten times more toxic than nitrates and supplants oxygen uptake by the cells.
"When unconditioned cattle consume plants containing high levels of nitrates, the the nitrate to nitrite conversion exceeds the ability of the rumen microbes to convert nitrites to ammonia. Blood levels of nitrites increase and alter the hemoglobin in blood cells to produce methemoglobin. Unlike hemoglobin, methemoglobin cannot carry oxygen to the tissues of the body.....
Many species are susceptible to nitrate and nitrite poisoning, but cattle are affected most frequently...young pigs also have gastro-intestinal microflora capable of reducing nitrate to nitrite....
...in acute intoxication [from methemoglobin]...incapable of oxygen transport and resulting anoxia...secondary effects of vasodilation on vascular smooth muscle may occur. [blood 'pools' when veins are unable to contract and turns the tissue dark as in cyanosis]. The nitrite ion may also alter metabolic protein enzymes. Ingested nitrates may directly irritate the GI mucosa and produce abdominal pain and diarrhea.
[nitrate toxicosis] although usually acute, the effects...may be subacute or chronic and are reported to include retarded growth, lowered milk production, vitamin A deficiency, goitrogenic effects and increased susceptibility to infection."
 
Signs of nitrate/nitrite poisoning:
--usually appear suddenly due to tissue hypoxia and low blood pressure due to vasodilation.
--muscle tremors, weakness and ataxia; early signs when methemoglobin is 30-40%
--brown, cyanotic mucous membranes develop radiply as methemoglobin exceeds 50%
--dyspnea [irreg. breathing], tachypnea, anxiety, and frequent urination are common
--in some monogastrics, due to non-plant exposures; salivation, vomiting, diarrhea, abdominal pain and gastric hemorrhage
--anoxic convulsions within one hour after a clinical course of 12-24 hours....with a 'recovery' [that may] occur but then develop into interstitial pulmonary emphysema with continued respiratory distress; sudden collapse and death can occur
--sudden death without appearance of illness
 
"Differential diagnoses include poisonings by cyanide, urea, pesticides, toxic gases, chlorides, aniline dyes, aminophenols or pharmaceuticals (i.e. sulfanomides, phenacetin, and acetaminophen) as well as infectious or non-infectious diseases (i.e. grain overload, hypocalcemia, hypomagnesemia, pulmonary adenomatosis, or emphysema)"
_______________________________________________
 
An explanation of the nitrogen disease process in humans is best explained by 'catabolism', the complement of anabolism and is much of what Dr. Lanka is addressing. This is the 'energy system' of cellular metabolism.
 
In my general research and articles, I was interested in highlighting the scope of nitrogen-based products which exploded into use after the Haber-Bosch process (1910) made atmospheric nitrogen extraction a reality. Though requiring immense inputs of industrial power to do so, Haber-Bosch made nitrogen excessively available and cheap by 1913 and was incorporated into commercial use on a wide scale in 1913 by I.G. Farben.
 
I'm working on a (personal) theory that nitrate toxicosis is the orginal source of the swine influenza virus as we know it and that the bacterial 'phage' work showed the way. Nitrites are salts of nitrous acid. The reason this went undiscovered in the 1918 flu, as the Merck vet manual points out, is that nitrate can be 'lost' in plasma or postmortem serum and "must be measured promptly". In live patients methemoglobin can convert back to hemoglobin within 2 hours. Since a viral response is an adaptive measure of the tissue to deal with cell damage, in this case in the gut of nitrogen poisoned swine, an original but mutant 'swine influenza virus' resulted.
 
A previous post about bacterial infection from the intestines (from even imperceptible lesions) made a point that these infections can concentrate in the heart and lungs, noted in autopsies of pnuemonia deaths. Influenza, and the Hemophilus Influenzae bacterium are considered pneumonia and "atypical pneumonia" which is presented in the army records on Spanish Flu. The 'secondary bacterial infection' deaths in cases of swine flu, today and in the past are primarily pneumonia. The harvested mucous from the lungs and resp. tracts of sick animals is the source of the experimental 'influenza virus'.

[Jenny Lake]

A question I posed earlier in this thread about 'polio' as the 'flu'; in 1915 and 1916 polio erupted and led to the largest quarantines known in US history (to my knowledge). The 1916 epidemic in New York City and the response by health officials is still the only one of its kind.
 
There's reason to think that 'nitrate toxicosis' also played a large role in this event. In the profile of this epidemic, it struck hardest at the very young, but included teenagers. NYC would not allow anyone sixteen or under leave the city. On the record this illness is recorded predominantly as 'atypical pneumonia', but the polio component of paralysis is a manifestation of acute toxicity.
 
At the time, the US was stockpiling munitions for the Allies on the Jersey shore side of the Hudson across from Manhattan until the night of July 30-31 when the cache at Black Tom Island was blown sky-high and incinerated to dust. What had previously been a few dozen cases of 'polio' accelerated within 2 weeks to thousands of cases. Child victims of this so-called polio epidemic had their remains turned into 'filtrate' by Simon Flexner of the Rockefeller Institute who created a new disease with it --experimental polio. Flexner had an inner conviction that polio was a respiratory tract infection because the victims came down with 'flu'.
 
Decades went by before poliovirus was affirmed as a disease agent in the 30s (though 'virus' was distinctively absent in polio epidemics), and it was determined to be an intestinal microbe. Poliovirus, they said, enters the bloodstream in the same way that bacteria do, ironically (?) written up by Simon Flexner himself in 1896 as microbes [bacteria] that "wander through the intestinal walls with great regularity". This is evidence that an intestinal 'agent' in humans, carrying human DNA, manifests as the flu, and it was already known that gut bacteria 'cause' pneumonia.
 
How does this fit the profile of Spanish Flu that broke out 2 years later? The historical 'standard tutorial' that I posted previously (on page 3 of this thread) had this to say about the 1918 flu:
"Spanish Flu killed more rapidly than any other form of influenza known up to that time. This particular strain of influenza was especially dangerous to young adults....morbidity changed dramatically and was now highest for the very young, and higher yet for persons between the ages of twenty and forty. The elderly appeared to be spared for the most part".
 
---Here I'll say that the 'standard tutorial' I posted is alot of disinfo from composite versions on flu BUT this statement is a KEY feature of polio! The 1916 polio epidemic affected 3 to 6 year olds in greater proportion, but that was rapidly changing to include older and older persons. Originally, "infantile paralysis" in the 1800s was prevalent among even younger children, infants and toddlers. By 1916, young adults were contracting the disease and by the 1950s the 20-40 demographic was 80% of polio victims. FDR, who had the Spanish Flu as asst. Sec of the Navy in 1918, got polio 3 years later at the age of 39.
The sentence, "and higher yet for persons between the ages of twenty and forty" is deceptively worded and placed,  clearly the meaning is that this group saw the largest increase in flu compared to itself as not normally susceptible to flu. A normal flu does, and did, kill the elderly, but the elderly are not a representative group of victims in polio outbreaks.
 
Spanish Flu appears to be multiple ailments: bacterial pneumonias, nitrate toxicosis and polio.  Viral agents were never found!

[LordLindsey]

Jenny, is NO2 dangerous as well?  I assume that one of the reasons that nitrogen is not good for the body is because it displaces the O2 levels in the blood and tissue, but this is just my guess.  Can you PLEASE elaborate on this and other nitrates' toxicity and WHY these are so terrible for the health of animal/human life?

LINDSEY

NB:  Thank you for your contributions, but I have to tell you that much of it is lost to me because it IS confusing to go through so much information that is COMPLETELY contradictory to what I have been taught, but I am willing to have an open-mind.

[Jenny Lake]

Lindsey, I hope to sort through this, deal with the confusion and present it more cohesively as I go along. I have more to say about nitrogen but a chemistry lesson wasn't what I had in mind because it makes for more confusion --and yes, nitrous oxide (NO2) is also dangerous. Nitrogen compounds readily decompose and recombine under the right circumstances. I'm not an organic chemist, though I have one to consult from time to time.


....and I should add to my previous statement, "normal flu"; "Spanish Flu appears to be multiple ailments: bacterial pneumonias, nitrate toxicosis, polio and 'normal flu'", since the US Army wants us to know that "Influenza after 1918 had reverted to its normal behavior of recurrent epidemics at intervals of a few years...commonly mild."
 
But, not counted here are cases of 'mystery' illness reported in 1918 such as in Switzerland where the word was "plague" --pneumonic plague, credited to the same organism that causes the bubonic version.
 
Its also interesting to note from research that the previous pandemic of influenza in 1889-1892 in the US corresponds to the first New England outbreaks of polio in Vermont, which recurred thereafter in the same manner as flu.
 
George K. Hirst, posted in the thread giving a speech in 1961 (sponsored by Pfizer pharm.) mentions three viruses in his address used by the experimenters:
Newcastle disease virus
poliovirus
and influenza virus
 
and what's Newcastle disease? http://en.wikipedia.org/wiki/Newcastle_disease
"...a highly contagious zoontic bird disease affecting many domestic and wild avian species...also called "avian paramyxovirus"...discovered in Newcastle upon Tyne, England in 1926...exposure of humans to infected birds can cause mild conjunctivitis and influenza-like symptoms...transmission occurs by exposure to fecal/other excretions...
[AND] In 2006 researchers from Hebrew University have succeeded in isolating a variant of the Newcastle Disease Virus (NDV-HUJ) in order to specifically target cancer cells...
Newcastle disease was one of more than a dozen agents that the US researched as potential biological weapons before the nation suspended its biological weapons program."

[CrackSmokeRepublican]

Hi Jenny,
Very interesting. I remembered an old link from my Weightlighting research that may be of interest. I take L-Arginine for Weightlighting but this has got me thinking twice about it and Nitric Oxide.  :shock:
-------------------------------------------------
Stresses of Daily Living and high levels of Nitric Oxide can actually induce mild brain damage according to Dr. Michael Colgan:

http://www.vistamagonline.com/vista_art ... n_-_part_2


Here's another article on Nitric Oxide by Dr. Colgan.

Article by Dr. Michael Colgan ( famous nutritionist ) on Nitric Oxide

-------
I chose this topic as I have been getting a lot of questions about nitric oxide, so I thought everyone might like to know the real chemistry. There are several l-arginine products on the market claiming to raise nitric oxide levels. This is not really something you want to do if you want to preserve your brain. However, taking l-arginine supplements does not dramatically increase nitric oxide, despite the marketing hype, because the body has built-in controls. If it didn't, every time you ate some protein food high in l-arginine, your body's chemistry would be out of control.
Nitric Oxide

Nitric oxide is one of the many gaseous chemicals in the human body, which attest to the old jibe that we are full of hot air. It is manufactured by an enzyme called nitric oxide synthase, which turns the amino acid L-arginine into citrulline and nitric oxide, both of which serve multiple bodily functions. Throughout the brain, nitric oxide is an essential chemical messenger, which improves communication between neurons, release of neurotransmitters, and transmission and storage of information.1,2
Nitric oxide is also a free radical, what is called a reactive nitrogen species (RNS), but is relatively benign.1,3 Like many other biochemicals, however, it can multiply out of control. Then it cooks your brain. It happens like this. Various stressors, such as banging your head against a brick wall, cause certain defensive genes to turn on and cause the brain to manufacture pro-inflammatory gremlins called cytokines. These nasty little beggars stimulate the glial cells to produce large amounts of the inducible form of the enzyme nitric oxide synthase. The enzyme then gobbles up all the spare L-arginine and produces a ton of nitric oxide, which overwhelms other control chemicals and causes raging inflammation. Result: damaged brain cells all around.
If you bang your head ve-r-r-r-y carefully against a brick wall for years on end, as some martial artists do, then, after a while, the defensive genes continue to sleep through it, and no inflammation occurs. So you can take severe blows to the head without much damage. At least that's the theory. Don't try this at home.

By Thought Alone
You don't need a wall or any other blunt object to cause brain damage. A typical brain stressor common to modern urban life, is the automatic fear and anger reaction at a near miss on the freeway. The wise realize they are unhurt, calm down immediately, and move back to the real purpose of life, a state of joyful ease. Those who let their emotions balloon into "road rage", however, irreversibly damage their own brains.
Numerous animal studies show that fearful and angry thoughts readily cause brain damage, by the same process that occurs with the physical damage from banging your head on a wall. In a new study, representative of the evidence, De Cristobal and colleagues at Universidad Complutense, Madrid, restrained rats, but did not physically harm them. The rats went ballistic with fear and rage, and severely damaged their brains by excess production of nitric oxide.4
Being dumb animals, rats could not understand what was going on. Being not quite so dumb, we know that fear and anger do not exist in any object or situation, but are creations of our own consciousness. Thus, in any event where no physical harm occurs, we always have the choice to avoid negative emotions. By now gentle reader you are coming to appreciate, that by lifestyle choices alone, even your choice of thoughts, you can profoundly influence gene expression, and either protect or endanger the physical structure of your brain.

Physical Damage
Air pollution provides a good example of a physical brain stressor just as damaging as a brick wall, yet unfelt and invisible. It is also impossible to avoid in urban life. In a typical recent study by the Toxicology Department of the University of North Carolina, researchers measured the brains of new-born dogs exposed to the air pollution of Mexico City, and compared them with dogs living in an unpolluted area. The dogs living in polluted air, showed large increases in the enzyme nitric oxide synthase, with a consequent cascade of events that damaged neurons throughout the brain. They also showed deposition of plaque and neurofibrillary tangles, and increased apoptosis (cell death), very like those found in Alzheimer's disease.5
Highly polluted cities such as Los Angeles, New York or Toronto produce similar brain damage in everyone who lives there. I have urged readers in previous books to arrange their lives so as to flee the city, to protect their health against cancer and cardiovascular disease. The new discoveries of unavoidable urban sources of brain damage, give you even more reason for doing so.

The Glutamate- Nitric Oxide Link
Fear, anger and air pollution, also damage the mitochondria and reduce the supply of ATP.2,4,5 The protective electric fences around outer cell membranes lose power, and unwanted substances leak into the cell. Particularly opportunistic is the neurotransmitter glutamate, responsible for fast, excitatory neural transmission, just the sort of brain activity that increases in fear and anger situations. Glutamate attacks what is called the n-methyl-d-aspartate (NMDA) receptors on neurons, making a sort of hole through which calcium and other nasties can leak into the cell.2
Calcium is very nasty when it gets into the wrong place, as anyone who has had a heel spur or a calcified artery can attest. In brain cells it converts an enzyme called xanthine dehydrogenase to xanthine oxidase, a process which produces a mass of superoxide free radicals.6,7 Then all hell breaks loose. The excess nitric oxide already being produced by the brain stressor, combines with the superoxide to make the extremely damaging free radical peroxynitrite (0N00-).6,7 Peroxynitrite damages mitochondria, DNA, other proteins in brain cells and any other tissues that get in its way.6,8
Some of these clues come from recent research on the brain damage caused by drugs such as methamphetamine, damage that is very like early Alzheimer's. In a representative study, Imam and colleagues at the US National Center for Toxicological Research, in Jefferson, Arkansas, showed that peroxynitrite is the major culprit.8 With every step of evidence, science is tying the brain damage caused by a wide variety of stressors to the major forms of dementia.

Links To Alzheimer's
Cholinergic neurons in the hippocampus of our basal forebrain, express the neurotransmitter acetylcholine. These cells are more primitive in evolution than cholinergic cells in the cerebral cortex. They evolved in the brains of short-lived, ferocious animals, and are designed for shorter, more violent life than those in the cerebral cortex. They have higher levels of nitric oxide, to speed neural transmission for violent action, and lower levels of endogenous antioxidants, because they did not have to last very long. So they are more vulnerable to damage, and are the first to go in neurodegeneration.
It is exactly these hippocampus structures that show the most damage in Alzheimer's disease, with large numbers of dead and dying cells, amyloid plaque blocking neural transmission, damage to mitochondrial DNA, and useless tangles of neurofibrils.9 In cell culture studies, the amyloid plaque itself causes further release of nitric oxide, thereby creating a vicious and progressive cycle of damage.10 Alzheimer's patients also have increased brain levels of inflammatory cytokines, which as we saw above, increase production of nitric oxide even further.11

Links To Other Dementias   
Similar mechanisms have now been found in multiple sclerosis. Inflammatory cytokines stimulate glial cells to produce nitric oxide by way of the enzyme nitric oxide synthase, which then increases peroxynitrite to cause extensive mitochondrial damage.12 Bagastra and colleagues at Thomas Jefferson University, recently found excess levels of nitric oxide synthase in every one of the brains of deceased multiple sclerosis patients, but in none of the control brains of people who had died without brain disease.13 Induced Parkinson's disease in animals in which the substantia nigra cells are deliberately damaged, shows the same pattern of enzyme activation.14 So does Huntington's disease.15
Stroke patients also show large increases in inflammatory cytokines and nitric oxide synthase, even up to three months after the stroke.16 Cerebral ischemia (restriction of blood supply) is also related to excessive glutamate stimulation of the NMDA receptor, with elevation of intracellular calcium and induction of nitric oxide synthase, which then raises nitric oxide levels.7
There are now hundreds of similar studies in the medical literature. In a major review of the research in October 2000, renowned expert on brain chemistry, Vittorio Calabrese, of the University of Catana in Italy, shows how this process occurs repeatedly with the stresses of usual urban life. He also reviews numerous other studies, showing that damage caused by excess nitric oxide is crucially involved in Alzheimer's, Parkinson's, Lou Gehrig's disease (amyotrophic lateral sclerosis, ALS) Huntington's disease and multiple sclerosis.1 Other researchers have shown that the same process of damage is a major determinant of the dementia caused by stroke, and by other forms of oxygen deprivation of the brain, and of various forms of brain seizure.15,16 Finally, the same process is implicated in common forms of epilepsy.17

Overall, the evidence shows that the brain degeneration caused in almost every one of us by excess nitric oxide, is also a major part of all common dementias, stroke and even epilepsy. I have covered only a fraction of these new discoveries in this short chapter, but I hope it is a representative and convincing fraction. If you fail to protect the brain from excess nitric oxide, then all other efforts to maintain your intelligence will come to naught.

Protecting Yourself from Nitric Oxide
The discovery that excess nitric oxide is a major cause of the brain damage of usual aging, and of all major neurodegenerative diseases, has pharmaceutical companies scrabbling like rats up a curtain, to be first to market with drugs that inhibit nitric oxide synthase, the enzyme that makes nitric oxide in your body. To formulate these drugs, and to prove that they work, researchers have to give animals poisons that damage their brains in similar ways to the damage found in Alzheimer's, Parkinson's and other diseases.
One particular toxin that produces the same brain damage in the substantia nigra, and the same symptom as Parkinson's, is methyl-phenyl-tetrahydropyradine (MPTP). This poison works in two major ways. First, it increases nitric oxide production. Second, it reduces ATP production by the mitochondria, thereby reducing power to the electric fences protecting brain cells and their receptors. The neurotransmitter glutamate then attacks the NMDA receptor, allowing calcium to leak into the cell and produce the superoxide free radical. Superoxide then combines with nitric oxide to make the free radical peroxynitrite. This Satan of free radicals promptly kills large numbers of cells in the substantia nigra, causing irreversible tremor, weakness, and loss of muscle, and eventually dementia.
From numerous animal studies over the last five years, we know that anything which inhibits nitric oxide synthase can stop this whole scenario. In a typical study, baboons were given the nitric oxide synthase inhibitor 7-nitroindazole. When subsequently given the poison MPTP, they were completely protected against cell death in the substantia nigra, and showed no physical symptoms of Parkinson's.18 7-nitroindazole is not yet commercially available, and has some nasty side-effects. But simpler, non-toxic substances work equally well. Genistein, extracted from soybeans, specifically inhibits nitric oxide production.19 Genistein is also neuroprotective in mouse models of Lou Gehrig's disease (amyotrophic lateral sclerosis), and stroke, and in protecting post-menopausal women from Alzhiemer's.20,21
Another inexpensive, non-toxic chemical that strongly inhibits nitric oxide synthase is allicin, extracted from garlic. In the latest study, Schwartz and colleagues at Tel Aviv Sourasky Medical Center in Israel, show that allicin also inhibits the transport of arginine, from which nitric oxide is manufactured. So this simple herbal offers double-whammy brain protection.22
A third non-toxic herbal that regulates nitric oxide levels is ginkgo. In animal experiments, ginkgo effectively prevents the changes in nitric oxide levels caused by induced brain trauma, such as subarachnoid hemorrhage.23 In studies of Alzheimer's patients, gingko stabilizes, and in less severe cases, improves cognitive performance.24
The final herbal I want to include in this chapter is the known liver protective agent Silymarin (milk thistle extract). It does not inhibit nitric oxide production, but can indirectly stop nitric oxide turning into peroxynitrite. Silymarin specifically inhibits production of the enzyme xanthine oxidase which, as a side-effect, produces the superoxide radical, the other half of peroxynitrite.25
One of the so-called smart drugs, aminoguanidine, is also an inhibitor of nitric oxide synthase. This chemical has low toxicity and is now being tried against multiple sclerosis. In the mouse model of multiple sclerosis called, encephalomyelitis, aminoguanidine suppresses nitric oxide production very effectively and reduces the disease.26
Then there is aspirin. For the last 18 years most clients of the Colgan Institute over age 35, have been taking a baby aspirin each day to inhibit platelet aggregation and clot formation, and prevent heart attacks. Little did they know that they are also protecting their brains. Recent animal studies show that small amounts of aspirin, the equivalent in humans of one adult aspirin per day (325 mg), effectively prevent the rise in nitric oxide which occurs in response to fear and anger caused by stressors such as immobilization.4
Another non-toxic substance that inhibits the excess nitric oxide scenario, is the omega-3 fat, docosohexaenoic acid (DHA) in fish oil. This nutrient works by inhibiting release of inflammatory cytokines that trigger nitric oxide production by brain glial cells.27
Thus we have an arsenal of substances with virtually no toxicity which can stop nitric oxide running amok in the brain, genistein, allicin, gingko, silymarin, aminoguanidine, aspirin, and docosohexaenoic acid. Make sure that you only take these in conjunction with a good multiple vitamin and mineral program.
You need to add to these supplements by fleeing the city and its stressors. You also need to program your mind, as detailed in a chapter ahead, to eliminate negative emotions. Follow these steps plus the strategies in previous chapters, and your brain will likely be good for more than a hundred years.
References
1. Calabrese V, et al. NO synthase and NO-dependent signal pathways in brain aging and neurodegenerative disorders: the role of oxidant/antioxidant balance. Neurochem Res, 2000;25:1315-1341.
2. Bashkatova VG, Rayevsky KS. Nitric oxide in mechanisms of brain damage induced by neurotoxic effect of glutamate. Biochemistry, 1998;63:866-873.
3. Iadecola C, Alexander M. Cerebral ischemia and inflammation. Curr Opin Neurol, 2001;14:89-94.
4. De Cristobal J, et al. Aspirin inhibits stress-induced increase in plasma glutamate, brain oxidative damage and ATP fall in rats. Neuroreport, 2002;13:217-221.
5. Calderon-Garciduenas L, et al. Air pollution and brain damage. Toxicol Pathol, 2002;30:373-389.
6. Beckman JS. The double role of nitric oxide in brain function and superoxide mediated injury. J Dev Physiol, 1991;15:53-59.
7. Chan PH, et al. SOD-1 transgenic mice as a model for studies of neuroprotection in stroke and brain trauma. Ann N Y Acad Sci, 1994;738:97-103.
8. Imam SZ, et al. Prevention of dopaminergic neurotoxicity by targeting nitric oxide and peroxynitrite: implications for the prevention of methamphetamine-induced neurotoxic damage. Ann N Y Acad Sci, 2000;914:157-171.
9. Sugaya K. Glial activation and brain aging. Nippon Yakurigaku Zasshi, 2001;118:251-257.
10. Goodwin H, et al. Microglial release of nitric oxide by the synergistic action of beta amyloid and INF-gamma. Brain Res, 1995;692:207-214.
11. Tarkowski E, et al. Intrathecal release of nitric oxide in Alzheimer's disease and vascular dementia. Dement Geriatr Cogn Disord, 2000;11:322-326.
12. Heales SJ, et al. Nitric oxide, mitochondria and neurological disease. Biochim Biophys Acta, 1999;1410:215-228.
13. Bagastra G, et al. Activation of the inducible form of nitric oxide synthase in the brains of patients with multiple sclerosis. Proc Nat Acad Sci, USA, 1995;92:12041-12045.
14. Wu DC, et al. Blockade of microglial activation is neuroprotective in the l-methyl-4-phenyl-1,2,3,6-tetrahydopyridine mouse model of Parkinson disease. J Neurosci, 2002;22:1763-1771.
15. Beal MF. Mitochondria, NO and neurodegeneration. Biochem Soc Symp, 1999;66:43-54.
16. Tarkowski E, et al. Intrathecal release of nitric oxide and its relation to final brain damage in patients with stroke. Cerebrovasc Dis, 2000;10:200-206.
17. Raevskii KS, et al. The role of nitric oxide in brain glutaminergic pathology. Vestn Ross Akad Med Nauk, 2000;(4):11-15.
18. Hantraye P, et al. Inhibition of neuronal nitric oxide synthase prevents MPTP-induced Parkinsonism in baboons. Nat Med, 1996;2:1017-1021.
19. Sheu F, et al. Suppression effect of soy isoflavones on nitric oxide production in RAW 264.7 macrophages. J Agric Food Chem, 2001;49:1767-1772.
20. Trieu VN, Uckun FM. Genistein is neuroprotective in murine models of familial amytrophic lateral sclerosis and stroke. Biochem Biophys Res Commun, 1999;258:685-688.
21. Kim H, et al. Attenuation of neurodegeneration-relevant modifications of brain proteins by dietary soy. Biofactors, 2000;12:243-250.
22. Schwartz IF, et al. Garlic attenuates nitric oxide production in rat cardiac myocytes through inhibition of inducible nitric oxide synthase and the arginine transporter CAT-2 (cationic amino acid transporter-2). Clin Sci, 2002;102:487-493.
23. Sun BL, et al. Effects of Gingko biloba extract on somatosensory evoked potential, nitric oxide levels in serum and brain tissue in rats with cerebral vasospasm after subarachnoid hemorrhage. Clin Hemorheol Microcirc, 2000;23:139-144.
24. Le Bars PH, et al. A placebo-controlled double-blind trial of an extract of gingko biloba for dementia. JAMA, 1997;278:1327-1332.
25. Sheu SY, et al. Inhibition of xanthine oxidase by purpurogallin and silymarin group. Anti-cancer Res, 1998;18:263-267.
26. Cross AH, et al. Aminoquanidine, an inhibitor of inducible nitric oxide synthase ameliorates experimental encephalopathies in SIL Mice. Clin Invest, 1994;93:2684-2690.
27. Perlmutter D. Functional therapies in neurodegenerative disease. J Appl Nutr. 1999;51:3-13.
28. Saito K, Yoshioka H. Protective effect of spin trap agent, N-tert-butyl-alpha-phenylnitrone on hyperoxia-induced oxidative stress and its potential as a nitric oxide donor. Free Rad Res, 2002;36:143-149.

http://forum.bodybuilding.com/showthread.php?t=442330

L-arginine binding to nitric-oxide synthase. The role of H-bonds to the nonreactive guanidinium nitrogens.
Babu BR, Frey C, Griffith OW.

Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.

Nitric-oxide synthase (NOS) catalyzes the oxidation of L-arginine to nitric oxide and L-citrulline. Because overproduction of nitric oxide causes tissue damage in neurological, inflammatory, and autoimmune disorders, design of NOS inhibitors has received much attention. Most inhibitors described to date include a guanidine-like structural motif and interact with the guanidinium region of the L-arginine-binding site. We report here studies with L-arginine analogs having one or both terminal guanidinium nitrogens replaced by functionalities that preserve some, but not all, of the molecular interactions possible for the -NH(2), =NH, or =NH(2)(+) groups of L-arginine. Replacement groups include -NH-alkyl, -alkyl, =O, and =S. Binding of L-canavanine, an analog unable to form hydrogen bonds involving a N(5)-proton, was also examined. From our results and previous work, we infer the orientation of these compounds in the L-arginine-binding site and use IC(50) or K(i) values and optical difference spectra to quantitate their affinity relative to L-arginine. We find that the non-reactive guanidinium nitrogen of L-arginine binds in a pocket that is relatively intolerant of changes in the size or hydrogen bonding properties of the group bound. The individual H-bonds involved are, however, weaker than expected (<2 versus 3-6 kcal). These findings elucidate substrate binding forces in the NOS active site and identify an importan

http://www.ncbi.nlm.nih.gov/pubmed/10464242

[Jenny Lake]

What are the possibilities that a TAB vaccine caused the Spanish Flu?
 
Despite claims in favor of that, I've seen no evidence myself. Anyone know? Why didn't the Spanish flu break out in and after 1911 when the army made the vaccine mandatory?
 
Typhoid Fever and Typhus are two different diseases...the vaccine was for Typhoid. Wikipedia states that "Typhus should not be confused with Typhoid Fever as the diseases are unrelated" here for Typhus--http://en.wikipedia.org/wiki/Rickettsia and here for Typoid Fever-- http://en.wikipedia.org/wiki/Typhoid
...indeed they look unrelated, although some of the signs of both appear as elements in Spanish Flu, neither one of them runs a similar clinical course. Both Typhoid Fever and Typhus have a long clinical course lasting 2-3 weeks. The Spanish Flu was killing people in 12 hours up to 3 days. Polio and nitrogen poisoning can kill people with that kind of speed.
 
Incidentally, the story of 'Typhoid Mary' is interesting. Typhoid fever, an intestinal illness caused by Salmonella typhi, was/is thought to be carried by a percentage of 'healthy' people....Mary Mallon, a household cook-for-hire, spread the disease to 6 households that she worked for before being arrested and incarcerated in hospital quarantine for 3 years on North Brother Island in the East River of NYC....she negotiated a release on the grounds of never cooking for others again, changed her last name, got a job cooking at the Sloane Hospital for Women where she was blamed for infecting 25 more people with Typhoid....her victims at Sloane were nurses and staff. ?? This resulted in her re-incarceration at the island for the rest of her life.
 
Vaccines, however, are not off-the-hook.
 
In Simon Flexner's papers at the American Philosophical Society is a curious entry listing Frederick L. Gates (John D. Rockefeller Sr.'s right-hand-man) as sending Flexner "daily reports of work with meningitis vaccine and case histories for 1918" from Fort Riley Kansas!
http://www.amphilsoc.org/library/mole/f/flexner2.xml
(scroll way down to 'Gates')
The experimental meningitis vaccine created by Flexner is an unrepeatable phenomena, it's said. Note also in this listing an entry marked "postvaccinal encephalitis"
 
Army history from the same link previously posted, by Thomas Francis, Jr. continues:
 
"Influenza then, in the 20 years since 1919, had returned to its former status of recurrent epidemics at short intervals, often so mild as to be unnoticed but with certain episodes of pandemic distribution and of sufficient severity to cause considerable alarm and disturbance in the general population.....Reports based on clinical diagnoses were, as always, unreliable since many factors, including publicity or special instructions, had a large influence in this respect. Army data show this effect clearly...in the lack of reports of influenza from some areas when an epidemic was known to be occurring, or high reports of influenza in prevalences of acute respiratory disease known not to be identifiable as influenza".

[Jenny Lake]

Typhus is caused by one of two types of bacteria: Rickettsia typhi or Rickettsia prowazekii. The form of typus depends on which type of bacteria causes the infection.

Rickettsia typhi causes murine or endemic typhus. Endemic typhus is uncommon in the United States. It is usually seen in areas where hygiene is poor and the temperature is cold. Endemic typhus is sometimes called "jail fever." Lice and fleas of flying squirrels spread the bacteria.

Murine typhus occurs in the southeastern and southern United States, often during the summer and fall. It is rarely deadly. Risk factors for murine typhus include:

Exposure to rat fleas or rat feces
Exposure to other animals (such as cats, opossums, raccoons, skunks, and rats)
Rickettsia prowazekii causes epidemic typhus and Brill-Zinsser disease. Brill-Zinsser disease is a mild form of epidemic typhus. It occurs when the disease re-activates in a person who was previously infected. It is more common in the elderly.

Typhus, found at http://www.umm.edu/ency/article/001363.htm

And hi! CSR, thanks for posting about nitrogen here AND in the 'Health, Diseases, Poisons" thread.
The bad news about nitrogen in the body is that it dramatically increases RADIOSENSITIVTY...part of the unaccounted for effects in Spanish Flu would be medical treatment from X-rays and Radium, which was very widespread and unregulated. I'll try posting some more interesting studies about this.

[Jenny Lake]

George Hirst, in his Pfizer speech, also mentions experiments done by 'Burnet' in 1931 --Frank MacFarlane Burnet-- as well as viruses used. Burnet was born in Victoria Australia, son of (banker father) Frank Burnet and (mother) Hadassah Pollack Mackay.
 
Burnet is notorious for setting up Australia's bioweapons program and is quoted in newspaper clippings from the 40s advising/suggesting his government develop 'intestinal agents' for biowarfare. He wrote a seminal and original work on immunity called "The Production of Antibodies" that later helped earn him a Nobel (1960). In 1931 through 1933, Burnet was a Rockefeller-funded researcher in London specializing in animal viruses. In this time period he isolated 'new' strains of poliovirus and influenza.
Read this essay entitled "Burnet's Solution: the Plan to Poison Southeast Asia"
http://www.theage.com.au/articles/2002/ ... 52044.html
 
The viruses he worked with include vaccinia (cowpox), herpes, polio, influenza, and his own discovery of "Q fever", which he isolated in 1928. Q fever virus was named for him, coxiella burnetii, and is designated as a biowarfare agent by the US.
A story about discovering Q fever describes that "there was a disaster in the country town of Bundeberg in Queensland, when 18 of 21 children who had received injections of a toxin-antitoxin mixture became ill within the next twelve hours and 12 [children] died." The Q infection is 'typhoid-like' determined to be rickettsial (from bacteria that produce 'cocci') and shares a relationship with the 'spotted fever' illnesses....somewhat like Typhus, interestingly enough.
 
Vaccinia Virus is the agent used for smallpox eradication of which the wiki states "The precise origin of vaccinia virus is unknown however, due to the lack of record-keeping as the virus was repeatedly cultivated and passaged in research laboratories....there is also speculation that vaccinia virus was originally isolated from horses".
 
Burnet's contribution to influenza experimentation is perhaps more than any other person:
"Burnet's team unravelled the function of influenza virus neuraminidase and (Gordon) Ada demonstrated that the influenza virus genome was RNA, while Burnet himself concentrated on influenza virus genetics. ...he demonstrated that when cells were mixedly infected with strains with different properties they recombined readily. Indeed, they recombined with such high frequency that other scientists, believing that what happened with bacteriophages must happen with all other viruses, did not believe it. Always ready to speculate, Burnet himself suggested that perhaps the genome of influenza virus 'may fracture and the fragments replicate themselves independently'. Some ten years later it was demonstrated that the influenza virus genome was indeed fragmented and that high frequency recombination was due to reassortment of these fragments..."
 
In 1944 he was offered a Chair at Harvard and in 1957 he published his "clonal selection theory" which help shapes our understanding of immunity:
"Burnet pointed out that this was the first clear recognition that the differentiation of 'self' from 'not-self' was very important in immunology and that, to a large extent, it was developed in birds and mammals during embryonic life....He predicted that an antigen artificially introduced into an immature immune system would lead to the animal believing that the antigen was not foreign".
 
http://www.asap.unimelb.edu.au/bsparcs/ ... burnet.htm
http://www.worldandi.com/public/1988/september/ns6.cfm

[Jenny Lake]

UPDATE

The situation report from the WHO, as of July 6 shows a total death toll standing at 429, accounting the 'spike' in deaths from Argentina.
The link for updates is here:
http://www.who.int/csr/disease/swineflu ... index.html
 
___________________________________________________________________________________
 
April comment on calling this current outbreak 'swine flu'...from within pork industry sources:
 
http://centaur.vri.cz/docs/cnfi/2009-04-28-108.mht
 

So, in summary, the reason that we are calling this virus swine flu is the history and evolution of the virus. It also rests on the fact that some of the genetic analysis indicates that elements from viruses that have traditionally been found in swine populations are incorporated. However since we know nothing of how this particular virus has gotten into the human population but there apparently is no history of swine exposure, it probably makes more sense epidemiologically to refer to this simply as an H1N1 influenza virus.
 
To some extent a similar nomenclatural history has occurred over time with the H5N1 virus becoming known by its viral strain, rather than bird flu. At least with the H5N1 it can most often be traced to exposure to avian species. But in the case of this so called swine flu, there really does appear to be no exposure to swine and some evidence (father, daughter pair in the US) of transmission without exposure to animals. Realistically, however, the name seems to have stuck in the popular media already and the terms swine flu does reflect what we know about the history of some very important H1N1 viruses. Unfortunately, this name will imply a simple, zoonotic transmission between swine and people, when in reality is origin and epidemiology is liking to be much more complex.

_____________
 
I posted this quote above because the media treated it as important to state in the initial reports that novel 'swine flu' victims had no known contact with swine, heightening the perceived fear of a mutant causing 'human to human' transmission, but in this experiment from the 30s (published 1938) it shows how the experimenters prepared a transmissible virus to cross species:

http://www.jem.org/cgi/reprint/67/5/739.pdf

"When....amounts of a culture of Hemophilus Influenzae suis (5) were administered with the human virus, a more prostrating febrile illness, similar to true swine influenza although never so severe, usually resulted."

The researchers were giving human influenza to pigs using bacteria.
 
_____________

The name of "swine influenza" has its origins here. Before being called a flu it was called "hog cholera".

http://www.jem.org/cgi/reprint/54/3/349.pdf

"Swine influenza (hog flu) was first recognized as a clinical entity in the fall of 1918. Because of the prevalence at the same time of human influenza and a marked resemblance in the symptoms of the two diseases, (J.S.)Koen became convinced that they were the same. He therefore gave the name of 'flu' to the new malady of hogs".

"The term 'hog flu' as popularly used, embraces more than one clinical entity...."

"Swine influenza has been established without difficulty by experimental infection of swine with eight separate strains of the disease brought from Iowa...."

"All of the transmission work was conducted at Princeton, New Jersey..." [at the Rockefeller (RIMR)]

[LordLindsey]

http://www.recombinomics.com/News/07130 ... _1918.html

"These data further support the observation that the 90% of the polymorphisms in sequences of all 8 gene segments from the 1918 pandemic strain can be found in a human H1N1 isolate, WSN/33 or a swine H1N1 isolate, A/swine/Iowa/15/1930.  These data support a scenario that mimics the data for 2009, which involves a swine H1N1 moving into a human population and spreading efficiently."

There is ZERO doubt for me that this is it, folks.  Whatever plans you have for when this begins to affect you and/or your family, you had better begin to make them NOW.  You will have to read this a couple of times to understand how important it is, perhaps, but the virus that was extracted from those frozen miners in Alaska and used to create this deadly virus several years ago is what is going to follow the same pattern as its predecesor.  That interview in Youtube form that Daryl has on his site is very good evidence of what I am saying, but just the fact that a "pandemic" has been called when there is seemingly no need is enough for me to know that very big plans are in the works for this to get much worse.

"Commentary

1918 and 2009 H1N1 Similarities Confirm Recombination
Recombinomics Commentary 14:41
July 13, 2009


The new Nature report also assessed the immune response of different groups to the new virus. The most intriguing finding, according to Kawaoka, is that those people exposed to the 1918 virus, all of whom are now in advanced old age, have antibodies that neutralize the H1N1 virus. "The people who have high antibody titers are the people born before 1918," he notes.

The above comments are in association with an upcoming publication in Nature demonstrating that patients born prior to 1918 still have antibodies that not only neutralize the 1918 pandemic virus, but also cross react with the 2009 pandemic swine H1N1.  Similarly, the 2009 pandemic strain replicates more efficiently in the lungs of experiment mice and ferrets, which may explain the frequent deaths of previously healthy young adults.  The targeting of this age group also parallels data from 1918.

These data further support the observation that the 90% of the polymorphisms in sequences of all 8 gene segments from the 1918 pandemic strain can be found in a human H1N1 isolate, WSN/33 or a swine H1N1 isolate, A/swine/Iowa/15/1930.  These data support a scenario that mimics the data for 2009, which involves a swine H1N1 moving into a human population and spreading efficiently.

Data worldwide identify previously healthy young adults dying from the pandemic H1N1 infection.  However, as the swine H1N1 spreads throughout the human population, opportunities for adaption to human host arise via acquisition of human polymorphisms.  Interestingly, many of the new acquisitions of can be found in early H1H1 isolates, raising additional concerns that the 2009 pandemic H1N1 is following a path similar to the evolutionary path of 1918.

A recent isolate from Japan, A/Sapporo/1/2009 has a genetic HA backbone matching the recent oseltamilvir resistant isolate A/Hong Kong/1269/2009, but has acquired a new polymorphism found in WSN/33 as well as an additional polymorphism found in swine/Iowa/15/1930, further supporting evolution along the 1918 pathway.

Thus, the growing list of similarities between 2009 pandemic H1N1 and 1918 pandemic H1N1 continues to cause concern."

LINDSEY

NB:  http://www.youtube.com/watch?v=fA5NSbbu ... r_embedded

http://www.youtube.com/watch?v=U9qV5TrT ... r_embedded

REALLY listen to what is being said and tell me that I am wrong...

[abduLMaria]

i am not surprised at all that there is a similarity between any of the flu strains in the news and the 1918 flue.

USAMRiiD travelled to Norway in the 1990's to dig up graves of 1918 flu casualties.  came home with live samples, retrieved from lung tissue of people who died so long go.

somehow USAMRiiD having these samples does not make me feel any safer.

TO THE CONTRARY.

reported on in 1997 New Yorker Mag.
http://www.geocities.com/abdu1maria/191 ... hunt__.jpg
http://www.geocities.com/abdu1maria/191 ... unt_2_.jpg

USAMRiiD = Zionist Occupied Territory.

[Jenny Lake]

http://drbroxmeyer.netfirms.com/001pdfB ... LISHED.pdf

Camp Devens, Massachusetts Surgical
Ward, 29th September 1918
In 1918, Camp Devens, near Boston was supposed
to have 50,000 men, or did have before the epidemic
broke loose. Starting with a flu-like illness
in what appeared to be grippe or Influenza, soldiers
brought to the hospital seemed to quickly develop
the most viscous type of pneumonia ever recorded.
Two hours after admission mahogany spots appeared
over their cheekbones leading within hours
to a blue cyanosis extending from their ears to
spread all over the face until racial differentiation
was impossible. From that point, it was only a matter
of hours until death came, following the struggle
for air and suffocation. Camp Devens was now
seeing close to 100 such deaths a day, including
an outrageous number of doctors and nurses among
them.

[Jenny Lake]

The quote above is but one small part of a very good essay about 1918 flu. Please read it, I urge you. No one, repeat no one, really knows if such a thing as a 1918 "Influenza virus" existed...it has never been found. The essay addresses a probability that tuberculosis was a statistically significant contributor to Spanish Flu.

Dr. Andrew Noymer and Michel Garenne, UCBerkeley demographers, reported in 2000 convincing statistics showing that undetected tuberculosis may have been the real killer in the 1918 flu epidemic. Aware of recent attempts to isolate the "Influenza Virus" on human cadavers and their specimens, Noymer and Garenne summed that: "Frustratingly, these findings have not answered the question why the 1918 virus was so virulent, noe do they offer an explanation for the unusual age profile of deaths." Bird flu would certainly be diagnosed in the hospital today as Acute Respiratory Distress Syndrom (ARDS). Roger and others favor suspecting tuberculosis in all cases of acute respiratory failure of unknown origin

....so where have the professionals gotten in their understanding of 1918 "virus"?? No further than speculation.

the essay continues:

There is an old adage which rings particularly true for even state of the art science. It reads: "You get what you look for". It is also a trap that no scientist should fall into. Specifically, if you are looking for a viral cause for the lethal Pandemic of 1918 and ignoring any evidence of bacteria....you will not only ignore evidence of bacterial disease in specimens but you will use agents such as phenol which will kill every bacteria that crawls. You will be sure that the 'virus' passes a filter [etc. etc.]...to once and for all nail down your argument. But does that mean in reality what you have seen and labeled a virus is in certainty a virus? Not at all. The fact that tuberculosis killed an estimated 1 billion people by itself between 1850 and 1950, the approximate mid-point of which was the Pandemic, is immaterial....

...by the 1950s the word 'virus' had become so mouldable a concept that one could speak of virus workers without the existence of any concensus whatsoever of what viruses were. Extremely supportive of this mouldability among virologists was Max Delbruck....

Statements coming from pioneer virologist Andre Lwoff in 1957 such as "viruses should be considered as viruses because viruses are viruses" were totally unacceptable. Also under the gun was Thomas M. Rivers, the Father of American Virology....Rivers was wrong....some bacteria could pass through filters that some of the larger viruses could not.

The experimentalists have not met the criteria that biological standards require.....and the media, in this current round, is not meeting the requisite evidence to back up a claim of "previously healthy young adults dying from the pandemic H1N1 infection...

It's the BIG LIE, folks....and they repeat and repeat and on and on "thus the growing list of similarities between 2009 pandemic H1N1 and the 1918 pandemic H1N1 continues to cause concern"

[Jenny Lake]

thanks Nobe, good finds on flu germs!


And what about the viruses, knowing from the present how important they are for genetic transfer--
 
Dr. Lanka explains:

...the first genetic molecule of life was RNA, and only later in evolution did DNA come into existence. Every one of our genomes..is the product of so-called reverse transcription: RNA transcribed into DNA...
 
In the early 1960s they came up with the central dogma of genetics, which tries to uphold even today....this kind of thought came from research funded by the seed-producing industry of the United States, and that a whole body of existing knowledge --namely that of cytogenetics before WWII-- was just suppressed or even slandered.... This kind of  science well established that the genetic material is not stable. It is subject to change, and this means the genetic material is reverse-transcribed. It goes in both directions.
 
...I quickly realized that reverse transcription is common to all forms of life, and in fact is the basis of all higher living. Later I learned that reverse transcription is a repair mechanism for chromosomal DNA....

http://educate-yourself.org/cn/stefanla ... ay09.shtml

suppressed and slandered?...and then, as Hirst points out (1961), the favored type of flu research was "dropped" in the mid-1950s. ?? At this time Dr. Richard E. Shope, hog cholera/flu expert, was in charge of Ft. Detrick's biowar program...

[Jenny Lake]

We KNOW since 'September 11' that the US government is involved in very elaborate and expensive HOAXes that take years and years of planning. Why would this Swine Flu Plan-demic be any different?

"What if you threw a Big Party and nobody came?"...do you think that's going to happen? I've been exploring the Austrian lawsuit filed by Jane Burgermeister and her friends; Dr. Bill Deagle, Dr. True Ott, Dr. Rebecca Carley, Alexander S. Jones, Carmen Reynolds, and various doctors Ridenour, Eisenstein, and others... and will have news about it posted soon on my new blog http://www.jenniferlake.wordpress.com

Jones' interview on "The Awakening" indicates that these 'lawsuit' documents were directed at the "American Patriot Movement". Besides sounding unprofessional about his own profession (computational bioinformatics), Jones's word use is exceptionally reminiscent of September 11th "eyewitnesses" on the streets in New York who volunteered how "fire caused the buildings to collapse"...

[LordLindsey]

So far, Burgemeister is the only person who has gone so far as to get the police and courts involved in what appears to be an orchestrated pandemic, and I commend her for that.  As for the people associated with her, especially Deagle and Ott, I am very leery of that, but it seems that she is accepting help from wherever it comes--which is understandable.

Jenny, why don't you contact her and tell her what you think about all of this?  If she is hanging-out with the wrong people, or if she is wrong in something, your advice would be helpful.  

LINDSEY

[hurensohn]

The only ones who died from the 1918 flu pandemic were the idiots who took the vaccine.