Katz says this is still gong on today: Morgellons come to mind, we cannot be treated by doctors? Was syphilis delusional too?
The study 1932 to 1972, in 1972 the transmembrane protein fluid mosiac model was established.
Was that the outcome of this study, to carry it right into HIV? then The spirochete exactly like the syphilis spirochete could be made? Lymes Disease.......HIV in 70s. that study set the stage for what we are suffereing from. A way to make things like other diseases, but, never to be uncovered.
John Heller John Cutler
who were they and who followed them?
Morgellons folks are treated similarily........is it due to certain genetics? now? Nothing has changed has it? Bad blood? really! the Horror done in Africa and here, and elsewhere is beyond forgiveness.
====================================TODAY, the Cytoskeletal Rearrangement or restructuring.......
Dendritic cells (DC) are key cells of the innate immune system required to prime adaptive immunity. Central DC functions including antigen uptake and presentation and DC migration are critically dependent on dynamic cytoskeletal reorganisation, the regulation of which remains poorly understood. Cytoskeletal studies are complicated by the fact that DC cytoarchitecture is altered considerably by maturation stimuli, including many tools employed for biological manipulation.
Lentiviral vectors, capable of transducing non-dividing cells such as DC, hold promise both for experimental and therapeutic manipulation of DC gene and protein expression but controversy remains about their effect on DC maturation. Here, we have examined the potential of lentiviral vectors as tools for gene delivery to monocyte derived human DC with preservation of immature DC cytoskeletal structure and function. We show that vesicular stomatitis virus G glycoprotein (VSVG)-pseudotyped lentivectors are most efficient at transducing immature DC and their precursor monocytes.
Even Howard Taylor Ricketts talked of this "syphilic virus" Is it related to typhus or rickettsia prow. the origin of human mitochondria? Syphilic roseola?
........ in 1903, Ricketts’ handwritten draft states:
"Recently Metchnikoff and Roux have given a concise statement of their observations which are most interesting and which may be of great importance to furthering the study of syphilis. The ﬁrst chimpanzee was infected with “syphilitic virus.” After 25 days a hard sore developed which Fournier and others were willing to consider of syph- ilitic nature. About a month later about 15 papules [appeared] on various parts of the body and remained until the death of the animal, 14 weeks after the inoculation was made. see page 4 of blastomycosis:
THIS IS INTERESTING THE TWO TOP DOGS>>>>>>>>>>>R AND R........
Rufus Cole in New York City invited Ricketts to consider moving to the Rockefeller Institute, where his work would be better funded. Ricketts turned down that invitation, explaining: There are some features regarding the bacil- lus I have found in spotted fever which will have to be worked out before I would want to leave the subject. Particularly there is the possibility of avirulent strains existing in ticks naturally, which has been suggested by some observations, and which would need to be determined before the bacillus could feel perfectly sure of its ground. I am still inclined to think that typhus should come next after spotted fever, and that was incor- porated in the plan which I presented to the University [of Chicago]. . .It ismy plan to go to Mexico City as soon as things can be arranged after I return from the West. . .
On 11 September 1909, Ricketts wrote to N. Charles Rothschild in England:“I have become interested in the transmission of infections by mosquitos, ﬂeas&c. and contemplate taking up the study of typhus fever on the basis of insect transmission.” By 23 December, Ricketts was hard at work in Mexico, again separated from his family. He explained to his professional mentor and closest conﬁdant Ludwig Hektoen, who was still in Chicago:
"Of course I am rushing into this heels over head because of the manifest success of the transfer of the disease to monkeys by the direct innoculation [sic] of human blood on the part of the government men. As to whether the susceptibility of the monkey is high enough or of the right quality to permit of insect transfer is of course not deﬁnitely known and of course we take chances on this to a certain extent. Shall deal with lice (vestamentorum), ﬂeas and bedbugs and shall try to carry all three along at the same time; incidentally shall try ticks. . ." Handwritten at the bottom of this letter is Ricketts’ ﬁrst suspicion in writing of the ﬁlter- able infectious culprit: “It may be that I have found a faintly staining bipolar bacillus [in the louse] (p. 92), but it is too uncertain to justify much excitement.” On 25 January 1910,Hektoen sent a telegram to Ricketts at the American Club in Mexico City: “McCampbells assistant dead. Typhus. No insect bite. Be careful.” Ricketts answered: We were shocked to hear of the death from typhus of McCampbell’s friend. It is impos- sible to be certain that one is not bitten by a louse, and this does not shake our faith in insect transmission. We shall, of course, be as careful as possible, the chief element of care being in spending as little time as pos- sible in the typhus ward, where the condi- tions are most excellent for the acquisition of lice. . . A few days later, he wrote to Myra: “. . .I think we undoubtedly have transmission by lice. . . Obtained it by the bite of the lice, and also by rubbing into incisions contents of the alimentary canal, or rather of the whole body cavity. . .” Despite the care taken, Ricketts, in his tent in the hospital yard, was close enough to lice to be bitten and on 18 April, only a few days before he was scheduled to return home, he fell ill.
In the American Hospital in Mexico City, Ricketts had been sleeping in a tent erected at his suggestion near the isolation wing. Always the acute observer, he took notes on his progress and thought he had survived the crisis. At the end he succumbed to heart failure, perhaps ag- gravated by the altitude.WhenMyra arrived, he told her that he was so glad that she could take charge. He also said that there was something that he had been longing to tell her. . .but she interrupted him and insisted that he rest. A few minutes later, his heart failed. Myra wondered for the rest of her life—another 40 years—what it was that he wanted to tell her. And she and others often wondered what he would have ac- complished if he had lived. The Legacy of Ricketts The importance of his work on the “bipolar bacilli” puts Ricketts among microbiology’s im- mortals. Rickettsia, named after his death, later proved to be obligate intracellular symbionts found in a wide range of insects. Several distin- guishable morphological and serological types of Rickettsia may coexist within the same ani- mal cell.
Today Rickettsia are known to be close free- living relatives of the mitochondria. These nearly ubiquitous organelles, present in all oxygen- respiring nucleated organisms, including fungi, animals, plants, and most protoctists, resemble avirulent and pathogenic Rickettsia in many Today Rickettsia are known to be close free- living relatives of the mitochondria. These nearly ubiquitous organelles, present in all oxygen- respiring nucleated organisms, including fungi, animals, plants, and most protoctists, resemble avirulent and pathogenic Rickettsia in many etts was always acutely sensitive to all as- pects of the environment in which the disease was detected. Although he would not recognize current terminology and would be bafﬂed by the large number of scientists required to investigate arthropod- bacterial symbionts compared to what he did virtually alone, we conclude that he was one of the ﬁrst, and one of the world’s greatest microbial ecologists.
Figure 7. Schematic diagram of the relationship of HIV-1 coat proteins to extracellular receptors. The close proximity of the putative neurotoxic domain of gp41 to the fusion peptide places it in an ideal position for cell /cell interaction.
Still thinking of the syphilic virus.....................ticks and lice................... ricketts.... mitochondria..........cytoskeletal changes...............coxsackie, lentivirus and pico rna viruses. leishmania virus, wolbachia in lice..........protozoa??? RNAP RNA vector takes over for the tick or lice, yet the tick or lice still eject the virus...........are the co factors symbiotic parasites, like typhus? ricketts? spirochetes?
Mycoplasma of what? mycoplasm fermentans............what is it actually? where is it from?
Leishmaniasis virus, syphilis virus, the pico rna viruses, mycoplasma genetalium, RNA virus, RNA vector in reduvids released in environments of selected areas.
I just found two reduvid bugs, one when I smashed it, had teal colored fluid coming out of it. That is not normal. That is either DNA tagged in the reduvid, for control measures, meaning these are being dropped in areas they do not belong. These are generally found in Mid East, sandfly vectors, or South, Central America, Mexico, and were used to bring leishmaniasis there, as they are doing here.
They will blame on global warming, when these were experiments from universities, not bioweapons. However, military did use them as well. In Africa, loaded with leishmaniasis, connnection to trypansoma. In fact was very thing Darwin suffered from, he let a reduviid type bug bite him, he suffered from skin condition rest of his life. Chagas does that to you, however the combination of RNA vector, leishmaniasis, and trypanasoma is devastating, and if oncho added, we in America are in for some nasty diseases.
They say Morgellons goes back to 60s what were the universities, including Cold Spring Harbor, MIT, UC, UT, MSU, Stanford, especially U of C at Irvine, closed down for a few years to cover the damage? doing at that time? Where did Convergence tech come in?
Those hippie, yippie, preppies and yuppies went where? they were the dot com people, took over San Jose, remember them, same people. Yet, they too are part of the Global Warming Scheme!
That would be the Bill Joy, Kurzweil, Tavistock, those academics who run the wars, they never go to war, but they run them, create the latest tech to use in those wars, but never sacrifice themselves to delivering them, only creating them, then measure the damage or those suffering, just like Tuskegee, they refuse to treat them, because they are still government experiments. No chemtrails needed for this operation, is done geologically, selection of certain areas and release of experiment into environment.
If you change the environment who present 'acquired diseases, parasites, fungi, etc" There is no trail, because the genetically modified bugs, and bacteria and viruses are in a different form. Genetically we accept and produce the new adaptive proteins, by bug bite, by fungal invasion, by pollen invasion. Would you call that a bioweapon? Or Experimental Biology in the new form of Inorganic biology? Or the convergence of Bio/chem/geo/physics?
All universal forms, both animal, insect, human plant...........The universal genes!
Just looking where we dare not go, because evolutionists are behind the decimation of the "selfish gene found non other than in the "junk dna". They only place this extracellular machine could work.
Of course, it doesn't affect our DNA, it just controls it by phosphorylation, methylation and acetylation, the epigenetic manifestations. Yet, they control what the DNA does.
AMP of the new transformed human.
Those falling by the waysides are part of Syndromes that are perpetuated by the HIV or AIDS process, you don't get the nasties, but your immune system goes down, so the new RNA can feed through the back door, thereby giving you either disease or integration of the new RNA which is Artificial Intelligence. You are now part of the machine or you fade away with one of the Syndromes. Aids, Lymes, Alzheimers, or Morgellons..........senesence sets in or integration of artificial takes hold and you get to live for a long time.
Kissing bugs (Family Reduviidae) can be the source of nocturnal dermatologic wounds in the mid to southern latitudes in the United States. The insects are obligate blood feeders and though the bites may be asymptomatic, a variety of dermatologic eruptions or death from anaphylaxis can result. The various dermatologic forms of the bite can be mistaken for herpes zoster, erythema multiforme and the ubiquitous catch-all diagnoses of "spider-bite."
Figure 1 Paratriatoma hirsuta (family Hemiptera) identified by Rick Vetter, UCR Entomology. Collected in the Mojave Desert east of Indio.
In true entomologic terminology, the word "bug" strictly refers only to the large order of insects (Hemiptera) which are characterized by having sucking mouthparts. Most hemipterans are familiar to us as plant feeders (leafhoppers, aphids, stinkbugs), however, the family Reduviidae consists of predatory and parasitic insects, one group of which are obligatory blood-feeders that seek out mammals for their meals. They are known by a variety of colloquial names (kissing bug, cone-nosed bug, Mexican bed bug, etc.) and can be a cause of dermatologic wounds. The assaults are usually nocturnal and reactions are due to salivary proteins. The most common kissing bugs in the United States are in the genus Triatoma with the less common Paratriatoma found in the southwest.
Life cycle and biology There are 16 species and 18 subspecies of Triatoma in the United States, distributed in the southern 2/3 of the country; additional related species and genera are common in Central and South America. The kissing bug is dorso-ventrally flattened and is armed with a long, piercing proboscis. Although its mouthparts are only capable of sucking and there are no opposing structures capable of biting, its feeding wounds are still referred to as bites. Triatoma insects go through 5 molts before reaching maturity. Their typical North American animal hosts include woodrats, opossum, raccoons and armadillos.[2,3] The insects are suspected to also feed off of many domestic pets and the wild animals that are abundant around human habitats. They are most often found in direct association with their animal host; for example, inside the large debris nests of pack rats. However, they are also capable of taking blood meals from humans. Because of their association with wild animal hosts, interactions with humans are more probable in areas that are surrounded by a natural environment in comparison to the disrupted landscaping of urban areas.
Triatoma are predominantly nocturnal and feed off of a sleeping person's exposed human body parts. They will not feed through clothing, although they will feed through large-weave laboratory cloth.[4,5] Typically, they position themselves next to the recumbent human, rather than on top of the host, to feed with the proboscis being the only contacting body part. Subjects describe the bite of Triatoma as virtually painless with a slight tingling sensation.[1,5,6] In laboratory observations, the insects fed for 8 to 15 minutes on humans before repletion and interfeeding duration was typically 3 weeks. However, the insects were able to survive 3 to 6 months between meals. In a large experimental study exposing 464 test subjects to 4 species of Triatoma nymphs and adults, most subjects exhibited no reactions to reduviid feeding with the number of symptomatic subjects being minimal (pruritus 0-4.2%, edema 0-3.2%, erythema 0-6.9%) 0 to 72 hours postbite for the variety of insect species tested. Ryckman attributes this low response to lack of prior exposure of subjects to Triatoma salivary antigens. However, Triatoma can cause severe wounds via exposure to its salivary compounds and death from anaphylaxis is possible. Most sleeping victims are not aware of the insect's presence during feeding, although for the few hypersensitive victims, severe allergic reaction to the insect's salivary secretions is sufficient to awaken them.[4,9]
Human interactions with Triatoma are considered to be incidental encounters and not deliberate infestations as the insects are typically found singularly inside homes and not as multiple intruders. Of definitive diagnostic importance, the engorged culprit is often found when sought; all 45 Texas patients and 95% of 110 California patients were able to recover the offending Triatoma when the home was thoroughly searched.[1,4] The insect often sought shelter in and around bedding or under sofa cushions. This high frequency of detection should readily allow one to confirm or exclude the bite of this reduviid insect.
For most victims, reaction to Triatoma feeding is unremarkable. However, for a minority, significant dermatologic injury occurs. Clinical expression has been divided into 4 categories and is summarized from Shields and Walsh.[1,4] Typically, feeding wounds are multiple (2 to 15 in number), grouped, and most common on hands, arms, feet, head and trunk in that order.
* Papular lesions are similar to insect bites but have non-specific lymphocytic infiltration atypical of insect bite. Grouped lesions are often misdiagnosed as herpes zoster. * Small vesicles surround the bite within 2 to 3 cm, commonly seen on the arms. No definite central puncture mark but wound is erythematous with moderate edema. Concomitant wounds elsewhere on the body can help with the diagnosis. Shields and Walsh list a patient with a hemorrhagic bullous lesion on the thumb who also had small vesicles on the arms. * Large urticarial-type lesions (10 to 16 cm diameter)are also seen. Puncture wound may or may not be visible and in many patients and the lesion is erythematous. Lymphangitis and lymphadenitis may be associated with this type of wound. * The most severe bite reaction exhibits hemorrhagic nodular-to-bullous lesions, typically on the hands and feet. The multiple lesions might be confused with erythema multiforme, however, in Triatoma bite, they are usually unilateral in occurrence. This type of wound is often attributed to the catch-all term, "spider-bite." Lymphangitis and lymphadenitis may be associated with this type of wound also.
In addition, the triatomine bugs of Central and South America are vectors of Chagas' disease (trypanosomiasis) which is caused by the parasitic protozoan Trypanosoma cruzi.[1,10] The mechanism of infection from Chagas' disease is not via feeding but instead through contamination of the wound or other bodily portals by fecal material during or shortly after feeding. Although North American Triatoma species have tested positive for T. cruzi, Chagas' disease is much less of a concern in the U.S. because the North American Triatoma delay defecation until 20-30 minutes post-feeding. By this time, they are usually no longer in contact with the sleeping human.[1,10] Hence, vectoring of the protozoan is much less likely. Although T. cruzi is not difficult to find in both North American triatomine insects and their mammalian hosts (e.g., raccoons, opossums), the incidence of Chagas' disease in humans is extremely low, though in Central and South America, it is of genuine epidemiologic concern. However, North Americans still need to be aware of the disease as infected immigrants enter the country and transmission has also occurred through blood transfusion.
An extensive, annotated bibliography of the medical aspects of triatomine insects has been compiled. [8,12]
A skin biopsy from the new lesions was performed and Leishmania spp was detected by imprint and culture. Hemoculture and PCR using DNA extracted from peripheral mononuclear cells or skin with a set of primers directed towards the minicircle conserved region, were positive. Parasites isolated from the biopsy specimen were submitted to in vitro culture and DNA was extracted. Electrophoresis of parasite enzymes identified L. chagasi as the causative agent.
cutaneous infection of a visitor to Surinam. The infection subsequently produced satellite lesions and symptoms of lymph node involvement but was cured by Pentostam treat- ment. Passage of the isolate through a hamster produced a mucocutaneous infection. There is as yet, however, no correlation between the presence of LR1 and any disease characteristic, host range, or growth characteristic of L. braziliensis guyanensis. The origin of LR1 is also unknown, although it is intriguing that the sandfly, the vector for Leishmania, is also a known vector of RNA viruses.
The initial characterization presented here is insufficient to de- termine whether LR1 belongs to an existing class or consti- tutes an additional class of RNA virus. Perhaps of most significance, however, is the potential for LR1 to serve as a transformation vector for Leishmania and possibly other kinetoplastids. This would aid the molecular biological stud- ies of these parasites immeasurably.
We are talking RNA viruses.............. RNA can vector them in.
This nucleic acid was absent from Trypanosoma brucei and Trypanosoma cruzi (data not shown). The high fluorescent intensity of this nucleic acid in L. braziliensis guyanensis CUMC1-lA relative to its size and the fluorescdhce of the chromosomal DNA in ethidium bromide staited gels indi- cates that it has a high copy number, estimated to be >500 copies per cell, based upon its relatiye fluorescence com- pared to that of the rRNAs. It is degraded by RNase A and alkali but not by DNase (Fig. 2A) showing that it is RNA. It was designated LR1 and examined in greater detail. LR1 is
Leishmania RNA Viruses in Leishmania of the Viannia Subgenus
Mucocutaneous leishmaniasis is caused by infections with intracellular parasites of the Leishmania Viannia subgenus, including Leishmania guyanensis. The pathology develops after parasite dissemination to nasopharyngeal tissues, where destructive metastatic lesions form with chronic inflammation. Currently, the mechanisms involved in lesion development are poorly understood. Here we show that metastasizing parasites have a high Leishmania RNA virus–1 (LRV1) burden that is recognized by the host Toll-like receptor 3 (TLR3) to induce proinflammatory cytokines and chemokines. Paradoxically, these TLR3-mediated immune responses rendered mice more susceptible to infection, and the animals developed an increased footpad swelling and parasitemia. Thus, LRV1 in the metastasizing parasites subverted the host immune response to Leishmania and promoted parasite persistence.
Leishmania protozoan parasites cause a diversity of tropical and subtropical diseases, ranging from disseminated visceral infections to disfiguring facial lesions. Ives et al. found that the Leishmania guyanensis parasites that cause mucocutaneous lesions are themselves infected by viruses, which seem to act as the trigger for pathology. The host’s Toll-like receptors 3 and 7 are activated in virus-infected L. guyanensis infections to promote expression of proinflammatory mediators, and the parasites are then able to persist within the inflammatory cells. The viruses might thus offer a tractable target for diagnostic, drug, or vaccine development for a group of widespread but neglected infections.
A. Ives, C. Ronet, F. Prevel, G. Ruzzante, S. Fuertes-Marraco, F. Schutz, H. Zangger, M. Revaz-Breton, L.-F. Lye, S. M. Hickerson, S. M. Beverley, H. Acha-Orbea, P. Launois, N. Fasel, S. Masina, Leishmania RNA virus controls the severity of mucocutaneous leishmaniasis. Science 331, 775–778 (2011).
Now, we have Morgellon's nose buggers, we have skin issues, we have megacolons, we have not only a protozoan parasite, but we have the virus inside the protozoan parasite, and we most likely have wolbachia associated onco, carrier status. so, this protozoan, plant, insect, bacteria and virus,..... mmmmmm
So, they were working on this in the 60s?....lets see what kind of studies were going on then.
=================well Google kindly gave me this: Principles of Molecular Virology mirror.lib.unair.ac.id/.../Cann_... by C Luciano - Related articles 1950s and 1960s of many viruses and their association with human ...... fied tobacco mosaic virus (TMV) RNA and coat protein were incubated together ...... bacterial genomes (e.g., Mycoplasma). Unlike the genomes of all cells, which are ..... Experiments involving chemical mutagens suffer from a number of drawbacks ..
Novel Approaches to Vaccine Research
Jun 20, 2011 – The L1 protein coat binds to the available receptor. ...... global campaign in the 1960s and 1970s by the World Health Organization (WHO) ...... DNA/Modified vaccinia virus Ankara vaccine expressing recombinant Leishmania ...... The concept arose from experiments designed to observe the effect of ...
Mar 13, 2009 – General Virology Viruses as Human Pathogens 7 8. V Parasitology .... II-inhibiting protein cell-mediated immunity cytomegaly virus (cytomegalovirus) ...... Mycoplasmas. Mycoplasmas are bacteria without rigid cell walls. ...... including for example Leishmania, Toxoplasma, Microspora, Echinococcus, ...
Ah yes............this is even better THE ULTIMATE SUBVERSION!
Muco-cutaneous leishmaniasis in the New World: the ultimate subversion August 23, 2011
Leishmania RNA Virus controls the severity of mucocutaneous leishmaniasis. [/b] "ABSTRACT
Infection by the human protozoan parasite Leishmania can lead, depending primarily on the parasite species, to either cutaneous or mucocutaneous lesions, or fatal generalized visceral infection. In the New World, Leishmania (Viannia) species can cause mucocutaneous leishmaniasis (MCL). Clinical MCL involves a strong hyper-inflammatory response and parasitic dissemination (metastasis) from a primary lesion to distant sites, leading to destructive metastatic secondary lesions especially in the nasopharyngal areas. Recently, we reported that metastasizing, but not nonmetastatic strains of Leishmania (Viannia) guyanensis, have high burden of a non-segmented dsRNA virus, Leishmania RNA Virus (LRV). Viral dsRNA is sensed by the host Toll-like Receptor 3 (TLR3) thereby inducing a pro-inflammatory response and exacerbating the disease. The presence of LRV in Leishmania opens new perspectives not only in basic understanding of the intimate relation between the parasite and LRV, but also in understanding the importance of the inflammatory response in MCL patients. "
LRV...........Leishmaniasis RNA Virus.......... MCL : mucocutaneous leishmaniasis.......Wonder what Old World is Like, this is the NWO disease, don't you think they would keep the theme going? NEW World Leishmaniasis....... yup! Ding Dongs!
~~~~~~~~~~~~~~~ more snippets:
MCL: Morgellon's Cutaneous Leishmaniasis? Bet they use this?
So, the WHO was working on this in 60s. Who are their scientists? Why is Leprosy soled out? And who are the scientists? Who sets standards? Who in the h are they really? Are those world-renown scientists, Nobel Peace Prize winners? Do they work for Wellcome Trust? or Kaiser? or the People of the World, or are the Stadholders, oops, Stakeholders, the ones with the money, WHO run the WHO show? Those scientists must have names!
"The organization relies on the expertise and experience of many world-renowned scientists and professionals to inform its work, such as the WHO Expert Committee on Biological Standardization, the WHO Expert Committee on Leprosy, and the WHO Study Group on Interprofessional Education & Collaborative Practice."
The World Health Organization (WHO) is a specialized agency of the United Nations (UN) that acts as a coordinating authority on international public health. Established on 7 April 1948, with headquarters in Geneva, Switzerland, the agency inherited the mandate and resources of its predecessor, the Health Organization, which was an agency of the League of Nations. It is a member of the United Nations Development Group.
The WHO's constitution states that its objective "is the attainment by all people of the highest possible level of health." The flag features the Rod of Asclepius as a symbol for healing. ==== "The rod of Asclepius (⚕; sometimes also spelled Asklepios or Aesculapius), also known as the asklepian, is an ancient symbol associated with astrology, the Greek god Asclepius, and with medicine and healing. It consists of a serpent entwined around a staff. The name of the symbol derives from its early and widespread association with Asclepius, the son of Apollo, who was a practitioner of medicine in ancient Greek mythology. His attributes, the snake and the staff, sometimes depicted separately in antiquity, are combined in this symbol. Hippocrates himself was a worshipper of Asclepius"......
The ambiguity of the serpent as a symbol, and the contradictions it is thought to represent, reflect the ambiguity of the use of drugs, which can help or harm, as reflected in the meaning of the term pharmakon, which meant "drug", "medicine" and "poison" in ancient Greek. Products deriving from the bodies of snakes were known to have medicinal properties in ancient times, and in ancient Greece, at least some were aware that snake venom that might be fatal if it entered the bloodstream could often be imbibed. Snake venom appears to have been 'prescribed' in some cases as a form of therapy.
Cornutus, a philosopher probably active in the first century CE, in the Theologiae Graecae Compendium (Ch. 33) offers a view of the significance of both snake and staff: “ Asclepius derived his name from healing soothingly and from deferring the withering that comes with death. For this reason, therefore, they give him a serpent as an attribute, indicating that those who avail themselves of medical science undergo a process similar to the serpent in that they, as it were, grow young again after illnesses and slough off old age; also because the serpent is a sign of attention, much of which is required in medical treatments. The staff also seems to be a symbol of some similar thing. For by means of this it is set before our minds that unless we are supported by such inventions as these, in so far as falling continually into sickness is concerned, stumbling along we would fall even sooner than necessary. ”
—Asclepius: A Collection and Interpretation of the Testimonies, Baltimore, 1945
In any case the two symbols certainly merged in antiquity as representations of the snake coiled about the staff are common. It has been claimed that the snake wrapped around the staff was a species of rat snake, Elaphe longissima.
============================================= contin........WHO through all the bs, can find some interesting controversies. ==========
The World Health Organization (WHO) is one of the original agencies of the United Nations, its constitution formally coming into force on the first World Health Day, (7 April 1948), when it was ratified by the 26th member state. Jawaharlal Nehru, a major freedom fighter of India had given an opinion to start WHO. Prior to this its operations, as well as the remaining activities of the League of Nations Health Organization, were under the control of an Interim Commission following an International Health Conference in the summer of 1946. The transfer was authorized by a Resolution of the General Assembly. The epidemiological service of the French Office International d'Hygiène Publique was incorporated into the Interim Commission of the World Health Organization on 1 January 1947.
The organization develops and promotes the use of evidence-based tools, norms and standards to support Member States to inform health policy options. It oversees the implementation of the International Health Regulations, and publishes a series of medical classifications including the International Statistical Classification of Diseases (ICD), the International Classification of Functioning, Disability and Health (ICF), and the International Classification of Health Interventions (ICHI). The WHO regularly publishes a World Health Report including an expert assessment of a specific global health topic. The organization has published tools for monitoring the capacity of national health systems and health workforces to meet primary health care goals. The organization has endorsed the world's first official HIV/AIDS Toolkit for Zimbabwe (from 3 October 2006), making it an international standard.
NOW THIS IS IMPORTANT>>>>>>>>THIS IS WHY PEOPLE IN JAPAN ARE NOT HELPED BY WHO>>>>>>> ESPECIALLY CONCERNING THE Fukushima disaster. They are left to die! Just like Chernobyl! THE WHO is ACTUALLY prevented from assisting them. Somewhat by design wouldn't you say?
IAEA - Agreement WHA 12-40 Demonstration on Chernobyl disaster day near WHO in Geneva
In 1959, the WHO signed Agreement WHA 12-40 with the International Atomic Energy Agency (IAEA), which some have claimed prevents the WHO from independently researching the effects on human health of radiations caused by the use of nuclear power, for examples after nuclear disasters.
The agreement states - specifically in Article 1, Paragraph 2 - that the WHO recognises the IAEA as having responsibility for peaceful nuclear energy without prejudice to the roles of the WHO of promoting health. However, the following paragraph adds: "Whenever either organization proposes to initiate a programme or activity on a subject in which the other organization has or may have a substantial interest, the first party shall consult the other with a view to adjusting the matter by mutual agreement." This last statement, which stresses the requirement for mutual agreement, has led some observers to question whether this effectively jeopardizes the WHO's independence when assessing matters relating to nuclear power.
Intermittent Preventive Therapy
The aggressive support of the Bill & Melinda Gates Foundation for intermittent preventive therapy of malaria which included the commissioning a report from the Institute of Medicine triggered a memo from the former WHO malaria chief Dr. Akira Kochi. Dr. Kochi wrote, “although it was less and less straightforward that the health agency should recommend IPTi, the agency’s objections were met with intense and aggressive opposition from Gates-backed scientists and the foundation”.
Now lets get into the meat of what the WHO does! This may surprise you!
"Progress in international health will require further research involving human subjects, and this may often take place in developing countries. In recent years, human experimentation has been dogged by controversy. Scientists from industrialized countries, where strict ethical standards protect participants in research and help to win public trust, have been accused of using double standards in carrying out research in poorer countries that they would not be permitted to perform at home.
Even as these debates continue in scientific journals and in the popular press, it is worth while to recall that participants in research in the wealthiest countries have not always been afforded such protection. In his essay ‘‘Ethics and clinical research’’ in 1966 (1), Henry K. Beecher identified ethical lapses in research carried out by physician–scientists in renowned universities and published in the world’s leading journals. In this paper, which has rightly been deemed the most influential single paper ever written about experimentation involving human subjects
Beecher demonstrated that poor treatment of human subjects was not confined to the barbaric practices of Nazi doctors that had been documented by the Nuremberg war crimes tribunal after the Second World War. Beecher’s paper prompted a reconsidera- tion of research practices that laid the groundwork for today’s ethical codes and review committees.
In 1936 at the age of 32, four years after graduating from Harvard Medical School, Beecher became anaesthetist-in-chief at Massachusetts Gen- eral Hospital and joined the medical faculty; in 1941 Harvard installed him in the world’s first endowed professorship in anaesthesiology. During his career, he trained over 300 anaesthesiologists, 50 of whom became professors at other medical schools around the world.When Beecher published this paper he had been the world’s foremost figure in anaesthesiology for almost three decades. Beecher made many original scientific contributions in his chosen field, but his research also had broader implications for medical science: he developed a number of tech- niques for the quantitative measurement of clinical responses that researchers had previously viewed as largely subjective, including pain, thirst, nausea, and even mood. He was also a pioneer in recognizing the placebo effect inmedical practice, andwas among the most influential early advocates of the need for double-blind controlled studies to account for this phenomenon in clinical research.
It was towards the end of the 1950s that Beecher became increasingly concerned with the ethical aspects of human experimentation. Historian David Rothman has emphasized that Beecher’s specialty played a role in this orientation, as well as his commitment to high quality research and the fear that unethical research would bring discredit to the scientific enterprise (3). Beecher’s deep Christian faith (he is said to have read a chapter of the Bible every day) may also have encouraged his excursion into research ethics (4). It also seems possible that he harboured some guilt over experiments that had taken place under his supervision; in a 1965 public lecture, he found himself ‘‘obliged to say that, in years gone by, work in my laboratory could have been criticized’’ on ethical grounds (5)
Beecher’s first major publication on research ethics appeared in the Journal of the American Medical Association in 1959 (6), but this extensive scholarly consideration of research ethics did not create much of a professional or public stir. Beecher’s agitation over the widespread moral laxity he perceived among his peers grew to a point where he was no longer satisfied with academic discourse, and he exercised his capacity for drama in the spring of 1965, when he chose to explore the problems and complexities of clinical research before a group of journalists convened by the Upjohn Pharmaceutical Company at the Brook Lodge Conference Center in rural Michigan (5). His speech must have rocked his conservative corporate conference sponsors. ‘‘What seem to be breaches of ethical conduct in experi- mentation’’, he informed his audience, ‘‘are by no means rare, but are almost, one fears, universal.’’ The body of his presentation centred on a review of eighteen examples of clinical research that he deemed unethical. Beecher claimed that these ethical pro- blems were not restricted to remote corners but were found in the nation’s leading medical schools, health centres, military hospitals, and industry.
Several of the nation’s most prominent news- papers soon carried stories written by reporters who had attended the conference; the Boston Globe published a front-page article that was headlined ‘‘Are humans used as guinea pigs not told?’’ Beecher faced harsh and immediate criticism from some of his colleagues who believed that he had violated profes- sional etiquette by airing his concerns in public and that he had incorrectly characterized ethically dubious clinical research as common rather than exceptional. He submitted a revised version of his presentation, with 32 additional examples of ‘‘unethical research’’, to the Journal of the American Medical Association, which rejected it (5). Undaunted, Beecher redirected the manuscript to The New England Journal of Medicine, where, after a few rounds of revision, the paper appeared in 1966 with 22 examples, as reprinted here.
In his expose ´ of clinical experimentation practices, Beecher deliberately did not furnish the names of investigators nor did he provide journal citations to their research. He explained to English physician Maurice Pappworth that he had adopted this policy in order to forestall criminal proceedings against the investigators. Four years earlier, in 1962, Pappworth had sounded his own warning in the British press about clinical experimentation. In 1967 his book Human guinea pigs (7, 8), which harshly criticized clinical research practices in both Britain and the United States, identified researchers by name and provided their institutional affiliations. The less aggressive strategy used by Beecher who, unlike Pappworth, was perceived as a member of the academic and social elite in spite of his humble origins (the son of Henry Unangst, a night watchman and carpenter in Kansas City, Beecher adopted the illustrious surname of a distant relative when he moved to Boston (4)), proved to have greater immediate influence on the conduct of research (9).
Both Beecher’s and Pappworth’s efforts at reforming clinical research reflect the turbulent status of human experimentation in the decades after the development of the Nuremberg Code. In 1964, after years of deliberation and committee discussion, the World Medical Association, an international body representing physicians and researchers from coun- tries around the world, adopted the Declaration of Helsinki which established new rules for human experimentation. This Declaration, in the words of Henry Beecher, offered ‘‘a more broadly useful instrument’’ than the ‘‘rigid set of legalistic demands’’ set out in the Nuremberg Code. The Declaration of Helsinki has been amended five times since its adoption. For the most recent version, ratified in October 2000 in Edinburgh, Scotland, consult www.wma.net/e/policy/17-c_e.html.
Beecher’s 1966 article played a significant role in the implementation of federal rules governing the conduct of human experimentation in the USA, including a clear call for fully informed consent from research subjects. This development ironically did not sit well with Henry Beecher. Although he believed that obtaining consent from research subjects was a worthy and necessary ideal, he expressed scepticism that ‘‘consent in any fully informed sense’’ was obtainable.
Rather than formal rules for human experimentation, Beecher argued that the presence of an intelligent, informed, conscientious, compassionate, and responsible in- vestigator offered the best protection for human research subjects. For the same reason, Beecher was not an advocate of the mechanism of the ethical review committee, now a fixture in health research. The publications of Beecher and Pappworth did not resolve all controversies in research ethics, as the periodic revisions of the Declaration of Helsinki and national regulations demonstrate. But they did prompt the public and the health professions to recognize that questionable research practices could be carried out, and even rewarded, in advanced, democratic states, and that careful attention to ethics should be part of every scientist’s approach to research. n
References 1. Beecher HK. Ethics and clinical research. The New England Journal of Medicine, 1966, 274: 1354–1360. 2. Moreno J. Undue risk: secret state experiments on humans. New York, WH Freeman, 1999: 242. 3. Rothman R. Strangers at the bedside: a history of how law and bioethics transformed medical decision making. New York, Basic Books, 1991. 4. Harkness J. Henry Beecher. In: Garraty JA, Carnes MC, eds. American national biography, vol. 2. New York, Oxford University Press, 1999: 465–467. 5. BeecherHK. Ethics and the explosion of human experimentation. 1965. In the Beecher papers, Francis A. Countway Library of Medicine, Harvard University. 6. Beecher HK. Experimentation in man. Journal of the American Medical Association, 1959, 169 (5): 461–478. 7. Pappworth M. Human guinea pigs: experimentation on man. London, Routledge & Kegan Paul, 1967. 8. PappworthMH. Human guinea pigs—a history. BritishMedical Journal, 1990, 301: 1456–1460. 9. Edelson P. Henry K. Beecher and Maurice Pappworth: informed consent in human experimentation and the physician’s response. In: Doyal L, Tobias JS, eds. Informed consent in medical research. London, BMJ Books, 2000.
These are the ones that may lead to Morgellons.......issues........not nec bioweapons, but biologicial agents used in human experiments, unrelated to war.
Ugly past of U.S. human experiments uncovered Tests included exposing mental patients, prisoners to infectious diseases
ATLANTA — Shocking as it may seem, U.S. government doctors once thought it was fine to experiment on disabled people and prison inmates. Such experiments included giving hepatitis to mental patients in Connecticut, squirting a pandemic flu virus up the noses of prisoners in Maryland, and injecting cancer cells into chronically ill people at a New York hospital.
Much of this horrific history is 40 to 80 years old, but it is the backdrop for a meeting in Washington this week by a presidential bioethics commission. The meeting was triggered by the government's apology last fall for federal doctors infecting prisoners and mental patients in Guatemala with syphilis 65 years ago.
U.S. officials also acknowledged there had been dozens of similar experiments in the United States — studies that often involved making healthy people sick.
An exhaustive review by The Associated Press of medical journal reports and decades-old press clippings found more than 40 such studies. At best, these were a search for lifesaving treatments; at worst, some amounted to curiosity-satisfying experiments that hurt people but provided no useful results.
Inevitably, they will be compared to the well-known Tuskegee syphilis study. In that episode, U.S. health officials tracked 600 black men in Alabama who already had syphilis but didn't give them adequate treatment even after penicillin became available.
These studies were worse in at least one respect — they violated the concept of "first do no harm," a fundamental medical principle that stretches back centuries.
"When you give somebody a disease — even by the standards of their time — you really cross the key ethical norm of the profession," said Arthur Caplan, director of the University of Pennsylvania's Center for Bioethics.
Attitude similar to Nazi experiments Some of these studies, mostly from the 1940s to the '60s, apparently were never covered by news media. Others were reported at the time, but the focus was on the promise of enduring new cures, while glossing over how test subjects were treated.
Attitudes about medical research were different then. Infectious diseases killed many more people years ago, and doctors worked urgently to invent and test cures. Many prominent researchers felt it was legitimate to experiment on people who did not have full rights in society — people like prisoners, mental patients, poor blacks. It was an attitude in some ways similar to that of Nazi doctors experimenting on Jews.
"There was definitely a sense — that we don't have today — that sacrifice for the nation was important," said Laura Stark, a Wesleyan University assistant professor of science in society, who is writing a book about past federal medical experiments.
The AP review of past research found:
* A federally funded study begun in 1942 injected experimental flu vaccine in male patients at a state insane asylum in Ypsilanti, Mich., then exposed them to flu several months later. It was co-authored by Dr. Jonas Salk, who a decade later would become famous as inventor of the polio vaccine.
Some of the men weren't able to describe their symptoms, raising serious questions about how well they understood what was being done to them. One newspaper account mentioned the test subjects were "senile and debilitated." Then it quickly moved on to the promising results.
* In federally funded studies in the 1940s, noted researcher Dr. W. Paul Havens Jr. exposed men to hepatitis in a series of experiments, including one using patients from mental institutions in Middletown and Norwich, Conn. Havens, a World Health Organization expert on viral diseases, was one of the first scientists to differentiate types of hepatitis and their causes.
A search of various news archives found no mention of the mental patients study, which made eight healthy men ill but broke no new ground in understanding the disease.
* Researchers in the mid-1940s studied the transmission of a deadly stomach bug by having young men swallow unfiltered stool suspension. The study was conducted at the New York State Vocational Institution, a reformatory prison in West Coxsackie. The point was to see how well the disease spread that way as compared to spraying the germs and having test subjects breathe it. Swallowing it was a more effective way to spread the disease, the researchers concluded. The study doesn't explain if the men were rewarded for this awful task. * A University of Minnesota study in the late 1940s injected 11 public service employee volunteers with malaria, then starved them for five days. Some were also subjected to hard labor, and those men lost an average of 14 pounds. They were treated for malarial fevers with quinine sulfate. One of the authors was Ancel Keys, a noted dietary scientist who developed K-rations for the military and the Mediterranean diet for the public. But a search of various news archives found no mention of the study. * For a study in 1957, when the Asian flu pandemic was spreading, federal researchers sprayed the virus in the noses of 23 inmates at Patuxent prison in Jessup, Md., to compare their reactions to those of 32 virus-exposed inmates who had been given a new vaccine. * Government researchers in the 1950s tried to infect about two dozen volunteering prison inmates with gonorrhea using two different methods in an experiment at a federal penitentiary in Atlanta. The bacteria was pumped directly into the urinary tract through the flipper, according to their paper.
The men quickly developed the disease, but the researchers noted this method wasn't comparable to how men normally got infected — by having sex with an infected partner. The men were later treated with antibiotics. The study was published in the Journal of the American Medical Association, but there was no mention of it in various news archives.
Though people in the studies were usually described as volunteers, historians and ethicists have questioned how well these people understood what was to be done to them and why, or whether they were coerced. Victims for science Prisoners have long been victimized for the sake of science. In 1915, the U.S. government's Dr. Joseph Goldberger — today remembered as a public health hero — recruited Mississippi inmates to go on special rations to prove his theory that the painful illness pellagra was caused by a dietary deficiency. (The men were offered pardons for their participation.)
But studies using prisoners were uncommon in the first few decades of the 20th century, and usually performed by researchers considered eccentric even by the standards of the day. One was Dr. L.L. Stanley, resident physician at San Quentin prison in California, who around 1920 attempted to treat older, "devitalized men" by implanting in them testicles from livestock and from recently executed convicts. Newspapers wrote about Stanley's experiments, but the lack of outrage is striking. "Enter San Quentin penitentiary in the role of the Fountain of Youth — an institution where the years are made to roll back for men of failing mentality and vitality and where the spring is restored to the step, wit to the brain, vigor to the muscles and ambition to the spirit. All this has been done, is being done ... by a surgeon with a scalpel," began one rosy report published in November 1919 in The Washington Post. Story: Doctors order tests to fend off lawsuits, says study
Around the time of World War II, prisoners were enlisted to help the war effort by taking part in studies that could help the troops. For example, a series of malaria studies at Stateville Penitentiary in Illinois and two other prisons was designed to test antimalarial drugs that could help soldiers fighting in the Pacific.
It was at about this time that prosecution of Nazi doctors in 1947 led to the "Nuremberg Code," a set of international rules to protect human test subjects. Many U.S. doctors essentially ignored them, arguing that they applied to Nazi atrocities — not to American medicine. The late 1940s and 1950s saw huge growth in the U.S. pharmaceutical and health care industries, accompanied by a boom in prisoner experiments [/b]funded by both the government and corporations. By the 1960s, at least half the states allowed prisoners to be used as medical guinea pigs.
But two studies in the 1960s proved to be turning points in the public's attitude toward the way test subjects were treated.
The first came to light in 1963. Researchers injected cancer cells into 19 old and debilitated patients at a Jewish Chronic Disease Hospital in the New York borough of Brooklyn to see if their bodies would reject them.
The hospital director said the patients were not told they were being injected with cancer cells because there was no need — the cells were deemed harmless. But the experiment upset a lawyer named William Hyman who sat on the hospital's board of directors. The state investigated, and the hospital ultimately said any such experiments would require the patient's written consent.
At nearby Staten Island, from 1963 to 1966, a controversial medical study was conducted at the Willowbrook State School for children with mental retardation. The children were intentionally given hepatitis orally and by injection to see if they could then be cured with gamma globulin.
Those two studies — along with the Tuskegee experiment revealed in 1972 — proved to be a "holy trinity" that sparked extensive and critical media coverage and public disgust, said Susan Reverby, the Wellesley College historian who first discovered records of the syphilis study in Guatemala. 'My back is on fire!' By the early 1970s, even experiments involving prisoners were considered scandalous. In widely covered congressional hearings in 1973, pharmaceutical industry officials acknowledged they were using prisoners for testing because they were cheaper than chimpanzees.
Holmesburg Prison in Philadelphia made extensive use of inmates for medical experiments. Some of the victims are still around to talk about it. Edward "Yusef" Anthony, featured in a book about the studies, says he agreed to have a layer of skin peeled off his back, which was coated with searing chemicals to test a drug. He did that for money to buy cigarettes in prison.
"I said 'Oh my God, my back is on fire! Take this ... off me!'" Anthony said in an interview with The Associated Press, as he recalled the beginning of weeks of intense itching and agonizing pain.
The government responded with reforms. Among them: The U.S. Bureau of Prisons in the mid-1970s effectively excluded all research by drug companies and other outside agencies within federal prisons.
As the supply of prisoners and mental patients dried up, researchers looked to other countries.
It made sense. Clinical trials could be done more cheaply and with fewer rules. And it was easy to find patients who were taking no medication, a factor that can complicate tests of other drugs. Story: FDA defends actions at plant that made tainted wipes
Additional sets of ethical guidelines have been enacted, and few believe that another Guatemala study could happen today. "It's not that we're out infecting anybody with things," Caplan said.
Still, in the last 15 years, two international studies sparked outrage.
One was likened to Tuskegee. U.S.-funded doctors failed to give the AIDS drug AZT to all the HIV-infected pregnant women in a study in Uganda even though it would have protected their newborns. U.S. health officials argued the study would answer questions about AZT's use in the developing world. The other study, by Pfizer Inc., gave an antibiotic named Trovan to children with meningitis in Nigeria, although there were doubts about its effectiveness for that disease. Critics blamed the experiment for the deaths of 11 children and the disabling of scores of others. Pfizer settled a lawsuit with Nigerian officials for $75 million but admitted no wrongdoing.
Last year, the U.S. Department of Health and Human Services' inspector general reported that between 40 and 65 percent of clinical studies of federally regulated medical products were done in other countries in 2008, and that proportion probably has grown. The report also noted that U.S. regulators inspected fewer than 1 percent of foreign clinical trial sites.
Monitoring research is complicated, and rules that are too rigid could slow new drug development. But it's often hard to get information on international trials, sometimes because of missing records and a paucity of audits, said Dr. Kevin Schulman, a Duke University professor of medicine who has written on the ethics of international studies.
Syphilis study These issues were still being debated when, last October, the Guatemala study came to light.
In the 1946-48 study, American scientists infected prisoners and patients in a mental hospital in Guatemala with syphilis, apparently to test whether penicillin could prevent some sexually transmitted disease. The study came up with no useful information and was hidden for decades.
Story: U.S. apologizes for Guatemala syphilis experiments
The Guatemala study nauseated ethicists on multiple levels. Beyond infecting patients with a terrible illness, it was clear that people in the study did not understand what was being done to them or were not able to give their consent. Indeed, though it happened at a time when scientists were quick to publish research that showed frank disinterest in the rights of study participants, this study was buried in file drawers. "It was unusually unethical, even at the time," said Stark, the Wesleyan researcher.
"When the president was briefed on the details of the Guatemalan episode, one of his first questions was whether this sort of thing could still happen today," said Rick Weiss, a spokesman for the White House Office of Science and Technology Policy.
That it occurred overseas was an opening for the Obama administration to have the bioethics panel seek a new evaluation of international medical studies. The president also asked the Institute of Medicine to further probe the Guatemala study, but the IOM relinquished the assignment in November, after reporting its own conflict of interest: In the 1940s, five members of one of the IOM's sister organizations played prominent roles in federal syphilis research and had links to the Guatemala study.
So the bioethics commission gets both tasks. To focus on federally funded international studies, the commission has formed an international panel of about a dozen experts in ethics, science and clinical research. Regarding the look at the Guatemala study, the commission has hired 15 staff investigators and is working with additional historians and other consulting experts.
The panel is to send a report to Obama by September. Any further steps would be up to the administration.
Some experts say that given such a tight deadline, it would be a surprise if the commission produced substantive new information about past studies. "They face a really tough challenge," Caplan said.
..."I WOULD LIKE to issue the following statement about the polio vaccine situation. The last week has been both eventful and encouraging. A committee of scientists is now screening polio vaccine before it is released for public use. The Surgeon General of the Public Health Service tells me that it is hoped to release some vaccine within a few days. Batches of vaccine must pass the most careful tests that scientists can devise and be as safe and effective as man can make the vaccine.
According to Dr. Francis' report on last year's field tests, the child who was vaccinated had a three times better chance of avoiding polio than the child who was not vaccinated.
There has been delay in the vaccination program. But remember-we are dealing in this field with the lives of our children and our grandchildren. Because of scientific work that was done during that delay science has learned new things about the way viruses behave in large scale manufacture and about the way we should make vaccine. Scientists have been able to design testing techniques of greater sensitivity and production techniques which build in a greater factor of safety and additional checks on the final product. So from that delay science has gained new knowledge, new safeguards.
I want to caution the people of our nation about two things: First: No vaccination program can prevent all cases of the disease against which it is directed. Let us not forget that Dr. Francis reported the polio vaccine as used in the 1954 field trial was found to be 60 to 90 percent--not 100 percent--effective in the field trials last year.
Second: Although the manufacturers are now moving toward full scale production and distribution of this vaccine, it will take them varying periods of time to "retool" to meet the revised production standards. During the months immediately ahead we must be patient while our limited supply of vaccine is used first to help protect those who need it most.
Every parent and every child should be grateful to those scientists who have been working without rest and without relief during recent weeks to find answers to the problems that caused the delay. They have found these answers and another battle in the continuing fight against polio has been won.
Since April 12 the National Foundation for Infantile Paralysis has been furnishing free vaccine for children in the first and second grades, and for children in the third grade who participated in the field tests of vaccine last year. More than 5Ѕ million children have been vaccinated--including one of my grandchildren, a first grader. This free vaccination program is the initial method for getting the vaccine to our children. No vaccine is now being distributed in any other way.
Sufficient vaccine to complete the Foundation's program should be released within 60 days. Until it is finished all vaccine produced will go to the Foundation.
The fact that some children do not get their second injection promptly will not reduce the effectiveness of the first injection. Dr. Salk, himself, stated last week that the level of immunity developed by the first injection would last many months.
DISTRIBUTION WHEN THE FOUNDATION PROGRAM IS COMPLETED
As soon as the Foundation program is completed, distribution must continue to proceed in a fair and orderly manner. The Secretary of Health, Education and Welfare presented to me two weeks ago a sound plan for the distribution of the vaccine. I promptly endorsed that plan and made it public.
Briefly the voluntary control plan for distribution will work as follows: 1. Priorities. The vaccine must be used first for those most susceptible to polio. Not only is this just, but also by reducing the incidence of the disease among those most likely to get it we increase the protection for all of us. The National Advisory Committee on Poliomyelitis Vaccine and the Secretary of Health, Education and Welfare have recommended that the vaccine be administered first to children of the ages of 5 to 9, inclusive.
I strongly endorse this recommendation and call upon our people to adhere strictly to the age 5 to 9 priority during the months ahead. No person not in the 5 to 9 age group should be vaccinated until the children of these age groups have received two vaccinations. The doctors of the country, through the American Medical Association, have pledged their support of these priorities.
The age group of second priority will be established and announced in due course.
2. Output of the Manufacturers. Each of the manufacturers of the vaccine has individually agreed to distribute his entire output of vaccine in accordance with this overall plan adopted by the Secretary of Health, Education and Welfare on the recommendation of the National Advisory Committee.
3. Allocation to States. The Secretary of Health, Education and Welfare will compile reports on the total output of the manufacturers and allocate the vaccine to each State on the basis of its population of unvaccinated children within the 5 through 9 age group, and subsequently, for other age groups.
4. State Responsibility. The States will advise the Secretary of Health, Education and Welfare as to their general plans for distribution of the vaccine and, specifically, their shipping instructions for manufacturers. This information then will be transmitted to the manufacturers.
5. Vaccination Programs. To assure that no child is denied vaccination by reason of its cost, some states and localities may operate mass free public vaccination programs for all children.
Other states may provide free vaccination only for children whose parents are unable to pay, through clinics, schools and preschool programs, or by furnishing free vaccine to private physicians. In those States, a portion of the State allocation of vaccine will flow into normal drug distribution channels for the exclusive use of children in the priority age brackets--to be administered by family doctors.
To assist the States in providing free vaccinations, I have recommended that the Congress enact legislation making $28 million available to the States for the purchase of vaccine. This legislation is now being considered by the appropriate Committees of the Congress and I urge its immediate adoption.
6. Keeping of Records. Doctors, as well as all manufacturers and distributors of the vaccine, will keep records of the vaccine they handle. Cooperation to this end has been pledged by the doctors, the manufacturers and the distributors.
This plan for distribution of the vaccine can go into effect as soon as the free vaccination program of the National Foundation for Infantile Paralysis is completed. Under it, the Federal Government will assume responsibility for the equitable allocation of the vaccine among the States, and the States will assume responsibility for the direction of distribution within their borders.
The program will operate in a sure and orderly way, given the full cooperation of the State officials, the manufacturers, the distributors, the medical profession, and the people of the Nation. I am confident that the program will receive that support.
For these reasons I do not believe that regulatory legislation in this field is necessary.
We all hope that the dread disease of poliomyelitis can be eradicated from our society. With the combined efforts of all, the Salk vaccine will be made available for our children in a manner in keeping with our highest traditions of cooperative national action. Note: The report referred to early in this message was prepared by Dr. Thomas F. Francis, Director, Poliomyelitis Vaccine Evaluation Center, University of Michigan. Entitled "An Evaluation of the 1954 Poliomyelitis Vaccine Trials," the report, dated April 12, 1955, was published by the Center.
Dr. Urnovitz revealed significant evidence that human immunodeficiency virus type 1 (HIV-1) is a monkey hybrid virus which was produced when 320,000 Africans were injected with polio virus contaminated with live simian immunodeficiency virus (SIV) in the late 1950's. Apparently, viral fragments combine easily with other viruses to produce these hybrids called "chimeras." Prior to this revelation, health officials were blaming AIDS on the habit of certain Africans to consume monkey flesh.
Ancient Egyptian paintings and carvings depict otherwise healthy people with withered limbs, and children walking with canes at a young age. It is theorized that the Roman Emperor Claudius was stricken as a child, and this caused him to walk with a limp for the rest of his life. Perhaps the earliest recorded case of poliomyelitis is that of Sir Walter Scott. In 1773 Scott was said to have developed "a severe teething fever which deprived him of the power of his right leg." At the time, polio was not known to medicine. A retrospective diagnosis of polio is considered to be strong due to the detailed account Scott made.
The symptoms of poliomyelitis have been described by many names. In the early nineteenth century the disease was known variously as: Dental Paralysis, Infantile Spinal Paralysis, Essential Paralysis of Children, Regressive Paralysis, Myelitis of the Anterior Horns, Tephromyelitis (from the Greek tephros, meaning "ash-gray") and Paralysis of the Morning. In 1789 the first clinical description of poliomyelitis was provided by the British physician Michael Underwood—he refers to polio as "a debility of the lower extremities". The first medical report on poliomyelitis was by Jakob Heine, in 1840; he called the disease Lähmungszastände der unteren Extremitäten. Karl Oskar Medin was the first to empirically study a poliomyelitis epidemic in 1890. This work, and the prior classification by Heine, led to the disease being known as Heine-Medin disease.
Dr. Hiram M. Hiller, Jr., was one of the physicians in several cities who realized what they were dealing with, but the nature of the disease remained largely a mystery. The 1916 epidemic caused widespread panic and thousands fled the city to nearby mountain resorts; movie theaters were closed, meetings were canceled, public gatherings were almost nonexistent, and children were warned not to drink from water fountains, and told to avoid amusement parks, swimming pools, and beaches. From 1916 onward, a polio epidemic appeared each summer in at least one part of the country, with the most serious occurring in the 1940s and 1950s.
The field trial set up to test the Salk vaccine was, according to O'Neill, "the most elaborate program of its kind in history, involving 20,000 physicians and public health officers, 64,000 school personnel, and 220,000 volunteers." Over 1,800,000 school children took part in the trial. When news of the vaccine's success was made public on April 12, 1955, Salk was hailed as a "miracle worker", and the day "almost became a national holiday." His sole focus had been to develop a safe and effective vaccine as rapidly as possible, with no interest in personal profit. When he was asked in a televised interview who owned the patent to the vaccine, Salk replied: "There is no patent. Could you patent the sun?"
In 1960, he founded the Salk Institute for Biological Studies in La Jolla, California, which is today a center for medical and scientific research. He continued to conduct research and publish books, including Man Unfolding (1972), The Survival of the Wisest (1973), World Population and Human Values: A New Reality (1981), and Anatomy of Reality: Merging of Intuition and Reason (1983). Dr. Salk's last years were spent searching for a vaccine against HIV.
" Instead, he became absorbed in research, even taking a year off to study biochemistry
laboratory of Dr. Thomas Francis. Francis had recently joined the faculty of the medical school after working for the Rockefeller Foundation, where he had discovered the Type B influenza virus. According to Bookchin, "the two month stint in Francis's lab was Salk's first introduction to the world of virology—and he was hooked.":25
After graduating from medical school he began his residency at New York's Mount Sinai Hospital, where he again worked in Francis's laboratory. Few hospitals in Manhattan had the status of Mount Sinai, particularly among the city's Jews. Oshinsky interviewed a friend of Salk's, who said, "to intern there was like playing ball for the New York Yankees ... only the top men from the nation's medical schools dared apply. Out of 250 who sought the opportunity, only a dozen were chosen."
According to Oshinsky, "Salk quickly made his mark." Although focused mainly on research, "he showed tremendous skills as a clinician and a surgeon." But it was "his leadership as president of the house staff of interns and residents at Mount Sinai that best defined him to his peers." The key issue for many of them in 1939, for example, was not the fate of the hospital, but rather the future of Europe after Nazi Germany's invasion of Poland. In one instance, "several interns responded by wearing badges to signify support for the Allies", but the hospital's director told them to remove them lest they upset some of the patients.
The interns then took the matter to Salk, where he said that "everyone should wear the badge as an act of solidarity." One intern recalled, "Jonas was a very staunch guy. He never took a backward step on that issue or any other issue of principle between us and the hospital." The hospital administrators backed off and there was no further interference from the director.  Research career
At the end of his residency, Salk began applying for permanent research positions. But he discovered that many of the jobs he desired were closed to him due to Jewish quotas, which, according to Bookchin, "prevailed in so much of the medical research establishment." Nor could he apply at Mount Sinai as their policy prevented hiring their own interns. As a last resort, he contacted Dr. Francis for help. But Francis had left New York University a year earlier after accepting an offer to direct the University of Michigan's School of Public Health.
However, "Francis did not let him down,"writes Bookchin. "He secured extra grant money and offered Salk a job" working on an army-commissioned project in Michigan to develop an influenza vaccine. He and Francis eventually perfected a vaccine that was soon widely used at army bases, where "Salk had been responsible for discovering and isolating one of the flu strains that was included in the final vaccine.:26
By 1947, Salk decided to find an institution where he could direct his own laboratory. After three institutions turned him down, he received an offer from William McEllroy, the dean of the University of Pittsburgh School of Medicine, which included a promise that he would run his own lab. He accepted, and in the fall of that year left Michigan and relocated to Pennsylvania. But the promise was not quite what he expected. After Salk arrived at Pittsburgh, "he discovered that he had been relegated to cramped, unequipped quarters in the basement of the old Municipal Hospital", writes Bookchin. As time went on, however, he began securing grants from the Mellon family and was able to build a working virology laboratory, where he continued his research on flu vaccines.
Salk's work on influenza viruses has been associated with ethical controversy. The Associated Press reported that Salk authored a research paper, describing a federally-funded study that began in 1942. Salk injected patients in a state insane asylum in Ypsilanti, Michigan with an experimental influenza vaccine, then exposed them to influenza virus months later to check the vaccine's efficacy. It is questionable at best whether any of these patients could have understood what was being done to them, or why.
It was SALK who did the Ypsilanti human experiment..................................as shown in Ugly Truth................................ ==================================
Are we getting to the bottom of this??notice he was working with Influ B...........
He was later approached by the director of research at the National Foundation for Infantile Paralysis and asked if he would like to participate on the foundation's polio project, which had earlier been established by President Franklin D. Roosevelt, at the time thought to be a victim of polio himself. He quickly accepted the offer saying he "would be happy to work on this important project."
In 1956, Wisdom magazine ran a cover story about Salk, summarizing some of the reasoning behind his desire to do research:
There are two types of medical specialists. There are those who fight disease day and night, who assist mankind in times of despair and agony and who preside over the awesome events of life and death. Others work in the quiet detachment of the laboratory; their names are often unknown to the general public, but their research may have momentous consequences.
Polio was a medical oddity that baffled researchers for years. It was first recorded in 1835 and grew steadily more prevalent. It took a long time to learn that the virus was transmitted by fecal matter and secretions of the nose and throat. It entered the victim orally, established itself in the intestines, and then traveled to the brain or spinal cord.
The research by Salk was not without controversey. Esther Lederberg's research with lambda phage and plasmids was well known and used by Salk. However, Dr. Esther Lederberg felt that Salk needed detailed records to ensure that his vaccine was as effective as claimed.   Discovering a vaccine Main article: Polio vaccine Newspaper headlines about polio vaccine tests (13 April 1955).  Test results announced
On April 12, 1955, Dr. Thomas Francis, Jr., of the University of Michigan, the monitor of the test results, "declared the vaccine to be safe and effective." The announcement was made at the University of Michigan, exactly 10 years to the day after the death of President Roosevelt. Five hundred people, including 150 press, radio, and television reporters, filled the room; 16 television and newsreel cameras stood on a long platform at the back; and 54,000 physicians, sitting in movie theaters across the country, watched the broadcast on closed-circuit television. Eli Lilly and Company paid $250,000 to broadcast the event.
What an adventure.............reading between the lines.......The info about Lederberg is interesting. more snippets:
"Although he is distinctly future-oriented, Dr. Salk has not lost sight of the institute's immediate aim, which is the development and use of the new biology, called molecular and cellular biology, described as part physics, part chemistry and part biology. The broad-gauged purpose of this science is to understand man's life processes.
"There is talk here of the possibility, once the secret of how the cell is triggered to manufacture antibodies is discovered, that a single vaccine may be developed to protect a child against many common infectious diseases. There is speculation about the power to isolate and perhaps eliminate genetic errors that lead to birth defects.
"Dr. Salk, a creative man himself, hopes that the institute will do its share in probing the wisdom of nature and thus help enlarge the wisdom of man. For the ultimate purpose of science, humanism and the arts, in his judgment, is the freeing of each individual to cultivate his full creativity, in whichever direction it leads. . . As if to prepare for Socratic encounters such as these, the institute's architect, Louis Kahn, has installed blackboards in place of concrete facings on the walls along the walks."
The New York Times, in a 1980 article celebrating the 25th anniversary of the Salk vaccine, described the current workings at the facility:
"At the institute, a magnificent complex of laboratories and study units set on a bluff overlooking the Pacific, Dr. Salk holds the titles of founding director and resident fellow. His own laboratory group is concerned with the immunologic aspects of cancer and the mechanisms of autoimmune disease, such as multiple sclerosis, in which the immune system attacks the body's own tissues.
Salk describes his "biophilosophy" as the application of a "biological, evolutionary point of view to philosophical, cultural, social and psychological problems." He went into more detail in two of his books, Man's Unfolding, and The Survival of the Wisest. In an interview in 1980, he described his thoughts on the subject, including his feeling that a sharp rise and an expected leveling off in the human population would take place and eventually bring a change in human attitudes:
"I think of biological knowledge as providing useful analogies for understanding human nature.... People think of biology in terms of such practical matters as drugs, but its contribution to knowledge about living systems and ourselves will in the future be equally important.... In the past epoch, man was concerned with death, high mortality; his attitudes were antideath, antidisease", he says. "In the future, his attitudes will be expressed in terms of prolife and prohealth. The past was dominated by death control; in the future, birth control will be more important. These changes we're observing are part of a natural order and to be expected from our capacity to adapt. It's much more important to cooperate and collaborate. We are the co-authors with nature of our destiny."
His definition of a "bio-philosopher" is "Someone who draws upon the scriptures of nature, recognizing that we are the product of the process of evolution, and understands that we have become the process itself, through the emergence and evolution of our consciousness, our awareness, our capacity to imagine and anticipate the future, and to choose from among alternatives."
Okay now this gets interesting, a vaccine for flu was done before the polio vaccine. That flu vaccine had dead virus in it....
While still a student, Salk became interested in vaccines. At the time it was acknowledged that bacterial vaccines could be made from a preparation of dead bacteria, which would immunize without inducing an infection. But scientists believed that a live vaccine had to be used in order to immunize against a virus. These ideas seemed contradictory to Salk. After his internship he joined Dr. Thomas Francis's influenza vaccine project at the University of Michigan. As a result of Salk's efforts, the influenza vaccine became the first killed-virus vaccine.
However, I am think of the waterborne like in streams, rivers, ponds, lakes, swamps etc.
even back then........ WWII, after war, was worse,.......also UFO time as well. 1947 Roswell.
"How do you patent the Sun?....."
Was radiation used?
Polio Diplomacy describes the complex activities of building a modern global medical infrastructure in the twentieth century; activities that intensified in the 1930s as radiation-assisted genetic science expanded and then virtually exploded alongside the Atomic Bomb. The spread of polio is a means of tracking nuclear proliferation and as we shall see, especially during the Cold War, nuclear intentions. The ‘year 2000′ redoubled effort to eradicate polio by vaccination has become a tyranny of the first order. More than any other aspect of the Polio Story, polio diplomacy reveals the depth of covert globalization and humanity’s present “genetic crisis”. Polio vaccinations should have been stopped. They were going to be in 2000. Most of world’s circulating disease-associated polioviruses are acknowleged to be vaccine-derived, but there never was a really “wild type” of natural poliovirus. The artifice begun in the first decade of the 20th century is now the artifice of the 21st. Polio, cancer, AIDS, vaccines, transgenics and ”equalized” populations have ended the domain of the once free-living species known as ourselves.
Before this is in fly, where is it found? I bet the amstigote form was in the dust, due to dust storms.
Leishmanial illnesses similar to those we have described may not be recognized as such when they occur in populations in which they are endemic, because of their protean clinical manifestations, insensitive diagnostic tests, and infrequent examination of bone marrow for amastigotes.Another possibility is that nearly universal infection in childhood leads to resistance to disease in adult life.
The exposure of more than 500,000 nonimmune adults during Operation Desert Storm may therefore have revealed more of the clinical spectrum of infection caused by L. tropica.
We have described a systemic illness caused by L. tropica. We call this illness “viscerotropic” leishmaniasis to distinguish it from “visceral” leishmaniasis, which is frequently considered to be the same as classic kala-azar18,47. The natural history of this illness is not yet defined, and the prevalence of infection among returning troops is not known. Diagnosis still requires an invasive procedure, such as a bone marrow aspiration or a lymph-node biopsy, and specialized laboratory support that is not widely available. This disorder should be included in the differential diagnosis of unexplained systemic illness in patients who have returned from areas of the world where leishmaniasis is endemic.
In different areas of the world, certain Leishmania species tend to be most commonly associated with the visceral form of the disease: L. donovani (in India), L. infantum (Middle East), L. chagasi (Latin America), and L. amazonensis (Brazil). After inoculation of pro-mastigotes into the skin, a small papule may be noticed. Leishmania amastigotes subsequently silently invade macrophages throughout the reticuloendothelial system. Usually 3 to 8 months pass before the burden of organisms increases to a level that causes symptoms.
The onset of symptoms can be gradual or sudden. In subacute cases, the patient will experience slow but progressive enlargement of the abdomen as a result of hepatosplenomegaly. Increased abdominal girth is accompanied by intermittent fever, weakness, loss of appetite, and weight loss. This presentation can be mistaken for lymphoma, infectious mononucleosis, brucellosis, chronic malaria, and hepatosplenic schistosomiasis. In acute cases, an abrupt onset of high fever and chills mimics malaria or an acute bacterial infection. On physical examination, the spleen may be massively enlarged, hard, and nontender. Hepatomegaly is also present. The skin tends to be dry and thin, and in light-skinned individuals, it takes on a grayish tint. This characteristic accounts for the Indian name Kala-azar, which means “black fever.” On laboratory examination anemia, leukopenia, and hypergam-maglobulinemia are common.
====================== The acidocalcisome is rich in pyrophosphate, short- and long-chain polyphosphate (poly P), magnesium, calcium, sodium and zinc. An exopolyphosphatase (PPX), a pyrophosphatase (PPase) and a polyphosphate kinase (PPK) may also be present. A question mark was added to indicate the lack of biochemical evidence for their presence. rstb.royalsocietypublishing.org/content/365/1541/775/F4.large.jpg
PolyP and hydrogen exchangers? in the Poly II or RNAP????Is this what was borrowed from the Trypanasome? Could be? it would be from T. Bruceii......
GalNac? modification of glycogen, sugar backbones, with sugar snakes? O-GalNAc Glycans
O-glycosylation is a common covalent modification of serine and threonine residues of mammalian glycoproteins. This chapter describes the structures, biosynthesis, and functions of glycoproteins that are often termed mucins. In mucins, O-glycans are covalently α-linked via an N-acetylgalactosamine (GalNAc) moiety to the -OH of serine or threonine by an O-glycosidic bond, and the structures are named mucin O-glycans or O-GalNAc glycans. The focus of this chapter is on mucins and mucin-like glycoproteins that are heavily O-glycosylated, although glycoproteins that carry only one or a few O-GalNAc glycans are also briefly discussed. There are also several types of nonmucin O-glycans, including α-linked O-fucose, β-linked O-xylose, α-linked O-mannose, β-linked O-GlcNAc (N-acetylglucosamine), α- or β-linked O-galactose, and α- or β-linked O-glucose glycans (discussed in Chapters 12 and 16–18). In this chapter, however, the term O-glycan refers to mucin O-glycans, unless otherwise specified. Mucin glycoproteins are ubiquitous in mucous secretions on cell surfaces and in body fluids. So, the epitope from T. Bruceii was used for what?
. Using this enzymatic probe and other methods, we and others (for review, Hart et al, 1989, 1995a-c) have now docu- mented that O-GlcNAc is ubiquitous and abundant on nuclear and cytoskeletal proteins of virtually all eukaryotes, including protozoans (Ortega-Barria et al, 1990; Dieckmann-Schuppert etal, 1993, 1994; Stanley etal, 1995) and fungi (Machida and Jigami, 1994).
In addition, O-GlcNAc is highly dynamic, with turnover rates much higher than the protein backbones to which it is attached (Kearse and Hart, 1991; Chou et al, 1992; Roquemore et al, 19%). Virtually all O-GlcNAc proteins ex- amined to date are also phosphoproteins, and in some instances Ser(Thr)-O-GlcNAc and Ser(Thr)-O-phosphate appear to re- ciprocally occupy the same hydroxyl groups (Kelly et al, 1993; Chou et al, 1995a,b). The dynamic characteristics of O-GlcNAc, and the importance of O-GlcNAcylated proteins in cellular regulation and in cytoskeletal structure, have led us to hypothesize that O-GlcNAc is a regulatory modification that not only regulates protein phosphorylation, but also is involved in modulating protein multimerization (Hart et al, 1995b,c).
Here we are:::::::::::::::::THE CYTOSKELETON::::::::::::::::::::::::::::::::The BRIDGING PROTEINS> Glycosylation, POL II, Intermediate filaments, tumor supression oncogenes, Viral proteins teguments fibers, HSP and nuclear pores..........All ya need for cell, heh?
Analyses of c-Myc Tryptic Glycopeptides trypsln GT I RP-HPLC, pH7.0 ^''RP-HPLC, pH2.0 "RP-HPLC, pH4.0 Gas-Phase' Microsequenclng amino acid sequence Manual Edman Degradation Mass Spectrometry position of OGIcNAc molecular weight
Recently, the p53 tumor suppressor was shown to bear O-GlcNAc (Shaw et ai, 1996). These studies suggested that the O-GlcNAcylated form of p53 has higher biological activity and higher DNA binding activity than the non-O-GlcNAcylated species of p53. Recent studies have also shown that SV40 Large T antigen is O- GlcNAcylated (Medina-Vera and Haitiwanger, 1994). Several O-GlcNAcylated DNA-binding proteins have also been de- scribed in the filamentous fungus, Aspergillus orzae, suggest- ing that O-GlcNAcylation may be important in the functions of transcription factors from even the most primitive eukaryotes (Machida and Jigami, 1994).
. A putative role for O-GlcNAcylation in Alzheimer disease is even more intriguing with the recent finding of O- GlcNAc on the p-amyloid precursor protein (Griffith et al, 1995), and the direct demonstration of altered O-GlcNAc levels in Alzheimer patients (Griffith and Schmitz, 1995). Likewise, a possible role for O-GlcNAc in generally mediating the associations of microtubule binding proteins must be consid- ered in the light of recent reports describing the O- GlcNAcylation of the high molecular weight MAP proteins, including MAP2 (Ding and Vandre, 1996). It is noteworthy that several of the O-GlcNAcylated cytoskeletal proteins, such as band 4.1 (Holt et al, 1987a), vinculin (Vostal and Kras- newich, 1996), talin (Hagmann et al, 1992), synapsin (Luthi et al, 1991), and others are involved in the phosphorylation- dependent reversible bridging of the cytoskeleton to the mem- brane or other structures. Thus, while direct data are still lack- ing, it is our working hypothesis that O-GlcNAcylation plays an important role in mediating protein—protein interactions in- volved in a wide variety of cellular functions, including the organization of the cytoskeleton.
flagella protein from t. bruceii or O-GalNac? Cell proliferation; diabetes; glycosyl-phosphatidylinositol; growth factors; insulin metabolic effects; phospholipases; signal transduction; synthetic inositol-sugars That would be the oligosaccharides and where do they come from?
=========================== The identity and origin of oligosaccharides present in the faeces and urine of sick infants
Received 19 April 1979; Available online 20 January 2003. Abstract
A systematic identification scheme, based on improved paper and thin-layer chromatography, acidic and enzymatic hydrolysis, and the reaction of carbohydrates with several location reagents, has been applied to the analysis of oligosaccharides present in the urine and faeces of sick children and the diets they are fed.
The identity and origin of these oligosaccharides is described and their relevance to the diagnosis and treatment of children with suspected disorders of carbohydrate metabolism is discussed.
~~~~~~~~~~~~~~~~~~ mycelial wall of fungi: oligosacharrides: called elicitors.
...."Thus, elicitors are likely to be molecules present in many different microbes and, n fact, the elicitor to be described in this paper is a structural polysaccharide of the mycelial walls of many fungi ."...........
......"soybean pathogen Phytophthora megasperma var. sojae (Pms), the causal agent of root and stem rot. "........
...."that glyceollin will also stop the growth of three Gram-negative bacteria, Pseudomonas glycinea, Rhizobium trifolii, and Rhizobium japonicum, of the Gram-positive bacterium, Bacillus subtilis, and of baker's yeast, Saccharomyces cerevisiae. Inter- estingly, it requires about 25 /~g/ml of glyceollin to inhibit by 50% and 100 /xg/ml to inhibit by 100% the growth of all of these different orga- nisms (Fig. 3). The fact that it requires the same concentration of glyceollin to inhibit the growth of a variety of cell types suggests that the mechanism of action of glyceollin is a chemically catalyzed reaction (such as the photosensitized furanocou- marins or such as disruption of membranes) rather ".........
GLYCEOLLIN? ========================== "Glyceollins are a family of prenylated pterocarpan found in ineffective types of nodule in soybean in response to symbiotic infection. They are phytoalexins with an antiestrogenic activity.
Molecules found in the family are :
* Glyceollin I * Glyceollin II * Glyceollin III * Glyceollin IV
Metabolism Glycinol is the direct precursor of glyceollins through the action of a prenyltransferase. Glyceollin synthase then transforms those prenylated precursors into glyceollins.".....
The T. bruceii could be part of the Pol II: ===========================
RNA editing is believed to be catalyzed by a ribonucleoprotein complex containing endonucleolytic, terminal uridylyl transferase (TUTase), 39 uridine-specific exonucleolytic (U-exo), and ligase activities. None of the catalytic enzymes for RNA editing have been identified. Here we describe the identification of two candidate RNA ligases (48 and 52 kDa) that are core catalytic components of the T. brucei ribonucleoprotein editing complex. Both enzymes share homology to the covalent nucleotidyl transferase superfamily and contain five key signature motifs, including the active site KXXG. In this report, we present data on the proposed 48 kDa RNA editing ligase. We have prepared polyclonal antibodies against recombinant 48 kDa ligase that specifically recognize the trypanosome enzyme. When expressed in trypanosomes as an epitope-tagged fusion protein, the recombinant ligase localizes to the mitochondrion, associates with RNA editing complexes, and adenylates with ATP. These findings provide strong support for the enzymatic cascade model for kinetoplastid RNA editing.
Expression and analysis of epitope-tagged p48 in T. brucei Recombinant p48 expressed in E. coli is largely insol- uble and lacks ligase activity+ ........
Because the RNA editing ligase is only found in large RNP complexes, we hypothesized that accessory trypanosomal proteins or cofactors might be necessary for activity+ Therefore, to study activity, an epitope-tagged recombinant p48 was expressed in trypanosomes+ We created two trypano- some expression vectors: one in which the p48 con- tained a C-terminal His(10) epitope, and a second in which the p48 contained a C-terminal HA epitope (Fig+ 3A; McDowell et al+, 1998)+ Both constructs con- tained sequences of the a-b tubulin intergenic region for site-specific integration, the PARP promoter for high- level expression, and the neomycin resistance gene
An oligosaccharide (from the Greek oligos, a few, and sacchar, sugar) is a saccharide polymer containing a small number (typically three to ten of component sugars, also known as simple sugars (monosaccharides). Oligosaccharides can have many functions; for example, they are commonly found on the plasma membrane of animal cells where they can play a role in cell-cell recognition.In general, they are found either O- or N-linked to compatible amino acid side-chains in proteins or to lipid moieties . e.g.Fructo-oligosaccharides (FOS), which are found in many vegetables, consist of short chains of fructose molecules. (Inulin has a much higher degree of polymerization than FOS and is a polysaccharide.) Galactooligosaccharides (GOS), which also occur naturally, consist of short chains of galactose molecules. These compounds can be only partially digested by humans.
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