A Review of the impacts of antibiotics on mitochondria leads to the conclusion that there is a risk of increased cancers and heart disease. 2022-04-30. Jorma Jyrkkanen BSc PDP

A Review of the impacts of antibiotics on mitochondria leads to the conclusion that there is a risk of increased cancers and heart disease resulting from exposure at a later time due to harm to DNA, tumor suppressor genes, microbiomes, immune systems and sugar metabiolism which probably varies with the type and amount of usage encountered. Thee risks are also amplified by pesticides that may rupture mitochondria and spike proteins and covid viruses which do the wame. See also my article on these topics for further information. https://www.researchgate.net/publication/346505752_Antibiotic_induced_changes_to_mitochondria_result_in_potential_contributions_to_carcinogenesis_heart_pathologies_other_medical_conditions_and_ecosystem_risks

Computing Eigenvalues and Eigenvectors for Squamish River Wintering Bald Eagles. Jorma Jyrkkanen, jjyrkkanen76@outlook.com

Computing Eigenvalues and Eigenvectors for Squamish River Wintering Bald Eagles. Jorma Jyrkkanen, jjyrkkanen76@outlook.com 3 Dec 2018 Background I fiddled with my 4 years of Squamish Wintering Eagles demographic data and fudged a bit of the model to add males in the Reproduction and got an interesting growth rate, lambda1 and a great Eigenvector or stable age distribution. Here it is. Will play with it until I am happy with data fit and may extend it out to 15-20 years age classes. It’s a dynamic model amenable to gaming based on thousands of field observations.

Discussion What I saw from year to year though were what looked like compensatory density dependent adjustments in age specific survival so it flip flopped p due to competition from yr to yr.

This fact is not amenable to deterministic Markov models like Leslie UNLESS you ‘game it’ or program in ‘if Sxi > or < Sxi critical-then-change-Sxi+ or-n’ ie compensatory survival feedbacks to other age classes. I urge population biology students to try it and watch amazing responses to population and age structure. I used an online Calculator bandicoot.maths.adelaide page written by Mathew Roughan.

Figure 1. Sample Leslie Matrix and Start Population Vector with test age specific reproductive rates for a Female Population based on Hypothetical Statistics to Observe Deterministic Model Responses in Total Population, Age Classes and Growth Rates (Primary Eigenvalue) and proportional age class structure (Eigenvectors).December 3, 2018Created by Jorma A. Jyrkkanen Note. The last three age classes are all adults and there is some presumption of productivity from four year class Bald Eagles ie R4=0.1

Eagles Run 2 with a Working Survivorship Population Vector but discrepancy in observed and model that works.

This latter run has a high crash potential (CP) in 8 yrs and a lot of fluctuation. For a more realistic model I have to incorporate my field data.

The bottom box has the stable age structure eigenvector and age specific eigenvalues. The latter more realistic run works but stability hangs on a few percentage survivorships of juveniles age classes and only includes 8 Age classes total. Conclusion I concluded that the dynamic nature of feedbacks assures high survival of recruits to replace low adult mortality. Note how with even static Survivorships (Sij diagonals in L) there is an innate generation of wild fluctuations in age-class abundance in the curves at the bottom but I caution that in the field this is difficult to tease apart from random effects of migration linked as it is to weather and food availability. This phenomenon no doubt leads a lot of people to think a population is in trouble when only short-term observations are made and it is not true. Time lags are working to smooth out the age class distributions and real population. You only come to know these statistics as probably true after years of observation. I did 4 with thousands of observations and it was just starting to sink in. Keep in mind that these parameters apply only to the female side of the population. If you add the males it will approximately double.

Russia Presents Evidence at UN Security Council Meeting on Biowarfare Labs. 2022-04-26. Jorma Jyrkkanen.

https://www.youtube.com/watch?v=9_EHI2syUbs See Youtube https://www.youtube.com/watch?v=9_EHI2syUbs https://www.youtube.com/watch?v=9_EHI2syUbs See also https://www.youtube.com/watch?v=olHRu_Ou4WI See also America's Response to the accusation of Bioweapons in Ukrainian Labs. https://www.newsweek.com/tulsi-gabbard-bio-labs-ukraine-russia-conspiracy-1687594

The USA Coronvirus Patent Story. Who Got there First? Work Leading to Patents Started Around 2003. 2022-04-26. Jorma Jyrkkanen.

https://pubchem.ncbi.nlm.nih.gov/patent/US-2006257852-A1 United States Patent Application 20060257852 Kind Code A1 Rappuoli; Rino ; et al. November 16, 2006 Severe acute respiratory syndrome coronavirus Abstract An outbreak of a virulent respiratory virus, now known as Severe Acute Respiratory Syndrome (SARS), was identified in Hong Kong, China and a growing number of countries around the world in 2003. The invention relates to nucleic acids and proteins from the SARS coronavirus. These nucleic acids and proteins can be used in the preparation and manufacture of vaccine formulations, diagnostic reagents, kits, etc. The invention also provides methods for treating SARS by administering small molecule antiviral compounds, as well as methods of identifying potent small molecules for the treatment of SARS. Inventors: Rappuoli; Rino; (Castelnuovo Berardenga, IT) ; Masignani; Vega; (Siena, IT) ; Stadler; Konrad; (Scharnstein, AU) ; Gregersen; Jens Peter; (Wetter, DE) ; Chien; David; (Alamo, CA) ; Han; Jang; (Lafayette, CA) ; Polo; John M.; (Danville, CA) ; Weiner; Amy; (Fairfield, CA) ; Houghton; Michael; (Danville, CA) ; Song; Hyun Chul; (Berkeley, CA) ; Seo; Mi-Young; (Yongin-si, KR) ; Donnelly; John; (Moraga, CA) ; Klenk; Hans Dieter; (Marburg, DE) ; Valiante; Nicholas; (Fremont, CA) Correspondence Address: Chiron Corporation;Intellectual Property - R440 P.O. Box 8097 Emeryville CA 94662-8097 US Assignee: Chiron Corporation Emeryville CA Family ID: 33304326 Appl. No.: 10/822303 Filed: April 9, 2004 Related U.S. Patent Documents Application Number Filing Date Patent Number 60462218 Apr 10, 2003 60462465 Apr 11, 2003 60462418 Apr 12, 2003 60462748 Apr 13, 2003 60463109 Apr 14, 2003 60463460 Apr 15, 2003 60463668 Apr 16, 2003 60463983 Apr 17, 2003 60463971 Apr 18, 2003 60464899 Apr 22, 2003 60464838 Apr 22, 2003 60465273 Apr 23, 2003 60465535 Apr 24, 2003 60468312 May 5, 2003 60473144 May 22, 2003 60495024 Aug 14, 2003 60505652 Sep 23, 2003 60510781 Oct 11, 2003 60529464 Dec 11, 2003 60536177 Jan 12, 2004 60560757 Apr 7, 2004 Current U.S. Class: 435/5 ; 435/325; 435/456; 435/69.3; 530/350; 536/23.72 Current CPC Class: A61K 2039/545 20130101; A61K 39/12 20130101; C12N 2770/20022 20130101; G01N 2333/165 20130101; G01N 2469/20 20130101; A61K 2039/55566 20130101; C12N 2770/20021 20130101; C12N 2770/20043 20130101; A61K 2039/5252 20130101; A61K 2039/55505 20130101; A61K 39/215 20130101; A61K 39/00 20130101; C12N 7/00 20130101; A61K 2039/55511 20130101; C12N 2770/20034 20130101; C12N 2770/20063 20130101; C12Q 1/701 20130101; C07K 2319/21 20130101; C07K 14/005 20130101; C12N 2770/20051 20130101; C07K 2317/76 20130101; C07K 2317/34 20130101; C07K 16/10 20130101 Class at Publication: 435/005 ; 435/069.3; 435/456; 435/325; 530/350; 536/023.72 International Class: C12Q 1/70 20060101 C12Q001/70; C07H 21/04 20060101 C07H021/04; C12N 15/86 20060101 C12N015/86; C07K 14/165 20060101 C07K014/165 Claims 1. An isolated polypeptide of the SARS virus. 2. The polypeptide of claim 1, wherein the polypeptide is a Spike (S) polypeptide, an Env (E) polypeptide, a Membrane (M) polypeptide, a hemagglutinin-esterase polypeptide (HE), a nucleocapsid (N) polypeptide, a ORF1a polypeptide, a ORF1ab polypeptide, a proteolytic fragment of a ORF1a polypeptide, or a proteolytic fragment of a ORF1ab polypeptide. 3. The polypeptide of claim 1, wherein the polypeptide comprises an amino acid sequence selected from the group consisting of SEQ ID NOS: 6039, 7232, 9766, 9767, 9768, 9769, 9770, 9771, 9772, 9773, 9774, 9775, 9776, 9777, 9778, 9779, 6042, 6043, 6044, 6045, 6046, 6047, 6048, 6049, 6050 or 6052. 4. The polypeptide of claim 1, wherein the polypeptide comprises an amino acid sequence having >75% sequence identity to an amino acid sequence selected from the group consisting of SEQ ID NOS: 6042, 6043, 6044, 6045, 6046, 6047, 6048, 6049, 6050, 6052, 9766, 9767, 9768, 9769, 9770, 9771, 9772, 9773, 9774, 9775, 9776, 9777, 9778, 9779, 9997, 9998, 10149, 10316, 10338, 10339, 10340, 10341, 10342, 10532, 10533, 10571, 10572, 10573, 10574, 10575, 10576, 10577, 10578, 10579, 11561, 11562, 11618, 11619, 11620, 11627, 11630, 11633 & 11636. 5. The polypeptide of claim 1, wherein the polypeptide comprises a fragment of at least 10 consecutive amino acids of an amino acid sequence selected from the group consisting of SEQ ID NOS: 6042, 6043, 6044, 6045, 6046, 6047, 6048, 6049, 6050, 6052, 9766, 9767, 9768, 9769, 9770, 9771, 9772, 9773, 9774, 9775, 9776, 9777, 9778, 9779, 9997, 9998, 10149, 10316, 10338, 10339, 10340, 10341, 10342, 10532, 10533, 10571, 10572, 10573, 10574, 10575, 10576, 10577, 10578, 10579, 11552, 11561, 11562, 11618, 11619, 11620, 11627, 11630, 11633 & 11636. 6. A polypeptide comprising an amino acid sequence having >80% sequence identity to an amino acid sequence selected from the group consisting of SEQ ID NOS: 6042, 6043, 6044, 6045, 6046, 6047, 6048, 6049, 6050, 6052, 9766, 9767, 9768, 9769, 9770, 9771, 9772, 9773, 9774, 9775, 9776, 9777, 9778, 9779, 9997, 9998, 10149, 10316, 10338, 10339, 10340, 10341, 10342, 10532, 10533, 10571, 10572, 10573, 10574, 10575, 10576, 10577, 10578, 10579, 11552, 11561, 11562, 11618, 11619, 11620, 11627, 11630, 11633 & 11636. 7. A polypeptide comprising an amino acid sequence that comprises a fragment of at least 10 consecutive amino acids of an amino acid sequence selected from the group consisting SEQ ID NOS: 6042, 6043, 6044, 6045, 6046, 6047, 6048, 6049, 6050, 6052, 9766, 9767, 9768, 9769, 9770, 9771, 9772, 9773, 9774, 9775, 9776, 9777, 9778, 9779, 9997, 9998, 10149, 10316, 10338, 10339, 10340, 10341, 10342, 10532, 10533, 10571, 10572, 10573, 10574, 10575, 10576, 10577, 10578, 10579, 11552, 11561, 11562, 11618, 11619, 11620, 11627, 11630, 11633 & 11636. 8. A polypeptide comprising an amino acid sequence having >80% sequence identity to SEQ ID NO: 6042, and/or comprising an amino acid sequence that comprises a fragment of at least 10 consecutive amino acids of SEQ ID NO: 6042, wherein the polypeptide is in the form of a trimer. 9. Nucleic acid encoding the polypeptide of any one of claims 1 to 8. 10. Nucleic acid according to claim 9, comprising a nucleotide sequence selected from the group consisting of SEQ ID NOS: 7191, 7273, 7275, 7277, 7279, 7281, 7283, 7285, 7287, 7289, 7291, 7292, 7293, 9968, 10066, 10084, 10299, 10505, 11323, 11563, 11639 & 11640. 11. A polynucleotide comprising a nucleotide sequence having >80% sequence identity to the nucleic acid of claim 9 or claim 10. 12. A polynucleotide comprising a fragment of at least 10 consecutive nucleotides of the nucleic acid of claim 9 or claim 10. 13. Antibody that recognizes the polypeptide of any one of claim 1 to 8. 14. The antibody of claim 13, wherein said antibody recognizes the polypeptide comprising the amino acid sequence of SEQ ID NO: 6042 or a fragment thereof. 15. The antibody of claim 14, wherein said antibody recognizes the polypeptide comprising the amino acid sequence of SEQ ID NO: 6042 or a fragment thereof in trimeric form. 16. The antibody of claim 13, wherein the antibody is a monoclonal antibody. 17. The antibody of claim 13, wherein the antibody is a human antibody. 18. An immunoassay for detecting a SARS virus antigen in a sample, comprising the step of contacting the sample with the antibody of any one of claims 13 to 17. 19. An immunoassay for detecting an antibody against a SARS virus antigen in a sample, comprising the step of contacting the sample with the polypeptide of any one of claims 1 to 8. 20. A method of detecting an antibody against a SARS virus antigen in a sample comprising contacting said sample with the polypeptide of any one of claims 1 to 8, under conditions suitable for binding said polypeptide to said antibody, if present, and detecting the binding of said polypeptide to said antibody. 21. A method for detecting a SARS virus antigen in a sample comprising contacting said sample with the antibody of any one of claims 13 to 17, under conditions suitable for binding said antibody to said antigen, if present, and detecting the binding of said antibody to said antigen. 22. A vaccine for the treatment or prevention of severe acute respiratory syndrome (SARS), comprising an inactivated SARS virus, a killed SARS virus, an attenuated SARS virus, a split SARS virus preparation, or at least one purified SARS virus antigens. 23. The vaccine of claim 22, comprising a purified polypeptide according to any one of claims 1 to 8. 24. The vaccine of claim 22 or claim 23, wherein the antigen is a purified SARS virus antigen in the form of a VLP. 25. The vaccine of any one of claims 22 to 24, further comprising an adjuvant. 26. The vaccine of claim 25, wherein the adjuvant is an aluminium salt or is MF59. 27. The vaccine of any one of claims 22 to 26, comprising more than one SARS virus antigen. 28. The vaccine of claim 27, wherein the antigens are selected from S, E, N and M. 29. The vaccine of claim 22, comprising an inactivated SARS virus. 30. The vaccine of claim 29, wherein said virus is inactivated by chemical or physical means. 31. The vaccine of claim 30, wherein said inactivation comprises treatment of the virus with an effective amount of one or more of the following agents selected from the group consisting of detergents, formaldehyde, formalin, .beta.-propriolactone, and UV light. 32. The vaccine of claim 30, wherein said inactivation comprises treatment of the virus with an effective amount of one or more of the following agents selected from the group consisting of methylene blue, psoralen and carboxyfullerene (C60). 33. The vaccine of claim 30, wherein said inactivation comprises treatment of the virus with an effective amount of one or more of the following agents selected from the group consisting of binary ethylamine, acetyl ethyleneimine and gamma irradiation. 34. The vaccine of claim 31, wherein said inactivation comprises treatment with .beta.-propriolactone. 35. The vaccine of claim 34, wherein said .beta.-propriolactone is used at a concentration of 0.01 to 0.5%. 36. The vaccine of claim 34, wherein said .beta.-propriolactone is used at a concentration of 0.5 to 0.2%. 37. The vaccine of claim 34, wherein said .beta.-propriolactone is used at a concentration of 0.025 to 0.1%. 38. A method of inactivating SARS virus comprising exposing the virus to an inactivation agent for 12 to 24 hours at refrigeration temperatures followed hydrolysis of any residual inactivating agent by elevating the temperature for three hours. 39. The method of claim 38, wherein the inactivation agent is .beta.-propriolactone. 40. The method of claim 38, wherein the refrigeration temperature is between 0.degree. C. and 8.degree. C. 41. The method of claim 38, wherein the elevated temperature is between 33.degree. C. and 41.degree. C. 42. A method for making an inactivated SARS vaccine comprising: a. innoculating a mammalian cell culture with SARS virus; b. cultivating the infected cells; c. harvesting SARS virus containing supernatant; d. inactivating the SARS virus; and e. purifying the inactivated SARS virus. 43. The method of claim 42, wherein said mammalian cell culture is derived from one or more of the cell types selected from the group consisting of fibroblast cells, endothelial cells, hepatocytes, keratinocytes, immune cells, mammary cells, smooth muscle cells, melanocyte cells, neural cells, prostate cells, renal cells, skeletal cells, liver cells, retinoblast cells and stromal cells. 44. The method of claim 42, wherein said mammalian cell culture is derived from a cell culture selected from the group consisting of human cells, non-human primate cells, HeLa cells, human diploid cells, fetal rhesus lung cells, human embryonic kidney cells, VERO cells, horse cells, cow cells, sheep cells, dog cells, cat cells or rodent cells. 45. The method of claim 42, wherein said mammalian cell culture is derived from VERO cells or fetal rhesus kidney cells. 46. The method of claim 42, wherein said mammalian cells are cultured in serum free media. 47. The method of claim 42, wherein said mammalian cells are cultured in protein free media. 48. The method of claim 42, wherein said inoculating step comprising absorbing the SARS virus onto the cell culture for 60 to 300 minutes. 49. The method of claim 42, wherein said inoculating step is conducted at 25.degree. C. to 40.degree. C. 50. The method of claim 42, wherein said purification step comprises one or more of the treatments selected from the group consisting of gradient centrifugation, ultracentrifugation, continuous-flow ultracentrifugation, chromatography, polyethylene glycol precipitation, and ammonium sulfate precipitation. 51. The method of claim 42, wherein said purification step comprises one or more of the treatments selected from the group consisting of ultrafiltration and dialfiltration. 52. The method of claim 50, wherein said chromatography treatment includes one or more of the chromatography treatments selected from the group consisting of ion exchange chromatography, size exclusion chromatography, and liquid affinity chromatography. 53. The method of claim 52, wherein said chromatography treatment includes use of one more chromatographic resins selected from the group consisting of an an anionic resin and a cationic resin. 54. The method of claim 52, wherein the ion exchange chromatography treatment includes a first step using a strong anion exchange resin and a second step using a strong cation exchange resin. 55. The method of claim 50, wherein said gradient centrifugation purification step comprises density gradient centrifugation. 56. The method of claim 42, wherein said purification step comprises a first step of chromatography purification and a second step of gradient centrifugation. 57. The method of claim 56, wherein said first chromatography purification step comprises liquid affinity chromatography. 58. The method of claim 56, wherein said second gradient centrifugation step comprises density gradient centrifugation. 59. A single-stranded oligonucleotide comprising a nucleotide sequence selected from the group consisting of SEQ ID NOS: 21-6020, 6076-6568, 6586-6587, 7292-7301, 7325-7328, 7332-7352, 7353-7385, 10235-10298, 10352-10504, 10580-11322 and 11325-11551. 60. A single-stranded oligonucleotide comprising the complement of the oligonucleotide of claim 59. 61. The oligonucleotide of claim 59 or claim 60, comprising 10-30 nucleotides. 62. The oligonucleotide of claim 61, comprising the nucleotide sequence of SEQ ID NO: 7292, SEQ ID NO: 7293, the complement of SEQ ID NO: 7292 or the complement of SEQ ID NO: 7293. 63. A kit comprising primers for amplifying a template sequence contained within a SARS virus nucleic acid target, the kit comprising a first primer and a second primer, wherein the first primer comprises a sequence substantially complementary to a portion of said template sequence and the second primer comprises a sequence substantially complementary to a portion of the complement of said template sequence, wherein the sequences within said primers which have substantial complementarity define the termini of the template sequence to be amplified. 64. The kit of claim 63, wherein the template sequence is contained within SEQ ID NO: 1 and/or SEQ ID NO: 2. 65. The kit of claim 63 or claim 64, wherein the first primer comprises a fragment of 8 or more nucleotides of SEQ ID NO: 1, and the second primer comprises a fragment of 8 or more nucleotides of the complement of SEQ ID NO: 1. 66. The kit of claim 63 or claim 64, wherein the first primer comprises a fragment of 8 or more nucleotides of SEQ ID NO: 2, and the second primer comprises a fragment of 8 or more nucleotides of the complement of SEQ ID NO: 2. 67. The kit of claim 63, wherein the first primer is an oligonucleotide according to any one of claims 59 to 62 and the second primer is an oligonucleotide according to any of claims 59 to 62. 68. The kit of any one of claims 63 to 67, further comprising a labeled probe that comprises either a fragment of 8 or more nucleotides of SEQ ID NO: 1 and/or SEQ ID NO: 2, or the complement of said fragment, which fragment is located within the template sequence. 69. The kit of any one of claims 63 to 68, wherein the first primer and/or the second primer comprises a nucleotide sequence selected from the group consisting of SEQ ID NOS: 21-6020, 6076-6568, 6586-6587, 7292-7301, 7325-7328, 7332-7352, 7353-7385, 10235-10298, 10352-10504, 10580-11322 and 11325-11551. 70. The kit of any one of claims 63 to 68, wherein the first primer and/or the second primer comprises the complement of a nucleotide sequence selected from the group consisting of SEQ ID NOS: 21-6020, 6076-6568, 6586-6587, 7292-7301, 7325-7328, 7332-7352, 7353-7385, 10235-10298, 10352-10504, 10580-11322 and 11325-11551. 71. A method of detecting the presence of SARS virus in a sample comprising providing a sample suspected of containing a SARS virus nucleic acid target, amplifying a template sequence contained within said SARS virus nucleic acid target with the kit of any one of claims 63 to 70, and detecting the amplified template sequence, wherein the presence of the amplified template sequence indicates the presence of SARS virus in said sample. 72. The method of claim 71, wherein said amplifying is accomplished using polymerase chain reaction, transcription mediated amplification, reverse transcription PCR, ligase chain reaction, strand displacement amplification or nucleic acid sequence-based amplification. 73. A double-stranded RNA molecule with a length from about 10 to about 30 nucleotides which is able to inactivate the SARS coronavirus in a mammalian cell. 74. The double-stranded RNA of claim 73, wherein the sequence of one of the strands is at least 90% identical to a target sequence, wherein the target sequence is a fragment of SEQ ID NO: 1 and/or SEQ ID NO: 2. 75. The double-stranded RNA of claim 73 or claim 74, wherein the target sequence comprising a nucleotide sequence selected from the group consisting of SEQ ID NOS: 7292, 7293, 7294, 7295, 7296, 7297, 7298, 7299, 7300 and 7301. 76. The double-stranded RNA of any one of claims 73 to 75, comprising at least one modified nucleotide. 77. A method for treating a patient suffering from SARS, comprising: administering to the patient a therapeutically effective dose of a molecule of less than 1000 g/mol. 78. The method of claim 77, wherein the molecule has an aromatic region and greater than one heteroatom selected from O, S, or N. 79. A method for treating a patient suffering from SARS, comprising: administering to the patient a therapeutically effective dose of a compound selected from: a nucleoside analog, a peptoid, an oligopeptide, a polypeptide a protease inhibitor, a 3C-like protease inhibitor, a papain-like protease inhibitor, or an inhibitor of an RNA dependent RNA polymerase. 80. A method for treating a patient suffering from SARS, comprising: administering to the patient a steroidal anti-inflammatory drug in combination with at least one antiviral compound. 81. A method for treating a patient suffering from SARS, comprising: administering to the patient a therapeutically effective dose of a compound selected from: acyclovir, gancyclovir, vidarabidine, foscamet, cidofovir, amantidine, ribavirin, trifluorothymidine, zidovudine, didanosine, zalcitabine, an antiviral compound listed in Table 1; an antiviral compound listed in Table 2; or an interferon. 82. The method of claim 81, wherein the interferon is an interferon-.alpha. or an interferon-.beta.. 83. The method of any one of claims 77 to 82, wherein the molecule or compound is delivered by inhalation. 84. A method of identifying a therapeutically active agent comprising the steps of: (a) contacting a therapeutically active agent with a cell infected with the SARS virus; (b) measuring attenuation of a SARS related enzyme. 85. A viral vector or particle for in vivo delivery of a nucleic acid of claim 9 or claim 10. 86. The viral vector of claim 85, wherein the vector is an adenovirus vector, a poxvirus vector or an alphavirus vector. 87. An alphavirus replicon particle comprising one or more SARS viral antigens. 88. The replicon particle of claim 87, wherein said SARS viral antigen is a spike protein. 89. The replicon particle of claim 87, wherein said particle comprises a replicon derived from Venezuelan Equine Encephalitis (VEE) and further comprises an envelope derived from Sindbus virus (SIN) or Semliki Forest Virus (SFV). 90. A vaccine comprising one or more SARS virus antigens and one or more respiratory virus antigens. 91. The vaccine of claim 90, wherein said respiratory virus antigens are selected from the group consisting of influenza virus, human rhinovirus (HRV), parainfluenza virus (PIV), respiratory syncytial virus (RSV), adenovirus, metapneumovirus, and rhinovirus. 92. The vaccine of claim 91, wherein said respiratory virus antigen is from influenza virus. 93. The vaccine of claim 90, wherein said respiratory virus antigen is from a coronavirus other than the SARS virus. 94. A polypeptide comprising an immunogenic, surface exposed fragment of the amino acid sequence SEQ ID NO: 6042. 95. The polypeptide of claim 94, wherein said fragment does not include the last 50 amino acids of the C-terminus of SEQ ID NO: 6042. 96. The polypeptide of claim 94, wherein said fragment does not include a transdomain region of SEQ ID NO: 6042. 97. The polypeptide of claim 94, wherein said fragment does not include a C-terminus cytoplasmic domain of SEQ ID NO: 6042. 98. The polypeptide of claim 94, wherein said fragment does not include a N-terminus signal sequence. 99. An isolated polynucleotide comprising a nucleic acid sequence selected from the group consisting of SEQ ID NOS: 9968 and 10066. 100. The polynucleotide of claim 99, wherein the polynucleotide comprising a nucleic acid sequence having >80% sequence identity to a polynucleotide sequence selected from the group consisting of SEQ ID NOS: 9968 and 10066. 101. An isolated polynucleotide comprising a fragment of at least 15 consecutive nucleic acids of a nucleic acid sequence selected from the group consisting of SEQ ID NOS: 9968 and 10066 and wherein said fragment does not consist entirely of SEQ ID NO: 10033. 102. An isolated polypeptide comprising an amino acid sequence encoded by any one of claims 99-101. 103. The polypeptide of claim 102, comprising an amino acid sequence selected from the group consisting of SEQ ID NOS: 9969-10032, 10067, and 10015. 104. The polypeptide of claim 103, wherein the amino acid sequence is selected from the group consisting of SEQ ID NOS: 9997, 9998 and 10015. 105. An expression construct for recombinant expression of a SARS virus spike protein wherein said construct comprises a nucleic acid sequence selected from the group consisting of SEQ ID NOS: 6578-6583. 106. A mammalian cell line stably expressing a SARS viral antigen. 107. The cell line of claim 106, wherein said cell line is a Chinese Hamster Ovary (CHO) cell. 108. The cell line of claim 106, wherein the SARS viral antigen is a spike protein or fragment thereof. 109. The cell line of claim 106, wherein the spike protein is truncated to remove the transmembrane sequence. 110. A method of identifying a therapeutically active agent comprising the steps of: (a) contacting a therapeutically active agent with a buffer comprising SARS enzyme; and (b) measuring attenuation of the SARS enzyme. 111. The method of claim 110 wherein the SARS enzyme is a SARS protease. 112. The method of claim 111 wherein the buffer further comprises a peptide with a SARS protease cleave site. 113. The method of claim 110 wherein the measurement is made by the measurement of fluorescence. 114. A vaccine of one of claims 22 to 37, and 90 to 93 further comprising an adjuvant. 115. The vaccine of claim 114 wherein the adjuvant is a SMIP. 116. The vaccine of claim 115 wherein the SMIP compound is selected from the group consisting of an acylpiperazine, a tryptanthrin, an indoledione, a tetrahydroisoquinoline, a benzocyclodione, an amino azavinyl compound, a thiosemicarbazone, a lactam, an aminobenzimidazole quinolinone, a hydropthalamide, a benzophenone, an isoxazole, a sterol, a quinazolinone, a pyrole, an anthraquinone, a quinoxaline, a triazine, an benzazole, and a pyrazolopyrimidine, or a pharmaceutically acceptable salt, ester, or prodrug thereof. 117. A method of vaccinating a subject comprising administering a vaccine of one of claims 22 to 37, and 90 to 93. 118. The method of claim 117 further comprising administering a SMIP. 119. A method for treating a patient of one of claims 77 to 82 further comprising administering at least one SMEP compound. 120. A method for treating a patient of one of claims 77 to 82 further comprising administering at least one SMIS compound. SUMMARY OF THE INVENTION [0008] The invention relates to nucleic acids and proteins from Severe Acute Respiratory Syndrome (SARS) virus. These nucleic acids and proteins can be used in the preparation and manufacture of vaccine formulations for the treatment or prevention of SARS. Such vaccine formulations may include an inactivated (or killed) SARS virus, an attenuated SARS virus, a split SARS virus preparation and a recombinant or purified subunit formulation of one or more SARS viral antigens. Expression and delivery of the polynucleotides of the invention may be facilitated via viral vectors and/or viral particles. [0009] The invention also relates to diagnostic reagents, kits (comprising such reagents) and methods which can be used to diagnose or identify the presence or absence of a SARS virus in a biological sample. The invention further includes non-coding SARS viral polynucleotide sequences, SARS viral sequences encoding for non-immunogenic proteins, conserved and variant SARS viral polynucleotide sequences for use in such diagnostic compositions and methods. [0010] The invention further relates to vaccine formulations comprising one or more SARS virus antigens and one or more other respiratory virus antigens. Additional respiratory virus antigens suitable for use in the invention include antigens from influenza virus, human rhinovirus (HRV), parainfluenza virus (PIV), respiratory syncytial virus (RSV), adenovirus, metapneumovirus, and rhinovirus. The additional respiratory virus antigen could also be from a coronavirus other than the SARS coronavirus. Preferably, the additional respiratory virus antigen is an influenza viral antigen. [0011] The compositions of the invention may further comprise one or more adjuvants. Adjuvants suitable for use in the invention include mucosal, transdermal or parenteral adjuvants. Mucosal adjuvants suitable for use in the invention include detoxified bacterial ADP-ribosylating toxins, such as E. coli heat labile toxoids (e.g., LTK63), chitosan and derivatives thereof, and non-toxic double mutant forms of Bordetella pertussis toxoids. Parenteral adjuvants suitable for use in the invention include MF59 and aluminum or aluminum salts. [0012] The invention also provides methods for treating SARS by administering small molecule compounds, as well as methods of identifying potent small molecules for the treatment of SARS. [0013] In one aspect of the invention a method of identifying a therapeutically active agent is provided comprising: (a) contacting the therapeutically active agent with a cell infected with the SARS virus; (b) measuring attenuation of a SARS related enzyme. [0014] In a more particular embodiment, the therapeutically active agent is a small molecule. In another more particular embodiment, the therapeutically active agent is a nucleoside analog. In another more particular embodiment the therapeutically active agent is a peptoid, oligopeptide, or polypeptide. In another embodiment the SARS related enzyme is SARS protease. In another embodiment the SARS related enzyme is SARS polymerase. In still another embodiment the SARS related enzyme is a kinase. Methods of identifying therapeutically active agents for treatment of SARS virus infection are further discussed in Section V below. [0015] In another aspect of the invention a method of treating a human infected with SARS is provided comprising administering a small molecule to a patient in need thereof. In one embodiment the small molecule is an inhibitor of SARS protease. In another embodiment the small molecule is an inhibitor of SARS polymerase. In another embodiment the SARS related enzyme is a kinase. In still another embodiment the small molecule is administered orally or parenterally. [0016] The invention also provides the use of such small molecules in the manufacture of a medicament for the treatment of severe acute respiratory syndrome. [0017] Small molecule compounds of the present invention include those of less than 1000 g/mol, preferably with an aromatic region and greater than one heteroatom selected from O, S, or N. Preferred small molecules include, but are not limited to acyclovir, gancyclovir, vidarabidine, foscamet, cidofovir, amantidine, ribavirin, trifluorothymidine, zidovudine, didanosine, zalcitabine, and combinations thereof. Interferons may also be used for treating patients, including interferon-.alpha. and interferon-.beta.. Interferon treatment has shown promise in treating SARS in monkeys (Enserink (2004) Science 303:1273-1275), particularly when pegylated (Haagmans et al. (2004) Nature Medicine 10:290-293). [0018] One aspect of the present invention relates to methods for identifying individuals exposed to, and biological samples containing SARS virus (SARSV), and to kits for carrying out the methods. Such methods can utilize nucleic acid detection techniques such as PCR, RT-PCR (the Coronaviridae are RNA viruses), transcription-mediated amplification (TMA), ligase chain reaction (LCR), branched DNA signal amplification assays, isothermal nucleic acid sequence based amplification (NASBA), other self-sustained sequence replication assays, boomerang DNA amplification, strand-displacement activation, cycling probe technology, or combinations of such amplification methods. Such nucleic acid detection techniques utilize oligonucleotides having nucleotide sequence similar to, or complementary to, the SARS viral genome, as primers (e.g., for amplification) and as probes (e.g., for capture or detection), as is well known in the art. [0019] Alternatively, or in addition to the nucleic acid detection methods described supra, the methods of the present invention can utilize various immunoassay techniques for detection of SARSV antigens and/or antibodies. [0020] Accordingly, the present invention relates to methods of identifying individuals exposed to SARSV, or biological samples containing SARSV, by detecting the presence of SARSV antigens using antibodies which specifically bind to the same. The antibodies are preferably monoclonal antibodies. Quantification of the amount of viral antigens present in a sample of an individual may be used in determining the prognosis of an infected individual. Preferably, the SARSV antigens to be detected are generally one of the structural proteins, particularly those present on the surface of the viral particles and include, for example, the spike glycoprotein (S), also called E2; the envelope (small membrane) protein (E), also called sM; the membrane glycoprotein (M), also called E1 ; the hemagglutinin-esterase glycoprotein (HE); also called E3; and the nucleocapsid phosphoprotein (N). In preferred embodiments, the antigens to be detected are the S, E and M proteins using antibodies to the same. [0021] The present invention relates to kits for identifying individual SARSV and reagents used in such kits. The kits comprise a first container which contains antibodies which specifically bind to a SARSV antigen and a second container which contains the SARSV antigen. The antibodies are preferably monoclonal antibodies. The kits may be adapted for quantifying the amount of antigen in a sample of an individual. Such information may be used in determining the prognosis of an infected individual. [0022] The present invention relates to methods of identifying individuals exposed to SARS virus, or biological samples containing SARSV, by detecting the presence of antibodies against SARS virus antigen in a sample using SARS antigen. Quantification of the amount of anti-SARS protein from SARS antibodies present in a sample of an individual may be used in determining the prognosis of an infected individual. Any one or more of the viral proteins (structural proteins or nonstructural proteins) may be used as antigen to detect the SARSV antibodies; preferably a SARSV antigen that is conserved amoung SARSV isolates is preferred. In this regard, nonstructural protein (e.g., Pol, Hel, 3CLp, MP, PLP1, PLP2) may be particularly useful. [0023] The present invention relates to kits for identifying individuals exposed to SARS and reagents used therein. The kits comprise a first container which contains antibodies which were produced in response to exposure to an antigen from SARS virus and a second container which contains the SARS antigen(s). The kits may be adapted for quantifying the amount of anti-SARS antibodies present in a sample of an individual. Such information may be used in determining the prognosis of an infected individual. [0024] The present invention relates to methods of identifying individuals exposed to SARS virus, or biological samples containing SARSV, by detecting the presence of nucleic acid from SARS virus. Quantification of the amount of SARS nucleic acid present in a sample of an individual may be used in determining the prognosis of an infected individual. The methods utilize oligonucleotide probes and/or primers that are similar or complementary in sequence to the SARSV genome or transcription or replication products. Preferred probes and primers are described herein. Also included in the present invention are kits for carrying out the methods of detecting the SARSV nucleic acid. [0025] The invention further includes a method for the treatment and/or prevention of SARS through the administration of a therapeutically effective amount of at least one antiviral compound from among those described in the US patents and published international patent applications listed in Table 1 and Table 2. In one embodiment of the method, the antiviral compound is a small molecule. In another embodiment, the antiviral compound is a protease inhibitor. In a further embodiment, the antiviral protease inhibitor is a 3C-like protease inhibitor and/or a papain-like protease inhibitor. In another embodiment, the antiviral compound is an inhibitor of an RNA-dependent RNA polymerase. In another embodiment, a first antiviral compound which is a protease inhibitor is administered with a second antiviral compound which is an RNA-dependent RNA polymerase inhibitor. The invention further provides for the administration of a steroidal anti-inflammatory drug in combination with at least one antiviral compound, for example, from the antiviral compounds described in the documents listed in Table 1 and Table 2. [0026] The invention further provides for a method for the treatment and/or prevention of SARS through the administration of a therapeutically effective amount of at least one antiviral compound from among those described in the US patents and published international patent applications listed in Table 1 and Table 2 by inhalation. In one embodiment of the method, the antiviral compound is a small molecule. In another embodiment, the antiviral compound is a protease inhibitor. In a further embodiment, the antiviral protease inhibitor is a 3C-like protease inhibitor and/or a papain-like protease inhibitor. In another embodiment, the antiviral compound is an inhibitor of an RNA dependent RNA polymerase. In another embodiment, a first antiviral compound which is a protease inhibitor is administered with a second antiviral compound which is an RNA-dependent RNA polymerase inhibitor. The invention further provides for the administration of a steroidal anti-inflammatory drug in combination with at least one antiviral compound, for example, from the antiviral compounds described in the documents listed in Table 1 and Table 2 by inhalation. The steroidal anti-inflammatory drug may be administered by inhalation for a local effect or administered for systemic absorption such as via an oral or intravenous route. [0027] The invention further provides the use of an antiviral compound, as defined above, in the manufacture of a medicament for the treatment of severe acute respiratory syndrome. [0028] The invention further provides for a kit for use by a consumer for the treatment and/or prevention of SARS. Such a kit comprises: (a) a pharmaceutical composition comprising a therapeutically effective amount of at least one antiviral compound from among those described in the US patents and published international patent applications listed in Table 1 and Table 2 and a pharmaceutically acceptable carrier, vehicle or diluent; (b) a container for holding the pharmaceutical composition; and, optionally; (c) instructions describing a method of using the pharmaceutical compositions for the treatment and or the prevention of SARS. The kit may optionally contain a plurality of antiviral compounds for the treatment of SARS wherein the anti viral compounds are selected from 3C-like protease inhibitors and papain-like protease inhibitors. In a further embodiment, the kit contains an antiviral compound which is an RNA-dependent RNA polymerase inhibitor. When the kit comprises more than one antiviral compound, the antiviral compounds contained in the kit may be optionally combined in the same pharmaceutical composition. [0029] An additional aspect of the invention provides for the use of at least one of the antiviral compounds described in the US patents and published international patent applications listed in Table 1 and Table 2 for the manufacture of a medicament for the treatment or prevention of SARS.

CIA Planning Included Regime Change in Pakistan to Favour American Empire Expansion. 2022-04-19. Jorma Jyrkkanen, BSc PDP

https://www.globalresearch.ca/the-destabilization-of-pakistan/7705?fbclid=IwAR2V337Ca3ZAxIv4cwPMqXJeUxiJCqytZ_x51452NQhxKIG9WdgVjHo5kUc The Destabilization of Pakistan By Prof Michel Chossudovsky Global Research, April 16, 2022 30 December 2007 Region: Asia Theme: Terrorism, US NATO War Agenda In-depth Report: PAKISTAN [print] 88 30 7 138 Author’s Note The Biden White House was behind Prime Minister Imran Khan‘s political demise. “We know which are the places from where the pressure is being exerted on us. We will not compromise on the interest of the country. I [Khan] am not levelling allegations, I have the letter which is the proof,” Under Imran Khan, a major geopolitical shift had occurred, which Washington is intent upon reversing, Pakistan is no longer America’s staunchest ally. Washington’s actions in Pakistan go far beyond the narrow objective of “regime change”. Historically, the thrust of US foreign policy actions consisted in weakening the central government, fracturing the country as well as sabotaging Pakistan’s strategic and economic relations with China and Russia. The current crisis is a continuation of Washington’s resolve to retain Pakistan as a neo-colonial entity. It goes back to America’s design to trigger the collapse of Pakistan as a nation state following the assassination of Benazir Bhutto on December 27, 2007. According to a 2005 report by the US National Intelligence Council and the CIA, Pakistan was slated to become a “failed state” by 2015, “as it would be affected by civil war, complete Talibanisation and struggle for control of its nuclear weapons”. That was Washington’s strategic objective. It didn’t happen as planned. The following article published on December 30th, 2007 three days after the assassination of Benazir Bhutto, examines Washington’s scenario of disintegration and civil war in Pakistan. Michel Chossudovsky, April 16, 2022 *** The Destabilization of Pakistan By Prof Michel Chossudovsky Global Research, 30 December 2007 The assassination of Benazir Bhutto has created conditions which contribute to the ongoing destabilization and fragmentation of Pakistan as a Nation. The process of US sponsored “regime change”, which normally consists in the re-formation of a fresh proxy government under new leaders has been broken. Discredited in the eyes of Pakistani public opinion, General Pervez Musharaf cannot remain in the seat of political power. But at the same time, the fake elections supported by the “international community” scheduled for January 2008, even if they were to be carried out, would not be accepted as legitimate, thereby creating a political impasse. There are indications that the assassination of Benazir Bhutto was anticipated by US officials: “It has been known for months that the Bush-Cheney administration and its allies have been maneuvering to strengthen their political control of Pakistan, paving the way for the expansion and deepening of the “war on terrorism” across the region. Various American destabilization plans, known for months by officials and analysts, proposed the toppling of Pakistan’s military… The assassination of Bhutto appears to have been anticipated. There were even reports of “chatter” among US officials about the possible assassinations of either Pervez Musharraf or Benazir Bhutto, well before the actual attempts took place. (Larry Chin, Global Research, 29 December 2007) Political Impasse “Regime change” with a view to ensuring continuity under military rule is no longer the main thrust of US foreign policy. The regime of Pervez Musharraf cannot prevail. Washington’s foreign policy course is to actively promote the political fragmentation and balkanization of Pakistan as a nation. A new political leadership is anticipated but in all likelihood it will take on a very different shape, in relation to previous US sponsored regimes. One can expect that Washington will push for a compliant political leadership, with no commitment to the national interest, a leadership which will serve US imperial interests, while concurrently contributing under the disguise of “decentralization”, to the weakening of the central government and the fracture of Pakistan’s fragile federal structure. The political impasse is deliberate. It is part of an evolving US foreign policy agenda, which favors disruption and disarray in the structures of the Pakistani State. Indirect rule by the Pakistani military and intelligence apparatus is to be replaced by more direct forms of US interference, including an expanded US military presence inside Pakistan. This expanded military presence is also dictated by the Middle East-Central Asia geopolitical situation and Washington’s ongoing plans to extend the Middle East war to a much broader area. The US has several military bases in Pakistan. It controls the country’s air space. According to a recent report: “U.S. Special Forces are expected to vastly expand their presence in Pakistan, as part of an effort to train and support indigenous counter-insurgency forces and clandestine counterterrorism units” (William Arkin, Washington Post, December 2007). The official justification and pretext for an increased military presence in Pakistan is to extend the “war on terrorism”. Concurrently, to justify its counterrorism program, Washington is also beefing up its covert support to the “terrorists.” The Balkanization of Pakistan Already in 2005, a report by the US National Intelligence Council and the CIA forecast a “Yugoslav-like fate” for Pakistan “in a decade with the country riven by civil war, bloodshed and inter-provincial rivalries, as seen recently in Balochistan.” (Energy Compass, 2 March 2005). According to the NIC-CIA, Pakistan is slated to become a “failed state” by 2015, “as it would be affected by civil war, complete Talibanisation and struggle for control of its nuclear weapons”. (Quoted by former Pakistan High Commissioner to UK, Wajid Shamsul Hasan, Times of India, 13 February 2005): “Nascent democratic reforms will produce little change in the face of opposition from an entrenched political elite and radical Islamic parties. In a climate of continuing domestic turmoil, the Central government’s control probably will be reduced to the Punjabi heartland and the economic hub of Karachi,” the former diplomat quoted the NIC-CIA report as saying. Expressing apprehension, Hasan asked, “are our military rulers working on a similar agenda or something that has been laid out for them in the various assessment reports over the years by the National Intelligence Council in joint collaboration with CIA?” (Ibid) Continuity, characterized by the dominant role of the Pakistani military and intelligence has been scrapped in favor of political breakup and balkanization. US Cuts off Aid to Pakistan, Obstructing Pakistan’s Economic Cooperation with China According to the NIC-CIA scenario, which Washington intends to carry out: “Pakistan will not recover easily from decades of political and economic mismanagement, divisive policies, lawlessness, corruption and ethnic friction,” (Ibid) . The US course consists in fomenting social, ethnic and factional divisions and political fragmentation, including the territorial breakup of Pakistan. This course of action is also dictated by US war plans in relation to both Afghanistan and Iran. This US agenda for Pakistan is similar to that applied throughout the broader Middle East Central Asian region. US strategy, supported by covert intelligence operations, consists in triggering ethnic and religious strife, abetting and financing secessionist movements while also weakening the institutions of the central government. The broader objective is to fracture the Nation State and redraw the borders of Iraq, Iran, Syria, Afghanistan and Pakistan. Pakistan’s Oil and Gas reserves Pakistan’s extensive oil and gas reserves, largely located in Balochistan province, as well as its pipeline corridors are considered strategic by the Anglo-American alliance, requiring the concurrent militarization of Pakistani territory. Balochistan comprises more than 40 percent of Pakistan’s land mass, possesses important reserves of oil and natural gas as well as extensive mineral resources. The Iran-India pipeline corridor is slated to transit through Balochistan. Balochistan also possesses a deap sea port largely financed by China located at Gwadar, on the Arabian Sea, not far from the Straits of Hormuz where 30 % of the world’s daily oil supply moves by ship or pipeline. (Asia News.it, 29 December 2007) Pakistan has an estimated 25.1 trillion cubic feet (Tcf) of proven gas reserves of which 19 trillion are located in Balochistan. Among foreign oil and gas contractors in Balochistan are BP, Italy’s ENI, Austria’s OMV, and Australia’s BHP. It is worth noting that Pakistan’s State oil and gas companies, including PPL which has the largest stake in the Sui oil fields of Balochistan are up for privatization under IMF-World Bank supervision. According to the Oil and Gas Journal (OGJ), Pakistan had proven oil reserves of 300 million barrels, most of which are located in Balochistan. Other estimates place Balochistan oil reserves at an estimated six trillion barrels of oil reserves both on-shore and off-shore (Environment News Service, 27 October 2006) . Covert Support to Balochistan Separatists Balochistan’s strategic energy reserves have a bearing on the separatist agenda. Following a familiar pattern, there are indications that the Baloch insurgency is being supported and abetted by Britain and the US. The Baloch national resistance movement dates back to the late 1940s, when Balochistan was invaded by Pakistan. In the current geopolitical context, the separatist movement is in the process of being hijacked by foreign powers. British intelligence is allegedly providing covert support to Balochistan separatists (which from the outset have been repressed by Pakistan’s military). In June 2006, Pakistan’s Senate Committee on Defence accused British intelligence of “abetting the insurgency in the province bordering Iran” [Balochistan]..(Press Trust of India, 9 August 2006). Ten British MPs were involved in a closed door session of the Senate Committee on Defence regarding the alleged support of Britain’s Secret Service to Baloch separatists (Ibid). Also of relevance are reports of CIA and Mossad support to Baloch rebels in Iran and Southern Afghanistan. It would appear that Britain and the US are supporting both sides. The US is providing American F-16 jets to the Pakistani military, which are being used to bomb Baloch villages in Balochistan. Meanwhile, British alleged covert support to the separatist movement (according to the Pakistani Senate Committee) contributes to weakening the central government. The stated purpose of US counter-terrorism is to provide covert support as well as as training to “Liberation Armies” ultimately with a view to destabilizing sovereign governments. In Kosovo, the training of the Kosovo Liberation Army (KLA) in the 1990s had been entrusted to a private mercenary company, Military Professional Resources Inc (MPRI), on contract to the Pentagon. The BLA bears a canny resemblance to Kosovo’s KLA, which was financed by the drug trade and supported by the CIA and Germany’s Bundes Nachrichten Dienst (BND). The BLA emerged shortly after the 1999 military coup. It has no tangible links to the Baloch resistance movement, which developed since the late 1940s. An aura of mystery surrounds the leadership of the BLA. Distribution of Balochs is marked in pink. Baloch population in Pink: In Iran, Pakistan and Southern Afghanistan Washington favors the creation of a “Greater Balochistan” which would integrate the Baloch areas of Pakistan with those of Iran and possibly the Southern tip of Afghanistan (See Map above), thereby leading to a process of political fracturing in both Iran and Pakistan. “The US is using Balochi nationalism for staging an insurgency inside Iran’s Sistan-Balochistan province. The ‘war on terror’ in Afghanistan gives a useful political backdrop for the ascendancy of Balochi militancy” (See Global Research, 6 March 2007). Military scholar Lieutenant Colonel Ralph Peters writing in the June 2006 issue of The Armed Forces Journal, suggests, in no uncertain terms that Pakistan should be broken up, leading to the formation of a separate country: “Greater Balochistan” or “Free Balochistan” (see Map below). The latter would incorporate the Pakistani and Iranian Baloch provinces into a single political entity. In turn, according to Peters, Pakistan’s North West Frontier Province (NWFP) should be incorporated into Afghanistan “because of its linguistic and ethnic affinity”. This proposed fragmentation, which broadly reflects US foreign policy, would reduce Pakistani territory to approximately 50 percent of its present land area. (See map). Pakistan would also loose a large part of its coastline on the Arabian Sea. Although the map does not officially reflect Pentagon doctrine, it has been used in a training program at NATO’s Defense College for senior military officers. This map, as well as other similar maps, have most probably been used at the National War Academy as well as in military planning circles. (See Mahdi D. Nazemroaya, Global Research, 18 November 2006) “Lieutenant-Colonel Peters was last posted, before he retired to the Office of the Deputy Chief of Staff for Intelligence, within the U.S. Defence Department, and has been one of the Pentagon’s foremost authors with numerous essays on strategy for military journals and U.S. foreign policy.” (Ibid) Map: click to enlarge It is worth noting that secessionist tendencies are not limited to Balochistan. There are separatist groups in Sindh province, which are largely based on opposition to the Punjabi-dominated military regime of General Pervez Musharraf (For Further details see Selig Harrisson, Le Monde diplomatique, October 2006) “Strong Economic Medicine”: Weakening Pakistan’s Central Government Pakistan has a federal structure based on federal provincial transfers. Under a federal fiscal structure, the central government transfers financial resources to the provinces, with a view to supporting provincial based programs. When these transfers are frozen as occurred in Yugoslavia in January 1990, on orders of the IMF, the federal fiscal structure collapses: “State revenues that should have gone as transfer payments to the republics [of the Yugoslav federation] went instead to service Belgrade’s debt … . The republics were largely left to their own devices. … The budget cuts requiring the redirection of federal revenues towards debt servicing, were conducive to the suspension of transfer payments by Belgrade to the governments of the Republics and Autonomous Provinces. In one fell swoop, the reformers had engineered the final collapse of Yugoslavia’s federal fiscal structure and mortally wounded its federal political institutions. By cutting the financial arteries between Belgrade and the republics, the reforms fueled secessionist tendencies that fed on economic factors as well as ethnic divisions, virtually ensuring the de facto secession of the republics. (Michel Chossudovsky, The Globalization of Poverty and the New World Order, Second Edition, Global Research, Montreal, 2003, Chapter 17.) It is by no means accidental that the 2005 National Intelligence Council- CIA report had predicted a “Yugoslav-like fate” for Pakistan pointing to the impacts of “economic mismanagement” as one of the causes of political break-up and balkanization. “Economic mismanagement” is a term used by the Washington based international financial institutions to describe the chaos which results from not fully abiding by the IMF’s Structural Adjustment Program. In actual fact, the “economic mismanagement” and chaos is the outcome of IMF-World Bank prescriptions, which invariably trigger hyperinflation and precipitate indebted countries into extreme poverty. Pakistan has been subjected to the same deadly IMF “economic medicine” as Yugoslavia: In 1999, in the immediate wake of the coup d’Etat which brought General Pervez Musharaf to the helm of the military government, an IMF economic package, which included currency devaluation and drastic austerity measures, was imposed on Pakistan. Pakistan’s external debt is of the order of US$40 billion. The IMF’s “debt reduction” under the package was conditional upon the sell-off to foreign capital of the most profitable State owned enterprises (including the oil and gas facilities in Balochistan) at rockbottom prices . Musharaf’s Finance Minister was chosen by Wall Street, which is not an unusual practice. The military rulers appointed at Wall Street’s behest, a vice-president of Citigroup, Shaukat Aziz, who at the time was head of CitiGroup’s Global Private Banking. (See WSWS.org, 30 October 1999). CitiGroup is among the largest commercial foreign banking institutions in Pakistan. There are obvious similarities in the nature of US covert intelligence operations applied in country after country in different parts of the so-called “developing World”. These covert operation, including the organisation of military coups, are often synchronized with the imposition of IMF-World Bank macro-economic reforms. In this regard, Yugoslavia’s federal fiscal structure collapsed in 1990 leading to mass poverty and heightened ethnic and social divisions. The US and NATO sponsored “civil war” launched in mid-1991 consisted in coveting Islamic groups as well as channeling covert support to separatist paramilitary armies in Bosnia, Kosovo and Macedonia. A similar “civil war” scenario has been envisaged for Pakistan by the National Intelligence Council and the CIA: From the point of view of US intelligence, which has a longstanding experience in abetting separatist “liberation armies”, “Greater Albania” is to Kosovo what “Greater Balochistan” is to Pakistan’s Southeastern Balochistan province. Similarly, the KLA is Washington’s chosen model, to be replicated in Balochistan province. The Assassination of Benazir Bhutto Benazir Bhutto was assassinated in Rawalpindi, no ordinary city. Rawalpindi is a military city host to the headquarters of the Pakistani Armed Forces and Military Intelligence (ISI). Ironically Bhutto was assassinated in an urban area tightly controlled and guarded by the military police and the country’s elite forces. Rawalpindi is swarming with ISI intelligence officials, which invariably infiltrate political rallies. Her assassination was not a haphazard event. Without evidence, quoting Pakistan government sources, the Western media in chorus has highlighted the role of Al-Qaeda, while also focusing on the the possible involvement of the ISI. What these interpretations do not mention is that the ISI continues to play a key role in overseeing Al Qaeda on behalf of US intelligence. The press reports fail to mention two important and well documented facts: 1) the ISI maintains close ties to the CIA. The ISI is virtually an appendage of the CIA. 2) Al Qaeda is a creation of the CIA. The ISI provides covert support to Al Qaeda, acting on behalf of US intelligence. The alleged involvement of either Al Qaeda and/or the ISI would suggest that US intelligence was cognizant and/or implicated in the assassination plot. [Part Two: Pakistan and the “Global War on Terrorism” Michel Chossudovsky is the author of the international bestseller America’s “War on Terrorism” Global Research, 2005. He is Professor of Economics at the University of Ottawa and Director of the Center for Research on Globalization.

Chinas Social Credit System compared to Facebook Social Media Community Standards Boycott System and the Wests Tax System. 2022-04-13 Jorma Jyrkkanen, BSc, PDP

Chinas Social Credit System Punishment and Denial of Priviliges for Disobedience. For speaking against the system. Tianamin Square massacre was the best known example of frank outright put-down of free speech where protestors were killed. Training camps for Uighurs are another example. The Abolition of protest in Hong Kong is a conctinuation of that autocratic domination. There are more subtle wayw China punishes free speakers. China's 'social credit' system ranks citizens and punishes them with throttled internet speeds and flight bans if the Communist Party deems them untrustworthy. The Chinese Communist Party has been constructing a moral ranking system for years that will monitor the behavior of its enormous population — and rank them all based on their "social credit." The "social credit system," first announced in 2014, is "an important component part of the Socialist market economy system and the social governance system" and aims to reinforce the idea that "keeping trust is glorious and breaking trust is disgraceful," according to a 2015 government document. The rankings are decided by China's economics planning team, the National Development and Reform Commission (NDRC), the People's Bank of China, and the Chinese court system, according to the South China Morning Post. The system can be used for individual people, but also for companies and government organizations. The private sector, including the burgeoning tech world in China, has their own non-governmental scoring systems that they implement, as Wired reported. For example, Sesame Credit, which is owned by Jack Ma's Ant Group, uses its own unofficial scoring system for its employees, such as studying shopping habits, according to the think tank Merics. The program has been piloted for millions across the country in recent years, as CNBC reported, and was expected to become fully operational and integrated by 2020. But at the moment the system is piecemeal and voluntary, though the plan is for it to eventually be mandatory and unified across the nation, with each person given their own unique code used to measure their social credit score in real-time, per Wired. Denial of Privileges for Speaking, Writing, Publishing and Protesting Behaviors offending Tribunals and Government in the West If you write material the goes against so called community standards or is deemed false on Facebook, you may be punished by banning permanently any number of days by people who you don't know, whose knowledge you cannot check, whose motives are potentially suspect, who you cannot really challenge because you are denied access to the social media. Science cannot be done this way so science is ruled out as an activity that has any credibility. Who and how are community standards determined? I have never been asked for input. This leaves only one conclusion. The system is geared for manipulation for profit and censorship. This is neither science nor journalism and violates Freedoms of speech, the press and association in the western world, both guaranteed by Charter and Constitutional rights. Criticisms may be misinterpreted as hate speech so that vast areas of contention are out of bounds for public discussion. This is clear attempt to muzzle intellectual debate and evade discovery of inconvenient truths. The most clear violation I have seen is the use of Bank denials and removal of drivers work priviliges and trucks being seized and freedoms being squashed by legislation in Canada for truckers daring to protest what some would call excessive impositions on Charter freedoms and rights over covid among truckers who never were demonstrated to spread the virus. Similar draconian measures are being used against Russia for aggressive retaliatory war of Russia against an American coup imposed fascist regime in the Ukraine which has discriminated against Russian speakers in the Donbass region. The Wests Tax System Poor people are inordinately taxed relatively more draconianly than the rich and corporations leading to vast inequity, indenturement to corporations and money lenders and tedious shorter lives with less opportunity. This is a form of punishment for no other sin than fortuitous birth place. This is a proxy punitive social credit system that punishes people based on economic class.

WHAT HUMAN ENDOGENOUS RETROVIRUS's SAY ABOUT WHAT WE ARE. A HETEROGENOUS VIBORG? 2022-04-12 Jorma Jyrkkanen, BSc, PDP

Viborg Chimaeral Variant Implications of HERV for The Human Species. This is Pure Conjecture. Original 11 February 2011 There is Mendelian genetics and then there is the following and we must also account for epigenetics which I don't discuss here though its possibly a great player in the whole genome story. Because we share genes in common with everything from a banana to chimps and bacteria to viruses is logical to deduce that science is on the cusp of a great discovery of the human race. We are a pluripotent genetic chimaera. How I arrived at this INTRIGUING IDEA is from a long standing consideration of trying to find an explanation for autism, schizophrenia, and the 26 genes for mental retardation on the human X chromosome and several days ago, finding out that we have 50,000 human endogenous retroviruses HERV's in the non-coding regions of our DNA genome. It was reading this article and watching undisciplined children's behavior change to more infective mode with flu virus infections that brought me to this eureka moment. http://www.autoimmune.com/HMTVGen.html It occured to me that these HERV's must from time to time manifest themselves in altering human behavior as well as the cancers like murine breast cancer MMTV and HMTV, the 95% similar human variant we have come to associate with them. Multicellular organisms that have mitchondria, golgi apparatae, amoeboid cells are really a symbiont of a variety of cell types each contributing something vital to the organism including quite possibly a behavioral component. This makes eukaryotes a chimaera, a bizarre hybrid of species and classes of organisms. With the discovery of HERV's, we must accept that we are also hybridized with endogenous retroviruses, some so deeply incorporated into our genomes, that they are not recognized by the immune system as other when they happen to produce their proteins in a reading frame and they may in fact through mutations and selection, provide benefits to evolutionary fitness. The Retrovirus Life Cycle Unlike most other organisms, the genome of a retrovirus is composed of RNA instead of DNA. This means that infectious retroviral particles contain RNA. After infection of a cell by a retrovirus, the viral RNA is released into the cell along with several proteins which are required for the initial steps of viral replication. One of these proteins is called reverse transcriptase. After the release of the RNA, the reverse transcriptase makes, or transcribes, a DNA copy of the viral genome. This DNA copy is then inserted somewhat randomly into the DNA of the infected cell. The insertions occur in areas of the cell's DNA that are undergoing the normal DNA replication that happens prior to cell division, so only actively growing cells can support insertion of viral DNA. After the DNA copy is inserted into the cell's DNA, viral sequences then direct the expression of the viral genome. During this process, which in the case of MMTV occurs in response to estrogen, a complete RNA copy of the entire viral genome is produced. This RNA is then packaged into infectious viral particles, and the viral particles are subsequently released from the cell where they can infect another cell and start the whole cycle again. Insertional Mutagenesis During the viral life cycle the insertion of the viral genome occurs most of the time within "silent" regions of the cell's DNA. These silent regions, which account for the vast majority of the DNA within a cell, have no known function. Sometimes, however, the insertion occurs within or very near the DNA base pairs that make up a gene, and the presence of the virus's inserted DNA alters the function of that gene. The altered gene is said to have been mutated, and this process is called insertional mutagenesis. If the normal function of a gene is critical to the survival of the cell, then a mutation of the gene will kill the infected cell. But if the gene controls a non-critical function of the infected cell, such as its growth, the cell can survive the insertion despite the fact that the cell's physiology has been permanently altered. In some cases this mutation has no outward effect on the cell, but in other cases the mutation can have profound effects on how the cell grows and behaves. Other HERV's are known to cause autoimmune diseases and there are quite a number of them. I thought why not diseases that affect human consiousness and behavior as well and of course they must, because like the mitochondria, golgi, plasmid of old, each addition to the mix that is eukaryotes must bring a behavioral component as well. I think now that I have identified that we humans have pluripotent chimaeral variants in existence and what we call disease in some cases is really the HERV taking over the ape inherited behavioral component of our species making us a HERV human hybrid, Herv-Borgs or short hand Viborgs if you will. 50,000 HERV's that live in our DNA cannot be ignored regarding their potential to alter our being. I think it is entirely within the frame of reality to postulate here and now that human virus hybrids, HERV-Borgs or Viborgs can and do exist and we simply didn't realize this until molecular genetics had advanced to where it is today. Mysterious psychological diseases that have bizarre unexplained elements coud possibly be cases of Viborgs. Conversely if an individuals behavior is ape_like, simian if you will, then they are a Simborg. Simply put. More variants of humans exist than we have recognized previously by manifestation of HERV product and they may be HERV-Ape hybrids. The Ape lineage is too narrow a perspective for what it is to be Human. Some proportion of psychopathologies that manifest clearly un-ape like behavior are potentially Viborgs, this other variant whose HERV DNA is not in the silent region sleeping at all but is the virus very much producing protein product. Is this an example of saltatory evolution testing the variant field? An interesting new development is that bacteria can incorporate segments of human DNA into their genomes! http://www.medicalnewstoday.com/articles/216442.php The profound ramification of this is that other organisms are chimaeras too, made up not only of genes they themselves have inherited and mutated but genes they have copied or stolen or had injected by phages or symbionts or pathogens from other species. Was a human endogenous retrovirus virus involved in the transfer? Raises the profound question is there a pure species or is every creature a chimaera? In further reading from the internet, I have found an ancient lemur retrovirus in the human genome called HERV-W that is associated with schizophrenia psychosis. http://discovermagazine.com/2010/jun/03-the-insanity-virus/article_view?b_start:int=2&-C
“Research shows that infections may play a role in chronic psychiatric illnesses such as schizophrenia, with the Herpes virus family.” (See MedWireNews, Schizophrenia Research, 2011) (4) (4) Davenport, L. EBV infection linked to subclinical psychosis symptoms. Published June 16, 2011. How does EBV cause schizophrenia? Scientists are not entirely certain. However, one theory suggests that viruses like EBV actually integrate with the genome (the genetic material) of those they infect. “The insertion of viral DNA into the human genome had until recently been thought to be the preserve of retroviruses. However the incorporation of DNA into mammalian genomes has recently been demonstrated on a large scale for both RNA and DNA viruses.” (See the Journal of Pathogens, from 2011) (5) EBV is a double stranded DNA virus. The result of the integration of EBV into the genome is that “upon infection, these pathogens are thus able to interfere with the function of their human counterparts in a number of ways.” (5) For example, “Repeated viral insertion could well explain copy number variations, which are associated with a number of diseases, including schizophrenia.” (5) Carter, C.J. Schizophrenia: A Pathogenetic Autoimmune Disease Caused by Viruses and Pathogens and Dependent on Genes. Journal of Pathogens. Published 2011. Q.E.D. Thesis confirmed. We are a chimaera and a psychotic viral variant, a Viborg, exists. The clinical and legal ramifications are enormous stemming from my discovery. Psychosis can be contagious triggered by infections, pathogens and human endogenous retrovirus becoming active. There is a very important ramification for our understanding of evolution speaking to us from this lateral gene injection. It is this. Evolution is both intraspecific and interspecific, that is linear and lateral across species, and I would call it transpecific evolutionary genome transfer. Viborgs and Simborgs cry out that evolution is linear with inherited genomes and lateral with acquired genomes as is the case when our primal plasmids acquired the mitochondria or a virus inserted or newly asserts itself into our inherited genome. Darwin would shake in his boots at this conclusion.

Conversely, Perrons genome, HERV-W on chromosomes 6, 7 when inactivated, is probably the main cause of rationality in the human species and if coupled to neoteny of infantile imprinting, can explain our ability to learn over a lifetime and make scientific deductions. My conclusion is that there is no such thing as pure species. All life owes its existence to the web of life around us. Copyright 2011 Jorma Jyrkkanen. All rights reserved. Tags: HERV, endogenous retroviruses, chimaera, humans, psychologicaal, disease, pluripotential, hybrids, HERV-Borg, Viborg, Jorma Jyrkkanen Addendum: These chaps showe that MYRPH in the brain can alter gene expression. MYRF encodes a transcription factor, a protein which binds to the DNA of other genes and switches them on or off. Without it, many of the genes needed for myelination don't get turned on and the whole process goes awry, leading to major neurological problems. Recently, two research teams independently teased apart how MYRF works and discovered that a core part of the gene originally came from a virus which preys upon bacteria. This line of work has led to major changes to our understanding of evolution as attested to by a Sept tweet by this reporter. This raises the question does modifying gene expression in the brain alter behavioural expression? http://www.nature.com/scitable/blog/accumulating-glitches/viruses_genes_in_our_brain Tags: chimaera, disease, endogenous retroviruses, herv, herv-borg, humans, hybrids, jorma jyrkkanen, pluripotential, psychologicaal, viborg

How Exososmes Spike Protein May Account for Cardiomyopathy Long After Exposure to Vaccine or Virus. 2022-04-05

I assembled this Powerpoint Video to demonstrate a possible pathway to high cardiomyopathy from exposure by either one or both virus or vaccine spike fragments. It points to the need for clarification in the research.