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FTR #694 The Perfect War Machine

MP3 Side 1 [1] | Side 2 [2]

Intro­duc­tion: Past broad­casts have dealt with the sub­ject of can­cer as a weapon of assas­si­na­tion, as well as the con­t­a­m­i­na­tion of vac­cines with SV40, a dead­ly can­cer-caus­ing simi­an virus [3]. This pro­gram details the mech­a­nisms through which SV40 caus­es can­cer. It is impor­tant to remem­ber that this virus has, in all prob­a­bil­i­ty, been “weaponized” through the research detailed by Ed Haslam in Dr. Mary’s Mon­key [4].

To under­stand how a virus can cause can­cer, it is help­ful to under­stand how the body and its cells defend them­selves against becom­ing can­cer­ous. There are mech­a­nisms which func­tion as cel­lu­lar brakes, work­ing to pre­vent the prop­a­ga­tion of dam­aged and poten­tial­ly can­cer­ous cells and oth­ers that act as “accel­er­a­tors,” work­ing to pro­duce vir­tu­al­ly unlim­it­ed and patho­log­i­cal cell growth.

SV40 neu­tral­izes the Rb and p53 genes, two of the body’s most impor­tant defens­es against cells becom­ing can­cer­ous. Neu­tral­iz­ing the Rb pro­teins and p53 gene is essen­tial to cause a cell to become can­cer­ous. Act­ing in tan­dem, they assure that a cell that under­goes abnor­mal repro­duc­tion will die, rather than repro­duce and pass on the devel­op­men­tal abnor­mal­i­ty and any asso­ci­at­ed risk for can­cer.

In addi­tion to neu­tral­iz­ing p53 and the Rbs, SV40 and its T‑antigen pro­tein scram­ble the nuclei of infect­ed cells. With P53 and the Rb pro­teins neu­tral­ized by large T‑antigen, the result­ing abnor­mal cells are free to repro­duce.

In addi­tion to neu­tral­iz­ing the P53 gene and the Rb proteins–the cel­lu­lar “brakes”–SV40 acti­vates two “oncogenes”–Met and Notch‑1, which func­tion as cel­lu­lar accel­er­a­tors per­mit­ting the uncon­trolled growth char­ac­ter­iz­ing can­cer cells.

In yet anoth­er fash­ion, SV40 facil­i­tates onco­ge­n­e­sis by pre­vent­ing the pro­gres­sive short­en­ing of the telom­eres as cells repeat­ed­ly divide. A spin­dle of fibers at the end of each chro­mo­some, the telom­eres are essen­tial for cel­lu­lar repro­duc­tion and they short­en pro­gres­sive­ly as cells repro­duce. Even­tu­al­ly, they short­en to the point where cel­lu­lar repro­duc­tion becomes impos­si­ble and the cell line per­ish­es. SV40 pre­vents this pro­gres­sive short­en­ing, facil­i­tat­ing the for­ma­tion of can­cer cells.

[4]Yet anoth­er remark­able and dead­ly fea­ture of SV40 is its “stealth” abil­i­ty to cause can­cer, infect­ing cells, trans­form­ing them and then dis­ap­pear­ing, thus escap­ing the immune sys­tem’s nat­ur­al mech­a­nisms for attack­ing large T‑antigen. With the now malig­nant cells no longer man­i­fest­ing large T‑antigen, those cells can escape neu­tral­iza­tion by the immune sys­tem.

On top of the oth­er can­cer-caus­ing mech­a­nisms that SV40 man­i­fests, the virus stim­u­lates the pro­duc­tion of VEGF, which caus­es the growth of blood ves­sels that nour­ish tumors.

Yet anoth­er dev­as­tat­ing aspect of SV40 is the fact that there are two major varieties–”slow growth” and “fast growth” SV40. Slow growth SV40 takes 19 days to mature, evad­ing the screen­ing process which eval­u­ates cell cul­tures after the four­teen days that the faster grow­ing vari­ant of the virus takes to reach matu­ri­ty and dam­age cells in such a way as to become evi­dent to the screen­ing pro­ce­dures of the time.

Pro­gram High­lights Include: An overview of the mol­e­c­u­lar sim­plic­i­ty of SV40’s struc­ture; review of the appar­ent weaponiza­tion of SV40 dis­cussed by Ed Haslam [5]; review of the appar­ent soft-tis­sue can­cer-epi­dem­ic [6] stem­ming from SV40 vac­cine con­t­a­m­i­na­tion; dis­cus­sion of the inter­ac­tion of envi­ron­men­tal car­cino­gens with SV40 to pro­duce mesothe­lioma and oth­er can­cers.

1. The SV40 is as sim­ple as it is dead­ly.

Mag­ni­fied fifty thou­sand times under an elec­tron micro­scope, SV40 does­n’t seem par­tic­u­lar­ly men­ac­ing. In con­trast to the por­ten­tous, worm­like shape of some more noto­ri­ous virus­es, such as Ebo­la, SV40 looks almost pretty–bluish snowflakes against a field of white. It owes its del­i­cate appear­ance to its isosa­he­dral tri­an­gu­lar scaf­fold­ing, a geo­met­ric, twen­ty-sided pro­tein skin that sur­rounds its lone cir­cu­lar dou­ble strand of DNA. Com­pact and effi­cient, the DNA strand con­tains only 5,243 base pairs–a lean life form com­pared to the four mil­lion base pairs of DNA con­tained in even a sim­ple bac­teri­um. SV40 is as sim­ple as it is small. The human genome codes for 150,000 pro­teins while SV40 codes for just six (although some sci­en­tists believe they have recent­ly dis­cov­ered a sev­enth), three of which make up its pro­tein skin. Of the remain­ing pro­teins, one reg­u­lates the virus’s growth and the two oth­ers are the virus’s tumor-caus­ing pro­teins, hence the name: T‑antigen, for tumor-caus­ing anti­gen. The large T‑antigen, dis­tin­guished by its cap­i­tal T, is about 700 amino acids in length, while its sis­ter pro­tein, the small t‑antigen, des­ig­nat­ed with a low­er-case t, embod­ies 174 amino acids. Sci­en­tists often refer to these two tumor-caus­ing pro­teins by short­hand des­ig­na­tions of “Tag,” for the large T‑antigen and “tag” for the small t‑antigen. These tumor anti­gens, par­tic­u­lar­ly the large T‑antigen are high­ly onco­genic. [Pio­neer SV40 researcher Dr. Michele] Car­bone describes large T‑antigen as “the most onco­genic pro­tein ever dis­cov­ered. It is unique”, he says, “in its abil­i­ty to cause can­cer when set loose inside cer­tain cells.”

(The Virus and the Vac­cine; Deb­bie Bookchin and Jim Schu­mach­er; St. Martin’s Press [HC]; Copy­right 2004 by Deb­bie Bookchin and Jim Schu­mach­er; ISBN 0–312-27872–1; pp. 204–205.) [3]

2. As stat­ed by the authors, to under­stand how a virus can cause can­cer, it is help­ful to under­stand how the body and its cells defend them­selves against becom­ing can­cer­ous. There are mech­a­nisms which func­tions as cel­lu­lar brakes, work­ing to pre­vent the prop­a­ga­tion of dam­aged and poten­tial­ly can­cer­ous cells and oth­ers that act as “accel­er­a­tors,” work­ing to pro­duce vir­tu­al­ly unlim­it­ed and patho­log­i­cal cell growth.

To under­stand how a cell becomes can­cer­ous, it helps to know some­thing about the mul­ti­lay­ered pro­tec­tions bequeathed by nature to help pre­vent cells from becom­ing can­cer­ous. It is only when these pro­tec­tive mech­a­nisms are breached that the cell takes its dead­ly turn toward immor­tal­i­ty.

Sim­ply put, for a cell to become can­cer­ous three things have to hap­pen. The first is that the cell has to lose the func­tion of those genes that restrain cell growth and pre­vent malignancy–the cel­lu­lar “brakes,” so to speak. Sec­ond­ly, the cell has to receive a stim­u­lat­ing sig­nal from those genes–called oncogenes–that cause tumor cells to grow. Final­ly, the cel­l’s nor­mal lim­it on now many times it can divide must be over­come.

Ibid.; p.205. [7]

3. SV40 neu­tral­izes the Rb and p53 genes, two of the body’s most impor­tant defens­es against cells becom­ing can­cer­ous.

The first of these pro­tec­tions involve a series of tumor sup­pres­sor genes known as p53 and the Rb genes. When­ev­er a cell begins to divide, in the process known as mito­sis, a small army of qual­i­ty con­trol agents goes to work. Run­ning up and down the cel­l’s DNA, like a band of fre­net­ic elec­tri­cians look­ing for loose wiring in an apart­ment com­plex, these genes and pro­teins work togeth­er in a suc­ces­sion of intri­cate­ly linked mech­a­nisms to scru­ti­nize the DNA’s integri­ty. If at any stage of cell divi­sion they detect DNA abnor­mal­i­ties, mito­sis is halt­ed and the dam­age is repaired. If the dam­age can­not be repaired, anoth­er set of genes is acti­vat­ed and the cell under­goes “apop­to­sis,” the term for pro­grammed cell death–the cell essen­tial­ly com­mits sui­cide.

Idem. [7]

4. Neu­tral­iz­ing the Rb pro­teins and p53 gene is essen­tial to cause a cell to become can­cer­ous. More about how p53 and the Rbs work and their role in main­tain­ing nor­mal cel­lu­lar repro­duc­tion:

The prin­ci­pal in this elab­o­rate reg­u­la­to­ry ance is called p53. Arnold J. Levine, for­mer pres­i­dent of Rock­e­feller Uni­ver­si­ty, in New York City, and one of the dis­cov­er­ers of p53, says that 60 per­cent of all can­cers involve some sort of dam­age, muta­tion, or inac­ti­va­tion of the gene. “The p53 gene is cen­tral to human can­cers,” he explains, describ­ing it is “the first line of defense against can­cer for­ma­tion.” If p53 is not func­tion­ing prop­er­ly, a cell with altered DNA may under­go mito­sis instead of dying as it should. If the DNA alter­ations are such that the cell con­tin­ues to repro­duce wild­ly, that is the begin­ning of a can­cer.

In July 1997, in two ground­break­ing papers pub­lished in the jour­nal Nature Med­i­cine, Car­bone and his col­lab­o­ra­tors exam­ined how SV40’s large T‑antigen is able to stran­gle p53 and oth­er cru­cial tumor sup­pres­sor genes in human mesothe­lial cells. one of the para­dox­es about mesothe­lioma is that human mesothe­liomas are rich in nor­mal p53, yet they are one of the most dead­ly human can­cers. Why, if there is an abun­dance of this can­cer-sup­press­ing gene, is the can­cer so aggres­sive? Car­bone’s exper­i­ments showed that in human mesothe­liomas, large T‑antigen attacks p53, bind­ing to it so that it can­not func­tion prop­er­ly even though the gene is present in large quan­ti­ties. In effect, it does­n’t mat­ter how much p53 is present in the mesothe­liomas; SV40 pro­duces enough T‑antigen to dis­able all of it. In the com­pan­ion Nature Med­i­cine study, Anto­nio Gior­dano, then at the Kim­mel Can­cer Can­cer in Philadel­phia, described how large T‑antigen inhibits a sec­ond series of anti­cancer pro­teins called Rbs, which togeth­er serve as the final gate­keep­ers in cel­lu­lar divi­sion they thus serve as a sec­ond lay­er of cel­lu­lar pro­tec­tion against against can­cer. If p53 fails, the Rbs can step in and stop genet­i­cal­ly defec­tive cells from divid­ing. Gior­dano found that in mesothe­liomas, SV40 T‑antigen was crip­pling the Rbs.

Togeth­er, the Car­bone and Gior­dano stud­ies estab­lished that SV40 is unique­ly onco­genic in human mesothe­liomas. Using a sin­gle protein–large T‑antigen–SV0 can dis­able the body’s most impor­tant can­cer sup­press­ing sys­tems simul­ta­ne­ous­ly. No oth­er can­cer-caus­ing virus has that capac­i­ty. For exam­ple, human papil­lo­ma virus, which caus­es cer­vi­cal can­cer, must pro­duce two pro­teins, E6 and E7, to inac­ti­vate p53 and the Rbs respec­tive­ly. SV40 needs only one–large
T‑antigen. For this rea­son, Arnold Levine calls large T‑antigen “a remark­able pro­tein.” . . .

Ibid.; p. 206. [7]

5. In addi­tion to neu­tral­iz­ing p53 and the Rbs, SV40 and T‑antigen scram­ble the nuclei of infect­ed cells.

. . . What makes a cell malig­nant? Once again, SV40 can serve as the source of the actu­al genet­ic changes that make nor­mal cells can­cer­ous. Again, the virus can do it in more than one way. One is through human chro­mo­some damage–by adding or delet­ing whole sec­tions of DNA or reshuf­fling the genes on the twen­ty-three pairs of chro­mo­somes con­tained in the cel­l’s nucle­us. Joseph R. Tes­ra, direc­tor of the Human Genet­ics Pro­gram at Fox Chase Can­cer Cen­ter in Philadel­phia, says that once SV40 is fin­ished with a cell, “it looks like some­body set off a bomb inside the cel­l’s nucle­us, because of all these chro­mo­some rearrange­ments.”

Ibid.; pp. 207–208. [7]

6. In addi­tion, SV40 accel­er­ates cell growth, anoth­er con­di­tion for can­cer-for­ma­tion. SV40 acti­vates two “onco­genes” or can­cer-caus­ing genes, Met and Notch‑1.

Anoth­er way SV40 induces malig­nan­cy is to accel­er­ate cell growth. An Ital­ian team of sci­en­tists dis­cov­ered that T‑antigen trig­gers an “acti­va­tion” sig­nal (or onco­gene) in the cell called Met that stim­u­lates growth fac­tors. This caus­es the mesothe­o­lial cell to go from a rest­ing phase to a repli­cat­ing phase–essentially flip­ping the switch for cel­lu­lar growth to fast for­ward. And just as cells have more than one brake (p53 and Rbs), they also have more than one accel­er­a­tor. Car­bone’s col­league, Boc­chet­ta, dis­cov­ered that SV40 can also acti­vate a gene called Notch‑1 that push­es the cell divide. SV40 thus can inac­ti­vate two key cel­lu­lar brakes and acti­vate two key accel­er­a­tors, all by itself.

Ibid.; p. 208. [7]

7. In yet anoth­er fash­ion, SV40 facil­i­tates onco­ge­n­e­sis by pre­vent­ing the pro­gres­sive short­en­ing of the telom­eres as cells repeat­ed­ly divide. A spin­dle of fibers at the end of each chro­mo­some, the telom­eres are essen­tial for cel­lu­lar repro­duc­tion and they short­en pro­gres­sive­ly as cells repro­duce. Even­tu­al­ly, they short­en to the point where cel­lu­lar repro­duc­tion becomes impos­si­ble and the cell line per­ish­es. SV40 pre­vents this pro­gres­sive short­en­ing, facil­i­tat­ing the for­ma­tion of can­cer cells.

Knock­ing out a cel­l’s brakes and kick­ing on its accel­er­a­tor is still not suf­fi­cient to pro­duce unchecked tumor growth. Nature blessed the body with an addi­tion­al anti­cancer fea­ture: cells have a lim­it­ed life span. A healthy cell will repro­duce itself only a finite num­ber of times before dying. That is because each time a cell divides, the telom­eres, a spin­dle of microfibers on the ends of each chro­mo­some, short­en a lit­tle bit. In clas­si­cal mythol­o­gy, three goddesses–the Fates–wove togeth­er the fab­ric of a per­son­’s life, deter­min­ing how long he or she would live. Telom­eres are lit­er­al­ly the threads of life; they deter­mine the nat­ur­al life span of all cells. Each time a cell divides, a lit­tle piece of the thread gets used up, and the telom­eres get short­er. Once they have short­ened beyond a cer­tain point, the cell–and all the daugh­ter cells, which derived from it–have used up all their allot­ted thread. They can­not divide any longer, and they die. This is why most sci­en­tists believe that all human beings, no mat­ter how healthy have an upper lim­it to their life spans. . . .

. . . Car­bone and Rudy Fod­dis, a post­doc­tor­al stu­dent in his lab­o­ra­to­ry, found that SV40 acti­vates telom­erase, an enzyme that allows the telom­eres to be changed every time the cell divides instead of becom­ing shortened–in effect, allow­ing the mesothe­lial cells to divide end­less­ly. Iron­i­cal­ly, it was the virus’s con­t­a­m­i­na­tion of the polio vac­cine that led to the search for an alter­na­tive sub­strate by Hayflick, which in turn led to the dis­cov­ery of the impor­tance of telom­eres. Now it turns out that it is SV40’s inter­fer­ence with the nat­ur­al behav­ior of telom­eres that allows malig­nant cells to become immor­tal, instead of dying as they should. . . .

Ibid.; pp. 208–209. [7]

8. Yet anoth­er remark­able and dead­ly fea­ture of SV40 is its “stealth” abil­i­ty to cause can­cer.

. . . . Mean­while, oth­er research shows that SV40 has addi­tion­al can­cer-caus­ing tricks. Some­times the virus sets off the chain reac­tion that leads to tumor for­ma­tion, yet man­ages to leave no trace that it was ever present. In virol­o­gy, this is described as a hit-and-run mech­a­nism: The virus can cause so much dam­age that the cell per­pet­u­ates its own malig­nant growth long after the virus has dis­ap­peared.

A team of sci­en­tists from Bonn has demon­strat­ed this mech­a­nism in rats, show­ing that SV40 is able to inflict dam­age in cells and then van­ish com­plete­ly. The Ger­man team inject­ed fetal rat brain cells that had been ren­dered can­cer­ous by large T‑antigen into the brains of adult rats. Eighty per­cent of the adult rats devel­oped a brain can­cer that is the rodent equiv­a­lent of human medul­loblas­toma, one of the pedi­atric brain can­cers with which SV40 has been asso­ci­at­ed and the same type that afflict­ed Alexan­der Hor­win. When the Bonn researchers searched for large T‑antigen in the tumors, it was no longer present in some of the cells. Yet these par­tic­u­lar sets of trans­formed (or malig­nant) cells appeared to be even more malig­nant than those that were still express­ing the T‑antigen–evidently because with­out the pres­ence of T‑antigen, the immune sys­tem could no longer rec­og­nize them as a threat. Thanks to SV40, and per­haps oth­er virus­es, can induce can­cer and yet not be read­i­ly detectable once tumor start pro­lif­er­at­ing rapid­ly. With­out the pres­ence of an immuno­genic pro­tein like T‑antigen, can­cer cels are less prone to immune sys­tem attack. Thus, after a cer­tain point in tumor­o­ge­n­e­sis, can­cer cells that have rid them­selves of the virus have high­er sur­vival rates than those that still con­tain SV40, even­tu­al­ly replac­ing SV40-infect­ed cells as the dom­i­nant sub­set in some expand­ing tumors. Yet the ulti­mate source for the aggres­sive, “stealth” can­cer was still SV40.

Stud­ies from Italy sup­port this nov­el hypoth­e­sis: SV40 is dan­ger­ous as long as it is in the right tis­sue, even if it is not actu­al­ly present in every, or even most cells. A team led by Luciano Mut­ti and Gio­van­ni Gaudi­no dis­cov­ered that a small num­ber of SV40-infect­ed mesothe­lial cells can induce malig­nan­cy in much larg­er num­bers of near­by non­in­fect­ed cells. Mut­ti and Gaudi­no found that once SV40 invades the mesothe­lial cells, the virus not only turns on the Met onco­gene with­in the cells it has infect­ed, it also stim­u­lates those cells to send chem­i­cal sig­nals to their neigh­bors, forc­ing them to turn on Met. Now these neigh­bor­ing, unin­fect­ed cells have also been arti­fi­cial­ly switched on from a rest­ing phase into an unnat­ur­al, hyper­ac­tive growth phase. Thus, even if only a few tumor cells con­tain SV40, growth fac­tors pro­duced by these cells will spur the malig­nant growth of near­by cells that do not con­tain the virus.

Ibid.; pp. 211–212. [7]

9. On top of the oth­er can­cer-caus­ing mech­a­nisms that SV40 man­i­fests, the virus stim­u­lates the pro­duc­tion of VEGF, which caus­es the growth of blood ves­sels that nour­ish tumors.

Mut­ti also found that once tumor for­ma­tion is under way, SV40 sub­verts one more cel­lu­lar reg­u­la­to­ry sys­tem in order to ensure that the tumor con­tin­ues to grow. SV40, Mut­ti dis­cov­ered, stim­u­lates mesothe­lioma cells to pro­duce vas­cu­lar epithe­lial growth fac­tor or VEGF. VEGF is a chem­i­cal that pro­motes blood ves­sel growth. Mut­ti found that in mesothe­lioma biop­sies that test­ed neg­a­tive for the pres­ence of SV40, lit­tle VEGF is pro­duced, while tumor cells that con­tained SV40 man­u­fac­ture high lev­els of the growth fac­tor. In this way, SV40, by encour­ag­ing blood ves­sels to grow toward the tumor, helps secure for the bur­geon­ing can­cer an ample sup­ply of blood and nutri­ents. . . .

Idem. [7]

10. Yet anoth­er dev­as­tat­ing aspect of SV40 is the fact that there are two major varieties–“slow growth” and “fast growth” SV40. Slow growth SV40 takes 19 days to mature, evad­ing the screen­ing process which eval­u­ates cell cul­tures after the four­teen days that the faster grow­ing vari­ant of the virus takes to reach matu­ri­ty and dam­age cells in such a way as to become evi­dent to the screen­ing pro­ce­dures of the time.

. . . In 1999, when Car­bone test­ed his vials of 1955 vac­cine for SV40 and real­ized he had detect­ed slow-grow­ing SV40 vari­ants that were present in the oral vac­cine, he became curi­ous. Sup­pose a slow-grow­ing SV40 vari­ant were present in the oral vac­cine? Were cur­rent FDA reg­u­la­tions, which required only four­teen-day cell cul­ture cycles, ade­quate to detect all SV40 types, includ­ing SV40 that was slow grow­ing? Car­bone con­duct­ed his own test. He dis­cov­ered  that the slow-grow­ing strain of SV40 that he had recov­ered from Her­bert Rat­ner’s 1955 vac­cine took nine­teen days to grow out–or become appar­ent in tis­sue cul­tures. That means FDA-man­dat­ed tests as like­ly as not would have failed to detect it or oth­er slow-grow­ing vari­ants present in a vac­cine.

Using the FDA’s test­ing pro­to­col, here’s what might have hap­pened in the case of the slow-grow­ing vari­ant of SV40 such as the type Car­bone found in his 1955 vac­cine vials: A sam­ple of a lot from which the final triva­lent vac­cine batch was derived would have been inoc­u­lat­ed into a test cul­ture and held for four­teen days. Because the virus con­tained in the lot was Car­bone’s nine­teen-day, slow-grow­ing type, after four­teen days, lit­tle, if any, of the virus would have infect­ed cells and repli­cat­ed to the point where it would burst the cells and release SV40 into the flu­ids that sur­round the tis­sue cul­ture cells. There would be no appar­ent sign of viral growth and this pri­ma­ry cul­ture, there­fore, would be regard­ed as neg­a­tive. On the four­teenth day, the flu­ids that sur­round the cell cul­ture would be inoc­u­lat­ed into a sec­ond cul­ture, the sub­cul­ture. But these flu­ids from the first cul­ture (pri­ma­ry cul­ture) still con­tained either no SV40  or only a very small amount of the virus. If there were no SV40 in the flu­ids from the first cul­ture, this sec­ond sub­cul­ture, too, would be neg­a­tive. In the event that some SV40 actu­al­ly was in the flu­ids of the pri­ma­ry cul­ture, the sub­cul­ture would still appear to be neg­a­tive, even after four­teen days of obser­va­tion, since this par­tic­u­lar slow-grow­ing SV40 vari­ant takes nine­teen days to grow out. Thus, an SV40-con­t­a­m­i­nat­ed lot would pass the one safe­ty test designed to catch the virus, and it would be released.

Slow-grow­ing SV40 hap­pens to be the type most often found in brain and bone cell tumors–tumor types that often afflict chil­dren, includ­ing the brain can­cer that killed Alexan­der Hor­win. (Faster-grow­ing vari­ants of SV40 have been found in these tumor types as well.) Car­bone’s tests on his vin­tage vac­cine sup­port the the­o­ry that if slow­er-grow­ing SV40 was present in the lots used to make the oral polio vac­cine admin­is­tered to Alexan­der, it might not have been detect­ed fol­low­ing the test pro­to­cols required  by the FDA. It is cer­tain­ly sci­en­tif­i­cal­ly pos­si­ble, there­fore, that Alexan­der’s dose of oral vac­cine was a pos­si­ble source for the SV40 in his medul­loblas­toma.

Ibid.; pp. 268–269. [7]