
Masayuki
1.2.3.4
Okumura
,
Marcelo
1
Mester
and Joaquim
1
Gama-Rodrigues
Departments: Gastroenterology1 and Pathology2 of Faculdade de Medicina da Universidade de S. Paulo;
Instituto de Medicina Tropical de S. Paulo3 and Instituto Adolfo Lutz, S. Paulo4 – Brazil.
INTRODUCTION
The moment the scientists expose the lab animals to the X-ray, they are destroying the cellular matrix. Due to the lack of cells, they admit the cellular dedifferentiation or
“plasticity”1, which consist of changing grown-up cells into primitive totipotent cells, they also call them embryos stem or trunk cells. “Stem or trunk cells” remind us of part
of a tree with pre-established genetic code and they should develop into specific fruits according to the seeds, without behavior of fertile grounds.
HYPOTHESIS
Our daily contact with two of the endemic tropical diseases of Brazil has permitted us to propose the following hypothesis: a “Fruitful Jelly or Amorphous Primitive Mass”
is precursor of the “Stem or Trunk Cells” of modern scientists
BACKGROUND
During the second half of the last century (1958) we initiated:
1) the surgical treatment of portal hypertension in patients with Hepatosplenic schistosomiasis (Schistosoma mansoni) with one the techniques employed: Splenectomy + spleno-renal shunt. The
patients frequently presented changes of their hemograms, often presenting pancytopenia (anemia with RBC values of 2,500,000 – 3,000,000/mm3; leucopenia with RBC values of 2,000 –
3,000/mm3 and trombopenia with platelet values of 20,000 – 40,000/mm3). We noted that two to four days posoperatively, the patient’s hemogram had already been corrected. Some patients
even presented platelet levels of 500,000 to 1,000,000 units/mm3. Our “FRUITFUL JELLY or AMORPHOUS PRIMITIVE MASS” remained at rest, quiescent, undifferentiated until summoned
by a splenectomy, they reacted roughly by liberating billion cells.
2) And we began to study the correlation between experimental Chagas’ disease2 and “megas” of the digestive system in laboratory animals.When researching experimental Chagas’ disease
and inoculating Trypanosoma cruzi3 in mice, we found that the protozoan enters the organism’s cell for its reproduction:
7
Ring – Shaped and evolutive forms
resulting from unwinding.
Auerbach plexus; integral
neuron with parasites without
inflammatory reaction.
c)
3
Bone Marrow, imprint:parasite evolved by
an “unwiding or indirect mechanism”
Giemsa. Kodak Film (Immersion).
4
Liver: Slide with free parasites in the
capillaries and sinusoids.
5
Spherical and developing forms
resulting from elongation.
If entering the liver (Fig. 4), it develops a spheric shape with basophil-particles (Fig. 5) forming a bulge (Fig. 5) in the membrane followed by the flagellum and
undulating membrane, acquiring the shape of a tadpole and evolving by a “direct or elongation mechanism”9 (Fig. 6) Hepatic figure. The presence of ring-shaped
figures was unusual. The ratio was hundred of hepatic forms to only one medullar; the opposite occurred in the bone marrow, leading us to suppose that the
amorphous primitive mass remained at rest, quiescent state, undifferentiated, until summoned by an abrupt aggression (roughly) they reacted by liberating the two
forms. We can presume the trunk or stem cells work like joined antibodies, therefore, they do not exist normally, but only after stimulation.
2
1
Bone Marrow filled with free forms.
b)
6
Evolutionary form resulting from
elongation – resembling tadpoles.
8
Rupture of nest within parasitic neuron and
ruptured of host cell without inflammatory reaction
(cytokine should be forming at this time).
9
Ruptured neuron without reaction.
10
Start of acute inflammatory process.
11
Llymphocytes stained by cytokine.
12
Granuloma formation.
In any other cell, the parasites transformed from a flagellate (tripomastigote) (Fig. 15), into an elliptical one (amastigote) and during the reproduction remains
grouped forming a pseudocyst or parasite nest10.(Fig. 7 and 17) The increase in volume causes the nest to break, releasing a cytokine-like substance4 (constitute by
conjugation of a procytokine originating from the parasite nest with its DNA (Fig.8), with another procytokine of host cell lesion and, with its genetic code) (Fig. 9).
When forming in the interstitial space, the cytokine-like substance11, by an autocrine or paracrine mechanism attracts the WBC’s (neutrophils, lymphocytes naïve
and monocytes) from the local capillaries, forming the first organic reaction, constituting the acute inflammatory process (Fig. 10). If the reaction is inadequate, the
cytokine substance (Fig. 11) in the general circulation (pleiotropy), will stimulate the hematopoietic organs, activate our “FRUITFUL JELLY or AMORPHOUS
PRIMITIVE MASS” (Fig. 13 - 14) and transform it into WBC’s (lymphocytes “activated” and macrophages). The later oriented by the original host cells genetic code,
is directed to the respective organ, constituting the second acute lymphomonocytic reaction. When this defense mechanism were also insufficient, the third
mechanism would be activated with special combination of cytokines, as an attempt to surround the lesion which may form incipient granuloma (Fig. 12), with
macrophages, mastocytes, proliferation of fibroblasts leading to fibrosis and residual scars. Because of the cyclical nature of the disease, its repetition determines
the chronic inflammatory reaction, with the increase in volume of the affected organs, originating the respective “megas”12 (megaesophagus, megastomach,
megaduodenum (Fig. 18), megacolon, cardiomegaly, in addition to hepatosplenomegaly showing the potentiality according to the enviroment.
13
Gel or primitive amorphous mass.
14
Gel or primitive amorphous mass.
15
Blood stream - two adults of T. cruzi.
17
16
Macrophage filled with ring shaped
Trypanosoma cruzi.
Macrophage filled with amastigotes.
18
Megastomach and Duodenal:
animal preserve informalin.
BRAZILIAN
CLONING THEORY
For the purpose of understanding the cloning, let us hypothesize that our amorphous mass has a behavior similar to the ovular cytoplasm. When scientists remove
the nucleus to initiate cloning, they are transforming into our “Fruitful jelly or amorphous primitive mass” (with the capacity of changing into any of the organism’s cells
- totipotent), they introduce the cell to be cloned, producing a stem or trunk cells (Fig. 1 and Fig.3).
THE DREAMS OF HUMAN
ORGANS TRANSPLANTS
Our opinion is that only molecular biology will be able to definitely clarify the participation of our ”Fruitful jelly or Amorphous primitive mass”, in the genesis, repair and
transformation tissues. This will certainly be an important step on the way to producing tissues “in vitro” and even changing the transplants to repair by the simple
lesion (cut or biopsy) of target organs, for the realization of ours dreams, the pioneers in human organs transplants.
SUMMARY AND
CONCLUSION
REFERENCES
We can admit that our primitive amorphous mass, is the precursor of the trunk or stem cells, emphasizing: 1) its potential for furnishing the raw material for forming:
a) the cell, b) the body of the parasites, c) the red and white blood cells and the platelets, d) the energy, and e) their extra-cellular enviroment.; 2) its versatility for
change of shape: tripomastigotes (flagellate- elongated), amastigotes (elliptical), epithelial (cubic, squamous and columnar), connective tissue and muscle
(elongated), star-shaped nerve with its branches, bone (calcified), etc, and 3) besides the daily variety in number and size.
Note: Trypanosoma cruzi was chosen because it is easily visible under the ordinary optical microscope due to its
size, it has great mobility, functioning us a biological marker, and even eliminating the use of stains.
1- HOLDEN, C. & V0GEL, G.- Plasticity: Time for A Reappraisal? Science, 2002, 296:2126-2129
2- OKUMURA , M. & COREA NETTO, A- Produção experimental de “megas” em animais inoculados com Trypanosoma cruzi. Rev. Hosp. Clin. Fac. Med. S. Paulo, 1961, 16: 338-341.
3- CHAGAS, C.- Nova tripanosomiase humana. Estudo sobre a morfologia e o ciclo evolutivo do Schizotrypanum cruzi, n. gen, n. sp, agente etiológico de nova entidade mórbida do homem. Mem. Inst. Oswaldo Cruz,
1909, 2: 1-62.
4- SILVA, L.H.P & CAMARGO, E. P.- Ciclo evolutivo do Trypanosoma cruzi . In CANÇADO, J.R.- Doença de Chagas. Imprensa Oficial de Belo Horizonte, Minas Gerais, 1968, 87-99.
5- PINTO, P.L.S. et al. – Life cycle of Trypanosoma cruzi (Y strain) in mice. Rev. Hosp. Clin. Fac. Méd. S. Paulo, 1999, 54: 141-146.
6- KONDO, M. et al.- Cell-fate conversion of lymphoid - commited progenitors by instructive actions of cytokines. Nature, 2000, 407: 383-386.
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ROSSANT, J.- Stem cells in the Early Embryo. A.A.A.S – Annual Meeting. and Science innovation Exposition, 14-19 February, Boston, MA, 2002:56.
GOLDMAN, S.A.- Neural Stem and Progenitor Cells of the Human Brain. A.A.A.S. – Annual Meeting and Science Innovation Exposition, 14-19 February, Boston, MA, 2002:56.
RIBEIRO, R.B.- et al. – Relato sobre a infecção crônica pelo Trypanosoma cruzi (cepa Y) em camundongos Swiss. Rev. Brasileira de Medicina Tropical, 1999, 32 sup. 1:334.
VIANNA, G.- Contribuição para o estudo da anatomia patolojica da “Moléstia de Carlos Chagas” Mem. Inst. Oswaldo Cruz, 1911, 3: 276-294.
OKUMURA,M. et al. – Cytokine-Like substance: origin and fate in Chagas’disease. New hypothesis about the local inflammatory reaction. Rev. Hosp. Clin. Fac. Med. S. Paulo,
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12- OKUMURA, M.- Doença de Chagas Experimental. In RAIA, A-A,- Manifestações Digestivas na Moléstia de Chagas. Sarvier, S. Paulo, 1983, pp. 35-59.
by Inout Informática – (011) 3284-7233
a) If the parasite enters the bone marrow (Fig. 1) or spleen, it
progress freely in the shape of an eosinophil-ring (Fig. 2)
which upon breaking, acquires the shape of truncated “C”
and an elongated “C”, seeming to develop by an “indirect or
uncoiling mechanism”;4 (Fig. 3), Medullar figure.