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. INTRODUCTION 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 HYPOTHESIS 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 organisms cells - totipotent), they introduce the cell to be cloned, producing a stem or trunk cells (Fig. 1 and Fig.3). BRAZILIAN CLONING THEORY 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. THE DREAMS OF HUMAN ORGANS TRANSPLANTS 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. SUMMARY AND CONCLUSION 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. REFERENCES 1-HOLDEN, C. & V0GEL, G.- Plasticity: Time for A Reappraisal? Science, 2002, 296: OKUMURA, M. & COREA NETTO, A- Produção experimental de megas em animais inoculados com Trypanosoma cruzi. Rev. Hosp. Clin. Fac. Med. S. Paulo, 1961, 16: 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: 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, PINTO, P.L.S. et al. – Life cycle of Trypanosoma cruzi (Y strain) in mice. Rev. Hosp. Clin. Fac. Méd. S. Paulo, 1999, 54: KONDO, M. et al.- Cell-fate conversion of lymphoid - commited progenitors by instructive actions of cytokines. Nature, 2000, 407: ROSSANT, J.- Stem cells in the Early Embryo. A.A.A.S – Annual Meeting. and Science innovation Exposition, February, Boston, MA, 2002:56. 8-GOLDMAN, S.A.- Neural Stem and Progenitor Cells of the Human Brain. A.A.A.S. – Annual Meeting and Science Innovation Exposition, February, Boston, MA, 2002:56. 9-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: VIANNA, G.- Contribuição para o estudo da anatomia patolojica da Moléstia de Carlos Chagas Mem. Inst. Oswaldo Cruz, 1911, 3: OKUMURA,M. et al. – Cytokine-Like substance: origin and fate in Chagasdisease. New hypothesis about the local inflammatory reaction. Rev. Hosp. Clin. Fac. Med. S. Paulo, 1999, 54: OKUMURA, M.- Doença de Chagas Experimental. In RAIA, A-A,- Manifestações Digestivas na Moléstia de Chagas. Sarvier, S. Paulo, 1983, pp Departments: Gastroenterology 1 and Pathology 2 of Faculdade de Medicina da Universidade de S. Paulo; Instituto de Medicina Tropical de S. Paulo 3 and Instituto Adolfo Lutz, S. Paulo 4 – Brazil. Masayuki Okumura , Marcelo Mester 1 and Joaquim Gama-Rodrigues 1 by Inout Informática – (011) During the second half of the last century (1958) we initiated: BACKGROUND 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/mm 3 ; leucopenia with RBC values of 2,000 – 3,000/mm 3 and trombopenia with platelet values of 20,000 – 40,000/mm 3 ). We noted that two to four days posoperatively, the patients hemogram had already been corrected. Some patients even presented platelet levels of 500,000 to 1,000,000 units/mm 3. 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 disease 2 and megas of the digestive system in laboratory animals.When researching experimental Chagas disease and inoculating Trypanosoma cruzi 3 in mice, we found that the protozoan enters the organisms cell for its reproduction: b)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. 8 Rupture of nest within parasitic neuron and ruptured of host cell without inflammatory reaction (cytokine should be forming at this time). 7 Auerbach plexus; integral neuron with parasites without inflammatory reaction. 9 Ruptured neuron without reaction. 10 Start of acute inflammatory process. 11 Llymphocytes stained by cytokine. 12 Granuloma formation. c)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 nest 10.(Fig. 7 and 17) The increase in volume causes the nest to break, releasing a cytokine-like substance 4 (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 substance 11, by an autocrine or paracrine mechanism attracts the WBCs (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 ) and transform it into WBCs (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 Gel or primitive amorphous mass. Macrophage filled with ring shaped Trypanosoma cruzi. Blood stream - two adults of T. cruzi.Macrophage filled with amastigotes.Megastomach and Duodenal: animal preserve informalin. 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. 1 2 Bone Marrow filled with free forms. Bone Marrow, imprint:parasite evolved by an unwiding or indirect mechanism Giemsa. Kodak Film (Immersion). 4 3 Ring – Shaped and evolutive forms resulting from unwinding. Liver: Slide with free parasites in the capillaries and sinusoids. 6 5 Spherical and developing forms resulting from elongation. Evolutionary form resulting from elongation – resembling tadpoles.