No abstract

Trypanosoma cruzi undergoes a biphasic life cycle that consists of four alternate developmental stages. In vitro conditions to obtain a synchronic transformation and efficient rates of pure intermediate forms (IFs), which are indispensable for further biochemical, biological, and molecular studies, have not been reported. In the present study, we established an improved method to obtain IFs from secondary amastigogenesis. During the transformation kinetics, we observed progressive decreases in the size of the parasite body, undulating membrane and flagellum that were concomitant with nucleus remodeling and kinetoplast displacement. In addition, a gradual reduction in parasite movement and acquisition of the amastigote-specific Ssp4 antigen were observed. Therefore, our results showed that the in vitro conditions used obtained large quantities of highly synchronous and pure IFs that were clearly distinguished by morphometrical and molecular analyses. Obtaining these IFs represents the first step towards an understanding of the molecular mechanisms involved in amastigogenesis.

Irregular antibodies are produced by alloimmunization because of pregnancies or blood transfusions. They are called "irregular" due to target erythrocyte antigens from "rare blood systems," those different from the ABO system. Irregular antibodies have been widely investigated in immunohematology since their presence in blood donors may lead to difficulties in blood typing and in blood cross-matching, or to induce hemolytic transfusion reactions. Nevertheless, their incidence and participation in the physiopathology of autoimmune diseases have not been thoroughly studied. In this work, we analyzed the presence and pro-hemolytic capabilities of irregular antibodies in patients with different autoimmune diseases lacking signs of hemolytic anemia, in comparison with healthy multiparous women. Five of 141 autoimmune patients (3.5 %) and two of 77 multiparous women (2.6 %) were positive. Although frequency was relatively low and similar in both populations, the targeted antigens were Kell (k, Kp, Js) and Luth (Lu) in multiparous women, and the same plus Duffy (Fy), Kidd (Jk) and MNS (M, s) in autoimmune patients. Irregular antibodies from autoimmune patients did not induce complement-mediated hemolysis (intravascular), but they were able to induce macrophages-mediated phagocytosis (extravascular hemolysis) in vitro. It is the first approach exploring the presence of irregular antibodies associated with the loss of immune tolerance and demonstrating their hemolytic potential in autoimmune patients without hemolytic manifestations. The presence of irregular antibodies targeted to Duffy (Fya), Kidd (Jka) and MNS (M, s) antigens only in autoimmune patients suggests a loss of immune tolerance to these erythrocyte antigens.

Las enfermedades cardiovasculares (ECV) son la primera causa de muerte de las enfermedades no transmisibles en el mundo, figurando las dislipidemias como una irregularidad frecuente y principal factor de riesgo. El gen SCARB1 codifica el receptor SR-B1, el cual participa en la depuración del colesterol y captación selectiva de HDL. La sobre expresión del SR-B1 disminuye el HDL-C y la aterosclerosis, mientras que su ausencia incrementa el HDL-C y eleva la aterosclerosis. Objetivo. Identificar el tipo de asociación de las dislipidemias con el SNP rs5888 del gen SRB1 (exón 8) en población aparentemente sana del estado de Morelos México. Metodología. De un total de 258 muestras, se extrajo ADN para su purificación y cuantificación, posteriormente se realizó la genotipificación del exón 8 mediante PCR en tiempo real y utilizando el software applied biosystems, las asociaciones genotípicas (con SNP y sin SNP) se realizaron por la prueba estadística de Razón de Momios. Resultados. El 72.87 % de la población estudiada presenta dislipidemias, siendo la hipoαlipoproteinemia la más frecuente, mayormente en hombres (78.19 %). Se encontró asociación protectora limítrofe para hipoαlipoproteinemia quienes presenten el SNP rs5888 y asociación de riesgo en hipercolesterolemia e hipertrigliceridemia, concluyendo que un cambio en el mismo gen, pueden aumentar o disminuir la probabilidad de desarrollar enfermedades cardiovasculares.