Strength, Elastic Properties and Fiber-Matrix Interaction Mechanism in Geopolymer Composites.

The current geopolymers have limited mechanical strength against the effect of tension, which makes them susceptible to brittle failure. However, owing to their potential as a sustainable construction material, there is growing interest in improving the poor mechanical properties of geopolymers. This study experimentally investigated crucial properties of polypropylene-fiber-reinforced fly ash-based geopolymer composites. The effects of polypropylene fibers (PPF) addition (0.5%, 1.0% and 1.5% by volume) on the mechanical properties of the geopolymer composites were investigated with respect to compressive and flexural strength, deformation behavior of Young's and shear moduli, and resilience capacity. In addition, scanning electron microscopy was performed to establish the morphology of the geopolymeric matrix and the fiber-matrix interfacial interaction. The addition of PPF significantly increased the flexural strength: compared with the control, at 7 days it was 27% greater for the 0.5% PPF composite and 65% greater for the 1.0% PPF composite. By 14 days it was 31% and 61% greater, respectively. By contrast, the 1.5% PPF composite had lower strength parameters compared with the control because the fiber dispersion increased the porosity. Similar trends were seen for resilience. The SEM observations showed the dispersion of the fibers and helped elucidate the fiber-matrix interaction mechanism.

Impaired Gene Expression Due to Iodine Excess in the Development and Differentiation of Endoderm and Thyroid Is Associated with Epigenetic Changes.

Background: Thyroid hormone (TH) synthesis is essential for the control of development, growth, and metabolism in vertebrates and depends on a sufficient dietary iodine intake. Importantly, both iodine deficiency and iodine excess (IE) impair TH synthesis, causing serious health problems especially during fetal/neonatal development. While it is known that IE disrupts thyroid function by inhibiting thyroid gene expression, its effects on thyroid development are less clear. Accordingly, this study sought to investigate the effects of IE during the embryonic development/differentiation of endoderm and the thyroid gland. Methods: We used the murine embryonic stem (ES) cell model of in vitro directed differentiation to assess the impact of IE on the generation of endoderm and thyroid cells. Additionally, we subjected endoderm and thyroid explants obtained during early gestation to IE and evaluated gene and protein expression of endodermal markers in both models. Results: ES cells were successfully differentiated into endoderm cells and, subsequently, into thyrocytes expressing the specific thyroid markers Tshr, Slc5a5, Tpo, and Tg. IE exposure decreased the messenger RNA (mRNA) levels of the main endoderm markers Afp, Crcx4, Foxa1, Foxa2, and Sox17 in both ES cell-derived endoderm cells and embryonic explants. Interestingly, IE also decreased the expression of the main thyroid markers in ES cell-derived thyrocytes and thyroid explants. Finally, we demonstrate that DNA methyltransferase expression was increased by exposure to IE, and this was accompanied by hypermethylation and hypoacetylation of histone H3, pointing to an association between the gene repression triggered by IE and the observed epigenetic changes. Conclusions: These data establish that IE treatment is deleterious for embryonic endoderm and thyroid gene expression.

First report of a KELnull phenotype in Peru and a lesson of invisible genetic disparity.

Blood banks in developing countries have limited capability to typify common blood groups creating disparities in the access to blood units for patients with rare blood genotypes. We report the case of a Peruvian woman with metastatic breast cancer with KELnull phenotype (K0), a rare blood group characterized by the lack of expression of all Kell antigens on the red blood cells (RBCs). The molecular studies identified that the patient's RBCs were homozygous for the nonsense c.1546C > T mutation predicted to encode p.Arg516Ter (KEL*02 N.17 allele), which confirmed the K0 phenotype. We conducted a local and international search of compatible blood units. Finally, the Japanese Red Cross donated the blood units for the patient. We present here the first report for a K0 phenotype in Peru and the challenging genetic disparities that many patients have to face to access to blood units in our country.

Ameloblastoma uniquístico plexiforme: a propósito de un caso / Plexiform unicystic ameloblastoma: a propos of a case

El ameloblastoma es un tumor odontogénico benigno de origen epitelialcon estroma fi broso maduro sin ectomesénquima odontogénico, decomportamiento localmente agresivo e infi ltrante con alta capacidad de recidiva. Representa entre 11 y 13 por ciento de los tumores odontogénicosmandibulares y 1 por ciento de los tumores y quistes maxilomandibulares. El tratamiento debe orientarse de acuerdo con el potencial del tumor,las características del crecimiento según su variable clínica y el tipo histológico. Debe ser un tratamiento que asegure un mejor pronóstico para el paciente

The ameloblastoma is a benign odontogenic tumor of epithelial origin with mature fi brous stroma, without odontogenic ectomesenchyme. It exhibits locally aggressive and invasive behavior, with a high level of recurrence. Ameloblastomata account for between 11 and 13% of mandibular odontogenic tumors, and 1% of maxillo-mandibular tumors and cysts. Treatment should be guided by the potential of the tumor and its growth characteristics based on the clinical variable and histological type, the preferred treatment being that which ensures the best prognosis for the patient.