Double-setting alpha-tricalcium phosphate cement provided with interconection channels in rabbits after enucleation: a potential implant for the anophthalmic socket

The purpose of this study was to evaluate the macroscopy and microstructure of a double setting alpha-tricalcium phosphate bone cement sphere provided with interconnection channels (alpha-TCP-i), as well as the integration of the implant with the rabbits' orbital tissue, through macroscopic analysis and histopathology. The external and internal surfaces of the alpha-TCP-i were evaluated macroscopically and by electron microscopy. Twelve New Zealand rabbits received 12mm implants of alpha-TCP-i following enucleation of the left eye. The clinical assessment was undertaken daily during the first 15 days, followed by fortnightly assessment until the end of the study period. For the morphological analysis, exenteration was performed in 3 animals per experimental period (15, 45, 90 and 180 days). The external and internal surfaces of the implant appeared solid, smooth and compact, with six channels which interconnected centrally. The micro-architecture was characterized by the formation of columns of hexagonal crystals. No signs of infection, exposure, dehiscence of sutures or extrusion of the implant were noted in any of the animals during the entire period of the study. The morphological evaluation demonstrated the presence of a thin capsule around the implant, from whence appeared fibro-vascular projections, which penetrated it through the interconnecting channels. In the first days after the insertion of the implant, an intense inflammatory reaction was noted. At 180 days, however, there were no signs of inflammation. The alpha-tricalcium phosphate cement implant was well tolerated in this rabbit model and appeared to be relatively inert with some fibrovascular ingrowth through the large channels.

Hemoglobin I-Philadelphia [alpha 16 (A14) LYS→GLU] heterozygote among blood donors from Brazil

We describe a heterozygous case of Hb I-Philadelphia [alpha 16 (A14) LYS-->GLU] in a blood donor from the Acre State Blood Bank, in the Brazilian Amazon region. We confirmed the mutation by electrophoretic and chromatographic methods and by DNA sequencing. A literature search showed that this is the first description of this alpha globin mutant in a Brazilian Caucasian group. We also emphasize the importance of the hemoglobin study in blood donors for the purpose of the genetic counseling and quality assurance of the blood to be transfused. Screening tests for hemoglobin mutants are also important for gathering anthropological information about the Brazilian population.

Changes in the TNF-alpha/IL-10 ratio in hyperglycemia-associated pregnancies

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Changes in gene expression in PBMCs profiles of PPAR alpha target genes in obese and non-obese individuals during fasting

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effect of adding a gonadotropin-releasing-hormone treatment at the beginning and a second prostaglandin F-2 alpha treatment at the end of an estradiol-based protocol for timed artificial insemination in lactating dairy cows during cool or hot seasons of the year

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by alpha(2)-adrenergic activation in the lateral parabrachial nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Diabetes reduces mesenchymal stem cells in fracture healing through a TNF alpha-mediated mechanism

Diabetes interferes with bone formation and impairs fracture healing, an important complication in humans and animal models. The aim of this study was to examine the impact of diabetes on mesenchymal stem cells (MSCs) during fracture repair.Fracture of the long bones was induced in a streptozotocin-induced type 1 diabetic mouse model with or without insulin or a specific TNF alpha inhibitor, pegsunercept. MSCs were detected with cluster designation-271 (also known as p75 neurotrophin receptor) or stem cell antigen-1 (Sca-1) antibodies in areas of new endochondral bone formation in the calluses. MSC apoptosis was measured by TUNEL assay and proliferation was measured by Ki67 antibody. In vitro apoptosis and proliferation were examined in C3H10T1/2 and human-bone-marrow-derived MSCs following transfection with FOXO1 small interfering (si)RNA.Diabetes significantly increased TNF alpha levels and reduced MSC numbers in new bone area. MSC numbers were restored to normal levels with insulin or pegsunercept treatment. Inhibition of TNF alpha significantly reduced MSC loss by increasing MSC proliferation and decreasing MSC apoptosis in diabetic animals, but had no effect on MSCs in normoglycaemic animals. In vitro experiments established that TNF alpha alone was sufficient to induce apoptosis and inhibit proliferation of MSCs. Furthermore, silencing forkhead box protein O1 (FOXO1) prevented TNF alpha-induced MSC apoptosis and reduced proliferation by regulating apoptotic and cell cycle genes.Diabetes-enhanced TNF alpha significantly reduced MSC numbers in new bone areas during fracture healing. Mechanistically, diabetes-enhanced TNF alpha reduced MSC proliferation and increased MSC apoptosis. Reducing the activity of TNF alpha in vivo may help to preserve endogenous MSCs and maximise regenerative potential in diabetic patients.