Chemical modification of keratin using Schiff bases to prepare cation exchangers and study their adsorption activity.

In this research, keratin was chemically modified by Grafting keratin with 4-nitro-aniline, and then a reducing reaction was carried out to reduce the nitro group in order to generate an aromatic amino group on keratin structure to be used in the preparation of Schiff bases. Four exchangers of Schiff bases then were synthesized by reacting five derivatives of benzaldehyde with the crafted keratin. The FTIR, DSC spectra of the prepared exchanges were recorded.

An experimental model of partial insulin-like growth factor-1 deficiency in mice.

Insulin-like growth factor-1 (IGF-1) is responsible for many systemic growth hormone (GH) functions although it has an extensive number of inherent activities (anabolic, cytoprotective, and anti-inflammatory). The potential options for IGF-1 therapy arise as a promising strategy in a wide list of human diseases. However, deeper studies are needed from a suitable animal model.

Hepatoprotection and neuroprotection induced by low doses of IGF-II in aging rats.

Background: GH and IGFs serum levels decline with age. Age-related changes appear to be associated to decreases in these anabolic hormones. We have previously demonstrated that IGF-I replacement therapy improves insulin resistance, lipid metabolism and reduces oxidative damage (in brain and liver) in aging rats.

RasGRF1 disruption causes retinal photoreception defects and associated transcriptomic alterations.

RasGRF1 null mutant mice display impaired memory/learning and their hippocampus transcriptomic pattern includes a number of differentially expressed genes playing significant roles in sensory development and function. Odour avoidance and auditory brainstem response tests yielded normal results but electroretinographic analysis showed severe light perception impairment in the RasGRF1 knockouts. Whereas no structural alterations distinguished the retinas of wild-type and knockout mice, microarray transcriptional analysis identified at least 44 differentially expressed genes in the retinas of these Knockout animals.

The protein kinase DYRK1A regulates caspase-9-mediated apoptosis during retina development.

The precise regulation of programmed cell death is critical for the normal development of the nervous system. We show here that DYRK1A (minibrain), a protein kinase essential for normal growth, is a negative regulator of the intrinsic apoptotic pathway in the developing retina. We provide evidence that changes in Dyrk1A gene dosage in the mouse strongly alter the cellularity of inner retina layers and result in severe functional alterations.