European Journal of Molecular & Clinical Medicine

Nowadays, there is a continuous and progressive global public exposure to acrylamide (ACR) due its presence in fried and backed food. Thermal preparation of sugar-rich food mostly initiates chemical reactions that yield dangerous chemicals. Of these chemicals arise acrylamide and its metabolite glycidamide. Those having a high
affinity for binding to nervous tissues. The acrylamide-induced neurotoxicity involves reduction in proliferation of neuronal progenitor cells associated with apoptotic cell death. Concerning acrylamide-induced toxicity, preventive medicine research focused on natural antioxidants. Studies on active constituents of Saffron showed obvious antioxidant, and anti-toxic properties. Here, we designed this study to investigate the possible protective
effect of saffron against acrylamide-induced neurotoxicity in hippocampal area of brain. Adult male albino rats were assigned equally into 4 groups (n = 8); control; saffron group; acrylamide (ACR)-administered group and combined ACR and saffron- treated group. Our results recorded molecular changes as a significant decrease on genomic DNA fragmentation in saffron co-administered group as compared to ACR-exposed group. The changes on DNA mutagenicity were studied by analyzing the random amplification of polymorphism of DNA that showed an elevated genomic integrity on rat co -administered saffron with ACR in contrast to those exposed to ACR only.

In this research , the energy loss of electronic to projected carbon, oxygen and protons were calculated in targets (Adipose tissue, Skeletal muscle, and Brain)With using Bohr equation and Bethe equation with Bloch correction and Shell correction at the energy range of (20_500) MeV . The calculations were compared with the experimental data of the SRIM 2012 .Since Bohr equation is classic, its results were a difference from the results of the practical program. As for Bethe's quantum equation, its results were Bloch correction that was closest to the practical program. As for the shell correction, it recorded a difference at specific energies and then began to approach with increasing range of used energy.

Corpus callosum includes a large amount of axons with various degrees of myelination, interconnecting cerebral hemispheres. Tumors, demyelinating diseases, infections, trauma and metabolic diseases as well as vascular lesions may affect corpus callosum, often extending to other white matter areas of the brain. We describe the case of a 76 years old male patient with history of arterial hypertension, diabetes mellitus and normal pressure hydrocephalus, developing dysphagia during hospitalization. Ab-ingestis pneumonia caused brain hypoxia and coma; brain magnetic resonance disclosed isolated demyelination of corpus callosum that was not present before hypoxia. Compared to neurons and astrocytes, oligodendrocytes are reported as particularly sensitive to hypoxia. Respiratory involvement without blood flow impairment could have lead to a prevalent oligodendrocytes damage, resulting in a selective demyelination of corpus callosum. Our patient indeed evolved into persistent vegetative state and died five months after hypoxic episode. This case report could give some insight about in vivo brain susceptibility to hypoxic damage.