Modifying Mesoporous SBA-15 by a Microencapsulation Method in the Matrix of Sodium Alginate

The present work represents hydrogel as a composite based on sodium alginate and mesoporous SBA-15. The hydrogel was obtained by modifying mesoporous SBA-15 by a microencapsulation method of the SBA-15 in the sodium alginate matrix. The solution of CaCl2 provided a gelation complex of sodium alginate/SBA-15 in a rigid gel-like structure. The sodium alginate/SBA-15 hydrogels beads of about 3 mm diameter were prepared. Composite material was characterized by using powder X- ray diffraction, scanning electron microscopy and energy dispersive X-ray analysis. This composite material may have potential application in removal of metal ions – pollutants from aqueous solutions.XVI International Conference on Fundamental and Applied Aspects of Physical Chemistry : Proceedings, Vol. 2, September 26-30, Belgrad

Regional distribution of cytochrome c oxidase activity and copper in sclerotic hippocampi of epilepsy patients

Introduction Disruption of copper homeostasis and dysfunction of mitochondria have been documented in sclerotic hippocampi (HS) of patients with mesial temporal lobe epilepsy (mTLE). However, a potential link between these pathological changes has not been tackled so far. Herein, we analyzed regional distribution of neuron somata density, copper concentration, and the activity of cytochrome c oxidase (CCO), a component of mitochondrial electron transport chain and copper-containing metalloprotein, in HS. Methods Histochemical staining and laser ablation inductively coupled plasma mass spectrometry were carried out to construct comparable maps of these parameters in coronal sections of hippocampi of 3 mTLE-HS patients and 3 control subjects. Results Copper levels were decreased in all regions of HS with pyramidal neuron somata. CCO activity was significantly reduced in stratum pyramidale (PY) 1 and cornu Ammonis field 4, the two regions with significant reduction in neuron somata density. CCO activity was also lower in layers that contain apical dendrites of pyramidal neurons and mossy fibers. It appears that copper deficiency in PY2 and PY3 comes before CCO activity reduction and neuronal loss. A strong positive correlation was found between neuron density, Cu concentration, and CCO activity. Conclusions Presented results imply that pathological alterations in Cu and energy metabolism could be involved in the development of HS. A limitation of this study was the relatively small number of patients. However, presented results underline copper deficiency as a component of pathological mechanisms of epilepsy and warrant further investigation of cuproproteins and members of copper transport machinery