Elzbieta Rebas has completed her PhD and DSc from Medical University of Lodz. Currently she is an Associate Professor of Department of Molecular Neurochemistry at Medical University of Lodz. She has published a number of papers related to brain function in reputed international journals and participated in many international conferences, congresses and symposia. She has more than 20 years of teaching experience in the field of Biochemistry. She is a Member of FEBS and Council of Polish Biochemical Society.
Many neurodegenerative and affective diseases are related to disturbed metabolism of - aminobutyric acid (GABA) and GABA-shunt enzymes: glutamate decarboxylase (GAD), GABA aminotransferase (GABA-T) and succinate-semialdehyde dehydrogenase (SSADH). Neurological diseases are also often accompanied by impaired calcium conditions. Traditional drugs are not always efficient and may evoke adverse side effects. Chemicals naturally occurring in plants can provide an attractive alternative target in modulating of neurotransmission via affecting of GABA-shunt enzymes activity. The aim of this study was to investigate an effect of selected phytochemicals: genistein and zeaxanthin on activity of GABA-shunt enzymes. In our study we used stably transfected pseudoneuronal PC12 cells with reduced expression of neuron-specific isoforms of calcium membrane pumps: PMCA2 or PMCA3 and increased intracellular calcium concentration. Cells were incubated with 10 M and 20 M of tested compounds during 10 and 20 minutes, a short time precluding genomic action or during 4 and 12 hours. Enzymes activity was determined with fluorimetric and spectrophotometric methods. Additionaly, during GAD activity determination we used vigabatrin, inhibitor of GABA-T. Our results indicate that genistein and zeaxhantin can modulate activity of GABA-shunt, especially glutamate decarboxylase and this way change balance between to oppositely acting neurotransmitters. Genistein decreases GAD activity in all studied lines, but cells with reduced expression of PMCA are more sensitive to genistein. Zeaxhantin inhibits GAD under disturbed calcium homeostasis but increases GAD activity in normal cells. Due to short time of incubation we suggest non-genomic action of studied phytochemicals.
Francesca Morelli was born in 1983 in a small town in Tuscany (Italy). She grew up nearby the sea and, after Classical studies; she graduated at the Medical School of Pisa in 2008. She then moved to The Netherlands and started her Internal Medicine Residency, at the Erasmus Medical Center, Rotterdam. During this residency, she has been working for 5 months at the Department of Infectious Diseases of Tygerberg Hospital, Cape Town. In 2017 she started a fellowship Intensive Care at the Erasmus Medical Center, which she will conclude in April this year. Nowadays, she is moving to Trento with her partner and their son, to enjoy the beauty and calm of the Dolomites.
Once traumatic brain injury (TBI) has occurred, management at the Intensive Care Unit aims to reduce intracranial hypertension and cerebral edema, and improve cerebral perfusion. Medical treatment for raised intracranial pressure (ICP) includes hyperosmolar therapy, which shifts fluids from the cerebral- to the vascular compartment. Next to the effect of osmotic agents on sodium and water balance, TBI itself can lead to sodium disorders, mainly due to pituitary dysfunction. Since both hypo- and hypernatremia are associated with increased morbidity and mortality, prompt recognition and adequate treatment are mandatory. Actually, management of dysnatremia in TBI patients can be challenging. Firstly, osmotic therapy makes interpretation of clinical and laboratory findings uncertain. Secondly, sodium fluctuation after treatment may worsen cerebral injury. In order to discuss these diagnostic and therapeutic dilemmas, we present the emblematic case of a young woman with severe TBI. While on high dose Mannitol, patient developed severe hypernatremia and polyuria. In this setting, osmotic diuresis and diabetes insipidus were difficult to recognize. Later on during admission hyponatremia occurred, probably due to syndrome of inappropriate antidiuretic hormone secretion (SIAD) or glucocorticoid insufficiency. This case clearly shows how challenging sodium disorders can be, especially in the delicate phase of post-TBI management.