Maurizio Previati was born in Ferrara in 1961; he graduated in Biology at Ferrara University in 1987. In 1991 he was employed as technician at the Human Anatomy Institute of Ferrara University. Since 1st November 2001 he works as full time researcher at the Faculty of Medicine of Ferrara University. . He has taken part in n. 23 national and international congresses and published n. 23 papers on international scientific magazines. His research activities include studies on: the role of inositides as signal transductors; efficiency of histamine as tumor marker; phenotype-genotype correlation in normal and thromboembolic subjects carrying mutations in the gene of methylenetetrahydrofolate reductase; study of the pathways induced by gentamicin and cisplatin in immortalized cell line from inner ear.
He is member of Interdepartmental Bioacustic Center, Doctorate in Biomedical Endocrynological and Neurophysiological Sciences, and of Italian anatomical Society.
Since 1997 he is lecturer of the course of Anatomy and Histology at the Faculty of Medicine.
From 98 to 2002 he had been lecturer in Neuroanatomy, la parte di Neuroanatomia degree in Medicine and Surgery.
Since 2002-03 he is lecture of Anatomy in the courses ofMorfology and Embryology like as Anatomy and Physiology in the degree in Biotechology.
He has taken part in n. 23 national and international congresses and published n. 23 papers on international peer-reviewed scientific magazines.
His research activities include studies on: the role of inositides as signal transductors; efficiency of histamine as tumor marker; phenotype-genotype correlation in normal and thromboembolic subjects carrying mutations in the gene of methylenetetrahydrofolate reductase; study of the pathways induced by gentamicin and cisplatin in immortalized cell line from inner ear.
In particular, in the latter topic he worked both on immortalized cell lines from Immorthomause inner ear and organotypic ex vivo cultures. On immortalized cell lines he investigated the intracellular emchanisms underderlying the cell death due to gentamicin and cisplatin (1. BERTOLASO et al.,(2003). gentamin-induced cytotoxicity involves protein kinase c activation, glutathione extrusion and malondialdehyde production in an immortalized cell line from the organ of corti. AUDIOLOGY AND NEURO-OTOLOGY 8:38-48; BERTOLASO et al.,(2001) Apoptosis in the OC-k3 immortalized cell line treated with different agents. AUDIOLOGY. 40:327-335).
In particular, it has been shown the involvement of PKC activation and tanslocation in gentamicin toxicity, as well as ERK 1/2 phosphorylation in cispaltin induced cell death. In addition, trascriptional changes after cisplatin challange, monitored by gene array analysis (PREVIATI et al.,(2004). RNA expression induced by cisplatin in an organ of Corti-derived immortalized cell line. HEARING RESEARCH 196:8-18) suggested the existence of lipidic peroxidation pathways in cisplatin damage. The existence of nuclear fragmentation, the early appearance of lipidic peroxidation and the observation scavengers prevent both lipid peroxidation and cell death occurrence show that lipid peroxidation is not a trivial postnecrotic process but on the contrary is a key step into a cisplatin-induced apoptotic cascade.
The organotypic culture from inner ear involves the explant and culture of organ of Corti together with the peripheral filaments, the cellular bodies and part of central filaments of spiral ganglion neurons. On these cultures we studied a model of gentamicin and cispaltin toxicity. In particular, it was found that minocycline protects from gentamicin (CORBACELLA Eet al.,(2004) Minocycline attenuates gentamicin induced hair cell loss in neonatal cochlear cultures HEARING RESEARCH 197:11-118)and confirmed a role for ERK phosphorylation in cisplatin toxicity. These latter resulats was shown at ARO (Association for Research in Otolaryngology) Midwinter Meeting (Ding et al., PD98059 protects hair cells from csiaplatin).
Again, organotypic cultures like as neuronal differentiation models were utilized to test the safety range of neurotrophins (GDNF; BDNF and NT3) and antioxidants (ascorbic acid and tocopherols). This waork constituted 2 specific deliverables in the RTD programme “Quality of
life and management of living resources”, progetto europeo QLRT -2001-01563, "BIOEAR". focused on the preparation of a cochlear implant prototype able to delivery drugs together with electrical stimulation, in order to prevent spiral ganglio neuron loss and stimulate peripheral process regeneration. dr. previati work showed a cytotoxic effect of both antioxidants (but not of neurotrophins)at higher concentrations, probably for a Fenton-like metal catalysed prooxidative behaviour, suggesting the need to finely tune the cochlear implant mediated antioxidant delivery.
He is member of Interdepartmental Bioacustic Center, Doctorate in Biomedical Endocrynological and Neurophysiological Sciences, and of Italian anatomical Society.
Since 1997 he is lecturer of the course of Anatomy and Histology at the Faculty of Medicine.
From 98 to 2002 he had been lecturer in Neuroanatomy, la parte di Neuroanatomia degree in Medicine and Surgery.
Since 2002-03 he is lecture of Anatomy in the courses ofMorfology and Embryology like as Anatomy and Physiology in the degree in Biotechology.
He has taken part in n. 23 national and international congresses and published n. 23 papers on international peer-reviewed scientific magazines.
His research activities include studies on: the role of inositides as signal transductors; efficiency of histamine as tumor marker; phenotype-genotype correlation in normal and thromboembolic subjects carrying mutations in the gene of methylenetetrahydrofolate reductase; study of the pathways induced by gentamicin and cisplatin in immortalized cell line from inner ear.
In particular, in the latter topic he worked both on immortalized cell lines from Immorthomause inner ear and organotypic ex vivo cultures. On immortalized cell lines he investigated the intracellular emchanisms underderlying the cell death due to gentamicin and cisplatin (1. BERTOLASO et al.,(2003). gentamin-induced cytotoxicity involves protein kinase c activation, glutathione extrusion and malondialdehyde production in an immortalized cell line from the organ of corti. AUDIOLOGY AND NEURO-OTOLOGY 8:38-48; BERTOLASO et al.,(2001) Apoptosis in the OC-k3 immortalized cell line treated with different agents. AUDIOLOGY. 40:327-335).
In particular, it has been shown the involvement of PKC activation and tanslocation in gentamicin toxicity, as well as ERK 1/2 phosphorylation in cispaltin induced cell death. In addition, trascriptional changes after cisplatin challange, monitored by gene array analysis (PREVIATI et al.,(2004). RNA expression induced by cisplatin in an organ of Corti-derived immortalized cell line. HEARING RESEARCH 196:8-18) suggested the existence of lipidic peroxidation pathways in cisplatin damage. The existence of nuclear fragmentation, the early appearance of lipidic peroxidation and the observation scavengers prevent both lipid peroxidation and cell death occurrence show that lipid peroxidation is not a trivial postnecrotic process but on the contrary is a key step into a cisplatin-induced apoptotic cascade.
The organotypic culture from inner ear involves the explant and culture of organ of Corti together with the peripheral filaments, the cellular bodies and part of central filaments of spiral ganglion neurons. On these cultures we studied a model of gentamicin and cispaltin toxicity. In particular, it was found that minocycline protects from gentamicin (CORBACELLA Eet al.,(2004) Minocycline attenuates gentamicin induced hair cell loss in neonatal cochlear cultures HEARING RESEARCH 197:11-118)and confirmed a role for ERK phosphorylation in cisplatin toxicity. These latter resulats was shown at ARO (Association for Research in Otolaryngology) Midwinter Meeting (Ding et al., PD98059 protects hair cells from csiaplatin).
Again, organotypic cultures like as neuronal differentiation models were utilized to test the safety range of neurotrophins (GDNF; BDNF and NT3) and antioxidants (ascorbic acid and tocopherols). This waork constituted 2 specific deliverables in the RTD programme “Quality of
life and management of living resources”, progetto europeo QLRT -2001-01563, "BIOEAR". focused on the preparation of a cochlear implant prototype able to delivery drugs together with electrical stimulation, in order to prevent spiral ganglio neuron loss and stimulate peripheral process regeneration. dr. previati work showed a cytotoxic effect of both antioxidants (but not of neurotrophins)at higher concentrations, probably for a Fenton-like metal catalysed prooxidative behaviour, suggesting the need to finely tune the cochlear implant mediated antioxidant delivery.
