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Sebastiano Cavallaro

Publications and source records attributed to Sebastiano Cavallaro.

17 recordsLinked to original sources
PubMed2006

Nickel Gluconate-Mercurius Heel-Potentised Swine Organ Preparations: a new therapeutical approach for the primary treatment of pediatric ranula and intraoral mucocele.

OBJECTIVE: Many authors consider surgical therapy of pediatric ranula and intraoral mucocele as the election treatment. Recently, an intracystic sclerosing injection with OK-432 has been proposed as a ranula primary treatment. This preliminary study evaluates the effectiveness of the use of Nickel Gluconate-Mercurius Heel-Potentised Swine Organ Preparations as the primary treatment of pediatric ranula and intraoral mucocele. METHODS: Eighteen children (9 ranulas, 9 labial mucoceles, 2 lingual mucoceles) were treated with oral administration of Nickel Gluconate-Mercurius Heel-Potentised Swine Organ Preparations D10/D30/D200. RESULTS: Eighty-nine percent ranulas (8 out of 9), 67% labial mucoceles (6 out of 9) completely responded to the therapy. One ranula, that interrupted therapy after only 4 weeks, was subjected to marsupialization in another hospital. A double mucocele case partially responded (one of the two was extinguished), another case incompletely responded, decreasing the size beyond 50%, and just one case, changing volume, resisted the therapy. Lingual mucocele healed at once. Blandin-Nuhn polypoid congenital mucocele responded to the treatment with gradual reabsorption, permitting surgical excision of the atrophic polypoid remnant, without removing glands of origin. No solved case showed recurrence (follow up range: 4-32 months). CONCLUSION: Homotoxicological therapy with Nickel Gluconate-Mercurius Heel-Potentised Swine Organ Preparations D10/D30/D200 is an effective primary treatment of pediatric ranula and intraoral mucocele.

Adolescent↗
PubMed2006

Genomic profiling of cortical neurons following exposure to beta-amyloid.

In vitro and in vivo studies have shown that beta-amyloid peptide induces neuronal cell death. To explore the molecular basis underlying beta-amyloid-induced toxicity, we analyzed gene expression profiles of cultured rat cortical neurons treated for 24 and 48 h with synthetic beta-amyloid peptide. From the 8740 genes interrogated by oligonucleotide microarray analysis, 241 genes were found to be differentially expressed and segregated into distinct clusters. Functional clustering based on gene ontologies showed coordinated expression of genes with common biological functions and metabolic pathways. The comparison with genes differentially expressed in cerebellar granule neurons following serum and potassium deprivation indicates the existence of common regulatory mechanisms underlying neuronal cell death. Our results offer a genomic view of the changes that accompany beta-amyloid-induced neurodegeneration.

Amyloid beta-Peptides↗
PubMed2006

A genomic approach to investigate neuronal apoptosis.

Apoptosis has been postulated to play a possible causal role in the onset of Alzheimer's disease due to shortage of trophic supply, deafferentation and excessive production of free radicals. Many experiments in the past have demonstrated the requirement of de novo gene expression during neuronal apoptosis. In view of the possible involvement of apoptotic processes in Alzheimer's disease and to begin a comprehensive survey of the gene-based molecular mechanisms that underlie these events we have used genome scale screening by DNA microarray technology in cerebellar granule neurons following serum and potassium deprivation. From the 8740 genes interrogated by the microarrays, 423 genes were found regulated both at the transcriptional and post-transcriptional level and segregated into distinct clusters. Functional clustering based on gene ontologies showed coordinated expression of genes with common biological functions and metabolic pathways. Among the genes implicated in apoptotic cerebellar granule neurons, 70 were in common with those differentially expressed in cortical neurons exposed to amyloid beta-protein, indicating the existence of common mechanisms responsible of neuronal cell death. This new approach offer a genomic view of the changes that accompany neuronal apoptosis and yield new insights into the molecular basis underlying it.

Alzheimer Disease↗
PubMed2005

Tracheomalacia in oesophageal atresia: morphological considerations by endoscopic and CT study.

OBJECTIVE: A Tracheomalacia complicates 11-33% of cases of Oesophageal Atresia with distal Tracheo-Oesophageal Fistula. The lesion generally involves only the thoracic segment of the trachea, and it has close anatomical relationships with the mediastinal structures, specially with the aortic arch. We therefore tried to define the most important morphotypes of tracheobronchial malacia by using dynamic fiberoptic bronchoscopy (DFB) and spiral multilayer computed tomography (CT). METHODS: Between 1999 and 2003 we studied 40 children from two different institutions who had been operated on at birth for oesophageal atresia. All patients were been submitted to DFB, and the positive cases underwent examination by CT with an iodinated contrast medium. CT angiographic images of great vessels and multiplanar and three-dimensional images of the airways (virtual broncoscopy and broncography) were obtained for morphological evaluation. RESULTS: Twenty-five patients (62%) tested positive for malacia using DBF and all were also confirmed by CT study. In 11 cases (46%), the malacia was located at the thoracic section of the trachea, which was occluded by compression of the aorto-innominate complex. A simple intrinsic tracheomalacia without any vascular compression was present in eight cases (33%), while in five cases (21%), the malacia was complex. CONCLUSIONS: A correct morphological analysis of the malformed segment permitted 'tailored surgery' for each individual patient, allowing us to take account of the type of malacia, its length, and the compressive action exercised by the mediastinal great vessels.

Bronchoscopy↗
PubMed2004

Gene expression profiles of apoptotic neurons.

The multigenic program underlying neuronal apoptosis is mostly unknown. To study the program, we used genome-scale screening by oligonucleotide microarrays during serum and potassium deprivation-induced apoptosis of cerebellar granule neurons. From the 8740 genes interrogated by the arrays, 423 genes were found to be regulated at both the transcriptional and the posttranscriptional level and segregated into distinct clusters. Semantic clustering based on gene ontologies showed coordinated expression of genes with common biological functions and metabolic pathways. Among the genes implicated in apoptotic cerebellar granule neurons, 70 were in common with those differentially expressed in cortical neurons exposed to amyloid beta-protein, indicating the existence of common mechanisms responsible for neuronal cell death. Our results offer a genomic view of the changes that accompany neuronal apoptosis and yield new insights into the underlying molecular basis.

Amyloid beta-Peptides↗
PubMed2004

Genomic portraits of the nervous system in health and disease.

As the human genome project moves toward its goal of sequencing the entire human genome, gene expression profiling by DNA microarray technology is being employed to rapidly screen genes for biological information. In this review, we will introduce DNA microarray technology, outline the basic experimental paradigms and data analysis methods, and then show with some examples how gene expression profiling can be applied to the study of the central nervous system in health and disease.

Algorithms↗
PubMed2004

Parkin transcript variants in rat and human brain.

Alternative splicing has an important role in expanding protein diversity. We have identified complementary DNA species from adult rat and fetal human brain encoding seven new splice variants of parkin, a gene mutated in autosomal recessive juvenile parkinsonism (ARJP). Alternative splicing affects almost all previously characterized exons, plus 3 new exons of 72, 156, and 180 nucleotides. This creates the potential to express hundreds of different isoforms. The encoded parkin isoforms have different amino acid composition, post-translational modifications, and, most important, molecular architectures. They diverge for the presence or absence of the ubiquitin-like domain, one or two C3HC4 ring fingers, the in-between ring fingers (IBR) domain, and a thiol proteases active site, which has not been previously characterized. Distinct expression patterns occur in primary cultures of neuronal and glial cells. Extensive splicing of parkin produces regional and structural diversity and may have important implications for the pathogenetic mechanisms underlying ARJP.

Alternative Splicing↗
PubMed2003

Quantification and distribution of beta-secretase alternative splice variants in the rat and human brain.

Beta-amyloid (Abeta) is formed by sequential cleaving of the amyloid precursor protein by two proteolytic enzymes, beta- and gamma-secretases. Beta-secretase (BACE) is a type I transmembrane aspartic proteinase that is highly expressed in the mammalian brain. Four alternative splice variants of BACE are currently known and each encodes for a protein isoform with a different enzymatic activity. In Alzheimer's disease (AD) patients, the enzymatic activity and protein levels of BACE are increased in the neocortex, suggesting their differential expression may have a role in Abeta plaque formation. We have determined the differential expression of BACE mRNA and its splice variants in eight regions of the rat and two of the human brain. In humans, the frontal cortex which shows Abeta deposition in AD, expressed three-fold more BACE than the cerebellum and four fold more than the rats' frontal cortex both of which do not form Abeta plaques. The highest BACE levels of rats were found in the frontal cortex and less in other areas. Although most human and rat brain regions expressed all four BACE variants, the human cerebellum did not express the I-457 BACE variant. Human and rat frontal cortex expressed high levels of the I-501 and I-457 variants, but I-432 was highly expressed only in the rat. Species-specific differences were evident between human and rat brain areas, suggesting that BACE transcript variants may have different evolutionary conservation. Differential expression of BACE variants may explain the broad spectrum of phenotypic abnormalities and possible pathogenetic mechanisms underlying Alzheimer's disease.

Alternative Splicing↗
PubMed2003

Opposing effects by pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide on hippocampal synaptic transmission.

Pituitary adenylate cyclase-activating polypeptide (PACAP), vasoactive intestinal peptide (VIP), and their receptors have been localized within the hippocampus but their physiological function on synaptic transmission is still unclear. We investigated the effects of PACAP and VIP on evoked excitatory postsynaptic currents (EPSCs) recorded with patch clamp from CA1 pyramidal neurons in rat hippocampal slices. Bath application of PACAP reversibly reduced EPSC amplitude. This effect was partly prevented by intracellular addition of (R)-adenosine, cyclic 3',5'-hydrogenphosphorothioate (cAMPS-Rp), a cAMP antagonist inhibiting protein kinase A, but not by the calcium chelator 1,2-bis (2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). Application of VIP induced a long-lasting increase of EPSC amplitude that was completely abolished when cAMPS-Rp was included in the intracellular solution. PACAP and VIP effects on EPSCs were mimicked by the cAMP agonist 8-bromoadenosine-3',5'-cyclic monophosphate (8-Br-cAMP). The differing abilities of PACAP and VIP to modulate transmission efficiency over long periods of time, through the cAMP/PKA pathway, suggest that these neuropeptides may exert opposing roles in synaptic plasticity.

Animals↗
PubMed2003

Hippocampal gene expression profiles in passive avoidance conditioning.

Many experiments in the past have demonstrated the requirement of de novo gene expression during the long-term retention of learning and memory. Although previous studies implicated individual genes or genetic pathways in learning and memory, the collective behaviours of the genes is mostly unknown. We have used genome-scale screening by microarray analysis to examine the hippocampal expression of more than 1200 genes relevant to neurobiology during instrumental conditioning. Training rats on a step-through passive avoidance task led to unique patterns of gene expression when compared to naïve animals or those exposed to the conditioned or the unconditioned stimulus alone. The newly identified genes afford a quantitative view of the changes which accompany conditioning at the genomic level and enable deeper insights into the molecular basis underlying learning and memory.

Animals↗
PubMed2002

Memory-specific temporal profiles of gene expression in the hippocampus.

Many experiments in the past have demonstrated the requirement of de novo gene expression during the long-term retention of learning and memory. Although previous studies implicated individual genes or genetic pathways in learning and memory, they did not uncover the collective behaviors or patterns of the genes. We have used genome-scale screening to analyze gene expression during spatial learning of rats in the Morris water maze. Our results show distinct temporal gene expression profiles associated with learning and memory. Exogenous administration of one peptide whose sustained increase during memory retention was implicated by microarray analysis, fibroblast growth factor (FGF)-18, improved spatial learning behavior, suggesting that pharmacological modulation of pathways and targets identified may allow new therapeutic approaches for improving learning and memory. Results of this study also suggest that while learning and physical activity involve common groups of genes, the behavior of learning and memory emerges from unique patterns of gene expression across time.

Animals↗
PubMed2002

Gene expression profiles of heme oxygenase isoforms in the rat brain.

In the last decade the heme oxygenase (HO) system has been strongly highlighted for its potential significance in maintaining cellular homeostasis. Nevertheless the physiological relevance of the three isoforms cloned to date, HO-1, HO-2 and HO-3, and their reciprocal interrelation have been poorly understood. In the brain the HO system has been reported to be very active and its modulation seems to play a crucial role in the pathogenesis of neurodegenerative disorders. To discriminate the regional and cellular distribution of HO isoforms in the CNS, we have developed a real time quantitative reverse transcription-polymerase chain reaction (RT-PCR) protocol. With this highly sensitive methodology we have assessed for the first time the expression of all known HO isoform mRNAs in different rat brain areas. Although they presented a highly dissimilar range of expression, with HO-2>HO-1>HO-3, all three HO isoform transcripts demonstrated high level of expression in the cerebellum and the hippocampus, showing in a different scale, a strikingly parallel distribution gradient. We have also quantified the expression of HO mRNAs in primary culture of cortical neurons and type I astrocytes. While HO-1 and HO-2 were detected in both cellular types, HO-3 transcript was uniquely found in astrocytes. To further investigate the regional brain expression of this elusive and poorly studied isoform, we have performed in situ hybridization using an HO-3 specific riboprobe. HO-3 mRNA was expressed mainly in hippocampus, cerebellum and cortex. The initial elucidation of HO isoforms distribution should facilitate further research on their pathophysiological role in the nervous system.

Animals↗
PubMed2002

Gene expression profiles in a transgenic animal model of fragile X syndrome.

Fragile X syndrome is the most common inherited form of mental retardation. Although this syndrome originates from the absence of the RNA-binding protein FMRP, the molecular mechanisms underlying the cognitive deficits are unknown. The expression pattern of 6789 genes was studied in the brains of wild-type and FMR1 knockout mice, a fragile X syndrome animal model that has been associated with cognitive deficits. Differential expression of more than two-fold was observed for the brain mRNA levels of 73 genes. Differential expression of nine of these genes was confirmed by real-time quantitative reverse transcription-polymerase chain reaction and by in situ hybridization. In addition to corroborating the microarray data, the in situ hybridization analysis showed distinct spatial distribution patterns of microtubule-associated protein 2 and amyloid beta precursor protein. A number of differentially expressed genes associated with the fragile X syndrome phenotype have been previously involved in other memory or cognitive disorders.

Amyloid beta-Protein Precursor↗
PubMed2002

Distribution of parkin in the adult rat brain.

A mutation in the parkin gene has been identified as the cause for an autosomal recessively inherited form of Parkinson's disease (PD). The authors have recently isolated the mRNA coding for the rat homolog of parkin and showed its widespread expression in the central nervous system (CNS) by in situ hybridization. In the present study, we investigated the distribution of parkin in the rat CNS with a polyclonal antibody that reacts with a approximately 52-kDa protein, mainly localized in the cytoplasm and corresponding to the predicted molecular mass of parkin. Immunohistochemistry on adult rat brain sections showed a widespread distribution of parkin. This included labeling of cell bodies, nuclei as well as processes in the hippocampus, cerebral cortex, cerebellum, and several nuclei in the brainstem. The regional expression of parkin-immunoreactivity (IR) correlated well with the parkin-mRNA levels assessed by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). This study provides the detailed analysis of the regional and cellular distribution of parkin in the rat brain and may be useful in elucidating its pathophysiological role.

Animals↗
PubMed2002

Programs of gene expression during the laying down of memory formation as revealed by DNA microarrays.

Many experiments in the past have demonstrated the requirement of de novo gene expression during memory formation. In contrast to the initial reductionistic view that genes relevant to learning and memory would be easily found and would provide a simple key to understand this brain function, it is becoming apparent that the genetic contribution to memory is complex. Previous approaches have been focused on individual genes or genetic pathways and failed to address the massively parallel nature of genome activities and collective behavior of the genes that ultimately control the molecular mechanisms underlying brain function. In view of the broad variety of genes and the cross talk of genetic pathways involved in this regulation, only gene expression profiles may reflect the complete behavior of regulatory pathways. In this review we illustrate how DNA microarray-based gene expression profiling may help to dissect and analyze the complex mechanisms involved in gene regulation during the acquisition and storage of memory in the mammalian brain.

Animals↗
PubMed2002

Gene expression profiles--a new dynamic and functional dimension to the exploration of learning and memory.

Many experiments in the past have demonstrated the requirement of de novo gene expression during the long-term retention of learning and memory. Although previous studies implicated individual genes or genetic pathways in learning and memory they did not uncover the collective behaviors of the genes. In view of the broad variety of genes and the cross-talk of genetic pathways, gene expression profiles offer a new dynamic and functional dimension to the exploration of learning and memory. This review illustrates how DNA microarray-based gene expression profiling may help to dissect and analyze the complex mechanisms involved in gene regulation during the acquisition and storage of memory.

Animals↗