22 research outputs found
Non uniqueness of non runaway solutions of Abraham–Lorentz–Dirac equation in an external laser pulse
No full textIn the paper cite{carati95} it was shown that, for motions on a line under the action of a potential barrier, the third-order ALD equation presents the phenomenon of non uniqueness of non runaway solutions. Namely, at least for a sufficiently steep barrier, the physical solutions of the equation are not determined by the ``mechanical state'' of position and velocity, and knowledge of the initial acceleration too is required. Due to recent experiments, both in course and planned, on the interactions between strong laser pulses and ultra relativistic electrons, it becomes interesting to establish whether such a non uniqueness phenomenon extends to the latter case, and for which ranges of the parameters. In the present work we will consider just the simplest model, i.e., the case of an electromagnetic plane wave, and moreover the ALD equation will be dealt with in the non relativistic approximation. The result we found is that the non uniqueness phenomenon occurs if, at a given frequency of the incoming wave, the field intensity is sufficiently large. An analytic stimate of such a threshold is also given. At the moment it is unclear whether such a phenomenon applies also in the full relativistic case, which is the one of physical interest
Searching for centaurin-α2 interacting proteins: evidence of interaction with tubulin-β
No full textCentaurin-α2 belongs to the centaurin family and is characterized by a
zinc binding domain similar to Arf-GAP and by two PH domains. Its expression
pattern and function have not yet been extensively investigated.
Centaurin-α2 was shown to bind PIP2 and PIP3 and to localize at
plasma membrane, promoting the release of GTP and the consequent
inactivation of Arf-6, a protein involved in the regulation of intracellular
vesicular trafficking and in cytoskeletal rearrangement. We recently
studied the expression profile of CENTA2 mRNA by in situ hybridization,
during mouse embryo development and we found it is expressed
in early developmental stages of encephalon and heart.
With the final aim of elucidating the centaurin-α2 molecular pathways
and its biological role/s, we searched for interactors by means of the
yeast two-hybrid assay.
An interaction with the C-terminal region of tubulin-β has been observed
and confirmed by co-immunoprecipitation. This portion of tubulin-
β is involved in the binding of MAPs and motor proteins. Considering
that tubulin-β was found to bind phospholipase Cγ1 through
its PH domains, we hypothesized an interaction between centaurin-α2
mediated by this domain.
The yeast two-hybrid assay allowed us also to detect an interaction
with nucleoporin NUP53, a component of the nuclear pore complex,
that will be confirmed by co-immunoprecipitation.
According to our evidence, that will be further investigated, we propose
that centaurin-α2 can be localized at the plasma membrane, the cytoplasm and the perinuclear region, and can translocate through microtubules
anchoring, according to its hypothesized role in vesicular
trafficking
Ricerca di interattori molecolari della centaurina-α2 : evidenze di associazione con la tubulina β
No full textRADIOMICS AND MACHINE LEARNING FOR PRETREATMENT EVALUATION OF ESSENTIAL TREMOR RESPONSE TO MRGFUS THALAMOTOMY
No full textEvaluation of 1p36 markers and clinical outcome in a skull base chordoma study
No full textChordomas are rare embryogenetic tumors, arising from remnants of the notochord, characterized by local invasiveness and variable tendency for recurrence. No molecular markers are currently used in a clinical setting to distinguish chordomas with an indolent or an aggressive
pattern. Among the genetic lesions observed in this tumor, one of the most commonly detected is 1p loss. In a previous study we observed 1p36 loss of heterozygosity(LOH) in 85% of the analyzed chordomas. We studied a group of 16 homogeneously treated skull base chordomas
(SBCs), reporting 1p36 LOH in 75% of them and determining
the expression pattern of eight apoptotic genes
mapped at 1p36. No tumors shared a common expression profile with nucleus pulposus, which is considered the only adult normal tissue deriving from notochord. In particular, tumor necrosis factor receptor superfamily
genes TNFRSF8, TNFRSF9, and TNFRSF14 were differently expressed compared with control in a higher percentage of tumors (40%–53%) than were the remaining
analyzed genes, suggesting that the deregulation of these
three genes might have a role in chordoma tumorigenesis.
The presence/absence of LOH and the expression/
nonexpression of each apoptotic gene were studied in
a survival analysis. Our results suggest that the lack
of 1p36 LOH or the presence of TNFRSF8 expression
might be associated with a better prognosis in patients
with SBCs
Centa2 is expressed during heart development and is a candidate gene for CVMs
No full textCardiovascular malformations (CVMs) have a greater incidence in NF1 microdeletion syndrome compared to classical NF1, because of haploinsufficiency of one or more genes inside the deletion. We previously identified by RT-PCR and Northern blot the expression of Centa2, Suz12 and Utp6, mapping in the deletion interval, in human fetal and embryonic mouse heart. To characterize their expression pattern we carried out in situ hybridizations on mouse embryos and sections. Centa2 is expressed in the heart from 9 to 15.5 dpc and displays a strong hybridizations signal at 9-9.5 dpc, while the heart tube is looping. Suz12 is weakly detectable in the heart at 10 dpc, while Utp6 is not detectable in heart. In zebrafish, we detected by RT-PCR only Centa2 expression in adult heart, while in situ hybridizations at different embryonic stages demonstrate that both Centa2 and Suz12 are expressed in CNS. Only a faint Centa2 signal is visible in 48 hpf heart. Little is known about the molecular functions of Centaurin α 2; preliminary yeast two-hybrids results indicate Tubulin β as a possible interactor. Our data suggest a role of Centa2 in heart development and an implication in the onset of CVMs
Breakpoint characterization of a novel NF1 multiexonic deletion : a case showing expression of the mutated allele
No full textNeurofibromatosis type 1 (NF1) is a common genetic disease caused by haploinsufficiency of the NF1 tumor-suppressor gene. Different pathogenetic mechanisms have been identified, with the majority (95%) causing intragenic lesions. Single or multiexon NF1 copy number changes occur in about 2% of patients, but little is known about the molecular mechanisms behind these intragenic deletions. We report here on the molecular characterization of a novel NF1 multiexonic deletion. The application of a multidisciplinary approach including multiplex ligation-dependent probe amplification, allelic segregation analysis, and fluorescent in situ hybridization allowed us to map the breakpoints in IVS27b and IVS48. Furthermore, the breakpoint junction was characterized by sequencing. Using bioinformatic analysis, we identified some recombinogenic motifs in close proximity to the centromeric and telomeric breakpoints and predicted the presence of a mutated messenger ribonucleic acid, which was deleted between exons 28 and 48 and encodes a neurofibromin that lacks some domains essential for its function. Through reverse transcriptase- polymerase chain reaction, the expression of the mutated allele was verified, showing the junction between exons 27b and 49 and, as expected, was not subjected to nonsense-mediated decay. Multiexonic deletions represent 2% of NF1 mutations, and until now, the breakpoint has been identified in only a few cases. The fine characterization of multiexonic deletions broadens the mutational repertoire of the NF1 gene, allowing for the identification of different pathogenetic mechanisms causing NF1
Evaluation of 1p36 LOH, apoptotic genes’ expression and clinical outcome in a skull base chordoma prospective study
No full textStudio di espressione dei recettori tirosin-kinasici target dell’Imatinib mesilato in cordomi della base cranica
No full text
