171,346 research outputs found
The magi: Gentiles or Jews?
No full textFrom the second century onwards the Chrisian tradition has almost without exception accepted that the magi in Matthew's infancy narrative were Gentiles, and this view also completely dominates modern Matthean studies. Yet this idenification of the magi as Gentiles is built upon a number of unconvincing arguments, which fail to stand up to closer scrutiny. A re-assessment of the evidence reveals that the evangelist did not sipulate the racial origins of the magi. They may have been Gentiles, but it is equally plausible that they were Jews
Considerazioni ed osservazioni al microscopio elettronico a scansione sui fili ortodontici in nichel-titanio.
No full textFili ortodontici al confronto: proprietà meccaniche e caratteristiche morfologiche superficiali dei fili in acciaio, beta-titanio e nichel-titanio.
No full text
Neuron-specific regulation of associative learning and memory by MAGI-1 in C. elegans
No full textBACKGROUND: Identifying the molecular mechanisms and neural circuits that control learning and memory are major challenges in neuroscience. Mammalian MAGI/S-SCAM is a multi-PDZ domain synaptic scaffolding protein that interacts with a number of postsynaptic signaling proteins and is thereby thought to regulate synaptic plasticity [1], [2], [3]. PRINCIPAL FINDINGS: While investigating the behavioral defects of C. elegans nematodes carrying a mutation in the single MAGI ortholog magi-1, we have identified specific neurons that require MAGI-1 function for different aspects of associative learning and memory. Various sensory stimuli and a food deprivation signal are associated in RIA interneurons during learning, while additional expression of MAGI-1 in glutamatergic AVA, AVD and possibly AVE interneurons is required for efficient memory consolidation, i.e. the ability to retain the conditioned changes in behavior over time. During associative learning, MAGI-1 in RIA neurons controls in a cell non-autonomous fashion the dynamic remodeling of AVA, AVD and AVE synapses containing the ionotropic glutamate receptor (iGluR) GLR-1 [4]. During memory consolidation, however, MAGI-1 controls GLR-1 clustering in AVA and AVD interneurons cell-autonomously and depends on the ability to interact with the beta-catenin HMP-2. SIGNIFICANCE: Together, these results indicate that different aspects of associative learning and memory in C. elegans are likely carried out by distinct subsets of interneurons. The synaptic scaffolding protein MAGI-1 plays a critical role in these processes in part by regulating the clustering of iGluRs at synapses
E6 targets the PDZ domains of Magi.
No full textTransgenes were expressed in the wing disc under the control of apterous-Gal4 driver in the dorsal compartment. Discs are oriented in all panels with dorsal to the left and ventral to the right. (A-B) Full length Magi::Cherry was distributed around the membrane and found in prominent intracellular puncta (A,A’). When coexpressed with E6+UBE3A, Magi::Cherry levels in the membrane and puncta were reduced (B,B’) with regions of little or no expression (B’ arrow). (C-D) Magi∆WW is uniformly distributed around the membrane (C,C’). When expressed with E6+UBE3A (D,D’) the levels of Magi∆WW are reduced with regions of little or no expression (D’ arrow). (E, F) The localization and levels of Magi∆PDZ were not affected in E6+UBE3A expressing compartment (F,F’) similar to Magi∆PDZ expression alone (E,E’). (G) Cartoon of the Magi transgenic constructs with the WW (yellow), PDZ (blue) and epitope tags (Cherry–red; FLAG–black) indicated. Scale bars indicate 10μm. Inserts were digitally magnified 200%.</p
MAGI-MS: multiple seed-centric module discovery
No full textSUMMARY: Complex disorders manifest by the interaction of multiple genetic and environmental factors. Through the construction of genetic modules that consist of highly coexpressed genes, it is possible to identify genes that participate in common biological pathways relevant to specific phenotypes. We have previously developed tools MAGI and MAGI-S for genetic module discovery by incorporating coexpression and protein interaction networks. Here, we introduce an extension to MAGI-S, denoted as Merging Affected Genes into Integrated Networks—Multiple Seeds (MAGI-MS), which permits the user to further specify a disease pathway of interest by selecting multiple seed genes likely to function in the same molecular mechanism. By providing MAGI-MS with seed genes involved in processes underlying certain classes of neurodevelopmental disorders, such as epilepsy, we demonstrate that MAGI-MS can reveal modules enriched in genes relevant to chemical synaptic transmission, glutamatergic synapse and other functions associated with the provided seed genes. AVAILABILITY AND IMPLEMENTATION: MAGI-MS is free and available at https://github.com/jchow32/MAGI-MS. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics Advances online
43rd NATIONAL CONGRESS OF THE ITALIAN SOCIETY OF MICROBIOLOGY
No full textIntroduction: Capsaicin (8-methyl-N-vanillyl-
6-nonenamide) is the active component responsible
for the fruit pungency of Capsicum plants,
cultivated for food and also for medicinal uses since
ancient times. Besides its multiple pharmacological
and physiological properties (pain relief, cancer
prevention, weight reduction, cardiovascular, and
gastrointestinal benefits), capsaicin has recently
received attention because of its antimicrobial activity
and anti-virulence properties. The aim of the
present study was to investigate the effects of capsaicin
on Streptococcus pyogenes, the most common
cause of acute bacterial pharyngotonsillitis.
Materials and Methods: The erythromycin-resistant
[erm(B)/cMLS], high cell-invasive, and strong
biofilm producer S. pyogenes pharyngeal isolate
SP1070 was used throughout the study. Capsaicin
was purchased from Sigma-Aldrich and stored (10
mg/mL stock solution) in absolute ethanol at -20°C.
The MIC and MBC were determined according to
the CLSI guidelines. Survival in presence of capsaicin
was studied by the live/dead assay. Biofilm
formation was tested by a microtiter assay and
quantified by measuring the absorbance at 690 nm.
Cell experiments were performed using the human
alveolar carcinoma A549 cell line.
Results: The MIC and the MBC of capsaicin were
both 128 μg/mL. In the live/dead assay, several red
cells were detected as early as 15 min after incubation
with capsaicin at MIC; all cells were red after
60 min of incubation. At capsaicin sub-MICs (1/2– 1/16 × MIC), a significant increase in biofilm production
and in the number of streptococci adherent
to A549 cells was observed; whereas a strong reduction
in the number of intracellular bacteria was
detected.
Discussion and Conclusions: Our findings reveal
that capsaicin has a dual effect on S. pyogenes.
High-level capsaicin exerts a bactericidal effect,
probably due to the disruption of the cell membrane,
this result being in agreement with previous
studies on Gram-positive and Gram-negative
pathogens; while sub-lethal capsaicin modifies
virulence properties in vitro, such as the ability to
form biofilm and to adhere/invade epithelial cells.
Capsaicin-induced effects on biofilm formation
seem to be similar to those observed for a variety of
antibiotics that at sub-lethal concentrations can act
as agonists of bacterial biofilm production in vitro.
Overall, capsaicin-induced effects on S. pyogenes
deserve further studies
Article A Genome-wide Functional Screen Shows MAGI-1 Is an L1CAM-Dependent Stabilizer of Apical Junctions in C. elegans
No full textSummary Background: In multicellular organisms, cell-cell junctions are involved in many aspects of tissue morphogenesis. a-catenin links the cadherin-catenin complex (CCC) to the actin cytoskeleton, stabilizing cadherin-dependent adhesions. Results: To identify modulators of cadherin-based cell adhesion, we conducted a genome-wide RNAi screen in C. elegans and uncovered MAGI-1, a highly conserved protein scaffold. Loss of magi-1 function in wild-type embryos results in disorganized epithelial migration and occasional morphogenetic failure. MAGI-1 physically interacts with the putative actin regulator AFD-1/afadin; knocking down magi-1 or afd-1 function in a hypomorphic a-catenin background leads to complete morphogenetic failure and actin disorganization in the embryonic epidermis. MAGI-1 and AFD-1 localize to a unique domain in the apical junction and normal accumulation of MAGI-1 at junctions requires SAX-7/L1CAM, which can bind MAGI-1 via its C terminus. Depletion of MAGI-1 leads to loss of spatial segregation and expansion of apical junctional domains and greater mobility of junctional proteins. Conclusions: Our screen is the first genome-wide approach to identify proteins that function synergistically with the CCC during epidermal morphogenesis in a living embryo. We demonstrate novel physical interactions between MAGI-1, AFD-1/afadin, and SAX-7/L1CAM, which are part of a functional interactome that includes components of the core CCC. Our results further suggest that MAGI-1 helps to partition and maintain a stable, spatially ordered apical junction during morphogenesis
A Genome-wide Functional Screen Shows MAGI-1 Is an L1CAM-Dependent Stabilizer of Apical Junctions in C. elegans
No full textSummaryBackgroundIn multicellular organisms, cell-cell junctions are involved in many aspects of tissue morphogenesis. α-catenin links the cadherin-catenin complex (CCC) to the actin cytoskeleton, stabilizing cadherin-dependent adhesions.ResultsTo identify modulators of cadherin-based cell adhesion, we conducted a genome-wide RNAi screen in C. elegans and uncovered MAGI-1, a highly conserved protein scaffold. Loss of magi-1 function in wild-type embryos results in disorganized epithelial migration and occasional morphogenetic failure. MAGI-1 physically interacts with the putative actin regulator AFD-1/afadin; knocking down magi-1 or afd-1 function in a hypomorphic α-catenin background leads to complete morphogenetic failure and actin disorganization in the embryonic epidermis. MAGI-1 and AFD-1 localize to a unique domain in the apical junction and normal accumulation of MAGI-1 at junctions requires SAX-7/L1CAM, which can bind MAGI-1 via its C terminus. Depletion of MAGI-1 leads to loss of spatial segregation and expansion of apical junctional domains and greater mobility of junctional proteins.ConclusionsOur screen is the first genome-wide approach to identify proteins that function synergistically with the CCC during epidermal morphogenesis in a living embryo. We demonstrate novel physical interactions between MAGI-1, AFD-1/afadin, and SAX-7/L1CAM, which are part of a functional interactome that includes components of the core CCC. Our results further suggest that MAGI-1 helps to partition and maintain a stable, spatially ordered apical junction during morphogenesis
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