Institution
University of Milano-Bicocca
Education•Milan, Italy•
About: University of Milano-Bicocca is a education organization based out in Milan, Italy. It is known for research contribution in the topics: Population & Blood pressure. The organization has 8972 authors who have published 22322 publications receiving 620484 citations. The organization is also known as: Università degli Studi di Milano-Bicocca & Universita degli Studi di Milano-Bicocca.
Topics: Population, Blood pressure, Large Hadron Collider, Branching fraction, Ambulatory blood pressure
Papers published on a yearly basis
Papers
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TL;DR: The data suggest that signaling through BMPR1A;B performs at least two roles in early respiratory development: first, it promotes tracheal formation through repression of Sox2; and second, it restricts the site of lung bud initiation.
Abstract: The mammalian foregut gives rise to the dorsally located esophagus and stomach and the ventrally located trachea and lung. Proper patterning and morphogenesis of the common foregut tube and its derived organs is essential for viability of the organism at birth. Here, we show that conditional inactivation of BMP type I receptor genes Bmpr1a and Bmpr1b (Bmpr1a;b) in the ventral endoderm leads to tracheal agenesis and ectopic primary bronchi. Molecular analyses of these mutants reveal a reduction of ventral endoderm marker NKX2-1 and an expansion of dorsal markers SOX2 and P63 into the prospective trachea and primary bronchi. Subsequent genetic experiments show that activation of canonical WNT signaling, previously shown to induce ectopic respiratory fate in otherwise wild-type mice, is incapable of promoting respiratory fate in the absence of Bmpr1a;b. Furthermore, we find that inactivation of Sox2 in Bmpr1a;b mutants does not suppress ectopic lung budding but does rescue trachea formation and NKX2-1 expression. Together, our data suggest that signaling through BMPR1A;B performs at least two roles in early respiratory development: first, it promotes tracheal formation through repression of Sox2; and second, it restricts the site of lung bud initiation.
202 citations
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TL;DR: Analyses of effective connectivity indicated that these results were due to a failure of attention to modulate connectivity between extrastriate areas and V1, which may suggest a mechanism to explain the reduced salience of social stimuli in ASD.
201 citations
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TL;DR: Molecular and functional evidence for feasible and seamless gene editing in HSPCs is provided and p53-mediated DDR pathway activation was the predominant response to even single-nuclease-induced DSBs across all HSPC subtypes analyzed.
201 citations
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TL;DR: Mortality risk for patients receiving VV ECMO is correlated to the extrapulmonary organ function at the time of ECMO initiation, and the ECMOnet score is a tool for the evaluation of the appropriateness and timing of VVECMO in acute lung failure.
Abstract: Purpose
The decision to start venovenous extracorporeal membrane oxygenation (VV ECMO) is commonly based on the severity of respiratory failure, with little consideration of the extrapulmonary organ function. The aim of the study was to identify predictors of mortality and to develop a score allowing a better stratification of patients at the time of VV ECMO initiation.
199 citations
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TL;DR: The findings support the previous evidence indicative for a contribution of glial TLR4 to the initiation of neuropathic pain, suggest it as potential innovative target to treat this debilitating disease, and propose FP‐1 as lead compound for the development of new effective drugs.
Abstract: Neuropathic pain remains a prevalent clinical problem because it is often poorly responsive to the currently used analgesics, thus it is crucial the identification of new potential targets and drugs. Recent evidence indicated that microglial cells in the spinal cord are critically involved in the development and maintenance of neuropathic pain, with a pivotal role of toll-like receptor 4 (TLR4). Binding of an endogenous ligand to TLR4 might be considered an important step in the regulation of microglia activity in pain facilitation, suggesting that a mechanism aimed to inhibit such a binding could be effective against neuropathic pain. We have synthesized new ligands to TLR4 with antagonistic activity. In the present work we evaluated the efficacy of the most potent TLR4 antagonist synthesized by us (FP-1), administered in mice with painful neuropathy. The repeated treatment of neuropathic mice with FP-1 (5-10 mg/kg, i.p.) evoked a relief of both thermal hyperalgesia and mechanical allodynia, whereas the administration of the highest dose to TLR4 knockout neuropathic mice revealed that in the absence of TLR4 receptor, the compound lost its efficacy. As consequence of TLR4 binding, the repeated treatment with FP-1 prevented the activation of the transcription factor NF-kB and the TNFalpha overproduction in the spinal cord. Together, our findings support the previous evidence indicative for a contribution of glial TLR4 to the initiation of neuropathic pain, suggest it as potential innovative target to treat this debilitating disease, and propose FP-1 as lead compound for the development of new effective drugs.
199 citations
Authors
Showing all 9226 results
Name | H-index | Papers | Citations |
---|---|---|---|
Carlo Rovelli | 146 | 1502 | 103550 |
Giuseppe Mancia | 145 | 1369 | 139692 |
Marco Bersanelli | 142 | 526 | 105135 |
Teruki Kamon | 142 | 2034 | 115633 |
Marco Colonna | 139 | 512 | 71166 |
M. I. Martínez | 134 | 1251 | 79885 |
A. Mennella | 132 | 463 | 93236 |
Roberto Salerno | 132 | 1197 | 83409 |
Federico Ferri | 132 | 1376 | 89337 |
Marco Paganoni | 132 | 1438 | 88482 |
Arabella Martelli | 131 | 1318 | 84029 |
Sandra Malvezzi | 129 | 1326 | 84401 |
Andrea Massironi | 129 | 1115 | 78457 |
Marco Pieri | 129 | 1285 | 82914 |
Cristina Riccardi | 129 | 1627 | 91452 |