Bruno Bonetti
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View article: Intranasal Administration of Extracellular Vesicles Derived from Adipose Mesenchymal Stem Cells Has Therapeutic Effect in Experimental Autoimmune Encephalomyelitis
Intranasal Administration of Extracellular Vesicles Derived from Adipose Mesenchymal Stem Cells Has Therapeutic Effect in Experimental Autoimmune Encephalomyelitis Open
Adipose stem cells (ASCs) are a subset of mesenchymal stem cells with validated immunomodulatory and regenerative capabilities that make them attractive tools for treating neurodegenerative disorders, such as multiple sclerosis (MS). Sever…
View article: Intrathecal Inflammatory Profile and Gray Matter Damage Predict Progression Independent of Relapse Activity in Early Multiple Sclerosis
Intrathecal Inflammatory Profile and Gray Matter Damage Predict Progression Independent of Relapse Activity in Early Multiple Sclerosis Open
A specific intrathecal inflammatory profile associated with TNF superfamily markers, CLn, and atrophy of several cortical and deep gray matter regions, assessed at time of diagnosis, is predictive of PIRA in early MS.
View article: Multiple sclerosis diagnosis and its differential diagnosis in patients presenting with type four ‘mirror pattern’ CSF oligoclonal bands
Multiple sclerosis diagnosis and its differential diagnosis in patients presenting with type four ‘mirror pattern’ CSF oligoclonal bands Open
Background Presence of oligoclonal bands (OCBs) restricted to cerebrospinal fluid (CSF) characterizes most patients with multiple sclerosis (MS). Few data are available on the frequency of MS diagnosis and the main alternative diagnoses in…
View article: CD103–CD8+ T cells promote neurotoxic inflammation in Alzheimer’s disease via granzyme K–PAR-1 signaling
CD103–CD8+ T cells promote neurotoxic inflammation in Alzheimer’s disease via granzyme K–PAR-1 signaling Open
Immune mechanisms contribute to the neuropathology of Alzheimer’s disease (AD) but the role of adaptive immune cells is unclear. Here we show that the brain CD8+ T cell compartment is dysregulated in AD patients and in a mouse model with t…
View article: Left Atrial Appendage Occlusion vs Standard of Care After Ischemic Stroke Despite Anticoagulation
Left Atrial Appendage Occlusion vs Standard of Care After Ischemic Stroke Despite Anticoagulation Open
Importance Patients with atrial fibrillation (AF) who have ischemic stroke despite taking oral anticoagulation therapy (OAT) have a very high risk of recurrence. Left atrial appendage occlusion (LAAO) is a mechanical stroke prevention stra…
View article: Association of Levels of CSF Osteopontin With Cortical Atrophy and Disability in Early Multiple Sclerosis
Association of Levels of CSF Osteopontin With Cortical Atrophy and Disability in Early Multiple Sclerosis Open
These data confirm and expand our knowledge on the prognostic role of the CSF inflammatory profile in predicting changes in cortical pathology and disease activity in early MS. The data emphasize a crucial role of OPN.
View article: A Cellular Model of Amyotrophic Lateral Sclerosis to Study the Therapeutic Effects of Extracellular Vesicles from Adipose Mesenchymal Stem Cells on Microglial Activation
A Cellular Model of Amyotrophic Lateral Sclerosis to Study the Therapeutic Effects of Extracellular Vesicles from Adipose Mesenchymal Stem Cells on Microglial Activation Open
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive degeneration of upper and lower motor neurons (MNs) in the brain and spinal cord, leading to progressive paralysis and death. Increas…
View article: Magnetic resonance-guided focused ultrasound unilateral thalamotomy for medically refractory essential tremor: 3-year follow-up data
Magnetic resonance-guided focused ultrasound unilateral thalamotomy for medically refractory essential tremor: 3-year follow-up data Open
Introduction Magnetic resonance–guided focused ultrasound (MRgFUS) thalamotomy of the ventralis intermediate (Vim) nucleus is an “incisionless” treatment for medically refractory essential tremor (ET). We present data on 49 consecutive cas…
View article: CSF levels of Chitinase3like1 correlate with early response to cladribine in multiple sclerosis
CSF levels of Chitinase3like1 correlate with early response to cladribine in multiple sclerosis Open
Background Cladribine has been introduced as a high-efficacy drug for treating relapsing-remitting multiple sclerosis (RRMS). Initial cohort studies showed early disease activity in the first year after drug initiation. Biomarkers that can…
View article: Prevalence of Fabry disease and GLA variants in young patients with acute stroke: The challenge to widen the screening. The Fabry-Stroke Italian Registry
Prevalence of Fabry disease and GLA variants in young patients with acute stroke: The challenge to widen the screening. The Fabry-Stroke Italian Registry Open
In this large multicenter cohort the frequency of FD and GLA variants was consistent with previous reports. Limiting the screening for GLA variants to patients with cryptogenic stroke may miss up to 80% of diagnoses. Some easily recognizab…
View article: Extracellular vesicles from adipose mesenchymal stem cells target inflamed lymph nodes in experimental autoimmune encephalomyelitis
Extracellular vesicles from adipose mesenchymal stem cells target inflamed lymph nodes in experimental autoimmune encephalomyelitis Open
Background aimsAdipose mesenchymal stem cells (ASCs) represent a promising therapeutic approach in inflammatory neurological disorders, including multiple sclerosis (MS). Recent lines of evidence indicate that most biological activities of…
View article: Supplementary Figure 3 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 3 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 1554K, Cap-dependent translation is enhanced by EGFRvIII expression and CC214-1 strongly inhibits P-4E-BP1 phosphorylation.
View article: Supplementary Figure 2 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 2 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 5300K, CC214-1 synergizes at low doses with rapamycin. Quantification of the blots shown in Fig. 2B. PTEN detection on DEAL captured GBM39 cells upon CC214-1 treatment.
View article: Data from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Data from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
Purpose: mTOR pathway hyperactivation occurs in approximately 90% of glioblastomas, but the allosteric mTOR inhibitor rapamycin has failed in the clinic. Here, we examine the efficacy of the newly discovered ATP-competitive mTOR kinase inh…
View article: Supplementary Figure 4 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 4 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 1694K, EGFRvIII expression sensitizes cells to CC214-1 mediated inhibition of proliferation and to autophagy.
View article: Supplementary Figure 7 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 7 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 5321K, In vitro and in vivo pharmacological inhibition of autophagy sensitizes U87EGFRvIII cells and orthotopic xenografts to CC214-1/CC214-2 mediated apoptosis.
View article: Supplementary Figure 1 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 1 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 3457K, Time course dependent CC214-1 treatment in a panel of isogenic GBM cell lines, U87EGFRvIII, U251 and LN229.
View article: Supplementary Figure 2 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 2 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 5300K, CC214-1 synergizes at low doses with rapamycin. Quantification of the blots shown in Fig. 2B. PTEN detection on DEAL captured GBM39 cells upon CC214-1 treatment.
View article: Supplementary Figure 3 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 3 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 1554K, Cap-dependent translation is enhanced by EGFRvIII expression and CC214-1 strongly inhibits P-4E-BP1 phosphorylation.
View article: Supplementary Figure 6 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 6 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 2561K, Treatment with CC214-1, leads to induction of autophagy in GBM39 cells and genetic inhibition of autophagy sensitizes U87EGFRvIII cells to apoptosis.
View article: Data from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Data from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
Purpose: mTOR pathway hyperactivation occurs in approximately 90% of glioblastomas, but the allosteric mTOR inhibitor rapamycin has failed in the clinic. Here, we examine the efficacy of the newly discovered ATP-competitive mTOR kinase inh…
View article: Supplementary Figure 1 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 1 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 3457K, Time course dependent CC214-1 treatment in a panel of isogenic GBM cell lines, U87EGFRvIII, U251 and LN229.
View article: Supplementary Figure Legend from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure Legend from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 91K
View article: Supplementary Figure 7 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 7 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 5321K, In vitro and in vivo pharmacological inhibition of autophagy sensitizes U87EGFRvIII cells and orthotopic xenografts to CC214-1/CC214-2 mediated apoptosis.
View article: Supplementary Figure Legend from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure Legend from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 91K
View article: Supplementary Figure 5 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 5 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 2080K, Tunable expression of EGFRvIII in genetically modified models correlates with autophagy induction upon CC214-1 treatment.
View article: Supplementary Figure 6 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 6 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 2561K, Treatment with CC214-1, leads to induction of autophagy in GBM39 cells and genetic inhibition of autophagy sensitizes U87EGFRvIII cells to apoptosis.
View article: Supplementary Figure 5 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas
Supplementary Figure 5 from The mTOR Kinase Inhibitors, CC214-1 and CC214-2, Preferentially Block the Growth of EGFRvIII-Activated Glioblastomas Open
PDF file - 2080K, Tunable expression of EGFRvIII in genetically modified models correlates with autophagy induction upon CC214-1 treatment.