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Article ; Online: Nonrandomised controlled trial in recurrent glioblastoma patients: the promise of autologous tumour lysate-loaded dendritic cell vaccination.

Pasqualetti, Francesco / Zanotti, Sofia

2023 Volume 129, Issue 6, Page(s) 895–896

Abstract: Recently, Liau et al. reported the results of Phase 3 clinical trial testing DCVax-L vaccines on patients with glioblastoma. Despite the promising and significant results obtained, the study design and the long-lasting period of recruitment of this work ... ...

Abstract	Recently, Liau et al. reported the results of Phase 3 clinical trial testing DCVax-L vaccines on patients with glioblastoma. Despite the promising and significant results obtained, the study design and the long-lasting period of recruitment of this work deserve some reflection.
MeSH term(s)	Humans ; Glioblastoma/therapy ; Brain Neoplasms/therapy ; Neoplasm Recurrence, Local/therapy ; Cancer Vaccines/therapeutic use ; Vaccination ; Dendritic Cells
Chemical Substances	Cancer Vaccines
Language	English
Publishing date	2023-02-15
Publishing country	England
Document type	Controlled Clinical Trial ; Journal Article
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-023-02194-1
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Article: Traumatic Brain Injury Triggers Neurodegeneration in a Mildly Symptomatic MELAS Patient: Implications on the Detrimental Role of Damaged Mitochondria in Determining Head Trauma Sequalae in the General Population.

Zanotti, Simona / Velardo, Daniele / Sciacco, Monica

Metabolites

2022 Volume 13, Issue 1

Abstract: Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a maternally inherited genetic mitochondrial disease with a typical onset in the first two decades of life and a major involvement of central nervous system ( ... ...

Abstract	Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a maternally inherited genetic mitochondrial disease with a typical onset in the first two decades of life and a major involvement of central nervous system (CNS). We present the case of a man affected with an oligosymptomatic, genetically determined MELAS syndrome, whose clinical picture dramatically and irreversibly worsened following a mild head injury. We hypothesize that the CNS metabolic stress induced by the brain injury activated an irreversible cascade of events leading to progressive neurodegeneration because damaged mitochondria were unable to restore the balance between energy requirements and availability.
Language	English
Publishing date	2022-12-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662251-8
ISSN	2218-1989
ISSN	2218-1989
DOI	10.3390/metabo13010046
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Article ; Online: Peculiar histological and ultrastructural skeletal muscle alterations in a patient with CMV infection and autoimmune myositis: case evaluation and brief literature review.

Ripolone, Michela / Napoli, Laura / Mantero, Vittorio / Sciacco, Monica / Zanotti, Simona

Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology

2022 Volume 41, Issue 1, Page(s) 41–47

Abstract: We report the case of a young woman with CMV infection, high level of creatine kinase and myopathy. Electromyography showed a myopathic pattern. Muscle biopsy showed a marked increase of NADH enzymatic activity in the central area of almost all type I ... ...

Abstract	We report the case of a young woman with CMV infection, high level of creatine kinase and myopathy. Electromyography showed a myopathic pattern. Muscle biopsy showed a marked increase of NADH enzymatic activity in the central area of almost all type I fibres, few degenerative and necrotic fibres and scattered mononuclear cell infiltrates. Ultrastructural analysis showed a marked disarrangement of sarcomeric structure and large inclusions of thin filaments in some fibres, while immunohistochemistry evidenced alteration in desmin, actin and αB-crystallin protein signals. PCR for CMV detection on muscle sections was negative. Histological, immunological and ultrastructural evaluations were compatible with a necrotic inflammatory myopathy. The correlations between CMV liver infection and the myopathic pattern are discussed. This case underscores the need to consider CMV infection in the differential diagnosis of myopathy with undetermined aetiology, quickly providing directions for a targeted muscle pharmacological intervention.
MeSH term(s)	Autoimmune Diseases ; Cytomegalovirus Infections/complications ; Cytomegalovirus Infections/diagnosis ; Cytomegalovirus Infections/metabolism ; Female ; Humans ; Muscle, Skeletal/pathology ; Muscular Diseases/metabolism ; Myositis/diagnosis ; Myositis/pathology
Language	English
Publishing date	2022-03-31
Publishing country	Italy
Document type	Case Reports
ZDB-ID	2102328-1
ISSN	2532-1900 ; 1128-2460
ISSN (online)	2532-1900
ISSN	1128-2460
DOI	10.36185/2532-1900-068
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Article ; Online: Polarization states and far-field optical properties in dielectric photonic crystal slabs.

Zagaglia, Luca / Zanotti, Simone / Minkov, Momchil / Liscidini, Marco / Gerace, Dario / Claudio Andreani, Lucio

Optics letters

2023 Volume 48, Issue 19, Page(s) 5017–5020

Abstract: We study the role of topological singularities like Bound States in a Continuum (BICs) or Circularly Polarized States (CPSs) in determining ellipticity of the far-field polarization in dielectric metasurfaces. Using finite-difference time-domain as well ... ...

Abstract	We study the role of topological singularities like Bound States in a Continuum (BICs) or Circularly Polarized States (CPSs) in determining ellipticity of the far-field polarization in dielectric metasurfaces. Using finite-difference time-domain as well as rigorous coupled-wave analysis simulations, we determine the behavior of the Stokes parameter S
Language	English
Publishing date	2023-09-29
Publishing country	United States
Document type	Journal Article
ISSN	1539-4794
ISSN (online)	1539-4794
DOI	10.1364/OL.501595
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Article ; Online: Interleukin 6 mediates selected effects of Notch in chondrocytes.

Zanotti, S / Canalis, E

Osteoarthritis and cartilage

2013 Volume 21, Issue 11, Page(s) 1766–1773

Abstract: Objective: Notch receptors determine cell fate by regulating transcription, an event mediated by the Notch intracellular domain (NICD), which is generated by proteolysis brought about by Notch-ligand interactions. Since Notch activation or exposure to ... ...

Abstract	Objective: Notch receptors determine cell fate by regulating transcription, an event mediated by the Notch intracellular domain (NICD), which is generated by proteolysis brought about by Notch-ligand interactions. Since Notch activation or exposure to interleukin (Il)6 have similar effects in chondrocytes, we explored whether interleukin 6 (Il6) contributes to the mechanisms of Notch action in these cells. Method: NICD was overexpressed in primary chondrocytes from Rosa(Notch) mice, where the Rosa26 promoter precedes a loxP-flanked STOP cassette followed by the NICD coding sequence. Cells were infected with adenoviral vectors expressing Cre to induce NICD or green fluorescent protein (GFP) as control. Gene expression was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Il6 protein concentration in the culture media was determined by enzyme-linked immunosorbent assay (ELISA). To test the mechanisms of Notch action on Il6 expression, cells were transfected with a fragment of the Il6 promoter or control vector pGL3, or transcriptionally arrested with 5,6-dichloro-1-β-d-ribofuranosylbenzimidazole. Il6 was inhibited with a neutralizing antibody, whereas a normal immunoglobulin G (IgG) was used as control. Results: NICD induced Il6 mRNA and protein, and transactivated the Il6 promoter without affecting Il6 mRNA stability. Il6 neutralization had no impact on gene expression under basal conditions, and did not modify the effects of NICD on sex determining region-Y-related high mobility group-box gene (Sox)9, collagen type II α1 (Col2a1) and collagen type X α1 (Col10a1) expression. Conversely, Il6 neutralization opposed aggrecan (Acan) suppression and prevented matrix metalloprotease (Mmp)13 induction by NICD. Conclusion: Il6 mediates suppression of Acan and induction of Mmp13 expression by Notch in chondrocytes.
MeSH term(s)	Aggrecans/biosynthesis ; Animals ; Chondrocytes/metabolism ; Female ; Gene Expression Regulation/physiology ; Interleukin-6/antagonists & inhibitors ; Interleukin-6/biosynthesis ; Interleukin-6/genetics ; Interleukin-6/physiology ; Male ; Matrix Metalloproteinase 13/biosynthesis ; Mice ; Mice, Inbred C57BL ; RNA, Messenger/genetics ; Receptors, Notch/physiology ; Transcriptional Activation ; Transfection
Chemical Substances	Acan protein, mouse ; Aggrecans ; Interleukin-6 ; RNA, Messenger ; Receptors, Notch ; Matrix Metalloproteinase 13 (EC 3.4.24.-) ; Mmp13 protein, mouse (EC 3.4.24.-)
Language	English
Publishing date	2013-08-14
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1167809-4
ISSN	1522-9653 ; 1063-4584
ISSN (online)	1522-9653
ISSN	1063-4584
DOI	10.1016/j.joca.2013.08.010
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Article ; Online: Activation of Notch3 in osteoblasts/osteocytes causes compartment-specific changes in bone remodeling.

Canalis, Ernesto / Zanotti, Stefano / Schilling, Lauren / Eller, Tabitha / Yu, Jungeun

The Journal of biological chemistry

2021 Volume 296, Page(s) 100583

Abstract: Notch receptors maintain skeletal homeostasis. NOTCH1 and 2 have been studied for their effects on bone remodeling. Although NOTCH3 plays a significant role in vascular physiology, knowledge about its function in other cellular environments, including ... ...

Abstract	Notch receptors maintain skeletal homeostasis. NOTCH1 and 2 have been studied for their effects on bone remodeling. Although NOTCH3 plays a significant role in vascular physiology, knowledge about its function in other cellular environments, including bone, is limited. The present study was conducted to establish the function of NOTCH3 in skeletal cells using models of Notch3 misexpression. Microcomputed tomography demonstrated that Notch3 null mice did not have appreciable bone phenotypes. To study the effects of the NOTCH3 activation in the osteoblast lineage, BGLAP-Cre or Dmp1-Cre transgenics were crossed with Rosa
MeSH term(s)	Animals ; Bone Remodeling ; Gene Expression Regulation ; Mice ; Osteoblasts/cytology ; Osteoblasts/metabolism ; Osteocytes/cytology ; Osteocytes/metabolism ; Receptor, Notch3/metabolism
Chemical Substances	Receptor, Notch3
Language	English
Publishing date	2021-03-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1016/j.jbc.2021.100583
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Article: MERRF Mutation A8344G in a Four-Generation Family without Central Nervous System Involvement: Clinical and Molecular Characterization.

Ripolone, Michela / Zanotti, Simona / Napoli, Laura / Ronchi, Dario / Ciscato, Patrizia / Comi, Giacomo Pietro / Moggio, Maurizio / Sciacco, Monica

Journal of personalized medicine

2023 Volume 13, Issue 1

Abstract: A 53-year-old man approached our Neuromuscular Unit following an incidental finding of hyperckemia. Similar to his mother who had died at the age of 77 years, he was diabetic and had a few lipomas. The patient's two sisters, aged 60 and 50 years, did not ...

Abstract	A 53-year-old man approached our Neuromuscular Unit following an incidental finding of hyperckemia. Similar to his mother who had died at the age of 77 years, he was diabetic and had a few lipomas. The patient's two sisters, aged 60 and 50 years, did not have any neurological symptoms. Proband's skeletal muscle biopsy showed several COX-negative fibers, many of which were "ragged red". Genetic analysis revealed the presence of the A8344G mtDNA mutation, which is most commonly associated with a maternally inherited multisystem mitochondrial disorder known as MERRF (myoclonus epilepsy with ragged-red fibers). The two sisters also carry the mutation. Family members on the maternal side were reported healthy. Although atypical phenotypes have been reported in association with the A8344G mutation, central nervous system (CSN) manifestations other than myoclonic epilepsy are always reported in the family tree. If present, our four-generation family manifestations are late-onset and do not affect CNS. This could be explained by the fact that the mutational load remains low and therefore prevents tissues/organs from reaching the pathologic threshold. The fact that this occurs throughout generations and that CNS, which has the highest energetic demand, is clinically spared, suggests that regulatory genes and/or pathways affect mitochondrial segregation and replication, and protect organs from progressive dysfunction.
Language	English
Publishing date	2023-01-11
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2662248-8
ISSN	2075-4426
ISSN	2075-4426
DOI	10.3390/jpm13010147
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Article ; Online: The Profiling of 179 miRNA Expression in Serum from Limb Girdle Muscular Dystrophy Patients and Healthy Controls.

Magri, Francesca / Napoli, Laura / Ripolone, Michela / Ciscato, Patrizia / Moggio, Maurizio / Corti, Stefania / Comi, Giacomo Pietro / Sciacco, Monica / Zanotti, Simona

International journal of molecular sciences

2023 Volume 24, Issue 24

Abstract: Limb girdle muscular dystrophies (LGMDs) are a group of genetically inherited neuromuscular diseases with a very variable clinical presentation and overlapping traits. Over the last few years there has been an increasing interest in the use of non- ... ...

Abstract	Limb girdle muscular dystrophies (LGMDs) are a group of genetically inherited neuromuscular diseases with a very variable clinical presentation and overlapping traits. Over the last few years there has been an increasing interest in the use of non-invasive circulating biomarkers to monitor disease progression and to evaluate the efficacy of therapeutic approaches. Our aim was to identify the miRNA signature with potential value for LGMD patient screening and stratification. Using miRCURY LNA miRNA qPCR Serum/Plasma Panel, we analyzed 179 miRNAs from 16 patients, divided in four pools based on their genetic diagnosis, and from healthy controls. The miRNAs analysis showed a total of 107 dysregulated miRNAs in LGMD patients when compared to the healthy controls. After filtering via skeletal tissue expression and gene/pathways target analysis, the number of dysregulated miRNAs drastically reduced. Six selected miRNAs-let-7f-5p (in LGMDR1), miR-20a-5p (in LGMDR2), miR-130b-5p, miR-378a-5p (both in LGMDR3), miR-376c-3p and miR-382-5p (both in LGMDR4)-whose expression was significantly lower compared to controls in the different LGMD pools, were further investigated. The bioinformatic analysis of the target genes in each selected miRNA revealed ECM-receptor interaction and TGF-beta signaling as the most involved pathways. The correlation analysis showed a good correlation of let-7f-5p with fibrosis and with the cross sectional area of type I and type II fibers, while miR-130b-5p showed a good correlation with the age of onset of the disease. The receiver operating characteristic curves showed how single miRNAs were able to discriminate a specific group of LGMD patients and how the combination of six miRNAs was able to discriminate LGMD patients from controls.
MeSH term(s)	Humans ; MicroRNAs/genetics ; Gene Expression Profiling ; Biomarkers ; Muscular Dystrophies, Limb-Girdle/diagnosis ; Muscular Dystrophies, Limb-Girdle/genetics ; ROC Curve
Chemical Substances	MicroRNAs ; Biomarkers
Language	English
Publishing date	2023-12-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms242417402
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Article ; Online: Test of Antifibrotic Drugs in a Cellular Model of Fibrosis Based on Muscle-Derived Fibroblasts from Duchenne Muscular Dystrophy Patients.

Zanotti, Simona / Mora, Marina

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1687, Page(s) 205–217

Abstract: An in vitro model of muscle fibrosis, based on the use of primary human fibroblasts isolated from muscle biopsies of patients affected by Duchenne muscular dystrophies (DMD) and cultivated in monolayer and 3D conditions, is used to test the potential ... ...

Abstract	An in vitro model of muscle fibrosis, based on the use of primary human fibroblasts isolated from muscle biopsies of patients affected by Duchenne muscular dystrophies (DMD) and cultivated in monolayer and 3D conditions, is used to test the potential antifibrotic activity of pirfenidone (PFD). This in vitro model may be usefully also to evaluate the toxicity and efficacy of other candidate molecules for the treatment of fibrosis. The drug toxicity is evaluated using a colorimetric assay based on the conversion of tetrazolium salt (MTT) to insoluble formazan, while the effect of the drug on cell proliferation is measured with the bromodeoxyuridine incorporation assay. The efficacy of the drug is evaluated in fibroblast monolayers by quantitating synthesis and deposition of intracellular collagen with a spectrophotometric picrosirius red-based assay, and by quantitating cell migration using a "scratch" assay. The efficacy of PFD as antifibrotic drug is also evaluated in a 3D fibroblast model by measuring diameters and number of nodules.
MeSH term(s)	Cell Movement/drug effects ; Cell Proliferation/drug effects ; Collagen/metabolism ; Fibroblasts/drug effects ; Fibroblasts/pathology ; Fibrosis/complications ; Fibrosis/drug therapy ; Fibrosis/pathology ; Humans ; Muscles/drug effects ; Muscular Dystrophy, Duchenne/complications ; Muscular Dystrophy, Duchenne/drug therapy ; Muscular Dystrophy, Duchenne/pathology ; Primary Cell Culture ; Pyridones/administration & dosage ; Pyridones/adverse effects
Chemical Substances	Pyridones ; Collagen (9007-34-5) ; pirfenidone (D7NLD2JX7U)
Language	English
Publishing date	2017-12-12
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-7374-3_15
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Article ; Online: Hairy and Enhancer of Split-Related With YRPW Motif-Like (HeyL) Is Dispensable for Bone Remodeling in Mice.

Canalis, Ernesto / Zanotti, Stefano

Journal of cellular biochemistry

2017 Volume 118, Issue 7, Page(s) 1819–1826

Abstract: Notch induces Hairy Enhancer of Split (Hes)1 and Hes-related with YRPW motif (Hey) Hey1, Hey2 and Hey-like (HeyL) expression in osteoblasts, but it is not known whether any of these target genes mediates the effect of Notch in the skeleton. We ... ...

Abstract	Notch induces Hairy Enhancer of Split (Hes)1 and Hes-related with YRPW motif (Hey) Hey1, Hey2 and Hey-like (HeyL) expression in osteoblasts, but it is not known whether any of these target genes mediates the effect of Notch in the skeleton. We demonstrated that Notch1 activation in osteoblasts/osteocytes induces Hes1, Hey1, Hey2, and HeyL, but HeyL was induced to a greater extent than other target genes. To characterize HeyL null mice for their skeletal phenotype, microcomputed tomography (µCT) and histomorphometric analysis of HeyL null and sex-matched littermate controls was performed. µCT demonstrated modest cancellous bone osteopenia in 1 month old male mice and normal microarchitecture in 3 month old male HeyL null mice. Female HeyL null mice were not different from controls at either 1 or 3 months of age. Bone histomorphometry did not demonstrate differences between HeyL null mice of either sex and littermate controls. In conclusion, HeyL null mice do not exhibit an obvious skeletal phenotype demonstrating that HeyL is dispensable for skeletal homeostasis. J. Cell. Biochem. 118: 1819-1826, 2017. © 2016 Wiley Periodicals, Inc.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Bone Remodeling/genetics ; Bone Remodeling/physiology ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Osteoblasts/metabolism ; Osteocytes/metabolism ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Transcription Factor HES-1/genetics ; Transcription Factor HES-1/metabolism ; X-Ray Microtomography
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Cell Cycle Proteins ; Hes1 protein, mouse ; Hey1 protein, mouse ; Hey2 protein, mouse ; Heyl protein, mouse ; Notch1 protein, mouse ; Receptor, Notch1 ; Repressor Proteins ; Transcription Factor HES-1
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.25859
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