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A Commemorative Special Issue in Honor of Prof. Giovanni De Toni: A Pediatrician and Innovator at the Gaslini Children’s Hospital, Genoa, Italy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 1546

Special Issue Editors

Prof. Dr. Consolato M. Sergi

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Guest Editor
Div. of Anat. Pathology, Children’s Hospital of Eastern Ontario, Univ. of Ottawa, ON, Canada, and Dept. of Lab. Med. and Pathology, Univ. of Alberta, Edmonton, AB, Canada
Interests: gastrointestinal/biliary diseases; metabolic diseases; congenital heart disease; mitochondrial DNA-related cardiomyopathies; carcinogenesis (bone/liver)
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Angelo Ravelli

E-Mail Website
Guest Editor
Department of Neurosciences, Rehabilitation, Ophthalmology, Genetics and Maternal-Infantile Sciences (DiNOGMI), University of Genoa, Genoa, Italy
Interests: childhood rheumatic diseases; lupus nephritis; autoantibodies
Dr. Luca Pio

E-Mail Website
Guest Editor
Department of Surgery, St. Jude Children’s Research Hospital, MS 133, 262 Danny Thomas Place, Memphis, TN 38105, USA
Interests: pediatric surgical oncology; neuroblastoma; robotic surgery; translational surgery; precision surgery; image-guided surgery
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Living in Liguria, gathering that the sea may be a metaphor for the human condition is not difficult. The Nobel Prize winner for literature (1975), Eugenio Montale, was born in Genoa in 1896 and spent his childhood and youth between his hometown and the picturesque village of Monterosso, in Cinque Terre. Paraphrasing Mengaldo here, the ego feels almost pulled in by the sea, and simultaneously, it is ejected and confined to the land-dwelling. Montale’s collection “Ossi di Seppia” is an evocation and allegory of the misery and marginalization of the human condition, which moved Giovanni De Toni into action.

Two years before Montale won his Nobel Prize for literature, Giovanni de Toni, an outstanding pediatrician and director of one of the largest children’s hospitals worldwide, passed away. Born in Venice in 1895, Giovanni De Toni was an Italian pediatrician. Known internationally for describing the so-called De Toni–Fanconi–Debré syndrome, he was a prominent figure in Italy, so much so that the Department of Pediatric Sciences of the University of Genoa bears his name. With his wife, Prof. Dr. De Toni also launched the “Villa Santa Chiara” in Genoa to assist disabled children. In 1933, he described a new type of pathology later known as “De Toni–Fanconi–Debré syndrome”. The disease established a cornerstone in vitamin D-resistant rickets. Later, he characterized children affected by hyperosteogenesis and was an authentic innovator in auxologic studies. According to many scholars, De Toni identified a form of infantile cortical hyperostosis, also studied in 1945 by John Caffey and William Silverman (the so-called “Caffey–De Toni disease”). In 1942, Prof. De Toni assumed the director position at the Istituto Gaslini, where he creatively transformed the approach to pediatric healthcare by instituting a free outpatient clinic within the hospital. His prominence rose during the tuberculosis epidemic, as he was the forerunner in detecting a cure with streptomycin. In the 1950s, Giovanni De Toni was remembered as a fervent breastfeeding supporter. On 1 November 1965, the pediatrician left his role at the pediatric institution. He subsequently became president of the Italian Society of Pediatrics (SIP), a position he held from 1966 to the time of his death in Genoa on 8 January 1973. This Special Issue is dedicated to his legacy at the Gaslini Children’s Hospital and to his descendants, Ettore and Teresa, who followed in his footsteps on the scientific journey.

Prof. Dr. Consolato M. Sergi
Prof. Dr. Angelo Ravelli
Dr. Luca Pio
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at mdpi.longhoe.net by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • bone
  • soft tissue sarcomas
  • neuroblastoma

Published Papers (3 papers)

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Research

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14 pages, 13074 KiB  
Article
Ectopic Activation of Fgf8 in Dental Mesenchyme Causes Incisor Agenesis and Molar Microdontia
by Yu Wang, **g**g Wang, Tian Xu, Shuhui Yang, **nran Wang, Lei Zhu, Nan Li, Bo Liu, **g **ao and Chao Liu
Int. J. Mol. Sci. 2024, 25(13), 7045; https://doi.org/10.3390/ijms25137045 - 27 Jun 2024
Viewed by 192
Abstract
Putatively, tooth agenesis was attributed to the initiation failure of tooth germs, though little is known about the histological and molecular alterations. To address if constitutively active FGF signaling is associated with tooth agenesis, we activated Fgf8 in dental mesenchyme with Osr-cre knock-in [...] Read more.
Putatively, tooth agenesis was attributed to the initiation failure of tooth germs, though little is known about the histological and molecular alterations. To address if constitutively active FGF signaling is associated with tooth agenesis, we activated Fgf8 in dental mesenchyme with Osr-cre knock-in allele in mice (Osr2-creKI; Rosa26R-Fgf8) and found incisor agenesis and molar microdontia. The cell survival assay showed tremendous apoptosis in both the Osr2-creKI; Rosa26R-Fgf8 incisor epithelium and mesenchyme, which initiated incisor regression from cap stage. In situ hybridization displayed vanished Shh transcription, and immunostaining exhibited reduced Runx2 expression and enlarged mesenchymal Lef1 domain in Osr2-creKI; Rosa26R-Fgf8 incisors, both of which were suggested to enhance apoptosis. In contrast, Osr2-creKI; Rosa26R-Fgf8 molar germs displayed mildly suppressed Shh transcription, and the increased expression of Ectodin, Runx2 and Lef1. Although mildly smaller than WT controls prenatally, the Osr2-creKI; Rosa26R-Fgf8 molar germs produced a miniature tooth with impaired mineralization after a 6-week sub-renal culture. Intriguingly, the implanted Osr2-creKI; Rosa26R-Fgf8 molar germs exhibited delayed odontoblast differentiation and accelerated ameloblast maturation. Collectively, the ectopically activated Fgf8 in dental mesenchyme caused incisor agenesis by triggering incisor regression and postnatal molar microdontia. Our findings reported tooth agenesis resulting from the regression from the early bell stage and implicated a correlation between tooth agenesis and microdontia. Full article
(This article belongs to the Special Issue A Commemorative Special Issue in Honor of Prof. Giovanni De Toni: A Pediatrician and Innovator at the Gaslini Children’s Hospital, Genoa, Italy)
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16 pages, 8895 KiB  
Article
Zebrafish as a Human Muscle Model for Studying Age-Dependent Sarcopenia and Frailty
by Paula Aranda-Martínez, Ramy K. A. Sayed, José Fernández-Martínez, Yolanda Ramírez-Casas, Yang Yang, Germaine Escames and Darío Acuña-Castroviejo
Int. J. Mol. Sci. 2024, 25(11), 6166; https://doi.org/10.3390/ijms25116166 - 3 Jun 2024
Viewed by 524
Abstract
Currently, there is an increase in the aging of the population, which represents a risk factor for many diseases, including sarcopenia. Sarcopenia involves progressive loss of mass, strength, and function of the skeletal muscle. Some mechanisms include alterations in muscle structure, reduced regenerative [...] Read more.
Currently, there is an increase in the aging of the population, which represents a risk factor for many diseases, including sarcopenia. Sarcopenia involves progressive loss of mass, strength, and function of the skeletal muscle. Some mechanisms include alterations in muscle structure, reduced regenerative capacity, oxidative stress, mitochondrial dysfunction, and inflammation. The zebrafish has emerged as a new model for studying skeletal muscle aging because of its numerous advantages, including histological and molecular similarity to human skeletal muscle. In this study, we used fish of 2, 10, 30, and 60 months of age. The older fish showed a higher frailty index with a value of 0.250 ± 0.000 because of reduced locomotor activity and alterations in biometric measurements. We observed changes in muscle structure with a decreased number of myocytes (0.031 myocytes/μm2 ± 0.004 at 60 months) and an increase in collagen with aging up to 15% ± 1.639 in the 60-month group, corresponding to alterations in the synthesis, degradation, and differentiation pathways. These changes were accompanied by mitochondrial alterations, such as a nearly 50% reduction in the number of intermyofibrillar mitochondria, 100% mitochondrial damage, and reduced mitochondrial dynamics. Overall, we demonstrated a similarity in the aging processes of muscle aging between zebrafish and mammals. Full article
(This article belongs to the Special Issue A Commemorative Special Issue in Honor of Prof. Giovanni De Toni: A Pediatrician and Innovator at the Gaslini Children’s Hospital, Genoa, Italy)
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Review

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27 pages, 1592 KiB  
Review
A Glimpse into Humoral Response and Related Therapeutic Approaches of Takayasu’s Arteritis
by Shuning Guo, Yixiao Tian, **g Li and **aofeng Zeng
Int. J. Mol. Sci. 2024, 25(12), 6528; https://doi.org/10.3390/ijms25126528 - 13 Jun 2024
Viewed by 563
Abstract
Takayasu’s arteritis (TAK) manifests as an insidiously progressive and debilitating form of granulomatous inflammation including the aorta and its major branches. The precise etiology of TAK remains elusive, with current understanding suggesting an autoimmune origin primarily driven by T cells. Notably, a growing [...] Read more.
Takayasu’s arteritis (TAK) manifests as an insidiously progressive and debilitating form of granulomatous inflammation including the aorta and its major branches. The precise etiology of TAK remains elusive, with current understanding suggesting an autoimmune origin primarily driven by T cells. Notably, a growing body of evidence bears testimony to the widespread effects of B cells on disease pathogenesis and progression. Distinct alterations in peripheral B cell subsets have been described in individuals with TAK. Advancements in technology have facilitated the identification of novel autoantibodies in TAK. Moreover, emerging data suggest that dysregulated signaling cascades downstream of B cell receptor families, including interactions with innate pattern recognition receptors such as toll-like receptors, as well as co-stimulatory molecules like CD40, CD80 and CD86, may result in the selection and proliferation of autoreactive B cell clones in TAK. Additionally, ectopic lymphoid neogenesis within the aortic wall of TAK patients exhibits functional characteristics. In recent decades, therapeutic interventions targeting B cells, notably utilizing the anti-CD20 monoclonal antibody rituximab, have demonstrated efficacy in TAK. Despite the importance of the humoral immune response, a systematic understanding of how autoreactive B cells contribute to the pathogenic process is still lacking. This review provides a comprehensive overview of the biological significance of B cell-mediated autoimmunity in TAK pathogenesis, as well as insights into therapeutic strategies targeting the humoral response. Furthermore, it examines the roles of T-helper and T follicular helper cells in humoral immunity and their potential contributions to disease mechanisms. We believe that further identification of the pathogenic role of autoimmune B cells and the underlying regulation system will lead to deeper personalized management of TAK patients. We believe that further elucidation of the pathogenic role of autoimmune B cells and the underlying regulatory mechanisms holds promise for the development of personalized approaches to managing TAK patients. Full article
(This article belongs to the Special Issue A Commemorative Special Issue in Honor of Prof. Giovanni De Toni: A Pediatrician and Innovator at the Gaslini Children’s Hospital, Genoa, Italy)
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