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Bone is a richly vascularized connective tissue. As the main source of oxygen, nutrients, hormones, neurotransmitters and growth factors delivered to the bone cells, vasculature is indispensable for appropriate bone development, regeneration and remodeling. Bone vasculature also orchestrates the process of hematopoiesis. Blood supply to the skeletal system is provided by the networks of arteries and arterioles, having distinct molecular characteristics and localizations within the bone structures. Blood vessels of the bone develop through the process of angiogenesis, taking place through different, bone-specific mechanisms. Impaired functioning of the bone blood vessels may be associated with the occurrence of some skeletal and systemic diseases, i.e., osteonecrosis, osteoporosis, atherosclerosis or diabetes mellitus. When a disease or trauma-related large bone defects appear, bone grafting or bone tissue engineering-based strategies are required. However, a successful bone regeneration in both approaches largely depend s on a proper blood supply. In this paper, we review the most recent data on the functions, molecular characteristics and significance of the bone blood vessels, with a particular emphasis on the role of angiogenesis and blood vessel functioning in bone development and regeneration, as well as the consequences of its impairment in the course of different skeletal and systemic diseases.

Pulmonary alveolar type I (AT1) cells cover more than 95% of alveolar surface and are essential for the air–blood barrier function of lungs. AT1 cells have been shown to retain developmental plasticity during alveolar regeneration. However, the development and heterogeneity of AT1 cells remain largely unknown. Here, we conducted a single-cell RNA-seq analysis to characterize postnatal AT1 cell development and identified insulin-like growth factor-binding protein 2 (Igfbp2) as a genetic marker specifically expressed in postnatal AT1 cells. The portion of AT1 cells expressing Igfbp2 increases during alveologenesis and in post pneumonectomy (PNX) newly formed alveoli. We found that the adult AT1 cell population contains both Hopx⁺Igfbp2⁺ and Hopx⁺Igfbp2⁻ AT1 cells,which have distinct cell fates during alveolar regeneration. Using an Igfbp2-CreER mouse model, we demonstrate that Hopx⁺Igfbp2⁺ AT1 cells represent terminally differentiated AT1 cells that are not able to transdifferentiate into AT2 cells during post-PNX alveolar regeneration. Our study provides tools and insights that will guide future investigations into the molecular and cellular mechanism or mechanisms underlying AT1 cell fate during lung development and regeneration.

The 21st Annual Meeting of the Interuniversity Institute of Myology (IIM), held in Assisi, Italy, from September 4–7, 2024, gathered 123 experts, including basic and clinical myologists, pharmaceutical representatives, and patient organizations from Italy, Europe, Canada, and USA. The meeting fostered a proactive, collaborative and dynamic atmosphere, promoting scientific exchange and international partnerships focused on muscle research, from physiology to disease mechanisms, and eventually therapeutic approaches. The 21st IIM Meeting featured 6 main scientific sessions, showcasing 30 oral presentations and 45 always-on-display posters, all reporting original and unpublished research. The program was enriched by four keynote lectures from internationally renowned speakers and talks from delegates of the Société Française de Myologie, adding depth to the scientific discussions. As part of the IIM Meeting organization, this year there was also a free-access educational convention titled “Physical exercise as prevention”. Leading IIM experts shared insights on exercise-based lifestyle interventions aimed at improving public health, with the participation of the Italian former boxer Roberto Cammarelle. The event drew a large in-person and online audience. This IIM Meeting edition strongly emphasized the involvement and growth of young researchers, with 50% of the attendees being <35, reinforcing IIM’s commitment to fostering the next generation of myologists. Along this line, and to further support young researchers, awards for Best Talk, Best Poster Blitz, and Best Poster were presented. The winners joined the IIM Young Committee, contributing to the scientific organization of future IIM meetings together with the IIM Scientific Committee. The meeting was also integrated into the “Advanced Myology Update 2024” high-training course, organized by the University of Perugia in collaboration with IIM. The 11 trainees enrolled in the course participated in dedicated roundtables and exclusive lessons led by IIM’s invited speakers. In this report are included the abstracts of both oral and poster presentations, with some being withheld for patent-related reasons. Through its annual congress and educational initiatives, IIM played a crucial role in shaping the future of myology research, fostering innovation, collaboration, and scientific excellence on an international scale. We invite you to save the date for the 22nd IIM meeting that will be held in the beautiful Assisi, September 11-14, 2025. We can’t wait to welcome you!

The 2023 represented a milestone for the Interuniversity Institute of Myology (IIM) since it marked twenty years of IIM activity joined with the 20th annual meeting organized by the association. The 20th IIM meeting took place in the fascinating town of Assisi, in the heart of central Italy, from 12 to 15 October. The commemorative 20th edition of the meeting represented a success in terms of participation and contributions as it brought together 160 myologists, clinicians, pharmaceutical companies, and patient organization representatives from Italy, several European countries (especially France), the United Kingdom, Brazil, and the USA. Four main scientific sessions hosted 36 oral communications and 54 always-on-display posters reporting original and unpublished results. Four main lectures from internationally renowned invited speakers and talks from delegates of the Societé Française de Myologie gave particular interest and emphasis to the scientific discussion. In line with the traditional policy of the IIM to encourage the participation of young researchers, about 50% of the attendees were under 35 years old. Moreover, the 20th IIM meeting was part of the high-training course in “Advanced Myology Update 2023”, reserved to young trainees and managed by the University of Perugia (Italy) in collaboration with the IIM. In addition to the meeting scientific sessions, the 29 attendees to the course had a dedicated round table and dedicated lessons with the IIM invited speakers as teachers. Awards for the best talk, best poster blitz, and best poster have been conferred to young attendees, who became part of the IIM Young Committee, involved in the scientific organization of the IIM meetings. To celebrate the 20th IIM anniversary, a special free-access educational convention on “Causes and mechanisms of muscle atrophy. From terrestrial disuse to Space flights” has been organized, in which IIM experts in the field have illustrated the current knowledge about the muscle atrophy process in several atrophying conditions, and the former Italian astronaut, Paolo Nespoli shared his incredible experience in Space fascinating the large audience attending both in presence and online live stream. The meeting was characterized by a vibrant, friendly, and inclusive atmosphere, and stimulated discussion on emerging areas of muscle research, fostering international collaborations, and confirming the IIM meeting as an ideal venue to discuss around muscle development, function, and diseases pointing to the development of efficacious therapeutic strategies. Here, the abstracts of the meeting illustrate the most recent results on basic, translational, and clinical research in the myology field. Some abstracts are missing as per authors’ decision due to the patentability of the results.

Experiments in zebrafish have shed new light on the relationship between development and regeneration in the heart.Experiments in zebrafish have shed new light on the relationship between development and regeneration in the heart.

Although the light‐induced melatonin suppression response is well characterized in adults, studies examining the dynamics of this effect in children are scarce. The purpose of this study was to quantify the magnitude of evening light‐induced melatonin suppression in preschool‐age children. Healthy children (n = 10; 7 females; 4.3 ± 1.1 years) participated in a 7‐day protocol. On days 1–5, children followed a strict sleep schedule. On day 6, children entered a dim light environment (<15 lux) for 1‐h before providing salivary samples every 20‐ to 30‐min from the afternoon until 50‐min after scheduled bedtime. On day 7, subjects remained in dim light conditions until 1‐h before bedtime, at which time they were exposed to a bright light stimulus (~1000 lux) for 1‐h and then re‐entered dim light conditions. Saliva samples were obtained before, during, and after bright light exposure and were time anchored to samples taken the previous evening. We found robust melatonin suppression (87.6 ± 10.0%) in response to the bright light stimulus. Melatonin levels remained attenuated for 50‐min after termination of the light stimulus (P < 0.008). Furthermore, melatonin levels did not return to 50% of those observed in the dim light condition 50‐min after the light exposure for 7/10 children. Our findings demonstrate a robust light‐induced melatonin suppression response in preschool‐age children. These findings have implications for understanding the role of evening light exposure in the development of evening settling difficulties and may serve as experimental evidence to support recommendations regarding light exposure and sleep hygiene practices in early childhood. In this study, we examined melatonin suppression in response to 1‐h of bright light exposure before bedtime and found that this exposure suppressed children's melatonin secretion by ~88%. Furthermore, melatonin levels remained attenuated for 50‐min after termination of the evening bright light stimulus. We believe our findings have important implications for understanding fundamental circadian physiology in young children and the role of light in childhood sleep disturbances

Volumetric muscle injury (VML) causes an irrecoverable loss of muscle fibers, persistent strength deficits, and chronic disability. A crucial challenge to VML injury and possible regeneration is the removal of all of the in situ native elements necessary for skeletal muscle regeneration. Our first goal was to establish a reliable VML model in the mouse tibialis anterior (TA) muscle. In adult male wild‐type and nude mice, a non‐repaired ≈20% VML injury to the TA muscle resulted in an ≈59% loss in nerve evoked muscle strength, ≈33% loss in muscle mass, and ≈29% loss of muscle fibers at 28 day post‐injury. Our second goal was to investigate if minced muscle grafts (≈1 mm3 tissue fragments) promote recovery of muscle fibers after VML injury and to understand if the graft‐derived progenitor cells directly contribute to fiber regeneration. To assess donor cell contribution, donor muscle tissue was derived from UBC‐GFP mice in a subset of experiments. Minced grafts restored ≈34% of the lost fibers 28 days post‐injury. The number of GFP+ fibers and the estimated number of regenerated fibers were similar, regardless of host mouse strain. The muscle tissue regeneration promoted by minced grafts did not improve TA muscle strength at this time post‐injury. These findings demonstrate the direct contribution of minced muscle graft‐derived myogenic stem/progenitor cells to recovery of muscle fibers after VML injury and signify the utility of autologous myogenic stem cell therapies for this indication. Our study demonstrates the direct contribution of minced muscle graft‐derived myogenic stem/progenitor cells to de novo muscle fiber regeneration after VML injury and signify the utility of autologous myogenic stem cell therapies for this indication.

We present data from two experiments that examined how the developmental processes of smoltification and sexual maturation proceed in parallel in domesticated Atlantic salmon. Onset of maturation and smoltification was stimulated using temperature and photoperiod. Our observations on gonadosomatic index (GSI), spermatogenic activity, gill Na+, K+‐ATPase enzyme (NKA) activity, and plasma 11‐ketotestosterone (11‐KT), Na, Cl, and Ca show that smoltification and maturation were both triggered and developed in parallel in male Atlantic salmon, but that the progressing maturation impaired hypoosmoregulation. Female maturation started after completion of smoltification. Furthermore, we present data showing that domesticated salmon can physiologically smoltify–desmoltify–resmoltify within a short period of time, and that development of a secondary sexual characteristic, such as a kype, depends on size in male postsmolts.

Congenital microtia is a birth defect characterized by auricular underdevelopment, with unclear pathogenesis and unidentified pathogenic genes. Differential expression analysis, weighted co-expression network analysis (WGCNA), protein-protein interaction (PPI) networks and support vector machine recursive feature elimination (SVM-RFE) identified the key biomolecules in microtia. Single-cell and intercellular communication analysis were used to decipher the key intercellular signaling pathway. We extracted primary cells and conducted Immuno precipitation mass spectrometry (IP-MS), co-Immuno precipitation (Co-IP) and RNA-sequencing (RNA-seq) to confirmed the mechanism. The intercellular communication network was confirmed through the cell co-culture system. Organoid and animal models further validated the role of key biomolecules. We found that IL-6 may be the key biomolecule in microtia. Normal ear cartilage tissue is mainly composed of chondrocytes, but microtia auricular ear tissue contained chondrocytes and stem cells. IL-6 signaling pathway is the main intercellular communication pathways in microtia. We extracted primary chondrocytes and stem cells, and proved that IL-6 promotes the growth and migration of primary cells. The binding of IL-6 and IL-6R and Glycoprotein 130 (GP130) and the activation of their downstream were confirmed. Furthermore, IL-6 signaling pathway was proved to involve in the intercellular communication of microtia. Cartilage microspheres demonstrated the role of IL-6 in regeneration of ear cartilage. The preventive intervention of adeno-associated virus (AAV) on pregnant mice confirmed the role of IL-6 . IL-6 signaling is the key biomolecule in the development and regeneration of auricular cartilage in microtia. IL-6 is a potential biomarker and preventive and therapeutic target for microtia patients.

The psychoactive component in cannabis, delta‐9‐tetrahydrocannabinol, can restrict fetal growth and development. Delta‐9‐tetrahydrocannabinol has been shown to negatively impact cellular proliferation and target organelles like the mitochondria resulting in reduced cellular respiration. In the placenta, mitochondrial dysfunction leading to oxidative stress prevents proper placental development and function. A key element of placental development is the proliferation and fusion of cytotrophoblasts to form the syncytium that comprises the materno‐fetal interface. The impact of delta‐9‐tetrahydrocannabinol on this process is not well understood. To elucidate the nature of the mitochondrial dysfunction and its consequences on trophoblast fusion, we treated undifferentiated and differentiated BeWo human trophoblast cells, with 20 µM delta‐9‐tetrahydrocannabinol for 48 hr. At this concentration, delta‐9‐tetrahydrocannabinol on BeWo cells reduced the expression of markers involved in syncytialization and mitochondrial dynamics, but had no effect on cell viability. Delta‐9‐tetrahydrocannabinol significantly attenuated the process of syncytialization and induced oxidative stress responses in BeWo cells. Importantly, delta‐9‐tetrahydrocannabinol also caused a reduction in the secretion of human chorionic gonadotropin and the production of human placental lactogen and insulin growth factor 2, three hormones known to be important in facilitating fetal growth. Furthermore, we also demonstrate that delta‐9‐tetrahydrocannabinol attenuated mitochondrial respiration, depleted adenosine triphosphate, and reduced mitochondrial membrane potential. These changes were also associated with an increase in cellular reactive oxygen species, and the expression of stress responsive chaperones, HSP60 and HSP70. These findings have important implications for understanding the role of delta‐9‐tetrahydrocannabinol‐induced mitochondrial injury and the role this might play in compromising human pregnancies. THC disrupted mitochondrial function, increased markers of mitochondrial fission and cellular stress in BeWo cells. This was coincident with reduced BeWo cell fusion and secretion of important fetal growth signals, hPL and IGF2. These changes were mediated, in part, via the CB1 receptor in syncytialized BeWo cells.