Eating disorder in children: Impact on quality of life, with a spotlight on autism spectrum disorder.

Eating behavior, which includes eating habits and preferences, frequency of eating, and other features related to diet, is a major characteristic not only of a person's nutritional status, but also of health in general. In recent years, the prevalence of eating disorders in children has tended to increase; they also require cross-system approaches in diagnosis by a variety of specialists and correction requires appropriate selection of optimal methods. Maladaptive eating attitudes formed at an early age can contribute to the formation of eating disorders, which can lead to or worsen various neuropsychiatric diseases, digestive diseases, and other related conditions. In children with autism spectrum disorder (ASD), eating disorders often appear earlier than other major symptoms of the condition. However, the clinical manifestations of eating disorders in children with ASD are varied and differ in severity and duration, whereas these disorders in neurotypical children might present as short-lived and may not lead to serious consequences. Nevertheless, cases of progressive eating disorders accompanied by a child presenting as under- or overweight and/or with macronutrient and micronutrient deficiencies cannot be excluded. Given the high prevalence of eating disorders in children, many researchers have highlighted the lack of a valid and universally accepted instruments to assess atypical eating behaviors in this population. Therefore, in this review, we wanted to highlight the problems and causes of eating disorders in children, and also to analyze the existing approaches to the validation of these problems, taking into account the existing behavioral features in children with ASD.

Comparative Analysis of Cytokine Profiles in Cerebrospinal Fluid and Blood Serum in Patients with Acute and Subacute Spinal Cord Injury.

BACKGROUND: Cytokines are actively involved in the regulation of the inflammatory and immune responses and have crucial importance in the outcome of spinal cord injuries (SCIs). Examining more objective and representative indicators of the patient's condition is still required to reveal the fundamental patterns of the abovementioned posttraumatic processes, including the identification of changes in the expression of cytokines. METHODS: We performed a dynamic (3, 7, and 14 days post-injury (dpi)) extended multiplex analysis of cytokine profiles in both CSF and blood serum of SCI patients with baseline American Spinal Injury Association Impairment Scale grades of A. RESULTS: The data obtained showed a large elevation of IL6 (>58 fold) in CSF and IFN-γ (>14 fold) in blood serum at 3 dpi with a downward trend as the post-traumatic period increases. The level of cytokine CCL26 was significantly elevated in both CSF and blood serum at 3 days post-SCI, while other cytokines did not show the same trend in the different biosamples. CONCLUSIONS: The dynamic changes in cytokine levels observed in our study can explore the relationships with the SCI region and injury severity, paving the way for a better understanding of the pathophysiology of SCI and potentially more targeted and personalized therapeutic interventions.

Intrathecal Injection of Autologous Mesenchymal Stem-Cell-Derived Extracellular Vesicles in Spinal Cord Injury: A Feasibility Study in Pigs.

Spinal cord injury (SCI) remains one of the current medical and social problems, as it causes deep disability in patients. The use of mesenchymal stem cell (MSC)-derived extracellular vesicles (EVs) is one strategy for stimulating the post-traumatic recovery of the structure and function of the spinal cord. Here, we chose an optimal method for obtaining cytochalasin B-induced EVs, including steps with active vortex mixing for 60 s and subsequent filtration to remove nuclei and disorganized inclusions. The therapeutic potential of repeated intrathecal injection of autologous MSC-derived EVs in the subacute period of pig contused SCI was also evaluated for the first time. In this study, we observed the partial restoration of locomotor activity by stimulating the remyelination of axons and timely reperfusion of nervous tissue.

A Comparative Study of Mesenchymal Stem Cell-Derived Extracellular Vesicles' Local and Systemic Dose-Dependent Administration in Rat Spinal Cord Injury.

Spinal cord injury (SCI) is a serious neurological condition that causes severe disability. One of the approaches to overcoming the complications of SCI is stem cell-derived extracellular vesicle (EV) therapy. In this research, we performed a comparative evaluation of rat spinal cord post-traumatic regeneration efficacy using different methods of mesenchymal stem cell-derived EV transplantation (local vs. systemic) followed by evaluation of their minimal therapeutic dose. The results suggested that MSC-EV therapy could improve locomotor activity over 60 days after the SCI, showing a dose-dependent effect on the recovery of spinal cord motor pathways. We also established the possibility of maintaining a population of mature oligodendrocytes by MSC-EVs. It was observed that in the spinal cord injury area, intravenous transplantation of MSC-EVs showed more pronounced therapeutic effects compared to the treatment of fibrin matrix-encapsulated MSC-EVs.

Cellular and Molecular Gradients in the Ventral Horns With Increasing Distance From the Injury Site After Spinal Cord Contusion.

To identify cellular and molecular gradients following spinal cord injury (SCI), a rat contusion model of severe SCI was used to investigate the expression of NG2 and molecules that identify astrocytes and axons of the ventral horns (VH) at different distances on 7 and 30 days post-injury (dpi). A gradient of expression of NG2+/Olig2+ cells was determined, with the highest concentrations focused close to the injury site. A decrease in NG2 mean intensity correlates with a decrease in the number of NG2+ cells more distally. Immunoelectron microscopy subsequently revealed the presence of NG2 in connection with the membrane and within the cytoplasm of NG2+ glial cells and in large amounts within myelin membranes. Analysis of the astrocyte marker GFAP showed increased expression local to injury site from 7 dpi, this increase in expression spread more distally from the injury site by 30 dpi. Paradoxically, astrocyte perisynaptic processes marker GLT-1 was only increased in expression in areas remote from the epicenter, which was traced both at 7 and 30 dpi. Confocal microscopy showed a significant decrease in the number of 5-HT+ axons at a distance from the epicenter in the caudal direction, which is consistent with a decrease in ß3-tubulin in these areas. The results indicate significant cellular and molecular reactions not only in the area of the gray matter damage but also in adjacent and remote areas, which is important for assessing the possibility of long-distance axonal growth.

Extracellular Matrix in Neural Plasticity and Regeneration.

The extracellular matrix (ECM) is a fundamental component of biological tissues. The ECM in the central nervous system (CNS) is unique in both composition and function. Functions such as learning, memory, synaptogenesis, and plasticity are regulated by numerous ECM molecules. The neural ECM acts as a non-specific physical barrier that modulates neuronal plasticity and axon regeneration. There are two specialized types of ECM in the CNS, diffuse perisynaptic ECM and condensed ECM, which selectively surround the perikaryon and initial part of dendritic trees in subtypes of neurons, forming perineuronal nets. This review presents the current knowledge about the role of important neuronal ECM molecules in maintaining the basic functions of a neuron, including electrogenesis and the ability to form neural circuits. The review mainly focuses on the role of ECM components that participate in the control of key events such as cell survival, axonal growth, and synaptic remodeling. Particular attention is drawn to the numerous molecular partners of the main ECM components. These regulatory molecules are integrated into the cell membrane or disposed into the matrix itself in solid or soluble form. The interaction of the main matrix components with molecular partners seems essential in molecular mechanisms controlling neuronal functions. Special attention is paid to the chondroitin sulfate proteoglycan 4, type 1 transmembrane protein, neural-glial antigen 2 (NG2/CSPG4), whose cleaved extracellular domain is such a molecular partner that it not only acts directly on neural and vascular cells, but also exerts its influence indirectly by binding to resident ECM molecules.

The Function of NG2/CSPG4-expressing Cells in the Rat Spinal Cord Injury: An Immunoelectron Microscopy Study.

Emerging evidence supports an increased role for NG2/CSPG4-expressing cells in the process of neuroregeneration and synaptic plasticity, due to the increased production of multifunctional chondroitin sulfate proteoglycan (NG2/CSPG4). However, the response of NG2/CSPG4-expressing cells in spinal cord injury (SCI) remains to be elcudiated. Expression and distribution of NG2/CSPG4-expressing cells were studied by immunoelectron microscopy in the ventral horns (VH) of an intact and injured rat spinal cord. In the intact spinal cord, NG2/CSPG4 expression was detected on the cell membrane and in the cytoplasm of NG2 glia and was absent in neurons. Large amounts of NG2/CSPG4 were found on myelin membranes. The ability of intact astrocytes to produce NG2/CSPG4 was shown, although to a lesser extent than oligodendrocytes and NG2 glia. At 7 days after SCI at the Th8 level in the reactive glial zone of VH, the expression of NG2/CSPG4 sharply increased in NG2 glia at a distance of 3-5 mm and in reactive astrocytes were observed at all investigated distances caudally from the epicenter of injury. The obtained results indicate the presence of NG2/CSPG4-positive astrocytes in the intact spinal cord, and in the case of damage, an increase in the ability of reactive astrocytes to produce NG2/CSPG4. SCI leads to increased expression of NG2/CSPG4 by NG2 glia in the early stages after injury, which decreases with distance from the epicenter of the injury, as well as at later stages.