The phase composition and mechanical properties of the Ti–38Zr–13Nb alloy subjected to quenching and quenching followed by low-temperature annealing are studied. The alloy is found to consist of the stable β phase; after annealing, no ω- and α'-phases are detected. In this case, the microstructure is represented by elongated grains having no signs of recrystallization. Tensile tests show that the annealing does not reduce the plasticity, but increases the ultimate strength by 18
This article examines the influence of the secretory and humoral activity of the major salivary glands on the pathogenesis of experimental periodontitis in rats with induced hyposalivation. Saliva, with its immune and cleansing properties, serves as a key factor in protecting periodontal tissues. Decreased saliva secretion (hyposalivation) is considered a significant risk factor; however, the complex impact of this condition on the pathogenesis of periodontitis requires further study. Aim: The aim of this study was to examine the role of the secretory and humoral activity of the major salivary glands in the pathogenesis of experimental periodontitis in rats with induced hyposalivation. Materials and methods: The experiment was performed on 35 Wistar rats divided into 7 groups. Hyposalivation was induced by daily subcutaneous injections of atropine sulfate at a dose of 2 mg/kg for 30 days. Periodontitis was induced by subperiosteal ligation. Morphological, biochemical, and immune changes in the salivary glands and gums were studied. Statistical data processing was performed using one-way analysis of variance (ANOVA) with Tukey's post-hoc test. Results: In the hyposalivation groups, a 55–65 % decrease in salivary gland weight and a 50 % decrease in IgA secretion were recorded. Concurrently, an increase in biochemical markers of inflammation and oxidative stress was noted: malondialdehyde (MDA) levels increased by 70–80 %, and tumor necrosis factor-alpha (TNF-α) concentrations increased by 60 %. In the combined models, worsening signs of periodontitis were observed, including increased neutrophil infiltration and destruction of the dental ligament apparatus. These changes were significant compared to the control group (p 0.05). Conclusion: It has been established that hyposalivation contributes to the progression of periodontitis by disrupting the protective functions of saliva and activating inflammatory mechanisms. This is associated with a weakening of local immunity (decreased IgA) and activation of systemic inflammation (increased TNF-α and MDA). The results confirm the key role of the salivary glands in maintaining periodontal health and indicate the need to develop strategies for correcting xerostomia to prevent periodontitis.
Brain death in children after clinical death is one of the most complex and urgent problems of modern pediatric intensive care. Immaturity of the nervous system, high metabolic activity, functional instability of the blood–brain barrier, and incomplete myelination determine the increased vulnerability of the child’s brain to ischemia and hypoxia. This article reviews the main pathogenetic mechanisms: primary (global ischemia, energy deficit, ion imbalance, excitotoxicity), secondary (mitochondrial dysfunction, reperfusion injury, oxidative stress, blood–brain barrier disruption, neuroinflammation), as well as different forms of cell death (apoptosis, necrosis, pathological autophagy). Particular attention is paid to the morphological consequences for the developing brain, including white matter injury, delayed myelination, and loss of neuronal networks. In children, the transition from reversible to irreversible damage occurs faster than in adults, which significantly complicates prognosis and therapeutic interventions. Current understanding of the molecular and morphological mechanisms of brain death has practical significance for improving diagnostics, prognosis, and treatment in pediatric intensive care.
Pain syndrome (PS) poses a serious challenge in children and adolescents admitted in ICUs. This review describes the outcomes of analgesic ketamine administration in pediatric patients with various PS. It discusses the advantages and disadvantages of this drug for pain relief in childhood. The mechanisms of analgesic effect through the effect on NMDA and opiate receptors are described. Pharmacokinetics of ketamine is described. The main dosages and routes of administration for PS relief in children and adolescents are indicated. The authors analyze clinical data on ketamine versus other analgesics for relief of intraoperative and postoperative pain, PS associated with cancer and chronic PS. Pediatric anesthesiologists should consider this analgesic for PS relief in children and adolescents.
The aim of this review was to systematize current pathophysiological mechanisms of sepsis-associated acute kidney injury (SA-AKI) in children and their relevance for early recognition of renal dysfunction. A review of 44 literature sources, published predominantly between 2021 and 2026, was conducted. SA-AKI cannot be explained solely by arterial hypotension or reduced renal perfusion. Its pathogenesis involves systemic inflammation, endothelial dysfunction, endothelial glycocalyx damage, intrarenal microcirculatory disturbances, coagulopathy, mitochondrial insufficiency, and inflammatory-metabolic injury to the tubular epithelium. Even after macrohemodynamic stabilization, capillary stasis, local hypoxia, interstitial edema, and heterogeneous renal perfusion may persist. Glycocalyx degradation increases vascular permeability, leukocyte-platelet adhesion, and microthrombus formation. Impaired fatty-acid β-oxidation, reduced mitochondrial ATP synthesis, oxidative stress, and altered phospholipid metabolism contribute to tubular dysfunction before a marked rise in serum creatinine. Complement and inflammasome activation, apoptosis, pyroptosis, necroptosis, ferroptosis, and disturbances of autophagy, mitophagy, and tissue repair play a distinct role in sustaining renal injury. In newborns and young children, these mechanisms are important because of immature immune and vascular regulation, susceptibility to fluid overload, and limited functional renal reserve. The delayed rise in creatinine and the variable diagnostic value of urine output restrict early detection; therefore, risk assessment should consider age, baseline renal reserve, fluid exposure, and the severity of multiple organ dysfunction. SA-AKI should be regarded as an early manifestation of profound tissue dysregulation rather than only as a late laboratory complication of sepsis.
