The article presents a comparative analysis of the results of guided bone regeneration operations using individual titanium skeleton membranes, where in one group, soft tissue plastic surgery was not performed before alveolar bone reconstruction, and in the other group, it was performed accordingly. Soft tissue plastic surgery was performed using the technique of an apically displaced flap with the transfer of a free gingival graft to the wound surface. The individual titanium frame membrane was manufactured using the technology of direct laser sintering of metals on a 3D printer. In patients of the 1st group, 7 cases of complications were registered within a month after the direct bone regeneration (GBR) such as suture divergence and membrane densification. In group 2, after two months, all patients had a keratinized gum attachment with a width of 4–5 mm and a thickness of at least 1.5 mm; then, all patients underwent reconstruction of the alveolar ridge using individually manufactured titanium membranes. In the second group, 1 case of a complication in the form of membrane exposure was registered within a month after the GBR. According to a comparative analysis of the number of complications between the 1st and 2nd groups, statistically significant results were obtained in reducing the number of complications, in the form of suture divergence and membrane exposure, 28 and 4%, respectively, p = 0.049.
Neuroinflammation is regarded as a central mechanism driving the progression of neurodegenerative diseases, integrating age-associated inflammation, glial dysfunction, blood–brain barrier disruption, mitochondrial stress, and systemic factors. Activation of microglia and astrocytes, involvement of the NLRP3 inflammasome, dysregulation of TREM2 signaling, disturbances in iron and lipid metabolism, as well as the influence of the microbiota and metabolic comorbidities together form a self-sustaining pathological network that exacerbates neuronal loss in Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis. Emerging therapeutic strategies include modulation of microglia, inhibition of inflammasome-related cascades, epigenetic approaches, and nanotechnology-based delivery systems for anti-inflammatory compounds; however, their clinical efficacy remains limited. A deeper understanding of the architecture of neuroinflammation opens avenues for the development of targeted and personalized interventions.
Nootropics represent a heterogeneous group of substances that affect cognitive functions primarily through modulation of neuroplasticity. Classic agents improve neuronal metabolism and, in experimental models, increase neurotrophin levels, but their clinical efficacy in dementia and other cognitive disorders remains moderate. Psychostimulants provide short-term improvement in attention and performance; however, they do not strengthen long-term plasticity and may adversely affect the developing brain. Herbal and nutraceutical agents exert mild and delayed effects, predominantly manifesting in individuals with mild cognitive complaints or deficits. Despite growing interest in pharmacological cognitive enhancement, convincing evidence of a clinically meaningful improvement in cognitive functions in healthy individuals is lacking, whereas the strongest effects on neuroplasticity continue to be demonstrated by non-pharmacological interventions.
Nasal congestion is a common condition in which reduced nasal patency alters respiratory aerodynamics, increases upper airway resistance, and promotes a shift to mouth breathing, particularly during sleep. These changes impair ventilation–perfusion matching, decrease gas-exchange efficiency, and may lead to systemic or local hypoxia, especially in sleep-disordered breathing and in children who are obligate nasal breathers. Clinical evidence demonstrates that both chronic and acute nasal obstruction are associated with reduced SpO2, increased intermittent hypoxemia, sleep disruption, and cognitive and behavioral consequences. Medical and surgical relief of obstruction improves nasal airflow, decreases the severity of hypoxic episodes, and enhances the effectiveness of sleep-disordered breathing treatment. Thus, maintaining nasal patency is a key component in the prevention and correction of hypoxia across diverse patient populations.
Obstructive sleep apnea (OSA) is a common sleep-related breathing disorder characterized by recurrent episodes of upper airway obstruction leading to apnea and hypopnea. A combination of anatomical and functional factors contributes to the development of OSA: narrowing of the upper airway (e.g., due to obesity or craniofacial features), reduced tone of pharyngeal dilator muscles during sleep, increased ventilatory drive (ventilatory control instability, high loop gain), and a low arousal threshold. These factors promote pharyngeal collapse during sleep with episodes of hypoxia and arousals. Recurrent intermittent hypoxia and sleep fragmentation trigger a cascade of reactions – sympathetic activation, oxidative stress, systemic inflammation, endothelial dysfunction — which underlie cardiovascular complications (hypertension, atherosclerosis, arrhythmias), metabolic disturbances (insulin resistance, appetite-related hormonal imbalance), and neurocognitive consequences (daytime sleepiness, cognitive dysfunction).
