Sarcopenia currently affects 10–27% of people worldwide and 30–37% in the Russian Federation. Its social burden is considerable: the condition is associated with fractures, disability, and increased mortality. Sarcopenia nonetheless remains underdiagnosed. Diagnosis is hindered by the absence of universal criteria, standardized cutoff values, and widely available screening tools, while applying non-adapted foreign reference values to the Russian population may cause both under- and overdiagnosis.

Aim. To analyze the evolution of international and Russian approaches to sarcopenia diagnosis, assess the diagnostic value and limitations of available screening and instrumental methods, and formulate proposals for optimizing diagnostic strategies in clinical practice in the Russian Federation.

Materials and methods. A literature review on sarcopenia diagnosis was conducted using PubMed/MEDLINE, Scopus, Google Scholar, and eLibrary.ru for 2006–2026. Systematic reviews, meta-analyses, randomized controlled trials and cohort studies, consensus documents, and clinical guidelines were included.

Results. A shift was observed from the isolated assessment of muscle mass toward diagnostic models in which muscle strength serves as the primary criterion and physical performance as an indicator of disease severity. Handgrip dynamometry cutoff values varied across populations. In particular, muscle strength in Russians older than 65 years was at the lower limit of European reference values. No screening instrument demonstrated both high sensitivity and high specificity. The most balanced instrument, SARC-CalF, has not been validated in the Russian population. Instrumental methods are highly accurate; however, their use is limited by high cost, limited availability, dependence on hydration status, and the lack of standardized protocols.

Conclusion. To improve the effectiveness of sarcopenia diagnosis in Russia, national reference values should be developed, diagnostic protocols standardized, and screening instruments validated.

Blood-based biomarkers are increasingly explored for their ability to distinguish non-small cell lung cancer (NSCLC) from non-malignant conditions. Single markers, however, often show limited performance, which has led to growing interest in combining multiple biological features.

Aim. To develop a multivariable diagnostic model based on serum biomarkers and assess its discriminatory performance in an exploratory TRIPOD Type 1a study.

Materials and methods. This study represents a secondary analysis of a previously published case–control cohort, focusing on multivariable model development rather than single biomarker assessment. A total of 275 participants were enrolled in this retrospective case–control study supplemented by prospectively collected samples, including 85 patients with histologically confirmed NSCLC and 190 controls. Serum concentrations of 20 biomarkers representing tumor-associated, inflammatory, and metabolic pathways were analyzed. Univariable logistic regression was performed, followed by multivariable modeling including variables with p < 0.10. Model discrimination was evaluated using receiver operating characteristic analysis and the area under the curve (AUC), and internal validation was performed by bootstrap resampling on complete-case data.

Results. Three independent variables were retained in the final multivariable model: human epididymis protein 4 (HE4), apolipoprotein A4 (ApoA4), and age. The final model showed high apparent discrimination within the study dataset (AUC = 0.975; 95% CI: 0.958–0.992). Bootstrap internal validation demonstrated minimal optimism, with an optimism-corrected AUC of 0.972. HE4 and age were positively associated with NSCLC, whereas ApoA4 showed an inverse association. In the age-matched sensitivity analysis, HE4 and ApoA4 retained essentially unchanged associations while age lost independent significance, supporting a biomarker-driven rather than age-driven contribution to model discrimination. The multivariable model demonstrated improved discrimination compared with individual biomarkers.

Conclusion. This exploratory model derivation study identified a candidate serum biomarker combination associated with NSCLC. The findings should be considered hypothesis-generating. Independent validation in clinically representative populations is required before any clinical interpretation or application.

The neural plexus located on the ependyma’s apical surface of the cerebral ventricles may be an important link in the extra-barrier signal transmission and regulation of the cerebrospinal fluid composition, but to date it remains a poorly understood part of the central nervous system.

Aim. To investigate signs of functional activity of the supraependymal nerve plexus in early postnatal development using immunohistochemical methods.

Materials and methods. Coronal brain sections of adult rats and rats on postnatal days 1, 7, and 10 (n = 16) were used for immunohistochemical analysis. Antibodies to tyrosine hydroxylase, tryptophan hydroxylase, and synaptophysin were used to identify supraependymal fibers and structures exhibiting potential synaptic activity.

Results. There was no immunopositive reaction observed in the supraependymal plexus of neonatal rats regardless of the marker used. Synaptophysin-containing puncta or fibers with varicosities on the surface of ependymal cells were first detected by the end of the first week of postnatal development. Tryptophan hydroxylase-positive structures were also observed at this stage of postnatal development. Fibers and puncta were located throughout the walls of the lateral and third ventricles, with the exception of the infundibular recess. Only on the 10^th day of postnatal development were tyrosine hydroxylase-containing granules detected on the apical surface of the ependyma. A double immunofluorescence assay demonstrated that the tryptophan hydroxylase distribution matched with synaptophysin. Moreover, at none of the studied periods were neurons found on the surface of the ependyma.

Conclusion. The supraependymal plexus exhibits the capacity for synaptic transmission and serotonin synthesis by the end of the first week of postnatal development. By the 10^th day of postnatal development, supraependymal nerve fibers may participate in catecholaminergic neurotransmission.

Aim. To study morphological changes in the stomach and intestines of transgenic mice with amyloid precursor protein with the Swedish mutation and presenilin 1 deleted exon 9 line (APPswe/PS1dE9) used as a model of Alzheimer's disease.

Materials and methods. To assess cognitive impairment in animals, behavioral tests “Open Field”, “Elevated plus maze” and “Morris water maze” were performed. Brain and samples of the stomach, small intestine, and colon were collected from 1-year-old APPswe/PS1dE9 mice (n = 5) and wild-type C57BL/6J mice (n = 5) and fixed in Carnoy's fluid. The presence of amyloid deposits in the brain was assessed after staining the sections with sulfated alcian blue and using antibodies against amyloid beta. Antibodies against peripherin, synaptophysin, glial fibrillary acidic protein (GFAP), and S100 calcium-binding protein B (S100B) were used to assess the morphological characteristics of cells of the enteric nervous system. The number of positively stained structures was assessed. The distribution of variables in the samples was assessed using the Shapiro–Wilk test. Student's t-test and one-way analysis of variance (ANOVA) were used to assess intergroup differences.

Results. Amyloid deposits were found in the brain of experimental animals. In comparison with the control group, the deposition of amyloid beta in intramural ganglia neurons was noted in all studied organs of the gastrointestinal tract in animals of the APPswe/PS1dE9 line. These animals also showed increased synaptophysin immunoreactivity in neurons of the small and large intestines, accompanied by activation of GFAP⁺ glial cells. An increase in the number of S100B⁺ cells was found in all parts of the gastrointestinal tract outside the intermuscular plexus.

Conclusion. In APPswe/PS1dE9 mice, morphological changes in the structural components of the enteric nervous system largely reflect changes characteristic of central nervous system structures in this model.