BACKGROUND: Dental assistants are often susceptible to musculoskeletal disorders due to their professional duties; however, data on ergonomic risks for them are limited. AIM: To compare the severity of pain syndrome in dental assistants while working on chairs of different designs. METHODS: The study involved eight dental assistants who worked for two months on chairs of various designs and subjectively assessed pain severity using the visual analog scale (VAS). Before the start of each work shift, each assistant received one of two types of dental chair using a random number generator: a chair with armrests or a chair without armrests. Randomization was conducted independently for each shift and each participant. The resulting 221 observations were divided into two groups depending on the type of chair used during the shift: group 1 included 106 measurements obtained after a shift on a chair without armrests, and group 2 included 115 measurements obtained after a shift on a chair with armrests. Statistical analysis included assessment of normality of distribution (Shapiro–Wilk test), group comparisons (Student t-test, Mann–Whitney U test), and ROC analysis. Differences were considered statistically significant at p ≤ 0.05. RESULTS: Neck pain was the most common symptom in dental assistants (70%). Shoulder pain ranked second in frequency (52% of cases), and upper back pain ranked third (35%). When working on a chair with armrests, the median pain severity on the VAS was significantly lower in the neck (3.0 vs 5.0 points; p 0.001), right (3.0 vs 5.0 points; p 0.001) and left (2.5 vs 5.0 points; p 0.001) shoulders, as well as in the upper back on the right (4.0 vs 5.0 points; p = 0.030). For the upper back on the left, the differences did not reach statistical significance (p = 0.086). ROC analysis showed the best predictive ability of the model for the shoulders (AUC = 0.802 on the right; AUC = 0.804 on the left), moderate for the neck (AUC = 0.739–0.745) and the upper back on the right (AUC = 0.705). CONCLUSION: When comparing the groups, work on a chair with armrests was characterized by lower pain severity in the neck, shoulders, and upper back on the right than work on chairs of other designs.
BACKGROUND: Poor oral hygiene exacerbates existing periodontal disease and dental hard tissue pathology, promotes exacerbation of chronic odontogenic infection and the formation of new foci, which can lead to tooth loss and the development of osteonecrosis foci. AIM: To assess dental status in patients with medicationrelated osteonecrosis of the jaw. METHODS: A crosssectional study was conducted. Inclusion criteria were a confirmed diagnosis of medicationrelated osteonecrosis of the jaw. A total of 99 patients were examined. All patients (100%) had received bonemodifying agents (bisphosphonates and denosumab) for bone metastases from malignant neoplasms of various primary sites. Exclusion criteria were decompensated comorbid conditions and progression of the malignant neoplasm. Dental status was assessed using the caries intensity index, the Simplified Oral Hygiene Index of GreeneVermillion, and the papillarymarginalalveolar index. Calculations were performed using MS Excel 10 and Statistica 10. We determined the mean (M), median (Me), and standard deviation (σ). Distribution normality was assessed using skewness and kurtosis values and the Shapiro–Wilk test (W). The Mann–Whitney U test was used to compare between groups. Correlation was assessed using the Pearson correlation coefficient and Spearman's rank correlation test. Results were considered statistically significant at p ≤ 0.5. RESULTS: The mean Simplified Oral Hygiene Index score was 2.38 ± 0.56 (Me 2.26; 2.5) (W = 0.96; p = 0.027). The mean papillarymarginalalveolar index was 50.86 ± 17.09 (95% CI: 47.26; 54.47) (W = 0.94, p = 0.0005). In 38.2% of cases (n = 34), the index exceeded 60%. The prevalence of caries was 100%. The mean caries intensity index was 20.13 ± 5.67 (95% CI: 18.99; 21.26) (W = 0.95, p = 0.002). Complete secondary edentulism was diagnosed in 10 (10.1%) patients. CONCLUSION: The condition of dental hard tissues and periodontal tissues has a significant impact on the development and progression of medicationrelated osteonecrosis of the jaw.
This ceremonial speech presents current data on the diagnosis and treatment of myocardial infarction. Attention is given to the most important modifiable risk factors for coronary heart disease. Data are presented on the organization of care for patients with myocardial infarction in the region. The remaining problems in the management of patients with myocardial infarction are outlined. The speech also focuses on the prevention of myocardial infarction.
This review analyzes current scientific data on the application of a systems approach to the development of polytarget medicinal products of plant origin. The need for a methodological rationale for this line of research is driven by growing interest in polypharmacological strategies in clinical practice. Drugs with narrow molecular specificity demonstrate limited effectiveness in the treatment of multifactorial diseases, which determines the need for the development of agents that provide simultaneous action on multiple pathogenetic links. This review is to propose a unified research methodology employing a systems approach for the development of polytarget medicinal products and their subsequent use. Based on an analysis of published data and the authors’ own experimental data, the key components of the systems approach to phytopharmaceutical development are identified: investigation of the chemical composition of raw material sources; establishment of the relationship “substance structure/chemical composition of the phytosubstance—properties” and the production of standardizable pharmacologically active substances; assessment of the safety and activity profiles of drug candidates from the standpoint of systemic regulation of the body, with reference to mechanisms of action across the hierarchy of levels of biological organization and the interrelatedness of processes. In this context, the class of phenylpropanoids is considered to illustrate the systems approach as an example of biologically active compounds with a broad spectrum of action. The interaction between part and whole is demonstrated: known constituents are integrated into a unified architecture of the etiopathogenesis of impairments in specific and nonspecific resistance of the body and into a corresponding architecture of sanogenesis reflecting the pharmacodynamics of phenylpropanoids. The presented architectures constitute an original conceptual model requiring further experimental validation; in particular, at the preclinical stage this implies the use of clinically relevant etiopathogenetic models. Overall, the methodology discussed aligns with the principle “treat the patient, not the disease” and, in combination with modern digital technologies, expands the possibilities for the targeted development of complexcomposition medicinal products and the subsequent personalization of pharmacotherapy, including phytotherapy.
Interest in studying uric acid stems from its central role in the pathogenesis of a large number of chronic non-communicable diseases. Elevated uric acid levels are directly linked to an increased incidence of gout, nephrolithiasis (10%–20% of cases), chronic kidney disease, and cardiovascular events, myocardial infarction and stroke. Uric acid can have dual effects: as an antioxidant at physiological concentrations and as a trigger for inflammation and oxidative stress when its concentration increases, leading to increased manifestations of atherosclerosis and metabolic syndrome. It is known that renal transporters maintain the balance of urate reabsorption and secretion, but the mechanisms of their interactions, the role of rare genetic variants, and regulatory factors such as microRNAs remain poorly understood, limiting the potential for personalized therapy and prevention. The novelty of this search and analytical work lies in the systematization of modern data on the molecular mechanisms of urate transport, including the analysis of mutations associated with hyperuricemia and hypouricemia. This review examines in detail the key renal transporters: URAT1 (SLC22A12) and GLUT9 (SLC2A9) as the main systems of urate reabsorption in the proximal tubules; OAT1, OAT3, OAT4, OAT10 (SLC22 family) and ABCG2, responsible for the secretion of uric acid from cells into the tubular lumen; NPT1 and NPT4 (SLC17A family), located on the apical membrane of the proximal renal tubules and responsible for sodiumphosphate cotransport. The operation of urate “transportosomes” of the proximal renal tubules, which ensure efficient transport and metabolism of uric acid, is described. Particular attention is paid to genetic variants: a common ABCG2 polymorphism (rs2231142), which increases the risk of hyperuricemia and urolithiasis, and rare mutations in URAT1 (G774A, c.1400CT) and GLUT9 (c.374CT), which lead to hypouricemia types 1 and 2 with the risk of acute renal failure under exercise. The roles of microRNAs (miR1433p, miR4770 for GLUT9; miR301a/b for URAT1) in posttranscriptional regulation and GWAS loci (GCKR, KCNK5, etc.) associated with urate homeostasis disorders are analyzed. The review provides a deeper understanding of the paradoxical nature of uric acid, reflecting its dual biological role: a powerful antioxidant at physiological concentrations and a trigger for inflammation and oxidative stress when its serum concentration increases. A comprehensive consideration of urate transport mechanisms will reveal gaps in our understanding of key mutations associated with urate urolithiasis, as well as present current approaches to the management of patients with gout, urate nephrolithiasis, and hyperuricemia.
