Restoration of the motor function of the musculoskeletal system impaired due to innervation damageis an important clinical problem. In the study the potential therapeutic effect of C60 fullerene application was estimated in the Wistar rat model of neurogenic muscle atrophy caused by nervus ischiadicus injury. The animals were divided into the following: control, injury, injury+С60 groups. C60 fullerene aqueous solution was administrated orally for 30 days after ischiadicus injury at a daily dose of 1 mg/kg. Biomechanical parameters of gastrocnemius muscle contraction and biochemical indices (creatinine, lactate, reduced glutathione content as well as creatine phosphokinase, lactate dehydrogenase, catalase and superoxide dismutase activity) in the blood of rats were estimated on day 30 after nerve transection. It has been found that muscle strength response in the injury+С60 group was significantly enhanced, in particular, the muscle force impulse was increased by more than 30 ± 2% compared to the injury group. The studied biochemical indices of the muscle
fatigue and oxidative stress in the blood of experimental animals had a pronounced tendency to increase after the initiation of the muscle neurogenic atrophy, while under the influence of C60 fullerene they decreased compared with the injury group. In our opinion, C60 fullerene prevented significant dysfunction of the gastrocnemius muscle after neurogenic atrophy by exerting an antioxidant effect and improving its contractile activity.
K e y w o r d s: C60 fullerene, muscle gastrocnemius, neurogenic atrophy, muscle contraction, biochemical indicators.

УДК: 616.716.4-001-089.843-018
   Відновлення кісткової тканини залишається складним завданням для сучасної медицини. Унікальні властивості хітозану, його вплив на регенерацію кісток щелепно-лицевої ділянки, механізми та динаміка залишаються не до кінця вивченими, потребують уточнення і деталізації. Мета дослідження – визначити динаміку морфологічних, рентгенологічних, та лектиногістохімічних характеристик кістково-керамічного регенерату після трансплантації октакальційфосфату з додаванням хітозан-ацетату з ампіциліном в експериментальний дефект нижньої щелепи кролика. Матеріали і методи. Для дослідження використовували статевозрілих кролів-самців віком 6-7 місяців, вагою 2,5-3 кг. До контрольної групи увійшли тварини з дефектом кісткової тканини, який загоювався під кров’яним згустком. Експериментальну групу складали кролі, у яких кістковий дефект заповнювали остеотропним матеріалом з октакальційфосфатом з додаванням хітозан-ацетату з ампіциліном (ОКФ-Н-Хітозан-Ампіцилін). Контроль посттравматичного стану кісткової тканини в ділянці дефекту здійснювали впродовж 84 діб. Серед методик були використані: моделювання кісткового дефекту, оцінка макроструктури щелеп, рентгенографічне дослідження, радіовізіографічне дослідження, вивчення мікропрепаратів шліфів кістки та лектиногістохімічні дослідження зрізів декальцинованої кістки. Результати. Дослідження макроструктури експериментального кісткового дефекту нижньої щелепи після імплантації матеріалу з октакальційфосфатом, хітозан-ацетатом та ампіциліном (ОКФ-Н-Хітозан-Ампіцилін) дозволило виявити регенераційні зміни, що відбувалися після нанесення травми та корелювали з даними рентгенографічного, радіовізіографічного дослідження. Вивчення мікропрепаратів шліфів кістки дозволило встановити фазовий характер динаміки досліджуваних регенеративних змін та складу регенерату.
   Висновки. Встановлено, що в експериментальній групі тварин, у яких пластику дефекту проводили з використанням матеріалу ОКФ-Н-Хітозан-Ампіцилін, спостерігалося скорочення реактивної фази посттравматичного запального процесу, що забезпечило активний початок остеорегенерації. Застосування даної комбінації препаратів засвідчило пришвидшену репаративну регенерацію нижньої щелепи та прилеглої слизової.
   Ключові слова: нижня щелепа, зубощелепний апарат, кісткова тканина, регенерація, остеопластичні матеріали, хітозан, морфологічне дослідження, рентгенографічний метод, лектиногістохімія.

УДК 616.61–036.12–06:616.12–008.9] –092–036–07–038–037–08(048.8)

Introduction. Cardiorenal metabolic syndrome (CRMS) is a complex, multisystem disorder resulting from the intricate interplay between cardiovascular, renal, and metabolic dysfunctions. In individuals with chronic kidney disease (CKD), CRMS markedly elevates the risk of cardiovascular events, progressive kidney function decline, and overall mortality. Despite its clinical relevance, CRMS remains underdiagnosed, and both its pathophysiological mechanisms and management approaches continue to evolve. Accordingly, a thorough and up-to-date synthesis of the available scientific evidence is essential.

The aim of the study. To conduct a comprehensive review of current scientific information on the pathogenesis, diagnostic approaches, risk factors, prognosis, and therapeutic perspectives of cardiorenal metabolic syndrome in patients with chronic kidney disease, based on an analysis of the literature and the description of a clinical case.

Results. The review identified the key pathophysiological mechanisms underlying CRMS in CKD, including hemodynamic disturbances, neurohormonal activation, chronic inflammation, and endothelial dysfunction. Current diagnostic strategies—encompassing both conventional methods and emerging biomarkers—were analyzed. Particular emphasis was placed on risk stratification models, prognostic indicators, and therapeutic perspectives, including the use of SGLT2 inhibitors and comprehensive renoprotective approaches. The presented clinical case further illustrated the typical course and management challenges of CRMS in the context of CKD.

Conclusions. CRMS in patients with CKD necessitates an interdisciplinary approach to both diagnosis and treatment, incorporating clinical evaluation, laboratory testing, and instrumental diagnostics. Early identification, accurate risk stratification, and the application of modern therapeutic strategies are critical for improving patient outcomes and slowing the progression of the disease.

UDC: 617.77-002:616-056.3]-06-07 

Abstract. Blepharitis is a very common disease in ophthalmology, dermatology, and allergist practice. It can be acute or chronic. Acute blepharitis is most often caused by viruses (Herpes simplex and Varicella zoster) and bacteria (Staphylococcus). Chronic blepharitis is a symptom of allergies, metabolic syndromes most often associated with liver disease, autoimmune diseases, fungal infections, and Demodex. The liver is a vital organ that supports immunity, metabolism, digestion, stores vitamins, and is responsible for detoxification. Therefore, liver dysfunction can also cause skin lesions around the eyes. Stress, through the activation of the pituitary-hypothalamic-adrenal system, promotes cell activation and the release of biologically active cytokines, which in turn
is a factor in skin damage. Clinically, blepharitis is manifested by redness, itching, and swelling of the eyelids, sometimes the formation of scales on the eyelids. As a rule, both eyes are affected and the disease has a recurrent course. In most cases, blepharitis does not pose a threat to the patient's life, but it reduces the quality of life and is dangerous for the development of such complications as conjunctival lesions and the formation of corneal marginal ulcers.
The article presents clinical cases of patients with chronic blepharitis who had similar symptoms but differed in etiology and treatment regimens.
Key words: blepharitis, contact dermatitis, toxic blepharitis.

Background and objectives. Recent evidence has demonstrated that mildly elevated bilirubin concentrations are protective against various oxidative stress-mediated diseases, including autoimmune disorders. Based on this, the present study aimed to investigate the association between serum bilirubin levels, albumin-based inflammatory ratios, and the presence of primary antiphospholipid syndrome (APS) in women with a history of spontaneous miscarriages.
Materials and methods. This cross-sectional observational study included 72 women aged 21–40 years (median age 27) with a history of spontaneous miscarriages in the first trimester. Based on clinical and laboratory findings, 47 women were diagnosed with APS, and 25 were classified as non-APS. All participants underwent a complete evaluation, including blood count, coagulation tests, glucose and lipid profiles, CRP, vitamin D, and assessments of thyroid, liver, and kidney function.
Results. A total bilirubin level below 8 μmol/L was observed in 53% of APS patients, significantly higher than in non-APS women (24%, p = 0.024). Total, direct, and indirect bilirubin concentrations were significantly lower, while inflammatory markers such as fibrinogen, CRP, and CRP/albumin ratio were significantly higher in APS patients (p < 0.05). Logistic regression and ROC analysis confirmed the diagnostic value of these markers. The AUC values for total bilirubin, bilirubin/albumin ratio, fibrinogen, albumin/fibrinogen ratio, CRP, and CRP/albumin ratio demonstrated moderate diagnostic
accuracy (AUC = 0.723, 0.793, 0.693, 0.828, 0.761, and 0.699, respectively).
Conclusions. Serum bilirubin levels and the bilirubin/albumin ratio were negatively associated with APS in women with a history of spontaneous miscarriage. These findings suggest impaired antioxidant and anti-inflammatory defenses in APS patients. Serum bilirubin combined with albumin-based inflammatory ratios may serve as additional screening tools for APS in this population.

Keywords: antiphospholipid syndrome, total bilirubin, total bilirubin to albumin ratio, oxidative stress