Abstract. This study presents an artificial intelligence (AI)-assisted historical andbiographical  investigation  of  the  surgical  aspects  of Yurii  Lypa's  medical  practice, confirms his place in the history of Ukrainian medicine, and evaluates his contribution to  the  development  of  national  medical  science  and  practice.  Using  historical  and biographical  methods  combined  with AI-assisted  analysis  of  archival  sources  and scholarly  literature,  the  study  reconstructs  the  academic  environment  that  shaped Lypa's  professional  education  and  clinical  training.  Particular  attention  is  paid  to surgical  education  at  the  University  of  Poznań  during 1922–1929, including  the organization  of  clinical  instruction,  demonstration  operations,  bedside  teaching, clinical ward rounds, and the acquisition of practical skills in operative surgery, asepsis, antisepsis,  and  surgical  technique.  The  contribution  of  Professors Antoni  Tomasz Jurasz,  Franciszek  Raszeja, Adam Wrzosek,  and  other  members  of  the  Faculty  of Medicine to the formation of Lypa's clinical thinking and professional competencies is examined.  The  study  demonstrates  that  the  clinical  education  he  received  at  the University  of  Poznań  became  the  foundation  of  his  subsequent  medical  practice, scientific  interests,  and  publications  on  phytotherapy,  which  combined  the achievements of academic medicine with the rational use of medicinal plants. It is concluded that the University of Poznań and its surgical school exerted a profound influence  on  Lypa's  professional  development  as  a  physician,  military  medical practitioner, and representative of the Ukrainian medical intelligentsia during the firsthalf of  the twentiethcentury. Particular emphasis  is placed on  his  medical service during  the  Second  World  War,  his  contribution  to  the  development  of  Ukrainian military  medicine,  and  his  promotion  of  scientifically  grounded  phytotherapy. The study also substantiates the need for further historical-medical investigations of Lypa'sprofessional legacy through the expanded use of archival materials preserved at the University of Poznań. Overall, Yurii Lypa's medical career illustrates the successful integration  of  clinical  competence,  scientific  inquiry,  humanistic  medical  values, patriotic service, and professional responsibility.

УДК: 616-071:616.72-002-036-08

Резюме. Мета: узагальнити сучасні можливості лабораторної діагностики реактивного артриту та продемонструвати їх значення для етіологічної верифікації, прогнозування перебігу й персоналізації лікування на прикладі клінічного випадку РеА єрсиніозної етіології. Об’єкт і методи дослідження. Проведено аналіз сучасних наукових джерел щодо патогенезу, лабораторної діагностики та лікування РеА. Наведено результати клінічного, лабораторного та інструментального обстеження 21-річної пацієнтки із суглобовим синдромом, шкірними проявами та перенесеним тяжким ентероколітом. Визначали маркери системного запалення, ревматоїдний фактор, anti-CCP, anti-MCV, ANA, HLA-B27 та антитіла IgA й IgG до Yersinia enterocolitica методом Western Blot; проведено магнітно-резонансну томографію крижово-клубових суглобів. Результати. Виявлено HLA-B27, позитивні IgA та IgG до кількох антигенів Y. enterocolitica, зокрема плазмідокодованого YopD, і МРТ-ознаки двобічного сакроілеїту. Маркери ревматоїдного артриту та системних захворювань сполучної тканини не підтверджено. Сукупність анамнестичних, серологічних, генетичних та візуалізаційних даних дала змогу діагностувати хронічний HLA-B27-асоційований РеА єрсиніозної етіології з аксіальним ураженням. Висновки. Комплексне використання серологічних, молекулярно-генетичних та інструментальних методів підвищує точність етіологічної діагностики РеА, сприяє оцінці ризику хронізації та обґрунтованому вибору персоналізованої лікувальної тактики.

UDC 616.13‑004.6‑02:577.112.85]-038:616.12‑008.331.1(048.8)

Introduction. Elevated lipoprotein(a) has emerged as an important determinant of cardiovascular risk because of its roles in atherosclerotic disease, vascular inflammation, endothelial dysfunction, arterial stiffening, and vascular calcification. Increasing evidence suggests that the clinical significance of Lp(a) extends beyond atherosclerosis, as higher concentrations have also been linked to vascular remodeling and adverse cardiovascular outcomes in patients with arterial hypertension.

Aim. To evaluate the current scientific evidence on the role of lipoprotein(a) in vascular remodeling and its effects on endothelial function, arterial stiffness, and cardiovascular risk among patients with arterial hypertension.

Materials and methods. The MEDLINE database via PubMed was searched for articles published between 2016 and 2026 using a predefined set of keywords. The search yielded 86 articles, which were initially screened and assessed based on their titles and abstracts. After evaluating relevance, we selected 56 articles for detailed assessment. Finally, 31 articles were included in the review.

Results. Elevated Lp(a) concentrations are linked to multiple mechanisms that drive vascular remodeling and cardiovascular injury. A substantial part of Lp(a)'s pathogenic activity is attributed to oxidized phospholipids, which contribute to endothelial dysfunction, vascular inflammation, extracellular matrix remodeling, fibrosis, and vascular calcification. Research indicates associations between elevated Lp(a) levels and increased pulse pressure, reduced nocturnal blood pressure decline, arterial stiffness, vascular calcification, and hypertensive target-organ damage. These findings suggest that elevated Lp(a) may influence the development of a less favorable vascular profile in arterial hypertension and contribute to cardiovascular risk beyond that explained by traditional lipid markers. The development of RNA-based therapeutic approaches, including antisense oligonucleotides and small interfering RNA agents, has enabled substantial reductions in circulating Lp(a) levels and may provide new opportunities for individualized cardiovascular risk management.

Conclusions. Elevated lipoprotein(a) levels should be regarded as an important genetically determined factor in vascular remodeling and cardiovascular risk in patients with arterial hypertension. Increased lipoprotein(a) concentrations contribute to endothelial dysfunction, vascular inflammation, arterial stiffness, vascular fibrosis, and calcification through multiple mechanisms, predominantly mediated by oxidized phospholipids.

ABSTRACT A 16-year-old male (ASA II, BMI 31) underwent reconstructive osteoplasty with insertion of a polymethylmethacrylate (PMMA) spacer. Shortly after cement application, he developed sudden hypotension, tachycardia, and decreased end-tidal CO₂, consistent with Grade II BCIS. Supportive management with fluids, ketamine, and norepinephrine stabilized the patient. Postoperatively, he experienced recurrent hypotension, acute kidney injury, and elevated liver enzymes and creatine kinase. Intensive care treatment resulted in recovery, and he was discharged from the ICU on day five. Bone cement implantation syndrome, though exceptionally uncommon in pediatric patients, may develop during orthopedic procedures involving polymethylmethacrylate. Early recognition, continuous anesthetic vigilance, and timely multidisciplinary intervention are crucial to reduce morbidity and improve perioperative outcomes.

KEY WORDS: bone cements, anesthesia, hypotension, acute kidney injury, vasopressors, creatine kinase

Aim: To determine the significance of growth factors (TGF-β1 and CTGF) in the development and progression of diabetic retinopathy (DR) in carriers of different genotypes of the TGFB1 rs1800470 polymorphism in type 2 diabetes mellitus (T2DM).

Materials and Methods: 102 individuals with T2DM and DR were examined, who were divided into 3 groups: 1st – with non-proliferative DR (NPDR, 35 individuals), 2nd – with preproliferative (PPDR, 34 individuals) and 3rd – with proliferative (PDR,33 individuals); 61 individuals were included in the control group. The patients underwent standard ophthalmological examinations. Determination of TGF-β1 in blood serum and intraocular fluid (IOF) and CTGF in IOP was performed by enzyme-linked immunosorbent assay (Invitrogen Thermo Fisher Sci., USA). Alleles rs1800470 (T869C) were determined by polymerase chain reaction (TaqMan Mutation Detection Assays Life-Technology test system, USA). For statistical studies, the MedStat and MedCalc v.15.1 software packages (MedCalc Software bvba) were used.

Results: Rs1800470 A/Acarriers had worse visual acuity (p=0.016) and higher central retinal thickness and volume (p<0.001) compared to G/G carriers. In DR the content of TGF-β1 in the blood and IOF and CTGF in IOF significantly exceeded that in controls (by 1.5-5.2 times; p<0.05). The highest content of both factors in DR compared to controls was determined in G/Aand A/Ars1800470 carriers. By stages of DR, a significant increase in the content of TGF-β1 in the blood and IOF and CTGF in IOF was established with maximum values in PDR. A higher content of both factors was established in G/Aand A/Acarriers compared to G/Gcarriers. In PDR, the blood content of TGF-β1 in A/A carriers was 1.2 times higher (p<0.05) than in G/Gcarriers. The increase in CTGF content in the IOF when comparing NPDR and PPDR was characteristic only for A/A carriers compared to G/Aand G/Gcarriers (1.2-1.5 times; p<0.05). In PDR, the content of this factor was equally high in G/Aand A/Acarriers compared to G/Grs1800470 carriers (1.3 times; p<0.05).

Conclusions: Thus, the content of both TGF-β1 and CTGF was higher in carriers of the G/Aand A/Agenotypes compared with the ancestral G/Ggenotype. Therefore, the clinically worse course of DR in carriers of the SNP rs1800470 of the TGFB1gene could be associated with a higher concentration of TGF-β1 and CTGF in the IOF of such patients.