UDC 616.379-008.64:617.735:576.3:611-018

Abstract

Background. Diabetic retinopathy (DR) is increasingly recognized as a heterogeneous neurovascular disorder, yet preclinical models often fail to distinguish between the distinct pathophysiological clusters of type 2 diabetes. Recent clinical evidence demonstrates that patients with different metabolic phenotypes, specifically Severe Insulin-Resistant Diabetes (SIRD) versus Severe Insulin-Deficient Diabetes (SIDD), exhibit divergent patterns of retinal complications. However, the specific cytomorphometric signatures that distinguish these phenotypes at the cellular level remain poorly characterized.

Aim: to determine whether specific systemic metabolic phenotypes, SIRD versus SIDD, induce distinguishable cytomorphometric signatures of retinal neurodegeneration in experimental models.

Materials and Methods. Male Wistar rats were stratified into three metabolic models: (1) Chronic High-Fat Diet (HFD, 150-180 days) mimicking the SIRD phenotype; (2) HFD combined with low-dose streptozotocin (STZ, 30 days post-induction) mimicking the SIDD phenotype; and (3) HFD with supplemental glucose loading. Systemic phenotyping included longitudinal profiling of lipids, liver function, and protein status. Retinal cytoarchitecture was quantified using a computational pathomics pipeline (QuPath/StarDist) with deep learning-based segmentation of >90,000 nuclei, analyzed via Bayesian hierarchical modelling.

Results. The HFD model exhibited a "lipotoxicity-first" trajectory where dyslipidemia and hepatic steatosis preceded hyperglycemia. This SIRD-like phenotype was characterized by progressive retinal atrophy, specifically an 18-46% reduction in Inner Nuclear Layer neuronal density, accompanied by nuclear hyperchromasia indicative of epigenetic condensation. In contrast, the HFD+STZ model, characterized by acute hyperglycemia and significant hypoproteinemia, exhibited a paradoxical 1.54-fold increase in Ganglion Cell Layer density and thickening. This SIDD-like signature reflected cytotoxic edema driven by osmotic and oncotic failure, confirmed morphologically by severe irregular karyomegaly and profound chromatin dissolution (hypochromasia).

Conclusions. Retinal neurodegeneration is not a monolithic process but mirrors specific systemic metabolic trajectories. Chronic insulin resistance (SIRD) drives progressive atrophy via lipotoxicity, while insulin deficiency (SIDD) precipitates acute edema driven by hemodynamic oncotic failure. These findings establish retinal morphometry as a sensitive biomarker for systemic metabolic phenotyping, supporting a precision medicine approach to diabetic retinopathy.

Aim: to evaluate the histomorphology of the eyes of rabbits with experimental autoimmune uveitis (EAU) of varying severity.

Materials and Methods: The study was conducted on 30 Chinchilla rabbits with EAU, which were divided into two groups according to the severity of the disease. Histomorphological examination of the rabbit eyes was performed.

Results: In general, the inflammatory process can be characterized as a humoral-type hypersensitivity reaction. An inflammatory process was observed, predominantly affecting the inner ocular layers – mainly the choroid and retina. Inflammatory changes in the iris were sporadic, minimal, and primarily consisted of a few scattered lymphocyte-like cells. In the ciliary body, inflammation predominantly involved the ciliary processes. Damage to the retinal pigment epithelium was predominantly observed in the optical part. The involvement of the choroidal vasculature was evident, accompanied by stromal exudation. Retinal alterations predominantly involved the inner layers. The bipolar and ganglion cell layers were essentially destroyed, while the photoreceptor layer was largely preserved. Destruction of the retinal pigment epithelium was associated with damage to Bruch’s membrane.

Conclusion: Overall, histomorphological alterations in EAU showed a time-dependent progression, peaking between Days 3 and 10, particularly in moderate and severe cases. Although inflammatory activity decreased from Day 14 onward, complete morphological recovery was not observed. Persistent intergroup differences indicate sustained, partially irreversible ocular tissue damage associated with disease severity.

Key words: histomorphology, experimental model, autoimmune uveitis, tissue damage

UDC 616.37-002-036.11-06-07:616.37-031.63.-008.8-091.8-07

 Abstract. Purpose. To study the character and peculiarities of cytomorphological changes of cellular
sediment material of fluid collections (FC) as criterion for objective assessment of the clinical course
severity in acute complicated pancreatitis (ACP).
Materials and methods. The results of cytological researches of peripancreatic sediments of FC
obtained during interventional ultrasonography in 51 (88%) and videolaparoscopy in 7 (12%) observations in 58 patients on ACP were analysed.
Results. It was found that in intraabdominal FC (n=37) in 10 (27%) cases the dominating of proliferative mesothelium with its polymorphism was observed. In 15 cases (41%) degenerative-dystrophic
changes of cytoplasm whippings with the appearance of large “ring-similar” cells were manifested. In
12 studies (32%), atypically altered mesothelium cells with anisocytosis and anisonucleosis, as well as
cytomorphological changes similar to the neoplastic process were detected. In retroperitoneal localization
of FC (n=21) more significant changes were observed in granulocyte-nuclei cells, in particular, in 9 cases
(43%), irreversible violations of their structure were identified as phenomena of cariopicnosis, carioresix
and cariolysis. Was established that depth of structural changes of mesotheliocyte cells and neutrophil
granulocytes depended on degree of ACP severity.
Conclusions. Estimation of cytomorphological changes of the FC cell components can serve as objective criterion of the ACP severity.
Key words: acute complicated pancreatitis, fluid collections, cytological research.

UDC 616.37-002-036.11-06-089-085.456.7

Abstract.

Aim – to evaluate the effectiveness of early enteral nutrition (EEN) in patients with acute complicated pancreatitis (ACP), including clarification of its therapeutic rationale and optimization of administration strategies.Materials and Methods. The outcomes of EEN were analyzed in 82 patients with ACP, including 28(34%) with moderately severe disease and 54(66%) with severe disease. Two patient groups were identified: the main group (n=58), in whom EEN was implemented as a part of comprehensive treatment during preoperative and postoperative periods, and the comparison group (n=24), which received conventional treatment.EEN was performed using various methods: placement of a probe during esophago-gastro-duodenoscopy into the proximal part of the small intestine (n=25), suboperative nasogastrointestinal intubation of the small intestine (n=12), and also the formation of a suspended jejunostoma according to Witzel technique (n=21). nutritional formulas were used in combination with the probiotic Saccharomyces boulardii (I-745) and the metabolic modulator – citrulline malate, including according to the original method.Commercially available enteral Results. The positive effect of the implemented EEN methods was manifested by a more rapid recovery of the motor-evacuatory function of the small intestine, normalization of leukocyte counts and blood protein levels, and attenuation of microstructural changes in the intestinal mucosa. In particular, a reduction in the number of necrotized villi was observed, from 16 (94%) to 5 (29%) (χ² = 12.454; p = 0.004). Decreasing of the frequency of basal/apical enterocyte membrane detachment – from 15 (88%) to 6 (35%) (χ² = 7.971; p = 0.004), and erosive changes – from 13 (76%) to 5 (29%) (χ² = 5.785; p = 0.01) was observed, as well as cleansing of purulent-necrotic focus.Conclusions. EEN represents an effective component of the surgical management of patients with ACP during both the preoperative and postoperative periods.Enteral nutrition via Witzel-type jejunostomy demonstrated the highest efficacy and was fully aligned with contemporary principles of surgical patient management within– «Fast-Track» – surgery.Key words: acute complicated pancreatitis, early enteral nutrition

ABSTRACT
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).

Material and methods:
A study examined 102 individuals with T2DM and DR, divided into three groups: non-proliferative DR (35), preproliferative DR (34), and proliferative DR (33), with 61 as controls. Standard ophthalmological exams and enzyme-linked immunosorbent assays were conducted. Alleles rs1800470 were determined using polymerase chain reaction. Statistical analyses were done using MedStat and MedCalc v.15.1.

Results:
Results showed rs1800470 A/A carriers had worse visual acuity and higher retinal thickness than G/G carriers. TGF-β1 and CTGF levels in DR patients were significantly higher than in controls, especially in G/A and A/A carriers. TGF-β1 levels were highest in proliferative DR, and CTGF levels increased in A/A carriers compared to G/A and G/G carriers.

Conclusions:
Thus, the content of both TGF-β1 and CTGF was higher in carriers of the G/A and A/A genotypes compared with the ancestral G/G genotype. Therefore, the clinically worse course of DR in carriers of the SNP rs1800470 of the TGFB1 gene could be associated with a higher concentration of TGF-β1 and CTGF in the IOF of such patients.