Aim - an appropriate experimental model is required to investigate the development of chronic heart failure in the elderly and to evaluate pharmacological interventions. Models based on aged animals remain insufficiently characterized. To assess the degree of impairment in myocardial contractility and morphological changes in vital organs in 24-month-old rats with isoproterenol-induced chronic heart failure. Chronic heart failure was induced in 24-month-old male Wistar rats (550-600 g) by subcutaneous injections of isoproterenol hydrochloride (ISO; Sigma-Aldrich, USA). Animals in the experimental group (n=7) received ISO at a dose of 10 mg/kg four times at 3-day intervals. Control animals (n=7) received equivalent volumes of saline according to the same protocol. Sixty days after the final injection, cardiac pump function was assessed in isolated hearts using the Langendorff perfusion technique. Tissue samples from the myocardium, kidneys, lungs, and brain were fixed in formalin, stained with hematoxylin and eosin, and subjected to histopathological examination. Cardiomyocyte myofibrillar structure was evaluated using polarization microscopy. Heart rate was significantly higher in the experimental group compared with controls. At the same time, no statistically significant differences were observed in contractility parameters of isolated perfused hearts between the groups. Histological examination of myocardial, renal, pulmonary, and brain tissues revealed changes characteristic of chronic heart failure. Repeated administration of ISO (10 mg/kg, four injections) induces a compensated chronic heart failure phenotype in 24-month-old rats by day 60, characterized by morphological alterations in the myocardium and multiple organs in the absence of myocardial contractile dysfunction.

A retrospective study included 171 patients with acute coronary syndrome who underwent primary percutaneous coronary intervention between 2019 and 2023. Elderly and long-lived patients with ST-ECS and NSTE-ACS are characterized by significant comorbidity, with significantly more severe coronary pathology, as measured by the Syntax Score. In-hospital and long-term mortality were significantly higher in patients over 75 years of age. However, the incidence of late stroke and bleeding did not differ statistically between the study groups. Patients 75 years and older are a complex, heterogeneous group with a very high risk of in-hospital and long-term mortality, requiring a balanced and individualized approach from medical personnel at all stages of treatment.

The analysis of the progression of chronic kidney disease (CKD) and cardiovascular events was performed in 318 patients aged 80 years and older during 12 months after myocardial infarction (MI). Patients were divided into 2 groups: with CKD (n=164) and without CKD (n=154). It was found that in patients with CKD, the urinary concentration of KIM-1 and the level of microalbuminuria (UACR) were significantly higher and remained elevated during the year, correlating with the rate of eGFR decline (r=-0,47; p<0,01) and NT-proBNP level. The median time to cardiovascular event in the CKD group was 198 [112; 289] days versus 312 [245; 358] days in the comparison group (p<0,001). The risk of the composite endpoint (death, recurrent MI, stroke) in the CKD group was 2,9 times higher (p<0,001). Independent predictors of adverse outcomes were KIM-1 >1,5 ng/ml (HR=2,3), UACR >30 mg/g (HR=2,1) and anemia (HR=1,8). The obtained data confirm that KIM-1 and microalbuminuria are significant predictors of adverse renal and cardiac prognosis in geriatric patients.

The presence of aortic valve defects in patients is associated with a more severe course of coronary heart disease and heart failure. This article examines the impact of aortic valve defects on the risk of developing and progressing coronary heart disease. The study was conducted based on a retrospective statistical assessment of own clinical experience (a sample of 193 patients in whom the most significant indicators of cardiac function and hemodynamics were determined) and literature data. A significant decrease in the heart's ability to relax and, consequently, greater severity of diastolic dysfunction, manifested by an increase in the size of the left atrium and the diastolic diameter of the LV, were found in patients with aortic valve defects. A relationship between aortic valve defects and the presence of multivessel atherosclerotic lesions was established. For all parameters, p<0,05. The presence of aortic valve defects negatively impacts the course of coronary artery disease, leading to disruption of myocardial structure and function. This fact must be taken into account when assessing the severity of the disease, choosing treatment strategies, and determining the patient's prognosis.

Biotechnology in modern medicine and pathology encompasses molecular diagnostics, multi-omics analysis, nanotechnology-enabled platforms, digital pathology, bioinformatics, and computational approaches that support disease detection, therapeutic development, and clinical decision-making. This review examines how these technologies have contributed to diagnostic workflows, therapeutic development, disease classification, and clinical decision-making in contemporary healthcare. The integration of molecular biology, nanotechnology, and computational sciences has expanded the evaluation of disease-related processes such as genetic variation, biomarker expression, tumor heterogeneity, immune regulation, and molecular pathway alterations in conditions including cancer, inherited disorders, infectious diseases, cardiovascular disease, and autoimmune disease. Therapeutic innovations such as gene editing, nanomedicine, immunotherapy, biologics, and targeted drug delivery systems have further supported mechanism-based treatment strategies by improving tissue targeting, reducing off-target toxicity, and enabling more individualized therapeutic planning. Artificial intelligence (AI) and bioinformatics approaches, including machine learning, deep learning, computational pathology, digital whole-slide image analysis, and omics-data integration, have supported biomarker discovery, disease classification, diagnostic image analysis, risk stratification, and pathology-based clinical decision support. Additionally, molecular and digital pathology have improved disease subclassification and prognostic assessment by integrating histomorphologic findings with molecular and computational data. Despite these advances, high costs, technical complexity, data standardization challenges, infrastructure limitations, and ethical concerns continue to restrict widespread clinical adoption. Future work should prioritize low-cost point-of-care molecular and biosensor platforms for resource-limited settings, interoperable standards for omics and digital pathology data, multicenter prospective validation of AI-assisted diagnostic tools and nanomedicine-based therapies, transparent reporting of algorithm provenance, and regulatory pathways addressing data privacy, clinical accountability, and equitable access. Overall, biotechnology represents an important component of precision healthcare, with the potential to strengthen diagnostic accuracy, targeted therapy, disease monitoring, and patient-centered clinical outcomes.

Orthostatic hypertension is an under-recognized abnormal blood pressure phenotype defined by a paradoxical increase in systolic blood pressure after standing. Consensus definitions describe an exaggerated orthostatic pressor response as a systolic blood pressure increase of at least 20 mmHg after standing, with orthostatic hypertension present when standing systolic blood pressure reaches at least 140 mmHg. Although orthostatic hypertension has been associated with adverse cardiovascular and cerebrovascular outcomes, acute symptomatic presentations resembling a hypertensive emergency remain poorly characterized.

This study describes the clinical characteristics, hemodynamic profile, management, and follow-up outcomes of hospitalized patients with symptomatic orthostatic hypertensive emergency in the setting of severe obesity and obesity-related heart failure with preserved ejection fraction (HFpEF).

We conducted a single-center retrospective observational study of hospitalized adult patients evaluated by cardiology who had orthostatic blood pressure measurements obtained during routine clinical care. Patients were included if they had an orthostatic systolic blood pressure increase of at least 20 mmHg from supine to standing, a standing systolic blood pressure of at least 140 mmHg, and associated neurological or cardiac symptoms. Patients were excluded if they were critically ill, unable to stand, or receiving vasopressor therapy or lacked complete orthostatic blood pressure documentation. Demographics, comorbidities, symptoms, blood pressure values, echocardiographic findings, cardiac catheterization results when available, treatment strategies, lifestyle adherence, weight change, and follow-up outcomes were abstracted from the medical record.

Seven patients met the inclusion criteria. The median age was 56 years, and body mass index ranged from 44.1 to 78.2 kg/m². Initial orthostatic systolic blood pressure increases ranged from 21 to 44 mmHg, with a peak standing systolic blood pressure ranging from 148 to 194 mmHg at index presentation. One patient later developed recurrent severe orthostatic hypertension, with systolic blood pressure increasing from 109 mmHg supine to 188 mmHg standing. Presenting symptoms included dyspnea, chest pain, pulmonary edema, syncope or near-syncope, confusion, and stroke-like symptoms. All patients had severe obesity and clinical features consistent with obesity-related cardiometabolic disease and HFpEF. Patients who adhered to structured cardiometabolic lifestyle and medical therapy demonstrated weight loss and improvement or resolution of orthostatic symptoms and blood pressure abnormalities. Patients who were non-adherent experienced persistent symptoms, recurrent hospitalization, or loss to follow-up.

 Orthostatic hypertensive emergency may represent an under-recognized acute phenotype of postural blood pressure dysregulation in patients with severe obesity, cardiometabolic disease, and HFpEF. Routine orthostatic blood pressure assessment in hospitalized patients with obesity-related heart failure symptoms may improve the recognition of clinically significant blood pressure variability. The very small sample size of our experience serves as a hypothesis-generating report. Larger prospective studies are needed to define prevalence, prognosis, mechanisms, and optimal treatment strategies.

Atherosclerosis progression is driven by the plasticity of plaque macrophages, making the suppression of M1-like macrophage polarization a promising therapeutic goal. While inhibiting the M1-regulator microRNA-155 (miR-155) is a viable strategy, its clinical application is limited with inadequate systemic bioavailability and off-target organ damage. Herein, we developed YC/ANM-155, an orally delivered biomimetic system that utilizes yeast microcapsules (YC) to specifically transport AntagomiR-155 (ANM-155) to aortic plaques. This targeted strategy demonstrated superior efficacy compared to free ANM-155 in alleviating the atherosclerotic burden. Mechanistically, the treatment suppressed local miR-155 expression, inhibited M1-like macrophage polarization, and downregulated key pro-inflammatory cytokines at both the lesional and systemic levels. Complementary in vitro studies showed that miR-155 inhibition reduced M1-like macrophage polarization and attenuated inflammatory activation. The formulation showed improved stability under simulated gastrointestinal conditions and favorable biosafety under the present experimental settings. Collectively, our findings suggest that yeast-mediated oral delivery of miRNA antagomirs may serve as a promising preclinical strategy for RNA-based AS therapy and warrant further evaluation in larger-scale preclinical models.

Urolithin A (UA) is an important bioactive metabolite generated by the gut microbiota from ellagic acid and ellagitannins. In recent years, it has attracted widespread attention because of its potential value in aging intervention and the prevention and treatment of multisystem diseases. This review systematically summarizes the molecular mechanisms of UA, its effects in disease intervention, and progress in human clinical studies. Existing studies have shown that, with mitochondrial quality control as the core, UA exerts multi-target biological effects through the synergistic regulation of pathways related to inflammatory responses, oxidative stress, mitophagy, and programmed cell death. Findings from in vitro mechanistic studies and animal models suggest that UA may influence pathological processes relevant to degenerative musculoskeletal diseases, cardiovascular diseases, neurological disorders, and cancers, whereas current human clinical evidence remains preliminary and is mainly concentrated in muscle function, exercise-related outcomes, selected metabolic biomarkers, and short- to medium-term safety and tolerability. In addition, this review discusses the bioavailability of UA and its relationship with individual gut microbiota metabolic phenotypes. Future research should focus on high-quality, long-term randomized controlled trials with extended follow-up to promote the application of UA in precision nutrition and its clinical translation.

Congenital esophageal stenosis is a rare and heterogenous malformation often associated with esophageal atresia (EA). Failure of conservative endoscopic treatment leads to surgery. Transthoracic approach is rarely advocated due to the peridiaphragmatic localization of the stricture. Robotic-assisted thoracoscopic surgery (RATS) may offer enhanced precision in confined spaces; its application in patients under 10 kg is still considered a challenge. We report the first description of RATS resection of cartilaginous congenital stenosis and esophagoesophagostomy in a 9.5 kg patient. A female patient with a history of EA type III was corrected via videothoracoscopy, two cardiac surgeries via sternotomy, and laparoscopic treatment of duodenal atresia. During weaning, she did not tolerate thickened food, and endoscopy revealed a patent anastomosis but a distal esophageal stricture. A course of pneumatic dilation was attempted. Persistent clinical and radiological findings indicated the need for surgery. At 15 months, the patient underwent three-trocar thoracoscopy with the da Vinci Xi system. Esophagoscopy helped the identification of the stricture. A longitudinal incision exposed a 2-cm segment of thickened esophageal wall requiring complete excision. A tension-free end-to-end anastomosis was performed using 4/0 PDS. Tracheobronchial remnants were confirmed at histopathologIcal finding. Esophageal contrastography demonstrated a good diameter anastomosis. One month after the operation, she was able to swallow solid food. Surgery for congenital stenosis is indicated when endoscopic management fails. RATS for esophageal diseases in patients under 10 kg is feasible, and peridiahragmatic esophagus particularly suits to this technique. Previous accesses to the thorax seems not to be a limitation.

Ischemic stroke (IS) is a complex cerebrovascular disease with multifactorial etiology and pathological mechanisms, characterized by high morbidity, disability, and mortality rates. Although mechanical thrombectomy, intravenous thrombolysis, and neuroprotective interventions have improved acute management, effective brain-targeted delivery remains limited by the blood-brain barrier, short therapeutic windows, heterogeneous ischemic lesions, and secondary injury after reperfusion. Biomimetic nanomedicines have emerged as promising platforms for IS therapy because they can inherit biological functions from cell membranes, extracellular vesicles, or endogenous ligands, thereby improving biocompatibility, immune evasion, circulation stability, and lesion targeting. However, their clinical translation is still constrained by biosafety and immunogenicity concerns, uncertain pharmacokinetics and reproducible large-scale manufacturing, quality control, and regulatory requirements. Moreover, the balance between drug-loading capacity and target release efficiency remains a key challenge. Excessive cargo loading may compromise nanocarrier stability, whereas insufficient loading may fail to achieve therapeutic efficacy. Therefore, rational nanocarrier design for IS should coordinate brain accumulation, stable systemic circulation, lesion-selective activation, efficient loading, and controllable release. In this review, we discuss how stimuli-responsive biomimetic nanomedicines exploit pathological cues such as reactive oxygen species, acidosis, enzymes, inflammatory mediators, or external stimuli for spatiotemporally controlled therapy and combined therapy. This review critically summarizes IS pathophysiology, major biomimetic nanocarrier types, and the design principles and response mechanisms of stimuli-responsive biomimetic systems. Finally, current limitations and future directions are discussed, with emphasis on biosafety evaluation, standardized characterization, scalable manufacturing, clinically relevant models, and rational integration of precision-responsive designs to accelerate translation.