Medical Research" is a peer-reviewed scientific journal of the Faculty of Medicine of the University of Belgrade, which was first published in 1971, that is, half a century ago. The journal "Medical Research" is primarily dedicated to publishing the results of the scientific research work of teachers and associates of the Faculty of Medicine, as well as other scientists in the field of biomedical research. The journal "Medical Research" publishes scientific papers in English with an abstract in Serbian and has an open access policy. It is published three times a year, while the fourth volume also publishes summaries of the presentations at the "Aspirations and Innovations in Medicine" symposium. Original and previously unpublished works are published in the journal "Medical Research": a. original works in which the results of own research are published for the first time; b. review papers (Review), critically and originally presented (with self-citations); c. presentations of patients and cases (Case report). The works published in the journal "Medical Research" belong to the fields of: basic biomedical research, clinical research and preventive medicine. For the purpose of expert review of submitted papers, the Editorial Board of the journal is divided into three sections: basic, clinical and preventive sciences, and their work is coordinated by the Section Editors. The section for statistical data analysis will be involved in the evaluation of the statistical data of the submitted works.
Medicinski fakultet Univerzitet u Beogradu
Nasal Polyposis: An Overview of Etiology, Diagnosis, and Modern Treatment Options
Chronic rhinosinusitis with nasal polyps (CRSwNP) is a chronic, heterogeneous inflammatory disease associated with substantial impairment of nasal breathing, olfaction, and patients’ quality of life. Its etiology and pathogenesis are multifactorial and involve epithelial barrier dysfunction, impaired mucociliary clearance, dysbiosis, biofilm formation, Staphylococcus aureus, eosinophilic/type 2 inflammation, local IgE production, tissue remodeling, environmental factors, and numerous comorbidities. The coexistence of asthma and intolerance to aspirin and/or nonsteroidal anti-inflammatory drugs is particularly important within the unified airway concept. Diagnosis is established by correlating characteristic symptoms with objective findings obtained by clinical and/or endoscopic examination of the nose and computed tomography of the paranasal sinuses. Assessment of disease severity, comorbidities, and relevant differential diagnoses is essential. The cornerstone of treatment is intranasal corticosteroid therapy and nasal saline irrigation, whereas systemic corticosteroids, endoscopic sinus surgery, and biologic therapy are reserved for more severe, recurrent, or uncontrolled disease. The diagnostic and therapeutic approach to CRSwNP requires differentiation between disease phenotypes and endotypes, recognition of type 2 inflammation, active management of associated conditions, and continuous monitoring of treatment response based on symptoms, endoscopic findings, quality of life, and the need for additional interventions. This review summarizes current evidence on the etiology, pathogenesis, clinical presentation, quality of life, diagnostic criteria, and modern treatment options for CRSwNP, based on systematic reviews, clinical guidelines, and original studies. An individualized approach, adequate control of local disease and comorbidities, and regular follow-up are key to improving long-term treatment outcomes.
Burden of tuberculosis in Europe due to migrant crisis: urgent integration of global health perspectives into national TB control program
Global migration has increased in recent decades owing to war, conflict, persecution and natural disasters, but also secondary to increased opportunities related to work or study. Migrants’ risk of tuberculosis (TB) differs depending on migration, socioeconomic status, mode of travel and TB risk in transit, TB incidence and healthcare provision in country of origin. A narrative review summarized current evidence on the diagnosis of active TB in migrants entering the European Union/European Economic Area and UK, including clinical presentation and diagnostic delay, treatment outcomes of drug-susceptible TB and multidrug-resistant/ rifampicin-resistant TB, prevalence and TB/ humam immunodeficiency virus (HIV) co-infection. We documented that migrants had higher vulnerability for TB, including an increased risk of extrapulmonary TB, multidrug-resistant/rifampicin-resistant TB, TB/HIV co-infection and worse TB treatment outcomes compared to host populations. Consensus recommendations include screening migrants for TB/latent TB infection according to country data, a minimal package for TB care in drug-susceptible and multidrug-resistant/rifampicin-resistant TB, implementation of migrant-sensitive strategies and free healthcare and preventive treatment for migrants with HIV co-infection. Dedicated care for TB prevention and treatment in migrant populations within the European Union/European Economic Area and UK is essential. Key words: tuberculosis, migrants, multi-drug resistance, HIV
Predictive Value of CT Morphological Features For Metastatic Risk Stratification of Gastrointestinal stromal tumors: Independent Dual- Reader Analysis
Background: Gastrointestinal stromal tumors (GISTs) exhibit variable biological behavior, from indolent lesions to aggressive tumors with metastatic potential. Preoperative risk assessment is important for treatment planning. Therefore, this study evaluated the predictive value and reproducibility of CT morphological features in identifying high-risk GISTs using independent dual-reader analysis. Materials and Methods: This retrospective study included 26 patients with histopathologically confirmed gastric GISTs who underwent biphasic contrast-enhanced MDCT. Two radiologists independently evaluated CT morphological features, including tumor size, mucosal integrity, internal structure, shape, growth pattern, and enlarged feeding or draining vessels (EFDV). Based on disrupted mucosa and EFDV, tumors were stratified into high-risk (HR) and low-risk (LR) groups and correlated with histopathological findings. Results: Histopathological analysis confirmed HR GISTs in 10 and LR GISTs in 16 patients. Excellent interobserver agreement was observed for mucosal integrity (κ=0.843) and tumor structure (κ=0.923), with substantial agreement for EFDV, shape, growth pattern, and predicted risk. Both radiologists demonstrated high sensitivity (90%) for identifying HR GISTs. Larger tumor size, disrupted mucosa, heterogeneous structure, irregular shape, endophytic growth, and EFDV were associated with HR tumors, although specificity remained limited due to overlapping imaging features. Conclusion: CT-derived morphological features are valuable imaging biomarkers for preoperative risk stratification of gastric GISTs. Disrupted mucosa and enlarged peri-/intratumoral vessels were the strongest predictors of high-risk tumors. Despite overlapping imaging features between low- and high-risk lesions, conventional CT analysis may aid in identifying aggressive tumors and guiding treatment planning.
CLINICAL SPECTRUM AND MANAGEMENT OUTCOMES OF SUPRARENAL MASSES IN INFANTS: A 17-YEAR TERTIARY CENTER EXPERIENCE
Introduction/Aim: The detection of suprarenal masses (SRM) in neonates and infants has increased due to widespread prenatal and postnatal ultrasonography. While surgery was historically the standard treatment, a conservative approach is now advocated for small, asymptomatic masses. This study aimed to analyze the management and clinical outcomes of SRM at a single tertiary care center over the last two decades. Material and Methods: Retrospective analysis of 39 patients diagnosed with SRM between 2006 and 2023 was conducted. Clinical, radiological (US, CT, MRI), and laboratory data (urinary VMA/HVA, NSE) were evaluated. The follow-up protocol consisted of ultrasonography every two weeks during the first three months of age, followed by monthly or quarterly evaluations until complete resolution, with a median follow-up of 16.6 months (range: 1.9–89). Patients were managed via upfront surgery or a conservative protocol. Results: SRM larger than 5 cm were identified in 18% of patients (7/39), out of which five underwent surgery confirming neuroblastoma (NBL) and in remaining two patients spontaneous resolution of mass occurred. For the 32 patients with masses smaller than 5 cm, a conservative approach was initially adopted. Eight of these patients (25%) eventually required surgery, due to elevated urinary catecholamines, which proved to be a reliable indicator of NBL. Complete regression was observed in all other cases managed conservatively. Conclusion: Close observation of small SRM is safe in carefully selected patients and effectively reduces unnecessary surgical interventions. Urinary catecholamine metabolites remain a valuable tool for identifying high-risk patients requiring surgical treatment.
BK POLYOMAVIRUS (BKPyV) INFECTION IN RENAL TRANSPLANTATION: VIRAL CHARACTERISTICS, DIVERSITY, REACTIVATION, RISK FACTORS AND LABORATORY DIAGNOSIS
BK polyomavirus (BKPyV) is a ubiquitous human polyomavirus, and more than 80% of the human population is seropositive for BKPyV. Following primary infection, which is usually asymptomatic, BKPyV establishes lifelong persistence in renal epithelial cells. In recent years, the use of potent immunosuppressive drugs after transplantation has led to an increasing incidence of BKPyV reactivation in patients with organ transplants, placing BKPyV among the major risk factors for graft loss in kidney transplant recipients. This review provides an overview of BKPyV infection in the context of renal transplantation from a virologist's perspective. The first part of the review covers basic virology, including virion structure, genome organisation, life cycle, mechanisms of lifelong BKPyV persistence, and basic epidemiology. The meeting points of basic and clinical virology are explained through BKPyV diversity and its clinical implications. The clinical aspects are discussed, including donor- and recipient-related risk factors for BKPyV reactivation, the clinical importance of BKPyV subtyping, and serotype-specific immunity. In the second part of the review, emphasis is placed on the possibilities of laboratory diagnostics of BKPyV infection. Finally, the review provides current international recommendations for screening and monitoring of BKPyV infection in the post-transplant period. By combining virological, clinical, and diagnostic aspects, this review highlights the complexity of BKPyV infection after kidney transplantation, underscoring the need for optimised monitoring strategies, further research into the clinical importance of viral diversity, and improvements in therapeutic protocols to control BKPyV infection after kidney transplantation.
Editorial for the second issue of volume 59 of the medical journal “Medical Research”
SNAKE BITE WITH A FATAL OUTCOME IN WESTERN SERBIA – A RARE CASE REPORT
Introduction: Snakebites can lead to a wide range of clinical manifestations, from local tissue effects to systemic complications, including rhabdomyolysis, coagulopathy, acute kidney injury, neurological, and cardiac events. Although snakebites in Western Serbia are generally not a major public health issue, severe cases may occur, with potentially fatal outcomes. Patient review: We report the case of a 71-year-old man bitten by Vipera ammodytes in ####, Western Serbia. He presented with fatigue, vomiting, and swelling of the left hand one hour after the bite. His past medical history included diabetes mellitus, ischemic stroke, and cerebral aneurysm repair. On admission, he was hypotensive and dehydrated, with a local hematoma and thrombocytopenia. He received antivenom, corticosteroids, dopamine, antibiotics, and supportive care. Despite initial stabilization, the patient developed acute respiratory distress, acute kidney injury, hypotension, and peripheral cyanosis, requiring mechanical ventilation and dual inotropic support. Laboratory findings indicated coagulopathy and rising markers of organ injury. Despite intensive management, the patient succumbed to complications. Conclusion: This represents the first reported fatal snakebite in Western Serbia in the past 30 years. The primary pathogenic mechanism was likely disseminated intravascular coagulation triggered by the venom. This case highlights the importance of prolonged clinical and laboratory monitoring, timely supportive therapy, and awareness of severe systemic complications following snakebites, even in regions with historically low incidence.
Distant Metastasis–Free Interval and Overall Survival in Breast Sarcoma: A Single-Institution Retrospective Study
Background: Breast sarcomas (BS) are rare malignant tumors with aggressive behavior and limited evidence guiding outcome assessment. Data on distant metastasis–free interval (DMFI) in this population are scarce. This study aimed to describe oncologic outcomes and to explore clinicopathologic factors associated with DMFI and overall survival (OS) in patients with BS treated with curative intent. Methods: Patients with primary or secondary breast sarcoma treated at a single tertiary cancer center between 2013 and 2025 were retrospectively analyzed. Patients with metastatic disease at diagnosis were excluded. DMFI was the primary endpoint and OS was secondary. Survival was estimated using Kaplan–Meier methods and compared with log-rank tests. Exploratory receiver operating characteristic analyses were performed for descriptive stratification. Results: Twenty-six patients met inclusion criteria. Angiosarcoma was the most common histologic subtype, predominantly occurring as secondary disease after prior breast radiotherapy. Median DMFI was not reached during follow-up, with 71.5% of patients remaining metastasis free at 3 years, whereas median OS was 31 months with a 3-year OS of 46.9%. Shorter DMFI was associated with higher pathological T stage, larger tumors, tumor necrosis, younger age, and narrower resection margins. Overall survival was significantly associated only with resection margins, which was the sole variable related to both DMFI and OS. Exploratory Cox regression analyses were inconclusive because of limited event numbers. Conclusions: Tumor burden–related factors, tumor necrosis, and surgical margin width were associated with metastasis-related outcomes and survival in breast sarcoma. Adequate surgical resection remains critical in this rare and heterogeneous disease.
INTRAVENOUS IRON THERAPY IN HEART FAILURE WITH REDUCED EJECTION FRACTION: EVIDENCE FROM RECENT TRIALS AND META-ANALYSES
Anemia is a frequently observed comorbidity in patients with heart failure (HF) and contributes to increased morbidity and mortality. Even though the etiology of anemia in HF patients is polymorphic, chronic inflammation and iron deficiency (ID) are reported as the most frequent underlying causes. Anemia is a strong prognostic marker in both acute and chronic HF, while ID, even in the absence of anemia, has a negative impact on patients’ symptoms, functional capacity, and quality of life (QOL). In chronic HF, functional ID is often present due to impaired iron utilization, but it may coexist with absolute ID, where iron stores are depleted. Intravenous (IV) iron therapy, has shown its beneficial effect in improving functional status, reducing symptoms, and lowering the rate of hospital readmissions. This has led to its inclusion in the latest guidelines of the European Society of Cardiology (ESC) as a recommended treatment for symptomatic patients with heart failure with reduced ejection fraction (HFrEF). Several studies have also described a consistent trend toward reduced mortality. The aim of this paper is to summarize current knowledge on the importance of ID and the therapeutic effects of iron supplementation in HFrEF patients. Timely recognition and correction of ID should be considered a cornerstone of individualized HfrEF management.
TARGETED DRUG DEVELOPMENT IN FRAGILE X SYNDROME: MOLECULAR MEDICINE AS A KEY TOOL IN CLINICAL PHARMACOLOGY
The full mutation and epigenetic silencing of the FMR1 gene lead to a deficiency of its protein, FMRP, resulting in Fragile X Syndrome (FXS). Although significant advances have been made in understanding the molecular mechanisms underlying FXS, no cure or targeted pharmacological treatments have yet been approved for this neurodevelopmental disorder. Current clinical management primarily relies on symptomatic therapies, which often offer limited benefits and do not address the core molecular causes of the condition, especially given the multifaceted roles of the FMRP. This review highlights the crucial role of molecular insights in guiding the development of drugs for FXS. It provides an overview of existing pharmacotherapies, discusses their benefits and limitations, and emphasizes the unmet need for interventions that target the specific pathways disrupted by FMR1 dysfunction. Recent and ongoing clinical trials were examined, focusing on how a deeper understanding of FXS molecular biology can inform the design of more effective and precise therapeutic strategies. In summary, key molecular pathways relevant to FXS are presented, and the potential synergy between clinical pharmacology and molecular medicine is discussed as a means to promote the advancement of tailored therapeutic approaches.
NINE MOST COMMON MISCONCONCEPTIONS IN THE DIAGNOSIS AND TREATMENT OF GLAUCOMA
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2 Accent 5"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 5"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 5"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 5"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light Accent 6"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 6"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 6"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 6"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 6"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful Accent 6"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful Accent 6"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hashtag"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Unresolved Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Link"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> Diagnosis and treatment of glaucoma have advanced significantly in the last 20 years, but there are still some misconceptions about this group of diseases in everyday ophthalmological practice. The goal of this review is to point out the most common misconceptions in the diagnosis and treatment of glaucoma, which should improve the quality of treatment for our patients. A review of research articles with key words glaucoma, misconception, intraocular pressure measurement, published in PubMed database until June 30th, 2025 was done. Some of the most common misconceptions in the diagnosis and treatment of glaucoma are related to the method of measuring intraocular pressure, the time when the measurement is performed, subtracting/adding values according to the nomogram for pachymetry, banning caffeine intake for glaucoma patients and recommendations for physical activity in all forms of glaucoma. While significant advancements have been made in the diagnosis and treatment of glaucoma, persistent misconceptions among ophthalmologists must be addressed to improve patient outcomes and quality of life.
Assessment of Left Main Coronary Artery Luminal Diameter Using Quantitative Coronary Analysis and Optical Coherence Tomography
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Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hashtag"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Unresolved Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Link"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> Introduction: Accurate assessment of left main (LM) coronary lumen dimensions is essential during percutaneous coronary intervention (PCI). Quantitative coronary analysis (QCA) is routinely used, yet its agreement with high-resolution intravascular imaging modalities such as optical coherence tomography (OCT) in the LM segment remains incompletely defined. Methods: Thirty patients who underwent LM PCI were evaluated using follow-up angiography and OCT. Eight matched lumen parameters were assessed using 2D QCA, 3D QCA, and OCT. Differences between modalities were analyzed using repeated-measures ANOVA for normally distributed variables and Friedman’s test for minimal lumen area (MLA). Linear correlations were assessed descriptively, and agreement was evaluated using Bland–Altman analysis. Results: Significant modality-dependent differences were observed across most lumen parameters. QCA demonstrated strong linear associations with OCT for reference- and mean-based lumen metrics, whereas correlations were weaker for extreme (minimal and maximal) dimensions. Bland–Altman analysis revealed minor mean differences between QCA and OCT but wide limits of agreement, indicating substantial inter-individual variability despite consistency at the group level. Conclusion: QCA provides reasonably consistent estimates of reference and mean lumen dimensions in the LM segment but shows limited association with OCT for extreme measurements. Despite strong linear associations, individual variability remains considerable, supporting OCT as the preferred modality for precise lumen assessment, stent sizing, and procedural optimization in LM PCI.
The effect of the most abundant bioactive compounds of the mediterranean diet on the osteoblast-mediated osteoclast differentiation signaling pathway: in silico analysis
Introduction: Bones are fundamental components of the skeletal system that continuously remodel throughout life. Osteoclasts are responsible for bone resorption, while osteoblasts form new bone matrix and indirectly influence osteoclast differentiation through signaling pathways involving molecules such as M-CSF, c-Fms, GRB2, ERK, PI3K, and Akt. To maintain bone health, increasing attention is being given to nutritional interventions, including the Mediterranean diet, which is rich in bioactive compounds. The aim of this study was to perform an in silico analysis of potential interactions between the most prevalent bioactive compounds of the Mediterranean diet and the key proteins of the osteoclast differentiation signaling pathway. Materials and Methods: A library comprising 115 predominant bioactive compounds from the Mediterranean diet was constructed based on literature data. Protein structures obtained via crystallography were used as targets in molecular docking simulations to predict interactions between ligands and receptors. Results: Most ligands did not show significant interactions with the investigated proteins (ΔG > −7 kcal/mol), except in the case of Akt protein. For this protein, a larger number of ligands demonstrated ΔG values < −7 kcal/mol. The five most potent ligands (salvianolic acid, apigenin, diosmin, mangiferin and sylbin) bound to amino acid sequences forming the active site of the receptor, indicating a potential inhibitory effect. Conclusion: The in silico analysis suggests that bioactive components of the Mediterranean diet possess potential to inhibit Akt protein (protein kinase B), thereby opening new perspectives for their application in modulating osteoclast activity and developing novel strategies for maintaining bone health.
THE ROLE AND SIGNIFICANCE OF CARDIAC MAGNETIC RESONANCE IN HYPERTROPHIC CARDIOMIOPATHY
Introduction: Hypertrophic cardiomyopathy (HCM) is an autosomal dominant disorder of cardiomyocytes that leads to myocardial thickening. Aims: The aims of this study were to establish the diagnosis of HCM in patients with hypertrophic left ventricle walls, to evaluate myocardial tissue, and to assess the degree of myocardial fibrosis using cardiac magnetic resonance (CMR). Material and Methods: The study included 51 patients diagnosed with HCM by CMR (27 males, 24 females) and was carried out in the University Clinical Centre of Serbia, Center of Radiology. All collected patient data was obtained from official medical documentation for this retrospective observational study. CMR confirmed HCM in 51 pts based on a standard imaging protocol performed on a 1.5T Siemens scanner, with the contrast agent Gadolinium. Regarding Late Gadolinium Enhancement (LGE) distribution, CMR enables the detection of focal fibrosis and helps to differentiate the etiology of the hypertrophied myocardium. Results: Left ventricular outflow tract obstruction was observed in 9 (17.6%) patients. Asymmetric HCM was noted in 41 (80.4%) patients. LGE presence was detected in 39 (76.5%) patients, most notably in the septal region (62.7%). The degree of fibrosis was estimated at a median of 6% of the left ventricular mass and a median of 11 grams of fibrosis per gram of left ventricular mass. Conclusion: CMR as a non-invasive method represents the gold standard for myocardial tissue characterization. The detection of myocardial fibrosis, a major trigger for the development of malignant arrhythmias, positions CMR as a risk stratification method in HCM patients.
The role of the optical coherence tomography angiography in diseases of the posterior segment of the eye
Optical coherence tomography angiography (OCTA) is a noninvasive, quantitative tool for imaging the retina and choroid, capable of visualizing the microvasculature in three dimensions. It is widely used for diagnosing and monitoring treatment response for various diseases of anterior and posterior segment of the eye. A systematic search of the relevant literature was conducted emphasizing a period of the most intensive development and clinical application of OCT angiography. This paper aims to summarize current knowledge regarding the applications of OCTA in the diagnosis and monitoring of posterior segment retinal pathologies, and to discuss its advantages over traditional imaging techniques.
PREOPERATIVE HEALTH-RELATED QUALITY OF LIFE IN PATIENTS UNDERGOING ELECTIVE SURGERY FOR COLORECTAL CANCER
Introduction/Aim: Health-related quality of life (HRQoL) is an important multidimensional, patient-centered concept in colorectal cancer (CRC). However, data on preoperative HRQoL in Southeast European surgical populations remain limited. The aim of this study was to describe preoperative HRQoL in patients undergoing elective surgery for CRC, compare HRQoL between colon and rectal cancer, and identify sociodemographic and clinical factors associated with preoperative HRQoL. Material and Methods: Preoperative HRQoL was assessed using the Functional Assessment of Cancer Therapy–Colorectal (FACT-C) and the Cleveland Clinic Colorectal Cancer Quality of Life questionnaire (CCF-CaQL). Sociodemographic and clinical data were collected using a structured questionnaire and medical records. Group comparisons were performed according to tumor localization, while factors associated with FACT-C total score were evaluated using univariable and multivariable linear regression. Results: The mean CCF-CaQL total score was 92.3±20.4, and the mean FACT-C total score was 98.8±18.2. No significant differences in HRQoL were observed between patients with colon and rectal cancer across any questionnaire domains (all p>0.05). In multivariable analysis, higher ASA physical status was independently associated with lower FACT-C total score (B=-5.05; 95% CI -9.70 to -0.40; p=0.033). Conclusion: Preoperative HRQoL in patients undergoing elective CRC surgery was moderate and did not differ significantly by tumor localization. Higher ASA physical status was independently associated with poorer preoperative HRQoL.
In silico investigation of the effects of gentamicin on lysosmal lipid degradation and the transport system between lysosomes and smooth endoplasmic reticulum
Introduction: Gentamicin, an aminoglycoside antibiotic has limited clinical use due to accompanying side effects: nephrotoxicity and ototoxicity. The damage caused by gentamicin accumulates over time and leads to cell death. Cells of renal proximal tubules are most affected, as are hair cells of the inner. One of the presumed mechanisms of toxicity is phospholipidosis, a disorder characterized by accumulation of phospholipids in the cell. The Aim: The aim of this study is to investigate, in silico, the mechanism of gentamicin action in the development of phospholipidosis through interactions with key proteins responsible for lipid transport between the smooth endoplasmic reticulum and late endosomes, as well as enzymes involved in lipid degradation. Material and Methods: We defined target proteins in the KEGG database and their expression profiles and tissue specificities were examined through the Human Atlas database. Nine proteins met the final criteria and were further examined by molecular docking using AutoDock Vina program. Results: Most of the examined proteins showed high expression in the kidney and corresponding structures of the central nervous system. Docking analysis indicated that the interaction between gentamicin and ORP1L protein exhibited the lowest Gibbs free energy value of - 8.1kCal/mol, while the STARD3 protein had the highest Gibbs free energy value of -5.2kCal/mol. Amino acid sequences to which gentamicin binds on the selected proteins were similar within the same protein families. Conclusion: Observed under in silico conditions, gentamicin interacts with proteins that participate in lysosomal lipid degradation and transport between lysosomes and smooth endoplasmic reticulum.
Telehealth for Adolescent Mental Health: A Narrative Review of effectiveness, acceptability, and ethical–legal considerations
Adolescents experience a high burden of mental health problems but face substantial barriers to care. Telehealth—encompassing synchronous teletherapy, telephone contacts, and digital mental health interventions (apps, internet CBT)—has expanded rapidly, especially since the COVID-19 pandemic. The primary purpose of this narrative review was to synthesize current evidence on the effectiveness, acceptability/engagement, clinical safety, and ethical-legal aspects of telehealth interventions in adolescent mental health, with attention to regional regulatory gaps. The reviewed data suggests that telehealth modalities (video, telephone, and digital interventions) can deliver clinically meaningful improvements for common adolescent conditions (depression, anxiety) and, in many settings, achieve outcomes comparable to those of treatment-as-usual. Acceptability among adolescents is generally high but variable and depends on privacy, platform usability, and perceived therapeutic relationship. Remote care raises distinct safety challenges (managing suicidality and crisis response), and the ethical-legal landscape remains underdeveloped in many regions: data protection, consent/assent rules for minors, professional licensure across jurisdictions, and reimbursement policies are recurrent concerns. The supplied reports emphasize important local/regional gaps—limited regulation, infrastructure barriers, and the need for formal protocols and clinician training. In conclusion, telehealth is a viable modality for adolescent mental health care when implemented with clear clinical protocols, robust data‑security safeguards, and attention to consent and crisis pathways. Policy action is required to standardize legal and ethical frameworks, ensure equitable access, and integrate telehealth within routine adolescent mental health services. Keywords: telehealth, adolescents, mental health
Changes in the hemostatic system in severely ill COVID-19 patients
Introduction/research objective: COVID-19 coagulopathy is a disorder of the hemostatic system that occurs in critically ill patients infected with the SARS-CoV 2 virus and increases the risk of mortality. The goal of the research is to evaluate changes in hemostatic parameters and determine their prognostic significance in patients with a severe form of the COVID-19 disease. Methods: The study was designed as a retrospective cohort study, which included 146 patients treated from June to September 2020 in the Intensive Care Unit (ICU) of the Clinical Hospital Center ”Bežanijska Kosa” in Belgrade, diagnosed with COVID-19 pneumonia. Inclusion criteria were age over 18 years, proven current SARS-CoV2 infection and admission to ICU. Results: 82 patients (56.2%) died during the treatment, while 64 (43.8%) were discharged. Significantly higher D-dimer values ​​on admission to the ICU were recorded in subjects who died during treatment 888 (1226.5)ng/ml compared to persons who were discharged from treatment 666 (1207.3)ng/ml (p = 0.03). Differences were not demonstrated for INR, aPTT and fibrinogen. D-dimer values ​​on admission to the ICU greater than or equal to 760ng/ml are a statistically significant predictor of death during hospitalization (p = 0.04). Conclusion: COVID coagulopathy is a complication that increases the mortality of people infected with the SARS-CoV2 virus. The main feature is a state of hypercoagulability, which is detected by elevated D-dimer values. D-dimer greater than or equal to 760 ng/ml on admission to the ICU may have prognostic significance for survival during hospitalization.
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THE IMPACT OF PHYSICAL ACTIVITY ON INTRAOCULAR PRESSURE: A REVIEW OF THE LITERATURE
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Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="List Continue 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="List Continue 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="List Continue 4"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="List Continue 5"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Message Header"/> <w:LsdException Locked="false" Priority="11" QFormat="true" Name="Subtitle"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Salutation"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Date"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text First Indent"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text First Indent 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Note Heading"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text Indent 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text Indent 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Block Text"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="FollowedHyperlink"/> <w:LsdException Locked="false" Priority="22" QFormat="true" Name="Strong"/> <w:LsdException Locked="false" Priority="20" QFormat="true" Name="Emphasis"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Document Map"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Plain Text"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="E-mail Signature"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Top of Form"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Bottom of Form"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Normal (Web)"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Acronym"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Address"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Cite"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Code"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Definition"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Keyboard"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Preformatted"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Sample"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Typewriter"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Variable"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Normal Table"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="annotation subject"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="No List"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Outline List 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Outline List 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Outline List 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table 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Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 4"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 5"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 4"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 5"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 6"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 7"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 8"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 4"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 5"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 6"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 7"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table List 8"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table 3D effects 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table 3D effects 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table 3D effects 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Contemporary"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Elegant"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Professional"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Subtle 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Subtle 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Web 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Web 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Web 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Balloon Text"/> <w:LsdException Locked="false" Priority="39" Name="Table Grid"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Theme"/> <w:LsdException Locked="false" SemiHidden="true" Name="Placeholder Text"/> <w:LsdException Locked="false" Priority="1" QFormat="true" Name="No Spacing"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading"/> <w:LsdException Locked="false" Priority="61" Name="Light List"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3"/> <w:LsdException Locked="false" Priority="70" Name="Dark List"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 1"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 1"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 1"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 1"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 1"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 1"/> <w:LsdException Locked="false" SemiHidden="true" Name="Revision"/> <w:LsdException Locked="false" Priority="34" QFormat="true" Name="List Paragraph"/> <w:LsdException Locked="false" Priority="29" QFormat="true" Name="Quote"/> <w:LsdException Locked="false" Priority="30" QFormat="true" Name="Intense Quote"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 1"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 1"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 1"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 1"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 1"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 1"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 1"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 1"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 2"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 2"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 2"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 2"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 2"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 2"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 2"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 2"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 2"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 2"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 2"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 2"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 2"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 2"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 3"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 3"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 3"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 3"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 3"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 3"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 3"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 3"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 3"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 3"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 3"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 3"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 3"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 3"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 4"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 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Name="Plain Table 4"/> <w:LsdException Locked="false" Priority="45" Name="Plain Table 5"/> <w:LsdException Locked="false" Priority="40" Name="Grid Table Light"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light Accent 1"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 1"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 1"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 1"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 1"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful Accent 1"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful Accent 1"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light Accent 2"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 2"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 2"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 2"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 2"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful Accent 2"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful Accent 2"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light Accent 3"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 3"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 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Locked="false" Priority="47" Name="Grid Table 2 Accent 5"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 5"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 5"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 5"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light Accent 6"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 6"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 6"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 6"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 6"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful Accent 6"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful Accent 6"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light Accent 1"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 1"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 1"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 1"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 1"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful Accent 1"/> 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<w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 5"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 5"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light Accent 6"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 6"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 6"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 6"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 6"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful Accent 6"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful Accent 6"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> Glaucoma is a chronic, progressive optic neuropathy and one of the leading causes of irreversible blindness worldwide. Intraocular pressure (IOP) remains the most important and only proven modifiable risk factor for the development and progression of glaucoma. Physical activity exerts a wide range of systemic effects that may directly or indirectly influence IOP and ocular perfusion. The effect of physical activity on IOP depends on the type, intensity, and duration of exercise, as well as individual patient characteristics. Aerobic exercise is consistently associated with acute IOP reductions of 1 to 5 mmHg, mediated by increased aqueous humor outflow, osmotic shifts, and sympathetic modulation of aqueous production. Long-term aerobic training may produce sustained baseline IOP reductions of approximately 2 to 4 mmHg, with concurrent improvements in ocular perfusion pressure. In contrast, high-intensity anaerobic and isometric exercise, as well as inverted body positions such as specific yoga postures, can transiently elevate IOP to clinically concerning levels, primarily through Valsalva maneuver-induced increases in episcleral venous pressure. The relationship between physical activity and ocular perfusion pressure further underscores the complexity of exercise-ocular interactions. The clinical significance of these findings lies in the potential application of physical activity as an adjunctive strategy in glaucoma management. Moderate aerobic exercise should be encouraged in most patients, while certain high-intensity activities and inverted positions should be carefully considered. Further research is needed to establish standardized guidelines and to better understand the long-term impact of physical activity on glaucoma progression.
Evolution of the SYNTAX score (I, II and II 2020): development, application and limitations in everyday clinical practice
Surgical myocardial revascularization is the gold standard for myocardial revascularization in chronic coronary syndrome (CCS). The first randomized trials comparing bare metal stent (BMS) implantation and aorto-coronary bypass graft surgery (CABG) resulted in similar mortality and myocardial infarction rate, and lower rate of repeat revascularization after CABG compared to BMS implantation, directed the development of drug eluting stents (DES) with the lower rate of clinical restenoses. Over the years, there was a need for objective assessment and calculation of risk and benefit of both surgical and percutaneous myocardial revascularization, and giving an advantage to one of these two methods, or equipoise for a specific patient. SYNTAX score I was used for the quantitative assessment of coronary stenoses complexity in a patient with CCS. However, two major flaws of the SYNTAX score I, (1) absence of the assessment of functional significance of coronary stenosis, and (2) absence of clinical variables that may influence perioperative mortality rate, were partially overcome with development of SYNTAX score II including clinical variables that showed the greatest association with mortality (age, creatinine clearance, left ventricular ejection fraction, unprotected left main coronary artery disease, female gender, peripheral vascular disease and chronic obstructive pulmonary disease) and SYNTAX score II 2020 predicting 10-year mortality rate. The SYNTAX score II and II 2020 potentially can change the recommendation for myocardial revascularization based on SYNTAX score I alone. This review focuses on development of these scores, their accuracy, predicitve value and limitations in practical applications in an individual patient with CCS.
Unilateral genu recurvatum: A case report
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Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hashtag"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Unresolved Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Link"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> Introduction: Genu recurvatum is characterized by knee hyperextension, gait instability, and pain. It is rarely encountered in routine orthopedic practice, and evidence regarding optimal treatment strategies remains limited. In this case, the absence of trauma, associated varus malalignment, and the unilateral presentation further increased the complexity, with progressive worsening observed over a three-year follow-up period. This report presents a rare case of unilateral genu recurvatum of unknown etiology, treated with corrective proximal tibial osteotomy and posterior tibial slope adjustment, along with postoperative outcomes and a brief review of the literature. Case Presentation: A 32-year-old male patient presented with unilateral genu recurvatum and an intact posterior cruciate ligament (PCL), confirmed by MRI and arthroscopy. Preoperative planning was based on MSCT analysis. An open-wedge proximal tibial corrective osteotomy with plate fixation was performed. Under C-arm–guided fluoroscopy, the planned correction and posterior tibial slope were achieved. The posterior tibial tilt increased from 94° to 101°, improving knee stability and correcting the deformity. Conclusion: Corrective proximal tibial osteotomy with posterior slope adjustment represents an effective treatment option for unilateral genu recurvatum of unknown etiology. This technique provides reliable mechanical axis correction, joint stabilization, and favorable clinical outcomes with relatively rapid postoperative recovery.
Ovarian Hyperstimulation Syndrome: Contemporary Approach to Pathophysiology, Risk Stratification, Prevention and Management
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UnhideWhenUsed="true" Name="Body Text First Indent 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Note Heading"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text Indent 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Body Text Indent 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Block Text"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="FollowedHyperlink"/> <w:LsdException Locked="false" Priority="22" QFormat="true" Name="Strong"/> <w:LsdException Locked="false" Priority="20" QFormat="true" Name="Emphasis"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Document Map"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Plain Text"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="E-mail Signature"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Top of Form"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Bottom of Form"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Normal (Web)"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Acronym"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Address"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Cite"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML Code"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="HTML 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SemiHidden="true" UnhideWhenUsed="true" Name="Outline List 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Simple 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Simple 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Simple 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Classic 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Classic 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Classic 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Classic 4"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Colorful 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Colorful 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Colorful 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 4"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Columns 5"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 1"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 2"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 4"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Grid 5"/> <w:LsdException 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Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Web 3"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Balloon Text"/> <w:LsdException Locked="false" Priority="39" Name="Table Grid"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Table Theme"/> <w:LsdException Locked="false" SemiHidden="true" Name="Placeholder Text"/> <w:LsdException Locked="false" Priority="1" QFormat="true" Name="No Spacing"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading"/> <w:LsdException Locked="false" Priority="61" Name="Light List"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3"/> <w:LsdException Locked="false" Priority="70" Name="Dark List"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 1"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 1"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 1"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 1"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 1"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 1"/> <w:LsdException Locked="false" SemiHidden="true" Name="Revision"/> <w:LsdException Locked="false" Priority="34" QFormat="true" Name="List Paragraph"/> <w:LsdException Locked="false" Priority="29" QFormat="true" Name="Quote"/> <w:LsdException Locked="false" Priority="30" QFormat="true" Name="Intense Quote"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 1"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 1"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 1"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 1"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 1"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 1"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 1"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 1"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 2"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 2"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 2"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 2"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 2"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 2"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 2"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 2"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 2"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 2"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 2"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 2"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 2"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 2"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 3"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 3"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 3"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 3"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 3"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 3"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 3"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 3"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 3"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 3"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 3"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 3"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 3"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 3"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 4"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 4"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 4"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 4"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 4"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 4"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 4"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 4"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 4"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 4"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 4"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 4"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 4"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 4"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 5"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 5"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 5"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 5"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 5"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 5"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 5"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 5"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 5"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 5"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 5"/> <w:LsdException Locked="false" Priority="71" Name="Colorful Shading Accent 5"/> <w:LsdException Locked="false" Priority="72" Name="Colorful List Accent 5"/> <w:LsdException Locked="false" Priority="73" Name="Colorful Grid Accent 5"/> <w:LsdException Locked="false" Priority="60" Name="Light Shading Accent 6"/> <w:LsdException Locked="false" Priority="61" Name="Light List Accent 6"/> <w:LsdException Locked="false" Priority="62" Name="Light Grid Accent 6"/> <w:LsdException Locked="false" Priority="63" Name="Medium Shading 1 Accent 6"/> <w:LsdException Locked="false" Priority="64" Name="Medium Shading 2 Accent 6"/> <w:LsdException Locked="false" Priority="65" Name="Medium List 1 Accent 6"/> <w:LsdException Locked="false" Priority="66" Name="Medium List 2 Accent 6"/> <w:LsdException Locked="false" Priority="67" Name="Medium Grid 1 Accent 6"/> <w:LsdException Locked="false" Priority="68" Name="Medium Grid 2 Accent 6"/> <w:LsdException Locked="false" Priority="69" Name="Medium Grid 3 Accent 6"/> <w:LsdException Locked="false" Priority="70" Name="Dark List Accent 6"/> 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Name="Plain Table 2"/> <w:LsdException Locked="false" Priority="43" Name="Plain Table 3"/> <w:LsdException Locked="false" Priority="44" Name="Plain Table 4"/> <w:LsdException Locked="false" Priority="45" Name="Plain Table 5"/> <w:LsdException Locked="false" Priority="40" Name="Grid Table Light"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light Accent 1"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 1"/> <w:LsdException Locked="false" Priority="48" 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Name="Grid Table 7 Colorful Accent 4"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light Accent 5"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 5"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 5"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 5"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 5"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful Accent 5"/> <w:LsdException Locked="false" Priority="46" Name="Grid Table 1 Light Accent 6"/> <w:LsdException Locked="false" Priority="47" Name="Grid Table 2 Accent 6"/> <w:LsdException Locked="false" Priority="48" Name="Grid Table 3 Accent 6"/> <w:LsdException Locked="false" Priority="49" Name="Grid Table 4 Accent 6"/> <w:LsdException Locked="false" Priority="50" Name="Grid Table 5 Dark Accent 6"/> <w:LsdException Locked="false" Priority="51" Name="Grid Table 6 Colorful Accent 6"/> <w:LsdException Locked="false" Priority="52" Name="Grid Table 7 Colorful Accent 6"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light Accent 1"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 1"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 1"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 1"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 1"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful Accent 1"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful Accent 1"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light Accent 2"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 2"/> <w:LsdException Locked="false" Priority="48" Name="List Table 3 Accent 2"/> <w:LsdException Locked="false" Priority="49" Name="List Table 4 Accent 2"/> <w:LsdException Locked="false" Priority="50" Name="List Table 5 Dark Accent 2"/> <w:LsdException Locked="false" Priority="51" Name="List Table 6 Colorful Accent 2"/> <w:LsdException Locked="false" Priority="52" Name="List Table 7 Colorful Accent 2"/> <w:LsdException Locked="false" Priority="46" Name="List Table 1 Light Accent 3"/> <w:LsdException Locked="false" Priority="47" Name="List Table 2 Accent 3"/> <w:LsdException Locked="false" Priority="48" 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Name="List Table 7 Colorful Accent 6"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hashtag"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Unresolved Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Link"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> Ovarian hyperstimulation syndrome (OHSS) is a potentially serious iatrogenic complication of controlled ovarian stimulation in assisted reproductive technology procedures. Despite substantial progress in stimulation protocols and preventive strategies, OHSS remains an important clinical and safety concern in contemporary IVF practice. The purpose of this narrative review is to summarize and critically analyze current knowledge regarding the pathophysiology, risk factors, clinical presentation, prevention, and management of OHSS. Relevant literature was identified through searches of the PubMed/MEDLINE, Scopus, and Web of Science databases, including clinical studies, cohort analyses, systematic reviews, and professional society guidelines published between 2019 and 2026, with selective inclusion of earlier landmark studies essential for understanding the basic mechanisms of the syndrome. Current evidence indicates that the key pathophysiological mechanism of OHSS is increased vascular permeability mediated by vascular endothelial growth factor (VEGF), most commonly triggered by exposure to human chorionic gonadotropin. Identification of high-risk patients using ovarian reserve biomarkers, individualized gonadotropin dosing, the use of GnRH antagonist protocols and GnRH agonist trigger, as well as freeze-all embryo strategies, have substantially reduced the incidence of moderate and severe forms of the syndrome. Contemporary management of OHSS is therefore primarily based on prevention and individualized stimulation strategies aimed at optimizing reproductive outcomes while ensuring maximal patient safety.
IMAGING OF VASCULAR ANOMALIES OF THE AORTA AND VESSELS OF THE HEAD AND NECK- REVIEW ARTICLE
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Locked="false" Priority="21" SemiHidden="false" UnhideWhenUsed="false" QFormat="true" Name="Intense Emphasis"/> <w:LsdException Locked="false" Priority="31" SemiHidden="false" UnhideWhenUsed="false" QFormat="true" Name="Subtle Reference"/> <w:LsdException Locked="false" Priority="32" SemiHidden="false" UnhideWhenUsed="false" QFormat="true" Name="Intense Reference"/> <w:LsdException Locked="false" Priority="33" SemiHidden="false" UnhideWhenUsed="false" QFormat="true" Name="Book Title"/> <w:LsdException Locked="false" Priority="37" Name="Bibliography"/> <w:LsdException Locked="false" Priority="39" QFormat="true" Name="TOC Heading"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> This review article aims to present the most common vascular anomalies of the head and neck arteries, detailing their clinical presentations, the diagnostic advantages of current imaging modalities, and the selection of appropriate therapeutic interventions. Vascular malformations result from localized errors in the development of blood and lymphatic vessels, leading to the formation of abnormal structures prior to birth. They typically grow proportionally with the child, though they may occasionally undergo rapid expansion. Vascular malformations are classified based on their hemodynamic characteristics into two major categories: slow-flow anomalies (comprising capillary, lymphatic, and venous malformations) and fast-flow anomalies (arteriovenous and arterial malformations). The incidence of arteriovenous malformations (AVMs) is increasing; many remain clinically asymptomatic, though approximately 12% are symptomatic. In cases involving hemorrhage, the mortality rate is 10–15%, with morbidity ranging from 30% to 50%. There is no gender predilection. Computed Tomographic Angiography (CTA) and Magnetic Resonance Imiging (MRI) are essential for therapeutic planning and risk assessment across surgical, endovascular, and radiological interventions. These modalities allow for the visualization of complications such as hemorrhage, stroke, and cerebral atrophy. Furthermore, magnetic resonance imaging is critical for assessing the reduction of the nidus size, the extent of post-therapeutic edema, and the presence of radiation necrosis within the treatment field. While surgery remains the primary definitive treatment, embolization has become a significant therapeutic component in recent years.
PERIOPERATIVE ACUTE KIDNEY INJURY AFTER MAJOR NON-CARDIAC SURGERY: RISK FACTORS, CLINICAL OUTCOMES, AND PREDICTIVE PERFORMANCE OF PERIOPERATIVE SCORING SYSTEMS
Background: Perioperative acute kidney injury (AKI) is a serious complication after major non-cardiac surgery, associated with increased mortality, prolonged ICU stay, and the need for renal replacement therapy (RRT). Objective: To assess the impact of AKI severity and associated risk factors on clinical outcomes after major abdominal surgery and to evaluate the prognostic performance of SPARK, APACHE II, and SOFA scores, including sepsis-associated AKI. Materials and Methods: This prospective cohort study was conducted in the Surgical ICU of University Hospital Center Bežanijska Kosa (Belgrade) from January to June 2024. Thirty adult patients who developed perioperative AKI after major abdominal surgery were analyzed. AKI was defined according to KDIGO criteria and sepsis according to Sepsis-3. Disease severity was assessed using APACHE II and SOFA, and preoperative AKI risk using the SPARK index. Results: AKI occurred in 30 operated patients. KDIGO stages were: stage 1 in 26.7%, stage 2 in 30.0%, and stage 3 in 43.3%. In-hospital mortality was 30.0% and occurred exclusively in patients older than 60 years. Mortality was significantly higher in KDIGO stage 3 (61.5% vs. 5.9%, p=0.0016). KDIGO stage 3 and age >60 years were strongly associated with death. SPARK showed good discrimination for severe AKI (AUC≈0.78), while APACHE II demonstrated excellent performance for severe AKI and mortality (AUC≈0.97). RRT use was more frequent in advanced AKI stages. Conclusions: Perioperative AKI was infrequent but severe, with high mortality driven by KDIGO stage 3 and advanced age. SPARK and particularly APACHE II were useful for risk stratification.
Sphenoid sinus pneumatization · Vidian canal · Anterior clinoid process · Pterygoid process · Multidetector computed tomography.
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Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hashtag"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Unresolved Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Link"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> Background: Multidetector computed tomography of the sphenoid sinus is the most accurate method for visualizing sinus pneumatization and all anatomical variations. Objective: To characterize the patterns of pneumatization of the sphenoid sinus and assess the association with variations in the bony structures of the sinus in relation to gender and age groups. Methods: Retrospective CT analysis of 127 patients (43 men and 84 women). Pneumatization patterns, skull base extensions, and Vidian canal types were classified. Results: Bilateral increased sphenoid sinus pneumatization shows a very strong age association (p = 0.001), with clustering in middle-aged (40–52) and elderly (≥ 66) groups. Right-sided preserved sphenoid sinus pneumatization shows a statistically significant association with gender (χ² = 3.90, p = 0.048), with a higher proportion of males than females. Bilateral pneumatization (BPP) showed a statistically significant association with age (p = 0.019); individuals with BPP were significantly younger. Sellar type predominated (67.7%), with frequent posterior and lateral extensions. The dorsal sphenoid sinus configuration is the only variant showing a statistically significant association with age (χ² = 8.17, p = 0.043). Complete sellar type shows a strong, consistent positive association with both anterior clinoid and pterygoid process pneumatization on all sides (p ≤ 0.015, often < 0.001). Type III Vidian canal occurred in ~ 40%. Vidian canal Type I is strongly associated with pterygoid process pneumatization, especially bilaterally (p < 0.001 in all cases). Conclusions: The cohort exhibits a highly pneumatized, surgically relevant sphenoid sinus phenotype, primarily developmental rather than symptom-driven.
PREDICTORS OF CARDIAC ARREST IN CHILDREN
The incidence of cardiac arrest (CA) in pediatric patients is lower than in the adult population. The unique anatomical and physiological characteristics of children contribute to differences in the etiology of CA and the outcomes of resuscitation. Key factors for surviving a life-threatening event include the rapid recognition of CA and the prompt initiation of effective resuscitation. Therefore, identifying predictors of CA is crucial, as they indicate the potential for such an event and help differentiate affected patients from others. It is possible to prevent the occurrence of CA by appropriate treatment in these situations. Moreover, there are significant differences in the approach, implementation of resuscitation procedures, treatment, outcomes, and education regarding CA events that occur in children, whether they take place in-hospital or out-of-hospital.
RETINAL VASCULAR CHANGES IN PATIENTS WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE
INTRODUCTION/AIM Chronic obstructive pulmonary disease (COPD) is a progressive and inflammatory disease of the airways that often leads to cardiovascular and microvascular changes. This study aimed to analyze retinal microcirculation in patients with COPD using optical coherence tomography angiography (OCTA) MATERIALS AND METHODS Cross-sectional study. A total of 44 subjects were analyzed, including 28 with COPD and 16 healthy controls. Inclusion criteria were subjects older than 18 years with a confirmed COPD diagnosis based on spirometric parameters RESULTS The statistically significant differences were observed between the groups for the following parameters: deep capillary plexus macular (p = 0.009), parafoveal (p = 0.026), and perifoveal region (p = 0.034). A significant negative correlation was observed between the ratio of residual volume to total lung capacity (RV/TLC) and the vessel density in the macular and perifoveal superficial capillary plexus regions (p<0.05). The choriocapillaris Flow also demonstrates a significant inverse relationship with the RV/TLC ratio. Regarding the deeper retinal layers, our analysis revealed a significant negative correlation between outer retina Flow and forced vital capacity (FVC). CONCLUSION Monitoring changes in the OCTA parameters, particularly in relation to lung volume parameters like RV/TLC and FVC, we conclude that OCTA may provide valuable insights into systemic vascular progression and overall severity of the disease in COPD patients
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Name="List Table 7 Colorful Accent 6"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Hyperlink"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Hashtag"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Unresolved Mention"/> <w:LsdException Locked="false" SemiHidden="true" UnhideWhenUsed="true" Name="Smart Link"/> </w:LatentStyles> </xml><![endif]--><!-- [if gte mso 10]> <![endif]--> Ischemic heart disease (IHD), or coronary artery disease, ranks as the primary global cause of mortality and disability. This narrative review summarizes the epidemiology of IHD, focusing on global distribution, risk factors, and prevention. A literature search was conducted using PubMed, Scopus, and Google Scholar databases to identify relevant studies from the past decade. In 2019, IHD affected 197.2 million individuals, resulting in 9.1 million deaths, and 182.0 million disability-adjusted life years (DALYs) worldwide. While age-standardized mortality rates, DALYs, and prevalence have declined, the number of reported cases continues to rise. The highest prevalence was reported in Central and Eastern Europe and Central Asia, while the lowest was in South Asia. Modifiable and non-modifiable risk factors influence IHD. The main causal risk factors, such as hypertension, dyslipidemia, diabetes, smoking, and age, are independently associated with IHD development. Environmental factors (air pollution, noise exposure, and climate change) further increase the risk of IHD. The emerging concept of the exposome emphasizes that the cumulative and combined influence of environmental risk factors plays a crucial role in the development of IHD. IHD can be prevented from developing through primordial (targeting social determinants like urbanization, poverty, illiteracy, living conditions) and primary prevention (management of risk factors through lifestyle interventions, pharmacotherapies). IHD is a growing global health and economic challenge, disproportionately affecting low-income regions, as a result of population aging, limited access to healthcare, and the presence of numerous risk factors that require appropriate prevention and treatment.
EFFECTS OF NMDA RECEPTOR ANTAGONISTS ON ACUTE POSTOPERATIVE PAIN
Introduction/Aim of the paper: Pain represents a multifactorial process with detrimental effects on the entire organism. This randomized, open-label pilot study investigated the effect of preemptive administration of ketamine and magnesium-sulfate on the intensity of postoperative pain after laparoscopic colon tumor resection. Methods: Sixty patients were randomized into the ketamine-magnesium (KM) and the control (C) groups. After the introduction to anesthesia, patients in the KM group received an i.v. bolus dose of 0.5 mg/kg ketamine, followed by a continuous infusion of 0.6 mg/kg/h lasting until the end of surgery. After a bolus dose of ketamine, they received magnesium-sulfate 20 mg/kg in an intravenous infusion (5-10 minutes). Group C received only 0.9% NaCl infusion. After the patients were awakened (0h), the pain intensity was compared (0- 46h) between the two groups. Results: The Mann-Whitney test implied significantly (p<0.05) lower visual analog scale (VAS) scores, in KM group at 0, 1, 2, 10, 22 and 30 hours after the surgery, and no statistical significance (p>0.05) for VAS scores after 6, 14, 18, 38 and 46 hours, compared to C group. Ketamine and magnesium-sulfate significantly (p<0.05) reduced the postoperative consumption of analgesics, increased the sedation level at 0h postoperatively, and increased the overall patient satisfaction with the treatment. Conclusion: Preemptive administration of ketamine and magnesium-sulfate combination has beneficial effect on postoperative pain after laparoscopic colon tumor resection.