Biomedical Papers-Olomouc最新文献

Background: Recent regenerative studies imply conflicting results on knee osteoarthritic (OA) chondrocytes and mesenchymal stem cells (MSC)-mediated cartilage constructs in terms of compressive properties and tensile strength. This could be attributed to different gene expression patterns between MSC and OA chondrocytes during chondrogenic differentiation. Therefore, we analyzed differentially expressed genes (DEGs) between OA and MSC-derived chondrocytes using bioinformatics tools.

Methods: We downloaded and analyzed the GSE19664 dataset from the Gene Expression Omnibus to identify DEGs. DAVID was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, while a protein-protein interaction network of DEGs was constructed through the Search Tool for the Retrieval of Interacting Genes (STRING) and identified hub genes by CytoHubba.

Results: A total of 43 DEGs identified (15 downregulated and 28 upregulated) were found to be deregulated between OA and MSC-derived chondrocytes. KEGG analysis revealed the enrichment of complement and coagulation cascades and other pathways among the studied chondrocytes. The pathway enrichment identified top KEGG, gene ontology biological process, molecular function, and cellular component. The hub networks identified the top 5 hub genes involved in chondrogenesis, including CLU, PLAT, CP, TIMP3, and SERPINA1.

Conclusions: Our results identified significant genes involved in chondrogenesis. These findings provide new avenues for exploring the genetic mechanism underlying cartilage synthesis and novel targets for preclinical intervention and clinical treatment.

Backround and aims: Early evaluation of cardiac remodeling may be useful in predicting heart failure in patients with arterial hypertension. The identification of biomarkers as useful clinical tools in this regard is ongoing. The aim of this study was to evaluate the association of selected cardiac biomarkers levels with parameters of cardiac structure and function in patients with arterial hypertension.

Patients and methods: Included in the study were patients with arterial hypertension with normal left ventricular ejection fraction (LV EF) and absence of signs of heart failure. The levels of selected biomarkers: NT-proBNP, sST2, Galectin-3, GDF-15, Cystatin C, TIMP-1 and ceruloplasmin were measured and assessed together with other biochemical and echocardiographic parameters.

Results: A total of 92 patients (61% men) mean age 61.5 years were included. Mean LV EF was 64.7% and mean LV mass index was 91.7 g/m2. NT-proBNP level correlated significantly with the parameters of LV diastolic function: velocity of E wave (r=0.377, P<0.002), and with E/A ratio, (r=0.455, P<0.0001), with E lat (r=-0.354, P=0.006), E/E' ratio, r=0.393, P<0.002, with ePAP (r=0.390, P=0.014), and with age (r=0.384, P<0.0001). Statistically significant correlations for GDF-15 were as follows: with age (r=0.426, P<0.0001) and left atrial diameter (LA) (r=0.401, P<0.0001), for Cystatin C there are statistically significant correlation with age (r=0.288, P=0.006) and LA (r=0.329, P=0.004). Only sST2 level correlated significantly with parameters of cardiac structure: with LV mass (r=0.290, P<0.01) and LV mass index (r=0.307, P=0.012) and with posterior wall thickness PW (r=0.380, P<0.001). No other observed variables including Galectin-3 and TIMP-1, correlated significantly with age or echocardiographic variables. In a comparison of patients with and without left ventricular hypertrophy, statistically significant differences were found only in LA (P<0.0001) and sST2 (P=0.004). In a multivariate logistic regression, sST2 and TIMP were independent predictors of left ventricular hypertrophy.

Conclusion: NT-proBNP level as a biomarker of cardiac remodeling correlated with parameters of LV diastolic function in patients with arterial hypertension. Soluble ST2 correlated with parameters of cardiac structure. Biomarkers sST2 and TIMP-1 were associated with left ventricular hypertrophy.

Background: Nearly 50% of ST elevation myocardial infarction (STEMI) patients have multivessel coronary artery disease. The optimal selection of non-culprit lesions for complete revascularization is a matter of current debate. Little is known about the predictive value of myocardial perfusion study (MPS) in this scenario.

Methods: We enrolled 49 STEMI patients (61.5 ± 10.3 years) with at least one major non-culprit lesion (50-90%) other than left main coronary artery lesions. Overall 63 non-infarct- related artery (IRA) stenoses (65.2 ± 11.9%) were recommended for further evaluation using Fractional Flow Reserve (FFR) measurement as is standard in our institution. Prior to FFR, all patients were scheduled for non-invasive MPS using single-photon emission computed tomography (SPECT). Both FFR and MPS were performed 4-8 weeks after STEMI with MPS preceding FFR within no more than 48 hours. An FFR value of ≤0.80 was considered significant and guided the final revascularization strategy. The results of MPS were correlated to FFR as well as to the clinical and angiographic characteristics of both culprit and non-infarct-related lesions.

Results: Based on FFR, 30 out of 63 stenoses (47.6%) in 27 patients were considered hemodynamically significant (FFR 0.69 ± 0.08, range 0.51-0.79) compared to residual 33 stenoses considered negative (FFR 0.87 ± 0.04, range 0.81-0.96). The MPS revealed abnormal myocardium (23.6% average, range 5-56%) in 21 patients (42.8%). Among those patients, only 9 showed the evidence of ischemic myocardium (average 10.8%, range 4-18%) with low sensitivity of MPS in predicting positive FFR. Besides that, higher proportion of patients (71.4% vs. 42.9%, P=0.047) with overall lower FFR values (0.73 vs. 0.80, P=0.014, resp.) in non-IRAs as well as higher proportion of patients with more severely compromised flow in IRAs (P=0.048) during STEMI had MPS-detected abnormal myocardium.

Conclusion: In STEMI patients with multivessel coronary artery disease, we observed rather weak correlation between MPS using SPECT and invasive hemodynamic measurement using FFR in ischemia detection.

Aim: The main objective of this study was to determine whether urinary trauma increases the risk of acute kidney injury (AKI) in patients with severe trauma. As a secondary objective, we assessed the reliability of neutrophil gelatinase-associated lipocalin (NGAL) in the early prediction of AKI in this patient population.

Methods: Retrospective analysis of two prospective observational studies involving 179 adult patients with severe trauma (Injury Severity Score >16). NGAL levels were measured by taking a blood sample 24 h after admission. AKI was diagnosed according to the Kidney Disease Improving Global Outcomes (KDIGO) classification.

Results: The overall incidence of AKI was 29%. Kidney or vascular injury was an independent risk factor for AKI (risk ratio [RR] = 3.1, 95% confidence interval [CI] 1.93-4.90). Trauma to urinary passages was also associated with an increased risk of AKI (RR = 4.2, 95% CI 2.70-6.46). Among patients without urinary tract injury, serum NGAL levels were significantly higher in trauma patients who developed AKI during the first 5 days in the intensive care unit (ICU) compared to patients without this organ dysfunction (214.6 µg/L [IQR 167.3] vs. 90.6 µg/L [IQR 58.4]; P<0.001). In patients with urinary tract trauma, there was no difference in the NGAL levels between the two groups (184.6 µg/L [IQR 139.9] vs. 118.3 µg/L [IQR 118.1]; P=0.216). NGAL was not a reliable predictor of AKI in patients with urinary trauma (AUC 0.660).

Conclusion: Urinary tract injury is associated with a significant increase in AKI in patients with severe trauma during the first 5 days of hospitalization in the intensive care unit. In these patients, NGAL is not a reliable predictor of the development of AKI.

Background and aim: In a previous follow-up of glaucoma patients taking carteolol or latanoprost, we found a greater progression of visual field changes with the prostaglandin than the betablocker. In the present study we compared the impact of carteolol and latanoprost on peripapillary vessel density in newly diagnosed primary open-angle glaucoma (POAG) patients.

Methods: The study consisted of two groups of POAG patients. There were 46 patient eyes treated with carteolol (Carteol LP 2%) in the first group and 52 eyes treated with latanoprost (Xalatan 0.005%) in the second. Intraocular pressure (IOP), vessel density (VD) and visual field were assessed in all patients. VD was measured peripapillary by optical coherence tomography angiography (OCTA) with the Avanti RTVue XR in eight segments: Inferior Temporal - IT (1); Temporal Inferior -TI (2); Temporal Superior - TS (3); Superior Temporal - ST (4); Superior Nasal - SN (5); Nasal Superior - NS (6); Nasal Inferior - NI (7) and Inferior Nasal - IN (8). The measurements were compared before and after three months of treatment. The visual field was examined with a fast threshold glaucoma program using a Medmont M 700 instrument from Medmont International Pty Ltd. and only when a diagnosis of POAG was done. The overall defect (OD) was assessed.

Results: Before treatment, there was no difference between groups in either OD or VD. After treatment, there was a decrease in IOP in both groups. In the carteolol-treated group, the mean decrease was 5.8 mmHg and in the latanoprost-treated eyes, the mean decrease was 7 mmHg. The difference was not statistically significant (P=0.133). After treatment with carteolol, there was a statistically significant increase in VD in segments 4, 5 and 6. After latanoprost treatment, VD was statistically significantly improved only in segment 5. A greater increase in VD values was found in eyes treated with carteolol than in eyes treated with latanoprost.

Conclusion: Carteolol had a better effect on vessel density than latanoprost.

Traumatic brain injury (TBI) has long-term consequences, including neurodegenerative disease risk. Current diagnostic tools are limited in detecting subtle brain damage. This review explores emerging biomarkers for TBI, including those related to neuronal injury, inflammation, EVs, and ncRNAs, evaluating their potential to predict clinical outcomes like mortality, recovery, and cognitive impairment. It addresses challenges and opportunities for implementing biomarkers in clinical practice, aiming to improve TBI diagnosis, prognosis, and treatment.

Background and aims: Early diagnosis and management of the ever-increasing global consequences of diabetes is of concern to all nations. The populations of developing countries in particular, account for about 75% of the estimated total number of those afflicted. The Middle East and North Africa Region have around 35.4 (24.3-47.4) million diabetics with a prevalence of around 10.5% in the Middle East. A high proportion of these are undiagnosed. The aim of this study was to assess the awareness of and knowledge about the ocular impacts of diabetes as diabetic retinopathy (DR) in Jordanians by comparing those with and those without diabetes.

Methods: In this cross-sectional study, diabetic and non-diabetic patients attending different clinics at the National Center for Diabetes, Endocrinology and Genetics (NCDEG) were interviewed face-to-face using a questionnaire, to assess the level of knowledge about diabetic retinopathy (DR). The questionnaire was assessed beforehand by ophthalmologists from the School of Medicine, the University of Jordan, in Amman Results. A total of 214 subjects participated in this study (108 males:106 females). The mean age was 58.2 ± 10.6 years; (28 to 88 years) ~70% were diabetic. More than 98% were aware that diabetes can have ocular consequences. Only 17.3% however, had an adequate knowledge of DR. Around 40% did not know the treatment options although 75.7% of the diabetics carried out regular blood sugar checks in <6 months, and 73.4% had their last eye checkups in

Conclusions: The participants in this study had good awareness of DR but their knowledge of this ocular condition and treatment options is limited. Health-education programs and awareness campaigns should be initiated at health and eye care centers. Enrichment of social media and internet websites with evidence-based information by medical professionals are promising options for upgrading knowledge about this common global cause of blindness.

Introduction: Congenital hypofibrinogenemia (CH) and congenital dysfibrinogenemia (CD) are rare coagulation disorders caused by quantitative or qualitative defects in the fibrinogen gene. The aim of this study was to characterize the genetic background and the clinical manifestations of congenital fibrinogen disorders in the patients from Slovakia registered at the National Haemophilia Centre.

Materials and methods: Results of genetic analysis of the fibrinogen genes FGA, FGB and FGG using polymerase chain reaction followed by direct sequencing were evaluated in 36 patients.

Results: Molecular-genetic analysis revealed six novel variants - FGA c.923_968dup p.(Gly324Lysfs*44) and FGG c.1105C>T p.(His369Tyr) were identified in CD patients. In CH patients, in the FGG gene c.8G>A p.(Trp3*), c.823G>T p.(Glu275*) and c.323C>A p.(Ala108Asp) variants were detected. In the FGB gene c.1427C>T p.(Ser476Leu) was identified.

Conclusion: This study is a positive contribution towards expanding knowledge about genetic variants in patients with congenital fibrinogen disorders.

Background: The aim of this study was to evaluate the significance of testing the gain of chromosome 8 and the gain of chromosome 6 as prognostic markers in histopathological samples of enucleated eyes in with uveal melanoma.

Methods: This is a retrospective study of 54 enucleated eyes. The status of chromosomes 3, 8 and 6 was tested by CISH, and FISH was used in a few samples. A follow-up for the detection of metastases was conducted in all patients. The statistical significance of chromosomal abnormalities as a prognostic factor for the development of metastases was determined.

Results: The study group consists of 54 patients (average age 63 years), 28 men (51.9%) Monosomy 3 together with gain of chromosome 8 was found in 10 samples (18.5%). Both chromosomal abnormalities were detected in 6 (11%) patients. No chromosomal abnormality in 3 or 8 was detected in 21 (38.9%) patients. Abnormalities of chromosome 6 were present in 6 (11%) patients. Progression free survival after 5 years was 33.3% (95% CI 0.0; 83.3) in these patients.

Conclusions: Our findings indicate a correlation between progression-free survival and the presence of changes in chromosome 3 and e 8 in uveal melanomas. The results underline the necessity of testing for both chromosomal aberrations.

Background: Patients with extensive-stage small-cell lung cancer (ES-SCLC) have a poor prognosis. The standard palliative treatment for four decades has been chemotherapy as a combination of etoposide with carboplatin or cisplatin, and in recent years, immunotherapy in addition.

Aims: To determine whether there is a difference in the efficacy of palliative chemotherapy as cisplatin or carboplatin in combination with etoposide in patients with ES-SCLC in real-world practice in the Czech Republic.

Methods: This was a retrospective analysis of a cohort of 348 patients from the LUCAS project with ES-SCLC. 79 were treated with etoposide plus cisplatin and 265 were treated with etoposide plus carboplatin. Kaplan-Meier curves and the Cox regression model were used for analysis.

Results: No statistically significant difference in median overall survival (mOS) or median progression free survival (mPFS) was found between groups or between patients grouped according to age and performance status (PS) in mOS. The Cox regression result was similar.

Conclusion: This study shows that cisplatin and carboplatin do not differ in efficacy in a given indication, thus when choosing a treatment, the physician should consider the expected toxicity in a particular patient, assessing the patient's general condition and comorbidities.