Ahmet Mentese

Tr en Amaç: Bu çalışmanın amacı endotel hasarı sonucu trombosit aktivasyonu ve kümeleşmesinin patofizyolojisinde rol oynadığı bilinen pulmoner emboli (PE) hastalığında; endotel disfonksiyonu, platelet adezyonu ve arterial trombüs ile ilişkelendirilen siklofilin A (CYPA) ve vasküler adezyon protein- 1 (VAP-1) adlı biyokimyasal belirteçlerin tanısal değerini araştırmaktır. Gereç ve Yöntem: Prospektif olarak yapılan bu klinik çalışmada acil servise akut PE şüphesi ile başvurarak çalışmaya alınan ve spiral bilgisayarlı tomografi anjiografi ile PE varlığı değerlendirilen 165 hastanın serum CYPA ve VAP-1 düzeyi ölçüldü. Bilgisayarlı tomografi sonuçlarına göre, PE (+) ve PE (-) olarak 2 gruba ayrılan bu hastaların ölçülen CYPA ve VAP-1 düzeyleri birbirleriyle karşılaştırıldı. Bulgular: Her iki grup ölçümleri birbiriyle karşılaştırıldığında VAP-1 düzeyi bakımından gruplar arası fark istatistiksel anlamlı bulunurken (p=0.0001), CYPA düzeyinin bakımından bu fark istatistiksel olarak anlamlı değildi. (p=0.381). Sonuç: Akut PE’de serum VAP-1 düzeyinin tanısal olarak kullanılabileceği tespit edilmiştir. Serum CYPA düzeyinin ise akut PE’de tanısal değeri bulunmamaktadır. Aim: To investigate the diagnostic value of the biochemical markers cyclophilin A (CYPA) and VAP-1, associated with endothelial dysfunction, platelet adhesion, and arterial thrombus in pulmonary embolism (PE), in whose pathophysiology platelet activation and aggregation resulting from endothelial damage are known to be involved. Material and Method: Serum CYPA and VAP-1 levels of 165 patients presenting to the emergency department with suspected acute PE and with presence of PE investigated at spiral computerized tomography angiography were measured in this prospective clinical study. These patients were assigned into two groups, PE (+) and PE (-), based on the tomography results, and their CYPA and VAP-1 levels were then compared. Results: Comparison of the two groups’ measurements revealed a significant difference in terms of VAP-1 levels (p=0.0001), but none for CYPA (p=0.381). Conclusion: Diagnostic value was determined for serum VAP-1 levels in acute PE, but CYPA levels are of no such value.

Objective: The purpose of this study was to investigate the value of signal peptide-CUB-EGF domain-containing protein 1 (SCUBE1) in the diagnosis of angina pectoris in patients presenting to the emergency department.Material and Methods: This prospective research was planned as a cross-sectional, single-center clinical study. Patients presenting to the emergency department with angina pectoris symptoms over a period of five months from receipt of ethical committee approval were included. Patients presenting with ischemic chest pain were divided on the basis of etiology into stable angina pectoris (SAP), unstable angina pectoris (UAP), non-ST elevation myocardial infarction (NSTEMI), and ST segment elevation myocardial infarction (STEMI) groups. Clinical, laboratory and demographic characteristics were recorded. SCUBE1 levels from each group were compared with a healthy control group.Results: 118 individuals were enrolled in the study, 78 patients meeting the inclusion criteria and 40 healthy controls. Patients’ mean age was 54.36 ± 14.03 years, and 88.5% (n=69) were male. Hypertension (59%) and smoking (62%) predomination over other risk factors. NSTEMI was the most common factor (46.1%) in patients enrolled due to ischemic chest pain. No statistically significant difference was determined between patients’ serum SCUBE1 levels at time of presentation and at 6 h and 12 h and the control group (p>0.05).Conclusion: On the basis of our study findings, SCUBE1 is of no value in the diagnosis of ischemic chest pain etiologies.

Crimean-Congo Hemorrhagic Fever (CCHF) may exhibit a mild clinical course or a severe profile like mortal bleeding. The pathogenesis of the illness and reason of bleeding are unclear. However, endothelial injury is a key factor in the pathogenesis of the illness. Transforming growth factor beta (TGF-β) is one of the materials involved in repairing injured endothelium. This is a significant polypeptide released in pretty much all cells and important for the regulation of cellular events, epithelium formation, inflammation, blood coagulation, and collagen synthesis. This study aimed to determine the prognostic significance of serum TGF-β1 levels in CCHF patients. We examined 120 patients hospitalized with CCHF diagnosis and their serum TGF-β1 was investigated, retrospectively. Patients were put into two groups according to the existence of hemorrhage. Forty-four (36.7%) patients had hemorrhage. TGF-β1 levels in patients with bleeding were 5.2 ± 1.8, and 7.1 ± 2.2 for non-bleeding (P < 0.0001). When ROC analysis was performed in patients with CCHF alone in order to identify patients with bleeding, at a TGF-β1 cut-off point of 4.9, AUC was 0.762 (0.675–0.835), sensitivity 59.1%, specificity 85.5%, PPV 70.3%, and NPV 78.3%. We summarize that TGF-β1 level and endothelial dysfunction can be related. A decreased TGF-β1 level is a likely prognostic and diagnostic factor for bleeding in CCHF patients. Therefore, this marker should be considered in the treatment strategy for these patients. J. Med. Virol.

Context: Erythrocyte membranes regulate many enzyme activities, including carbonic anhydrase II (CA II). Membrane fluidity is associated with alterations in protein function and protein-protein interactions. Objective: The purpose of this study was to show the human CA II (hCA II) activity regulation by human erythrocyte membranes from diabetic and hypercholesterolemic subjects. Materials and methods: Erythrocyte membranes were obtained from diabetic, hypercholesterolemic, and healthy subjects. hCA II activity was measured using the electrometric method. Results: hCA II activity was increased in vitro by membranes from both diabetic and hypercholesterolemic patients, with hypercholesterolemic membranes exhibiting a greater increase. Conclusion: Changes in membrane composition may affect the erythrocyte membranes’ capacity to increase in vitro hCA II activity.

The aim of this study was to investigate the effects of homocysteine (Hcy), a risk factor for cardiovascular diseases, hypertension, stroke and obesity, on expression of CD36 that regulates uptake of oxidized low-density lipoprotein (Ox-LDL) by adipocytes and differentiation of 3T3-L1 cells to adipocytes. Cell viability was determined using MTT assay, and density of triglycerides were measured with Oil Red O staining. The expression levels of CD36 were analyzed using SYBR green assay by quantitative RT-PCR. Our results showed that the addition of Hcy inhibited differentiation of 3T3-L1 preadipocytes in a dose-dependent manner without a significant cell toxicity (p < 0.05). Percentage CD36 gene expression increased in the Hcy treatment groups, but not statistically significantly (p > 0.05) compared to differentiated adipocytes. Hcy reduced adipocyte differentiation, but had no effect on the expression level of CD36 in vitro conditions. The effect of Hcy on uptake and clearance of Ox-LDL by adipose tissue now needs to be investigated in vivo.