Erhan Arıkan

Objectives: In patients presenting to the emergency department with acute ischemic stroke (AIS), there is a growing need for practical and rapid biomarkers that can effectively predict prognosis and infarct volume, complementing neurological examination and imaging methods. Methods: This study retrospectively evaluates patients diagnosed with AIS at the emergency department of Bilecik Training and Research Hospital between 1 March 2022, and 30 September 2023. Patients who were transferred for reperfusion therapy were excluded, as thrombolysis and mechanical thrombectomy were not available at our institution during the study period. The systemic immune–inflammation index (SII) and the systemic inflammation response index (SIRI) scores were calculated based on patients’ laboratory values. Additionally, infarct volumes were independently assessed by two experienced radiologists and calculated by multiplying the hyperintense areas on diffusion-weighted magnetic resonance imaging by slice thickness. Results: Of the 349 patients diagnosed with AIS during this study period, 257 who met the inclusion criteria were analyzed. The median age was 76 years (IQR: 66–83), and 130 (51%) patients were female. Lacunar infarction was present in 109 patients (42.4%), while 148 (57.6%) had non-lacunar infarction. The all-cause mortality rates at 1 month, 1 year, and 2 years were 7.8%, 21.4%, and 29.6%, respectively. SII and SIRI scores were significantly higher in deceased patients compared to survivors across all time points for mortality. Conclusions: The findings of this study suggest that SII and SIRI values, derived from complete blood count parameters, may contribute to the early identification and management of high-risk AIS patients.

This study was designed to examine the metaphorical perceptions and meaning-making schemas of hemodialysis patients regarding the concept of death. The study, designed qualitatively through metaphor analysis, included 38 hemodialysis patients. Data were collected using forms on semi-structured interviews employing writing and drawing techniques to explore perceptions of death. The data were analyzed using content analysis. It was determined that hemodialysis patients participating in the study produced four metaphors (The end of life and reaching union, Nightmare and despair, Sense of disappearance and emptiness, and The journey of life) each using the writing technique and drawing technique. The study revealed that hemodialysis patients interpret death within the framework of complex cognitive schemas, intense anxiety and multidimensional meanings. The findings indicate that this process of interpretation is strongly shaped by religious and spiritual interpretations. In this regard, recognizing and strengthening patients' psychological, social, and spiritual coping resources is of great importance. Psychosocial nursing interventions based on metaphors, person centered care, and spiritual care components can make meaningful contributions to reducing death-related anxiety and strengthening emotional well-being.

Aim: In acute appendicitis (AA), early differentiation between complicated AA (CA) and uncomplicated AA (UCA) directly affects the treatment process. This study investigated the diagnostic performance of the Systemic Immune-Inflammation Index (SII) and the Systemic Inflammatory Response Index (SIRI) in distinguishing CA from UCA, as well as the association between door-to-surgery time (DST) and clinical outcomes.Materials and Methods: Patients who presented to the emergency department and underwent surgery with a diagnosis of AA between January 1, 2020, and December 31, 2024, were retrospectively evaluated. According to the pathology reports, cases of perforated or gangrenous appendicitis were classified as CA, whereas cases of simple or suppurative/phlegmonous AA were classified as UCA. DST, defined as the time (minutes) from the patient’s admission to the emergency department until the start of surgery, was calculated for each patient.Results: After applying exclusion criteria, 556 patients were included in the analysis. Of the patients, 16.9% (n=94) were classified as CA, and 83.1% (n=462) as UCA. In the CA group, median age, monocyte count, C-reactive protein (CRP), SII, and SIRI were significantly higher, whereas lymphocyte count was significantly lower. In ROC analysis, CRP showed the highest diagnostic performance (AUC: 0.741; threshold: 39.1 mg/L; sensitivity: 61.7%; specificity: 79.3%). SII (AUC: 0.597) and SIRI (AUC: 0.612) yielded statistically significant AUC values but showed limited discriminative ability. No significant association was found between DST and CA, whereas a weak positive correlation was found between CRP and length of hospital stay (r=0.285; p<0.001).Conclusions: SII and SIRI were significantly elevated in CA, but their diagnostic performance was lower than that of CRP. The findings suggest that moderate in-hospital delay was not associated with increased rates of CA in this cohort. Prospective studies evaluating the combined use of these indices with CRP and their integration into clinical scoring systems are needed.

Ejmi Eurasian Journal of Medical Investigation

Cardiovascular diseases (CVDs) are the leading cause of global morbidity and mortality, with oxidative stress and redox imbalance playing pivotal roles in their initiation and progression. In this comprehensive review, we explore the molecular mechanisms by which reactive oxygen and nitrogen species disrupt vascular homeostasis, promote endothelial dysfunction, and drive adverse cardiac remodeling. We highlight key redox-sensitive pathways, including NADPH oxidase activation, mitochondrial dysfunction, endothelial nitric oxide synthase uncoupling, and endoplasmic reticulum stress. Emerging oxidative stress biomarkers, such as 8-iso-prostaglandin F2α, oxidized low-density lipoprotein, and myeloperoxidase, are critically examined for their diagnostic and prognostic relevance. Additionally, we discuss therapeutic strategies targeting oxidative stress, ranging from conventional antioxidants to novel mitochondrial-directed and enzyme-specific interventions. Despite advances in understanding the redox landscape of CVDs, challenges remain in translating these insights into effective clinical therapies. Future research integrating omics technologies, precision medicine, and combined lifestyle-pharmacological approaches may offer new opportunities for redox-based cardiovascular interventions.

Background/Objectives: Severe COVID-19 pneumonia damages alveolar type II cells and disrupts surfactant homeostasis, contributing to acute respiratory distress syndrome (ARDS). Surfactant proteins (SP-A, SP-B, SP-C, SP-D) are critical for reducing alveolar surface tension and for innate immune defense. We aimed to evaluate whether surfactant protein gene expression varies with the severity of COVID-19. Methods: Peripheral blood was collected from 122 adults with confirmed COVID-19, categorized as asymptomatic (no symptoms), mild (requiring hospitalization), or severe (requiring ICU admission). We quantified mRNA expression of surfactant protein genes (SFTPA1, SFTPA2, SFTPB, SFTPC, SFTPD) in blood cells using RT-qPCR. Relative expression was normalized to GAPDH and compared among the groups using the 2^−ΔΔCt method. Outliers (Ct values > 3 SD from the mean) were excluded before analysis. Results: Distinct surfactant gene expression patterns were markedly associated with disease severity. Transcripts of SFTPB and SFTPC decreased with increasing severity of the disease. Notably, SFTPC expression was ~49-fold higher in mild cases compared to asymptomatic COVID-19-positive patients (p < 0.0001), but then decreased by ~54-fold in severe cases relative to mild (p < 0.0001), returning to near-baseline levels. In contrast, SFTPA2 and SFTPD were dramatically upregulated in severe cases. SFTPA2 was ~50-fold higher in severe versus mild cases (p < 0.0001), and SFTPD was ~4346-fold higher in severe versus asymptomatic cases (p < 0.0001; ~9.6-fold higher than in mild). SFTPA1 showed only a modest ~1.4-fold decrease in severe cases (vs. mild). All noted differences remained statistically significant after outlier exclusion. Conclusions: COVID-19 severity is correlated with profound changes in surfactant gene expression in blood. Critically ill patients exhibit loss of key surfactant components (SP-B and SP-C transcripts) alongside an excessive SP-D response. These preliminary findings suggest an imbalance that may contribute to lung injury in severe disease. However, further validation is needed to establish surfactant proteins, such as SP-D, as biomarkers of COVID-19 severity.

Background/Objectives: Severe COVID-19 pneumonia causes alveolar type II cell damage and surfactant dysfunction, contributing to acute respiratory distress syndrome (ARDS). Surfactant proteins (SP-A, SP-B, SP-C, SP-D) are critical for reducing alveolar surface tension and defending against infection. We aimed to evaluate how surfactant protein gene expression affects COVID-19 severity Methods: Peripheral blood was collected from 122 adults with confirmed COVID-19, categorized as asymptomatic (no symptoms), mild (hospitalized), or severe (ICU admission). We quantified mRNA expression of surfactant protein genes (SFTPA1, SFTPA2, SFTPB, SFTPC, SFTPD) by RT-qPCR and compared relative expression levels between groups. Results: Surfactant gene expression patterns differed markedly with disease severity. SFTPB and SFTPC transcripts decreased as severity increased. Notably, SFTPC was ~49-fold higher in mild cases than asymptomatic controls, but then dropped ~54-fold in severe cases relative to mild, returning to near-baseline levels. In contrast, SFTPA2 and SFTPD were dramatically upregulated in severe illness. SFTPD expression in severe patients was ~4346-fold higher than in asymptomatic individuals (and ~9.6-fold higher than in mild cases). SFTPA2 was ~50-fold higher in severe versus mild cases. By comparison, SFTPA1 showed a modest ~1.4-fold decrease in severe cases (vs. mild). All noted differences were statistically significant (p < 0.05). Conclusion: COVID-19 severity is associated with distinct surfactant gene expression changes. Critically ill patients exhibited loss of key surfactant components (SP-B and SP-C) alongside an excessive SP-D response. This imbalance in the surfactant system likely contributes to alveolar collapse in severe COVID-19, and elevated SP-D may serve as a biomarker of lung injury severity.