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In this study, the relationship between IL-1β [-31 C / T] gene polymorphisms in the herniated lumbar disc is offered to investigate. IL-1β [-31 C / T] gene was amplified with by PCR [Polymerase Chain Reaction] the method. Polymorphic site Cut with the restriction enzyme Alu I and genotyping was performed. Fifteen subjects (15%) were homozygous for the C/C allele at -31 position of IL1B gene. Of the remaining 85 subjects, 64 (64%) were heterozygous for C/T and 21 (21%) were homozygous for T/T. In LDH group, fifteen subjects (30%) were homozygous for the T/T allele at -31 position of IL1B gene. 35 subjects were heterozygous for C/T (70%). There were significant differences between control and LDH group. In LDH group, C/T and T/T genotype were higher than the control group, however in control group C / C genotype was higher. C/C genotype was not determined in LDH group. In this study, IL-1b -31T allele is shown to be associated with the Lumbar herniated disc.

Background This study seeks to investigate the distribution of the angiotensin-converting enzyme (ACE) gene polymorphism and serum levels in patients with viral pneumonia and predict which polymorphism will lead to severe progression of the disease. Methodology The serum ACE levels and ACE gene polymorphisms were successfully evaluated with respect to subsequent viral pneumonia using records of 100 patients with viral pneumonia and 100 healthy controls. Results ACE serum concentration was statistically significantly elevated. ACE serum concentration with a cut-off value of ≥5,256.05 pg/mL had 85.3% sensitivity and 83.2% selectivity. In addition, patients with ACE genotype D/D were 0.08 times more likely to manifest severe lung involvement than those with I/I, and patients with the I/D genotype were 0.02 times more likely than their counterparts with I/I. The computed tomography findings of the patients revealed that ACE serum concentration was significantly effective in discriminating between mild and moderate-to-severe lung involvement. No significant difference was observed between the blood parameters and ACE genotype distributions. Conclusions I/D polymorphism likely affects the expression of the ACE gene and/or the function of the angiotensin I converting enzyme. The D/D genotype is associated with vessel wall thickness and higher blood pressure. Strong evidence was found between D/D and I/D genotypes in the patient cohort concerning genotypes and ACE serum concentration. Further analysis showed that ACE serum levels were more elevated in the D/D genotype compared to the I/D genotype in the patient cohort.

Various biomarkers are used when evaluating the hospitalization needs of patients diagnosed with Coronavirus disease (COVID-19). Ischemia-modified albumin (IMA) is a biomarker that causes blood levels to increase as a result of hypoxia and acidosis. We think that an increase in IMA in the blood may be caused by hypoxia stemming from lung damage. This study aimed to compare the mean/median of the blood IMA value in patients with pneumonia due to COVID-19 infection with a control group.The case group included patients with COVID-19 pneumonia detected by lung imaging and a positive COVID test. Demographic information of the case group, the severity of pneumonia, and their PCR test results were recorded in the data set.A total of 150 people, 90 of whom were in the case group and 60 of whom were in the control group, participated in the study. No statistically significant differences were found between the blood IMA levels of the case group and the control group. When the blood IMA levels of the case group were compared according to pneumonia severity, no statistically significant differences were found between the mild-moderate and severe pneumonia groups.Blood IMA levels are not a diagnostic biomarker for patients with COVID-19 pneumonia and are not helpful in predicting the severity of pneumonia.

Purpose: Serum surfactant protein D (SP-D) plays roles in the body such as protection against viral infection,bacterial and fungal clearance, clearance of apoptotic cells and suppression of inflammation. This study aims toexamine the relationship between SP-D level and coronavirus disease (COVID-19) severity.Methods: 80 patients (30 with mild disease and 50 with severe/critical COVID-19), and 50 healthy volunteerswere enrolled in the study. SP-D levels were analyzed by ELISA in serum samples.Results: The median of SP-D was found to be 2.47 (1.67-7.79) ng/ml in mild disease and 5.65 (3.09-16.55) ng/ml in severe/critical disease groups, while 2.89 (10.8-6.24) ng/ml in the healthy controls. The differences in SP-Dlevels between the severe/critical disease group compared to both mild disease and control groups were foundstatistically significant (p=0.007 and 0.001, respectively). ROC analysis showed greater AUC for the serumSP-D levels of the severe/critical COVID-19 patients compared to mild COVID-19 disease patients (AUC=0,691,95% CI=0.56-0,822; p=0.004). Furthermore, SP-D levels were 86% sensitive and 51.6% specific at 2.44 ng/mllevel (p=0.004) to detect severe/critical patients.Conclusion: SP-D levels is useful for COVID-19 patients in the prediction of clinical severity and prognosis.SP-D is a valuable biomarker for predicting the clinical severity and prognosis., Amaç: Serum surfaktan protein D (SP-D) vücutta viral enfeksiyona karşı koruma, bakteriyel ve fungal klirens,apoptotik hücrelerin temizlenmesi ve inflamasyonun baskılanması gibi roller oynar. Bu çalışma, SP-D düzeyi ilekoronavirüs hastalığı (COVID-19) şiddeti arasındaki ilişkiyi incelemeyi amaçlamaktadır.Gereç ve yöntem: Çalışmaya 80 hasta (30 hafif hastalığı ve 50 ağır/kritik COVID-19) ve 50 sağlıklı gönüllü dahiledildi. Serum örneklerinde SP-D seviyeleri ELISA ile analiz edildi.Bulgular: SP-D düzeyi ortanca değeri hafif hastalıkta 2,47 (1,67-7,79) ng/ml, ağır/kritik hastalık gruplarında5,65 (3,09-16,55) ng/ml iken, sağlıklı control grubunda 2,89 (10,8-6,24) ng/ml olarak bulundu. Ağır/kritik hastalıkgrubu hem hafif hastalık hem de kontrol grubu ile karşılaştırıldığında SP-D düzeylerindeki farklılıklar istatistikselolarak anlamlı bulundu (sırasıyla p=0,007 ve 0,001). ROC analizi, hafif COVID-19 hastalığı hastalarına kıyaslaşiddetli/kritik COVID-19 hastalarında serum SP-D seviyeleri için eğri altında kalan alan daha yüksek saptandı(AUC=0.691, %95 CI=0,56-0.822; p=0,004). Ayrıca, ağır/kritik hastaları saptamak için SP-D düzeyleri 2,44 ng/ml düzeyinde (p=0,004) %86 duyarlı ve %51,6 özgül saptandı.Sonuç: SP-D seviyeleri, COVID-19 hastaları için klinik şiddeti ve prognozu tahmin etmede faydalıdır. SP-D,klinik şiddeti ve prognozu tahmin etmek için değerli bir biyobelirteçtir.

This study aims to evaluate the relationship between peroxisome proliferator-activated receptor (PPAR) alpha and gamma gene polymorphisms and acute coronary syndrome (ACS) clinically.Peripheral blood samples were collected from a total of 200 people, including 100 acute coronary syndrome patients and 100 controls aged 19 to 93 years, admitted to the Pamukkale University Emergency Medicine Department. The healthy volunteers had no known chronic or acute diseases, no history of drug use, and no recent history of coronary artery disease (CAD). PPAR alpha L162V and PPAR gamma C161T gene polymorphic regions were detected using DNA sequencing analyses. In addition, data collected from the hemogram and biochemical parameters and comorbidities of the patients were statistically analyzed.PPAR gamma C161T polymorphisms were compared between groups. The CT heterozygous rate in the patient group (74%) was higher than in the control group (7%). The T allele was more common in the patient group (0.37) compared to the control group (0.03). When PPAR alpha L162V polymorphism was compared, VV homozygous individuals were %19 in the patient group and none in the control group. The V allele was found to be statistically higher in patients with ACS (p0.01).The findings revealed that elevated PPAR alpha L162V and PPAR gamma C161T gene polymorphisms were associated with a progressive risk of ACS.

Background Recent studies have investigated the importance of Galetin-3 in inflammation, fibrosis, cell proliferation, cardiac disease, diabetes, and tumor formation. Aims This study aims to investigate the role of the Galectin-3 level in the diagnosis of COVID-19 pneumonia and the value of the Galectin-3 level in predicting the clinical course of the patient. Methods This study employed a prospective, case-control study design and was conducted at Bakircay University Ciğli Training and Research Hospital. A total of 100 patients (40 had moderate and 60 had severe/critical COVID-19 disease according to World Health Organisation guidelines) and 50 non-symptomatic healthy volunteers participated in the study. Blood samples were taken from patients at the time of hospital admission, after which serum was isolated. Following the isolation of serum, Galectin-3 levels were evaluated using the enzyme-linked immunosorbent assay (ELISA) method. Results The serum Galectin-3 level was measured as 13.57 (10.9-16.4) ng/mL in the control group, 13.52 (10.69-16.6) ng/mL in the moderate disease group, and 11.65 (6.09-14.33) ng/mL in the severe/critical disease group. Serum Galectin-3 levels were significantly lower in the severe/critical disease group compared to the control and moderate disease groups (p=0.001 and p=0.019, respectively). Using ROC analysis, a larger area under the curve (AUC) for the serum Galectin-3 levels of the control group (AUC=0.622, 95% CI =0.529-0.714; p=0.015) was calculated compared to the COVID-19 patient group for the diagnosis of COVID-19 disease. The Galectin-3 level was found to be 75% sensitive and 50% specific at a cut-off level of 11.3 ng/mL in predicting the need for ICU treatment. Conclusion Galectin-3 levels may be a beneficial biomarker in predicting the clinical severity of COVID-19 disease when used in conjunction with other known biomarkers, at the time of admission to the emergency department (ED).

Inflammatory processes play an important role in the pathogenesis of heart failure. The accumulation of unfolded protiens in the endoplasmic reticulum lumen and the unfolded protien response signal path is activated. The IL-IB gene is located in the Chromsone 2.q14 region. -31 and -511 single nucleotide polymorphisms (SNPs) were detected in the IL-IB Promoter region. These two SNPs affect IL-1expression. This Study aims to investigate the presence of IL-IB (-511 C / T) and IL-IB (-31 T / C) gene polymorphisms and the relationship between ER Stress markers and the inflammatory markers. Patients who applied to the department of emergency medicine with the findings of acute decompensated heart failure. Polymorphic sites of the IL-IB gene were determined by DNA sequencing. In all study, individuals with IL-IB (-31 T / C) T allele have higher serum PERK, GRP-78, CHOP AND CRP levels median values than individuals with IL-IB (-31 T/C) C allele (p = 0.00001, p = 0.0002, p = 0.002 and p = 0.011, respectively). Serum ERK and GRP-78 Values in HF Group were higher in individuals with IL-IB (-31 T / C) T allele compared to individuals with C alle (p = 0.0001 and p = 0.0006). There was a statistically difference in serum CHOP levels in the control group with the IL-IB (-511 C / T) T allele and the individuals with the C allele in the HF group (p= 0.002). In Cnclusion we consider that the inflammatory response caused by IL-IB (-31 T / C) gene polymorphism increased and the ER stress response increased, inflammatory pathway and stress of having IL-IB (-31 T / C) T / T genotype or T allele.

Aim: Angiopoietins play an important role in the regulation of inflammation, angiogenesis and increased vascular permeability, which are the main steps in the pathogenesis of malignant pleural effusions (MPEs). The present study investigates the diagnostic value of pleural fluid angiopoietin-2 (Ang-2) levels in the differentiation of malignant pleural effusions from other effusions.Methods: This research was designed as case-control study in a single-center. The study included a total of 66 patients (13 had transudate, 28 had benign exudate and 25 had malignant pleural effusions). The patient group involved 25 patients diagnosed with MPE, based on the criteria of lung cancer and other organ malignancies, and malignant pleural effusion. The control group consisted of 41 patients, 13 with transudate according to the Light criteria and 28 with exudate other than MPE (parapneumonic, tuberculous pleurisy, embolism, etc.). Results: Pleural fluid Ang-2 levels were found to be higher in both the benign and malignant exudates than in the transudative pleural effusions (P=0.001). Pleural fluid Ang-2 levels were higher in the benign exudate group than in the malignant exudate group, although the difference was not statistically significant (P=0.874). A patient with an exudative pleural effusion and a pleural fluid Ang-2 level of higher than 13.84 was found to be 1.87 times more likely to have a malignant pleural effusion.Conclusion: Despite the use of Ang-2 levels in the differentiation of transudative and exudative pleural effusions, the present study found that Ang-2 level cannot be used to differentiate between malignant and benign exudative pleural fluids., Amaç: Anjiopoietinler, malign plevral efüzyon (MPE) patogenezinde ana basamaklar olan inflamasyon, anjiyogenez ve vaskuler permeabilite artışının düzenlenmesinde önemli bir rol oynamaktadır. Çalışmamızda, malign plevral efüzyonların diğer efüzyonlardan ayrımında plevra sıvı anjiopoietin 2 (Ang-2) seviyelerinin tanısal değerini araştırdık.Yöntemler: Bu çalışma, tek merkezli vaka kontrol çalışması olarak tasarlandı. Çalışmamıza, 13 transüda, 28 benign eksüda ve 25 malign plevral sıvıya sahip (malign eksüda) toplam 66 hasta alındı. Çalışmaya hasta grubu olarak olarak MPE tanısı konulmuş 25 hasta alındı. MPE tanılı hastalar; akciğer veya diğer organ maligniteleri mevcut olan ve plevral sıvının maligniteye bağlı olarak olarak geliştiği hastalardan oluştu. Kontrol grubu olarak, Light kriterlerine göre transüda olduğu saptanan 13 hasta ve MPE dışındaki eksüda vasıflı (parapnomonik, tüberküloz plörezi, emboli vb) 28 hasta olmak üzere toplam 41 hasta dahil edildi.Bulgular: Plevral sıvı Ang-2 seviyeleri, hem benign eksüda hem de malign eksüda vasfındaki sıvılarda transüda vasfındaki plevral sıvılara göre belirgin olarak yüksek bulundu (P=0,001). Benign eksüda grubunda plevra Ang-2 seviyeleri malign eksüda grubuna göre yüksek olarak saptandı ancak bu durum istatistiksel olarak anlamlı değildi (P=0,874). Eksüda vasıflı plevral sıvılarda Ang-2 düzeyi 13,84 değerinin üzerinde saptanmış olan bir hastada malign plevral efüzyon olma riski, 13,84 değerinin altında olan bir hastaya göre 1,87 kat fazla bulundu.Sonuç: Ang-2’nin, transüda ve eksüda özelliğindeki plevral sıvıların ayrımında kullanılabilir olmasına rağmen, eksüdatif plevral sıvılarda, malign ya da benign ayrımı yapmada yetersiz olduğu saptandı.

Background/Aim: This study aimed to measure the DNA methylation state of thousands of CpG islands in the blood of two monozygotic twins that were discordant for cardiovascular disease (CVD). Twin 1 had suffered myocardial infarction, while the other was healthy. Patients and Methods: Since the aim of this study was to identify differentially methylated regions which might act as potential markers, reduced-representation bisulfite libraries were used for whole-genome methylation analysis. Results: According to the analysis, 11 genes lipid droplet associated hydrolase (LDAH), apolipoprotein B (APOB), acyl-CoA synthetase medium chain family member 2A (ACSM2A), acyl-CoA synthetase medium chain family member 5(ACSM5), acylCoA synthetase family member 3 (ACSF3), carboxylesterase 1 (CES1 ), carboxylesterase 1 pseudogene 1 (CES1P1), AFG3 like matrix AAA peptidase subunit 2 (AFG3L2), iron-sulfur cluster assembly enzyme (ISCU), SEC14 like lipid binding 2 (SEC14L2) and microsomal triglyceride transfer protein (MTTP) were all hypomethylated in DNA from twin 2, the unaffected twin. Methylation changes were observed at different multiple loci between the twins, suggesting loci that are affected by disease status in identical genetic backgrounds. Conclusion: This twin study may contribute significantly to the understanding of the genetic basis of CVD and resulting myocardial infarction. This approach may allow identification of possible target loci associated with aberrant epigenetic regulation in CVD. C1 [Koseler, Aylin] Pamukkale Univ, Dept Biophys, Sch Med, Denizli, Turkey. [Ma, Feiyang; Morselli, Marco; Pellegrini, Matteo] Univ Calif Los Angeles, David Geffen Sch Med, Dept Mol Cell & Dev Biol, Box 951606, Los Angeles, CA 90095 USA. [Kilic, Ismail Dogu; Kilic, Oguz] Pamukkale Univ, Dept Cardiol, Sch Med, Denizli, Turkey.

SARS-CoV-2 Spike protein was predicted by molecular docking to bind the host cell surface GRP78, which was suggested as a putative good molecular target to inhibit Covid-19. We aimed to confirm that GRP78 gene expression was increased in blood of SARS-CoV-2 (+) versus SARS-CoV-2 (-) pneumonia patients. In addition, we aimed to identify drugs that could be repurposed to inhibit GRP78, thus with potential anti-SARS-CoV-2 activity. Gene expression studies were performed in 10 SARS-CoV-2 (-) and 24 SARS-CoV-2 (+) pneumonia patients. A structure-based virtual screen was performed with 10,761 small molecules retrieved from DrugBank, using the GRP78 nucleotide binding domain and substrate binding domain as molecular targets. Results indicated that GRP78 mRNA levels were approximately four times higher in the blood of SARS-CoV-2 (+) versus SARS-CoV-2 (-) pneumonia patients, further suggesting that GRP78 might be a good molecular target to treat Covid-19. In addition, a total of 409 compounds were identified with potential as GRP78 inhibitors. In conclusion, we found preliminary evidence that further proposes GRP78 as a possible molecular target to treat Covid-19 and that many clinically approved drugs bind GRP78 as an off-target effect. We suggest that further work should be urgently carried out to confirm if GRP78 is indeed a good molecular target and if some of those drugs have potential to be repurposed for SARS-CoV-2 antiviral activity. C1 [Palmeira, Andreia; Sousa, Emilia; Pinto, Madalena M.] Univ Porto, Fac Pharm, Dept Chem Sci, Lab Organ & Pharmaceut Chem LQOF, Rua Jorge Viterbo Ferreira 228, P-4050313 Porto, Portugal. [Palmeira, Andreia; Sousa, Emilia; Pinto, Madalena M.] Interdisciplinary Ctr Marine & Environm Res CIIMA, P-4450208 Matosinhos, Portugal. [Koseler, Aylin] Pamukkale Univ, Dept Biophys, Fac Med, TR-20190 Denizli, Turkey. [Sabirli, Ramazan] Kafkas Univ, Dept Emergency Med, Fac Med, TR-36000 Kars, Turkey. [Goren, Tarik; Turkcuer, Ibrahim] Pamukkale Univ, Dept Emergency Med, Fac Med, TR-20190 Denizli, Turkey. [Kurt, Ozgur] Acibadem Mehmet Ali Aydinlar Univ, Dept Microbiol, Sch Med, TR-34752 Istanbul, Turkey. [Helena Vasconcelos, M.] Univ Porto, Inst Invest & Inovacao Saude i3S, P-4200135 Porto, Portugal. [Helena Vasconcelos, M.] Univ Porto IPATIMUP, Canc Drug Resistance Grp, Inst Mol Pathol & Immunol, P-4200135 Porto, Portugal. [Helena Vasconcelos, M.] Univ Porto, Fac Pharm, Dept Biol Sci, Lab Microbiol, P-4050313 Porto, Portugal.

Background/Aim: A novel human coronavirus, named SARS-COV-2, has recently caused thousands of deaths all around the world. Endoplasmic reticulum (ER) stress plays an important role in the development of diseases. Patients and Methods: We aimed to to investigate the relationship between ER stress markers in patients infected with SARS-COV-2 and patients with pneumonia. A total of 9 patients (4 patients diagnosed with pneumonia and 5 patients diagnosed with SARS-COV-2 infection) who admitted to the emergency Department with symptoms of pneumonia and SARS-COV-2 were included in the study. A total of 18 healthy individuals without any known chronic or acute disease and drug use were included as the healthy control group. Serum human glucose regulated protein 78 (GRP78), serum human C/EBP homologous protein (CHOP) and serum human phospho extracellular signal regulated kinase (PERK) levels were measured using enzyme-linked immunosorbent assay (ELISA). Results: GRP78 levels were found to be significantly higher in SARS-COV-2 positive cases compared to individuals in other groups. Serum GRP78 level median value was statistically significantly higher in SARS-COV-2-positive group compared to the other groups (p=0.0003). Serum PERK level was statistically significantly higher in SARS-COV-2-positive pneumonia cases (p=0.046). Conclusion: An association was shown between GRP78 and SARS-COV-2 infection. Although a small number of patients was investigated, these results will be important and guide future treatments of SARS-COV-2. C1 [Koseler, Aylin] Pamukkale Univ, Fac Med, Dept Biophys, Denizli, Turkey. [Sabirli, Ramazan] Kafkas Univ, Dept Emergency Med, Fac Med, Kars, Turkey. [Goren, Tarik; Turkcuer, Ibrahim] Pamukkale Univ, Dept Emergency Med, Fac Med, Denizli, Turkey. [Kurt, Ozgur] Acibadem Mehmet Ali Aydinlar Univ, Sch Med, Dept Microbiol, Istanbul, Turkey.

Aims:Nondiabetic patients were studied to determine whether modest elevations in plasma mannose may be associated with a greater incidence of coronary artery disease (CAD). Materials and Methods:Plasma insulin, mannose, glucose, hexokinase 1-2, GLUT1-GLUT4 levels, and serum mannose phosphate isomerase enzyme levels were evaluated with respect to subsequent CAD using records from 120 nondiabetic CAD patients and 120 healthy volunteers. CAD was identified from myocardial infarction and new diagnoses of angina. Results:Of 120 nondiabetic CAD patients studied, their plasma GLUT4 and HK1 levels were significantly lower than those of the control group. A significant increase in plasma mannose levels was found in the patient group compared to the control group. Conclusion:Our findings showed that elevated baseline mannose levels in plasma are associated with an increased risk of CAD over time. C1 [Koseler, Aylin] Pamukkale Univ, Fac Med, Dept Biophys, TR-20020 Denizli, Turkey. [Arslan, Idris] Bulent Ecevit Univ, Dept Biomed Engn, Zonguldak, Turkey. [Sabirli, Ramazan] Kafkas Univ, Fac Med, Dept Emergency Med, Kars, Turkey. [Zeytunluoglu, Ali] Pamukkale Univ, Vocat Sch Tech Sci, Dept Elect & Automat, Denizli, Turkey. [Kilic, Oguz] Doc Dr Ismail Karakuyu State Hosp, Dept Cardiol, Kutahya, Turkey. [Kilic, Ismail Dogu] Pamukkale Univ, Fac Med, Dept Cardiol, Denizli, Turkey.