journal: Turkish Journal of Biochemistry

Impact Factor: 0.7

Zeitschrift Open Access

Turkish Journal of Biochemistry

Türk Biyokimya Dergisi

Editor-in-Chief: Doğan Yücel

Sprache: Englisch

Erstveröffentlichung: 1. Januar 1976

Neuestes Heft anzeigen

Veröffentlicht von

Veröffentlichen auch Sie bei De Gruyter Brill

Manuskript einreichen Informationen für Autor*innen Erkunden Sie dieses Fachgebiet

Über diese Zeitschrift

Objective
The Turkish Journal of Biochemistry (TJB) is the official journal of the Turkish Biochemical Society. The aim of the journal is to promote the international research and publication culture. TJB publishes contributions in the field of medical sciences, including clinical biochemistry, hematology, immunology, microbiology and molecular biology and genetics. TJB is published bi-monthly. All articles submitted for publication in TJB are subject to double-anonymized peer review by at least two experts in the field, selected and invited by the Editor-in-Chief and a dedicated editorial team. TJB publishes only English-language articles.
TJB is an open access journal. To sustain the publication of all fully peer-reviewed manuscripts, each article accepted for publication in TJB is subject to an article processing charge (APC), paid by the authors' affiliated institutions, funders, sponsors or institutions that have an agreement with us.
Open Researcher and Contributor ID (ORCID) is mandatory for submission.

Topics
Biomarkers // Cellular and molecular biochemistry // Clinical biochemistry // Clinical hematology and coagulation // Clinical immunology and autoimmunity // Clinical laboratory management // Clinical microbiology // Laboratory medicine in diseases // Medical biochemistry // Medical metrology // Molecular biology // Molecular genetics // Molecular mechanisms of diseases // New technologies, methodologies, reagents, and instrumentation // Therapeutic drug monitoring // Training and education in biochemistry and clinical biochemistry // Translational laboratory medicine

Article formats
Research Article // Review Article/Mini Review // Opinion Paper // Editorial // Short Communication // Letter to the Editor and Reply // Case Report // Guidelines and Recommendations // Congress Abstracts

Ihre Vorteile

Wide-ranging platform for promoting local and global research in biochemistry
Basic and applied research in the field of biochemistry
High quality peer-review
Archive of volumes 1-40 (1976-2015)
Authors retain copyright – articles published under the Creative Commons Attribution (CC-BY-4.0) License
Each article easily discoverable because of Search Engine Optimization (SEO) and comprehensive abstracting and indexing services
Secure archiving by De Gruyter and the independent archiving service Portico

Open Access
Study on the roles of glycolipid metabolism indicators and microRNAs in benign prostatic hyperplasia

17. Oktober 2025

Yanping Li, Hongyan Zhang, Yanjun Yue

PDF downloaden

Objectives As a highly prevalent disease in older men, the incidence of benign prostatic hyperplasia (BPH) is increasing as aggravating aging of the global population. This study aimed to explore the pathogenesis of BPH and its potential biomarkers. Methods Expression of miR-96-5p/miR-181a-5p and glycolipid metabolism indicators (GLMI) were detected by collecting the peripheral blood samples from 100 healthy volunteers and 110 patients with BPH. The diagnostic value of clinical factors for BPH was evaluated through the receiver operating characteristic (ROC) curve. The inhibitors of miR-96-5p and miR-181a-5p were introduced to detect their roles in BPH pathogenesis and regulation of FOXP2 expression. Interaction between miR-96-5p/miR-181a-5p and FOXP2 mRNA was verified through dual luciferase assay. Silencing FOXP2 to explore its role in the progression of BPH. Results GLMI, miR-96-5p, and miR-181a-5p levels are high in BPH patients and increased with the severity of disease, and their blood levels are positively correlated with International Prostate Symptom Score (IPSS). MiR-96-5p combined with miR-181a-5p is a good prediction model for the occurrence and severe progression of BPH, with area under curve (AUC) of 0.901 and 0.927, respectively; and they combined with GLMI showed a high authenticity, with AUC of 0.927 and 0.962, respectively. MiR-96-5p/miR-181a-5p inhibited FOXP2 expression by adsorption of its mRNA, and their inhibition reduced the viability and promoted apoptosis of WPMY-1 and BPH-1 cells, which was reversed by the silence of FOXP2. Conclusions GLMI, miR-96-5p, and miR-181a-5p presented a close clinical correlation with BPH, which are valuable biomarkers of BPH, and these two miRNAs may contribute to BPH progression by regulating FOXP2 negatively.
Open Access
Serum aberrant expression of microRNA-125b-5p and its association with carotid artery stenosis

2. September 2025

Xiaoling Guo, Tong Zhang, Shaoteng Li, Jiahui Guo, Lihua Xu, Huan Deng, Shaojie Yuan

PDF downloaden

Objectives This study focused on the aberrantly expressed miR-125b-5p and explored its diagnostic and prognostic value in CAS patients. Methods 218 individuals with informed consent were enrolled including 92 healthy individuals (control) and 126 patients with CAS and they provided blood samples willingly. The miR-125b-5p level was computed through qRT-PCR. For assessing the diagnostic capacity of miR-125b-5p, the receiver operator characteristic (ROC) was adopted, supplemented by correlation analysis. The prognostic performance of miR-125b-5p was appraised with the help of the Kaplan-Meier curve plotted according to 5-year follow-up and multivariate Cox regression. Results The expression of serum miR-125b-5p was aberrantly lower in CAS patients than that in the control group. There was a negative correlation between the miR-125b-5p level and the severity of CAS. The ROC curve proved a high credibility in miR-125b-5p diagnosis. The area under the curve (AUC) reached 0.969 with high sensitivity (96.44 %) as well as specificity (86.81 %). Kaplan-Meier curve verified that CAS patients having lower miR-125b-5p were at a higher risk of developing cerebrovascular events (CEs). Both miR-125b-5p and degree of CAS were identified as independent risk factors of developing CEs for CAS patients via multivariate Cox regression analysis. Conclusions The serum miR-125b-5p was aberrantly lower in CAS patients. Lower miR-125b-5p possessed high diagnostic along with prognostic value in CAS patients.
Open Access
To investigate the action mechanism of lncRNA CDKN2B-AS1/hsa-miR-134-5p/CCND1 axis in cervical cancer based on bioinformatics

23. Mai 2025

Weiwei Xiong, Meixing Wang, Xiaohua Wen, Xijuan Wang, Ye Guo, Xingmei Ma, Yanru Liu

PDF downloaden

Objectives Cervical cancer (CC) is a malignant tumor that poses a serious threat to women’s lives and has a complex pathogenesis. This study aims to investigate the mechanism underlying the lncRNA CDKN2B-AS1 in CC. Methods The expression of CDKN2B-AS1, hsa-miR-134-5p, and CCND1 was detected by RT-qPCR and western blotting, and their targeted regulatory relationships were verified by dual-luciferase reporter assay and overexpression/knockdown assay. CCK-8, Transwell, and Annexin V-FITC/PI staining experiments were used to assess the proliferation, migration, invasion and apoptosis of CC cells (HeLa and SiHa), respectively. The Kaplan-Meier survival curve was used to evaluate the clinical value of CDKN2B-AS1 in CC. Results CDKN2B-AS1, CCND1 were high-expressed, and hsa-miR-134-5p was low-expressed in CC cells and tissues. Silencing CDKN2B-AS1 significantly inhibited the growth and metastasis of HeLa and SiHa cells, and induced their apoptosis. The overall survival time of CC patients with high CDKN2B-AS1 was shorter (log rank p<0.05). Hsa-miR-134-5p mimic attenuated the luciferase activity of cells transfected with wild-type CDKN2B/CCND1 luciferase vector. Overexpression of CDKN2B-AS1 decreased the intracellular level of hsa-miR-134-5p, while its knockdown was inverse. The inhibition of hsa-miR-134-5p promoted CCND1 expression. Conclusions High CDKN2B-AS1 level predicted a poor prognosis of CC patients, and it promoted CC development by down-regulating hsa-miR-134-5p to enhance CCND1 expression.
Open Access
Lactobacillus acidophilus ATCC4356 inhibits thyroid cancer via E3 ubiquitin-protein ligase Mdm2 (MDM2)

31. Oktober 2025

Rui-Sheng Ke, Wei-Hao Zhang, Yan-ling Tu, Zhao-Hui Liu, Fu-Xing Zhang, Kun-Zhai Huang

PDF downloaden

Objectives Emerging evidence suggests that Lactobacillus species exhibit anticancer properties against various malignancies, including gastric and breast cancers. However, their effects on thyroid cancer remain unexplored. This study investigates the antitumor potential of Lactobacillus acidophilus ( L. acidophilus ) ATCC 4356 culture supernatants against thyroid cancer and elucidates its underlying molecular mechanism. Methods L. acidophilus culture supernatants were prepared at 24, 48, and 72 h. The supernatants were used to culture thyroid cancer cells at different concentrations. Cell viability was measured via CCK-8 assay, with IC50 values calculated for subsequent experiments. Cell senescence was evaluated using β-galactosidase staining. Potential molecular targets were predicted through bioinformatics analysis and validated by rescue experiments with MDM2 overexpression. Results L. acidophilus supernatants demonstrated concentration-dependent growth inhibition on thyroid cancer cells. The 48 h supernatant showed optimal efficacy, with 16 and 22 % concentrations significantly suppressing proliferation (p<0.01), and triggering cellular senescence in SA-β-gal + cells vs. control (p<0.001). Mechanistically, MDM2 was identified as the key target, as its overexpression partially rescued the antitumor effects in proliferation inhibition and cellular senescence induction. Conclusions These findings establish L. acidophilu s ATCC 4356 as a novel MDM2 -targeting probiotic with therapeutic potential against thyroid cancer, providing a molecular basis for further preclinical development.
Open Access
MicroRNA-766-3p modulates the progression of delayed fracture healing by targeting TGFBR1

26. August 2025

Guorui Zhang, Laicong Liao, Peijie Liu, Jianhua Ren, Yuan Ruan

PDF downloaden

Objectives A certain number of patients frequently encounter delayed fracture healing (DFH) following surgery. This study intended to investigate the functionality of miR-766-3p in the progression of DFH. Methods The research encompassed 100 normal tibial fracture healing patients and 95 DFH patients. RT-qPCR was implemented to measure the expression, and the ROC was used to determine the diagnostic value of miR-766-3p for DFH patients. Cox regression was performed to identify the independent risk factors associated with DFH. Moreover, we further analyzed the regulatory effects of miR-766-3p and TGFBR1 on osteogenic markers. The CCK-8 method and flow cytometry were utilized to detect proliferation and apoptosis. The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) were quantified using enzyme-linked immunosorbent assay (ELISA). The dual-luciferase reporter gene assay was carried out to detect the targeted relationship. Results In DFH patients, miR-766-3p exhibited a downward movement. miR-766-3p served as an independent prognostic factor influencing DFH. miR-766-3p increased after the induction and differentiation of MC3T3-E1 cells. Elevated miR-766-3p could enhance the expression of osteogenic markers, facilitate proliferation and differentiation, inhibit inflammatory reactions, and reduce apoptosis. Additionally, when TGFBR1 was upregulated, it reversed the effect of miR-766-3p on osteoblasts. miR-766-3p may emerge as a feasible predictive biomarker for patients with DFH. Conclusions miR-766-3p exerted its regulatory function on DFH by targeting TGFBR1 .
Open Access
Dysregulation of miR-709 in diabetic kidney disease and its role in inflammatory response

23. Mai 2025

Fang Zhou, Lanlan Chen, Meng Xie, Sen Meng, Jiaze Sun

PDF downloaden

Objectives Research has shown that miRNAs play an essential role in the pathophysiology diabetic kidney disease (DKD). This study primarily explored the expression of miR-709 in DKD and elucidated its potential clinical significance for patients with DKD. Methods A total of 95 patients with DKD were included in the case group, while 102 T2DM patients constituted the control group. 50 healthy individuals were selected as the healthy group. Real-time quantitative PCR was employed to assess the expression levels of miR-709. The receiver operating characteristic curve was used to evaluate the diagnostic value of miR-709 in DKD. Spearman correlation analysis was performed to explore the relationship between serum miR-709 levels and various clinical data variables. Furthermore, an in vitro DKD cell model was developed to investigate the effect of miR-709 expression in DKD. Results In DKD patients, serum miR-709 levels are markedly reduced and have high diagnostic value. MiR-709 associated with clinical features and inflammation in DKD. Up-regulation of miR-709 significantly suppressed HG-induced proliferation and inflammatory factor levels in human mesangial cells (HMCs). Conclusions The decreased level of miR-709 is closely linked to DKD and its inflammation, which is expected to become a potential biomarker for clinical screening and a target for therapeutic intervention.
Open Access
Study on the mechanism of Wuji Baifeng pill in alleviating rosuvastatin-induced liver injury via SREBF2

27. August 2025

Xinyang Li, Wang Chen, Junying Zhao, Zhongjun Jing, Xiaoying Li, Ludan Deng

PDF downloaden

Objectives This study aims to elucidate the mechanism by which Wuji Baifeng pill alleviates rosuvastatin-induced liver injury, with the goal of providing a reference for precise clinical treatment. Methods This study utilized a high-fat diet (HFD) rat model to assess serum liver function indicators and the levels of inflammatory factors and oxidative stress markers in liver tissues. Additionally, quantitative reverse transcription PCR (qRT-PCR) was employed to measure the expression changes of key genes. Results Wuji Baifeng pill and rosuvastatin reduce triglycerides, low-density lipoprotein cholesterol (LDL-C) levels and diacylglycerol acyltransferase 1 ( DGAT1 ) expression, while increasing CGI-58 expression and high-density lipoprotein cholesterol (HDL-C) levels, with combined treatment showing the most significant effect. Wuji Baifeng pill significantly reverses rosuvastatin-induced increasing serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) activities. It significantly reduces rosuvastatin-induced inflammation and oxidative stress. Ten intersection genes were identified, with sterol regulatory element binding protein 2 ( SREBF2 ) as a key therapeutic target of Wuji Baifeng pill. Wuji Baifeng pill significantly reversed rosuvastatin-induced increases in SREBF2 mRNA and protein levels. Overexpression of SREBF2 reversed Wuji Baifeng pill’s antioxidant and anti-inflammatory effects, reducing glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) levels and increasing IL-6 and IL-1β secretion. Conclusions Wuji Baifeng pill significantly inhibits drug-induced liver injury (DILI)-related inflammation and protects against rosuvastatin-induced liver injury through SREBF2 , offering a foundation for developing new therapies for DILI using its active ingredients.
Open Access
miR-30c-5p serves a diagnostic biomarker in chronic heart failure patients and its regulatory role in vascular endothelial

9. September 2025

Dan Xiong, Yi Mei, Yao Zhu, Pan Deng

PDF downloaden

Objectives Chronic heart failure (CHF) is a syndrome of conflicting organ supply and demand caused by cardiac insufficiency. Previous studies have demonstrated that miR-30c-5p is strongly associated with cardiovascular diseases such as cardiac hypertrophy and acute coronary syndrome. The aim of this study was to explore the meaning of miR-30c-5p in the diagnosis of CHF patients and its effect on vascular endothelial cells. Methods Serum miR-30c-5p levels were detected in 113 CHF patients and 98 healthy individuals by RT-qPCR. ROC curve and logistic regression analysis were conducted to estimate the diagnostic ability and risk factors of miR-30c-5p for CHF. The relationship of miR-30c-5p with BNP and LVEF was analyzed by Pearson correlation. The influence of miR-30c-5p on HUVECs cell lines was explored by transfection with miR-30c-5p mimic/inhibitor. Cell apoptosis and proliferation were detected by flow cytometry and CCK8 assay. Transwell assay was used to detect the migration and invasion abilities of cells. Results miR-30c-5p was reduced in CHF patients’ serum and progressively decreased with increasing NYHA grade. The ROC curve demonstrated that miR-30c-5p had high sensitivity (83.19 %) and specificity (84.69 %) to diagnose CHF. Logistic regression revealed that miR-30c-5p was a pivotal risk factor for CHF development. Pearson correlation analysis suggested that miR-30c-5p was negatively related to BNP and positively correlated with LVEF. Transfection of miR-30c-5p mimic suppressed apoptosis and promoted cell proliferation, migration, and invasion in HUVECs. Conclusions Reduced serum miR-30c-5p levels in CHF patients may be a biomarker for CHF diagnosis. Aberrant miR-30c-5p expression may influence CHF development by affecting the HUVECs function.
Open Access
Unravelling the significance of natural products with antiosteoporetic action: a recent review

21. November 2025

Biwen Dong, Yuyan Wang

PDF downloaden

Introduction Degeneration of bone microarchitecture and decreased bone mineral density are hallmarks of osteoporosis, a prevalent skeletal disorder. The promise of natural compounds derived from medicinal plants as safe and efficient treatments has drawn attention due to the drawbacks and adverse effects of existing pharmaceutical medicines. Therefore, knowledge of medicinal plants and phytochemicals with antiosteoporosis potential is crucial. Thus, this article’s goal was to compile the mechanisms and efficacy of medicinal plants and their many types of phytochemicals in the fight against osteoporosis. Content This article reviews current studies on natural substances with anti-osteoporosis properties, discussing their mechanisms such as regulating bone resorption, preventing osteoclastogenesis, encouraging osteoblast differentiation, and reducing inflammatory processes from sources like ScienceDirect, Google Scholar and PubMed. Summary Flavonoids, polyphenols, alkaloids, terpenoids, and vitamins are naturally occurring compounds with promising anti-osteoporotic properties. They inhibit NF-κB, PI3K/Akt, MAPK, and Wnt/β-catenin pathways, regulating bone turnover and inhibiting resorption. Some phytochemicals also protect bones with antioxidant and anti-inflammatory properties. However, challenges remain in translating these findings into clinical practice. Outlook By finding natural products that help fight osteoporosis, this review seeks to increase therapy choices, especially for older persons with osteoporosis. These therapies may lessen health issues, enhance wellbeing, and provide an affordable substitute for pricey prescription drugs. People with chronic illnesses may find natural products attractive since they may have fewer adverse effects than synthetic medications.
Open Access
The role of MiR-361-5p in delayed fracture healing and its clinical predictive value

30. September 2025

Yanqi Shang, Qianqian Cheng, Hongqing Wang, Meng Han

PDF downloaden

Objectives Delayed fracture healing (DFH) is a common clinical complication in orthopedic trauma. This study aims to investigate the expression patterns and regulatory mechanisms of miR-361-5p in DFH. Methods Patients with normal fracture healing (NFH) and DFH were included in this study. miR-361-5p levels in the subjects were detected using RT-qPCR, and the predictive value of miR-361-5p for DFH was evaluated through Receiver Operating Characteristic (ROC) curve. MC3T3-E1 cells were induced to undergo osteogenic differentiation in vitro , and the functional role of miR-361-5p in this process was investigated. The expression levels of osteogenic differentiation markers, including alkaline phosphatase (ALP), osteocalcin (OCN), osteopontin (OPN), and runt-related transcription factor 2 (RUNX2), in the cells were quantitatively assessed using RT-qPCR. Dual luciferase reporter assay and RNA immunoprecipitation assay were used to verify the targeted binding relationship between miR-361-5p and FGF7. Results miR-361-5p significantly increased in patients with DFH. Serum miR-361-5p had a sensitivity of 87.93 % and a specificity of 74.14 % for the prediction of DFH. During the process of osteogenic induction, we observed that the expression level of miR-361-5p gradually decreased. And this molecule is negatively correlated with the level of osteogenic markers. We found that miR-361-5p directly targets FGF7. Transfection with miR-361-5p inhibitor can enhance the activity of ALP and increase the levels of osteogenic markers. However, specific inhibition of FGF7 partially counteracted these effects. Conclusions MiR-361-5p can be used as a potential predictor of DFH. miR-361-5p inhibits osteogenic differentiation by targeting FGF7, thereby delaying the process of fracture healing.
Open Access
Potential of the FOX gene family and LncRNAs as biomarkers in differentiated thyroid cancer treated with I-131

11. Juli 2025

Tugba Agbektas, Ayca Tas, Baris Sariakcali, Zekiye Hasbek, Yavuz Silig

PDF downloaden

Objectives Forkhead box (FOX) transcription factors and long non-coding RNAs (lncRNAs) localize within tumor cell nuclei in various cancers, suggesting their involvement in transcriptional regulation. This study aimed to investigate expression changes of FOX family members and selected lncRNAs to explore their potential regulatory roles in differentiated thyroid cancer (DTC). Methods Expression levels of FOX genes and lncRNAs were analyzed using RT-PCR, and protein levels were measured via ELISA in patients diagnosed with DTC who received radioactive iodine (RAI) therapy. Results RT-PCR analysis revealed significant differences in FOXO1 and HOXA11-AS expression before and after RAI therapy (p<0.05). FOXO3 , FOXP1 , FOXP2 , and CASC21 showed significant expression differences in pre-RAI samples, while MEG3 and KCNQ1OT1 differed significantly post-RAI (p<0.05). Moreover, strong correlations were identified between FOXO3 , FOXP2 , and key lncRNAs including MEG3 , KCNQ1OT1 , CASC21 , and HOXA11-AS (p<0.05). ELISA results showed a significant change in FOXP1 protein levels, and TSH and Tg levels differed significantly across treatment stages (p<0.05). CASC21 exhibited the highest AUC in ROC analysis. Conclusions Despite the limited sample size, the findings suggest the potential of these genes, particularly CASC21, as biomarkers in DTC. These results may contribute to enhancing RAI therapy efficacy and advancing personalized treatment approaches.
Open Access
Novel prostaglandin and isoprostane panel for evaluating Wilson’s Disease

25. September 2025

Merve Banu Polat, Bekir Mert Durukan, Sabir İsrafilov, Gül Yalçın Çakmaklı, İlkay S. İdilman, Osman Dağ, Muşturay Karçaaltıncaba, Cenk Sökmensüer, Bülent Elibol, Hatice Yasemin Balaban, Aslı Pınar

PDF downloaden

Objectives Wilson’s Disease (WD) leads to copper accumulation in the liver and brain. It generates oxidative stress, which can damage the liver and central nervous system (CNS). The concentrations of oxidized lipid products, such as prostaglandins and isoprostanes, in blood and urine can indicate both the presence and the extent of damage. However, there is limited research specifically investigating these oxidative stress biomarkers in WD, making this study a novel contribution to the field. Methods In this study, serum and 24-h urine samples were collected from a total of 64 individuals, including 22 WD patients with hepatic involvement (HI-WD), 17 with neurological-hepatic involvement (NHI-WD), and 25 healthy controls (HC). A Liquid Chromatography Mass Spectrometry (LC-MS/MS) method was developed and validated to quantify specific prostaglandins and isoprostanes in serum and urine samples. Results The results showed significant differences in the levels of iPF 2α -III, 2,3-dinor-iPF 2α -III, 5-iPF 2α -VI in serum as well as PGE 2 , PGD 2 , PGF 2α , iPF 2α -III and 5-iPF 2α -VI in 24-h urine samples between WD and HC groups. Notably, the concentration of PGD 2 in urine was significantly higher in the NHI-WD group compared to both the HC and HI-WD groups. Our novel urine biomarker panel has the potential to be used for grading disease severity, monitoring therapy and assessing CNS involvement in WD. Conclusions It represents one of the first to explore a panel of oxidative stress biomarkers, particularly prostaglandins and isoprostanes, in both serum and urine samples in WD patients, making it an original contribution to the current literature on WD.
Open Access
Rapid diagnosis of pulmonary Chlamydia psittaci infection using metagenomic next-generation sequencing: a case report and literature review

29. April 2025

Xinying Wang, Xiaohong Wang, Ren Ren, Xiangfeng XU

PDF downloaden

Objectives To present the clinical diagnosis and treatment of a case of Chlamydia psittaci pneumonia, review relevant literature, assess the diagnostic value of metagenomic next-generation sequencing (mNGS) in this condition, and enhance clinical understanding of the disease. Methods A case of Chlamydia psittaci pneumonia treated at Tai’an Central Hospital, affiliated with Qingdao University, was analyzed. The terms “Chlamydia psittaci” and “pneumonia” were used to search PubMed for case reports published from 2019 to 2024, and 41 selected cases were summarized and analyzed. Results The patient, a 61-year-old female, was diagnosed with Chlamydia psittaci pneumonia through mNGS of alveolar lavage fluid. Following treatment with levofloxacin and doxycycline, she was discharged from the hospital. A review of the literature identified 41 related cases. The primary clinical manifestations of Chlamydia psittaci pneumonia included fever (100 %), cough (51.2 %), headache (17.1 %), and dyspnea (14.6 %). A history of poultry exposure was noted in 90.2 % of patients. Chest CT imaging revealed bilateral lung involvement in 10 patients (24.3 %), pleural effusion in seven patients (17.1 %), and unilateral lung inflammation in 31 patients (75.6 %). The diagnosis was achieved by mNGS in 38 patients. Most were treated with doxycycline, minocycline, or moxifloxacin, with favorable outcomes. Improvement was observed in 40 patients (97.6 %) following timely and accurate treatment. Conclusions In summary, mNGS is a primary method for detecting Chlamydia psittaci clinically. The main treatment for infections caused by this pathogen involves tetracyclines or combinations of tetracyclines and fluoroquinolones.
Open Access
Exercise combined with cognitive rehabilitation training affects miR-103a-3p/BDNF expression to improve Alzheimer’s disease

20. November 2025

Hui Xu, Xue-Ping Wang, Song-Li Mei, Zhu Song, Jie Yang

PDF downloaden

Objectives Exercise and cognitive rehabilitation exercises (EC) have been shown to slow the progression of Alzheimer’s disease (AD). To evaluate the regulation of EC for the miR-103a-3p/BDNF expression to delay the progression of AD. Methods AD patients were assigned to control (n=30) and EC groups (n=30) using a random number table method. Cognition was assessed using the Mini-Mental State Examination (MMSE), ‌Activity of Daily Living (ADL), and the Alzheimer’s Disease Assessment Scale–Cognition (ADAS-Cog) before and after treatment.in AD patients. The expression of miR-103a-3p in AD patients was detected by the RT-qPCR method. The expression of amyloid β-protein (Aβ), phosphorylated Tau proteins (p-Tau), BDNF, Tumor Necrosis Factor-α (TNF-α), and Interleukin-1 beta (IL-1β) in the serum of AD patients was measured by ELISA. Results After six months of EC treatment for them, MMSE and ALD scores were elevated, and ADAS-cog scores were reduced in AD patients. In addition, serum Aβ 1-42 was elevated and p-Tau was decreased in AD patients after EC treatment. RT-qPCR results indicated that the expression of miR-103a-3p was reduced in AD patients after EC treatment. The results of ELISA indicated that the expression of BDNF was increased while TNF-α and IL-1β were decreased in AD patients after EC treatment. Dual-luciferase reporter assay confirmed miR-103a-3p targeting of BDNF. Conclusions EC may affect miR-103a-3p/BDNF expression to inhibit the expression of pro-inflammatory factors (TNF-α and IL-1β), thus alleviating AD.
Open Access
Relationship between glycosylated hemoglobin level and prognostic cardiac function in diabetic patients complicated with myocardial infarction

11. September 2025

Feng Liu, Huan Yu, Yajun Qin

PDF downloaden

Objectives The study aimed to explore the correlation between glycated hemoglobin (HbA1c) levels and cardiac function in diabetic individuals who have experienced a heart attack. Methods Eighty diabetic patients with myocardial infarction admitted between March 2021 and November 2022 were divided into two groups: low HbA1c (<6.5 %, n=33) and high HbA1c (>6.5 %, n=47). Patient data were collected. Left ventricular function, Including left ventricular ejection fraction (LVEF), left ventricular end systolic volume (LVESV), and left ventricular end diastolic volume (LVEDV), which infarct size, and global peak strain (radial, circumferential, longitudinal) were measured using CMRI. Cardiac troponin and BNP/NT-proBNP levels were measured by ELISA. Pearson correlation and multivariate linear regression analyzed the relationship between HbA1c levels and left ventricular function. Results No significant variation in overall data between groups (p>0.05). High HbA1c group had lower LVEF and higher LVESV and LVEDV (p<0.05). Infarct size was larger in the high HbA1c group (p<0.05). Peak strains in all directions were significantly lower in the high HbA1c group (p<0.05). BNP and NT-proBNP levels were higher in the high HbA1c group (p<0.05). HbA1c level negatively correlated with left ventricular strain parameters (p<0.05). HbA1c independently predicted decreased LVEF and strain value (p<0.05). Conclusions Higher HbA1c levels in diabetic myocardial infarction patients are closely correlated with decreased left ventricular function, weakened cardiac deformability, and increased myocardial injury.
Open Access
miR-15b-5p affects the innate immune response through PAQR3 in patients with reflux esophagitis

27. Mai 2025

Ye Wei, Yixin Zhang, Xiaowen Zheng, Chunlei Li, Qianqian Peng

PDF downloaden

Objectives Reflux esophagitis (RE) arises from the regurgitation of gastric fluid that contains acids, bile, and other damaging components, significantly impacting on the quality of life. This study aimed to investigate the functions of miR-15b-5p and AdipoQ receptor family member 3 (PAQR3) in reflux esophagitis, as well as to delve into the effect on innate immune response. Methods The study enrolled 54 patients with RE and 33 healthy subjects. qRT-PCR was used to detect the expression level of miR-15b-5p, PAQR3, TLR2, TLR4 and MyD88. The ELISA kits were employed to assess the alterations in the levels of IFN-β, IL-6, and IL-8. Additionally, a dual-luciferase reporter assay was used to verify the binding relationship between miR-15b-5p and PAQR3. Results miR-15b-5p was significantly elevated in RE patients. Cell model tests demonstrated that miR-15b-5p was upregulated in cells treated with acid medium. Inhibition of miR-15b-5p significantly suppressed the expression of innate immunity related genes induced by acid medium. miR-15b-5p targets and regulates PAQR3. In addition, miR-15b-5p activated innate immune responses by blocking PAQR3. Conclusions miR-15b-5p may be involved in the innate immune response of reflux esophagitis by regulating PAQR3.
Open Access
Evaluation of TNF (rs1800629), TLR2 (rs111200466), and TLR4 (rs4986790) gene polymorphisms in adult patients with acute appendicitis

7. Oktober 2025

Yusuf Ertugrul Aslan, Elif Funda Şener, Nahide Ekici Günay, Emre Tuğhan, Tuğba Coşkun Aslan, Şeniz Demiryürek

PDF downloaden

Objectives Acute appendicitis (AA) is the primary cause of urgent surgery. The goal of this case-control study was to establish the possible associations of tumor necrosis factor (TNF), toll-like receptor-2 (TLR2), and toll-like receptor-4 (TLR4) gene polymorphisms in cases of AA in a Turkish population. Methods This prospective research was performed on 160 AA cases admitted into the Erciyes University Emergency Medicine Department. A total of 197 healthy volunteers were also included as a control group. TNF –308 G>A (rs1800629), TLR2 −196 to −174 del/ins (rs111200466), and TLR4 (Asp299Gly, 896A>G, rs4986790) polymorphisms were analyzed using real-time polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLR) methods. Results The TNF rs1800629 polymorphism had significant increases in the patient group’s A allele frequencies and AA genotype (p<0.001). However, for the TLR2 (−196 to −174 del/ins) and TLR4 Asp299Gly polymorphisms (p>0.05), no significant correlations were found in the genotype frequencies. Conclusions This research demonstrated that TNF −308G>A, but not the TLR2 (−196 to −174 del/ins) or TLR4 Asp299Gly variant, is a contributing factor to the susceptibility of AA development in the Turkish population.
Open Access
Clinical value of miR-31-5p in predicting vascular calcification in patients with end-stage renal disease

20. Oktober 2025

Rongna Li, Renping Guan, Yanhui Lv

PDF downloaden

Objectives Vascular calcification (VC) significantly elevates the mortality risk in patients with end-stage renal disease (ESRD). This study was to explore the clinical utility of miR-31-5p in the diagnosis and prognostication of VC. Methods According to the occurrence of VC, all patients with ESRD were categorized into a VC group and a non-VC group. Subsequently, the levels of miR-31-5p in these patients were evaluated using RT-qPCR. The ability of miR-31-5p to diagnose VC patients was assessed through receiver operating characteristic curve. To investigate whether miR-31-5p serves as a risk factor influencing the progression of VC, we employed Kaplan-Meier survival analysis in conjunction with binary logistic regression analysis. Results In a cohort of 90 patients suffering from ESRD, 63 individuals were diagnosed with VC. Notably, the duration of dialysis in VC patients was significantly prolonged compared to non-VC patients. Conversely, levels of Fetuin-A, albumin, and miR-31-5p were found to be lower in VC patients. Furthermore, a positive correlation emerged between miR-31-5p and both fetuin-A and albumin. Importantly, miR-31-5p demonstrated a proficient capacity to differentiate between VC and non-VC patients. More critically, a decline in miR-31-5p serves as a significant risk factor influencing the progression of VC, subsequently contributing to its exacerbation. Conclusions Patients with ESRD exhibiting low levels of miR-31-5p are at an increased risk for the deterioration of VC. Consequently, we propose that the dysregulation of miR-31-5p serves as a potential predictor for VC risk in individuals with ESRD.
Open Access
Comparison between free light chains and immunofixation electrophoresis: one-year data from a tertiary hospital

25. Juli 2025

Fatmagül Can, Fatma E. Koçak, Yavuz Çoban

PDF downloaden

Objectives Immunofixation electrophoresis (IFE) is a biochemical diagnostic method used in the diagnosis, treatment, and follow-up of monoclonal gammopathies. Paraproteinaemias involve overproduction of immunoglobulins, known as paraproteins or monoclonal proteins (M-proteins). M-protein can be detected as a sharp band on serum protein electrophoresis (SPE). Paraprotein types produced in monoclonal gammopathies can be detected by the IFE method. In our study, we aimed to retrospectively evaluate the types of paraproteinaemia detected by the IFE method in the laboratory and to compare our data with the literature. Methods A retrospective evaluation of the IFE results of a medical biochemistry laboratory of a tertiary care education and research hospital in Turkey in terms of the frequency and type of monoclonal gammopathy was performed in 2022. Serum free kappa/lambda ( κ / λ ) ratios and IFE results were compared. Results In our study, 1,169 serum IFE results were retrospectively analyzed, and paraprotein bands were detected in 116 different cases. The frequency of detected paraproteins was determined to be 10 %. A comparison between serum free κ / λ ratios and IFE results yielded 87 % concordance. Conclusions In our retrospective analysis, we obtained results similar to those reported in the literature in terms of serum immunofixation data, age, gender, and immunoglobulin types. We identified IgG- κ (20 %) as the most common paraprotein type. We believe that our study will contribute to the literature in terms of the frequency and variety of paraproteinemia. The κ / λ ratio is of limited use, since most abnormal IFE sera have normal free light chain (FLC) ratios.
Open Access
Geniposide effect on cardiac zinc level, oxidative stress, inflammation, and apoptosis in rats with obesity-linked heart injury

11. Juli 2025

Lu Li, Pan Liu

PDF downloaden

Objectives Geniposide (GNP) is a natural compound that possesses both antioxidant and anti-inflammatory activities. Here, we examined GNP effect on obesity-induced cardiac injury in Wistar rats. Methods Wistar rats were grouped into control, high fat diet (HFD) and HFD+GNP. Levels of cardiac total antioxidants and malondialdehyde (MDA) were measured. TUNEL assay was applied to detect cardiac cells apoptosis. Gene expression analysis was performed for catalase (CAT), tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD), interleukin-10 (IL-10), Caspase-3 and -9, B-cell lymphoma-2 (Bcl2) and Bcl-2-associated X protein (Bax) by Real Time PCR and fold-change ratio was calculated using 2 −ΔΔCt method. Results GNP administration not only decreased hyperlipidemia, atherogenic coefficient (0.65±0.06 vs. 1.70±0.31; p<0.001) and cardiac risk ratio (1.65±0.23 vs. 2.70±0.29; p<0.01), but also it attenuated inflammatory cell infiltration and cardiomyocyte vacuolization, and cardiac apoptotic cells (8.22±1.05 % vs. 21.46±2.44 %; p<0.001) compared to HFD alone. GNP significantly increased cardiac TAC (578.11±36.2 μM/g tissue; p<0.01) and zinc (144.17±8.57 vs. 102.13±5.81 ng/g tissue; p<0.001) contents, but significantly decreased MDA content (3.02±0.5 vs. 4.71±0.38 nmol/mg protein, p<0.01). A significant trend was found toward overexpression of Caspase-8, Bax, Caspase-3 and TNF-α in HFD group, but IL-10, SOD, CAT and Bcl2 expression was significantly decreased. Conclusions GNP is a safe and effective natural product that protects obesity-induced cardiac injury by elevating total antioxidant pools, suppressing inflammation, oxidative stress and apoptosis.
Open Access
The association of miR-191-5p in acne vulgaris and its predictive value for disease progression

8. September 2025

Xiang Luo, Tao Chen, Yan-yan Feng, Pei-mei Zhou, Bei Kan, Li Han, Li-wen Zhang

PDF downloaden

Objectives Acne vulgaris is a common chronic inflammatory skin disease predominantly affecting adolescents. This study aims to investigate the diagnostic value of miR-191-5p in acne vulgaris and its predictive potential for disease progression. Methods Relative expression of miR-191-5p was evaluated using reverse transcription-polymerase chain reaction. The diagnostic value was calculated via the receiver operating characteristic (ROC) curve, with the area under the ROC curve (AUC), sensitivity, and specificity. Spearman’s rank correlation coefficient analyzed the correlation between miR-191-5p and clinical features. Results miR-191-5p was increased in acne vulgaris patients than in controls. miR-191-5p had high diagnostic value for acne vulgaris (AUC=0.852, sensitivity=83.93 %, specificity=80.00 %, and cutoff value=1.285). miR-191-5p levels were enhanced in moderate to severe acne vulgaris when compared to those with mild cases. The miR-191-5p can effectively distinguish patients experiencing moderate plus severe acne vulgaris from those with mild stage (AUC=0.805, sensitivity=77.42 %, specificity=76.00 %, and cutoff value=1.490). miR-191-5p expression was notably related to total cholesterol (TC) ( r =0.211, p=0.023), high-density lipoprotein cholesterol (HDL-C) ( r =−0.188, p=0.043), low density lipoprotein-cholesterol (LDL-C) ( r =0.184, p=0.048), dihydrotestosterone (DHT) ( r =0.478, p<0.001), dehydroepiandrosterone (DHEA) ( r =0.473, p<0.001), and androstadienedione (AD) ( r =0.314, p=0.001) levels. Conclusions miR-191-5p is upregulated in acne vulgaris and possesses high diagnostic value for acne vulgaris and severity grades. The correlation with clinical features suggests its involvement in lipid metabolism and hormonal balance.
Open Access
Does modifying energy metabolism alter cellular signaling and proliferation in KRAS mutant NSCLCs?

4. Juni 2025

Sahika Cingir Koker, Irem Dogan Turacli

PDF downloaden

Objectives The capacity to sense and respond to cellular energy stress is an important factor in tumorigenesis. We aimed to investigate the proliferation patterns of KRAS-mutant NSCLC cell lines (A549, Calu-1, H2009) under high (HG) and low glucose (LG) conditions w/wo DCA, which alters metabolic pathways and promotes oxidative phosphorylation. Methods Cell viability was detected by MTT assay, protein expressions were determined by Western Blot and RNA expressions were analyzed by RT-qPCR. Results NSCLCs exhibited lower proliferation in HG compared to LG conditions. The effect of DCA in reducing the proliferation of the cells, was higher in HG compared to LG condition. We detected lower pRB levels in LG and in DCA treated conditions. LG conditions also showed higher p21 levels w/wo DCA while AMPK activation was more pronounced in 48 h. p-JAK2 was dominant in conditions having LG and p-Stat3 activation varied between all cells. The eIF4e activation was induced in LG w/wo DCA in all the cells. Despite p21-mediated cell cycle arrest, eIF4e and JAK2 signaling promoted proliferation. Conclusions Our results clearly showed the potential for increased aggressiveness and the delicate balance of cellular metabolic adjustments in response to energy stress in KRAS-mutant NSCLC cells.
Open Access
Evaluation of the cytotoxic effects of atorvastatin and oleuropein combination in head and neck cancer cells

12. Dezember 2025

Buse Aktas, Mesut Akyuz, Sila Ektas Kalayci, Adem Kara

PDF downloaden

Objectives Head and neck squamous cell carcinoma (HNSCC) remain a major clinical challenge, with limited efficacy of current therapeutic regimens. Natural compounds such as oleuropein and pharmacological agents like atorvastatin have shown anticancer potential individually, yet their combined effects in HNSCC remain unexplored. This study aimed to evaluate the cytotoxic, antimigratory, and molecular effects of atorvastatin and oleuropein, alone and in combination, in FaDu pharyngeal carcinoma cells. Methods FaDu cells were treated with oleuropein, atorvastatin, or their combination. Cell viability was assessed by cell viability detection kit-8 (CVDK-8), migration by wound healing assay, and mRNA expression of apoptosis, proliferation, and signaling-related genes by real-time PCR. Results Oleuropein significantly reduced cell viability, induced BAX and PTEN expression, and suppressed CDK2 and CDK4 , consistent with apoptosis induction and cell-cycle arrest. Atorvastatin alone exhibited minimal cytotoxicity but downregulated AKT and mTOR . Combination treatment attenuated oleuropein’s cytotoxicity and increased BCL-2 expression, suggesting a potential antagonistic interaction. Neither atorvastatin nor its combination with oleuropein significantly inhibited cell migration. Conclusions This is the first study to investigate atorvastatin and oleuropein co-treatment in HNSCC cells. While oleuropein alone demonstrated potent anticancer effects, atorvastatin partially counteracted these activities, highlighting the complexity of drug–natural product interactions. Future studies should expand dose–response analyses, validate protein level mechanisms, and test in vivo models to clarify the translational potential of this novel combination.
Open Access
Clinical value of serum LncRNA EPB41L4A-AS1 in high-risk carotid artery stenosis and analysis of its mechanism

8. September 2025

Lin Zhao, Yufeng He, Huhe Bateer, Bingqiao Li, Changjing Wu, Pengfei Li, Yan Gao

PDF downloaden

Objectives To investigate the diagnostic value of erythrocyte membrane protein band 4.1 like 4A gene antisense RNA 1 (EPB41L4A-AS1) for carotid artery stenosis (CAS) and its mechanism of action. Methods 157 patients with CAS and 65 healthy individuals were included. Color doppler ultrasound determined the degree of carotid artery stenosis and plaque stability of the patients. Real-time quantitative PCR (RT-qPCR) detected the expression of EPB41L4A-AS1. Receiver operating characteristic (ROC) curve assessed the diagnostic value of EPB41L4A-AS1 for CAS. Cell counting kit-8 (CCK-8) observed the proliferative ability of the cells, Transwell detected the migration, and enzyme-linked immunoassay (ELISA) validated the expression of inflammatory factors. Results Blood pressure and low-density lipoprotein cholesterol (LDL-C) indexes were significantly elevated in CAS patients, and EPB41L4A-AS1 was significantly down-regulated, which was more pronounced in patients with heavy and unstable plaques. EPB41L4A-AS1 has diagnostic significance for the degree of carotid stenosis and plaque stability in CAS patients. Oxidized low-density lipoprotein (ox-LDL) induced cell proliferation and migration, and promotes inflammatory levels. However, overexpression of EPB41L4A-AS1 inhibited cell function and downregulated inflammatory levels. Conclusions Low EPB41L4A-AS1 was positively associated with the degree of carotid artery stenosis and plaque vulnerability in patients with CAS. Overexpression of EPB41L4A-AS1 may alleviate the degree of CAS by downregulating the expression of inflammatory factors.
Open Access
Effects of l-carnitine, taurine and vitamin E in cellular Non-alcoholic fatty liver disease models

3. November 2025

Eray Ozgun, Gulben Sayilan Ozgun, Kıymet Tabakcioglu, Selma Suer Gokmen, Sevgi Eskiocak

PDF downloaden

Objectives We aimed to evaluate the effects of l -carnitine, taurine, and vitamin E in steatosis, protein oxidation, endoplasmic reticulum (ER) stress, and paraoxonase enzymes in fatty acid-induced NAFLD models. We also investigated the role of AMP-activated protein kinase (AMPK) in these effects. Methods HepG2 cells were incubated for 24 h with 1 mM palmitic acid (PA) or a 1 mM oleic acid (OA) and PA mixture to generate NAFLD models, representing acute lipotoxicity and benign chronic steatosis, respectively. l -carnitine, taurine, or vitamin E was applied together with fatty acids. Also, tunicamycin (ER stress inducer), 4-phenylbutyrate (ER stress inhibitor), or compound C (AMPK inhibitor) treatments were used. MTT test was used to evaluate cell viability. Measurement of triglyceride levels and oil red O staining of cells were used to determine steatosis. Protein carbonyl (PC), activating transcription factor 4 (ATF4), and C/EBP-homologous protein (CHOP), PON1-3, phosphorylated/total AMPK were evaluated by Western blotting. Results l -carnitine, taurine, and vitamin E reduced triglyceride levels in both models. Taurine and vitamin E also decreased PC levels in both models. Additionally, vitamin E lowered 1 mM PA-induced ATF4 and CHOP levels. Neither the models nor the treatments with l -carnitine, taurine, and vitamin E caused significant changes in PON1-3 or phosphorylated/total AMPK levels. Conclusions l -carnitine, taurine, and vitamin E attenuated lipid accumulation, with vitamin E demonstrating superior efficacy by significantly reducing both protein oxidation and ER stress. No changes in PON1-3 levels or AMPK phosphorylation were observed in the models or treatments under the conditions of this study.
Open Access
LncRNA EBLN3P inhibits myocardial inflammation and apoptosis after acute myocardial infarction via targeting miR-675-3p

15. September 2025

Wanrong Bi, Qing Peng, Yushi Feng, Jingjing Liu

PDF downloaden

Objectives Acute myocardial infarction (AMI) is myocardial necrosis caused by acute and persistent ischemia and hypoxia of the coronary arteries. This study aimed to investigate the potential mechanisms of lncRNA EBLN3P in the development of AMI. Methods This study recruited 109 patients with AMI and 117 healthy controls. The hypoxia/reoxygenation (H/R) cell model was primarily utilized to simulate in vivo ischemia-reperfusion injury of tissues and organs. The expression levels of EBLN3P were assessed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The concentrations of TNF-α, IL-6, and IL-1β were quantified via enzyme-linked immunosorbent assay (ELISA). Apoptosis was evaluated using flow cytometry. Additionally, the dual-luciferase reporter assay was utilized to confirm the targeting relationship between EBLN3P and miR-675-3p. Results EBLN3P was significantly downregulated in the serum of AMI patients. The receiver operating characteristic (ROC) curve analysis demonstrated that EBLN3P exhibited high diagnostic accuracy for AMI. Hypoxia/reoxygenation (H/R) treatment led to a marked decrease in EBLN3P expression levels, which could be significantly restored by transfecting EBLN3P post H/R treatment. H/R treatment significantly elevated the levels of TNF-α, IL-1β, and IL-6, but EBLN3P transfection partially reversed this effect. Additionally, H/R treatment resulted in a significant increase in the apoptosis rate, which EBLN3P transfection markedly reduced following H/R. EBLN3P targeted and regulated miR-675-3p, with their expression levels being negatively correlated. Furthermore, under H/R conditions, co-expression of EBLN3P and miR-mimic partially alleviated the effects of EBLN3P on cell behavior. Conclusions EBLN3P was involved in the regulatory mechanism of AMI by targeting miR-675-3p.
Open Access
Homocysteine induces iNOS and oxLDL accumulation in murine immune cells

22. Mai 2025

Yusuf Elma, İshak Ozel Tekin, Nilgün Solak, Tunç Hakan Sipahi, Emine Yilmaz Can

PDF downloaden

Objectives Increased levels of homocysteine (Hcy) in the blood are considered to be a risk factor for atherosclerosis. Endothelial damage induced by Hcy can lead to deterioration of coronary, cerebral, and peripheral vascular beds, contributing to cardiovascular morbidity and mortality. However, the mechanisms underlying Hcy-induced damage have not been fully elucidated. This study aimed to investigate the effect of Hcy on low-density lipoprotein (LDL) oxidation and inducible nitric oxide synthase (iNOS) expression, both of which are thought to play a role in the pathogenesis of atherosclerotic plaque formation and regulation of inflammation. Methods L-929 fibroblast-like cells and RAW 264.7 macrophages were treated with varying concentrations of Hcy (50, 100 and 200 μg/mL for L-929 cells, 10, 25, 100, 200 μg/mL for RAW 264.7 cells) to assess LDL oxidation and iNOS expression using immunocytochemical and immunofluorescence methods. Images obtained from cell culture experiments were quantitatively analyzed using color and brightness histograms, followed by statistical evaluation. Results Hcy significantly and dose-dependently increased LDL oxidation and intracellular oxidized LDL (ox-LDL) accumulation in both cell groups. Hcy also significantly increased iNOS expression in both cell groups in a dose-dependent manner. Conclusions These findings suggest that Hcy may play a role in the pathogenesis of atherosclerosis and inflammatory processes. The increased levels of ox-LDL and the elevated iNOS expression, particularly in macrophages, may contribute to the exacerbation of atherosclerosis and related diseases.
Open Access
Evaluation of leptin, neuregulin 4, FGF21, and vitamin D levels in patients with lichen planus

23. Oktober 2025

Fatma Tuncez Akyurek, Fikret Akyurek, Gözde Ulutas Demirbas

PDF downloaden

Objectives Lichen planus (LP) is a chronic inflammatory skin disease associated with metabolic disorders. This study aimed to investigate the relationship between LP and metabolic diseases through the evaluation of insulin resistance, adipocytokines, and vitamin D levels in addition to routine biochemical tests. Methods The study included 37 LP patients and 41 healthy controls. Serum fibroblast growth factor-21 (FGF-21), leptin, and neuregulin-4 (Ng-4) were measured using Enzyme-Linked Immuno Sorbent Assay (ELISA) methods. Levels of 25-hydroxyvitamin D (25-OH vitamin D) and were determined by chemiluminescence method on a Beckman Coulter DXI 800 (USA), while the glucose and lipid parameters were analyzed using photometric methods on a Beckman Coulter AU5800 Series (Japan). Results Significant differences were observed between patients and controls in body mass index (BMI), triglycerides, high-density lipoprotein cholesterol (HDL-C), glucose, insulin, HOMA-IR, and Ng-4 (p<0.05). LP patients had higher BMI, triglycerides, glucose, insulin, and HOMA-IR, but lower HDL-C and Ng-4. In cases with both mucosal and cutaneous involvement, glucose and FGF-21 were significantly lower (p<0.05). ROC analysis for Ng-4 showed modest diagnostic value (AUC=0.624), with a cut-off of 7.127 ng/mL (sensitivity 51.2 %, specificity 73.7 %). Conclusions LP patients displayed impaired carbohydrate and lipid metabolism, characterized by increased glucose, insulin, triglycerides, HOMA-IR, and BMI, along with reduced HDL-C and Ng-4. Although FGF-21 and leptin did not differ significantly, subgroup analyses suggested potential roles in disease heterogeneity. Ng-4 alone showed limited diagnostic utility but may gain importance within a biomarker panel for LP-related metabolic disturbances.
Open Access
Study on the association of LINC00924 with prognosis and malignant progression of thyroid cancer

5. September 2025

Luwei Niu, Qing Lu, Ran Li, Jiaxin Zhang

PDF downloaden

Objectives This study aimed to investigate the role of LINC00924 and its prognostic value in thyroid cancer (TC). Methods The study included cancer tissues from 101 TC patients and four TC cell lines. LINC00924 and miR-454-3p levels were measured using qRT-PCR. Patients were categorized into two groups according to LINC00924 levels. Cox regression analysis and Kaplan–Meier survival analysis were conducted to assess the correlation of LINC00924 with the pathological features of TC patients and its prognostic value. Additionally, validation of LINC00924 and miR-454-3p targeting relationship using dual luciferase reporter assay, and CCK-8 and Transwell assays were performed to evaluate TC cell proliferation, migration, and invasion. Results LINC00924 downregulated in TC tissues and cell lines, while miR-454-3p exhibited a marked upregulation. Lower LINC00924 expression correlated with advanced TNM stage, lymph node metastasis, and poorer overall survival. Cox analysis Kaplan-Meier survival analysis identified LINC00924 as an independent prognostic factor. Mechanistically, LINC00924 directly bound and negatively regulated miR-454-3p, acting as a molecular sponge. Functional experiments showed that LINC00924 suppressed TC cell proliferation, migration, and invasion, effects that were partially reversed by miR-454-3p. Conclusions LINC00924 may affect TC cell activity by regulating miR-454-3p. Furthermore, LINC00924 had potential as a clinical prognostic marker for TC.
Open Access
A cross-sectional study on physicians’ laboratory test request behaviors

8. September 2025

Adil Aydoğdu, Bayram Şahin

PDF downloaden

Objectives Since laboratory tests are an important component of health expenditures, it is important to understand the factors that cause unnecessary test use and take the necessary precautions in order to control health expenditures. The aim of this study is to determine physicians’ views on factors affecting unnecessary laboratory test orders. Methods A survey method was used to examine unnecessary laboratory test use from the physician’s perspective. The construct validity of the survey, which consists of 28 items, was tested with exploratory factor analysis and a 5-factor structure was reached. The reliability of the survey was tested with the internal consistency coefficient and the Cronbach’s alpha coefficient was found to be 0.85. Multivariate regression analysis was used to determine whether physicians’ level of agreement with the possible reasons for unnecessary test use differed according to their personal characteristics. Results Among the possible reasons for unnecessary test use, the dimension in which the physicians who responded to the survey agreed most was “Risk avoidance and patient demands”, and the dimension they agreed least on was “Excessively skeptical and detailed thinking”. Regression analyzes determined that physicians’ opinions about unnecessary test use varied significantly according to the demographic characteristics of physicians. Conclusions The findings obtained as a result of the study are thought to be important for decision makers to understand the factors that cause unnecessary laboratory test use and to take the necessary managerial measures.
Open Access
Reviewer Acknowledgment

9. Dezember 2025

PDF downloaden
Open Access
The impact of circadian rhythms on biomolecular set points: implications for disease diagnosis and monitoring

13. November 2025

Abdurrahman Coskun, Zelal Zuhal Kaya, Giuseppe Lippi

PDF downloaden

Laboratory data must be both analytically accurate and interpreted with clinically accuracy for safeguarding patient safety. However, variations – both analytical and biological – are inherent in all measurements obtained from patient samples. Biological variation observed in laboratory data can be broadly classified into two main categories: random and systematic variation. Among the systematic sources, in particular, circadian rhythms may have a significant influence on laboratory measurements. Understanding and recognizing the effects of circadian rhythms on both reference intervals and measurement results of analytes in both healthy individuals and patients is hence essential for enabling the accurate interpretation of laboratory data. In this review, we briefly discuss the major types of variation influencing laboratory data, with particular emphasis on systematic variation. We provide a detailed analysis of circadian rhythms and their impact on analyte concentrations and reference intervals, discuss the concept of set points and their variability in the context of diagnosis and monitoring of diseases, and examine mathematical models used to estimate physiological rhythms along with their respective advantages and limitations.
Open Access
Protective effects of thymoquinone and carvacrol against the cadmium toxicity in the liver tissues of rats

15. Dezember 2025

Gözde Öğütçü, Nadire Kıyak, Gülten Tuncel, Erblina Nikshiqi, Ferda Topal Çelikkan, Sevda Müftüoğlu, Selin Işık, Aysel Kükner

PDF downloaden

Objectives Structural, molecular and immunohistochemical changes in the liver of rats after acute cadmium (Cd) exposure and the effects of carvacrol (Car) and thymoquinone (TQ) were studied in this research. Methods Control, DMSO, Cd-treated (3.5 mg/kg by subcutane), Car (50 mg/kg gavage)-Cd treated, TQ (5 mg/kg by gavage)- Cd treated, carvacrol, and thymoquinone groups were formed.H&E and Masson’s Trichrome stainings were performed. Histological scoring was performed in liver. On the liver sections TNF-a, IL-6, and NF-kB immunostainings were carried out. Also sections of liver tissue were evaluated by electron microscopy. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and triglyceride (TG), oxidative stress parameters, MDA and GPx, were evaluated. Tnf-a, Nfkb1, IL6, mTor and Casp3 mRNA gene expression levels were examined using RT-PCR. The obtained data was statistically analyzed using GraphPad Prism software. Results Treatment groups showed significant reduction in ALT and TG when compared to cadmium group.In the cadmium group, MDA levels increased significantly and GPX1 levels decreased compared to the control group. As a results of the microscopic studies, cellular and structural defects by cadmium were decreased in the presence of carvacrol and thymoquinone. NF-kB, TNF-a and IL-6 immunostained surface area increased in cadmium compared to the control group. Cd-Car and Cd+Thymoquinone alleviated these inflammatory expressions. In treatment groups, Nfkb1, Tnf-a, IL6, mTor, Casp3 expressions reduced compared to cadmium alone. Conclusions The study results indicate that carvacrol and thymoquinone alleviate the toxic effects of liver tissue induced by cadmium.
Open Access
The possible link between endocannabinoid system gene polymorphisms and overweight/obesity susceptibility in individuals living in the Marmara Region

22. Mai 2025

Beril Altun, İsmet Cok, Cemal Onur Noyan, Ela Kadioglu, Alptekin Cetin, Tijen Sengezer, Merih Altintas, Samet Kurnaz, Nesrin Dilbaz

PDF downloaden

Objectives Obesity is a global health problem related to reduced life quality and shorter life expectancy. Given the fact that genetic factors play a role in obesity development, studies have suggested that polymorphisms of Cannabinoid Receptor 1 ( CNR1 ), Monoacylglycerol lipase ( MGLL ), and Fatty Acid Amide Hydrolase ( FAAH ) genes located in the endocannabinoid system (ECS) are related to overweight/obesity risk. Accordingly, we aimed to assess the genetic susceptibility to overweight/obesity in individuals with Turkish ancestral origin concerning these ECS genes. Methods The present study comprised 194 unrelated individuals with Turkish ancestral origin living in the Marmara Region. The study population is categorized into two groups according to their body mass index (BMI) overweight/obese group (BMI≥25) and normal weight group (18.5<BMI<25). Genotyping of the CNR1 rs1049353 , MGLL rs60430 , and FAAH rs324420 polymorphisms was performed using the Real-Time Polymerase Chain Reaction (RT-PCR). Results The GG genotype frequency of CNR1 rs1049353 was significantly higher in overweight/obese individuals than in normal weight individuals (75.5 vs. 61.4 %, respectively; p=0.034 ). No difference was observed in terms of MGLL rs604300 and FAAH rs324420 polymorphisms between the groups ( p>0.05 ). The genotype distributions of CNR1 , MGLL , and FAAH genes were compatible with the Hardy–Weinberg equilibrium ( p>0.05 ). Conclusions Our findings supported that individuals with AA/AG genotype of CNR1 rs1049353 have reduced overweight/obesity risk; however, neither FAAH rs324420 nor MGLL rs604300 showed any association. A relatively smaller sample size and lack of inclusion of obesity-related measurements could be considered the limitations of this study. Further research is needed to confirm or disprove our results.
Open Access
Serum fatty acid synthase and GLP-1 levels in prostate cancer and benign prostatic hyperplasia

21. November 2025

Abdullah Üner, Tevfik Noyan, Erdal Benli

PDF downloaden

Objectives This study aimed to investigate the differences in serum fatty acid synthase (FASN) and glucagon-like peptide-1 (GLP-1) levels among patients diagnosed with prostate cancer, benign prostatic hyperplasia (BPH), and healthy controls. Methods A total of 60 male patients and 28 healthy male subjects were included in the study. Based on biopsy results, the patients were divided into two groups: prostate cancer (n = 30) and BPH (n = 30). Results The mean FASN level was 6.71 ± 0.81 ng/mL in the prostate cancer group, 3.84 ± 0.21 ng/mL in the BPH group, and 3.57 ± 0.29 ng/mL in the control group. There was no statistically significant difference in FASN levels between the BPH and control groups (p > 0.05). However, FASN levels were significantly higher in the prostate cancer group compared to both the control and BPH groups (p < 0.001). The mean GLP-1 level was 9.69 ± 0.65 pmol/L in the prostate cancer group, 11.40 ± 0.77 pmol/L in the BPH group, and 7.03 ± 0.62 pmol/L in the control group. Compared to the control group, GLP-1 levels were significantly elevated in both the BPH and prostate cancer groups (p < 0.001 for both); however, there was no significant difference between the BPH and prostate cancer groups (p > 0.05). Conclusions Our findings suggest that FASN and GLP-1 levels may contribute to the diagnostic accuracy of prostate diseases when used in conjunction with PSA and its derivatives.
Open Access
Hair cortisol concentration, psychological distress and resilience in women with premenstrual dysphoric disorder and premenstrual syndrome

9. Dezember 2025

Kevser Yildirim Ciftci, Elif Akcay, Ceylan Bal, Raziye Desdicioglu, Gulsum Akdeniz, Gulsen Yilmaz

PDF downloaden

Objectives Women frequently experience premenstrual dysphoric disorder (PMDD) and premenstrual syndrome (PMS), which can lead to both physical symptoms and severe psychological distress that can impact daily functioning. Also, these women may be exposed to chronic stress, for which hair cortisol concentration (HCC) serves as a potential biomarker. In the present study, the relationship between HCC, psychological distress and resilience in women with PMDD and PMS were evaluated. Methods A total of 80 women older than 18 years ages and menstruating regularly for at least two years participated in this study. Sociodemographic characteristics and menstrual cycle features were self-reported by all participants. Premenstrual syndrome symptoms were assessed with the Premenstrual Symptoms Screening Tool (PSST). Resilience, perceived stress, depression, anxiety, stress and loneliness were evaluated using the Brief Resilience Scale (BRS), Perceived Stress Scale (PSS), Depression, Anxiety, Stress Scale (DASS-21) and UCLA Loneliness Scale. HCC was measured using ELISA. Results Participants of study were divided into three groups based on PSST as follows: PMDD (n = 20, 25 %), PMS (n = 25, 31.3 %), and control (n = 35, 43.8 %). In the PMDD group, perceived stress and anxiety were higher compared to the control group and anxiety scores were higher than the PMS group. Out of the three groups, HCC had negative moderate correlation with resilience scores only in the PMDD group (r = −0.509, p = 0.022). Conclusions Women with PMDD experience severe affective symptoms and exhibit higher resilience as HCC concentrations decrease. These findings highlighted that enhancing resilience through psychological support could be a beneficial intervention for the PMDD group.
Open Access
Study on the role of miR-146b-3p in the occurrence and development of endometriosis

17. Oktober 2025

Yan Zhang, Dongxiang Han

PDF downloaden

Objectives A chronic inflammatory disease, endometriosis is recognized by the ectopic tissue growth of endometrium, but its pathogenesis has not been fully elucidated. Recently, miRNAs have been identified as a key regulator in the pathological process of endometriosis. This study investigated the function and molecular mechanism of miR-146b-3p in the occurrence and development of endometriosis. Methods In this study, 90 patients with endometriosis and 90 age-matched patients who had surgery for uterine fibroids or simple ovarian cysts were selected for the research objects. miR-146b-3p and UNC5C levels were examined by qRT-PCR in clinical endometriotic tissues and normal tissues. The impact of miR-146b-3p on endometriotic cells was verified through transfection of miR-146b-3p mimic or inhibitor. Apoptosis and proliferation were detected using flow cytometry and CCK8 assay. Transwell method was employed for examination of cell migration and invasion. The interaction of miR-146b-3p and UNC5C was detected via luciferase activity. Results miR-146b-3p levels were significantly elevated in endometriotic tissues and gradually raised with increasing rASRM grade. In endometriotic cells, up-regulation of miR-146b-3p inhibited apoptosis, facilitated cell proliferation, migration and invasion, and elevated IL-6 and TNF-α, whereas downregulation of miR-146b-3p exhibited opposite trend. In addition, miR-146b-3p targeted UNC5C, which altered the influences of miR-146b-3p on apoptosis, proliferation, migration, invasion, and inflammatory responses. Conclusions This study found that miR-146b-3p regulates inflammatory response and progression of endometriosis by targeting UNC5C, which provided a theoretical basis for the exploitation of new diagnostic biomarkers or searching for potential therapeutic targets.
Open Access
Dysregulated serum miR-384-5p as a diagnostic biomarker for Alzheimer’s disease

7. November 2025

Yue Miao, Jie Zheng, Ting Huang, Xichun Wang, Ren Zhang

PDF downloaden

Objectives Alzheimer’s disease (AD) is classified as a neurodegenerative disorder. Studies have found that miR-384-5p plays a role in neurological diseases such as Parkinson’s. This study investigated the dysregulation of circulating miR-384-5p in Alzheimer’s disease patients through serum analysis. We investigated its diagnostic significance in AD, neuroprotective effects, and underlying mechanisms. Methods SH-SY5Y cells were treated with Aβ25-35 to model AD, and qRT-PCR quantified miR-384-5p expression in both serum and cellular components. The diagnostic potential of miR-384-5p for Alzheimer’s disease was evaluated through combined analysis of cognitive assessment (MMSE) and diagnostic accuracy validation (ROC curve). miR-384-5p demonstrated cytotoxic activity (MTT/flow cytometry) and target regulation (luciferase assay). Results miR-384-5p expression was significantly elevated in both AD patient serum and Aβ25-35-exposed SH-SY5Y cells (p<0.001). A significant inverse correlation was observed between miR-384-5p expression levels and MMSE scores (r=−0.615, p<0.001). ROC analysis revealed strong diagnostic efficacy with an AUC of 0.877 at the optimal cutoff value of 0.582, demonstrating 78.0 % sensitivity and 80.2 % specificity. miR-384-5p suppression attenuated Aβ-induced cytotoxicity and apoptosis (p<0.001), with SIRT1 identified as its direct target. Conclusions Altered serum levels of miR-384-5p were identified as a potential diagnostic biomarker in AD patients. Mechanistic investigations revealed that miR-384-5p downregulation exerts neuroprotective effects through targeted regulation of SIRT1, suggesting its dual significance in both disease detection and pathological mechanisms of AD.
Open Access
Fetuin-A-to-adiponectin ratio, progranulin, and CTRP-3 in overweight individuals: links to adipose tissue inflammation

30. Juni 2025

Yıldız Öner-İyidoğan, Nur Çınar-Şirin, Selda Can Arkaya, Pınar Kural Enç

PDF downloaden

Objectives This study aimed to investigate serum Fetuin-A (FetA) and adiponectin levels, the FetA/adiponectin ratio (FAR), and their roles in inflammation and insulin resistance in overweight individuals. Instead of evaluating FAR as a predictive biomarker, this study aimed to explore its association with metabolic parameters in this population. Materials The study included 57 participants aged 24–56 years, divided into control (BMI<25 kg/m 2 , n=27) and overweight (BMI 25–30 kg/m 2 , n=30) groups. Anthropometric measurements and body composition analyses were performed after a 12-h fasting period. Serum FetA, adiponectin, progranulin, and CTRP-3 levels were measured using ELISA. Insulin resistance was assessed using the HOMA-IR index. Statistical analyses included Mann–Whitney U tests, correlation analyses, and ROC curve analysis. Results Overweight individuals showed significantly higher waist circumference, body fat mass, and HOMA-IR compared to controls, while adiponectin levels were significantly lower (p=0.006). The FAR was elevated in the overweight group (p=0.023) and positively correlated with BMI, body fat mass, and HOMA-IR (p<0.05). Progranulin and CTRP-3 levels showed no significant differences between groups, but a negative correlation between these two adipokines was observed. ROC analysis revealed an optimal FAR cut-off of 40.5 for predicting increased BMI, with 60 % sensitivity and 80 % specificity. Conclusions The findings suggest that FAR is associated with insulin resistance and metabolic parameters in overweight individuals. Although promising, its clinical utility as a diagnostic biomarker requires further investigation.
Open Access
Tanshinone ⅡA suppresses hypoxia-induced human pulmonary artery smooth muscle cell over-proliferation via the LINC01013/miR-548c-3p/IL6 pathway

3. November 2025

Nuan Zhang, Kai Xing

PDF downloaden

Objectives The high proliferation of pulmonary artery endothelial cells and smooth muscle cells (PASMCs) is one of the mechanisms of pulmonary hypertension (PH), which can eventually lead to death. The purpose of this study is to explore the effect of tanshinone ⅡA on PASMC proliferation and its action mechanism. Methods PASMCs were treated with hypoxia to simulate the PH cell model, and they were cultured by the medium containing different concentrations of tanshinone ⅡA to evaluate its effect on cell viability. CCK-8 reagent was for the viability detection of PASMCs. The expressions of LINC01013, miR-548c-3p, and interleukin 6 (IL6) were detected by RT-qPCR or western blotting, and their targeting relationships were demonstrated by a dual-luciferase reporter assay. The proliferation capacity of PASMCs was evaluated by CCK-8 and the expressions of markers. Glycolysis was measured by detecting phosphofructokinase-1 (PFK-1) activity and pyruvic acid level. Results Tanshinone ⅡA restrained hypoxic PASMC viability in a concentration-dependent manner. Overexpression of LINC01013 decreased miR-548c-3p level by binding to it. IL6 was a target of miR-548c-3p, and its expression was hindered by the miR-548c-3p mimics. LINC01013 and IL6 promoted the proliferation and glycolysis of hypoxic PASMCs, and miR-548c-3 acted with inhibiting effects on which. Tanshinone ⅡA suppressed LINC01013/IL6 expression and up-regulated miR-548c-3p. Conclusions Tanshinone ⅡA inhibited the glycolysis-mediated growth in hypoxic PASMCs by regulating the LINC01013/miR-548c-3p/IL6 pathway.
Open Access
Effect of luer-lock access device on hemolysis during blood collection via intravenous catheters in the emergency department

5. November 2025

Havva Yasemin Cinpolat, Canan Akman, Eda Sahin

PDF downloaden

Objectives Emergency departments are the units where hemolysis is most frequently observed, and blood collection from intravenous catheters increases the hemolysis rate. This study aimed to compare the effects of two different blood collection methods from an intravenous catheter (an adapter and a syringe) on serum indices, complete blood count, and routine clinical chemistry tests in an emergency department. Methods The study encompassed 104 patients from the yellow and green zones of the Emergency Department at Canakkale Onsekiz Mart University Hospital. Blood samples were obtained from an intravenous catheter with a standard syringe and an adapter into serum separator tubes and dipotassium ethylenediaminetetraacetic acid (K 2 EDTA) tubes. Serum index, aspartate aminotransferase (AST), creatine kinase (CK), lactate dehydrogenase (LDH), potassium, high-sensitivity (hs) Troponin T, and complete blood count were evaluated. Passing-Bablok regression analysis was performed, and the mean percentage difference was calculated and compared to target values via a Bland-Altman plot. Results A statistically higher hemolysis rate was observed when blood was collected with a syringe, compared to collecting blood with an adapter (p<0.001). When the results were categorized according to the parameter-specific hemolysis index, AST, CK, potassium, LDH, and hs Troponin T results were more affected by hemolysis when blood was collected with a syringe (p<0.001). The mean percentage difference for AST and LDH exceeded the minimum target values based on biological variation. Conclusions Using a catheter-compatible adapter in emergency departments may reduce the rate of hemolysis and provide reliable results for tests frequently affected by hemolysis.
Open Access
Integrated bioinformatics analysis reveals convergent molecular networks and therapeutic targets in hepatocellular carcinoma and sepsis

14. November 2025

Dilek Dulger, Tugba Gurkok-Tan, Serhat Sirekbasan, Seda Ekici, Bekir Eren Cetin

PDF downloaden

Objectives Hepatocellular carcinoma (HCC) and sepsis are significant global health challenges, both involving complex molecular mechanisms that may overlap. Identifying shared differentially expressed genes (DEGs) between these conditions could provide novel insights into disease progression and therapeutic targets. This study aimed to determine common DEGs between HCC and sepsis using microarray datasets and to explore their biological implications through bioinformatics analyses. Methods Publicly available microarray datasets for HCC and sepsis were retrieved from gene expression repositories. After preprocessing and normalization, DEGs were identified using statistical approaches, and overlapping genes were determined through comparative analysis. Functional enrichment analysis was performed with the DAVID platform to assess associated biological processes and pathways. A protein–protein interaction (PPI) network was then constructed to identify hub genes, and transcription factor (TF)–gene interaction analysis was carried out to evaluate potential regulatory mechanisms shared between the two conditions. Results A total of 379 common DEGs were identified between HCC and sepsis. Functional enrichment analysis indicated that these DEGs were mainly related to immune response, cell cycle regulation, and antigen presentation pathways. PPI network analysis revealed hub genes including CCNA2, NUSAP1, TOP2A, and CDK1, all of which were significantly upregulated in both diseases. TF–gene interaction analysis highlighted convergent transcriptional regulatory mechanisms linking immune dysregulation in sepsis with tumorigenesis in HCC. Conclusions This study demonstrates molecular similarities between HCC and sepsis, emphasizing shared DEGs and regulatory networks. The identification of hub genes and enriched pathways provides potential diagnostic markers and therapeutic targets, underscoring the importance of transcriptional dysregulation in both cancer development and sepsis pathophysiology.
Open Access
Shenfu injection combats pathological myocardial hypertrophy by targeting TNF and TGFB1 to inhibit angiotensin II-induced autophagy

29. September 2025

Tiansheng Su, Jihong Luo, Candong Li, Zhangwu Xiao

PDF downloaden

Objectives This study aimed to explore the mechanism of action of Shenfu injection (SFI) on pathological myocardial hypertrophy. Methods The compound targets of the active ingredients in SFI were collected and intersected with the gene targets related to pathological myocardial hypertrophy. We performed protein-protein interactions (PPI), network construction, KEGG pathway enrichment analysis, and molecular docking on these targets. We used RT-qPCR and Western blot to measure the number of related genes and proteins and analyze their mechanisms of action. Results SFI relieved the hypertrophy of H9C2 cells induced by angiotensin II (Ang II). Eleven possible targets of SFI against myocardial hypertrophy were obtained. After conducting KEGG pathway enrichment analysis, these genes are closely related to heart disease-related pathways. SFI reversed the increase in the expression levels of TNF , TGFB1 , mTORC1 , and p-ULK1-Ser555 caused by Ang II. SFI can reduce the Ang II-induced increase in LC3-positive cells. Conclusions Our findings demonstrate that SFI inhibits Ang II-induced myocardial hypertrophy by attenuating pathological autophagy, an effect mediated through targeting TNF and TGFB1 pathways. These results position SFI as a promising multi-target therapeutic strategy targeting dysregulated cytokine signaling and autophagy in cardiac remodeling.
Open Access
Comparison of HLA-G levels for cord blood derived-MSC and Wharton’s jelly derived-MSC

17. September 2025

Figen Abatay Sel, Ayşe Erol Bozkurt, Şule Karataş, Mediha Süleymanoğlu, Beril Yaşa, Cenk Yaşa, Hayriye Şentürk Çiftçi, Fatma Savran Oğuz

PDF downloaden

Objectives A special group of stem cells with multipotent and immunomodulatory properties are mesenchymal stem cells (MSCs). Many modulatory factors are thought to mediate immunomodulatory properties of MSCs. One of these modulatory factors is thought to be HLA-G, one of human leukocyte antigens (HLA). This study aimed to compare HLA-G levels in both stimulated and unstimulated of peripheral blood mononuclear cell (PBMC) cultures with “cord blood-MSC” (CB-MSC) and “Wharton’s jelly-MSC” (WJ-MSC) at different rates and different incubation periods. Methods WJ-MSCs were obtained by explant method, and CB-MSCs using Ficoll-paque. They were characterized by flow cytometry. MSCs and PBMCs were directly co-cultured for 24 and 72 h at 1:5 and 1:10, respectively. After incubations, the media were collected and HLA-G levels were measured by ELISA. Results In the unstimulated group, the highest HLA-G level was found in the PBMC:WJ-MSC-72-1:5 group, while the lowest HLA-G level was found in the PBMC:CB-MSC-72-1:5. When 24-1:5 and 72-1:5 groups were examined, the HLA-G level decreased significantly in CB-MSC groups compared to WJ-MSC, while it increased significantly in the 24-1:10 and 72-1:10 groups (p<0.05). In stimulated groups, the highest HLA-G level was observed in the PBMC:CB-MSC-24-1:5. Conclusions Our study aimed to evaluate the immunomodulatory effect of MSCs via HLA-G molecule. HLA-G levels changed with different incubation times of two different MSC sources. In this study, we suggest that MSCs as a cell therapy, in particular for immune system-related disease, may be a preliminary in vitro approach to evaluate the immunomodulatory effect via HLA-G.
Open Access
Effect of ADSC exosome-loaded sustained-release nanosphere gel on cartilage repair: a study using chondrosarcoma cell line SW1353

2. Dezember 2025

Yuyang Li, Beibei Wang, Li Hong, Shuping Wang, Yanwei Gao

PDF downloaden

Objectives This study aims to explore the function of ADSCs-derived exosomes within a hyaluronic acid (HA) hydrogel on chondrocytes. Methods ADSCs-Exo were isolated and characterized through western blot analysis. An HA hydrogel encapsulating ADSCs-Exo (HA@ADSCs-Exo) was formulated. To simulate cartilage injury, an IL-1β-induced cell model was constructed. MTT assay, flow cytometry, ELISA, and RT-qPCR were used to detect the cell viability, apoptosis, as well as inflammatory factors, oxidative stress indexes, and the levels of degradation-related proteins and synthesis-related proteins in SW1353 chondrocytes. Results In comparison to IL-1β induction, the presence of HA@ADSCs-Exo improved cell viability and mitigated cell apoptosis. HA@ADSCs-Exo significantly restricted the production of TNF-α and IL-6 in the context of IL-1β stimulation. Moreover, the addition of HA@ADSCs-Exo inhibited the intracellular leakage of MDA and promoted the formation of SOD. Ultimately, HA@ADSCs-Exo effectively suppressed the expression of chondrocyte degradation markers (MMP-13 and ADAMTS-1), while simultaneously facilitating the upregulation of chondrocyte reconstruction marker (Aggrecan). Conclusions HA@ADSCs-Exo demonstrates remarkable efficacy in mitigating chondrocyte damage induced by IL-1β. This innovative drug delivery system, which intricately combines HA-hydrogels with exosomes derived from ADSCs, offers a novel approach to addressing cartilage injury and has exhibited promising potential for facilitating cartilage repair.
Open Access
Clinical value of abnormal expression of serum lncRNA HOTTIP rs1859168 in recurrent spontaneous abortion

30. September 2025

Mingchen Jin, Junhua Hou, Limin Sun, Zhimin Huang, Chunyou Qiao, Jingya Liu

PDF downloaden

Objectives The objective of this research was to investigate the correlation between HOTTIP polymorphisms and recurrent spontaneous abortion (RSA) susceptibility. Methods This study included 265 RSA patients as the case group and 260 healthy volunteers as the control group. Genotyping was performed using the TaqMan probe-based polymerase chain reaction (PCR) method. Serum HOTTIP expression in subjects was detected using reverse transcription quantitative polymerase chain reaction (RT-qPCR). The clinical diagnostic value of HOTTIP for RSA was evaluated by a receiver operating characteristic (ROC) curve. Results The frequency of C alleles in the case group was lower than that of the control group, and the frequency of A alleles was higher than that of the control group, and the A allele was a risk factor for the onset of RSA (p<0.05). The rs1859168 gene polymorphism was correlated with RSA susceptibility under the codominant, dominant, and recessive inheritance models (p<0.05). Serum HOTTIP expression was elevated in RSA patients. The ROC curve showed that serum HOTTIP had good diagnostic value for RSA, with an area under the curve (AUC) of 0.903, a sensitivity of 87.5 % and a specificity of 81.2 %. Conclusions HOTTIP rs1859168 gene polymorphism is associated with RSA susceptibility. People bearing the AC and AA genotypes have a higher risk of RSA.
Open Access
Novel pediatric within-subject biological variation estimates derived from laboratory data using an indirect method

7. November 2025

Coskun Cavusoglu

PDF downloaden

Objectives Biological variation (BV) is critical for interpreting lab results and setting analytical performance specifications. However, within-subject BV (CV I ) data are limited in pediatric populations. This study aimed to estimate pediatric CV I values for selected lab tests using an indirect method. Materials and methods In this retrospective study at Umraniye Education and Research Hospital (Istanbul), 69,984 results from 11,535 pediatric patients (0–19 years) over 20 months were analyzed for CBC and selected biochemical analytes (glucose, urea, creatinine, ALT, AST) within reference intervals. Patients with 5–15 results were included, with outliers (Q test) and trends (regression) excluded. Person-specific CVs were calculated and then further improved by removing values outside the 2.5–97.5 percentile of the Gaussian distribution, combined to obtain CVpooled, and adjusted by subtracting analytical variation (CV A ) to estimate CV I , which was subsequently compared with CALIPER BV and EFLM-BVD data using the <0.5 or >1.5 ratio threshold. Results Overall, pediatric CV I s estimated by the indirect method were generally high. For CBC parameters, Hgb, Hct, and MCHC ratios were within the threshold (1.0±0.5), whereas others exceeded it; for biochemical parameters, all ratios compared to CALIPER exceeded the threshold. Conclusions This study provides novel pediatric CV I estimates using an indirect method. Elevated CV I values may reflect physiological variability and pre-analytical factors in children. Indirect approaches are useful alternatives for BV estimation where direct sampling is challenging.
Open Access
LINC01711 facilitated gastric carcinoma progression by sponging miR-140-3p

9. Dezember 2025

Weikang Su, Jiahuan Wang, Yan-Hui Sun, Xiao-Xiao Wang, Cong Wu, Liping Liu

PDF downloaden

Objectives Gastric carcinoma (GC) remains a high-mortality malignancy that needs efficient ways for the prognosis and therapy of the disease. LncRNAs are biomolecules that participate in cancer progression by regulating gene expression. This study thus investigated the role of lncRNA LINC01711 in GC progression and the underlying mechanisms. Methods GC tumor and normal tissues were collected from 150 GC patients. qRT-PCR was used to test the expression of biomolecules. LncBook, Miranda, and starBase databases were employed to explore miRNAs that interact with LINC01711. The association between the biomolecules was validated via a dual luciferase reporter assay. Biological functions of biomolecules in GC cells were measured by the Cell Counting Kit-8 (CCK-8) and the transwell migration and invasion assays. Results This study found an upregulation of LINC01711 in GC tumor tissues compared to normal tissues. The upregulation of LINC01711 was an indicator of adverse clinical outcomes in GC patients. The miRNA that interacted with LINC01711 in GC was hsa-miR-140-3p. There was a negative correlation between the expression levels of LINC01711 and hsa-miR-140-3p in both GC tumor tissues and cells. LINC01711 promoted GC tumor cell proliferation, migration, and invasion by sponging hsa-miR-140-3p. Conclusions LINC01711 might be an ideal prognostic marker and treatment target for GC. The upregulation of LINC01711 was a negative prognostic indicator for GC patients. LINC01711 facilitated GC tumor cell activities related to GC progression by sponging hsa-miR-140-3p.
Open Access
Xanthohumol inhibits extracellular matrix degradation via the Nrf2/PERK/ATF4/C/EBPβ pathway in osteoarthritis

4. Dezember 2025

Tiansheng Zheng, Shuo Niu, Qingluo Zhou, Jishang Huang, Jun Yi, Runhong Mei, Xuefeng Yu

PDF downloaden

Objectives This study aims to explore the therapeutic potential of Xanthohumol (XH) in mitigating osteoarthritis (OA) progression by inhibiting extracellular matrix (ECM) degradation. Specifically, it investigates the role of XH in reducing matrix metalloprotease-13 (MMP-13) activity and modulating the PRKR-like endoplasmic reticulum kinase/activating transcription factor 4 (PERK/ATF4) pathway while enhancing nuclear factor-erythroid 2-related factor 2 (Nrf2) activity. Methods In vitro experiments were conducted on OA chondrocytes (CTs) to evaluate MMP-13 production and collagen II expression following XH treatment. In vivo , XH was administered intraperitoneally, and cartilage degradation was assessed. Molecular analysis examined the expression of C/EBPβ, a downstream effector of the PERK/ATF4 pathway, and Nrf2 activity. Overexpression and knockdown experiments were performed to elucidate XH’s mechanistic effects. Results XH treatment reduced MMP-13 production by 46 % and increased collagen II expression by 38 % in vitro . In vivo , XH administration resulted in a 31 % decrease in cartilage degradation scores compared to controls. Mechanistically, XH decreased C/EBPβ expression and increased Nrf2 activity by 52 %. Overexpression of C/EBPβ or activation of the PERK/ATF4 pathway nullified XH’s protective effects, while Nrf2 knockdown abolished its benefits. Conclusions XH inhibits ECM degradation in OA by suppressing the PERK/ATF4/C/EBPβ pathway and activating Nrf2, demonstrating its potential as a low-cytotoxicity therapeutic agent for OA treatment. This approach offers a promising strategy for mitigating cartilage damage and advancing OA management.
Open Access
The potential role and mechanism of miR-1910-5p in the prognosis of glioma

15. August 2025

Qinxuan Xu, Dong Li, Zeng Liu

PDF downloaden

Objectives The suboptimal prognosis of glioma patients after treatment underscores the critical significance of elucidating the intricate molecular mechanisms underlying glioma progression. This study endeavors to excavate reliable biomarkers in order to advance the treatment of gliomas. Methods A total of 133 glioma patients were enrolled in this study, with glioma tissues and adjacent normal tissues collected during surgery. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect miR-1910-5p expression, and Kaplan-Meier analysis was conducted to assess its predictive value for patient survival within 5 years post- surgery. Bioinformatic approaches were utilized to identify potential targets of miR-1910-5p, which were subsequently validated using a luciferase reporter gene system. Ultimately, the influence of miR-1910-5p/GPX8 on cell proliferation and metastasis was analyzed by CCK8 and Transwell assays. Results miR-1910-5p expression was markedly down-regulated in glioma tissues and cells. Notably, a lower miR-1910-5p level was associated with a poorer 5-year prognosis for glioma patients. GPX8, on the other hand, was significantly up-regulated in gliomas and exhibited a negative correlation with miR-1910-5p expression, suggesting a unidirectional negative regulation of GPX8 by miR-1910-5p. Further analysis revealed that miR-1910-5p overexpression suppressed glioma cell proliferation and metastasis, with these effects being significantly reversed by GPX8 overexpression. Conclusions miR-1910-5p has the potential to serve as a prognostic marker of glioma and may exert its inhibitory effects on glioma cellular behaviors by targeting GPX8.
Open Access
A mini review: the trio of artichoke (Cynara scolymus L.), cytotoxicity, and apoptosis

17. Oktober 2025

Taygun Dayi, Müjgan Kuşi, Fatma Hacet

PDF downloaden

The artichoke, also known as C scolymus L. , is an edible plant that is commonly grown worldwide, particularly in the Mediterranean region. C scolymus L . has different nutritious by-products , and while it depends on the culture, nearly all of them are consumable. Cancer is the second leading cause of death worldwide, and many molecular pathways are effective in both the development and prevention of cancer. This narrative article aims to review the effects of C scolymus L . on cytotoxicity and apoptosis, also known as programmed cell death. Current in vitro studies published in the last decade have shown that different by-products of C scolymus L. extracts increase cytotoxicity, which is the specific destructive action of an agent on cancer cells, and may also induce apoptosis. Moreover, C scolymus L . causes the stimulation of pro-apoptotic and suppression of anti-apoptotic cancer pathways. It increases initiating caspases 8 and 10 activities in the extrinsic pathway of apoptosis. While different C scolymus L. extracts potentially increase Bax expression, they suppress Bcl-2 in the intrinsic pathway of apoptosis. These effects cause an increase in caspase 9 activity. Increased activities of these initiating caspases (8-9-10) stimulate effector caspases 3 and 7, thus apoptosis. These are important beneficial effects for apoptosis and thus preventing cancer. However, these potential effects are limited to the results of in vitro studies. More in vitro studies on different cancer cell lines, in vivo studies, and randomised controlled human trials are therefore necessary to increase the level of evidence.
Open Access
Tephrosin attenuates breast cancer via the modulation of TRAP1/HIF-1α/SDHA expression: in vitro and in vivo approach

9. Oktober 2025

Gang Nie, Longjie Zhang, Hongai Wang

PDF downloaden

Objectives Breast cancer is the most commonly diagnosed malignancy among women worldwide. Our study explored the chemotherapeutic activity of tephrosin in breast cancer treatment. Methods The in vitro study has been performed on MCF-7 cell line through cell viability and flow cytometry assay. The toxicity study was conducted by acute and subacute toxicity study to determine LD50 and ED50 doses of tephrosin for further chemotherapeutic study. In in vivo assessment, the breast cancer has been induced in rat via the single i.v administration of 7,12-Dimethylbenz[a]anthracene (DMBA) with dose of 0.5 mg/100 g body weight in corn oil. Subsequently, the tephrosin treatment through oral route has been commenced in carcinogen-induced rats that sustained for 24 weeks. The immunohistochemistry, histopathology, cell proliferation study and apoptosis assay via TUNEL method have been performed to evaluate the restoration of normal cellular architecture of breast tissues through upregulation of succinate dehydrogenase subunit A (SDHA) expression. Results Our results showed that the treatment with tephrosin causes the downregulation of tumor necrosis factor receptor-associated protein 1 (TRAP1) expression in mitochondrial matrix and decreases the stabilization of succinate-dependent HIF-1α, leading to the upstream of SDHA protein levels in breast cancer tissues. Conclusions In conclusion, the progression of breast cancer has been attenuated by the initiation of apoptotic events and distortion of cellular proliferation, which is permissible for the development of a suitable molecular mechanistic pathway of tephrosin in breast cancer chemotherapy.
Open Access
Pregnancy associated plasma protein-A: a promising biomarker in kidney diseases

30. September 2025

Betül Ceylaner, İrem Nur Savaş, Meral Meşe, Zerrin Bicik Bahçebaşı

PDF downloaden

Kidney diseases are a worldwide public health problem with more than 850 million patients all over the world. Therefore, early diagnosis is essential for effective treatment of any renal disease. Most biomarkers have the potential to be used in diagnosis, screening, prognosis, and follow-up, but it is challenging to confirm associations with certain diseases. Although some biomarkers such as urea and creatinine are used in clinical practice for kidney diseases, these molecules’ sensitivity and specificity are not at the desirable level. Pregnancy-associated plasma protein-A (PAPP-A) is being used for the screening of Down’s syndrome in the first trimester of pregnancy, however, increased expressions have been reported in various kidney diseases. This study aimed to evaluate the clinical significance of PAPP-A as a potential biomarker for diagnosing and monitoring renal diseases. We searched Pubmed and Web of Science databases using PAPP-A, kidney diseases, acute kidney injury, chronic kidney disease, hemodialysis, peritoneal dialysis, kidney transplant, diabetic nephropathy, polycystic kidney disease, and kidney cancer. According to our search, PAPP-A seems to be a candidate biomarker for diabetic nephropathy and chronic kidney disease, yet further studies are needed to detect diseases in the early stage.
Open Access
Diagnostic value and bioinformatics-based mechanistic exploration of serum miR-7977 in diabetic peripheral neuropathy

31. Juli 2025

Ziye Lin, Li Liu

PDF downloaden

Objectives Peripheral neuropathy, as a complication in patients with type 2 diabetes mellitus (T2DM), is easily overlooked in the early stage. The aim of this study was to investigate the significance of microRNA-7977 (miR-7977) for early warning of T2DM combined with diabetic peripheral neuropathy (DPN). Methods The study included T2DM patients two groups: those without DPN (n=63) and those with DPN (n=62). Quantitative Real-Time Polymerase Chain Reaction was used to detect serum levels of miR-7977 and mouse double minute 2 homolog (MDM2). Receiver Operating Characteristic Curve was used to assess their diagnose potential for DPN. Serum levels of malondialdehyde (MDA) and antioxidant markers (glutathione peroxidase and superoxide dismutase) were measured. Bioinformatics and dual luciferase reporter assays were used to validate MDM2 as a target of miR-7977. Results Serum miR-7977 levels were elevated in T2DM patients compared to healthy controls and further increased in DPN patients. Elevated miR-7977 was an independent risk factor for DPN and was positively correlated with MDA and negatively correlated with antioxidant markers in patients. MDM2, as a target gene of miR-7977, showed an opposite trend of expression to that in patients. Serum MDM2 combined with miR-7977 can efficiently diagnose T2DM combined with DPN. Conclusions miR-7977 and MDM2 may serve as a novel biomarker for early DPN diagnosis. miR-7977 may promote oxidative stress process by targeting MDM2, suggesting a potential therapeutic pathway.
Open Access
Systems biology based elucidation and experimental validation of anticancer effects of warfarin in vulvar cancer

26. August 2025

Jianwei Liang, Qiang Yao, Xingtao Pi, Yuan Liu, Wendong Cao, Shanchen Wei, Wendong Feng

PDF downloaden

Objectives To evaluate the efficacy of warfarin in inhibiting vulvar cancer cell growth and explore its molecular mechanisms, including effects on immune-infiltration and pathways utilizing both computational and experimental approaches. Methods The pharmacokinetic and toxicity profiles of warfarin were computationally evaluated to confirm drug-likeness and safety. Biological targets were then predicted, and the resulting genes were analyzed using a systems biology framework to construct a protein–protein interaction network, identifying key hub-genes. These genes underwent survival analysis to assess prognostic significance and were further analyzed for immune cell infiltration, indicating possible immunomodulatory effects. Molecular docking simulations examined warfarin’s binding affinity to the PD-1/PD-L1 immune checkpoint complex, suggesting immune regulatory potential. Experimental validation using SW-962 (vulvar-cancer) and HaCaT (normal) cell lines assessed cytotoxicity, oxidative stress, nuclear morphology, and cell cycle dynamics. Results Warfarin has promising physicochemical properties: high GI-absorption, BBB-permeability, and drug-likeness. Its predicted targets overlap with 20-vulvar cancer-related genes and form a PPI-network of key cancer-related pathways. GO and KEGG analyses reveal that the genes’ involvement in stress response, structural components, and cancer pathways. The top hub genes include AKT1 and CASP3, both of which have poor survival, and studies on immune infiltration show that warfarin interacts with immune cells. The docking analysis shows a strong binding affinity to the PD-1/PD-L1-complex, whereas cytotoxicity tests show selective action against cancer cells through oxidative stress, apoptosis, and G0/G1-cell cycle arrest. Conclusions Warfarin demonstrates promising anti-cancer effects by promoting apoptosis, cell cycle arrest, ROS-generation, and immune modulation, therefore warranting further clinical studies.
Open Access
Inflammatory markers in treated obese and non-obese pediatric hypertensive patients

10. Dezember 2025

Belen Ates, Selcuk Sen, Hasan Dursun, Semih Tek, Gizem Guvener, Baris Ozdemir, Yagiz Uresin

PDF downloaden

Objectives This study aimed to investigate the association between obesity, blood pressure (BP), and inflammatory markers, including tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1), in pediatric patients with hypertension receiving antihypertensive treatment. Methods A cross-sectional study was conducted involving 40 hypertensive pediatric patients aged 10–18 years, all undergoing at least three months of antihypertensive treatment. Participants were categorized into obese and non-obese groups based on body mass index (BMI). Group comparisons were performed, and correlations between BMI, BP, and inflammatory markers were analyzed. Serum IL-1 and TNF-α levels were quantified via enzyme-linked immunosorbent assay (ELISA). Results Both systolic BP (p=0.002) and diastolic BP (p<0.001) were significantly higher in obese patients. Median serum TNF-α was 2.37 (1.98–3.04) pg/mL in non-obese group, it was 3.04 (2.37–4.89) pg/mL, (p=0.032) in obese group. Median serum IL-1 was 1.23 (0.56–3.71) pg/mL in non-obese group, it was 2.47 (1.23–4.89) pg/mL, (p=0.035) in obese group. BMI showed a moderate correlation with SBP (r=0.484, p=0.002) and DBP (r=0.465, p=0.003), while its correlation with TNF-α was weak and borderline significant (r=0.312, p=0.05). No significant correlation was found between BMI and IL-1 (r=0.217, p=0.179). Conclusions Obesity in pediatric hypertension patients is associated with increased BP and elevated inflammatory markers, IL-1 and TNF-α. Effective weight management strategies should be integrated into pediatric hypertension treatment to mitigate inflammatory risks.
Open Access
Awareness and knowledge levels of patients regarding pre-analytical errors

22. April 2025

Esin Avci, Sena Yeşildağ Demir, Burak Akdeniz, Neziye Topcu, Ahmet Burak Dağaşan, Hande Şenol

PDF downloaden

Objectives Efforts to minimize pre-analytical errors remain significant in laboratory procedures. However, the existing literature has not thoroughly explored the awareness of errors that could influence the process before patients submit samples, and there is yet to be an internationally recognized standard on this matter. In this study, a set of 20 questions was posed to participants in the waiting area to assess their knowledge and awareness regarding the pre-analytical process. Methods In this study, voluntary participants were administered an awareness survey consisting of 4 open-ended and 16 multiple-choice questions. Four voluntary pollsters conducted a 20-item survey of voluntary individuals aged 18 and over who came to the blood sampling department of Pamukkale University Hospital to provide samples. The data obtained were analyzed using SPSS 25.0. Results The average age of the 328 participants was 30 ± 14 years, with 55.9 % of them being female. 68 % of the participants responded that they knew the rules before sampling. The % of those who believed fasting would not affect the sample result was 42.7. The 89 % of the participants mostly answered “yes” to the survey’s last question, which asked, “The questions directed to me showed that there may be points I do not know about blood sample giving.” Conclusions This article, which mentions assessing awareness and knowledge levels before blood sampling, highlights the necessity for education among healthcare professionals and patients.
Open Access
Targeting SASP with FDA-approved agents: minoxidil and diazoxide as potential senomorphic agents in cancer therapy

4. Dezember 2025

Yaprak Dilber Simay Demir, Islam Mohammed Ahmed, Tugce Tayyar, Aysun Ozdemir, Mustafa Ark

PDF downloaden

Objectives Chemotherapy-induced senescent cells are recognized to lead to cancer progression and resistance to treatment by releasing factors associated with the senescence-associated secretory phenotype (SASP). Therefore, targeting SASP via senomorphic agents is an emerging therapeutic strategy. In this study, we evaluated the potential of L-type Ca 2+ channel blockers, nifedipine and verapamil, and K + ATP channel openers, minoxidil and diazoxide, to influence senescence development and SASP-related secretory activity. Methods Senescence development was evaluated by beta-galactosidase activity and senescent cell morphology. Senomorphic activity was evaluated by measuring the secretion levels of total protein and IL-6, which are considered indicators of the SASP. Additionally, the effects of SASP were tested for cancer cell proliferation using the transwell system and cell migration using wound healing methods. Results Our findings indicate that neither L-type Ca 2+ channel blockers, nifedipine and verapamil, nor K + ATP channel openers, minoxidil and diazoxide, influence the induction of senescence by doxorubicin or alter senescent cell morphology. The K + ATP channel openers minoxidil and diazoxide notably inhibit the secretion of the proinflammatory cytokine IL-6 and VEGF-A in senescent HeLa cells, implying potential senomorphic properties. Moreover, although minoxidil and diazoxide did not reduce the proliferative effects of SASP on cancer cells, these drugs modulated the secretory phenotype of senescent cells to reduce HeLa cell migration significantly. Conclusions We suggest that minoxidil and diazoxide may have potential as senomorphic adjuvants in cancer therapy. If confirmed by invivo and clinical studies, these drugs may be repurposed to attenuate SASP-induced tumor progression. Moreover, K + ATP channels represent potential targets for senotherapy.
Open Access
Analysis of clinical application value of miR-1284 in type 2 diabetes mellitus

31. Oktober 2025

Yangyang Li, Yang Yang, Yinpei Ma, Lixin Yan

PDF downloaden

Objectives Type 2 diabetes mellitus (T2DM) is a chronic disease caused by insufficient use or low efficiency of insulin. With the improvement of people’s living standards, the prevalence of T2DM is increasing, which causes a huge burden to patients and society. The aim of this study is to explore the diagnostic and prognostic value of miR-1284 in T2DM by analyzing its expression level. Methods The study included 106 patients with T2DM and 98 healthy individuals as study subjects. The expression level of miR-1284 was detected by RT-qPCR in venous blood, and the biochemical indicators were determined. The receiver operating characteristic (ROC) curve and binary logistic analysis were used to evaluate the diagnostic value of miR-1284 in T2DM. Kaplan–Meier survival curve, multivariate Cox regression analysis, and ROC curve were used to analyze the prognostic value of miR-1284 in T2DM. Results miR-1284 was upregulated in T2DM patients. ROC results indicated that upregulation of miR-1284 expression in serum was one of the factors for diagnosing T2DM. Compared with the good prognosis group, the expression of miR-1284 was increased in the poor prognosis group. Multivariate Cox analysis showed that miR-1284 was associated with the occurrence of T2DM complications. Conclusions miR-1284 has high diagnostic and prognostic value for T2DM patients and may become a biomarker for clinical treatment of T2DM.
Erfordert eine Authentifizierung Nicht lizenziert
Lizenziert

Acid phosphatases from the breadfruit Artocarpus communis seeds as novel plant phosphorylating biocatalysts

4. September 2019

Hubert Kouassi Konan, Michel Djary Koffi, Desire Yapi Assoi Yapi, Lucien Patrice Kouame

Artikelnummer: 20170108

PDF downloaden

Objective Investigation on the phosphotransferase activity of two non-specific acid phosphatases (EC 3.1.3.2) designated as AP1 and AP2, previously isolated from breadfruit ( Artocarpus communis ) seeds for further biotechnological and industrial applications. Methods Transphosphorylation reactions were tested with sodium pyrophosphate as the phosphoryl donor and phenol as its acceptor. Transfer products were quantified by using high performance liquid chromatography. Results The two acid phosphatases were able to catalyze phosphoconjugates synthesis using pyrophosphate as the phosphoryl donor and phenol as acceptor. The optimal conditions of transphosphorylation reactions indicated that this synthesis was highly dependent on pH, temperature, time course, donor and acceptor concentrations and enzyme amount. A very short period (1.25 h) was observed for these synthesis reactions catalyzed by acid phosphatases isolated from breadfruit ( Artocarpus communis ) seeds. This suggested energy saving during biotransformation processes. The high average yields of 84.20 and 66.78% obtained for AP1 and AP2, respectively, made them useful to phosphorylate a wide range of nucleophile compounds such as nucleotides often used as food additives and pharmaceutical intermediates. Conclusion The acid phosphatase AP1 would be the most promising on the basis the better synthesis product yield (84.20%). The two biocatalysts could be considered as new valuable tools for bioprocesses.
Open Access
Effect of caffeine on acrylamide-induced cellular hepatotoxicity

20. Juni 2025

Tugce Karabas, Gulben Sayilan Ozgun

PDF downloaden

Objectives This study aims to determine the effects of caffeine on protein oxidation and endoplasmic reticulum (ER) stress in acrylamide (AA)-induced cellular hepatotoxicity. Methods First, HepG2 cells were incubated with 10 1 , 10 3 , and 10 4   µM AA. MTT assay was used to evaluate the cell viability. The western blot method was used to measure protein carbonyl (PC) levels to evaluate protein oxidation, and glucose-regulated protein 78 (GRP78), activating transcription factor 4 (ATF4), and C/EBP homologous (CHOP) levels to evaluate ER stress. Then, according to our results, cells were incubated with 10, 50, and 200 µM caffeine simultaneously with 10 4  µM AA and cell viability, PC, GRP78, ATF4 and CHOP levels were measured with the same methods. Results 10 3 and 10 4  µM AA caused a significant decrease in cell viability (p<0.05 and p<0.001, respectively). 10 4  μM AA caused a significant increase in PC (p<0.05), GRP78 (p<0.01), ATF4 (p<0.001), and CHOP (p<0.001) levels. 50 and 200 μM caffeine significantly reduced PC levels in AA-incubated cells (p<0.05 and p<0.01, respectively). Caffeine concentrations did not significantly change in cell viability, GRP78, ATF4, and CHOP levels (p>0.05 for all). Conclusions Our study showed that; AA, especially at higher concentrations, caused an increase in cytotoxicity, protein oxidation, and ER stress, and caffeine decreases protein oxidation without changing AA-induced cytotoxicity and ER stress.
Open Access
MiR-26b-5p and its association with inflammatory markers in infants and toddlers with bronchiolitis and respiratory symptoms

11. Juli 2025

Lanlan Li, Yanrui Yan, Shuge Wang, Wenlong Yi

PDF downloaden

Objectives The aim of this study was to investigate the impact of miR-26b-5p on diagnosis of bronchiolitis as well as its relationship with inflammatory factors. Methods This study conducts a retrospective study of infants and toddlers with bronchiolitis, coughing and wheezing as the main symptoms (RSV-positive and RSV-negative). The qRT-PCR was used to examine miR-26b-5p expression levels. Diagnostic accuracy of miR-26b-5p in infant and toddler respiratory diseases was assessed by ROC curve. Pearson correlation analysis was applied to demonstrate the relationship between miR-26b-5p and clinical severity markers, along with immune-related genes such as PTGS2 and TRAF3 . RSV-infected HBECs were used to validate the effect of miR-26b-5p on inflammatory factors. IL-6, IL-10 and TNF-α were measured by ELISA kits. Results MiR-26b-5p expression was reduced in infant and toddler respiratory diseases including bronchiolitis, coughing and wheezing. The ROC curve indicated that miR-26b-5p had a high diagnostic accuracy for differentiating respiratory diseases from healthy infants and toddlers. Notably, miR-26b-5p returned to baseline in infants and toddlers who had recovered from bronchiolitis. Pearson correlation analysis revealed a negative relationship of miR-26b-5p with PTGS2 and TRAF3 . RSV infection of HBECs reduced miR-26b-5p expression, and transfection with miR-26b-5p mimic reversed this trend. Furthermore, IL-6 and TNF-α levels were significantly elevated and IL-10 levels were reduced in RSV-infected HBECs, which was reversed by overexpression of miR-26b-5p. Conclusions MiR-26b-5p may be involved in disease progression through modulation of inflammatory responses and may be a diagnostic biomarker for infant and toddler respiratory diseases.
Open Access
Developing and evaluation of a novel machine learning-derived formula for LDL-C estimation

5. September 2025

Şaban Yayla, Alper Yayla, Hakan Ayyıldız

PDF downloaden

Objectives The Friedewald, Martin, and Sampson equations are widely used for calculating low-density lipoprotein cholesterol (LDL-C). We aimed to develop a new machine-learning-based formula to address errors and uncertainties associated with these equations. Methods We collected LDL-C, total cholesterol, triglyceride (TG), and high-density lipoprotein cholesterol measurements from 2,270 patients using the Abbott Architect c16000 analyzer for the training dataset. Three independent test datasets were generated using the homogeneous enzymatic method: 40,941 results from Architect c16000, 42,520 from Beckman Coulter AU5800, and 5,813 from Cobas c501 analyzers. Equations were developed using machine learning and symbolic regression in Python. Results The novel equation (mg/dL): (Y-LDL-C)=TC – HDL_C – (√TG) xTC/100. The formula demonstrated better performance across all datasets with the lowest root mean square error (9.9, 8.1, 16.0), mean absolute error (6.8, 5.9, 12.8), and mean absolute percentage error (5.2, 4.6, 9.9 %), along with the highest R 2 values (0.94, 0.95, 0.84) and accuracy rates (95.7, 95.3, 71.1 %). For samples with TG<400 mg/dL(<4.516 mmol/L), analytical accuracy was 96.3, 95.4, and 71.5 %, with minimal clinical error rates (0.6, 0.6, 3.5 %). Even with TG>400 mg/dL(>4.516 mmol/L), accuracy remained high (72.7, 91.2, 65.3 %) with low clinical error rates (3.9, 1.3, 11.7 %). The novel formula consistently outperformed the Friedewald, Sampson, and extended Martin equations. A key limitation is that the equation was derived using enzymatic LDL-C rather than beta-quantification. Conclusions The novel formula shows improved concordance in LDL-C estimations compared to existing equations, demonstrating better performance across diverse patient populations and laboratory systems.
Open Access
LncRNA MALAT1 regulates the inflammatory response of dry eye disease via sponging miR-302d

10. Juli 2025

Yuling Bai, Xingshuang Li, Qingjie Gai, Yue Hao, Xilan Chen, Yongxin Du

PDF downloaden

Objectives Dry eye disease (DED) is a prevalent ocular surface, and its pathogenesis remains inadequately elucidated. This research examined the possible regulatory mechanisms of lncRNA MALAT1 in DED to provide biomarkers for DED treatment. Methods qPCR was employed to assess the expression levels of MALAT1 and miR-302d in DED patients’ serum and HCECs cells. ELISA was utilized to measure the levels of IL-1β, IL-6, IL-8, and IFN-γ in DED patients’ serum and in various cell transfection groups. The effects of different cell transfection groups on the proliferation and apoptosis of HCECs were analyzed using the CCK-8 assay and flow cytometry. Furthermore, potential regulatory pathways were explored through GO and KEGG enrichment analyses of the target genes of miR-302d. Results MALAT1 exhibited a significant up-regulation in DED patients’ serum, while miR-302d was notable down-regulation, with a significant negative correlation between two molecules. MALAT1 was positively correlated with the Ocular Surface Disease Index (OSDI) and Symptom Assessment in Dry Eye (SANDE), suggesting its potential utility in evaluating the severity of DED. MALAT1 inhibited the proliferation of TNF-α-induced HCECs, promoted apoptosis, and enhanced the release of inflammatory factors. However, the suppression of miR-302d mitigated the impact of MALAT1 silencing on the function of HCECs. Enrichment analysis revealed that the target gene of miR-302d played a role in regulating cellular homeostasis and growth in HCECs. Conclusions The sponging effect of MALAT1 on miR-302d caused changes in HCECs cell function, and led to DED. MALAT1 was an important parameter reflecting the severity of DED patients.
Open Access
Low microRNA-338-3p expression drives cutaneous squamous cell carcinoma progression and predicts poor prognosis

17. Oktober 2025

Dongshuo Ji, Dayong Chen, Shaocong Lv, Liling Shen

PDF downloaden

Objectives To explore the clinical significance and influence of miR-338-3p in cSCC. Methods The content of miR-338-3p in cSCC was quantified using qRT-PCR. Prognostic relevance of miR-338-3p in cSCC was evaluated via Kaplan-Meier curve analysis. Functional roles of miR-338-3p in cSCC cell behavior were assessed through MTT assays, transwell assays. Results miR-338-3p was low-expressed in cSCC, with levels linked with lymph node metastasis, TNM stage, and disease progression. Statistically, miR-338-3p was a predictor of poor prognosis in cSCC. Functionally, miR-338-3p restoration weakened cSCC cellular viability and metastatic potential in vitro . Conclusions In cSCC, miR-338-3p exhibited downregulated expression, which suppressed cell viability, migratory behaviors, and invasive abilities. It has potential as a predictor for prognosis and a therapeutic target in cSCC.
Open Access
A bibliometric analysis of biochemistry theses in Türkiye: comparison with global trends

8. September 2025

Muammer Özdemіr, Sedat Abuşoğlu, Ali Ünlü

PDF downloaden

Objectives This study aims to examine the trends and distribution of research areas and methodologies in biochemistry theses over time by performing a bibliometric analysis in the CoHE database and comparing them with PubMed trends. Methods The study includes biochemistry theses from Türkiye spanning 1969 to 2023, totalling 5,543 theses in the CoHe database. Also, the PubMed database is used to compare the world’s and our country’s scientific trends. Google Sheets, AppSheets and Python are used for data analysis. The study employed various bibliometric techniques like performance analysis, cluster analysis, science mapping and co-occurrence analysis. Results Although several diseases exhibited insignificant associations, pregnancy demonstrated a significant positive correlation between CoHE and PubMed trends (ρ=0.455, p=0.0022). The noted negative associations for atherosclerosis (ρ = −0.429, p=0.0041) and hypertension (ρ = −0.470, p=0.0015) suggest that national trends in thesis production differ from international publication trends for these conditions. Furthermore, oxidant-antioxidant system studies at CoHe have held the first place for over 30 years, despite being decreasing after the 2000s and having a positive but statistically irrelevant connection with global trends (ρ=0.100; p=0.873). Conclusions We propose that biochemistry studies should prioritise diseases such as atherosclerosis and osteoarthritis in parallel with the findings in our work, particularly considering increasing life expectancy. Moreover, placing increased focus on microbiota studies and the utilisation of animal models within research methodologies will be crucial for advancing our understanding in the field.
Open Access
MiR-101-3p alleviates TGF-β1-induced fibrosis of renal tubular epithelial cells by inhibiting EZH2 in chronic kidney disease

15. Dezember 2025

Li Xu, Xinsheng Xie, Yong Li, Peng Zhou, Wei An, Danan Sun, Xinxin Qu

PDF downloaden

Objectives Renal fibrosis (RF) is a critical pathway in the progression of chronic kidney disease (CKD) to end-stage kidney diseases. This study aimed to investigate the role of miR-101-3p in the progression of fibrosis in renal tubular epithelial cells (RTECs) and to elucidate the underlying molecular mechanisms. Methods An RF cell model was established by induction with transforming growth factor-β1 (TGF-β1). The expression levels of miR-101-3p and fibrosis-associated proteins were measured using quantitative real-time reverse transcription polymerase chain reaction. Cell migration ability was detected by Transwell assay. The potential target genes of miR-101-3p were predicted through bioinformatic analysis. The interaction between miR-101-3p and EZH2 was verified using the luciferase assay and RNA immunoprecipitation (RIP) assay. Results HK-2 cells treated with TGF-β1 showed downregulated expression of miR-101-3p. Overexpression of miR-101-3p reduced cell migration and decreased the production of fibronectin, collagen IV and α-smooth muscle actin (α-SMA). EZH2 was identified as a downstream target gene of miR-101-3p. The interaction between miR-101-3p and EZH2 was confirmed by luciferase assay and RIP assay. EZH2 was upregulated in TGF-β1-induced cells. Upregulation of EZH2 partially reversed the anti-fibrotic effects caused by miR-101-3p overexpression. Conclusions miR-101-3p alleviates TGF-β1-induced fibrosis in RTECs by inhibiting EZH2. This study provides new insights into the molecular mechanisms of RF and suggests potential therapeutic targets for CKD.
Open Access
MiR-221-3p improves the prognostic value of lung ultrasound score in acute respiratory distress syndrome and modulates the inflammatory response

19. August 2025

Dan Liu, Di Yang, Yufeng Zhang, Yu Wang, Huijuan Yu, Caimei Liu, Jianhang Ge

PDF downloaden

Objectives Acute respiratory distress syndrome (ARDS) is linked to high mortality rates, with effective assessment of the condition critical to improving patient prognosis. The aim is to explore the value of serum miR-221-3p and lung ultrasound (LUS) score on the prognosis of ARDS, with the aim of providing meaningful references for clinical evaluation and therapeutic strategies. Methods The study cohort comprised 156 patients diagnosed with sepsis-induced ARDS. MiR-221-3p levels were quantified using RT-qPCR. Prognostic significance was determined by the ROC curve and Logistic analysis. Furthermore, a cell injury model was established in human pulmonary microvascular endothelial cells (HPMECs) induced by LPS, and the effects of miR-221-3p on cell viability and apoptosis of HPMECs were examined utilizing CCK-8 and flow cytometry. ELISA was utilized to evaluate the role of miR-221-3p on inflammatory factors and cell adhesion molecules. Results In deceased ARDS patients, elevated levels of serum miR-221-3p demonstrated a notable positive correlation with APACHE II score, SOFA score, procalcitonin, and LUS score. Notably, miR-221-3p and LUS score were identified as prognostic factors associated with patient mortality, and the integration of these two assays resulted in a more accurate assessment of patient prognoses. In HPMECs exposed to LPS, miR-221-3p silencing enhanced cell survival, suppressed apoptosis, and reduced levels of inflammatory cytokines (TNF-α, IL-6, IL-1β) and adhesion molecules (ICAM-1, E-selectin). Conclusions MiR-221-3p, combined with LUS assessment, holds prognostic value in ARDS. Its involvement in inflammation and cellular damage suggests a modulatory effect on disease advancement.
Open Access
Protective effect of N-acetylcysteine on retinal cell apoptosis, oxidative stress and inflammation in type 1 diabetic rats

17. September 2025

Lina Ma, Yantao Jin

PDF downloaden

Objectives The purpose of the current study is to explore the therapeutic role of N-acetylcysteine (NAC) against retinal cell apoptosis in a rat model of type 1 diabetes mellitus (T1DM) and to evaluate possible mechanisms of action. Methods A total of 18 Wistar rats (16-months-old) were divided into three groups in equal numbers: Control (group 1), T1DM (Group 2) and T1DM + NAC (group 3). In group 2 and 3 rats, T1DM was induced by intraperitoneal (IP) injection of streptozotocin (65 mg/kg). Group 3 was given oral NAC (60 mg/kg once daily) for 5 months. Serum and retina were collected for further use. Results NAC administration significantly declined fasting glucose level, hyperlipidemia, atherogenic coefficient and cardiac risk ratio, but improved weight gain and fasting insulin level in T1DM rats. Associated with these effects, NAC significantly improved levels of total antioxidant capacity, while significantly decreased malondialdehyde, protein carbonyls and 8-hydroxy-2′-deoxyguanosine contents in the retina of T1DM animals. NAC significantly diminished the percentage of retinal cell apoptosis in T1DM rats. A significant enhancement was found in Bax, TNF-α, and Caspase expression, but IL-10, superoxide dismutase, catalase and Bcl2 expression was significantly decreased in T1DM rats. However, NAC treatment considerably improved the expression of these genes in retina of T1DM rats. Conclusions NAC protects retinal cell by enhancing antioxidant pool, attenuating inflammation, oxidative stress and apoptosis in T1DM.
Open Access
Magnolia officinalis and neuronal mitochondrial dysfunction: a potential therapeutic approach for aging or chemotherapy-induced peripheral neuropathy

23. September 2025

Simge Unay, Metin Caliskan, Gülsen Bayrak, Erkan Tuncay, Belma Turan

PDF downloaden

Objectives Peripheral neuropathy caused by aging and chemotherapy significantly reduces quality of life. Magnolia officinalis (MAGO), a traditional Chinese medicinal plant, is renowned for its anti-inflammatory, antioxidant, and anticancer properties. However, its effects on aging- and chemotherapy-induced peripheral neuropathy remain poorly understood. Therefore, this study aimed to investigate the impact of MAGO on peripheral neuropathy induced by aging or chemotherapy at the cellular level. Methods PC12 cell lines were used to establish models of D-galactose (D-gal)-induced aging and cisplatin-induced peripheral neuropathy. Cells in these models were treated with MAGO at concentrations of 5 µM or 10 µM. The effects of MAGO were evaluated by assessing cell viability, immunocytochemistry, RT-PCR, and mitochondrial function through measurement of mitochondrial membrane potential. Results MAGO treatment significantly improved cell viability in both D-gal-induced aging (5 µM: 82.2 ± 1.3 %; 10 µM: 78.9 ± 1.0 %) and cisplatin-induced peripheral neuropathy (CIPN5 µM: 74.7 ± 0.3 %; 10 µM: 70.3 ± 0.2 %) model cells. Treatment with MAGO significantly alleviated cellular viability in D-gal-induced aging (5 µM; 82.2 ± 1.3 or 10 µM; 78.9 ± 1.0) or cisplatin-induced peripheral neuropathy (5 µM; 74.7 ± 0.3 or 10 µM; 70.3 ± 0.2) model cells. Treatment with MAGO (5 µM) significantly prevented the upregulation of the apoptosis marker caspase-3 (Cas-3) and mitochondrial uncoupling protein 3 (UCP3), as determined by immunostaining and subsequent quantification. The analysis showed that the elevated levels of these two proteins in the model cells were effectively reduced following MAGO treatment. Additionally, the expression of a mitofusin 1 (MFN1), a key gene involved in mitochondrial function, was also restored in the treated groups. This recovery was consistent with the observed improvement in mitochondrial membrane potential, suggesting a protective role of MAGO in maintaining mitochondrial integrity. Conclusions Overall, our data suggest that MAGO has potential in reducing aging-related cellular damage and chemotherapy-induced neuropathy by modulating apoptosis and mitochondrial dysfunction.

XXXI Meeting of Balkan Clinical Laboratory Federation 35th National Biochemistry Congress 28 October - 1 November 2024, Antalya, Türkiye

2nd National Nutrition and Metabolism Symposium 2023

Heft 3

Heft 2

Heft s2

VIII. Turkey in vitro Diagnostic (IVD) Symposia: Preclinical Models 29 Kasım - 1 Aralık 2023 Izmir

Heft s1

International Biochemistry Congress 2023 34th National Biochemistry Congress 29 October - 1 November 2023, Fethiye, Türkiye

Heft 1

Heft s4

I.International Nutrition and Metabolism Symposia 16-17 December 2022 Istanbul

Heft s3

IN MEMORY OF PROF GUNES T. YUREGIR 2nd KAHRAMANMARAS BI0CHEMISTRY DAYS

Heft s2

TBS International Biochemistry Congress 2022 - 33rd National Biochemistry Congress

Heft 6

Heft s1

VII. Türkiye in vitro Diagnostic (IVD) Symposia: Inflammation 27-29 April 2022 Izmir

TBS International Biochemistry Congress 2021 - 32nd National Biochemistry Congress

Heft s1

3rd International Cancer and Ion channels Congress 2021

XXXI National Congress of The Turkish Biochemical Society 2020

Heft 6

Heft s1

V. Turkey in vitro Diagnostic (IVD) Symposium: Health Biotechnology

XXVII. Balkan Clinical Laboratory Federation Meeting BCLF 2019, XXX. National Congress of the Turkish Biochemical Society TBS 2019

Workshop on PhD Supervision in Biomedicine and Health Sciences: ORPHEUS Perspective

Heft s5

TBS International Biochemistry Congress 2018, 29th National Biochemistry Congress

Heft s2

TBD-BD Preanalytic Phase Symposium 2018

Heft 5

Heft s4

FEBS Workshop on Molecular Life Sciences: Training Tomorrow's Scientists

Heft s1

III. Turkey in vitro Diagnostic (IVD) Symposium Endocrine and Metabolic Diseases Biomarkers From Diagnostic To Therapy

Insulin Resistance Symposium | in vitro Diagnostic Biomarkers Symposium

Heft s1

International Biochemical Congress 2017 | 28th National Biochemistry Congress

1st International Cell Death Research Congress-Turkey: Abstract Issue

Heft s4

Heft s3

TBS Biochemical Days: Abstract Issue

Journal Impact Factor	0.7	2024, Journal Citation Reports (Clarivate, 2025)
5-year Journal Impact Factor	0.7	2024, Journal Citation Reports (Clarivate, 2025)
Journal Citation Indicator	0.13	2024, Journal Citation Reports (Clarivate, 2025)
CiteScore	1.3	2024, Scopus (Elsevier B.V., 2025)
SCImago Journal Rank	0.23	2024, SJR (Scimago Lab, 2025; Data Source: Scopus)
Source Normalized Impact per Paper	0.328	2024, CWTS Journal Indicators (CWTS B.V., 2025; Data Source: Scopus)

Weitere Informationen über Zeitschriftenmetriken

You can easily submit your manuscript online. Simply go to https://mc.manuscriptcentral.com/tjbiochem and you will be guided through the entire submission and publishing process.
Prepare your manuscript according to the Instructions for Authors and Submission Checklist.
The Turkish Journal of Biochemistry follows Tier 3 of our Data Sharing Policy. Authors are required to provide a data availability statement. Please refer to the Data Sharing Policy for guidance on how to write a data availability statement.
As a condition of submission, the Template for Ethical and Legal Declarations must be customized by the submitting author on behalf of all others and uploaded as a separate Word file.
The title page should be submitted as separate file (main title, short title, author names and affiliations, full address of corresponding author, keywords).
If you have any general questions please visit our FAQ page for authors.
For more detailed information please contact editor@turkjbiochem.com.

EDITOR IN CHIEF
Doğan Yücel, Department of Medical Biochemistry, Faculty of Medicine, Lokman Hekim University, Ankara, TÜRKIYE

VICE EDITORS
Aylin Sepici Dinçel, Department of Medical Biochemistry, Faculty of Medicine, Gazi University, Ankara, TÜRKIYE
Merve Sibel Güngören, Duzen Lab., Ankara, TÜRKIYE
Güneş Özhan, İzmir Institute of Technology, Molecular Biology and Genetics, Gulbahce Campus, İzmir, TÜRKIYE
Oytun Portakal, Department of Medical Biochemistry, Faculty of Medicine, Hacettepe University, Ankara, TÜRKIYE
Mehmet Şeneş, Department of Biochemistry, Ankara Education and Research Hospital, Ankara, TÜRKIYE
Muhittin Serdar, Department of Medical Biochemistry, School of Medicine, Acıbadem University, İstanbul, TÜRKIYE

ASSOCIATE EDITORS
Sedat Abuşoğlu, Department of Medical Biochemistry, Faculty of Medicine, Selçuk University, Konya, TÜRKIYE
Hamit Hakan Alp, Department of Biochemistry, Yuzuncu Yil Universitesi Tip Fakultesi, Van, TÜRKIYE
Sreeparna Banerjee, Department of Biological Sciences, Middle East Technical University, Ankara, TÜRKIYE
Burak Barut, KTÜ Eczacılık Fakültesi, Karadeniz Teknik Universitesi Pharmacy, Trabzon, TÜRKIYE
Tülin Bayrak, Department of Medical Biochemistry, Faculty of Medicine, Ordu University, Ordu, TÜRKIYE
Murat Bolayırlı, Department of Biochemistry, Faculty of Medicine, Cerrahpaşa İstanbul University, İstanbul, TÜRKIYE
Abdurrahman Coşkun, Department of Medical Biochemistry, School of Medicine, Acıbadem University, İstanbul,TÜRKIYE
Özlem Dalmızrak, Department of Medical Biochemistry, Faculty of Medicine, Near East University, Nicosia, TRNC
Birsen Can Demirdöğen, Department of Biomedical Engineering, TOBB University of Economics and Technology, Ankara, TÜRKIYE
Halef Okan Doğan, Tıp fakültesi, Cumhuriyet Üniversitesi Sivas, TÜRKIYE
Perinur Bozaykut Eker, Department of Molecular Biology and Genetics, Acibadem Mehmet Ali Aydinlar University, Istanbul, TÜRKIYE
Suat Erdoğan, Department of Medical Biology, School of Medicine, Trakya University, Edirne, TÜRKIYE
Uzay Görmüş, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Solna, SWEDEN
Gürcan Günaydın, Basic Oncology, Hacettepe University Cancer Institute, Ankara, TÜRKIYE
Semra Koçtürk, Department of Medical Biochemistry, School of Medicine, Dokuz Eylül University, İzmir, TÜRKIYE
Işıl Aksan Kurnaz, Department of Molecular Biology and Genetics, Gebze Technical University, Kocaeli, TÜRKIYE
Melek Özkan, Department of Environmental Engineering, Gebze Technical University, Kocaeli, TÜRKIYE
Ebru Saatçi, Department of Biology, Faculty of Arts & Sciences, Erciyes University, Kayseri, TÜRKIYE
Alaattin Şen, Department of Biology, Faculty of Arts & Sciences, Pamukkale University, Denizli, TÜRKIYE
Çağdaş Son, Department of Computer Engineering, Middle East Technical University, Ankara, TÜRKIYE
Deniz İlhan Topçu, Biochemistry Laboratory, Baskent University, İzmir, TÜRKIYE
Serenay Elgün Ülkar, Department of Medical Biochemistry, Faculty of Medicine, Ankara University, Ankara, TÜRKİYE
Ali Ünlü, Medical Biochemistry, Selcuk Universitesi, Konya, TÜRKIYE
Hamdi Uysal, Department of Biochemistry, Faculty of Veterinary Medicine, Ankara University, Ankara, TÜRKIYE
İlhan Yaylım, Department of Molecular Medicine, Aziz Sancar Institute of Experimental Medicine, İstanbul University, İstanbul, TÜRKIYE
Fatma Meriç Yılmaz, Department of Medical Biochemistry, Faculty of Medicine, Ankara Yıldırım Beyazıt University, Ankara, TÜRKIYE
Meral Yüksel, Department of Medical Laboratory Techniques, Vocational School of Health Services, Marmara University, Istanbul, TÜRKIYE

STATISTICS EDITORS
Erdal Coşgun, Microsoft Genomics Research Group, Redmond, WA, USA
Sevilay Karahan, Department of Biostatistics, Faculty of Medicine, Hacettepe University, Ankara, TÜRKIYE
Jale Karakaya, Department of Biostatistics, Faculty of Medicine, Hacettepe University, Ankara, TÜRKIYE

TECHNICAL EDITORS
Serkan Bolat, Department of Medical Biochemistry, Sivas Cumhuriyet University, Sivas, TÜRKİYE
Gizem Yılmaz Çalık, Medical Biochemistry Laboratory, Tokat Zile State Hospital, Tokat, TÜRKİYE
Merve Sibel Güngören, Duzen Lab., Ankara, TÜRKIYE
Duygu Eryavuz Onmaz, Department of Medical Biochemistry, Faculty of Medicine, Selçuk University, Konya, TÜRKIYE
Duygu Şahin, Department of Medical Biochemistry, Istanbul Aydın University, Istanbul, TÜRKIYE
Emel Çolak Samsum, Medical Biochemistry Laboratory, Pursaklar State Hospital, Ankara, TÜRKİYE
İsmail Sarı, Department of Medical Biochemitry, Faculty of Medicine, Kırklareli University, Kırklareli, TÜRKİYE
Z. Onur Uygun, Department of Medical Biochemistry, Faculty of Medicine, Ege University, Kars, TÜRKIYE
Oğuzhan Zengi, Department of Medical Biochemistry, Bağcılar Training and Research Hospital, İstanbul, TÜRKIYE

CORRESPONDENCE
Nermin Şahan, Hirfanlı Sokak 9/3 Gaziosmanpaşa 06700 Ankara, TÜRKİYE

EDITORIAL BOARD
Khosrow Adeli, Molecular Medicine, Research Institute, The Hospital for Sick Children, University of Toronto, Toronto, Ontario, CANADA
Cezmi Akdiᶊ, University Zurich, Swiss Institute of Allergy and Asthma Research (SIAF), Davos, SWITZERLAND
Mübeccel Akdiᶊ, University Zurich, Swiss Institute of Allergy and Asthma Research (SIAF), Davos, SWITZERLAND
Reᶊat Apak, Department of Chemistry, Faculty of Engineering, İstanbul University Cerrahpaºa Research Information System, İstanbul, TURKEY
Diler Aslan, Department of Biochemistry, Faculty of Medicine, Pamukkale University, Denizli, TÜRKIYE
Anyla Bulo-Kasneci, Laboratory Department, University Hospital Center "Mother Teresa", Tirana, ALBANIA
Elif Demirkan, Department of Biology, Faculty of Arts & Sciences, Uludağ University, Bursa, TÜRKIYE
Z. Günnur Dikmen, Department of Biochemistry, Faculty of Medicine, Hacettepe University, Ankara, TÜRKIYE
Mustafa B.A. Djamgoz, Department of Life Sciences, Faculty of Natural Sciences, Imperial College, London, UNITED KINGDOM
Gökhan Hotamışlıgil, Department of Genetics and Complex Diseases, Harvard School of Public Healt, Boston, USA
Ivan G. Ivanov, Institute of　Molecular Biology, Bulgarian Academy of Sciences, Sofia, BULGARIA
Erdal Karaöz, Department of Histology and Embryology, Faculty of Medicine, Istinye University, İstanbul, TÜRKIYE
Mehmet Kesimer, Department of Pathology and Laboratory Medicine, Marsico Lung Institute, University of North Carolina at Chapel Hill, NC, USA
İrfan Küfrevioğlu, Department of Chemistry, Faculty of Art & Sciences, Atatürk University, Erzurum, TÜRKIYE
Nada Majkic-Singh, Institute of Medical Biochemistry, Pharmaceutical Faculty and Clinical Centre of Serbia, Belgrade, SERBIA
Gülgün Oktay, Department of Medical Biochemistry, Faculty of Medicine, University of Dokuz Eylül, İzmir, TÜRKIYE
Yeşim Özarda, Department of Medical Biochemistry, Faculty of Medicine, Uludağ University, Istanbul, TÜRKIYE
Tomris Özben, Department of Medical Biochemistry, Faculty of Medicine, Akdeniz University, Antalya, TÜRKIYE
Nazmi Özer, Faculty of Pharmacy, Girne American University, Nicosia TRNC
Mario Plebani, Department of Medical Sciences, University of Padova, Padova, ITALY
Demetrios Rizos, Hormonal and Biochemical Laboratory, Aretaieio Hospital, University of Athens, Athens, GREECE
George Russev, Bulgarian Academy of Sciences, Institute of Molecular Biology, Sofia, BULGARIA
Fahri Saatçioğlu, Department of Biosciences, University of Oslo, Oslo, NORWA
Ferhan Girgin Sağın, Department of Medical Biochemistry, Faculty of Medicine, University of Ege, İzmir, TÜRKIYE
Aziz Sancar, Deparment of Biochemistry and Biophysics, University of North Carolina School of Medicine, Chapel Hill, NC, USA
Praveen Sharma, All India Institute of Medical Sciences, Jodhpur, INDIA
Emin Sofic, Department of Chemistry, Faculty of Science,University of Sarajevo, Sarajevo, BOSNIA AND HERZEGOVIA
Eser Yıldırım Sözmen, Department of Medical Biochemistry, Faculty of Medicine, Tınaztepe University, İzmir, TÜRKIYE
Sedef Yenice, Department of Clinical Chemistry, Group Florence Nightingale Hospitals, İstanbul, TÜRKIYE

Editorial Office
submission@turkjbiochem.com

Heike Jahnke
E-mail: heike.jahnke@degruyter.com

Turkish Journal of Biochemistry ist in den folgenden Services indiziert:

Baidu Scholar
Cabells Journalytics
CABI (over 50 subsections)
Chemical Abstracts Service (CAS) - CAplus
Chemical Abstracts Service (CAS) - SciFinder
CNKI Scholar (China National Knowledge Infrastructure)
CNPIEC - cnpLINKer
Dimensions
DOAJ (Directory of Open Access Journals)
EBSCO (relevant databases)
EBSCO Discovery Service
EMBASE
FSTA - Food Science & Technology Abstracts
Genamics JournalSeek
Google Scholar
Index Copernicus
Japan Science and Technology Agency (JST)
J-Gate
Journal Citation Reports/Science Edition
JournalGuide
Naver Academic
Naviga (Softweco)
Primo Central (ExLibris)
Publons
QOAM (Quality Open Access Market)
ReadCube
ScienceON (Korea Institute of Science and Technology Information)
Scilit
SCImago (SJR)
SCOPUS
Semantic Scholar
Sherpa/RoMEO
Summon (ProQuest)
TDNet
TEMA Technik und Management
TÜBITAK/ULAKBIM
TÜRK MEDLINE-ULUSAL ATIF INDEKSI ve TÜRKIYE ATIF DIZINI
Ulrich's Periodicals Directory/ulrichsweb
WanFang Data
Web of Science - Science Citation Index Expanded
WorldCat (OCLC)
X-MOL
Yewno Discover

Medizin Klinische Medizin Klinische Medizin, andere

Online Submission of Manuscripts

Zeitschriften Informationen

Weitere Informationen

eISSN:

1303-829X

ISSN:

0250-4685

Sprache:

Englisch

Verlag:

De Gruyter

Weitere Informationen

Erstveröffentlichung:

1. Januar 1976

eISSN: 1303-829X

ISSN: 0250-4685

Zielgruppe(n) für diese Zeitschrift

researchers in chemistry, physics, engineering, pharmacology, molecular biology, biomedicine, and clinicians, addressing recipients in academic, industrial, and regulatory environments, the informed public and policymakers.

Sicherheits- und Produktressourcen

Herstellerinformationen:
Walter de Gruyter GmbH
Genthiner Straße 13
10785 Berlin
productsafety@degruyterbrill.com

Creative Commons

BY 4.0

Turkish Journal of Biochemistry

Über diese Zeitschrift

Ihre Vorteile

Zusatzmaterial

Fachgebiete

Turkish Journal of Biochemistry

Übersicht

Über diese Zeitschrift

Ihre Vorteile

Ahead-of-Publication / Just-Accepted

Ausgaben

Metriken

Einreichen

Editorial

Abstracting und Indexing

Zusatzmaterial

Zusatzmaterial

Fachgebiete

Fachgebiete

Externe Links

Bibliographische Daten