journal: Turkish Journal of Biochemistry

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Turkish Journal of Biochemistry

Türk Biyokimya Dergisi

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Sprache: Englisch

Erstveröffentlichung: 1. Januar 1976

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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
Effects of monosodium glutamate administration during childhood period on learning, memory, and neurobehaviour

19. Mai 2026

Halil İbrahim Büyükbayram, Duygu Kumbul, İlter İlhan, Yonca Sönmez, Fatih Gültekin

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Objectives This study aimed to evaluate the effects of monosodium glutamate (MSG) exposure during the childhood-equivalent period on learning, memory, and neurobehaviour, considering potential sex-related differences. Methods Sixty-six post-weaning Wistar Albino rats were randomly assigned to Control (C), Low Dose (LD; 25 mg/kg/day), and High Dose (HD; 2,500 mg/kg/day) groups for 6 weeks. Behavioral assessments included the Morris Water Maze (MWM), Open Field Test (OFT), and Forced Swim Test (FST). Following behavioral testing, hippocampal tissues were collected to measure NR2A, NR2B, nAChR α7, and 5-HT2A receptor levels. Results While all groups improved spatial learning over time, the HD group showed a delayed learning curve. In the OFT, HD rats exhibited reduced exploratory activity, suggesting anxiety-like behavior. In the FST, both LD and HD groups had increased immobility durations, indicating behavioral despair. Receptor analysis revealed significantly increased NR2A expression in both sexes in the HD group. Additionally, 5-HT2A density was elevated in LD males, and nAChR α7 was reduced in LD and HD females. These changes suggest MSG may disrupt neurotransmitter systems involved in mood and cognition. Conclusions MSG exposure, even at dietary-relevant doses, can alter neurobehavioral outcomes and receptor expression during early development. High doses impaired learning and induced anxiety- and depression-like behaviors, potentially mediated by NR2A upregulation. Low doses may also increase vulnerability to affective disturbances. These findings raise concerns about the long-term neurodevelopmental effects of MSG in children.
Open Access
Biological evaluation of an artemisinin-benzothiophene derivative: anti-cancer and anti-inflammatory effects

18. Mai 2026

Kübra Kocabıyık, Omrüye Özok-Arici, Arif Kivrak, Şevki Arslan

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Objectives Cancer is a leading global health issue with complex causes. Conventional treatments often face challenges like drug resistance and toxicity. Plant-derived compounds such as artemisinin have gained interest due to their diverse anticancer mechanisms, including ROS generation and apoptosis induction. In this study, the biological activities of ART-FB, a hybrid compound combining benzothiophene and artemisinin, were systematically investigated for the first time. Methods ART-FB’s cytotoxicity was tested on various human cancer cell lines (Caco-2, LNCaP, HeLa, A549) and HUVEC via MTT assay. Colony formation, scratch-wound, and Annexin V/PI assays were used to assess proliferation, migration, and apoptosis. Apoptotic gene expression was analyzed by qPCR. Anti-inflammatory effects were studied in LPS-stimulated RAW264.7 cells via Griess assay and qPCR. Results ART-FB showed selective cytotoxicity in Caco-2, LNCaP, HeLa, and A549 cancer cell lines, with lower toxicity in non-cancerous HUVEC cells. It effectively suppressed proliferation, colony formation, and migration, especially in LNCaP and A549 cells, suggesting potential anti-metastatic activity. Annexin V/PI staining and gene expression analysis confirmed that ART-FB induces apoptosis via both intrinsic and extrinsic pathways, with the strongest effects in LNCaP and Caco-2 cells. In LPS-stimulated RAW264.7 macrophages, ART-FB significantly reduced nitric oxide levels and downregulated iNOS , COX-2 , TNF-α , and IL-6 , while upregulating IL-10 , suggesting dual anticancer and anti-inflammatory action. Conclusions ART-FB exhibits both anticancer and anti-inflammatory properties, targeting key pathways involved in tumor growth and immune response. These findings indicate that ART-FB is a promising candidate for further preclinical development as a multifunctional therapeutic agent.
Open Access
Rabdosia serra alleviates intrahepatic cholestasis via activation of the CAR/MRP2 pathway in a rat model

18. Mai 2026

Da-kun Zhang, Yuan-yuan Cai

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Objectives This study aimed to investigate the pharmacological effects and mechanisms of Xihuangcao (XHC) in a rat model of Intrahepatic cholestasis (IC). Methods Network pharmacology analysis was conducted to identify the main active ingredients and key targets of XHC in alleviating IC, validated through molecular docking. An IC rat model was then established to evaluate the efficacy of XHC. The potential mechanisms were verified using hematoxylin-eosin (HE) staining, real-time quantitative polymerase chain reaction (RT-qPCR), and Western blotting (WB). Results Network analysis identified CAR as the key target for XHC’s effects on IC, with active ingredients including luteolin, quercetin, isorhamnetin, kaempferol, a quercetin derivative, and skrofulein. Molecular docking confirmed the strong binding affinity of these components to CAR. Compared to the model group, high-dose XHC significantly increased the body weight of rats (p<0.01), and decreased serum biochemical markers related to IC, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and bilirubin levels (p<0.01). HE staining showed reduced hepatocyte necrosis and inflammation. Additionally, RT-qPCR and WB confirmed increased mRNA and protein levels of MRP2 and CAR in the high-dose XHC group (p<0.001). Conclusions XHC may alleviate IC through the CAR/MRP2 signaling pathway, providing pharmacological support for its use in treating IC.
Open Access
Diagnostic accuracy of the Dirui FUS-3000 plus in proteinuria screening: a retrospective evaluation

15. Mai 2026

Muhammed Seyithanoğlu

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Objectives Proteinuria is a key biomarker for early detection, staging, and monitoring of chronic kidney disease (CKD). This study aimed to evaluate the diagnostic accuracy of the Dirui FUS-3000 Plus automated urine analyzer by comparing urine dipstick test results with the spot urine protein-to-creatinine ratio (PCR) as the reference method. Methods A retrospective cross-sectional analysis was conducted on 6,543 spot urine samples. Dipstick results were assessed in two ways by categorizing “trace” as either negative or positive. Diagnostic parameters including sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and Cohen’s kappa were calculated for two PCR cut-off values (150 mg/g and 200 mg/g). Results Diagnostic performance of the dipstick test varied according to the PCR cut-off value and the interpretation of trace results. When trace was classified as negative, sensitivity and specificity were 71.3 % and 98.3 % at a PCR cut-off of 200 mg/g, and 60.2 % and 99.1 % at a cut-off of 150 mg/g, with Cohen’s kappa values of 0.703 and 0.554, respectively (all p<0.001). When trace was classified as positive, sensitivity and specificity were 85.3 % and 88.8 % at a PCR cut-off of 200 mg/g, and 75.8 % and 92.7 % at a cut-off of 150 mg/g, with corresponding kappa values of 0.741 and 0.662 (all p<0.001). McNemar’s test was statistically significant in all analyses. Conclusions The Dirui FUS-3000 Plus provides competitive diagnostic performance in proteinuria screening. Consideration of trace results and urine concentration is crucial to minimize misclassification, especially in borderline proteinuria cases.
Open Access
lncRNA DLEU2 facilitates clear cell renal cell carcinoma progression by regulating miR-186-5p

6. Mai 2026

Zhengke Zhu, Yamei Feng, Muyang Cao, Jianbin Zhang, Wenjin Du

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Objectives The dysregulation and function of lncRNA DLEU2 (DLEU2) in human cancers have been widely reported. Its functional role in ccRCC remains unclear. The significance of DLEU2 in ccRCC and its potential molecular mechanism were investigated to explore a reliable biomarker. Methods One hundred and six ccRCC patients were included, and the expression of DLEU2 in tissues was evaluated by qPCR. The biological effect of DLEU2 on related cellular processes was assessed. The regulation of miR-186-5p by DLEU2 was studied with the luciferase-reporter assay. Results DLEU2 showed a significantly higher expression in ccRCC in comparison with normal samples. The upregulation of DLEU2 indicates advanced TNM stage and positive lymph node metastasis of patients. DLEU2 was an independent prognostic biomarker of ccRCC. Silencing DLEU2 significantly suppressed the proliferation, migration, and invasion of ccRCC cells. The negative regulation of miR-186-5p by DLEU2 was considered the underlying mechanism of DLEU2. Conclusions Upregulated DLEU2 indicated malignant development and poor prognosis of ccRCC. Moreover, DLEU2 acted as a tumor promoter via modulating miR-186-5p.
Open Access
MiR-134-5p serves as an early diagnostic biomarker and prognostic predictor for sepsis-associated acute kidney injury

4. Mai 2026

Shuxian Chen, Shaowei Guan, Jifang Liang, Fangfang Gao

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Objectives Sepsis-associated acute kidney injury (SA-AKI) poses significant challenges in early diagnosis and prognosis evaluation due to the lack of reliable biomarkers. This study focused on miR-134-5p to explore its potential as a novel biomarker for SA-AKI. Methods Serum miR-134-5p levels of sepsis patients (64 simple sepsis and 65 SA-AKI) were detected via qRT-PCR. Diagnostic value was evaluated by the receiver operator characteristic (ROC) curve analysis. Logistic regression analysis identified risk factors. Kaplan-Meier curves and Cox regression analysis evaluated the prognostic value of miR-134-5p in SA-AKI. Results miR-134-5p is upregulated in SA-AKI patients and exhibits diagnostic value (AUC=0.885). The miR-134-5p expression was positively correlated with the levels of serum creatinine (Scr, r=0.702), blood urea nitrogen (BUN, r=0.604), kidney injury molecule-1 (KIM-1, r=0.568), and negatively correlated with estimated glomerular filtration rate (eGFR, r=−0.315). miR-134-5p (OR=10.788) and eGFR (OR=0.368) were identified as risk factors for the development of AKI in sepsis patients. Compared with patients in the high-expression group, SA-AKI patients in the low miR-134-5p expression group exhibited better prognosis (log-rank test p=0.008). miR-134-5p could serve as an independent prognostic factor (HR=6.518) along with Scr (HR=4.491), BUN (HR=5.164), eGFR (HR=0.218), and KIM-1 (HR=5.662). Conclusions miR-134-5p was upregulated in SA-AKI and associated with the severity of SA-AKI. MiR-134-5p showed a diagnostic and prognostic value on SA-AKI.
Open Access
Downregulation of serum LINC00487 as a biomarker for predicting onset and short-term prognosis in acute coronary syndrome

4. Mai 2026

Li Ma, Yongning Zhao, Na Lv, Huifang Sun, Yang Gao

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Objectives long non-coding RNAs (lncRNAs) are critically involved in the pathogenesis of acute coronary syndrome (ACS) and have been linked to major adverse cardiovascular events (MACE). This study was designed to examine the diagnostic precision of LINC00487 in ACS patients and its ability to predict MACE. Methods a cohort of 120 participants was recruited, comprising 75 ACS patients and 45 healthy controls. Serum levels of LINC00487 were quantified via reverse transcription quantitative real-time PCR (RT-qPCR). Predictive utility of LINC00487 for ACS was assessed using receiver operating characteristic (ROC) curves and multivariate logistic regression. Participants were monitored over 6 months to document incident MACE. Correlational analyses were carried out to examine the association between LINC00487 expression and ACS severity. Prognostic relevance of LINC00487 in ACS was evaluated via Kaplan-Meier (K-M) curves. Additionally, multivariate Cox proportional hazards regression was employed to identify predictors of MACE. Results expression of LINC00487 was markedly reduced in ACS patients and demonstrated a negative correlation with cardiac troponin I (cTnI), SYNTAX score, and Gensini score. LINC00487 exhibited high discriminative power between ACS patients and healthy controls (AUC=0.843). Reduced LINC00487 expression was significantly associated with MACE development among ACS subjects (p=0.027). K-M analysis further underscored a pronounced relationship diminished LINC00487 expression and MACE incidence. LINC00487 was established a protective factor against MACE in ACS (HR=0.204, 95 % CI: 0.083–0.500, p=0.001). Conclusions serum LINC00487 expression is associated with ACS severity, and its downregulation has diagnostic and prognostic value for ACS.
Open Access
Hsa_circ_0008667 exerts a mediating effect on the hypertrophic scar-associated fibroblast functions through targeting miR-324-5p/HOXA9

4. Mai 2026

Xiaolin Miao, Suwen Zhang

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Objectives Hypertrophic scar (HS), a type of pathological scar, arises from excessive fibrosis in the process of skin wound repair. Circular RNAs (circRNAs) are involved in regulating fibroblast functions in HS, but the role of circ_0008667 remains unclear. To investigate the expression and regulatory mechanism of circ_0008667 in hypertrophic scar fibroblasts (HSFs). Methods This study employed HSFs and normal skin fibroblasts (NSFs). The expression levels of circ_0008667, miR-324-5p, HOXA9 , and collagen-related genes were detected using RT-qPCR. After cell transfection, the impacts of the relevant factors on HSFs proliferation and apoptosis were examined using CCK-8 and apoptosis assay. The target binding relationship is determined using the dual-luciferase reporter assay. Results Circ_0008667 was highly expressed in HSFs. Its silencing inhibited HSF proliferation, promoted apoptosis, and reduced collagen-related genes, including Collagen Type I ( Col I ), Collagen Type III ( Col III ), and α-smooth muscle actin ( α-SMA ) expression. Circ_0008667 can directly interact with miR-324-5p and negatively regulate its expression. MiR-324-5p reverses the promoting effects of circ_0008667 on HSFs. HOXA9 is a target of miR-324-5p, and when overexpressed, it can reverse the inhibitory effects of miR-324-5p. Conclusions Circ_0008667 mediates excessive proliferation and fibrosis of HSFs via regulating the miR-324-5p/ HOXA9 axis, suggesting its potential as a target for HS treatment.
Open Access
Relationship between asprosin and insulin resistance in hypothyroidism

4. Mai 2026

Filiz Alkan Baylan, Mehmet Yaşar, Mehmet Bankir

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Objectives Thyroid dysfunction is a common disorder associated with changes in body metabolism and low-grade inflammation. Associated with insulin resistance (IR), asprosin is a newly discovered peptide hormone. Asprosin promotes hepatic glucose production. This study was designed to evaluate the relationship between asprosin and IR in patients with overt and subclinical hypothyroidism and to compare the findings with a euthyroid healthy control group. Methods The study included 30 patients diagnosed with hypothyroidism, 29 patients diagnosed with subclinical hypothyroidism, and 30 healthy individuals. Serum asprosin concentrations, glucose concentrations, and HOMA-IR indices of the groups were compared. Results The mean age was 37.8 years, and 77.5 % (69/89) of participants were female. We found that circulating asprosin concentrations were elevated in patients with overt and subclinical hypothyroidism compared to controls. Asprosin concentrations were positively correlated with TSH, Anti TPO, Anti TG, glucose, insulin, HOMA-IR and negatively correlated with FT4 and FT3. Conclusions For the first time in the literature, this study has shown that asprosin concentration is increased in patients with hypothyroidism, and that increased asprosin concentrations are associated with increased serum glucose concentration and HOMA-IR index. Therefore, asprosin may be a useful new marker for early metabolic disorders in hypothyroid patients.
Open Access
Evaluation of lysyl oxidase G473A polymorphism with inflammatory cytokines in atherosclerotic coronary artery ectasia patients

4. Mai 2026

Onur Kilicarslan, Ahmet Yildiz, Ozgur Selim Ser, Omer Dogan, Gulcin Ozkara, Ezgi Irmak Aslan, Hulya Yilmaz-Aydogan, Cuneyt Kocas, Mehmet Tugay Yumuk

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Objectives Coronary artery ectasia (CAE) is characterised by an increase in the diameter of a coronary artery of ≥1.5 times its diameter at the adjacent vessel. It is evident that alterations in the extracellular matrix changes contribute to the development of CAE. Lysyl oxidases (LOXs) are copper-dependent monoamine oxidase enzymes that play a crucial role in the regulation of connective tissue. Deficiencies in these enzymes have been linked to vascular changes, consequently leading to cardiovascular diseases. The objective of this study was to assess the association between the LOX -G473A (rs1800449) variation and inflammatory markers in CAE development. Methods The current cross-sectional study includes 88 patients whom CAE was confirmed in one of the coronary arteries by coronary angiography and 75 controls with positive exercise tests and angiographically normal coronary arteries without any typical ischemic symptoms and family history of cardiac diseases. Luminex technology was used to detect inflammatory markers. The fluorescence end-point PCR method was used for genotyping. Results Significantly higher plasma levels of TNF-α, sE-selectin, and hypercholesterolemia were observed in the CAE group (p<0.05). Male gender was found as risk factor for CAE. Although the genotype and allele distributions did not showed statistical significance, CAE patients with GA genotype had significantly higher levels of TNF-α and sP-selectin compared to patients with GG genotype. In addition, patients with right coronary artery (RCA) ectasia had higher TNF-α levels than patients with non-RCA ectasia. Conclusions Our findings could suggest that LOX -G473A polymorphism could be associated with the increase in inflammatory markers and CAE development.
Open Access
Clinical utility of non-invasive markers in the assessment of liver fibrosis among type 2 diabetes mellitus patients

30. April 2026

Thilak Priyantha Weerarathna, Keddagoda Gamage Piyumi Wasana, Iroshani Kodikara, Suneth Ruwan Weerarathna

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Objectives To explore the utility of several readily available, cost-effective, non-invasive tests in assessing liver fibrosis, as measured by fibro scan, in patients with type 2 diabetes mellitus (DM). Methods A total of 120 type 2 DM patients were enrolled in the present cross-sectional study. Liver fibrosis was assessed using FibroScan via liver stiffness measure (LSM). Serum-based non-invasive measures and ultrasound scan results were collected. Results Moderate or advanced fibrosis (LSM≥7 kPa) was detected in 24.2 % of patients. These patients had significantly higher triglyceride (p=0.020) and glycated hemoglobin (HbA 1C ) (p=0.020) than those without fibrosis. Factors associated with LSM were total cholesterol (95 % CI 0.001–0.056, p=0.042) and HbA 1C (95 % CI 0.143–1.810, p=0.022). Fibrosis-4 index (FIB-4), aspartate aminotransferase-to-platelet ratio index (APRI), and non-alcoholic fatty liver disease (NAFLD) fibrosis score were significantly and positively correlated with LSM. A new index; FibroMet, showed a positive and significant correlation with FIB-4, NAFLD fibrosis score, and APRI. Ultrasonically diagnosed grade of liver fibrosis didn’t show any correlations with LSM. When LSM is served as the reference, the area under the ROC curve of FIB-4 was 0.630 (95 % CI 0.521–0.740, p=0.035), NAFLD fibrosis score was 0.647 (95 % CI 0.540–0.754, p=0.018), APRI was 0.629 (95 % CI 0.504–0.754, p=0.036), and FibroMet was 0.686 (95 % CI 0.574–0.798, p=0.003) to identify moderate and advanced fibrosis. Long-term glucose and lipid control are associated with reduced LSM in type 2 DM patients. Conclusions Serum-based non-invasive scores and FibroMet index have better clinical sensitivity and validity over ultrasound scan in terms of assessing liver fibrosis in type 2 DM patients.
Open Access
NEAT1 promotes the development of high myopia by targeting miR-28-3p to regulate human scleral fibroblasts

18. März 2026

Lifei Xu, Wenwei Li, Ruting Jiang, Shuangshuang Hu, Bin Wang

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Objectives High myopia (HM) can lead to serious complications that are hazardous to the health of adolescents. LncRNA nuclear-enriched abundant transcript 1 (NEAT1) and miR-28-3p exhibit abnormal expression in multiple ocular structures. Investigating the effects of NEAT1 and miR-28-3p on human corneal fibroblasts (HSF) may provide new theoretical foundations and directions for myopia management. Methods 102 patients with HM and 100 patients with myopia were included. The expression of NEAT1, miR-28-3p, transforming growth factor-β 1 (TGF-β1) and collagen Ι in aqueous humor was assessed by RT-qPCR. Cell Counting Kit-8 (CCK-8) and flow cytometry were used to detect cell proliferation and apoptosis, respectively. Dual luciferase reporter (DLR) and RNA Immunoprecipitation (RIP) assays were detected the target-binding relationship of NEAT1 and miR-28-3p. Results NEAT1 levels were higher and miR-28-3p levels were notably downregulated in the HM group than control. NEAT1 binds to miR-28-3p target and the levels were negatively correlated. Elevated NEAT1 suppressed cellular activity, markedly reducing TGF-β1 and collagen I levels. Knockdown of NEAT1 increased miR-28-3p expression, enhanced cell proliferation, reduced apoptosis, and boosted extracellular matrix synthesis. Conversely, silencing miR-28-3p significantly decreased cellular viability and extracellular matrix production. Conclusions Patients with HM have elevated levels of NEAT1. High NEAT1 levels suppress cellular activity and inhibit extracellular matrix production. Following NEAT1 silencing, miR-28-3p levels increase, thereby enhancing HSF cellular activity and promoting extracellular matrix production. This may delay HM progression.
Open Access
The role of LINC01943 in tumor progression and prognosis of triple-negative breast cancer

18. März 2026

Jiayang Wei, Rong Zhou, Jing Zhai, Liang An, Dengyuan Zhong, Xiao Chen

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Objectives This study explored the functional role of LINC01943 in triple-negative breast cancer (TNBC) development and prognosis to improve patient survival outcomes. Methods This study included 111 TNBC patients. LINC01943 and miR-224-5p expression levels in tumor tissues and TNBC cell lines (BT-549, MDA-MB-231, SUM-159, HCC1806) were analyzed by real-time quantitative PCR. Cox regression analyses and Kaplan-Meier survival curves confirmed the association between LINC01943 and TNBC prognosis. Luciferase assays validated the interaction between LINC01943 and miR-224-5p, while functional assays assessed their impact on proliferation, invasion, and apoptosis of TNBC cells. Bioinformatics analysis combined with luciferase assays preliminarily validated PLOD2 as a direct target of miR-224-5p. Western blot was used to detect protein expression levels. Results Compared with adjacent normal tissues and MCF-10, LINC01943 is upregulated in TNBC tissues and cell lines, while miR-224-5p is downregulated, and the two are negatively correlated in TNBC tumor tissues. Elevated LINC01943 expression correlated with advanced tumor node metastasis (TNM) stage, lymph node metastasis (LNM), and poorer 5-year survival in TNBC patients. LINC01943, TNM stage, and LNM were identified as prognostic predictors for TNBC. LINC01943 promoted tumor growth by enhancing cell proliferation and invasion while suppressing apoptosis through miR-224-5p regulation. PLOD2 was identified as the direct functional target of miR-224-5p, serving as the key downstream mediator of the LINC01943/miR-224-5p axis in regulating EMT and FAK signaling in TNBC. Conclusions LINC01943 is a novel prognostic biomarker for TNBC. The LINC01943/miR-224-5p/PLOD2 axis promotes tumor progression by activating FAK signaling and EMT, offering a promising therapeutic target.
Open Access
Exercise improves cognitive function in Alzheimer’s disease via the CRNDE/miR-338-3p axis

18. März 2026

Siye Wang, Jiahua Chen, Xiaolan Wang, Yankui Xu, Tianxiang He

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Objectives Alzheimer’s disease (AD) is imposing a substantial burden on families. This study aimed to investigated the association between the lncRNA CRNDE/miR-338-3p axis, exercise-induced changes, and AD. Methods 100 AD patients and 100 healthy controls were recruited for the study. An AD mouse model was utilized. Both the human participants diagnosed with AD and the AD mice underwent an exercise intervention. The mRNA levels were quantified using RT-qPCR. Interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) levels were assessed via enzyme-linked immunosorbent assay (ELISA). Cognitive function in the mice was evaluated using the Morris water maze (MWM) test. The interaction was validated through a dual-luciferase reporter assay. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analyses were performed to elucidate the potentially related signaling pathways. Results CRNDE expression was significantly upregulated in AD. Exercise enhanced cognition and reduced inflammation in AD patients, concurrently lowering CRNDE levels. In vivo, experiments in AD mice confirmed that exercise exerted ameliorative effects on cognitive function and inflammatory response via downregulating CRNDE, but the influences were abolished by the miR-338-3p axis. GO analysis and KEGG pathway analysis further demonstrated that exercise influenced the CRNDE/miR-338-3p axis, which may be involved in the MAPK signaling pathway. Conclusions Exercise intervention could enhance the cognitive function of AD patients, and this effect was associated with the CRNDE/miR-338-3p axis.
Open Access
Silencing lncRNA XIST enhances MiR-146a-5p expression levels to promote cutaneous acute wound healing

12. März 2026

Yang Yu, Huajiang Liu

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Objectives Surgical skin wounds impair patient mobility and pose a risk of infection. Long non-coding RNA XIST shows abnormal expression in burned skin. This study explores its expression in acute wounds and its impact on wound healing (WH). Methods An in vitro skin injury model was established by treating human immortalized keratinocytes (HaCaT) cells with 6 μg/mL lipopolysaccharide (LPS). Cell proliferation, apoptosis, and migration were evaluated using cell counting kit-8 (CCK-8), flow cytometry, and Transwell assay, respectively. Binding sites between XIST and miR-146a-5p were predicted using the ENCORI database. Dual-luciferase reporter assays confirmed their interaction. XIST and miR-146a-5p levels were quantified via real-time quantitative reverse transcription PCR (RT-qPCR). Enzyme-linked immunosorbent assay (ELISA) assay was used to measure the levels of inflammatory and growth factors in cells. Results XIST was overexpressed in the skin acute wound model, whereas miR-146a-5p was at a low level in the wound model. XIST is bound directly to miR-146a-5p. Silencing XIST elevated miR-146a-5p levels. LPS treatment restored the proliferation and migration of damaged HaCaT cells, reduced apoptosis rates, decreased inflammatory factors levels, and increased growth factors levels. Conclusions XIST may be detrimental to WH. Knocking down XIST to enhance miR-146a-5p expression could boost HaCaT cells physiological activity, offering a potential therapeutic target for promoting WH.
Open Access
High expression of lncRNA LINC00963 is associated with advanced cervical cancer through the miR-612/FOXM1 axis

12. März 2026

Xiaoming Ma, Chi Zhang, Bo Li

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Objectives Cervical cancer is a highly prevalent malignant tumor among women, with an increasing incidence. LINC00963 is aberrantly expressed as a cancer-promoting long non-coding RNA (lncRNA) in a variety of cancers, but its role in cervical cancer is unclear. This study revealed the expression characteristics, clinical significance, and cancer promotion mechanism of LINC00963 in cervical cancer and provided new ideas for targeted therapy. Methods The expression of LINC00963 , miR-612 , and FOXM1 was detected using quantitative reverse transcription polymerase chain reaction (qRT-PCR), and the clinical significance of LINC00963 was analyzed using the chi-square (χ 2 ) test and Cox regression analysis. The interaction between LINC00963 and miR-612 was validated through dual-luciferase assays, and the changes in cervical cancer cell phenotypes were assessed using Cell Counting Kit-8 (CCK-8) and Transwell experiments. Results The expression of LINC00963 in cervical cancer tissues was significantly higher than that in adjacent non-cancerous tissues, and it was significantly associated with tumor recurrence, staging, and lymph node metastasis. Upregulation of LINC00963 can predict poor prognosis in patients with cervical cancer, and its expression is negatively correlated with the expression of miR-612 . Silencing LINC00963 significantly inhibited the growth, migration, and invasion of HeLa cells, while inhibiting miR-612 weakened this effect. LINC00963 promotes the expression of FOXM1 by directly suppressing miR-612 . Conclusions LINC00963 is highly expressed in cervical cancer and promotes tumor progression. It regulates cancer cell functions by modulating the miR-612 / FOXM1 pathway, suggesting that the LINC00963 / miR-612 / FOXM1 axis could serve as a potential diagnostic biomarker and therapeutic target for cervical cancer.
Open Access
miR-15a-5p as a potential biomarker for hypertrophic cardiomyopathy and its bioinformatics analysis

12. März 2026

Xianghua Wang, Danna He, Ying Wang

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Objectives Hypertrophic cardiomyopathy (HCM) is a common clinical Cardiac abnormality manifested as myocardial hypertrophy and diastolic dysfunction. This study investigated the role and clinical relevance of miR-15a-5p in HCM. Methods 220 participants were enrolled, including 110 HCM patients and 110 healthy controls. The abundance of miR-15a-5p and IRS1 were quantified by qRT-PCR. Pearson correlation and ROC curve was used to evaluate clinical relevance and diagnostic potential. The interaction between miR-15a-5p and IRS1 was confirmed through a dual-luciferase reporter assay. An isoproterenol (ISO)-induced hypertrophic model was established in H9c2 cardiomyocytes. The impacts of miR-15a-5p/IRS1 axis on hypertrophy-related genes (ANP, BNP, β-MHC) were quantified. Results miR-15a-5p was significantly elevated in HCM patients and positively correlated with disease severity, particularly maximum wall thickness. miR-15a-5p exhibited strong diagnostic potential and was shown to promote cardiomyocyte hypertrophy by directly targeting and downregulating IRS1. Functional experiments confirmed that suppression of miR-15a-5p alleviated ISO-induced level of hypertrophy markers, while IRS1 silencing reversed these effects. Enrichment analysis further suggested that miR-15a-5p is potentially implicated in key hypertrophy-related signaling pathways, including the AMPK pathway. Conclusions This study demonstrates that miR-15a-5p contributes to HCM progression by negatively regulating IRS1 and promoting cardiomyocyte hypertrophy. miR-15a-5p holds promise as a diagnostic candidate for myocardial hypertrophy in HCM.
Open Access
Analytical performance comparison of Roche Cobas t 711 and Sysmex CS-2500 with assessment of interference effects

12. März 2026

Humeyra Ozturk Emre, Oguzhan Zengi, Kamil Taha Ucar, Beyazit Semih Yesil

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Objectives Coagulation tests are essential for diagnosing bleeding disorders and for monitoring anticoagulant therapy. However, analyzer-dependent variability and pre-analytical interferences such as hemolysis and lipemia may affect test accuracy. This study aimed to compare the analytical performance of Roche Cobas t 711 and Sysmex CS-2500 analyzers for Prothrombin Time (PT), International Normalized Ratio (INR), Activated Partial Thromboplastin Time (APTT), and fibrinogen measurements, and to evaluate the effect of hemolysis and lipemia on test results. Methods Plasma samples from 100 patients were used. Repeatability and intermediate precision were assessed, and method comparison was performed using Passing-Bablok regression and Bland-Altman analysis according to Clinical and Laboratory Standards Institute (CLSI) EP09-A3 guideline. Artificial hemolysis and lipemia were induced to simulate pre-analytical interference. Results Both analyzers showed acceptable precision (coefficient of variation [CV] <5 %). Fibrinogen measurements showed strong agreement (median difference −2.17 %), while PT and APTT results differed significantly (PT: −25.21 %; APTT: 22.76 %). PT was more affected by hemolysis (>6 g/L) and lipemia (>11.3 mmol/L) than APTT. These interferences appeared to affect Roche Cobas t 711 to a greater degree because of its optical detection method. Conclusions Although both devices performed reliably under standard conditions, significant differences were observed in PT and APTT measurements. Hemolysis and lipemia also caused clinically relevant bias at certain levels, especially in PT. Local validation and awareness of interference effects are essential for accurate coagulation testing, highlighting the need for careful testing of multiple measurands when transitioning between systems.
Open Access
miR-25-3p promotes the proliferation and metastasis of oral squamous cell carcinoma tumor cells

9. März 2026

Li Xiang, Liu Yi, Ting Yang

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Objectives Nearly 90 % of oral cancers are squamous cell carcinomas, which are malignant tumors that occur in the oral cavity. The present work is intended to explore the clinical relevance of miR-25-3p in oral squamous cell carcinoma (OSCC) and to uncover potential targets. Methods In the research, a total of 78 participants were recruited, including 48 OSCC patients and 30 controls. By RT-qPCR, we analyzed the distribution of miR-25-3p in OSCC tissues and cells and estimated the clinical diagnostic value of miR-25-3p using the ROC curve. The expression of miR-25-3p in OSCC was characterized by RT-qPCR. Cell proliferation and migration were evaluated using CCK-8, RT-qPCR, and Transwell assay. In addition, knockdown and over-expression models were established to verify that miR-25-3p affects OSCC progression by modulating CD69 . Results miR-25-3p expression was higher in OSCC patients compared with normal controls (NC). miR-25-3p was able to effectively distinguish OSCC patients. In OSCC patients, miR-25-3p expression was significantly increased and served to accelerate the proliferation and metastasis of OSCC cell lines by targeting CD69 . The use of miR-25-3p inhibitors significantly inhibited cell migration, whereas overexpression of miR-25-3p had the opposite effect. Knockdown of CD69 resulted in the reversal of proliferation and migration induced by miR-25-3p overexpression. Conclusions The current study demonstrated the diagnostic relevance of miR-25-3p. miR-25-3p regulates OSCC development via targeting CD69 , implying that CD69 may serve a critical function in OSCC pathogenesis.
Open Access
Aberrant expression of miR-200b-3p in polycystic ovary syndrome and its effect on disease progression

9. März 2026

Junqiao Jiang, Jing Hu, Qiuxia Xu, Liyuan Huang

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Objectives Polycystic ovary syndrome (PCOS) is a polygenic, multifactorial inflammatory disorder involving steroid regulation dysfunction, affecting tens of thousands of women of reproductive age. The considerable potential demonstrated by miR-200b-3p in regulating gynecological disorders has captured our attention. We aim to explore the diagnostic value of miR-200b-3p in PCOS, with the aspiration to advance medical progress. Methods A total of 208 patients with PCOS were included. Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR) was used to detect miRNA and mRNA levels. Radioimmunoassay and Enzyme-Linked Immunosorbent Assay (ELISA) were employed to determine the concentrations of hormones and inflammatory cytokines respectively. The inflammatory models were established by inducing KGN cell line with LPS. Cell proliferation was detected by the Cell Counting Kit-8 (CCK-8) assay. The target relationship was detected by dual-luciferase reporter assay. Results Compared with healthy women, PCOS patients exhibit abnormally elevated hormone levels. miR-200b-3p is up-regulated in the serum and follicular fluid of PCOS patients and demonstrates good diagnostic value. Cell experiments indicate that miR-200b-3p inhibitor promote KNG cell proliferation activity whilst simultaneously suppressing estradiol (E2) concentrations and inhibiting inflammatory responses. The miR-200b-3p targets zinc finger E-box binding homologue 1 (ZEB1). Silencing ZEB1 partially reversed the effects exerted by the miR-200b-3p inhibitor on KGN cell line. Conclusions Inhibition of miR-200b-3p promotes KNG cell line proliferation and suppresses inflammation by targeting ZEB1, potentially alleviating the progression of PCOS.
Open Access
Serum nicotine metabolite profiles and their association with hematological, biochemical, and cardiovascular parameters in smokers

6. März 2026

Mustafa Onmaz, Duygu Eryavuz Onmaz, Nur Demirbas, Ali Unlu

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Objectives Cigarette smoking remains a major contributor to preventable cardiovascular morbidity and mortality. While the Fagerström Test for Nicotine Dependence (FTND) evaluates behavioral addiction, objective biochemical markers linking dependence severity to cardiovascular risk remain limited. This study investigated associations between serum nicotine metabolites, FTND, and Framingham Risk Score (FRS) in male smokers. Methods A cross-sectional study was performed in 104 male smokers aged 18–65 years. Nicotine dependence was assessed using the FTND. Serum nicotine, cotinine, norcotinine, and 3-hydroxycotinine levels were quantified by a validated LC–MS/MS method. Cardiovascular risk was estimated using the FRS, and correlations among metabolites, FTND scores, and smoking duration (pack-years) were analyzed. Results Nicotine metabolite concentrations across FTND dependence categories demonstrated increasing trends for cotinine and norcotinine. However, after adjustment for multiple comparisons using the Benjamini–Hochberg false discovery rate, only norcotinine levels differed significantly between FTND groups (q=0.030), with higher concentrations observed in individuals with greater dependence severity. Smoking duration expressed as pack-years showed a positive association with serum norcotinine concentrations, and this relationship remained statistically significant following FDR correction (r=0.327, q=0.008). Conclusions Norcotinine emerged as the most robust biochemical marker of nicotine dependence and cumulative tobacco exposure, linking behavioral addiction severity with long-term metabolic burden. The absence of associations between nicotine metabolites and FRS highlights the limited capacity of single time-point exposure markers to reflect multifactorial cardiovascular risk. These findings support the need for integrated behavioral and metabolic approaches in addiction assessment.
Open Access
Sevoflurane alleviates hypoxia/reoxygenation-induced myocardial injury by regulating miR-208a-3p: an in vitro study

6. März 2026

Dan Sun, Jianlin He, Ruina Guo, Xueli Zhao, Xizhong Ma, Jianghong Liu, Zhixun Hu, Xiangyu Xu

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Objectives Myocardial hypoxia/reoxygenation (H/R) injury is a common pathological process in cardiovascular diseases. This study investigates whether sevoflurane alleviates H/R-induced myocardial injury by regulating miR-208a-3p and reveals the underlying molecular mechanisms. The findings may provide new therapeutic strategies for myocardial protection. Methods This study used neonatal rat cardiomyocytes as a model with 6-hour hypoxia treatment to simulate myocardial hypoxia. Cell viability was measured by CCK-8 assay, and miR-208a-3p expression levels were assessed by qRT-PCR. Inflammatory markers, myocardial injury markers, and oxidative stress markers were quantified by ELISA. The interaction between miR-208a-3p and its target gene was confirmed through dual-luciferase assays. Finally, the effects of sevoflurane and H/R treatment on the target gene were examined. Results This experiment found that the expression of miR-208a-3p reached its peak at 6 h of hypoxia. Sevoflurane preconditioning can concentration-dependently enhance cell viability, inhibit the upregulation of miR-208a-3p, and reduce the levels of myocardial injury markers cTnI and LDH. However, overexpression of miR-208a-3p inhibited cell activity, increased the levels of inflammatory, and promoted inflammatory responses. Meanwhile, overexpression of miR-208a-3p decreased SOD activity, increased MDA levels, and significantly enhanced oxidative stress. Mechanistically, sevoflurane enhances myocardial protection by targeting the 3′UTR of STC1 and upregulating STC1 expression. Conclusions Sevoflurane significantly alleviates H/R-induced myocardial injury by modulating miR-208a-3p, and this finding provides a new molecular target and potential therapeutic strategy for myocardial protection.
Open Access
Effects of LINC00607-miR-103a-3p/miR-16-5p pathway on proliferation, apoptosis, and inflammation of fibroblast-like synoviocytes in rheumatoid arthritis

6. März 2026

Meng Xie, Fang Zhou, Lan Li

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Objectives Rheumatoid arthritis (RA) is an autoimmune disease characterized by joint lesions caused by inflammation of the synovial membrane. This study investigates the potential mechanisms underlying RA pathogenesis. Methods The serum samples were collected from 66 healthy volunteers and 66 patients with RA for clinical expression analysis. RA-fibroblast-like synoviocytes (RA-FLS) were treated with 20 ng/mL TNF-α to construct an RA cell model. The method of 5-bromo-2′-deoxyuridine (BrdU) insertion was used to evaluate cell proliferation capacity. Cell apoptosis was determined by double staining with Annexin V-FITC/propidium iodide (PI). The inflammatory response was evaluated by measuring IL-6, IL-12, and IFN-γ levels. The dual luciferase reporter assay and the overexpressing plasmid transfection experiment were used to the targeted regulation verification of LINC00607 on miR-103a-3p and miR-16-5p. The effect of LINC00607-miR-103a-3p/miR-16-5p pathway in RA was evaluated by co-transfecting miR-103a-3p/miR-16-5p mimic and LINC00607 plasmid. Results LINC00607 was down-regulated in RA patients, whose overexpression reversed the abnormal proliferation, anti-apoptosis, and inflammation response in TNF-α-treated RA-FLS. The overexpression of LINC00607 decreased the cellular levels of miR-103a-3p and miR-16-5p. Transfecting miR-103a-3p or miR-16-5p mimic intensified the TNF-α-induced RA phenotypes in RA-FLS, which was rescued by the co-transfection of LINC00607 plasmid. Conclusions LINC00607 restrained the growth and inflammation of RA-FLS and accelerated apoptosis by regulating miR-103a-3p and miR-16-5p negatively, which may suppress RA development.
Open Access
Expression of miR-1908-5p in breast cancer and its correlation with survival outcome and chemosensitivity

4. März 2026

Yan Chang, Yujie Chang, Jianjun Han, Jumei Li, Shengli Cui

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Objectives One dangerous tumor that can seriously harm a woman’s health is breast cancer, and adriamycin resistance is a critical factor contributing to poor prognosis. Because of their role in the mechanisms underlying tumor treatment resistance, miRNAs have attracted more attention in recent years. This work aims to investigate the role of miR-1908-5p in the DOX resistance mechanism of breast cancer cells. Methods Quantitative PCR was performed to detect miR-1908-5p expression levels in cancerous and paracancerous tissues. The association of miR-1908-5p expression with clinicopathological characteristics and patient outcomes was assessed using Cox regression models and Kaplan-Meier survival analysis. The possible targets of miR-1908-5p were identified using TargetScanHuman and further confirmed by dual-luciferase reporter assays. Cell growth, programmed cell death, movement, and infiltration were evaluated using the CCK-8 method, flow cytometry analysis, and Transwell experiments, respectively. Results The expression of miR-1908-5p was markedly elevated in tumor tissues and showed a close relationship with the TNM stage, lymph node metastasis, tumor size, and unfavorable survival outcomes, acting as an independent prognostic indicator. Inhibition of miR-1908-5p enhanced the suppressive effects of DOX on cancer cells, which were reversed upon ASCL3 reintroduction, thereby confirming ASCL3 as a downstream target. Conclusions miR-1908-5p regulates DOX sensitivity by targeting ASCL3, and its high expression correlates with adverse clinicopathological features and worse prognosis. The miR-1908-5p/ASCL3 axis highlights a promising target for precision therapy against breast cancer drug resistance.
Open Access
Impact of hypothyroidism and thyroid autoimmunity on serum anti-mullerian hormone levels

3. März 2026

Ilkay Cakir, Alev Kural, Zeynep Ceyhanli, Evin Bozkur, Felemez Arslan, Muge Bilge

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Objectives Chronic Autoimmune Thyroiditis (AIT) is a prevalent etiology of hypothyroidism and is postulated to affect ovarian reserve (OR). Ovarian reserve in patients with hypothyroidism secondary to total thyroidectomy has not yet been specifically investigated. Anti-Mullerian hormone (AMH) is a verified and well-known biomarker reflecting OR. We aimed to investigate AMH levels in patients with hypothyroidism resulting from AIT or total thyroidectomy, and to assess the impact of both hypothyroidism and thyroid autoimmunity on ovarian reserve. Methods A cross-sectional study conducted at Bakırköy Dr. Sadi Konuk Education and Research Hospital in Istanbul, Turkey, between June 2022-June 2024. The study cohort comprised 56 euthyroid women with established hypothyroidism (30 cases with AIT and 26 post-total thyroidectomy) and 30 age- and BMI-matched healthy women. Parameters measured included AMH, FSH,LH, estradiol, fT3, fT4, TSH, TPOAbs, and TgAbs. Results No statistically significant difference was detected in AMH levels when comparing hypothyroid patients (irrespective of etiology) and healthy controls. Furthermore, no correlation was observed between AMH levels and TSH and/or thyroid autoantibodies. Conclusions Regardless of the underlying etiology, women with hypothyroidism demonstrate comparable AMH concentrations of healthy women. Furthermore, thyroid autoimmunity itself does not appear to exert an additional detrimental effect on AMH.
Open Access
Characterization of ZJ12 as a BRD4 ligand and its cellular effects in the MV4-11 leukemia cells

3. März 2026

Maofeng Zhang, Jiahui Du, Yan Zhang, Liguang Zhang, Songbai Liu

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Objectives Bromodomain-containing protein 4 (BRD4), a canonical epigenetic reader, is implicated in regulating the expression of various genes. The current research aimed to analyze the binding mechanism of ZJ12 to the BRD4 bromodomain. Another purpose was to explore the anticancer activity and underlying mechanisms of ZJ12 in acute myeloid leukemia (AML) cell lines, as well as to evaluate the drug-like properties of ZJ12. Methods The cocrystal structure of ZJ12-BRD4 was resolved via X-ray crystallography. The CellTiter-GLO method was employed to evaluate the viability of cells. Intracellular protein levels of cellular myelocytomatosis oncogene (c-Myc) and B-cell lymphoma 2 (Bcl-2) were examined through western blot, while mRNA levels of c-Myc and cyclin-dependent kinase 4 (CDK4) were quantified by quantitative real-time PCR (qPCR). Cell cycle and apoptosis rate were examined using flow cytometry. The in-silico tools SwissADME and ADMETlab were utilized to predict the drug-likeness and toxicity profile of ZJ12. Results The small molecule ZJ12 bound to the pocket of the BRD4 bromodomain in a shape-matched manner, forming critical interactions with key amino acids. ZJ12 significantly downregulated c-Myc as well as Bcl-2 expression in MV4-11. Concomitantly, ZJ12 suppressed cell growth, triggered cell cycle arrest at the G 0 /G 1 phase and increased the apoptosis ratio of MV4-11. Furthermore, ZJ12 exhibits favorable drug-likeness and promising predicted safety profiles. Conclusions ZJ12 is an effective small-molecule inhibitor of BRD4 bromodomain with good drug-likeness and safety profiles. ZJ12 promotes the downregulation of c-Myc and Bcl-2 levels by targeting BRD4 in MV4-11, which ultimately contributes to its antitumor activity.
Open Access
Association of serum vitamin D level and Fokl VDR gene polymorphism with temporomandibular joint disorders

23. Februar 2026

Ömer Ekici, Evrim Suna Arıkan Söylemez

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Objectives The aim of this study is to investigate the association of 25-hydroxy (25-OH) vitamin D level, FokI vitamin-D receptor (VDR) gene polymorphism, and painful temporomandibular joint (TMJ) disc displacement with reduction (DDwR). Methods This cross-sectional study comprised 49 people with temporomandibular disorders (TMDs) and 48 healthy controls of comparable age and gender. DDwR was diagnosed based on TMD diagnostic criteria (DC/TMD). Using genomic DNA extracted from blood, a genotyping analysis of the FokI (rs2228570) polymorphisms was conducted utilizing DNA sequencing and the Applied Biosystems 3130XL Genetic Analyzer (USA). The serum 25-hydroxy vitamin D levels and the FokI VDR gene polymorphism were compared between the two groups. Results There was not a noticeable distinction in the mean 25-hydroxy vitamin D levels between the two groups, the TMD group had substantially more persons with severe vitamin-D insufficiency (<10 ng) compared to the control group (p<0.05). The genotype and allele frequency of the FokI VDR polymorphism did not differ significantly between the TMD and control groups. However, The GG genotype and G allele were significantly more prevalent in the severe vitamin D deficiency (<10 ng) group than in the normal group (20–60 ng) and mild deficiency group (10–20 ng) (p<0.05). Conclusions Differences between groups in serum 25-hydroxy vitamin D levels indicate that indicating that vitamin-D insufficiency might be linked to TMD. Although the FokI (rs2228570) VDR polymorphism was associated with severe vitamin-D deficiency, no significant relationship existed between TMJ DDwR and FokI VDR polymorphism.
Open Access
Combined effects of bisphosphonates and rehabilitation exercise on osteoporosis management: a systematic review and meta-analysis

18. Februar 2026

Na Wang, Yichun Wu, Qibin Zhang

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Introduction Postmenopausal osteoporosis, defined by reduced bone mineral density and fracture risk, is a major health concern. Bisphosphonates are standard therapy, but the added value of exercise is uncertain. This study examined their combined effects on BMD, bone turnover, body composition, strength, and balance in postmenopausal women. Content PubMed, Embase, and Cochrane Central were systematically searched for RCTs on bisphosphonates, exercise, or their combination in postmenopausal osteoporosis. Primary outcomes were changes in BMD at lumbar spine, femoral neck, and total hip. Secondary outcomes included bone turnover markers (ALP-B, NTx), body composition (fat and lean mass), and leg extensor strength. Study quality was assessed with Cochrane Risk of Bias tool. Mean differences with 95 % confidence intervals (CI) were calculated using a random-effects model, with heterogeneity evaluated by I 2 . Summary Six RCTs with 1,059 subjects qualified for inclusion. Bisphosphonate + exercise treatment showed small and non-significant improvement in lumbar spine and femoral neck BMD (p=0.41 and p=0.11, respectively), and no significant change in total hip BMD (p=0.48). Levels of ALP-B significantly increased (p=0.0008), reflecting bone turnover rather than a direct clinical benefit; NTx showed non-significant trend (p=0.10). Fat mass significantly decreased (p<0.00001), leg strength significantly increased (p<0.00001), and lean mass showed no significant change (p=0.14). Outlook Combined exercise and bisphosphonates yield modest yet consistent improvements in site-specific BMD, fat loss, and strength in postmenopausal osteoporosis, supporting exercise as an adjunct to pharmacologic therapy for musculoskeletal health.
Open Access
Diagnostic value of lncRNA LINC00900 in papillary thyroid carcinoma metastasis and its oncogenic role through sponging miR-545-3p

11. Februar 2026

Yinglei Cui, Nuerbol Aslibek, Ying Yang

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Objectives Papillary Thyroid carcinoma (PTC) is a common endocrine malignancy, often with lymph node metastasis. This study aims to investigate the regulatory mechanism between LINC00900 and miR-545-3p in TC with lymph node metastasis, thereby providing novel insights for the diagnosis and therapeutic intervention of this disease. Methods A study involving 218 patients divided into low (n=106) and high (n=112) LINC00900 expression groups, utilized qPCR to analyze the levels of LINC00900 and miR-545-3p. Pearson correlation, chi-square test and ROC curve analysis were performed to estimate clinical associations and diagnostic value. Binding sites were predicted and confirmed via dual-luciferase assays. Functional tests (CCK-8, transwell) assessed cell proliferation, migration, and invasion. Results In PTC, elevated LINC00900 expression shows significant correlations with aggressive pathological features, including larger tumor size, advanced TNM stage, microcalcifications, and abnormal lymph node ultrasound findings. Patients with TC and lymph node metastasis exhibit higher blood and tissue levels of LINC00900 compared to those with benign nodules and adjacent tissue, respectively. A negative correlation exists between LINC00900 and miR-545-3p in tumor tissues, and ROC curve analysis confirms LINC00900’s diagnostic potential. Mechanistically, dual-luciferase reporter assays demonstrate that LINC00900 directly binds to miR-545-3p. Functional studies reveal that LINC00900 knockdown upregulates miR-545-3p and significantly suppresses tumor cell proliferation, migration, and invasion, while the miR-545-3p inhibitor reverses these effects. Conclusions LINC00900 is a potential diagnostic biomarker for PTC with lymph node metastasis and promotes tumor progression by interacting with miR-545-3p, offering both diagnostic and therapeutic value.
Open Access
Correlation of epigenetic markers with glioblastoma patients’ survival and molecular subtypes: insights from methylation-specific MLPA analysis

6. Februar 2026

Saoussen Trabelsi, Abdelbasset Amara, Imen Chabchoub, Mohamed Ladib, Hedi Krifa, Nadia Mama, Kalthoum Tlili, Moncef Mokni, Mohamed Tahar Yaacoubi, Chris Jones, Sergey Popov, Ali Saad, Dorra H’mida Ben Brahim

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Objectives Glioblastoma (GB) is a heterogeneous group of tumors with poor patient’s outcome. The epigenetic markers could influence patient’s outcome and add more precision in sub-typing. Methods The study aims to determine a correlation between the methylation status of 65 genes and the overall survival (OS) in 50 GB Tunisian patients using methylation specific-multiplex ligation-dependent probe amplification (MS-MLPA) technique. Results OS was significantly longer for patients with tumors harboring unmethylated tumor suppressor genes ATM , BRCA1 , BRCA2 , TP53 and TP73 and the DNA repairing gene MSH6 . Furthermore, simultaneous unmethylation of ATM , BRCA2 , CD44 and VHL genes was associated with GB presenting normal EGFR status. This subgroup exhibits a better prognosis (OS=15 months, p=0.005). Our results also showed that, combined methylation of TP73 , THBS1 , GSTP1 and ESR1 genes in amplified EGFR GB subtype resulted in a poor prognosis group (OS=3 months, p=0.041). Simultaneous methylation of HLTF and SFRP5 genes was associated with wild-type IDH1 GB defining therefore a very poor prognosis group (OS=1 month, p=0.026). Besides, BRCA1 methylation in wild-type IDH1 group was significantly associated with poor prognosis (OS=6 months, p=0.002). Interestingly, RBM14 and PCCA genes were co-methylated in 80 % of prolonged survival cases (GB+). In absence of EGFR amplification and with unmethylation of BRCA1 , BRCA2 , ATM , VHL , CD44 , HLTF and SFRP5 genes, GB+ tumors seemed to respond better to treatment, avoiding the relapse and conferring prolonged survival (>36 months). Conclusion Combining genes methylation status of GB with EGFR and IDH1 profiles will refine subtyping, predict patient’s outcomes and guide personalized therapy.
Open Access
Urinary procalcitonin, Pentraxin-3 and heparin binding protein levels in urinary tract infection

2. Februar 2026

Elif Börekci, Cevval Ulman, Mahmut Kılıç, Serkan Erdal, Zeki Arı

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Objectives Recent studies have indicated that the levels of procalcitonin (PCT) can rise in various body fluids, depending on the site of infection. However, there has been no investigation or publication to date on the urinary PCT levels in urinary tract infections (UTIs). Our aim is to evaluate the possible increase in PCT in the urine of patients diagnosed with UTI, in comparison with pentraxin 3 (PTX3) and heparin binding protein (HBP). Methods Sixty patients with UTI, and 30 healthy controls were included. PCT, PTX3 and HBP in the urine and PCT, PTX3 in the serum samples were measured and the groups were compared among themselves. The diagnostic performances of biomarkers were analyzed via receiver operating characteristic (ROC) curve analysis. Results While PTX3 and HBP levels were significantly elevated in the urine of patients with UTI (p<0.01), the anticipated increase in PCT was not observed. Urinary PCT showed only a weak positive correlation with WBC (rho=0.264). Although there was no difference in serum PCT levels between UTI patients and controls, within the UTI group, serum PCT was positively correlated with serum PTX3 (rho=0.335), CRP (r=0.472), creatinine (rho=0.258), and ESR (r=0.441). A urine PTX3 level ≥0.599 pg/mL indicated UTI diagnosis with 93 % sensitivity and specificity. Conclusions Our findings indicate that urinary PCT is not a reliable diagnostic marker for UTI. However, PTX3 and HBP, especially PTX3, serve as effective markers for detecting UTIs.
Open Access
Cuscuta chinensis Lam. Alleviates transforming growth factor beta-induced endometrial fibrosis and inflammation in vitro

30. Januar 2026

Xiuli Tian, Jindong Miao, Wenyan Zhang, Jing Xiao, Yunyun Jiang

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Objectives In this study, we intend to investigate and report the effect of Cuscuta chinensis Lam. (CCL) treatment on transforming growth factor beta (TGF-β)-induced endometrial fibrosis and inflammation. Methods Human endometrial stromal cells (HESCs) were treated with CCL. The efficacy of CCL on TGF-β-induced endometrial fibrosis and inflammation was assessed by detecting the expression levels of fibrosis and THP-1 inflammatory markers in HESCs using western blot and quantitative real-time reverse transcription polymerase chain reaction. The active ingredients and corresponding targets of the drugs were obtained from TCMSP and ETCM 2.0 databases. The relevant targets of IUA were collected using DisGeNET and GeneCards databases. Possible therapeutic targets of CCL in IUA were analyzed using R-based gene ontology (GO) and KEGG enrichment analysis. The top six targets ranked by degree were validated in HESCs and THP-1 cells. Results CCL treatment can significantly reverse the levels of TGF-β-induced fibrosis markers in HESCs, including α-SMA, COL1A1, vimentin, and E-cadherin (p<0.01). In addition, HESCs treated with CCL can reduce M1 polarization levels in THP-1 cells, represented as the decreased CCL-2 mRNA, ADGRE1 mRNA, and F4/80 ratio (p<0.001). 32 possible therapeutic targets of CCL in IUA were obtained. These 32 therapeutic targets were enriched in multiple GO terms and KEGG pathways. CCL decreased TGFB1, AKT1, and MMP9 expression levels in HESCs cells (p<0.001), as well as IL-1β, TNF-α, and IL-6 releases in THP-1 (p<0.01). Conclusions CCL inhibits fibrosis and inflammation, and it may be a potentially effective therapeutic strategy for the treatment of endometrial fibrosis.
Open Access
Downregulation of miR-1256 promotes breast cancer progression by targeting IL-22 and is associated with poor prognosis

30. Januar 2026

Yi Zhao, Qian Wang, Murong Liu, Wei Zhao

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Objectives Breast cancer (BC) poses a serious threat to women’s health, but its clinical prognosis is not ideal. miR-1256 has been shown to act as a tumor suppressor in various cancers, but its role in BC remains unknown. This study primarily explores the prognostic value of miR-1256 in BC. Methods The study included a total of 152 BC patients. RT-qPCR was employed to assay miR-1256 and interleukin-22 (IL-22) levels. Kaplan-Meier curves and Cox Proportional-Hazards Model (Cox) analysis were utilized to assess prognostic value. Cell Counting Kit-8 (CCK-8) and Transwell assays were used to study the proliferation and transfer capabilities of BC cells. Enzyme-linked immunosorbent assay (ELISA) assay for IL-22 protein content. The dual-luciferase reporter assay was employed to validate the relationship of miR-1256 with IL-22. Results miR-1256 level was significantly down-regulated in BC patients. The level of miR-1256 is closely related to clinical indicators, and high levels indicate a better prognosis. Overexpression of miR-1256 inhibits proliferation, migration, and invasion of breast cancer cells. Furthermore, IL-22 identified as a downstream target of miR-1256, is markedly up-regulated in BC patients and BC cells. Overexpression of IL-22 can reverse the suppression of malignant behavior in BC cells induced by miR-1256 mimic. Conclusions miR-1256 may inhibit malignant proliferation and transfer of BC cells by suppressing IL-22 levels. Furthermore, it holds promise as a potential target for clinical prognostication.
Open Access
A biochemical perspective on bone-implant interface healing after cemented knee arthroplasty: role of serum calcium and ALP

30. Januar 2026

Mehmet Can Gezer, Mahircan Demir, Merve Sibel Güngören, Mehmet Batu Ertan, Ali Kemal Us

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Objectives Osteointegration at the bone-cement interface is essential for the long-term success of implants following cemented total knee arthroplasty (TKA). This study aims to assess the time-dependent changes in serum calcium (Ca) and alkaline phosphatase (ALP) levels after TKA and to explore their relationship with functional recovery and osteointegration potential. Methods This prospective study involved 100 patients who underwent primary cemented TKA. Serum Ca and ALP levels were measured before surgery and at postoperative days 1, 3 weeks, 6 weeks, 6 months, and 1 year. Functional outcomes were evaluated using the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC), while pain levels were recorded with a 10-point Visual Analog Scale (VAS). Knee range of motion (ROM) was measured with a goniometer. Correlation and multivariate regression analyses were conducted to assess links between biochemical markers and clinical outcomes. Radiographic osteolysis was evaluated through standard X-rays. Results Serum Ca levels significantly declined over time (p<0.001), while ALP showed a biphasic pattern. Clinical outcomes, including WOMAC, VAS, and ROM, improved markedly (all p<0.001). However, no significant correlations were observed between Ca or ALP levels and these outcomes (all p>0.05). Conclusions Although measurable changes in serum calcium and ALP levels are observed following cemented TKA, these parameters demonstrate limited clinical utility as systemic markers of osteointegration or predictors of functional recovery. is warranted to assess implant integration and postoperative bone healing better.
Open Access
MiR-134-3p alleviates nerve damage and neurological deficits after ischemic stroke by targeting MMP-8

26. Januar 2026

Tianrui Yu, Yanping Ding, Juyao Liu

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Objectives Ischemic stroke is a major global cause of mortality and long-term disability, resulting in irreversible neuronal damage, cognitive impairment, and reduced quality of life. To investigate the neuroprotective role of miR-134-3p in ischemic stroke and elucidate its regulatory mechanism targeting MMP-8. Methods The middle cerebral artery occlusion (MCAO) model was established in mice to simulate ischemic stroke injury. Neuronal cell models subjected to oxygen-glucose deprivation (OGD) simulated ischemic conditions in vitro . The modified neurological severity score (mNSS), inflammation marker assays, cell viability tests, and luciferase reporter assays assessed functional outcomes and molecular interactions. Results MiR-134-3p expression was downregulated following ischemic injury both in vivo and in vitro . Overexpression of miR-134-3p improved neuronal survival, reduced inflammatory cytokine levels, and mitigated neurological deficits. Mechanistic studies demonstrated that miR-134-3p negatively regulated MMP-8 expression by binding its 3′ UTR directly. Furthermore, miR-134-3p overexpression reversed the detrimental effects induced by MMP-8 upregulation on neuronal viability. Conclusions MiR-134-3p showed a protective effect against ischemic stroke-induced neural damage through targeted suppression of MMP-8. And the therapeutic potential for targeting the miR-134-3p/MMP-8 axis as an intervention strategy for ischemic brain injury.
Open Access
TM4SF1 modulates the TGF-β1/Smad3 signaling pathway to affect malignant biological activity and autophagy of nasopharyngeal carcinoma cells

20. Januar 2026

Huadong Mao, Jianyong Chen

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Objectives To explore whether transmembrane 4 superfamily 1 (TM4SF1) can modulate the transforming growth factor β1 (TGF-β1)/mothers against decapentaplegic homolog 3 (Smad3) signaling pathway to influence nasopharyngeal carcinoma (NPC) cells from the aspect of malignant biological activity and autophagy. Methods Reverse transcriptase-polymerase chain reaction was utilized for measuring the relative expression of TM4SF1 in human nasopharyngeal epithelial cell line (NP69) as well as human NPC cells (5–8F, CNE2, and 6–10B). A small interfering-negative control (si-NC) group, a si-TM4SF1 group, a si-TM4SF1 + TGF-β1 group, and a control group (not transfected with any plasmid) were established for the assignment of 5–8F cells in a random manner. Cell proliferation, apoptosis, autophagy, and protein expression were evaluated by Cell Counting Kit-8 assay, flow cytometry, monodansylcadaverine (MDC) staining/transmission electron microscopy (TEM), and Western blotting, respectively. Results We found that TM4SF1 expression was higher in human NPC 5–8F, CNE2, and 6–10B cells than in NP69 cells, and its relative expression significantly rose in 5–8F cells compared with 6–10B and CNE2 cells (p<0.05). In comparison to the si-TM4SF1 group, the cell viability, number of invaded cells, and relative expression of TM4SF1, p-Smad3/Smad3 ratio and protein expressions of p62, TGF-β1 and N-cadherin in cells were elevated in the si-TM4SF1 + TGF-β1 group, together with the reductions in apoptosis rate, relative fluorescence intensity, number of autophagosomes, and LC3-II/LC3-Ι ratio and protein expressions of Beclin1 and E-cadherin in cells (p<0.05). Conclusions TM4SF1 knockdown is able to influence NPC cells by repressing their proliferation and infiltration while inducing their apoptosis.
Open Access
Fertilizing role of leuprolide acetate in assisted human reproduction among infertile patients with endometriosis

19. Januar 2026

Yaning Jiang, Jialin Li, Li Liu, Yuan Li, Lanjun Feng

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Objectives This study investigated the fertilizing potential of leuprolide acetate in infertile patients with endometriosis (EMS). Methods This study included 116 patients with the EMS infertility, who were randomly divided into the control group and the leuprolide acetate group. Patients of the former only underwent laparoscopic surgery, while those in the latter were additionally administered leuprolide acetate subcutaneous injections. The serum luteinizing hormone, estradiol, follicle-stimulating hormone, and cancer antigen 125 (CA125) levels of all subjects were measured using commercial ELISA kits. And Kaplan-Meier analysis was conducted to show the cumulative pregnancy rate within one year of follow-up. Furthermore, the recurrence rate and incidence of adverse events after treatment were analyzed. Results The serum luteinizing hormone, estradiol, and follicle-stimulating hormone levels were statistically insignificant in both groups before treatment (p > 0.05). However, their levels were typically suppressed after treatment, with a greater decrease observed in the leuprolide acetate group than in the control group (p < 0.05). The pregnancy rate was significantly higher in the leuprolide acetate group (62.07 %) than in the control group (20.69 %) after treatment. Additionally, the former exhibited a higher pregnancy rate in the one-year follow-up (log-rank p < 0.001). It also had a significantly lower recurrence rate and CA125 level compared to the control group (p < 0.05). Conclusions Treatment involving leuprolide acetate after laparoscopic surgery can improve the chance of pregnancy and reduce the endometriosis recurrence rate in infertile endometriosis patients.
Open Access
Evaluation of vascular tone in patients with menorrhagia: the role of apelin and norepinephrine

12. Januar 2026

Zeynep Guctekin, Mehmet Erdem, Umran Karabulut Dogan, Engin Yildirim, Tugba Raika Kiran

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Objectives Menorrhagia, characterized by excessive menstrual bleeding, impacts 30 % of women of childbearing period and is frequently linked to anemia and discomfort in the pelvic region. Understanding the vascular and hormonal mechanisms underlying this condition could aid in developing non-surgical treatment options. This research focused on exploring the role of apelin and norepinephrine (NE), along with nitric oxide (NO) and prostacyclin (PGI 2 ), in the pathophysiology of menorrhagia. Methods The study included 44 women diagnosed with menorrhagia and 44 healthy controls. Blood specimens were taken on the 2nd or 3rd day of menstruation, and serum specimens were prepared. The levels of apelin, NE, NO, and PGI 2 were determined using commercially available ELISA kits. Furthermore, standard biochemical analyses were conducted on all specimens. Results Apelin and NE levels were significantly reduced in the menorrhagia group compared to control group (p<0.05). The comparison of NO and PGI 2 levels showed no statistically significant difference between the menorrhagia and control groups (p>0.05). In the menorrhagia group, total cholesterol, iron-binding capacity, platelet count, and FSH concentrations were markedly higher than those in control individuals, conversely, albumin, iron, hemoglobin, MCV, hematocrit, and progesterone levels were notably reduced (p<0.05). Conclusions The study identified apelin and NE as moderately discriminative markers in menorrhagia and suggested that these markers could potentially contribute to impaired vasoconstriction and excessive menstrual bleeding. Future research should focus on evaluating biomarkers across different menstrual phases and exploring new therapeutic strategies for uterine protection.
Open Access
Anti-lung cancer effect of Ornithogalum caudatum Jacq. via the CRHBP and regulation of M2 macrophage polarization

9. Januar 2026

Guanglei Wang, Yihua Zhang, Xikai Tao, Tingting Dong, Lei Du, Zekai Tang

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Objectives This study aimed to validate OCJ’s anti-lung cancer effect and CRHBP regulation mechanism in vitro . Methods The ETCM database was searched to identify the main components and specific targets of OCJ. According to the HPA database, the immunohistochemical (IHC) images of normal lung cells and lung cancer cells were screened. The CCK-8 assay and flow cytometry were employed to evaluate the impact of OCJ on cancer cell viability, proliferation, and apoptosis before and following CRHBP knockout. Finally, the mechanisms by which OCJ regulates M2 macrophages were explored. Results The major component of OCJ was Caudaside A, and the specific target was CRHBP, according to the ETCM database. CRHBP was found to be expressed at a lower level in lung cancer tissue and cells compared to normal tissue and cells. However, the expression level of CRHBP was increased by the addition of OCJ. In the cell functional assay, OCJ failed to effectively suppress cell proliferation or induce cell apoptosis following CRHBP knockdown. The inhibitory effects of OCJ on the M2 polarization markers of macrophages rescued by CRHBP suppression. Conclusions OCJ can promote the overexpression of CRHBP to inhibit the polarization of M2 macrophages, thus inhibiting lung cancer cell proliferation and inducing apoptosis.
Open Access
LncRNA NBAT1 affects the progression of diabetic retinopathy by targeting miR-140-3p

8. Januar 2026

Huili Cheng, Min Chen

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Objectives Diabetic retinopathy (DR) is a serious threat to vision, with rising prevalence worldwide. Non-coding RNAs play a role in DR development. This study investigates how the lncRNA NBAT1/miR-140-3p axis regulates DR. Methods NBAT1 expression levels in serum were measured using RT-qPCR. Binding sites between miR-140-3p and NBAT1 were predicted using the LncRNASNP2 database. To simulate DR in vitro , a high glucose (HG)-induced ARPE-19 cell model was established. The expressions of NBAT1 and miR-140-3p under HG conditions were detected and the regulatory effect of NBAT1 on miR-140-3p was examined by dual luciferase reporter assay. After overexpressing NBAT1 and miR-140-3p in the HG model, TNF-α, IL-1β, and IL-6 levels were measured by ELISA. Results NBAT1 was significantly upregulated in DR patients compared to those with diabetes alone. The area under the ROC curve (AUC) of 0.7745 indicates its diagnostic potential for DR. Under HG condition, NBAT1 expression increased while miR-140-3p decreased. Dual luciferase reporter assay confirms that NBAT1 negatively regulates miR-140-3p. HG induction promoted inflammatory cytokine release in ARPE-19 cells, an effect that was amplified by NBAT1 overexpression. Importantly, transfection with miR-140-3p mimics reversed the pro-inflammatory effects induced by NBAT1. Conclusions NBAT1 is a risk factor for DR. In vitro studies show that NBAT1 worsens inflammatory responses in DR by negatively regulating miR-140-3p.
Open Access
The expression profile and clinical relevance of miR-486-5p in individuals with chronic periodontitis

8. Januar 2026

Shiliang Guo, Xingtao Wen, Huadan Jin, Fenglin Chen, Ling Li

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Objectives The development of chronic periodontitis (CP) is closely connected with the abnormal expression of microRNA. Here, we attempted to determine the levels of miR-486-5p in CP patients and to evaluate the function of miR-486-5p on the proliferation and apoptosis of human periodontal ligament cells (PDLCs). Methods A total of 80 patients with CP and 100 periodontally healthy individuals were enrolled. Gingival crevicular fluid samples (GCFs) were collected. PDLCs were stimulated with lipopolysaccharide (LPS) to establish an in vitro model of cells mimicking CP. The GCFs miR-486-5p expression was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The receiver operating characteristic curve was conducted to explore the diagnostic utility of miR-486-5p. Cell proliferation, apoptosis, and inflammatory factors were assessed by cell counting kit-8 assay, flow cytometry assay, and enzyme-linked immunosorbent assay. The interactions between miRNA and targets were investigated by dual luciferase reporter assay. Results The expression of miR-486-5p was increased in CP patients compared to controls. The area under the curve value was 0.878, which had a certain diagnostic value in CP. In vitro, cell experiments confirmed that the elevation of miR-486-5p diminished cell proliferation and enhanced apoptosis. Similarly, overexpression of miR-486-5p stimulated the release of inflammatory cytokines. PTEN was the target of miR-486-5p. Conclusions miR-468-5p had a certain value and significance as a biomarker for CP diagnosis, and its elevated expression correlates with the progression of the disease.
Open Access
Distinct epigenetic analysis of mRNA 5-methylcytosine in the hippocampi of healthy young and aged mice

6. Januar 2026

Xuan Zhang, Wenhui He, Sanwei Jiang, Junmei Li, Qinbin Hu, Chengzhang Li, Lingtong Zhi, Chengbiao Lu

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Objectives To profile the mRNA m 5 C modification landscape in hippocampi from young and aged mice. Methods MeRIP-seq (Methylated RNA Immunoprecipitation Sequencing) technology was conducted to profile m 5 C-tagged peaks and genes in young and aged hippocampi. M 5 C methylation-related enzymes were detected using Western blot. Results The numbers of m 5 C methylation peaks and genes were increased during aging. Among 2010 different m 5 C peaks, 830 methylated peaks in 782 genes were upregulated and 1,180 methylated peaks in 1,088 genes were downregulated in the aged hippocampi. Most of the m 5 C sites in the hippocampal transcriptome were distributed at the coding sequence, while the fewest m 5 C sites found in the 5′ untranslated regions (5′ UTRs). Young and aged mice showed a similar enrichment of the most credible motif. The protein level of the m 5 C demethylase TET2 was downregulated during aging, suggesting that TET2 may potentially influence neuronal health and even cognitive function through epigenetic mechanisms. Conclusions Our data demonstrated different m 5 C-enriched regions in the young and aged hippocampi, providing novel insight into the possible functions of m 5 C methylation in brain aging.
Open Access
Relation between hOGG1 rs1052133 polymorphism with the susceptibility of hepatocellular carcinoma: a meta-analysis

29. Dezember 2025

Haomiao Xu, Hong Zhang, Fei Wang, Yichuan Zhang, Susu Ye

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Objectives Human 8-hydroxy guanine DNA glycosylase (hOGG1) is a DNA repair enzyme associated with hepatocellular carcinoma (HCC). This study aimed to investigate the pooled relationship between hOGG1 rs1052133 polymorphism and HCC susceptibility. Methods Eligible articles were searched from PubMed, EMBASE, China Knowledge Network (CNKI), and WanFang databases. Random or fixed effects models were employed to assess pooled odds ratios (ORs) and 95 % confidence intervals (95 % CIs) of the association. Subgroup analysis based on ethnicity and control source was performed to assess the source of heterogeneity. Results High heterogeneity was discovered in five genetic models. Therefore, the pooled association was discovered under the random-effect model. hOGG1 rs1052133 was significantly related to HCC vulnerability under CG + GG vs. CC (OR=1.38, 95 % CI=1.04–1.83), CG vs. CC (OR=1.44, 95 % CI=1.12–1.84) genetic models. Subgroup analysis based on ethnicity indicated that rs1052133 was linked to elevated HCC risk in the Caucasian subgroup under G vs. C (OR=1.76, 95 % CI=1.22–2.56), CG + GG vs. CC (OR=2.72, 95 % CI=1.48–4.99), GG vs. CC (OR=2.51, 95 % CI=1.10–5.72), CG vs. CC (OR=2.66, 95 % CI=1.19–5.96) genetic models. Notably, the ORs were modest when considering the 95 % CIs. The study was largely free of publication bias. Conclusions The hOGG1 rs1052133 was significantly associated with HCC risk, especially in Caucasians.
Open Access
Application of abnormal expression of serum LINC00968 in early identification of childhood obesity risk

25. Dezember 2025

Hongbo Wu, Wei Liu, Zhenni Lu, Lihua Li

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Objectives This study investigates the dysregulated expression of long non-coding RNA LINC00968 in pediatric populations with early-onset obesity or metabolic syndrome (MS), while evaluating its potential utility as a clinical biomarker. Methods The study enrolled children with obesity (classified as simple obesity or obesity-MS) and healthy controls. The level of serum LINC00968 and miR-17-5p were quantified by RT-qPCR. Receiver operating characteristic (ROC) curve was employed to assess the serum LINC00968’s capacity for risk identification in obese children and the prediction of obesity-MS. Dual luciferase reporter ( DLR) and RNA immunoprecipitation (RIP) experiments confirmed that LINC00968 can target miR-17-5p. Logistic regression analysis was employed to evaluate the potential risk factors influencing the occurrence of obesity-MS. Results Serum LINC00968 levels were significantly higher in children with obesity compared to controls, with the higher expression observed in those with obesity-MS. In contrast, miR-17-5p expression was significantly downregulated. LINC00968 demonstrated a sensitivity of 86.67 % and a specificity of 90.28 % in distinguishing obese children from healthy controls. In children with obesity, LINC00968 exhibited a significant positive correlation with TG and BMI, and a negative correlation with HDL-C. Molecularly, LINC00968 directly targets miR-17-5p, which is negatively correlated with miR-17-5p in children with obesity. Conclusions Our findings suggest that elevated serum LINC00968 levels could serve as a biomarker for pediatric obesity and MS, potentially driving disease progression via miR-17-5p targeting.
Open Access
Early diagnostic and prognostic potential of miR-200c in acute kidney injury

23. Dezember 2025

Feifei Wang, Zijian Tian, Jingjing Gong, Zhenwen Chen

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Objectives Acute kidney injury (AKI) is a serious clinical condition characterized by rapid renal dysfunction and high mortality. Although the dysregulation of microRNAs is well-established in AKI, the clinical significance of microRNA-200c in this condition remains poorly defined. Methods RT-qPCR detected miR-200c and inflammatory factors (TNF-α, IL-6, IL-8) in serum from 75 patients with AKI and 72 controls. ROC curves assessed miR-200c’s diagnostic value. Multivariate Cox regression identified independent survival risk factors. Kaplan-Meier curves analyzed miR-200c-survival links. Establishment of an in vitro cell model induced by LPS. To assess cell proliferation and apoptosis, CCK-8 assays and flow cytometry were employed. Results miR-200c expression was significantly elevated in AKI patients. Serum miR-200c effectively distinguishes AKI patients from controls. Compared with the group of patients with good prognosis, the miR-200c expression was significantly higher in the group of patients with poor prognosis. Survival analysis showed that higher miR-200c levels in AKI cases correlated with a notable decline in 90-day survival. Suppression of miR-200c expression enhanced cell proliferation, attenuated apoptosis, and reduced inflammatory factor levels, thereby ameliorating AKI progression. Conclusions miR-200c shows promising application potential in the diagnosis and prognosis assessment of AKI. Suppressing miR-200c expression effectively curbs aberrant cellular behaviors and pro-inflammatory responses.
Open Access
AI-supported quantitative anti-müllerian hormone measurement with lateral flow biosensor

23. Dezember 2025

Samet Kırat, Zihni Onur Uygun

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Objectives This study aims to develop a mobile-integrated, paper-based biosensor for the quantitative detection of anti-müllerian hormone (AMH), providing a reliable and objective tool to support reproductive health assessment. Rather than serving as a stand-alone diagnostic for a specific condition, the system focuses on accurate AMH quantification to assist broader hormonal biomarker monitoring in both clinical and decentralized settings. Methods An antibody-based lateral flow biosensor was combined with a deep learning-powered image analysis pipeline. Smartphone-captured images of the test strip were processed using a YOLOv8-based object detection model to localize the test line and extract RGB intensity values. These features were then analyzed by a random forest regression model trained to map image intensities to AMH concentrations. Image standardization and lighting correction algorithms were implemented to ensure measurement robustness under variable field conditions. Results The developed biosensor achieved quantitative AMH detection within a concentration range of 0.05–20 ng/mL, exhibiting a strong correlation with standard laboratory immunoassays (R 2 =0.9966). The YOLOv8-integrated analytical pipeline demonstrated excellent selectivity, repeatability, and stability under different illumination scenarios. Receiver operating characteristic analysis (AUC=0.962) confirmed high diagnostic reliability for AMH level stratification, emphasizing the system’s potential in reproductive endocrinology. Conclusions This AI-integrated biosensor represents a robust and accessible tool for AMH monitoring at the point of care. The combination of paper-based sensing and deep learning-driven quantification offers a scalable platform for hormonal biomarker analysis, paving the way for broader applications in personalized reproductive health management.
Open Access
Luteolin alleviates lung cancer pain in mice by modulating AKT1

23. Dezember 2025

Haiyan Tu, Shanshan Qi, Cheng Zhang, Jie Yang

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Objetives The treatment of lung cancer pain (LCP) faces the double challenge of high side effects of analgesics and unclear mechanisms. Luteolin (LUT), an active ingredient of Salvia miltiorrhiza Bge., has anti-tumor potential, but its mechanism in alleviating LCP has not been elucidated completely. To elucidate the molecular mechanism of LUT in alleviating LCP by modulating the AKT1. Methods Based on the network pharmacology strategy, potential active ingredients of Salvia miltiorrhiza Bge. and their targets for the treatment of LCP were collected from the TCMSP, HERB, and CTD databases. A protein-protein interaction (PPI) network was constructed in the STRING database to identify the hub genes. Detection of AKT1 expression was performed by RT-qPCR or western blot. The degree of pain in lung cancer patients was quantified using the Numeric Rating Scale (NRS). The CCK-8 and Transwell assays were used to assess human lung carcinoma epithelial cell (A549) viability and invasiveness. The sensitivity to pain in bone metastasis mice was assessed by measuring the mechanical paw withdrawal threshold. Results AKT1 had the highest node degree value in the PPI network. The clinical analysis showed that AKT1 expression level was positively correlated with LCP. Cellular experiments showed that LUT concentration-dependently inhibited the cell viability of A549 cells and hindered cell invasion by down-regulating AKT1. The in vivo experiments showed that LUT treatment alleviated the pain of bone metastasis mice and decreased AKT1 expression. Conclusions LUT suppressed lung cancer cell invasion and relieved LCP through AKT1 inhibition.
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

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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
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

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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
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

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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
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

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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
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

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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
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

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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
Serum fatty acid synthase and GLP-1 levels in prostate cancer and benign prostatic hyperplasia

21. November 2025

Abdullah Üner, Tevfik Noyan, Erdal Benli

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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
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

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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
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

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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
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

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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
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

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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
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

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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 mini review: the trio of artichoke (Cynara scolymus L.), cytotoxicity, and apoptosis

17. Oktober 2025

Taygun Dayi, Müjgan Kuşi, Fatma Hacet

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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
Study on the role of miR-146b-3p in the occurrence and development of endometriosis

17. Oktober 2025

Yan Zhang, Dongxiang Han

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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
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

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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
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

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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.
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

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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.
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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

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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.

3rd NATIONAL NUTRITION AND METABOLISM SYMPOSIUM 2025

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INTERNATIONAL LABORATORY MEDICINE SUMMIT ERZURUM 2025

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

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

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

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

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

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TBS International Biochemistry Congress 2022 - 33rd National Biochemistry Congress

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

TBS International Biochemistry Congress 2021 - 32nd National Biochemistry Congress

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3rd International Cancer and Ion channels Congress 2021

XXXI National Congress of The Turkish Biochemical Society 2020

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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

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TBS International Biochemistry Congress 2018, 29th National Biochemistry Congress

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TBD-BD Preanalytic Phase Symposium 2018

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

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

Insulin Resistance Symposium | in vitro Diagnostic Biomarkers Symposium

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International Biochemical Congress 2017 | 28th National Biochemistry Congress

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

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TBS Biochemical Days: Abstract Issue

Journal Impact Factor	0.7	2024, Journal Citation Reports (Clarivate, 2025)
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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

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submission@turkjbiochem.com

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

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eISSN:

1303-829X

ISSN:

0250-4685

Sprache:

Englisch

Verlag:

De Gruyter

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Erstveröffentlichung:

1. Januar 1976

eISSN: 1303-829X

ISSN: 0250-4685

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

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