Explore the vast range of titles available.

Purpose To evaluate the serum levels of vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1) after intravitreal injection of aflibercept (IVA) and the transition of aflibercept into systemic circulation in infants with severe retinopathy of prematurity (ROP). Study design Prospective study. Methods This single-centered prospective cohort study included infants who received IVA for the treatment of type 1 ROP in zone I and posterior zone II. Blood samples were collected before IVA and at 1 day and 1, 2, 4, and 8 weeks after IVA. VEGF, IGF-1 and aflibercept levels were measured. Results Thirty eyes of 15 infants received IVA of 1 mg/0.025 mL. Serum VEGF levels decreased significantly at 1 day and 1, 2, 4, and 8 weeks after IVA compared with baseline ( P  < 0.05). Serum aflibercept levels decreased significantly 1, 2, 4, and 8 weeks after IVA compared with the level at 1 day after IVA ( P  < 0.05) and increased significantly at 1 day, 1, 2, and 4 weeks after IVA compared with the baseline level ( P  < 0.05). No significant difference was detected between serum IGF-1 levels any time in any infant ( P  > 0.05). Conclusion Serum VEGF levels are suppressed for at least 8 weeks, and aflibercept could be detected in the systemic circulation at 4 weeks after injection. Clinicians should be cautious about changes in systemic VEGF levels and passage of the agent into systemic circulation after IVA in infants.

Osteoarthritis (OA) represents a degenerative joint disease which advances through cartilage breakdown, synovial inflammation, and subchondral bone transformation until it causes persistent pain and mobility loss. The scientific community lacks complete knowledge about OA disease mechanisms and post-operative healing processes despite arthroplasty surgery providing effective symptom relief. This study investigated plasma proteomic changes in OA patients before and after arthroplasty. The cohort included eight OA patients undergoing knee or hip arthroplasty and ten age-, sex-, and body mass index-matched healthy controls. Plasma proteins were analyzed using liquid chromatography–tandem mass spectrometry following enzymatic digestion and depletion of high-abundance components. The bioinformatic analysis together with quantitative methods showed that OA patients experienced changes in inflammatory pathways, extracellular matrix remodeling, immune system regulation and coagulation processes. A total of 93 proteins were differentially abundant in the pre-operative comparison. Among these, 63 proteins were consistently up-regulated and 23 were consistently down-regulated across both pre- and post-operative time points. In addition, 20 proteins exhibited post-operative-specific changes. These findings highlight both persistent disease-associated alterations and transient proteomic shifts linked to post-operative recovery. Overall, this study identifies candidate plasma proteomic signatures associated with OA and surgical intervention, providing exploratory insights into disease monitoring and potential personalized therapeutic strategies.

Diabetic nephropathy (DN) is a leading cause of end-stage renal disease, characterized by progressive kidney dysfunction. Early detection and targeted therapies remain key challenges in managing DN. This study aims to identify proteomic alterations in DN patients compared to healthy controls, focusing on proteins involved in inflammation, oxidative stress, immune response, and metabolic dysregulation. Using mass spectrometry and advanced bioinformatics, we identified significant upregulation of proteins associated with platelet activation, immune regulation, and extracellular matrix remodeling, as well as downregulation of proteins linked to lipid metabolism, immune regulation, and structural stability. These findings highlight the molecular complexity of DN and suggest that altered protein expression plays a critical role in the progression of kidney damage. The identified proteins may serve as potential biomarkers for early diagnosis and therapeutic targets for DN. Our results underline the importance of proteomic analyses in advancing the understanding of DN pathogenesis and in developing strategies for personalized treatment to improve patient outcomes. Future research should focus on further elucidating these molecular mechanisms and their implications for clinical management.

Background The incidence of non-alcoholic fatty liver disease (NAFLD) is increasing with obesity, and it is believed that the ongoing low-grade inflammation in obesity and alterations in the enterohepatic axis contributing this process. This study aimed to determine the role of fecal calprotectin (FC) as inflammatory biomarker in obesity and NAFLD. Methods Between November 2022-August 2023, 31 obese and 10 healthy adolescents aged between 10 and 18 years enrolled in this prospective controlled study. Body mass index higher than 2 standard deviation is considered as obesity. Obese adolescents were divided into two subgroups: obese adolescents ( n  = 11) and Obese + NAFLD group ( n  = 20). NAFLD diagnosis was made with biochemical analysis or ultrasonography. FC levels and laboratory parameters analyzed in study group, while only FC samples taken from control group. Anthropometric and laboratory parameters were compared between groups. This study was registered in ClinicalTrials.gov (NCT06229184). Results The median (IQR P25-75) FC levels in the obese + NAFLD, obese and the healthy controls were 136.23 (43.36-332.04), 61.77 (29.70-285.92) and 38.95 (27.59–50.52) µg/g feces, respectively ( p  = 0.018). Subgroup analyses revealed that the significant difference was between the obese + NAFLD group and the control group ( p  = 0.02), while no significant differences were observed between the control and obese groups, or between the obese and obese + NAFLD groups. FC positivity rates were 20% ( n  = 2) in the control group, 54.5% ( n  = 6) in the obese group, and 75% ( n  = 15) in the Obese + NAFLD group ( p  = 0.018). Conclusions FC is significantly higher in obese adolescents compared to healthy peers, but no significant difference was observed between obese and obese + NAFLD groups. Further studies needed on this subject. Trial registration This trial is registered in ClinicalTrials.gov (Trial registration number [ClinicalTrials.gov ID] NCT06229184).

Background: Cigarette smoking disrupts cellular energy metabolism and remains a major global health problem. The Mediterranean diet, characterized by antioxidant and anti-inflammatory properties, has been implicated in the regulation of metabolic pathways. Objective: This study aimed to examine the association between adherence to the Mediterranean diet and the expression of energy metabolism-related genes in smokers aged 18–55 years. Methods: Smokers were classified according to their Mediterranean Diet Adherence Screener (MEDAS) scores into an adhering group (n = 24) and a non-adhering group (n = 24). Participant characteristics were recorded, blood samples were collected, and total RNA was isolated. Gene expression analysis was performed using a custom RT-qPCR array targeting energy metabolism-related genes. Pathway enrichment analysis was conducted using EnrichR Reactome 2024, and gene–metabolite relationships were explored using MetaboAnalyst 6.0 to support pathway-level interpretation. Results: Smoking was associated with coordinated upregulation of genes involved in glycolysis, glucose transport, lipid metabolism, amino acid metabolism, the pentose phosphate pathway, and redox regulation, consistent with a metabolically stressed state. In contrast, adherence to the Mediterranean diet was associated with lower expression of genes related to glycolytic flux, lipid β-oxidation, and amino acid turnover, alongside relatively higher engagement of tricarboxylic acid cycle-related pathways and reduced activation of redox-associated processes. Conclusions: Adherence to the Mediterranean diet was associated with differences in the expression of genes involved in cellular energy metabolism among smokers, suggesting a potential modulatory role of dietary patterns in smoking-related metabolic alterations.

Introduction and hypothesisThe association between overactive bladder (OAB) and uterine prolapse remains unclear. The extent of the role of serum nerve growth factor (NGF) levels in this relationship is also not known. Therefore, our study evaluated the association among OAB, high-grade uterine prolapse and serum NGF levels.MethodsA total of 90 patients participated in our study and were grouped as follows. Group I included patients with high-grade uterine prolapse and OAB, group II included patients with only high-grade uterine prolapse, and group III included healthy women without uterine prolapse or OAB. Serum NGF level analysis was performed in all groups.ResultsSerum NGF levels varied greatly among the three groups, with significantly higher levels in group 1 than in groups 2 and 3 (p < 0.001). Serum NGF levels with a cutoff point of 120.49 pg/ml identified women with significant OAB symptoms to discriminate among groups with a sensitivity of 80%, specificity of 86.7%, positive predictive value of 75.0%, negative predictive value of 89.7% and positive likelihood ratio of 6.01 (p < 0.001).ConclusionsOur study showed that NGF-related pathways may play an active role in the pathophysiology of OAB with high-grade uterine prolapse patients based on obstruction hypothesis.

Decoy receptor 3 (DcR3) is a supermember of tumor necrosis receptor (TNF) factor. DcR3 acts as a binding partner in multiple apoptotic ligands that inhibit apoptosis. TNF-associated apoptosis-inducing ligand (TRAIL)-induced apoptosis has been demonstrated to be sensitized by DcR3. DcR3 has been found to be a ‘‘pleiotropic’’ soluble factor with ‘‘decoy’’ and ‘‘non-decoy’’ activities that control cell functions. The connection between Fas and FasL can be inhibited by recombinant DcR3 coupled with an IgG1 Fc domain. TNF superfamily FasL can inhibit apoptosis and increase angiogenesis through neutralizing members of LIGHT and TL1A. DcR3 serum level is almost undetectable in most normal individuals without inflammatory diseases and cancer. According to several research, the level of DcR3 in the blood is linked to cancer stage in cancer patients. High DcR3 levels in serum or tissues have been found to be associated with poor prognosis and/or resistance to therapy in some cancer patients. As a result, identifying the cut-off value of the DcR3 serum level will provide to able to forecast the severity of disease in the future. While inhibiting DcR3 expression may slow tumor growth, improving DcR3-mediated effector functions could be a viable strategy for reducing autoimmunity and promoting tissue healing. Thus, recombinant DcR3 is a promising immunotherapeutic agent; yet, in the malignant environment, turning off DcR3 expression may improve cancer therapy success. The purpose of this review is to provide clinical convenience by collecting the findings of studies on DcR3 so far. These discoveries could help with cancer diagnosis, differentiation, metastasis, and stage detection. Furthermore, these may provide new therapeutic approaches to target carcinomas in the future.

Background. Vitamin B12, an indispensable micronutrient, is pivotal in numerous physiological processes, with particular significance during pregnancy and fetal development. The increasing adoption of vegetarian diets and the economic challenges associated with accessing animal-based food sources contribute to the prevalence of vitamin B12 deficiency. This study aims to examine the levels of vitamin B12 and homocysteine in pregnant women upon admission for delivery and to analyze corresponding cord blood samples from their newborn infants in a substantial sample within the Istanbul metropolitan area. Materials and Methods. This cross-sectional multicenter study included women aged ≥16 years admitted for delivery and their newborns ≥34 weeks. The demographic data and the results of complete blood counts within the previous 24 hours before birth were recorded. Vitamin B12 and homocysteine levels were measured in maternal and cord blood samples. The study parameters were compared between the groups based on the mothers’ and babies’ homocysteine and vitamin B12 levels. Results. The study included 832 pregnant women and 832 neonates. Anemia affected 36% of pregnant women, with a higher frequency in mothers with vitamin B12 deficiency. Seventy-eight mothers and 48.9% of neonates showed Vitamin B12 levels below 200 pg/mL, while elevated homocysteine levels were observed in 30% of mothers and 26% of neonates. Maternal vitamin B12 deficiency was significantly correlated with cord blood B12 deficiency and elevated homocysteine. The median cord blood vitamin B12 level was inversely correlated with the number of previous pregnancies. Conclusion. Vitamin B12 deficiency is extremely common in pregnant women before delivery, significantly correlating to cord blood homocysteine and vitamin B12 levels. However, homocysteine alone is not a reliable marker for maternal vitamin B12 status. Implementing strategies to detect vitamin B12 deficiency and supplying adequate vitamin B12 supplementation during pregnancy holds the potential to enhance maternal and neonatal health in Türkiye. 

Degenerative joint disease is a condition that affects joints and is commonly referred to as osteoarthritis (OA). This form of arthritis is most prevalent among women and tends to become more frequent as people age. The pathogenesis of OA involves an imbalance of cytokines in favor of pro-inflammatory cytokines. However, the steroid hormone dehydroepiandrosterone (DHEA) exerts chondroprotective effects and regulates the balance of catabolic factors such as thrombospondin motif disintegrin and metalloproteinase (ADAMTS), thereby playing a role against OA. Pro-inflammatory cytokines induce aggrecanases, such as ADAMTS5, which degrade the extracellular matrix and contribute to OA. The molecule nerve growth factor (NGF), associated with pain in OA, is important for cartilage homeostasis, and DHEA can modulate pain by interfering with NGF receptors. This review covers the roles of DHEA, ADAMTS5, and NGF in the pathogenesis of OA, their relationship with pain pathways, and their use in current treatments. We also anticipate that these pathways will be crucial in developing new strategies to prevent and treat OA, and understanding their interactions may make it possible to enhanced the quality of life of patients with OA.