Human Pentraxin 3 ,PTX3 ELISA Kit
- Known as:
- Human Pentraxin 3 ,PTX3 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 201-12-1939
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Sunredbio SunBT Sun red bio
- Gene target:
- Human Pentraxin 3 PTX3 ELISA Kit
Related genes to: Human Pentraxin 3 ,PTX3 ELISA Kit
- Gene:
- PTX3 NIH gene
- Name:
- pentraxin 3
- Previous symbol:
- TNFAIP5
- Synonyms:
- TSG-14
- Chromosome:
- 3q25.32
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2016-10-05
Related products to: Human Pentraxin 3 ,PTX3 ELISA Kit
Related articles to: Human Pentraxin 3 ,PTX3 ELISA Kit
- Oocyte in vitro maturation (IVM) is a critical step for in vitro embryo production. Compared with the in vivo system, conventional IVM lacks paracrine support, resulting in reduced oocyte quality. Insulin-like peptide 3 (INSL3), an ovarian paracrine factor, has been shown to be involved in follicular development and oocyte maturation. However, whether INSL3 plays a role in sheep oocyte IVM remains unclear. This study investigated the effects of INSL3 on IVM of sheep oocytes and subsequent embryonic development. Our results showed that supplementation with 10 ng/mL INSL3 significantly increased the polar body extrusion (PBE) rate compared with the control group (77.71% vs. 52.74%, P < 0.05), reaching levels comparable to the EGF group. INSL3 also enhanced cumulus expansion and upregulated expansion-related genes (PTX3, HAS2, PTGS2, TNFαIP6). In addition, INSL3 reduced intracellular reactive oxygen species (ROS), improved mitochondrial function, and decreased early apoptosis, as indicated by a lower BAX/BCL-2 ratio. Following in vitro fertilization, oocytes matured with 10 ng/mL INSL3 exhibited higher cleavage (78.62% vs. 67.68%), morula (52.64% vs. 36.64%), and blastocyst rates (35.07% vs. 25.28%) than the control group (P < 0.05), with results comparable to EGF. In conclusion, INSL3 supplementation during IVM improves oocyte quality and developmental competence in sheep, potentially through regulation of cumulus cell function, oxidative status, and mitochondrial activity, and may serve as a promising factor in sheep embryo production technologies. - Source: PubMed
Publication date: 2026/07/14
Yang QiZhang Rui-FengJiang Zhao-YuSun DuiTang Rui-HaoZhang Xiao-YiLi Yi-TongLi Wen-YingLiu AoZhang Chun-LanJia Zhi-WenFeng Meng-LeiXue Fang-RuiSong Chun-RuZhang Xiao-JieLiang Cheng-Guang - Pre-Eclampsia (PE) is characterized by an imbalance of angiogenic and inflammatory modulators, with clinical symptoms emerging after 20 weeks of gestation. Fibroblast Growth Factor-2 (FGF2) promotes angiogenesis, whereas the acute-phase protein Pentraxin-3 (PTX3) binds FGF2 and blocks its interaction with receptors. In this cross-sectional case-control study, we compared plasma levels of PTX3 and FGF2 in normotensive (NT) and PE pregnancies and evaluated their ability to discriminate early-onset (<34 weeks) from late-onset PE (≥ 34 weeks). PTX3 and FGF2 concentrations were quantified by sandwich ELISA in non-pregnant women (NP, n = 19) and in third-trimester samples from NT women (n = 29) and women with PE (n = 30; early-onset PE = 11, late-onset PE = 19). Both PTX3 and FGF2 levels were significantly higher (p < 0.05) in PE compared to NT pregnancies. Moreover, their concentrations in early-onset PE were, on average, twice as high as those observed in NT and late-onset PE groups. Pearson's correlation analysis revealed a negative association between PTX3 and FGF2 levels in PE (r = -0.5160; p = 0.0167). In conclusion, PTX3 and FGF2 are both elevated in PE, particularly in early-onset cases. Their inverse correlation suggests a disrupted PTX3-FGF2 axis that may contribute to the angiogenic deficit found in PE. These findings suggest that PTX3 and FGF2 are candidate biomarkers associated with disease severity and may contribute to a molecular signature related to early-onset PE. Further prospective studies are required to establish their predictive value and clinical applicability. - Source: PubMed
Publication date: 2026/07/16
de Oliveira Flávia SantiagoPerucci Luiza OliveiraAlpoim Patrícia NessrallaSant'Ana Dusse Luci MariaDias Adriana Abalen Martins - Patients undergoing maintenance hemodialysis face annual mortality rates of 15-27%, with cardiovascular causes accounting for more than half of all deaths. Despite advances in dialytic technology, conventional prognostic models derived from the general population systematically underestimate risk in end-stage renal disease, failing to capture the complexity of uremic pathophysiology that drives this excess mortality: immune dysregulation, chronic inflammation, oxidative stress, vascular calcification, uremic cardiomyopathy, protein-energy wasting, and accelerated vascular aging. This narrative review synthesizes current evidence on biomarkers predicting all-cause and cardiovascular mortality in haemodialysis patients, spanning established markers (albumin, CRP, ferritin, hemoglobin, high-sensitivity troponins, and NT-proBNP) to an emerging frontier encompassing IL-6, PTX3, sST2, galectin-3, FGF-23, Klotho, and multi-omics signatures. We further examine composite neutrophil-derived indices, adipokines, and mineral metabolism markers as tools for pathway-specific risk interrogation. The evidence converges on a clear practical message: combination and dynamics outperform single, static measurements. Multi-biomarker models consistently outperform individual markers, and longitudinal trajectories carry prognostic information, with divergence between survivors and non-survivors detectable many months before death, that a single time-point value cannot replicate. Advances in artificial intelligence and multi-omics further support this shift toward dynamic, personalized risk stratification, though these approaches remain at an early, largely exploratory stage. Critically, clinical translation remains limited by the lack of dialysis-specific thresholds, poor standardization, and the absence of randomized evidence demonstrating that biomarker-guided strategies improve outcomes. Bridging this gap between prognostic insight and clinical application remains the central challenge of precision nephrology. - Source: PubMed
Publication date: 2026/07/15
Ramoni DavideScuricini AlessandroLiberale LucaCarbone FedericoMontecucco Fabrizio - Reproductive efficiency in swamp buffalo () remains constrained by the lack of molecular tools to identify fertile females before service. The aim of this study was to discover biologically grounded biomarkers of fertility. - Source: PubMed
Publication date: 2026/05/14
Yusuf MuhammadToleng Abdul LatiefHasrin HasrinBaharun AbdullahDiansyah Athhar ManabiKaiin Ekayanti MulyatiMasturi MasturiSahiruddin SahiruddinJannah Miftahul - The cardiovascular-kidney-metabolic (CKM) syndrome represents a continuum linking metabolic dysfunction, chronic kidney disease, and cardiovascular disease, in which chronic inflammation plays a central role. However, conventional inflammatory biomarkers may not fully capture local inflammatory processes involved in CKM stage transitions. Pentraxin 3 (PTX3), a long pentraxin produced locally at sites of inflammation, may provide complementary information, yet its association with CKM staging has not been systematically evaluated. In this cross-sectional study, circulating PTX3 levels were measured in 240 adults, including healthy controls (stage 0, S0; n = 60) and individuals with stage 2 (S2; n = 60), stage 3 (S3; n = 60), and stage 4 (S4; n = 60) CKM, classified according to the CKM staging framework. Associations between PTX3 and inflammatory, metabolic, cardiac, and renal biomarkers were assessed using Spearman correlation analysis. Multivariable logistic regression models were constructed within the CKM population (S2-S4) to distinguish early-stage CKM (S2) from mid-advanced-stage CKM (S3 + S4). Model discrimination and calibration were evaluated using receiver operating characteristic (ROC) analysis and the Hosmer-Lemeshow goodness-of-fit test. PTX3 levels were significantly elevated in early-stage CKM (S2) compared with healthy controls (p < 0.001) and showed further differentiation between S2 and S3 (p < 0.01). PTX3 showed moderate correlations with biomarkers reflecting inflammatory activation, metabolic dysregulation, myocardial injury, and renal dysfunction, including high-sensitivity C-reactive protein (hs-CRP; r = 0.361, p < 0.001), glycated hemoglobin (HbA1c; r = 0.434, p < 0.001), triglycerides (TG; r = 0.296, p < 0.001), and high-sensitivity cardiac troponin T (hs-cTnT; r = 0.411, p < 0.001), and was inversely correlated with estimated glomerular filtration rate (eGFR; r = -0.419, p < 0.001). In multivariable logistic regression models adjusting for demographic factors, metabolic indices, and cardiorenal biomarkers, PTX3 remained independently associated with classification into mid-advanced-stage CKM (S3 + S4 vs S2; odds ratio [OR] per unit increase = 1.05, 95% confidence interval [CI]: 1.03-1.08; p < 0.001), whereas hs-CRP and procalcitonin (PCT) showed no independent associations. Compared with the clinical base model, addition of PTX3 improved model discrimination, increasing the AUC from 0.833 to 0.892 (ΔAUC = 0.059; DeLong p = 0.008), without evidence of impaired calibration. Circulating PTX3 is cross-sectionally associated with CKM stage classification and demonstrates incremental discriminative value beyond demographic, metabolic, and cardiorenal variables, as well as conventional inflammatory markers, in distinguishing early-stage from mid-advanced-stage CKM. These findings suggest that PTX3 may reflect inflammatory processes not fully captured by systemic markers, supporting its potential role in CKM risk stratification. - Source: PubMed
Publication date: 2026/07/04
Xu ZhenYang ShuoTan YuanZhang QianWang HeTao JingjinLiu QiLi ZhongxinWang ChongCui Liyan