Rat COMP ELISA
- Known as:
- Rat COMP Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-51102
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Rat COMP ELISA
Related genes to: Rat COMP ELISA
- Gene:
- COMP NIH gene
- Name:
- cartilage oligomeric matrix protein
- Previous symbol:
- PSACH, EDM1, EPD1
- Synonyms:
- MED, THBS5
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-24
- Date modifiied:
- 2016-10-05
Related products to: Rat COMP ELISA
Related articles to: Rat COMP ELISA
- Frailty is a critical geriatric syndrome associated with disability and mortality, yet the associations and mechanisms between environmental metal co-exposure with frailty remain unclear. This cross-sectional study included 4484 adults aged ≥ 60 years from China. Metal concentrations were measured by inductively coupled plasma mass spectrometry (ICP-MS), and frailty was assessed using a frailty index (FI). Single-metal analyses used generalized linear models (GLMs). For multi-metal analyses, we applied machine-learning-based variable selection, followed by Bayesian kernel machine regression (BKMR) and quantile g-computation (qg-comp) model. Potential explanatory pathways involving inflammatory markers, as well as interactions with age, sex, and lifestyle, were also explored. Positive associations were observed for magnesium (Mg), molybdenum (Mo), and vanadium (V) with FI, whereas rubidium (Rb) showed an inverse association (P < 0.001). Significant effect modification by age, sex, and lifestyle was identified. Positive metal‑FI associations were stronger in older females, while the inverse Rb‑FI correlation was more evident in participants with unhealthy lifestyles (P for interaction < 0.05). Multi-metal models showed overall positive co-exposure effects on frailty, with Mo (positive) and Rb (negative) contributing the largest weights. In exploratory mediation analyses, the neutrophil-to-high-density lipoprotein ratio (NHR) accounted for 2.09% of the Rb-FI association and 1.81% of the Mo-FI association. The platelet-to-albumin ratio (PAR) accounted for 1.52% of the Mo-FI association and 5.30% of the Mg-FI association (P < 0.05). These findings suggest that metal co-exposure is positively associated with frailty, with inflammation as a potential explanatory pathway. Metal‑frailty associations vary by age, sex and lifestyle, with distinct patterns for different metals. Although longitudinal studies are needed to establish temporality and causal pathways, these findings identify high-risk subgroups for future investigation. - Source: PubMed
Publication date: 2026/07/12
Yu DongmeiWei YueZhou Yan-FengHe JunxiuBao YuLiang LunFeng DongyiLi YujinCheng HongCai HaiqingChen XingYang Xiaobo - Vascular calcification (VC), a common complication of chronic kidney disease (CKD), substantially contributes to cardiovascular morbidity. Although distinct forms of programmed cell death have been implicated in VC, the role of PANoptosis remains unclear. This study investigated the involvement of PANoptosis in CKD-associated VC and explored its regulatory mechanisms. Transcriptomic analysis of the GSE146638 dataset combined with machine learning algorithms was used to identify key PANoptosis-related genes associated with VC. CKD-associated VC was established in adenine/high-phosphate-fed mice and 5/6-nephrectomized rats fed a high-phosphate diet. In vitro, vascular smooth muscle cells (VSMCs) transfected with cartilage oligomeric matrix protein (COMP) small interfering RNA (siRNA) were subsequently stimulated with β-glycerophosphate (β-GP), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) to induce calcification-associated PANoptosis. Protein interactions and downstream signaling pathways were explored using co-immunoprecipitation (Co-IP). CKD-associated VC was characterized by concurrent activation of apoptosis, pyroptosis, and necroptosis in VSMCs, indicating PANoptosis activation in vivo and in vitro. Through an integrative bioinformatics strategy, COMP was identified as a hub gene exhibiting markedly reduced expression in calcified vessels. COMP deficiency aggravated VSMC calcification and enhanced PANoptotic signaling. Mechanistically, COMP directly interacted with angiotensin II type 1 receptor (AT1R) and restrained β-arrestin-2-dependent signaling, thereby limiting PANoptosome assembly. Conversely, COMP depletion promoted PANoptosis and calcification, whereas β-arrestin-2 inhibition largely reversed these effects. Collectively, these findings demonstrate that PANoptosis contributes to CKD-associated VC. COMP protects against VC by restraining AT1R-dependent β-arrestin-2 signaling, thereby suppressing PANoptosis, identifying the COMP-AT1R-β-arrestin-2 axis as a potential therapeutic target for cardiovascular complications in CKD. - Source: PubMed
Publication date: 2026/07/11
Ding WeiLiu JiaxinWang XiaoqianGuan ChenZhang NingxinXin YanluGu MinghaoSong ZhuoYang ChengyuBu QuandongWang LitingXu Yan - Environmental change causes physiological effects that can last years in long-lived species, yet there is a dearth of methods for quantifying such effects and their population consequences across the necessary decadal timescales. The Population Consequences of Multiple Stressors (PCoMS) framework is intended to link short-term responses to stressors to health, then to vital rates and from there to population-level effects. To date, implementations of the PCoMS framework have primarily focused on behavioral responses of marine mammals to stressors, enabled by data available from biologging devices. However, technological advances have facilitated the collection of physiological data, particularly hormones, through techniques such as extraction and quantification of hormones in respiratory vapor (blow), feces, vibrissae, blubber, skin, and baleen, amongst others. Using baleen specimens from bowhead whales (Balaena mysticetus) that were sampled for stable isotopes and adrenal, thyroid, and reproductive hormones, we demonstrate how these individual histories can be used within the PCoMS framework to begin modelling the linkages between ecological change, anthropogenic actions, individual physiology, and potential population impacts. - Source: PubMed
Publication date: 2026/07/11
New LeslieReed JoshuaJelincic JenniferBuck C LorenPirotta EnricoHunt Kathleen - Patient involvement in routine outcome monitoring (ROM) is vital for collaborative treatment and understanding differences between patient and clinician perspectives. This study assessed the agreement between patient and clinician ratings using the Instrument for Forensic Treatment Evaluation (IFTE) and its self-report version (IFTE-S) in high-security forensic psychiatric centers in Flanders, Belgium. Results showed concordance in domains like protective behavior and resocialization skills, but patients rated their problematic behavior as less severe than clinicians did. Item-level analyses revealed a more differentiated pattern, identifying more concordance on observable items and discordance in subjective or stigmatized behaviors. Discrepancies remained stable over the first 15 months of treatment and were not influenced by primary psychiatric diagnosis. The study underscores the importance of addressing such differences in treatment to enhance shared understanding, promote feedback-informed care, and support patient engagement. Further longitudinal research is needed to confirm these findings and improve ROM practices in forensic settings. - Source: PubMed
Publication date: 2026/07/11
Verschueren Sophievan den Ameele RubenJeandarme Inge - Neurodegenerative diseases (NDDs) exhibit considerable molecular heterogeneity, making it difficult to pinpoint robust, disease-specific biomarkers. Although proteomic studies have deepened our understanding of individual disorders, systematic cross-disease comparisons with cross-platform validation remain scarce, especially for rare conditions like spinal and bulbar muscular atrophy (SBMA). To address this gap, we conducted a comparative plasma proteomic analysis using liquid chromatography-tandem mass spectrometry (LC-MS/MS) in 264 participants across major neurodegenerative and related diagnostic groups, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), SBMA, and cognitively healthy controls. This unified framework allowed us to capture both disease-specific and shared protein signatures across neurodegenerative conditions. Candidate proteins were then validated in the UK Biobank (Olink Explore) and the Global Neurodegeneration Proteomics Consortium (SomaScan). Of 23 proteins assessed in the UK Biobank, four unique proteins (yielding six disease-protein associations) showed nominally significant and directionally concordant changes; of 20 proteins represented by 27 probes tested in the Global Neurodegeneration Proteomics Consortium, seven proteins reached nominal significance, all with full directional concordance across both cohorts. Notably, IGFBP2 was consistently elevated in AD and PD across independent datasets, pointing to shared metabolic dysregulation, while ADIPOQ showed parallel increases in the same conditions, reinforcing convergent shifts in energy metabolism. By contrast, CRTAC1 and COMP were selectively reduced in motor neuron diseases, suggesting disease-enriched alterations in extracellular matrix composition. Taken together, our findings provide a cross-disease, cross-platform framework for uncovering reproducible proteomic biomarkers and shed light on both overlapping and distinct molecular pathways in neurodegeneration. - Source: PubMed
Publication date: 2026/07/10
Choi YoungtaeLee ShinryeAshim JanbolatYu WookyungCho EunjiLee Ho-WonPark Jin-SungYoon Jong HyukKim Hyung-JunCheon Mookyung