Rat ICAM1 ELISA Kit
- Known as:
- Rat ICAM1 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- 55r-1589
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- Rat ICAM1 ELISA Kit
Related genes to: Rat ICAM1 ELISA Kit
- Gene:
- ICAM1 NIH gene
- Name:
- intercellular adhesion molecule 1
- Previous symbol:
- -
- Synonyms:
- BB2, CD54
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1989-04-24
- Date modifiied:
- 2016-01-15
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- Astrocytes are essential regulators of central nervous system (CNS) homeostasis, and their dysfunction can amplify neuroinflammation and neurodegeneration. HIV and methamphetamine (Meth) are known to downregulate β-catenin signaling and induce astrocyte senescence, but whether this senescent state is functionally pathogenic and contributes directly to neuroinflammatory processes remains unclear. Here, we investigated how senescent astrocytes respond across prototypical astrocytic functions.In vitro, human iPSC-derived astrocytes infected with HIV and/or exposed to Meth developed a senescence phenotype (increased p16) accompanied by reduced expression of the phagocytic receptor MEGF10 and impaired engulfment of apoptotic neurons. HIV/Meth exposure also shifted astrocyte secretomes toward proinflammatory profiles (IL-6, CCL2, CXCL1, and ICAM-1), and astrocyte-conditioned media decreased neuronal PSD95 and NFL and disrupted endothelial adherens and tight junction proteins (VE-cadherin, occludin, claudin-5), resulting in increased monocyte transmigration. Mechanistically, pharmacologic activation or lentiviral expression of active β-catenin protected astrocytes from senescence, preserving MEGF10 expression and phagocytic capacity under HIV/Meth exposure, while MEGF10 overexpression independently restored phagocytosis. In a human-mouse chimera model (NSG mice xenotransplanted with human iPSC-derived astrocytes), HIV infection and/or Meth administration increased p16 and reduced MEGF10 expression in engrafted human astrocytes, recapitulating in vitro findings.Together, these studies demonstrate that HIV and Meth suppress β-catenin signaling to drive a functionally disruptive astrocyte senescence program linked to impaired MEGF10-dependent phagocytosis, diminished neuronal support, and compromised blood-brain barrier integrity. Restoring β-catenin signaling and preserving MEGF10 function emerge as rational strategies to prevent astrocyte-driven neuroinflammation and neuropathogenesis in HIV/Meth co-morbidity. - Source: PubMed
Publication date: 2026/06/15
Jana ArundhatiNarasipura Srinivas DSzczerkowski JamesMamede João IAl-Harthi Lena - Commonly measured cardiometabolic biomarkers have not been systematically characterized across the long-term continuum of the postprandial and postabsorptive phases. The aim of the present study was to evaluate how the exact time since last meal impacts test results for lipoprotein particles and inflammatory biomarkers. - Source: PubMed
Publication date: 2026/06/03
Jensen Silje-MarieHolven Kirsten BUlven Stine MAnfinsen Åslaug MatreDierkes JuttaLysne VegardChristensen Jacob J - Osteoarticular tuberculosis (OATB) accounts for 10-15% of extrapulmonary TB cases and causes progressive bone destruction, neurological compromise, and persistent disability. No validated host-based framework currently identifies patients at high risk of complicated disease course at baseline, and the integrated role of cellular, cytokine, endothelial, and fibrinolytic axes in OATB has not been systematically characterized. - Source: PubMed
Publication date: 2026/05/29
Bozorov ShuhratKhamdamov BakhtiyorUsmanov IsomiddinFaizullaeva NigoraShodiyeva Musharraf - Doxorubicin (DOX) is a widely used chemotherapeutic agent, but its severe cardiotoxicity limits its clinical application. Many biological processes and molecular mechanisms have been implicated in DOX-induced cardiotoxicity. However, the mechanisms underlying DOX-induced cardiotoxicity remain largely unknown. This study aimed to identify key regulatory genes and select targeted drugs for DOX-induced cardiotoxicity. - Source: PubMed
Publication date: 2026/06/14
Mao CongZhang ZhuoXiao DabaoHe JunruLeng XuZhao WenzhenZeng MengyaZhong KeyanChen Yuewu - Millions of U.S. troops and supporting personnel have been deployed to military bases in the Middle East. Essentially all personnel on military bases were exposed to the combustion emissions generated by open pit waste burning. Chronic multisymptom illness (CMI) is a term advanced to characterize the complex health effects of inhalation exposures to military burn pits (BP). Because of the diversity of geography, environmental conditions, and deployment operations, it is very challenging to estimate the number of Veterans affected by CMI, but it has been reported to be in the range of ~ 40-60%. Despite this overwhelming number of patients, the underlying causes of CMI remain to be identified. The purpose of this study was to replicate BP combustion and deliver these representative emissions to a whole-body inhalation exposure chamber with Sprague Dawley rats. We hypothesized that because the microcirculation is a critical component of health and disease, that normal microvascular function may be disrupted after BP inhalation exposures. A surrogate BP emission generator was used to combust mixtures of wood, rubber, plastic and jet fuel. Resultant emissions were complex mixtures of volatile organic chemicals, polyaromatic hydrocarbons, fine and ultrafine particles. The particle aerodynamic count median diameter was 113 nm with a geometric standard deviation of 2.21. The particle mobility diameter was 78.1 nm with a geometric standard deviation of 1.69. The aerosol mass-size size distribution had a mass median aerodynamic diameter of 288 nm with a geometric standard deviation of 1.72 nm. Rats were exposed for ~ 4 h/d at BP emission concentrations of 15.4 ± 1.6 mg/m, for 2, 3, or 6 days. Twenty-four hours later, the spinotrapezius muscle was prepared for intravital microscopy. Tissues were also harvested from different rats in these groups for thorough mechanistic analyses. After 3-6 days of exposure, endothelium-dependent arteriolar dilation was abolished. Adrenergic vasoconstrictor sensitivity was augmented by as much as 50% in the BP exposure groups. Bronchoalveolar lavage revealed robust pulmonary inflammation and cellular infiltration. High-performance liquid chromatography with plasma samples demonstrated significant increases (> 50%) in circulating xanthine oxidase, a known driver of oxidative stress, disruptor of vascular nitric oxide, and thus mediator of endothelial dysfunction. After 3 days of BP exposure, RNA sequencing tissue analyses revealed transcriptional markers of lung inflammation as well as an altered transcriptional immune response in both the lung and spleen. BP inhalation exposure also led to elevated RNA transcripts for the vascular growth factor Vegfa and the immune cell trafficking factor Icam1 in brain hippocampal tissue. These initial microvascular observations demonstrate disruption of typical function and mechanisms that may link pulmonary insult with diverse systemic syndromes characteristic with CMI in Veterans. - Source: PubMed
Publication date: 2026/06/12
Nguyen VanRanpara AnandGoldsmith William TBatchelor Thomas PHoyer JacobLeonard Howard DRazazan AtefehLewis Sara EKrafcheck JacobBurns RobertNelson Randy JSharma PallaviWalton James CBeru NeeharikaBain WilliamCruz Charles DelaWilson MarkKelley Eric EHussain SalikNurkiewicz Timothy R