AGER Pre-design Chimera RNAi
- Known as:
- AGER Pre-design Chimera RNAi
- Catalog number:
- H00000177-R02
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- AGER Pre-design Chimera RNAi
Related genes to: AGER Pre-design Chimera RNAi
- Gene:
- AGER NIH gene
- Name:
- advanced glycosylation end-product specific receptor
- Previous symbol:
- -
- Synonyms:
- RAGE, SCARJ1
- Chromosome:
- 6p21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1994-10-17
- Date modifiied:
- 2016-10-05
Related products to: AGER Pre-design Chimera RNAi
Related articles to: AGER Pre-design Chimera RNAi
- Speech Sound Disorder (SSD) reduces speech intelligibility, affecting a child's ability to make themselves understood. If SSD is not resolved in the early years it will negatively impact children's education and general well-being. Effective and efficient speech and language therapy is known to resolve SSD and mitigate these risks. Intervention for SSD is often provided in inadequate dosages to be effective or efficient. Quantitative dosage is an overarching term for the different aspects of intensity of intervention which may impact outcomes. Existing literature on quantitative dosage indicates that more intensive therapy approaches for SSD appear to be more effective and efficient than less intensive delivery. A scoping review of current research in this area will serve to clarify evidence-based knowledge and understanding about quantitative dosage, how it works, and how different components potentially interact to contribute to outcomes for children with phonological impairment (PI) (a sub-type of SSD), informing future service developments and research. - Source: PubMed
Titterington JillRudd SarahStringer HelenPagnamenta EmmaRobinson TomosHarding Sam - Abdominal aortic aneurysm (AAA) is a life-threatening vascular condition driven by interactions between genetic regulation and environmental influences, yet reliable biomarkers are lacking. Although individual programmed cell death (PCD) pathways have been implicated in AAA, their integrated dysregulation, particularly in environmental and toxicological contexts, remains unclear. Here, we conducted an integrative multi-omics analysis combining bulk transcriptomic datasets, single-cell RNA sequencing cohorts, and independently sequenced clinical samples to systematically characterize PCD dysregulation in AAA. Our results revealed widespread activation of cell-death and inflammatory signaling, cell type-specific enrichment of multiple PCD modalities, and two distinct PCD-related molecular subtypes with distinct immune infiltration patterns. Using machine learning approaches, we identified four core PCD genes (AGER, CX3CR1, LEP, and SATB1) and incorporated them into an artificial neural network-based AAA risk model, which demonstrated robust diagnostic performance across multiple cohorts and revealed potential therapeutic relevance. Chemical‑gene interaction analysis further prioritized three environmental compounds (triphenyl phosphate, sodium arsenite, and propylthiouracil) as high‑risk exposures linked to these PCD core genes. Notably, LEP consistently emerged as a key gene across predictive modeling and subsequent experimental validation. It exhibited marked upregulation in AAA tissues, predominant localization to inflammatory cells, and significantly elevated circulating levels in both an independent clinical cohort and the UK Biobank population. Together, this work supports PCD dysregulation as a central feature of AAA and positions LEP as a potential candidate biomarker linking molecular alterations, environmental exposures, and disease risk. Our findings provide new insights into biomarker-guided evaluation and implicate environmental toxicants in AAA progression via PCD-centric networks. - Source: PubMed
Publication date: 2026/09/29
Jing JingjingLin TianyiWang LeiDong NannanChen ZhuoLi ZhuoyuanMa ChunyanLi Tan - Anaemia is a common modifiable risk factor in surgery, yet how it is recognized and managed in women across different surgical pathways is unknown. This study aimed to evaluate anaemia prevalence in women and its management across surgical pathways and life stages, examine associations with 30-day outcomes, and estimate the potential benefit of anaemia correction. - Source: PubMed
Kamarajah Sivesh KathirHapangama Dharani - Epigenetic mechanisms underlying susceptibility to abdominal aortic aneurysm (AAA) remain poorly understood. Identifying causal DNA methylation markers for AAA can elucidate the regulatory processes that drive aneurysm formation and accelerate translational applications. We leveraged the Veterans Affairs (VA) Million Veteran Program to identify methylation biomarkers and delineate underlying pathways. - Source: PubMed
Publication date: 2026/09/29
Yuan ShuaiClark Michael GShakt GabrielleLevin Michael GHartmann KatherineJudy RenaeDinatale TiaVoorhees AmyLynch Julie APyarajan SaijuLevy DanielJoehanes RobyChang Kyong-MiBrody Jennifer ABis Joshua CPsaty Bruce MVoight Benjamin FTsao Philip SJones Gregory TDamrauer Scott M - Myocardial ischemia-reperfusion (MI/R)-induced lung injury is a major pulmonary complication after cardiac surgery. We aimed to verify this phenomenon in rats and to investigate whether electroacupuncture (EA) pretreatment at bilateral Feishu (BL13) and Zusanli (ST36) acupoints (once daily for 3 days) exerts protective effects. In an MI/R-induced lung injury model in SD rats, EA pretreatment significantly improved lung function and reduced pathological damage (p < 0.05 and p < 0.01, respectively). It also attenuated the pulmonary inflammatory response and decreased the expression of high mobility group box 1 (HMGB1) and receptor for advanced glycation end products (RAGE) (p < 0.05 or p < 0.01). Intratracheal administration of recombinant HMGB1 (rHMGB1) to upregulate lung HMGB1/RAGE signaling impaired the pulmonary protective effect of EA (p < 0.05, p < 0.01). Together, these findings demonstrate that EA pretreatment mitigates MI/R-induced lung injury by inhibiting HMGB1/RAGE signaling. - Source: PubMed
Xie ChenlongZhang JiaojiaoZhang YujiaoChi HaoYong YueSong Jiangang