ACHE Antibody
- Known as:
- ACHE Antibody
- Catalog number:
- AF1017a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ACHE Antibody
Ask about this productRelated genes to: ACHE Antibody
- Gene:
- ACHE NIH gene
- Name:
- acetylcholinesterase (Cartwright blood group)
- Previous symbol:
- YT
- Synonyms:
- -
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-02
- Date modifiied:
- 2019-04-23
Related products to: ACHE Antibody
Related articles to: ACHE Antibody
- Chronic post-surgical pain (CPSP) after total knee arthroplasty (TKA) remains a significant clinical challenge. This study aimed to investigate the association between concurrent lumbar degenerative disease (LDD) and CPSP after TKA for knee osteoarthritis (KOA). - Source: PubMed
Publication date: 2026/05/19
Zhang XichenZhu XinfeiRao DunliangSha LeiHao LiangJiang ShouhaiZhang ZiyangZhang Chuankai - Sex disparities in young adults aged 20-40 with acute coronary syndrome (ACS) are rarely known in China. We aimed to explore these sex-based differences, using a nationwide, population-based database. - Source: PubMed
Publication date: 2026/05/19
Nawsherwan Hu YangChen XiaohanBin WangLe ZhangSang MangmangJiyi LinHuang ShuangjieLi SichengXinli LiHuo YongGe JunboZhuang WeifenYan Wang - Chronic pelvic pain syndrome (CPPS) is a multifactorial condition with unclear pathophysiology and a lack of objective biomarkers for assessing disease activity. To investigate its molecular basis, we generated patient-derived prostate organoids from biopsy tissues of nine patients with CPPS, categorized as mild, moderate, or severe according to the NIH CP Symptom Index scores. The organoids were treated with Eviprostat or tadalafil, followed by transcriptomic profiling, quantitative RT-PCR validation, and immunohistochemical analysis of candidate genes. Among the differentially expressed genes, monoamine oxidase A (MAOA) and calbindin-D28K (CALB1) were consistently associateds with symptom severity. Expression of both genes decreased in organoids and prostate tissues as symptom severity increased, whereas serum MAOA levels were significantly elevated in patients with severe CPPS. These findings suggest that MAOA and CALB1 reflect molecular alterations linked to symptom intensity and may serve as potential biomarkers for CPPS. Furthermore, patient-derived prostate organoids offer a valuable experimental platform for elucidating disease mechanisms and evaluating therapeutic interventions in prostatitis-related disorders. - Source: PubMed
Publication date: 2026/05/19
Kitano HiroyukiSekino YoheiYukihiro KazumaOkazaki MaiNomura NaofumiHatayama TomoyaShikuma HiroyukiNakano YoshinoriTasaka ShinsakuIwane KyosukeTasaka RyoKohada YukiMiyamoto SyunsukeNaito MikiKobatake KoheiMorihara NagisaHinata Nobuyuki - Attention distraction mitigates pain, yet its neural basis remains elusive. We established cricket hunting as an attention-demanding paradigm that alleviates acute and chronic pain in male mice. Activity tagging revealed that cricket hunting activated a subset of glutamatergic neurons in the superior colliculus (SC). Selective stimulation of these hunting-activated neurons alleviated chronic hyperalgesia, primarily mediated by their projections to the zona incerta (ZI). Notably, repeated engagement, either through the hunting paradigm or by repeatedly activating hunting-activated SC-ZI projections, induced sustained analgesia (lasting at least 6 hours), linked to potentiated glutamatergic inputs to ZI GABAergic neurons. Furthermore, SC-ZI projections originating from SC neurons expressing tachykinin precursor 1 (Tac1) selectively elevated neuropathic pain thresholds via substance P release and neurokinin 1 (NK1) receptor-dependent excitatory synaptic transmission onto ZI GABAergic neurons. Together, we show that a specific SC-ZI circuit drives attention-induced analgesia, highlighting the SC-ZI pathway as a therapeutic target for chronic pain. - Source: PubMed
Publication date: 2026/05/19
Zhang XueLiu Xiao-JuanYin CuiZhou QiangqiangZhang JiaqiWang LiweiCao Jun-LiXiao ChengZhou Chunyi - Antibiotic shortages are increasing worldwide. Their impact on individual health and bacterial ecology is unknown, but it could be significant, and there is a lack of epidemiological evidence. Here, we assess the impact of beta-lactam shortage management on pneumococcal resistance and the incidence of invasive pneumococcal disease (IPD). We developed a mechanistic model of S. pneumoniae paediatric colonization and transmission, accounting for beta-lactam and macrolide exposure. We explored the effects of four antibiotic allocation strategies following a one-year beta-lactam shortage: lowering consumption frequency, shortening treatment duration, reducing the daily dose, or substituting beta-lactams with macrolides. These strategies were analyzed in different European pharmaco-epidemiological settings. We found heterogeneous impacts of allocation strategies, amplified at high shortage intensity. The adverse outcomes of shortages increased with baseline antibiotic consumption and the main determinants of the optimal strategy were the initial prevalence of resistance. Reducing beta-lactam frequency most effectively limited resistance, lowering penicillin-non-susceptible and multidrug-resistant strains by up to 21% in Spain during a 50% shortage. The optimal strategy for minimizing IPD incidence was country-dependent: either lowering the daily dose or beta-lactam-to-macrolide substitution. However, the latter significantly increased macrolide resistance, reaching up to 26.2% in Denmark, for a 50% shortage. Our results show that public health priorities and country-specific pharmaco-epidemiological factors should guide antibiotic management strategies during antimicrobial shortages. - Source: PubMed
Publication date: 2026/05/19
Maurin AurélieDelory TristanLe Bel JosselinGuillemot DidierSofonea Mircea TTemime LauraOpatowski Lulla