ACHE
- Known as:
- ACHE
- Catalog number:
- 001007A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACHE
Ask about this productRelated genes to: ACHE
- 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
Related articles to: ACHE
- A 9-year-old boy initially presented with a closed metaphyseal transverse fracture of the distal right femur following a fall from a trampoline. Due to the adequate trauma and lack of initial radiological indications for an underlying pathological bone lesion, the fracture was primarily treated with antegrade elastic stable intramedullary nailing (ESIN). Postoperatively, the patient developed persistent pain, progressive soft tissue swelling and highly atypical callus formation accompanied by osteolytic lesions. Following referral to our pediatric trauma center, the radiological diagnostics of the surrounding region raised the suspicion of a telangiectatic osteosarcoma, further complicated by iatrogenic tumor cell seeding along the intramedullary path of the ESIN in the sense of a skip lesion. The diagnosis was confirmed by reference histopathology. Following neoadjuvant chemotherapy according to the EURAMOS/COSS protocol, the iatrogenic tumor cell dissemination necessitated a total femoral en bloc resection and reconstruction using a modular total endoprosthesis. - Source: PubMed
Publication date: 2026/09/11
Jung FelixVoith Katrin LuiseFerandez Francisco - Percutaneous spinal cord epidural stimulation (pSCES) is an effective modality for managing pain. However, the use of pSCES in restoration of motor control after SCI is still under research exploration. Today, the effects of postural changes on pSCES-motor control are still controversial. - Source: PubMed
Publication date: 2026/09/11
Hessavi SohaleSchroeder WillAlazzam AhmadUzair Rehman MuhammadTrainer RobertGorgey Ashraf S - - Source: PubMed
Publication date: 2026/09/11
Lehmann ChristianConnes Philippe - Preeclampsia (PE) is a leading cause of maternal and neonatal morbidity, with immune dysregulation at the maternal-fetal interface central to its pathogenesis. The highly polymorphic HLA region mediates maternal immune tolerance of the semi-allogeneic fetus, yet the contribution of HLA diversity to PE risk remains poorly defined. Whether the HLA heterozygote advantage observed in other immune disorders is relevant to PE has not been systematically evaluated. Using data from the multi-ancestry TOPMed Boston-Colombia Collaborative for Adverse Pregnancy Outcomes (n = 12,790; 4770 PE, 8020 controls; 10,808 maternal, 1982 fetal, including 1848 pairs), we evaluated associations between heterozygosity across eight classical HLA loci and PE and four sub-phenotypes, adjusting for genetic ancestry. HLA heterozygosity was common across most loci (> 80%). No individual maternal HLA locus was associated with overall PE; however, heterozygosity across Class I loci showed a protective effect in preterm PE (OR = 0.81, 95% CI: 0.68-0.97), with a similar pattern for HLA-A heterozygosity (OR = 0.78, 95% CI: 0.64-0.97). In contrast, fetal heterozygosity at HLA-DQB1 was nominally associated with increased risk of PE (OR = 1.36, 95% CI: 1.03-1.80) and preterm PE (OR = 1.73, 95% CI: 1.13-2.74). No individual maternal or fetal HLA alleles were associated with PE. Maternal-fetal mismatch analysis demonstrated locus-specific associations with preterm PE, including increased risk with HLA-DQA1 mismatch and reduced risk with HLA-C mismatch. These findings highlight distinct maternal and fetal immunogenetic contributions to PE risk and underscore the importance of considering HLA diversity-rather than individual alleles alone-in studies of PE aetiology. - Source: PubMed
Cao ChangMaher MatthewHu JieKeating Brendan JBurwick Richard MKarumanchi S AnanthMaxwell G LarryPowe Camille EMcElrath Thomas FCantonwine David ESerrano NormaColmenares ClaudiaCasas Juan PSaxena RichaGray Kathryn J - The cold pressor test (CPT) is a painful test used to assess cardiovascular and cerebrovascular reactivity. Past studies examined between-visit reproducibility of cardiovascular reactivity during the CPT but not cerebrovascular reactivity. Therefore, we performed a retrospective analysis to test the hypothesis that cerebrovascular responses during the CPT would not differ and would have moderate relative agreement between visits. Fifty young adults free from overt disease, not taking pain-modifying medications, completed two trials ≥48 hours apart. We measured middle cerebral artery blood velocity (MCAv) via transcranial Doppler ultrasound, beat-to-beat blood pressure (BP) via photoplethysmography, and end-tidal CO2 (ET-CO2) via capnography during a five-minute baseline and two-minute CPT. We calculated reactivity as the change (Δ) from baseline to the first and second minute of the CPT. There were no between-visit differences in baseline mean BP, mean MCAv, or ET-CO2 (Ps≥0.24). There were no between-visit differences for Δmean MCAv (Ps>0.75) or Δmean BP (Ps>0.07). Relative agreement between visits was moderate for Δmean MCAv (intraclass correlation coefficient (ICC): Δmin-1=0.68, Δmin-2=0.72) and moderate/good Δmean BP (ICC: Δmin-1=0.65, Δmin-2=0.80). Our data suggest that Δmean MCAv to the CPT isnot different between visits while the relative agreement is similar to BP reactivity. Further, relative agreement was higher during minute two than minute one for key variables. These data extend our knowledge of the reproducibility of CPT reactivity. These findings will inform future research aimed at comparing cardiovascular and cerebrovascular reactivity as health markers between groups. - Source: PubMed
Publication date: 2026/09/11
Vondrasek Joseph DHoch Jonathan WHuang MuBelval Luke NJarrard Caitlin PCrandall Craig GWatso Joseph C