AChE antibody
- Known as:
- AChE (anti-)
- Catalog number:
- 10-1855
- Product Quantity:
- 200 ul
- Category:
- -
- Supplier:
- Fitzgerald
- 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
- High‑frequency spinal cord stimulation (HF‑SCS) is an effective method for treating neuropathic pain (NP), but its specific mechanism of action in treating spinal cord injury (SCI) remains unclear. The present study aimed to explore the therapeutic effect of early HF‑SCS in a rat model of SCI and its potential molecular mechanism. A Sprague‑Dawley rat model of T10 spinal cord contusion was established and stimulation electrodes were implanted epidurally, which was followed by HF‑SCS treatment (40% movement threshold at a frequency of 10 kHz). Through behavioral assessments, histopathological analysis and immunofluorescence staining, the present study demonstrated that HF‑SCS markedly alleviated post‑SCI NP, facilitated functional recovery and accelerated axonal regeneration and myelin repair. Mechanistic studies employing RNA sequencing, western blotting and immunofluorescence further revealed that HF‑SCS exerted its neuroprotective effect by downregulating the reactive oxygen species/p38 MAPK/NF‑κB signaling pathway to reduce microglial activation and decrease the release of proinflammatory factors; simultaneously, it inhibited the activation of the C‑X‑C motif chemokine ligand 10/C‑X‑C motif chemokine receptor 3 axis to alleviate central sensitization. These findings suggest that early HF‑SCS intervention can improve the functional prognosis after SCI by suppressing neuroinflammation and reducing central sensitization, thereby providing a theoretical basis for the treatment of SCI with HF‑SCS. - Source: PubMed
Publication date: 2026/08/14
Su SitongLiu TaoLei HonghuiYu YangMa CaizhiWang XinglangChen HaoyuanHuang ZebinCheng MeilingQian TongtongWang Fangyong - C-fibre nociceptors display low-level spontaneous firing in the context of tissue injury. Microneurography studies have demonstrated that such low frequency firing can dynamically regulate the activity-dependent slowing (ADS) or temporal pain signal relay of C-fibre nociceptors, thus providing a memory trace of prior activity levels. Here we explore whether low-frequency 'manipulation' can alter C-fibre ADS, in response to subsequent short higher frequency stimulus trains, in compound action potential (CAP) 'population' recordings from isolated rodent dorsal roots of both sexes. In CAP recordings from rat dorsal roots, manipulation (1 Hz, 2 min) increased or decreased ADS in response to short stimulus trains (10 Hz, ×40). This dynamic memory was not sex-dependent. The manipulation-induced change in C-fibre ADS correlated with the level of C-fibre ADS pre-manipulation. In CAP recordings from mouse dorsal roots, manipulation (1 Hz, 1 min) increased C-fibre ADS in response to short stimulus trains (2 Hz, ×40). This dynamic memory was not sex-dependent, despite a more pronounced ADS in males. The impact of dynamic memory on spinal processing was explored through patch-clamp recording of noxious heat responsive neurons with monosynaptic C-fibre inputs in spinal slices. Manipulation (1 Hz, 1 min) increased monosynaptic C-fibre ADS in response to stimulus trains (2 Hz, ×16). This was independent of sex and was associated with synaptic failures. Current-clamp recordings demonstrated that this monosynaptic C-fibre dynamic memory altered action potential firing in noxious heat responsive spinal neurons. In summary, dynamic memory in rodent C-fibres, is not regulated by sex and is communicated to and can alter activity in spinal pain circuits. KEY POINTS: Human studies have previously demonstrated that the peripheral nerve C-fibres, which detect potential tissue-damaging stimuli, are able to retain a memory of prior activity levels that influences their subsequent relay of 'warning' signals. This study demonstrates that this 'memory' is also present in rat and mouse tissue damage-detecting peripheral nerve C-fibres and that this memory is not sex-dependent. We demonstrate that this 'memory' is evident in the C-fibres that directly activate spinal cord neurons responsive to potential tissue damaging heat stimuli and can dynamically regulate their activity. This suggests that ongoing firing of these tissue damage-detecting C-fibres in the context of injury can dynamically regulate how the spinal cord processes pain. - Source: PubMed
Publication date: 2026/08/14
Velichkova Atanaska NTorsney Carole - - Source: PubMed
Publication date: 2026/08/14
Gallego-Peñalver Francisco JoséRomero-de-la-Higuera Silvia BeatrizGómez-Trullén Eva María - Arthritis, characterised by inflammation, pain, and joint stiffness, is emerging as a significant health concern in ageing populations worldwide. While many studies have examined the effects of outdoor environmental risk factors on arthritis, fewer have investigated the effects of residential ecological factors. - Source: PubMed
Publication date: 2026/08/14
Jia XiangbinXiong XinJiang ZichaoYang Haoze - People with chronic illnesses are at elevated risk of suicide. Prior research has focused on risk with specific diagnoses and/or comparisons with living controls; the profiles of medically ill people who die by suicide remain largely unknown. This study aims to identify characteristics and subgroups among suicide decedents with medical illnesses. - Source: PubMed
Publication date: 2026/08/14
Tahir UmairSanchez Morales DanielChan Prudence Po MingSchaffer AyalDmetrichuk Jennifer MMitchell Rachel H BSteinberg RosalieFiksenbaum LisaHatcher SimonSinyor Mark