ACHE polyclonal antibody
- Known as:
- ACHE pab (anti-)
- Catalog number:
- PAB6747
- Product Quantity:
- 100 ug
- Category:
- -
- Supplier:
- Abno
- Gene target:
- ACHE polyclonal antibody
Related genes to: ACHE polyclonal 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 polyclonal antibody
Related articles to: ACHE polyclonal antibody
- To compare the efficacy and safety of computed tomography-guided percutaneous thoracic sympathetic radiofrequency thermocoagulation (RFT) targeting the upper versus lateral margin of the fourth rib head for severe primary palmar hyperhidrosis (PPH). - Source: PubMed
Publication date: 2026/08/26
Wu YueXing QianqianHuang HuaTian SumingHe FeifangWang YongjieChen Gang - To systematically assess the prevalence of sexual dysfunction among patients suffering from endometriosis. - Source: PubMed
Zhang YujieLiu ZiyueHan QianWei ZhijieJiang YantingCui LiweiWang MengLi Hui - Central post-stroke pain (CPSP) remains difficult to treat due to limited understanding of its underlying mechanisms. Emerging evidence implicates microglia-driven neuroinflammation in CPSP development. Mitogen-activated protein kinase phosphatase-1 (MKP-1) negatively regulates MAPK signaling and modulates inflammation in neurological disorders, yet its role in CPSP is unclear. Using a mouse model of thalamic hemorrhage, we examined MKP-1 expression and function in CPSP. Behavioral testing assessed pain hypersensitivity and affective disturbances. Immunofluorescence and western blot evaluated MKP-1 expression, microglial activation, and inflammatory signaling in the thalamus. Pharmacological MKP-1 inhibition was employed to assess functional contributions. Thalamic hemorrhage induced persistent mechanical hypersensitivity and anxiety-like behaviors, accompanied by pronounced microglial activation in the peri-lesional thalamus. MKP-1 expression increased significantly after stroke and localized primarily to microglia. MKP-1 inhibition exacerbated pain behaviors and enhanced microglial activation, with corresponding increases in pro-inflammatory mediators and p38 MAPK phosphorylation. These findings suggest that MKP-1 may function as an endogenous negative regulator of microglia-mediated neuroinflammation following thalamic hemorrhage. Pharmacological modulation of MKP-1 signaling warrants further investigation as a potential approach for CPSP. - Source: PubMed
Publication date: 2026/08/26
Fei YongMeng XiChen MengjiaoFan HanruiXu PingYu MingqingZhang HaonanZhang YinanBu FanXu LongshengLi Xiang-Yao - Spinal adhesive arachnoiditis (SAA) is a severe and potentially disabling complication of neurocysticercosis (NCC), but it remains poorly characterised. We conducted a retrospective descriptive case series including patients evaluated between 2000 and 2025 at a tertiary care hospital in Mexico City. Inclusion criteria includeda definitive NCC diagnosis, SAAconfirmedby magnetic resonance imaging(MRI), complete clinical and radiological data, and a minimum follow-up of 12 months. Eight patients were included. All presented the basal subarachnoid form of NCC with parasites located in the pontobulbar cisterns. At NCC diagnosis, all patients had intracranial hypertension and markedly abnormal cerebrospinal fluid. SAA was diagnosed concomitantly with NCC in three patients, while in the remaining five,diagnosis was established between 12 and 108 months later. At SAA diagnosis, all patients presented lumbar pain, motor deficits were observed in five, and sensory deficits in six. MRI confirmed lumbosacral SAA in all patients. Despite antiparasitic and symptomatic treatment, functional outcomes were generally poor: mean Karnofsky Performance Scale score decreased from 81.25 at SAA diagnosis to 71.25 after a mean follow-up of 128 months, with four patients showing progressive functional decline. In conclusion, SAA is a rare but disabling and likely underdiagnosed complication of extraparenchymal-NCC, characterised by delayed onset, persistent inflammation, and progressive functional decline despite treatment. The large volume of the lumbar intradural subarachnoid space may explain the frequent asymptomatic period preceding SAA diagnosis. Early recognition through systematic spinal MRI in patients with pontobulbar cistern NCC may represent a critical window for intervention. - Source: PubMed
Publication date: 2026/08/26
Rosales-Mayorga DylanCandelas-Juarez AlanBaez-Osorio DianaMegchun-Vázquez XimenaCarrillo Mezo RogerFleury Agnès - Lytic cell death pathways drive hepatic ischemia-reperfusion injury (IRI). The transmembrane protein ninjurin-1 (NINJ1) aggregates in the plasma membrane to permeabilize the cell during multiple cell death pathways implicated in hepatic IRI. We hypothesized that NINJ1 mediates liver IRI and that its inhibition would mitigate injury. We found that NINJ1 is highly expressed in human liver tissue and that its up-regulation and activation correlate with early allograft dysfunction in liver transplant patients. Using a segmental hepatic IRI model in mice and rats, genetic deletion or pharmacologic inhibition diminished acute injury. Mice with hepatocyte- or macrophage-specific knockout had reduced hepatocellular injury following IRI, suggesting that NINJ1 within both populations contributes to the resulting liver injury. Mechanistically, we found that hepatocytes and Kupffer cells are susceptible to hypoxia-induced NINJ1-mediated plasma membrane rupture, which can be pharmacologically prevented. We therefore position NINJ1 as a potential new therapeutic target to limit hepatic IRI, with important implications for liver transplantation. - Source: PubMed
Publication date: 2026/08/26
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