Ask about this productRelated genes to: NONO antibody
- Gene:
- NONO NIH gene
- Name:
- non-POU domain containing octamer binding
- Previous symbol:
- -
- Synonyms:
- NRB54, NMT55, P54NRB, P54, PPP1R114
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-02-06
- Date modifiied:
- 2017-05-12
Related products to: NONO antibody
Related articles to: NONO antibody
- To explore the clinical phenotypes and genetic etiology of a child with MRXS34 syndrome due to a variant of NONO gene. - Source: PubMed
Chen XintongXue HuiqinYue HaoMa TianjiaoGao JingboSun XiayuGuo RongLu HongyongWu Jianrui - Nerinetide is a neuroprotective agent recently evaluated in the ESCAPE-NEXT (Efficacy and Safety of Nerinetide in Participants With Acute Ischemic Stroke Undergoing Endovascular Thrombectomy Excluding Thrombolysis) trial (NCT04462536), which was terminated after failing to meet its Day 90 primary end point; however, by that time, Year 1 follow-up outcomes were already available for 513 participants. - Source: PubMed
Publication date: 2026/06/23
Adams CoreyHeard KathyKohli YatikaVatanpour ShabnamBerrouschot JorgBuck BrianDemchuk AndrewDippel DiederikDorn FranziskaField ThaliaMuto MarioPham MirkoRyckborst Karla JSwartz Richard Hvan Adel Brian AMenon BijoyGoyal MayankHill Michael DTymianski Michael - - Source: PubMed
Publication date: 2026/06/22
Hill Michael DNguyen Thanh NCampbell Bruce C VBroderick Joseph P - Plasmodium falciparum malaria remains a major cause of morbidity and mortality in endemic regions, with outcomes influenced by host genetic factors. The ABO blood group system has been linked to clinical severity, though findings differ regarding blood groups and severe malaria susceptibility. This analysis aims to synthesise evidence on ABO blood group's role in severe P. falciparum malaria (SM) through meta-analysis and trial sequential analysis. - Source: PubMed
Publication date: 2026/06/19
Ranjan ShovitDubey MadhaviSharma ShardaBehera Sweety RaniMeher SanjayaPanda Aditya K - Autoimmune hemolytic anemia (AIHA) is an uncommon but recognized complication of intravenous immunoglobulin (IVIG) therapy in Kawasaki disease (KD). The mechanism is thought to involve passive transfer of donor isohemagglutinins that bind to recipient red blood cell (RBC) antigens, causing immune-mediated hemolysis. We describe four pediatric cases of IVIG-induced AIHA following treatment for KD. We retrospectively reviewed four KD patients who developed hemolytic anemia temporally associated with IVIG administration. Clinical data included age, blood type, transfusion requirement, and outcomes. All four patients were non-O blood types. Hemolysis developed within days of IVIG infusion, confirmed by a positive direct antiglobulin test. Two patients required red blood cell transfusions for symptomatic anemia. The lowest recorded hemoglobin levels ranged from 6.6 to 7.9 g/dL. None required corticosteroids or additional immunosuppression. All patients achieved full recovery with iron and folate supplementation. No coronary aneurysms or long-term complications were observed. IVIG-induced AIHA is a rare but clinically significant complication of KD therapy, particularly in non-O blood group patients. Routine post-infusion hemoglobin monitoring and early recognition of anemia are essential. Supportive management alone is typically sufficient, and prognosis remains excellent when the condition is promptly identified and managed. - Source: PubMed
Publication date: 2026/05/17
Pastrana Echevarria ItzamarGarcía JesusHenriquez Gabriela MCondor YesabeliVelazquez Vylma