University of New Mexico

About: University of New Mexico is a education organization based out in Albuquerque, New Mexico, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 28870 authors who have published 64767 publications receiving 2578371 citations. The organization is also known as: UNM & Universitatis Novus Mexico.

TH17 responses in cytokine storm of COVID-19: An emerging target of JAK2 inhibitor Fedratinib.

Abstract: COVID-19 emerges as a pandemic disease with high mortality. Development of effective prevention and treatment is an urgent need. We reviewed TH17 responses in patients with SARS-CoV-2 and proposed an FDA approved JAK2 inhibitor Fedratinib for reducing mortality of patients with TH17 type immune profiles.

Mutations in the cardiac transcription factor NKX2.5 affect diverse cardiac developmental pathways

Abstract: Heterozygous mutations in NKX2.5, a homeobox transcription factor, were reported to cause secundum atrial septal defects and result in atrioventricular (AV) conduction block during postnatal life. To further characterize the role of NKX2.5 in cardiac morphogenesis, we sought additional mutations in groups of probands with cardiac anomalies and first-degree AV block, idiopathic AV block, or tetralogy of Fallot. We identified 7 novel mutations by sequence analysis of the NKX2.5-coding region in 26 individuals. Associated phenotypes included AV block, which was the primary manifestation of cardiac disease in nearly a quarter of affected individuals, as well as atrial septal defect and ventricular septal defect. Ventricular septal defect was associated with tetralogy of Fallot or double-outlet right ventricle in 3 individuals. Ebstein’s anomaly and other tricuspid valve abnormalities were also present. Mutations in human NKX2.5 cause a variety of cardiac anomalies and may account for a clinically significant portion of tetralogy of Fallot and idiopathic AV block. The coinheritance of NKX2.5 mutations with various congenital heart defects suggests that this transcription factor contributes to diverse cardiac developmental pathways. J. Clin. Invest. 104:1567–1573 (1999).