Anthropogenic Fingerprint Detectable in Upper Tropospheric Ozone Trends Retrieved from Satellite.

Tropospheric ozone (O) is a strong greenhouse gas, particularly in the upper troposphere (UT). Limited observations point to a continuous increase in UT O in recent decades, but the attribution of UT O changes is complicated by large internal climate variability. We show that the anthropogenic signal ("fingerprint") in the patterns of UT O increases is distinguishable from the background noise of internal variability.

deficiency disrupts V(D)J recombination to cause SCID and Omenn syndrome.

Inborn errors of T cell development present a pediatric emergency in which timely curative therapy is informed by molecular diagnosis. In 11 affected patients across four consanguineous kindreds, we detected homozygosity for a single deleterious missense variant in the gene NudC domain-containing 3 () Two infants had severe combined immunodeficiency with the complete absence of T and B cells (TB SCID), whereas nine showed classical features of Omenn syndrome (OS). Restricted antigen receptor gene usage by residual T lymphocytes suggested impaired V(D)J recombination.

Air quality related equity implications of U.S. decarbonization policy.

Climate policies that target greenhouse gas emissions can improve air quality by reducing co-emitted air pollutant emissions. However, the extent to which climate policy could contribute to the targets of reducing existing pollution disparities across different populations remains largely unknown. We quantify potential air pollution exposure reductions under U.

Tracking Cardiovascular Comorbidity in Models of Chronic Inflammatory Disease.

Immune-mediated inflammatory diseases (IMIDs) are commonly associated with complex coexisting conditions, and cardiovascular comorbidities are a common cause of mortality in systemic inflammation. Experimental models of disease provide an opportunity to dissect inflammatory mechanisms that promote damage to vascular tissues affected by comorbidity. Here, we describe methods to recover the thoracic aorta from mice during experimental inflammatory arthritis and assess vascular constriction responses by isometric tension myography.

Canagliflozin impairs T cell effector function via metabolic suppression in autoimmunity.

Augmented T cell function leading to host damage in autoimmunity is supported by metabolic dysregulation, making targeting immunometabolism an attractive therapeutic avenue. Canagliflozin, a type 2 diabetes drug, is a sodium glucose co-transporter 2 (SGLT2) inhibitor with known off-target effects on glutamate dehydrogenase and complex I. However, the effects of SGLT2 inhibitors on human T cell function have not been extensively explored.