Odynophagia after Cardiac Catheterization: A Rare Complication in the Presence of Aberrant Subclavian Artery

Background. Vascular complications from transradial cardiac catheterization are uncommon. Mediastinal hematoma is a rare complication with life-threatening potential. We present a case of a patient who underwent cardiac catheterization and subsequently experienced odynophagia from injury to an aberrant subclavian artery that led to a mediastinal hematoma. Case Report. A 59-year-old female with past medical history of coronary artery disease presented with complaints of angina and underwent a transradial cardiac catheterization. Immediately after the procedure, the patient complained of chest pain and odynophagia. EKG and echocardiogram were unremarkable, and a CT scan of the chest demonstrated an ill-defined fluid collection present in the superior mediastinum and an aberrant right subclavian artery. The patient was closely monitored in the Intensive Care Unit, and the patient remained hemodynamically stable throughout the admission. The patient was subsequently discharged home in good condition and did well on outpatient follow-up. Conclusion. Vascular injuries associated with delivery of standard radial catheters in the subclavian artery are rare, with very few cases reported in the literature. We presented the case of a patient who had a previously unidentified right aberrant subclavian artery with a retroesophageal course which precipitated the hematoma and subsequently resulted in odynophagia despite an uncomplicated catheterization. This rare complication of a commonplace procedure necessitates prompt recognition, appropriate hemodynamic management, and possible repair of the injured vessel to appropriately manage a potentially life-threatening condition

Hydrogen Intensity and Real-Time Analysis Experiment: 256-element array status and overview

International audienceThe Hydrogen Intensity and Real-time Analysis Experiment (HIRAX) is a radio interferometer array currently in development, with an initial 256-element array to be deployed at the South African Radio Astronomy Observatory Square Kilometer Array site in South Africa. Each of the 6 m, f  /  0.23 dishes will be instrumented with dual-polarization feeds operating over a frequency range of 400 to 800 MHz. Through intensity mapping of the 21 cm emission line of neutral hydrogen, HIRAX will provide a cosmological survey of the distribution of large-scale structure over the redshift range of 0.775  <  z  <  2.55 over ∼15,000 square degrees of the southern sky. The statistical power of such a survey is sufficient to produce ∼7  %   constraints on the dark energy equation of state parameter when combined with measurements from the Planck satellite. Additionally, HIRAX will provide a highly competitive platform for radio transient and HI absorber science while enabling a multitude of cross-correlation studies. We describe the science goals of the experiment, overview of the design and status of the subcomponents of the telescope system, and describe the expected performance of the initial 256-element array as well as the planned future expansion to the final, 1024-element array

Lung adenocarcinoma promotion by air pollutants

A complete understanding of how exposure to environmental substances promotes cancer formation is lacking. More than 70 years ago, tumorigenesis was proposed to occur in a two-step process: an initiating step that induces mutations in healthy cells, followed by a promoter step that triggers cancer development1. Here we propose that environmental particulate matter measuring ≤2.5 μm (PM2.5), known to be associated with lung cancer risk, promotes lung cancer by acting on cells that harbour pre-existing oncogenic mutations in healthy lung tissue. Focusing on EGFR-driven lung cancer, which is more common in never-smokers or light smokers, we found a significant association between PM2.5 levels and the incidence of lung cancer for 32,957 EGFR-driven lung cancer cases in four within-country cohorts. Functional mouse models revealed that air pollutants cause an influx of macrophages into the lung and release of interleukin-1β. This process results in a progenitor-like cell state within EGFR mutant lung alveolar type II epithelial cells that fuels tumorigenesis. Ultradeep mutational profiling of histologically normal lung tissue from 295 individuals across 3 clinical cohorts revealed oncogenic EGFR and KRAS driver mutations in 18% and 53% of healthy tissue samples, respectively. These findings collectively support a tumour-promoting role for PM2.5 air pollutants and provide impetus for public health policy initiatives to address air pollution to reduce disease burden