Delays in Recommended Follow-Up after Positive Findings in Lung Cancer Screening.

Rationale: Lung cancer screening (LCS) is an effective tool to reduce mortality. However, barriers along the LCS care continuum, including delay in follow-up care, may reduce effectiveness. Objectives: The primary goals of this study were to evaluate delays in follow-up in patients with positive findings on LCS and to examine the impact of delay on lung cancer staging. Methods: This was a retrospective cohort study of patients enrolled in a multisite LCS program with positive LCS findings, defined as Lung Computed Tomography Screening Reporting and Data System (Lung-RADS) 3, 4A, 4B, or 4X. Time to first follow-up was evaluated with delay considered >30 days beyond the standardized Lung-RADS recommendation. Multivariable Cox models were used to evaluate the likelihood of delay by Lung-RADS category. Participants with resultant non-small cell lung cancer were evaluated to determine if delay in follow-up was associated with clinical upstaging. Results: Three hundred sixty-nine patients with 434 examinations had positive findings; 16% of findings were ultimately diagnosed as lung cancer. In 47% of positive examinations, there was a delay in follow-up (median delay, 104 d), representing 59% (210 d) of Lung-RADS 3 examinations, 35% (64 d) of Lung-RADS 4A examinations, and 40% (34 d) of Lung-RADS 4B/4X examinations (P < 0.001). In the 54 patients diagnosed with non-small cell lung cancer through LCS, delay was associated with increased likelihood of clinical upstaging (P < 0.001). Conclusions: In this study of delay in follow-up after positive LCS findings, we found that nearly half of patients had delays in follow-up and that delay was associated with clinical upstaging in patients whose positive findings represented lung cancer. Further targeted interventions to ensure timely follow-up after positive LCS examination are critical.

Trends in Labor Unionization Among US Health Care Workers, 2009-2021.

Importance: Labor unionization efforts have resurged in the US, and union membership has been shown to improve worker conditions in some industries. However, little is known about labor unionization membership and its economic effects across the health care workforce. Objectives: To examine the prevalence of labor unionization among health care workers and its associations with pay, noncash benefits, and work hours. Design, Setting, and Participants: This cross-sectional study was conducted using data from the Current Population Survey and Annual Social and Economic Supplement from 2009 through 2021. The US nationally representative, population-based household survey allowed for a sample of 14 298 self-identified health care workers (physicians and dentists, advanced practitioners, nurses, therapists, and technicians and support staff). Exposures: Self-reported membership status or coverage in a labor union. Main Outcomes and Measures: Prevalence and trend in labor unionization. Further comparisons included mean weekly pay, noncash benefits (pension or other retirement benefits; employer-sponsored, full premium-covered health insurance; and employer's contribution to the worker's health insurance plan), and work hours. Results: The 14 298 respondents (81.5% women; 7.1% Asian, 12.0% Black, 8.5% Hispanic, 70.4% White individuals; mean [SD] age, 41.6 [13.4] years) included 1072 physicians and dentists, 981 advanced practitioners, 4931 nurses, 964 therapists, and 6350 technicians and support staff. After weighting, 13.2% (95% CI, 12.5% to 13.8%) of respondents reported union membership or coverage, with no significant trend from 2009 through 2021 (P = .75). Among health care workers, those who were members of a racial or ethnic minority group (Asian, Black, or Hispanic individuals compared with White individuals) and those living in metropolitan areas were more likely to report being labor unionized. Reported unionization was associated with significantly higher reported weekly earnings ($1165 vs $1042; mean difference, $123 [95% CI, $88 to $157]; P < .001) and higher likelihood of having a pension or other retirement benefits at work (57.9% vs 43.4%; risk ratio [RR], 1.33 [95% CI, 1.26 to 1.41]; P < .001) and having employer-sponsored, full premium-covered health insurance (22.2% vs 16.5%; RR, 1.35 [95% CI, 1.17 to 1.53]; P < .001). Union members reported more work hours (37.4 vs 36.3; mean differences, 1.11 [95% CI, 0.46 to 1.75]; P < .001) per week. White workers reported mean weekly earnings that were significantly more than members of racial and ethnic minority groups among nonunionized workers ($1066 vs $1001; mean difference, $65 [95% CI, $40 to $91]; P < .001), but there was no significant difference between the 2 groups among unionized workers ($1157 vs $1170; mean difference, -$13 [95% CI, -$78 to $52]; P = .70). Conclusions and Relevance: From 2009 through 2021, labor unionization among US health care workers remained low. Reported union membership or coverage was significantly associated with higher weekly earnings and better noncash benefits but greater number of weekly work hours.

Report: A Pox Presenting Without Pox.

ABSTRACT: A man with virally suppressed human immunodeficiency virus (HIV) presented with an erythematous, morbilliform rash without pustules in the setting of fever, fatigue, and myalgias after recent travel to Mexico and Puerto Rico. He was diagnosed with nonvariola orthopoxvirus (monkeypox) infection. This case report highlights an atypical presentation in the 2022 outbreak.

Tle1 tumor suppressor negatively regulates inflammation in vivo and modulates NF-κB inflammatory pathway.

Tle1 (transducin-like enhancer of split 1) is a corepressor that interacts with a variety of DNA-binding transcription factors and has been implicated in many cellular functions; however, physiological studies are limited. Tle1-deficient (Tle1(Δ/Δ)) mice, although grossly normal at birth, exhibit skin defects, lung hypoplasia, severe runting, poor body condition, and early mortality. Tle1(Δ/Δ) mice display a chronic inflammatory phenotype with increased expression of inflammatory cytokines and chemokines in the skin, lung, and intestine and increased circulatory IL-6 and G-CSF, along with a hematopoietic shift toward granulocyte macrophage progenitor and myeloid cells. Tle1(Δ/Δ) macrophages produce increased inflammatory cytokines in response to Toll-like receptor (TLR) agonists and lipopolysaccharides (LPS), and Tle1(Δ/Δ) mice display an enhanced inflammatory response to ear skin 12-O-tetradecanoylphorbol-13-acetate treatment. Loss of Tle1 not only results in increased phosphorylation and activation of proinflammatory NF-κB but also results in decreased Hes1 (hairy and enhancer of split-1), a negative regulator of inflammation in macrophages. Furthermore, Tle1(Δ/Δ) mice exhibit accelerated growth of B6-F10 melanoma xenografts. Our work provides the first in vivo evidence, to our knowledge, that TLE1 is a major counterregulator of inflammation with potential roles in a variety of inflammatory diseases and in cancer progression.

A novel in vitro model to study alveologenesis.

Many pediatric pulmonary diseases are associated with significant morbidity and mortality due to impairment of alveolar development. The lack of an appropriate in vitro model system limits the identification of therapies aimed at improving alveolarization. Herein, we characterize an ex vivo lung culture model that facilitates investigation of signaling pathways that influence alveolar septation. Postnatal Day 4 (P4) mouse pup lungs were inflated with 0.4% agarose, sliced, and cultured within a collagen matrix in medium that was optimized to support cell proliferation and promote septation. Lung slices were grown with and without 1D11, an active transforming growth factor-ß-neutralizing antibody. After 4 days, the lung sections (designated P4 + 4) and noncultured lung sections were examined using quantitative morphometry to assess alveolar septation and immunohistochemistry to evaluate cell proliferation and differentiation. We observed that the P4 + 4 lung sections exhibited ex vivo alveolarization, as evidenced by an increase in septal density, thinning of septal walls, and a decrease in mean linear intercept comparable to P8, age-matched, uncultured lungs. Moreover, immunostaining showed ongoing cell proliferation and differentiation in cultured lungs that were similar to P8 controls. Cultured lungs exposed to 1D11 had a distinct phenotype of decreased septal density when compared with untreated P4 + 4 lungs, indicating the utility of investigating signaling in these lung slices. These results indicate that this novel lung culture system is optimized to permit the investigation of pathways involved in septation, and potentially the identification of therapeutic targets that enhance alveolarization.