Determination of ultrafine particle number emission factors from building materials in standardized conditions.

When comparing the particle emissivity for different materials and/or mechanical activities, a serious methodological issue emerges due to the dynamic nature of solid aerosols. Particle size distribution and concentration depend on initial particle emission that constantly evolves due to aerodynamic collisions. In this context, we propose a methodological approach and an experimental setup that enables to assess the release of fine/ultra-fine particles maintaining a steady-state inhalable mass concentration, here chosen at the Swiss occupational exposure level value for biopersistent granular particles (OEL: 10 mg/m3) in a controlled ventilation chamber.

Human induced pluripotent stem cell-derived planar neural organoids assembled on synthetic hydrogels.

The tailorable properties of synthetic polyethylene glycol (PEG) hydrogels make them an attractive substrate for human organoid assembly. Here, we formed human neural organoids from iPSC-derived progenitor cells in two distinct formats: (i) cells seeded on a Matrigel surface; and (ii) cells seeded on a synthetic PEG hydrogel surface. Tissue assembly on synthetic PEG hydrogels resulted in three dimensional (3D) planar neural organoids with greater neuronal diversity, greater expression of neurovascular and neuroinflammatory genes, and reduced variability when compared with tissues assembled upon Matrigel.

Preclinical Models of Anal Cancer Combined-Modality Therapy.

Introduction: There have been no significant changes in anal cancer treatment options in 4 decades. In this study, we highlight two preclinical models designed to assess anal cancer treatments.

Materials And Methods: Transgenic K14E6/E7 mice were treated with 7, 12-dimethylbenz(a)anthracene until anal tumors developed.

Metabolomics revealed the influence of breast cancer on lymphatic endothelial cell metabolism, metabolic crosstalk, and lymphangiogenic signaling in co-culture.

Breast cancer metastasis occurs via blood and lymphatic vessels. Breast cancer cells 'educate' lymphatic endothelial cells (LECs) to support tumor vascularization and growth. However, despite known metabolic alterations in breast cancer, it remains unclear how lymphatic endothelial cell metabolism is altered in the tumor microenvironment and its effect in lymphangiogenic signaling in LECs.