Diesel exhaust particles alter mitochondrial bioenergetics and cAMP producing capacity in human bronchial epithelial cells.

Air pollution from diesel combustion is linked in part to the generation of diesel exhaust particles (DEP). DEP exposure induces various processes, including inflammation and oxidative stress, which ultimately contribute to a decline in lung function. Cyclic AMP (cAMP) signaling is critical for lung homeostasis.

SARS-CoV-2 Spike-specific IFN-γ T-cell Response After COVID-19 Vaccination in Patients With Chronic Kidney Disease, on Dialysis, or Living With a Kidney Transplant.

Unlabelled: Studies have shown that coronavirus disease 2019 (COVID-19) vaccination is associated with a lower humoral response in vulnerable kidney patients. Here, we investigated the T-cell response following COVID-19 vaccination in kidney patients compared with controls.

Methods: Patients with chronic kidney disease (CKD) stage G4/5 [estimated glomerular filtration rate <30 mL/min/1.

Epithelial 3D-spheroids as a tool to study air pollutant-induced lung pathology.

Cigarette smoke (CS) and air pollutants (AP) activate pathological processes in bronchial epithelial cells resulting in lung function decline which severely impacts human health. Knowledge about the molecular mechanism(s) by which CS and AP induce pathology is limited. Our previous studies in 2D cultures of human bronchial epithelial (BEAS-2B) cells showed that CS exposure activates transforming growth factor-β1 (TGF-β1) release and signaling.

Human/robotic interaction: vision limits performance in simulated vitreoretinal surgery.

Purpose: Compare accuracy and precision in XYZ of stationary and dynamic tasks performed by surgeons with and without the use of a tele-operated robotic micromanipulator in a simulated vitreoretinal environment. The tasks were performed using a surgical microscope or while observing a video monitor.

Method: Two experienced and two novice surgeons performed tracking and static tasks at a fixed depth with hand-held instruments on a Preceyes Surgical System R0.

Elevated pCO2 causes a shift towards more toxic microcystin variants in nitrogen-limited Microcystis aeruginosa.

Elevated pCO2 may promote phytoplankton growth, and potentially alleviate carbon limitation during dense blooms. Under nitrogen-limited conditions, elevated pCO2 may furthermore alter the phytoplankton carbon-nitrogen (C:N) balance and thereby the synthesis of secondary metabolites, such as cyanobacterial toxins. A common group of these toxins are the microcystins, with variants that differ not only in C:N stoichiometry, but also in toxicity.