Biphasic response of human iPSC-derived neural network activity following exposure to a sarin-surrogate nerve agent.

Organophosphorus nerve agents (OPNA) are hazardous environmental exposures to the civilian population and have been historically weaponized as chemical warfare agents (CWA). OPNA exposure can lead to several neurological, sensory, and motor symptoms that can manifest into chronic neurological illnesses later in life. There is still a large need for technological advancement to better understand changes in brain function following OPNA exposure.

Host tracheal and intestinal microbiomes inhibit growth .

Unlabelled: Coccidioidomycosis, also known as Valley fever, is a disease caused by the fungal pathogen . Unfortunately, patients are often misdiagnosed with bacterial pneumonia, leading to inappropriate antibiotic treatment. The soil -like species exhibits antagonistic properties against ; however, the antagonistic capabilities of host microbiota against are unexplored.

Mef2c regulates bone mass through Sost-dependent and -independent mechanisms.

Mef2c is a transcription factor that mediates key cellular behaviors that promote endochondral ossification and bone formation. Previously, Mef2c has been shown to regulate Sost transcription via its osteocyte-specific enhancer, ECR5, and conditional deletions of Mef2c with either Col1-Cre or Dmp1-Cre produced generalized high bone mass (HBM) consistent with Van Buchem Disease phenotypes. However, Sost; Mef2c; Dmp1-Cre mice produced a significantly higher bone mass phenotype that Sost alone suggesting that Mef2c modulates bone mass through additional mechanisms, independent of Sost.

Host tracheal and intestinal microbiomes inhibit growth .

Coccidioidomycosis, also known as Valley fever, is a disease caused by the fungal pathogen . Unfortunately, patients are often misdiagnosed with bacterial pneumonia leading to inappropriate antibiotic treatment. Soil bacteria -like species exhibits antagonistic properties against ; however, the antagonistic capabilities of host microbiota against are unexplored.

Loss of Cadherin-11 in pancreatic ductal adenocarcinoma alters tumor-immune microenvironment.

Pancreatic ductal adenocarcinoma (PDAC) is one of the top five deadliest forms of cancer with very few treatment options. The 5-year survival rate for PDAC is 10% following diagnosis. Cadherin 11 (Cdh11), a cell-to-cell adhesion molecule, has been suggested to promote tumor growth and immunosuppression in PDAC, and Cdh11 inhibition significantly extended survival in mice with PDAC.