RAGE is a key regulator of ductular reaction-mediated fibrosis during cholestasis.

Ductular reaction (DR) is the hallmark of cholestatic diseases manifested in the proliferation of bile ductules lined by biliary epithelial cells (BECs). It is commonly associated with an increased risk of fibrosis and liver failure. The receptor for advanced glycation end products (RAGE) was identified as a critical mediator of DR during chronic injury.

CAF Specific Expression of Podoplanin May Be Dispensable for the Malignancy of Malignant Melanoma.

Within the tumor microenvironment (TME), cancer-associated fibroblasts (CAFs) were shown to be an active and pivotal cell population, supporting many protumorigenic mechanisms. Podoplanin (PDPN)-positive CAFs are of special interest since their abundance correlated with a worse prognosis for patients of different cancer entities, including malignant melanoma. In this study, we applied a loss-of-function approach in an in vivo mouse melanoma model to evaluate the contribution of CAF-specific PDPN expression to melanoma formation and progression.

Initial response to the COVID-19 pandemic on real-life well-being, social contact and roaming behavior in patients with schizophrenia, major depression and healthy controls: A longitudinal ecological momentary assessment study.

The COVID-19 pandemic strongly impacted people's daily lives. However, it remains unknown how the pandemic situation affects daily-life experiences of individuals with preexisting severe mental illnesses (SMI). In this real-life longitudinal study, the acute onset of the COVID-19 pandemic in Germany did not cause the already low everyday well-being of patients with schizophrenia (SZ) or major depression (MDD) to decrease further.

Podoplanin is required for tumor cell invasion in cutaneous squamous cell carcinoma.

The invasiveness of late-stage cutaneous squamous cell carcinoma (cSCC) is associated with poor patients' prognosis and linked to strong upregulation of the glycoprotein Podoplanin (PDPN) in cancer cells. However, the function of PDPN in these processes in cSCC carcinogenesis has not been characterized in detail yet. Employing a CRISPR/Cas9-based loss-of-function approach on murine cSCC cells, we show that the loss of Pdpn results in decreased migration and invasion in vitro.