Endothelial identity not found - Beyond passage 38, commercial cardiac microvascular endothelial cells do not express CD31 and VE-cadherin.

Few immortalized cardiac microvascular endothelial cell (CMEC) lines are available, particularly mouse lines. We purchased the CLU510 mCMEC line (Cedarlane), isolated by fluorescence-activated cell sorting for CD31 and VE-cadherin. The cell line has been used in previous studies, although none report CD31 or VE-cadherin expression.

Impact of the Number of Positive Pelvic Lymph Nodes on Risk of Para-Aortic Recurrence in Patients with Clinically Early Cervical Cancer Treated by a Radical Hysterectomy and Pelvic Lymphadenectomy.

Background: Guidelines recommend the extension of the pelvic radiotherapy volume to the para-aortic region in locally advanced cervical cancer and ≥3 suspicious pelvic lymph nodes (PLN) on imaging. Whether this recommendation is also valid for clinically early stages is uncertain. The objective of this study was to investigate the para-aortic (PAO) lymph node recurrence rate in patients with early-stage cervical cancer, ≥3 metastatic PLN, and negative common iliac nodes after a radical hysterectomy followed by pelvic (chemo)radiotherapy without extension to the PAO region.

Early adipose tissue wasting in a novel preclinical model of human lung cancer cachexia.

Cancer cachexia (CC), a syndrome of skeletal muscle and adipose tissue wasting, reduces responsiveness to therapies and increases mortality. There are no approved treatments for CC, which may relate to discordance between pre-clinical models and human CC. To address the need for clinically relevant models, we generated tamoxifen-inducible, epithelial cell specific ( ) mice.

Glycogen synthase kinase-3 inhibition and insulin enhance proliferation and inhibit maturation of human iPSC-derived cardiomyocytes via TCF and FOXO signaling.

Embryonic signaling pathways exert stage-specific effects during cardiac development, yet the precise signals for proliferation or maturation remain elusive. To uncover the cues for proliferation, we performed a combinatory cell-cycle screen for insulin and glycogen synthase kinase-3 (GSK3) inhibition in spontaneously beating human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Our analysis for proliferation, and subsequential downstream sarcomere development, gene expression analysis, and molecular interventions identified a temporal interplay between insulin/Akt/FOXO and CHIR99021/Wnt/GSK3/TCF signaling.