Results 221 to 230 of about 938,873 (282)
Targeting Hyperglycemic Bone Pre‐Metastatic Niche for Breast Cancer Bone Metastasis Therapy
This study reveals that breast cancer creates a hyperglycemic pre‐metastatic niche in bone prior to colonization and amplifies glucose metabolism post‐metastasis. To target this mechanism, a biomimetic enzyme‐engineered nanoplatform that disrupts tumor glycolytic pathways, proposing a therapeutic strategy to inhibit breast cancer bone metastasis by ...
Jianxin Ye+13 more
wiley +1 more source
Repeated neonatal sevoflurane exposure impairs adolescent fear memory through Igfbp2 downregulation in paraventricular thalamus‐central amygdala glutamatergic projections. Restoring Igfbp2 or activating this circuit rescues memory deficits, neuronal excitability, and spine density, identifying a precise molecular target for preventing anesthesia ...
Weiming Zhao+16 more
wiley +1 more source
A Subcircuit in the Suprachiasmatic Nucleus Generates Wakefulness
This study identifies a sub‐circuit within the circadian pacemaker suprachiasmatic nucleus (SCN) that promotes arousal. This sub‐circuit is labeled by the clock output molecule mWAKE, which suppresses its excitability in a time‐dependent manner. mWAKE‐expressing cells in the SCN (SCNmWAKE cells) project to the subparaventricular zone (SPZ) to mediate ...
Qiang Liu+6 more
wiley +1 more source
Translation of a Human‐Based Malaria‐on‐a‐Chip Phenotypic Disease Model for In Vivo Applications
Inoculation of the Malaria‐on‐a‐Chip model with human erythrocytes infected with Plasmodium falciparum can support the entire intraerythrocytic lifecycle for 7 days in vitro. Utilizing this human‐based, serum‐free model provides an alternative to animal testing by introducing a human‐based, preclinical alternative for antimalarial therapeutic delivery.
Michael J. Rupar+15 more
wiley +1 more source
Ovarian cancer patients with high levels of mortalin protein in their tumors have worse survival. The investigational drug SHetA2 interferes with mortalin's support of mitochondria. The resulting mitochondrial damage causes a process called mitophagy that contributes to how SHetA2 kills cancer cells. Noncancerous cells repair their mitochondria through
Vishal Chandra+9 more
wiley +1 more source