Numerous prodrugs have been developed and used for cancer treatments to reduce side effects and promote efficacy. In this work, we have developed a new photoactivatable prodrug system based on intracellular photoinduced electron transfer-reversible addition-fragmentation chain-transfer (PET-RAFT) polymerization. This unique polymerization process provided a platform for the synthesis of structure-predictable polymers with well-defined structures in living cells. The intracellularly generated poly(,-dimethylacrylamide)s were found to induce cell cycle arrest, apoptosis, and necroptosis, inhibit cell proliferation, and reduce cancer cell motilities. This polymerization-based "prodrug" system efficiently inhibits tumor growth and metastasis both and and will promote the development of targeted and directed cancer chemotherapy.
Allergic inflammation is closely related to the activation of mast cells (MCs), which is regulated by its intracellular Ca level, but the intake and effects of the intracellular Ca remain unclear. The Ca influx is controlled by members of Ca channels, among which calcium voltage-gated channel subunit alpha1 C (Ca1.2) is the most robust.
Testosterone signaling mediates diseases such as androgenetic alopecia and prostate cancer and is controlled by the activation of the androgen receptor (AR) and nuclear translocation of the ligand-receptor complex. This study established an immortalized dermal papilla cell line that stably expresses the AR labeled with a monomeric green fluorescence marker. The cells expressed the histone H2B protein as visualized using a red fluorescence marker, enabling the Detection of nuclear translocation under live cell conditions using image analysis.
KCNN4, a Ca-activated K channel, is involved in various physiological and pathological processes. It is essential for epithelial transport, immune system and other physiological mechanisms but its activation is also involved in cancer pathophysiology as well as red blood cell disorders (RBC). The activation of KCNN4 in RBC leads to loss of KCl and water, a mechanism known as the "Gardos effect" described seventy years ago.
Background: Increased cardiac after load and multiple non-hemodynamic stimuli implicate in adverse left ventricular remodeling (LVR). This is particularly identifiable in treatment-resistant and secondary hypertension contexts, like primary hyperaldosteronism (PA), however little data exists on post-treatment residual LVR in these individuals.
Methods: Cardiac magnetic resonance (CMR) with T1 mapping were performed in 14 patients with treated PA matched with 15 treated patients with primary hypertension (PH) and 15 healthy individuals.
