Effectiveness of palatal anchorage device (PAD) for maxillary anterior retraction with clear aligners using finite element study.

The palatal anchorage device (PAD) is commonly used in fixed appliance for anchorage, but the biomechanics of PAD in patients treated with clear aligners(CAs)remains poorly understood, especially in its elastic mode and force magnitude. This study aimed to assess the biomechanical effects of using PAD for retraction during clear aligner treatment (CAT) with the extraction of two maxillary first premolars. Four finite element models were created: (1) Incisors retraction (IR) with active contraction of the clear aligner only; (2) IR with PAD using different forces (50,75,100 g) or not; (3) PAD without IR (forces of 50,75,100 g), and (4) Different elastic directions (D1, D2, D3) from aligner to PAD without IR.

USP49 inhibits ischemia-reperfusion-induced cell viability suppression and apoptosis in human AC16 cardiomyocytes through DUSP1-JNK1/2 signaling.

Dual-specificity protein phosphatases (DUSP) also known as mitogen-activated protein kinase (MAPK) phosphatases (MKPs) can dephosphorylate MAPKs, including extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and p38. DUSP1-mediated JNK dephosphorylation has been found to play an antiapoptotic role against cardiac ischemia-reperfusion (I/R) injury. However, the regulation of DUSP1-JNK pathway remains unclear.

Involvement of JNK1/2-NF-κBp65 in the regulation of HMGB2 in myocardial ischemia/reperfusion-induced apoptosis in human AC16 cardiomyocytes.

JNK1/2 and NF-κB signal are essential signaling pathways that mediate a variety of cellular processes, including cell survival, apoptosis, inflammation and angiogenesis. JNK1/2 activation and NF-κBp65 nuclear translocation have been found in ischemia/reperfusion (I/R)-induced injury. However, the regulation of JNK1/2-NF-κBp65 signaling pathway remains unclear.