The data suggest that the ethanol extracts of Artemisia asiatica exerted significant protection from alcohol-induced gastric mucosal injury through bio-regulation, which is essential for cytoprotection and anti-inflammation.

A nerve block is an effective tool for diagnostic and therapeutic methods. If a diagnostic nerve block is successful for pain relief and the subsequent therapeutic nerve block is effective for only a limited duration, the next step that should be considered is a nerve ablation or modulation. The nerve ablation causes iatrogenic neural degeneration aiming only for sensory or sympathetic denervation without motor deficits. Nerve ablation produces the interruption of axonal continuity, degeneration of nerve fibers distal to the lesion (Wallerian degeneration), and the eventual death of axotomized neurons. The nerve ablation methods currently available for resection/removal of innervation are performed by either chemical or thermal ablation. Meanwhile, the nerve modulation method for interruption of innervation is performed using an electromagnetic field of pulsed radiofrequency. According to Sunderland's classification, it is first and foremost suggested that current neural ablations produce third degree peripheral nerve injury (PNI) to the myelin, axon, and endoneurium without any disruption of the fascicular arrangement, perineurium, and epineurium. The merit of Sunderland's third degree PNI is to produce a reversible injury. However, its shortcoming is the recurrence of pain and the necessity of repeated ablative procedures. The molecular mechanisms related to axonal regeneration after injury include cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules, and their receptors. It is essential to establish a safe, long-standing denervation method without any complications in future practices based on the mechanisms of nerve degeneration as well as following regeneration.

Although recent studies have suggested that cessation of imatinib (IM) in chronic myeloid leukemia patients can be associated with sustained response, further validation is needed to explore predictive factors. In a prospective, multicenter study, chronic phase patients were eligible for cessation of IM therapy after more than 3 years if they had no detectable BCR-ABL1 transcript for at least 2 years. A total of 48 patients with a median age of 47 years (19-74 years) were enrolled. Twenty patients received IM for post-transplant relapse. After a median follow-up of 15.8 months (1.4-28.2 months) after IM discontinuation, nine of the non-transplant group lost undetectable molecular residual disease (UMRD) and major molecular response (MMR), whereas none of the 20 patients in the transplant group experienced UMRD loss. Probabilities for sustained MMR and UMRD were 64.4% and 66.3% in the non-transplant group, respectively. Of nine patients re-treated with IM, eight patients re-achieved MMR at a median of 1.7 months (0.9-2.8 months). Seven of these patients re-achieved UMRD at a median of 5.6 months (2.8-12.1 months). Previous transplantation, IM duration, and UMRD duration were significantly associated with sustained molecular responses. Our data strongly suggest that immunological control contributes to sustained suppression of residual leukemia cell expansion and that IM can be safely discontinued in patients with post-transplant relapse. Am. J.

Background: Catechins in green tea have a beneficial effect in bone formation, but the detailed mechanism is not fully understood. Results: ECG, a major compound of green tea, stimulates TAZ-and RUNX2-mediated osteogenic gene transcription through PP1A. Conclusion: ECG stimulates osteoblast differentiation through a transcriptional activation. Significance: A novel mechanism for green tea-stimulated osteoblast differentiation is revealed.

dTranscriptional coactivator with PDZ-binding motif (TAZ) physically interacts with a variety of transcription factors and modulates their activities involved in cell proliferation and mesenchymal stem cell differentiation. TAZ is highly expressed in the kidney, and a deficiency of this protein results in multiple renal cysts and urinary concentration defects; however, the molecular functions of TAZ in renal cells remain largely unknown. In this study, we examined the effects of osmotic stress on TAZ expression and activity in renal cells. We found that hyperosmotic stress selectively increased protein phosphorylation at tyrosine 316 of TAZ and that this was enhanced by c-Abl activation in response to hyperosmotic stress. Interestingly, phosphorylated TAZ physically interacted with nuclear factor of activated T cells 5 (NFAT5), a major osmoregulatory transcription factor, and subsequently suppressed DNA binding and transcriptional activity of NFAT5. Furthermore, TAZ deficiency elicited an increase in NFAT5 activity in vitro and in vivo, which then reverted to basal levels following restoration of wild-type TAZ but not mutant TAZ (Y316F). Collectively, the data suggest that TAZ modulates cellular responses to hyperosmotic stress through fine-tuning of NFAT5 activity via tyrosine phosphorylation.T ranscriptional coactivator with PDZ-binding motif (TAZ), also known as WW domain-containing transcription regulator 1 (WWTR1), was first identified as a 14-3-3-interacting phosphoprotein (16). Phosphorylation of TAZ at serine 89 is required for its interaction with 14-3-3 and for substantial retention in the cytoplasm (16). In addition to the 14-3-3-binding motif, TAZ contains multiple functional domains, including a WW domain, a coiled-coil domain, and a PDZ-binding motif, through which it modulates the activity of transcription factors involved in stem cell differentiation (13). For example, TAZ interacts with runt-related transcription factor 2 (RUNX2) and MyoD during osteoblast and myogenic differentiation and promotes cell lineage-specific gene transcription (6, 13, 15). During adipogenic differentiation, TAZ suppresses the activity of peroxisome proliferator-activated receptor (PPAR), thus inhibiting adipogenic differentiation from mesenchymal stem cells (13). TAZ also controls organ development, including thyroid, cardiac, and limb development, by association with thyroid transcription factor 1 (TTF-1), paired box gene 8 (PAX8), and PAX3 (7,(28)(29)(30). Furthermore, TAZ promotes cell proliferation through activation of TEAD transcription factors, resulting in tumor cell growth and epithelialmesenchymal transition (4,5,19,22,37). Much of our understanding of the physiological function of TAZ in vivo has been derived from studies using TAZ knockout (KO) mice, which develop significant pathogenic phenotypes, such as lung emphysema and multiple kidney cysts (14,24). Although the pathogenic mechanisms at play in TAZ KO mice largely remain to be explored, TAZ is known to suppress the expression and activity of the tran...