Thermal bleaching of photodarkening and heat-induced loss and spectral broadening in Tm3+-doped fibers.

We demonstrate the thermal bleaching effect on a photodarkened thulium-doped fiber (TDF) in detail. The bleaching effect on visible transmission initiates at 250 °C and a complete recovery is achieved at 550 °C. Prior to the recovery, a post-irradiation heat-induced spectral loss is observed. It indicates that an intermediate energy state is generated in the TDF under exposure to near-infrared (NIR) radiation, exhibiting the spectral attenuation in visible (VIS) and NIR region as driven by color center after thermal activation. And, with thermal treatment, the bleached TDF shows a partial photodarkening (PD) resistance when it is subject to photoirradiation again. In addition, the temperature-dependent spectral broadening and red shift that may distort the measured decay curve of excess loss is observed and discussed.

Bleaching of photodarkening in Tm-doped silica fiber with deuterium loading.

We demonstrate the rapid photodarkening (PD) phenomenon in Tm-doped fiber (TDF) core pumped by a laser at 1080 nm and the bleaching effect of deuterium (${{\rm D}_2}$D2) on PD TDF. By ${{\rm D}_2}$D2 loading for seven days, the PD-induced excess loss (PIEL) in the visible (VIS) and near-infrared (NIR) region have been largely eliminated, and no degradation was observed within 30 days. PD resistance of the ${{\rm D}_2}$D2 pretreated TDF has been investigated as well. The formation of color centers based on defects and precursors in the silica matrix and the mechanism of ${{\rm D}_2}$D2 bleaching are discussed.

Stat3 Regulates Liver Progenitor Cell-Driven Liver Regeneration in Zebrafish.

After liver injury, regeneration manifests as either (1) hepatocytes proliferating to restore the lost hepatocyte mass or (2) if hepatocyte proliferation is compromised, biliary epithelial cells (BECs) dedifferentiating into liver progenitor cells (LPCs), which subsequently differentiate into hepatocytes. Following pharmacogenetic ablation of hepatocytes in Tg(fabp10a:CFP-NTR) zebrafish, resulting in severe liver injury, signal transducer and activator of transcription 3 (Stat3) and its target gene and negative regulator, socs3a, were upregulated in regenerating livers. Using either Stat3 inhibitors, JSI-124 and S3I-201, or stat3 zebrafish mutants, we investigated the role of Stat3 in LPC-driven liver regeneration. Although Stat3 suppression reduced the size of regenerating livers, BEC dedifferentiation into LPCs was unaffected. However, regenerating livers displayed a delay in LPC-to-hepatocyte differentiation and a significant reduction in the number of BECs. While no difference in cell death was detected, Stat3 inhibition significantly reduced LPC proliferation. Notably, stat3 mutants phenocopied the effects of Stat3 chemical inhibitors, although the mutant phenotype was incompletely penetrant. Intriguingly, a subset of socs3a mutants also displayed a lower number of BECs in regenerating livers. We conclude that the Stat3/Socs3a pathway is necessary for the proper timing of LPC-to-hepatocyte differentiation and establishing the proper number of BECs during LPC-driven liver regeneration.

Radical passive bleaching of Tm-doped silica fiber with deuterium.

We demonstrate the almost complete 2 µm laser power recovery of the gamma-ray-irradiated thulium (Tm)-doped silica fiber under deuterium loading. The optical-optical slope efficiency and the cladding absorption spectra of the Tm-doped fiber with gamma-ray irradiation and deuterium treatment have been measured for comparison. It was found that the slope efficiency of the irradiated Tm-doped fiber could be recovered to 96.1% of the pristine after deuterium bleaching, which significantly degraded from 60.7% to 25.3% after irradiation. Meanwhile, the additional absorption attenuation of the irradiated Tm-doped with D2 treatment completely vanished. Based on the comprehensive comparison of cladding absorption spectra, the probable mechanism of the deuterium bleaching effect on irradiated Tm-doped fiber has also been discussed.

Stat3/Cdc25a-dependent cell proliferation promotes embryonic axis extension during zebrafish gastrulation.

Cell proliferation has generally been considered dispensable for anteroposterior extension of embryonic axis during vertebrate gastrulation. Signal transducer and activator of transcription 3 (Stat3), a conserved controller of cell proliferation, survival and regeneration, is associated with human scoliosis, cancer and Hyper IgE Syndrome. Zebrafish Stat3 was proposed to govern convergence and extension gastrulation movements in part by promoting Wnt/Planar Cell Polarity (PCP) signaling, a conserved regulator of mediolaterally polarized cell behaviors. Here, using zebrafish stat3 null mutants and pharmacological tools, we demonstrate that cell proliferation contributes to anteroposterior embryonic axis extension. Zebrafish embryos lacking maternal and zygotic Stat3 expression exhibit normal convergence movements and planar cell polarity signaling, but transient axis elongation defect due to insufficient number of cells resulting largely from reduced cell proliferation and increased apoptosis. Pharmacologic inhibition of cell proliferation during gastrulation phenocopied axis elongation defects. Stat3 regulates cell proliferation and axis extension in part via upregulation of Cdc25a expression during oogenesis. Accordingly, restoring Cdc25a expression in stat3 mutants partially suppressed cell proliferation and gastrulation defects. During later development, stat3 mutant zebrafish exhibit stunted growth, scoliosis, excessive inflammation, and fail to thrive, affording a genetic tool to study Stat3 function in vertebrate development, regeneration, and disease.

Berberine inhibits the proliferation of colon cancer cells by inactivating Wnt/ß-catenin signaling.

Colon cancer is one of the most common malignancies, mainly initiated by the abnormal activation of Wnt/ß-catenin signaling. In this study, we investigated the proliferation inhibitory effect of berberine on colon cancer cells and the molecular basis underlying this effect. With the viability, apoptosis and cell cycle assay, we demonstrated that berberine can inhibit proliferation, induce apoptosis and cell cycle arrest in colon cancer cells. In in vivo investigation, we demonstrated that berberine can prevent the colon cancer formation initiated by dimethylhydrazine (DMH) and dextran sodium sulfate (DSS) in rats. We employed western blotting, reverse transcription and polymerase chain reaction, special antagonist, overexpression and knockdown techniques to dissect the possible molecular mechanisms mediating the function of berberine. We found that the protein levels of ß-catenin in the nucleus and cytoplasm were all reduced after treating the colon cancer cells with berberine, and this may not result from accelerating the degradation of ß-catenin in the cytoplasm, but from inhibiting the mRNA expression of ß-catenin. Our results indicate that berberine can be a potential chemoprevention and chemotherapy agent for human colon cancer by targeting Wnt/ß-catenin signaling.

Phloroglucinol protects gastric mucosa against ethanol-induced injury through regulating myeloperoxidase and catalase activities.

It has been shown that oxidative stress plays an important role in the pathogenesis of ethanol-induced acute gastric mucosal injury, and phloroglucinol, a smooth muscle relaxant, has been reported to possess anti-oxidative properties. In this study, we explored the effect of phloroglucinol on ethanol-induced gastric mucosal injury and the possible underlying mechanisms. The rat model of gastric mucosal injury was induced by oral administration of acidified ethanol, and the gastric tissues were collected for analysis of gastric ulcer index (UI), cellular apoptosis, anti-O(2) ˙ or OH˙ formation activity, malondialdehyde (MDA) content, and the activities of myeloperoxidase (MPO), catalase and glutathione peroxidase. The results showed that acute administration of ethanol significantly increased gastric UI concomitantly with the increased cellular apoptosis, MDA contents, MPO activity as well as the decreased activities of catalase and anti-O(2) ˙ or OH˙ formation, which was reversed by pretreatment with phloroglucinol. Although ethanol treatment significantly decreased the activity of glutathione peroxidase, pretreatment with phloroglucinol did not significantly affect the activity of the same. The results suggest that phloroglucinol could protect the gastric mucosa against ethanol-induced injury, which is related to inhibiting the MPO activity and increasing the catalase activity in the gastric tissues.

miR-8 microRNAs regulate the response to osmotic stress in zebrafish embryos.

MicroRNAs (miRNAs) are highly conserved small RNAs that act as translational regulators of gene expression, exerting their influence by selectively targeting mRNAs bearing complementary sequence elements. These RNAs function in diverse aspects of animal development and physiology. Because of an ability to act as rapid responders at the level of translation, miRNAs may also influence stress response. In this study, we show that the miR-8 family of miRNAs regulates osmoregulation in zebrafish embryos. Ionocytes, which are a specialized cell type scattered throughout the epidermis, are responsible for pH and ion homeostasis during early development before gill formation. The highly conserved miR-8 family is expressed in ionocytes and enables precise control of ion transport by modulating the expression of Nherf1, which is a regulator of apical trafficking of transmembrane ion transporters. Ultimately, disruption of miR-8 family member function leads to an inability to respond to osmotic stress and blocks the ability to properly traffic and/or cluster transmembrane glycoproteins at the apical surface of ionocytes.