Full-Stokes Retrieving and Configuration Optimization in a Time-Integration Imaging Polarimeter.

A time-integration imaging polarimeter with continuous rotating retarder is presented, and its full-Stokes retrieving and configuration optimization are also demonstrated. The mathematical expression between the full-Stokes vector and the time-integration light intensities is derived. As a result, the state of polarization of incident light can be retrieved by only one matrix calculation. However, the modulation matrix deviates from the initial well-conditioned status due to time integration. Thus, we re-optimize the nominal angles for the special retardance of 132° and 90° with an exposure angle of 30°, which results in a reduction of 31.8% and 16.8% of condition numbers comparing to the original configuration, respectively. We also give global optimization results under different exposure angles and retardance of retarder; as a result, the 137.7° of retardance achieves a minimal condition number of 2.0, which indicates a well-conditioned polarimeter configuration. Besides, the frame-by-frame algorithm ensures the dynamic performance of the presented polarimeter. For a general brushless DC motor with a rotating speed of over 2000 rounds per minute, the speed of polarization imaging will achieve up to 270 frames per second. High precision and excellent dynamic performance, together with features of compactness, simplicity, and low cost, may give this traditional imaging polarimeter new life and attractive prospects.

Cardioprotective effects of timosaponin B-II isolated from Anemarrhena rhizome in a zebrafish model.

Timosaponin B-II (TB-II; (25S)-26-(ß-D-glucopyranosyloxy)-3ß-[(2-O-ß-D-glucopyranosyl-ß-D-galactopyranosyl) oxy]-5ß-furostan-22-ol is extracted from Anemarrhena. Its anti-inflammation, anti-oxidation, and anti-asthma properties have been widely explored. However, its effect on the heart has not been reported. In this study, we used zebrafish as a research model to determine the effects of TB-II on the heart and its toxic and anti-inflammatory effects. To explore the cause of cardioprotective effects of TB-II, we used transgenic zebrafish with macrophages and neutrophils labeled with fluorescent protein. We found for the first time that TB-II had a protective effect on the zebrafish heart. It did not affect the survival and hatching rates of zebrafish embryos, indicating its low toxicity. Results showed that TB-II may have cardioprotective effects, which might be related to its anti-inflammatory effects.

Tissue regeneration promotion effects of phenanthroimidazole derivatives through pro-inflammatory pathway activation.

A chemotherapeutic drug exerts favorable antitumor activity and simultaneously exhibits expectable inhibition on wound healing process. Phenanthroimidazole derivatives possess potent anticancer activity. However, only a few studies focused on the discovery of its potential effects on promoting tissue regeneration. In this study, four novel phenanthroimidazole derivatives were synthesized and characterized, and they exhibited evident inhibition on different tumor cells; compound 3 is the most active one. Moreover, 3 can promote wound healing of zebrafish in a dose-dependent manner. Further study demonstrated that 3 promoted the recruitment of inflammatory cells, formation of angiogenesis, and generation of reactive oxygen species and also influenced the motor behavior of zebrafish. Results indicated that 3 can accelerate the occurrence of pro-inflammation, angiogenesis, oxidative stress, and innervation, which play key roles in the facilitation of wound healing. Therefore, 3 can act as a bifunctional drug in inhibiting tumor and promoting tissue regeneration.

Parietal stimulation reverses age-related decline in exploration, learning, and decision-making.

Aging can compromise decision-making and learning, potentially due to reduced exploratory behaviors crucial for novel problem-solving. We posit that invigorating exploration could mitigate these declines. Supporting this hypothesis, we found that older mice mirrored human aging, displaying less exploration and learning during decision-making, but optogenetic stimulation of their posterior parietal cortex boosted initial exploration, subsequently improving learning. Thus, enhancing exploration-driven learning could be a key to countering cognitive aging.

Notch3 regulates ferroptosis via ROS-induced lipid peroxidation in NSCLC cells.

Ferroptosis is type of programmed cell death, which is known to be involved in certain cancers. Notch3 signaling is reported to be involved in the tumorigenesis of non-small-cell lung cancer (NSCLC) and regulates iron metabolism, lipid synthesis, and oxidative stress in some tissues. However, whether Notch3 signaling regulates ferroptosis is unclear. In this study, we found that ferroptosis inhibitors, ferrostatin-1 and liproxstatin-1, protected against cell death induced by Notch3 knockdown and that Notch3 knockdown initiated ferroptosis in NSCLC cells by increasing reactive oxygen species (ROS) levels, lipid peroxidation, and Fe2+ levels, accompanied by downregulation of glutathione peroxidase 4 (GPX4) and peroxiredoxin6 (PRDX6). Conversely, Notch3 intracellular domain overexpression suppressed erastin-induced ferroptosis, which was synergistically enhanced by MJ33 in H1299 cells via a decrease in ROS levels and lipid peroxidation, accompanied by upregulation of GPX4 and PRDX6. Moreover, Notch3 knockdown decreased tumorigenesis in vivo with downregulation of GPX4 and PRDX6. In summary, here we have identified Notch3 as a potential negative regulator of ferroptosis in NSCLC.

Effects of customized resin base on bonding strength of spherical self-ligating brackets.

PURPOSE: Fabricating resin bases has become an easy and economical method to achieve the customization of brackets. This study aimed to assess the effect of the resin base on bonding strength of spherical self-ligating brackets. METHODS: A defined amount of adhesive was bonded to the bracket base and constituted the new resin base. The thickness of the adhesive was measured and controlled at 0.5, 1.0, 1.5 and 2.0 mm, and a group without a resin base was used as a control. Sixty extracted human premolars were randomly divided into five groups. The brackets in each group were bonded to the specimen, and debonding tests were conducted. The shear bond strength (SBS) was calculated according to the measured debonding force in relation to the base area. The adhesive remnant index (ARI) score and the residual location of the fractured resin base were recorded. Enamel damage was also analyzed by scanning electron microscopy. After assessing for data normality and homogeneity, statistical comparisons between the groups and correlations among parameters were determined. P < 0.05 was regarded as significant. RESULTS: The correlation analysis revealed an inverse correlation between the resin base thickness and the SBS (Coeff = -0.719, P < 0.01). The highest SBS was 9.33 MPa, in the control group, which was significantly greater than the lowest SBS (6.03 MPa), in the 2.0-mm group (P < 0.05). Multiple comparisons analysis revealed no differences in SBS between the 1.0-, 1.5- and 2.0-mm groups. Nonparametric analysis found that only the ARI score in the 0.5-mm group (2.92) was significantly different (P < 0.05) from that in the control group (1.25). As the thickness of the resin base increased, the fractured resin base tended to remain at the bracket base, and the risk of enamel damage decreased. CONCLUSIONS: As the thickness of the resin base increased, the bonding strength of the spherical bracket decreased. However, the required clinical bonding strength was still satisfied when the thickness was less than 2.0 mm. The existence of a resin base could protect the enamel surface from damage caused by debonding. The customization of spherical brackets by tailoring a resin base can be applied in clinical practice because of the clinically acceptable bonding strength.

Notch3 is involved in the proliferation of renal cancer cells via regulation of cell cycle progression and HIF-2α.

Renal cell carcinoma (RCC) is one of the most common malignant tumors of the urinary system. Although deregulation of the Notch signaling pathway is common in RCC and is involved in the tumorigenic process, the exact role of Notch3 and its underlying molecular mechanism in RCC, particularly in hypoxia, remain unknown. In the present study, RO4929097, a Notch3 inhibitor, was used to alter NICD3 expression. A Cell Counting Kit-8 assay, EdU incorporation assay, colony formation assay, flow cytometry and western blot analysis were used to investigate the effects of altered NICD3 expression on cell proliferation, cell cycle progression and HIF-2α protein expression. The results of western blot analysis showed that RO4929097 dose-dependently decreased the expression of Notch3 intracellular domain (NICD3) in 786-O and ACHN cells, which originate from clear cell RCC (ccRCC). The results of the Cell Counting Kit-8, EdU incorporation and colony formation assays demonstrated that downregulation of NICD3 significantly suppressed cell proliferation in both normoxia and hypoxia. In addition, flow cytometry and western blot analysis demonstrated that hypoxia (2% O2) promoted cell cycle progression in ccRCC cells with the increased expression of G1-S transition-associated proteins, namely cyclin-dependent kinase (CDK)4 and cyclin D1, while downregulation of NICD3 exerted negative effects on cell cycle progression, and the expression levels of CDK4 and cyclin D1. Furthermore, western blot analysis revealed that 2% O2-induced upregulated hypoxia-inducible factor-2α (HIF-2α) expression decreased following downregulation of NICD3 in 786-O and ACHN cells. Following transfection of the vector containing the NICD3 coding sequence, HIF-2α, CDK4, cyclin D1 and proliferating cell nuclear antigen expression, that were inhibited by RO4929097 in hypoxia, were rescued. Collectively, the results of the present study suggest that Notch3 is closely associated with the cell proliferation of ccRCC cells by regulating the cell cycle and HIF-2α.

Sirt1 improves heart failure through modulating the NF-κB p65/microRNA-155/BNDF signaling cascade.

Heart failure (HF) affects over 26 million people worldwide, yet the pathologies of this complex syndrome have not been completely understood. Here, we investigated the involvement of deacetylase Sirtuin 1 (Sirt1) in HF and its downstream signaling pathways. A HF model was induced by the ligation of the left coronary artery in rats, where factors associated with left ventricular echocardiography, heart hemodynamics and ventricular mass indexes were recorded. Collagen volume fraction in heart tissues was determined by Masson's trichrome staining. Cell models of HF were also established (H2O2, 30 min) in cardiomyocytes harvested from suckling rats. HF rats presented with downregulated expressions of Sirt1, brain-derived neurotrophic factor (BDNF) and exhibited upregulated expressions of NF-κB p65 and miR-155. Repressed Sirt1 expression increased acetylation of NF-κB p65, resulting in the elevation of NF-κB p65 expression. NF-κB p65 silencing improved heart functions, decreased ventricular mass and reduced apoptosis in cardiomyocytes. MiR-155 inhibition upregulated its target gene BDNF, thereby reducing cardiomyocyte apoptosis. Sirt1 overexpression upregulated BDNF, improved heart function, and reduced apoptosis in cardiomyocytes. In conclusion, Sirt1 alleviates HF in rats through the NF-κB p65/miR-155/BDNF signaling cascade.