Activation of autophagy and IL-10 production are regulated by Jun N-terminal kinase 1 and 2 and p38 mitogen activated protein kinase signaling pathways during Talaromyces marneffei infection within dendritic cells.

Previous study have shown that Talaromyces marneffei (T. marneffei) induced activation of autophagy. Therefore, we explore signaling pathway that regulates activation of autophagy by intracellular signaling mechanisms during T. marneffei infection. Further, we examine c-Jun N-terminal kinase 1 and 2 (JNK1/2) and p38 signaling pathways that regulate IL-1ß and IL-10 production and activation of autophagy during T. marneffei infection in human dendritic cells (DCs). We found that T. marneffei induced activation of JNK1/2 and p38 in human DCs. Furthermore, the inhibition of JNK1/2 and p38 increased activation of autophagy and decreased the replication of T. marneffei in T. marneffei-infected human DCs. Moreover, IL-1ß secretion in T. marneffei-infected human DCs was dependent on JNK1/2 and autophagy pathways, whereas IL-10 secretion was dependent on JNK1/2, p38 and autophagy pathways. These data suggest that JNK1/2 and p38 pathways play critical roles in activation of autophagy, the multiplication of T. marneffei and subsequent cytokine production during T. marneffei infection.

Optical properties of electrically controlled arc-electrode liquid-crystal microlens array for wavefront measurement and adjustment.

An electrically controlled arc-electrode liquid-crystal microlens array (AE-LCMLA), with tuning and swing focus, is proposed, which can be utilized to replace the traditional mechanically controlled microlenses and also cooperate with photosensitive arrays to solve the problems of measuring and further adjusting a strong distortion wavefront. The top patterned electrode of a single LC microlens is composed of three arc-electrodes distributed symmetrically around a central microhole for constructing the key controlling structures of the LC cavity in the AE-LCMLA. All the arc-electrodes are individually controlled, and then the focal spot of each microlens can be moved freely in a three-dimensional fashion including along the optical axial direction and over the focal plane by simply adjusting the driving signal voltage applied over each arc-electrode, independently. The featured performances of the AE-LCMLA in a wavelength range of ∼501-561 nm are the driving signal voltage being relatively low (less than ∼11 Vrms), the focal length tuning range being from ∼2.54 mm to ∼3.50 mm, the maximum focus swing distance being ∼52.92 µm, and the focus swing ratio K being ∼20‰.

Resveratrol induces p53 in colorectal cancer through SET7/9.

Resveratrol is one of the most promising phytoalexins for use as an anti-cancer agent, which is present in the skin of red grapes and berries. Resveratrol has been demonstrated to modulate a number of signalling pathways that are involved in carcinogenesis. In the present study, the function of resveratrol as a pro-apoptotic agent in colorectal cancer cell lines, including HCT116, CO115 and SW48, was investigated. The results revealed that resveratrol supressed cell viability. Additionally, resveratrol enhanced the expression of tumour protein p53 (p53) and p53 target genes, including Bcl2 associated X, apoptosis regulator and Bcl2 binding component 3 that have a pivotal role in p53-dependent apoptosis. Furthermore, treating cells with resveratrol upregulated SET domain containing lysine methyltransferase 7/9 (SET7/9) expression, which positively regulates p53 through its mono-methylation at lysine 372, compared with untreated cells. Furthermore, treating cells with resveratrol induced the expression of apoptotic markers including cleaved caspase-3 and poly (ADP-ribose) polymerases (PARP) compared with untreated cells. However, the genetic knockdown of SET7/9 by short hairpin RNA attenuated the resveratrol-driven overexpression of p53, cleaved caspase-3 and PARP. Collectively, these results reveal the molecular mechanisms by which resveratrol induces p53 stability in colon cancer that results in the activation of p53-mediated apoptosis.

Research on a Dual-Mode Infrared Liquid-Crystal Device for Simultaneous Electrically Adjusted Filtering and Zooming.

A new dual-mode liquid-crystal (LC) micro-device constructed by incorporating a Fabry⁻Perot (FP) cavity and an arrayed LC micro-lens for performing simultaneous electrically adjusted filtering and zooming in infrared wavelength range is presented in this paper. The main micro-structure is a micro-cavity consisting of two parallel zinc selenide (ZnSe) substrates that are pre-coated with ~20-nm aluminum (Al) layers which served as their high-reflection films and electrodes. In particular, the top electrode of the device is patterned by 44 × 38 circular micro-holes of 120 µm diameter, which also means a 44 × 38 micro-lens array. The micro-cavity with a typical depth of ~12 µm is fully filled by LC materials. The experimental results show that the spectral component with needed frequency or wavelength can be selected effectively from incident micro-beams, and both the transmission spectrum and the point spread function can be adjusted simultaneously by simply varying the root-mean-square value of the signal voltage applied, so as to demonstrate a closely correlated feature of filtering and zooming. In addition, the maximum transmittance is already up to ~20% according the peak-to-valley value of the spectral transmittance curves, which exhibits nearly twice the increment compared with that of the ordinary LC-FP filtering without micro-lenses.

Silencing of Tctex1 impairs autophagy lysosomal degradation of α-synuclein and cell viability.

Tctex1 is an important element of the dynein motor unit in mammalian cells that helps move targets along microtubules and toward the centrosome for degradation. Here, we analyzed the role of Tctex1 in the α-synuclein autophagy-lysosome degradation pathway using Tctex1-siRNA in SH-SY5Y cells. Results showed that siRNA silencing of Tctex1 suppressed cellular viability and promoted cell apoptosis. Protein and mRNA expression of Tctex1 and dynein decreased after Tctex1 knockdown, whereas α-synuclein, LC3-II, and LAMP2 increased. Consistently, fluorescence intensity of Tctex1 was weaker in siRNA-Tctex1-transfected cells, and that of α-synuclein, LC3-II, and LAMP2 was increased. Tctex1 inhibition reduced cell viability and promoted apoptosis. These results show that Tctex1 plays an important role in α-synuclein autophagic degradation and in maintaining cellular homeostasis.