SDSS-IV MaNGA : spatial evolution of star formation triggered by galaxy interactions

Galaxy interaction is considered a key driver of galaxy evolution and star formation (SF) history. In this paper, we present an empirical picture of the radial extent of interaction-triggered SF along the merger sequence. The samples under study are drawn from the integral field spectroscopy survey SDSS-IV MaNGA, including 205 star-forming galaxies in pairs/mergers and ~1350 control galaxies. For each galaxy in pairs, the merger stage is identified according to its morphological signatures: incoming phase, at first pericenter passage, at apocenter, in merging phase, and in final coalescence. The effect of interactions is quantified by the global and spatially resolved SF rate (SFR) relative to the SFR of a control sample selected for each individual galaxy (Δlog SFR and Δlog sSFR(r), respectively). Analysis of the radial Δlog sSFR(r) distributions shows that galaxy interactions have no significant impact on Δlog sSFR(r) during the incoming phase. Right after the first pericenter passage, the radial Δlog sSFR(r) profile decreases steeply from enhanced to suppressed activity for increasing galactocentric radius. Later on, SF is enhanced on a broad spatial scale out to the maximum radius we explore (~6.7 kpc) and the enhancement is in general centrally peaked. The extended SF enhancement is also observed for systems at their apocenters and in the coalescence phase, suggesting that interaction-triggered SF is not restricted to the central region of a galaxy. Further explorations of a wide range in parameter space of merger configurations (e.g., mass ratio) are required to constrain the whole picture of interaction-triggered S

SiMMap: a web server for inferring site-moiety map to recognize interaction preferences between protein pockets and compound moieties

The protein–ligand interacting mechanism is essential to biological processes and drug discovery. The SiMMap server statistically derives site-moiety map with several anchors, which describe the relationship between the moiety preferences and physico-chemical properties of the binding site, from the interaction profiles between query target protein and its docked (or co-crystallized) compounds. Each anchor includes three basic elements: a binding pocket with conserved interacting residues, the moiety composition of query compounds and pocket–moiety interaction type (electrostatic, hydrogen bonding or van der Waals). We provide initial validation of the site-moiety map on three targets, thymidine kinase, and estrogen receptors of antagonists and agonists. Experimental results show that an anchor is often a hot spot and the site-moiety map can help to assemble potential leads by optimal steric, hydrogen bonding and electronic moieties. When a compound highly agrees with anchors of site-moiety map, this compound often activates or inhibits the target protein. We believe that the site-moiety map is useful for drug discovery and understanding biological mechanisms. The SiMMap web server is available at http://simfam.life.nctu.edu.tw/

Capacitive and non-capacitive faradaic charge storage

This article aims to offer a critical overview of selected literature on capacitive and non-capacitive faradaic charge storage. It is particularly relevant to the concept of pseudocapacitance that is generally described as a result of fast surface faradaic processes. In general, faradaic processes represent electron transfer reactions at the interface between an electrode and its contacting solid or liquid electrolyte phase that is able to accept or donate electrons. Obviously, not all faradaic processes can be associated with pseudocapacitance. The question is how to differentiate pseudocapacitance related faradaic charge storage from the others. Therefore, attempts have been made to apply the band model for semiconductors to account qualitatively for the origin of pseudocapacitance. Capacitive and non-capacitive faradaic processes are then proposed to define and differentiate different charge storage mechanisms in supercapacitor and battery. On the other hand, the unequal electrode capacitance approach and the use of Ca2+ in aqueous electrolytes are discussed in relation with enhanced energy capacity of supercapacitors. In addition, the principle of supercapattery as a hybrid device is explained with recent literature examples

A Nanodot Array Modulates Cell Adhesion and Induces an Apoptosis-Like Abnormality in NIH-3T3 Cells

Micro-structures that mimic the extracellular substratum promote cell growth and differentiation, while the cellular reaction to a nanostructure is poorly defined. To evaluate the cellular response to a nanoscaled surface, NIH 3T3 cells were grown on nanodot arrays with dot diameters ranging from 10 to 200 nm. The nanodot arrays were fabricated by AAO processing on TaN-coated wafers. A thin layer of platinum, 5 nm in thickness, was sputtered onto the structure to improve biocompatibility. The cells grew normally on the 10-nm array and on flat surfaces. However, 50-nm, 100-nm, and 200-nm nanodot arrays induced apoptosis-like events. Abnormality was triggered after as few as 24 h of incubation on a 200-nm dot array. For cells grown on the 50-nm array, the abnormality started after 72 h of incubation. The number of filopodia extended from the cell bodies was lower for the abnormal cells. Immunostaining using antibodies against vinculin and actin filament was performed. Both the number of focal adhesions and the amount of cytoskeleton were decreased in cells grown on the 100-nm and 200-nm arrays. Pre-coatings of fibronectin (FN) or type I collagen promoted cellular anchorage and prevented the nanotopography-induced programed cell death. In summary, nanotopography, in the form of nanodot arrays, induced an apoptosis-like abnormality for cultured NIH 3T3 cells. The occurrence of the abnormality was mediated by the formation of focal adhesions

Broad targeting of resistance to apoptosis in cancer

Apoptosis or programmed cell death is natural way of removing aged cells from the body. Most of the anti-cancer therapies trigger apoptosis induction and related cell death networks to eliminate malignant cells. However, in cancer, de-regulated apoptotic signaling, particularly the activation of an anti-apoptotic systems, allows cancer cells to escape this program leading to uncontrolled proliferation resulting in tumor survival, therapeutic resistance and recurrence of cancer. This resistance is a complicated phenomenon that emanates from the interactions of various molecules and signaling pathways. In this comprehensive review we discuss the various factors contributing to apoptosis resistance in cancers. The key resistance targets that are discussed include (1) Bcl-2 and Mcl-1 proteins; (2) autophagy processes; (3) necrosis and necroptosis; (4) heat shock protein signaling; (5) the proteasome pathway; (6) epigenetic mechanisms; and (7) aberrant nuclear export signaling. The shortcomings of current therapeutic modalities are highlighted and a broad spectrum strategy using approaches including (a) gossypol; (b) epigallocatechin-3-gallate; (c) UMI-77 (d) triptolide and (e) selinexor that can be used to overcome cell death resistance is presented. This review provides a roadmap for the design of successful anti-cancer strategies that overcome resistance to apoptosis for better therapeutic outcome in patients with cancer

The Anti-Apoptotic Bcl-xL Protein, a New Piece in the Puzzle of Cytochrome C Interactome

A structural model of the adduct between human cytochrome c and the human anti-apoptotic protein Bcl-xL, which defines the protein-protein interaction surface, was obtained from solution NMR chemical shift perturbation data. The atomic level information reveals key intermolecular contacts identifying new potentially druggable areas on cytochrome c and Bcl-xL. Involvement of residues on cytochrome c other than those in its complexes with electron transfer partners is apparent. Key differences in the contact area also exist between the Bcl-xL adduct with the Bak peptide and that with cytochrome c. The present model provides insights to the mechanism by which cytochrome c translocated to cytosol can be intercepted, so that the apoptosome is not assembled

The histone H3K36 demethylase Rph1/KDM4 regulates the expression of the photoreactivation gene PHR1

The dynamics of histone methylation have emerged as an important issue since the identification of histone demethylases. We studied the regulatory function of Rph1/KDM4 (lysine demethylase), a histone H3K36 demethylase, on transcription in Saccharomyces cerevisiae. Overexpression of Rph1 reduced the expression of PHR1 and increased UV sensitivity. The catalytically deficient mutant (H235A) of Rph1 diminished the repressive transcriptional effect on PHR1 expression, which indicates that histone demethylase activity contributes to transcriptional repression. Chromatin immunoprecipitation analysis demonstrated that Rph1 was associated at the upstream repression sequence of PHR1 through zinc-finger domains and was dissociated after UV irradiation. Notably, overexpression of Rph1 and H3K36A mutant reduced histone acetylation at the URS, which implies a crosstalk between histone demethylation and acetylation at the PHR1 promoter. In addition, the crucial checkpoint protein Rad53 acted as an upstream regulator of Rph1 and dominated the phosphorylation of Rph1 that was required for efficient PHR1 expression and the dissociation of Rph1. The release of Rph1 from chromatin also required the phosphorylation at S652. Our study demonstrates that the histone demethylase Rph1 is associated with a specific chromatin locus and modulates histone modifications to repress a DNA damage responsive gene under control of damage checkpoint signaling

Effect of Temperature Gradient Direction in the Catalyst Nanoparticle on CNTs Growth Mode

To improve the understanding on CNT growth modes, the various processes, including thermal CVD, MP-CVD and ECR-CVD, have been used to deposit CNTs on nanoporous SBA-15 and Si wafer substrates with C2H2 and H2 as reaction gases. The experiments to vary process parameter of ΔT, defined as the vector quantities of temperature at catalyst top minus it at catalyst bottom, were carried out to demonstrate its effect on the CNT growth mode. The TEM and TGA analyses were used to characterize their growth modes and carbon yields of the processes. The results show that ΔT can be used to monitor the temperature gradient direction across the catalyst nanoparticle during the growth stage of CNTs. The results also indicate that the tip-growth CNTs, base-growth CNTs and onion-like carbon are generally fabricated under conditions of ΔT > 0, <0 and ~0, respectively. Our proposed growth mechanisms can be successfully adopted to explain why the base- and tip-growth CNTs are common in thermal CVD and plasma-enhanced CVD processes, respectively. Furthermore, our experiments have also successfully demonstrated the possibility to vary ΔT to obtain the desired growth mode of CNTs by thermal or plasma-enhanced CVD systems for different applications

Dehydrocostuslactone Suppresses Angiogenesis In Vitro and In Vivo through Inhibition of Akt/GSK-3β and mTOR Signaling Pathways

The traditional Chinese medicine component dehydrocostuslactone (DHC) isolated from Saussurea costus (Falc.) Lipschitz, has been shown to have anti-cancer activity. Angiogenesis is an essential process in the growth and progression of cancer. In this study, we demonstrated, for the first time, the anti-angiogenic mechanism of action of DHC to be via the induction of cell cycle progression at the G0/G1 phase due to abrogation of the Akt/glycogen synthase kinase-3β (GSK-3β)/cyclin D1 and mTOR signaling pathway. First, we demonstrated that DHC has an anti-angiogenic effect in the matrigel-plug nude mice model and an inhibitory effect on human umbilical vein endothelial cell (HUVEC) proliferation and capillary-like tube formation in vitro. DHC caused G0/G1 cell cycle arrest, which was associated with the down-regulation of cyclin D1 expression, leading to the suppression of retinoblastoma protein phosphorylation and subsequent inhibition of cyclin A and cdk2 expression. With respect to the molecular mechanisms underlying the DHC-induced cyclin D1 down-regulation, this study demonstrated that DHC significantly inhibits Akt expression, resulting in the suppression of GSK-3β phosphorylation and mTOR expression. These effects are capable of regulating cyclin D1 degradation, but they were significantly reversed by constitutively active myristoylated (myr)-Akt. Furthermore, the abrogation of tube formation induced by DHC was also reversed by overexpression of Akt. And the co-treatment with LiCl and DHC significantly reversed the growth inhibition induced by DHC. Taken together, our study has identified Akt/GSK-3β and mTOR as important targets of DHC and has thus highlighted its potential application in angiogenesis-related diseases, such as cancer