NH3-Sensing Mechanism Using Surface Acoustic Wave Sensor with AlO(OH) Film

In this study, AlO(OH) (boehmite) film was deposited onto a surface acoustic wave (SAW) resonator using a combined sol-gel and spin-coating technology, and prepared and used as a sensitive layer for a high-performance ammonia sensor. The prepared AlO(OH) film has a mesoporous structure and a good affinity to NH3 (ammonia gas) molecules, and thus can selectively adsorb and react with NH3. When exposed to ammonia gases, the SAW sensor shows an initial positive response of the frequency shift, and then a slight decrease of the frequency responses. The sensing mechanism of the NH3 sensor is based on the competition between mass-loading and elastic-loading effects. The sensor operated at room temperature shows a positive response of 1540 Hz to 10 ppm NH3, with excellent sensitivity, selectivity and stability

Physical Exercise Regulates p53 Activity Targeting SCO2 and Increases Mitochondrial COX Biogenesis in Cardiac Muscle with Age

The purpose of this study was to outline the timelines of mitochondrial function, oxidative stress and cytochrome c oxidase complex (COX) biogenesis in cardiac muscle with age, and to evaluate whether and how these age-related changes were attenuated by exercise. ICR/CD-1 mice were treated with pifithrin-μ (PFTμ), sacrificed and studied at different ages; ICR/CD-1 mice at younger or older ages were randomized to endurance treadmill running and sedentary conditions. The results showed that mRNA expression of p53 and its protein levels in mitochondria increased with age in cardiac muscle, accompanied by increased mitochondrial oxidative stress, reduced expression of COX subunits and assembly proteins, and decreased expression of most markers in mitochondrial biogenesis. Most of these age-related changes including p53 activity targeting cytochrome oxidase deficient homolog 2 (SCO2), p53 translocation to mitochondria and COX biogenesis were attenuated by exercise in older mice. PFTμ, an inhibitor blocking p53 translocation to mitochondria, increased COX biogenesis in older mice, but not in young mice. Our data suggest that physical exercise attenuates age-related changes in mitochondrial COX biogenesis and p53 activity targeting SCO2 and mitochondria, and thereby induces antisenescent and protective effects in cardiac muscle

Laser-Induced Damage Initiation and Growth of Optical Materials

The lifetime of optical components is determined by the combination of laser-induced damage initiation probability and damage propagation rate during subsequent laser shots. This paper reviews both theoretical and experimental investigations on laser-induced damage initiation and growth at the surface of optics. The damage mechanism is generally considered as thermal absorption and electron avalanche, which play dominant roles for the different laser pulse durations. The typical damage morphology in the surface of components observed in experiments is also closely related to the damage mechanism. The damage crater in thermal absorption process, which can be estimated by thermal diffusion model, is typical distortion, melting, and ablation debris often with an elevated rim caused by melted material flow and resolidification. However, damage initiated by electron avalanche is often accompanied by generation of plasma, crush, and fracture, which can be explained by thermal explosion model. Damage growth at rear surface of components is extremely severe which can be explained by several models, such as fireball growth, impact crater, brittle fracture, and electric field enhancement. All the physical effects are not independent but mutually coupling. Developing theoretical models of multiphysics coupling are an important trend for future theoretical research. Meanwhile, more attention should be paid to integrated analysis both in theory and experiment

Hexavalent Chromium Cr(VI) Up-Regulates COX-2 Expression through an NFκB/c-Jun/AP-1–Dependent Pathway

Background: Hexavalent chromium [Cr(VI)] is recognized as a human carcinogen via inhalation. However, the molecular mechanisms by which Cr(VI) causes cancers are not well understood

A New Allele of the SPIKE1 Locus Reveals Distinct Regulation of Trichome and Pavement Cell Development and Plant Growth

The single-celled trichomes of Arabidopsis thaliana have long served as an elegant model for elucidating the mechanisms of cell differentiation and morphogenesis due to their unique growth patterns. To identify new components in the genetic network that governs trichome development, we carried out exhaustive screens for additional Arabidopsis mutants with altered trichome morphology. Here, we report one mutant, aberrantly branched trichome1-1 (abt1-1), with a reduced trichome branching phenotype. After positional cloning, a point mutation in the SPIKE1 (SPK1) gene was identified in abt1-1. Further genetic complementation experiments confirmed that abt1-1 is a new allele of SPK1, so abt1-1 was renamed as spk1-7 according to the literatures. spk1-7 and two other spk1 mutant alleles, covering a spectrum of phenotypic severity, highlighted the distinct responses of developmental programs to different SPK1 mutations. Although null spk1 mutants are lethal and show defects in plant stature, trichome and epidermal pavement cell development, only trichome branching is affected in spk1-7. Surprisingly, we found that SPK1 is involved in the positioning of nuclei in the trichome cells. Lastly, through double mutant analysis, we found the coordinated regulation of trichome branching between SPK1 and two other trichome branching regulators, ANGUSTIFOLIA (AN) and ZWICHEL (ZWI). SPK1 might serve for the precise positioning of trichome nuclei, while AN and ZWI contribute to the formation of branch points through governing the cMTs dynamics. In summary, this study presented a fully viable new mutant allele of SPK1 and shed new light on the regulation of trichome branching and other developmental processes by SPK1

Transcriptome profile of halofuginone resistant and sensitive strains of Eimeria tenella

The antiparasitic drug halofuginone is important for controlling apicomplexan parasites. However, the occurrence of halofuginone resistance is a major obstacle for it to the treatment of apicomplexan parasites. Current studies have identified the molecular marker and drug resistance mechanisms of halofuginone in Plasmodium falciparum. In this study, we tried to use transcriptomic data to explore resistance mechanisms of halofuginone in apicomplexan parasites of the genus Eimeria (Apicomplexa: Eimeriidae). After halofuginone treatment of E. tenella parasites, transcriptome analysis was performed using samples derived from both resistant and sensitive strains. In the sensitive group, DEGs associated with enzymes were significantly downregulated, whereas the DNA damaging process was upregulated after halofuginone treatment, revealing the mechanism of halofuginone-induced parasite death. In addition, 1,325 differentially expressed genes (DEGs) were detected between halofuginone resistant and sensitive strains, and the DEGs related to translation were significantly downregulated after halofuginone induction. Overall, our results provide a gene expression profile for further studies on the mechanism of halofuginone resistance in E. tenella

Identification of Introgressed Alleles Conferring High Fiber Quality Derived From Gossypium barbadense L. in Secondary Mapping Populations of G. hirsutum L.

The improvement of fiber quality is an essential goal in cotton breeding. In our previous studies, several quantitative trait loci (QTLs) contributing to improved fiber quality were identified in different introgressed chromosomal regions from Sea Island cotton (Gossypium barbadense L.) in a primary introgression population (Pop. A) of upland cotton (G. hirsutum L.). In the present study, to finely map introgressed major QTLs and accurately dissect the genetic contribution of the target introgressed chromosomal segments, we backcrossed two selected recombinant inbred lines (RILs) that presented desirable high fiber quality with their high lint-yielding recurrent parent to ultimately develop two secondary mapping populations (Pop. B and Pop. C). Totals of 20 and 27 QTLs for fiber quality were detected in Pop. B and Pop. C, respectively, including four and five for fiber length, four and eight for fiber micronaire, two and four for fiber uniformity, five and four for fiber elongation, and six and four for fiber strength, respectively. Two QTLs for lint percentage were detected only in Pop. C. In addition, seven stable QTLs were identified, including two for both fiber length and fiber strength and three for fiber elongation. Five QTL clusters for fiber quality were identified in the introgressed chromosomal regions, and negative effects of these chromosomal regions on lint percentage (a major lint yield parameter) were not observed. Candidate genes with a QTL-cluster associated with fiber strength and fiber length in the introgressed region of Chr.7 were further identified. The results may be helpful for revealing the genetic basis of superior fiber quality contributed by introgressed alleles from G. barbadense. Possible strategies involving marker-assisted selection (MAS) for simultaneously improving upland cotton fiber quality and lint yield in breeding programs was also discussed

E3 Ligase Activity of XIAP RING Domain Is Required for XIAP-Mediated Cancer Cell Migration, but Not for Its RhoGDI Binding Activity

Although an increased expression level of XIAP is associated with cancer cell metastasis, the underlying molecular mechanisms remain largely unexplored. To verify the specific structural basis of XIAP for regulation of cancer cell migration, we introduced different XIAP domains into XIAP−/− HCT116 cells, and found that reconstitutive expression of full length HA-XIAP and HA-XIAP ΔBIR, both of which have intact RING domain, restored β-Actin expression, actin polymerization and cancer cell motility. Whereas introduction of HA-XIAP ΔRING or H467A mutant, which abolished its E3 ligase function, did not show obvious restoration, demonstrating that E3 ligase activity of XIAP RING domain played a crucial role of XIAP in regulation of cancer cell motility. Moreover, RING domain rather than BIR domain was required for interaction with RhoGDI independent on its E3 ligase activity. To sum up, our present studies found that role of XIAP in regulating cellular motility was uncoupled from its caspase-inhibitory properties, but related to physical interaction between RhoGDI and its RING domain. Although E3 ligase activity of RING domain contributed to cell migration, it was not involved in RhoGDI binding nor its ubiquitinational modification

WldS Reduces Paraquat-Induced Cytotoxicity via SIRT1 in Non-Neuronal Cells by Attenuating the Depletion of NAD

WldS is a fusion protein with NAD synthesis activity, and has been reported to protect axonal and synaptic compartments of neurons from various mechanical, genetic and chemical insults. However, whether WldS can protect non-neuronal cells against toxic chemicals is largely unknown. Here we found that WldS significantly reduced the cytotoxicity of bipyridylium herbicides paraquat and diquat in mouse embryonic fibroblasts, but had no effect on the cytotoxicity induced by chromium (VI), hydrogen peroxide, etoposide, tunicamycin or brefeldin A. WldS also slowed down the death of mice induced by intraperitoneal injection of paraquat. Further studies demonstrated that WldS markedly attenuated mitochondrial injury including disruption of mitochondrial membrane potential, structural damage and decline of ATP induced by paraquat. Disruption of the NAD synthesis activity of WldS by an H112A or F116S point mutation resulted in loss of its protective function against paraquat-induced cell death. Furthermore, WldS delayed the decrease of intracellular NAD levels induced by paraquat. Similarly, treatment with NAD or its precursor nicotinamide mononucleotide attenuated paraquat-induced cytotoxicity and decline of ATP and NAD levels. In addition, we showed that SIRT1 was required for both exogenous NAD and WldS-mediated cellular protection against paraquat. These findings suggest that NAD and SIRT1 mediate the protective function of WldS against the cytotoxicity induced by paraquat, which provides new clues for the mechanisms underlying the protective function of WldS in both neuronal and non-neuronal cells, and implies that attenuation of NAD depletion may be effective to alleviate paraquat poisoning