A new mechanical structural damage feature index based on HHT

A new damage feature index is presented for the structural health monitoring based on Hilbert-Huang transform (HHT). The energy marginal spectrum of the dynamic signal is used to construct damage characteristic parameter, which can reflect the signal energy variation and benefit the structural damage detection. A sinusoidal wave with frequency change and a composite plate vibration experiment with pre-defined damage are designed to verify the effectiveness of characteristic parameter in damage detection. Results obtained from simulation and test show that the extracted non-model-based damage feature index is available and sensitive in damage detection of time-varying system.Peer Reviewe

Afadin orients cell division to position the tubule lumen in developing renal tubules

In many types of tubules, continuity of the lumen is paramount to tubular function, yet how tubules generate lumen continuity in vivo is not known. We recently found the F-actin binding protein Afadin is required for lumen continuity in developing renal tubules, though its mechanism of action remains unknown. Here we demonstrate Afadin is required for lumen continuity by orienting the mitotic spindle during cell division. Using an in vitro 3D cyst model, we find Afadin localizes to the cell cortex adjacent to the spindle poles and orients the mitotic spindle. In tubules, cell division may be oriented relative to two axes, longitudinal and apical-basal. Unexpectedly, in vivo examination of early stage developing nephron tubules reveals cell division is not oriented in the longitudinal (or planar polarized) axis. However, cell division is oriented perpendicular to the apical-basal axis. Absence of Afadin in vivo leads to misorientation of apical-basal cell division in nephron tubules. Together these results support a model whereby Afadin determines lumen placement by directing apical-basal spindle orientation, which generates a continuous lumen and normal tubule morphogenesis

Electronic Structures of N-doped Graphene with Native Point Defects

Nitrogen doping in graphene has important implications in graphene-based devices and catalysts. We have performed the density functional theory calculations to study the electronic structures of N-doped graphene with vacancies and Stone-Wales defect. Our results show that monovacancies in graphene act as hole dopants and that two substitutional N dopants are needed to compensate for the hole introduced by a monovacancy. On the other hand, divacancy does not produce any free carriers. Interestingly, a single N dopant at divacancy acts as an acceptor rather than a donor. The interference between native point defect and N dopant strongly modifies the role of N doping regarding the free carrier production in the bulk pi bands. For some of the defects and N dopant-defect complexes, localized defect pi states are partially occupied. Discussion on the possibility of spin polarization in such cases is given. We also present qualitative arguments on the electronic structures based on the local bond picture. We have analyzed the 1s-related x-ray photoemission and adsorption spectroscopy spectra of N dopants at vacancies and Stone-Wales defect in connection with the experimental ones. We also discuss characteristic scanning tunneling microscope (STM) images originating from the electronic and structural modifications by the N dopant-defect complexes. STM imaging for small negative bias voltage will provide important information about possible active sites for oxygen reduction reaction.Comment: 40 pages, 2 tables, 16 figures. The analysis of Clar sextets is added. This version is published on PHYSICAL REVIEW B 87, 165401(2013

Interplay between Nitrogen Dopants and Native Point Defects in Graphene

To understand the interaction between nitrogen dopants and native point defects in graphene, we have studied the energetic stability of N-doped graphene with vacancies and Stone-Wales (SW) defect by performing the density functional theory calculations. Our results show that N substitution energetically prefers to occur at the carbon atoms near the defects, especially for those sites with larger bond shortening, indicating that the defect-induced strain plays an important role in the stability of N dopants in defective graphene. In the presence of monovacancy, the most stable position for N dopant is the pyridinelike configuration, while for other point defects studied (SW defect and divacancies) N prefers a site in the pentagonal ring. The effect of native point defects on N dopants is quite strong: While the N doping is endothermic in defect-free graphene, it becomes exothermic for defective graphene. Our results imply that the native point defect and N dopant attract each other, i.e., cooperative effect, which means that substitutional N dopants would increase the probability of point defect generation and vice versa. Our findings are supported by recent experimental studies on the N doping of graphene. Furthermore we point out possibilities of aggregation of multiple N dopants near native point defects. Finally we make brief comments on the effect of Fe adsorption on the stability of N dopant aggregation.Comment: 10 pages, 5 figures. Figure 4(g) and Figure 5 are corrected. One additional table is added. This is the final version for publicatio

Data-driven Exploration of New Pressure-induced Superconductivity in PbBi2_2Te4_4 with Two Transition Temperatures

Candidates compounds for new thermoelectric and superconducting materials, which have narrow band gap and flat bands near band edges, were exhaustively searched by the high-throughput first-principles calculation from an inorganic materials database named AtomWork. We focused on PbBi$_2$Te$_4$ which has the similar electronic band structure and the same crystal structure with those of a pressure-induced superconductor SnBi2Se4 explored by the same data-driven approach. The PbBi$_2$Te$_4$ was successfully synthesized as single crystals using a melt and slow cooling method. The core level X-ray photoelectron spectroscopy analysis revealed Pb2+, Bi3+ and Te2- valence states in PbBi$_2$Te$_4$. The thermoelectric properties of the PbBi$_2$Te$_4$ sample were measured at ambient pressure and the electrical resistivity was also evaluated under high pressure using a diamond anvil cell with boron-doped diamond electrodes. The resistivity decreased with increase of the pressure, and two pressure-induced superconducting transitions were discovered at 3.4 K under 13.3 GPa and at 8.4 K under 21.7 GPa. The data-driven approach shows promising power to accelerate the discovery of new thermoelectric and superconducting materials

Simultaneous Identification of Multiple Causal Mutations in Rice

Next-generation sequencing technologies (NGST) are being used to discover causal mutations in ethyl methanesulfonate (EMS)-mutagenized plant populations. However, the published protocols often deliver too many candidate sites and sometimes fail to find the mutant gene of interest. Accurate identification of the causal mutation from massive background polymorphisms and sequencing deficiencies remains challenging. Here we describe a NGST-based method, named SIMM, that can simultaneously identify the causal mutations in multiple independent mutants. Multiple rice mutants derived from the same parental line were back-crossed, and for each mutant, the derived F2 individuals of the recessive mutant phenotype were pooled and sequenced. The resulting sequences were aligned to the Nipponbare reference genome, and single nucleotide polymorphisms (SNPs) were subsequently compared among the mutants. Allele index (AI) and Euclidean distance (ED) were incorporated into the analysis to reduce noises caused by background polymorphisms and re-sequencing errors. Corrections of sequence bias against GC- and AT-rich sequences in the candidate region were conducted when necessary. Using this method, we successfully identified seven new mutant alleles from Huanghuazhan (HHZ), an elite indica rice cultivar in China. All mutant alleles were validated by phenotype association assay.Guangdong Innovative Research Team Program [201001S0104725509]; Ministry of Agriculture Transgenic Project [2012ZX08001001]; National Program on Key Basic Research Project of China [973 Program] [2011CB100101, 2013CBA01402]; National High Technology Research and Development Program of China [863 Program] [2014AA10A602]; Natural Science Foundation of China [31110103917]; Shenzhen Commission on Innovation and Technology [KQF201109160004A, CXZZ20140411140647863]SCI(E)ARTICLE

REGULATION OF IMMEDIATE EARLY AND EPITHELIAL-MESENCHYMAL TRANSITION GENES EXPRESSION BY ADIPOCYTOKINES IN THE FEMALE REPRODUCTIVE TRACT

Individuals who are overweight or obese are at increased risk for cancer. However, the mechanistic link between obesity and cancer is poorly defined. Adipose tissue produces hormones and pro-inflammatory cytokines with mitogenic properties. Many of these hormones and cytokines are altered in obese individuals and may lead to disruption of the normal balance between cell proliferation, differentiation, and apoptosis. Thus, the objective of this study was to determine how adipocyte-derived factors regulate the expression of genes that contribute to cell proliferation and migration. To compare immediate early gene (cell proliferation) and epithelial-mesenchymal transition (cell migration) gene expression between untreated and treated cells, HeLa cells were exposed to IGF-1 (100ng/ml), leptin (100ng/ml), TNFa (10ng/ml), or IL-6 (10ng/ml) and QPCR analyses were carried out. Immediate early gene expression was regulated by all four hormones. Specifically, IGF-1 increased Jun, Fos, and Il-8; leptin increased Jun and Il-6; IL-6 increased Fos, Il-6, and Il-8; and TNFa increased Jun, Fos, Il-6, and Il-8 mRNA abundance. Genes that regulate the epithelial-mesenchymal transition were also regulated by IGF-1, IL-6, and TNF. Specifically, IGF-1 increased Snail1 and Snail2; IL-6 increased Snail1; and TNF increased Jag1 mRNAs. Interestingly, the expression of Snail1, Snail2, JUN, and FOS was increased in the uterus of age-matched obese compared to normal-weight mice. Western blot analyses demonstrated that these changes in mRNA abundance were associated with increased phosphorylation of Akt, Erk1/2, Jnk, and Stat3 in treated compared to untreated cells suggesting that these signaling factors play a role in the regulation of immediate early and epithelial-mesenchymal transition gene expression. These studies demonstrate for the first time a mechanistic link between factors produced and secreted by adipocytes and the expression of genes associated with cell transformation, proliferation, and migration. These cell functions play an important role in tumorigenesis and therefore changes in their expression may provide a plausible mechanism for obesity-dependent increases in a myriad of cancer

REGULATION OF IMMEDIATE EARLY AND EPITHELIAL-MESENCHYMAL TRANSITION GENES EXPRESSION BY ADIPOCYTOKINES IN THE FEMALE REPRODUCTIVE TRACT

Individuals who are overweight or obese are at increased risk for cancer. However, the mechanistic link between obesity and cancer is poorly defined. Adipose tissue produces hormones and pro-inflammatory cytokines with mitogenic properties. Many of these hormones and cytokines are altered in obese individuals and may lead to disruption of the normal balance between cell proliferation, differentiation, and apoptosis. Thus, the objective of this study was to determine how adipocyte-derived factors regulate the expression of genes that contribute to cell proliferation and migration. To compare immediate early gene (cell proliferation) and epithelial-mesenchymal transition (cell migration) gene expression between untreated and treated cells, HeLa cells were exposed to IGF-1 (100ng/ml), leptin (100ng/ml), TNFa (10ng/ml), or IL-6 (10ng/ml) and QPCR analyses were carried out. Immediate early gene expression was regulated by all four hormones. Specifically, IGF-1 increased Jun, Fos, and Il-8; leptin increased Jun and Il-6; IL-6 increased Fos, Il-6, and Il-8; and TNFa increased Jun, Fos, Il-6, and Il-8 mRNA abundance. Genes that regulate the epithelial-mesenchymal transition were also regulated by IGF-1, IL-6, and TNF. Specifically, IGF-1 increased Snail1 and Snail2; IL-6 increased Snail1; and TNF increased Jag1 mRNAs. Interestingly, the expression of Snail1, Snail2, JUN, and FOS was increased in the uterus of age-matched obese compared to normal-weight mice. Western blot analyses demonstrated that these changes in mRNA abundance were associated with increased phosphorylation of Akt, Erk1/2, Jnk, and Stat3 in treated compared to untreated cells suggesting that these signaling factors play a role in the regulation of immediate early and epithelial-mesenchymal transition gene expression. These studies demonstrate for the first time a mechanistic link between factors produced and secreted by adipocytes and the expression of genes associated with cell transformation, proliferation, and migration. These cell functions play an important role in tumorigenesis and therefore changes in their expression may provide a plausible mechanism for obesity-dependent increases in a myriad of cancer

Nel positively regulates the genesis of retinal ganglion cells by promoting their differentiation and survival during development

Peer reviewedPublisher PD