bluuebunny/crossref_metadata_2025_split huggingface dataset:
The chemical states and atomic structure evolution of ultralow-energy high-dose Boron implanted Si(110) via laser annealing
Authors: Lee Fu-Ying , Wu Zong-Zhe , Kao Li-Chi , Chang Feng-Mei , Chen Sheng-Wen , JangJian Shiu-Ko , Cheng Hui-Yu , Chen Wei-Liang , Chang Yu-Ming , Lo Kuang Yao 
Published: October 2017

AbstractFurther scale down the dimension of silicon-based integrated circuit is a crucial trend in semiconductor fabrication. One of the most critical issues in the nano-device fabrication is to confirm the atomic structure evolution of the ultrathin shallow junction. In this report, UV Raman spectroscopy, X-ray photoelectron spectroscopy (XPS), X-ray absorption near edge structure (XANES) and reflective second harmonic generation (RSHG) are utilized to monitor the pulse laser induced atomic structure evolution of ultralow-energy high-dose Boron implanted Si(110) at room and cold substrate temperature. A peak feature around 480 cm−1 resolved in UV Raman spectra indicates the formation of Si-B bond after the laser irradiation. The red shift of binding energy of Si element (~99 eV) in XPS and the evolution of absorption peak (~196.2 eV) in XANES reveal that the changes in the chemical states of ultra shallow junction strongly correlate to the activation process of Boron implantation, which is confirmed by RSHG measurement. The substrate temperature effect in the recrystallization of Boron implanted region is also realized by cross-section high-resolution TEM (HRTEM). The phenomena of Si-B bond formation and ultra-shallow junction recrystallization can be traced and applied to improve the reliability of Si ultra shallow junction in the future.
Vascular Endothelial Growth Factor in Cartilage Development and Osteoarthritis
Authors: Nagao Masashi , Hamilton John L. , Kc Ranjan , Berendsen Agnes D. , Duan Xuchen , Cheong Chan Wook , Li Xin , Im Hee-Jeong , Olsen Bjorn R. 
Published: October 2017

AbstractGenome wide studies indicate that vascular endothelial growth factor A (VEGF) is associated with osteoarthritis (OA), and increased VEGF expression correlates with increased disease severity. VEGF is also a chondrocyte survival factor during development and essential for bone formation, skeletal growth and postnatal homeostasis. This raises questions of how the important embryonic and postnatal functions of VEGF can be reconciled with an apparently destructive role in OA. Addressing these questions, we find that VEGF acts as a survival factor in growth plate chondrocytes during development but only up until a few weeks after birth in mice. It is also required for postnatal differentiation of articular chondrocytes and the timely ossification of bones in joint regions. In surgically induced knee OA in mice, a model of post-traumatic OA in humans, increased expression of VEGF is associated with catabolic processes in chondrocytes and synovial cells. Conditional knock-down of Vegf attenuates induced OA. Intra-articular anti-VEGF antibodies suppress OA progression, reduce levels of phosphorylated VEGFR2 in articular chondrocytes and synovial cells and reduce levels of phosphorylated VEGFR1 in dorsal root ganglia. Finally, oral administration of the VEGFR2 kinase inhibitor Vandetanib attenuates OA progression.
Characterization of Fluorescein Arsenical Hairpin (FlAsH) as a Probe for Single-Molecule Fluorescence Spectroscopy
Authors: Fernandes Dennis D. , Bamrah Jasbir , Kailasam Senthilkumar , Gomes Gregory-Neal W. , Li Yuchong , Wieden Hans-Joachim , Gradinaru Claudiu C. 
Published: October 2017

AbstractIn recent years, new labelling strategies have been developed that involve the genetic insertion of small amino-acid sequences for specific attachment of small organic fluorophores. Here, we focus on the tetracysteine FCM motif (FLNCCPGCCMEP), which binds to fluorescein arsenical hairpin (FlAsH), and the ybbR motif (TVLDSLEFIASKLA) which binds fluorophores conjugated to Coenzyme A (CoA) via a phosphoryl transfer reaction. We designed a peptide containing both motifs for orthogonal labelling with FlAsH and Alexa647 (AF647). Molecular dynamics simulations showed that both motifs remain solvent-accessible for labelling reactions. Fluorescence spectra, correlation spectroscopy and anisotropy decay were used to characterize labelling and to obtain photophysical parameters of free and peptide-bound FlAsH. The data demonstrates that FlAsH is a viable probe for single-molecule studies. Single-molecule imaging confirmed dual labeling of the peptide with FlAsH and AF647. Multiparameter single-molecule Förster Resonance Energy Transfer (smFRET) measurements were performed on freely diffusing peptides in solution. The smFRET histogram showed different peaks corresponding to different backbone and dye orientations, in agreement with the molecular dynamics simulations. The tandem of fluorophores and the labelling strategy described here are a promising alternative to bulky fusion fluorescent proteins for smFRET and single-molecule tracking studies of membrane proteins.
Trk-fused gene (TFG) regulates pancreatic β cell mass and insulin secretory activity
Authors: Yamamotoya Takeshi , Nakatsu Yusuke , Kushiyama Akifumi , Matsunaga Yasuka , Ueda Koji , Inoue Yuki , Inoue Masa-Ki , Sakoda Hideyuki , Fujishiro Midori , Ono Hiraku , Kiyonari Hiroshi , Ishihara Hisamitsu , Asano Tomoichiro 
Published: October 2017

AbstractThe Trk-fused gene (TFG) is reportedly involved in the process of COPII-mediated vesicle transport and missense mutations in TFG cause several neurodegenerative diseases including hereditary motor and sensory neuropathy with proximal dominant involvement (HMSN-P). The high coincidence ratio between HMSN-P and diabetes mellitus suggests TFG to have an important role(s) in glucose homeostasis. To examine this possibility, β-cell specific TFG knockout mice (βTFG KO) were generated. Interestingly, βTFG KO displayed marked glucose intolerance with reduced insulin secretion. Immunohistochemical analysis revealed smaller β-cell masses in βTFG KO than in controls, likely attributable to diminished β-cell proliferation. Consistently, β-cell expansion in response to a high-fat, high-sucrose (HFHS) diet was significantly impaired in βTFG KO. Furthermore, glucose-induced insulin secretion was also markedly impaired in islets isolated from βTFG KO. Electron microscopic observation revealed endoplasmic reticulum (ER) dilatation, suggestive of ER stress, and smaller insulin crystal diameters in β-cells of βTFG KO. Microarray gene expression analysis indicated downregulation of NF-E2 related factor 2 (Nrf2) and its downstream genes in TFG depleted islets. Collectively, TFG in pancreatic β-cells plays a vital role in maintaining both the mass and function of β-cells, and its dysfunction increases the tendency to develop glucose intolerance.
Revealing the Saline Adaptation Strategies of the Halophilic Bacterium Halomonas beimenensis through High-throughput Omics and Transposon Mutagenesis Approaches
Authors: Chen Yan-Huey , Lu Chia-Wei , Shyu Yuan-Tay , Lin Shih-Shun 
Published: October 2017

AbstractStudies on the halotolerance of bacteria are attractive to the fermentation industry. However, a lack of sufficient genomic information has precluded an investigation of the halotolerance of Halomonas beimenensis. Here, we describe the molecular mechanisms of saline adaptation in H. beimenensis based on high-throughput omics and Tn5 transposon mutagenesis. The H. beimenensis genome is 4.05 Mbp and contains 3,807 genes, which were sequenced using short and long reads obtained via deep sequencing. Sixteen Tn5 mutants with a loss of halotolerance were identified. Orthologs of the mutated genes, such as nqrA, trkA, atpC, nadA, and gdhB, have significant biological functions in sodium efflux, potassium uptake, hydrogen ion transport for energy conversion, and compatible solute synthesis, which are known to control halotolerance. Other genes, such as spoT, prkA, mtnN, rsbV, lon, smpB, rfbC, rfbP, tatB, acrR1, and lacA, function in cellular signaling, quorum sensing, transcription/translation, and cell motility also shown critical functions for promoting a halotolerance. In addition, KCl application increased halotolerance and potassium-dependent cell motility in a high-salinity environment. Our results demonstrated that a combination of omics and mutagenesis could be used to facilitate the mechanistic exploitation of saline adaptation in H. beimenensis, which can be applied for biotechnological purposes.
Mitochondrial glycerol 3-phosphate facilitates bumblebee pre-flight thermogenesis
Authors: Masson Stewart W. C. , Hedges Christopher P. , Devaux Jules B. L. , James Crystal S. , Hickey Anthony J. R. 
Published: October 2017

AbstractBumblebees (Bombus terrestris) fly at low ambient temperatures where other insects cannot, and to do so they must pre-warm their flight muscles. While some have proposed mechanisms, none fully explain how pre-flight thermogenesis occurs. Here, we present a novel hypothesis based on the less studied mitochondrial glycerol 3-phosphate dehydrogenase pathway (mGPDH). Using calorimetry, and high resolution respirometry coupled with fluorimetry, we report substrate oxidation by mGPDH in permeabilised flight muscles operates, in vitro, at a high flux, even in the absence of ADP. This may be facilitated by an endogenous, mGPDH-mediated uncoupling of mitochondria. This uncoupling increases ETS activity, which results in increased heat release. Furthermore, passive regulation of this mechanism is achieved via dampened temperature sensitivity of mGPDH relative to other respiratory pathways, and subsequent consumption of its substrate, glycerol 3-phosphate (G3P), at low temperatures. Mitochondrial GPDH may therefore facilitate pre-flight thermogenesis through poor mitochondrial coupling. We calculate this can occur at a sufficient rate to warm flight muscles until shivering commences, and until flight muscle function is adequate for bumblebees to fly in the cold.
Small-angle neutron scattering modeling of spin disorder in nanoparticles
Authors: Vivas Laura G. , Yanes Rocio , Michels Andreas 
Published: October 2017

AbstractMagnetic small-angle neutron scattering (SANS) is a powerful technique for investigating magnetic nanoparticle assemblies in nonmagnetic matrices. For such microstructures, the standard theory of magnetic SANS assumes uniformly magnetized nanoparticles (macrospin model). However, there exist many experimental and theoretical studies which suggest that this assumption is violated: deviations from ellipsoidal particle shape, crystalline defects, or the interplay between various magnetic interactions (exchange, magnetic anisotropy, magnetostatics, external field) may lead to nonuniform spin structures. Therefore, a theoretical framework of magnetic SANS of nanoparticles needs to be developed. Here, we report numerical micromagnetic simulations of the static spin structure and related unpolarized magnetic SANS of a single cobalt nanorod. While in the saturated state the magnetic SANS cross section is (as expected) determined by the particle form factor, significant deviations appear for nonsaturated states; specifically, at remanence, domain-wall and vortex states emerge which result in a magnetic SANS signal that is composed of all three magnetization Fourier components, giving rise to a complex angular anisotropy on a two-dimensional detector. The strength of the micromagnetic simulation methodology is the possibility to decompose the cross section into the individual Fourier components, which allows one to draw important conclusions regarding the fundamentals of magnetic SANS.
Work and information from thermal states after subtraction of energy quanta
Authors: Hloušek J. , Ježek M. , Filip R. 
Published: October 2017

AbstractQuantum oscillators prepared out of thermal equilibrium can be used to produce work and transmit information. By intensive cooling of a single oscillator, its thermal energy deterministically dissipates to a colder environment, and the oscillator substantially reduces its entropy. This out-of-equilibrium state allows us to obtain work and to carry information. Here, we propose and experimentally demonstrate an advanced approach, conditionally preparing more efficient out-of-equilibrium states only by a weak dissipation, an inefficient quantum measurement of the dissipated thermal energy, and subsequent triggering of that states. Although it conditionally subtracts the energy quanta from the oscillator, average energy grows, and second-order correlation function approaches unity as by coherent external driving. On the other hand, the Fano factor remains constant and the entropy of the subtracted state increases, which raise doubts about a possible application of this approach. To resolve it, we predict and experimentally verify that both available work and transmitted information can be conditionally higher in this case than by arbitrary cooling or adequate thermal heating up to the same average energy. It qualifies the conditional procedure as a useful source for experiments in quantum information and thermodynamics.
Metabolic Responses of Eisenia Fetida to Individual Pb and Cd Contamination in Two Types of Soils
Authors: Tang Ronggui , Ding Changfeng , Ma Yibing , Wang Junsong , Zhang Taolin , Wang Xingxiang 
Published: October 2017

AbstractTo characterize the potential toxicity of low Pb- and Cd-contaminated arable soils, earthworms were exposed to Pb contaminated ferrosol, cambosol or Cd contaminated ferrosol for two weeks. Polar metabolites of earthworms were detected by nuclear magnetic resonance. Data were then analyzed with principal component analysis followed by orthogonal signal correction-partial least squares-discriminant analysis and univariate analysis to determine possible mechanisms for the changes in metabolites. The survival rates, metal concentrations and bioaccumulation factor (BAF) of the earthworms were also measured and calculated as auxiliary data. The results showed that the metabolite profiles were highly similar in Pb-contaminated ferrosol and cambosol (R2 = 0.76, p < 0.0001), which can be attributed to similar response mechanisms. However, there was a more intense response in ferrosol likely due to higher Pb concentrations in earthworms. Metabolic pathways and BAFs exhibited apparent distinctions between Pb- and Cd-contaminated ferrosol, likely because they bind to different bio-ligands. The affected metabolic pathways were involved in alanine-aspartate-glutamate, purine, glutathione, valine-leucine-isoleucine biosynthesis and degradation and nicotinate and nicotinamide metabolism. Regarding the bioavailability in earthworms, Pb availability was higher for ferrosol than for cambosol. We confirmed that the potential toxicity of low Pb/Cd-contaminated soils can be characterized using earthworm metabolomics.
Growth hormone secretagogues hexarelin and JMV2894 protect skeletal muscle from mitochondrial damages in a rat model of cisplatin-induced cachexia
Authors: Sirago Giuseppe , Conte Elena , Fracasso Flavio , Cormio Antonella , Fehrentz Jean-Alain , Martinez Jean , Musicco Clara , Camerino Giulia Maria , Fonzino Adriano , Rizzi Laura , Torsello Antonio , Lezza Angela Maria Serena , Liantonio Antonella , Cantatore Palmiro , Pesce Vito 
Published: October 2017

AbstractChemotherapy can cause cachexia, which consists of weight loss associated with muscle atrophy. The exact mechanisms underlying this skeletal muscle toxicity are largely unknown and co-therapies to attenuate chemotherapy-induced side effects are lacking. By using a rat model of cisplatin-induced cachexia, we here characterized the mitochondrial homeostasis in tibialis anterior cachectic muscle and evaluated the potential beneficial effects of the growth hormone secretagogues (GHS) hexarelin and JMV2894 in this setting. We found that cisplatin treatment caused a decrease in mitochondrial biogenesis (PGC-1α, NRF-1, TFAM, mtDNA, ND1), mitochondrial mass (Porin and Citrate synthase activity) and fusion index (MFN2, Drp1), together with changes in the expression of autophagy-related genes (AKT/FoxO pathway, Atg1, Beclin1, LC3AII, p62) and enhanced ROS production (PRX III, MnSOD). Importantly, JMV2894 and hexarelin are capable to antagonize this chemotherapy-induced mitochondrial dysfunction. Thus, our findings reveal a key-role played by mitochondria in the mechanism responsible for GHS beneficial effects in skeletal muscle, strongly indicating that targeting mitochondrial dysfunction might be a promising area of research in developing therapeutic strategies to prevent or limit muscle wasting in cachexia.
Associations of interactions between NLRP3 SNPs and HLA mismatch with acute and extensive chronic graft-versus-host diseases
Authors: Takahashi Hidekazu , Okayama Naoko , Yamaguchi Natsu , Miyahara Yuta , Morishima Yasuo , Suehiro Yutaka , Yamasaki Takahiro , Tamada Koji , Takahashi Satoshi , Tojo Arinobu , Asano Shigetaka , Tanabe Tsuyoshi 
Published: October 2017

AbstractHLA matching is a well-known genetic requirement for successful bone marrow transplantation (BMT). However, the importance of non-HLA single-nucleotide polymorphisms (SNPs) remains poorly understood. The NLR family pyrin domain–containing 3 (NLRP3) inflammasome, a key regulator of innate immunity, is associated with multiple diseases. We retrospectively genotyped SNPs of NLRP1–3 and caspase recruitment domain family member 8 (CARD8), which are implicated in the interleukin 1β (IL-1β) signaling, in 999 unrelated BMT donor–recipient pairs. We identified an association of the interaction between the recipient NLRP3 SNP CC genotype and total HLA mismatches with grade 2–4 acute graft-versus-host disease (AGVHD), and an association of the interaction between the donor NLRP3 SNP T allele and HLA-C mismatch with extensive chronic GVHD (ECGVHD), in both adjusted and unadjusted regressions (P < 0.005). Importantly, the ECGVHD risk associated with HLA-C mismatch was not elevated when the donor NLRP3 genotype was CC. We also identified an association of the interaction between recipient NLRP3 SNP and donor cytomegalovirus seropositivity with overall survival in adjusted regressions (P < 0.005). These results suggest the importance of certain SNP–covariate interactions in unrelated BMT. The three identified interactions may be useful for donor selection or outcome prediction.
Spectrum of spontaneous photon emission as a promising biophysical indicator for breast cancer research
Authors: Zhao Xiaolei , Yang Meina , Wang Yong , Pang Jingxiang , Wijk Eduard Van , Liu Yanli , Fan Hua , Zhang Liewei , Han Jinxiang 
Published: October 2017

AbstractIn this study, we investigated the spectral characteristics of Spontaneous Photon Emission (SPE) from the body surface of a human breast cancer-bearing nude mice model during the overall growth process of breast cancers. By comparing and analyzing the data, we found that there was a striking difference between tumor mice and healthy controls in the spectral distribution of SPE from the body surface of lesion site, even when the morphological changes at the lesion site were not obvious. The spectral distribution of SPE from the healthy site of the tumor mice also differed from that of the healthy controls as the breast cancer developed to a certain stage. In addition, the difference in spectrum was related with different growth states of tumors. Interestingly, there was a positive correlation between the spectral ratio (610–630/395–455 nm) and the logarithm of the tumor volume for both the lesion site (R2 = 0.947; p < 0.001) and the normal site (R2 = 0.892; p < 0.001) of the tumor mice. The results suggested that the spectrum of SPE was sensitive to changes in the tumor status.
Bortezomib promotes KHSV and EBV lytic cycle by activating JNK and autophagy
Authors: Granato Marisa , Romeo Maria Anele , Tiano Mariangela Sara , Santarelli Roberta , Gonnella Roberta , Gilardini Montani Maria Saveria , Faggioni Alberto , Cirone Mara 
Published: October 2017

AbstractKSHV and EBV are gammaherpesviruses strictly linked to human cancers. Even if the majority of cancer cells harbor a latent infection, the few cells that undergo viral replication may contribute to the pathogenesis and maintenance of the virus-associated malignancies. Cytotoxic drugs used for the therapies of cancers harboring virus-infection often have, as side effect, the activation of viral lytic cycle. Therefore it is important to investigate whether they affect viral reactivation and understand the underlying mechanisms involved. In this study, we found that proteasome inhibitor bortezomib, a cytotoxic drug that efficiently target gammaherpesvirus-associated B cell lymphomas, triggered KSHV or EBV viral lytic cycle by activating JNK, in the course of ER stress, and inducing autophagy. These results suggest that the manipulation of these pathways could limit viral spread and improve the outcome of bortezomib treatment in patients affected by gammaherpesvirus-associated lymphomas.
In vivo noninvasive microscopy of human leucocytes
Authors: Winer Matan M. , Zeidan Adel , Yeheskely-Hayon Daniella , Golan Lior , Minai Limor , Dann Eldad J. , Yelin Dvir 
Published: October 2017

AbstractLeucocytes play a key role in our immune system, protecting the body against infections using a wide range of biological mechanisms. Effective imaging and identification of leucocytes within the blood stream in patients is challenging, however, because of their low volume fraction in the blood, the high tissue scattering and the rapid blood flow. Spectrally encoded flow cytometry (SEFC) has recently been demonstrated effective for label-free high-resolution in vivo imaging of blood cells using an optical probe that does not require mechanical scanning. Here, we use SEFC to noninvasively image leucocytes at different imaging depths within small vessels in human volunteers, and identify visual differences in cell brightness and nuclei shapes, that would help distinguish between the two most abundant leucocyte types. The observed differences match the in vitro characteristics of isolated granulocytes and mononuclear cells. The results prove the potential of the system for conducting differential leucocyte count and as an effective research tool for studying the function and distribution of leucocytes in humans.
Ultraintense UV emission from ZnO-sheathed ZnS nanorods
Authors: Lee Jae Kyung , Sun Gun-Joo , Lee Woo Seok , Hyun Soong Keun , Kim Kyoung-Kook , Choi Seung-Bok , Lee Chongmu 
Published: October 2017

AbstractShort-wavelength luminescence is essential for high-performance optoelectronic device applications. There have been efforts to obtain intense ultraviolet (UV) emission by encapsulating ZnO one-dimensional (1D) nanostructures with materials such as ZnS. However, the encapsulation of ZnS 1D nanostructures with ZnO has not been reported. In this paper, we report ultraintense UV emission from ZnS nanorods coated with ZnO, i.e., ZnS-core/ZnO-shell nanorods. UV emission from the ZnS-core/ZnO-shell nanorods was much more intense than that obtained from the extensively studied ZnO-core/ZnS-shell nanorods. The highest intensity of the near-band-edge emission from the ZnS-core/ZnO-shell nanorods was obtained with a ZnO shell layer thickness of 35 nm, which is ∼16 times higher than that of pristine ZnS nanorods. Moreover, the deep level (DL) emission was suppressed completely. The substantial enhancement of the UV emission from the ZnS nanorods and the complete suppression of the DL emission by ZnO sheathing can be rationalized by combining the following four effects: the reinforcement of the UV emission by the overlap of the UV emissions from the ZnS core and ZnO shell, enhancement of the emission from the ZnO shell by the carrier transfer from the ZnS core to the ZnO shell, suppression of the capture of carriers by the surface states on the ZnS surface, and suppression of the visible emission and nonradiative recombination in ZnS.