bluuebunny/crossref_metadata_2025_split huggingface dataset:
A novel ruthenium (II)-derived organometallic compound, TQ-6, potently inhibits platelet aggregation: Ex vivo and in vivo studies
Authors: Hsia Chih-Hsuan , Velusamy Marappan , Sheu Joen-Rong , Khamrang Themmila , Jayakumar Thanasekaran , Lu Wan-Jung , Lin Kuan-Hung , Chang Chao-Chien 
Published: August 2017

AbstractArterial thrombosis plays a key role in cardiovascular diseases. Hence, developing more effective antithrombotic agents is necessary. We designed a ruthenium (II)-derived complex, [Ru(η6-cymene)2-(1H-benzoimidazol-2-yl)-quinoline Cl]BF4 (TQ-6), as a new antiplatelet drug. TQ-6 (0.3 µM) exhibited extremely strong inhibitory activity against platelet aggregation, Src, and Syk phosphorylation stimulated by agonists in human platelets. In collagen-activated platelets, TQ-6 also inhibited ATP-release, [Ca+2]i, P-selectin expression, FITC-PAC-1 binding, and hydroxyl radical formation, as well as the phosphorylation of phospholipase Cγ2, protein kinase C, mitogen-activated protein kinases, and Akt. Neither FITC-JAQ1 nor FITC-triflavin binding or integrin β3 phosphorylation stimulated by immobilized fibrinogen were diminished by TQ-6. Furthermore, TQ-6 had no effects in cyclic nucleotide formation. Moreover, TQ-6 substantially prolonged the closure time in whole blood, increased the occlusion time of thrombotic platelet plug formation and bleeding time in mice. In conclusion, TQ-6 has a novel role in inhibiting platelet activation through the inhibition of the agonist receptors-mediated inside-out signaling such as Src-Syk-PLCγ2 cascade and subsequent suppression of granule secretion, leading to disturb integrin αIIbβ3-mediated outside-in signaling, and ultimately inhibiting platelet aggregation. Therefore, TQ-6 has potential to develop as a therapeutic agent for preventing or treating thromboembolic disorders.
Circulating endothelial cell-derived extracellular vesicles mediate the acute phase response and sickness behaviour associated with CNS inflammation
Authors: Couch Yvonne , Akbar Naveed , Roodselaar Jay , Evans Matthew C. , Gardiner Chris , Sargent Ian , Romero Ignacio A. , Bristow Adrian , Buchan Alastair M. , Haughey Norman , Anthony Daniel C. 
Published: August 2017

AbstractBrain injury elicits a systemic acute-phase response (APR), which is responsible for co-ordinating the peripheral immunological response to injury. To date, the mechanisms responsible for signalling the presence of injury or disease to selectively activate responses in distant organs were unclear. Circulating endogenous extracellular vesicles (EVs) are increased after brain injury and have the potential to carry targeted injury signals around the body. Here, we examined the potential of EVs, isolated from rats after focal inflammatory brain lesions using IL-1β, to activate a systemic APR in recipient naïve rats, as well as the behavioural consequences of EV transfer. Focal brain lesions increased EV release, and, following isolation and transfer, the EVs were sequestered by the liver where they initiated an APR. Transfer of blood-borne EVs from brain-injured animals was also enough to suppress exploratory behaviours in recipient naïve animals. EVs derived from brain endothelial cell cultures treated with IL-1β also activated an APR and altered behaviour in recipient animals. These experiments reveal that inflammation-induced circulating EVs derived from endothelial cells are able to initiate the APR to brain injury and are sufficient to generate the associated sickness behaviours, and are the first demonstration that EVs are capable of modifying behavioural responses.
Neuroprotective effect of kinin B1 receptor activation in acute cerebral ischemia in diabetic mice
Authors: Desposito Dorinne , Zadigue Georges , Taveau Christopher , Adam Clovis , Alhenc-Gelas François , Bouby Nadine , Roussel Ronan 
Published: August 2017

AbstractActivation of the kallikrein-kinin system enhances cardiac and renal tolerance to ischemia. Here we investigated the effects of selective agonists of kinin B1 or B2 receptor (R) in brain ischemia-reperfusion in diabetic and non-diabetic mice. The role of endogenous kinins was assessed in tissue kallikrein deficient mice (TK−/−). Mice underwent 60min-middle cerebral artery occlusion (MCAO), eight weeks after type 1-diabetes induction. Treatment with B1R-, B2R-agonist or saline was started at reperfusion. Neurological deficit (ND), infarct size (IS), brain water content (BWC) were measured at day 0, 1 and 2 after injury. MCAO induced exaggerated ND, mortality and IS in diabetic mice. B2R-agonist increased ND and mortality to 60% and 80% in non-diabetic and diabetic mice respectively, by mechanisms involving hemodynamic failure and renal insufficiency. TK−/− mice displayed reduced ND and IS compared to wild-type littermate, consistent with suppression of B2R activity. B1R mRNA level increased in ischemic brain but B1R-agonist had no effect on ND, mortality or IS in non-diabetic mice. In contrast, in diabetic mice, B1R-agonist tested at two doses significantly reduced ND by 42–52% and IS by 66–71%, without effect on BWC or renal function. This suggests potential therapeutic interest of B1R agonism for cerebral protection in diabetes.
Hyperspectral data processing improves PpIX contrast during fluorescence guided surgery of human brain tumors
Authors: Bravo J. J. , Olson J. D. , Davis S. C. , Roberts D. W. , Paulsen K. D. , Kanick S. C. 
Published: August 2017

AbstractFluorescence guided surgery (FGS) using aminolevulinic-acid (ALA) induced protoporphyrin IX (PpIX) provides intraoperative visual contrast between normal and malignant tissue during resection of high grade gliomas. However, maps of the PpIX biodistribution within the surgical field based on either visual perception or the raw fluorescence emissions can be masked by background signals or distorted by variations in tissue optical properties. This study evaluates the impact of algorithmic processing of hyperspectral imaging acquisitions on the sensitivity and contrast of PpIX maps. Measurements in tissue-simulating phantoms showed that (I) spectral fitting enhanced PpIX sensitivity compared with visible or integrated fluorescence, (II) confidence-filtering automatically determined the lower limit of detection based on the strength of the PpIX spectral signature in the collected emission spectrum (0.014–0.041 μg/ml in phantoms), and (III) optical-property corrected PpIX estimates were more highly correlated with independent probe measurements (r = 0.98) than with spectral fitting alone (r = 0.91) or integrated fluorescence (r = 0.82). Application to in vivo case examples from clinical neurosurgeries revealed changes to the localization and contrast of PpIX maps, making concentrations accessible that were not visually apparent. Adoption of these methods has the potential to maintain sensitive and accurate visualization of PpIX contrast over the course of surgery.
Overexpression of miR-210 and its significance in ischemic tissue damage
Authors: Zaccagnini G. , Maimone B. , Fuschi P. , Maselli D. , Spinetti G. , Gaetano C. , Martelli F. 
Published: August 2017

AbstractHypoxia-induced miR-210 displays a pro-survival, cytoprotective and pro-angiogenic role in severalin vitrosystems.In vivo, we previously found that miR-210 inhibition increases ischemic damage. Here we describe the generation of a versatile transgenic mouse model allowing the evaluation of miR-210 therapeutic potential in ischemic cardiovascular diseases. We generated a Tet-On miR-210 transgenic mouse strain (TG-210) by targeted transgenesis in the ROSA26 locus. To functionally validate miR-210 transgenic mice, hindlimb ischemia was induced by femoral artery dissection. Blood perfusion was evaluated by power Doppler while tissue damage and inflammation were assessed by histological evaluation. We found that miR-210 levels were rapidly increased in TG-210 mice upon doxycycline administration. miR-210 overexpression was maintained over time and remained within physiological levels in multiple tissues. When hindlimb ischemia was induced, miR-210 overexpression protected from both muscular and vascular ischemic damage, decreased inflammatory cells density and allowed to maintain a better calf perfusion. In conclusion, we generated and functionally validated a miR-210 transgenic mouse model. Albeit validated in the context of a specific cardiovascular ischemic disease, miR-210 transgenic mice may also represent a useful model to assess the function of miR-210 in other physio-pathological conditions.
GsCHX19.3, a member of cation/H+ exchanger superfamily from wild soybean contributes to high salinity and carbonate alkaline tolerance
Authors: Jia Bowei , Sun Mingzhe , DuanMu Huizi , Ding Xiaodong , Liu Beidong , Zhu Yanming , Sun Xiaoli 
Published: August 2017

AbstractCation/H+ exchangers (CHX) are characterized to be involved in plant growth, development and stress responses. Although soybean genome sequencing has been completed, the CHX family hasn’t yet been systematically analyzed, especially in wild soybean. Here, through Hidden Markov Model search against Glycine soja proteome, 34 GsCHXs were identified and phylogenetically clustered into five groups. Members within each group showed high conservation in motif architecture. Interestingly, according to our previous RNA-seq data, only Group IVa members exhibited highly induced expression under carbonate alkaline stress. Among them, GsCHX19.3 displayed the greatest up-regulation in response to carbonate alkaline stress, which was further confirmed by quantitative real-time PCR analysis. We also observed the ubiquitous expression of GsCHX19.3 in different tissues and its localization on plasma membrane. Moreover, we found that GsCHX19.3 expression in AXT4K, a yeast mutant lacking four ion transporters conferred resistance to low K+ at alkali pH, as well as carbonate stress. Consistently, in Arabidopsis, GsCHX19.3 overexpression increased plant tolerance both to high salt and carbonate alkaline stresses. Furthermore, we also confirmed that GsCHX19.3 transgenic lines showed lower Na+ concentration but higher K+/Na+ values under salt-alkaline stress. Taken together, our findings indicated that GsCHX19.3 contributed to high salinity and carbonate alkaline tolerance.
Bacterial Community Structure in the Asian Rice Gall Midge Reveals a Varied Microbiome Rich in Proteobacteria
Authors: Ojha Abhishek , Sinha Deepak Kumar , Padmakumari A. P. , Bentur J. S. , Nair Suresh 
Published: August 2017

AbstractThe Asian rice gall midge (ARGM) has emerged as a model gall forming pest of rice. The ARGM infestation of rice results in failure of panicle formation and economic loss. Understanding the molecular basis of ARGM-rice interactions is very crucial in order to control this devastating pest of rice. The current investigation was devised to identify bacterial communities present in the ARGM and in addition the bacterial diversity in the maggots during their interaction with susceptible or resistant rice varieties. Sequencing of 16S rRNA bacterial gene (V3-V4 region) revealed differences in the microflora of the ARGM maggots feeding on susceptible or resistant rice hosts. Results revealed that Wolbachia was the predominant bacterium in pupae and adults while Pseudomonas was predominant in maggots. Further, we observed that members of proteobacteria were predominant across all the samples. There was high species diversity in maggots isolated from susceptible rice and a high representation of unclassified bacteria in maggots isolated from resistant rice. This is the first study that reports variation of microbiome of the ARGM, based on host phenotype from which it was isolated, and results suggest that these variations could have an important role in host’s susceptibility.
Universal linear-temperature resistivity: possible quantum diffusion transport in strongly correlated superconductors
Authors: Hu Tao , Liu Yinshang , Xiao Hong , Mu Gang , Yang Yi-feng 
Published: August 2017

AbstractThe strongly correlated electron fluids in high temperature cuprate superconductors demonstrate an anomalous linear temperature (T) dependent resistivity behavior, which persists to a wide temperature range without exhibiting saturation. As cooling down, those electron fluids lose the resistivity and condense into the superfluid. However, the origin of the linear-T resistivity behavior and its relationship to the strongly correlated superconductivity remain a mystery. Here we report a universal relation $$d{\boldsymbol{\rho }}/{\boldsymbol{dT}}=({{\boldsymbol{\mu }}}_{{\bf{0}}}{{\boldsymbol{k}}}_{{\boldsymbol{B}}}/{\boldsymbol{\hslash }})\,{{\boldsymbol{\lambda }}}_{{\boldsymbol{L}}}^{{\bf{2}}}$$

d
ρ

/

dT

=
(

μ

0

k

B

/
ℏ

)

λ

L

2

, which bridges the slope of the linear-T-dependent resistivity (dρ/dT) to the London penetration depth λ
L
at zero temperature among cuprate superconductor Bi2Sr2CaCu2O8+δ
and heavy fermion superconductors CeCoIn5, where μ0 is vacuum permeability, k
B
is the Boltzmann constant and ħ is the reduced Planck constant. We extend this scaling relation to different systems and found that it holds for other cuprate, pnictide and heavy fermion superconductors as well, regardless of the significant differences in the strength of electronic correlations, transport directions, and doping levels. Our analysis suggests that the scaling relation in strongly correlated superconductors could be described as a hydrodynamic diffusive transport, with the diffusion coefficient (D) approaching the quantum limit D ~ ħ/m*, where m* is the quasi-particle effective mass.
Exciton-polariton Josephson junctions at finite temperatures
Authors: Lebedev M. E. , Dolinina D. A. , Hong Kuo-Bin , Lu Tien-Chang , Kavokin A. V. , Alodjants A. P. 
Published: August 2017

AbstractWe consider finite temperature effects in a non-standard Bose-Hubbard model for an exciton- polariton Josephson junction (JJ) that is characterised by complicated potential energy landscapes (PEL) consisting of sets of barriers and wells. We show that the transition between thermal activation (classical) and tunneling (quantum) regimes exhibits universal features of the first and second order phase transition (PT) depending on the PEL for two polariton condensates that might be described as transition from the thermal to the quantum annealing regime. In the presence of dissipation the relative phase of two condensates exhibits non-equilibrium PT from the quantum regime characterized by efficient tunneling of polaritons to the regime of permanent Josephson or Rabi oscillations, where the tunneling is suppressed, respectively. This analysis paves the way for the application of coupled polariton condensates for the realisation of a quantum annealing algorithm in presently experimentally accessible semiconductor microcavities possessing high (105 and more) Q-factors.
Characterization and RNAi-mediated knockdown of Chitin Synthase A in the potato tuber moth, Phthorimaea operculella
Authors: Mohammed Ahmed M. A. , Diab Mervat R. , Abdelsattar Mohamed , khalil Sayed M. S. 
Published: August 2017

AbstractChitin is a major component of insect exoskeleton, tracheal system and gut where it is synthesized by chitin synthase (CHS) enzymes. In this paper, we report the isolation and RNAi of chitin synthase A (PhoCHSA) from the potato tuber moth Phthorimaea operculella. The full-length cDNA of PhoCHSA is 5,627 bp with 4,689 bp open reading frame coding for 1,563 amino acids. Structural analysis of conceptual amino acid translation showed three distinct regions found in all known insect CHS proteins; N-terminus region having 9 transmembrane helices, middle catalytic region containing several conserved domains identified in insect CHS enzymes, and C-terminus region containing seven transmembrane spans. Phylogenetic analysis showed that PhoCHSA protein clustered with CHSA enzymes identified from insects from different insect orders. RNAi targeting three different regions of the gene showed different efficacy against potato tuber moth larvae and dsRNA targeting the 5′ region has the highest efficacy. Results were verified by qRT-PCR which showed that dsRNA targeting the 5′ region caused the highest reduction in PhoCHSA mRNA level. Our results show the importance of selecting the RNAi target region and that chitin synthase A can be a suitable RNAi target for the potato tuber moth control.
SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis
Authors: Yu Jianhua , Zhang Weiguang , Qian Hongwei , Tang Haijun , Lin Weiguo , Lu Baochun 
Published: August 2017

AbstractAcute obstructive cholangitis (AOC) is a common and severe infectious diseases that occurs in an obstructed biliary system. The suppressors of cytokine signaling (SOCS) family include well-known negative regulators of cytokine receptor signaling. However, few studies have been conducted to determine their function in AOC. In this study, we showed that SOCS1 expression aberrantly changed and was associated with AOC prognosis in rat models. Decreased SOCS1 expression enhances regenerative response after biliary drainage (BD) resulting from AOC by upregulating hepatocyte growth factor (HGF) signaling. To detect SOCS1 expression in the liver less invasively and to predict the prognosis for AOC after BD, miR-221 and miR-222 were investigated. Ectopic SOCS1 expression indirectly decreases miR-221/222 expression through Met in vitro. An inverse correlation between SOCS1 expression and miR-221/222 expression in liver tissue or in serum was verified in rats. Serum from AOC patients showed that lower expression of circulating miR-221/222 after endoscopic nasobiliary drainage was associated with delayed restoration of liver function. Our results showed that SOCS1 regulates hepatic regenerative response, and indirectly detecting downstream molecules, such as miR-221/222, may provide prognostic makers for AOC.
Bone marrow-derived cells and their conditioned medium induce microvascular repair in uremic rats by stimulation of endogenous repair mechanisms
Authors: Golle Lina , Gerth Hans U. , Beul Katrin , Heitplatz Barbara , Barth Peter , Fobker Manfred , Pavenstädt Hermann , Di Marco Giovana S. , Brand Marcus 
Published: August 2017

AbstractThe reduced number of circulating stem/progenitor cells that is found in chronic kidney disease (CKD) patients may contribute to impaired angiogenic repair and decreased capillary density in the heart. Cell therapy with bone marrow-derived cells (BMDCs) has been shown to induce positive effects on the microvasculature and cardiac function, most likely due to secretion of growth factors and cytokines, all of which are present in the conditioned medium (CM); however, this is controversial. Here we showed that treatment with BMDC or CM restored vascular density and decreased the extent of fibrosis in a rat model of CKD, the 5/6 nephrectomy. Engraftment and differentiation of exogenous BMDCs could not be detected. Yet CM led to the mobilization and infiltration of endogenous circulating cells into the heart. Cell recruitment was facilitated by the local expression of pro-inflammatory factors such as the macrophage chemoattractant protein-1, interleukin-6, and endothelial adhesion molecules. Consistently, in vitro assays showed that CM increased endothelial adhesiveness to circulating cells by upregulating the expression of adhesion molecules, and stimulated angiogenesis/endothelial tube formation. Overall, our results suggest that both treatments exert vasculoprotective effects on the heart of uremic rats by stimulating endogenous repair mechanisms.
Accuracy of deep learning, a machine-learning technology, using ultra–wide-field fundus ophthalmoscopy for detecting rhegmatogenous retinal detachment
Authors: Ohsugi Hideharu , Tabuchi Hitoshi , Enno Hiroki , Ishitobi Naofumi 
Published: August 2017

AbstractRhegmatogenous retinal detachment (RRD) is a serious condition that can lead to blindness; however, it is highly treatable with timely and appropriate treatment. Thus, early diagnosis and treatment of RRD is crucial. In this study, we applied deep learning, a machine-learning technology, to detect RRD using ultra–wide-field fundus images and investigated its performance. In total, 411 images (329 for training and 82 for grading) from 407 RRD patients and 420 images (336 for training and 84 for grading) from 238 non-RRD patients were used in this study. The deep learning model demonstrated a high sensitivity of 97.6% [95% confidence interval (CI), 94.2–100%] and a high specificity of 96.5% (95% CI, 90.2–100%), and the area under the curve was 0.988 (95% CI, 0.981–0.995). This model can improve medical care in remote areas where eye clinics are not available by using ultra–wide-field fundus ophthalmoscopy for the accurate diagnosis of RRD. Early diagnosis of RRD can prevent blindness.
A missense MT-ND5 mutation in differentiated Parkinson Disease cytoplasmic hybrid induces ROS-dependent DNA Damage Response amplified by DROSHA
Authors: Pignataro Daniela , Francia Sofia , Zanetta Francesca , Brenna Giulia , Brandini Stefania , Olivieri Anna , Torroni Antonio , Biamonti Giuseppe , Montecucco Alessandra 
Published: August 2017

AbstractGenome integrity is continuously threatened by endogenous sources of DNA damage including reactive oxygen species (ROS) produced by cell metabolism. Factors of the RNA interference (RNAi) machinery have been recently involved in the cellular response to DNA damage (DDR) in proliferating cells. To investigate the impact of component of RNAi machinery on DDR activation in terminally differentiated cells, we exploited cytoplasmic hybrid (cybrid) cell lines in which mitochondria of sporadic Parkinson’s disease patients repopulate neuroblastoma SH-SY5Y-Rho(0) cells. Upon differentiation into dopaminergic neuron-like cells, PD63 cybrid showed increased intracellular level of ROS and chronic DDR activation, compared to other cybrids with the same nuclear background. Importantly, DDR activation in these cells can be prevented by ROS scavenging treatment suggesting that ROS production is indeed causative of nuclear DNA damage. Sequence analysis of the mitogenomes identified a rare and heteroplasmic missense mutation affecting a highly conserved residue of the ND5-subunit of respiratory complex I, which accounts for ROS increase. We demonstrated that the assembly of nuclear DDR foci elicited by oxidative stress in these cells relies on DROSHA, providing the first evidence that components of RNAi machinery play a crucial role also in the mounting of ROS-induced DDR in non-replicating neuronal cells.
Work Function Modulation of Molybdenum Disulfide Nanosheets by Introducing Systematic Lattice Strain
Authors: Shakya Jyoti , Kumar Sanjeev , Kanjilal D. , Mohanty Tanuja 
Published: August 2017

AbstractTuning the surface electronic properties of 2D transition metal dichalcogenides such as Molebdenum disulfide (MoS2) nanosheets is worth exploring for their potential applications in strain sensitive flexible electronic devices. Here in, the correlation between tensile strain developed in MoS2 nanosheets during swift heavy ion irradiation and corresponding modifications in their surface electronic properties is investigated. With prior structural characterization by transmission electron microscopy, chemically exfoliated MoS2 nanosheets were exposed to 100 MeV Ag ion irradiation at varying fluence for creation of controlled defects. The presence of defect induced systematic tensile strain was verified by Raman spectroscopy and X-ray Diffraction analysis. The effect of ion irradiation on in–plane mode is observed to be significantly higher than that on out-of-plane mode. The contribution of irradiation induced in-plane strain on modification of the surface electronic properties of nanosheets was analyzed by work function measurement using scanning Kelvin probe microscopy. The work function value is observed to be linearly proportional to tensile strain along the basal plane indicating a systematic shifting of Fermi surface with fluence towards the valence band.