bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reassortment compatibility between PB1, PB2, and HA genes of the two influenza B virus lineages in mammalian cells
Authors: Kim Jin Il , Lee Ilseob , Park Sehee , Bae Joon-Yong , Yoo Kirim , Lemey Philippe , Park Mee Sook , Song Jin-Won , Kee Sun-Ho , Song Ki-Joon , Park Man-Seong 
Published: June 2016

AbstractIn addition to influenza A subtypes, two distinct lineages of influenza B virus also cause seasonal epidemics to humans. Recently, Dudas et al. have done evolutionary analyses of reassortment patterns of the virus and suggested genetic lineage relationship between PB1, PB2, and HA genes. Using genetic plasmids and reassortant viruses, we here demonstrate that a homologous lineage PB1-PB2 pair exhibits better compatibility than a heterologous one and that the lineage relationship between PB1 and HA is more important for viral replication than that between PB2 and HA. However, co-adaptation of PB1-PB2-HA genes appears to be affected by complete gene constellation.
Numerical research on the anisotropic transport of thermal neutron in heterogeneous porous media with micron X-ray computed tomography
Authors: Wang Yong , Yue Wenzheng , Zhang Mo 
Published: June 2016

AbstractThe anisotropic transport of thermal neutron in heterogeneous porous media is of great research interests in many fields. In this paper, it is the first time that a new model based on micron X-ray computed tomography (CT) has been proposed to simultaneously consider both the separation of matrix and pore and the distribution of mineral components. We apply the Monte Carlo method to simulate thermal neutrons transporting through the model along different directions, and meanwhile detect those unreacted thermal neutrons by an array detector on the other side of the model. Therefore, the anisotropy of pore structure can be imaged by the amount of received thermal neutrons, due to the difference of rock matrix and pore-filling fluids in the macroscopic reaction cross section (MRCS). The new model has been verified by the consistent between the simulated data and the pore distribution from X-ray CT. The results show that the evaluation of porosity can be affected by the anisotropy of media. Based on the research, a new formula is developed to describe the correlation between the resolution of array detectors and the quality of imaging. The formula can be further used to analyze the critical resolution and the suitable number of thermal neutrons emitted in each simulation. Unconventionally, we find that a higher resolution cannot always lead to a better image.
Dynamical control on helicity of electromagnetic waves by tunable metasurfaces
Authors: Xu He-Xiu , Sun Shulin , Tang Shiwei , Ma Shaojie , He Qiong , Wang Guang-Ming , Cai Tong , Li Hai-Peng , Zhou Lei 
Published: June 2016

AbstractManipulating the polarization states of electromagnetic (EM) waves, a fundamental issue in optics, attracted intensive attention recently. However, most of the devices realized so far are either too bulky in size, and/or are passive with only specific functionalities. Here we combine theory and experiment to demonstrate that, a tunable metasurface incorporating diodes as active elements can dynamically control the reflection phase of EM waves, and thus exhibits unprecedented capabilities to manipulate the helicity of incident circular-polarized (CP) EM wave. By controlling the bias voltages imparted on the embedded diodes, we demonstrate that the device can work in two distinct states. Whereas in the “On” state, the metasurface functions as a helicity convertor and a helicity hybridizer within two separate frequency bands, it behaves as a helicity keeper within an ultra-wide frequency band in the “Off” state. Our findings pave the way to realize functionality-switchable devices related to phase control, such as frequency-tunable subwavelength cavities, anomalous reflectors and even holograms.
Low palaeoelevation of the northern Lhasa terrane during late Eocene: Fossil foraminifera and stable isotope evidence from the Gerze Basin
Authors: Wei Yi , Zhang Kexin , Garzione Carmala N. , Xu Yadong , Song Bowen , Ji Junliang 
Published: June 2016

AbstractThe Lhasa terrane is a key region for understanding the paleoelevation of the southern Tibetan Plateau after India-Asia collision. The Gerze Basin, located in the northern part of the Lhasa terrane, is a shortening-related basin. We discovered Lagena laevis (Bandy) fossils in upper Eocene strata of the Gerze Basin. This type of foraminifera is associated with lagoon and estuarine environments, indicating that the northern part of the Lhasa terrane was near sea level during the late Eocene. We speculate that these foraminifera were transported inland by storm surges to low elevation freshwater lakes during times of marine transgressions. This inference is consistent with the relatively positive δ18O values in carbonate from the same deposits that indicate low palaeoelevations close to sea level. Considering the palaeoelevation results from the nearby Oligocene basins at a similar latitude and the volcanic history of the Lhasa terrane, we infer that large-magnitude surface uplift of the northern Lhasa terrane occurred between late Eocene and late Oligocene time.
Histone acetyltransferase HAT4 modulates navigation across G2/M and re-entry into G1 in Leishmania donovani
Authors: Yadav Aarti , Chandra Udita , Saha Swati 
Published: June 2016

AbstractHistone acetyltransferases impact multiple processes. This study investigates the role of histone acetyltransferase HAT4 in Leishmania donovani. Though HAT4 was dispensable for survival, its elimination decreased cell viability and caused cell cycle defects, with HAT4-nulls experiencing an unusually long G2/M. Survival of HAT4-nulls in macrophages was also substantially compromised. DNA microarray analysis revealed that HAT4 modestly regulated the expression of only a select number of genes, thus not being a major modulator of global gene expression. Significantly, cdc20 was among the downregulated genes. To ascertain if decreased expression of cdc20 was responsible for HAT4-null growth and cell cycle defects we expressed LdCdc20 ectopically in HAT4-nulls. We found this to alleviate the aberrant growth and cell cycle progression patterns displayed by HAT4-nulls, with cells navigating G2/M phase and re-entering G1 phase smoothly. HAT4-nulls expressing LdCdc20 ectopically showed survival rates comparable to wild type within macrophages, suggesting that G2/M defects were responsible for poor survival of HAT4-nulls within host cells also. These are the first data analyzing the in vivo functional role of HAT4 in any trypanosomatid. Our results directly demonstrate for the first time a role for Cdc20 in regulating trypanosomatid G2/M events, opening avenues for further research in this area.
Involvement of the neuronal phosphotyrosine signal adaptor N-Shc in kainic acid-induced epileptiform activity
Authors: Baba Shiro , Onga Kazuko , Kakizawa Sho , Ohyama Kyoji , Yasuda Kunihiko , Otsubo Hiroshi , Scott Brian W. , Burnham W. McIntyre , Matsuo Takayuki , Nagata Izumi , Mori Nozomu 
Published: June 2016

AbstractBDNF-TrkB signaling is implicated in experimental seizures and epilepsy. However, the downstream signaling involved in the epileptiform activity caused by TrkB receptor activation is still unknown. The aim of the present study was to determine whether TrkB-mediated N-Shc signal transduction was involved in kainic acid (KA)-induced epileptiform activity. We investigated KA-induced behavioral seizures, epileptiform activities and neuronal cell loss in hippocampus between N-Shc deficient and control mice. There was a significant reduction in seizure severity and the frequency of epileptiform discharges in N-Shc deficient mice, as compared with wild-type and C57BL/6 mice. KA-induced neuronal cell loss in the CA3 of hippocampus was also inhibited in N-Shc deficient mice. This study demonstrates that the activation of N-Shc signaling pathway contributes to an acute KA-induced epileptiform activity and neuronal cell loss in the hippocampus. We propose that the N-Shc-mediated signaling pathway could provide a potential target for the novel therapeutic approaches of epilepsy.
Role of Cystathionine Gamma-Lyase in Immediate Renal Impairment and Inflammatory Response in Acute Ischemic Kidney Injury
Authors: Markó Lajos , Szijártó István A. , Filipovic Milos R. , Kaßmann Mario , Balogh András , Park Joon-Keun , Przybyl Lukasz , N’diaye Gabriele , Krämer Stephanie , Anders Juliane , Ishii Isao , Müller Dominik N. , Gollasch Maik 
Published: June 2016

AbstractHydrogen sulfide (H2S) is known to act protectively during renal ischemia/reperfusion injury (IRI). However, the role of the endogenous H2S in acute kidney injury (AKI) is largely unclear. Here, we analyzed the role of cystathionine gamma-lyase (CTH) in acute renal IRI using CTH-deficient (Cth−/−) mice whose renal H2S levels were approximately 50% of control (wild-type) mice. Although levels of serum creatinine and renal expression of AKI marker proteins were equivalent between Cth−/− and control mice, histological analysis revealed that IRI caused less renal tubular damage in Cth−/− mice. Flow cytometric analysis revealed that renal population of infiltrated granulocytes/macrophages was equivalent in these mice. However, renal expression levels of certain inflammatory cytokines/adhesion molecules believed to play a role in IRI were found to be lower after IRI only in Cth−/− mice. Our results indicate that the systemic CTH loss does not deteriorate but rather ameliorates the immediate AKI outcome probably due to reduced inflammatory responses in the kidney. The renal expression of CTH and other H2S-producing enzymes was markedly suppressed after IRI, which could be an integrated adaptive response for renal cell protection.
Caffeine administration prevents retinal neuroinflammation and loss of retinal ganglion cells in an animal model of glaucoma
Authors: Madeira Maria H. , Ortin-Martinez Arturo , Nadal-Nícolas Francisco , Ambrósio António F. , Vidal-Sanz Manuel , Agudo-Barriuso Marta , Santiago Ana Raquel 
Published: June 2016

AbstractGlaucoma is the second leading cause of blindness worldwide, being characterized by progressive optic nerve damage and loss of retinal ganglion cells (RGCs), accompanied by increased inflammatory response involving retinal microglial cells. The etiology of glaucoma is still unknown and despite elevated intraocular pressure (IOP) being a major risk factor, the exact mechanisms responsible for RGC degeneration remain unknown. Caffeine, which is an antagonist of adenosine receptors, is the most widely consumed psychoactive drug in the world. Several evidences suggest that caffeine can attenuate the neuroinflammatory responses and afford protection upon central nervous system (CNS) injury. We took advantage of a well characterized animal model of glaucoma to investigate whether caffeine administration controls neuroinflammation and elicits neuroprotection. Caffeine or water were administered ad libitum and ocular hypertension (OHT) was induced by laser photocoagulation of the limbal veins in Sprague Dawley rats. Herein, we show that caffeine is able to partially decrease the IOP in ocular hypertensive animals. More importantly, we found that drinking caffeine prevented retinal microglia-mediated neuroinflammatory response and attenuated the loss of RGCs in animals with ocular hypertension (OHT). This study opens the possibility that caffeine or adenosine receptor antagonists might be a therapeutic option to manage RGC loss in glaucoma.
A microscopic landscape of the invasive breast cancer genome
Authors: Ping Zheng , Xia Yuchao , Shen Tiansheng , Parekh Vishwas , Siegal Gene P. , Eltoum Isam-Eldin , He Jianbo , Chen Dongquan , Deng Minghua , Xi Ruibin , Shen Dejun 
Published: June 2016

AbstractHistologic grade is one of the most important microscopic features used to predict the prognosis of invasive breast cancer and may serve as a marker for studying cancer driving genomic abnormalities in vivo. We analyzed whole genome sequencing data from 680 cases of TCGA invasive ductal carcinomas of the breast and correlated them to corresponding pathology information. Ten genetic abnormalities were found to be statistically associated with histologic grade, including three most prevalent cancer driver events, TP53 and PIK3CA mutations and MYC amplification. A distinct genetic interaction among these genomic abnormalities was revealed as measured by the histologic grading score. While TP53 mutation and MYC amplification were synergistic in promoting tumor progression, PIK3CA mutation was found to have alleviated the oncogenic effect of either the TP53 mutation or MYC amplification, and was associated with a significant reduction in mitotic activity in TP53 mutated and/or MYC amplified breast cancer. Furthermore, we discovered that different types of genetic abnormalities (mutation versus amplification) within the same cancer driver gene (PIK3CA or GATA3) were associated with opposite histologic changes in invasive breast cancer. In conclusion, our study suggests that histologic grade may serve as a biomarker to define cancer driving genetic events in vivo.
M2-polarized macrophages contribute to neovasculogenesis, leading to relapse of oral cancer following radiation
Authors: Okubo Makiko , Kioi Mitomu , Nakashima Hideyuki , Sugiura Kei , Mitsudo Kenji , Aoki Ichiro , Taniguchi Hideki , Tohnai Iwai 
Published: June 2016

AbstractDespite the fact that radiation is one of the standard therapies in the treatment of patients with oral cancer, tumours can recur even in the early stages of the disease, negatively impacting prognosis and quality of life. We previously found that CD11b+ bone marrow-derived cells (BMDCs) were recruited into human glioblastoma multiforme (GBM), leading to re-organization of the vasculature and tumour regrowth. However, it is not yet known how these cells contribute to tumour vascularization. In the present study, we investigated the role of infiltrating CD11b+ myeloid cells in the vascularization and recurrence of oral squamous cell carcinoma (OSCC). In a xenograft mouse model, local irradiation caused vascular damage and hypoxia in the tumour and increased infiltration of CD11b+ myeloid cells. These infiltrating cells showed characteristics of M2 macrophages (M2Mφs) and are associated with the promotion of vascularization. M2Mφs promoted tumour progression in recurrence after irradiation compared to non-irradiated tumours. In addition, we found that CD11b+ myeloid cells, as well as CD206+ M2Mφs, are increased during recurrence after radiotherapy in human OSCC specimens. Our findings may lead to the development of potential clinical biomarkers or treatment targets in irradiated OSCC patients.
Realization of Plasmonic Microcavity with Full Transverse and Longitudinal Mode Selection
Authors: Liu Ju , Chen Yue-Gang , Gan Lin , Xiao Ting-Hui , Li Zhi-Yuan 
Published: June 2016

AbstractSurface plasmon polaritons (SPPs) manipulation is of vital importance to construct ultracompact integrated micro/nano-optical devices and systems. Here we report the design, fabrication and characterization of a SPP microcavity with full transverse and longitudinal mode selection and control on the surface of gold film. The designed microcavity supports the fundamental and first-order transverse modes of Gaussian mode beam with controllable longitudinal modes, respectively. The transverse mode is determined by two holographic mirrors made from deliberately designed groove patterns via the surface electromagnetic wave holography methodology, while the longitudinal mode is determined by the length of cavity. Both numerical simulations and leaky-wave SPP mode observations confirm the realization of full mode selection in the fabricated cavity. Our work opens up a powerful way to fully explore longitudinal and transverse mode control in SPP microcavities, which will be beneficial for light-matter interaction enhancement, construction of novel SPP nanolaser and microlaser, optical sensing and optical information processing.
IDH-mutant glioma specific association of rs55705857 located at 8q24.21 involves MYC deregulation
Authors: Oktay Yavuz , Ülgen Ege , Can Özge , Akyerli Cemaliye B. , Yüksel Şirin , Erdemgil Yiğit , Durası İ. Melis , Henegariu Octavian Ioan , Nanni E. Paolo , Selevsek Nathalie , Grossmann Jonas , Erson-Omay E. Zeynep , Bai Hanwen , Gupta Manu , Lee William , Turcan Şevin , Özpınar Aysel , Huse Jason T. , Sav M. Aydın , Flanagan Adrienne , Günel Murat , Sezerman O. Uğur , Yakıcıer M. Cengiz , Pamir M. Necmettin , Özduman Koray 
Published: June 2016

AbstractThe single nucleotide polymorphism rs55705857, located in a non-coding but evolutionarily conserved region at 8q24.21, is strongly associated with IDH-mutant glioma development and was suggested to be a causal variant. However, the molecular mechanism underlying this association has remained unknown. With a case control study in 285 gliomas, 316 healthy controls, 380 systemic cancers, 31 other CNS-tumors, and 120 IDH-mutant cartilaginous tumors, we identified that the association was specific to IDH-mutant gliomas. Odds-ratios were 9.25 (5.17–16.52; 95% CI) for IDH-mutated gliomas and 12.85 (5.94–27.83; 95% CI) for IDH-mutated, 1p/19q co-deleted gliomas. Decreasing strength with increasing anaplasia implied a modulatory effect. No somatic mutations were noted at this locus in 114 blood-tumor pairs, nor was there a copy number difference between risk-allele and only-ancestral allele carriers. CCDC26 RNA-expression was rare and not different between the two groups. There were only minor subtype-specific differences in common glioma driver genes. RNA sequencing and LC-MS/MS comparisons pointed to significantly altered MYC-signaling. Baseline enhancer activity of the conserved region specifically on the MYC promoter and its further positive modulation by the SNP risk-allele was shown in vitro. Our findings implicate MYC deregulation as the underlying cause of the observed association.
Generation of an ultra-short electrical pulse with width shorter than the excitation laser
Authors: Shi Wei , Wang Shaoqiang , Ma Cheng , Xu Ming 
Published: June 2016

AbstractWe demonstrate experimentally a rare phenomenon that the width of an electrical response is shorter than that of the excitation laser. In this work, generation of an ultrashort electrical pulse is by a semi-insulating GaAs photoconductive semiconductor switch (PCSS) and the generated electrical pulse width is shorter than that of the excitation laser from diode laser. When the pulse width and energy of the excitation laser are fixed at 25.7 ns and 1.6 μJ respectively, the width of the generated electrical pulse width by 3-mm-gap GaAs PCSS at the bias voltage of 9 kV is only 7.3 ns. The model of photon-activated charge domain (PACD) is used to explain the peculiar phenomenon in our experiment. The ultrashort electrical pulse width is mainly relevant to the time interval of PACD from occurrence to disappearance in the mode. The shorter the time interval is, the narrower the electrical pulse width will become. In more general terms, our result suggests that in nonlinear regime a response signal can have a much short width than the excitation pulses. The result clearly indicates that generating ultrashort electrical pulses can be achieved without the need of ultrashort lasers.
Interleukin-1β induced Stress Granules Sequester COX-2 mRNA and Regulates its Stability and Translation in Human OA Chondrocytes
Authors: Ansari Mohammad Y. , Haqqi Tariq M. 
Published: June 2016

AbstractEnhanced and immediate expression of cyclooxygenase-2 (COX-2) mRNA is observed in IL-1β-stimulated OA chondrocytes but the synthesis of protein found significantly delayed. Here we investigated the role of stress granules (SGs), ribonucleoprotein complexes that regulate mRNA translation, in the delayed translation of COX-2 mRNAs in IL-1β-stimulated OA chondrocytes. Stimulation of human chondrocytes with IL-1β activated the stress response genes and the phosphorylation of eIF2α that triggered the assembly of SGs. Using combined immunofluorescence staining of SGs markers and COX-2 protein, RNA fluorescence in situ hybridization and RNA immunoprecipitation, the COX-2 mRNAs were found sequestered in SGs in IL-1β-stimulated OA chondrocytes. No increase in COX-2 protein expression was observed during the persistence of SGs but enhanced expression of COX-2 protein was noted upon clearance of the SGs. Inhibition of SGs clearance blocked COX-2 mRNA translation whereas blocking the assembly of SGs by TIA-1 depletion resulted in rapid and increased production of COX-2 and PGE2. Our findings show for the first time assembly of SGs and sequestration of COX-2 mRNAs in human OA chondrocytes under pathological conditions. Post-transcriptional regulation of COX-2 mRNAs translation by SGs indicates a role in IL-1β-mediated catabolic response that could be therapeutically targeted in OA.
Natural killer cells regulate eosinophilic inflammation in chronic rhinosinusitis
Authors: Kim Ji Heui , Choi Go Eun , Lee Bong-Jae , Kwon Seog Woon , Lee Seung-Hyo , Kim Hun Sik , Jang Yong Ju 
Published: June 2016

AbstractEosinophils play a major pathologic role in the pathogenesis of diverse inflammatory diseases including chronic rhinosinusitis (CRS). Dysregulated production of prostaglandin (PG), particularly PGD2, is considered to be an important contributing factor to eosinophilic inflammation in CRS primarily through proinflammatory and chemotactic effects on eosinophils. Here, we provide evidence that PGD2 can promote eosinophilic inflammation through a suppression of Natural killer (NK) cell effector function and NK cell-mediated eosinophil regulation. Eosinophil apoptosis mediated by NK cells was significantly decreased in CRS patients compared with healthy controls. This decrease was associated with NK cell dysfunction and eosinophilic inflammation. Tissue eosinophils were positively correlated with blood eosinophils in CRS patients. In a murine model of CRS, NK cell depletion caused an exacerbation of blood eosinophilia and eosinophilic inflammation in the sinonasal tissue. PGD2 and its metabolite, but not PGE2 and a panel of cytokines including TGF-β, were increased in CRS patients compared with controls. Effector functions of NK cells were potently suppressed by PGD2-dependent, rather than PGE2-dependent, pathway in controls and CRS patients. Thus, our results suggest decreased NK cell-mediated eosinophil regulation, possibly through an increased level of PGD2, as a previously unrecognized link between PG dysregulation and eosinophilic inflammation in CRS.