bluuebunny/crossref_metadata_2025_split huggingface dataset:
DNA Methylation mediated down-regulating of MicroRNA-33b and its role in gastric cancer
Authors: Yin Haixin , Song Peng , Su Rui , Yang Guihua , Dong Lei , Luo Min , Wang Bin , Gong Bei , Liu Changzheng , Song Wei , Wang Fang , Ma Yanni , Zhang Junwu , Wang Weibin , Yu Jia 
Published: January 2016

AbstractThe discovery of microRNAs (miRNAs) provides a new and powerful tool for studying the mechanism, diagnosis and treatment of human cancers. Currently, down-regulation of tumor suppressive miRNAs by CpG island hypermethylation is emerging as a common hallmark of cancer. Here, we reported that the down-regulation of miR-33b was associated with pM stage of gastric cancer (GC) patients. Ectopic expression of miR-33b in HGC-27 and MGC-803 cells inhibited cell proliferation, migration and invasion, which might be due to miR-33b targeting oncogene c-Myc. Moreover, enhanced methylation level of the CpG island upstream of miR-33b in GC patients with down-regulated miR-33b was confirmed by methylation-specific PCR (MSP) amplification. Furthermore, re-introduction of miR-33b significantly suppressed tumorigenesis of GC cells in the nude mice. In conclusion, miR-33b acts as a tumor suppressor and hypermethylation of the CpG island upstream of miR-33b is responsible for its down-regulation in gastric cancer.
Overexpression of sonic hedgehog in the triple negative breast cancer: clinicopathological characteristics of high burden breast cancer patients from Bangladesh
Authors: Noman A. S. , Uddin M. , Rahman M. Z. , Nayeem M. J. , Alam S. S. , Khatun Z. , Wahiduzzaman M. , Sultana A. , Rahman M. L. , Ali M. Y. , Barua D. , Ahmed I. , Islam M. S. , Aboussekhra A. , Yeger H. , Farhat W. A. , Islam S. S. 
Published: January 2016

AbstractDysregulation of Hedgehog (Hh) signaling pathway has been documented in mammary gland development and breast cancer (BC) progression. Despite the remarkable progress in therapeutic interventions, BC related mortality in Bangladesh increased in the last decade. Triple negative breast cancer (TNBC) still presents a critical therapeutic challenge. Thus effective targeted therapy is urgently needed. In this study, we report the clinicopathological characteristics and prognosis of BC patients from Bangladesh. Routine immunohistochemical analysis and high throughput RNA-Seq data from the TCGA library were used to analyze the expression pattern and association of high and low level of Shh expression in a collection of BC patients with a long-term follow-up. High levels of Shh were observed in a subset of BC tumors with poor prognostic pathological features. Higher level of Shh expression correlated with a significantly poorer overall survival of patients compared with patients whose tumors expressed a low level of Shh. These data support the contention that Shh could be a novel biomarker for breast cancer that is involved in mediating the aggressive phenotype of BC. We propose that BC patients exhibiting a higher level of Shh expression, representing a subset of BC patients, would be amenable to Shh targeted therapy.
Apoptosis signal-regulating kinase 1 mediates striatal degeneration via the regulation of C1q
Authors: Cho Kyoung Joo , Cheon So Young , Kim Gyung Whan 
Published: January 2016

AbstractApoptosis signal-regulating kinase-1 (ASK1), an early signaling element in the cell death pathway, has been hypothesized to participate in the pathology of neurodegenerative diseases. The systemic administration of 3-nitropropionic acid (3-NP) facilitates the development of selective striatal lesions. However, it remains unclear whether specific neurons are selectively targeted in 3-NP-infused striatal degeneration. Recently, it has been proposed that complement-mediated synapse elimination may be reactivated aberrantly in the pathology of neurodegenerative diseases. We hypothesized that ASK1 is involved in striatal astrocyte reactivation; reactive astrocyte secretes molecules detrimental to neuron; and striatal neurons are more susceptible to these factors. Our results indicate that striatal astrocyte is reactivated and ASK1 level increases after 3-NP general and chronic infusion. Reactive striatal astrocyte increases TGF-beta differentially to cortex and striatum. ASK1 may be involved in regulation of astrocyte TGF-beta and it is linked to the C1q level in spatial and temporal and moreover in the earlier stage of progressing striatal neuronal loss. Conclusively the present study suggests that ASK1 mediates 3-NP toxicity and regulates C1q level through the astrocyte TGF-beta. And also it may suggest that C1q level may be a surrogate of prediction marker representing neurodegenerative disease progress before developing behavioral impairment.
Origin of the Avalanche-Like Photoluminescence from Metallic Nanowires
Authors: Ma Zongwei , Yu Ying , Shen Shaoxin , Dai Hongwei , Yao Linhua , Han Yibo , Wang Xia , Han Jun-Bo , Li Liang 
Published: January 2016

AbstractSurface plasmonic systems provide extremely efficient ways to modulate light-matter interaction in photon emission, light harvesting, energy conversion and transferring, etc. Various surface plasmon enhanced luminescent behaviors have been observed and investigated in these systems. But the origin of an avalanche-like photoluminescence, which was firstly reported in 2007 from Au and subsequently from Ag nanowire arrays/monomers, is still not clear. Here we show, based on systematic investigations including the excitation power/time related photoluminescent measurements as well as calculations, that this avalanche-like photoluminescence is in fact a result of surface plasmon assisted thermal radiation. Nearly all of the related observations could be perfectly interpreted with this concept. Our finding is crucial for understanding the surface plasmon mediated thermal and photoemission behaviors in plasmonic structures, which is of great importance in designing functional plasmonic devices.
State-dependent and cell type-specific temporal processing in auditory thalamocortical circuit
Authors: Sakata Shuzo 
Published: January 2016

AbstractOngoing spontaneous activity in cortical circuits defines cortical states, but it still remains unclear how cortical states shape sensory processing across cortical laminae and what type of response properties emerge in the cortex. Recording neural activity from the auditory cortex (AC) and medial geniculate body (MGB) simultaneously with electrical stimulations of the basal forebrain (BF) in urethane-anesthetized rats, we investigated state-dependent spontaneous and auditory-evoked activities in the auditory thalamocortical circuit. BF stimulation induced a short-lasting desynchronized state, with sparser firing and increased power at gamma frequency in superficial layers. In this desynchronized state, the reduction in onset response variability in both AC and MGB was accompanied by cell type-specific firing, with decreased responses of cortical broad spiking cells, but increased responses of cortical narrow spiking cells. This onset response was followed by distinct temporal evolution in AC, with quicker rebound firing in infragranular layers. This temporal profile was associated with improved processing of temporally structured stimuli across AC layers to varying degrees, but not in MGB. Thus, the reduction in response variability during the desynchronized state can be seen subcortically whereas the improvement of temporal tuning emerges across AC layers, emphasizing the importance of state-dependent intracortical processing in hearing.
Resistin, a fat-derived secretory factor, promotes metastasis of MDA-MB-231 human breast cancer cells through ERM activation
Authors: Lee Jung Ok , Kim Nami , Lee Hye Jeong , Lee Yong Woo , Kim Su Jin , Park Sun Hwa , Kim Hyeon Soo 
Published: January 2016

AbstractResistin, an adipocyte-secreted factor, is known to be elevated in breast cancer patients. However, the molecular mechanism by which resistin acts is not fully understood. The aim of this study was to investigate whether resistin could stimulate invasion and migration of breast cancer cells. Here, we report that resistin stimulated invasion and migration of breast cancer cells as well as phosphorylation of c-Src. Inhibition of c-Src blocked resistin-induced breast cancer cell invasion. Resistin increased intracellular calcium concentration and chelation of intracellular calcium blocked resistin-mediated activation of Src. Resistin also induced phosphorylation of protein phosphatase 2A (PP2A). Inhibition of c-Src blocked resistin-mediated PP2A phosphorylation. In addition, resistin increased phosphorylation of PKCα. Inhibition of PP2A enhanced resistin-induced PKCα phosphorylation, demonstrating that PP2A activity is critical for PKCα phosphorylation. Resistin also increased phosphorylation of ezrin, radixin and moesin (ERM). Additionally, ezrin interacted with PKCα and resistin promoted co-localization of ezrin and PKCα. Either inhibition of c-Src and PKCα or knock-down of ezrin blocked resistin-induced breast cancer cells invasion. Moreover, resistin increased expression of vimentin, a key molecule for cancer cell invasion. Knock-down of ezrin abrogated resistin-induced vimentin expression. These results suggest that resistin play as a critical regulator of breast cancer metastasis.
Ultrahigh Performance of Novel Capacitive Deionization Electrodes based on A Three-Dimensional Graphene Architecture with Nanopores
Authors: Shi Wenhui , Li Haibo , Cao Xiehong , Leong Zhi Yi , Zhang Jun , Chen Tupei , Zhang Hua , Yang Hui Ying 
Published: January 2016

AbstractIn order to achieve optimal desalination during capacitive deionization (CDI), CDI electrodes should possess high electrical conductivity, large surface area, good wettability to water, narrow pore size distribution and efficient pathways for ion and electron transportation. In this work, we fabricated a novel CDI electrode based on a three-dimensional graphene (3DG) architecture by constructing interconnected graphene sheets with in-plane nanopores (NP-3DG). As compared to 3DG, NP-3DG features a larger specific surface area of 445 m2 g−1 and therefore the higher specific capacitance. The ultrahigh electrosorptive capacity of NP-3DG predicted from Langmuir isotherm is 17.1 mg g−1 at a cell potential of 1.6 V. This can be attributed to the interconnected macropores within the graphene networks and nanopores on graphene sheets. Both of macropores and nanopores are favorable for enhancing CDI peroformance by buffering ions to reduce the diffusion distances from the external electrolyte to the interior surfaces and enlarging the surface area.
CRISPR/Cas9 facilitates investigation of neural circuit disease using human iPSCs: mechanism of epilepsy caused by an SCN1A loss-of-function mutation
Authors: Liu J , Gao C , Chen W , Ma W , Li X , Shi Y , Zhang H , Zhang L , Long Y , Xu H , Guo X , Deng S , Yan X , Yu D , Pan G , Chen Y , Lai L , Liao W , Li Z 
Published: January 2016

AbstractMutations in SCN1A, the gene encoding the α subunit of Nav1.1 channel, can cause epilepsies with wide ranges of clinical phenotypes, which are associated with the contrasting effects of channel loss-of-function or gain-of-function. In this project, CRISPR/Cas9- and TALEN-mediated genome-editing techniques were applied to induced pluripotent stem cell (iPSC)-based-disease model to explore the mechanism of epilepsy caused by SCN1A loss-of-function mutation. By fluorescently labeling GABAergic subtype in iPSC-derived neurons using CRISPR/Cas9, we for the first time performed electrophysiological studies on SCN1A-expressing neural subtype and monitored the postsynaptic activity of both inhibitory and excitatory types. We found that the mutation c.A5768G, which led to no current of Nav1.1 in exogenously transfected system, influenced the properties of not only Nav current amount, but also Nav activation in Nav1.1-expressing GABAergic neurons. The two alterations in Nav further reduced the amplitudes and enhanced the thresholds of action potential in patient-derived GABAergic neurons, and led to weakened spontaneous inhibitory postsynaptic currents (sIPSCs) in the patient-derived neuronal network. Although the spontaneous excitatory postsynaptic currents (sEPSCs) did not change significantly, when the frequencies of both sIPSCs and sEPSCs were further analyzed, we found the whole postsynaptic activity transferred from the inhibition-dominated state to excitation in patient-derived neuronal networks, suggesting that changes in sIPSCs alone were sufficient to significantly reverse the excitatory level of spontaneous postsynaptic activity. In summary, our findings fill the gap of our knowledge regarding the relationship between SCN1A mutation effect recorded on exogenously transfected cells and on Nav1.1-expressing neurons, and reveal the physiological basis underlying epileptogenesis caused by SCN1A loss-of-function mutation.
Postoperative Delayed Cervical Palsies: Understanding the Etiology
Authors: Planchard Ryan F. , Maloney Patrick R. , Mallory Grant W. , Puffer Ross C. , Spinner Robert J. , Nassr Ahmad , Fogelson Jeremy L. , Krauss William E. , Clarke Michelle J. 
Published: January 2016

Study Design Retrospective study. Objective This study reviews 1,768 consecutive cervical decompressions with or without instrumented fusion to identify patient-specific and procedural risk factors significantly correlated with the development of delayed cervical palsy (DCP). Methods Baseline demographic and procedural information was collected from the electronic medical record. Particular attention was devoted to reviewing each chart for recognized risk factors of postsurgical inflammatory neuropathy: autoimmune disease, blood transfusions, diabetes, and smoking. Results Of 1,669 patients, 56 (3.4%) developed a DCP. Although 71% of the palsies involved C5, 55% of palsies were multimyotomal and 18% were bilateral. Significant risk factors on univariate analysis included age ( p = 0.0061, odds ratio [OR] = 1.07, 95% confidence interval [CI] 1.008 to 1.050), posterior instrumented fusion ( p < 0.0001, OR = 3.30, 95% CI 1.920 to 5.653), prone versus semisitting/sitting position ( p = 0.0036, OR = 3.58, 95% CI 1.451 to 11.881), number of operative levels ( p < 0.0001, OR = 1.42, 95% CI 1.247 to 1.605), intraoperative transfusions ( p = 0.0231, OR = 2.57, 95% CI 1.152 to 5.132), and nonspecific autoimmune disease ( p = 0.0107, OR = 3.83, 95% CI 1.418 to 8.730). On multivariate analysis, number of operative levels ( p = 0.0053, OR = 1.27, 95% CI 1.075 to 1.496) and nonspecific autoimmune disease ( p = 0.0416, OR 2.95, 95% CI 1.047 to 7.092) remained significant. Conclusions Although this study partially supports a mechanical etiology in the pathogenesis of a DCP, we also describe a notable correlation with autoimmune risk factors. Bilateral and multimyotomal involvement provides additional support that some DCPs may result from an inflammatory response and thus an underlying multifactorial etiology for this complication.
Limited tolerance by insects to high temperatures across tropical elevational gradients and the implications of global warming for extinction
Authors: García-Robledo Carlos , Kuprewicz Erin K. , Staines Charles L. , Erwin Terry L. , Kress W. John 
Published: January 2016

Significance
Tolerance to high temperatures will determine the survival of animal species under projected global warming. Surprisingly little research has been conducted to elucidate how this trait changes in organisms living at different elevations of similar latitudes, especially in the tropics. DNA barcodes demonstrate that insect species previously thought to have broad elevational distributions and phenotypically plastic thermal tolerances actually comprise cryptic species complexes. These cryptic species occupy discrete elevational ranges, and their thermal tolerances seem to be locally adapted to temperatures in their life zones. The combination of high species endemism and local adaptation to temperature regimes may increase the extinction risk of high-elevation insects in a warming world.
Using decision pathway surveys to inform climate engineering policy choices
Authors: Gregory Robin , Satterfield Terre , Hasell Ariel 
Published: January 2016

SignificanceA growing number of scientists now believe that climate engineering technologies could be required to control global temperatures and protect ecosystems. Decision makers often rely on surveys to inform them about citizens’ views, but when novel technologies are involved results can fail to reflect the assumptions, knowledge, and values that underlie people’s choices. To bridge this gap, we describe a new, behaviorally and cognitively responsive “decision pathway” survey (n= 800) that mimics the conversational depth of small-group deliberations by adopting a broader context that includes competing objectives, civic priorities, factual information, and risk–benefit tradeoffs. Results yield important insights into citizens’ reasoning strategies and the ethical and governance concerns influencing the conditional nature of climate engineering policy choices.
Social relationships and physiological determinants of longevity across the human life span
Authors: Yang Yang Claire , Boen Courtney , Gerken Karen , Li Ting , Schorpp Kristen , Harris Kathleen Mullan 
Published: January 2016

Significance
Although much evidence has accrued in research over the past 20 years on the strong causal associations between social relationships and health and longevity, important gaps remain in our understanding of the mechanisms, timing, and duration of these associations. This study integrates social and biological disciplinary perspectives and research to examine how social relationships “get under the skin” to affect physiological well-being as individuals age. By combining data from and harmonizing measurement across four large nationally representative, population-based, contemporary surveys using an innovative longitudinal life course design, this study provides previously unidentified evidence on the biological and life course mechanisms linking social relationship patterns with health. As such, our findings advance explanations of the emergence and progression of diseases across the human life span.
Changing climates of conflict: A social network experiment in 56 schools
Authors: Paluck Elizabeth Levy , Shepherd Hana , Aronow Peter M. 
Published: January 2016

Significance
Despite a surge in policy and research attention to conflict and bullying among adolescents, there is little evidence to suggest that current interventions reduce school conflict. Using a large-scale field experiment, we show that it is possible to reduce conflict with a student-driven intervention. By encouraging a small set of students to take a public stance against typical forms of conflict at their school, our intervention reduced overall levels of conflict by an estimated 30%. Network analyses reveal that certain kinds of students (called “social referents”) have an outsized influence over social norms and behavior at the school. The study demonstrates the power of peer influence for changing climates of conflict, and suggests which students to involve in those efforts.
Revealing the burden of obesity using weight histories
Authors: Stokes Andrew , Preston Samuel H. 
Published: January 2016

SignificanceThere is substantial uncertainty about the association between obesity and mortality. A major issue is the treatment of reverse causation, a phrase referring to the loss of weight among people who become ill. Weight histories are vital to addressing reverse causality, but few studies incorporate them. Here we introduce nationally representative data on lifetime maximum weight to distinguish individuals who were never obese from those who were formerly obese and lost weight. We formally investigate the performance of various models, finding that models that incorporate history perform better than the conventional approach based on a single observation of weight at the time of survey. We conclude that the burden of obesity is likely to be greater than is commonly appreciated.
Long-term clinical study and multiscale analysis of in vivo biodegradation mechanism of Mg alloy
Authors: Lee Jee-Wook , Han Hyung-Seop , Han Kyeong-Jin , Park Jimin , Jeon Hojeong , Ok Myoung-Ryul , Seok Hyun-Kwang , Ahn Jae-Pyoung , Lee Kyung Eun , Lee Dong-Ho , Yang Seok-Jo , Cho Sung-Youn , Cha Pil-Ryung , Kwon Hoon , Nam Tae-Hyun , Han Jee Hye Lo , Rho Hyoung-Jin , Lee Kang-Sik , Kim Yu-Chan , Mantovani Diego 
Published: January 2016

Significance
In the past decade, countless studies have been performed to control the mechanical and corrosion property of magnesium-based alloy, which degrades in the physiological environment, to overcome the flaws of the inert implant materials and shift the paradigm of conventional bone fixation devices. Controlled degradation of Mg-5wt%Ca-1wt%Zn alloy results in the formation of biomimicking calcification matrix at the degrading interface to initiate the bone formation process. This process facilitates early bone healing and allows the complete replacement of biodegradable Mg implant by the new bone within 1 y of implantation, as demonstrated in 53 cases of successful long-term clinical study.
Heparanase-neutralizing antibodies attenuate lymphoma tumor growth and metastasis
Authors: Weissmann Marina , Arvatz Gil , Horowitz Netanel , Feld Sari , Naroditsky Inna , Zhang Yi , Ng Mary , Hammond Edward , Nevo Eviatar , Vlodavsky Israel , Ilan Neta 
Published: January 2016

Significance
Heparanase is the predominant enzyme that cleaves heparan sulfate (HS) in mammals, a linear polysaccharide that is normally attached to a core protein, forming HS proteoglycans (HSPGs) that are abundant in the cell surface and extracellular matrix (ECM). Cleavage of HS by heparanase results in structural alterations of the ECM and release of ECM-bound factors that together stimulate cancer metastasis and angiogenesis. Here we provide evidence that heparanase is expressed by B-lymphomas, and heparanase inhibitors restrain tumor growth. Furthermore, we describe, for the first time to our knowledge, the development and characterization of heparanase-neutralizing monoclonal antibodies (mAbs) that inhibit cell invasion and tumor metastasis. Moreover, we show that these mAbs attenuate lymphoma growth by targeting heparanase in the tumor microenvironment.
Exploring why Costa Rica outperforms the United States in life expectancy: A tale of two inequality gradients
Authors: Rosero-Bixby Luis , Dow William H. 
Published: January 2016

SignificanceRecent National Academies of Sciences reports have summarized evidence to understand why US health indicators lag those of other countries, in an effort to explore the fundamental question of why some populations live longer than others. However, this literature has failed to engage in the potentially more striking comparisons with countries that outperform the United States despite wielding many fewer resources. Costa Rica is one of a handful of middle-income countries with data to conduct this comparison. The finding that socioeconomic inequality in mortality is wider in the United States than in Costa Rica, and that people lower on the hierarchy in Costa Rica live longer than people in the equivalent position in the United States, is startling.