bluuebunny/crossref_metadata_2025_split huggingface dataset:
ELAVL1 regulates alternative splicing of eIF4E transporter to promote postnatal angiogenesis
Authors: Chang Sung-Hee , Elemento Olivier , Zhang Jiasheng , Zhuang Zhen W. , Simons Michael , Hla Timothy 
Published: November 2014

Significance
Angiogenesis, or new blood vessel formation, is critical not only for normal processes such as embryonic development but also for progression of diseases such as tumor growth, metastasis, and chronic inflammatory disease. This work elucidated a molecular mechanism that is important in postnatal angiogenesis in tumor growth and ischemia–reperfusion injury in the hind limb. Specifically, we identified a posttranscriptional gene regulatory mechanism that controls the activity of a potent suppressor of gene expression, named eIF4e transporter (4E-T). Alternative splicing of 4E-T controls the level of the active form of 4E-T, which suppresses gene expression in endothelial cells. This mechanism may be targeted to control angiogenesis-dependent diseases.
The cholesterol-dependent cytolysins pneumolysin and streptolysin O require binding to red blood cell glycans for hemolytic activity
Authors: Shewell Lucy K. , Harvey Richard M. , Higgins Melanie A. , Day Christopher J. , Hartley-Tassell Lauren E. , Chen Austen Y. , Gillen Christine M. , James David B. A. , Alonzo Francis , Torres Victor J. , Walker Mark J. , Paton Adrienne W. , Paton James C. , Jennings Michael P. 
Published: November 2014

SignificanceThe pneumococcus accounts for 25% of deaths in children under 5 y of age in developing countries. One of the most important virulence factors expressed by this pathogen is the pore-forming toxin, pneumolysin (Ply), an example of a Gram-positive cholesterol-dependent cytolysin (CDC). We show that Ply interacts with the Lewis histo-blood group antigen sialyl LewisX and that blocking this interaction can protect RBCs from lysis. We also identify glycan receptors on RBCs for the CDC streptolysin O from group A streptococcus. Our study supports the emerging paradigm shift that CDCs have cellular receptors other than cholesterol that define target cell tropism.
Amazonian landscapes and the bias in field studies of forest structure and biomass
Authors: Marvin David C. , Asner Gregory P. , Knapp David E. , Anderson Christopher B. , Martin Roberta E. , Sinca Felipe , Tupayachi Raul 
Published: November 2014

SignificanceAlthough tropical forests absorb more carbon dioxide as biomass than any other terrestrial ecosystem, biomass estimates disagree substantially at landscape-to-regional scales. Current biomass maps rely upon field plots for extrapolations to larger scales, yet whether field plots accurately represent landscape-scale variables has not been assessed. To our knowledge, this is the first study to compare forest structural variables and aboveground biomass derived from field plots to those derived from their host landscapes using airborne 3D remote sensing. We found that typical field plots can produce substantially biased estimates and the number of plots needed to reduce this bias is impractical, positioning airborne remote sensing as a core tool for mapping forest structure and biomass across tropical landscapes.
Substrate recognition by the cell surface palmitoyl transferase DHHC5
Authors: Howie Jacqueline , Reilly Louise , Fraser Niall J. , Vlachaki Walker Julia M. , Wypijewski Krzysztof J. , Ashford Michael L. J. , Calaghan Sarah C. , McClafferty Heather , Tian Lijun , Shipston Michael J. , Boguslavskyi Andrii , Shattock Michael J. , Fuller William 
Published: November 2014

Significance
Dynamic palmitoylation at the cell surface by the acyl transferase DHHC5 regulates a plethora of physiological processes, from endocytosis to synaptic plasticity. Here we report that DHHC5 is abundantly expressed in cell surface caveolar microdomains in cardiac muscle, and that the Na pump regulator phospholemman is a substrate for DHHC5. Palmitoylation of phospholemman C40 by DHHC5 reduces Na pump activity. DHHC5 interacts with phospholemman independent of its PSD-95/Discs-large/ZO-1 homology (PDZ) binding motif, via a region of its intracellular carboxyl tail that has not hitherto been implicated in substrate recognition. This suggests that it may be possible to selectively manipulate DHHC5 activity by blocking the recruitment of specific substrates to the active site by the carboxyl tail.
Electric fingerprint of voltage sensor domains
Authors: Souza Caio S. , Amaral Cristiano , Treptow Werner 
Published: November 2014

Significance
A central paradigm in the subject of cellular excitability is whether or not a dynamic membrane voltage field contributes to the operation of voltage sensor proteins. This issue has challenged an entire generation of scientists because static and dynamic contributions of the field cannot be discriminated from electrophysiology measurements. The dilemma imposes that structure-based calculations are required to solve the issue. By following this approach, we report that reshaping or dynamics of the field does not impact significantly the domain energetics or operation. As such, the functional diversity of voltage sensors observed in nature originates from variations in the detailed atom–atom interactions of the domain (chemical free energy) rather than in its coupling with the membrane voltage.
A mechanical-biochemical feedback loop regulates remodeling in the actin cytoskeleton
Authors: Stachowiak Matthew R. , Smith Mark A. , Blankman Elizabeth , Chapin Laura M. , Balcioglu Hayri E. , Wang Shuyuan , Beckerle Mary C. , O'Shaughnessy Ben 
Published: November 2014

Significance
Cellular activities are regulated by signaling pathways in which information is transduced biochemically. Increasingly it is appreciated that regulation also involves mechanical signaling, where mechanical information is mechanotransduced into biochemical information. However, little is understood about the cooperation of mechanical and biochemical signaling in mixed pathways. We identified a pathway where the two types of signaling work in harmony to remodel actomyosin stress fibers in the cell’s cytoskeleton. We present evidence that expansion or contraction of fibers alters the actin filament overlap, a mechanical signal that is mechanotransduced into actin assembly or disassembly, which in turn alters the overlap. A mathematical model accurately describes our measurements and shows that this mechanical-biochemical feedback loop synchronizes actin remodeling with fiber length changes.
Molecular architecture of the αβ T cell receptor–CD3 complex
Authors: Birnbaum Michael E. , Berry Richard , Hsiao Yu-Shan , Chen Zhenjun , Shingu-Vazquez Miguel A. , Yu Xiaoling , Waghray Deepa , Fischer Suzanne , McCluskey James , Rossjohn Jamie , Walz Thomas , Garcia K. Christopher 
Published: November 2014

Significance
The T-cell receptor (TCR) does not signal on its own. Instead, it is constitutively associated with the CD3 coreceptors, which contain intracellular signaling motifs. Although antigen (Ag) recognition by the TCR and the activation of T cells after CD3 activation have been extensively studied, there is far less known about how the TCR relays the binding of Ag to initiate intracellular signaling. Detailed study of the eight-chain TCR–CD3 complex is hampered by limited structural information for how the components of the complex interact. We use complementary structural approaches to examine where the TCR–CD3 extracellular domains are placed relative to each other and the overall organization of the complex.
A calcium-dependent protease as a potential therapeutic target for Wolfram syndrome
Authors: Lu Simin , Kanekura Kohsuke , Hara Takashi , Mahadevan Jana , Spears Larry D. , Oslowski Christine M. , Martinez Rita , Yamazaki-Inoue Mayu , Toyoda Masashi , Neilson Amber , Blanner Patrick , Brown Cris M. , Semenkovich Clay F. , Marshall Bess A. , Hershey Tamara , Umezawa Akihiro , Greer Peter A. , Urano Fumihiko 
Published: November 2014

Significance
Wolfram syndrome is an autosomal recessive disorder characterized by juvenile diabetes and neurodegeneration, and is considered a prototype of human endoplasmic reticulum (ER) disease. Wolfram syndrome is caused by loss of function mutations of Wolfram syndrome 1 or Wolfram syndrome 2 genes, which encode transmembrane proteins localized to the ER. Despite its rarity, Wolfram syndrome represents the best human disease model currently available to identify drugs and biomarkers associated with ER health. Furthermore, this syndrome is ideal for studying the mechanisms of ER stress-mediated death of neurons and β cells. Here we report that the pathway leading to calpain activation offers potential drug targets for Wolfram syndrome and substrates for calpain might serve as biomarkers for this syndrome.
Absence of Handling-Induced Saprolegnia Infection in Juvenile Rainbow Trout with Implications for Catch-and-Release Angling
Authors: Schwabe Martin , Meinelt Thomas , Phan Thuy M. , Cooke Steven J. , Arlinghaus Robert 
Published: November 2014

Abstract
Catch-and-release angling is common in recreational fisheries. During handling and dehooking, fish are subjected to stress and dermal injuries, which may result in infections by pathogens after the fish is released. The objective of this study was to evaluate the consequences of common handling practices used by anglers on the postrelease behavior and fate, particularly the susceptibility to disease, of undersized Rainbow Trout Oncorhynchus mykiss. Behavior immediately following capture and subsequent release of fish was examined in a 40-L container, and long-term fate was studied for 2 weeks in tanks incubated with Saprolegnia parasitica zoospores. Trout were behaviorally impaired as indicated by the ease of being netted following the simulated fight associated with catch and release, but there were no further behavioral impacts due to subsequent handling. None of the Rainbow Trout developed fungal infections nor was any significant mortality observed after 2 weeks; only 1 out of 137 fish died. Our data indicate that juvenile hatchery-reared Rainbow Trout have a high resilience to Saprolegnia infection handling-induced stress.
Received February 9, 2014; accepted August 25, 2014
Effects of Sodium Chloride and Long-Term, Low-Concentration Exposures to Hydrogen Peroxide on New Zealand Mud Snails
Authors: Oplinger Randall W , Wagner Eric J 
Published: November 2014

Abstract
New Zealand mud snails Potamopyrgus antipodarum (NZMS) are an invasive species and keeping NZMS out of hatcheries is important because the snail can be spread through the stocking of fish. We conducted a series of experiments to evaluate the effectiveness of using hydrogen peroxide to kill NZMS and sodium chloride to force NZMS to withdraw into their shells. The lowest concentrations of hydrogen peroxide that produced 100% mortality of NZMS were 750 mg/L for a 24-h exposure and and 75 mg/L for a 96-h exposure. We found that NZMS treated with sodium chloride withdrew into their shell and released from the substrate. Treatments with sodium chloride (717 mg/L) caused 70% of NZMS to withdraw into their shells and release from the substrate within the first minute of exposure, which could be beneficial in flushing them from a hatchery system provided there is sufficient discharge.
Dietary change in Cape gannets reflects distributional and demographic shifts in two South African commercial fish stocks
Authors: Green David B. , Klages Norbert T. W. , Crawford Robert J. M. , Coetzee Janet C. , Dyer Bruce M. , Rishworth Gavin M. , Pistorius Pierre A. 
Published: November 2014

Abstract
Seabirds are upper trophic level predators, and are often highly sensitive to changes in the availability of their prey. Altered prey assemblages resulting from fluctuations in oceanographic conditions may be mirrored by shifts in seabird diet. Long-term studies of dietary change in seabirds therefore provide valuable insight into the nature of environmental shifts within the systems in which they forage. In recent decades, the Agulhas region in South Africa has undergone significant oceanographic change related to warming and intensification of the Agulhas current. Concurrent with this change, the population of Cape gannets Morus capensis at Bird Island, Algoa Bay, has grown rapidly, probably as a result of an increased availability of its dominant prey items, sardine Sardinops sagax and anchovy Engraulis encrasicolus. Using one of the longest and most complete time-series available on diet of a seabird (spanning 34 years), we tested for changes in composition and the abundance of dominant prey species of this population. These observed changes were also compared with acoustic survey estimates of their biomass, and annual catch data. Since 1979, the prey composition has remained similar, but the dietary contribution of sardine and anchovy, which fluctuated inversely to each other, increased over the study period. These shifts seem to be reflective of fluctuations in the stock size of sardine and anchovy. Conversely, a third species, saury Scomberesox saurus, dominant in the non-breeding diet of the 1980s, decreased significantly in dietary abundance over the following two decades. It is likely that dietary shifts of Cape gannets at Bird Island were related to climate-mediated oceanographic change. The implications of such changes are discussed.
Lichen planus pigmentosus‐inversus: Report of three Chinese cases and review of the published work
Authors: Chen Shumin , Sun Wenqi , Zhou Guizhi , Chen Shengli , Lu Xuanmei 
Published: November 2014

AbstractLichen planus pigmentosus‐inversus is a rare variant of lichen planus. So far, only 24 cases from 12 reports have been documented in the published work. The prominent characteristics of the disease are dark‐brown macules and patches confined to the non‐sun exposed, flexural areas and skin folds with lichenoid pathological changes and prominent melanin incontinence. We report three female Chinese patients with typical clinical and pathological manifestations and a miniature review of the published work.
‘Trophic whales’ as biotic buffers: weak interactions stabilize ecosystems against nutrient enrichment
Authors: Schwarzmüller Florian , Eisenhauer Nico , Brose Ulrich 
Published: November 2014

Summary

Human activities may compromise biodiversity if external stressors such as nutrient enrichment endanger overall network stability by inducing unstable dynamics. However, some ecosystems maintain relatively high diversity levels despite experiencing continuing disturbances.

This indicates that some intrinsic properties prevent unstable dynamics and resulting extinctions. Identifying these ‘ecosystem buffers’ is crucial for our understanding of the stability of ecosystems and an important tool for environmental and conservation biologists. In this vein, weak interactions have been suggested as stabilizing elements of complex systems, but their relevance has rarely been tested experimentally.

Here, using network and allometric theory, we present a novel concept for a priori identification of species that buffer against externally induced instability of increased population oscillations via weak interactions. We tested our model in a microcosm experiment using a soil food‐web motif.

Our results show that large‐bodied species feeding at the food web's base, so called ‘trophic whales’, can buffer ecosystems against unstable dynamics induced by nutrient enrichment. Similar to the functionality of chemical or mechanical buffers, they serve as ‘biotic buffers’ that take up stressor effects and thus protect fragile systems from instability.

We discuss trophic whales as common functional building blocks across ecosystems. Considering increasing stressor effects under anthropogenic global change, conservation of these network‐intrinsic biotic buffers may help maintain the stability and diversity of natural ecosystems.
β‐asarone and levodopa co‐administration protects against 6‐hydroxydopamine‐induced damage in parkinsonian rat mesencephalon by regulating autophagy: down‐expression Beclin‐1 and light chain 3B and up‐expression P62
Authors: Huang Li‐Ping , Deng Min‐Zhen , He Yu‐Ping , Fang Yong‐Qi 
Published: November 2014

SummaryIn this study, we investigated Beclin‐1, light chain (LC)3B, and p62 expression in 6‐hydroxydopamine (6‐OHDA)‐induced parkinsonian rats after β‐asarone and levodopa (l‐dopa) co‐administration. Unilateral 6‐OHDA injection into the medial forebrain bundle was used to create the models, except in sham‐operated rats. Rats were divided into eight groups: sham‐operated group; 6‐OHDA model group; madopar group (75 mg/kg, per os (p.o.)); l‐dopa group (60 mg/kg, p.o.); β‐asarone group (15 mg/kg, p.o.); β‐asarone + l‐dopa co‐administered group (15 mg/kg + 60 mg/kg, p.o.); 3‐methyladenine group (500 nmol, intraperitoneal injection); and rapamycin group (1 mg/kg, intraperitoneal injection). Then, Beclin‐1, LC3B, and p62 expression in the mesencephalon were detected. The mesencephalon was also observed by transmission electron microscope. The results showed that Beclin‐1 and LC3B expression decreased and that p62 expression increased significantly in the madopar, l‐dopa, β‐asarone, and co‐administered groups when compared with the 6‐OHDA model. Beclin‐1 and LC3B expression in the β‐asarone and co‐administered groups were less than in the madopar or l‐dopa groups, whereas p62 expression in the β‐asarone and co‐administered groups was higher than in the madopar or l‐dopa groups. In addition, a significant decrease in autophagosome was exhibited in the β‐asarone and co‐administered groups when compared with the 6‐OHDA group. Our findings indicate that Beclin‐1 and LC3B expression decreased, whereas p62 expression increased after co‐administration treatment. In sum, all data suggest that the co‐administration of β‐asarone and l‐dopa may contribute to the treatment of 6‐OHDA‐induced damage in rats by inhibiting autophagy activity.
Carvedilol promotes neurological function, reduces bone loss and attenuates cell damage after acute spinal cord injury in rats
Authors: Liu Da , Huang Ying , Li Bin , Jia Changqing , Liang Feng , Fu Qin 
Published: November 2014

SummaryAcute spinal cord injury (SCI) leads to permanent functional deficits via mechanical injury and secondary mechanisms, but the therapeutic strategy for SCI is limited. Carvedilol has been shown to possess multiple biological and pharmacological properties. The of the present study was to investigate the possible protective effect of carvedilol in SCI rats. An acute SCI rat model was established and neurological function was tested. After carvedilol (10 mg/kg, oral gavage) treatment for 21 days, the status of osteoporosis, neuron damage, astrocyte activation, inflammation, oxidative stress and apoptosis were evaluated in rats. Carvedilol significantly improved locomotor activity that was decreased by SCI. In addition, carvedilol promoted bone growth by regulating the expression of nuclear factor‐κB ligand (receptor activator of nuclear factor‐κB ligand; RANKL) and osteoprotegerin (OPG), inactivating osteoclasts and thereby increasing bone mineral density in tibias. In addition, carvedilol reduced SCI‐induced neural damage, increased neuron number and reduced astrocyte activation in the spinal cord. Furthermore, the production and mRNA expression of tumour necrosis factor‐α, interleukin (IL)‐1β and IL‐6 were significantly reduced, reduced glutathione content and superoxide dismutase activity were markedly increased and malondialdehyde content was markedly decreased in the spinal cords of carvedilol‐treated rats. These results indicate that carvedilol exhibits anti‐inflammatory and anti‐oxidative effects in SCI rats. In addition, the expression of Fas and Fas ligand was reduced by carvedilol treatment, which, in turn, reduced cleaved caspase 3 expression and finally decreased the number of apoptotic cells in the spinal cord. In conclusion, carvedilol promotes neurological function, reduces bone loss and attenuates cell damage after acute SCI in rats.
Antinociceptive properties of esculetin in non‐inflammatory and inflammatory models of pain in rats
Authors: Rzodkiewicz Przemyslaw , Gasinska Emilia , Maslinski Slawomir , Bujalska‐Zadrozny Magdalena 
Published: November 2014

SummarySome studies suggest that 5‐lipoxygenase (5‐LOX) inhibition or leukotriene receptor antagonism may effectively attenuate different kinds of pain. In the present study, we investigated whether esculetin (which, among other actions, potently inhibits 5‐LOX) possesses analgesic activity in acute non‐inflammatory pain and acute inflammatory pain models in rats. We also examined the effects of zileuton, a selective 5‐LOX inhibitor, on esculetin activity. Plasma concentrations of leukotriene B4 (LTB4) after administration of esculetin were also determined. Esculetin (1.25–20 mg/kg, i.p.) dose‐dependently alleviated hyperalgesia and exhibited antinociceptive effects in both experimental models. The greatest effect of esculetin was observed with a dose of 20 mg/kg. In carrageenan‐induced inflammatory pain in rats, 20 mg/kg esculetin reversed or mitigated hyperalgesia, increasing the threshold to mechanical stimuli from a control value of −23.8 ± 1.8% to 15.2 ± 2.2% (P < 0.01) and that to thermal stimuli from −52.5 ± 6.1% to −9.5 ± 3.9% (P < 0.01). In non‐inflammatory pain, after esculetin (20 mg/kg) administration the threshold values to mechanical and thermal stimuli increased to 75.9 ± 4.2% and 59.2 ± 4.3%, respectively (P < 0.01 for both). Zileuton (30 mg/kg, p.o.) alone slightly but significantly increased the pain threshold in the non‐inflammatory and inflammatory acute pain models. Pretreatment with 30 mg/kg, p.o., zileuton significantly enhanced the analgesic activity of 5 mg/kg, i.p., esculetin in both pain models. Moreover, esculetin (10 mg/kg, i.p.) decreased LTB4 concentrations in the blood from 244 ± 29 pg/mL in the control group to 185 ± 11 pg/mL (P < 0.005). The results of the present study suggest the involvement of the 5‐LOX pathway in esculetin analgesia.
The production of nitric oxide by marine ammonia‐oxidizing archaea and inhibition of archaeal ammonia oxidation by a nitric oxide scavenger
Authors: Martens‐Habbena Willm , Qin Wei , Horak Rachel E. A. , Urakawa Hidetoshi , Schauer Andrew J. , Moffett James W. , Armbrust E. Virginia , Ingalls Anitra E. , Devol Allan H. , Stahl David A. 
Published: November 2014

SummaryNitrification is a critical process for the balance of reduced and oxidized nitrogen pools in nature, linking mineralization to the nitrogen loss processes of denitrification and anammox. Recent studies indicate a significant contribution of ammonia‐oxidizing archaea (AOA) to nitrification. However, quantification of the relative contributions of AOA and ammonia‐oxidizing bacteria (AOB) to in situ ammonia oxidation remains challenging. We show here the production of nitric oxide (NO) by Nitrosopumilus maritimus SCM1. Activity of SCM1 was always associated with the release of NO with quasi‐steady state concentrations between 0.05 and 0.08 μM. NO production and metabolic activity were inhibited by the nitrogen free radical scavenger 2‐phenyl‐4,4,5,5,‐tetramethylimidazoline‐1‐oxyl‐3‐oxide (PTIO). Comparison of marine and terrestrial AOB strains with SCM1 and the recently isolated marine AOA strain HCA1 demonstrated a differential sensitivity of AOB and AOA to PTIO and allylthiourea (ATU). Similar to the investigated AOA strains, bulk water column nitrification at coastal and open ocean sites with sub‐micromolar ammonia/ammonium concentrations was inhibited by PTIO and insensitive to ATU. These experiments support predictions from kinetic, molecular and biogeochemical studies, indicating that marine nitrification at low ammonia/ammonium concentrations is largely driven by archaea and suggest an important role of NO in the archaeal metabolism.