bluuebunny/crossref_metadata_2025_split huggingface dataset:
Krill space: a comparative assessment of mesoscale structuring in polar and temperate marine ecosystems
Authors: Santora Jarrod A. , Sydeman William J. , Schroeder Isaac D. , Reiss Christian S. , Wells Brian K. , Field John C. , Cossio Anthony M. , Loeb Valerie J. 
Published: March 2012

Abstract
Santora, J. A., Sydeman, W. J., Schroeder, I. D., Reiss, C. S., Wells, B. K., Field, J. C, Cossio, A. M., and Loeb, V. J. 2012. Krill space: a comparative assessment of mesoscale structuring in polar and temperate marine ecosystems. – ICES Journal of Marine Science, 69: . The spatial organization, mesoscale variability, and habitat associations of krill within portions of the Antarctic Peninsula and California Current marine ecosystems are compared. Using a decade of acoustic observations and remotely sensed oceanography (2000–2009), the hypothesis that mesoscale spatial organization of krill in both systems closely relates to geospatial variability of the shelf break and is non-linearly related to geostrophic flow and positively related to chlorophyll a (Chl a) is tested. Directional-dependence analysis to measure spatial variability of krill is used along with spatially explicit generalized additive models to quantify and compare the spatial relationships among krill and habitat characteristics in both systems. The results suggest the following aspects of krill spatial organization: (i) areas of dense aggregation, i.e. hot spots, are present in both systems and are orientated in the direction of the shelf break, (ii) moderate levels of eddy kinetic energy seem to concentrate krill in favourable habitats and lessen the likelihood of advection away from the system, and (iii) variable responses to surface Chl a concentration suggest that real-time Chl a values may not be useful as a global predictor of important krill habitat. The results provide valuable reference points for marine spatial management of krill and for refining ecosystem and foodweb models.
Cardiac-specific knockout of ETA receptor mitigates low ambient temperature-induced cardiac hypertrophy and contractile dysfunction
Authors: Zhang Yingmei , Li Linlin , Hua Yinan , Nunn Jennifer M. , Dong Feng , Yanagisawa Masashi , Ren Jun 
Published: March 2012

Abstract
Cold exposure is associated with oxidative stress and cardiac dysfunction. The endothelin (ET) system, which plays a key role in myocardial homeostasis, may participate in cold exposure-induced cardiovascular dysfunction. This study was designed to examine the role of ET-1 in cold stress-induced cardiac geometric and contractile responses. Wild-type (WT) and ETA receptor knockout (ETAKO) mice were assigned to normal or cold exposure (4°C) environment for 2 and 5 weeks prior to evaluation of cardiac geometry, contractile, and intracellular Ca2+ properties. Levels of the temperature sensor transient receptor potential vanilloid (TRPV1), mitochondrial proteins for biogenesis and oxidative phosphorylation, including UCP2, HSP90, and PGC1α were evaluated. Cold stress triggered cardiac hypertrophy, depressed myocardial contractile capacity, including fractional shortening, peak shortening, and maximal velocity of shortening/relengthening, reduced intracellular Ca2+ release, prolonged intracellular Ca2+ decay and relengthening duration, generation of ROS and superoxide, as well as apoptosis, the effects of which were blunted by ETAKO. Western blotting revealed downregulated TRPV1 and PGC1α as well as upregulated UCP2 and activation of GSK3β, GATA4, and CREB in cold-stressed WT mouse hearts, which were obliterated by ETAKO. Levels of HSP90, an essential regulator for thermotolerance, were unchanged. The TRPV1 agonist SA13353 attenuated whereas TRPV1 antagonist capsazepine mimicked cold stress- or ET-1-induced cardiac anomalies. The GSK3β inhibitor SB216763 ablated cold stress-induced cardiac contractile (but not remodeling) changes and ET-1-induced TRPV1 downregulation. These data suggest that ETAKO protects against cold exposure-induced cardiac remodeling and dysfunction mediated through TRPV1 and mitochondrial function.
Active Emergence from Propofol General Anesthesia Is Induced by Methylphenidate
Authors: Chemali Jessica J. , Van Dort Christa J. , Brown Emery N. , Solt Ken 
Published: March 2012

Background
A recent study showed that methylphenidate induces emergence from isoflurane general anesthesia. Isoflurane and propofol are general anesthetics that may have distinct molecular mechanisms of action. The objective of this study was to test the hypothesis that methylphenidate actively induces emergence from propofol general anesthesia.

Methods
Using adult rats, the effect of methylphenidate on time to emergence after a single bolus of propofol was determined. The ability of methylphenidate to restore righting during a continuous target-controlled infusion (TCI) of propofol was also tested. In a separate group of rats, a TCI of propofol was established and spectral analysis was performed on electroencephalogram recordings taken before and after methylphenidate administration.

Results
Methylphenidate decreased median time to emergence after a single dose of propofol from 735 s (95% CI: 598-897 s, n = 6) to 448 s (95% CI: 371-495 s, n = 6). The difference was statistically significant (P = 0.0051). During continuous propofol anesthesia with a median final target plasma concentration of 4.0 μg/ml (95% CI: 3.2-4.6, n = 6), none of the rats exhibited purposeful movements after injection of normal saline. After methylphenidate, however, all six rats promptly exhibited arousal and had restoration of righting with a median time of 82 s (95% CI: 30-166 s). Spectral analysis of electroencephalogram data demonstrated a shift in peak power from δ (less than 4 Hz) to θ (4-8 Hz) and β (12-30 Hz) after administration of methylphenidate, indicating arousal in 4/4 rats.

Conclusions
Methylphenidate decreases time to emergence after a single dose of propofol, and induces emergence during continuous propofol anesthesia in rats. Further study is warranted to test the hypothesis that methylphenidate induces emergence from propofol general anesthesia in humans.
Phosphoproteomic Analysis of Seed Maturation in Arabidopsis, Rapeseed, and Soybean
Authors: Meyer Louis J. , Gao Jianjiong , Xu Dong , Thelen Jay J. 
Published: March 2012

Abstract
To characterize protein phosphorylation in developing seed, a large-scale, mass spectrometry-based phosphoproteomic study was performed on whole seeds at five sequential stages of development in soybean (Glycine max), rapeseed (Brassica napus), and Arabidopsis (Arabidopsis thaliana). Phosphopeptides were enriched from 0.5 mg of total peptides using a combined strategy of immobilized metal affinity and metal oxide affinity chromatography. Enriched phosphopeptides were analyzed by Orbitrap tandem mass spectrometry and mass spectra mined against cognate genome or cDNA databases in both forward and randomized orientations, the latter to calculate false discovery rate. We identified a total of 2,001 phosphopeptides containing 1,026 unambiguous phosphorylation sites from 956 proteins, with an average false discovery rate of 0.78% for the entire study. The entire data set was uploaded into the Plant Protein Phosphorylation Database (www.p3db.org), including all meta-data and annotated spectra. The Plant Protein Phosphorylation Database is a portal for all plant phosphorylation data and allows for homology-based querying of experimentally determined phosphosites. Comparisons with other large-scale phosphoproteomic studies determined that 652 of the phosphoproteins are novel to this study. The unique proteins fall into several Gene Ontology categories, some of which are overrepresented in our study as well as other large-scale phosphoproteomic studies, including metabolic process and RNA binding; other categories are only overrepresented in our study, like embryonic development. This investigation shows the importance of analyzing multiple plants and plant organs to comprehensively map the complete plant phosphoproteome.
Quantitative Phosphoproteome Profiling of Iron-Deficient Arabidopsis Roots
Authors: Lan Ping , Li Wenfeng , Wen Tuan-Nan , Schmidt Wolfgang 
Published: March 2012

Abstract
Iron (Fe) is an essential mineral nutrient for plants, but often it is not available in sufficient quantities to sustain optimal growth. To gain insights into adaptive processes to low Fe availability at the posttranslational level, we conducted a quantitative analysis of Fe deficiency-induced changes in the phosphoproteome profile of Arabidopsis (Arabidopsis thaliana) roots. Isobaric tags for relative and absolute quantitation-labeled phosphopeptides were analyzed by liquid chromatography-tandem mass spectrometry on an LTQ-Orbitrap with collision-induced dissociation and high-energy collision dissociation capabilities. Using a combination of titanium dioxide and immobilized metal affinity chromatography to enrich phosphopeptides, we extracted 849 uniquely identified phosphopeptides corresponding to 425 proteins and identified several not previously described phosphorylation motifs. A subset of 45 phosphoproteins was defined as being significantly changed in abundance upon Fe deficiency. Kinase motifs in Fe-responsive proteins matched to protein kinase A/calcium calmodulin-dependent kinase II, casein kinase II, and proline-directed kinase, indicating a possible critical function of these kinase classes in Fe homeostasis. To validate our analysis, we conducted site-directed mutagenesis on IAA-CONJUGATE-RESISTANT4 (IAR4), a protein putatively functioning in auxin homeostasis. iar4 mutants showed compromised root hair formation and developed shorter primary roots. Changing serine-296 in IAR4 to alanine resulted in a phenotype intermediate between mutant and wild type, whereas acidic substitution to aspartate to mimic phosphorylation was either lethal or caused an extreme dwarf phenotype, supporting the critical importance of this residue in Fe homeostasis. Our analyses further disclose substantial changes in the abundance of phosphoproteins involved in primary carbohydrate metabolism upon Fe deficiency, complementing the picture derived from previous proteomic and transcriptomic profiling studies.
The NADPH oxidase‐mediated production of hydrogen peroxide (H2O2) and resistance to oxidative stress in the necrotrophic pathogen Alternaria alternata of citrus
Authors: YANG SIWY LING , CHUNG KUANG‐REN 
Published: March 2012

SUMMARYIt has become increasingly apparent that the production of reactive oxygen species (ROS) by the NADPH oxidase (Nox) complex is vital for cellular differentiation and signalling in fungi. We cloned and characterized an AaNoxA gene of the necrotrophic fungus Alternaria alternata, which encodes a polypeptide analogous to mammalian gp91phox and fungal Noxs implicated in the generation of ROS. Genetic analysis confirmed that AaNoxA is responsible for the production of ROS. Moreover, deletion of AaNoxA in A. alternata resulted in an elevated hypersensitivity to hydrogen peroxide (H2O2), menadione, potassium superoxide (KO2), diamide and many ROS‐generating compounds. The results implicate the involvement of AaNoxA in cellular resistance to ROS stress. The impaired phenotypes strongly resemble those previously seen for the ap1 null mutant defective in a YAP1‐like transcriptional regulator and for the hog1 mutant defective in a HOG1‐like mitogen‐activated protein (MAP) kinase. The noxA null mutant was also hypersensitive to Nox inhibitors, nitric oxide (NO·) donors and NO· synthase inhibitors, implying a role of AaNoxA in the NO· signalling pathway. Expression of AaNoxA was activated by H2O2, menadione, KO2, NO· donors and l‐arginine (a substrate for NO· synthase). AaNoxA may be able to sense and respond to both ROS and nitric oxide. Moreover, AaNoxA is required for normal conidiation and full fungal virulence. AaNoxA promoted the expression of the AaAP1 and AaHOG1 genes in A. alternata. Inactivation of AaNoxA greatly reduced the transcriptional activation of AaAP1 in response to ROS stress. Thus, we conclude that the regulatory functions of AaNoxA conferring ROS resistance are modulated partially through the activation of the YAP1‐ and HOG1 MAP kinase‐mediated signalling pathways.
Prenatal exposure to acid‐suppressive drugs and the risk of childhood asthma: a population‐based Danish cohort study
Authors: Andersen A. B. T. , Erichsen R. , Farkas D. K. , Mehnert F. , Ehrenstein V. , Sørensen H. T. 
Published: March 2012

SummaryBackgroundProton pump inhibitors (PPIs) may activate the immune system and cause asthma.AimTo investigate the association of prenatal exposure to PPIs and histamine 2‐receptor antagonists (H2RAs) with risk of asthma.MethodsIn this cohort study, 197 060 singletons born between 1996 and 2008 in northern Denmark were followed until the end of 2009. Data were obtained through Danish medical registries. Asthma in offspring was defined as at least two prescriptions of both a β‐agonist and an inhaled glucocorticoid and/or a hospital diagnosis of asthma during the follow‐up. Cox proportional‐hazard regression was used to compute incidence rate ratios, adjusting for covariates.ResultsA total of 2238 (1.1%) children were prenatally exposed to PPIs and 24 506 (12.4%) children developed asthma during follow‐up (median follow‐up = 6.8 years). The adjusted IRR (aIRR) of asthma associated with prenatal exposure to PPIs was 1.41 (95% confidence interval (CI): 1.27–1.56), compared with those unexposed. The association did not vary by trimester of exposure, and prenatal exposure to H2RAs was associated with similar increase in risk. The aIRR for maternal PPI and H2RA use in the year after, but not during pregnancy was 1.32 (95% CI: 1.20–1.46) and 1.13 (0.93–1.36), respectively, compared with non‐use during and in the year after pregnancy.ConclusionsPrenatal exposure to both PPIs and H2RAs was associated with an increased risk of asthma in our study. Because the observed association is not drug specific and also observed for maternal postnatal use it may be explained by a ‘class effect’ or maternal underlying condition.
A Study of the Inheritance and Properties of an Electrophoretic Variant of NADH‐Methaemoglobin Reductase Associated with Congenital Methaemoglobinaemia
Authors: West C. A. 
Published: March 2012

Summary. Further investigation on the patient previously reported and on his family are described. It is shown that in this patient the disease is the result of a doubly heterozygous state in which both an electrophoretically slow enzyme variant (ma) and small amounts of electrophoretically normal NADH‐methaemoglobin reductase are present. Electrophoretic and kinetic studies showed that the abnormal enzyme variant ma possessed a significantly reduced capacity for binding NADH compared with the normal enzyme, which was found to consist of two distinct components when studied in an electrophoretic system incorporating NADH. The variant ma appeared to consist of only the minor of these components.The mother of the patient, and 13 other family members were identified as heterozygotes after electrophoretic analysis of haemoglobin free red cell extracts. The assay of red cell NADH‐methaemoglobin reductase in all the electrophoretically confirmed heterozygotes demonstrated the considerable overlap of their enzyme levels with the normal range, and therefore the inadvisability of utilizing NADH‐methaemoglobin reductase level alone as the criterion of the heterozygous state.
Immunological pathways in virus‐induced COPD exacerbations: a role for IL‐15
Authors: Zdrenghea Mihnea T. , Mallia Patrick , Johnston Sebastian L. 
Published: March 2012

Eur J Clin Invest 2012; 42 (9): 1010–1015AbstractBackground  Chronic obstructive pulmonary disease (COPD) is characterized by high levels of antiviral type 1 cytokine interferon‐γ and activated CD8+ T cells. COPD exacerbations are the major cause of morbidity and mortality, have a prolonged and intense effect on quality of life and may result in accelerated loss of lung function. Respiratory virus infections, frequently within a state of colonization by bacteria, are the major cause of COPD exacerbations, and there is also evidence of virus latency in ‘stable’ disease, suggesting that latent infection might be a cause of chronic inflammation in COPD.Design  This is an update of current literature concerning the role of interleukin‐15 and major histocompatibility complex class I‐related chain A and B molecules in type 1 immune responses, particularly to respiratory virus infections, which are the main cause of COPD exacerbations. We also present data from our own group suggesting a role for interleukin‐15 in virus‐induced COPD exacerbations.Results  Type 1 cytokine interleukin‐15 is produced by resident airway cells (epithelial cells and macrophages) in response to virus infection and bacteria. Virus infections modulate major histocompatibility complex class I‐related chain A and B molecules in respiratory epithelial cells.Conclusions  Interleukin‐15 could play a major role in the airway inflammation in COPD directly, via its own receptors, by amplifying the type 1 immune responses and decreasing apoptosis or indirectly, via modulating molecules associated with cytotoxic activity of natural killer and CD8+ T cells, such as major histocompatibility complex class I‐related chain A and B.
Localization and characterization of cracks in clay‐rocks using frequency and time‐domain induced polarization
Authors: Okay G. , Cosenza P. , Ghorbani A. , Camerlynck C. , Cabrera J. , Florsch N. , Revil A. 
Published: March 2012

ABSTRACTInduced polarization (IP) is a geophysical method that is potentially sensitive to the presence of cracks in porous rocks and therefore to damage. We performed time‐domain and frequency domain IP measurements at the Tournemire Underground Research Laboratory (URL, Aveyron, France) in areas where different types of cracks are observed. These cracks correspond to both tectonic fractures and new cracks associated with stress release and desiccation resulting from the excavation of a gallery. These measurements were performed both in eastern and northern galleries of the test site. The eastern gallery was excavated in 1996 while the northern gallery was excavated recently in 2008. This gives us the opportunity to study the electrical characteristics of the excavation damaged zone surrounding the galleries with respect to the age of the excavation. Longitudinal profiles were performed along the floor of the galleries with 48 Cu/CuSO4 electrodes separated by a distance of 20 cm. Chargeability and resistivity were inverted using a Gauss‐Newton iterative approach assuming an isotropic heterogeneous clay‐rock material. The resulting IP tomograms show a correlation between high values of chargeability and the presence of calcite‐filled tectonic fractures. X‐ray analysis indicates that the presence of pyrite in these fractures is a potential source of the observed IP signals. The cracks associated with the mechanical damage of the formation exhibit low values of chargeability, on the same order of magnitude than the chargeability of the clay‐rock matrix and are therefore hardly observable. A smaller IP response associated with the presence of these cracks is observed in the older gallery and this observation is qualitatively related to the desaturation process associated with these cracks. In a specific area of one of the galleries, the presence of calcareous nodules is observed to be an important source of anomalous chargeability. This signature seems to be associated with the presence of pyrite.
Aberrant cytokeratin 7 expression of centrilobular hepatocytes: a clinicopathological study
Authors: Matsukuma Susumu , Takeo Hiroaki , Kono Takako , Nagata Yuiko , Sato Kimiya 
Published: March 2012

Matsukuma S, Takeo H, Kono T, Nagata Y & Sato K  (2012) Histopathology 61, 857–862Aberrant cytokeratin 7 expression of centrilobular hepatocytes: a clinicopathological studyAims:  This study has attempted to elucidate the clinicopathological features of aberrant cytokeratin 7 (CK7) expression by centrilobular hepatocytes.Methods and results:  A total of 113 liver biopsy specimens from patients with common non‐neoplastic liver diseases, including hepatitis B or C, non‐alcoholic steatohepatitis, alcoholic liver disease and other diseases were examined. In 56 specimens (49.6%), CK7‐positive centrilobular hepatocytes (CK7 + CHs) were identified and sometimes showed binuclear features. CK7 + CHs were associated with patients’ older age (P = 0.004), higher serum levels of aspartate aminotransferase (P = 0.016) and γ‐glutamyltransferase (P = 0.006), centrilobular fibrosis (P < 0.001), prominent thickening of hepatocytic plates (P < 0.001) and higher scores of total and periportal CK7‐positive hepatocytes (both P < 0.001), but were not correlated with gender, steatosis, serum levels of total bilirubin or alanine aminotransferase. In 55 cases of hepatitis B and hepatitis C only, CK7 + CHs were related to a higher stage of fibrosis (P = 0.006).Conclusion:  CK7 + CHs occur relatively frequently in non‐neoplastic liver disease, associated with centrilobular scarring and the presence of CK7‐positive periportal hepatocytes, and appear to be a non‐specific phenomenon with respect aetiology of underlying disease. CK7 + CHs may represent age‐dependent activation of hepatic progenitor cells or a regenerative phenomenon of hepatocytes themselves, both of which might contribute to liver regeneration.
Long‐term use of HU210 adversely affects spermatogenesis in rats by modulating the endocannabinoid system
Authors: M Lewis S. E. , Paro R. , Borriello L. , Simon L. , Robinson L. , Dincer Z , Riedel G. , Battista N. , Maccarrone M. 
Published: March 2012

SummaryRecent societal acceptance of cannabinoids as recreational and therapeutic drugs has posed a potential hazard to male reproductive health. Mammals have a highly sophisticated endogenous cannabinoid (ECS) system that regulates male (and female) reproduction and exo‐cannabinoids may influence it adversely. Therefore it is imperative to determine their effects on male reproduction so that men can make informed choices as to their use. Here, an animal model was used to administer HU210, a synthetic analogue of Δ9‐tetrahydrocannabinol (THC) and potent cannabinoid receptor (CB) agonist to determine its effects on reproductive organ weights, spermatogenesis, testicular histology and sperm motility. Its effects on the physiological endocannabinoid system were also investigated. Spermatogenesis was markedly impaired with reductions in total sperm count after 2 weeks of exposure. Spermatogenic efficiency was depleted, and Sertoli cell number decreased as exposure time increased with seminiferous tubules showing germ cell depletion developing into atrophy in some cases. Sperm motility was also adversely affected with marked reductions from 2 weeks on. HU210 also acted on the sperm’s endocannabinoid system. Long‐term use of exo‐cannabinoids has adverse effects on both spermatogenesis and sperm function. These findings highlight the urgent need for studies evaluating the fertility potential of male recreational drug users. HU210, a selective agonist for CB1 and CB2 cannabinoid receptors impairs spermatogenesis and sperm motility and deregulates the endocannabinoid system