bluuebunny/crossref_metadata_2025_split huggingface dataset:
Macrophage Adipose Triglyceride Lipase Deficiency Attenuates Atherosclerotic Lesion Development in Low-Density Lipoprotein Receptor Knockout Mice
Authors: Lammers Bart , Chandak Prakash G. , Aflaki Elma , Van Puijvelde Gijs H.M. , Radovic Branislav , Hildebrand Reeni B. , Meurs Illiana , Out Ruud , Kuiper Johan , Van Berkel Theo J.C. , Kolb Dagmar , Haemmerle Guenter , Zechner Rudolf , Levak-Frank Sanja , Van Eck Miranda , Kratky Dagmar 
Published: October 2010

Objective—
The consequences of macrophage triglyceride (TG) accumulation on atherosclerosis have not been studied in detail so far. Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme for the initial step in TG hydrolysis. Because ATGL knockout (KO) mice exhibit massive TG accumulation in macrophages, we used ATGL KO mice to study the effects of macrophage TG accumulation on atherogenesis.

Methods and Results—

Low-density lipoprotein receptor (LDLr) KO mice were transplanted with bone marrow from ATGL KO (ATGL KO→LDLr KO) or wild-type (WT→LDLr KO) mice and challenged with a Western-type diet for 9 weeks. Despite TG accumulation in ATGL KO macrophages, atherosclerosis in ATGL KO→LDLr KO mice was 43% reduced associated with decreased plasma monocyte chemoattractant protein-1 (MCP-1) and macrophage interleukin-6 concentrations. This coincided with a reduced amount of macrophages, possibly because of a 39% increase in intraplaque apoptosis and a decreased migratory capacity of ATGL KO macrophages. The reduced number of white blood cells might be due to a 36% decreased Lin
−
Sca-1
+
cKit
+
hematopoietic stem cell population.

Conclusion—
We conclude that the attenuation of atherogenesis in ATGL KO→LDLr KO mice is due to decreased infiltration of less inflammatory macrophages into the arterial wall and increased macrophage apoptosis.
Stochastic Parameterization Schemes for Use in Realistic Climate Models
Authors: Culina Joel , Kravtsov Sergey , Monahan Adam H. 
Published: October 2010

Abstract
Stochastic parameterizations of fast-evolving, subgrid-scale processes are increasingly being used in a range of models from conceptual models to general circulation models. However, stochastic terms are generally included in an ad hoc fashion. In this study, a systematic method—“Hasselmann’s method”—of stochastic parameterization is developed through the direct application of rigorously justified limit theorems that predict the effective slow dynamics in systems with coupled slow and fast variables. The multiple Hasselmann models form a hierarchy of models ordered by the time scales over which they are expected to provide good approximations to the slowly evolving variables. Adaptable, efficient algorithms for integrating these reduced models are developed that require minimal changes to the unreduced model.
Hasselmann’s method is tested on an O(10 000)-dimensional (planetary and synoptic scale) quasigeostrophic model of atmospheric low-frequency variability. Low-dimensional deterministic and stochastic models in the planetary-scale modes alone are derived, which accurately generate the statistics of the corresponding modes of the unreduced model, including the statistical signatures of jet regime behavior. It is shown that deterministic nonlinearity through slow forcing averaged with respect to the fast modes distribution dominates over multiplicative noise in generating the regime behavior.
Ice–Ice Collisions: An Ice Multiplication Process in Atmospheric Clouds
Authors: Yano J.-I. , Phillips V. T. J. 
Published: October 2010

Abstract
Ice in atmospheric clouds undergoes complex physical processes, interacting especially with radiation, which leads to serious impacts on global climate. After their primary production, atmospheric ice crystals multiply extensively by secondary processes. Here, it is shown that a mostly overlooked process of mechanical breakup of ice particles by ice–ice collisions contributes to such observed multiplication. A regime for explosive multiplication is identified in its phase space of ice multiplication efficiency and number concentration of ice particles. Many natural mixed-phase clouds, if they have copious millimeter-sized graupel, fall into this explosive regime. The usual Hallett–Mossop (H–M) process of ice multiplication is shown to dominate the overall ice multiplication when active, as it starts sooner, compared to the breakup ice multiplication process. However, for deep clouds with a cold base temperature where the usual H–M process is inactive, the ice breakup mechanism should play a critical role. Supercooled rain, which may freeze to form graupel directly in only a few minutes, is shown to hasten such ice multiplication by mechanical breakup, with an ice enhancement ratio exceeding 104 approximately 20 min after small graupel first appear. The ascent-dependent onset of subsaturation with respect to liquid water during explosive ice multiplication is predicted to determine the eventual ice concentrations.
The Quasi-Biennial Oscillation in a Double CO2 Climate
Authors: Kawatani Yoshio , Hamilton Kevin , Watanabe Shingo 
Published: October 2010

AbstractThe effects of anticipated twenty-first-century global climate change on the stratospheric quasi-biennial oscillation (QBO) have been studied using a high-resolution version of the Model for Interdisciplinary Research on Climate (MIROC) atmospheric GCM. This version of the model is notable for being able to simulate a fairly realistic QBO for present-day conditions including only explicitly resolved nonstationary waves. A long control integration of the model was run with observed climatological sea surface temperatures (SSTs) appropriate for the late twentieth century, followed by another integration with increased atmospheric CO2 concentration and SSTs incremented by the projected twenty-first-century warming in a multimodel ensemble of coupled ocean–atmosphere runs that were forced by the Special Report on Emissions Scenarios (SRES) A1B scenario of future atmospheric composition. In the experiment for late twenty-first-century conditions the QBO period becomes longer and QBO amplitude weaker than in the late twentieth-century simulation. The downward penetration of the QBO into the lowermost stratosphere is also curtailed in the late twenty-first-century run. These changes are driven by a significant (30%–40%) increase of the mean upwelling in the equatorial stratosphere, and the effect of this enhanced mean circulation overwhelms counteracting influences from strengthened wave fluxes in the warmer climate. The momentum fluxes associated with waves propagating upward into the equatorial stratosphere do strengthen overall by ∼(10%–15%) in the warm simulation, but the increases are almost entirely in zonal phase speed ranges that have little effect on the stratospheric QBO but that would be expected to have important influences in the mesosphere and lower thermosphere.
A New Extratropical Tracer Describing the Role of the Western Pacific in the Onset of El Niño: Implications for ENSO Understanding and Forecasting
Authors: Ballester Joan , Rodríguez-Arias Miquel Àngel , Rodó Xavier 
Published: October 2010

AbstractA complex empirical orthogonal function analysis was applied to sea surface temperature data in the southern high-latitude Pacific to identify and isolate primary processes related to the onset of El Niño (EN) events. Results were compared to those of a lead–lag composite analysis of a new tracer of EN events in the southern high-latitude Pacific, the Ross–Bellingshausen (RB) dipole. Both techniques successfully isolate the main low-frequency features in the interaction among the tropical and southern extratropical Pacific during the onset of recent eastward-propagating EN events. Particularly, positive RB peaks were followed by EN events around 9 months later, on average. In turn, RB maxima were anticipated by local warm anomalies in the western tropical Pacific a year in advance, which enhance local convection and upper-troposphere divergence and generate an anomalous wave train extending eastward and poleward in the southern extratropics. In addition, circulation changes lead to a warm SST region in the central tropical Pacific, which is then strengthened by suppressed equatorial easterlies. Convection thus starts to move to the central Pacific and so the Walker circulation weakens, activating the positive Bjerknes feedback that ultimately leads to the development of an EN event. These results highlight the enormous potential of the interaction between the tropics and this high-latitude region in the Southern Hemisphere to increase El Niño–Southern Oscillation understanding and to improve the long-lead prediction skill of EN phenomenon.
Intraseasonal Modulation of the North Pacific Storm Track by Tropical Convection in Boreal Winter
Authors: Deng Yi , Jiang Tianyu 
Published: October 2010

Abstract
The modulation of the North Pacific storm track by tropical convection on intraseasonal time scales (30–90 days) in boreal winter (December–March) is investigated using the NCEP–NCAR reanalysis and NOAA satellite outgoing longwave radiation (OLR) data. Multivariate empirical orthogonal function (MEOF) analysis and case compositing based upon the principal components (PCs) of the EOFs reveal substantial changes in the structure and intensity of the Pacific storm track quantified by vertically (925–200 mb) averaged synoptic eddy kinetic energy (SEKE) during the course of a typical Madden–Julian oscillation (MJO) event. The storm-track response is characterized by an amplitude-varying dipole propagating northeastward as the center of the anomalous tropical convection moves eastward across the eastern Indian Ocean and the western-central Pacific. A diagnosis of the SEKE budget indicates that the storm-track anomaly is induced primarily by changes in the convergence of energy flux, baroclinic conversion, and energy generation due to the interaction between synoptic eddies and intraseasonal flow anomalies. This demonstrates the important roles played by eddy–mean flow interaction and eddy–eddy interaction in the development of the extratropical response to MJO variability. The feedback of synoptic eddy to intraseasonal flow anomalies is pronounced: when the center of the enhanced tropical convection is located over the Maritime Continent (western Pacific), the anomalous synoptic eddy forcing partly drives an upper-tropospheric anticyclonic (cyclonic) and, to its south, a cyclonic (anticyclonic) circulation anomaly over the North Pacific. Associated with the storm-track anomaly, a three-band (dry–wet–dry) anomaly in both precipitable water and surface precipitation propagates poleward over the eastern North Pacific and induces intraseasonal variations in the winter hydroclimate over western North America.
El Niño–Southern Oscillation’s Impact on Atlantic Basin Hurricanes and U.S. Landfalls
Authors: Klotzbach Philip J. 
Published: October 2010

Abstract
El Niño–Southern Oscillation (ENSO) has been shown in many previous papers to impact seasonal levels of Atlantic basin tropical cyclone activity. This paper revisits this relationship by examining a longer period (1900–2009) than has been examined in earlier analyses. Alterations in large-scale climate parameters, especially vertical wind shear, are shown to be the primary reasons why tropical cyclone activity in the Atlantic is reduced in El Niño years. Climate signals are found to be somewhat stronger in the Caribbean than for the remainder of the tropical Atlantic. The focus of the paper then shifts to U.S. landfalls, confirming previous research that U.S. landfalls are reduced in El Niño years. The reduction in landfall frequency is greater along the Florida peninsula and East Coast than it is along the Gulf Coast, especially for major hurricanes. The probability of each state being impacted by a hurricane and major hurricane is given for El Niño, La Niña, and neutral years. The most dramatic probability differences between warm and cold ENSO events lie along the East Coast and, in particular, the state of North Carolina. The relationship between ENSO and the Atlantic multidecadal oscillation (AMO) is also examined. In general, the negative phase of the AMO is characterized by a stronger ENSO modulation signal than a positive phase of the AMO.
Brainstem changes in 5-HT1A receptor availability during migraine attack
Authors: Demarquay G , Lothe A , Royet JP , Costes N , Mick G , Mauguière F , Ryvlin P 
Published: October 2010

Background: Among serotonin receptors, 5-HT1A receptors are implicated in the regulation of central serotoninergic tone and could be involved in the abnormal brain 5-HT turnover suspected in migraineurs. The aim of this study was to investigate 5-HT1A receptors’ availability during migraine attacks. Methods: Ten patients suffering from odor-triggered migraine attacks and 10 control subjects were investigated using positron emission tomography (PET) and [18F]MPPF PET tracer, a selective 5-HT1A antagonist. All subjects underwent calibrated olfactory stimulations prior to the PET study. Results: Four patients developed a migraine attack during the PET study. In these patients, statistical parametrical mapping and region of interest analyses showed an increased [18F]MPPF binding potential (BPND) in the pontine raphe when compared to headache-free migraineurs and control subjects. This ictal change was confirmed at the individual level in each of the four affected patients. In comparison with the headache-free migraineurs, patients with a migraine attack also showed significantly increased [18F]MPPF BPND in the left orbitofrontal cortex, precentral gyrus and temporal pole. No significant change in [18F]MPPF BPND was observed between headache-free migraineurs and controls. Conclusions: Our results emphasize the role of 5HT1A receptors in the pontine raphe nuclei during the early stage of migraine attacks.
Factors Affecting Healing Rates after Arthroscopic Double-Row Rotator Cuff Repair
Authors: Tashjian Robert Z. , Hollins Anthony M. , Kim Hyun-Min , Teefey Sharlene A. , Middleton William D. , Steger-May Karen , Galatz Leesa M. , Yamaguchi Ken 
Published: October 2010

Background Double-row arthroscopic rotator cuff repairs were developed to improve initial biomechanical strength of repairs to improve healing rates. Despite biomechanical improvements, failure of healing remains a clinical problem. Purpose To evaluate the anatomical results after double-row arthroscopic rotator cuff repair with ultrasound to determine postoperative repair integrity and the effect of various factors on tendon healing. Study Design Case series; Level of evidence, 4. Methods Forty-eight patients (49 shoulders) who had a complete arthroscopic rotator cuff repair (double-row technique) were evaluated with ultrasound at a minimum of 6 months after surgery. Outcome was evaluated at a minimum of 1-year follow-up with standardized history and physical examination, visual analog scale for pain, active forward elevation, and preoperative and postoperative shoulder scores according to the system of the American Shoulder and Elbow Surgeons and the Simple Shoulder Test. Quantitative strength was measured postoperatively. Results Ultrasound and physical examinations were performed at a minimum of 6 months after surgery (mean, 16 months; range, 6 to 36 months) and outcome questionnaire evaluations at a minimum of 12 months after surgery (mean, 29 months; range, 12 to 55 months). Of 49 repairs, 25 (51%) were healed. Healing rates were 67% in single-tendon tears (16 of 24 shoulders) and 36% in multitendon tears (9 of 25 shoulders). Older age and longer duration of follow-up were correlated with poorer tendon healing (P < .03). Visual analog scale for pain, active forward elevation, American Shoulder and Elbow Surgeons scores, and Simple Shoulder Test scores all had significant improvement from baseline after repair (P < .0001). Conclusion Increased age and longer duration of follow-up were associated with lower healing rates after double-row rotator cuff repair. The biological limitation at the repair site, as reflected by the effects of age on healing, appears to be the most important factor influencing tendon healing, even after maximizing repair biomechanical strength with a double-row construct.
Endothelial LSP1 is involved in endothelial dome formation, minimizing vascular permeability changes during neutrophil transmigration in vivo
Authors: Petri Björn , Kaur Jaswinder , Long Elizabeth M. , Li Hang , Parsons Sean A. , Butz Stefan , Phillipson Mia , Vestweber Dietmar , Patel Kamala D. , Robbins Stephen M. , Kubes Paul 
Published: October 2010

AbstractThe endothelium actively participates in neutrophil migration out of the vasculature via dynamic, cytoskeleton-dependent rearrangements leading to the formation of transmigratory cups in vitro, and to domes that completely surround the leukocyte in vivo. Leukocyte-specific protein 1 (LSP1), an F-actin–binding protein recently shown to be in the endothelium, is critical for effective transmigration, although the mechanism has remained elusive. Herein we show that endothelial LSP1 is expressed in the nucleus and cytosol of resting endothelial cells and associates with the cytoskeleton upon endothelial activation. Two-photon microscopy revealed that endothelial LSP1 was crucial for the formation of endothelial domes in vivo in response to neutrophil chemokine keratinocyte-derived chemokine (KC) as well as in response to endogenously produced chemokines stimulated by cytokines (tumor necrosis factor α [TNFα] or interleukin-1β [IL-1β]). Endothelial domes were significantly reduced in Lsp1−/− compared with wild-type (WT) mice. Lsp1−/− animals not only showed impaired neutrophil emigration after KC and TNFα stimulation, but also had disproportionate increases in vascular permeability. We demonstrate that endothelial LSP1 is recruited to the cytoskeleton in inflammation and plays an important role in forming endothelial domes thereby regulating neutrophil transendothelial migration. The permeability data may underscore the physiologic relevance of domes and the role for LSP1 in endothelial barrier integrity.
Vaccination with dendritic cell/tumor fusion cells results in cellular and humoral antitumor immune responses in patients with multiple myeloma
Authors: Rosenblatt Jacalyn , Vasir Baldev , Uhl Lynne , Blotta Simona , MacNamara Claire , Somaiya Poorvi , Wu Zekui , Joyce Robin , Levine James D. , Dombagoda Dilani , Yuan Yan Emily , Francoeur Karen , Fitzgerald Donna , Richardson Paul , Weller Edie , Anderson Kenneth , Kufe Donald , Munshi Nikhil , Avigan David 
Published: October 2010

AbstractWe have developed a tumor vaccine in which patient-derived myeloma cells are chemically fused with autologous dendritic cells (DCs) such that a broad spectrum of myeloma-associated antigens are presented in the context of DC-mediated costimulation. We have completed a phase 1 study in which patients with multiple myeloma underwent serial vaccination with the DC/multiple myeloma fusions in conjunction with granulocyte-macrophage colony-stimulating factor. DCs were generated from adherent mononuclear cells cultured with granulocyte-macrophage colony-stimulating factor, interleukin-4, and tumor necrosis factor-α and fused with myeloma cells obtained from marrow aspirates. Vaccine generation was successful in 17 of 18 patients. Successive cohorts were treated with 1 × 106, 2 × 106, and 4 × 106 fusion cells, respectively, with 10 patients treated at the highest dose level. Vaccination was well tolerated, without evidence of dose-limiting toxicity. Vaccination resulted in the expansion of circulating CD4 and CD8 lymphocytes reactive with autologous myeloma cells in 11 of 15 evaluable patients. Humoral responses were documented by SEREX (Serologic Analysis of Recombinant cDNA Expression Libraries) analysis. A majority of patients with advanced disease demonstrated disease stabilization, with 3 patients showing ongoing stable disease at 12, 25, and 41 months, respectively. Vaccination with DC/multiple myeloma fusions was feasible and well tolerated and resulted in antitumor immune responses and disease stabilization in a majority of patients.
Ewing sarcoma gene Ews regulates hematopoietic stem cell senescence
Authors: Cho Joonseok , Shen Hongmei , Yu Hui , Li Hongjie , Cheng Tao , Lee Sean Bong , Lee Byeong Chel 
Published: October 2010

AbstractThe longevity of organisms is maintained by stem cells. If an organism loses the ability to maintain a balance between quiescence and differentiation in the stem/progenitor cell compartment due to aging and/or stress, this may result in death or age-associated diseases, including cancer. Ewing sarcoma is the most lethal bone tumor in young patients and arises from primitive stem cells. Here, we demonstrated that endogenous Ewing sarcoma gene (Ews) is indispensable for stem cell quiescence, and that the ablation of Ews promotes the early onset of senescence in hematopoietic stem progenitor cells. The phenotypic and functional changes in Ews-deficient stem cells were accompanied by an increase in senescence-associated β-galactosidase staining and a marked induction of p16INK4a compared with wild-type counterparts. With its relevance to cancer and possibly aging, EWS is likely to play a significant role in maintaining the functional capacity of stem cells and may provide further insight into the complexity of Ewing sarcoma in the context of stem cells.
Active Rac1 improves pathologic VEGF neovessel architecture and reduces vascular leak: mechanistic similarities with angiopoietin-1
Authors: Hoang Mien V. , Nagy Janice A. , Senger Donald R. 
Published: October 2010

AbstractArchitecturally defective, leaky blood vessels typify pathologic angiogenesis induced by vascular endothelial growth factor-A (VEGF-A). Such neovascular defects aggravate disease pathology and seriously compromise the therapeutic utility of VEGF. Endothelial cell (EC) transduction with active L61Rac1 strongly improved VEGF-driven angiogenesis in vivo as measured by increased neovascular density, enhanced lumen formation, and reduced vessel leakiness. Conversely, transduction with dominant-negative N17Rac1 strongly inhibited neovascularization. In vitro, active L61Rac1 promoted organization of cortical actin filaments and vascular cords and improved EC-EC junctions, indicating that improved cytoskeletal dynamics are important to the mechanism by which active L61Rac1 rectifies VEGF-driven angiogenesis. SEW2871, a sphingosine 1-phosphate receptor-1 agonist that activates Rac1 in ECs, improved cord formation and EC-EC junctions in vitro similarly to active L61Rac. Moreover, SEW2871 administration in vivo markedly improved VEGF neovessel architecture and reduced neovascular leak. Angiopoietin-1, a cytokine that “normalizes” VEGF neovessels in vivo, activated Rac1 and improved cord formation and EC-EC junctions in vitro comparably to active L61Rac1, and a specific Rac1 inhibitor blocked these effects. These studies distinguish augmentation of Rac1 activity as a means to rectify the pathologic angioarchitecture and dysfunctionality of VEGF neovessels, and they identify a rational pharmacologic strategy for improving VEGF angiogenesis.