bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Hormonal Correlates of Implicit Motives
Authors: Schultheiss Oliver C. 
Published: January 2013

AbstractImplicit motives represent nonconsciously represented dispositions to seek specific classes of incentives and to avoid corresponding classes of disincentives. Growing evidence suggests that the implicit power motive is associated with basal levels and reactivity of the gonadal steroid hormones testosterone in men and estradiol in women. It is also associated with increased release of stress hormones (cortisol, norepinephrine) in response to dominance challenges and social defeat. The implicit affiliation motive is linked to the release of progesterone: increases in progesterone are followed by increases in affiliation motivation, and arousal of affiliation motivation is associated with concurrent or subsequent progesterone increases. There is limited evidence for a role of vasopressin in achievement motivation. These findings point to a key role of the hypothalamus for implicit motives, a role that is consistent with the existence of function‐specific nuclei within this brain area.
Investigation of three Fe–Ti oxide deposits associated with Grenvillian anorthosite massifs as potential source for lunar analogue ilmenite
Authors: Morisset Caroline-Emmanuelle , Williamson Marie-Claude , Hipkin Victoria 
Published: January 2013

Terrestrial ilmenite has been assessed for its suitability in the preparation of a simulant of lunar high-Ti mare regolith, which is needed to test oxygen production on the lunar surface during future missions. Petrographic observations using optical and electron microscopes revealed that ilmenite grains in the Mirepoix, Sanford Lake, and Degrosbois Fe–Ti oxide deposits from Grenvillian anorthosite massifs contain hercynite in their rims but that hematite exsolution is absent in three of eight studied samples. Electron microprobe analyses showed that the ilmenite grains vary in TiO2 from 38.82 to 52.34 wt.%; in FeO from 33.15 to 45.88 wt.%; in Fe2O3 (calculated from stoichiometry) from 2.18 to 27.03 wt.%; in MgO from 0.05 to 2.49 wt.%; and in MnO from 0.26 to 1.51 wt.% and are thus comparable in composition to lunar ilmenite. Ilmenite, free of hematite, in two samples was homogeneous in composition (e.g., sample SL1: 50.4–51.4 wt.% TiO2). Two sub-solidus reactions occurred amongst the oxide minerals in the studied deposits: (i) exsolution of hercynite in magnetite; and (ii) reaction between the hematite component in the ilmenite and the ulvöspinel component of the magnetite, forming new ilmenite, which includes the hercynite. The reaction between the hematite component in the ilmenite and the ulvöspinel component of the magnetite, when conditions are favorable for diffusion, produces ilmenite grains that are homogenous in composition and free of hematite exsolution. Ilmenite with little or no Fe3+ may occur in massive, fine-grained, and metamorphosed Fe–Ti oxide deposits and provide a terrestrial analogue source of ilmenite useful for the production of lunar mare simulant.
A Genome-Scale RNA Interference Screen Implicates NF1 Loss in Resistance to RAF Inhibition
Authors: Whittaker Steven R. , Theurillat Jean-Philippe , Van Allen Eliezer , Wagle Nikhil , Hsiao Jessica , Cowley Glenn S. , Schadendorf Dirk , Root David E. , Garraway Levi A. 
Published: January 2013

Abstract
RAF inhibitors such as vemurafenib and dabrafenib block BRAF–mediated cell proliferation and achieve meaningful clinical benefit in the vast majority of patients with BRAFV600E-mutant melanoma. However, some patients do not respond to this regimen, and nearly all progress to therapeutic resistance. We used a pooled RNA interference screen targeting more than 16,500 genes to discover loss-of-function events that could drive resistance to RAF inhibition. The highest ranking gene was NF1, which encodes neurofibromin, a tumor suppressor that inhibits RAS activity. NF1 loss mediates resistance to RAF and mitogen-activated protein kinase (MAPK) kinase kinase (MEK) inhibitors through sustained MAPK pathway activation. However, cells lacking NF1 retained sensitivity to the irreversible RAF inhibitor AZ628 and an ERK inhibitor. NF1 mutations were observed in BRAF–mutant tumor cells that are intrinsically resistant to RAF inhibition and in melanoma tumors obtained from patients exhibiting resistance to vemurafenib, thus showing the clinical potential for NF1-driven resistance to RAF/MEK-targeted therapies.
Significance: This work identifies functional loss of NF1 as a mediator of resistance to RAF inhibitors in BRAFV600E-mutant cancers. Furthermore, we nominate new therapeutic modalities to treat this mechanism of resistance. Cancer Discov; 3(3); 350–62. ©2012 AACR.
See related commentary by Gibney and Smalley, p. 260
This article is highlighted in the In This Issue feature, p. 239
Peptide Inhibitor of CXCL4–CCL5 Heterodimer Formation, MKEY, Inhibits Experimental Aortic Aneurysm Initiation and Progression
Authors: Iida Yasunori , Xu Baohui , Xuan Haojun , Glover Keith J. , Tanaka Hiroki , Hu Xiaolei , Fujimura Naoki , Wang Wei , Schultz Joshua R. , Turner Court R. , Dalman Ronald L. 
Published: January 2013

Objective—
Macrophages are critical contributors to abdominal aortic aneurysm (AAA) disease. We examined the ability of MKEY, a peptide inhibitor of CXCL4–CCL5 interaction, to influence AAA progression in murine models.

Approach and Results—
AAAs were created in 10-week-old male C57BL/6J mice by transient infrarenal aortic porcine pancreatic elastase infusion. Mice were treated with MKEY via intravenous injection either (1) before porcine pancreatic elastase infusion or (2) after aneurysm initiation. Immunostaining demonstrated CCL5 and CCR5 expression on aneurysmal aortae and mural monocytes/macrophages, respectively. MKEY treatment partially inhibited migration of adaptively transferred leukocytes into aneurysmal aortae in recipient mice. Although all vehicle-pretreated mice developed AAAs, aneurysms formed in only 60% (3/5) and 14% (1/7) of mice pretreated with MKEY at 10 and 20 mg/kg, respectively. MKEY pretreatment reduced aortic diameter enlargement, preserved medial elastin fibers and smooth muscle cells, and attenuated mural macrophage infiltration, angiogenesis, and aortic metalloproteinase 2 and 9 expression after porcine pancreatic elastase infusion. MKEY initiated after porcine pancreatic elastase infusion also stabilized or reduced enlargement of existing AAAs. Finally, MKEY treatment was effective in limiting AAA formation after angiotensin II infusion in apolipoprotein E–deficient mice.

Conclusion—
MKEY suppresses AAA formation and progression in 2 complementary experimental models. Peptide inhibition of CXCL4–CCL5 interactions may represent a viable translational strategy to limit progression of human AAA disease.
Subsequent Development of Fibroatheromas With Inflamed Fibrous Caps Can Be Predicted by Intracoronary Near Infrared Spectroscopy
Authors: Patel Dhavalkumar , Hamamdzic Damir , Llano Raul , Patel Daivesh , Cheng Lan , Fenning Robert S. , Bannan Khalid , Wilensky Robert L. 
Published: January 2013

Objective—
To prospectively evaluate whether the development of fibroatheromas exhibiting features of potential instability can be detected and predicted by serial invasive imaging.

Methods and Results—

Multivessel intravascular ultrasound and near infrared spectroscopy (NIRS) were performed in diabetic/hypercholesterolemic pigs 3, 6, and 9 months after induction. Animals were euthanized at 9 months and histological/immunohistochemical evaluation of the arteries was performed (n=304 arterial segments). Intravascular ultrasound demonstrated, over time, a progressive increase in plaque + media and necrotic core areas and positive vascular remodeling. By histology, NIRS+ lesions were significantly more likely to be a high-risk fibroatheroma (
P
=0.0001) containing larger plaque (
P
<0.0001) and necrotic core areas (
P
<0.0019) and thinner fibrous caps (
P
=0.04). NIRS + fibroatheromas possessed a greater concentration of inflammatory cells demonstrating protease activity (
P
=0.006), and proliferating (
P
=0.016), and apoptotic cells (
P
=0.04) within the fibrous cap. Eighty-eight percent of NIRS+ lesions at 3 and 6 months subsequently developed into a fibroatheroma at 9 months (
P
<0.01). By multivariate analysis NIRS positivity at 6 months predicted the subsequent presence of a fibroatheroma at 9 months (
P
=0.005; odds ratio, 2.71).

Conclusion—
The future development of inflamed fibroatheromas with thinner fibrous caps, greater plaque, and necrotic core areas, and posessing characteristics of increased plaque instability were detected by intravascular ultrasound/NIRS imaging.
Adrenergic Receptor Polymorphisms and Prevention of Ventricular Arrhythmias With Bucindolol in Patients With Chronic Heart Failure
Authors: Aleong Ryan G. , Sauer William H. , Robertson Alastair D. , Liggett Stephen B. , Bristow Michael R. 
Published: December 2012

Background—
β-blockers prevent cardiac arrhythmias in patients with chronic heart failure and reduced left ventricular ejection fraction, including ventricular tachycardia/ventricular fibrillation (VT/VF). We hypothesized that prevention of ventricular arrhythmias by the β-blocker/sympatholytic agent bucindolol is influenced by genetic variation in adrenergic receptors.

Methods and Results—

From a substudy of the β-Blocker Evaluation of Survival Trial (n=1040), we identified those with the high functioning 389Arg versus the lower function 389Gly β
1
adrenergic receptor variant, and the loss of function α
2c
322-325 adrenergic receptor deletion versus the 322 to 325 wild-type (Wt)/deletion variant. VT/VF was recorded on case report forms as an adverse event. There were 493 Arg 389 β
1
receptor homozygotes (β
1
389 Arg/Arg) versus 547 Gly389 carriers and 207 α
2c
322-325 deletion carriers versus 833 homozygous Wts (α
2c
322-325 Wt/Wt). In all genotypes bucindolol was associated with a lower incidence of VT/VF (subhazard ratio, 0.42 [0.27–0.64];
P
=0.00006). Bucindolol reduced VT/VF in β
1
389 Arg homozygotes (subhazard ratio, 0.26 [0.14–0.50];
P
=0.00005) but not in β
1
389 Gly carriers (subhazard ratio, 0.60 [0.34–1.07];
P
=0.09). For genotype combinations, the α
2c
322-325 polymorphism altered the VT/VF bucindolol response in β1389 Gly carriers, with α
2c
deletion genotypes associated with complete efficacy loss. A test of interaction was statistically significant (
P
=0.028) for the treatment group and a β
1
389/α
2c
322-325 three genotype construct, effectively identifying patients who exhibited enhanced response, no substantial response modification and loss of response.

Conclusions—

Bucindolol prevents VT/VF in subjects with heart failure and reduced left ventricular ejection fractions, and this effect is modulated by β
1
389 Arg/Gly and α
2c
322-325 Wt/deletion adrenergic receptor polymorphisms.
Novel Insights Into the Critical Role of Bradykinin and the Kinin B2 Receptor for Vascular Recruitment of Circulating Endothelial Repair–Promoting Mononuclear Cell Subsets
Authors: Kränkel Nicolle , Kuschnerus Kira , Müller Maja , Speer Timo , Mocharla Pavani , Madeddu Paolo , Bader Michael , Lüscher Thomas F. , Landmesser Ulf 
Published: December 2012

Background—

Endothelial injury is considered critical for progression of atherosclerosis and its complications in coronary artery disease (CAD). The endothelial-supportive effects of bradykinin have mainly been attributed to activation of the resident endothelium. Here we newly investigate the role of bradykinin and its B2 receptor for the recruitment and functional activation of circulating mononuclear cell subsets with endothelial-repair promoting capacity, such as CD34
+
CXCR4
+
cells, at sites of arterial injury.

Methods and Results—

Bradykinin-B2-receptor (B2R) blockade by icatibant substantially impaired recruitment of circulating CD34
+
CXCR4
+
mononuclear cells (expressing high levels of B2R) to endothelial cells in vitro and to injured arterial wall in vivo, whereas recruitment of CD14
hi
monocytes (expressing low levels of B2R) was unchanged. Moreover, the capacity of genetically
B2R
-deficient bone marrow cells to promote endothelial repair in vivo was markedly impaired as compared with wild-type bone marrow cells. B2R expression was reduced on CD34
+
CXCR4
+
mononuclear cells and endothelial repair–promoting early outgrowth cells, but not on CD14
hi
monocytes, from CAD patients as compared with healthy subjects. B2R stimulation induced CD18 activation in early outgrowth cells of healthy subjects, but not in early outgrowth cells of CAD patients. Adenoviral B2R overexpression enhanced in vivo vascular recruitment and rescued impaired endothelial repair capacity of early outgrowth cells from CAD patients.

Conclusions—
We newly report that bradykinin/B2R signaling may promote endothelial repair after arterial injury by selective recruitment and functional activation of B2R-expressing circulating mononuclear cell subsets. In CAD patients, B2R downregulation on endothelial repair–promoting circulating mononuclear cells substantially impairs the bradykinin-dependent endothelial repair, representing a novel mechanism promoting endothelial injury in CAD patients.
Statin Therapy and Outcome After Ischemic Stroke
Authors: Ní Chróinín Danielle , Asplund Kjell , Åsberg Signild , Callaly Elizabeth , Cuadrado-Godia Elisa , Díez-Tejedor Exuperio , Di Napoli Mario , Engelter Stefan T. , Furie Karen L. , Giannopoulos Sotirios , Gotto Antonio M. , Hannon Niamh , Jonsson Fredrik , Kapral Moira K. , Martí-Fàbregas Joan , Martínez-Sánchez Patricia , Milionis Haralampos J. , Montaner Joan , Muscari Antonio , Pikija Slaven , Probstfield Jeffrey , Rost Natalia S. , Thrift Amanda G. , Vemmos Konstantinos , Kelly Peter J. 
Published: January 2013

Background and Purpose—
Although experimental data suggest that statin therapy may improve neurological outcome after acute cerebral ischemia, the results from clinical studies are conflicting. We performed a systematic review and meta-analysis investigating the relationship between statin therapy and outcome after ischemic stroke.

Methods—
The primary analysis investigated statin therapy at stroke onset (prestroke statin use) and good functional outcome (modified Rankin score 0 to 2) and death. Secondary analyses included the following: (1) acute poststroke statin therapy (≤72 hours after stroke), and (2) thrombolysis-treated patients.

Results—

The primary analysis included 113 148 subjects (27 studies). Among observational studies, statin treatment at stroke onset was associated with good functional outcome at 90 days (pooled odds ratio [OR], 1.41; 95% confidence interval [CI], 1.29–1.56;
P
<0.001), but not 1 year (OR, 1.12; 95% CI, 0.9–1.4;
P
=0.31), and with reduced fatality at 90 days (pooled OR, 0.71; 95% CI, 0.62–0.82;
P
<0.001) and 1 year (OR, 0.80; 95% CI, 0.67–0.95;
P
=0.01). In the single randomized controlled trial reporting 90-day functional outcome, statin treatment was associated with good outcome (OR, 1.5; 95% CI, 1.0–2.24;
P
=0.05). No reduction in fatality was observed on meta-analysis of data from 3 randomized controlled trials (
P
=0.9). In studies restricted to of thrombolysis-treated patients, an association between statins and increased fatality at 90 days was observed (pooled OR, 1.25; 95% CI, 1.02–1.52;
P
=0.03, 3 studies, 4339 patients). However, this association was no longer present after adjusting for age and stroke severity in the largest study (adjusted OR, 1.14; 95% CI, 0.90–1.44; 4012 patients).

Conclusion—
In the largest meta-analysis to date, statin therapy at stroke onset was associated with improved outcome, a finding not observed in studies restricted to thrombolysis-treated patients. Randomized trials of statin therapy in acute ischemic stroke are needed.
One-Year Progression of Moderate Asymptomatic Carotid Stenosis Predicts the Risk of Vascular Events
Authors: Balestrini Simona , Lupidi Francesca , Balucani Clotilde , Altamura Claudia , Vernieri Fabrizio , Provinciali Leandro , Silvestrini Mauro 
Published: January 2013

Background and Purpose—
This study aimed at evaluating whether ultrasound monitoring of moderate asymptomatic carotid stenosis may help in identifying subjects at high risk for vascular events.

Methods—
We included 523 subjects with unilateral asymptomatic carotid stenosis of 50% to 69%. Follow-up carotid ultrasound was performed within 12 months from inclusion to detect the frequency and degree of stenosis progression. Subjects were prospectively evaluated for a median period of 42 months (interquartile range, 38–45) after a second ultrasound evaluation. Outcome measures were any stroke and transient ischemic attack, myocardial infarction, and death.

Results—

Carotid stenosis progression was associated with the occurrence of vascular events (hazard ratio, 21.57; 95% confidence interval, 11.81–39.39;
P
<0.001). During follow-up, 96.7% of subjects without progressive carotid stenosis remained free from vascular events. Among patients with progressive stenosis, 53.7% experienced a vascular event and 27.1% experienced an ipsilateral stroke.

Conclusions—
One-year moderate asymptomatic carotid stenosis progression is related to higher risk of vascular events, including ipsilateral stroke.
Vitamin K Antagonists–Associated Cerebral Hemorrhages
Authors: Dequatre-Ponchelle Nelly , Hénon Hilde , Pasquini Marta , Rutgers Matthieu P. , Bordet Régis , Leys Didier , Cordonnier Charlotte 
Published: January 2013

Background and Purpose—
The high prevalence of atrial fibrillation in aging populations leads to an increasing incidence of vitamin K antagonists-associated intracerebral hemorrhages (VKAs-ICH). It remains unclear whether VKAs are causes or risk factors for ICH. We aimed at identifying the specificities of VKAs-ICH.

Methods—
We compared baseline characteristics of 545 consecutive patients receiving or not receiving VKAs before admission for spontaneous ICH. To determine whether the influence of VKAs depends on the underlying vasculopathy, that is, cerebral amyloid angiopathy in lobar, and deep perforating arteries vasculopathy in deep ICH, we compared characteristics of ICH (including volume) according to the anatomic distribution of ICH in multiple linear regression.

Results—

VKAs-ICH accounted for 83 patients, that is, 15% (95% confidence intervals, 12–18) of ICH in our cohort. The use of VKAs did not influence anatomic distribution of ICH. The impact of VKAs on ICH volume differed according to ICH location: in nonlobar ICH, VKAs use was associated with significant larger ICH volumes (median volume 25 mL vs 12 mL;
P
=0.002). In lobar ICH, VKAs use did not influence the volume (median 26 mL vs 30 mL;
P
=0.507).

Conclusions—
A similar anatomic distribution of ICH in patients with or without VKAs suggests that VKAs should not be considered as a cause of ICH because both locations are usually due to different vasculopathies (deep perforating arteries vasculopathy in deep and cerebral amyloid angiopathy in lobar). The different impact of VKAs on ICH volumes according to location suggests a different susceptibility of these vasculopathies to VKAs. This finding may lead to specific therapeutic strategies.
Contributions of Individual Atmospheric Diabatic Heating Processes to the Generation of Available Potential Energy
Authors: Romanski Joy , Rossow William B. 
Published: January 2013

Abstract
The generation of zonal and eddy available potential energy (Gz and Ge) as formulated by Lorenz are computed on a global-, daily-, and synoptic-scale basis to consider the contribution of each diabatic heating component separately and in combination. Using global, mostly satellite-derived datasets for the diabatic heating components and the temperature enables us to obtain Gz and, especially, Ge from observations for the first time and at higher temporal and spatial resolution than previously possible. The role of clouds in maintaining G is investigated.
The global annual mean Gz is 1.52 W m−2. Values reach a minimum of 0.63 W m−2 in the Northern Hemisphere during spring and a maximum of 2.27 W m−2 in the Southern Hemisphere during winter. The largest contributors to Gz are latent heating in the tropical upper troposphere, associated with the intertropical convergence zone in the summer hemisphere and surface sensible heat fluxes in the winter pole. Diabatic cooling by radiative fluxes (mostly longwave) generally destroys Gz.
The value of Ge is negative and is about an order of magnitude smaller than Gz, with a global annual mean of −0.29 W m−2. However, the small value of Ge results from the cancellation of the contributions from the individual diabatic heating terms, which are actually roughly similar in magnitude to their Gz contributions.
The results presented herein suggest that the large-scale dynamics of the atmosphere organize the spatial and temporal distribution of clouds and precipitation in such a way as to increase the energy available to drive the circulation, a kind of positive feedback.
Pathogenesis of reproductive failure induced by Trypanosoma vivax in experimentally infected pregnant ewes
Authors: Silva Taciana MF , Olinda Roberio G , Rodrigues Carla MF , Câmara Antônio CL , Lopes Francisco C , Coelho Wesley AC , Ribeiro Múcio FB , Freitas Carlos IA , Teixeira Marta MG , Batista Jael S 
Published: January 2013

Abstract
The present study was aimed at investigating the effect of experimental infection by Trypanosoma vivax in different stages of pregnancy, determining the pathogenesis of reproductive failure, and confirming transplacental transmission. We used 12 pregnant ewes distributed into four experimental groups: G1, was formed by three ewes infected with T. vivax in the first third of pregnancy (30 days); G2 comprised three infected ewes in the final third of pregnancy (100 days); G3 and G4 were composed of three non-infected ewes with the same gestational period, respectively. Each ewe of G1 and G2 was inoculated with 1.25 × 105 tripomastigotes. Clinical examination, determination of parasitemia, serum biochemistry (albumin, total protein, glucose, cholesterol, and urea), packed cell volume (PCV), serum progesterone, and pathological examination were performed. Placenta, amniotic fluid, blood and tissues from the fetuses and stillbirths were submitted to PCR. Two ewes of G1 (Ewe 1 and 3) presented severe infection and died in the 34th and 35th days post-infection (dpi), respectively; but both fetuses were recovered during necropsy. In G2, Ewe 5 aborted two fetuses on the 130th day (30 dpi) of pregnancy; and Ewe 6 aborted one fetus in the 140th day (40 dpi) of gestation. Ewes 2 and 4 delivered two weak lambs that died five days after birth. Factors possibly involved with the reproductive failure included high parasitemia, fever, low PCV, body score, serum glucose, total protein, cholesterol, and progesterone. Hepatitis, pericarditis, and encephalitis were observed in the aborted fetuses. The presence of T. vivax DNA in the placenta, amniotic fluid, blood, and tissues from the fetuses confirms the transplacental transmission of the parasite. Histological lesion in the fetuses and placenta also suggest the involvement of the parasite in the etiopathogenesis of reproductive failure in ewes.