bluuebunny/crossref_metadata_2025_split huggingface dataset:
CRUELTY AND ITS VICISSITUDES: JACQUES DERRIDA AND THE FUTURE OF PSYCHOANALYSIS
Authors: ROTTENBERG ELIZABETH 
Published: August 2012

abstractThis paper discusses Jacques Derrida's Death Penalty Seminars (two consecutive seminars he gave at the École des hautes études en sciences sociales in 1999–2000 and 2000–2001), as well as his 2000 Paris address to the States General of Psychoanalysis entitled “Psychoanalysis Searches the States of Its Soul.” The paper is magnetized by two questions: what does it mean to say, as Derrida says in his provocative statement at the end of his 1999 seminar, “even when the death penalty will have been abolished . . . it will survive, there will still be some death penalty [même quand la peine de mort sera abolie . . . elle survivra, il y en aura encore]”? And why is psychoanalysis in a privileged position to address “this irreducible thing in the life of the animate being” that is the possibility of cruelty?
THE PHILOSOPHY AND LITERATURE OF THE DEATH PENALTY: TWO SIDES OF THE SAME SOVEREIGN
Authors: NAAS MICHAEL 
Published: August 2012

abstractThis essay demonstrates that in his 1999–2000 Death Penalty Seminar Jacques Derrida pursues the deconstruction of political theology that he had been pursuing in a more or less explicit fashion for more than two decades. Derrida's interest in the theme of the death penalty can be traced back in large part, it is argued, to the theological and essentially Judeo‐Christian origins that Derrida finds in discourses both for and against the death penalty. This emphasis on the theological origins of the death penalty helps explain why Derrida spends much more time questioning the principles, rhetoric, and images of abolitionist discourses than pro–death penalty discourses. For Derrida, this essay concludes, a critique or deconstruction of discourses surrounding the death penalty is never more critical than in a putatively postreligious, secular age. In the end, Derrida hopes to provide what may be the very first philosophical abolitionist discourse, one that argues against the death penalty without relying on the language, tropes, symbols, and images of Judeo‐Christian theology.
DERRIDA ON THE DEATH PENALTY
Authors: FRITSCH MATTHIAS 
Published: August 2012

abstractResponding to Derrida's Death Penalty Seminar of 1999–2000 and its interpretation by Michael Naas, in this paper I argue that Derrida's deconstruction of the theologico‐political concept of the sovereign right over life and death in view of abolishing capital punishment should be understood in terms of the unconditional renunciation of sovereignty that dominates Derrida's later political writings, Rogues (2005) in particular. My reading takes seriously what I call the functional need for a “theological” moment in sovereignty beyond a merely historicist or genealogical interpretation of the European monotheistic heritage. Further, I ask how Derrida can follow through on his goal of developing the allegedly first principled philosophical stance against capital punishment. To this end, I assemble some ingredients of this complex but “unconditional” abolitionism, one that doubts our comprehension of and active relation to death to the point of questioning the commonsense distinctions among murder, suicide, and legal putting to death. I conclude that, for Derrida, letting another die of hunger or AIDS may be understood as a form of a death sentence, so that a deconstructive abolitionism leaves no room for the development of a good conscience.
Hic‐5 affects proliferation, migration and invasion of B16 murine melanoma cells
Authors: Noguchi Fumihito , Inui Shigeki , Nakajima Takeshi , Itami Satoshi 
Published: August 2012

SummaryHic‐5 is a shuttling protein between the cell membrane and the nucleus which functions as a focal adhesion adaptor protein and a nuclear receptor coactivator. Although several studies have shown its involvement in other types of cancer, the role of Hic‐5 in melanoma is unknown. Herein, we show for the first time that Hic‐5 is expressed in B16‐F1 murine melanoma cells. To determine its function in melanoma cells, we used shRNA‐mediated RNA interference and established stable clones with down‐regulated Hic‐5 expression. These clones had impaired growth and metastatic potential compared with controls in vivo, which correlated with decreased proliferation, migration and invasion in vitro. Moreover, silencing of Hic‐5 expression in B16‐F1 activated RhoA with an amoeboid phenotypic change, indicating that Hic‐5 is a key regulator of B16‐F1 metastasis in the context of Rho‐dependent motility. These results provide new evidence that Hic‐5 is a possible molecular target for treatment of melanoma.
Validating plastic scintillation detectors for photon dosimetry in the radiologic energy range
Authors: Lessard François , Archambault Louis , Plamondon Mathieu , Després Philippe , Therriault‐Proulx François , Beddar Sam , Beaulieu Luc 
Published: August 2012

Purpose:Photon dosimetry in the kilovolt (kV) energy range represents a major challenge for diagnostic and interventional radiology and superficial therapy. Plastic scintillation detectors (PSDs) are potentially good candidates for this task. This study proposes a simple way to obtain accurate correction factors to compensate for the response of PSDs to photon energies between 80 and 150 kVp. The performance of PSDs is also investigated to determine their potential usefulness in the diagnostic energy range.Methods:A 1‐mm‐diameter, 10‐mm‐long PSD was irradiated by a Therapax SXT 150 unit using five different beam qualities made of tube potentials ranging from 80 to 150 kVp and filtration thickness ranging from 0.8 to 0.2 mmAl + 1.0 mmCu. The light emitted by the detector was collected using an 8‐m‐long optical fiber and a polychromatic photodiode, which converted the scintillation photons to an electrical current. The PSD response was compared with the reference free air dose rate measured with a calibrated Farmer NE2571 ionization chamber. PSD measurements were corrected using spectra‐weighted corrections, accounting for mass energy‐absorption coefficient differences between the sensitive volumes of the ionization chamber and the PSD, as suggested by large cavity theory (LCT). Beam spectra were obtained from x‐ray simulation software and validated experimentally using a CdTe spectrometer. Correction factors were also obtained using Monte Carlo (MC) simulations. Percent depth dose (PDD) measurements were compensated for beam hardening using the LCT correction method. These PDD measurements were compared with uncorrected PSD data, PDD measurements obtained using Gafchromic films, Monte Carlo simulations, and previous data.Results:For each beam quality used, the authors observed an increase of the energy response with effective energy when no correction was applied to the PSD response. Using the LCT correction, the PSD response was almost energy independent, with a residual 2.1% coefficient of variation (COV) over the 80–150‐kVp energy range. Monte Carlo corrections reduced the COV to 1.4% over this energy range. All PDD measurements were in good agreement with one another except for the uncorrected PSD data, in which an over‐response was observed with depth (13% at 10 cm with a 100 kVp beam), showing that beam hardening had a non‐negligible effect on the PSD response. A correction based on LCT compensated very well for this effect, reducing the over‐response to 3%.Conclusion:In the diagnostic energy range, PSDs show high‐energy dependence, which can be corrected using spectra‐weighted mass energy‐absorption coefficients, showing no considerable sign of quenching between these energies. Correction factors obtained by Monte Carlo simulations confirm that the approximations made by LCT corrections are valid. Thus, PSDs could be useful for real‐time dosimetry in radiology applications.
Satisfaction with the humanitarian response to the 2010 Pakistan floods: a call for increased accountability to beneficiaries
Authors: Kirsch Thomas , Siddiqui Muhammad Ahmed , Perrin Paul Clayton , Robinson W Courtland , Sauer Lauren M , Doocy Shannon 
Published: August 2012

ObjectiveAscertain recipients' level of satisfaction with humanitarian response efforts.DesignA multi-stage, 80×20 cluster sample randomized survey (1800 households) with probability proportional to size of households affected by the 2010 Indus river floods in Pakistan. The floods affected over 18 million households and led to more than 8 billion USD in response dollars.ResultsLess than 20% of respondents reported being satisfied with response, though a small increase in satisfaction levels was observed over the three time periods of interest. Within the first month, receipt of hygiene items, food and household items was most strongly predictive of overall satisfaction. At 6 months, positive receipt of medicines was also highly predictive of satisfaction. The proportion of households reporting unmet needs remained elevated throughout the 6-month period following the floods and varied from 50% to 80%. Needs were best met between 1 and 3 months postflood, when response was at its peak. Unmet needs were the greatest at 6 months, when response was being phased down.ConclusionsAccess-limiting issues were rarely captured during routine monitoring and evaluation efforts and seem to be a significant predictor in dissatisfaction with relief efforts, at least in the case of Pakistan, another argument in favor of independent, population-based surveys of this kind. There is also need to better identify and serve those not residing in camps. Direct surveys of the affected population can be used operationally to assess ongoing needs, more appropriately redirect humanitarian resources, and ultimately, judge the overall quality of a humanitarian response.
Association between pre-eclampsia and locally derived traffic-related air pollution: a retrospective cohort study
Authors: Pereira Gavin , Haggar Fatima , Shand Antonia W , Bower Carol , Cook Angus , Nassar Natasha 
Published: August 2012

BackgroundPre-eclampsia is a common complication of pregnancy and is a major cause of fetal–maternal mortality and morbidity. Despite a number of plausible mechanisms by which air pollutants might contribute to this process, few studies have investigated the association between pre-eclampsia and traffic emissions, a major contributor to air pollution in urban areas.ObjectiveThe authors investigated the association between traffic-related air pollution and risk of pre-eclampsia in a maternal population in the urban centre of Perth, Western Australia.MethodThe authors estimated maternal residential exposure to a marker for traffic-related air pollution (nitrogen dioxide, NO2) during pregnancy for 23 452 births using temporally adjusted land-use regression. Logistic regression was used to investigate associations with pre-eclampsia.ResultsEach IQR increase in levels of traffic-related air pollution in whole pregnancy and third trimester was associated with a 12% (1%–25%) and 30% (7%–58%) increased risk of pre-eclampsia, respectively. The largest effect sizes were observed for women aged younger than 20 years or 40 years or older, aboriginal women and women with pre-existing and gestational diabetes, for whom an IQR increase in traffic-related air pollution in whole pregnancy was associated with a 34% (5%–72%), 35% (0%–82%) and 53% (7%–219%) increase in risk of pre-eclampsia, respectively.ConclusionsElevated exposure to traffic-related air pollution in pregnancy was associated with increased risk of pre-eclampsia. Effect sizes were highest for elevated exposures in third trimester and among younger and older women, aboriginal women and women with diabetes.
From oceanic crust to exhumed mantle: a 40 year (1970–2010) perspective on the nature of crust under the Santos Basin, SE Brazil
Authors: Kumar Naresh , Danforth A. , Nuttall P. , Helwig J. , Bird D. E. , Venkatraman S. 
Published: August 2012

Abstract
The first comprehensive geological and geophysical surveys of the Brazilian continental margin during the 1970s recognized the crust in the SE Brazilian basins as ‘anomalous’ but models for the opening of the South Atlantic proposed at that time invoked a very narrow continent–ocean transition. Nevertheless, such studies established the presence of a thick sedimentary prism, including an extensive salt layer under the São Paulo Plateau. The earliest reconstructions for the South Atlantic invoked a seaward shift of the spreading axis to account for the asymmetric widths of the salt layer between the Brazilian margin and its conjugate in offshore Africa.

Although our understanding of continent–ocean transition has progressed since then, direct seismic imaging at crustal scale has only been possible recently through long offset (10 km), deep recording (18 s), pre-stack depth migrated (PSDM) to 40 km, seismic-reflection data. These data allow us to generally image the Moho from under thick continental crust (>30 km) to thin oceanic crust (
c.
5 km). Although the nature of the transitional crust is still contested, these seismic data allow for constraints on various models for continent–ocean transition. Future integrated studies utilizing PSDM and refraction-seismic data will further refine these models.
Discordant Cellular Response to Presurgical Letrozole in Bilateral Synchronous ER+ Breast Cancers with aKRASMutation orFGFR1Gene Amplification
Authors: Balko Justin M. , Mayer Ingrid A. , Sanders Melinda E. , Miller Todd W. , Kuba Maria G. , Meszoely Ingrid M. , Wagle Nikhil , Garraway Levi A. , Arteaga Carlos L. 
Published: August 2012

AbstractWe describe herein a patient presenting with bilateral estrogen-receptor–positive (ER+) breast tumors who was enrolled in a clinical trial exploring molecular aberrations associated with hormone-refractory tumor cell proliferation. Short-term (two week) hormonal therapy with the aromatase inhibitor letrozole substantially reduced proliferation as measured by Ki67 immunohistochemistry in one tumor, whereas the second was essentially unchanged. Extensive molecular and genetic work-up of the two tumors yielded divergent lesions in the two tumors: an activating KRAS mutation in the responsive tumor and an amplification of the fibroblast growth factor receptor-1 (FGFR1) locus in the treatment-refractory tumor. These findings provide an insight to possible mechanisms of resistance to antiestrogen therapy in ER+ breast cancers. First, they illustrate the necessity of clinically approved assays to identify FGFR1 gene amplification, which occur in approximately 5% of breast tumors and have been linked to antiestrogen resistance. It is quite possible that the addition of FGFR inhibitors to ER-targeted therapy will yield a superior antitumor effect and improved patient outcome. Second, they suggest that the role of activating mutations in RAS, although rare in breast cancer, may need to be explored in the context of ER+ breast tumors. Mol Cancer Ther; 11(10); 2301–5. ©2012 AACR.
Turn Off the IDO: Will Clinical Trials Be Successful?
Authors: Novitskiy Sergey V. , Moses Harold L. 
Published: August 2012

Abstract
Summary: Indoleamine 2,3-dioxygenase (IDO) is overexpressed in many human cancers and is believed to play a role in tumor immune evasion, but a requirement for IDO in tumor progression has not been formally shown. The study by Smith and colleagues in this issue of Cancer Discovery provides genetic evidence for the importance of IDO in tumorigenesis, which supports the use of IDO inhibitors in clinical trials in humans. Cancer Discov; 2(8); 673–5. ©2012 AACR.
Commentary on Smith et al., p. 722.
Visualization of Vascular Inflammation in the Atherosclerotic Mouse by Ultrasmall Superparamagnetic Iron Oxide Vascular Cell Adhesion Molecule-1–Specific Nanoparticles
Authors: Michalska Marta , Machtoub Lina , Manthey Helga D. , Bauer Elisabeth , Herold Volker , Krohne Georg , Lykowsky Gunthard , Hildenbrand Markus , Kampf Thomas , Jakob Peter , Zernecke Alma , Bauer Wolfgang R. 
Published: August 2012

Objective—
Noninvasive imaging of atherosclerosis remains challenging in clinical applications. Here, we applied noninvasive molecular imaging to detect vascular cell adhesion molecule-1 in early and advanced atherosclerotic lesions of apolipoprotein E–deficient mice.

Methods and Results—
Ultrasmall superparamagnetic iron oxide particles functionalized with (P03011) or without (P3007) vascular cell adhesion molecule-1−binding peptide were visualized by ultra high-field (17.6 T) magnetic resonance. Injection of P03011 resulted in a marked signal loss in the aortic root of apolipoprotein E–deficient mice fed a Western diet for 8 and 26 weeks in vivo and ex vivo, compared with preinjection measurements, P3007-injected mice, and P03011- or P3007-injected age-matched C57BL/6 controls. Histological analyses revealed iron accumulations in the intima, in colocalization with vascular cell adhesion molecule-1−expressing macrophages and endothelial cells. Coherent anti-Stokes Raman scattering microscopy demonstrated iron signals in the intima and media of the aortic root in the P03011-injected but not untreated apolipoprotein E–deficient mice, localized to macrophages, luminal endothelial-like cells, and medial regions containing smooth muscle cells. Electron microscopy confirmed iron particles enclosed in endothelial cells and in the vicinity of smooth muscle cells.

Conclusion—
Using a combination of innovative imaging modalities, in this study, we demonstrate the feasibility of applying P03011 as a contrast agent for imaging of atherosclerosis.
Adverse Alterations in Mitochondrial Function Contribute to Type 2 Diabetes Mellitus–Related Endothelial Dysfunction in Humans
Authors: Kizhakekuttu Tinoy J. , Wang Jingli , Dharmashankar Kodlipet , Ying Rong , Gutterman David D. , Vita Joseph A. , Widlansky Michael E. 
Published: August 2012

Objective—
Mitochondrial dysfunction plays a key pathophysiological role in type 2 diabetes mellitus (T2DM). Data delineating relationships between mitochondrial and endothelial dysfunction in humans with T2DM are lacking.

Methods and Results—

In 122 human subjects (60 with T2DM, 62 without T2DM), we measured endothelial function by brachial artery ultrasound (flow mediated dilation) and digital pulse amplitude tonometery. Endothelial function in arterioles isolated from gluteal subcutaneous adipose was measured by videomicroscopy. In arterioles and mononuclear cells, we measured inner mitochondrial membrane potential (Δψ
m
), mitochondrial mass, and mitochondrial superoxide production using fluorophores. Endothelial function was impaired in T2DM subjects versus control subjects. Δψ
m
magnitude was larger and mitochondrial mass was lower in arterioles and mononuclear cells in T2DM. Mononuclear mitochondrial mass correlated with flow-mediated dilation and pulse amplitude tonometery (
ρ
=0.38 and 0.33,
P
=0.001 and 0.02, respectively), and mononuclear mitochondrial superoxide production inversely correlated with flow-mediated dilation (
ρ
=−0.58,
P
=0.03). Low doses of 2 different mitochondrial uncoupling agents (carbonyl cyanide m-chlorophenyl hydrazone and 2,4-dinitrophenol) that reduce Δψ
m
magnitude and a mitochondrial-targeted antioxidant (MitoTEMPOL) improved endothelial function and reduced mitochondrial superoxide levels in T2DM arterioles.

Conclusion—
Mitochondrial dysfunction may play a central role in the impairment of endothelial dysfunction in T2DM.
Role of Thromboxane Receptor in C-Reactive Protein–Induced Thrombosis
Authors: Grad Etty , Pachino Rachel M. , FitzGerald Garret A. , Danenberg Haim D. 
Published: August 2012

Objective—

Thromboxane A
2
and prostacyclin are thromboregulatory prostaglandins. The inflammatory C-reactive protein (CRP) promotes thrombosis after vascular injury, presumably via potentiation of thromboxane activity. Using a genetic approach, we investigated the role of thromboxane receptor (TP) pathway in CRP-induced thrombosis.

Methods and Results—

Four genetically engineered mice strains were used:
C57BL
/
6
wild-type, human CRP transgenic (
CRPtg
), thromboxane receptor–deficient (
Tp
−/−
), and CRPtgTp
−/−
mice. CRP and TP expression were correlated, and suppression of CRP expression using small interfering RNA/CRP led to reduction in TP expression. Platelet–endothelial adherence was increased in CRPtg and suppressed in CRPtgTP
−/−
and CRPtg cells that were suppressed with TP small interfering RNA. TP deficiency in both platelets and endothelial cells was synergistic in affecting platelet–endothelial interactions. Time until arterial occlusion, measured after photochemical injury, was significantly shorter in CRPtg and prolonged in CRPtgTp
−/−
compared with controls (n=10–15, 35±3.4, 136±13.8, and 67±8.9 minutes, respectively;
P
<0.05).

Conclusion—
TP pathway is of major importance in CRP-induced thrombosis. The expression of TP is increased in CRPtg endothelial cells, and its blockade significantly suppresses the prothrombotic effect of CRP.
Aneurysms Increase the Risk of Rebleeding After Stereotactic Radiosurgery for Hemorrhagic Arteriovenous Malformations
Authors: Kano Hideyuki , Kondziolka Douglas , Flickinger John C. , Yang Huai-che , Park Kyung-Jae , Flannery Thomas J. , Liu Xiaomin , Niranjan Ajay , Lunsford L. Dade 
Published: August 2012

Background and Purpose—
The purpose of this study was to define the risk of rebleeding after stereotactic radiosurgery (SRS) for hemorrhagic arteriovenous malformations with or without associated intracranial aneurysms.

Methods—
Between 1987 and 2006, we performed Gamma Knife SRS on 996 patients with brain arteriovenous malformations; 407 patients had sustained an arteriovenous malformation hemorrhage. Sixty-four patients (16%) underwent prior embolization and 84 (21%) underwent prior surgical resection. The median target volume was 2.3 mL (range, 0.1–20.7 mL). The median margin dose was 20 Gy (range, 13.5–27 Gy).

Results—

The overall rate of total obliteration defined by angiography or MRI was 56%, 77%, 80%, and 82% at 3, 4, 5, and 10 years, respectively. Before obliteration, 33 patients (8%) sustained an additional hemorrhage after SRS. The overall annual hemorrhage rate until obliteration after SRS was 1.3%. The presence of a patent aneurysm was significantly associated with an increased rehemorrhage risk after SRS (annual hemorrhage rate, 6.4%) compared with patients with a clipped or embolized aneurysm (annual hemorrhage rate, 0.8%;
P
=0.033).

Conclusions—
When an aneurysm is identified in patients with arteriovenous malformations selected for SRS, additional endovascular or surgical strategies should be considered to reduce the risk of bleeding during the latency interval.