bluuebunny/crossref_metadata_2025_split huggingface dataset:
Homeless Parents’Perceptions of Parenting Stress
Authors: Gorzka Patricia A. 
Published: August 2007

PURPOSE. To describe homeless parents' perceptions of parenting stress as potential indicators of needs for support in parenting roles.SAMPLE. Forty‐seven homeless parents (30 mothers, 17 fathers).METHODS. Subjects completed the Parenting Stress Index to measure perceived parenting stress in the areas of child domain, parent domain, and life stress.FINDINGS. Homeless mothers and homeless fathers both identified the child domain as the most frequent source of stress. T tests showed a significant dierence between groups only in the parent domain sub‐ scale of competence.CONCLUSIONS. Findings from this study indicate the need to include parenting stress questions in an initial nursing or health assessment.
Childhood Memories About Food: The Successful Dieters Project
Authors: Brink Pamela J. , Ferguson Kristi , Sharma Anju 
Published: August 2007

PURPOSE. The Successful Dieters Project explored and described the characteristics of dieters. This paper reports the results of a content analysis of one question about childhood memories surrounding food.METHODS. All subjects were interviewed once with an intensive interview guide, were weighed, and were measured for height and waist‐hip ratios.SUBJECTS. Subjects (N = 162) were 76 men and 86 women, who ranged in age from 21 to 84 years.FINDINGS. Gender and weight histo y differences were noted in the areas of food rules, the age at which dieting to control weight began, family food rules, positive versus negative memories, and the use of food as a rmard or punishment. Parental experience with food deprivation was a strong force in shaping childrenS attitudes toward food.CONCLUSIONS. Childhood memories about food appear to contribute to diferences among the obese, the always‐normul‐weight, and the successful dieter. Further research into this area of investigation is uxtrrantd.
The Prevention of Eating Disorders: A Review of the Research on Risk Factors With Implications for Practice
Authors: White Jane H. 
Published: August 2007

TOPIC. Eating disorders are a significant health problem among children and adolescents. A synthesis of recent research findings on the risk factors for eating disorders describes prevention strategies for practice.PURPOSE. To present research findings on risk factors for eating disorders that specifically relate to prevention for advanced practice. Current investigations are reviewed and critiqued for biologic, psychological, family, and sociocultural risk factors. A critique of the research and findings from important studies describes strategies for prevention of eating disorders for aduanced practice.SOURCES. Published literature and clinical and research expertise of the author.CONCLUSIONS. Identifiable risk factors for eating disorders are found in children as well as adolescents. Findings from risk factor research provide the advanced practice nurse strategies for prevention of eating disorders. Few prevention programs exist; even fewer have been tested. An important clinical and research focus for advanced practice nurses is the prmention of eating disorders.
Trioxaquines and Heme-Artemisinin Adducts Inhibit the In Vitro Formation of Hemozoin Better than Chloroquine
Authors: Loup Christophe , Lelièvre Joël , Benoit-Vical Françoise , Meunier Bernard 
Published: August 2007

ABSTRACT
Trioxaquines, potential antimalarial agents, and heme-artemisinin adducts, resulting from the alkylation of heme by artemisinin, were evaluated as inhibitors of β-hematin formation in 10 M acetate medium at pH 5.
Fatty Acid Synthesis Is Essential for Survival of
Cryptococcus neoformans
and a Potential Fungicidal Target
Authors: Chayakulkeeree Methee , Rude Thomas H. , Toffaletti Dena L. , Perfect John R. 
Published: August 2007

ABSTRACT

Fatty acid synthase in the yeast
Cryptococcus neoformans
is composed of two subunits encoded by
FAS1
and
FAS2
genes. We inserted a copper-regulated promoter (P

CTR4
-
2

) to regulate
FAS1
and
FAS2
expression in
Cryptococcus neoformans
(strains P

CTR4
-
2

/
FAS1
and P

CTR4
-
2

/
FAS2
, respectively). Both mutants showed growth rates similar to those of the wild type in a low-copper medium in which
FAS1
and
FAS2
were expressed, but even in the presence of exogenous fatty acids, strains were suppressed in growth under high-copper conditions. The treatment of
C. neoformans
with fluconazole was shown to have an increased inhibitory activity and even became fungicidal when either
FAS1
or
FAS2
expression was suppressed. Furthermore, a subinhibitory dose of fluconazole showed anticryptococcal activity in vitro in the presence of cerulenin, a fatty acid synthase inhibitor. In a murine model of pulmonary cryptococcosis, a tissue census of yeast cells in P

CTR4
-
2

/
FAS2
strain at day 7 of infection was significantly lower than that in mice treated with tetrathiomolybdate, a copper chelator (
P
< 0.05), and a yeast census of P

CTR4
-
2

/
FAS1
strain at day 14 of infection in the brain was lower in the presence of more copper. In fact, no positive cultures from the brain were detected in mice (with or without tetrathiomolybdate treatment) infected with the P

CTR4
-
2

/
FAS2
strain, which implies that this mutant did not reach the brain in mice. We conclude that both
FAS1
and
FAS2
in
C. neoformans
are essential for in vitro and in vivo growth in conditions with and without exogenous fatty acids and that
FAS1
and
FAS2
can potentially be fungicidal targets for
C. neoformans
with a potential for synergistic behavior with azoles.
Targeting of the
Brucella suis
Virulence Factor Histidinol Dehydrogenase by Histidinol Analogues Results in Inhibition of Intramacrophagic Multiplication of the Pathogen
Authors: Joseph Pascale , Abdo Marie-Rose , Boigegrain Rose-Anne , Montero Jean-Louis , Winum Jean-Yves , Köhler Stephan 
Published: August 2007

ABSTRACT

Brucella suis
histidinol dehydrogenase (HDH) can be efficiently targeted by substrate analogues. The growth of this pathogen in minimal medium was inhibited and the multiplication in human macrophages was totally abolished in the presence of the drugs. These effects have been shown to be correlated with the previously described inhibition of
Brucella
HDH activity.
Respiration of
Escherichia coli
in the Mouse Intestine
Authors: Jones Shari A. , Chowdhury Fatema Z. , Fabich Andrew J. , Anderson April , Schreiner Darrel M. , House Anetra L. , Autieri Steven M. , Leatham Mary P. , Lins Jeremy J. , Jorgensen Mathias , Cohen Paul S. , Conway Tyrrell 
Published: August 2007

ABSTRACT

Mammals are aerobes that harbor an intestinal ecosystem dominated by large numbers of anaerobic microorganisms. However, the role of oxygen in the intestinal ecosystem is largely unexplored. We used systematic mutational analysis to determine the role of respiratory metabolism in the streptomycin-treated mouse model of intestinal colonization. Here we provide evidence that aerobic respiration is required for commensal and pathogenic
Escherichia coli
to colonize mice. Our results showed that mutants lacking ATP synthase, which is required for all respiratory energy-conserving metabolism, were eliminated by competition with respiratory-competent wild-type strains. Mutants lacking the high-affinity cytochrome
bd
oxidase, which is used when oxygen tensions are low, also failed to colonize. However, the low-affinity cytochrome
bo

3

oxidase, which is used when oxygen tension is high, was found not to be necessary for colonization. Mutants lacking either nitrate reductase or fumarate reductase also had major colonization defects. The results showed that the entire
E. coli
population was dependent on both microaerobic and anaerobic respiration, consistent with the hypothesis that the
E. coli
niche is alternately microaerobic and anaerobic, rather than static. The results indicate that success of the facultative anaerobes in the intestine depends on their respiratory flexibility. Despite competition for relatively scarce carbon sources, the energy efficiency provided by respiration may contribute to the widespread distribution (i.e., success) of
E. coli
strains as commensal inhabitants of the mammalian intestine.
Prolonged Colonization of Mice by
Vibrio cholerae
El Tor O1 Depends on Accessory Toxins
Authors: Olivier Verena , Salzman Nita H. , Satchell Karla J. Fullner 
Published: August 2007

ABSTRACT

Cholera epidemics caused by
Vibrio cholerae
El Tor O1 strains are typified by a large number of asymptomatic carriers who excrete vibrios but do not develop diarrhea. This carriage state was important for the spread of the seventh cholera pandemic as the bacterium was mobilized geographically, allowing the global dispersion of this less virulent strain. Virulence factors associated with the development of the carriage state have not been previously identified. We have developed an animal model of cholera in adult C57BL/6 mice wherein
V. cholerae
colonizes the mucus layer and forms microcolonies in the crypts of the distal small bowel. Colonization occurred 1 to 3 h after oral inoculation and peaked at 10 to 12 h, when bacterial loads exceeded the inoculum by 10- to 200-fold, indicating bacterial growth within the small intestine. After a clearance phase, the number of bacteria within the small intestine, but not those in the cecum or colon, stabilized and persisted for at least 72 h. The ability of
V. cholerae
to prevent clearance and establish this prolonged colonization was associated with the accessory toxins hemolysin, the multifunctional autoprocessing RTX toxin, and hemagglutinin/protease and did not require cholera toxin or toxin-coregulated pili. The defect in colonization attributed to the loss of the accessory toxins may be extracellularly complemented by inoculation of the defective strain with an isogenic colonization-proficient
V. cholerae
strain. This work thus demonstrates that secreted accessory toxins modify the host environment to enable prolonged colonization of the small intestine in the absence of overt disease symptoms and thereby contribute to disease dissemination via asymptomatic carriers.
Constitutive Acid Sphingomyelinase Enhances Early and Late Macrophage Killing of
Salmonella enterica
Serovar Typhimurium
Authors: McCollister Bruce D. , Myers Jesse T. , Jones-Carson Jessica , Voelker Dennis R. , Vázquez-Torres Andrés 
Published: August 2007

ABSTRACT

We have identified acid sphingomyelinase (ASM) as an important player in the early and late anti-
Salmonella
activity of macrophages. A functional ASM participated in the killing activity of macrophages against wild-type
Salmonella enterica
serovar Typhimurium. The role of ASM in early macrophage killing of
Salmonella
appears to be linked to an active NADPH phagocyte oxidase enzymatic complex, since the flavoprotein inhibitor diphenyleneiodonium not only blocked a productive respiratory burst but also abrogated the survival advantage of
Salmonella
in macrophages lacking ASM. Lack of ASM activity also increased the intracellular survival of an isogenic Δ
spiC::FRT Salmonella
strain deficient in a translocator and effector of the
Salmonella
pathogenicity island 2 (SPI2) type III secretion system, suggesting that the antimicrobial activity associated with ASM is manifested regardless of the SPI2 status of the bacteria. Constitutively expressed ASM is responsible for the role that this lipid-metabolizing hydrolase plays in the innate host defense of macrophages against
Salmonella
. Accordingly, the ASM activity and intracellular concentration and composition of ceramide, gangliosides, and neutral sphingolipids did not increase upon
Salmonella
infection.
Salmonella
triggered, nonetheless, a significant increase in the secreted fraction of ASM. Collectively, these findings have elucidated a novel role for constitutive ASM in the anti-
Salmonella
activity of murine macrophages.
Antibody-Independent, CD4
+
T-Cell-Dependent Protection against Pneumococcal Colonization Elicited by Intranasal Immunization with Purified Pneumococcal Proteins
Authors: Basset Alan , Thompson Claudette M. , Hollingshead Susan K. , Briles David E. , Ades Edwin W. , Lipsitch Marc , Malley Richard 
Published: August 2007

ABSTRACT

Immunity to pneumococcal colonization in mice by exposure to live or killed pneumococci has been shown to be antibody independent but dependent on CD4
+
T cells. Here we show that intranasal immunization with pneumococcal proteins (pneumococcal surface protein C, adhesin A, and a pneumolysoid) can elicit a similar mechanism of protection. Colonization could be significantly reduced in mice congenitally deficient in immunoglobulins after intranasal immunization with this mixture of proteins; conversely, the depletion of CD4
+
T cells in immunized wild-type mice at the time of challenge eliminated the protection afforded by immunization. Overall, our results show that intranasal immunization with a mixture of pneumococcal proteins protects against colonization in an antibody-independent, CD4
+
T-cell-dependent manner.
CONSTRUCTION OF WHISKERS FOR THE QUASIPERIODICALLY FORCED PENDULUM
Authors: STENLUND MIKKO 
Published: August 2007

We study a Hamiltonian describing a pendulum coupled with several anisochronous oscillators, giving a simple construction of unstable KAM tori and their stable and unstable manifolds for analytic perturbations. We extend analytically the solutions of the equations of motion, order by order in the perturbation parameter, to a uniform neighborhood of the time axis.
Ribotoxic Stress Sensitizes Glioblastoma Cells to Death Receptor–Induced Apoptosis: Requirements for c-Jun NH2-Terminal Kinase and Bim
Authors: Xia Shuli , Li Yang , Rosen Eliot M. , Laterra John 
Published: August 2007

Abstract
A prominent feature of glioblastoma is its resistance to death receptor–mediated apoptosis. In this study, we explored the possibility of modulating death receptor–induced cell death with the c-Jun-NH2-terminal kinase (JNK) activator anisomycin. Anisomycin activates JNK by inactivating the ribosome and inducing “ribotoxic stress.” We found that anisomycin and death receptor ligand anti-Fas antibody CH-11 or tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) synergistically induce apoptosis in multiple human glioblastoma cell lines. For example, in U87 cells, anisomycin reduced the IC50 of CH-11 by more than 20-fold (from 500 to 25 ng/mL). Cell viability in response to anisomycin, CH-11, and their combination was 79%, 91%, and 28% (P &lt; 0.001), respectively. Anisomycin and TRAIL were found to be similarly synergistic in glioblastoma cells maintained as tumor xenografts. The potentiation of death receptor–dependent cell death by anisomycin was specific because emetine, another ribosome inhibitor that does not induce ribotoxic stress or activate JNK, did not have a similar effect. Synergistic cell death was predominantly apoptotic involving both extrinsic and intrinsic pathways. Expression of Fas, FasL, FLIP, and Fas-associated death domain (FADD) was not changed following treatment with anisomycin + CH-11. JNK was activated 10- to 22-fold by anisomycin + CH-11 in U87 cells. Inhibiting JNK activation with pharmacologic inhibitors of JNKK and JNK or with dominant negative mitogen-activated protein kinase (MAPK) kinase kinase 2 (MEKK2) significantly prevented cell death induced by the combination of anisomycin + CH-11. We further found that anisomycin + CH-11 up-regulated the proapoptotic protein Bim by ∼14-fold. Simultaneously inhibiting Bim expression and JNK activation additively desensitized U87 cells to anisomycin + CH-11. These findings show that anisomycin-induced ribotoxic stress sensitizes glioblastoma cells to death receptor–induced apoptosis via a specific mechanism requiring both JNK activation and Bim induction. (Mol Cancer Res 2007;5(8):783–92)
c-Src/Histone Deacetylase 3 Interaction Is Crucial for Hepatocyte Growth Factor–Dependent Decrease of CXCR4 Expression in Highly Invasive Breast Tumor Cells
Authors: Matteucci Emanuela , Ridolfi Elisa , Maroni Paola , Bendinelli Paola , Desiderio Maria Alfonsina 
Published: August 2007

Abstract
Hepatocyte growth factor (HGF), a cytokine of tumor microenvironment, exerts opposite effects on CXCR4 expression in MCF-7 (low invasive) and MDA-MB231 (highly invasive) breast carcinoma cells, and here, we show that completely different molecular mechanisms downstream of c-Src activation were involved. As experimental models, we used cells transfected with two CXCR4 promoter constructs and treated with HGF or cotransfected with c-Src wild-type (Srcwt) expression vector; phospho–c-Src formation was enhanced in both cell lines. In MCF-7 cells, consistent with activations of CXCR4Luc constructs after HGF treatment and Srcwt expression, Ets1 and nuclear factor-κB (NF-κB) transcription factors were activated. In contrast, in MDA-MB231 cells, CXCR4Luc construct, Ets1 and NF-κB activities decreased. The divergence point seemed to be downstream of HGF/c-Src and consisted in the interaction between c-Src and the substrate histone deacetylase 3 (HDAC3). Only in MDA-MB231 cells, HDAC3 level was enhanced in membranes and nuclei 30 min after HGF and colocalized/coimmunoprecipitated with phospho–c-Src and phosphotyrosine. Thus, the CXCR4 induction by HGF in MCF-7 cells required NF-κB and Ets1 activations, downstream of phosphoinositide-3-kinase/Akt, whereas in HGF-treated MDA-MB231 cells, HDAC3 activation via c-Src probably caused a reduction of transcription factor activities, such as that of NF-κB. These results indicate possible roles of HGF in invasive growth of breast carcinomas. By enhancing CXCR4 in low invasive tumor cells, HGF probably favors their homing to secondary sites, whereas by suppressing CXCR4 in highly invasive cells, HGF might participate to retain them in the metastatic sites. (Mol Cancer Res 2007;5(8):833–45)
Le mur de Manassé (2 Ch xxxiii 14) entre archéologues et théologiens
Authors: Himbaza Innocent 
Published: August 2007

AbstractMost archaeological scholarship accepts as historical the information of 2Ch xxxiii 14, which claims that Manasseh built a fortification wall in Jerusalem. However, there is no unanimity as to its identification, since recent archaeological publications indicate at least two walls. Concerning theological publications, 63% of them do not include archaelogical data in their discussions on that point. This article points out this lack of balance and suggests a possible solution.
Connecting Central Eurasia to the Middle East in American Foreign Policy Towards Afghanistan and Pakistan: 1979-Present
Authors: Bromley Simon 
Published: August 2007

AbstractDuring the Cold War, United States (US) policies towards the Middle East and towards Afghanistan and Pakistan were largely unrelated. India's non-alignment and relations with the Soviet Union were reasons for close US-Pakistani relations, but the Chinese success in the war with India in 1962 also highlighted the importance to the West of India's position. 1979 marked a major turning point in US foreign policy towards the Middle East and Central Eurasia (CEA) because of the two events which were to shape so much of politics and geopolitics in those regions as well as in the wider international system: namely, the Iranian revolution in February and the Soviet invasion of Afghanistan in December. Taken together, these developments posed a major challenge to US strategy towards the Soviet Union, to the wider Middle East and to relations with China, Pakistan, and India. After the Soviet withdrawal from Afghanistan during 1988/89, the US lost interest in Afghanistan and followed the policies of Pakistan for most of the 1990s. Then came 9/11 and President Musharraf took the historic decision to break with the Taliban. In March 2003, the US began its second war against Iraq. Whatever the rationale for the conflict, the outcome has been to turn the future of Iraq into a key fault-line of geopolitics in the Greater Middle East. Now, with the instability following the collapse of the Soviet Empire in CEA, the defeat of the Taliban and the ongoing future of Iraq, the US faces what the Department of Defense describes as an "arc of instability" running from the Middle East through CEA to Northeast Asia. This is the region that lies at the centre of planning for the "long war" announced in the Pentagon's 2006 quadrennial review.
The Challenges of Modernity: The Case of Political Islam
Authors: Amineh Mehdi Parvizi 
Published: August 2007

AbstractSince the Industrial Revolution in the late eighteenth century in England, all traditional cultures at one point in history have been challenged by modernity. This happened first in Europe and later in the rest of the world as a result of the late nineteenth century expansion of European capitalism and civilization. When confronted with modernity, individual traditional cultures conflict with the increasing plurality of lifestyles and values. There are two ways to solve this conflict: either remain in the past or innovate. In the first case, tradition prevails. In the second case, the challenges of modernity are embraced by adapting to the new circumstances. This will eventually lead to the renewal of one's own culture. Since the late nineteenth century, the challenges of modernity have resulted in a variety of often contradictory Islamic political ideologies and practices. In contrast to the cultural-essentialist and a-historical assumptions of some scholars, such as Samuel Huntington, who see the phenomenon of political Islam as a characteristic of an inevitable "clash of civilizations"—according to which conflicts and threats to world peace and security in the twenty-first century will be carried out along "civilizational fault lines"—this article argues that the actual fault-lines are socio-economic, not geo-cultural, and that conflicts in today's world do not take place between cultures but within them. Those societies that are more successful in adapting to the challenges of modernity show a relatively stronger capacity to cope with the growing complexity of political and cultural pluralism.
The Maghreb: Social, Political, and Economic Developments
Authors: Dris-Aït-Hamadouche Louisa , Zoubir Yahia 
Published: August 2007

AbstractDue to its geographical position, events in the Middle East, the Sahel, and Europe have consequential effects on the Maghreb (Algeria, Libya, Morocco, and Tunisia). Hence, recent economic, political, and cultural changes are more or less inspired or encouraged by those developments taking place in the surrounding environment. Together with Mauritania, the four countries founded in 1989 the Arab Maghreb Union (UMA), which aimed at regional integration. Unfortunately, the UMA remains a distant wish; the conflict over Western Sahara and the political differences between Algeria and Morocco have prevented the UMA's advance.Each Maghrebi country witnessed particular events and reacted differently to identical stimuli. Undoubtedly, the countries' distinctive historical experiences provide a valuable understanding of the internal logic of the processes they have undergone and the way they sought to tackle them. This article will review the salient developments that occurred within each of the four Maghrebi countries and analyze the ways through which the regimes seek to resolve the challenges they are faced with. The main contention in the article is that the regimes in place have yet to open up the political space and allow genuine democratization to take place, for despite some genuine transformations in a few areas, the old rulers are still reluctant to loosen their grip over power. While they succeed in reestablishing order, the roots that generate cyclical uprisings remain intact. Civil society has yet to fulfill its full potential and enjoy genuine citizen participation.