bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cusps of Hilbert modular varieties
Authors: McREYNOLDS D. B. 
Published: February 2008

AbstractMotivated by a question of Hirzebruch on the possible topological types of cusp cross-sections of Hilbert modular varieties, we give a necessary and sufficient condition for a manifoldMto be diffeomorphic to a cusp cross-section of a Hilbert modular variety. Specialized to Hilbert modular surfaces, this proves that every Sol 3–manifold is diffeo morphic to a cusp cross-section of a (generalized) Hilbert modular surface. We also deduce an obstruction to geometric bounding in this setting. Consequently, there exist Sol 3–manifolds that cannot arise as a cusp cross-section of a 1–cusped nonsingular Hilbert modular surface.
Integral Riemann–Roch formulae for cyclic subgroups of mapping class groups
Authors: AKITA TOSHIYUKI , KAWAZUMI NARIYA 
Published: February 2008

AbstractThe first author conjectured certain relations for Morita–Mumford classes and Newton classes in the integral cohomology of mapping class groups (integral Riemann–Roch formulae). In this paper, the conjecture is verified for cyclic subgroups of mapping class groups.
Off Her Trolley? Frances Kamm and the Metaphysics of Morality
Authors: NORCROSS ALASTAIR 
Published: February 2008

Frances Kamm's aptly titled Intricate Ethics is a tour de force of what Peter Unger calls the ‘preservationist’ approach to ethical theory. Here is some of what she says about her methodology:
Consider as many case-based judgments of yours as prove necessary. Do not ignore some case-based judgments, assuming they are errors, just because they conflict with simple or intuitively plausible principles that account for some subset of your case-based judgments. Work on the assumption that a different principle can account for all of the judgments. Be prepared to be surprised at what this principle is . . . . I say, consider your case-based judgments, rather than a survey of everyone's judgments. This is because I believe that much more is accomplished when one person considers her judgments and then tries to analyze and justify their grounds than if we do mere surveys. (5)
Concurrent comparison of energy intake and expenditure among adults in Butajira District, Ethiopia
Authors: Tesfaye Fikru , Byass Peter , Wall Stig 
Published: February 2008

AbstractObjectiveTo estimate and compare dietary energy intake (DEI) and total energy expenditure (TEE) among adults, using questionnaires.DesignComparative, cross-sectional study.SettingCommunity-based, at the demographic surveillance site (DSS) in Butajira District of Ethiopia.SubjectsA total of 619 adults, 18–64 years of age, were randomly selected from among the urban and rural population of Butajira using the DSS sampling frame. Habitual dietary intake and physical activity were assessed using questionnaires. BMR was estimated using a regression equation, and TEE was calculated from BMR and the metabolic energy equivalent task (MET) and duration of reported activities. Physical activity level (PAL) was calculated as TEE/BMR, while food intake level (FIL) was calculated as DEI/BMR. The mean DEI:TEE ratio was used to evaluate reported DEI at the population level, while individual misreporters were identified by applying the Goldberg cut-off points at three levels of PAL.ResultsBased on the Goldberg method, 57 % of the study participants were identified as acceptable reporters of DEI, among whom mean TEE was 8·21 (95 % CI 8·01, 8·42) MJ (1963 (95 % CI 1914, 2012) kcal), mean DEI was 8·13 (95 % CI 7·93, 8·34) MJ (1944 (95 % CI 1895, 1993) kcal) and mean DEI:TEE was 1·01 (95 % CI 0·99, 1·04).ConclusionThe dietary history and physical activity questionnaires provide comparable estimates of mean energy intake and expenditure at a population level. Acceptable reporters have to be identified in order to obtain better estimates. Questionnaire-based estimates of energy intake should not be interpreted without an inherent system of comparison or validation.
Leucine 7 to proline 7 polymorphism in the neuropeptide Y gene and changes in serum lipids during a family-based counselling intervention among school-aged children with a family history of CVD
Authors: Salminen Marika , Lehtimäki Terho , Fan Yue-Mei , Vahlberg Tero , Kivelä Sirkka-Liisa 
Published: February 2008

AbstractObjectiveTo compare whether serum lipids and their changes during a health education intervention are associated with the Leu7Pro polymorphism in the signal peptide part of neuropeptide Y (NPY) in children with normal weight and in those with overweight.DesignAn intervention study.SettingA family-based intervention of risk factors for prevention of CHD in Finland.SubjectsSubjects were 443 children with a family history of CVD participating in family-based health education. The children were divided into two groups according to NPY genotype: children with Leu7/Pro7 or Pro7/Pro7 genotype (n50) and children with Leu7/Leu7 genotype (n393). The final sample of the follow-up study included 353 (80 %) children (Pro7 allelle carriers,n43; Leu7/Leu7,n310).ResultsAt baseline, the Leu7Pro polymorphism was not associated with serum lipid values after adjustment for body weight in boys or girls. There was a significant interaction of NPY genotype group by time and body weight (P= 0·043 for three-way interaction: time × NPY genotype × body weight) in LDL-cholesterol (LDL-C) concentration among boys. LDL-C decreased among boys with normal weight in both NPY groups and in overweight boys with the Leu7/Leu7 genotype, whereas it increased in overweight boys with the Pro7 allele. Two-way interaction (time × NPY genotype) showed no significant differences in changes of serum lipids between the NPY genotype groups among boys or girls.ConclusionsThe Leu7Pro polymorphism may be associated with dietary response to LDL-C concentration in overweight boys with a family history of early-onset CVD.
Perceived subject outcomes and impact on health-related quality of life associated with diet using the new Food Benefits Assessment (FBA©) questionnaire: development and psychometric validation
Authors: Guyonnet Denis , Chassany Olivier , Picard Céline , Guillemin Isabelle , Meunier Juliette , Seignobos Eva , Vigneux Marc , Lassel Taous , Trudeau Elyse 
Published: February 2008

AbstractObjectiveTo assess the perceived outcomes associated with diet/food intake in the general adult population.Design and subjectsThe Food Benefits Assessment (FBA©) questionnaire was developed from subjects’ verbatim transcripts (n 18) and after comprehension tests (n 5). Normal-weight (n 130) and overweight (n 67) subjects then completed the final questionnaire twice, 7 d apart. Psychometric properties were assessed, including construct validity by principal components analysis (PCA), concurrent validity (Spearman coefficient) with the Short Form-36 scale (SF-36), known-group validity by comparing FBA dimension scores according to lifestyle and clinical variables, internal consistency reliability (Cronbach’s α) and test–retest reproducibility in stable subjects over 1 week (intraclass correlation coefficient, ICC).ResultsPCA and Multitrait analysis confirmed the final version of the FBA comprising forty-one items split into seven dimensions (vitality; digestive comfort; physical appearance; well-being; snacking; disease prevention; aesthetics). All dimensions displayed good item convergent validity (0·44 to 0·80), good concurrent validity (highest correlation between well-being dimension of FBA and mental health scale of SF-36, r = 0·83) and good known-group validity and reproducibility (ICC ≥ 0·76); internal consistency reliability was good to excellent (Cronbach’s α = 0·79 to 0·91).ConclusionThe FBA is the first valid and reliable questionnaire that allows the assessment of diet effects and impact as perceived by subjects. It is a good candidate in the nutrition field for further use in specific population settings and with a particular food or daily diet. Linguistically validated English (UK and US) and German versions of the questionnaire are available.
How to achieve long-term breast-feeding: factors associated with early discontinuation
Authors: Camurdan Aysu Duyan , Ilhan Mustafa N , Beyazova Ufuk , Sahin Figen , Vatandas Nilgun , Eminoglu Sancar 
Published: February 2008

AbstractObjectivesTo evaluate the factors associated with discontinuation of breast-feeding before 12 months in order to make suggestions for achieving long-term breast-feeding.DesignA descriptive cross-sectional study.SettingGazi University Medical School, Ankara, Turkey.SubjectsMothers of 1230 children who discontinued breast-feeding at least 15 d before the last visit were asked to fill out a questionnaire about the discontinuation process. Logistic regression analysis was performed to assess the independent effects of factors that might influence breast-feeding discontinuation.ResultsMean breast-feeding duration of the study group was 11·04 (sd 7·45) months. Introduction of bottle-feeding correlated with discontinuation of breast-feeding (r = 0·507, P = 0·001). Important risk factors for discontinuation of breast-feeding before the first 12 months were not exclusively breast-feeding at 3 and 6 months, prematurity, not having a plan about breast-feeding duration and maternity leave duration of ≤91 d for working mothers. The common reasons for abandoning breast-feeding in the first and second 6 months were similar, namely the mother’s concerns about the sufficiency of breast milk. After 12 months and 18 months the reasons for discontinuation were the baby’s unwillingness to eat solid foods while breast-feeding and the mother’s perception that ‘the baby is old enough’, respectively.ConclusionThe factors that improve long-term breast-feeding are successful exclusive breast-feeding in the first few months, intention of the mother to breast-feed and sufficient duration of maternity leave. This study emphasizes the importance of successful breast-feeding counselling during the first few months to achieve the desired long-term breast-feeding.
N‐Acetylcysteine prevents ifosfamide‐induced nephrotoxicity in rats
Authors: Chen N , Aleksa K , Woodland C , Rieder M , Koren G 
Published: February 2008

Background and purpose:Ifosfamide nephrotoxicity is a serious adverse effect for children undergoing cancer chemotherapy. Our recent in vitro studies have shown that the antioxidant N‐acetylcysteine (NAC), which is used extensively as an antidote for paracetamol (acetaminophen) poisoning in children, protects renal tubular cells from ifosfamide‐induced toxicity at a clinically relevant concentration. To further validate this observation, an animal model of ifosfamide‐induced nephrotoxicity was used to determine the protective effect of NAC.Experimental approach:Male Wistar albino rats were injected intraperitoneally with saline, ifosfamide (50 or 80 mg kg−1 daily for 5 days), NAC (1.2 g kg−1 daily for 6 days) or ifosfamide+NAC (for 6 days). Twenty‐four hours after the last injection, rats were killed and serum and urine were collected for biochemical analysis. Kidney tissues were obtained for analysis of glutathione, glutathione S‐transferase and lipid peroxide levels as well as histology analysis.Key results:NAC markedly reduces the severity of renal dysfunction induced by ifosfamide with a significant decrease in elevations of serum creatinine (57.8±2.3 vs 45.25±2.1 μmol l−1) as well as a reduced elevation of β2‐microglobulin excretion (25.44±3.3 vs 8.83±1.3 nmol l−1) and magnesium excretion (19.5±1.5 vs 11.16±1.5 mmol l−1). Moreover, NAC significantly improved the ifosfamide‐induced glutathione depletion and the decrease of glutathione S‐transferase activity, lowered the elevation of lipid peroxides and prevented typical morphological damages in renal tubules and glomeruli.Conclusions and implications:Our results suggest a potential therapeutic role for NAC in paediatric patients in preventing ifosfamide nephrotoxicity.British Journal of Pharmacology (2008) 153, 1364–1372; doi:10.1038/bjp.2008.15; published online 18 February 2008
Agonists at PPAR‐γ suppress angiotensin II‐induced production of plasminogen activator inhibitor‐1 and extracellular matrix in rat cardiac fibroblasts
Authors: Hao G‐H , Niu X‐L , Gao D‐F , Wei J , Wang N‐P 
Published: February 2008

Background and purpose:Peroxisome proliferator‐activated receptor (PPAR)‐γ ligands have been shown to inhibit cardiac fibrosis. However, the underlying mechanisms are poorly understood. We investigated the regulation by PPAR‐γ ligands of angiotensin (Ang) II‐induced plasminogen activator inhibitor (PAI)‐1, extracellular matrix (ECM) production and cell growth in cardiac fibroblasts.Experimental approach:The effects of PPAR‐γ ligands on Ang II‐induced PAI‐1, ECM expression and cell growth were assessed in primary‐cultured rat cardiac fibroblasts; cardiac PAI‐1 and ECM production was examined in Ang II‐infused rats.Key results:In growth‐arrested cardiac fibroblasts, PPAR‐γ ligands rosiglitazone and 15‐deoxy‐Δ12,14‐prostaglandin J2 (15d‐PGJ2) dose‐dependently attenuated Ang II‐induced cell proliferation and expression of PAI‐1, collagen type‐I, collagen type‐III and fibronectin. An accompanying increase in PPAR‐γ expression and activation was also observed. These suppressive effects were attenuated by the PPAR‐γ antagonists GW9662 and bisphenol A diglycidyl ether (BADGE). Moreover, rosiglitazone and 15d‐PGJ2 inhibited in part the expression and phosphorylation of Ang II‐induced transforming growth factor (TGF)‐β1, Smad2/3 and c‐Jun NH(2)‐terminal kinase (JNK). Ang II infusion in rats markedly increased left ventricular production of PAI‐1, collagen and fibronectin, with a concurrent increase in the ratios of heart weight/body weight and left ventricle weight/body weight. Co‐treatment with rosiglitazone significantly decreased these levels and upregulated PPAR‐γ expression.Conclusions and implications:Rosiglitazone and 15d‐PGJ2 suppress Ang II‐induced production of PAI‐1 and ECM probably via interactions between PPAR‐γ and TGF‐β1/Smad2/3 and JNK signalling pathways. It is suggested that PPAR‐γ and its ligands may have potential applications in preventing cardiac fibrosis.British Journal of Pharmacology (2008) 153, 1409–1419; doi:10.1038/bjp.2008.21; published online 18 February 2008
Activation of ETBreceptors regulates the abundance of ET‐1 mRNA in vascular endothelial cells
Authors: Farhat N , Matouk C C , Mamarbachi A M , Marsden P A , Allen B G , Thorin E 
Published: February 2008

Background and purpose:The factors that influence the cellular levels of endothelin‐1 (ET‐1) include transcription, mRNA localization, stability and translation, post‐translational maturation of preproET‐1 and degradation of ET‐1. We investigated the regulation of ET‐1 mRNA abundance by extracellular ET‐1 in porcine aortic endothelial cells (PAECs).Experimental approach:Passsage one cultures of PAECs were incubated in starving medium in the presence or absence of ET‐1 and antagonists or pharmacological inhibitors. PreproET‐1 mRNA,endothelin‐1promoter activity, Erk and p38 MAPK activation were determined.Key results:Exogenous ET‐1 reduced cellular ET‐1 mRNA content: a reduction of 10 000‐fold was observed after 4 h. ET‐1 simultaneously reduced the stability of ET‐1 mRNA and increased the loading of RNA Polymerase II at theendothelin‐1promoter. In the absence of exogenous ET‐1, the ETB‐selective antagonist, BQ788, increased ET‐1 mRNA. An ETA‐selective antagonist had no effect. ET‐1 mRNA returned to control levels within 24 h. Whereas activation of p38 MAPK induced by ET‐1 peaked at 30 min and returned to control levels within 90 min, Erk1/2 remained active after 4 h of stimulation. Inhibition of p38 MAPK prevented the ET‐1‐induced decrease in ET‐1 mRNA. In contrast, Erk1/2 inhibition increased ET‐1 mRNA. Similarly, inhibition of receptor internalization increased ET‐1 mRNA in the presence or absence of exogenous ET‐1.Conclusions and implications:These results suggest that extracellular ET‐1 regulates the abundance of ET‐1 mRNA in PAECs, in an ETBreceptor‐dependent manner, by modulating both mRNA stability and transcription via mechanisms involving receptor endocytosis and both ERK and p38 MAPK pathways.British Journal of Pharmacology(2008)153, 1420–1431; doi:10.1038/bjp.2008.25; published online 18 February 2008
Physiology and pharmacology of alcohol: the imidazobenzodiazepine alcohol antagonist site on subtypes of GABAAreceptors as an opportunity for drug development?
Authors: Wallner M , Olsen R W 
Published: February 2008

Alcohol (ethanol, EtOH) has pleiotropic actions and induces a number of acute and long‐term effects due to direct actions on alcohol targets, and effects of alcohol metabolites and metabolism. Many detrimental health consequences are due to EtOH metabolism and metabolites, in particular acetaldehyde, whose high reactivity leads to nonspecific chemical modifications of proteins and nucleic acids. Like acetaldehyde, alcohol has been widely considered a nonspecific drug, despite rather persuasive evidence implicating inhibitory GABAAreceptors (GABAARs) in acute alcohol actions, for example, a GABAAR ligand, the imidazobenzodiazepine Ro15‐4513 antagonizes many low‐to‐moderate dose alcohol actions in mammals. It was therefore rather surprising that abundant types of synaptic GABAARs are generally not responsive to relevant low concentrations of EtOH. In contrast, δ‐subunit‐containing GABAARs and extrasynaptic tonic GABA currents mediated by these receptors are sensitive to alcohol concentrations that are reached in blood and tissues during low‐to‐moderate alcohol consumption. We recently showed that low‐dose alcohol enhancement on highly alcohol‐sensitive GABAAR subtypes is antagonized by Ro15‐4513 in an apparently competitive manner, providing a molecular explanation for behavioural Ro15‐4513 alcohol antagonism. The identification of a Ro15‐4513/EtOH binding site on unique GABAAR subtypes opens the possibility to characterize this alcohol site(s) and screen for compounds that modulate the function of EtOH/Ro15‐4513‐sensitive GABAARs. The utility of such drugs might range from novel alcohol antagonists that might be useful in the emergency room, to drugs for the treatment of alcoholism, as well as alcohol‐mimetic drugs to harness acute positive effects of alcohol.British Journal of Pharmacology(2008)154, 288–298; doi:10.1038/bjp.2008.32; published online 18 February 2008
A novel activity for substance P: stimulation of peroxisome proliferator‐activated receptor‐γ protein expression in human monocytes and macrophages
Authors: Amoruso A , Bardelli C , Gunella G , Ribichini F , Brunelleschi S 
Published: February 2008

Background and purpose: Substance P (SP) and peroxisome proliferator‐activated receptor‐γ (PPAR‐γ) play important roles in different inflammatory conditions and are both expressed in human monocytes and macrophages. However, it is not known whether or not they interact. This study was undertaken to evaluate the effects of SP on PPAR‐γ protein expression in monocytes and macrophages (MDMs: monocyte‐derived macrophages) from healthy smokers and non‐smokers.Experimental approach: PPAR‐γ protein was detected by western blot and quantified by calculating the ratio between PPAR‐γ and β‐actin protein expression. Constitutive tachykinin NK1 receptor expression in monocytes and MDMs from healthy smokers and non‐smokers was evaluated by western blot. Cytokine release was evaluated by ELISA.Key results: In the concentration range 10−10–10−6 M, SP stimulated PPAR‐γ protein expression in monocytes and MDMs, being more effective in cells from healthy smokers. Moreover, in these cells there was a constitutively increased expression of NK1 receptors. SP‐induced expression of the PPAR‐γ protein was receptor‐mediated, as it was reproduced by the NK1 selective agonist [Sar9Met(O2)11]SP and reversed by the competitive NK1 antagonist GR71251. SP‐induced maximal effects were similar to those evoked by 15‐deoxy‐Δ12,14‐prostaglandin J2; an endogenous PPAR‐γ agonist, and were significantly reduced by a PPAR‐γ antagonist. NK1 and PPAR‐γ agonists exerted opposite effects on TNF‐α release from monocytes and MDMs.Conclusions and implications: Enhancement of PPAR‐γ protein expression represents a novel activity for SP, which could contribute to a range of chronic inflammatory disorders.
Detrimental role of endogenous nitric oxide in host defence against Sporothrix schenckii
Authors: Fernandes Karla Simone S. , Neto Edward Helal , Brito Marcelly M. S. , Silva João S. , Cunha Fernando Q. , Barja‐Fidalgo Christina 
Published: February 2008

SummaryWe earlier demonstrated that nitric oxide (NO) is a fungicidal molecule against Sporothrix schenckii in vitro. In the present study we used mice deficient in inducible nitric oxide synthase (iNOS–/–) and C57BL/6 wild‐type (WT) mice treated with Nω‐nitro‐arginine (Nitro‐Arg‐treated mice), an NOS inhibitor, both defective in the production of reactive nitrogen intermediates, to investigate the role of endogenous NO during systemic sporotrichosis. When inoculated with yeast cells of S. schenckii, WT mice presented T‐cell suppression and high tissue fungal dissemination, succumbing to infection. Furthermore, susceptibility of mice seems to be related to apoptosis and high interleukin‐10 and tumour necrosis factor‐α production by spleen cells. In addition, fungicidal activity and NO production by interferon‐γ (IFN‐γ) and lipopolysaccharide‐activated macrophages from WT mice were abolished after fungal infection. Strikingly, iNOS–/– and Nitro‐Arg‐treated mice presented fungal resistance, controlling fungal load in tissues and restoring T‐cell activity, as well as producing high amounts of IFN‐γ Interestingly, macrophages from these groups of mice presented fungicidal activity after in vitro stimulation with higher doses of IFN‐γ. Herein, these results suggest that although NO was an essential mediator to the in vitro killing of S. schenckii by macrophages, the activation of NO system in vivo contributes to the immunosuppression and cytokine balance during early phases of infection with S. schenckii.
Soluble CD276 (B7‐H3) is released from monocytes, dendritic cells and activated T cells and is detectable in normal human serum
Authors: Zhang Guangbo , Hou Jianquan , Shi Jinfang , Yu Gehua , Lu Binfeng , Zhang Xueguang 
Published: February 2008

SummaryExpression of membrane CD276 (mB7‐H3) has been reported on dendritic cells (DCs), monocytes, activated T cells, and various carcinoma cells. However, reports concerning its in vivo function have been inconsistent. Moreover, whether there is a soluble form of this protein is not known. In this study, using a sensitive dual monoclonal antibody sandwich enzyme‐linked immunosorbent assay (ELISA) to detect the soluble form of B7‐H3 (sB7‐H3), we demonstrated the release of sB7‐H3 by monocytes, DCs, activated T cells, and various mB7‐H3+ but not mB7‐H3– carcinoma cells. Release from cells was blocked by addition of a matrix metalloproteinase inhibitor (MMPI), which concomitantly caused the accumulation of B7‐H3 on the cell surface. To determine the level of circulating sB7‐H3, more than 200 serum samples were included in the study. The results indicated that sB7‐H3 was present at high levels in all serum samples. Western blotting of sB7‐H3 from cell culture supernatants or sera of healthy donors indicated that the molecular size was approximately 16 kDa. Soluble B7‐H3 was able to bind to the B7‐H3 receptor (B7‐H3R) on activated T cells, which showed that sB7‐H3 is a functionally active form. These results indicate that release of sB7‐H3 from the cell surface is mediated by a matrix metalloproteinase and probably regulates B7‐H3R/B7‐H3 interactions in vivo. Cleavage of sB7‐H3 to an active soluble form would alter both proximal and distal cellular responses.