bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Slurry Characteristics on the Surface Tribology During Copper CMP Process
Authors: Mudhivarthi Subrahmanya R. , Kakireddy Veera Raghava , Kumar Ashok , Obeng Y. 
Published: December 2007

Tribological properties at the polishing interface during	chemical mechanical polishing (CMP) in different slurry chemical environments need to be studied in greater detail, to understand the mechanism and science of CMP. The chemical reactions in different environments significantly affect the actual tribological behavior at the interface. In the present research, slurry temperature, oxidizer percentage and complexing agent concentrations in the slurry are varied and their effect on the tribology at the interface on polyurethane pads has been studied. Specifically, the main goal of this research is to develop fundamental understanding about the role of coefficient of friction in CMP and the effect of slurry characteristics on the tribology at the interface. From the results the effect of slurry temperature was found to be very weak when compared to the other process parameters such as pressure and velocity.
Integrating a CMP Robust ILD Module
Authors: Naughton John J. , Towner Janet M. , Aytes S. , Nelson M. M. 
Published: December 2007

CMP (chemical mechanical planarization) micro-scratches are yield and reliability limiting defects in semiconductor manufacturing. Silicon oxide films doped with boron and phosphorus have been standard in pre-metal dielectric stacks but are prone to CMP micro-scratching. A novel film stack was integrated utilizing a thick,undoped PECVD cap layer to	mitigate device failure and reliability problems. The sequence	of depositing the integral film layers in conjunction with the densification proved critical in maintaining device	performance.
Galactosylation does not prevent the rapid clearance of long-term, 4°C-stored platelets
Authors: Wandall Hans H. , Hoffmeister Karin M. , Sørensen Anne Louise , Rumjantseva Viktoria , Clausen Henrik , Hartwig John H. , Slichter Sherrill J. 
Published: December 2007

AbstractCold storage of platelets for transfusion is desirable to extend platelet storage times and to prevent bacterial growth. However, the rapid clearance of cold-stored platelets prevents their use. A novel method for preventing the rapid clearance of cold-stored platelets has previously been developed in a murine model. Cold storage induces the clustering and recognition of exposed β-N-acetylglucosamine (βGlcNAc) on platelet surfaces. Glycosylation of βGlcNAc residues with uridine 5′-diphosphogalactose (UDP-galactose) results in the normal survival of short-term (2 h) 0°C-stored murine platelets. Based on this finding, we developed a similar glycosylation process by adding UDP-galactose to human apheresis platelets. A phase 1 clinical trial was conducted transfusing radiolabeled autologous apheresis platelets stored for 48 hours at 4°C with or without pretreatment with UDP-galactose. In contrast to the murine study, galactosylation of human platelets did not prevent the accelerated platelet clearance routinely observed after 4°C storage. We next developed a murine model of platelet storage for 48 hours at 4°C and showed that UDP-galactose treatment of murine platelets also did not prevent their rapid clearance, in agreement with the human platelet study. We conclude that different mechanisms of clearance may exist for short- and long-term cold-stored platelets.
DNA variants in the dihydrofolate reductase gene and outcome in childhood ALL
Authors: Dulucq Stéphanie , St-Onge Geneviève , Gagné Vincent , Ansari Marc , Sinnett Daniel , Labuda Damian , Moghrabi Albert , Krajinovic Maja 
Published: December 2007

Abstract
Dihydrofolate reductase (DHFR) is the major target of methotrexate (MTX), a key component in childhood acute lymphoblastic leukemia (ALL) treatment. A total of 15 polymorphisms in DHFR promoter were analyzed, and 3 sites (C−1610G/T, C−680A, and A−317G) were identified as sufficient to define observed haplotypes (tag single nucleotide polymorphisms [tagSNPs]). These polymorphisms were investigated for association with treatment response in 277 children with ALL. Lower event-free survival (EFS) was associated with homozygosity for the allele A−317 and C−1610 (P = .03 and .02), and with the haplotype *1, defined by both C−1610 and A−317 alleles (P = .03). The haplotype *1 conferred higher transcriptional activity (P < .01 compared with haplotypes generating minimal luciferase expression). Quantitative mRNA analysis showed higher DHFR levels for particular haplotype *1 carriers (P < .01). The analysis combining haplotype *1 with thymidylate synthase (TS) and cyclin D1 (CCND1) genotypes previously shown to affect ALL outcome showed that the number of event-predisposing genotypes was associated with increasingly lower EFS (P < .001). In conclusion, DHFR promoter polymorphisms are associated with worse ALL outcome, likely due to a higher DHFR expression. Combined effects among genes of the folate cycle can further accentuate differences in the response to the treatment.
Ongoing improvement in long-term survival of patients with Hodgkin disease at all ages and recent catch-up of older patients
Authors: Brenner Hermann , Gondos Adam , Pulte Dianne 
Published: December 2007

Abstract
Since the breakthroughs in combination chemotherapy of patients with Hodgkin disease (HD) starting in the 1960s, prognosis of patients has been rising steadily. Trends in long-term survival of patients with HD on the population level should therefore be monitored in an as timely as possible manner. We assessed trends in age specific 5- and 10-year relative survival of patients with HD in the United States from 1980-1984 to 2000-2004 from the 1973-2004 database of the Surveillance, Epidemiology, and End Results (SEER) Program. Period analysis was used to disclose recent developments with minimum delay. Overall, 5-year relative survival steadily increased from 73.5% to 85.2% (+11.7 percentage units), and 10-year relative survival increased from 62.1% to 80.1% (+18.0 percentage units) between 1980-1984 and 2000-2004, according to period analysis. The increase was particularly pronounced for patients aged 45 to 59 years and 60 years and older (increases in 10-year relative survival by 24.8 and 23.3 percentage points, respectively). Nevertheless, a strong age gradient persisted, with 10-year relative survival of 92.7%, 88.7%, 84.9%, 76.2%, and 44.9% in patients aged 15 to 24 years, 25 to 34 years, 35 to 44 years, 45 to 54 years, and 60 years and older, respectively, in 2000-2004. Our period analysis discloses ongoing, major improvement in long-term survival of patients with HD in recent years, particularly among older patients.
Somatic inactivation of the PHD2 prolyl hydroxylase causes polycythemia and congestive heart failure
Authors: Minamishima Yoji Andrew , Moslehi Javid , Bardeesy Nabeel , Cullen Darragh , Bronson Roderick T. , Kaelin William G. 
Published: December 2007

AbstractPharmacologic activation of the heterodimeric HIF transcription factor appears promising as a strategy to treat diseases, such as anemia, myocardial infarction, and stroke, in which tissue hypoxia is a prominent feature. HIF accumulation is normally linked to oxygen availability because an oxygen-dependent posttranslational modification (prolyl hydroxylation) marks the HIFα subunit for polyubiquitination and destruction. Three enzymes (PHD1, PHD2, and PHD3) capable of catalyzing this reaction have been identified, although PHD2 (also called Egln1) appears to be the primary HIF prolyl hydroxylase in cell culture experiments. We found that conditional inactivation of PHD2 in mice is sufficient to activate a subset of HIF target genes, including erythropoietin, leading to striking increases in red blood cell production. Mice lacking PHD2 exhibit premature mortality associated with marked venous congestion and dilated cardiomyopathy. The latter is likely the result of hyperviscosity syndrome and volume overload, although a direct effect of chronic, high-level HIF stimulation on cardiac myocytes cannot be excluded.
Lysosomal trafficking functions of mucolipin-1 in murine macrophages
Authors: Thompson Eric G , Schaheen Lara , Dang Hope , Fares Hanna 
Published: December 2007

AbstractBackgroundMucolipidosis Type IV is currently characterized as a lysosomal storage disorder with defects that include corneal clouding, achlorhydria and psychomotor retardation.MCOLN1, the gene responsible for this disease, encodes the protein mucolipin-1 that belongs to the "Transient Receptor Potential" family of proteins and has been shown to function as a non-selective cation channel whose activity is modulated by pH. Two cell biological defects that have been described in MLIV fibroblasts are a hyperacidification of lysosomes and a delay in the exit of lipids from lysosomes.ResultsWe show that mucolipin-1 localizes to lysosomal compartments in RAW264.7 mouse macrophages that show subcompartmental accumulations of endocytosed molecules. Using stable RNAi clones, we show that mucolipin-1 is required for the exit of lipids from these compartments, for the transport of endocytosed molecules to terminal lysosomes, and for the transport of the Major Histocompatibility Complex II to the plasma membrane.ConclusionMucolipin-1 functions in the efficient exit of molecules, destined for various cellular organelles, from lysosomal compartments.
MRPS18CP2 alleles and DEFA3absence as putative chromosome 8p23.1 modifiers of hearing loss due to mtDNA mutation A1555G in the 12S rRNA gene
Authors: Ballana Ester , Mercader Josep Maria , Fischel-Ghodsian Nathan , Estivill Xavier 
Published: December 2007

Abstract

Background
Mitochondrial DNA (mtDNA) mutations account for at least 5% of cases of postlingual, nonsyndromic hearing impairment. Among them, mutation A1555G is frequently found associated with aminoglycoside-induced and/or nonsyndromic hearing loss in families presenting with extremely variable clinical phenotypes. Biochemical and genetic data have suggested that nuclear background is the main factor involved in modulating the phenotypic expression of mutation A1555G. However, although a major nuclear modifying locus was located on chromosome 8p23.1 and regardless intensive screening of the region, the gene involved has not been identified.

Methods
With the aim to gain insights into the factors that determine the phenotypic expression of A1555G mutation, we have analysed in detail different genetic and genomic elements on 8p23.1 region (DEFA3 gene absence, CLDN23 gene and MRPS18CP2 pseudogene) in a group of 213 A1555G carriers.

Results
Family based association studies identified a positive association for a polymorphism on MRPS18CP2 and an overrepresentation of DEFA3 gene absence in the deaf group of A1555G carriers.

Conclusion
Although none of the factors analysed seem to have a major contribution to the phenotype, our findings provide further evidences of the involvement of 8p23.1 region as a modifying locus for A1555G 12S rRNA gene mutation.
Immune system responses and fitness costs associated with consumption of bacteria in larvae of Trichoplusia ni
Authors: Freitak Dalial , Wheat Christopher W , Heckel David G , Vogel Heiko 
Published: December 2007

Abstract

Background

Insects helped pioneer, and persist as model organisms for, the study of specific aspects of immunity. Although they lack an adaptive immune system, insects possess an innate immune system that recognizes and destroys intruding microorganisms. Its operation under natural conditions has not been well studied, as most studies have introduced microbes to laboratory-reared insects via artificial mechanical wounding. One of the most common routes of natural exposure and infection, however, is via food; thus, the role of dietary microbial communities in herbivorous insect immune system evolution invites study. Here, we examine the immune system response and consequences of exposing a lepidopteran agricultural pest to non-infectious microorganisms via simple oral consumption.

Results

Immune system response was compared between Trichoplusia ni larvae reared on diets with or without non-pathogenic bacteria (Escherichia coli and Micrococcus luteus). Two major immune response-related enzymatic activities responded to diets differently – phenoloxidase activity was inhibited in the bacteria-fed larvae, whereas general antibacterial activity was enhanced. Eight proteins were highly expressed in the hemolymph of the bacteria fed larvae, among them immune response related proteins arylphorin, apolipophorin III and gloverin. Expression response among 25 putative immune response-related genes were assayed via RT-qPCR. Seven showed more than fivefold up regulation in the presence of bacterial diet, with 22 in total being differentially expressed, among them apolipophorin III, cecropin, gallerimycin, gloverin, lysozyme, and phenoloxidase inhibiting enzyme. Finally, potential life-history trade-offs were studied, with pupation time and pupal mass being negatively affected in bacteria fed larvae.

Conclusion

The presence of bacteria in food, even if non-pathogenic, can trigger an immune response cascade with life history tradeoffs. Trichoplusia ni larvae are able to detect and respond to environmental microbes encountered in the diet, possibly even using midgut epithelial tissue as a sensing organ. Potential benefits of this immune system priming may outweigh the observed tradeoffs, as priming based on environmentally sensed bacterial may decrease risk of serious infection. These results show that food plant microbial communities represent a dynamic and unstudied part of the coevolutionary interactions between plants and their insect herbivores.
Cyclooxygenase inhibition lowers prostaglandin E2 release from articular cartilage and reduces apoptosis but not proteoglycan degradation following an impact load in vitro
Authors: Jeffrey Janet E , Aspden Richard M 
Published: December 2007

AbstractThis study investigated the release of prostaglandin E2 (PGE2) from cartilage following an impact load in vitro and the possible chondroprotective effect of cyclooxygenase-2 (COX-2) inhibition using non-steroidal anti-inflammatory drugs (NSAIDs).Explants of human articular cartilage were subjected to a single impact load in a drop tower, and then cultured for 6 days in the presence of either a selective COX-2 inhibitor (celecoxib; 0.01, 0.1, 1.0 and 10 μM) or a non-selective COX inhibitor (indomethacin; 0.1 and 10 μM). The concentrations of PGE2 and glycosaminoglycans (GAGs), a measure of cartilage breakdown, were measured in the explant culture medium at 3 and 6 days post-impact. Apoptotic cell death was measured in frozen explant sections by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) method.PGE2 levels were increased by more than 20-fold in the medium of explants at both 3 (p = 0.012) and 6 days (p = 0.004) following impact, compared with unloaded controls. In the presence of celecoxib and indomethacin, the PGE2 levels were reduced in a dose-related manner. These inhibitors, however, had no effect in reducing the impact-induced release of GAGs from the cartilage matrix. Addition of celecoxib and indomethacin significantly reduced the number of trauma-induced apoptotic chondrocytes in cartilage explant sections.In this study, a marked increase in PGE2 was measured in the medium following an impact load on articular cartilage, which was abolished by the selective COX-2 inhibitor, celecoxib, and non-selective indomethacin. These inhibitors reduced chondrocyte apoptosis but no change was observed in the release of GAGs from the explants, suggesting that the COX/PGE2 pathway is not directly responsible for cartilage breakdown following traumatic injury. Our in vitro study demonstrates that it is unlikely that COX-2 inhibition alone would slow down or prevent the development of secondary osteoarthritis.
The relationship between gastric emptying, plasma cholecystokinin, and peptide YY in critically ill patients
Authors: Nguyen Nam Q , Fraser Robert J , Bryant Laura K , Chapman Marianne J , Wishart Judith , Holloway Richard H , Butler Ross , Horowitz Michael 
Published: December 2007

Abstract
Background
Cholecystokinin (CCK) and peptide YY (PYY) are released in response to intestinal nutrients and play an important physiological role in regulation of gastric emptying (GE). Plasma CCK and PYY concentrations are elevated in critically ill patients, particularly in those with a history of feed intolerance. This study aimed to evaluate the relationship between CCK and PYY concentrations and GE in critical illness.

Methods
GE of 100 mL of Ensure® meal (106 kcal, 21% fat) was measured using a 13C-octanoate breath test in 39 mechanically ventilated, critically ill patients (24 males; 55.8 ± 2.7 years old). Breath samples for 13CO2 levels were collected over the course of 4 hours, and the GE coefficient (GEC) (normal = 3.2 to 3.8) was calculated. Measurements of plasma CCK, PYY, and glucose concentrations were obtained immediately before and at 60 and 120 minutes after administration of Ensure.

Results
GE was delayed in 64% (25/39) of the patients. Baseline plasma CCK (8.5 ± 1.0 versus 6.1 ± 0.4 pmol/L; P = 0.045) and PYY (22.8 ± 2.2 versus 15.6 ± 1.3 pmol/L; P = 0.03) concentrations were higher in patients with delayed GE and were inversely correlated with GEC (CCK: r = -0.33, P = 0.04, and PYY: r = -0.36, P = 0.02). After gastric Ensure, while both plasma CCK (P = 0.03) and PYY (P = 0.02) concentrations were higher in patients with delayed GE, there was a direct relationship between the rise in plasma CCK (r = 0.40, P = 0.01) and PYY (r = 0.42, P < 0.01) from baseline at 60 minutes after the meal and the GEC.

Conclusion
In critical illness, there is a complex interaction between plasma CCK, PYY, and GE. Whilst plasma CCK and PYY correlated moderately with impaired GE, the pathogenetic role of these gut hormones in delayed GE requires further evaluation with specific antagonists.
The Third Intracellular Loop of the Human Somatostatin Receptor 5 Is Crucial for Arrestin Binding and Receptor Internalization after Somatostatin Stimulation
Authors: Peverelli Erika , Mantovani Giovanna , Calebiro Davide , Doni Andrea , Bondioni Sara , Lania Andrea , Beck-Peccoz Paolo , Spada Anna 
Published: December 2007

AbstractSomatostatin (SS) is a widely distributed polypeptide that exerts inhibitory effects on hormone secretion and cell proliferation by interacting with five different receptors (SST1-SST5). β-Arrestins have been implicated in regulating SST internalization, but the structural domains mediating this effect are largely unknown. The aim of this study was to characterize the intracellular mechanisms responsible for internalization of human SST5 in the rat pituitary cell line GH3 and to identify the SST5 structural domains involved in this process. To this purpose we evaluated, by fluorescence microscopy and biochemical assay, the ability of wild-type, progressive C-terminal truncated and third cytoplasmatic loop mutants SST5-DsRed to associate with β-arrestin-enhanced green fluorescent protein and to internalize under SS28 stimulation. The truncated mutants were comparable to the wild-type receptor with respect to recruitment of β-arrestin-2 and internalization, whereas the third loop mutants R240W, S242A, and T247A showed the abolishment or reduction of arrestin association and a significant reduction of receptor internalization (14.4%, 29%, and 30.9% vs. 52.4% of wild type) and serine phosphorylation upon SS28 stimulation. Moreover, we evaluated the ability of simultaneous mutation of these three residues (R240, S242, and T247) and C-terminal truncated receptors to internalize. The progressive truncation of the C-terminal tail resulted in a progressive increased internalization (21.6%, 36.7%, and 41%, respectively) with respect to the full-length total third-loop mutant (15%). In conclusion, our results indicate the SST5 third intracellular loop as an important mediator of β-arrestin/receptor interaction and receptor internalization, whereas they suggest that residues 328–347 within the C terminus may play an inhibitory role in receptor internalization.
Glucocorticoid Prevents Brain-Derived Neurotrophic Factor-Mediated Maturation of Synaptic Function in Developing Hippocampal Neurons through Reduction in the Activity of Mitogen-Activated Protein Kinase
Authors: Kumamaru Emi , Numakawa Tadahiro , Adachi Naoki , Yagasaki Yuki , Izumi Aiko , Niyaz Madinyet , Kudo Motoshige , Kunugi Hiroshi 
Published: December 2007

Abstract
An increased level of glucocorticoid may be related to the pathophysiology of depressive disorder. The involvement of brain-derived neurotrophic factor (BDNF) in the antidepressive effect has also been suggested; however, the possible influence of glucocorticoid on the action of BDNF in the developing central nervous system has not been elucidated. In this study, we investigated the effect of glucocorticoid (dexamethasone, DEX) on synaptic maturation and function enhanced by BDNF in early developing hippocampal neurons. In the immature stage, BDNF increased the outgrowth of dendrites and the expression of synaptic proteins including glutamate receptors and presynaptic proteins. Pretreatment with DEX significantly inhibited the BDNF-dependent up-regulation of both dendritic outgrowth and synaptic proteins. In the more mature stage, the BDNF-reinforced postsynaptic Ca2+ influx was decreased by DEX. BDNF-enhanced presynaptic glutamate release was also suppressed. RU486, a glucocorticoid receptor antagonist, canceled the DEX-dependent blocking effect on the action of BDNF. After down-regulation of glucocorticoid receptor by small interfering RNA application, no inhibitory effect of DEX on the BDNF-increased synaptic proteins was observed. Interestingly, the BDNF-activated MAPK/ERK pathway, which is an essential intracellular signaling pathway for the BDNF-increased synaptic proteins, was reduced by DEX. These results suggest that BDNF-mediated synaptic maturation is disturbed after neurons are exposed to high-level glucocorticoid in their development stage.
Thomas Schmidt, Der Kalender und die Folgen. Uwe Johnsons Roman ‚Jahrestage‘. Ein Beitrag zum Problem des kollektiven Gedächtnisses. 2000
Authors: Kopfermann Thomas 
Published: December 2007

Die Kernfrage lautet: „Aus welchen Gründen, mit welchen Mitteln und zu welchen Zielen erinnert sich der einzelne einer Vergangenheit, die nicht die seine ist? Was fördert das Erinnern, und was steht ihm entgegen?“ Dieser Fragenkomplex wird als „Gretchenfragen jedes individuellen Umgangs mit der Vergangenheit“ etikettiert, „der über die eigene Beteiligung hinaus ins Feld etwa der politischen oder der kulturellen Geschichte reicht“ (S. 216). Auf eine solche Zentralfrage verallgemeinert, wird plötzlich sichtbar, in welchem aktuellen Diskussionsraum wir uns mit Gesine Cresspahl, auf die die Gretchenfragen gemünzt sind, und mit Johnsons Jahrestagen befinden. Die letzte, viel und heiß diskutierte Antwort stammte von Martin Walser, dem Freund-Feind Johnsons, in seinem Roman Ein springender Brunnen:
In Wirklichkeit wird der Umgang mit der Vergangenheit von Jahrzehnt zu Jahrzehnt strenger normiert. Je normierter dieser Umgang, umso mehr ist, was als Vergangenheit gezeigt wird, Produkt der Gegenwart … Die Vergangenheit als Fundus, aus dem man sich bedienen kann. Nach Bedarf. Eine komplett erschlossene, durchleuchtete, gereinigte, genehmigte, total gegenwartsgeeignete Vergangenheit. Ethisch, politisch durchkorrigiert … von allem befreit, was in ihr so war, wie wir es jetzt nicht mehr möchten. (S. 282f.)
Walsers Roman als Gegenmodell zu den Jahrestagen, als kritische Gegenposition?