bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of coagulation processes on properties of epoxidized natural rubber
Authors: Zong‐Qiang Zeng , He‐Ping Yu , Qi‐Fang Wang , Guang Lu 
Published: April 2008

AbstractThe epoxidized natural rubber (ENR) with epoxy group contents of 48.4% were coagulated with ethanol and steam and the structures, processing performances, antioxidative behaviors, cure characteristics, and dynamic mechanical properties were analyzed using infrared spectroscopy, rubber processing analyzer, thermogravimetric analyzer, rheometer, and dynamic thermomechanical analyzer, respectively. The results indicate that the ENR coagulated with ethanol (ENR‐e) exhibits a compact structure and the contents of residual low‐molecular‐weight matters are higher than those of unconsolidated ENR coagulated with steam (ENR‐s). Therefore, the processing performance and antioxidative behavior as well as the curing characteristics of ENR‐e compound are poorer than those of ENR‐s. Although the mechanical properties and wet skid resistance of ENR‐s vulcanizate are poorer than those of ENR‐e, the heat build‐up or rolling resistance of ENR‐s is better than that of ENR‐e. © 2008 Wiley Periodicals, Inc. J Appl Polym Sci, 2008
Unique Microanatomy of Ileal Peyer's Patches of the One Humped Camel (Camelus dromedarius) is not Age‐Dependent
Authors: Zidan Mohamed , Pabst Reinhard 
Published: April 2008

AbstractThe Peyer's patches (PP) have been intensely investigated in several species because this is an important entry site for antigens and infectious agents. There are many PP in the jejunum, and in some species such as ruminants, carnivores, and omnivores, a different continuous PP is found in the terminal ileum. This PP disappears with age in these species studied. So far the ileal PP (IPP) has only been examined in the camel by light microscopy. Therefore, the localization of ileal Peyer's patches in the dromedary camel at different ages, as well as the histology and ultrastructures were now investigated. The IPP were characteristically seen as dark rose‐colored isolated structures in the shape of a cup, arranged in three irregular rows. The central row was antimesenteric. Each patch was formed by several mainly elongated dome regions flanked by intestinal villi. In cross‐sections these domes appeared as short, wide villi. The domes were formed from lymphoid follicles covered with a typical dome‐associated epithelium of enterocytes and M cells without any goblet cells. The M cells showed variable appearance depending on the functional status. The lymphoid follicles expressed clear germinal centers. High endothelial venules were localized in the interfollicular region. In contrast to other species the IPP were still present with a comparable macroscopic and histological structure in camels of 25 years of age. Anat Rec, 291:1023–1028, 2008. © 2008 Wiley‐Liss, Inc.
Effectiveness of medial‐wedge insole treatment for valgus knee osteoarthritis
Authors: Rodrigues Priscilla T. , Ferreira Ana F. , Pereira Rosa M. R. , Bonfá Eloísa , Borba Eduardo F. , Fuller Ricardo 
Published: April 2008

AbstractObjectiveTo assess the efficacy of medial‐wedge insoles in valgus knee osteoarthritis (OA).MethodsThirty consecutive women with valgus‐deformity knee OA ≥8 degrees were randomized into 2 groups: medial insole (insoles with 8‐mm medial elevation at the rearfoot [n = 16]) and neutral insole (similar insole without elevation [n = 14]). Both groups also wore ankle supports. A blinded examiner assessed pain on movement, at rest, and at night with a visual analog scale (VAS), the Lequesne index, and Western Ontario and McMaster Universities Osteoarthritis (WOMAC) Index. Femorotibial, talocalcaneal, and talar tilt angles were evaluated at baseline and after 8 weeks of insole use.ResultsSignificant reductions in the medial insole group were observed for pain on movement (mean ± SD VAS pre‐ and postintervention 8.1 ± 1.5 versus 4.2 ± 2.4; P = 0.001), at rest (5.1 ± 2.3 versus 2.7 ± 2.4; P = 0.002), and at night (6.1 ± 2.7 versus 3.1 ± 2.1; P = 0.001). In addition, a decrease in Lequesne (14.7 ± 3.4 versus 9.6 ± 3.8; P = 0.001) and WOMAC scores (74.1 ± 14.2 versus 56.1 ± 14.9; P = 0.001) was observed for the medial insole group. In the neutral insole group, a significant reduction was observed only for night pain (mean ± SD VAS pre‐ and postintervention 5.8 ± 2.4 versus 4.6 ± 2.4; P = 0.019). An increase in femorotibial angle (169.0 ± 3.4 versus 170.8 ± 3.7; P = 0.001) occurred only in the medial insole group. Moreover, the difference in measured femorotibial angles pre‐ and postintervention was 1.84 ± 1.42 versus −0.18 ± 0.67 (P < 0.001) for the medial and neutral insole groups.ConclusionThe use of medial‐wedge insoles was highly effective in reducing pain at rest and on movement and promoted a functional improvement of valgus knee OA.
Reducing joint loading in medial knee osteoarthritis: Shoes and canes
Authors: Kemp Georgina , Crossley Kay M. , Wrigley Tim V. , Metcalf Ben R. , Hinman Rana S. 
Published: April 2008

AbstractObjectiveIncreased medial knee loading is associated with a much higher risk of disease progression in knee osteoarthritis (OA). Interventions that can reduce medial knee joint load have the potential to slow disease progression over time. We evaluated the effects of shoes and a cane on knee load in people with knee OA.MethodsForty people with medial knee OA underwent 3‐dimensional gait analysis to measure their peak knee adduction moment, an indicator of medial knee joint load. Results when walking in bare feet were compared with those obtained when walking in their own usual shoes. Twenty participants also underwent testing using a cane, and results were compared with walking unaided.ResultsCompared with barefoot, walking in shoes was associated with a significant increase in the peak knee adduction moment (mean ± SD N × m/BW × H% 3.49 ± 0.84 versus 3.77 ± 0.90; P < 0.001), although there was considerable individual variation. The use of a cane resulted in a 10% decrease in the knee adduction moment (mean ± SD N × m/BW × H% 3.76 ± 0.95 versus 3.38 ± 0.68; P = 0.001).ConclusionWearing shoes increases medial knee joint load compared with walking barefoot. Given the variable response to shoes observed, further research is required to ascertain which shoe types might be optimal for those with knee OA. The use of a cane significantly reduces medial knee loading and has the potential to reduce the risk of disease progression in knee OA.
Long‐Wavelength Fluorescence from 2‐Aminopurine‐Nucleobase Dimers in DNA
Authors: Bonnist Eleanor Y. M. , Jones Anita C. 
Published: April 2008

AbstractWhen 2‐aminopurine (2AP) is substituted for adenine in DNA, it is widely accepted that its fluorescence spectrum is essentially unchanged from that of the free fluorophore. We show that 2AP in DNA exhibits long‐wavelength emission and excitation bands, in addition to the familiar short‐wavelength spectra, as a result of formation of a ground‐state heterodimer with an adjacent, π‐stacked, natural base. The observation of dual emission from 2AP in a variety of oligodeoxynucleotide duplexes and single strands demonstrates the generality of this phenomenon. The photophysical and conformational properties of the long‐wavelength‐emitting 2AP‐nucleobase dimer are examined. Analogous long‐wavelength fluorescence is seen when 2AP π‐stacks with aromatic amino acid sidechains in the active sites of methyltransferase enzymes during DNA nucleotide flipping.
Heck Reactions of 6‐ and 2‐Halopurines
Authors: Tobrman Tomáš , Dvořák Dalimil 
Published: April 2008

AbstractUnder the conditions of the Heck reaction, 9‐benzyl‐6‐iodopurine affords mainly the corresponding 6,6′‐dimer, the Heck product being formed only in low yield (≤12 %). With 7‐benzyl‐6‐iodopurine the dimerization is suppressed and the Heck product is obtained in 32–91 % yield. 9‐Substituted 6‐chloro‐2‐iodopurines react smoothly, giving 2‐alkenyl‐6‐chloropurines in 71–97 % isolated yields. The reaction proceeds with alkenes bearing electron‐withdrawing substituents (like CO2Bu, COCH3, CN) and Ph, while vinyl acetate and dodec‐1‐ene are unreactive. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2008)
Nuclear proteome analysis of undifferentiated mouse embryonic stem and germ cells
Authors: Buhr Nicolas , Carapito Christine , Schaeffer Christine , Kieffer Emmanuelle , Van Dorsselaer Alain , Viville Stéphane 
Published: April 2008

AbstractEmbryonic stem cells (ESCs) and embryonic germ cells (EGCs) provide exciting models for understanding the underlying mechanisms that make a cell pluripotent. Indeed, such understanding would enable dedifferentiation and reprogrammation of any cell type from a patient needing a cell therapy treatment. Proteome analysis has emerged as an important technology for deciphering these biological processes and thereby ESC and EGC proteomes are increasingly studied. Nevertheless, their nuclear proteomes have only been poorly investigated up to now. In order to investigate signaling pathways potentially involved in pluripotency, proteomic analyses have been performed on mouse ESC and EGC nuclear proteins. Nuclei from ESCs and EGCs at undifferentiated stage were purified by subcellular fractionation. After 2‐D separation, a subtractive strategy (subtracting culture environment contaminating spots) was applied and a comparison of ESC, (8.5 day post coïtum (dpc))‐EGC and (11.5 dpc)‐EGC specific nuclear proteomes was performed. A total of 33 ESC, 53 (8.5 dpc)‐EGC, and 36 (11.5 dpc)‐EGC spots were identified by MALDI‐TOF‐MS and/or nano‐LC‐MS/MS. This approach led to the identification of two isoforms (with and without N‐terminal acetylation) of a known pluripotency marker, namely developmental pluripotency associated 5 (DPPA5), which has never been identified before in 2‐D gel‐MS studies of ESCs and EGCs. Furthermore, we demonstrated the efficiency of our subtracting strategy, in association with a nuclear subfractionation by the identification of a new protein (protein arginine N‐methyltransferase 7; PRMT7) behaving as proteins involved in pluripotency.
Polydrug use, cannabis, and psychosis‐like symptoms
Authors: Van Dam Nicholas T , Earleywine Mitch , DiGiacomo Greg 
Published: April 2008

AbstractObjectiveTo examine psychosis‐like symptoms in users of legal and illicit drugs.MethodsSchizotypal Personality Questionnaire (SPQ) scores were compared in groups of people with different exposure to cannabis, with the use of other drugs serving as a covariate. Supplemental analyses compared users of legal and illicit drugs with cannabis use as a covariate.ResultsWeekly (n = 111) and monthly (n = 136) cannabis users had higher scores on the SPQ than former (n = 143) and non‐users (n = 81). The use of other drugs accounted for the links between cannabis and schizotypy. Lifetime use of psychomotor stimulant drugs plus ecstasy accounted for associations between cannabis and scores on the SPQ and its different subscales. Dividing groups by type of drug use revealed that those who used only cannabis and legal drugs (CLDs) (n = 126) were no different from those who used only legal drugs (LDs) (n = 74) but both groups scored significantly lower on the SPQ than polydrug users (n = 247). When controlling for marijuana use in the last month, the significant difference across drug use groups remained.ConclusionsThe results suggest that research on marijuana and schizotypy requires careful assessment of the use of other drugs, especially psychomotor stimulants and ecstasy. Copyright © 2008 John Wiley & Sons, Ltd.
Characterization of BASP1‐mediated neurite outgrowth
Authors: Korshunova Irina , Caroni Pico , Kolkova Kateryna , Berezin Vladimir , Bock Elisabeth , Walmod Peter S. 
Published: April 2008

AbstractThe brain acid‐soluble protein BASP1 (CAP‐23, NAP‐22) belongs to the family of growth‐associated proteins, which also includes GAP‐43, a protein recently shown to regulate neural cell adhesion molecule (NCAM)‐mediated neurite outgrowth. Here, the effects of BASP1 overexpression were investigated in PC12E2 cells and primary hippocampal neurons. BASP1 overexpression stimulated neurite outgrowth in both cell types. The effects of BASP1 and trans‐homophilic NCAM interactions were additive, and BASP1‐induced neurite outgrowth was not inhibited by ectopic expression of cytoplasmic NCAM domains. Furthermore, inhibition of signaling via the fibroblast growth factor receptor, Src‐family nonreceptor tyrosine kinases, protein kinase C, or GSK3β, and expression of constructs of the cytoskeletal proteins spectrin and tau inhibited NCAM‐ but not BASP1‐induced neurite outgrowth. Expression of BASP1 mutated at the serine‐5 phosphorylation site stimulated neurite outgrowth to a degree comparable to that observed in response to overexpression of wild‐type BASP1, whereas expression of BASP1 mutated at the myristoylation site at glycine‐1 completely abrogated the stimulatory effects of the protein on neurite outgrowth. Finally, coexpression experiments with dominant negative and wild‐type versions of GAP‐43 and BASP1 demonstrated that the two proteins could substitute for each other with respect to induction of NCAM‐independent neurite outgrowth, whereas BASP1 was unable to replace the stimulatory effect of GAP‐43 on NCAM‐mediated neurite outgrowth. These observations demonstrate that BASP1 and GAP‐43 have overlapping, but not identical, functions in relation to neurite outgrowth and indicate that the main function of BASP1 is to regulate the organization and morphology of the plasma membrane. © 2008 Wiley‐Liss, Inc.
Age‐related decreases in NAD(P)H and glutathione cause redox declines before ATP loss during glutamate treatment of hippocampal neurons
Authors: Parihar Mordhwaj S. , Kunz Elizabeth A. , Brewer Gregory J. 
Published: April 2008

AbstractAge‐related glutamate excitotoxicity depends in an unknown manner on active mitochondria, which are key determinants of the cellular redox potential. Compared with embryonic and middle‐aged neurons, old‐aged rat hippocampal neurons have a lower resting reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) and a lower redox ratio (NAD(P)H/flavin adenine nucleotide). Glutamate treatment resulted in an initial increase in NAD(P)H concentrations in all ages, followed by a profound calcium‐dependent, age‐related decline in NAD(P)H concentration and redox ratio. With complex I of the electron transport chain inhibited by rotenone, treatment with glutamate or ionomycin only resulted in the increase in NAD(P)H fluorescence. High‐performance liquid chromatography analysis of adenine nucleotides in brain extracts showed 50% less nicotinamide adenine dinucleotide (NADH) and almost twice as much oxidized nicotinamide adenine dinucleotide, demonstrating a more oxidized ratio in old than middle‐aged brain. Resting glutathione content also declined with age and further decreased with glutamate treatment without accompanying changes in adenosine triphosphate levels. We conclude that age does not affect production of NADH by dehydrogenases but that old‐aged neurons consume more NADH and glutathione, leading to a catastrophic decline in redox ratio. © 2008 Wiley‐Liss, Inc.
Huperzine A attenuates mitochondrial dysfunction after middle cerebral artery occlusion in rats
Authors: Zheng Chun Yan , Zhang Hai Yan , Tang Xi Can 
Published: April 2008

AbstractMitochondrial dysfunction has been proved to contribute to ischemia‐induced brain damage. In this study, which used a rat middle cerebral artery occlusion (MCAO) model, the protective effects of huperzine A (HupA) against mitochondrial dysfunction and brain damage were investigated. MCAO for 45 min followed by 4 hr of reperfusion significantly impaired the activities of mitochondrial respiratory chain enzymes (complex I, complex II–III, and complex IV) and α‐ketoglutarate dehydrogenase, increased the production of reactive oxygen species (ROS), and induced mitochondrial swelling. Pretreatment of HupA at 0.1 mg/kg significantly preserved respiratory chain enzyme activities, decreased ROS production, and attenuated mitochondrial swelling. It could also significantly attenuate the neurological deficits (after 4 or 24 hr reperfusion) and reduce infarct volumes (after 24 hr reperfusion). Moreover, HupA protected isolated nonsynaptosomal mitochondria from calcium‐induced damage in vitro by preserving mitochondrial membrane potential and decreasing ROS production. Overall, the present study indicates that HupA can ameliorate MCAO‐induced mitochondrial dysfunction, and this might partially contribute to its protective effect on brain damage after 24 hr of reperfusion. © 2008 Wiley‐Liss, Inc.
Antipsychotic drugs up‐regulate tryptophan hydroxylase in ADF neurons of Caenorhabditis elegans: Role of calcium‐calmodulin‐dependent protein kinase II and transient receptor potential vanilloid channel
Authors: Donohoe Dallas R. , Phan Thang , Weeks Kathrine , Aamodt Eric J. , Dwyer Donard S. 
Published: April 2008

AbstractAntipsychotic drugs produce acute behavioral effects through antagonism of dopamine and serotonin receptors, and long‐term adaptive responses that are not well understood. The goal of the study presented here was to use Caenorhabditis elegans to investigate the molecular mechanism or mechanisms that contribute to adaptive responses produced by antipsychotic drugs. First‐generation antipsychotics, trifluoperazine and fluphenazine, and second‐generation drugs, clozapine and olanzapine, increased the expression of tryptophan hydroxylase‐1::green fluorescent protein (TPH‐1::GFP) and serotonin in the ADF neurons of C. elegans. This response was absent or diminished in mutant strains lacking the transient receptor potential vanilloid channel (TRPV; osm‐9) or calcium/calmodulin‐dependent protein kinase II (CaMKII; unc‐43). The role of calcium signaling was further implicated by the finding that a selective antagonist of calmodulin and a calcineurin inhibitor also enhanced TPH‐1::GFP expression. The ADF neurons modulate foraging behavior (turns/reversals off food) through serotonin production. We found that short‐term exposure to the antipsychotic drugs altered the frequency of turns/reversals off food. This response was mediated through dopamine and serotonin receptors and was abolished in serotonin‐deficient mutants (tph‐1) and strains lacking the SER‐1 and MOD‐1 serotonin receptors. Consistent with the increase in serotonin in the ADF neurons induced by the drugs, drug withdrawal after 24‐hr treatment was accompanied by a rebound in the number of turns/reversals, which demonstrates behavioral adaptation in serotonergic systems. Characterization of the cellular, molecular, and behavioral adaptations to continuous exposure to antipsychotic drugs may provide insight into the long‐term clinical effects of these medications. © 2008 Wiley‐Liss, Inc.
Interactive roles of fibroblast growth factor 2 and neurotrophin 3 in the sequence of migration, process outgrowth, and axonal differentiation of mouse cochlear ganglion cells
Authors: Hossain Waheeda A. , D'Sa Chrystal , Morest D. Kent 
Published: April 2008

AbstractA growth factor may have different actions depending on developmental stage. We investigated this phenomenon in the interactions of fibroblast growth factor 2 (FGF2) and neurotrophins on cochlear ganglion (CG) development. The portions of the otocyst fated to form the CG and cochlear epithelium were cocultured at embryonic day 11 (E11). Cultures were divided into groups fed with defined medium, with or without FGF2 and neurotrophin supplements, alone or in combination, for 7 days. We measured the number of migrating neuroblasts and distances migrated, neurite outgrowth, and axonlike processes. We used immunohistochemistry to locate neurotrophin 3 (NT3) and its high‐affinity receptor (TrkC) in the auditory system, along with FGF2 and its R1 receptor, at comparable developmental stages in vitro and in situ from E11 until birth (P1) in the precursors of hair cells, support cells, and CG cells. Potential sites for interaction were localized to the nucleus, perikaryal cytoplasm, and cell surfaces, including processes and growth cones. Time‐lapse imaging and quantitative measures support the hypothesis that FGF2 alone or combined with neurotrophins promotes migration and neurite outgrowth. Synergism or antagonism between NT3 and other factors suggest interactions at the receptor level. Formation of axons, endings, and synaptic vesicle protein 2 were increased by interactions of NT3 and FGF2. Similar experiments with a mutant overexpressor for FGF2 suggest that endogenous FGF2 supports migration and neurite outgrowth of CG neuroblasts as well as proliferation, leading to accelerated development. The findings suggest interactive and sequential roles for FGF2 and NT3. © 2008 Wiley‐Liss, Inc.
Runx2 is expressed in human glioma cells and mediates the expression of galectin‐3
Authors: Vladimirova Valentina , Waha Andreas , Lückerath Katharina , Pesheva Penka , Probstmeier Rainer 
Published: April 2008

AbstractRunx2 is a member of the Runx family of transcription factors (Runx1–3) with a restricted expression pattern. It has so far been detected predominantly in skeletal tissues where, inter alia, it regulates the expression of the β‐galactoside‐specific lectin galectin‐3. Here we show that, in contrast to Runx3, Runx1 and Runx2 are expressed in a variety of human glioma cells. Runx2 expression pattern in these cells correlated completely with that of galectin‐3, but not with that of other galectins. A similar correlation in the expression pattern of galectin‐3 and Runx2 transcripts was detected in distinct types of 70 primary neural tumors, such as glioblastoma multiforme, but not in others, such as gangliocytomas. In glioma cells, Runx2 is directly involved in the regulation of galectin‐3 expression, as shown by RNAi and transcription factor binding assays demonstrating that Runx2 interacts with a Runx2‐binding motif present in the human galectin‐3 promoter. Knockdown of Runx2 was thus accompanied by a reduction of both galectin‐3 mRNA and protein levels by at least 50%, dependent on the glial tumor cell line tested. Reverse transcriptase–polymerase chain reaction analyses, aimed at finding other potential target genes of Runx2 in glial tumor cells, revealed the presence of bone sialoprotein, osteocalcin, osteopontin, and osteoprotegerin. However, their expression patterns only partially overlap with that of Runx2. These data suggest a functional contribution of Runx‐2‐regulated galectin‐3 expression to glial tumor malignancy. © 2008 Wiley‐Liss, Inc.
Swedish amyloid precursor protein mutation increases cell cycle‐related proteins in vitro and in vivo
Authors: Ahn Kwang‐Woo , Joo Yuyoung , Choi Yoori , Kim Minji , Lee Sang Hyoung , Cha Seok‐Ho , Suh Yoo‐Hun , Kim Hye‐Sun 
Published: April 2008

AbstractReactivation of the cell cycle, including DNA replication, might play a major role in Alzheimer's disease. In this study, we report that the expressions of Swedish double mutation of amyloid precursor protein (Swe‐APP) or of the APP intracellular domain (AICD) into nerve growth factor (NGF)‐differentiated PC12 cells or rat primary cortical neurons increased mRNA and protein levels of cyclin D1 and cyclin B1. Treatment with lithium chloride (a glycogen synthase kinase‐3β inhibitor) down‐regulated cyclin B1 induced by Swe‐APP expression but up‐regulated cyclin D1 expression induced by Swe‐APP, suggesting that glycogen synthase kinase‐3β activity is involved in these expression changes of cyclins D1 and B1. Swe‐APP, which is a prevailing cause of familial Alzheimer's disease, is well known to increase amyloid beta peptide production both in vitro and in vivo, but the underlying molecular means whereby it leads to the pathogenesis of AD remains unknown. The finding that cyclin D1 and B1 expressions were up‐regulated by Swe‐APP in in vitro cultured cells was substantiated in the brain tissues of Tg2576 mice, which harbor the Swe‐APP mutation. These results suggest that some disturbances in cell cycle regulation may be involved in Swe‐APP or AICD‐induced neurodegeneration and that these contribute to the pathogenesis of AD. © 2008 Wiley‐Liss, Inc.