bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sequence Analysis of Bacterial Artificial Chromosome Clones from the Apospory-Specific Genomic Region ofPennisetumandCenchrus
Authors: Conner Joann A. , Goel Shailendra , Gunawan Gunawati , Cordonnier-Pratt Marie-Michele , Johnson Virgil Ed , Liang Chun , Wang Haiming , Pratt Lee H. , Mullet John E. , DeBarry Jeremy , Yang Lixing , Bennetzen Jeffrey L. , Klein Patricia E. , Ozias-Akins Peggy 
Published: May 2008

AbstractApomixis, asexual reproduction through seed, is widespread among angiosperm families. Gametophytic apomixis in Pennisetum squamulatum and Cenchrus ciliaris is controlled by the apospory-specific genomic region (ASGR), which is highly conserved and macrosyntenic between these species. Thirty-two ASGR bacterial artificial chromosomes (BACs) isolated from both species and one ASGR-recombining BAC from P. squamulatum, which together cover approximately 2.7 Mb of DNA, were used to investigate the genomic structure of this region. Phrap assembly of 4,521 high-quality reads generated 1,341 contiguous sequences (contigs; 730 from the ASGR and 30 from the ASGR-recombining BAC in P. squamulatum, plus 580 from the C. ciliaris ASGR). Contigs containing putative protein-coding regions unrelated to transposable elements were identified based on protein similarity after Basic Local Alignment Search Tool X analysis. These putative coding regions were further analyzed in silico with reference to the rice (Oryza sativa) and sorghum (Sorghum bicolor) genomes using the resources at Gramene (www.gramene.org) and Phytozome (www.phytozome.net) and by hybridization against sorghum BAC filters. The ASGR sequences reveal that the ASGR (1) contains both gene-rich and gene-poor segments, (2) contains several genes that may play a role in apomictic development, (3) has many classes of transposable elements, and (4) does not exhibit large-scale synteny with either rice or sorghum genomes but does contain multiple regions of microsynteny with these species.
SCAMPs Highlight the Developing Cell Plate during Cytokinesis in Tobacco BY-2 Cells
Authors: Lam Sheung Kwan , Cai Yi , Hillmer Stefan , Robinson David G. , Jiang Liwen 
Published: May 2008

Abstract
We previously demonstrated that rice (Oryza sativa) SECRETORY CARRIER MEMBRANE PROTEIN1 (OsSCAMP1)-yellow fluorescent protein in transgenic tobacco (Nicotiana tabacum) Bright Yellow-2 cells locates to the plasma membrane and to motile punctate structures, which represent the trans-Golgi network/early endosome and are tubular-vesicular in nature. Here, we now show that SCAMPs are diverted to the cell plate during cytokinesis dividing Bright Yellow-2 cells. As cells progress from metaphase to cytokinesis, punctate OsSCAMP1-labeled structures begin to collect in the future division plane. Together with the internalized endosomal marker FM4-64, they then become incorporated into the cell plate as it forms and expands. This was confirmed by immunogold electron microscopy. We also monitored for the Golgi apparatus and the prevacuolar compartment (PVC)/multivesicular body. Golgi stacks tend to accumulate in the vicinity of the division plane, but the signals are clearly separate to the cell plate. The situation with the PVC (labeled by green fluorescent protein-BP-80) is not so clear. Punctate BP-80 signals are seen at the advancing periphery of the cell plate, which was confirmed by immunogold electron microscopy. Specific but weak labeling was observed in the cell plate, but no evidence for a fusion of the PVC/multivesicular body with the cell plate could be obtained. Our data, therefore, support the notion that cell plate formation is mainly a secretory process involving mass incorporation of domains of the trans-Golgi network/early endosome membrane. We regard the involvement of multivesicular late endosomes in this process to be equivocal.
Case ascertainment and estimated incidence of drug‐induced long‐QT syndrome: study in Southwest France
Authors: Molokhia Mariam , Pathak Atul , Lapeyre‐Mestre Maryse , Caturla Laetitia , Montastruc Jean Louis ,   L'Association Française des Centres Régionaux de Pharmacovigilance (CRPV), McKeigue Paul 
Published: May 2008

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT • Drug‐induced long‐QT syndrome (LQTS) is a potentially fatal condition that has led to a number of postmarketing withdrawals in recent years.• However, many cases may not survive long enough to reach hospital, and only a small proportion are reported to pharmacovigilance agencies.• The extent to which genetic determinants of susceptibility to LQTS are specific to particular drugs, or common to several classes of drug, remains to be determined. WHAT THIS STUDY ADDS • We estimated population prevalence of drug‐induced LQTS in the Midi‐Pyrenees region, southwest France, using five different institutions and assessed feasibility of tracing potential cases (in addition to pharmacovigilance data), using hospital data and rigorous case definition.• These methods can be adapted to a wider region, used to augment pharmacovigilance reporting, and offer researchers the opportunity to study genetic susceptibility to drug‐induced LQTS.AIMSThe aim of this study was to investigate the incidence and reporting rate of drug‐induced long‐QT syndrome (LQTS) in France [defined by evidence of torsades de pointes (TdP), QT prolongation and exposure to a relevant drug] and to assess feasibility of case collection for drug‐induced LQTS.METHODSA retrospective population‐based study was carried out in Southwest France in five institutions: three main hospitals, one private clinic and one cardiac emergency unit, searched from 1 January 1999 to 1 January 2005 (population coverage of 614 000). The study population consisted of 861 cases with International Classification of Diseases‐10 diagnostic codes for ventricular tachycardia (I147.2), ventricular fibrillation (I149.0) and sudden cardiac death (I146.1) from hospital discharge summaries, supplemented by cases reported to national or regional pharmacovigilance systems, and voluntary reporting by physicians, validated according to internationally defined criteria for drug‐induced LQTS.RESULTSOf 861 patients coded with arrhythmias or sudden cardiac death, there were 40 confirmed surviving acquired cases of drug‐induced LQTS. We estimated that the incidence of those who survive to reach hospital drug‐induced LQTS is approximately 10.9 per million annually in France (95% confidence interval 7.8, 14.8).CONCLUSIONSMany cases of drug‐induced LQTS may not survive before they reach hospital, as the reporting rate for drug‐induced LQTS identified through the cardiology records and also reported to pharmacovigilance systems for the Midi‐Pyrenees area is 3/40 (7.5%). Using the methods outlined it is possible to assemble cases to study genetic susceptibility to drug‐induced LQTS and adapt these methods more widely.
Neuro‐mediators as predictors of paediatric atopic dermatitis
Authors: Wang I. J. , Hsieh W. S. , Guo Y. L. , Jee S. H. , Hsieh C. J. , Hwang Y. H. , Chen P. C. 
Published: May 2008

SummaryBackground
Attempts to identify predictors of atopic dermatitis (AD) have focused on genetic and immunologic factors. However, the role of neuro‐mediators remains to be elucidated.Objective
To evaluate nerve growth factor (NGF) and vaso‐active intestinal peptide (VIP) in predicting paediatric AD and assess their correlation with intrinsic and extrinsic types of AD.Methods
We performed a nested case–control study in the prospective Taiwan birth panel cohort study. Cord and maternal plasma and questionnaires were gathered at birth. During follow‐up, we identified 40 available AD cases, which were matched to 80 unaffected controls chosen from this cohort. The concentrations of IgE, NGF, and VIP in cord and maternal plasma of these subjects were performed by ELISA. Receiver‐operating characteristic (ROC) curves were generated to see how well each biomarker could predict AD.Results
The NGF levels were significantly higher in AD patients than controls (mean±SD: 65.47±44.45 vs. 49.21±12.18 pg/mL for cord plasma and 89.68±41.04 vs. 66.96±23.05 pg/mL for maternal plasma) (P<0.05). VIP levels were also higher but not statistically significant. Plasma NGF may be a better biomarker than IgE in detecting paediatric AD (area under the ROC curve=0.65 vs. 0.61 for cord plasma and 0.69 vs. 0.61 for maternal plasma). Maternal NGF levels were significantly higher in patients with both intrinsic (96.18±48.15 pg/mL) and extrinsic (86.18±37.23 pg/mL) types of AD compared with controls (66.96±23.05 pg/mL) (P<0.05). We assessed a significant correlation between self‐reported stress during pregnancy and maternal NGF levels (r=0.22, P=0.02).Conclusion
Our results suggest that NGF is a good alternative biomarker in predicting children with a risk of AD.
Multiple controls for the variability of hydrogen isotopic compositions in higher plant n‐alkanes from modern ecosystems
Authors: LIU WEIGUO , YANG HONG 
Published: May 2008

AbstractWe performed a global scale analysis of available leaf wax n‐alkane δD data compiled from our new results, as well as from the literature and expressed as average values of D/H ratios from three common lipids of n‐alkanes with odd carbon numbers (n‐C27, n‐C29, and n‐C31) from living higher plants. Our results clearly indicate multiple controls of hydrogen isotope composition and its variability in plants leaf wax. (1) At the global scale, precipitation δD values play a dominating factor that exercises the first order of control for hydrogen isotopic compositions in plant leaf wax. The hydrogen isotopic composition of plant leaf wax tracks the decreasing trend of precipitation δD with increasing latitude. (2) Because of different water acquisition systems, plant life form influences the hydrogen isotopic composition of leaf wax n‐alkanes with woody plants and grasses having different responses to the change of global precipitation δD. (3) Physiological difference, due to different photosynthesis pathways or different water usage strategies, can leave an imprint on δD patterns of plant leaf waxes, causing δD variations among plants using the same source water. While these results better explain the variability of hydrogen isotope composition in leaf wax, they also have important implications for the interpretation of n‐alkane δD data from fossils and ancient sediments.
Biological functions and clinical implications of oestrogen receptors alfa and beta in epithelial tissues
Authors: Morani A. , Warner M. , Gustafsson J.‐Å. 
Published: May 2008

Abstract.For the past 10 years it is known that oestrogen functions through the activation of two oestrogen receptors (ERα and ERβ). To the great surprise of endocrinologists, ERβ was found to be widely distributed in tissues throughout the body including tissues previously considered as ‘oestrogen insensitive’. The epithelium of the ventral prostate and lung as well as ovarian granulosa cells are ERα‐negative but ERβ‐positive and in these tissues ERβ seems to be involved in important physiological processes, like differentiation, extracellular matrix organization and stromal–epithelial communication. In tissues where both ERs are expressed, the two receptors seem to counteract each other. In the uterus, mammary gland and immune system, ERα promotes proliferation whereas ERβ has pro‐apoptotic and pro‐differentiating functions. The challenge of the future will be to develop specific agonists, which can selectively activate/inactivate either ERα or ERβ. These pharmaceuticals are likely to be of clinical importance in the prevention or treatment of various diseases.
Central nervous system involvement in severe congenital neutropenia: neurological and neuropsychological abnormalities associated with specific HAX1 mutations
Authors: Carlsson G. , Van’t Hooft I. , Melin M. , Entesarian M. , Laurencikas E. , Nennesmo I. , Trębińska A. , Grzybowska E. , Palmblad J. , Dahl N. , Nordenskjöld M. , Fadeel B. , Henter J‐I 
Published: May 2008

Abstract.Objectives.  Homozygous mutations in the HAX1 gene were recently identified in severe congenital neutropenia patients belonging to the original Kostmann family in northern Sweden. Our observations suggested that these patients also develop neurological and neuropsychological symptoms.Methods.  Detailed clinical studies and mutation analyses were performed in the surviving patients belonging to the Kostmann kindred and in two patients not related to this family, along with studies of HAX1 splice variant expression in normal human tissues.Results.  Five of six Kostmann family patients and one other patient from northern Sweden harboured homozygous HAX1 mutations (568C→T, Q190X) and one carried a heterozygous ELA2 gene mutation. One Swedish patient of Kurdish extraction carried alternative homozygous HAX1 mutations (131G→A, W44X). All the three patients with Q190X mutations who were alive and available for evaluation developed neurological disease with decreased cognitive function, and three of four patients who reached 10 years developed epilepsy. In contrast, the patients with the ELA2 and W44X HAX1 mutations, respectively, showed no obvious neurological abnormalities. Moreover, two alternative HAX1 splice variants were identified in normal human tissues, including the brain. Both transcripts contained exon 5, harbouring the Q190X mutation, whereas the 5′ end of exon 2 containing the W44X mutation was spliced out from the second transcript.Conclusions.  We describe neurological and neuropsychological abnormalities for the first time in Kostmann disease patients. These central nervous system symptoms appear to be associated with specific HAX1 mutations.
A common haplotype of the C‐C chemokine receptor 2 gene and HLA‐DRB1*0301 are independent genetic risk factors for Löfgren’s syndrome
Authors: Spagnolo P. , Sato H. , Grunewald J. , Brynedal B. , Hillert J. , Mañá J. , Wells A. U. , Eklund A. , Welsh K. I. , Du Bois R. M. 
Published: May 2008

Abstract.Aim.  Sarcoidosis is a heterogeneous disorder with a strong genetic influence. Genetic factors are also thought to influence disease severity and outcome. We sought to determine whether polymorphisms within CCR2 gene predispose to Löfgren’s syndrome – a clinically and genetically distinct sarcoidosis phenotype – and, importantly, whether this association is independent of the known association with the HLA‐DRB1*0301 allele.Methods.  We investigated 5 CCR2 variants and HLA‐DRB1*0301 by sequence‐specific primer (SSP) polymerase chain reaction (PCR) in 176 Spanish (76 Löfgren’s syndrome, 100 controls) and 387 Swedish subjects (126 Löfgren’s syndrome, 77 non‐Löfgren sarcoidosis, 184 controls).Results.  One of the deduced haplotypes (CCR2 haplotype 2) was associated with Löfgren’s syndrome in both Spanish (OR: 2.03, uncorrected P = 0.02; permuted P = 0.041 vs. controls) and Swedish patients (OR: 3.02, uncorrected P = 0.0007; permuted P = 0.0027 vs. non‐Löfgren sarcoidosis; OR: 2.46, uncorrected P = 0.0005; permuted P = 0.0031 vs. controls). HLA‐DRB1*0301 allele frequency was also increased in Spanish (OR: 3.52, P = 0.0004 vs. controls) and Swedish patients with Löfgren’s syndrome (OR: 10.98, P < 0.0001 vs. non‐Löfgren sarcoidosis, OR: 7.71, P < 0.0001 vs. controls). Finally, multivariate analysis revealed that the CCR2 association was independent of HLA‐DRB1*0301 in both Spanish (P = 0.02 vs. controls) and Swedish cohorts (P = 0.002 vs. non‐Löfgren sarcoidosis, P = 0.001 vs. controls).Conclusions.  This study confirms that CCR2 haplotype 2 and HLA‐DRB1*0301 are independent genetic risk factors for Löfgren’s syndrome.
Combined effects of obesity and physical activity in predicting mortality among men
Authors: Orsini N. , Bellocco R. , Bottai M. , Pagano M. , Michaelsson K. , Wolk A. 
Published: May 2008

Abstract.Objective.  We evaluated the hypothesis that higher levels of total daily physical activity can eliminate the increased mortality rate associated with overweight and obesity.Design.  Population‐based prospective cohort study.Setting.  Central Sweden.Subjects.  A total of 37 633 men at baseline 45–79 years of age and free of known cancer and cardiovascular disease and diabetes completed a self‐administered life‐style questionnaire, which included questions on body‐mass index (BMI) and physical activity. During 9.7 years of follow‐up, we identified a total of 4086 deaths.Main outcome measures.  Mortality rate ratios (RRs).Results.  Compared to men who were lean (BMI < 25 kg m−2) and active (top tertile of total physical activity level) the multivariable adjusted RRs (95% confidence interval) of death from all causes were 1.44 (1.11–1.86) for obese (BMI ≥ 30 kg m−2) and active men, 1.54 (1.34–1.77) for lean (BMI < 25 kg m−2) but inactive (bottom tertile) men, and 1.81 (1.48–2.23) for obese‐inactive men. After excluding the first 3 years of follow‐up, current and former smokers, those who had lost weight from age 20 years to age at baseline, and heavy manual workers, the adjusted RRs of death from all causes were 1.65 (1.20–2.27) for overweight‐to‐obese and active men, 2.15 (1.59–2.91) for lean‐inactive men, and 2.04 (1.52–2.74) for overweight‐to‐obese and inactive men compared to lean‐active men.Conclusions.  We conclude that both overweight and physical inactivity are important predictors of mortality. Our findings do not support the hypothesis that a higher level of physical activity compensates the excess mortality associated with overweight and obesity.
Introduction of a real‐time based blood group genotyping approach
Authors: Polin H. , Danzer M. , Pröll J. , Hofer K. , Heilinger U. , Zopf A. , Gabriel C. 
Published: May 2008

Background and Objective  Genotyping may be applied for rare blood group polymorphisms in a high‐throughput mode as well for the molecular determination of blood groups due to unclear serological results.Material and Methods  We developed and validated a DNA typing method for the determination of KEL1/2, JK1/2, FY1/2, FY0, MNS1/2, MNS3/4, DO1/2, CO1/2 and LU1/2 alleles using a melting curve analysis downstream from a fully automated DNA extraction. All assays were validated in terms of specificity, sensitivity, assay variability and robustness. The usability was proven by a batch of 200 blood samples with partially known phenotype.Results  Assays for all blood groups were within the range of specificity (100%), assay variability and robustness (coefficient of variance < 3%). Genotypes of 200 random platelet donors were fully consistent with existing phenotype data. The obtained genotype distribution is in complete concordance with existing data for the European population underlined by a complete absence of CO2 homozygous donors and the FY0 allele among the cohort.Conclusion  We introduce an approach for blood group genotyping of particular samples or gene loci in glass capillary format and for medium‐throughput analysis in 96/384‐well format. The advantages of this real‐time polymerase chain reaction method are its automation potential, the flexibility regarding hardware and the rapid cycling time.
Inflammatory pain is enhanced in delta opioid receptor‐knockout mice
Authors: Gavériaux‐Ruff Claire , Karchewski Laurie A. , Hever Xavier , Matifas Audrey , Kieffer Brigitte L. 
Published: May 2008

AbstractTo examine the involvement of opioid receptors in inflammatory pain, we compared Complete Freund’s Adjuvant‐induced hyperalgesia in mice lacking mu, delta or kappa receptors under the same experimental conditions. Mechanical allodynia and thermal hyperalgesia were measured using von Frey filaments and the plantar test, respectively. All three receptor‐knockout mice, as well as wild‐type animals, developed inflammatory hyperalgesia following Complete Freund’s Adjuvant administration. Mu‐receptor mutants showed similar hyperalgesia to wild‐types in the two tests. Kappa‐receptor mutants exhibited enhanced mechanical allodynia compared with wild‐type mice but similar thermal hyperalgesia. In contrast, mechanical allodynia and thermal hyperalgesia were both markedly augmented in delta‐receptor mutants, indicating a role for an endogenous delta‐receptor tone in the control of inflammatory pain. Treatment with the delta‐selective agonist SNC80 produced antihyperalgesia, and this effect was abolished in the delta‐receptor knockout mice. Altogether, these data demonstrate that delta receptors inhibit inflammatory pain when activated either endogenously or exogenously. We have previously shown enhanced neuropathic pain in delta‐receptor knockout mice. The delta receptor definitely represents a promising target for treating chronic pain conditions.
Changes in nucleus accumbens dopamine transmission associated with fixed‐ and variable‐time schedule‐induced feeding
Authors: Richardson Nicole R. , Gratton Alain 
Published: May 2008

AbstractWe examined the changes in nucleus accumbens (NAcc) dopamine (DA) transmission associated with non‐contingent meal presentations under conditions of high (fixed time‐, FT‐schedule) and low (variable time‐, VT‐schedule) predictability. Of interest were the changes in NAcc DA transmission associated with discrepancies between the time food is expected and when it is actually presented. We used in vivo voltammetry to monitor NAcc DA levels as rats received, on the first and second test days, 30‐s meals of condensed milk on a VT‐52 schedule (inter‐meal intervals of 32, 35, 40, 45, 52, 64, and 95 s). On the third and subsequent days meals were presented first on a VT‐52 s schedule and then on an FT‐52 s schedule. On day 1, monotonic increases in NAcc DA signals were observed during both meal consumption and the intervals between VT meal presentations. By day 2, however, meal presentations on the VT schedule elicited biphasic DA signal fluctuations; DA signals increased prior to each meal presentation but then started to decline during the feeding bout that followed. Fixed‐time meal presentations on day 3 disrupted this pattern, resulting in a concurrent escalation of DA signal fluctuations upon subsequent VT meal presentations. These findings provide further evidence that, in trained animals, NAcc DA transmission is activated by conditioned incentive cues rather than by primary rewards. They also suggest that the increases in NAcc DA transmission associated with reward expectancy are sensitive to temporal cues (e.g. interval timing) and to discrepancies between expected and actual outcomes.
Endomorphin‐2 is released from newborn rat primary sensory neurons in a frequency‐ and calcium‐dependent manner
Authors: Scanlin Heather L. , Carroll Elizabeth A. , Jenkins Victoria K. , Balkowiec Agnieszka 
Published: May 2008

AbstractRecent evidence indicates that endomorphins, endogenous mu‐opioid receptor (MOR) agonists, modulate synaptic transmission in both somatic and visceral sensory pathways. Here we show that endomorphin‐2 (END‐2) is expressed in newborn rat dorsal root ganglion (DRG) and nodose‐petrosal ganglion complex (NPG) neurons, and rarely co‐localizes with brain‐derived neurotrophic factor (BDNF). In order to examine activity‐dependent release of END‐2 from neurons, we established a model using dispersed cultures of DRG and NPG cells activated by patterned electrical field stimulation. To detect release of END‐2, we developed a novel rapid capture enzyme‐linked immunosorbent assay (ELISA), in which END‐2 capture antibody was added to neuronal cultures shortly before their electrical stimulation. The conventional assay was effective at reliably detecting END‐2 only when the cells were stimulated in the presence of CTAP, a MOR‐selective antagonist. This suggests that the strength of the novel assay is related primarily to rapid capture of released END‐2 before it binds to endogenous MORs. Using the rapid capture ELISA, we found that stimulation protocols known to induce plastic changes at sensory synapses were highly effective at releasing END‐2. Removal of extracellular calcium or blocking voltage‐activated calcium channels significantly reduced the release. Together, our data provide the first evidence that END‐2 is expressed by newborn DRG neurons of all sizes found in this age group, and can be released from these, as well as from NPG neurons, in an activity‐dependent manner. These results point to END‐2 as a likely mediator of activity‐dependent plasticity in sensory pathways.