bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prevalence, self‐efficacy and perceptions of conflicting advice and self‐management: effects of a breastfeeding journal
Authors: Hauck Yvonne , Hall Wendy A. , Jones Christine 
Published: January 2007

Abstract Title. Prevalence, self‐efficacy and perceptions of conflicting advice and self‐management: effects of a breastfeeding journal Aim.  This paper reports an assessment of the effects of a breastfeeding journal on breastfeeding prevalence and perceptions of conflicting advice, self‐management and self‐efficacy.Background.  Breastfeeding prevalence rates in most developed countries are not meeting recommendations. Women's concerns about inconsistent advice, limited involvement in decision‐making, accessibility of information and inappropriate follow‐up have been recognized. Research on evaluation of interventions addressing these concerns and including antenatal and early postnatal periods is required.Method.  An intervention study was conducted from July 2003 to April 2004, with control and intervention groups recruited sequentially. The intervention group received a breastfeeding journal at 36 weeks antenatally in breastfeeding classes that were attended at different times by intervention and control group members. The intervention and control groups were compared during postpartum hospitalization and 12 weeks for breastfeeding prevalence and perceptions of self‐efficacy, conflicting advice and self‐management.Findings.  No statistically significant differences were noted between the intervention and control groups in breastfeeding prevalence at 12 weeks or self‐efficacy during hospitalization. There was a statistically significant difference between groups in conflicting advice at both times. Although conflicting advice continues to present a dilemma for women, levels of conflicting advice did not explain breastfeeding self‐efficacy. Breastfeeding self‐management was a statistically significant contributor to breastfeeding prevalence prior to the addition of breastfeeding self‐efficacy.Conclusions.  Women's perceptions of their ability to manage and be actively involved in decision‐making explained breastfeeding prevalence at 12‐week postpartum. Efforts to encourage women's involvement in decision‐making about breastfeeding are a useful strategy to promote breastfeeding.
A dendritic cell‐based vaccine for treating HIV infection: background and preliminary results
Authors: Andrieu J. M. , Lu W. 
Published: January 2007

Abstract.  Antibody response against human immunodeficiency virus‐1 (HIV) is ineffective and cellular immune response is not strong enough to achieve the complete suppression or at least a strong control of viral replication in HIV‐ infected patients. In 2001, we showed in vitro that dendritic cells (DCs) of HIV‐infected patients loaded with autologous HIV chemically inactivated by aldrithiol‐2 were capable of raising an HIV‐specific cellular immune response powerful enough to allow the destruction of autologous HIV‐ infected CD4 T cells. In 2003, we showed that simian immunodeficiency virus (SIV)‐infected macaques vaccinated with inactivated SIV‐loaded autologous DCs raised a strong SIV‐specific cellular response. Ten months after vaccination, plasma viral load of 7 out of the 10 vaccinated monkeys remained 1000‐fold lower than initially.In December 2004, we published results observed in 18 untreated HIV‐infected patients vaccinated with autologous monocyte‐derived DCs loaded with autologous inactivated HIV. A year following vaccination, 8 patients had a plasma viral load decrease >90%; among them, 4 had viral load <1000 copies mL−1. Moreover, by one year, the viral load decline of the 18 patients was significantly correlated with their percentage of HIV‐1‐gag‐specific CD8+ T cells expressing perforin and that of HIV‐1‐specific CD4+ TH1 cells. This is the first demonstration of the capacity of a therapeutic vaccine to induce an effective HIV‐specific T cell response associated with sustained viral suppression in untreated viremic patients. The manipulation of antigen presenting cells to elicit virus‐specific cellular responses is a promising tool to control persistant viral infections.
The association between fibrinogen haplotypes and myocardial infarction in men is partly mediated through pleiotropic effects on the serum IL‐6 concentration
Authors: Mannila M. N. , Eriksson P. , Leander K. , Wiman B. , De Faire U. , Hamsten A. , Silveira A. 
Published: January 2007

Abstract.Background and objectives.  Fibrinogen haplotypes have been associated with risk of myocardial infarction (MI), independently of plasma fibrinogen concentration, and experimental data indicate that fibrinogen exerts pleiotropic effects on interleukin 6 (IL‐6) production. Also, the coagulation factor XIII (gene symbol F13A1) Val34Leu haplotype tag single nucleotide polymorphism (htSNP) has been reported to exert pleiotropic effects on serum IL‐6 concentration and to be associated with risk of MI. Therefore, in the present case–control study (a substudy to the Stockholm Heart Epidemiology Program), the effects of the fibrinogen gamma (FGG) 9340T>C [rs1049636], fibrinogen alpha (FGA) 2224G>A [rs2070011] and F13A1 Val34Leu [rs5985] htSNPs on concentrations of plasma fibrinogen and serum IL‐6 and risk of MI were assessed.Results.  There were no associations between these SNPs and the plasma fibrinogen concentration. In contrast, in male controls the FGA 2224G>A htSNP was significantly associated with serum IL‐6 concentration (P < 0.05). Also, in men the FGG‐FGA*1 haplotype (containing the major FGG 9340T and FGA 2224G alleles) was associated with increased risk of MI [adjusted odds ratio (OR) 95% confidence interval (CI): 1.29 (1.02, 1.62)] and with higher IL‐6 concentrations, whereas the least common FGG‐FGA*4 haplotype (containing the minor FGG 9340C and FGA 2224A alleles) conferred lowered risk [adjusted OR (95% CI): 0.70 (0.57, 0.86)] and lowered IL‐6 concentrations. In women, fibrinogen haplotypes were not associated with risk of MI after adjusting for cardiovascular risk factors.Conclusion.  In healthy men, fibrinogen haplotypes are associated with serum IL‐6 concentrations in a manner consistent with their impact on MI risk.
Use of inhaled and oral glucocorticoids, severity of inflammatory disease and risk of hip/femur fracture: a population‐based case–control study
Authors: De Vries F. , Pouwels S. , Lammers J. W. J. , Leufkens H. G. M. , Bracke M. , Cooper C. , Van Staa T. P. 
Published: January 2007

Abstract.Background.  Patients using higher dosages of inhaled or oral glucocorticoids (GCs) have an increased risk of hip/femur fractures. The role of the underlying disease in the aetiology of this increased risk has not been widely studied.Objective.  To evaluate the contribution of the underlying disease to the risk of hip/femur fracture in patients using inhaled or oral GCs.Design and subjects.  A case–control study within the Dutch PHARMO‐RLS database was conducted. Cases (n = 6763) were adult patients with a first hip/femur fracture during enrolment. Each case was matched to four controls by age, gender and region.Results.  The risk of hip/femur fracture increased with current use of inhaled GCs (crude OR 1.30, 95% CI:1.16–1.47) and with current use of oral GCs (crude OR 1.66, 95% CI: 1.46–1.90). After adjustment for disease severity, the risk of hip/femur fracture was no longer statistically significantly increased in inhaled GC users (adjusted OR 1.08, 95% CI: 0.91–1.27), whilst it remained elevated in oral GC users (adjusted OR 1.43, 95% CI: 1.22–1.67). Patients using inhaled GCs without any exposure to oral GCs had no increased risk of fracture (adjusted OR 0.98, 95% CI: 0.79–1.22).Conclusion.  Inhaled GC users had no increased risk of femur/hip fracture after adjustment for underlying disease severity. Our data suggest that, even at higher dosages, inhaled GC use is not an independent risk factor for fracture. In contrast, oral GC use was associated with an increased risk of fracture, which was not fully explained by the underlying disease severity.
Physical activity and exercise performance predict long‐term prognosis in middle‐aged women surviving acute coronary syndrome
Authors: Al‐Khalili F. , Janszky I. , Andersson A. , Svane B. , Schenck‐Gustafsson K. 
Published: January 2007

Abstract.Aim. To evaluate the importance of exercise testing (ET) parameters and leisure time physical activity in predicting long‐term prognosis in middle‐aged women hospitalized for acute coronary syndrome (ACS).Methods and results. Women aged <66 years recently hospitalized for ACS in the Greater Stockholm area in Sweden were recruited. All underwent baseline clinical examinations including ET and then were followed up for 9 years. Nonparticipation in ET had a hazard ratio of 4.26 (95% confidence interval 2.02–8.95) for total mortality and 3.03 (1.03–8.91) for cardiovascular mortality. All ET parameters were significantly different between survivors than nonsurvivors, except for chest pain and ST‐segment depression during ET. Sedentary lifestyle and ET parameters were related to total mortality and cardiovascular mortality in a multivariate analysis adjusting for potential confounders. Predictors of total mortality were sedentary lifestyle 2.94 (1.31–6.62), exercise time 1.75 (1.07–2.87) and inadequate haemodynamic responses: low increase in pulse rate 2.04 (1.16–3.60) and systolic blood pressure (SBP) 1.88 (1.19–2.95) from rest to peak exercise. Parameters that predicted cardiovascular mortality were sedentary lifestyle 3.15 (1.13–8.74) and poor increase in SBP 2.76 (1.30–5.86) from rest to peak exercise. The relation of sedentary lifestyle to survival was substantially weakened when exercise parameters were added to the multivariate analysis model.Conclusion. In female patients <66 years surviving ACS, important independent predictors of long‐term all‐cause mortality were sedentary lifestyle, low physical fitness and inadequate pulse rate and SBP increase during exercise. Predictors of cardiovascular mortality were sedentary lifestyle and inadequate blood pressure response during exercise.
Unilateral limited scleroderma‐like changes following formation of an arteriovenous fistula
Authors: Roberts Hugh , Curnow Paul A 
Published: January 2007

SUMMARYA 55‐year‐old man presented with a 1‐year history of progressive skin thickening involving the right hand associated with Raynaud’s phenomenon, sclerodactyly and painful cutaneous ulcers. An arteriovenous fistula for haemodialysis had been formed on the same arm 2 years previously. There were no symptoms or signs of systemic sclerosis or involvement of the contralateral arm. The limb was clinically ischaemic, attributed to a vascular steal phenomenon from the arteriovenous fistula, superimposed on occlusive arterial disease. A revascularization procedure was performed, which resulted in substantial improvement in the sclerodactyly, Raynaud’s phenomenon and hand function. Tissue hypoxia is believed to be a contributing factor in the pathogenesis of scleroderma, and this case demonstrates scleroderma‐like changes in the setting of limb ischaemia.
Kinases and phosphatases and tau sites involved in Alzheimer neurofibrillary degeneration
Authors: Wang Jian‐Zhi , Grundke‐Iqbal Inge , Iqbal Khalid 
Published: January 2007

AbstractMicrotubule associated protein (MAP) tau is abnormally hyperphosphorylated in Alzheimer's disease (AD) and related tauopathies; in this form it is the major protein subunit of paired helical filaments (PHF)/neurofibrillary tangles. However, the nature of protein kinases and phosphatases and tau sites involved in this lesion has been elusive. We investigated self‐assembly and microtubule assembly promoting activities of hyperphosphorylated tau isolated from Alzheimer disease brain cytosol, the AD abnormally hyperphosphorylated tau (AD P‐tau) before and after dephosphorylation by phosphoseryl/phosphothreonyl protein phosphatase‐2A (PP‐2A), and then rephosphorylation by cyclic AMP‐dependent protein kinase (PKA), calcium, calmodulin‐dependent protein kinase II (CaMKII), glycogen synthase kinase‐3β (GSK‐3β) and cyclin‐dependent protein kinase 5 (cdk5) in different kinase combinations. We found that (i) dephosphorylation of AD P‐tau by PP‐2A inhibits its polymerization into PHF/straight filaments (SF) and restores its binding and ability to promote assembly of tubulin into microtubules; (ii) rephosphorylation of PP‐2A‐dephosphorylated AD P‐tau by sequential phosphorylation by PKA, CaMKII and GSK‐3β or cdk5, and as well as by cdk5 and GSK‐3β, promotes its self‐assembly into tangles of PHF similar to those seen in Alzheimer brain, and (iii) phosphorylation of tau sites required for this pathology are Thr231 and Ser262, along with several sites flanking the microtubule binding repeat region. Phosphorylation of recombinant human brain tau441 yielded similar results as the PP‐2A dephosphorylated AD P‐tau, except that mostly SF were formed. The conditions for the abnormal hyperphosphorylation of tau that promoted its self‐assembly also induced the microtubule assembly inhibitory activity. These findings suggest that activation of PP‐2A or inhibition of either both GSK‐3β and cdk5 or one of these two kinases plus PKA or CaMKII might be required to inhibit Alzheimer neurofibrillary degeneration.
Restored plasticity in a mouse model of neurofibromatosis type 1 via inhibition of hyperactive ERK and CREB
Authors: Guilding Clare , McNair Kara , Stone Trevor W. , Morris Brian J. 
Published: January 2007

AbstractPatients with neurofibromatosis type 1 (NF1), resulting from neurofibromin gene mutations, frequently suffer from deficits in learning and spatial memory. Mice heterozygous for functional deletion of the NF1 gene (NF1+/– mice) also exhibit compromised spatial learning, and deficits in early‐stage hippocampal long‐term potentiation (LTP). Neurofibromin is a multifunctional protein which acts in part as an inhibitory constraint on Ras signalling, and the deficits in early‐stage LTP and spatial learning have been linked to Ras hyperactivation. However, the downstream targets of Ras hyperactivation that lead to cognitive disruption are unknown. The levels of activity of signalling molecules potentially downstream of Ras were therefore studied in NF1+/– mice. Elevated phospho‐ERK (pERK) levels were observed in the hippocampi from NF1+/– mice, while phospho‐Akt/PKB (pAkt) and phospho‐eIF4E (peIF4E) levels were unchanged relative to wild‐type mice. Hippocampal levels of phospho‐CREB (pCREB) were also increased, suggesting potential changes in late‐phase LTP in NF1+/– mice. Indeed, LTP was found to be impaired for at least 4 h following induction in NF1+/– mice, linking neurofibromin function with the long‐term maintenance of LTP. Remarkably, U0126, an inhibitor of ERK activation, at doses which reduced the hyperactive pERK levels in NF1+/– mice to the levels observed in control mice, caused a reduction in the deficits in early‐phase LTP and completely rescued the long‐term LTP deficits. In contrast to the abundant evidence that reductions in ERK activity lead to impaired plasticity, these data indicate that ERK hyperactivation in a partial model of type 1 neurofibromatosis leads to deficits in long‐lasting hippocampal plasticity.
Glycogen synthase kinase‐3 inhibition is integral to long‐term potentiation
Authors: Hooper Claudie , Markevich Vladimir , Plattner Florian , Killick Richard , Schofield Emma , Engel Tobias , Hernandez Felix , Anderton Brian , Rosenblum Kobi , Bliss Tim , Cooke Sam F. , Avila Jesús , Lucas José J. , Giese Karl Peter , Stephenson John , Lovestone Simon 
Published: January 2007

AbstractGlycogen synthase kinase‐3 (GSK‐3) is a serine/threonine kinase regulating diverse cellular functions including metabolism, transcription and cell survival. Numerous intracellular signalling pathways converge on GSK‐3 and regulate its activity via inhibitory serine‐phosphorylation. Recently, GSK‐3 has been involved in learning and memory and in neurodegeneration. Here, we present evidence that implicates GSK‐3 in synaptic plasticity. We show that phosphorylation at the inhibitory Ser9 site on GSK‐3β is increased upon induction of long‐term potentiation (LTP) in both hippocampal subregions CA1 and the dentate gyrus (DG) in vivo. The increase in inhibitory GSK‐3β phosphorylation is robust and persists for at least one hour postinduction. Furthermore, we find that LTP is impaired in transgenic mice conditionally overexpressing GSK‐3β. The LTP deficits can be attenuated/rescued by chronic treatment with lithium, a GSK‐3 inhibitor. These results suggest that the inhibition of GSK‐3 facilitates the induction of LTP and this might explain some of the negative effects of GSK‐3 on learning and memory. It follows that this role of GSK‐3β in LTP might underlie some of the cognitive dysfunction in diseases where GSK‐3 dysfunction has been implicated, including Alzheimer's and other dementias.
Earliest spontaneous activity differentially regulates neocortical GABAergic interneuron subpopulations
Authors: De Lima Ana D. , Lima Beatriz D. , Voigt Thomas 
Published: January 2007

AbstractAlthough less than one quarter of all neurons in the cerebral cortex are GABAergic, these neurons are morphologically diverse and their physiological complexity decisively moulds the network physiology. An important question is how different subpopulations of GABAergic neurons are regulated numerically during development. In rat neocortical cultures, neuronal precursors continue to divide, generating both GABAergic and non‐GABAergic neurons. In vitro generated GABAergic neurons form a population of uniquely small, mostly fusiform neurons that differ in size and morphology from older, in situ generated, large stellate GABAergic neurons. In a large series of experiments we investigated the impact of neuronal activity on the development of these two subpopulations of GABA interneurons present in cortical networks during the first 2 weeks in vitro. Here we show that a moderate increase in the generation of GABAergic neurons was achieved by blocking activity with tetrodotoxin, indicating that intrinsic spontaneous activity inhibits GABAergic neurogenesis in culture. Antagonists to ionotropic glutamate receptor and/or GABAA receptor did not significantly alter GABAergic generation but agonists to these receptors showed a time‐sensitive regulation of the size of small and large GABAergic neuronal subpopulations. Further, our results indicate that alterations of cell generation by activity manipulations might be overwritten by later activity effects on the survival of GABAergic cell populations.
Task‐dependent modulation of functional connectivity between hand motor cortices and neuronal networks underlying language and music: a transcranial magnetic stimulation study in humans
Authors: Sparing R. , Meister I. G. , Wienemann M. , Buelte D. , Staedtgen M. , Boroojerdi B. 
Published: January 2007

AbstractAlthough language functions are, in general, attributed to the left hemisphere, it is still a matter of debate to what extent the cognitive functions underlying the processing of music are lateralized in the human brain. To investigate hemispheric specialization we evaluated the effect of different overt musical and linguistic tasks on the excitability of both left and right hand motor cortices using transcranial magnetic stimulation (TMS). Task‐dependent changes of the size of the TMS‐elicited motor evoked potentials were recorded in 12 right‐handed, musically naive subjects during and after overt speech, singing and humming, i.e. the production of melody without word articulation. The articulation of meaningless syllables served as control condition. We found reciprocal lateralized effects of overt speech and musical tasks on motor cortex excitability. During overt speech, the corticospinal projection of the left (i.e. dominant) hemisphere to the right hand was facilitated. In contrast, excitability of the right motor cortex increased during both overt singing and humming, whereas no effect was observed on the left hemisphere. Although the traditional concept of hemispheric lateralization of music has been challenged by recent neuroimaging studies, our findings demonstrate that right‐hemisphere preponderance of music is nevertheless present. We discuss our results in terms of the recent concepts on evolution of language and gesture, which hypothesize that cerebral networks mediating hand movement and those subserving language processing are functionally linked. TMS may constitute a useful tool to further investigate the relationship between cortical representations of motor functions, music and language using comparative approaches.
A population of human brain parenchymal cells express markers of glial, neuronal and early neural cells and differentiate into cells of neuronal and glial lineages
Authors: Rieske Piotr , Azizi S. Ausim , Augelli Brian , Gaughan John , Krynska Barbara 
Published: January 2007

AbstractGlial fibrillary acidic protein (GFAP)‐positive cells derived from the neurogenic areas of the brain can be stem/progenitor cells and give rise to new neurons in vitro and in vivo. We report here that a population of GFAP‐positive cells derived from fetal human brain parenchyma coexpress markers of early neural and neuronal cells, and have neural progenitor cell characteristics. We used a monolayer culture system to expend and differentiate these cells. During the initial proliferative phase, all cells expressed GFAP, nestin and low levels of βIII‐tubulin. When these cells were cultured in serum and then basic fibroblast growth factor, they generated two distinct progenies: (i) βIII‐tubulin‐ and nestin‐positive cells and (ii) GFAP‐ and nestin‐positive cells. These cells, when subsequently cultured in serum‐free media without growth factors, ceased to proliferate and differentiated into two major neural cell classes, neurons and glia. In the cells of neuronal lineage, nestin expression was down‐regulated and βIII‐tubulin expression became robust. Cells of glial lineage differentiated by down‐regulating nestin expression and up‐regulating GFAP expression. These data suggest that populations of parenchymal brain cells, initially expressing both glial and neuronal markers, are capable of differentiating into single neuronal and glial lineages through asymmetric regulation of gene expression in these cells, rather than acquiring markers through differentiation.
Inhibition of Na+/K+ ATPase potentiates synaptic transmission in tactile sensory neurons of the leech
Authors: Scuri Rossana , Lombardo Paola , Cataldo Enrico , Ristori Chiara , Brunelli Marcello 
Published: January 2007

AbstractIncreasing evidence indicates that modulation of Na+/K+ ATPase activity is involved in forms of neuronal and synaptic plasticity. In tactile (T) neurons of the leech Hirudo medicinalis, Na+/K+ ATPase is the main determinant of the afterhyperpolarization (AHP), which characterizes the firing of these mechanosensory neurons. Previously, it has been reported that cAMP (3′,5′‐cyclic adenosine monophosphate), which mediates the effects of serotonin (5HT) in some forms of learning in the leech, negatively modulates Na+/K+ ATPase activity, thereby reducing the AHP amplitude in T neurons. Here, we show that a transient inhibition of Na+/K+ ATPase can affect the synaptic connection between two ipsilateral T neurons. Bath application of 10 nm dihydroouabain (DHO), an ouabain analogue, causes an increase in the amplitude of the synaptic potential (SP) recorded in the postsynaptic element when a test stimulus is applied in the presynaptic neuron. Iontophoretic injection of cAMP into the presynaptic T neuron also produces an increase of SP. Simulations carried out by using a computational model of the T neuron suggest that a reduction of the pump rate and a consequent depression of the AHP might facilitate the conduction of action potentials to the synaptic terminals. Moreover, nearly intact leeches injected with 10 nm DHO respond with a swimming episode more quickly to an electrical stimulation, which selectively activates T neurons exhibiting sensitization of swimming induction. Collectively, our results show that inhibition of Na+/K+ ATPase is critical for short‐term plasticity.