bluuebunny/crossref_metadata_2025_split huggingface dataset:
Short to long term mortality of patients hospitalised with heart failure in the Czech Republic—a report from the EuroHeart Failure Survey
Authors: Rosolova Hana , Cech Jakub , Simon Jaroslav , Spinar Jindrich , Jandova Ruzena , Widimský sen Jiri , Holubec Lubomir , Topolcan Ondrej 
Published: July 2005

AbstractBackground and aim:The European Society of Cardiology initiated the EuroHeart Failure Survey to obtain more data about the quality of care in patients hospitalised with suspected heart failure (HF). The Czech Republic was 1 of the 24 European Society countries included in the survey. The aim of this report is to extend the original follow‐up period of 12 weeks out to 4 years to assess mortality.Methods:All admitted patients were screened according to the EuroHeart Survey Protocol, over a 6‐week period in six hospitals in Pilsen, Prague and Brno in the year 2000. Annual mortality and cause of death were obtained from the Prague Institute for Health Statistical Information (UZIS Praha).Results:A total of 2365 patients were screened and about 25% of all admitted patients fulfilled the criteria for HF. About 14% of patients died between admission and the 12‐week follow‐up, 36% of male and 42% of female patients died during the 4‐year follow‐up (2000–2003). Cardiovascular diseases were the main causes of death (92%). Deceased patients were significantly older, had lower haemoglobin and total plasma cholesterol level, and had renal insufficiency and higher levels of big endothelin and BNP than the survivors. Mortality risk was increased independently by positive history of previous myocardial infarction OR=2.39 (1.59–3.59), by age OR=1.03 (1.01–1.05) and by plasma creatinine level OR=1.04 (1.01–1.07). Treatment with diuretics and digoxin was associated with a higher risk of death; by contrast, a protective effect of beta‐blockers and statins was found in these HF patients.Conclusion:Patients with HF were older and had a poor prognosis; approximately one third of the patients will die within 3 years.
Short‐ and long‐term results of a programme for the prevention of readmissions and mortality in patients with heart failure: Are effects maintained after stopping the programme?
Authors: Ojeda Soledad , Anguita Manuel , Delgado Mónica , Atienza Felipe , Rus Carmen , Granados Amador L. , Ridocci Federico , Vallés Federico , Velasco Jose A. 
Published: July 2005

AbstractAbstractThe objective of the study was to evaluate whether improvements obtained during an intervention programme were maintained after the programme was stopped. 153 patients discharged with a diagnosis of heart failure (HF) were randomized to either usual care or an intervention programme, which included patient education, consultation with the cardiologist and monitoring in the Heart Failure Unit. After an average period of 16±8 months, the intervention programme was stopped. One year later, all the patients were re‐examined to assess HF readmissions, all‐cause mortality, quality of life, and prescribed medical treatment. During the 16±8‐month treatment period, patients in the intervention group had a lower rate of HF readmissions (17% vs. 51%, p<0.01), less all‐cause mortality (13% vs. 27%, p=0.03), improvement in quality of life (1.5±0.8 vs. 1.9±1, p=0.03) and optimisation of medical treatment was achieved. One year after stopping the intervention, there was no difference in HF readmissions (28% vs. 25%, p=0.72), all‐cause mortality (14% vs. 17%, p=0.64) and quality of life (1.7±0.9 vs. 1.8±1, p=0.24) between the groups. Survival and the probability of not being readmitted due to HF were similar in both groups. There was also a reduction in the use of beta‐blockers and spironolactone in the intervention group.ConclusionsThe positive effects of an intervention programme are clearly reduced when it is stopped, due to less strict control of the patients and a decrease in the use of drugs with proven efficacy in HF.
Treatment of rectosigmoid endometriosis by laparoscopically assisted vaginal rectosigmoidectomy
Authors: Abrao M.S. , Sagae U.E. , Gonzales M. , Podgaec S. , Dias J.A. 
Published: July 2005

AbstractObjective: To describe the use of mechanical anastomoses in cases of laparoscopically assisted vaginal rectosigmoidectomy for the treatment of rectosigmoid endometriosis. Methods: Pilot study evaluating eight patients with rectosigmoid endometriosis referred for surgical treatment. All patients were submitted to laparoscopically assisted vaginal segmental resection of the rectosigmoid with anastomoses performed using linear and circular staplers. Results: The average length of the surgical procedure was 177.5 min and average duration of hospitalization was 4.13 days. There were no intra‐operative complications and integrity of the anastomoses was confirmed in all patients. One patient reported partial improvement of symptoms and 7 patients presented complete clinical remission 12 months following surgery. Conclusion: Laparoscopically assisted vaginal segmental resection of the sigmoid infiltrated by endometriosis is a feasible surgical procedure. The technique combines transvaginal access with mechanical intestinal anastomoses performed using linear and circular staplers, and achieves good results with low morbidity.
Stock returns and inflation in Greece: A Markov switching approach
Authors: Hondroyiannis George , Papapetrou Evangelia 
Published: July 2005

AbstractThe paper studies the dynamic relationship between real stock returns and expected and unexpected inflation utilizing a Markov Switching vector autoregressive model (MS‐VAR). The MS‐VAR model has the advantage that it is able to capture the dependence structure of the series both in terms of mean and variance. Univariate and multivariate innovation decompositions are employed to separate inflation into two components, the expected and unexpected. The empirical evidence suggests that real stock returns are not related to expected and unexpected inflation and this result is independent of the method used to separate inflation into the two components. Rather, the results suggest that stock market movements are regime dependent, implying that stock market performance is not predictable.
A direct interview family study of obsessive–compulsive disorder. I
Authors: FYER ABBY J. , LIPSITZ JOSHUA D. , MANNUZZA SALVATORE , ARONOWITZ BONNIE , CHAPMAN TIMOTHY F. 
Published: July 2005

Background. This and the companion paper present two sequential family studies of obsessive–compulsive disorder (OCD) conducted by the same research group, but with different sampling and best-estimate procedures. In addition to providing further data on familial transmission of OCD, we used comparison of disparate findings (moderate, specific familial aggregation in this first study versus a stronger effect for other anxiety disorders than for OCD alone in the second) to examine possible effects of proband characteristics and informant data on outcome.Method. In this initial study we interviewed 179 first-degree relatives of 72 OCD probands and 112 relatives of 32 never mentally ill (NMI) controls. Informant data were obtained on an additional 126 relatives (total ‘combined’ samples of 263 and 154 respectively). Analyses used best-estimate diagnoses made by consensus of two ‘blinded’ senior clinicians who reviewed all diagnostic materials including proband informant data about relatives.Results. Significantly higher risk for OCD but not other anxiety disorders was found in relatives of OCD probands compared to relatives of controls in both the directly interviewed and combined samples. There was no relationship between proband age at onset of OCD and strength of familial aggregation.Conclusions. These data indicate moderate familial aggregation of OCD, but do not support increased transmission by early onset probands, or a familial relationship between OCD and other anxiety disorders with the possible exception of generalized anxiety disorder.
Genetic and pharmacological inactivation of the adenosine A2A receptor attenuates 3‐nitropropionic acid‐induced striatal damage
Authors: Fink J. Stephen , Kalda Anti , Ryu Hoon , Stack Edward C. , Schwarzschild Michael A. , Chen Jiang‐Fan , Ferrante Robert J. 
Published: July 2005

AbstractAdenosine A2A receptor (A2AR) antagonism attenuates 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐induced dopaminergic neurodegeneration and quinolinic acid‐induced excitotoxicity in the neostriatum. As A2ARs are enriched in striatum, we investigated the effect of genetic and pharmacological A2A inactivation on striatal damage produced by the mitochondrial complex II inhibitor 3‐nitropriopionic acid (3‐NP). 3‐NP was administered to A2AR knockout (KO) and wild‐type (WT) littermate mice over 5 days. Bilateral striatal lesions were analyzed from serial brain tissue sections. Whereas all of the 3‐NP‐treated WT mice (C57BL/6 genetic background) had bilateral striatal lesions, only one of eight of the 3‐NP‐treated A2AR KO mice had detectable striatal lesions. Similar attenuation of 3‐NP‐induced striatal damage was observed in A2AR KO mice in a 129‐Steel background. In addition, the effect of pharmacological antagonism on 3‐NP‐induced striatal neurotoxicity was tested by pre‐treatment of C57Bl/6 mice with the A2AR antagonist 8‐(3‐chlorostyryl) caffeine (CSC). Although bilateral striatal lesions were observed in all mice treated either with 3‐NP alone or 3‐NP plus vehicle, there were no demonstrable striatal lesions in mice treated with CSC (5 mg/kg) plus 3‐NP and in five of six mice treated with CSC (20 mg/kg) plus 3‐NP. We conclude that both genetic and pharmacological inactivation of the A2AR attenuates striatal neurotoxicity produced by 3‐NP. Since the clinical and neuropathological features of 3‐NP‐induced striatal damage resemble those observed in Huntington's disease, the results suggest that A2AR antagonism may be a potential therapeutic strategy in Huntington's disease patients.
Lipopolysaccharide‐induced increase in signalling in hippocampus is abrogated by IL‐10 – a role for IL‐1β?
Authors: Lynch Aileen M. , Walsh Christine , Delaney Ada , Nolan Yvonne , Campbell Veronica A. , Lynch Marina A. 
Published: July 2005

AbstractParenterally administered lipopolysaccharide (LPS) increases the concentration of the pro‐inflammatory cytokine interleukin‐1β (IL‐1β) in the rat hippocampus and evidence suggests that this effect plays a significant role in inhibiting long‐term potentiation (LTP). The anti‐inflammatory cytokine IL‐10, antagonizes certain effects of IL‐1β, so if the effects of LPS are mediated through an increase in IL‐1β, it might be predicted that IL‐10 would also abrogate the effect of LPS. Here, we report that IL‐10 reversed the inhibitory effect of LPS on LTP and the data couple this with an inhibitory effect on the LPS‐induced increase in IL‐1β. LPS treatment increased hippocampal expression of IL‐1 receptor Type I protein. Consistent with the LPS‐induced increases in IL‐1β concentration and receptor expression, were downstream changes which included enhanced phosphorylation of IRAK and the stress‐activated kinases, JNK and p38; these LPS‐induced changes were reversed by IL‐10, which concurs with the idea that these events are triggered by increased activation of IL‐1RI by IL‐1β. We provide evidence which indicates that LPS treatment leads to evidence of cell death and this was reversed in hippocampus prepared from LPS‐treated rats which received IL‐10. The evidence is therefore consistent with the idea that IL‐10 acts to protect neuronal tissue from the detrimental effects induced by LPS.
The role of neutral sphingomyelinase produced ceramide in lipopolysaccharide‐mediated expression of inducible nitric oxide synthase
Authors: Won Je‐Seong , Im Yeong‐Bin , Khan Mushfiquddin , Singh Avtar K. , Singh Inderjit 
Published: July 2005

AbstractLipopolysaccharide (LPS) and interferon‐γ (IFN) treatment of C6 rat glioma cells increased the intracellular ceramide level and the expression of the inducible nitric oxide synthase (iNOS) gene. To delineate the possible role of ceramide in the induction of iNOS, we examined the source of intracellular ceramide and associated signal transduction pathway(s) with the use of inhibitors of intracellular ceramide generation. The inhibitor of neutral sphingomyelinase (3‐O‐methylsphingomyelin, MSM) inhibited the induction of iNOS, whereas inhibitor of acidic sphingomyelinase (SR33557) or that of ceramide de novo synthesis (fumonisin B1) had no effect on the induction of iNOS. MSM‐mediated inhibition of iNOS induction was reversed by the supplementation of exogenous C8‐ceramide, suggesting that ceramide production by neutral sphingomyelinase (nSMase) is a key mediator in the induction of iNOS. The MSM‐mediated inhibition of iNOS gene expression correlated with the decrease in the activity of ras. Inhibition of co‐transfected iNOS promoter activity by dominant negative ras supported the role of ras in the nSMase‐dependent regulation of iNOS gene. NF‐κB DNA binding activity and its transactivity were also reduced by MSM pretreatment, and were completely reversed by the supplementation of C8‐ceramide. As the dominant negative ras also reduced NF‐κB transactivity, NF‐κB activation may be downstream of ras. Our results suggest that ceramide generated by nSMase may be a critical mediator in the regulation of iNOS gene expression via ras‐mediated NF‐κB activation under inflammatory conditions.
Phospholipase D2 modulates agonist‐induced µ‐opioid receptor desensitization and resensitization
Authors: Koch Thomas , Brandenburg Lars‐Ove , Liang Yingjian , Schulz Stefan , Beyer Andrea , Schröder Helmut , Höllt Volker 
Published: July 2005

AbstractReceptor phosphorylation, arrestin binding, uncoupling from G protein and subsequent endocytosis have been implicated in G protein‐coupled receptor desensitization after chronic agonist exposure. In search of proteins regulating the µ‐opioid receptor endocytosis, we have recently established that activation of phospholipase D (PLD)2 is required for agonist‐induced µ‐opioid receptor endocytosis. In this study, we determined the effect of PLD2 activity on the desensitization and resensitization rate of the µ‐opioid receptor. We clearly demonstrated that inhibition of PLD2‐mediated phosphatidic acid formation by alcohol (1‐butanol or ethanol) or overexpression of a dominant negative mutant of PLD2 prevented agonist‐mediated endocytosis and resulted in a faster desensitization rate of the µ‐opioid receptor after chronic (d‐Ala2, Me Phe4, Glyol5)enkephalin treatment in human embryonic kidney 293 cells. Moreover, inhibition of PLD2 activity led to an impairment of the resensitization rate of the µ‐opioid receptor. In summary, our data strongly suggest that PLD2 is a modulator of agonist‐induced endocytosis, desensitization and resensitization of the µ‐opioid receptor.
Amyloid‐β‐induced toxicity of primary neurons is dependent upon differentiation‐associated increases in tau and cyclin‐dependent kinase 5 expression
Authors: Liu Tianbing , Perry George , Chan Hsien W. , Verdile Giuseppe , Martins Ralph N. , Smith Mark A. , Atwood Craig S. 
Published: July 2005

AbstractIt has previously been reported that amyloid‐β (Aβ) peptide is neurotrophic to undifferentiated but neurotoxic to differentiated primary neurons. The underlying reasons for this differential effect is not understood. Recently, the toxicity of Aβ to neurons was shown to be dependent upon the activation of cyclin‐dependent kinase 5 (Cdk5), thought to promote tau phosphorylation that leads to cytoskeletal disruption, morphological degeneration and apoptosis. Here we report that Cdk5, tau, and phosphorylated‐tau (P‐tau) are expressed at very low levels in undifferentiated primary neurons, but that the expression of Cdk5 and tau and the phosphorylation of tau increase markedly between 4 and 8 days of differentiation in vitro. Tau expression decreased after this time, as did the level of P‐tau, to low levels by 17 days. Aβ induced tau phosphorylation of neurons only after ≥ 4 days of differentiation, a time that coincides with the onset of Aβ toxicity. Blocking tau expression (and therefore tau phosphorylation) with an antisense oligonucleotide completely blocked Aβ toxicity of differentiated primary neurons, thereby confirming that tau was essential for mediating Aβ toxicity. Our results demonstrate that differentiation‐associated changes in tau and Cdk‐5 modulate the toxicity of Aβ and explain the opposite responses of differentiated and undifferentiated neurons to Aβ. Our results predict that only cells containing appreciable levels of tau are susceptible to Aβ‐induced toxicity and may explain why Aβ is more toxic to neurons compared with other cell types.
Homodimerization of adenosine A2A receptors: qualitative and quantitative assessment by fluorescence and bioluminescence energy transfer
Authors: Canals Meritxell , Burgueño Javier , Marcellino Daniel , Cabello Núria , Canela Enric I. , Mallol Josefa , Agnati Luigi , Ferré Sergi , Bouvier Michel , Fuxe Kjell , Ciruela Francisco , Lluis Carmen , Franco Rafael 
Published: July 2005

AbstractThe results presented in this paper show that adenosine A2A receptor (A2AR) form homodimers and that homodimers but not monomers are the functional species at the cell surface. Fluorescence resonance energy transfer (FRET) and bioluminescence resonance energy transfer (BRET) techniques have been used to demonstrate in transfected HEK293 cells homodimerization of A2AR, which are heptaspanning membrane receptors with enriched expression in striatum. The existence of homodimers at the cell surface was demonstrated by time‐resolved FRET. Although agonist activation of the receptor leads to the formation of receptor clusters, it did not affect the degree of A2AR–A2AR dimerization. Both monomers and dimers were detected by immunoblotting in cell extracts. However, cell surface biotinylation of proteins has made evident that more than 90% of the cell surface receptor is in its dimeric form. Thus, it seems that homodimers are the functional form of the receptor present on the plasma membrane. A deletion mutant version of the A2A receptor, lacking its C‐terminal domain, was also able to form both monomeric and dimeric species when cell extracts from transfected cells were analyzed by immunoblotting. This suggests that the C‐terminal tail does not participate in the dimerization. This is relevant as the C‐terminal tail of A2AR is involved in heteromers formed by A2AR and dopamine D2 receptors. BRET ratios corresponding to A2AR–A2AR homodimers were higher than those encountered for heterodimers formed by A2AR and dopamine D2 receptors. As A2AR and dopamine D2 receptors do indeed interact, these results indicate that A2AR homodimers are the functional species at the cell surface and that they coexist with A2AR/D2 receptor heterodimers.
Toll‐like receptor 2 (TLR2) mediates astrocyte activation in response to the Gram‐positive bacterium Staphylococcus aureus
Authors: Esen Nilufer , Tanga Flobert Y. , DeLeo Joyce A. , Kielian Tammy 
Published: July 2005

AbstractAstrocytes play an important role in initiating and regulating CNS immune responses through the release of proinflammatory cytokines and chemokines. Here we demonstrate that primary astrocytes are capable of recognizing the Gram‐positive bacterium Staphylococcus aureus and its cell wall product peptidoglycan (PGN) and respond by producing numerous proinflammatory mediators including interleukin‐1β (IL‐1β), tumor necrosis factor‐α (TNF‐α), macrophage inflammatory protein‐1β (MIP‐1β), MIP‐2, and monocyte chemoattractant protein (MCP‐1). Astrocytes have recently been shown to express Toll‐like receptor 2 (TLR2), a pattern recognition receptor important for recognizing structural components of various Gram‐positive bacteria, fungi, and protozoa. However, the functional significance of TLR2 in mediating astrocyte activation remains unknown. Primary astrocytes from TLR2 knockout mice were used to evaluate the role of TLR2 in astrocyte responses to S. aureus and PGN. The results demonstrate that TLR2 is essential for maximal proinflammatory cytokine and chemokine production, but not phagocytosis, in primary astrocytes following S. aureus and PGN exposure. In addition, both stimuli led to a significant increase in TLR2 mRNA expression in wild‐type astrocytes as assessed by real‐time quantitative RT–PCR. These findings suggest that astrocytes may play a key role in the initial antibacterial immune response in the CNS through engagement of TLR2.
Helicobacter pylori Colonization in Infants in a Periurban Community in Karachi, Pakistan
Authors: Nizami Shaikh Qamaruddin , Bhutta Zulfiqar Ahmed , Weaver Lawrence , Preston Tom 
Published: July 2005

ABSTRACTBackground:The prevalence and incidence of Helicobacter pylori in children in Pakistan is not known.Objectives:To measure the prevalence and age of acquisition of Helicobacter pylori infection/colonization in infants in a peri‐urban community in Karachi, Pakistan.Setting:Field based epidemiologic study in a peri‐urban community in Karachi, Pakistan.Methods:Infants aged 1 to 3 months were recruited from a birth cohort from the community. 13C‐urea breath test (13C‐UBT) was performed on recruitment, and the test was repeated at 2, 3, 6, and 9 months of age.Results:One hundred forty‐eight infants were recruited and had 13C‐UBT on 319 occasions over a period of 2 years. Two hundred thirty‐one = (72%) tests were positive: 80% (49/61) infants at 1 month of age, 79% (33/42) at 2 month of age, 76% (92/121) at 3 month of age, 58% (37/64) at 6 months of age, and 67% (20/30) at 9 months of age.Conclusions:The study reveals an early colonization/infection of infants and a high prevalence of Helicobacter pylori in a peri‐urban community in Karachi, Pakistan.
Whole Body Bone Mineral Content Is Similar at Discharge from the Hospital in Premature Infants Receiving Fortified Breast Milk or Preterm Formula
Authors: De Schepper Jean , Cools Filip , Vandenplas Yvan , Louis Olivia 
Published: July 2005

ABSTRACTBackground:Prematurely born infants, especially those with very low birth weight (<1500 g) are at risk for metabolic bone disease.Objectives:The influence of the type of oral feeding regimen and of other potential determinants of whole bone mineral content in prematurely born infants, when they approached full gestation, were evaluated. Previous studies have mainly examined effects at the level of regional bone.Methods:34 infants (21males and 13 females), all born between 25.4 and 33.7 weeks of gestation, were studied before discharge. Whole body bone mineral content measurements were made just before hospital discharge using a commercial densitometer (Hologic QDR 4500, Hologic Inc, Waltham, MA) at a median age of 40 days (range, 10 to 115 days) after birth.Results:Expressed as a percentage of whole body mass, bone mass ranged between 0.86% and 1.99%, was similar between girls and boys and correlated positively with birth weight SD (r = 0.42; P < 0.05) and body weight SD (r = 0.35; P < 0.05). No difference in bone mass percentage was found between the different types of oral feedings (fortified human milk and preterm formula) or medications studied (corticoids and diuretics).Conclusions:Whereas prenatal and postnatal weight gain determines the degree of bone mineralization of premature infants, it appears that the type of oral feeding does not affect differently the postnatal bone mineralization of premature infants, when assessed at the moment of discharge.