bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fracture risk associated with smoking: a meta‐analysis
Authors: Vestergaard P. , Mosekilde L. 
Published: November 2003

Abstract.Objectives.  To assess fracture risk associated with smoking.Design.  Systematic review.Data sources.  Cohort, case–control, and cross‐sectional studies identified by searching PubMed and EMBASE, and by recursive screening of reference lists.Subjects.  Fifty studies including 512 399 subjects were included.Main outcome measure.  Fracture occurrence in current, previous, and never smokers.Results.  Fracture risk was significantly increased in current smokers for all fracture types combined (pooled relative risk 1.26, 95% CI 1.12–1.42) and for hip (1.39, 95% CI 1.23–1.58) and spine fractures (1.76, 95% CI 1.10–2.82), but not for wrist fractures (0.86, 95% CI 0.46–1.60). In previous smokers the estimate was significantly lower for as well all types of fractures (1.02, 95% CI 0.85–1.22, P = 0.03 compared with current smokers), as for hip fractures (1.19, 95% CI 1.06–1.34, P = 0.04). There was a trend towards higher risk estimates in previous smokers for hip fractures in case–control studies than in cohort studies. A similar difference between case–control and cohort studies was not present for current smokers. There was a geographical heterogeneity: the risk of hip fractures associated with current smoking increased with latitude, i.e. the risk was higher in Northern Europe and the USA than in Southern Europe and countries close to the equator.Conclusions.  Smoking is associated with an increased overall fracture risk, an increased risk of hip and spine but not wrist fractures. Cessation of smoking seems associated with a decrease in fracture risk. The impact of smoking varied geographically with an increase with latitude.
Aspirin in the prevention of progressing stroke: a randomized controlled study
Authors: Rödén‐Jüllig Å. , Britton M. , Malmkvist K. , Leijd B. 
Published: November 2003

Abstract.Objectives.  In acute stroke, progression has a severe impact on patient outcome and no effective treatment is known. The main objective was to evaluate the efficacy of aspirin for prevention of stroke progression thereby improving outcome.Design.  The trial was randomized, double‐blind and placebo‐controlled.Setting.  The patients were treated in stroke units of four hospitals in Sweden.Subjects.  Patients with ischaemic stroke but not complete paresis were included. No antiplatelet drugs were allowed within the last 72 h before onset. Delay until first trial dosage was maximized to 48 h. The trial was designed to detect a 20% reduction of the rate of stroke progression, which was estimated to take place in 20% of cases. Totally, 441 patients (220 aspirin, 221 placebo) completed the trial. Baseline comparisons between the groups showed no differences.Interventions.  Aspirin (325 mg) or placebo was given once daily for five consecutive days.Main outcome measures.  Neurological assessments were carried out three times daily during the treatment period to detect progression of at least two points in the Scandinavian Stroke Supervision Scale. Patient outcome was followed up at discharge and at 3 months.Results.  Aspirin treatment did not significantly reduce the frequency of stroke progression. Amongst aspirin‐treated patients, stroke progression occurred in 15.9% as compared with 16.7% in the placebo group, which is less frequent than expected. The relative risk was 0.95 (95% CI 0.62–1.45) in the treatment group. As regards patient outcome at discharge and after 3 months, aspirin treatment did not show any difference.Conclusion.  No positive effect of aspirin, of the expected size, could be shown on the frequency of stroke progression or patient outcome.
Blunted increase in plasma adenosine levels following dipyridamole stress in dilated cardiomyopathy patients
Authors: Laghi‐Pasini F. , Guideri F. , Petersen C. , Lazzerini P. E. , Sicari R. , Capecchi P. L. , Picano E. 
Published: November 2003

Abstract.Background.  Heart failure is characterized by chronically increased adenosine levels, which are thought to express a protective anti‐heart failure activation of the adenosinergic system. The aim of the study was to assess whether the activation of adenosinergic system in idiopathic dilated cardiomyopathy (IDC) can be mirrored by a blunted increase in plasma adenosine concentration following dipyridamole stress, which accumulates endogenous adenosine.Methods.  Two groups were studied: IDC patients (n = 19, seven women, mean age 60 ± 12 years) with angiographically confirmed normal coronary arteries and left ventricular ejection fraction <35%; and normal controls (n = 15, six women, mean age 68 ± 5 years). Plasma adenosine was assessed by high‐performance liquid chromatography methods in blood samples from peripheral vein at baseline and 12 min after dipyridamole infusion (0.84 mg kg−1 in 10 min).Results.  At baseline, IDC patients showed higher plasma adenosine levels than controls (276 ± 27 nm L−1 vs. 208 ± 48 nm L−1, P < 0.001). Following dipyridamole, IDC patients showed lower plasma adenosine levels than controls (322 ± 56 nm L−1 vs. 732 ± 250 nm L−1, P < 0.001). The dipyridamole‐induced percentage increase in plasma adenosine over baseline was 17% in IDC and 251% in controls (P < 0.001). By individual patient analysis, 18 IDC patients exceeded (over the upper limit) the 95% confidence limits for normal plasma adenosine levels at baseline, and all 19 exceeded (below the lower limit) the 95% confidence limits for postdipyridamole plasma adenosine levels found in normal subjects.Conclusion.  Patients with IDC have abnormally high baseline adenosine levels and – even more strikingly – blunted plasma adenosine increase following dipyridamole infusion. This is consistent with a chronic activation of the adenosinergic system present in IDC, which can be measured noninvasively in the clinical theatre.
Puberty: A Period of Both Organizational and Activational Effects of Steroid Hormones On Neurobehavioural Development
Authors: Romeo R. D. 
Published: November 2003

AbstractDuring perinatal development, steroid hormones act on the central nervous system (CNS) to organize neural circuits. These circuits remain relatively dormant until hormonal stimulation received in adulthood acts on the CNS to activate adult reproductive physiology and behaviour. In this review, the proposal is put forward that, in addition to perinatal development, puberty serves as another period of neural maturation mediated by both steroid‐dependent and ‐independent events that further organize and shape the behavioural potential of the adult organism. In support of this thesis, data are summarized that clearly show the organizational effects of the pubertal rise in gonadal hormones on mating behaviour and other steroid‐mediated behaviours exhibited in adulthood, and on the neural pathways that mediate these behaviours. The importance of determining whether this sensitive period of neural development during puberty is a ‘critical period’ is also discussed, as well as whether perturbations of the nervous system during pubertal development may result in negative behavioural and physiological outcomes in adulthood. It is concluded that puberty is not merely a time when increasing levels of gonadal steroids activate the neural circuits organized during perinatal development, but also a time of further organization of the CNS, which allows for appropriate behaviours to emerge in adulthood.
The Inhibition of Inducible Nitric Oxide Synthase Reverts Arthritic‐Induced Decrease in Pituitary Growth Hormone mRNA But Not in Liver Insulin‐Like Growth Factor I mRNA Expression
Authors: De Cáceres I. Ibáñez , Priego T. , Martín A. I. , López‐Calderón A. , Villanúa M. A. 
Published: November 2003

AbstractExperimental arthritis induced by Freund‐adjuvant administration is a model of chronic inflammation and rheumatoid arthritis associated with a decrease in pituitary growth hormone (GH) and hepatic insulin‐like growth factor I (IGF‐I) gene expression. Excessive nitric oxide (NO) synthesis by inducible NO synthase (iNOS) has been implicated in the pathogenesis of inflammatory illness. Moreover, NO participates in the regulation of GH secretion at both the hypothalamus and the pituitary. We have examined the role of iNOS activation in producing the changes in the GH‐IGF‐I axis in arthritic rats. Adult male Wistar rats received aminoguanidine or vehicle from day 20, after adjuvant or vehicle injection, until day 28. Two hours and 30 min after the last aminoguanidine injection, all rats were killed by decapitation. Arthritis increased hypothalamic expression of somatostatin mRNA while it decreased pituitary GH mRNA expression, and both effects were prevented by aminoguanidine administration. In arthritic rats, the parallel decrease in serum IGF‐I, and in hepatic IGF‐I content and mRNA expression, correlates with the decrease in circulating GH concentrations. Aminoguanidine administration to arthritic rats did not modify either serum GH or serum IGF‐I concentrations, or hepatic IGF‐I mRNA expression. However, aminoguanidine administration to control rats resulted in a decrease in serum GH concentrations and in a decrease in both hepatic IGF‐I mRNA expression and serum IGF‐I concentrations. These data suggest that NO mediates the arthritis‐induced decrease in GH mRNA expression by acting at a hypothalamic level, but it is not involved in the decrease in hepatic IGF‐I mRNA expression.
Elevated CO2 mitigates chilling‐induced water stress and photosynthetic reduction during chilling
Authors: BOESE S. R. , WOLFE D. W. , MELKONIAN J. J. 
Published: November 2003

ABSTRACTBean, cucumber and corn plants were grown in controlled‐environment chambers at 25/18 °C day/night temperature and either ambient (350 μmol mol−1) or elevated (700 μmol mol−1) CO2 concentration, and at 20–30 d after emergence they were exposed to a 24 h chilling treatment (6.5 ± 1.5 °C) at their growth CO2 concentration. Whole‐plant transpiration rates (per unit leaf area basis) during the first 3 h of chilling were about 26,28 and 13% lower at elevated than at ambient CO2 for bean, cucumber and corn, respectively. The decline in leaf water potential (ψL) and visible wilting of bean and cucumber during chilling were significantly less at elevated than at ambient CO2. Corn ψL was not significantly affected by chilling, and corn did not exhibit any other symptoms of chilling‐induced water stress. Leaf osmotic potentials (measured before chilling only) of bean and cucumber were more negative at elevated than at ambient CO2, and the corresponding calculated leaf turgor potentials were significantly higher at elevated than at ambient CO2. Leaf relative water content (RWC) during chilling at ambient CO2fell to 62 and 48% for bean and cucumber, respectively. RWC during chilling at elevated CO2 was never below 79% for bean or 63% for cucumber. Corn RWC was not measured. After 24 h of chilling at ambient CO2, net photosynthetic rate (PN) reductions were 83, 89 and 24% for bean, cucumber and corn, respectively. PN reductions during chilling were less at elevated CO2: 53, 40 and 4% for bean, cucumber and corn, respectively. At ambient CO2, none of the species fully recovered to pre‐chilling PN, but at elevated CO2 both bean and corn recovered fully. The average percentage leaf area with visible leaf damage due to chilling was 20.6 and 9.6% at ambient and elevated CO2, respectively, for bean, and 32.4 and 23.6% at ambient and elevated CO2, respectively, for cucumber. Corn showed no significant permanent leaf damage from chilling at either CO2 concentration. These results indicate that cucumber was most sensitive to chilling as imposed in this study, followed by bean and corn. The results support the hypothesis that, at least in young plants under controlled‐environment conditions, elevated CO2 improves plant water relations during chilling and can mitigate photosynthetic depression and chilling damage. The implications for long‐term growth and reproductive success in managed and natural ecosystems will require testing of this hypothesis under field conditions.
Seasonal trends of light‐saturated net photosynthesis and stomatal conductance of loblolly pine trees grown in contrasting environments of nutrition, water and carbon dioxide
Authors: MURTHY R. , ZARNOCH S. J. , DOUGHERTY P. M. 
Published: November 2003

ABSTRACTRepeated measures analysis was used to evaluate the effect of long‐term CO2 enhancement on seasonal trends of light‐saturated rates of net photosynthesis (Asat) and stomatal conductance to water vapour (gsat) of 9‐year‐old loblolly pine (Pinus taeda L.) trees grown in a 2 × 2 factorial experimental design of nutrition and water. A significant interaction effect of CO2 and nutrition on mean Asat was observed for juvenile foliage. Also, juvenile foliage exposed to +350 μmol mol−1 CO2 had a higher rate of increase of Asat between late summer and early autumn. This would lead to a greater potential for recharging carbohydrate reserves for winter. Mature foliage was affected by COsat, water and nutrient treatments in two ways. First, Asat was significantly increased as a result of elevated CO2 in January, a period when stomatal conductance was only 47% of the maximum observed rate. Secondly, the rate of increase of Asat from winter to early spring was accelerated as a result of both nutrient + water and + 350 μmol mol−1 CO2 treatments. This accelerated response resulted in a greater potential for photosynthate production during the period when growth initiation occurred. Nutrient, water or carbon dioxide treatments did not significantly alter trends in gsat for mature or juvenile foliage. A significant nutrition × CO2 interaction was observed for the mature foliage, suggesting that gsat increased with increasing CO2 and nutrition. These results may have important consequences for the determination of the water use efficiency of loblolly pine. In spite of low gsat in the winter to early spring period, there was a substantial gain in Asat attributable to elevated CO2 concentrations.
Photosynthesis and photoprotection in mangroves under field conditions
Authors: CHEESEMAN J. M. , HERENDEEN L. B. , CHEESEMAN A. T. , CLOUGH B. F. 
Published: November 2003

ABSTRACTNet CO2 exchange and in vivo chlorophyll fluorescence were studied in mangrove (Rhizophora stylosa) leaves at a field site in Western Australia, and leaf samples were collected for the analysis of enzymes and substrates potentially involved in anti‐oxidant photoprotection. Photosynthesis saturated at 900 μmol quanta m−2 s−1 and at no more than 7.5 μmol CO2 m−2 s−1. However, fluorescence analysis indicated no chronic photoinhibition: Fv:Fm was 0.8 shortly after sunset, and quantum efficiencies of PSII were high up to 500 μmol quanta m−2 s−1. Electron flow through PSII was more than 3 times higher than electron consumption through Calvin cycle activity, however, even with photorespiration and temperature‐dependent Rubisco specificities taken into account.Acknowledging the growing body of literature attributing a role to antioxidant systems in photoprotection, we also assayed the activities of superoxide dismutase (SOD) and several enzymes potentially involved in H2O2 metabolism. Their levels of maximal potential activity were compared with those in greenhouse‐grown mangroves (R. mangle), and growth chamber‐grown peas. Monodehydroascorbate reductase activities were similar in all species, and glutathione reductase was lower, and ascorbate peroxidase ∼40% higher, in the mangroves. SOD activities in field‐grown mangroves were more than 40 times those in peas.Our results support the hypothesis that O2 may be a significant sink for photochemically derived electrons under field conditions, and suggest an important role for O2− scavenging in photoprotection. However, when relative patterns are compared between species, imbalances between SOD and the other enzymes in the mangroves suggest that more components of the system (e.g. phenolics or peroxidases) are yet to be identified.
Elongation by primary lateral roots and adventitious roots during conditions of hypoxia and high ethylene concentrations
Authors: VISSER E. J. W. , NABBEN R. H. M. , BLOM C. W. P. M. , VOESENEK L. A. C. J. 
Published: November 2003

ABSTRACTSoil flooding results in unusually low oxygen concentrations and high ethylene concentrations in the roots of plants. This gas composition had a strongly negative effect on root elongation of two Rumex species. The effect of low oxygen concentrations was less severe when roots contained aerenchymatous tissues, such as in R. palustris Sm. R. thyrsiflorus Fingerh., which has little root porosity, was much more affected. Ethylene had an even stronger effect on root elongation than hypoxia, since very small concentrations (0.1 cm3 m−3) reduced root extension in the two species, and higher concentrations inhibited elongation more severely than did anoxia in the culture medium. Thus, ethylene contributes strongly to the negative effects of flooding on root growth. An exception may be the highly aerenchymatous, adventitious roots of R. palustris. Aerenchyma in these roots provides a low‐resistance diffusion pathway for both endogenously produced ethylene and shoot‐derived oxygen. This paper shows that extension by roots of R. palustris in flooded soil depends almost completely on this shoot‐derived oxygen, and that aerenchyma prevents accumulation of growth‐inhibiting levels of ethylene in the root.
Multi‐element and multi‐site isotopic analysis of nicotine from tobacco leaves
Authors: JAMIN E. , NAULET N. , MARTIN G. J. 
Published: November 2003

ABSTRACTThe carbon, nitrogen and hydrogen stable‐isotope contents of nicotine extracted from tobacco leaves were determined by Isotope Ratio Mass Spectrometry (overall 2H, 13C and 15N contents) and by the SNIF‐NMR method (site‐specific deuterium content). In addition, nicotine was chemically degraded into nicotinic acid so that the intramolecular distribution of carbon and nitrogen isotopes could be studied. A prerequisite for reliable measurements is the use of experimental procedures free of isotopic fractionation. Therefore, it was ensured that isotopic integrity was maintained throughout extraction, purification and chemical degradation steps. The multi‐element and multi‐site information provided is tentatively interpreted in terms of biochemical isotopic effects on intramolecular distribution patterns and of the influence of environmental factors on nicotine isotopic parameters.
Interferon‐γ Tempers the Expression of Carcinoembryonic Antigen Family Molecules in Human Colon Cells: a Possible Role in Innate Mucosal Defence
Authors: Fahlgren A. , Baranov V. , Frängsmyr L. , Zoubir F. , Hammarström M.‐L. , Hammarström S. 
Published: November 2003

AbstractFour carcinoembryonic antigen‐related cell adhesion molecule (CEACAM)s, i.e. CEA, CEACAM1, CEACAM6 and CEACAM7, are localized to the apical glycocalyx of normal colonic epithelium and have been suggested to play a role in innate immunity. The expression of these molecules in colon carcinoma cells was studied at the mRNA and protein levels after treatment with interferon‐γ (IFN‐γ), interleukin‐1β, live bacteria or lipopolysaccharide. The colon carcinoma cell lines LS174T and HT‐29 were studied in detail using real‐time quantitative reverse transcriptase‐polymerase chain reaction, immunoflow cytometry and immunoelectron microscopy. IFN‐γ, but not the other agents, modified expression of CEA, CEACAM1 and CEACAM6. None of the agents upregulated CEACAM7 expression. Two expression patterns were seen. HT‐29 cells, which initially showed low quantities of mRNAs and proteins, displayed marked upregulation of both mRNAs and proteins. LS174T cells transcribed stable high levels of mRNA before and after treatment. Additionally, IFN‐γ induced increased cell surface expression of CEA, CEACAM1 and CECAM6. IFN‐γ has two important effects on the expression levels of the CEA family molecules in colon epithelial cells: direct upregulation of CEACAM1 and promotion of cell differentiation resulting in increased expression of CEA and CEACAM6 and decreased expression of CEACAM7.
Natural Killer Cell‐Mediated Basal and Interferon‐Enhanced Cytotoxicity against Liver Cancer Cells is Significantly Impaired Under In Vivo Oxygen Conditions
Authors: Fink T. , Ebbesen P. , Koppelhus U. , Zachar V. 
Published: November 2003

AbstractCurrent immunostimulatory treatment protocols of cancer are often met with little success. Several lines of evidence indicate that the tumour microenvironment may impair the cytotoxic activity of natural killer (NK) cells. In this study, the NK cell‐mediated killing of liver‐derived cells was investigated at oxygen concentrations conform to those present in the human body at physiological and pathological conditions. The in vivo‐relevant oxygen concentrations corresponding to 1, 2 and 6% were compared to those of the ambient air (21%) for their effect on the lysis of four liver‐derived cell lines and the highly susceptible K562 cells. Exposure to each of the hypoxic conditions had a significantly inhibitory effect on NK cytotoxicity. Treatment with interferon‐α (IFN‐α) in hypoxia enhanced the cytotoxic potential of the NK cells less than it enhanced the cytotoxicity at ambient oxygen conditions. In summary, the oxygen tension profoundly affects both the cytoxic activity of NK cells and their activation by IFN‐α.
Microglial activation with atypical proinflammatory cytokine expression in a rat model of Parkinson's disease
Authors: Depino Amaicha M. , Earl Chris , Kaczmarczyk Elke , Ferrari Carina , Besedovsky Hugo , Del Rey Adriana , Pitossi Fernando J. , Oertel Wolfgang H. 
Published: November 2003

AbstractMicroglial activation has been associated with the pathogenesis of Parkinson's disease (PD). Among the many components of this reaction, cytokines have been proposed as candidates to mediate neurodegenerative or neuroprotective effects. We investigated the interleukin‐1 system and tumour necrosis factor‐α mRNA and protein levels at different time intervals in the subacute intrastriatal 6‐hydroxydopamine rat model of PD, in parallel with the inflammatory response. Immunohistochemistry showed that microglial cells were activated from days 6–30 postlesion in the substantia nigra pars compacta. This microglial activation was accompanied by an atypical proinflammatory cytokine production: Interleukin‐1α and β mRNAs were found to be elevated 30 days post‐6‐hydroxydopamine injection (2‐ and 16‐fold, respectively), but no induction for interleukin‐1α or β at the protein level was detected by ELISA. As a control, a classical proinflammatory stimulus, namely endotoxin, was capable of inducing these cytokines at similar mRNA levels but also at the protein level. In addition, tumour necrosis factor‐α mRNA was hardly or not detected in the substantia nigra at any time point studied. Our data point out a tight control of key proinflammatory cytokine production in our model of PD. This work supports the notion that chronic neuronal death per se does not induce secretion of these proinflammatory cytokines but that an additional stimulus is necessary to stimulate proinflammatory cytokine production. The production of proinflammatory cytokines from “primed” microglia may in turn modulate disease progression as has been recently proposed in a model of prion disease.