bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intra‐guild predation relaxes natural enemy impacts on herbivore populations
Authors: Finke Deborah L. , Denno Robert F. 
Published: March 2003

Abstract. 1. To investigate the role of intra‐guild predation in mediating the impact of the natural enemy complex on herbivore populations, a manipulative field experiment was conducted using uncaged plots (islets of Spartina cordgrass) on a North American salt marsh. The densities (moderate or low) of two invertebrate predators, the generalist wolf spider Pardosa littoralis and the specialist mirid bug Tytthus vagus, were manipulated in a 2 × 2 factorial design, and the resulting treatment effects on the population growth of their herbivorous prey, Prokelisia planthoppers, were assessed.2. The abundance of wolf spiders on experimental islets was unaffected by the presence of mirid bugs, however the density of mirid bugs was influenced very negatively by the presence of the wolf spider.3. The negative effect of the wolf spider on mirid bugs most probably resulted from the intra‐guild predation of mirids by spiders because planthopper limitation by the wolf spider alone was significantly greater than when both predators were present.4. As a result of intra‐guild predation, planthopper population growth was positive in the presence of both predators, despite the fact that each predator alone promoted a decrease in planthopper population growth.5. Notably, the occurrence of intra‐guild predation diminished top‐down impacts on planthopper populations in a relatively simple food web where strong top‐down effects were expected. This result, however, was limited to habitats on the marsh with simply structured vegetation lacking leaf litter.
Endogenous dopaminergic activity in Child–Pugh A cirrhosis: potential role in renal sodium handling and in the maintenance of clinical compensation
Authors: Sansoè  , Ferrari  , Baraldi  , Grisolia  , De Santis  , Villa  , Manenti  
Published: March 2003

BackgroundWe studied the main determinants of aldosterone secretion in a group of 20 patients with biopsy‐proven Child–Pugh A cirrhosis without previous ascites or diuretic consumption.MethodsWe evaluated the plasma levels of adrenocorticotrophic hormone (ACTH), active renin and aldosterone (both supine at 07.00 h and after 30 min of upright posture),and active renin and aldosterone responses 30 min and 60 min after the administration of metoclopramide, a dopamine DA2 antagonist (10 mg e.v.). Nine normal subjects were also submitted to the metoclopramide stimulation test.ResultsCompared with control subjects, the patients showed significantly greater incremental aldosterone responses both 30 min and 60 min after metoclopramide (+30 min: 157.5 ± 73.3 vs. 83.5 ± 32.2 pg mL−1, P < 0.003; +60 min: 142.1 ± 87.2 vs. 36.8 ± 39.0 pg mL−1, P < 0.001). We found significant positive correlations between amplitude of aldosterone response 30 min after metoclopramide and 24‐h urinary fractional excretion of sodium (r= 0.61, P < 0.01) and basal morning aldosterone levels (r= 0.69, P < 0.001).ConclusionsThe higher incremental aldosterone responses observed after metoclopramide in cirrhotic patients are expressions of increased dopaminergic activity in these patients compared with control subjects. Moreover, the correlation we found between the degree of dopaminergic activity and 24‐h urinary fractional excretion of sodium suggests a role for endogenous dopamine as a relevant mediator of natriuresis in cirrhosis, at least in patients with compensated disease.
Human liver glycogen metabolism assessed with a 13C‐enriched diet and a 13CO2 breath test
Authors: Tanis  , Van Den Berg  , Kroneman  , Wattimena  , Rietveld  , Nieland  , Swart  
Published: March 2003

BackgroundAdequate liver glycogen stores to maintain hepatic glucose output by glycogenolysis in the post‐absorptive state are essential to prevent protein loss through gluconeogenesis. There are no simple techniques to monitor liver glycogen use.MethodsIn this study, we labelled liver glycogen with naturally 13C‐enriched carbohydrate and measured the pattern of 13CO2 excretion and the post‐prandial time during which oxidation of 13C‐labelled liver glycogen was demonstrable by 13CO2 enrichment in breath. Two experiments were performed in 24 healthy volunteers.ResultsIn the first experiment we observed that breath 13CO2 enrichment returned to baseline values at 20.3 (SD 2.3, n = 12) hours post‐prandially, indicating exhaustion of the 13C‐labelled liver glycogen at that time. In a second experiment, breath 13CO2 enrichment in the early hours of the post‐prandial phase was studied. After a steep decline, which started 2–4 h after the last meal, the 13CO2 enrichment reached a plateau phase 6 h post‐prandially. This plateau phase lasted for about 6–8 h, suggesting steady‐state glycogenolysis during this period. The plateau phase was followed by a further decline in 13CO2 excretion, suggesting a gradually diminishing contribution of 13C‐labelled liver glycogen to substrate oxidation.ConclusionIt is possible to label liver glycogen with a diet of naturally 13C‐enriched carbohydrate. The oxidation of the labelled liver glycogen can be monitored by measuring 13C‐enrichment in breath CO2.
Inhibition of platelet–vessel wall interactions by thromboxane receptor antagonism in a human in vitro system: potentiation of antiplatelet effects of aspirin
Authors: Escolar  , Albors  , Garrido  , Bioque  , Díaz Ricart  , Carretero  , Ordinas  
Published: March 2003

BackgroundPharmacological inhibition of arachidonic acid metabolism has proven therapeutically useful in the prevention of cardiovascular events.MethodsWe have investigated the ability of Bay u 3405, a synthetic thromboxane antagonist, to interfere with platelet aggregation and arachidonic acid metabolism. The antiplatelet action was also analysed in a perfusion system in which vascular subendothelium was exposed to circulating human blood (10 min; shear rate = 800 s−1). Platelet interactions were morphometrically analysed and results compared with those obtained in studies with blood from donors taking aspirin (acetylsalicylic acid, ASA) (500 mg day−1). The additional effect of Bay u 3405 on the antiplatelet action of ASA was also evaluated.ResultsBay u 3405 caused a dose‐dependent inhibition of platelet aggregation induced by U46619 with a maximal effect at concentrations ≥ 0.01 μg mL−1. Higher concentrations (≥ 0.05 μg mL−1) also inhibited aggregations induced by ADP or collagen. Bay u 3405 did not interfere with platelet arachidonic acid metabolism. In perfusion studies, Bay u 3405 (0.01 μg mL−1) significantly decreased the total surface of the vessel covered by platelets (%CS = 18.7 ± 1.09 vs. 24.4 ± 1.94; P < 0.05) and the formation of large aggregates (%T = 7.5 ± 0.87 vs. 19.3 ± 1.61; P < 0.01). ASA treatment reduced platelet aggregate formation (%T = 13.7 ± 2.06; P < 0.05) but did not affect the total surface covered by platelets. The in vitro addition of Bay u 3405 to blood from ASA‐treated donors further reduced the formation of large aggregates (%T = 2.7 ± 0.79; P < 0.01 vs. ASA).Conclusions In vitro effects of Bay u 3405 on platelet function were superior to those observed with ASA. The thromboxane antagonism provided by Bay u 3405 further enhanced the inhibition of platelet aggregate formation found after ASA treatment.
Cytokine regulation of the acute‐phase protein levels in multiple myeloma
Authors: Bíró  , Domján  , Falus  , Jakab  , Cseh  , Kalabay  , Tarkovács  , Tresch  , Malle  , Kramer  , Prohászka  , Jákó  , Füst  , Császár  
Published: March 2003

BackgroundInterleukin (IL) 6 has an important role in the regulation of acute‐phase proteins (APPs) during an acute‐phase response. We studied IL‐6 and other cytokines to determine if they regulate serum APP levels in the same way under the condition of the aberrant, long‐lasting ‘acute‐phase response’ that occurs in patients with chronic inflammation and cancer.MethodsSerum levels of nine positive APPs [CRP, SAA, C1‐INH, Bf, C5, C8, C9, α1‐acidic glycoprotein (AGP) and haptoglobin] and two negative APPs [transferrin and α2‐HS glycoprotein (AHSG)] were measured using immunochemical methods in 59 multiple myeloma patients and in 72 healthy control subjects. Serum IL‐6 and tumour necrosis factor (TNF) α levels were determined by bioassays.ResultsIL‐6 was negatively correlated with five out of nine (C1‐INH, C8, C9, AGP and haptoglobin) positive APPs but positively correlated with C‐reactive protein (CRP). When patients with high and low IL‐6 serum concentration were compared, CRP levels were higher, AGP and haptoglobin levels were lower in the high‐ than in the low‐L‐6 group, whereas no significant difference between the two groups was found in levels of the other positive and negative APPs. TNF‐α levels were negatively correlated with transferrin and AHSG levels. No difference in the levels of positive APPs was observed between patients with low and high TNF‐α serum concentration. By contrast, levels of both transferrin and AHSG were significantly lower in the high‐ than in the low‐TNF‐α group.ConclusionsThese findings indicate that, except for regulation of the negative APPs by TNF‐α, the mechanism of APP regulation is different under the conditions of the short‐term and the chronic, long‐lasting ‘acute‐phase reaction’.
Tumour necrosis factor β alleles and hyperinsulinaemia in coronary artery disease
Authors: Braun  , März  , Winkelmann  , Donner  , Henning Usadel  , Badenhoop  
Published: March 2003

BackgroundHyperinsulinaemia and dyslipoproteinaemia are markers and risk factors for coronary artery disease (CAD) and non‐insulin‐dependent diabetes mellitus (NIDDM). We investigated the influence of a tumour necrosis factor β (TNF‐β) gene polymorphism on serum parameters related to these metabolic disorders in patients with CAD.MethodsA total of 199 patients with CAD and 81 control subjects with angiographically normal coronary arteries were studied. A digestion of amplified DNA with NcoI revealed three fragment patterns: homozygosity for TNF‐β*1 or TNF‐β*2 and heterozygosity (TNF‐β*1/*2).ResultsPatients with CAD who had increased serum insulin or C‐peptide (fasting and after glucose load) were predominantly heterozygous for TNF‐β (72% vs. 47%) and less frequently homozygous for TNF‐β*2 (22% vs. 43%, P = 0.03).ConclusionThis study demonstrates an association of TNF‐β alleles with the risk factor hyperinsulinaemia in CAD. Genomic variants of TNF‐β may therefore contribute to the complex susceptibility for the metabolic syndrome in patients with CAD.
Evidence for a role of T‐helper type 2 cytokines in the acquisition of human immunodeficiency virus syncytium‐inducing phenotype
Authors: Torres  , Medrano  , Rey  , Calderón  , Sánchez‐Quijano  , Lissen  , Leal  
Published: March 2003

BackgroundThe objective of the present study was to investigate the relationship between the serum cytokine pattern of T‐helper (Th) response and the acquisition of syncytium‐inducing (SI) human immunodeficiency virus type 1 (HIV‐1) variants in HIV‐1‐seropositive patients treated with antiretroviral drugs.MethodsSerum cytokines of Th1/Th2 responses were analysed in a case–control study of 20 individuals selected from a cohort of HIV‐1‐infected patients without SI variants at entry, who developed or did not develop SI virus during a prospective follow‐up. A group of 10 patients with SI variants at study entry was also evaluated. Serum concentration of interferon (IFN) gamma, interleukin (IL) 2, IL‐4 and IL‐10 was evaluated by mean of a commercial enzyme immunoassay.ResultsDespite close matching for immunological (CD4+ cell count) and virological (p24 antigen, serum HIV viraemia) parameters, SI‐converting patients showed at baseline significantly lower serum levels of IL‐2 and higher concentrations of IL‐4 than those who remained persistently negative for SI variants. Shortly after the phenotype conversion, SI‐converting patients were characterized by significantly high serum concentration of IL‐4 and by low levels of IFN‐γ (Th2‐like pattern). Patients with SI phenotype at study entry featured lower mean levels of both IL‐4 and IL‐10, but mean IFN‐γ and IL‐2 values were higher, although the clinical and immunological baseline was also poorer and no statistical analysis could be applied.ConclusionSerum cytokine pattern of Th1/Th2 response differs between patients with NSI and SI phenotype. Our data strongly suggest that the Th2 cytokine pattern could be associated with the acquisition of the SI HIV‐1 phenotype.
Alterations in adhesion molecule (CD11b/CD18 and CD62L) expression on granulocytes after chemotherapy
Authors: Engervall  , Lundahl  
Published: March 2003

BackgroundInfections during chemotherapy‐induced granulocytopenia constitute a major threat to patients with malignant disorders. The aim of this study was to evaluate whether circulating granulocytes after chemotherapy have a normal expression of adhesion molecules or if the granulocytes, in addition to being present in low number, also present signs of qualitative alterations.MethodsWe have investigated the time course of adhesion molecule expression (CD11b/CD18 and CD62L) and in vitro mobilization [responsiveness against N‐formyl‐methionyl‐leucyl‐phenylalanine (fMLP) for CD11b/CD18] by flow cytometry in circulating granulocytes after chemotherapy in 12 patients with haematological malignancies. Blood samples for analysis were drawn before chemotherapy and at time points when granulocyte counts were < 0.5, 0.5–1.0 and > 1.0 × 109 L−1.ResultsThe quantitative level, expressed as mean fluorescence intensity (MFI), of CD11b/CD18 was significantly higher and of CD62L significantly lower at granulocyte nadir than before chemotherapy. The in vitro responsiveness to fMLP was significantly reduced at the same time point. These alterations were restored to pretreatment values at the time of granulocyte count recovery. Granulocytes from patients with bacteraemia (n = 6) exhibited lower CD11b/CD18 MFI values after fMLP stimulation than non‐bacteraemic patients after granulocyte count recovery. In addition, the MFI of CD62L was significantly lower both before chemotherapy and after granulocyte recovery in the bacteraemic group.ConclusionChemotherapy induces qualitative alterations in circulating granulocytes with respect to adhesion molecule expression and mobilization, and these alterations are more pronounced in patients with accompanying bacteraemia.
Beta‐blockers reduce the release and synthesis of endothelin‐1 in human endothelial cells
Authors: Garlichs  , Zhang  , Mügge  , Daniel  
Published: March 2003

BackgroundEndothelins play an important role in cardiovascular diseases, and clinical trials have shown a reduction in endothelin levels after long‐term treatment of chronic heart failure with β‐adrenergic antagonists. It is not known, however, whether this effect is caused by haemodynamic changes associated with the use of β‐adrenergic antagonists or by direct interaction of β‐blockers with human endothelial cells. The aim of this study was to determine whether β‐adrenergic antagonists have an influence on endothelin‐1 (ET‐1) synthesis and release in human endothelial cells.MethodsPretreatment of cultured endothelial cells from human umbilical veins (HUVECs) with different concentrations of the non‐selective β‐blocker propranolol, the β1‐blocker metoprolol and the β1‐blocker and β2‐agonist celiprolol (all 10−7–10−4 mol L−1) was found to reduce ET‐1 production. This ET‐1‐reducing effect was even more pronounced in thrombin‐stimulated cells (10−5 mol L−1 of propranolol, metoprolol and celiprolol: 19% ± 5.8%, 25% ± 4% and 37% ± 5.2 % respectively).ResultsQuantitative reverse transcriptase polymerase chain reaction and Northern blotting confirmed an inhibitory effect of the β‐blocker on biosynthesis. Furthermore, the ET‐1‐reducing effect of propranolol, metoprolol and celiprolol was not due to a compensatory increase in prostacyclin and was not reversible by N‐nitro‐
L‐arginine.ConclusionThe effect of β‐adrenergic antagonists on ET‐1 production of the endothelium may at least partially explain the efficacy of β‐blockers in the treatment of diseases such as advanced heart failure, essential hypertension as well as acute coronary syndromes.
Holotranscobalamin — a sensitive marker of cobalamin malabsorption
Authors: Lindgren  , Kilander  , Bagge  , Nexø  
Published: March 2003

BackgroundNo simple and reliable method of identifying patients with cobalamin malabsorption is available at present. The measurement of plasma holotranscobalamin, i.e. the metabolically active cobalamins bound to the transport protein transcobalamin, has been suggested as a means of fulfilling such criteria.DesignWe describe a method that directly quantifies cobalamins attached to transcobalamin. The method is evaluated in patients referred for gastrointestinal examination because of suspected cobalamin malabsorption.ResultsOf the 101 patients referred, all 48 with gastrointestinal conditions compatible with cobalamin malabsorption had plasma holotranscobalamin below 35 pmol L−1 (interval of 35–160pmol L−1). None of the patients with plasma holotranscobalamin above the lower reference limit had conditions compatible with cobalamin malabsorption.ConclusionThe values obtained for plasma holotranscobalamin showed a better correlation with possible malabsorption than the values obtained for plasma cobalamins. The specificity of the test, however, needs to be elucidated further.
An angiotensin‐converting enzyme gene polymorphism suggests a genetic distinction between ischaemic stroke and carotid stenosis
Authors: Kostulas K. , Huang W.‐X. , Crisby M. , Jin Y.‐P. , He B. , Lannfelt L. , Eggertsen G. , Kostulas V. , Hillert J. 
Published: March 2003

BackgroundIschaemic cerebrovascular disease (ICVD) is a heterogeneous syndrome to which different genetic factors may contribute. We have investigated the distribution of alleles of the angiotensin‐converting enzyme (ACE) gene, which has been suggested to be of possible importance in ischaemic stroke or cardiovascular disease, in groups of patients with ischaemic stroke and carotid artery stenosis (CS).Materials and methodsOne hundred and thirty patients with ischaemic stroke and 68 patients with more than 50% stenosis of the internal carotid artery were investigated and compared with age‐ and sex‐matched healthy control subjects. Alleles of an insertion/deletion polymorphism of the ACE gene were determined by one‐stage polymerase chain reaction and visualized on agarose gels.ResultsThere was a significant difference (P < 0.05) in the distribution of ACE alleles, homozygosity for the presumed susceptibility deletion allele being more common in patients with CS than in healthy control subjects. There was also a significant difference (P < 0.05) in patients with CS in comparison with matched ICVD patients without CS, both in allelic frequencies and in homozygosity for the deletion allele.ConclusionsOur results indicate that the ACE gene polymorphism may be a risk factor for the development of CS. The observed difference in ACE allele distribution may be seen as evidence for a genetic distinction between ICVD and CS, two clinically related conditions, which further supports the hypothesis that genetic factors are of importance for this group of diseases.
Anti‐neutrophil cytoplasmic antibodies in a rat model of trinitrobenzenesulphonic acid‐induced liver injury
Authors: Orth  , Neurath  , Schirmacher  , Treichel  , Meyer zum Büschenfelde  , Mayet  
Published: March 2003

BackgroundIn sera from patients with autoimmune liver diseases, e.g. primary sclerosing cholangitis (PSC) and autoimmune hepatitis, anti‐neutrophil cytoplasmic antibodies (ANCAs) can be found. Until now, no animal model of ANCA induction in liver disease has been described. In this study, we describe a novel rat model of acute liver injury and subsequent ANCA production.Materials and methodsThe hapten reagent 2,4,6‐trinitrobenzenesulphonic acid (TNBS) was injected into the portal vein of female Lewis rats. Two experimental groups were studied: group A (TNBS/ethanol) received different TNBS concentrations; control animals of group B (ethanol) were injected with 10% (v/v) ethanol/0.9% (w/v) NaCl.ResultsA dose‐dependent acute necrotizing liver injury occurred after injection of TNBS. Histopathological examination revealed acute hepatic injury with confluent parenchymal necrosis, mild bile duct proliferation and periportal infiltration. The periportal infiltration consisted mainly of macrophages and T lymphocytes. ANCAs were found in an allogenic test system between 1 and 8 weeks after TNBS injection in 11 out of 28 (39%) TNBS‐treated rats (group A) and did not correlate with the extent of liver injury or TNBS dose. Autoantibody specificities of IgG type were directed against catalase (29%), myeloperoxidase (14%) and actin (7%), as detected by enzyme‐linked immunosorbent assay and Western blotting. Moreover, autoantibodies against the asialoglycoprotein receptor were observed. Peripheral blood mononuclear cells and spleen lymphocytes from TNBS‐treated rats were shown to produce ANCAs.ConclusionIn summary, we were able to show that intraportal administration of the hapten reagent TNBS induces an acute necrotizing liver injury with subsequent ANCA production in Lewis rats. ANCA specificities were mainly directed against catalase, an autoantigen that has recently been identified in sera from patients with primary sclerosing cholangitis and autoimmune hepatitis. This animal model offers the opportunity to study the pathomechanisms of ANCA production in necrotizing liver injury.
L‐selectin in trauma patients: a marker for organ dysfunction and outcome?
Authors: Kerner  , Ahlers  , Spielmann  , Keh  , Bührer  , Gerlach  , Höfler  , Gerlach  
Published: March 2003

BackgroundSystemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS) are important factors affecting morbidity and mortality after trauma. Adhesion molecules, e.g. L‐selectin (CD62 L), play crucial roles in both conditions.Patients and methodsIn 51 multiple trauma patients, CD62 L surface expression on granulocytes, monocytes, lymphocytes, as well as sCD62 L plasma concentrations were determined during the first 6 days after trauma, starting at the site of accident. Clinical parameters were severity of injury scores (ISS, APACHE II), requirement of red blood cell transfusion, acute lung or liver failure, development of MODS or SIRS, early (≤ 6 d) or late (> 6 d), and outcome.ResultsCD62 L expression was reversibly elevated on granulocytes, T cells and monocytes in comparison with initial values. sCD62 L plasma concentrations did not show temporal variations but were depressed throughout observation period, in comparison with healthy controls. Lung failure within the first 6 days was associated with increased CD62 L expression on monocytes and B cells on admission and increased sCD62 L concentrations after 12 and 24 h. Patients with more severe injuries (APACHE II > 20 points) had higher sCD62 L concentrations after 24 h. Non‐survivors had decreased sCD62 L (on admission) and T‐cell CD62 L expression (after 4 h). Patients with early MODS or SIRS showed increased monocyte CD62 L expression after 6 days.ConclusionsIn multiple trauma patients, severe organ dysfunction is associated with altered CD62 L expression on leukocytes and circulating sCD62 L plasma concentrations. However, the obvious complexity of the pattern currently restricts use of CD62 L quantitation for clinical purposes.