bluuebunny/crossref_metadata_2025_split huggingface dataset:
Competition as a factor underlying the abundance of an uncommon phytophagous insect, the salt‐marsh planthopper Delphacodes penedetecta
Authors: Ferrenberg Scott M. , Denno Robert F. 
Published: March 2003

Abstract. 1. Recent reviews of experimental studies provide compelling evidence that competition should be retained as a potential factor influencing the success of phytophagous insects. In this context, the objective of the study was to determine the role of interspecific and intraspecific competition, both contemporaneous and plant mediated (feeding‐induced resistance), in limiting the population density of a consistently rare insect in a guild of abundant potential competitors.2. Competitive interactions were assessed experimentally between two phloem‐feeding planthoppers, the abundant Prokelisia dolus and the rare Delphacodes penedetecta (Hemiptera: Delphacidae). Both species are monophagous on the cordgrass Spartina alterniflora and overlap broadly in their use of habitats in the intertidal salt marshes along the Atlantic coast of North America.3. The two planthoppers partition their cordgrass host plant, with D. penedetecta feeding more on the basal stems (particularly females) and P. dolus occurring most often on the canopy leaves. Notably, there was no evidence for niche shifting in D. penedetecta because its distribution on the plant did not change in the presence or absence of P. dolus.4. Interspecific interactions with P. dolus had very little effect on the performance (development time and body size) and survival of D. penedetecta, a result demonstrated in both the laboratory and field. This result occurred both in contemporaneous interactions and on plants fed on previously by P. dolus. Only the males of D. penedetecta experienced weak competitive effects from P. dolus, as evidenced by reduced body size and slightly protracted development.5. By contrast, there were strong adverse effects of intraspecific crowding (both from contemporaneous interactions and on plants fed on previously by conspecifics), whereby the survival, development time, and body size of D. penedetecta were affected very adversely.6. These results suggest that interspecific competition is a weak force influencing the abundance of D. penedetecta in the field. Rather, strong intraspecific competition, a high requirement for plant nitrogen, and intrinsically low lifetime fecundity combine to explain the rarity of D. penedetecta.
Cytokine autoantibodies in multiple sclerosis, aseptic meningitis and stroke
Authors: Elkarim  , Mustafa  , Kivisäkk  , Link  , Bakhiet  
Published: March 2003

BackgroundWe have recently described the induction of anti‐cytokine autoantibodies during bacterial infections and autoimmune diseases as a mechanism for cytokine regulation.MethodsHerein, we study the occurrence of autoantibodies to pro‐ and anti‐inflammatory cytokines in cerebrospinal fluid and plasma from patients with multiple sclerosis, aseptic meningitis and stroke.ResultsIncreased levels of autoantibodies to interferon γ, tumour necrosis factor α, interleukin 4 and interleukin 10 were detected in both compartments of multiple sclerosis and aseptic meningitis patients. Interestingly, in cerebrospinal fluid from stroke patients, only autoantibodies to interleukin 4 and interleukin 10, but not interferon α or tumour necrosis factor α were detected. No significant autoantibody levels were registered in plasma from stroke patients against all four cytokines compared with healthy control subjects. The latter revealed very low autoantibody levels in plasma and no detectable autoantibodies in cerebrospinal fluid.ConclusionsOur data show for the first time the occurrence of cytokine autoantibodies in these diseases, but their biological significance is unclear.
Angiotensin‐converting enzyme gene polymorphism is not associated with coronary atherosclerosis and myocardial infarction in a sample of Italian patients
Authors: Arca  , Pannitteri  , Campagna  , Candeloro  , Montali  , Cantini  , Seccareccia  , Campa  , Marino  , Ricci  
Published: March 2003

BackgroundThe deletion (D) allele of the angiotensin‐converting enzyme (ACE) gene has been proposed as a genetic marker of the risk of ischaemic heart disease. However, the relationships between ACE genotypes, the development of coronary atherosclerosis and the occurrence of major coronary events are still controversial.MethodsTo investigate whether the ACE I/D (insertion/deletion) polymorphism predicts the risk of coronary stenosis and myocardial infarction (MI), ACE genotypes were determined in 394 consecutive patients who underwent coronary angiography. The presence of coronary artery disease (CAD) (defined by > 50% stenosis) was detected in 236 patients (CAD+); 85 of these individuals had a history of MI. Patients with coronary stenosis < 10% (n = 158) served as controls (CAD−). ACE genotypes were determined by agarose gel sizing after polymerase chain reaction (PCR) amplification.ResultsThe distribution of ACE genotypes in CAD+ patients was not significantly different from that in CAD− patients (χ2 = 2.63, P < 0.27). After controlling for other coronary risk factors, no significant increase in risk of CAD or MI was found to be associated with the D allele, regardless of whether the D allele was assumed to have a dominant, a co‐dominant or a recessive effect. Similar results were observed in CAD+ patients at lower risk because of low body mass index and apolipoprotein B concentrations. Smoking, apolipoprotein B and history of hypertension were found to be independent predictors of CAD and MI.ConclusionOur study did not provide evidence of a significant association between ACE genotypes and the development of coronary atherosclerosis. It also failed to support a role of ACE I/D polymorphism in favouring the conversion of coronary stenosis to MI.
The effect of smoking on post‐heparin lipoprotein and hepatic lipase, cholesteryl ester transfer protein and lecithin:cholesterol acyl transferase activities in human plasma
Authors: Freeman  , Caslake  , Griffin  , Hinnie  , Tan  , Watson  , Packard  , Shepherd  
Published: March 2003

IntroductionSmoking is associated with dyslipidaemia, particularly raised plasma triglycerides and reduced high‐density lipoprotein (HDL)‐cholesterol and a delayed clearance of triglyceride in fat tolerance tests. The aim of this study was to investigate whether these phenomena could be explained by a reduced lipoprotein lipase activity in smokers.MethodsA group of 40 healthy individuals [plasma cholesterol 5.07 (SD 0.90) mmol L−1, plasma triglyceride 1.02 (SD 0.39) mmol L−1)] was studied to examine the effects of smoking on plasma enzyme activities, particularly post‐heparin lipase activities. The group comprised 20 smokers and 20 non‐smokers, who were matched for age, gender and body mass index (BMI).ResultsPost‐heparin lipoprotein lipase (LPL) activity [3.89 (SD 1.58) vs. 5.85 (SD 2.30) μmol free fatty acids (FFA) mL−1 h−1, P < 0.005], but not post‐heparin hepatic lipase (HL) activity, was reduced in smokers. Plasma cholesteryl ester transfer protein (CETP) activity and lecithin:cholesterol acyl transferase (LCAT) activity were measured in a subgroup of 18 individuals, comprising nine smokers with nine matched non‐smokers. There was no difference in CETP activities between the two groups, but smokers had a significantly reduced plasma LCAT activity [112 (SD 23) vs. 152 (SD 24) nmol cholesterol mL−1 h−1, P < 0.005]. In both smokers (r = –0.53, P < 0.05) and non‐smokers (r = –0.54, P < 0.05), HDL2 concentration was negatively associated with HL activity. In non‐smokers, HDL3 concentration was negatively associated with CETP activity (r = –0.77, P < 0.05), whereas in smokers HDL3 concentration was negatively associated with LCAT activity (r = –0.78, P < 0.050).ConclusionIt was shown by direct measurement that the activity of plasma post‐heparin LPL is reduced in smokers, independently of age, gender and BMI. It is concluded that this enzyme perturbation associated with smoking may contribute to the development of the atherogenic lipoprotein phenotype seen in smokers.
Parathyroid hormone and ionized calcium levels are related to the severity of illness and survival in critically ill patients
Authors: Carlstedt  , Lind  , Rastad  , Stjernström  , Wide  , Ljunghall  
Published: March 2003

BackgroundThe present study explores serum parathyroid hormone (PTH) and blood ionized calcium (Ca2+) levels in relation to the severity of disease and mortality in the intensive care unit (ICU).MethodsIn a pilot study, 37 consecutive critically ill patients admitted to the ICU were studied with determinations of serum PTH and total serum calcium within the first 24 h. In a following prospective study, patients suffering from sepsis (n = 13) or subjected to major surgery (n = 13) were investigated daily for 1 week with determinations of serum PTH and ionized calcium (Ca2+). Severity of disease was assessed by the APACHE II score and hospital mortality was recorded.ResultsIn the pilot study, serum PTH levels were elevated (> 55 ng L−1) in 38% of the patients and were not related to serum calcium but showed a significant relationship to the APACHE II score (r = 0.39, P < 0.05). In the prospective study, serum PTH was elevated in 69% of the patients in both groups at inclusion, and 6 days later 87% of the septic and 37% of the surgery patients still showed elevated levels. Hypocalcaemia was more commonly seen in the septic patients [mean Ca2+ 1.03 ± 0.08 (SD) mmol L−1] than in the surgical patients (1.14 ± 0.06 mmol L−1) at inclusion. Both PTH and Ca2+ levels were significantly related to the APACHE II score (r = 0.46, P < 0.03, and r = –0.54, P < 0.009, respectively). Furthermore, PTH levels were significantly increased in non‐survivors (n = 5) compared with survivors (mean 161 ± 51 vs. 79 ± 51 ng L−1, P < 0.005).ConclusionHypocalcaemia and increased levels of PTH were common findings in critically ill patients. These alterations in calcium homeostasis were related to the severity of disease and increased PTH levels were associated with a poor outcome.
Purine metabolism in female heterozygotes for hypoxanthine–guanine phosphoribosyltransferase deficiency
Authors: Puig  , Mateos  , Torres  , Buño  
Published: March 2003

BackgroundFemale carriers of the X‐linked recessive disorder hypoxanthine–guanine phosphoribosyltransferase (HPRT) deficiency show somatic cell mosaicism, and this may cause an increased synthesis of purines. We have examined whether urinary oxypurines could be useful for carrier diagnosis.MethodsCarrier testing was performed in 35 women belonging to 16 unrelated Spanish families with at least one subject affected by the Lesch–Nyhan syndrome (11 families, 14 patients) or the Kelley–Seegmiller syndrome (five families, six patients) by means of HPRT and adenine phosphoribosyltransferase activities in hair follicles and/or molecular studies. Plasma and 24‐h urinary concentrations of hypoxanthine, xanthine and uric acid were measured while subjects were on a purine‐restricted diet.ResultsMean plasma urate concentrations and 24‐h urinary hypoxanthine, xanthine and uric acid excretion rates were significantly higher in 22 heterozygotes than in 13 non‐carriers (P < 0.02). Daily urinary oxypurine excretion rates were also significantly higher in heterozygotes than in 12 normal women (P = 0.0011). Cumulative 5‐day radioactivity excretion after [8‐14C]‐adenine infusion was markedly increased in 10 carrier women compared with five normal women (P = 0.0369). The sensitivity of 24‐h urinary hypoxanthine and xanthine excretion rates was 86% and 77%, respectively, and the specificity 100% for both tests.ConclusionFemale heterozygotes for HPRT deficiency show an enhanced purine nucleotide degradation and purine overproduction. An elevated hypoxanthine and/or xanthine excretion rate differentiated most heterozygotes for HPRT deficiency from non‐carrier women and thus could be useful for carrier diagnosis.
Direct in vivo gene transfer to healing rat patellar ligament by intra‐arterial delivery of haemagglutinating virus of Japan liposomes
Authors: Özkan  , Shino  , Nakamura  , Natsu‐ume  , Matsumoto  , Horibe  , Tomita  , Kaneda  , Ochi  
Published: March 2003

BackgroundManipulation of ligament healing has been a major focus of orthopaedic research. In recent years, gene transfer to healing ligament appears to be a feasible method for manipulating the healing process. In this study, we investigated the feasibility of gene transfer to healing rat patellar ligament by intra‐arterial delivery.MethodsAn attempt was made to transfer a reporter gene (Escherichia coli, β‐galactosidase gene) to healing rat patellar ligament using the haemagglutinating virus of Japan (HVJ) liposome‐mediated gene transfer method. Three days after cutting the patellar tendons of 25 14‐week‐old male Wistar rats, HVJ–liposome complexes containing β‐galactosidase (β‐gal) cDNA were injected into the femoral artery of 15 Wistar rats as the experimental group. HVJ liposomes without DNA were injected into the femoral artery of 10 Wistar rats as the control group. Three rats from the experimental group and two control rats were killed 3, 7, 14, 28 and 56 days after the injection.ResultsAfter X‐gal staining, the rate of transfection in the experimental group (mean ±  SEM) was found to be 12.1% ± 0.590%, 8.7% ± 0.217%, 10.2% ± 0.227%, 3.2% ± 0.247% and 0.7% ± 0.060% at post‐injection days 3, 7, 14, 28 and 56 respectively. In control sections the number of blue‐stained cells were very few at any point.ConclusionWe succeeded in introducing a reporter gene into healing rat patellar ligament by intra‐arterial delivery of HVJ–liposome complexes. This method appears to have the potential to be applicable for soft‐tissue healing studies and also healing studies of other tissues and organs.
Zymogen granule alterations in caerulein‐induced pancreatitis developed during continuous hydrocortisone administration
Authors: García‐Montero A. C. , Manso M. A. , Orfao A. , Vicente S. , De Dios I. 
Published: March 2003

BackgroundThe amount of enzymes stored in individual zymogen granules and the glycosylation of their membrane have been analysed in rats with acute pancreatitis induced by caerulein after hydrocortisone treatment. The consequences of prolonging hydrocortisone administration after pancreatitis and the use of the cholecystokinin (CCK) receptor antagonist, L‐364,718, have also been evaluated.Materials and methodsAnalysis was performed using flow cytometry.ResultsCaerulein‐induced pancreatitis in rats previously treated for 7 days with hydrocortisone (10 mg kg−1 per day) revealed alterations in enzyme storage in the pancreas. Significant increases in amylase and trypsinogen contents in zymogen granules were observed, an effect associated with a reduction in l‐fucose glycoconjugates. Pancreatitis persists 7 days later if hydrocortisone treatment is prolonged. At this stage, a reduced granule fucosylation was still observed, and a significant decrease in the amount of trypsinogen stored in the granules was found. However, hydrocortisone administration led to an increase in intragranular amylase quantities up to normal values, even when L‐364,718 was simultaneously administered, but it reverted to plasma as a consequence of pancreatitis. The amount of N‐acetyl d‐glucosamine in the zymogen granule membrane was not altered by caerulein acute pancreatitis induced under continuous hydrocortisone treatment, but it was decreased by the administration of L‐364,718 over 7 days after pancreatitis induction.ConclusionsThe administration of hydrocortisone after the development of pancreatitis prevented recurrence of the disease. L‐364,718 proved to be detrimental, not only failing to reduce the symptoms of pancreatitis but also altering the glycoproteins of zymogen granule membrane.
α2‐Macroglobulin reduces paracrine‐ and autocrine‐stimulated matrix synthesis of cultured rat hepatic stellate cells
Authors: Schüftan G. G. , Bachem M. G. 
Published: March 2003

BackgroundTransforming growth factor β1 (TGF‐β1) is considered to represent a major fibrogenic mediator in the liver. The aim of the present study was to investigate whether α2‐macroglobulin (α2M) might reduce paracrine‐ and autocrine‐stimulated matrix synthesis of cultured rat hepatic stellate cells (HSCs) by scavenging TGF‐β.Methods and resultsUsing native agarose electrophoresis, we demonstrated that α2M binds [125I]‐TGF‐β1 within minutes. Preincubation of transiently acidified supernatants of cultured Kupffer cells, secondary cultured (activated) HSC and platelet lysate with, respectively, 500 and 2000 μg mL−1α2M significantly reduced the concentration of active TGF‐β1 in these media. As a consequence of TGF‐β scavenging by α2M, paracrine‐stimulated proteoglycan synthesis of primary cultured HSCs was reduced significantly. Furthermore, addition of 200 μg mL−1α2M to passaged (activated) HSCs resulted in (a) a reduction in autocrine‐stimulated extracellular matrix synthesis (proteoglycan −52%, fibronectin −55%) and (b) increased cell proliferation. A similar reduction in matrix synthesis was observed after the addition of 5 μmol L−1 TGF‐β1 antisense oligonucleotide to activated HSCs.ConclusionWe conclude that α2M reduces paracrine‐and autocrine‐stimulated extracellular matrix synthesis of cultured HSCs by scavenging TGF‐β. These mechanisms might restrict liver fibrogenesis.
Expression pattern of tumour necrosis factor receptors in subcutaneous and omental human adipose tissue: role of obesity and non‐insulin‐dependent diabetes mellitus
Authors: Hube  , Birgel  , Lee  , Hauner  
Published: March 2003

BackgroundTumour necrosis factor α (TNF) mRNA expression has been reported to be up‐regulated in adipose tissue from several rodent models of obesity and diabetes and from obese humans. This elevated expression has been assumed to be associated with the development of insulin resistance. However, the biological signal of TNF may be influenced by the expression of the two TNF receptors: the p60 TNF receptor, TNFR60, and the p80 TNF receptor, TNFR80.DesignThe aim of this study was to investigate the mRNA expression pattern of the two TNF receptors and their ligand in two adipose tissue depots of glucose‐tolerant obese women [n = 18, body mass index (BMI) 48.2 ± 8.4 kg m−2], obese women with impaired glucose tolerance or overt non‐insulin‐dependent diabetes mellitus (NIDDM) (n = 10, BMI 49.1 ± 11.6 kg m−2) and healthy non‐obese control subjects (n = 12, BMI 25.8 ± 2.7 kg m−2). RNA expression was assessed by a semiquantitative reverse transcriptase polymerase chain reaction (RT‐PCR) technique.ResultsThe mean mRNA levels of both TNF receptors were two‐ to threefold higher in adipose tissue samples from the obese than from the non‐obese women (P < 0.01 for each). Although TNFR60 mRNA did not vary within each obese group, there was a wide variation in the levels of TNFR80 mRNA and of TNF mRNA. A comparison of the expression levels between the subcutaneous abdominal and the omental adipose tissue depots showed significantly higher expression in the former. The TNFR60 expression level was positively correlated with BMI and fat cell size, whereas TNFR80 and TNF mRNA levels showed positive associations with serum insulin and triglyceride concentrations. No significant differences in the expression levels were observed between obese individuals with and without impaired glucose tolerance/NIDDM.ConclusionThese results indicate that severe obesity in women is characterized by increased amounts of the two TNF receptor mRNAs. The role of this up‐regulation for the development of obesity‐associated insulin resistance remains to be elucidated.
Anti‐PR‐3 antibodies induce endothelial IL‐8 release
Authors: Mayet  , Schwarting  , Barreiros  , Schlaak  , Neurath  
Published: March 2003

BackgroundIt has been shown that interaction of anti‐PR‐3 antibodies with human endothelial cells (EC) leads to an activation of EC in vitro, i.e. induction of adhesion molecules like E‐selectin, VCAM‐1 and tissue factor. The aim of this study was to investigate the effect of anti‐PR‐3 antibodies on endothelial IL‐8 expression.Materials and methodsEC were cultured in 96‐well plates and stimulated with TNF‐α and IL‐1β for 1 h to induce membrane expression of endothelial PR‐3. Anti‐PR‐3 antibodies were purified from sera from patients with clinically active Wegener's granulomatosis. Purified anti‐Ro, anti‐centromere, anti‐dsDNA antibodies and a monoclonal anti‐PR‐3 antibody (WGM2) served as controls. Induction of IL‐8 mRNA was detected by RT‐PCR. IL‐8 was measured in the supernatant of EC by ELISA. In addition, induction of NFκB was investigated by PAGE of nuclear extracts of EC and Western blot with ab against p65.ResultsIn contrast to controls, interaction of anti‐PR‐3 antibodies (patients and WGM2) with cytokine activated EC led to the highest amount of IL‐8 synthesis. Priming of EC with cytokines alone induced a markedly lower IL‐8 level. The lowest levels of IL‐8 could be measured after incubation of unprimed EC with anti‐PR‐3 antibodies. Anti‐PR‐3 antibody induced endothelial IL‐8 expression could be inhibited by cycloheximide. In addition, we established that the activation of NF‐κB is critically involved in anti‐PR‐3 antibody induced endothelial IL‐8 production.ConclusionIn summary, we were able to show that anti‐PR‐3 antibodies induce endothelial IL‐8 synthesis by activating NF‐κB. As IL‐8 represents a powerful neutrophil chemoattractant, our data provide further evidence for a direct pathogenic effect of anti‐PR‐3 antibodies in ANCA related diseases.
Compound heterozygosity of Leu252Val and Leu252Arg causing lipoprotein lipase deficiency in a Chinese patient with hypertriglyceridemia
Authors: Chan  , Mak  , Tomlinson  , Baum  , Wu  , Masarei  , Pang  
Published: March 2003

BackgroundWe investigated lipoprotein lipase (LPL) gene mutations in a Chinese male with severe hypertriglyceridemia and recurrent pancreatitis.MethodsWe screened for LPL sequence mutation in the LPL gene in this patient, his relatives and 160 unrelated hypertriglyceridaemic subjects. We determined the postheparin plasma LPL activity of subjects carrying a LPL mutation and studied the in vitro expression of mutant LPL in COS‐1 cells.ResultsThe proband was found to be a compound heterozygote for a novel Leu252Val and a reported Leu252Arg mutation in the LPL gene. He had low plasma levels of postheparin LPL activity and mass. The two mutations segregated independently in his family. In vitro expression analysis showed that Leu252Arg abolished both the catalytic function and secretion of LPL, while Leu252Val abolished the catalytic function but only reduced secretion by about half. We have also detected heterozygous Leu252Val and Leu252Arg mutations each in one hypertriglyceridaemic individual.ConclusionThese results indicated that the leucine 252 is critical for the catalytic activity and secretion of LPL. Why the substitution by valine instead of arginine resulted only in a partial suppression of LPL secretion, remains to be investigated. Leu252Val and Leu252Arg are the likely cause of hypertriglyceridemia in these subjects because of their deleterious effects on LPL activity or secretion. Leu252Val/Leu252Arg is the first compound heterozygous mutation known to occur in the same codon of the LPL gene. So far they are found only in Chinese.