bluuebunny/crossref_metadata_2025_split huggingface dataset:
Apolipoprotein C‐ll deficiency syndrome due to apo C‐IIHamburg: clinical and biochemical features and Hphl restriction enzyme polymorphism
Authors: BEIL F. U. , FOJO S. S. , BREWER H. B. , GRETEN H. , BEISIEGEL U. 
Published: March 2008

Abstract. We have characterized the clinical and biochemical features of three siblings of a kindred with severe hypertriglyceridaemia due to apolipoprotein C‐II (apo C‐II) deficiency caused by the mutation described as apo C‐IIHumburg. The clinical syndrome is characterized by recurrent pancreatitis in two of three affected individuals, with discrete hepatosplenomegaly in all three patients and cholelithiasis in one. Eruptive xanthomas and lipemia retinalis were absent.Plasma lipoproteins were characterized by fasting chylomicronaemia, reduced low density lipoproteins (LDL) and low high density lipoproteins (HDL). The marked hypertriglyceridaemia could be corrected promptly by infusion of normal plasma. Apolipoprotein C‐II (apo C‐II) levels in homozygotes were very low (0.01 mg dl‐1), and mean apo C‐II levels in heterozygotes were lower (2.08 pM 0.11 mg dl‐1) than in normal family members (3.38 pM 0.75 mg dl‐1). Lipoprotein lipase and hepatic triglyceride lipase activities in post‐heparin plasma were normal. Zonal ultracentrifugation revealed a marked increase in triglyceriderich lipoproteins and reduced LDL and HDL. LDL consisted of two fractions with higher hydrated density of the main fraction compared with normals with a trend to normalization on a fat‐free diet.The molecular defect in the apo C‐II Hamburg gene has been previously identified as a donor splice site mutation in the second intron. This leads to abnormal splicing of the apo C‐II Hamburg mRNA and apo C‐II deficiency in plasma. The mutation causes the loss of an Hphl restriction enzyme site present in the normal apo C‐II gene. Digestion of polymerase chain reaction (PCR)‐amplified DNA of members of the Hamburg kindred with Hphl permitted the identification of non‐obligate heterozygote individuals which could not be recognized by either fasting triglyceride or apo C‐II plasma levels.
Oncogene‐mediated propagation of tracheal epithelial cells from two cystic fibrosis fetuses with different mutations. Characterization of CFT‐1 and CFT‐2 cells in culture
Authors: LEMNAOUAR M. , CHASTRE E. , PAUL A. , MERGEY M. , VEISSIÈRE D. , CHERQUT G. , BARBRY P. , SIMON‐BOUY B. , FANEN P. , GESPACH C. , PICARD J. 
Published: March 2008

Abstract. Primary tracheal epithelial cells obtained from two fetuses with cystic fibrosis (CF) were successfully transfected with a plasmid vector recombined with the large T oncogene of SV40. The resulting tracheal cells were propagated in culture for up to 25 passages and retained the mutations of the CF genes carried by the two fetuses, one heterozygous for the S549N and N1303K substitutions (CFT‐I cells), and the other homozygous for the most common deletion ΔF508 (CFT‐2 cells). The transfected cells: (a) expressed the SV40 large T oncogene, as determined by immunofluorescence and Northern blot analysis; (b) retained typical epithelial morphology, as assessed by the presence of microvilli, desmosomes, gap junctions, and cytokeratin expression; (c) were fully responsive to the cAMP‐stimulating agents isproterenol, forskolin and vasoactive intestinal peptide for cAMP production and PKA activation; (d) do not produce any tumour in the athymic nude mice; (e) were diploid and tetraploid with a normal chromosomal complement at early passages, and (f) exhibited the abnormal regulation of chloride conductance characteristic of CF.These results indicate that CFT‐1 and CFT‐2 cells constitute a suitable model for: (a) comparison of the maturation and function of the CFTR protein mutated in the two nucleotide‐binding domains; (2) analysis of the biochemical defect in CF epithelial airway cells, (c) development of new therapeutic agents, and correction of the CF defect by gene replacement therapy in vitro.
Relationship of alcohol consumption to changes in HDL‐subfractions
Authors: SILLANAUKEE P. , KOIVULA T. , JOKELA H. , MYLLYHARJU H. , SEPPÄ K. 
Published: March 2008

Abstract. Epidemiological studies have consistently shown an apparent protective effect of moderate alcohol consumption on coronary artery disease (CAD). This has been considered to be due to the rise in the high‐density cholesterol lipoprotein (HDL‐cholesterol). Since the response of the HDL‐subfractions to moderate or heavy dose of alcohol is less clear, we now compared the high‐density lipoprotein cholesterol status between groups consuming different amounts of alcohol. In this population‐based survey serum total high‐density lipoprotein cholesterol and its HDL2 and HDL3 subfractions were blindly compared between 264 consecutive middle‐aged men (37 teetotallers, 137 moderate drinkers, 90 heavy drinkers) participating in a voluntary health screening and 104 male alcoholics.Alcohol consumption correlated significantly (P<0.001) with total HDL‐cholesterol, HDL2, HDL3 when all subjects (n= 368) were included but the correlation disappeared when alcoholics were excluded (n = 264). In comparison with teetotallers, alcoholics had significantly higher total HDL‐cholesterol, HDL2 and HDL3 values (P < 0.001). Moderate or heavy intake of alcohol had no effect on HDL2 but increased the HDL3‐‐fraction.If the protective effect of moderate alcohol consumption is mediated by high‐density lipoprotein, it may not be accounted for by changes in the HDL2‐‐fraction. The observed increases in the concentration of the HDL3‐‐fraction, however, suggest that this subfraction may not be inert with respect to coronary disease and could possibly have a role in the protective effect.
Zinc and magnesium in liver cirrhosis
Authors: ROCCHI E. , BORELLA P. , BORGHI A. , PAOLILLO F. , PRADELLI M. , FARINA F. , CASALGRANDI G. 
Published: March 2008

Abstract. The Authors determined zinc (Zn) and magnesium (Mg) in the plasma, urine, erythrocytes (RBCs), mono‐ and polymorphonuclear cells (MNCs and PMNs) of patients with overt alcoholic and nonalcoholic liver cirrhosis. In order to obtain a clearer clinical picture, biochemical and nutritional parameters (retinol, tocopherol, six different carotenoids, creatinine‐height index and tricipital skinfold), as well as markers of portal hypertension (spleno‐portal size and platelet count) were also evaluated.The plasma levels of Zn and Mg were found to be reduced, as were the urine levels of Mg. Urine Zn, on the other hand, was higher than normal. Plasma Zn correlated inversely, and urine Zn directly, with the severity of the disease, rather than with alcohol consumption or treatment with diuretics. Protein metabolism impairment would appear to affect the plasma transport of Zn rather than its overall availability in the organism; the opposite was found in the case of Mg, the availability of which appeared to be reduced. Determination of the two elements in RBCs, MNCs and PMNs suggested that a true nutritional deficit cannot be demonstrated. MNCs, rather than RBCs or PMNs seem better to reflect tissue status of trace elements.
The relationship of serum total sialic acid with serum acute phase proteins and lipoprotein (a) in patients with severe hypertriglyceridaemia
Authors: CROOK M. , HAQ S. , HAQ M. , TUTT P. 
Published: March 2008

Abstract. Total serum sialic acid (TSA), recently shown to be a cardiovascular risk factor, was measured in 15 patients with severe hypertriglyceridaemia (fasting triglyceride > 2·3 mmol l‐1) and 15 age and sex matched normal control subjects.To test the hypothesis that serum TSA is related in some way to serum acute phase proteins we also measured five acute phase proteins, namely alpha‐1‐antichymotrypsin (ACT), alpha‐1‐acid‐glycoprotein (AGP), alpha‐2‐macroglobulin (AMG), C‐reactive protein (CRP) and haptoglobin (HAP) in both groups.Of note was the significantly elevated serum TSA in the severely hypertriglyceridaemic group as compared to normal subjects. Serum TSA being 71·9 ± 11·7 mg dl‐1 and 59·6 ± 10·2 mg dl‐1 respectively (P < 0·01 Mann‐Whitney test).Serum CRP was significantly elevated in the type IV patients as compared to controls (6·4 ± 4·5 mg l‐1 vs. 3·3 ± 1·9 mg l‐1P<0·05 Mann Whitney test) as was serum AMG (2·1 ± 0·89 g l‐1 vs. 1·5 ± 0·53 g l‐1P < 0·05 Mann Whitney test).There was no correlation between serum TSA and lipoprotein (a) in either the normal or severely hypertriglyceridaemic subjects. We suggest that serum TSA could in part be related to hypertriglyceridaemia and serum acute phase proteins but that its property as a cardiovascular risk factor is not related to serum lipoprotein (a) concentrations.
Ascorbic acid reduces the endotoxin‐induced lung injury in awake sheep
Authors: DWENGER A. , PAPE H. C. , BANTEL C. , SCHWEITZER G. , KRUMM K. , GROTZ M. , LUEKEN B. , FUNCK M. , REGEL G. 
Published: March 2008

Abstract Our aim was to investigate whether ascorbic acid can reduce reactive oxygen metabolite‐mediated acute lung injury.The effects of intravenous administration of Escherichia coli endotoxin were studied, with and without ascorbic acid infusion, on haemodynamics, lung lymph flow, cardio‐respiratory and neutrophil function in chronically instrumented sheep. Paired experiments were performed on eight sheep in which they received either endotoxin alone (0·5 μg kg‐1 b.w.) (ET group) or in combination with an ascorbic acid infusion (1 g kg‐1 b.w. bolus injection followed by 0·2 g kg‐1 h‐1 continuous infusion) (ET + ASC group) in random order. Four of the animals also received ascorbic acid alone (ASC group).As a result, for the ET + ASC group a general and mostly significant improvement (P < 0·05) in the early hypertensive phase (0·60 min, P values) and in the late permeability phase (2–4 h, *P values) of cardiorespiratory function (mean artery pressure: P/*P= 0·283/0·049; mean pulmonary artery pressure: P/*P= 0·0.0001; mean pulmonary artery wedge pressure: P/*P= 0·02/0·001; right ventricular stroke work index: P/*P= 0·02/0·0001; cardiac index: P/*P= 0·797/0·755; arterial oxygen saturation: P/*P= 0·0059/0·01; arterial‐venous difference of oxygen tension: P/*P= 0·011/0·0005), oxygen consumption: P/*P=0·013/0·035, lung lymph flow: P/*P=0·562/0·012, lymph/plasma protein ratio: P/*P= 0·304/0·008 and protein clearance: P/*P= 0·56/0·05 was observed in comparison with the ET group. The decrease of the neutrophil chemiluminescence response of the ET + ASC group in the late phase: P/*P= 0·419/0·026 was most likely due to ascorbic acid, whereas β‐N‐acetylglucosaminidase secretion was identical for both groups. In conclusion, we suggest that reactive oxygen metabolite scavenging by ascorbic acid is responsible for the improvement of endotoxin‐induced acute lung injury.
Smoking attenuates the vasoconstrictor response to noradrenaline in type I diabetic patients and normal subjects: possible relevance to diabetic nephropathy
Authors: BODMER C. W. , VALENTINE D. T. , MASSON E. A. , SAVAGE M. W. , LAKE D. , WILLIAMS G. 
Published: March 2008

Abstract Exaggerated vascular reactivity has been implicated in the pathogenesis of diabetic nephropathy, and several studies suggest that smoking accelerates its progression. We therefore assessed the vasoactive effects of smoking by comparing noradrenaline‐induced vasoconstriction in dorsal hand‐veins between smoking and non‐smoking groups of Type I diabetic patients with and without microalbuminuria and in non‐diabetic subjects. Smokers had a significantly higher dose causing 50% vasoconstriction (reduced sensitivity to noradrenaline) in all three groups: microalbuminuric diabetic smokers vs. non‐smokers, 20·2(4·6) (SEM) vs. 6·6(2·3) ng min‐1 (P = 0·02); normoalbuminuric, 76·9(29·4) vs. 22·8(9·1) ng min‐1 (P = 0·03); non‐diabetic subjects, 97·8(30·0) vs. 38·0(12·8) ng min‐1 (P = 0·01). Both microalbuminuric diabetic groups showed significantly greater sensitivity to noradrenaline‐induced vasoconstriction than the other smoking and non‐smoking groups, respectively (P<0·01).Vasoconstrictor responses to noradrenaline are attenuated in smokers, possibly due to α‐adrenoceptor down‐regulation. Smoking could increase urinary albumin losses and accelerate renal damage through catecholamine surges which raise systemic and, perhaps, intraglomerular blood pressure. This hypothesis deserves further consideration.
Contribution of glycaemic control, endogenous lipoproteins and cholesteryl ester transfer protein to accelerated cholesteryl ester transfer in IDDM
Authors: RITTER M. C. , BAGDADE J. D. 
Published: March 2008

Abstract In an earlier study we demonstrated that the transfer of cholesteryl ester (CET) estimated as the net mass of CE lost from HDL to the apoB‐containing lipoproteins (VLDL + LDL) during incubation of plasma is accelerated in normolipidaemic patients with insulin‐dependent diabetes mellitus (IDDM). Recombination experiments with isolated lipoprotein fractions employing this same mass transfer assay indicated that this disturbance resulted from dysfunction of VLDL and not from changes in the activity of CE transfer protein (CETP).In this study, we sought first to determine whether CET estimated with an isotopic method that measures the transfer of radiolabelled CE from exogenous HDL from non‐diabetic controls to endogenous VLDL + LDL was also increased in IDDM and, if so, the extent to which this disturbance was affected by glycaemic control, VLDL and CETP. As observed with the mass transfer assay, the rate of transfer of the HDL‐CE label to VLDL + LDL was also significantly accelerated in IDDM plasma (IDDM: k = 0·256±0·07; control: k = 0·092±0·05; mean±SD; P < 0·001). Fasting glucose and fructosamine correlated with both isotopic transfer (k) (r= 0·54, P= 0·009; r= 0·57, P= 0·005, respectively) and the mass of CE transferred at 2 h (r= 0·55, P= 0·006; r= 0·59, P= 0·004, respectively). Recombination experiments revealed that isotopic CET was accelerated when: (a) IDDM VLDL were combined with controls HDL and d > 1·21 fractions; and (b) IDDM d > 1·21 plasma fractions containing CETP were combined with controls VLDL + LDL and HDL. While CETP concentrations in a subset of the study group were higher in the diabetic than in the non‐diabetic controls, the difference was not statistically significant (IDDM 2·25±0·97 vs. control 1·58±0·58 μg ml‐1; mean±SD; P<0·1). These findings indicate that dysfunction of VLDL and increased CETP concentrations both contribute to the pathological acceleration of isotopic transfer in IDDM plasma and that the magnitude of this proatherogenic defect correlates closely with glycaemic control.
Circulating somatostatin‐28 is not a physiologic regulator of gastric acid production in man
Authors: HILDEBRAND P. , ENSINCK J. W. , BUETTIKER J. , DREWE J. , BURCKHARDT B. , GYR K. , BEGLINGER C. 
Published: March 2008

Abstract. Studies were designed to establish the acid inhibitory potency and plasma kinetics of somatostatin‐28 (S‐28) in humans and to determine whether the amount of S‐28 released into the circulation after a meal is sufficient to regulate gastric acid secretion. A liquid meal induced a significant increase of S‐28 (P < 0·01) whereas S‐14 levels did not change. Postprandial S‐28 concentrations were then mimicked by exogenous infusions and tested on basal and pentagastrin‐stimulated gastric acid secretion. Expressed in terms of circulating plasma concentrations measured by specific radioimmunoassays, S‐14 was 10 times more potent than S‐28 in inhibiting gastric acid production. The plasma half‐life of S‐28 (1·86 min) was longer than that of S‐14 (1·00 min) due to a slower plasma clearance rate. S‐28 did neither affect basal and stimulated gastric acid secretion nor postprandial intragastric acidity.These studies suggest that postprandial plasma concentrations of S‐28 are unlikely to regulate gastric acid secretion in man. They also show that S‐28 is several times less potent than S‐14 with respect to inhibition of gastric acid output.
The in vivo effect of interleukin‐1β on urea synthesis is mediated by glucocorticoids in rats
Authors: HEINDORFF H. , ALMDAL T. , VILSTRUP H. 
Published: March 2008

Abstract. Interleukin‐1β has been proposed as one mediator of parts of the catabolic response following surgery. However, it is not known whether such an effect is due to interleukin‐1β itself or the associated changes in glucocorticoids.The effect of interleukin‐1β on urea synthesis was investigated in rats given a high (10 μg kg‐1) and a low dose (0·1 μg kg‐1) of recombinant interleukin‐1β (NOVO, Denmark) 3 h prior to determination of the rate of urea synthesis in vivo. Urea synthesis increased dose‐dependently after the low dose from 4·0±0·3 (control) to 6·3±0·3 (P<0·01), and after the high dose to 7·7±0·3 μmol (min·100 gBW)‐1 (P<0·01). The blood concentration of amino acids fell during interleukin‐1β treatment, so the effect on urea synthesis was not due solely to increased proteolysis, but was exerted predominantly in the liver.Pharmacological glucocorticoid receptor blockade (hormone analogue RU486, Roussel–Uclaf, Paris, France) given 1 h prior to the interleukin treatment, completely abolished the interleukin‐1β induced increases in urea synthesis. The study demonstrates that interleukin‐1β stimulates urea synthesis in vivo, and that the major part of the effect depends on glucocorticoid action.
A meta‐analysis of latitudinal variations in life‐history traits of roach, Rutilus rutilus, over its geographical range: linear or non‐linear relationships?
Authors: LAPPALAINEN JYRKI , TARKAN ALI SERHAN , HARROD CHRIS 
Published: March 2008

Summary1. We collated information from the literature on life history traits of the roach (a generalist freshwater fish), and analysed variation in absolute fecundity, von Bertalanffy parameters, and reproductive lifespan in relation to latitude, using both linear and non‐linear regression models. We hypothesized that because most life history traits are dependent on growth rate, and growth rate is non‐linearly related with temperature, it was likely that when analysed over the whole distribution range of roach, variation in key life history traits would show non‐linear patterns with latitude.2. As fecundity depends strongly on length, and the length structure of females varied among populations, latitudinal patterns in fecundity were examined based on residuals from the length–fecundity relationship. The reproductive lifespan of roach was estimated as the difference between age at maturity and maximum age of females in each population.3. The three life history traits of roach analysed all varied among populations and were non‐linearly related to latitude. Only the relationship between reproductive lifespan and latitude was a better fit to a linear that to a quadratic model, although Loess smoothing curves revealed that this relationship was actually closer to biphasic than linear in form. A latitude of 50°N formed a break point in all three life history traits.4. The negative relationships we have described between (i) fecundity and reproductive lifespan and (ii) fecundity and egg mass suggest that lower fecundity is compensated for by longer lifespan, while lower fecundity is compensated for by an increased egg mass, when analysed independently of location.
Future novel threats and opportunities facing UK biodiversity identified by horizon scanning
Authors: Sutherland William J. , Bailey Mark J. , Bainbridge Ian P. , Brereton Tom , Dick Jaimie T. A. , Drewitt Joanna , Dulvy Nicholas K. , Dusic Nicholas R. , Freckleton Robert P. , Gaston Kevin J. , Gilder Pam M. , Green Rhys E. , Heathwaite A. Louise , Johnson Sally M. , Macdonald David W. , Mitchell Roger , Osborn Daniel , Owen Roger P. , Pretty Jules , Prior Stephanie V. , Prosser Havard , Pullin Andrew S. , Rose Paul , Stott Andrew , Tew Tom , Thomas Chris D. , Thompson Des B. A. , Vickery Juliet A. , Walker Matt , Walmsley Clive , Warrington Stuart , Watkinson Andrew R. , Williams Rich J. , Woodroffe Rosie , Woodroof Harry J. 
Published: March 2008

Summary

Horizon scanning is an essential tool for environmental scientists if they are to contribute to the evidence base for Government, its agencies and other decision makers to devise and implement environmental policies. The implication of not foreseeing issues that are foreseeable is illustrated by the contentious responses to genetically modified herbicide‐tolerant crops in the UK, and by challenges surrounding biofuels, foot and mouth disease, avian influenza and climate change.
A total of 35 representatives from organizations involved in environmental policy, academia, scientific journalism and horizon scanning were asked to use wide consultation to identify the future novel or step changes in threats to, and opportunities for, biodiversity that might arise in the UK up to 2050, but that had not been important in the recent past. At least 452 people were consulted.
Cases for 195 submitted issues were distributed to all participants for comments and additions. All issues were scored (probability, hazard, novelty and overall score) prior to a 2‐day workshop. Shortlisting to 41 issues and then the final 25 issues, together with refinement of these issues, took place at the workshop during another two rounds of discussion and scoring.
We provide summaries of the 25 shortlisted issues and outline the research needs.
We suggest that horizon scanning incorporating wide consultation with providers and users of environmental science is used by environmental policy makers and researchers. This can be used to identify gaps in knowledge and policy, and to identify future key issues for biodiversity, including those arising from outside the domains of ecology and biodiversity.
Synthesis and applications. Horizon scanning can be used by environmental policy makers and researchers to identify gaps in knowledge and policy. Drawing on the experience, expertise and research of policy advisors, academics and journalists, this exercise helps set the agenda for policy, practice and research.
Bacteriophage infection is targeted to cellular poles
Authors: Edgar Rotem , Rokney Assaf , Feeney Morgan , Semsey Szabolcs , Kessel Martin , Goldberg Marcia B. , Adhya Sankar , Oppenheim Amos B. 
Published: March 2008

SummaryThe poles of bacteria exhibit several specialized functions related to the mobilization of DNA and certain proteins. To monitor the infection of Escherichia coli cells by light microscopy, we developed procedures for the tagging of mature bacteriophages with quantum dots. Surprisingly, most of the infecting phages were found attached to the bacterial poles. This was true for a number of temperate and virulent phages of E. coli that use widely different receptors and for phages infecting Yersinia pseudotuberculosis and Vibrio cholerae. The infecting phages colocalized with the polar protein marker IcsA–GFP. ManY, an E. coli protein that is required for phage λ DNA injection, was found to localize to the bacterial poles as well. Furthermore, labelling of λ DNA during infection revealed that it is injected and replicated at the polar region of infection. The evolutionary benefits that lead to this remarkable preference for polar infections may be related to λ's developmental decision as well as to the function of poles in the ability of bacterial cells to communicate with their environment and in gene regulation.