bluuebunny/crossref_metadata_2025_split huggingface dataset:
(Peri)vascular production and action of pro-inflammatory cytokines in brain pathology
Authors: Konsman Jan P. , Drukarch Benjamin , Van Dam Anne-Marie 
Published: March 2007

In response to tissue injury or infection, the peripheral tissue macrophage induces an inflammatory response through the release of IL-1β (interleukin-1β) and TNFα (tumour necrosis factor α). These cytokines stimulate macrophages and endothelial cells to express chemokines and adhesion molecules that attract leucocytes into the peripheral site of injury or infection. The aims of the present review are to (i) discuss the relevance of brain (peri)vascular cells and compartments to bacterial meningitis, HIV-1-associated dementia, multiple sclerosis, ischaemic and traumatic brain injury, and Alzheimer's disease, and (ii) to provide an overview of the production and action of pro-inflammatory cytokines by (peri)vascular cells in these pathologies of the CNS (central nervous system). The brain (peri)vascular compartments are highly relevant to pathologies affecting the CNS, as infections are almost exclusively blood-borne. Insults disrupt blood and energy flow to neurons, and active brain-to-blood transport mechanisms, which are the bottleneck in the clearance of unwanted molecules from the brain. Perivascular macrophages are the most reactive cell type and produce IL-1β and TNFα after infection or injury to the CNS. The main cellular target for IL-1β and TNFα produced in the brain (peri)vascular compartment is the endothelium, where these cytokines induce the expression of adhesion molecules and promote leucocyte infiltration. Whether this and other effects of IL-1 and TNF in the brain (peri)vascular compartments are detrimental or beneficial in neuropathology remains to be shown and requires a clear understanding of the role of these cytokines in both damaging and repair processes in the CNS.
Enhanced cardiac production of matrix metalloproteinase-2 and -9 and its attenuation associated with pravastatin treatment in patients with acute myocardial infarction
Authors: Yasuda Satoshi , Miyazaki Shunichi , Kinoshita Hideyuki , Nagaya Noritoshi , Kanda Munetake , Goto Yoichi , Nonogi Hiroshi 
Published: March 2007

Previous experimental studies have demonstrated that MMPs (matrix metalloproteinases) contribute to LV (left ventricular) remodelling. We hypothesized that cardiac MMPs are activated in patients with AMI (acute myocardial infarction) and, if so, MMP production may be attenuated by statins (3-hydroxy-3-methylglutaryl-CoA reductase inhibitors) through their cardiovascular protective actions. We studied 30 patients, ten control patients with stable angina pectoris and 20 patients with AMI, in whom LV catheterization at the chronic stage was performed 22±12 days (value is mean±S.D.) after the onset of AMI. Blood samples were collected from the CS (coronary sinus) and a peripheral artery. In patients with AMI, the levels of MMP-2 and MMP-9 were significantly (P&lt;0.05) higher in the CS than the peripheral artery (MMP-2, 853±199 compared with 716±127 ng/ml; MMP-9, 165±129 compared with 98±82 ng/ml), whereas no significant differences were observed in the patients with angina pectoris. The CS–arterial concentration gradients of MMP-2 and MMP-9 correlated positively with BNP (brain natriuretic peptide) levels (MMP-2, R=0.68, P&lt;0.01; MMP-9, R=0.59, P&lt;0.05) and LV end-diastolic volume index (MMP-2, R=0.70, P&lt;0.01; MMP-9, R=0.70, P&lt;0.01). When patients with AMI treated with 10 mg of pravastatin or without (n=10 in each group) were compared, this statin therapy significantly (P&lt;0.05) decreased the CS–arterial concentration gradients of MMP-2 (69±43 compared with 213±185 ng/ml) and MMP-9 (14±27 compared with 119±84 ng/ml). In conclusion, the enhanced production of cardiac MMP-2 and MMP-9 is associated with LV enlargement and elevated BNP levels in patients with AMI. A pleiotropic effect of statins appears to be associated with the modulation of cardiac MMP activation, which may be potentially beneficial in the attenuation of post-infarction LV remodelling.
Chronic administration of genistein improves endothelial dysfunction in spontaneously hypertensive rats: involvement of eNOS, caveolin and calmodulin expression and NADPH oxidase activity
Authors: Vera Rocio , Sánchez Manuel , Galisteo Milagros , Villar Inmaculada Concepcion , Jimenez Rosario , Zarzuelo Antonio , Pérez-Vizcaíno Francisco , Duarte Juan 
Published: March 2007

The soya-derived phytoestrogen genistein has been suggested to be protective in cardiovascular diseases. In the present study, we have analysed whether chronic oral genistein might influence endothelial function in male SHRs (spontaneously hypertensive rats) via ERs (oestrogen receptors), changes in eNOS (endothelial NO synthase) activity and vascular O2− (superoxide) production. Rats (23-weeks old) were divided into the following groups: WKY (Wistar–Kyoto)-vehicle, SHR-vehicle, WKY-genistein (10 mg·kg−1 of body weight·day−1); SHR-genistein; SHR-genistein-faslodex (ICI 182780; 2.5 mg·kg−1 of body weight·day−1). Vascular expression of eNOS, caveolin-1 and calmodulin-1 were analysed by Western blotting, eNOS activity by conversion of [3H]arginine into L-[3H]citrulline and O2− production by chemoluminescence of lucigenin. In SHRs, after 5 weeks of treatment, genistein reduced systolic blood pressure and enhanced endothelium-dependent aortic relaxation to acetylcholine, but had no effect on the vasodilator responses to sodium nitroprusside. Compared with WKY rats, SHRs had up-regulated eNOS and down-regulated caveolin-1 and calmodulin-1 expression, increased NADPH-induced O2− production, but reduced eNOS activity. Genistein increased aortic calmodulin-1 protein abundance and eNOS activity, and reduced NADPH-induced O2− production in SHRs. The pure ERα and ERβ antagonist faslodex did not modify any of the changes induced by genistein in SHRs, suggesting that these effects are unrelated to ER stimulation. In conclusion, genistein reduced the elevated blood pressure and endothelial dysfunction in SHRs. This latter effect appears to be related to increased eNOS activity associated with increased calmodulin-1 expression and decreased O2− generation.
Growth hormone decreases phase II ventricular tachyarrhythmias during acute myocardial infarction in rats
Authors: Elaiopoulos Dimitrios A. , Tsalikakis Dimitrios G. , Agelaki Maria G. , Baltogiannis Giannis G. , Mitsi Agathokleia C. , Fotiadis Dimitrios I. , Kolettis Theofilos M. 
Published: March 2007

GH (growth hormone) administration during acute MI (myocardial infarction) ameliorates subsequent LV (left ventricular) dysfunction. In the present study, we examined the effects of such treatment on arrhythmogenesis. A total of 53 Wistar rats (218±17 g) were randomized into two groups receiving two intraperitoneal injections of either GH (2 international units/kg of body weight; n=26) or normal saline (n=27), given at 24 h and 30 min respectively, prior to MI, which was generated by left coronary artery ligation. A single-lead ECG was recorded for 24 h post-MI, using an implanted telemetry system. Episodes of VT (ventricular tachyarrhythmia) and VF (ventricular fibrillation) during the first hour (phase I) and the hours following (phase II) MI were analysed. Monophasic action potential was recorded from the lateral LV epicardium at baseline and 24 h post-MI, and APD90 (action duration at 90% of repolarization) was measured. Infarct size was calculated 24 h post-MI. Infarct size and phase I VT+VF did not differ significantly between groups, but phase II hourly duration of VT+VF episodes was 82.8±116.6 s/h in the control group and 18.3±41.2 s/h in the GH group (P=0.0027), resulting in a lower arrhythmic (P=0.016) and total (P=0.0018) mortality in GH-treated animals. Compared with baseline, APD90 was prolonged significantly 24 h post-MI in the control group, displaying an increased beat-to-beat variation, but remained unchanged in the GH group. We conclude that GH decreases phase II VTs during MI in the rat. This finding may have implications in cardiac repair strategies.
Induction of apoptosis in rat lymphocytes by starvation
Authors: Pires Juliana , Curi Rui , Otton Rosemari 
Published: March 2007

The aim of the present study was to investigate whether fasting for 24 and 48 h induces apoptosis of rat mesenteric lymph node lymphocytes similar to that observed previously in diabetic patients and alloxan-induced diabetic rats. Several features of lymphocyte death were evaluated by flow cytometry. Plasma levels of glucose, NEFAs (non-esterified fatty acids) and ketone bodies (acetoacetate and β-hydroxybutyrate) were determined in rats fasted for 24 and 48 h. Lymphocytes obtained from fasted rats had an increase in DNA fragmentation and phosphatidylserine externalization after 48 h of culture, although there was no loss of membrane integrity in lymphocytes even after 48 h of culture. Cytochrome c release from the mitochondrial intermembrane space into the cytosol was increased significantly in lymphocytes from fasted rats cultured for 24 h, whereas the levels of bcl-2 and bax proteins were not affected. Activities of caspases 3, 6, 8 and 9 were increased significantly in lymphocytes from rats fasted for 24 h, whereas only an increase in caspase 3 and 9 activities were observed in rats fasted for 48 h. In conclusion, fasting for 24 and 48 h caused a significant increase in the proportion of lymphocytes undergoing apoptosis. The occurrence of apoptosis was observed by DNA fragmentation, phosphatidylserine externalization, cytochrome c release from the mitochondria and activation of the caspase cascade. These findings support the hypothesis that conditions that raise plasma fatty acids levels (e.g. diabetes and starvation) may impair immune function by causing lymphocyte death.
Altered calcium signalling in platelets from bile-duct-ligated rats
Authors: Atucha Noemí M. , Iyú David , Alcaraz Antonia , Rosa Vladimir , Martínez-Prieto Concepción , Ortiz M. Clara , Rosado Juan Antonio , García-Estañ Joaquín 
Published: March 2007

In the present study, we have analysed the mechanisms of Ca2+ entry and release in platelets obtained from BDL (bile-duct-ligated) rats, 11–13 days and 4 weeks after surgery. Platelets were washed and loaded with fura-2, and [Ca2+]i (cytosolic Ca2+ concentration) was determined in cell suspensions by means of fluorescence spectroscopy. Basal [Ca2+]i was similar in platelets from BDL rats compared with those from their respective controls, both in the absence and presence of extracellular Ca2+. Platelet stimulation with thrombin in the absence and presence of extracellular Ca2+ induced a rapid rise in [Ca2+]i that was of greater magnitude in platelets from BDL rats than in controls. Ca2+ storage was significantly elevated in platelets from BDL rats, as well as the activity of SERCA (sarcoplasmic/endoplasmic-reticulum Ca2+-ATPase). Capacitative Ca2+ entry, as evaluated by inhibition of SERCA with thapsigargin, was also altered in platelets from BDL rats, having lower rates of Ca2+ entry. In conclusion, chronic BDL alters intracellular Ca2+ homoeostasis in platelets, such that an enhanced Ca2+ release is evoked by thrombin, which may be due to an increased amount of Ca2+ stored in the intracellular organelles and secondary to an enhanced activity of SERCA. These alterations are already evident before cirrhosis has completely developed and occurs during the cholestasis phase.
AT1 receptor blockade prevents the decrease in conduit artery flow-mediated dilatation during NOS inhibition in humans
Authors: Bellien Jeremy , Iacob Michele , Eltchaninoff Helene , Bourkaib Ryad , Thuillez Christian , Joannides Robinson 
Published: March 2007

Whether AT1 (angiotenin II type 1) receptor blockade can prevent the decrease in conduit artery FMD (flow-mediated dilatation) during NOS (nitric oxide synthase) inhibition by alternative endothelial pathways has not been explored previously in humans. In 12 healthy subjects, we measured radial artery diameter (echotracking) and flow (Doppler) during FMD induced by sustained reactive hyperaemia during a control period and following NOS inhibition [1.5 mg·min−1·l−1L-NMMA (NG-monomethyl-L-arginine)], after a single oral administration of telmisartan (80 mg) or placebo, using a randomized double-blind cross-over design. In six volunteers, we also assessed the roles of prostacyclin and EDHF (endothelium-derived hyperpolarizing factor) during radial FMD after AT1 receptor blockade by oral administration of aspirin (500 mg) alone, aspirin+L-NMMA or aspirin+L-NMMA+fluconazole (a cytochrome epoxygenases inhibitor; 0.37 mg·min−1·l−1). Telmisartan did not affect radial artery FMD in the control period (10.9±0.6% with placebo compared with 9.9±0.7% with telmisartan), but prevented its decrease after L-NMMA (9.3±0.8% with placebo compared with 12.6±1.2% with telmisartan; P&lt;0.05) with no modification in baseline parameters, hyperaemia and radial artery endothelium-independent dilatation to sodium nitroprusside. Moreover, in telmisartan-treated subjects, radial artery FMD, compared with control (9.0±1.0%), was not modified by aspirin alone (9.4±0.7%) or associated with L-NMMA (9.5±0.5%), but was reduced by the combination of aspirin, L-NMMA and fluconazole (7.5±0.6%; P&lt;0.05). These results demonstrate that AT1 receptor blockade prevents the decrease in conduit artery FMD during NOS inhibition in humans, suggesting the development of a compensatory endothelial mechanism. This mechanism appears to be independent of prostacyclin and could possibly be related to an EDHF release.
Leukotriene B4 production in healthy subjects carrying variants of the arachidonate 5-lipoxygenase-activating protein gene associated with a risk of myocardial infarction
Authors: Maznyczka Annette , Mangino Massimo , Whittaker Andrew , Braund Peter , Palmer Tom , Tobin Martin , Goodall Alison H. , Bradding Peter , Samani Nilesh J. 
Published: March 2007

Leukotrienes are implicated in the pathogenesis of coronary artery disease. Recently two haplotypes (HapA and HapB) in the gene encoding ALOX5AP (arachidonate 5-lipoxygenase-activating protein), the main regulator of 5-lipoxygenase, have been associated with a doubling of the risk of myocardial infarction. Studies have also shown that treatment with a leukotriene inhibitor reduces biomarkers of coronary risk in patients carrying HapA, raising the possibility of developing genotype-specific therapy. In the present study, we examined whether carriage of HapA or HapB is associated with increased LTB4 (leukotriene B4) production in healthy subjects. Age- and gender-matched healthy HapA carriers (n=21), HapB carriers (n=20) and non-A/non-B carriers (n=18), with no reported history of cardiovascular disease, were recruited following DNA screening of 1268 subjects from a population-based study. Blood neutrophils were isolated, and LTB4 production was measured in response to stimulation with 1 μmol/l of the calcium ionophore A23187. There was no difference in the mean level for LTB4 production in the three groups (non-A/non-B, 24.9±8.3 ng/106 cells; HapA, 22.2±11.9 ng/106 cells; HapB, 19.8±4.8 ng/106; P=0.14). The findings indicate that if either the HapA or the HapB haplotype of ALOX5AP indeed increases cardiovascular risk, then the mechanism is not simply due to a systematically observable effect of the haplotype on LTB4 production in response to stimulation. The results suggest that knowledge of a patient's haplotype may not provide useful information on the probable clinical response to ALOX5AP inhibitors.
Effects of glucagon-like peptide-1-(7–36)-amide on pancreatic islet and intestinal blood perfusion in Wistar rats and diabetic GK rats
Authors: Svensson Annika M. , Östenson Claes-Göran , Efendic Suad , Jansson Leif 
Published: March 2007

The aim of the present study was to evaluate the effects of GLP-1 [glucagon-like peptide-1-(7–36)-amide] on total pancreatic, islet and intestinal blood perfusion in spontaneously hyperglycaemic GK rats and normal Wistar rats using a microsphere technique. GK rats had hyperglycaemia and increased pancreatic and islet blood flow. Blood glucose concentrations were not affected when measured shortly (8 min) after GLP-1 administration in either GK or Wistar rats. GLP-1 had no effects on baseline pancreatic or islet blood flow in Wistar rats, but did prevent the blood flow increase normally seen following glucose administration to these animals. In GK rats, administration of GLP-1 decreased both pancreatic and islet blood flow. Glucose administration to the GK rats decreased pancreatic and islet blood flow. This decrease was not affected by pre-treatment with GLP-1. We conclude that administration of GLP-1 leads to a decrease in the augmented blood flow seen in islets of diabetic GK rats. The GLP-1-induced action on islet blood perfusion may modulate output of islet hormones and contribute to the antidiabetogenic effects of the drug in Type 2 diabetes (non-insulin-dependent diabetes).
The influence of family culture on eating in low income families
Authors: Mackereth Catherine J. , Milner Susan J. 
Published: March 2007

PurposeThe purpose of this paper is to explore the influence of family culture on eating in families with low incomes.Design/methodology/approachA total of 32 couples were investigated using semi‐structured interviews.FindingsA central, core category emerged from the data around family culture and families could be identified into different groups or types. These groups were labelled “individualist” where families cooked what was easy, quick and cheap to prepare. The “subordinated” families were particularly restrained by lack of time and resources and usually ate whatever was available.Research limitations/implicationsThe results should be regarded as illustrative and no statistical inferences have been made due to the sampling methodology.Practical implicationsThe findings highlight that communities are diverse and any health promotion should be directed in accordance with these differences, instead of using the “one type fits all” approach which is predominantly used in work with low‐income families.Originality/valueThis paper helps people understand family culture and challenges the notion that people from lower socio‐economic groups do not eat healthily. Further research based on the present research study has already commenced.
Consumer understanding of UK salt intake advice
Authors: Marshall Stephanie , Bower John A. , Schröder Monika J.A. 
Published: March 2007

PurposeThe purpose of this paper is to investigate the effectiveness of consumer information and advice issued by the UK Food Standards Agency (FSA) in terms of consumer understanding.Design/methodology/approachA total of 118 female respondents in Scotland completed a questionnaire investigating their knowledge about the role of dietary salt and testing their understanding of educational material supplied by the FSA.FindingsA significant proportion (p<0.01) of the respondents considered themselves to be health conscious and nutritionally aware, but they were less aware of their salt intake and specific “salt in the diet” details prior to FSA information.Research limitations/implicationsThe study is limited to a convenience sample of relatively advantaged consumers, so that further work is required with more vulnerable consumers.Originality/valueA survey tool was employed that may be adapted to evaluate consumer information campaigns in any area of food policy.
Semi‐synthetic motor oils derived from high paraffinic petroleum base stock
Authors: Sejidov F.T. , Mansoori Y. 
Published: March 2007

PurposeTo prepare semi‐synthetic oils satisfying the classification API SF/CC and SAE 10W30 from mineral base oils derived from high paraffinic petroleum, synthetic alkylbenzenes base oils, and suitable additives.Design/methodology/approachThe mixtures of base mineral oils of deep hydro‐isomerization derived from high‐paraffinic petroleum (viscosity at 100°C is 12.5 cSt) and the mixtures of the synthetic alkyl aromatics oils with the naphthenic components (viscosity at 100°C of 8.0 cSt) were used as base oil. viscosity‐temperature properties, pour points, and flash points were modified by mixing of suitable additives. Octan M‐1, Octan M‐2, Octan M‐3, and Octan M‐4 oils were obtained by application of suitable additives into the prepared base oils B‐C. In order to get the SAE 10W30 requirements the viscous additive was added (0.4‐0.6 mass percent) to prepared base oils. For obtaining the API/SF/CC grade oils, package additive (Hitec 9229) additive was added (4.7 mass percent) to the mixture. The oil (Octan M‐1) was tested in the engine of Mercedes‐Benz model 230 car and positive results over 20,000 km running.FindingsIt was observed that, viscosities and pour points change linearly as the mass percent of alkylbenzenes the in the base oil mixture is changed. This realizes the possibility of the creation of semi‐synthetic motor oil of desired properties in the case of lack of other low‐viscosity synthetic component such as poly‐á‐olefins, diester and polyester oil. The obtained oils are useful for service in relatively mild climatic conditions (average temperature of the winter period −15 to −30°C).Research limitations/implicationsThe obtained oils cannot fully satisfy the requirements of the engines by pour point and low‐temperature characteristics in the absence of additives.Practical implicationsBecause of complexity of obtained mixture, it was impossible to study the structure and composition of the obtained products by modern techniques such as high field NMR spectroscopy.Originality/valueDetails practical information on preparation of four semi‐synthetic oils satisfying the classification API SF/CC are reported.
From foundation to honours degree: the student experience
Authors: Greenbank Paul 
Published: March 2007

PurposeThis paper aims to examine how students from foundation degrees (FDs) run at local further education colleges coped (academically and to a lesser extent psychologically) with the transition to a final year honours degree at a university.Design/methodology/approachThis paper is based on the experience of FD graduates who joined the final year of a full‐time BSc (Hons) in Business and Management at Edge Hill University. The study utilised questionnaires and focus groups with the FD graduates. It also involved interviews with the lecturers at Edge Hill and the programme managers of the foundation degrees.FindingsThe study found that the transition from foundation to honours degree created considerable levels of stress for the students. This largely arose because of the different approaches to teaching and learning adopted in further and higher education. In particular, Edge Hill adopted a more academic approach; there was less support; and there was a greater emphasis on independent learning. This paper identifies the need for more support for students making the transition from foundation to honours degrees. It also discusses different options for improving the transition process and highlights issues requiring further research and debate.Originality/valueThe experience of students making the transition from foundation degrees to honours degrees is under‐researched. This paper addresses this gap in the research. It will be of interest to policy makers, those involved in delivering foundation degrees and those recruiting FD graduates on to their honours programmes.
Employer co‐funded training in the UK
Authors: Thomas Rhodri , Parsons David , Barry John , Rowe Valerie 
Published: March 2007

PurposeThis paper sets out to examine the contribution of employer co‐funding of publicly‐funded vocational education and training in the UK (i.e. training initiatives that are available to all qualified applicants but funded jointly by the public and private sectors).Design/methodology/approachThe paper draws on qualitative research undertaken with more than 30 employers in a cross‐section of economic sectors.FindingsThe evidence from this study suggests that there is no model for how and why employers start to become engaged in co‐funding publicly‐funded training.Originality/valueThe paper identifies key issues for public policy‐makers.