bluuebunny/crossref_metadata_2025_split huggingface dataset:
MECHANISMS FOR REDUCTION OF CARDIOVASCULAR RISK BY REGULAR EXERCISE
Authors: Jennings Garry L. R. 
Published: June 2007

SUMMARY1. Regular aerobic exercise causes cardiovascular, neural, humoral and metabolic changes. Many of these are likely to influence cardiovascular risk and the changes vary according to the level and duration of increased physical activity.2. The case for exercise exerting beneficial effects derives from epidemiological data showing that sedentary subjects have, on average, double the risk of cardiovascular disease of active individuals. Post‐infarct rehabilitation studies are also consistent with a beneficial effect of exercise. Large randomized controlled intervention studies have not been performed.3. These benefits may be due to the effects of regular exercise on risk factors, direct effects on atheromatous vessels, or improvement in survivability in established coronary heart disease by reducing arrythmias or increasing tolerance of ischaemia.4. There are direct effects of regular exercise on blood pressure (BP) and lipid profiles. These occur at different levels of physical activity. Other changes which would be expected to reduce cardiovascular risk include increased insulin sensitivity, reduced sympathetic activity and increased gain of the baro‐receptor‐heart rate reflex and increased arterial compliance.5. In hypertensives these changes may improve outcomes, irrespective of the reduction in BP reported in some randomized controlled intervention studies.
ASSESSMENT OF NUTRITION AND PHYSICAL ACTIVITY EDUCATION PROGRAMMES IN CHILDREN
Authors: Burke V. , Beilin L. J. , Milligan R. , Thompson C. 
Published: June 2007

SUMMARY1. Studies in children relating blood lipids to the extent of atherosclerosis at post‐mortem suggest a link between risk factors for cardiovascular disease in childhood and adult life. Tracking of blood pressure (BP) and cholesterol from childhood also supports this association. However, prospective studies have not yet established the outcome in children with increased levels of risk factors.2. In a controlled trial in Perth, Western Australia, involving over 1000 10–12 year old children, fitness was improved by physical activity programmes which were associated with a greater fall in diastolic BP and triceps skinfolds in girls compared with controls. Sugar intake decreased in boys and fat intake fell in girls, mainly affecting participants in home nutrition programmes.3. In higher risk children, identified by cluster analysis, major benefits were associated with the fitness and home nutrition programmes. Physical activity combined with involvement of the family in nutrition education is likely to be the most successful approach to modifying lifestyle in children, including those with higher levels of risk.4. Undernutrition by too rigid restriction of fat intake must be avoided in young children who need calorie‐dense foods. Undernutrition, in itself, may predispose to cardiovascular disease in later life. Programmes should aim to establish a prudent diet appropriate to the age of the child combined with physical activity. As regular activity and a healthy diet in adult life will reduce risks of cardiovascular disease it is likely that childhood education will establish lifestyle habits of potential long‐term benefit.
ECONOMIC COMPARISON OF DRUG AND LIFESTYLE TREATMENT OF CARDIOVASCULAR RISK FACTORS IN HIGH‐RISK PATIENTS
Authors: Millar J. A. 
Published: June 2007

SUMMARY1. Lifestyle interventions are routinely used in the treatment of cardiovascular risk factors in individual patients but their cost‐effectiveness relative to drug treatment is largely unknown.2. Drug treatment is effective at normalizing risk factors and is known to decrease morbidity and mortality though costs may be high. Lifestyle interventions carry a significant potential to reduce expenditure on drugs, but prospective studies on cost‐effectiveness of lifestyle interventions favour drug treatment.3. According to current evidence, lifestyle intervention in high‐risk patients is not more cost‐effective than drug treatment.
EFFECTS OF DIABETES ON CALCIUM UPTAKE BY RAT BRUSH BORDER MEMBRANE VESICLES
Authors: Schedl Harold P. , Christensen Karla K. , Ronnenberg William C. 
Published: June 2007

SUMMARY1. We investigated the mechanism of decreased transmucosal calcium transport in the gut of the diabetic rat by comparing calcium uptake by brush border membrane vesicles from control and streptozotocin diabetic rats at 5 days. Brush border calcium uptake consists of saturable and non‐saturable components. Saturable uptake is mediated by a specific mobile carrier mechanism and is defined by Vmax (saturable uptake of calcium at infinite medium calcium concentration) and KT (calcium concentration at Vmax/2). Non‐saturable uptake is defined by kD (rate constant for non‐saturable uptake per unit calcium concentration), and comprises both diffusive and surface binding components of calcium uptake.2. We found both saturable and non‐saturable calcium uptake to be decreased (P < 0.05) in diabetes. Comparing control and diabetic, Vmax was 247 compared to 152 (data are pmol/mg protein per 3 s); kD was 285 compared to 172 (data are pmol/mg protein per 3 s at 1 mmol/L calcium); and KT (mmol/L) did not differ between groups, 0.070 compared to 0.057.3. The decreased Vmax in the setting of unchanged Kt in vesicles from diabetics is consistent with decreased calcium transporter specific activity, rather than with altered transporter function.4. Since (i) Vmax is decreased by vitamin D deficiency in the normal rat, and (ii) circulating 1α,25‐dihydroxycholecalciferol is decreased in the diabetic rat, decreased Vmax in the diabetic may be related to the low 1α,25‐dihydroxycholecalciferol.5. Since vitamin D deficiency does not alter kD in the normal rat, the decreased kD in diabetes may be an effect of diabetes on the membrane. In conclusion, decreased transmucosal calcium transport in diabetes is, at least in part, the consequence of decreased brush border uptake.
REGULATION OF NUCLEAR TRANSCRIPTION FACTORS BY STRESS SIGNALS
Authors: Woodgett James R. , Avruch Joseph , Kyriakis John M. 
Published: June 2007

SUMMARY1. A diverse array of stressful stimuli induces changes in gene expression via post‐translational modification of transcription factors.2. Study of activator protein (AP‐1) transcription factor regulation has revealed a novel family of protein‐serine kinases. Molecular cloning and expression of these proteins have demonstrated their specific activation by stress stimuli such as UV irradiation, heat, ischaemia/reperfusion and metabolic toxins.3. Dissection of the regulation of the stress‐activated protein kinases has revealed a similar but distinct mechanism to mitogen‐activated protein kinases suggesting that cellular responses to stress may partially overlap with normal growth responses and have common nuclear targets.
PRACTICAL APPLICATIONS OF NEURONAL TISSUE CULTURE IN IN VITRO TOXICOLOGY
Authors: Sawyer Thomas W. 
Published: June 2007

SUMMARY1. Primary chick embryo forebrain neurones are relatively easy to culture and are quite resilient to treatment manipulation. These characteristics have allowed application in a surprisingly diverse number of areas.2. These cultures have been used to investigate the anti‐cholinesterase potencies of many organophosphate (OP) nerve agents and insecticides.3. These cultures have been used to quantitate levels of OP in ‘spiked’ unknowns and in OP‐contaminated soil samples.4. These cells have also been used to test a variety of compounds using the MTT and neutral red cytotoxicity assays.
Ca2+‐DEPENDENT AND ‐INDEPENDENT MECHANISMS OF ISCHAEMIA‐EVOKED RELEASE OF [3H]‐DOPAMINE FROM RAT STRIATAL SLICES
Authors: Kim K. W. , Kim D. C. , Kim Y. H. , Eun Y. A. , Kim H. I. , Cho K. P. 
Published: June 2007

SUMMARY1. Ischaemia was induced by 5 min of deprivation of glucose and an additional 5 min of deprivation of glucose and oxygen from Mg2+‐free artificial cerebrospinal fluid in vitro.2. During the ischaemic period, 11 ± 1.5% of the total [3H]‐dopamine ([3H]‐D A) was released into the incubation medium.3. Ischaemia‐evoked release of [3H]‐DA from striatal slices was attenuated by tetrodotoxin (TTX), MgSO4, dizocilpine, ketamine, 6,7‐dinitroquinoxaline‐2,3‐dione (DNQX), or carbetapentane.4. Release of [3H]‐DA was attenuated by verapamil, ω‐conotoxin GVIA and dantrolene.5. Nomifensin inhibited the ischaemia‐induced release of [3H]‐DA.6. Omission of Ca2+ from incubation media potentiated ischaemia‐evoked [3H]‐DA release. The inhibitory effect of nomifensin was potentiated in Ca2+‐free incubation media.7. These results suggest that ischaemia induces release of [3H]‐DA by dual mechanisms; one is Ca2+‐dependent exocytosis and the other is reversal of transporter.
GLUTAMATE‐INDUCED CALCIUM LOADS: EFFECTS ON ENERGY METABOLISM AND NEURONAL VIABILITY
Authors: Thayer Stanley A. , Wang Guang Jian 
Published: June 2007

SUMMARY1. Glutamate‐induced increases in intracellular free Ca2+ concentration ([Ca2+]i) were recorded from cultured rat hippocampal neurons with single cell microfluorometry. The [Ca2+]i increase did not correlate with glutamate‐induced cell death, consistent with the idea that Ca2+ accumulates in an intracellular store, and that loading this store might be toxic.2. Glutamate‐induced Ca2+ loads were buffered by a low‐affinity, high‐capacity process that was inhibited by the mitochondrial uncoupling agent FCCP and modulated by intracellular Na+.3. Glutamate‐induced Ca2+ loads also produced an intracellular acidification. The acidification was prevented by the metabolic inhibitor 2‐deoxyglucose, mimicked by Ba2+, and inhibited by microinjection of ruthenium red.4. These data are consistent with the hypothesis that mitochondria sequester glutamate‐induced Ca2+ loads producing a metabolic acidosis; metabolic stress may contribute to glutamate‐induced neuronal death.
CROMAKALIM SUPPRESSES HYPERTONIC SALINE‐INDUCED RENAL VASOCONSTRICTION IN ANAESTHETIZED DOGS
Authors: Ogasawara Aichi , Hirano Takahiro , Hisa Hiroaki , Satoh Susumu 
Published: June 2007

SUMMARY1. Intrarenal arterial infusion of hypertonic saline (HS) transiently increased and then gradually reduced renal blood flow (RBF) in anaesthetized dogs. Glomerular filtration rate (GFR) but not filtration fraction decreased at the end of the infusion.2. In the presence of a potassium channel opener cromakalim (0.3 μg/kg per min), HS infusion failed to reduce RBF; the initial increase in RBF was maintained throughout the infusion. Since cromakalim also prevented the decrease in GFR, HS infusion lowered filtration fraction.3. The results suggest that cromakalim inhibits both pre‐and postglomerular vasoconstriction induced by HS infusion.
ENDOTHELIN‐1 AND THE REGULATION OF VASCULAR TONE
Authors: La Mylinh , Reid Julianne J. 
Published: June 2007

SUMMARY1. In 1988, Yanagisawa et al. reported the presence of a potent peptide from the supernatant of porcine endothelial cells. This was later named endothelin‐1 (ET‐1) and was found to belong to a new family of vasoconstrictor peptides. There are at least three isoforms of endothelin: ET‐1, endothelin‐2 and endothelin‐3.2. ET‐1 is produced from a larger precursor molecule by endothelin converting enzyme (ECE); there may be a number of ECE but the most physiologically relevant appears to be a membrane‐bound neutral metalloprotease. The endothelin precursor is produced on demand and is regulated at the mRNA level.3. Two subtypes of mammalian endothelin receptors have been cloned and sequenced: ETa receptors which mediate vasoconstriction and ETe receptors which mediate both vasoconstriction and vasodilatation. However, functional studies have indicated that other subtypes of endothelin receptors may exist.4. ET‐1 has a wide range of biological actions apart from its direct effects on vascular tone, including constriction of non‐vascular smooth muscle, cardiac effects, mitogenesis and stimulation of the release of hormones such as atrial natriuretic peptide and prostacyclin. At low concentrations which have no direct vasoconstrictor action, ET‐1 potentiates the effect of other vasoconstrictor agonists.5. The precise role of ET‐1 in health and disease is not well defined at present; however, there are indications that it may have a role in the pathogenesis of some cardiovascular disease states, including subarachnoid haemorrhage, renal ischaemia and certain types of hypertension.
ELECTROPHYSIOLOGICAL EFFECTS OF CHANGROLIN, AN ANTIARRHYTHMIC AGENT DERIVED FROMDICHROA FEBRIFUGA, ON GUINEA‐PIG AND RABBIT HEART CELLS
Authors: Lu Ling‐Ling , Habuchi Yoshizumi , Tanaka Hideo , Morikawat Junichiro 
Published: June 2007

SUMMARY1. The electrophysiological effects of changrolin (CRL), a Chinese antiarrhythmic drug derived from a traditional anti‐malarial plant, were examined using the whole‐cell patch‐clamp method on single cells isolated from guinea‐pig and rabbit hearts.2. At a clinically relevant concentration of 50μmol/L changrolin inhibited Ica. by 19.3 ± 6.0% and 17.3 ± 2.6% in guinea‐pig and rabbit ventricular cells, respectively. The voltage‐dependent channel availability curve was not affected. The CRL effect was enhanced to a small extent during a repetitive stimulation at 2 Hz.3. Inawas resistant to CRL and the channel availability curve was also unaffected. A small use‐dependent inhibition was observed only when the Inawas elicited at 5 Hz in the presence of 300 μmol/L CRL.4. At 50 μmol/L, CRL did not affect the time‐independent inward rectifier and the delayed rectifier K+currents (Iki and Ik, respectively), but inhibited the transient outward current (Ito) by 17.7 ± 2.4%. Changrolin significantly shortened the action potential duration in both guinea‐pig and rabbit ventricular cells.5. In conclusion, CRL inhibits Icaand Ito but has little effect on Ina.
COMPARISON OF NEURITE OUTGROWTH WITH NEUROFILAMENT PROTEIN SUBUNIT LEVELS IN NEUROBLASTOMA CELLS FOLLOWING MERCURIC OXIDE EXPOSURE
Authors: Abdulla Elizabeth McFarlane , Calaminici Mariarita , Campbell Iain C. 
Published: June 2007

SUMMARY1. The objectives of the study were to establish that inhibition of neuronal differentiation in culture (assessed by neurite outgrowth) can be used as a broad spectrum in vitro measure of neurotoxicity.2. To establish whether a rapid measure of neurite outgrowth could be used. Thus the study examined the relationship between the degree of neurite outgrowth assessed directly by image analysis and neurofilament protein subunit levels measured by an ELISA.3. SKNSH neuroblastoma cells, exposed for up to 6 days to mercuric chloride during initiation and continuation of differentiation, had lower levels of neurofilament proteins than unexposed cells.4. Preliminary data from parallel examinations of neurite outgrowth assessed by image analysis and neurofilament protein subunit levels assessed by ELISA support a correlation when neurofilament protein levels are decreased by sub‐cytotoxic doses of mercuric chloride in SKNSH cells.
ALTERATION OF THE MORPHOLOGY AND NEUROCHEMISTRY OF THE DEVELOPING MAMMALIAN NERVOUS SYSTEM BY HYDROGEN SULPHIDE
Authors: Roth S. H. , Skrajny B. , Reiffenstein R. J. 
Published: June 2007

SUMMARY1. Hydrogen sulphide (H2S) is a broad spectrum toxicant that occurs widely in nature and is also released by a variety of industrial activities and processes.2. The central nervous system (CNS) appears to be the major target organ.3. There is great potential for insult or injury to the developing or immature CNS.4. The risks of chronic or repeated exposures to low concentrations have not been well defined.5. Exposure to low concentrations of H2S to time‐pregnant rats from day 5 postcoitus until day 21 postnatal results in architectural modification of cerebellar Purkinje cells, alteration of putative amino acid neurotransmitters and changes in monoamine levels in the developing rat brain up to day 21 postnatal.6. H2S‐induced alterations in monoamine tissue levels observed in the developing rat brain return to control values if exposure is discontinued during development, that is, at day 21 postnatal.
GENE EXPRESSION OF ENDOTHELIN RECEPTORS IN AORTIC CELLS FROM CYCLOSPORINE‐INDUCED HYPERTENSIVE RATS
Authors: Iwai Junko , Kanayama Yoshiharu , Negoro Nobuo , Okamura Mikio , Takeda Tadanao 
Published: June 2007

SUMMARY1. We examined preproendothelin‐1, ETA and ETb receptor mRNA levels in aortic endothelial and smooth muscle cells from cyclosporine (CyA)‐induced hypertensive rats using the reverse transcription polymerase chain reaction method.2. Aortic endothelial preproendothelin‐1 mRNA expression was about 1.5‐fold higher, while that of ETB receptor mRNA was markedly decreased in CyA‐treated rats compared with those in controls.3. The expression of ETA receptor mRNA in smooth muscle cells from CyA‐induced hypertensive rats was increased about two‐fold over that in cells from control animals.4. Thus, increased endothelial preproendothelin‐1, and ETa receptor mRNA levels in smooth muscle cells, which are concomitant with the decrease in ETB receptor mRNA levels in endothelium, may contribute to CyA‐induced hypertension in rats.
POSITIVE INOTROPIC RESPONSES OF THE SODIUM CHANNEL MODULATOR BDF 9148 IN DISEASED RAT MYOCARDIUM
Authors: Hoey Andrew , Nankervis Richard , Brown Lindsay 
Published: June 2007

SUMMARY1. This study has defined the positive inotropic responses to the sodium channel modulator BDF 9148 in rats with hypertension, thyroid dysfunction, diabetes or dwarfism. Concentration‐response curves to BDF 9148 and calcium chloride were determined in isolated left atria and left ventricular papillary muscles.2. BDF 9148 increased force of contraction in left ventricular papillary muscles in all disease states with maximal responses comparable to calcium chloride. BDF 9148 potency was significantly decreased in muscles from diabetic rats only.3. BDF 9148 produced similar responses in left atria except from hyperthyroid rats where negative inotropic responses only were measured. This exception confirms that the left atria is an imperfect model for ventricular responsiveness.4. Thus, the increase in force of contraction in the ventricles as a consequence of sodium channel modulation by BDF 9148 is maintained in these disease states unlike responses to α‐or β‐adrenoceptor agonists.
RENAL MEDULLA AND BRADYKININ DURING THE DEVELOPMENT OF HYPERTENSION IN SHR
Authors: O'Sullivan Joseph B. , Bertram John F. , Harrap Stephen B. 
Published: June 2007

SUMMARY1. The long‐term reduction in blood pressure following ACE inhibitor treatment in young spontaneously hypertensive rats (SHR) appears to depend on both the kidney and brady‐kinin.2. The aim of this experiment was to examine the effects of ACE inhibition and bradykinin on renal morphology and blood pressure in SHR.3. Between 6 and 10 weeks of age male SHR received one of four treatments: water (n = 26), ramipril (1 mg/kg per day; n = 24), ramipril (1 mg/kg per day) plus Hoe 140 (0.5 mg/kg per day; n = 25) or Hoe 140 (0.5 mg/kg per day; n= 25).4. Renal medullary and cortical volumes were determined stereologically at 10 and 20 weeks of age.5. After 4 weeks of treatment, ramipril reduced the size of the renal medulla while Hoe 140 increased medullary volumes compared to control. Ten weeks after treatment was stopped the renal medulla of the ramipril group had returned to normal, however, there was a persistent increase in medullary volume of both Hoe 140 treated groups.6. Our results imply that bradykinin may influence the size of the renal medulla which may have important effects on the development of hypertension in SHR.
THE EFFECT OF INDUCED REFLECTIONS ON HUMAN ARTERIAL WAVEFORMS
Authors: Kobler H. , Henderson R. , Lal S. , Hart M. , Hunyor S. 
Published: June 2007

SUMMARY1. External compression of the human brachial artery results in waveform reflection.2. Resonant waves are found superimposed on the original blood pressure signal.3. The mechanism may be likened to the operation of an organ pipe with reflections at both ends of an arterial segment.4. This has implications for measurements in arteries where external pressure is applied.
RENIN mRNA CONCENTRATION IN RAT HYPOTHALAMUS IS DECREASED BY ENALAPRIL
Authors: Lou Yi‐kun , Liu Dennis T. , Whitworth Judith A. , Morris Brian J. 
Published: June 2007

SUMMARY1. Renin mRNA is expressed in several extrarenal tissues, including brain. The aim of the present study was to quantify renin mRNA in the hypothalamus in response to a low NaCl diet and angiotensin converting enzyme inhibitor treatment, both of which are well‐known stimuli of renin mRNA in kidney.2. Groups of six Sprague‐Dawley rats were given either a normal diet, low NaCl chow (0.04% NaCl), enalapril (0.25 mg/mL in drinking water), or low NaCl + enalapril, for 7 days. Renin mRNA in the hypothalamus was quantified by a competitive reverse transcriptase‐polymerase chain reaction (RTPCR) technique.3. Renin mRNA concentration in the hypothalamus of rats receiving a normal diet was 52 ± 3 S.E. fg/μg total RNA. Low NaCl had no effect (57 ± 7), whereas values were significantly lower in rats treated with enalapril, either given alone (38 ± 2; P= 0.002) or combined with a low NaCl diet (33± 4; P= 0.003).4. In conclusion, we have quantified renin mRNA in the rat hypothalamus and shown that it can be suppressed significantly by enalapril. This response is opposite to that seen in the kidney after enalapril.
WIRING UP THE VISUAL SYSTEM
Authors: Beazley L. D. , Dunlop S. A. , Chelvanyagam D. K. , Ross W. M. 
Published: June 2007

SUMMARY1. In this review we describe some of our recent studies on the developing marsupial visual pathway. The description focuses on retinal ganglion cells, considering the formation of their dendritic trees, the outgrowth of axons and the formation of connections within the brain.2. Both dendritic trees and outgrowing axons undergo a period of exuberance, followed by one of refinement. The dendritic tree transiently develops a more complex branching pattern than is found in adults. Short side branches, referred to as spines, are a feature of immature dendrites and, to a lesser extent, of axons. These structures are mostly lost as development proceeds. However, they are retained on the dendritic trees of small‐field ganglion cells and, for a proportion of axons, on that part within the nerve fibre layer of the retina. Although most axons navigate fairly direct routes towards their targets, a minority follow inappropriate courses, such as doubling back towards the eye or entering the opposite optic nerve at the chiasm. As such errant axons are not seen in the adult, we assume that their parent cell bodies die during development.3. Throughout development, optic axons are arranged in an approximate retinotopic order along the length of the visual pathway; as a result, axons approach the visual centres aligned to form, at least, a crude retinotopic map. Axons from dorsal and ventral retina exchange locations along the optic nerve and in this way correct for the inversion of the image brought about by the lens.4. We also describe the topography of cells in the retinal ganglion cell layer and the organization of the optic nerve in an unusual marsupial, the honey possum (Tarsips rostratus). Unexpected features in the adult were the low proportion of displaced amacrine to ganglion cells and an unmyelinated macular outflow in the retro‐bulbar portion of the optic nerve.