1,757 research outputs found
Hole cutter
An adjustable hole cutter is described for use in forming circular openings in workpieces. The hole cutter is characterized by a mount of a substantially planar configuration, positionable into a plane paralleling the working plane of a selected workpiece. It also contains a shaft for imparting rotary motion to the mount about an axis of rotation normally related to the working plane, a plurality of stabilizing struts for resiliently supporting the mount in parallelism with the working plane as rotary motion is imparted thereto, a drill bit for drilling a pilot hole concentric with the axis of rotation, and an elongated cutting tool adjustably seated within a radially extended slot
A low-dose comprehensive cardiac CT protocol assessing anatomy, function, perfusion, and viability
AbstractRadiation exposure in cardiac imaging is a major healthcare concern and low-dose cardiac imaging has important implications for patients. We describe the application of a low-dose comprehensive cardiac computed tomography protocol that assesses anatomy, function, perfusion and viability with correlations to invasive coronary angiography and magnetic resonance imaging
Observation of surface states on heavily indium doped SnTe(111), a superconducting topological crystalline insulator
The topological crystalline insulator tin telluride is known to host
superconductivity when doped with indium (SnInTe), and for low
indium contents () it is known that the topological surface states are
preserved. Here we present the growth, characterization and angle resolved
photoemission spectroscopy analysis of samples with much heavier In doping (up
to ), a regime where the superconducting temperature is increased
nearly fourfold. We demonstrate that despite strong p-type doping, Dirac-like
surface states persist
Vascular effects of urocortins 2 and 3 in healthy volunteers
Background:
Urocortin 2 and urocortin 3 are endogenous peptides with an emerging role in cardiovascular pathophysiology. We assessed their pharmacodynamic profile and examined the role of the endothelium in mediating their vasomotor effects in vivo in man.
Methods and Results:
Eighteen healthy male volunteers (23±4 years) were recruited into a series of doubleâblind, randomized crossover studies using bilateral forearm venous occlusion plethysmography during intraâarterial urocortin 2 (3.6 to 120 pmol/min), urocortin 3 (1.2 to 36 nmol/min), and substance P (2 to 8 pmol/min) in the presence or absence of inhibitors of cyclooxygenase (aspirin), cytochrome P450 metabolites of arachidonic acid (fluconazole), and nitric oxide synthase (LâNMMA). Urocortins 2 and 3 evoked arterial vasodilatation (P<0.0001) without tachyphylaxis but with a slow onset and offset of action. Inhibition of nitric oxide synthase with LâNMMA reduced vasodilatation to substance P and urocortin 2 (Pâ€0.001 for both) but had little effect on urocortin 3 (P>0.05). Neither aspirin nor fluconazole affected vasodilatation induced by any of the infusions (P>0.05 for all). In the presence of all 3 inhibitors, urocortin 2â and urocortin 3âinduced vasodilatation was attenuated (P<0.001 for all) to a greater extent than with LâNMMA alone (Pâ€0.005).
Conclusions:
Urocortins 2 and 3 cause potent and prolonged arterial vasodilatation without tachyphylaxis. These vasomotor responses are at least partly mediated by endothelial nitric oxide and cytochrome P450 metabolites of arachidonic acid. The role of urocortins 2 and 3 remains to be explored in the setting of human heart failure, but they have the potential to have major therapeutic benefits
Systematic assessment in an animal model of the angiogenic potential of different human cell sources for therapeutic revascularization
INTRODUCTION: Endothelial progenitor cells (EPC) capable of initiating or augmenting vascular growth were recently identified within the small population of CD34-expressing cells that circulate in human peripheral blood and which are considered hematopoietic progenitor cells (HPC). Soon thereafter human HPC began to be used in clinical trials as putative sources of EPC for therapeutic vascular regeneration, especially in myocardial and critical limb ischemias. However, unlike HPC where hematopoietic efficacy is related quantitatively to CD34(+ )cell numbers implanted, there has been no consensus on how to measure EPC or how to assess cellular graft potency for vascular regeneration. We employed an animal model of spontaneous neovascularization to simultaneously determine whether human cells incorporate into new vessels and to quantify the effect of different putative angiogenic cells on vascularization in terms of number of vessels generated. We systematically compared competence for therapeutic angiogenesis in different sources of human cells with putative angiogenic potential, to begin to provide some rationale for optimising cell procurement for this therapy. METHODS: Human cells employed were mononuclear cells from normal peripheral blood and HPC-rich cell sources (umbilical cord blood, mobilized peripheral blood, bone marrow), CD34(+ )enriched or depleted subsets of these, and outgrowth cell populations from these. An established sponge implant angiogenesis model was adapted to determine the effects of different human cells on vascularization of implants in immunodeficient mice. Angiogenesis was quantified by vessel density and species of origin by immunohistochemistry. RESULTS: CD34(+ )cells from mobilized peripheral blood or umbilical cord blood HPC were the only cells to promote new vessel growth, but did not incorporate into vessels. Only endothelial outgrowth cells (EOC) incorporated into vessels, but these did not promote vessel growth. CONCLUSIONS: These studies indicate that, since EPC are very rare, any benefit seen in clinical trials of HPC in therapeutic vascular regeneration is predominantly mediated by indirect proangiogenic effects rather than through direct incorporation of any rare EPC contained within these sources. It should be possible to produce autologous EOC for therapeutic use, and evaluate the effect of EPC distinct from, or in synergy with, the proangiogenic effects of HPC therapies
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Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial
Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events
Cardiovascular Effects of Urocortin 2 and Urocortin 3 in Patients with Chronic Heart Failure
Aims:
Urocortin 2 and urocortin 3 may play a role in the pathophysiology of heart failure and are emerging therapeutic targets. We aimed to examine the local and systemic cardiovascular effects of urocortin 2 and urocortin 3 in healthy subjects and patients with heart failure.
Methods:
Patients with heart failure (n = 8) and age and gender-matched healthy subjects (n = 8) underwent bilateral forearm arterial blood flow measurement using forearm venous occlusion plethysmography during intra-arterial infusions of urocortin 2 (3.6â36 pmol minâ1), urocortin 3 (360â3600 pmol minâ1) and substance P (2â8 pmol minâ1). Heart failure patients (n = 9) and healthy subjects (n = 7) underwent non-invasive impedance cardiography during incremental intravenous infusions of sodium nitroprusside (573â5730 pmol kgâ1 minâ1 ), urocortin 2 (36â360 pmol minâ1 ), urocortin 3 (1.2â12 nmol minâ1) and saline placebo.
Results:
Urocortin 2, urocortin 3 and substance P induced dose-dependent forearm arterial vasodilatation in both groups (P < 0.05 for both) with no difference in magnitude of vasodilatation between patients and healthy subjects. During systemic intravenous infusions, urocortin 3 increased heart rate and cardiac index and reduced mean arterial pressure and peripheral vascular resistance index in both groups (P < 0.01 for all). Urocortin 2 produced similar responses to urocortin 3, although increases in cardiac index and heart rate were only significant in heart failure (P < 0.05) and healthy subjects (P < 0.001), respectively.
Conclusion:
Urocortins 2 and 3 cause vasodilatation, reduce peripheral vascular resistance and increase cardiac output in both health and disease. These data provide further evidence to suggest that urocortins 2 and 3 continue to hold promise for the treatment of heart failure
Manganese-Enhanced Magnetic Resonance Imaging in Takotsubo Syndrome
Acknowledgments The authors thank the Edinburgh Imaging Facility. Sources of Funding This work and T. Singh, S. Joshi, and Drs Dweck and Newby are supported by the British Heart Foundation (grants FS/17/19/32641, CS/17/1/32445, RG/16/10/32375, RE/18/5/34216, FS/ICRF/20/26002, and FS/SCRF/21/32010). T. Singh is supported by the Medical Research Council (grant MR/T029153/1). Dr Newby is the recipient of a Wellcome Trust Senior Investigator Award (WT103782AIA). Dr McCann is supported by an NIHR Research Professorship (08-2017-ST2-007). The Edinburgh Clinical Research Facilities and Edinburgh Imaging Facility are supported by the National Health Service Research Scotland through the National Health Service Lothian Health Board.Peer reviewe
Vascular effects of apelin in vivo in man
ObjectivesThis study was designed to establish the direct vascular effects of apelin in vivo in man.BackgroundApelin is the endogenous ligand for the previously orphaned G-proteinâcoupled receptor, APJ. This novel pathway is widely expressed in the cardiovascular system and is emerging as an important mediator of cardiovascular homeostasis. In pre-clinical models, apelin causes venous and arterial vasodilation.MethodsVascular effects of apelin were assessed in 24 healthy volunteers. Dorsal hand vein diameter was measured by the Aellig technique during local intravenous infusions (0.1 to 3 nmol/min) of apelin-36, (Pyr1)apelin-13, and sodium nitroprusside (0.6 nmol/min). Forearm blood flow was measured by venous occlusion plethysmography during intrabrachial infusions of apelin-36 and (Pyr1)apelin-13 (0.1 to 30 nmol/min) and subsequently in the presence or absence of a ânitric oxide clampâ (nitric oxide synthase inhibitor, L-NG-monomethylarginine [8 ÎŒmol/min], coinfused with nitric oxide donor, sodium nitroprusside [90 to 900 ng/min]), or a single oral dose of aspirin (600 mg) or matched placebo.ResultsAlthough sodium nitroprusside caused venodilation (p < 0.0001), apelin-36 and (Pyr1)apelin-13 had no effect on dorsal hand vein diameter (p = 0.2). Both apelin isoforms caused reproducible vasodilation in forearm resistance vessels (p < 0.0001). (Pyr1)apelin-13âmediated vasodilation was attenuated by the nitric oxide clamp (p = 0.004) but unaffected by aspirin (p = 0.7).ConclusionsAlthough having no apparent effect on venous tone, apelin causes nitric oxideâdependent arterial vasodilation in vivo in man. The apelin-APJ system merits further clinical investigation to determine its role in cardiovascular homeostasis
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