Emergency management of acute cardiac arrhythmias

Copyright to Australian Family Physician. Reproduced with permission. Permission to reproduce must be sought from the publisher, The Royal Australian College of General Practitioners.BACKGROUND Anything other than normal sinus rhythm can be classified as an arrhythmia. However not all arrhythmias need acute intervention. OBJECTIVE This article reviews which arrhythmias need intervention in an acute setting, and the various options available for intervention. DISCUSSION The impact of an arrhythmia upon perfusion determines what intervention should be considered. Conscious level, cardiac ischaemia secondary to poor perfusion of the coronary arteries and blood pressure need to be assessed. Patients with bradycardias with adequate perfusion are treated initially with oxygen and observation. Sinus bradycardia not responding to increased oxygenation is treated with atropine. For other bradycardias the two alternatives are to drive the inherent rate with a sympathomimetic drug or to pace the patient with an external or internal pacer. Usually supraventricular tachycardias are not life threatening. Unconscious patients with wide complex tachycardia should be treated in a standard cardiac arrest approach. Conscious patients in ventricular fibrillation however, can be treated either chemically or with synchronised cardioversion. If a patient is in cardiac arrest the approach is to establish effective resuscitation and early defibrillation as per Australian Resuscitation Council guidelines.Hugh JM Grantha

Neuronal response in Alzheimer's and Parkinson's disease: the effect of toxic proteins on intracellular pathways

Accumulation of protein aggregates is the leading cause of cellular dysfunction in neurodegenerative disorders. Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease, Prion disease and motor disorders such as amyotrophic lateral sclerosis, present with a similar pattern of progressive neuronal death, nervous system deterioration and cognitive impairment. The common characteristic is an unusual misfolding of proteins which is believed to cause protein deposition and trigger degenerative signals in the neurons. A similar clinical presentation seen in many neurodegenerative disorders suggests the possibility of shared neuronal responses in different disorders. Despite the difference in core elements of deposits in each neurodegenerative disorder, the cascade of neuronal reactions such as activation of glycogen synthase kinase-3 beta, mitogen-activated protein kinases, cell cycle re-entry and oxidative stress leading to a progressive neurodegeneration are surprisingly similar. This review focuses on protein toxicity in two neurodegenerative diseases, AD and PD. We reviewed the activated mechanisms of neurotoxicity in response to misfolded beta-amyloid and α-synuclein, two major toxic proteins in AD and PD, leading to neuronal apoptosis. The interaction between the proteins in producing an overlapping pathological pattern will be also discussed.Shohreh Majd, John H. Power and Hugh J.M. Grantha

The impact of tau hyperphosphorylation at Ser(262) on memory and learning after global brain ischaemia in a rat model of reversible cardiac arrest

An increase in phosphorylated tau (p-tau) is associated with Alzheimer's disease (AD), and brain hypoxia. Investigation of the association of residue-specific tau hyperphosphorylation and changes in cognition, leads to greater understanding of its potential role in the pathology of memory impairment. The aims of this study are to investigate the involvement of the main metabolic kinases, Liver Kinase B1 (LKB1) and Adenosine Monophosphate Kinase Protein Kinase (AMPK), in tau phosphorylation-derived memory impairment, and to study the potential contribution of the other tau kinases and phosphatases including Glycogen Synthase Kinase (GSK-3β), Protein kinase A (PKA) and Protein Phosphatase 2A (PP2A). Spatial memory and learning were tested in a rat global brain ischemic model of reversible cardiac arrest (CA). The phosphorylation levels of LKB1, AMPK, GSK-3β, PP2A, PKA and tau-specific phosphorylation were assessed in rats, subjected to ischaemia/reperfusion and in clinically diagnosed AD and normal human brains. LKB1 and AMPK phosphorylation increased 4 weeks after CA as did AMPK related p-tau (Ser262). The animals showed unchanged levels of GSK-3β specific p-tau (Ser202/Thr205), phospho-PP2A (Tyr307), total GSK-3β, PP2A, phospho-cAMP response element-binding protein (CREB) which is an indicator of PKA activity, and no memory deficits. AD brains had hyperphosphorylated tau in all the residues of Ser262, Ser202 and Thr205, with increased phosphorylation of both AMPK (Thr172) and GSK-3β (Ser9), and reduced PP2A levels. Our data suggests a crucial role for a combined activation of tau kinases and phosphatases in adversely affecting memory and that hyperphosphorylation of tau in more than one specific site may be required to create memory deficits.Shohreh Majd, John H.T.Power, Simon A.Koblar, Hugh J.M.Grantha

High-temperature optically activated GaAs power switching for aircraft digital electronic control

Gallium arsenide high-temperature devices were fabricated and assembled into an optically activated pulse-width-modulated power control for a torque motor typical of the kinds used in jet engine actuators. A bipolar heterojunction phototransistor with gallium aluminum arsenide emitter/window, a gallium arsenide junction field-effect power transistor and a gallium arsenide transient protection diode were designed and fabricated. A high-temperature fiber optic/phototransistor coupling scheme was implemented. The devices assembled into the demonstrator were successfully tested at 250 C, proving the feasibility of actuator-located switching of control power using optical signals transmitted by fibers. Assessments of the efficiency and technical merits were made for extension of this high-temperature technology to local conversion of optical power to electrical power and its control at levels useful for driving actuators. Optical power sources included in the comparisons were an infrared light-emitting diode, an injection laser diode, tungsten-halogen lamps and arc lamps. Optical-to-electrical power conversion was limited to photovoltaics located at the actuator. Impedance matching of the photovoltaic array to the load was considered over the full temperature range, -55 C to 260 C. Loss of photovoltaic efficiency at higher temperatures was taken into account. Serious losses in efficiency are: (1) in the optical source and the cooling which they may require in the assumed 125 C ambient, (2) in the decreased conversion efficiency of the gallium arsenide photovoltaic at 260 C, and (3) in impedance matching. Practical systems require improvements in these areas

Early glycogen synthase kinase-3beta and protein phosphatase 2A independent tau dephosphorylation during global brain ischaemia and reperfusion following cardiac arrest and the role of the adenosine monophosphate kinase pathway

Abnormal tau phosphorylation (p-tau) has been shown after hypoxic damage to the brain associated with traumatic brain injury and stroke. As the level of p-tau is controlled by Glycogen Synthase Kinase (GSK)-3β, Protein Phosphatase 2A (PP2A) and Adenosine Monophosphate Kinase (AMPK), different activity levels of these enzymes could be involved in tau phosphorylation following ischaemia. This study assessed the effects of global brain ischaemia/reperfusion on the immediate status of p-tau in a rat model of cardiac arrest (CA) followed by cardiopulmonary resuscitation (CPR). We reported an early dephosphorylation of tau at its AMPK sensitive residues, Ser(396) and Ser(262) after 2 min of ischaemia, which did not recover during the first two hours of reperfusion, while the tau phosphorylation at GSK-3β sensitive but AMPK insensitive residues, Ser(202) /Thr(205) (AT8), as well as the total amount of tau remained unchanged. Our data showed no alteration in the activities of GSK-3β and PP2A during similar episodes of ischaemia of up to 8 min and reperfusion of up to 2 h, and 4 weeks recovery. Dephosphorylation of AMPK followed the same pattern as tau dephosphorylation during ischaemia/reperfusion. Catalase, another AMPK downstream substrate also showed a similar pattern of decline to p-AMPK, in ischaemic/reperfusion groups. This suggests the involvement of AMPK in changing the p-tau levels, indicating that tau dephosphorylation following ischaemia is not dependent on GSK-3β or PP2A activity, but is associated with AMPK dephosphorylation. We propose that a reduction in AMPK activity is a possible early mechanism responsible for tau dephosphorylation.Shohreh Majd, John H. T. Power, Simon A. Koblar and Hugh J. M. Grantha

Beaufort/Bering 1979 microwave remote sensing data catalog report, 14-24 March 1979

The airborne microwave remote sending measurements obtained by the Langley Research Center in support of the 1979 Sea-Ice Radar Experiment (SIRE) in the Beaufort and Bering Seas are discussed. The remote sensing objective of SIRE was to define correlations between both active and passive microwave signatures and ice phenomena assocated with practical applications in the Arctic. The instruments used by Langley during SIRE include the stepped frequency microwave radiometer (SFMR), the airborne microwave scatterometer (AMSCAT), the precision radiation thermometer (PRT-5), and metric aerial photography. Remote sensing data are inventoried and cataloged in a user-friendly format. The data catalog is presented as time-history plots when and where data were obtained as well as the sensor configuration

ANALYTICAL INVESTIGATION AND PREDICTION OF SPIN AND RECOVERY CHARACTERISTICS OF THE NORTH AMERICAN X-15 AIRPLANE

Spin and recovery characteristics of north american x-15 aircraf

An operational satellite scatterometer for wind vector measurements over the ocean

Performance requirements and design characteristics of a microwave scatterometer wind sensor for measuring surface winds over the oceans on a global basis are described. Scatterometer specifications are developed from user requirements of wind vector measurement range and accuracy, swath width, resolution cell size and measurement grid spacing. A detailed analysis is performed for a baseline fan-beam scatterometer design, and its performance capabilities for meeting the SeaSat-A user requirements. Various modes of operation are discussed which will allow the resolution of questions concerning the effects of sea state on the scatterometer wind sensing ability and to verify design boundaries of the instrument

Localization of overexpressed c-myc mRNA in polycystic kidneys of the cpk mouse

Localization of overexpressed c-myc mRNA in polycystic kidneys of the cpk mouse. The C57BL/6J-cpk mouse has a form of autosomal-recessive polycystic kidney disease characterized by the rapid growth of large collecting duct cysts and the development of severe renal failure usually by three to four weeks of age. Previous studies had shown higher steady-state levels of proto-oncogene mRNA in these cystic kidneys. It is now shown using nuclear run-on transcription that the c-fos and c-myc proto-oncogenes are transcribed at higher rates in cystic kidneys, and thus that increased transcription, in part, may account for the increased mRNA levels. c-myc mRNA was detected by in situ hybridization in nephron anlagen and elongating tubules of normal and cystic kidneys during late fetal and early neonatal kidney development. Localization of c-myc expression in the normal kidney decreased with age over the three-week postnatal period. By contrast, c-myc mRNA was found in cysts as early as three days of age, with increased levels at two and three weeks, c-myc expression was also elevated in apparently normal, non-dividing proximal tubules in three-week-old cystic animals. On the basis of these findings, we suggest that c-myc expression is linked to the proliferation of cells engaged in the primary cystogenic process, and that expression of this gene in proximal tubule cells of severely azotemic animals reflects the compensatory response of residual tubular epithelial cells to progressive renal dysfunction