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ABC Juice (Apple, Beetroot, Carrot)
A for Apple, B for Beetroot, C for Carrot – 3 simple ingredients for ABC Juice
I chanced upon this interesting vegetable juice at reena's blog and I just know I had to try it. I thought it will be fun to post a recipe on ABC juice right after posting my ABC soup recipe, even though these two recipes are not related to each other besides the similar name. The "ABC" in this case stands for apples, beetroots and carrots, so this recipe is super easy to remember. Beetroot is a super healthy vegetable, but I've always preferred to "drink" beetroot rather than to eat it. I personally feel that this fuss-free recipe is the best way to consume beetroot and enjoy all its wonderful nutrients at the same time.
Known properties & benefits of beetroots (aka beets)
Info from Wiki & LoveBeetroot.co.uk
– Lowers blood pressure (therefore avoid/consume in moderation if you are anemic)
– Relaxes the mind (due to the substance betaine) and is used to treat depression. It also contains trytophan which contributes to a sense of well being.
– Contains aphrodisiac properties according to the Romans. The juice is a rich source of boron, which plays an important role in the production of human sex hormones.
The unique deep red/magenta hue of beetroot is due to the substance known as betanin, which is used industrially as a red food colourant – e.g. to improve the colour of tomato paste, sauces, jams and ice cream. To me, the beetroot looks as if it is "bleeding" when you cut into it, so do be careful about red stains. Betacyanin in beetroot may cause pink "side effects" in some people who are unable to break it down, however do not be alarmed if that happens.
(Makes one tall glass)
– 1 small (about 200g) beetroot, remove skin and cut to small chunks
– 2 medium carrots, skin peeled, cut to small chunks
– 1 large red unwaxed apple, cut to small chunks
1. Blend everything with a fruit juice extractor (not food blender) and serve immediately. That's all – it's as easy as ABC :-)
– You can use green apple instead of red apple for a sour taste.
– You can add 1 stalk of celery if you like the vegetable.
– Carrots and red apples make the juice sweet, so you can experiment with the quantity to adjust the sweetness.
70 comments on "ABC Juice (Apple, Beetroot, Carrot)"
bwoy di ABC un up mi nah lie
I have the tried ABC juice and it is very nice.
Hi, dyou know where can i get beetroot in singapore? My dad is having last stage cancer. Hope dis will at least boost up his system :(
Hi Juliana , I'm very sorry to hear that :( You can buy beetroot at wet markets or supermarkets (NTUC, Giant or Cold Storage). If you can't find, the more upmarket supermarket like Jasons should have. Please take care.
ABC Juice is so good, as 4 m,I drink a lot whisk, so every morning I take one glass of ABC Juice then my day will b alright
Brilliant! Do you cook the beets first or juice them raw?
Just raw :)
tried it, very nice, since it do good to the body so why not
I had been preparing this juice for my husband recently, may I know that can I give it to my sons age 12, 14 and 16?
its green apple not red apple from the beginning
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by Nick Brown
In the name of the Father and of the Son and the Holy Spirit
Todays Gospel reading (John 3:13-17) contains a preparatory reminder for the upcoming feast of the Holy Cross, which will be celebrated on 14th September. In one of the passages, Jesus tells us that just as Moses lifted up the serpent in the wilderness, even so must the Son of man be lifted up. This is a referral to the Old Testament Book of Numbers (21:9), where the Israelites, after they were released from bondage in Egypt and were wandering around in the desert wilderness, were overcome by venomous snakes. As a cure for the snakebites, God commanded Moses to fashion a brass serpent, to place it on a standard or post, and whosoever was to gaze upon the serpent would immediately be healed. Here Christ is again using the Old Testament as a pedagogical or teaching tool, to show us that He is the fulfilment of the Old Covenant.
Christ is showing us that just as the faithful Israelites were healed through this symbol of death (i.e, the serpent) so are we saved through Christ who was hung upon the Cross. And while the Cross was the symbol of death, like the serpent, it now becomes the symbol of life. In this instance, we are faced with another of those phenomenal paradoxes. Other examples of these paradoxes would be God becomes man or a virgin gives birth etc. Yet, as unfathomable as some of these things may be to us, the earthly existence of the Saviour was prefigured throughout the Old Testament. Christ becomes the new Adam; Jonah in the belly of the fish foreshadows Christ in the tomb after His crucifixion, as well as the brass serpent as prefiguring the saving act of Christs death on the Cross. While the serpent or snake symbolised sin and its deadly effect in the Old Testament, the brass serpent symbolised the bearing away of the curse and judgement of sin. Furthermore, the metal itself was figurative of the righteousness of Gods judgement. In case you were wondering where you might have seen the emblem of a serpent wrapped around a pole, it has been adopted by society as the symbol of the medical profession.
As Christians, we should never underestimate the importance of the Old Testament and its place within our lives, because, basically, without the Old Testament we would never be able to fully understand the message of the New Testament. Without the Old Testament we would not understand what Christ was referring to in tonights Gospel. Our Church Fathers have always emphasised the importance of the Old Testament and its message as being the inspired Word of God that points the way to our salvation. So if the message of the Old Testament is referred to in short as something that points the way, what then, in short, is the message of the New Testament?
Jesus sums it up entirely by saying, "For God so loved the world that He gave His only begotten Son, that whoever believes in Him will not perish but have everlasting life". That is ultimately the message of the Gospels summed up in 25 words. Gods love for us; God loving us so much that He sends His Son for us; our faith or belief in the Son; and our guaranteed eternal existence because of Gods love, because Jesus has come, and because of our faith in Him. This small but important passage is the essence of our faith. If someone who had never in their life heard of Christianity, what we believe, what we practice etc., this would be the primary passage which would illustrate everything about God, about us, and about our salvation.
Continuing on from this passage, Jesus states that, "For God did not send His Son into the world to condemn the world, but that the world through Him might be saved". Now Jesus never condemned anyone whilst here on earth. He was very stern with many, He even condemned the practices of some of the Pharisees, but He never condemned anyone to eternal suffering; to a hell. In fact, God doesnt send people to hell.
Our whole understanding of what heaven and hell is, has been so distorted and abused by the teachings of the Western churches that it has even entered our Church and made us blind to the teachings of the Gospel and the teachings of the Church Fathers. Heaven is not up there, and hell is not down there. You want to know what hell is? Hell is an absence of God (whether its here on this earth or in the afterlife), and it is a turning away from God. You want to know who condemns us to hell? We condemn ourselves. To find yourself in hell is to turn your back on God, to reject God, to reject His mercy. There are people out there who are living in hell on this earth right now, and the sad thing is that they often dont realise it. They love to blame society, those around them, even the Church, but the answers to their problems are inside of them! All they need to do is to discover God and His kingdom within them, and then will they realise what theyve been missing all this time. God cant condemn us to an eternity of misery. Its just not in His nature. He can only love, but He cant force you to love Him. If you choose to turn your back on God, turn your back on His unconditional love, then you will create your own hell.
Our relationship with Our Father in Heaven is very similar to that of a married couple. For a relationship to really work, you need the cooperation of both parties, but more importantly you need mutual love for each other. Its similar between God and us, with the only difference being that He cant do anything but love. Yet, so often we turn our relationship into a one sided affair. Its a case of too much me, me, me, and not enough of Him. We are in this 'marriage' together for eternity. Lets not let it end in divorce, but lets make it work. Better still, lets encourage and help those around us to maintain this relationship, this marriage with the Creator.
Greek Orthodox Church of
Saint George,
Brisbane QLD

subset: commoncrawl


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20090906-12009, digital image and unique archival pigment print
Copyright S.Monnier 2009
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A blog post related to this work:
September 9th 2009
Non-attenuated pattern piling
The "pattern piling" technique, used in all my work since around 2002, consists, starting from a pattern covering the plane, in generating rescaled copies of it and merging these copies together. Usually, the small copies of the pattern are attenuated. Indeed, the smallest copies are too small to be resolved on low resolution images and would produce a random noise which would hide the large scale structures if they were not attenuated. The attenuation is controlled by a parameter, traditionally called beta (B), whose effect can be visualized here. The smaller B is, the less attenuated small copies of the pattern are, B=0 corresponding to no attenuation at all.
As a consequence of attenuation, the resulting image is not scale invariant. At high magnification, the small copies of the pattern which produce the visible structure are attenuated, and the latter look washed out. An instance of this phenomenon is obvious in my older images, for instance this one, in which the smallest visible triangular pattern is barely noticeable.
During all the years that I've spent exploring this technique, the mean value of B decreased steadily. Back in 2002, 2003 or 2004, I often used values of B between 0.7 and 1. In 2008, B was still between 0.5 and 1, with occasional texture layers using lower beta value. My 2009 works often use values of B around 0.3. Recently, I tried B=0.1 in a few images, like the one below.
One can wonder if it is possible to make an image in which the smaller copies of the pattern are not attenuated and which does not look like random noise. Such an image would have the very elegant property of being scale invariant: the patterns would not fade out when zooming on them. It turns out that it is much more easy that I thought to create such images, provided one is a little bit careful when choosing the pattern to be piled. The image below uses randomly distributed squares. The density of squares is very low, so that the small scale patterns do not interfere significantly with the large scale pattern.
On the contrary, this image uses a smooth pattern, but a rather large magnification step (8).
The only trouble with these non-attenuated images is that they look rather different before and after anti-aliasing For instance, here is 20090907-1 without anti-aliasing, as it appears in Ultra Fractal.
I had several candidate works which looked great as raw images, but turned out to be boring when rendered. Some practice is still needed to be able to foresee the result of anti-aliasing.


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Infanticide and monogamy
Science writer Matt Ridley once described the human mating system as "monogamy plagued by adultery," which sounds a little judgmental. Perhaps we should just agree that we are an imperfectly pair-bonding species. Quite imperfectly – I am on my second marriage, and so is my wife – but the point is that we do form pairs: 89 percent of the world's people get married before the age of forty-nine.
Elsewhere in the animal world, monogamy is definitely a minority taste. Only 3 percent of mammals are monogamous. Even among our closest relatives, the primates, only a quarter of the species form pair bonds. Moreover, the very fragility of the pair bond in human beings suggests that it is a behavior we only adopted fairly recently in our evolutionary history. So when did we acquire it, and why?
There is a new explanation on the table. In a study published this week in the "Proceedings of the National Academy of Sciences", scientists argue that the main reason why human beings – more precisely, male human beings – became monogamous was to keep their babies from being killed by other men.
There are many species where an incoming male will kill a female's offspring by a previous male in order to make room for his own. It's especially common in mammals, where a female remains infertile while she is still producing milk for an existing baby. The new male is in a hurry to get on with fathering the bearers of his own genes, and if he kills her existing offspring she will become fertile again.
This may have been a particularly big problem in our own species, because human females may nurse a child for as long as two or three years. Infanticide is ugly, but unfortunately it makes sense as a male reproductive strategy. So it also makes sense for the father of the existing children to stick around and protect them from that fate.
This was the hypothesis of the scientists from University College London and Oxford, Manchester and Auckland Universities who published the article in "Proceedings". "You do not get monogamy unless you already have infanticide, and you do not get a switch to paternal care (by males) if you don't already have monogamy," wrote Dr. Christopher Opie of UCL.
This flies in the face of the previously dominant explanation, which was based on the remarkably long childhood of human offspring. As our brains got bigger and the amount of cultural learning that had to be imparted to our children grew greater, the portion of their lives that they spent as dependent children grew longer and longer. Male help was therefore needed to raise them successfully.
True enough, but why would the males commit in the first place? They were unlikely to be able make that kind of statistical calculation, and the normal male reproductive strategy in mammals is to impregnate as many females as possible and leave the mothers to raise them. Maybe they just stayed with the females to keep their children from being killed by other males.
So the researchers decided to test the rival hypotheses: did males commit to monogamy to prevent infanticide, or to ease the burden on females and thus improve the children's survival chances in a different way? The cynics among you will already know the answer to this, but scientists actually have to prove things.
What they did was to take a family tree of 230 mammals, including most of the primate species, and put in the details of their mating behavior, rates of infanticide, and amount of paternal care (i.e. monogamy). Then they simulated the evolution of those species over a period of 75 million years, running the program millions of times to see how monogamy rose or fell for each species under different circumstances.
The conclusion was clear: among primates, monogamy was always preceded by one thing and one thing only: infanticide by males. Once you have monogamy, there is usually a rise in the male commitment to caring for the offspring as well, but infanticide has to come first. It's not exactly romantic, but evolution isn't.
So here we are, living in couples and raising our offspring together as if we were birds. (90 percent of birds are monogamous.) It doesn't really matter how we got here, but it's definitely a better place to be. In the end, we even figured out how to love each other.


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Dr. Ruey Jen Sung is Professor Emeritus, Cardiovascular Medicine, Department of Medicine. Previously, he served as Director, Cardiac Electrophysiology and Arrhythmia Service at Stanford University Medical Center (Chair, Department of Medicine: the late Professor Edward "Ted" D. Harris, Jr)(1991-2001). He graduated from National Taiwan University (1968), completed Medical Residency at University of Wisconsin (Chair: the late Professor Robert F. Schilling)(1970-72) and Cardiology Fellowship, University of Miami (1972-74). Since then, he has devoted his research endeavors to Clinical Cardiac Electrophysiology. He was the first to define the distinct anatomic location of the slow pathway relative to fast pathway conduction in the human atrioventricular (AV) node (1981), the principle of which has provided the basis of selective ablation of slow pathway conduction for curing AV nodal reentrant tachycardia, the most common form of paroxysmal supraventricular tachycardia in humans. Subsequently, he described electrophysiological characteristics of the three different forms of ventricular tachycardia (i.e., reentry, automaticity, and triggered activity), their modes of initiation and termination, and responses to various pharmacological agents in the Clinical Electrophysiology laboratory (1983, 1988). In 1985, he was promoted to full Professor of Medicine in Residence at the University of California at San Francisco (Chair: the late Professor Lloyd "Holly" Smith, Jr)(1981-91). Between 2001 and 2007, he was recruited to the post of Dean, College of Medicine, and Vice-President, National Cheng Kung University, Taiwan. Over the past 40 years, he has authored and co-authored 200 original articles and 66 invited chapters and monographs pertaining to mechanisms and treatment of cardiac rhythm disorders. Additionally, he has co-authored a book with the late Dr. Michael R. Lauer, entitled "Fundamental Approaches to the Management of Cardiac Arrhythmias" (2000, dedicated to his early year mentor, the late Professor Agustin Castellanos, Jr. Notably, Dr. Sung is one of the Founders of the Heart Rhythm Foundation and is currently Fellows of the American College of Physicians, American College of Cardiology, American Heart Association, and Heart Rhythm Society.
Academic Appointments
Emeritus Faculty, Acad Council, Medicine
Administrative Appointments
Director, Pacemaker-Arrhythmia Clinic and Director,Cardiac Electrophysiology Laboratory, Jackson Memorial Hospital, University of Miami School of Medicine (1975 - 1981)
Director, Clinical Cardiac Electrophysiology Laboratory, H.C. Moffitt Hospital, University of California at San Francisco (1981 - 1983)
Director, Cardiac Electrophysiology, San Francisco General Hospital, University of California at San Francisco (1983 - 1991)
Director,Cardiac Electrophysiology and Arrhythmia Service, Stanford University Medical Center (1991 - 2001)
Director, Center of Biosciences and Biotechnology, National Cheng Kung University, Tainan, Taiwan (2001 - 2003)
Vice-president of the University and Dean, College of Medicine, National Cheng Kung University, Tainan, Taiwan (2001 - 2007)
Honors & Awards
Eminent Cardiologist Award, Asian-Pacific Heart Association (2013)
Best paper Award, The 4th CardioRhythm, HongKong (2009)
Martin H. Stein Memorial Award, Cardiology Fellowship, University of Miami School of Medicine, Miami, Florida (1974)
Holden Award, Rotating Internship, Bon Secours Hospital, Grosse Pointe, Michigan (1970)
Best Internship Award, College of Medicine, National Taiwan University (1968)
Boards, Advisory Committees, Professional Organizations
Fellow and Founders Club, Heart Rhythm Society (2000 - Present)
Fellow, American College of Chest Physicians (1989 - 1995)
Fellow, Council on Clinical Cardiology, American Heart Association (1977 - Present)
Fellow, American College of Physicians (1977 - Present)
Fellow, American College of cardiology (1976 - Present)
Peer Review Board, UpToDate in Cardiovascular Medicine (2000 - Present)
Editorial Board, Korean Journal of Cardiovascular Diseases (2000 - 2010)
Editorial Board, Journal of American College of Cardiology (2000 - 2004)
Editorial Board, Journal of Interventional Cardiac Electrophysiology (1997 - 2003)
Editorial Board, Journal of Formosan Medical Society (1994 - 2007)
Editorial Board, Cardiovascular Drugs and Therapy (1994 - 2001)
Editorial Board, Journal of Cardiovascular Electrophysiology (1991 - 1999)
Editorial Board, American Heart Journal (1991 - 1996)
Editorial Board, Clinical Progress in Pacing and Electrophysiology (1981 - 1989)
Professional Education
MD, College of Medicine, National Taiwan University Taipei, Taiwan, Medicine (1968)
Community and International Work
Board Member, Wuhan, P.R. China
Scientific Advisory Board
Partnering Organization(s)
Britton Chance Center for Biomedical Photonics (BC CBMP), Huazhong University of Science and Technology (HUST)
Ongoing Project
Opportunities for Student Involvement
Chair, Scientific Committee, Taipei, Taiwan
The 16th Asian-Pacific Congress of Cardiology, Taipei, Taiwan
Partnering Organization(s)
The Asian-Pacific Congress of Cardiology
Populations Served
Ongoing Project
Opportunities for Student Involvement
Chair, Research Committee, Taiwan
Taiwan Society of Cardiology, Taiwan
Partnering Organization(s)
Chair, Research Committee, Taiwan Society of Cardiology, Taipei, Taiwan
Ongoing Project
Opportunities for Student Involvement
Additional Info
Current Research and Scholarly Interests
Clinical and basic cardiac electrophysiology
All Publications
Targeting intracellular calcium cycling in catecholaminergic polymorphic ventricular tachycardia: a theoretical investigation
Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a malignant arrhythmogenic disorder linked to mutations in the cardiac ryanodine receptor (RyR2) and calsequestrin, predisposing the young to syncope and cardiac arrest. To define the role of β-adrenergic stimulation (BAS) and to identify potential therapeutic targeted sites relating to intracellular calcium cycling, we used a Luo-Rudy dynamic ventricular myocyte model incorporated with interacting Markov models of the L-type Ca(2+) channel (I(Ca,L)) and RyR2 to simulate the heterozygous state of mouse RyR2 R4496C mutation (RyR2(R4496C+/-)) comparable with CPVT patients with RyR2 R4497C mutation. Characteristically, in simulated cells, pacing at 4 Hz or faster or pacing at 2 Hz under BAS with effects equivalent to those of isoproterenol at ≥ 0.1 μM could readily induce delayed afterdepolarizations (DADs) and DAD-mediated triggered activity (TA) in RyR2(R4496C+/-) but not in the wild-type via enhancing both I(Ca,L) and sarcoplasmic reticulum (SR) Ca(2+) ATPase (I(UP)). Moreover, with the use of steady state values of isolated endocardial (Endo), mid-myocardial (M), and epicardial (Epi) cells as initial data for conducting single cell and one-dimensional strand studies, the M cell was more vulnerable for developing DADs and DAD-mediated TA than Endo and Epi cells, and the gap junction coupling represented by diffusion coefficient (D) of ≤ 0.000766*98 cm(2)/ms was required for generating DAD-mediated TA in RyR2(R4496C+/-). Whereas individual reduction of Ca(2+) release channel of SR and Na-Ca exchanger up to 50% was ineffective, 30% or more reduction of either I(Ca,L) or I(UP) could totally suppress the inducibility of arrhythmia under BAS. Of note, 15% reduction of both I(Ca,L) and I(UP) exerted a synergistic antiarrhythmic efficacy. Findings of this model study confirm that BAS facilitates induction of ventricular tachyarrhythmias via its action on intracellular Ca(2+) cycling and a pharmacological regimen capable of reducing I(Ca,L) could be an effective adjunctive to β-adrenergic blockers for suppressing ventricular tachyarrhythmias during CPVT.
View details for DOI 10.1152/ajpheart.00696.2010
View details for Web of Science ID 000295360100045
View details for PubMedID 21742998
Electrophysiological mechanisms of ventricular arrhythmias in relation to Andersen-Tawil syndrome under conditions of reduced I-K1: a simulation study
Patients with Andersen-Tawil syndrome (ATS) mostly have mutations on the KCNJ2 gene, producing loss of function or dominant-negative suppression of the inward rectifier K(+) channel Kir2.1. However, clinical manifestations of ATS including dysmorphic features, periodic paralysis (hypo-, hyper-, or normokalemic), long QT, and ventricular arrhythmias (VAs) are considerably variable. Using a modified dynamic Luo-Rudy simulation model of cardiac ventricular myocytes, we attempted to elucidate mechanisms of VA in ATS by analyzing effects of the inward rectifier K(+) channel current (I(K1)) on the action potential (AP). During pacing at 1.0 Hz with extracellular K(+) concentration ([K(+)](o)) at 4.5 mM, a stepwise 10% reduction of Kir2.1 channel conductance progressively prolonged the terminal repolarization phase of the AP along with gradual depolarization of the resting membrane potential (RMP). At 90% reduction, early afterdepolarizations (EADs) became inducible and RMP was depolarized to -52.0 mV (control: -89.8 mV), followed by emergence of spontaneous APs. Both EADs and spontaneous APs were facilitated by a decrease in [K(+)](o) and suppressed by an increase in [K(+)](o). Simulated beta-adrenergic stimulation enhanced delayed afterdepolarizations (DADs) and could also facilitate EADs as well as spontaneous APs in the setting of low [K(+)](o) and reduced Kir2.1 channel conductance. In conclusion, the spectrum of VAs in ATS may include 1) triggered activity mediated by EADs and/or DADs and 2) abnormal automaticity manifested as spontaneous APs. These VAs can be aggravated by a decrease in [K(+)](o) and beta-adrenergic stimulation and may potentially induce torsade de pointes and cause sudden death. In patients with ATS, the hypokalemic form of periodic paralysis should have the highest propensity to VAs, especially during physical activity.
View details for DOI 10.1152/ajpheart./00393.2006
View details for Web of Science ID 000241855900010
View details for PubMedID 16877549
Significance of inducible ventricular flutter/fibrillation in risk stratification in patients with coronary artery disease
2004; 94 (1): 67-71
Although inducible ventricular fibrillation (VF) has been used as an indication for prophylactic implantation of cardioverter-defibrillators (ICDs) in patients with coronary artery disease (CAD), the significance of inducible VF remains controversial.Among 364 CAD patients who underwent electrophysiologic (EP) study for risk stratification, 23 patients, 12 without any history of VF or cardiac arrest (group A) and 11 with previously documented VF or cardiac arrest (group B), exhibited inducible ventricular flutter (VFL) or VF and subsequently underwent ICD implantation. Additionally, 11 CAD patients without previous VF or cardiac arrest, who had no inducible ventricular tachyarrhythmias but received an ICD, were included for comparison (group C).During 2 years of follow-up, 1 (8%), 5 (45%), and 1 (9%) patients had appropriate ICD shocks in groups A, B, and C, respectively. The survival free from appropriate ICD shocks was significantly lower in group B compared to groups A and C (p<0.05). There were no significant differences in age, sex, ejection fraction (EF), or induction protocol between groups A and B or between groups A and C.In CAD patients with inducible VFL/VF, patients without any history of VF or cardiac arrest had significantly lower incidence of appropriate ICD shocks when compared to those with such clinical events. Conversely, in CAD patients without any history of VF or cardiac arrest, incidence of appropriate ICD shocks was similar regardless of inducible VFL/VF. Inducible VFL/VF is therefore not useful as an indication for prophylactic ICD implantation in this patient population.
View details for DOI 10.1016/j.ijcard.2003.04.008
View details for PubMedID 14996477
Spatial heterogeneity of action potential alternans during global ischemia in the rabbit heart
Cardiac ischemia causes beat-to-beat fluctuation in action potential duration (APD) alternans, which leads to T wave alternans and arrhythmias. Occurrence of APD alternans that is out of phase at two sites is especially important, but most APD alternans studies have involved rapid pacing of normal myocardium rather than ischemia. To determine the spatial features of APD alternans during ischemia, blood-perfused rabbit hearts were stained with 4-[beta-[2(di-n-butylamino)-6-napthyl]vinyl]pyridinium (di-4-ANEPPS) and imaged with a high-resolution camera. Hearts were perfused with oxygenated Tyrode solution at 37 degrees C for staining and then switched to a 50:50% blood/Tyrode mixture. Hearts were paced from the right ventricle at 3/s, and made ischemic by stopping flow for 6 min. Images of 10,000 pixels were obtained at 300 frames/s. Motion artifact was controlled by immobilization and by manual selection of undistorted single-pixel records. Upstroke propagation and conduction isochrones were displayed by computerized image processing. APD alternans was demonstrated in six of seven hearts, and was out of phase in different regions of the image in three hearts. The largest spatial variation in the onset of depolarization to 50% repolarization (APD50) was 155%. This caused beat-to-beat reversal of repolarization. An alternans map could be constructed for well-immobilized portions of the image. There were discrete regions of APD alternans separated by a boundary, as occurs with intracellular Ca2+ concentration alternans. Pixels as close together as 1.1 mm showed an APD alternans that was out of phase. The out-of-phase APD alternans was not due to conduction alternans, as shown by upstroke intervals and conduction isochrones. This contrasts with rapid pacing, where a causal relationship appears to exist. These new observations suggest distinct mechanisms for the genesis of arrhythmias during ischemia.
View details for DOI 10.1152/ajpheart.00369.2003
View details for Web of Science ID 000186521700056
View details for PubMedID 12907420
Facilitating electrical cardioversion of persistant atrial fibrillation by antiarrhythmic drugs: update on clinical trial results.
Cardiac electrophysiology review
2003; 7 (3): 300-303
Results from clinical trials suggest that antiarrhythmic drugs (AD) can facilitate electrical cardioversion (EC) for persistent atrial fibrillation (AF) (duration >48 hours, no spontaneous termination) by suppression of immediate reinitiation of AF following the procedure. Class IC agents may increase the atrial defibrillation threshold (DFT) by significantly reducing the availability of Na+-channel for depolarization. In contrast, class III agents may decrease the atrial DFT by markedly prolonging atrial refractoriness. Among all AD, ibutilide and amoidarone have been shown to be most effective in enhancing the acute outcome of EC. In patients who are over 65 years of age at high risks of stroke (e.g., atherosclerotic cardiovascular disease, diabetes, hypertension, previous thromboembolism, etc.), the rhythm control strategy offers no survival advantage over the rate control strategy and frequently subjects patients to serious adverse effects of AD therapy. It can not be overemphasized that adequate anticoagulation (INR 2.0-3.0) with warfarin is needed regardless of whichever strategy is chosen unless there are contraindications. On the other hand, in patients who are under 65 years of age without structural heart disease or other risk factors of stroke, rhythm control can be the treatment of choice. Specifically, if a patient has failed EC alone or if the patient has characteristics (e.g., duration of AF >6 months, left atrium >50 mm, etc.) that EC could fail, AD may be given before the procedure to facilitate EC. In the subgroup of patients who are symptomatic with hypertrophic cardiomyopathy and severe diastolic dysfunction requiring maintenance of sinus rhythm to have sufficient ventricular function for optimization of cardiac output, an aggressive approach for rhythm control with amiodarone along with adequate anticoagulation with warfarin should be encouraged.
View details for PubMedID 14739733
Limited predictive value of inducible sustained ventricular tachycardia for future occurrence of spontaneous ventricular tachycardia in patients with coronary artery disease and relatively preserved cardiac function
2003; 36 (3): 205-211
To evaluate the significance of inducible sustained ventricular tachycardia (VT) in patients with coronary artery disease and relatively preserved cardiac function, 33 patients who met the following criteria were studied; documented nonsustained VT but no history of life-threatening arrhythmia, inducible sustained VT at electrophysiologic study, and implantation of a cardioverter-defibrillator. Eighteen patients developed clinical sustained VT within 2 years. By univariate analysis, left ventricular ejection fraction (EF) and the cycle length of induced VT were associated with clinical VT occurrence. By multivariate analysis, however, EF was the only independent predictor. Among 23 patients with EF
40% (P <.01). In coronary artery disease patients with relatively preserved EF, the incidence of clinical VT is considerably low even though sustained VT is inducible. Inducible VT is therefore not appropriate for risk stratification in this patient population.
View details for DOI 10.1016/S0022-0736(03)00032-3
View details for PubMedID 12942482
Unidirectional conduction block at cavotricuspid isthmus created by radiofrequency catheter ablation in patients with typical atrial flutter
2002; 13 (11): 1098-1102
Although unidirectional conduction block at the cavotricuspid isthmus can be created by radiofrequency ablation for atrial flutter, its underlying mechanism has not been elucidated.Twenty-seven patients (22 men and 5 women; mean age 59 +/- 11 years) who met the following criteria were studied: (1) bidirectional isthmus conduction demonstrable at baseline; (2) at least one linear lesion attempted on the cavotricuspid isthmus with radiofrequency catheter ablation; and (3) conduction times at anterolateral and posteromedial portions of the isthmus measured for both clockwise and counterclockwise directions before the ablation procedure. Unidirectional conduction block was observed before achieving bidirectional block in 9 patients (group I); the remaining 18 patients did not exhibit unidirectional conduction block (group II). All unidirectional conduction blocks were demonstrated in the counterclockwise direction. Anterolateral isthmus conduction time in group I was significantly longer than that in group II in both directions. However, there were no significant differences in posteromedial isthmus conduction time between groups I and II in either direction. Anterolateral isthmus conduction time was significantly longer than posteromedial conduction time in group I but not in group II.There were significant differences in conduction properties at the cavotricuspid isthmus between patients who developed unidirectional conduction block and those who did not. Our results support the notion that anisotropy contributes to the genesis of unidirectional conduction block at the cavotricuspid isthmus during the radiofrequency ablation procedure.
View details for PubMedID 12475099
Importance of using standard rather than torso surface electrocardiographic leads for pacemapping at the right ventricular outflow tract
2002; 25 (5): 776-784
Although pacemapping has been used to localize the origin of ventricular tachycardia, the effect of changes in the position of ECG electrodes during ventricular pacing remains unknown. To clarify the relationship between the position of ECG limb electrodes and QRS configuration during pacemapping at the right ventricular outflow tract (RVOT), RVOT pacing was performed on 12 patients at eight pacing sites located in the anterior, septal, lateral, and posterior portions each in the high and low RVOT. Standard and torso ECGs were recorded simultaneously during each pacing protocol, and the QRS axis and amplitude were compared between the two ECGs. Differences between sites in the horizontal plane and in the longitudinal direction were also compared. The QRS axis on the torso ECG was significantly more rightward than that on the standard ECG at all eight pacing sites (72.1+/-17.4 vs 64.0+/-21.9 degrees). The magnitude of differences in the QRS axis and amplitude between the anterior and other sites at the same height was significantly greater in the standard ECG in all locations and in 7 of 18 comparable leads, respectively. The magnitude of differences between high and low sites was significantly greater in the standard ECG in three of four locations and in 5 of 12 comparable leads, respectively. In conclusion, the torso ECG is less sensitive to changes in pacing site at the RVOT than the standard ECG. The torso ECG is, therefore, not proper for pacemapping in attempts to ablate ventricular tachycardia arising from the RVOT.
View details for Web of Science ID 000175689700005
View details for PubMedID 12049368
Spatial heterogeneity of calcium transient alternans during the early phase of myocardial ischemia in the blood-perfused rabbit heart
2001; 104 (17): 2082-2087
Optical mapping of cytosolic calcium transients in intact mammalian hearts is now possible using long-wavelength [Ca(2+)](i) indicators. We propose that beat-to-beat [Ca(2+)](i) transient alternans during ischemia may lead to spatial and temporal heterogeneity of calcium-activated membrane currents.To test this hypothesis, isolated rabbit hearts were loaded with the fluorescent [Ca(2+)](i) indicator, rhod-2 AM, and imaged at 300 frames/sec during blood-perfused ischemic trials. High-quality [Ca(2+)](i) transients were recorded in each of 8 hearts.[Ca(2+)](i) transient alternans was never present in control records but occurred in each of the hearts during ischemia, with onset after 2 to 4 minutes. Alternans was confined to circumscribed regions of the heart surface 5 to 15 mm across. Multiple regions of alternans were found in most hearts, and regions that were out of phase with one another were found in 6 hearts. Quantitative maps of alternans were constructed by calculating an alternans ratio. This ratio behaved as a continuous variable that reached a maximum value in the center of the regions with alternans.These results demonstrate marked spatial heterogeneity of the [Ca(2+)](i) transient during the early phase of ischemia, which could produce electrical instability and arrhythmias in large mammalian hearts.
View details for Web of Science ID 000171828800019
View details for PubMedID 11673350
Influence of isoproterenol on the accelerated junctional rhythm observed during radiofrequency catheter ablation of atrioventricular nodal slow pathway conduction
2001; 142 (4): 664-668
Accelerated junctional rhythm (AJR) has been considered as a sensitive but rather nonspecific marker of successful radiofrequency (RF) ablation of slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). However, AJR also occurs commonly during isoproterenol infusion. We therefore investigated the effect of isoproterenol on the significance of AJR while attempting slow pathway ablation.Forty patients with AVNRT underwent slow pathway ablation. Sixty-nine RF applications accompanied by AJR were observed and were separated into 2 groups: applications performed without (group I, n = 26) and with (group II, n = 43) isoproterenol infusion. The specificity of AJR for successful ablation for each group was calculated.The specificity of AJR in groups I and II was 73% (19/26) and 49% (21/43), respectively (P <.05). There was no significant difference between the groups in the atrial electrogram width, atrial/ventricular electrogram amplitude ratio, the time from application onset to AJR emergence, or AJR cycle length. The catheter-tip temperature at AJR emergence was significantly lower (47 degrees C +/- 3 degrees C vs 52 degrees C +/- 3 degrees C, P <.001) and the ratio of junctional beats to total heart beats during RF application was significantly greater (46% +/- 24% vs 33% +/- 18%, P <.05) in group II compared with group I.Isoproterenol lowers the threshold of AJR emergence during RF application and thereby lowers the specificity of AJR for successful ablation. Complete washout of isoproterenol may therefore improve the specificity of AJR during RF ablation in patients with AVNRT.
View details for Web of Science ID 000171343100015
View details for PubMedID 11579357
Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia
2001; 12 (8): 928-934
Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT.During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness.During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.
View details for Web of Science ID 000170405400012
View details for PubMedID 11513445
Antiarrhythmic agents in facilitating electrical cardioversion of atrial fibrillation and promoting maintenance of sinus rhythm
2001; 95 (1): 1-8
Atrial fibrillation (AF) is a prevalent arrhythmia associated with significant morbidity and mortality. Electrical cardioversion of AF is a potentially definitive treatment, but as little as 67% of patients may be successfully cardioverted and, after normal sinus rhythm (NSR) is achieved, AF often recurs. Class IA, IC, and III antiarrhytmic agents are used for both facilitation of electrical cardioversion and subsequent maintenance of NSR. The mechanisms of these agents may be related to suppressing automaticity, prolonging the wavelength of reentrant wavelets, and preventing electrical remodeling. The possibility of proarrhythmia and other adverse effects complicates use of these drugs, and no large trials have been completed to elucidate definite indications. Several factors may predict failure with electrical cardioversion alone (duration of AF, atrial size, age, underlying disease, and factors that affect transthoracic impedance), calling for empiric pharmacotherapy to facilitate cardioversion. For this purpose, class IA agents hold some promise, evidence for class IC agents is conflicting, and class III agents are the most effective. Adverse effects are rare given the short course before cardioversion, but ibutilide, the most efficacious in this regard, may be proarrhythmic after only a single dose. In promoting maintenance of sinus rhythm, antiarrhythmics across the different classes have similar efficacies: NSR may be maintained in approximately 40-65% of patients compared to approximately 30-35% with placebo at 1 year. Amiodarone is distinct in its success, with approximately 60-80% of patients remaining in NSR. For all of these agents, long-term therapy may lead to proarrhythmia or other substantial adverse effects. Finally, a serial antiarrhythmic strategy may be effective, with maintenance of NSR and minimal adverse effects ultimately achieved by trial and error.
View details for Web of Science ID 000169197000001
View details for PubMedID 11385184
Effects of adenosine A(1)-receptor activation on torsade de pointes in rabbits
1999; 13 (5): 441-447
We tested whether the adenosine A1 receptor agonist, R-PIA, suppressed torsade de pointes (TdP) induced by the delayed rectifier potassium channel blocker clofilium. Furthermore, we studied the underlying mechanism: beta-adrenergic antagonism or ATP-sensitive K+ channel (IK-ATP) opening.In anesthetized rabbits, TdP was induced by simultaneous infusion of clofilium and the alpha1-adrenoceptor agonist methoxamine. Four groups were studied: (1) saline infusion after TdP induction; (2) R-PIA (1.3 mg/kg) infusion; (3) R-PIA infusion after propranolol (2 micromol/kg) pretreatment; (4) R-PIA infusion after glibenclamide (10 micromol/kg) pretreatment.TdP suppression rate was 0% in group 1, 78% in group 2 (p<0.01 vs. group 1), 67% in group 3 (p<0.05 vs. group 1, p = NS vs. group 2), 33% in group 4 (p = NS vs. group 1, p = 0.08 vs. group 2). TdP induction coincided with increased QT/QTc duration and QT dispersion. TdP suppression coincided with reduced QT dispersion, but further QT/QTc lengthening.R-PIA suppressed TdP, not by beta-adrenergic antagonism, but mostly by IK-ATP opening. QT dispersion correlated better with TdP induction/suppression than QT/QTc duration.
View details for Web of Science ID 000082322600008
View details for PubMedID 10547225
Multiple atrioventricular nodal pathways in humans: Electrophysiologic demonstration and characterization
1998; 9 (2): 129-140
Multiple AV nodal pathway physiology can be demonstrated in certain patients with clinical AV reentrant tachycardia.Evidence suggesting multiple AV nodal pathway conduction was present in seven (two males; age range 15 to 75 years) of 78 patients (9%) who underwent electrophysiologic studies for AV nodal tachycardia. The presence of two discrete discontinuities in the AV nodal conduction curves suggested triple AV nodal pathway conduction. Detailed mapping of their retrograde atrial activation sequence was performed along the tricuspid annulus from the coronary sinus ostium to the His-bundle electrogram recording site. Three zones (anterior, middle, and posterior) correspond to the upper, middle, and lower third of the triangle of Koch, respectively. The fast pathway exits were determined as anterior (4/7) or middle (3/7), the intermediate pathway exits as middle (4/7) or posterior (3/7), and the slow pathway exits as middle (1/7) or posterior (6/7). Other evidence suggesting multiple AV nodal pathway conduction includes: (1) triple ventricular depolarizations from a single atrial impulse; (2) sequential dual ventricular echoes; (3) spontaneous transformation between the slow-fast and fast-slow forms of AV nodal reentrant tachycardia; and (4) persistent cycle length alternans during AV nodal reentrant tachycardia. In four patients, all three pathways were shown to be involved in AV nodal echoes or reentrant tachycardia.Multiple AV nodal pathways are not uncommon and can be identified by careful electrophysiologic elucidation and mapping technique.
View details for Web of Science ID 000072148200003
View details for PubMedID 9511887
The role of intravenous amiodarone in the management of cardiac arrhythmias
1997; 127 (4): 294-303
To review the electropharmacology, clinical applications, side effects, and hemodynamic profile of intravenous amiodarone.The MEDLINE database was searched for English-language material, including reports of clinical trials and in vivo studies, review articles, and abstracts presented at national symposia, that was published between 1985 and 1996. Bibliographies of textbooks and articles were also examined.Studies that reported on the efficacy, toxicity, and hemodynamic profile of intravenous amiodarone and studies that examined the pharmacologic behavior of intravenous amiodarone in laboratory models were reviewed.Study design and quality and relevant data on efficacy of suppression and treatment of arrhythmias with oral and intravenous amiodarone therapy, the reported mechanisms of antiarrhythmic effect, and hemodynamic changes seen with therapy were analyzed.Amiodarone is a unique antiarrhythmic agent that is now available in oral and intravenous forms in the United States. The use of intravenous amiodarone in the short-term treatment of life-threatening or hemodynamically unstable rhythm disturbances has generated much interest. Amiodarone has many electropharmacologic actions, some of which differ between the oral and intravenous forms. The wide clinical application of amiodarone includes treatment and prevention of supraventricular and ventricular arrhythmias and arrhythmias related to myocardial infarction. Intravenous amiodarone is effective for supraventricular and ventricular arrhythmias that are resistant to other antiarrhythmic agents. The effectiveness of intravenous amiodarone as short-term treatment also suggests that the drug has an important role in protocols of advanced cardiac life support. Intravenous amiodarone seems to have an overall favorable hemodynamic profile and does not produce many of the unwanted long-term side effects associated with oral therapy.Intravenous amiodarone shows much promise for the short-term treatment of unstable arrhythmias. Its favorable hemodynamic effects and minimal short-term side effects make it an attractive option in the management of cardiac arrhythmias.
View details for Web of Science ID A1997XR26600009
View details for PubMedID 9265430
Intracoronary arterial occlusion: a novel technique potentially useful for ablation of cardiac arrhythmias.
Journal of interventional cardiac electrophysiology
1997; 1 (1): 7-14
To develop a new technique for ablating arrhythmias by interrupting coronary perfusion of the myocardium, we studied six mongrel dogs, weighing 20-35 kg. Under angiographic guidance a microcatheter (1.0 mm diameter) was introduced into a branch of the left anterior descending or posterior descending coronary artery. A detachable platinum coil (0.0254 cm diameter, 3 cm length) soldered onto a stainless-steel delivery wire (Guglielmi) was inserted through the microcatheter and advanced to occlude the arterial branch. A 0.5-mA electric current applied to the proximal end of the delivery wire resulted in intravascular thrombosis due to attraction of the negatively charged blood cells, platelets, and fibrinogen to the positively charged platinum coil. In approximately 4.5 minutes, as the thrombus was formed, electric current dissolved the soldering and detached the platinum coil from the delivery wire. Electrocardiograms showed focal ST-T changes but no ventricular tachyarrhythmias. Pathologic studies revealed thrombosis around the platinum coil and well-demarcated focal ischemia/infarction that was correlated with elevation of cardiac enzymes. We conclude that intracoronary arterial embolization and electrothrombosis using an electrolytic platinum coil can be selectively performed in a very small coronary arterial branch, resulting in a limited area of myocardial damage. This technique is potentially useful for ablating arrhythmias and may be safer and more controllable than intracoronary alcohol infusion.
View details for PubMedID 9869945
Clinical efficacy of propantheline bromide in neurocardiogenic syncope: Pharmacodynamic implications
67th Scientific Session of the American-Heart-Association
The pharmacological response with tilt-table testing predicts long-term efficacy in neurocardiogenic syncope. However, beta-blockers for neurocardiogenic syncope are often not tolerated or are ineffective. Since cholinergic tone is important in the efferent part of the neurocardiogenic reflex, we investigated the pharmacodynamics and efficacy of propantheline bromide in preventing neurocardiogenic syncope. We studied 16 patients (11 males) with a mean age of 48.8 (+/- 15.1) years with presyncope or syncope and who had positive baseline tilt-table studies at a mean of 15.8 (+/- 10.3) minutes into the upright 60 degrees tilt. They were given propantheline bromide orally, an anticholinergic agent, at a dose of 64.3 (+/- 21.8) mg/day for 7 days, and tilt-table testing was repeated 1 hour after readministration of propantheline bromide, 30 mg orally. After propantheline bromide treatment, 13 of 16 patients (81%) had no inducible presyncope or syncope on repeat tilt-table testing. In this group of responders, the mean minimum heart rate during upright tilt-table testing increased from 43.2 (+/- 77.3) beats/min to 77.3 (+/- 17.2) beats/min after propantheline bromide (p < 0.005). More significantly, the minimum mean arterial blood pressure increased from 42.2 (+/- 25) mmHg to 81.3 (+/- 16.7) mmHg (p < 0.0005) during upright tilt. At a follow-up of 15.2 (+/- 7.4) months, in the responder group (12 patients with long-term follow-up), the average dose of propantheline bromide was 32.5 (+/- 23.8) mg/day, which was significantly reduced from the initial dose (p < 0.05). A clinical recurrence of symptoms occurred in only 4 out of 12 patients on propantheline bromide (33%), none of which were directly attributable to drug failure. It was concluded from this study that propantheline bromide is highly effective in preventing neurocardiogenic syncope. In addition, propantheline bromide's effectiveness is more than would be expected by prevention of cardioinhibition in neurocardiogenic syncope and would support a role for direct cholinergic control of vascular tone.
View details for Web of Science ID A1997WT08000005
View details for PubMedID 9110111
Ventricular pacing threshold and refractoriness after defibrillation shocks in patients with implantable cardioverter-defibrillators
1996; 131 (6): 1121-1126
The aim of this study was to examine the effect of ventricular fibrillation and a subsequent defibrillation shock on ventricular excitability and refractoriness in human beings. We studied 16 consecutive patients with implantable cardioverter-defibrillators undergoing follow-up studies. The pre- and post-shock pacing threshold, ventricular effective refractory period, monophasic action potential duration, and serum catecholamine levels were measured. Compared with the baseline state, immediately after ventricular fibrillation, and a successful defibrillation shock: (1) the ventricular effective refractory period decreased from 251 +/- 24 ms to 222 +/- 30 ms (p < 0.01), (2) the monophasic action potential duration decreased from 210 +/- 16 ms to 179 +/- 23 ms (P < 0.01) at 50% repolarization and from 274 +/- 24 ms to 240 +/- 26 ms (P< 0.01) at 90% repolarization, (3) the pacing threshold was not significantly altered and, (4) serum levels of epinephrine and norepinephrine were elevated. These results show that although ventricular fibrillation and subsequent defibrillation had no effect on the ventricular pacing threshold in human beings, it was associated with a decrease in post-shock monophasic action potential duration and ventricular effective refractory period, contrary to some previously reported findings.
View details for Web of Science ID A1996UP98200011
View details for PubMedID 8644590
Correlation of p-wave polarity with underlying electrophysiologic mechanisms of long RP' tachycardia
1996; 77 (12): 1129-?
Analysis of surface electrocardiograms from patients with long RP' tachycardia due to either atypical atrioventricular node reentrant tachycardia, permanent junctional reciprocating tachycardia, or low atrial tachycardia was performed. Although a negative P wave in the inferior leads is common to all 3 mechanisms, the results suggest that a positive or isoelectric P wave in electrocardiographic lead I strongly supports a diagnosis of atypical atrioventricular node reentrant tachycardia, whereas a negative or biphasic P wave in lead I argues against this mechanism.
View details for Web of Science ID A1996UN62400022
View details for PubMedID 8644674
Spectrum of electrophysiologic and electropharmacologic characteristics of verapamil-sensitive ventricular tachycardia in patients without structural heart disease
1996; 77 (11): 967-973
Verapamil-sensitive ventricular tachycardia (VT) is a well-recognized clinical entity that some authorities believe may result from triggered activity. Despite its uniform response to verapamil, however, there is evidence that this uncommon form of VT may not be as homogeneous as first believed. Standard intracardiac electrophysiologic techniques were used to study verapamil-sensitive VT in 32 patients (aged 38 years +/- 20 years) without evidence of structural heart disease. More than half of these patients (69%) exhibited VT with a right bundle branch block-type QRS pattern, with the remainder (31%) displaying VT with a left bundle branch block pattern. In 31% of the patients the VT could be induced by fixed-cycle length atrial pacing, whereas in 59% of patients fixed-cycle length ventricular pacing was necessary. A critical range of cycle lengths for VT induction was required in 66% of the patients. Ventricular tachycardia was initiated with single atrial premature extrastimuli in 16% of patients, single ventricular extrastimuli in 50% of patients, and double ventricular premature extrastimuli in 9% of patients. Ventricular tachycardia displaying cycle-length alternans was observed in 28% of patients. In only 19% of patients was it possible to entrain VT during pacing from the right ventricular apex. Isoproterenol infusion was required for tachycardia induction in 50% of patients, 44% of whom had VT with a left bundle branch block QRS pattern, with the remaining 56% exhibiting VT with a right bundle branch block pattern. Beta-adrenergic blockers suppressed 53% of verapamil-sensitive VT in patients tested, whereas adenosine terminated VT in 50% of patients, with 81% of these patients exhibiting either a left bundle branch block QRS pattern or isoproterenol dependence. Ventricular tachycardia exhibiting a left bundle branch block pattern was more likely to be isoproterenol dependent (p <0.05) and adenosine sensitive (p <0.001). However, verapamil-sensitive, catecholamine-dependent VT was no more likely to be adenosine sensitive than the catecholamine-independent form of the arrhythmia (p >0.5). Verapamil-sensitive VT exhibits properties expected of both a reentrant and triggered arrhythmia, and it is inconsistently dependent on both exogenous catecholamines for induction and intravenous adenosine for termination. Verapamil-sensitive VT encompasses a heterogeneous group of tachycardias that may result from multiple cellular electrophysiologic mechanisms.
View details for Web of Science ID A1996UM49400011
View details for PubMedID 8644647
Localization of the origin of the atrioventricular junctional rhythm induced during selective ablation of slow-pathway conduction in patients with atrioventricular node reentrant tachycardia
1996; 131 (5): 937-946
During radiofrequency catheter ablation of slow atrioventricular node pathway conduction in patients with atrioventricular node reentrant tachycardia, an atrioventricular junction rhythm is frequently observed. The origin and relation to ablation success of this junctional rhythm was examined in this study. By using standard intracardiac electrophysiology techniques, we studied the radiofrequency energy-induced atrioventricular junctional rhythm in 43 consecutive patients with atrioventricular node reentrant tachycardia undergoing selective ablation of slow-pathway conduction. The frequency of atrioventricular junctional activity was correlated with successful and unsuccessful attempts at ablation of slow-pathway conduction. Also, we compared the sequence of retrograde atrial activation of radiofrequency energy-induced atrioventricular junctional beats in a subgroup of 22 patients with the retrograde activation sequence observed during pacing from the right ventricular apex and the site of successful ablation of slow-pathway conduction. A total of 201 radiofrequency-energy applications was delivered in 43 patients with > or = 5 atrioventricular junctional beat(s) induced during 110 (55%) of 201 ablation attempts. Atrioventricular junctional activity was noted during 98% of successful ablations but only 43% of the unsuccessful attempts (sensitivity, 98%; specificity, 57%; negative predictive value, 99%). The mean time to appearance of atrioventricular junctional beats was 8.8 +/- 4.1 sec (mean +/- SD) after the onset of radiofrequency-energy application. In 22 (100%) of 22 patients in whom detailed atrial mapping was performed, the retrograde atrial activation sequence of the radiofrequency-induced atrioventricular junctional beats was earliest in the anterior atrial septum, identical to that seen during pacing from the right ventricular apex. Earliest retrograde atrial activation was at the posterior septum in all patients during pacing from the successful ablation site, a markedly different activation pattern compared with that seen during either radiofrequency ablation or ventricular pacing. Whereas the occurrence of atrioventricular junctional activity during radiofrequency ablation does not necessarily herald a successful ablation of slow atrioventricular node pathway conduction, its absence strongly suggests that the energy is being applied in an unsuccessful fashion. Furthermore, it appears that radiofrequency energy-induced atrioventricular junctional beats originate not from the endocardium in contact with the ablating catheter tip but instead appear to exit remotely from the anterior atrial septal region. This finding supports the existence of specialized tissues in the atrioventricular junction that preferentially transmit the effects of radiofrequency energy to an anterior exit site, possibly identical to the atrial exit site of the retrograde fast atrioventricular node conduction pathway.
View details for Web of Science ID A1996UH93400015
View details for PubMedID 8615313
Role of atrial extrastimulation in the diagnosis of atrioventricular node reentrant tachycardia with antegrade atrioventricular conduction via bystander accessory connection
1996; 131 (4): 839-842
View details for Web of Science ID A1996UE42100037
View details for PubMedID 8721668
Characteristic electrocardiographic features of manifest left anterior paraseptal accessory atrioventricular connection
1996; 131 (4): 814-818
View details for Web of Science ID A1996UE42100027
View details for PubMedID 8721658
Electrophysiologic significance of discrete slow potentials in dual atrioventricular node physiology: Implications for selective radiofrequency ablation of slow pathway conduction
1996; 131 (3): 490-498
Atrioventricular (AV) node reentrant tachycardia is now routinely cured by selective radiofrequency ablation of slow AV node pathway conduction. However, debate remains concerning the optimum method for localizing the site at which radiofrequency energy should be delivered to eliminate slow-pathway conduction. Some investigators have proposed simple anatomy-guided ablations posteriorly near the ostium of the coronary sinus, whereas others suggest an electrophysiology-guided ablation using either recorded "slow potentials" or mapping of the retrograde atrial exit site of slow AV note pathway conduction when possible. To examine these issues, we systematically studied slow potentials recorded in the AV junction of patients undergoing radiofrequency catheter ablation for medically refractory AV node reentrant tachycardia. In 67 patients with the slow-fast form of AV note reentrant tachycardia, we performed detailed atrial mapping along the tricuspid annulus within the triangle of Koch. Two types of slow potentials were identified. Low-amplitude, low-frequency potentials, found in 48% of patients, were localized to the mid to posterior portions of the triangle of Koch, whereas high-amplitude, high-frequency potentials, observed in 22% of patients, were located only posteriorly near the ostium of the coronary sinus. In response to a bolus infusion of adenosine or incremental atrial pacing-induced AV node Wenckebach periodicity, the low-amplitude, low-frequency potentials showed an increased duration and further reduction in amplitude and frequency and often totally disappeared. In contrast, in spite of these maneuvers, the high-amplitude and high-frequency potentials remained unchanged. Of the 25 (37%) of 67 patients in whom the earliest retrograde atrial activation during ventriculoatrial slow AV nodal pathway conduction could be recorded, no patient exhibited low-amplitude, low-frequency potentials, and only 7 (28%) of 25 of these patients showed high-amplitude, high-frequency potentials. High-amplitude, high-frequency potentials persisted after successful radiofrequency ablation of slow pathway conduction. Fewer applications of radiofrequency energy were required for successful elimination of slow pathway conduction in patients in whom the retrograde atrial exit site of slow-pathway conduction could be localized, compared with those patients who only exhibited retrograde fast AV nodal pathway conduction. We conclude that high-amplitude, high-frequency potentials are part of atrial activity, whereas the origin of low-amplitude, low-frequency potentials is unclear and may represent either true intranodal biophysical electrical activity or merely artifact or far-field potentials. Regardless, the recording of high-amplitude or low-amplitude potentials is not required for successful ablation of slow-pathway conduction, although the ability to localize the retrograde atrial exit of slow-pathway conduction may assist in the ablation procedure.
View details for Web of Science ID A1996TZ29500009
View details for PubMedID 8604628
1995; 92 (9): 2558-2564
This study was designed to characterize the ventricular vulnerable period (VVP) and ventricular fibrillation (VF) threshold by use of T-wave shocks in patients undergoing implantation of cardioverter/defibrillators. A premature condensed shock applied during the VVP can induce VF. Most studies on the VVP and VF threshold have been conducted in animals rather than in humans.Twenty-one patients undergoing implantation of Medtronic PCD Jewel 7219D cardioverter/defibrillators because of ventricular tachycardia and/or VF were enrolled. All had structural heart disease. Their ages ranged from 42 to 85 years (mean, 69 +/- 11.3 years). Seventeen (80.9%) had atherosclerotic coronary artery disease. The right ventricle (RV) was driven at a cycle length (S1) of 400 ms, and monophasic shocks (S2) of 0.6 J were delivered through an RV apex lead (cathode) and a superior vena cava lead (anode) during the T wave of each cardiac cycle. The longest and shortest S1-S2 intervals that were capable of inducing sustained VF were defined as the outer and inner limits of the VVP at an energy level of 0.6 J, respectively. To determine the VF threshold, a shock of 0.2 J was applied at the midpoint of the VVP at 0.2-J increments until sustained VF was induced. The lowest energy setting capable of inducing sustained VF was defined as the VF threshold. Of the 21 patients, the VVP at an energy level of 0.6 J averaged 53.8 +/- 26.0 ms. Characteristically, the VVP started from the ascending limb of the T wave and ended at or slightly beyond the peak of the T wave, occupying 12.2 +/- 5.8% of the QT interval. The midpoint of the VVP used for determination of the VF threshold measured 0 to 90 ms (mean, 32.9 +/- 26.0 ms) before the peak of the T wave. Of the 21 patients, 16 (76.2%) had a VF threshold at < or = 0.2 J (estimated 57 V), 3 at 0.4 J (estimated 81 V), and 2 at 0.6 J (estimated 99 V).The VF threshold is low (< or = 0.2 J) in the majority of patients requiring implantation of cardioverter/defibrillators. Further studies are needed to define clinical usefulness of the study technique relative to its potential role for risk stratification and for assessing antifibrillatory properties of antiarrhythmic drugs in this subset group of patients.
View details for Web of Science ID A1995TC79600028
View details for PubMedID 7586357
1995; 79 (5): 1121-?
Nonpharmacologic approaches to the long-term management of SVTs have evolved rapidly and now offer to patients a safe, effective alternative for symptomatic relief from many SVTs. By far, radiofrequency catheter ablation, a technology less than 10 years old, offers the least invasive and most cost-effective nonpharmacologic alternative for many SVTs. Knowledge gained through electrophysiologic and ablation studies has enlarged the understanding of SVTs and may enable electrophysiologists to approach the more common and morbid condition of atrial fibrillation. From a societal standpoint, catheter ablation can remain a cost-effective mode of treatment if patient selection is stringent. The next 10 years should see further refinement in technique and in understanding of SVTs, improved technology, and enlarging applications of radiofrequency energy to cure or modify cardiac arrhythmias.
View details for Web of Science ID A1995RW54700009
View details for PubMedID 7674687
1995; 122 (9): 701-714
To review the current understanding of the mechanisms and treatment of the long QT interval syndromes and torsade de pointes.Personal databases of the authors and a search of the MEDLINE database from 1966 to 1994.Experimental and clinical studies and topical reviews on the electrophysiologic mechanisms and treatment of torsade de pointes were analyzed.The long QT interval syndromes have been classified into acquired and hereditary forms, both of which are associated with a characteristic type of life-threatening polymorphic ventricular tachycardia called torsade de pointes. The acquired form is caused by various agents and conditions that reduce the magnitude of outward repolarizing K+ currents, enhance inward depolarizing Na+ or Ca2+ currents, or both, thereby triggering the development of early afterdepolarizations that initiate the tachyarrhythmia. The hereditary form appears to result from an abnormal response to adrenergic or sympathetic nervous system stimulation. At least some cases of the hereditary long QT interval syndromes may result from a single gene defect that alters the intracellular regulatory proteins responsible for the modulation of K+ channel function. Treatment of the acquired form is primarily directed at identifying and withdrawing the offending agent, although emergent therapy using maneuvers and agents that favorably modulate transmembrane ion currents can be lifesaving. In torsade de pointes associated with the hereditary long QT interval syndromes, early diagnosis leading to treatments designed to both shorten the QT interval and block the beta-adrenergic-induced instability of the QT interval is essential.The long QT interval syndromes and torsade de pointes are potentially life-threatening conditions caused by various agents, conditions, and genetic defects. The mechanisms responsible for these conditions and available treatment options for them are reviewed.
View details for Web of Science ID A1995QV15100009
View details for PubMedID 7702233
1994; 8 (5): 773-774
Although amiodarone is the most effective antiarrhythmic agent for maintaining sinus rhythm in patients with atrial fibrillation, it is generally used as the drug of the last resort in the United States. This is because long-term amiodarone therapy can potentially cause serious noncardiac side effects, such as pulmonary fibrosis, thyroid dysfunction, hepatitis, and neurotoxicity. Furthermore, it may also cause adverse interaction with digoxin, coumadin, and other antiarrhythmic drugs. Atrial fibrillation is frequently associated with a variety of cardiac disease, and its triggering factors vary among patients. Treatment strategy should be tailored to each individual patient according to the clinical presentation, concomitant disease, left ventricular function, and response (efficacy and side effects) to each drug regimen.
View details for Web of Science ID A1994PR69500012
View details for PubMedID 7873476
1994; 17 (8): 1413-1430
With the advent of RF catheter modification of AV node conduction for the treatment of AV node reentrant tachycardia, considerable advances have been made with better understanding of the AV junctional anatomy, electrophysiology, and mechanism responsible for AV node reentrant tachycardia. Future studies should be designed to uncover the basic cellular electrophysiological mechanisms responsible for fast and slow AV node conduction, to define the exact tissue components of the reentrant circuit in order to make ablative procedures safer, and to study the long-term effects of RF catheter ablation on AV conduction. Special caution should be directed toward pediatric patients with more stringent indications for catheter ablation of the AV junctional area in these patients.
View details for Web of Science ID A1994PA52000010
View details for PubMedID 7971402
1994; 73 (8): 559-563
Many of the newest implantable cardioverter-defibrillators (ICDs) provide the option of programmable low-energy cardioversion for monomorphic ventricular tachycardia (VT). Whereas these devices may provide less myocardial damage and increased comfort in patients receiving frequent shocks for VT, the proarrhythmic effects of low-energy cardioversion from ICDs in patients with structural heart disease are not clear. The purpose of this study was to determine prospectively the per-patient incidence of ventricular fibrillation (VF) induction after low-energy cardioversion of VT by ICDs in patients with coronary artery disease. The estimated cardioversion energy requirement was determined during the course of routine predischarge ICD testing in 40 patients with newly implanted ICDs. Two groups of patients were identified during determination of the cardioversion energy requirement: (1) a non-VF group consisting of 26 of 40 patients (65%) without VF induced by low-energy shock and, (2) a VF group consisting of 14 of 40 patients (35%) who developed VF during low-energy cardioversion. There was no difference between the 2 groups in terms of patient age, sex, concurrent antiarrhythmic drug therapy, VT cycle length, or type of ICD system implanted. Compared with the non-VF group, the VF group was more likely to have both a lower ejection fraction (25 +/- 5% vs 33 +/- 8%; p = 0.005) and a cardioversion energy requirement > 2 J (79 vs 27%; p = 0.005). Our results suggest that low-energy cardioversion is associated with a high per-patient risk of VF induction, and the risk is higher in patients with poorer left ventricular function and, possibly, higher cardioversion energy requirement.(ABSTRACT TRUNCATED AT 250 WORDS)
View details for Web of Science ID A1994NB93500007
View details for PubMedID 8147300
1994; 73 (1): 38-42
The purpose of this study was to determine if adenosine is equally effective in terminating catecholamine-dependent and independent supraventricular tachycardia (SVT). The effect of adenosine on termination of SVT was studied in 21 patients: 12 with atrioventricular (AV) reciprocating tachycardia, and 9 with AV node reentrant tachycardia. Group 1 comprised 13 patients who had SVT induced in the absence of exogenous catecholamines, whereas group 2 comprised 8 who needed isoproterenol (1.6 +/- 0.4 micrograms/min) for induction. There was no statistical difference between the 2 groups regarding age, weight, mean arterial pressure during sinus rhythm and SVT, cycle length of SVT, or norepinephrine and epinephrine levels during sinus rhythm and SVT. Cycle length during sinus rhythm was significantly decreased in group 2. The mean dose of adenosine needed to terminate SVT was 52 +/- 6 micrograms/kg of body weight in group 1, and 61 +/- 12 micrograms/kg in group 2 (p > 0.05). In addition to isoproterenol not altering the minimal dose of adenosine necessary to terminate SVT, there was also no correlation between the dose of adenosine (mean 55 +/- 6 micrograms/kg) of each patient, and the corresponding endogenous epinephrine (273 +/- 59 pg/ml) (r = -0.19) and norepinephrine (400 +/- 58 pg/ml) (r = 0.01) levels during SVT, or cycle length of SVT (323 +/- 9 ms) (r = -0.35). The results show that adenosine is equally effective in terminating catecholamine-dependent and independent SVT; higher adenosine doses should not be needed to manage catecholamine-dependent SVT.(ABSTRACT TRUNCATED AT 250 WORDS)
View details for Web of Science ID A1994MP70300008
View details for PubMedID 8279375
1993; 72 (5): 471-475
View details for Web of Science ID A1993LT36100022
View details for PubMedID 8352195


text: Home Products Health & Pharmacy Foot Care VELVET SMOOTH ELECTRIC FOOT SYSTEM PURPL VELVET SMOOTH ELECTRIC FOOT SYSTEM PURPL Hover to zoom | Click for full image Details: Item code: SC03208881 Availability: IN STOCK RRP: £39.99 x OK This site uses cookies This website uses cookies to give you a better user experience. By clicking "Accept", with the tick box enabled, you agree to the storing of cookies on your device to enhance site navigation, analyse site usage, and assist in our marketing efforts. Please remember that if you turn cookies off, certain features of this website may not be available to you. Find out more about how we use cookies. https://www.murrayshealthandbeauty.com/terms-and-conditions/cookie-statement Non-essential cookies Accept


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Middlebury town employees sign three-year pact
MIDDLEBURY — The town of Middlebury and its 38 unionized workers have come to terms on a new, three-year contract that will afford employees annual pay increases of 2 percent but require them to contribute a little more toward their health insurance premiums.
The pact, retroactive to this past July 1, applies to fiscal years 2013 through 2015, according to Middlebury Town Manager Kathleen Ramsay. It applies to the various public works, clerical, police and library workers unionized under American Federation of State, County and Municipal Employees (ASCFME) Local 1201 of Council 93.
The contract does not include the municipality's 15 non-unionized workers.
"I think it is a pretty good deal," said Verna Watson, chapter chair of ASCFME Local 1201. "I think it was a good settlement for both parties."
Ramsay said contract negotiations began last March. When the sides were unable to make substantial progress, they agreed to bring in an independent mediator to help move things along. That mediator came on board Sept. 26 and was able to help bring the sides together that very day, according to Ramsay.
"I would say the negotiations were fairly amicable," Ramsay said. "I think both sides learned a lot in the process, heard each others' concerns and issues, and met in the middle."
Major terms of the contract, according to Ramsay, include:
• Cost Of Living Adjustment (COLA) increases of 2 percent during each of the three years of the pact. This was an advance for employees compared to terms of the previous contract, negotiated during tougher economic times. That two-year agreement, reached during the fall of 2010, called for a wage freeze (and no change in health benefits) during the first year. In year two, workers were granted a COLA adjustment of 1.5 percent. Also during that second year union employers were asked to assume 1-percent more of their health insurance premiums.
• A requirement that union workers again pay a little more of their health care premiums, beginning in the final year of the pact. The town's responsibility for the insurance premium payment at that time will decrease from the current 86 percent to 85 percent, according to Ramsay.
The new agreement will not cover the 15 town workers who have elected not to be part of the union, Ramsay noted. Those employees' salary raises are decided annually by the selectboard, based on prevailing economic trends in the Northeast. The board voted them a 2-percent COLA salary increase that took effect July 1.
Non-union employees currently pay 10 percent of their health insurance premium, according to Ramsay. She added town officials have elected to maintain this lower health insurance premium rate for non-union workers in recognition of the fact that they did not get raises during some of the slow economic times, while union employees did. This has been a sore subject at times during negotiations, according to union officials.
The hammering out of a contract comes at a good time for municipal budget planners.
"It was great for us going into next year's budget to have those factors known, so we can set them in the budget and have the stability over the next two years," Ramsay said.
Reporter John Flowers is at [email protected].
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JOHNSON CITY, Tenn. (Dec. 8, 2006) - The ETSU men's track and field team received an early Christmas gift Friday afternoon when the NCAA announced that James Rainer (Alcoa, Tenn.) will be able to compete in the 2007 outdoor season.
"We had a good idea that everything was going to work out for the best, and I am really excited for the team," said Rainer. "Once I found out the news this afternoon I was ecstatic. This will give me the chance to help our team win the outdoor conference championship."
After having a stellar 2005-06 season, Rainer will be the key part to the men's outdoor track team in 2007. He became the first Buc since 2000 to compete at the NCAA Championships last year, and was a four-time Atlantic Sun Athlete of the Week award winner. In addition to his success on the track, Rainer also shined in the classroom by being named to the U.S. Track and Field and Cross Country Coaches Association All-Academic Team in July.
Rainer helped the ETSU men's team win the inaugural Atlantic Sun Indoor Track and Field Championship last season. He earned gold medals in the 60- and 200-meter dashes at the A-Sun Indoor Championships, as well as winning "Most Outstanding Athlete" honors. Rainer also finished in the top-15 at the USA Indoor Track & Field Championships and was the only collegian to qualify for the semifinals.
During the 2006 outdoor season, Rainer cruised to three conference championships by winning the 100- and 200-meter events, and anchored the 4x100-meter relay team to a gold medal. He then set a personal-best in the 100 meters when he posted 10.16 in the preliminaries at NCAA Mid-East Regional Championships in May. Rainer ended with five individual-event titles in the spring.
He sat out the 2002-03 track and field season and was granted a medical hardship for the 2005 outdoor season.
"First I want to thank our support staff for putting in all the hard work, because without them none of this would have happened," added coach Michelle Byrne. "As for getting James back, this is a huge shot in the arm for us, because he is a true leader and works hard every day in practice. He energizes the team, and now this gives us a better chance to win the conference outdoor title."
The ETSU indoor track and field team will compete next in the Tennessee All-Comers meet on Jan. 5 in


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As we approach the back half of FLCL, the story finally starts to explain itself. Even these explanations, however, are couched in the same elliptical and intentionally confounding strategies that make watching FLCL an exercise in puzzling out plot points from subtle clues. While the last two episodes focused on Mamimi and Ninamori, respectively, the story in this episode shines light on the character of Haruko, revealing a few of her ulterior motives and highlighting her indifference to those standing in her way. We already know that despite her wacky Manic Pixie Dream Girl persona, she is a remarkably selfish and immature individual driven by unclear motives, but we did not know until this episode that her reckless-Vespa-driving, head-smashing-with-vintage-bass-guitar ways included a willingness to leave Kamon to die or to threaten the life of everyone in Mabase by knocking a bomb out of the sky. Both of these gambits are to the same end: She intends to force Naota into action. She gives him no choice other than to grow up fast and transcend his fears. Luckily for everyone, Naota is finally ready to swing the bat.
Although the key to Haruko's motives is still a mystery, some of the explanation come in the form of the newly introduced character of Amarao, the nori-eyebrowed Man In Black. Amarao starts to clear up a few things for Naota regarding the odd happenings in his life while hinting at the greater explanations to come. For one thing, he gives a name to Naota's portal, calling it an N.O. channel and explaining that it uses both hemispheres of his brain, while the screen flashes to the first episode's splash screen of a brain X-ray, presumably Naota's. Amarao knows quite a bit about Haruko, although he mostly hints at this. He shares Naota's preference for sweet foods over spicy ones, and hints that Haruko played a similar part in his childhood to the one she is playing in Naota's. Amarao is also the first to mention the Pirate Lord Atomsk to Naota. Since, as we shall see, the capture of Atomsk by Medical Mechanica is the catalyst for the action in FLCL, Amarao will be instrumental in making sense of this story, even though his own understanding is limited.
Baseball plays its most prominent role in the whole anime in this episode, being both a signifier of cool—similar to the role played by all the vintage guitars—and, more importantly, a metaphor for Naota's repression and growth. Haruko, by playing for the opposing team, is trying to make Naota jealous while also setting the plot into motion by beaning balls at the satellite she means to drop on Mabase. Her proficiency at the game is a direct counterpoint to Naota's untested skills, which is also connected to his N.O. channel. Haruko initiated his N.O. channel the first time she hit him, when Canti, who is also an excellent baseball player, emerged from Naota's N.O. channel. At the climax, when Haruko pulls from Naota's head his "bat"—a white, 1967 Gibson Flying V which is, incidentally, 15 kinds of awesome—the display causes Amarao's assistant Kitsurubami to swoon while all of the ladies in their secret alien-monitoring agency burst into sudden nosebleeds. Conflated in all of this imagery of baseball, vintage guitars, and sexual prowess is the connection between Naota's powerful N.O. channel and his imminent maturity. When Naota is preparing to hit the baseball-shaped bomb, he starts to say his brother's name (unless he is planning to call for help, as the Japanese word for help shares its first two syllables with Tasuku's name), but, unlike when he fought the eye-hand robots in the first two episodes, he stops himself. At that moment, Red Canti's symbol—which is, remember, a corruption of the symbol for "adult" in Japanese—appears on his forehead. Naota has decided that he does not need to invoke his brother to get through his fears. He is growing up.
The most disturbing sequence in the episode involves the Kamon-bot. Haruko's quasi-sexual cavorting with the Kamon-bot is obviously meant to upset Naota and prepare him to swing the bat, but her callous discarding of the real Kamon is the truly upsetting aspect of this part of the story. The scene where Naota destroys the Kamon-bot certainly appears to be an Oedipal murder, although the only things destroyed are a robot, a TV, and a clock. Since Naota destroyed the TV, which caused the robot to explode, it is unclear how the clock was broken, but the symbolism is rather perfect. When the Kamon-bot confronts Naota, spurring his jealousy, Naota imagines Haruko saying "mouth" and then becoming a mouse to be batted around by Miyu Miyu until she dies. Considering how the Galactic Space Patrol Brotherhood use both Miyu Miyu and Haruko, this may be a realistic metaphor for Haruko's role, although how Naota became the source of the vision is unclear. After destroying the Kamon-bot and having an odd interview with Amarao, Naota finds Kamon's desiccated corpse at the bottom of a closet with roaches all over him. As he races to the bathroom to rehydrate the corpse (which leads to an explosion!), Miyu Miyu acts oddly during this sequence, racing with Naota and seemingly getting in his way. It is a mystery how warm water revived Kamon, but there is a certain dream-logic to it. When Kamon is himself again, he explains that Haruko discarded him because his head did not work right. Only Naota alone has a strong enough N.O. channel for Haruko's plans. Her maniacal laughter at the end is because she thinks that she has figured out exactly how she is going to use Naota.
Stray observations:
- Naota accidentally pulls Mamimi's panties off when she races off to see Canti play baseball. As people do.
- There's a Dalek on Kamon's shelf when Naota peeks into his room.
- Haruko's suggestive language is at a fever pitch during this episode. "I didn't know that boys felt like this inside" is the mere tip of the iceberg.


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Food Police Demand Pop Stars Stop Promoting 'Disease-Causing' Pepsi
Pepsi and pop stars don't mix, according to one food police group.
The D.C.-based Center for Science in the Public Interest (CSPI) ran a full page "open letter" in Variety, telling pop singer Katy Perry to stop her work with Pepsi, on account of her influencing young fans. CSPI warned Perry that, "Soda companies are using you and other celebrities." The letter then bashed her for not caring about her fans. ''Drink Pepsi and you can be cool like Katy Perry' is the takeaway message for your young fans. 'Live for now' – and worry about the health consequences later." The letter ended by urging her not to "exploit that popularity by marketing a product that causes disease in your fans."
This was not the first time CSPI has made ridiculous demands. Last November, CSPI sued Dr. Pepper Snapple Group, makers of 7Up, for misleading customers about there being vitamins in the fruit flavored 7Up varieties because there were pictures of fruit on the cans.
In the past few years, CSPI has gone after McDonald's Happy Meals, Vitamin Water, and flavored cereals, among other things. The CSPI website warns of the dangers of milk, meat, salt, sugar, trans fats, food additives, artificial sugar, caffeine and alcohol, to name a few. Over the years, CSPI has gone after everything from vending machines to kids menus. It frequently equates common substances like sugar and salt to disease-causing agents, ignoring the fact that these foods can be enjoyed in moderation without adverse health effects. Though CSPI calls itself a consumer advocacy group, it has acted more like the food police.
It's not just that CSPI hypes up the dangers of certain foods, but that it wants the FDA and other government agencies to ban these foods and ingredients from being allowed in the free market. It has tried to control restaurant menus, school lunches, and hospital vending machines. The organization has even filed several lawsuits against soda companies and restaurants for not subscribing to its ideal healthy menu.
As an alarmist, pro-government regulation group, of course it has been a media favorite for years.
Michael Jacobson, the group's executive director, told CBS' "Morning News" February 14, 2013, about his group's campaigning for the FDA to require less sugar in sodas. "When you`re faced with a diabetes epidemic, the situation in which two-thirds of American adults are overweight or obese, the government has a responsibility to do something about that."
CSPI members have been frequently interviewed by TV news reporters with no introduction or explanation that they were food and drink regulating lobbyists. In the past year, CSPI members were interviewed on the morning and evening news 20 times, and a spokesperson from the business or industry CSPI was targeting was never interviewed in the same segment.
CSPI is also supporting a local ad campaign that singles out and bashes Coca-Cola The commercial, which will air in Maryland starting the last week in October, features campaign workers walking around and trading cans of Coke for water and lower-calorie beverages.
— Kristine Marsh is Staff Writer for MRC Culture at the Media Research Center. Follow Kristine Marsh on Twitter.


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Google's putting a quick patch on an Android security flaw that could leak contacts and calendar data through open Wi-Fi networks.
The patch will roll out to Android phones starting Wednesday. "Today we're starting to roll out a fix which addresses a potential security flaw that could, under certain circumstances, allow a third party access to data available in calendar and contacts. This fix requires no action from users and will roll out globally over the next few days," Google said in a statement.
Researchers at Ulm University's Institute of Media Forensics reported the flaw last week, and the tech press took notice on Monday and Tuesday. The issue lies in the way Android handles authentication tokens. If sent over an insecure http connection, a hacker on the same Wi-Fi network as the user could conceivably steal the authentication and gain access to the user's calendar, contacts and Picasa Web albums. Although the issue of contact and calendar leakage was already fixed in Android 2.3.4, the vast majority of Android phones run older versions of the software.
The odds of being attacked are unlikely, but it's not the type of issue Google would want to ignore. The patch only addresses calendar and contact data; Google is still trying to figure out how to address the issue within Picasa.
It's interesting to note that Google was able to patch the problem quickly on old versions of the Android software. Fragmentation may be an issue for app compatibility or getting the latest Android features, but at least it didn't stop Google from pushing out a fix to a security problem.
Follow Jared on Facebook and Twitter for even more tech news and commentary.


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Verizon Wireless said in March that its 4G LTE network was showing higher speeds than expected in real-world tests near Boston. On Tuesday, it did what a lot of people do these days to prove it: posted a YouTube video.
The Long-Term Evolution fourth-generation mobile network, scheduled for commercial availability in 25 to 30 markets later this year, proved to deliver between 5M bps (bits per second) and 12M bps downstream, and between 2M bps and 5M bps upstream, Verizon said earlier this year after conducting tests in Boston and Seattle.
The video posted Tuesday shows what appears to be a real speed test on a laptop in a pizza restaurant in Newton Center, Massachusetts, near Boston University. The result displayed is 8.55M bps downstream and 2.80M bps upstream, going over the Internet to Los Angeles. Next to that laptop is another one using 3G, which shows speeds of 2.21M bps downstream and 866K bps upstream.
Those speeds are more typical of wired broadband than wireless, as some users in the video, apparently customers at the pizzeria, point out as they rave about the service. LTE is designed as a fully mobile technology, though at first it will be limited to laptops and netbooks, with the first LTE handsets expected next year.
LTE will also be the next-generation mobile network for AT&T, beginning next year, and for many other carriers around the world. Much of the battle over 4G, between LTE and Clearwire's WiMax network, revolves around speed. Clearwire says its network offers an average of 3M bps to 6M bps downstream, with bursts of 10M bps or more, and up to 1M bps upstream. Informal tests on Clearwire's commercial network in Las Vegas during the CTIA Wireless trade show in March generally proved those estimates, at least in one area of the city.
But availability is another factor, and here Clearwire has a significant head start on Verizon. Between that company itself and partners Sprint Nextel, Comcast and Time Warner Cable, WiMax is already available in 32 markets around the U.S., reaching 41 million potential customers, according to the carrier. WiMax will be available in 19 more markets before the end of summer, Clearwire said last week.
Nevertheless, Clearwire has hinted it may eventually adopt LTE itself. The two systems are based on the same basic technology.