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  • August 6, 2014
  • 08:15 AM
  • 224 views

Fall Leaves And Orange Flamingos

by Mark Lasbury in As Many Exceptions As Rules

Flamingos are pink because of their diet, but greater and lesser flamingos eat different things – and neither food is pink. The spirulina food of the lesser flamingo is a cyanobacterium called Arthospira fusiformis. Unforunately, there have been large die offs in lesser flamingos. Recent research has shown that this may be due to toxic alga blooms and production of toxins even by A. fusiformis. In addition, a newer study has shown that a bacteriophage is responsible for large die offs of A. fusiformis and that this leads to a trophic cascade effect up the food chain.... Read more »

Anderson MJ, & Williams SA. (2010) Why do flamingos stand on one leg?. Zoo biology, 29(3), 365-74. PMID: 19637281  

Peduzzi P, Gruber M, Gruber M, Schagerl M. (2014) The virus's tooth: cyanophages affect an African flamingo population in a bottom-up cascade. ISME J. , 8(6), 1346-1351. info:/

  • August 6, 2014
  • 04:39 AM
  • 217 views

Gastrointestinal response to A1 vs A2 milk

by Paul Whiteley in Questioning Answers

I want to talk about the findings from Ho and colleagues [1] today, and in particular their observation of: "differences in gastrointestinal responses in some adult humans consuming milk containing beta-casein of either the A1 or the A2 beta-casein type". If you're wondering why such a paper finds it's way on to a blog predominantly about autism research, well stay with me on this rather long blogging entry...Start your engines... @ Wikipedia Before progressing, I am going to put a sort of COI (conflict of interest) statement into this blog post. As part of my day job, I have, down the years, been party to some conversations on A2 milk and how one might scientifically test some of the claims / assumptions made about this milk with specific populations in mind. That also our lab has been looking at analytical ways of differentiating A1 and A2 milk from each other is another COI, allowing for the fact that I am neither a consumer of, nor advocate for, anything to do with any of the white stuff.In case you're not up to speed with A1 and A2 milk, well, it all boils down to type of cow and type of milk produced. Anyone with a handle on autism research history will have probably heard about the opioid-excess hypothesis [2]. The long-and-short-of-it is that casein, the protein found in milk and dairy products, is eventually metabolised into it's constituent amino acids. Along the way, short chains of amino acids called peptides are formed. Some of these peptides look (chemically) similar to compounds like morphine and are hence referred to as the casomorphins (casein derived morphine-like). The opioid-excess hypothesis suggested that these exogenously derived peptides mimic some of our own naturally occurring morphine-like compounds that we all have, and disrupt typical functioning in this area to such an extent that it may correlate with some of the signs and symptoms called autism. I talked about something similar quite recently.Granted, such a model looks a little simplistic these days knowing what we think we know about the very plural autisms and the ESSENCE of cormorbidity. Still, such a hypothesis did seem to fit in well with the suggested effectiveness of a casein-free (and gluten-free) diet for some on the autism spectrum, and also some work looking at the opioid receptor blocker that is naltrexone (see here) and autism. It is with the structure of those peptides in mind that we come to the differences suggested for A1 and A2 milk. Y'see not every cow or other mammal produces the same kind of casein protein in their milk and hence peptide formulations can vary also. For A2 casein, the idea is that beta-casomorphin fragment 1-7 (BC 1-7), a peptide formed during digestion is not the same as the BC1-7 from A1 milk (see here) particularly when it comes to a single amino acid change (proline over histidine) [3].After such a long-winded explanation, we come back to the Ho paper and some interesting findings...First things first, this was a double-blind, randomised cross-over study looking at "gastrointestinal effects" in adults under conditions of either A1 or A2 milk consumption. Two weeks of either A1 or A2 milk consumption (with an appropriate washout period in between) were completed.The very informative Bristol Stool Chart was used to grade poop (stool) consistency alongside other more physiological measures such as faecal calprotectin.Results: "The A1 beta-casein milk led to significantly higher stool consistency values". That and a correlation between stool consistency and reports of abdominal pain for participants when on the A1 milk compared with when on A2 milk. Ergo, it didn't seem that A2 milk did anything over and above A1 milk, rather that consumption didn't seem to be linked to the symptoms noted when drinking A1 milk. Appreciating the authors' call for further study in this area, I was intrigued by these results. Not so many moons ago, I came across the paper by Barnett and colleagues [4] talking about greater gastrointestinal (GI) transit time in rats fed A1 milk over A2 milk (see here for some additional commentary from one of the study authors). One might very well overlap those rodent reports with the more recent Ho results in terms of how longer transit time from A1 milk might mean greater discomfort bearing in mind some of the literature on longer transit time and "pain and distension" [5] in certain conditions. Interestingly, the authors ask that research not only focus on confirmation of their results but: "confirmation in a larger study of participants with perceived intolerance to ordinary A1 beta-casein-containing milk" which begs the question: who and what ailments are being reported?That all being said, not all the literature on A2 milk is so directional. Take for example the paper by Crowley and colleagues [6] (open-access) looking at the question of milk consumption correlating with the functional bowel issue constipation. They concluded that: "that removal of CMP [cow's milk protein] from the diet of children with CFC [chronic functional constipation] significantly increased the number of bowel motions and improved constipation". Their results however did not show any significant effect based on casein type when looking at A1 and A2 milk. Constipation, by the way, is also something talked about with some autism in mind (see here) and particularly the findings from Afzal and colleagues [7] which concluded: "Multivariate regression analysis showed consumption of milk to be the strongest predictor of constipation in the autistic group".I am quite interested in this whole area of different milks from different animals potentially possessing different qualities which might impact on physiology particularly if eventually applied to conditions like autism, or at least some comorbidity. I think back to the post I did on milk derived opioid peptides and methylation status (see here) as also being important, as might be the work on something like the use of camel milk (see here) bearing in mind ... Read more »

  • August 6, 2014
  • 02:27 AM
  • 251 views

Does AA work for young people?

by DJMac in Recovery Review

Evidence has accumulated over the last couple of decades of the association between attendance at Alcoholics Anonymous and improved drinking outcomes, including abstinence. AA is sometimes seen as an organisation that is better suited to older drinkers seeking sobriety than to folk under thirty, though there are in fact young people’s meetings in various large [...]
The post Does AA work for young people? appeared first on Recovery Review.
... Read more »

  • August 6, 2014
  • 12:04 AM
  • 205 views

Female Athletic Trainers Balancing Life and Motherhood

by Nicole Cattano in Sports Medicine Research (SMR): In the Lab & In the Field

Female mentors/role models who are successfully maintaining work-life balance are critical to the success and retention of quality female athletic trainers at the NCAA Division I level.... Read more »

  • August 5, 2014
  • 11:00 PM
  • 197 views

What is the Best Way to Manage Cardiac Arrest According to the Evidence?

by Rogue Medic in Rogue Medic

There is an excellent review article by Dr. Bentley Bobrow and Dr. Gordon Ewy on the best management of sudden cardiac arrest from the bystander to the ICU (Intensive Care Unit).

They point out something that we tend to resist learning. Cardiac arrest that is not due to respiratory causes does not need respiratory treatment. A person who is unresponsive and gasping is exhibiting signs of cardiac arrest, not signs of respiratory problems.... Read more »

  • August 5, 2014
  • 01:28 PM
  • 184 views

Weight loss Stalled? Kick those Hunger Cravings!

by Gabriel in Lunatic Laboratories

Trying to drop the weight, but find yourself picking up more of it? Is your diet failing because you are so hungry you could eat a horse?  Well a new […]... Read more »

Li SS, Kendall CW, de Souza RJ, Jayalath VH, Cozma AI, Ha V, Mirrahimi A, Chiavaroli L, Augustin LS, Blanco Mejia S.... (2014) Dietary pulses, satiety and food intake: A systematic review and meta-analysis of acute feeding trials. Obesity (Silver Spring, Md.), 22(8), 1773-80. PMID: 24820437  

  • August 5, 2014
  • 12:29 PM
  • 106 views

Implanted Neurons Derived from Skin Become Part of the Brain

by beredim in Stem Cells Freak

Researchers at the Luxembourg Centre for Systems Biomedicine (LCSB) of the University of Luxembourg have grafted neurons reprogrammed from skin cells into the brains of mice for the first time with long-term stability. Six months after implantation, the neurons had become fully functionally integrated into the brain.This successful, lastingly stable, implantation of neurons raises hope for future therapies that will replace sick neurons with healthy ones in the brains of Parkinson's disease patients, for example.The Luxembourg researchers published their results in the current issue of Stem Cell Reports.The LCSB research group around Prof. Dr. Jens Schwamborn and Kathrin Hemmer is working continuously to bring cell replacement therapy to maturity as a treatment for neurodegenerative diseases. Sick and dead neurons in the brain can be replaced with new cells. This could one day cure disorders such as Parkinson's disease. The path towards successful therapy in humans, however, is long.Read More... Read more »

Hemmer, K., Zhang, M., van Wüllen, T., Sakalem, M., Tapia, N., Baumuratov, A., Kaltschmidt, C., Kaltschmidt, B., Schöler, H., Zhang, W.... (2014) Induced Neural Stem Cells Achieve Long-Term Survival and Functional Integration in the Adult Mouse Brain. Stem Cell Reports. DOI: 10.1016/j.stemcr.2014.06.017  

  • August 5, 2014
  • 12:17 PM
  • 95 views

Frankfurt-Based Researchers Discover Weakness of Leukemic Stem Cells

by beredim in Stem Cells Freak

Despite improvements in therapy, only one out of every two adult patients survive acute myeloid leukaemia (AML). The mean survival time for this disease, which predominantly occurs in the elderly, is less than a year for patients over 65 years. It is assumed that leukaemic stem cells, which cannot be completely eliminated during treatment, are the origin of relapse. However, as has been discovered by a team of Frankfurt-based researchers, these cells do have a weakness: In the current edition of the high impact journal "Cancer Research", they report that the enzyme 5-lipoxygenase (5-LO) plays a significant role in the survival of leukaemic AML stem cells.5-LO is known for its role in inflammatory diseases like asthma. A team led by Dr. Marin Ruthardt from the Haematology Department of the Medical Clinic II and Dr. Jessica Roos, Prof. Diester Steinhilber and Prof. Thorsten Jürgen Maier from the Institute for Pharmaceutical Chemistry showed that the leukaemic stem cells in a subgroup of AML could be selectively and efficiently attacked by 5-LO inhibitors. This was demonstrable in cell culture models as well as in leukaemia mouse models.Read More... Read more »

  • August 5, 2014
  • 04:05 AM
  • 183 views

Bipolar disorder is frequent in adult Asperger syndrome

by Paul Whiteley in Questioning Answers

"BD [bipolar disorder] in AS [Asperger syndrome] patients is frequent, usually it onsets during adolescence and is often characterized by atypical presentation, making its correct identification particularly difficult".Maybe I'm better suited as a brunette? @ WikipediaThat was the primary finding reported by Vannucchi and colleagues [1] based on their systematic review of the relevant peer-reviewed research literature in this area. They found that the prevalence of BD ranged between 6 - 20% depending on the studies included for review. They also reported that "BD assumes peculiar features which might shape its under-recognition or misdiagnosis" in cases of AS. In short, this is an area which perhaps requires a little more investigation.Bipolar disorder, previously called manic depression, is concerned with mood and how it can 'swing' between extremes of depression and mania. Although discussions about the 'causes' of BD parallel discussions on the causes of lots of conditions which manifest psychiatric symptoms, research like that from Faedda and colleagues [2] talking about "generalized anxiety disorders" as risk factors for BD might be important. I've mentioned BD a few times on this blog: be it in relation to the genetic 'common ground' of psychiatry (see here) or the interesting work coming out of Johns Hopkins on gastrointestinal (GI) inflammation and immune activation in cases of BD (see here). Suffice to say that there may be quite a bit more to BD [3] than what just goes on the old grey-pinkish matter.Asperger syndrome probably needs little introduction to regular readers of this blog. In case you don't know, here is the UK National Autistic Society (NAS) description of the condition. As per the growing acceptance that comorbidity, some medical comorbidity, might be elevated when a diagnosis on the autism spectrum is received (see here), there is also a realisation that the presence of autism or AS might also elevate the risk of psychiatric comorbidity too. The paper by Rosenberg and colleagues [4] (open-access here) corroborates this view, and indeed highlights how BD represents one such comorbid psychiatric diagnosis. At the risk of going off at a tangent, I was also intrigued by the finding by Rosenberg et al that: "Autistic regression was associated with lower risk of any comorbidity" which might imply different factors or weightings (genetic, environment) being involved in different types of autism...The comment in the Vannucchi review about "atypical presentation" of BD in cases of AS got me thinking quite a bit. The case report detailed by Frazier and colleagues [5] (open-access) offers some insight into how this atypical presentation might manifest; in particular: "Bipolar disorder should be entertained as a possible diagnosis when there is deterioration in cognition, language, behavior, or activity; when there is a clear pattern of fluctuation or cyclicity in activity, behavior, and interests (with "good times" and "bad times"); and when observed behavior indicates a mood problem". They go on to mention: "His affective [mood] disorder exacerbated the underlying symptoms of Asperger’s [syndrome]" and that: "Once comorbid bipolar disorder was diagnosed and appropriate treatment occurred, Abraham gradually began to recover and his self-injury, aggression, and intense pressured obsessiveness disappeared". Self-injury and aggression eh?I'm not necessarily saying that everyone with AS who has BD will fit into the description provided by Frazier et al in terms of presentation or intervention (which, by the way, was made up of "oral clonazepam... lithium... and risperidone"). But this and other reports do offer some good starting points to looking at the issue of BD as comorbid to cases of AS or other autism spectrum diagnoses. Oh and if one is to assume that something like immune function might be related to cases of BD, maybe, just maybe, one might consider looking at some of the correlates of immune activation as per reports like the one from Emily Severance and colleagues [6] on food potentially being a factor. Food and psychiatry... now where have I heard about that before?Music to close. When You Were Young by The Killers.----------[1] Vannucchi G. et al. Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. J Affect Disord. 2014 Jul 8;168C:151-160.[2] Faedda GL. et al. Clinical risk factors for bipolar disorders: A systematic review of prospective studies. J Affect Disord. 2014. July 18.[3] Rege S. & Hodgkinson SJ. Immune dysregulation and autoimmunity in bipolar disorder: Synthesis of the evidence and its clinical application. Aust N Z J Psychiatry. 2013 Dec;47(12):1136-51.[4] Rosenberg RE. et al. Parent report of community psychiatric comorbid diagnoses in autism spectrum disorders. Autism Res Treat. 2011;2011:405849.[5] Frazier JA. et al. Treating a child with Asperger's disorder and comorbid bipolar disorder. Am J Psychiatry. 2002 Jan;159(1):13-21[6] Severance EG. et al. Immune activation by casein dietary antigens in bipolar disorder. Bipolar Disord. 2010 Dec;12(8):834-42.----------Vannucchi G, Masi G, Toni C, Dell׳Osso L, Erfurth A, & Perugi G (2014). Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. Journal of affective disorders, 168C, 151-160 PMID: 25046741... Read more »

Vannucchi G, Masi G, Toni C, Dell׳Osso L, Erfurth A, & Perugi G. (2014) Bipolar disorder in adults with Asperger׳s Syndrome: A systematic review. Journal of affective disorders, 151-160. PMID: 25046741  

  • August 4, 2014
  • 09:32 PM
  • 183 views

The effects of shoes and barefoot on postural stability

by Craig Payne in Running Research Junkie

The effects of shoes and barefoot on postural stability... Read more »

  • August 4, 2014
  • 03:00 PM
  • 92 views

One Gene, One Cancer

by Viputheshwar Sitaraman in Draw Science

A mutation in the BRAF gene, called V599E, is purportedly the cause of several different cell pathways leading to the symptoms of melanoma. This mutation is present in many patients with melanoma, and stopping it could mean a cure or treatment.... Read more »

Hingorani SR, Jacobetz MA, Robertson GP, Herlyn M, & Tuveson DA. (2003) Suppression of BRAF(V599E) in human melanoma abrogates transformation. Cancer research, 63(17), 5198-202. PMID: 14500344  

  • August 4, 2014
  • 02:02 PM
  • 191 views

Want a Larger Brain: How About an Implant?

by Gabriel in Lunatic Laboratories

Feel like you could use some extra grey matter? Maybe get a dash of genius added to all those cobwebs in the brain? Well then science might just have the […]... Read more »

Hemmer, K., Zhang, M., van Wüllen, T., Sakalem, M., Tapia, N., Baumuratov, A., Kaltschmidt, C., Kaltschmidt, B., Schöler, H., Zhang, W.... (2014) Induced Neural Stem Cells Achieve Long-Term Survival and Functional Integration in the Adult Mouse Brain. Stem Cell Reports. DOI: 10.1016/j.stemcr.2014.06.017  

  • August 4, 2014
  • 10:45 AM
  • 188 views

Who said beer is just for drinking?

by Sarah Wilson in The 'Scope

An alternative use for beer that will "get under your skin"!... Read more »

Chen, W., Becker, T., Qian, F., & Ring, J. (2014) Beer and beer compounds: physiological effects on skin health. Journal of the European Academy of Dermatology and Venereology, 28(2), 142-150. DOI: 10.1111/jdv.12204  

  • August 4, 2014
  • 10:43 AM
  • 190 views

Unpacking Eating Disorder Recovery Part 1: The Recovery Model

by Andrea in Science of Eating Disorders


What does eating disorder recovery really look like? When you say the word “recovery,” differences of opinion loom large. The lack of definitional clarity around the concept of recovery came up many times at ICED, and continues to surface in discussions among researchers, clinicians, and individuals with eating disorders themselves. We’ve looked at recovery on the blog before (for example, Gina looked at how patients define recovery here; Tetyana surveyed readers about their perspectives on whether or not they thought of themselves as being in recovery and wrote about it here; I wrote about men’s experiences after recovery here) it’s something of a hot topic in the research literature, too.
My Master’s thesis focused primarily on recovery, with one “take home message” being that there can be a disconnect between what recovery means in treatment settings, in popular understanding, and among individuals who have experienced eating disorders. Of course, my study was qualitative and from a critical feminist standpoint, so it is still unclear how well my findings map onto the larger dynamics of recovery. Still, understanding …

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... Read more »

Dawson L, Rhodes P, & Touyz S. (2014) The recovery model and anorexia nervosa. The Australian and New Zealand journal of psychiatry. PMID: 24927735  

  • August 4, 2014
  • 09:17 AM
  • 116 views

Knowing what to keep and what to trash: How the Dis3l2 protein distinguishes cellular messages

by beredim in Stem Cells Freak

Every once in a while, we are forced to sort that stack of papers on the kitchen counter. Interspersed between the expired coupons and dozens of takeout menus are important documents like your car insurance or electric bill. So it isn't an option to simply drop it all in the trash at once – you need to read through the messages to be sure that you don't lose vital information.In the cell, proteins similarly read through messages to distinguish what needs to be saved and what needs to be discarded. But, here, the process takes on a much more important role. More than just clutter, messages that are marked for disposal can drastically alter the fate of a cell. In fact, stem cells use just such a mechanism to maintain their identity. So how does a protein detect the difference between two seemingly similar messages? Today, a team of Cold Spring Harbor Laboratory (CSHL) scientists, led by Professor and Howard Hughes Medical Institute Investigator Leemor Joshua-Tor, describe how the protein Dis3l2 uses numerous recognition sites to capture messages that are flagged for decay.Read More... Read more »

  • August 4, 2014
  • 09:07 AM
  • 180 views

Coxsackie Virus Depletes Cardiac Stem Cells

by beredim in Stem Cells Freak

There is epidemiological evidence that links type B coxsackie virus (CVB) infection with heart disease, and research published on July 31st in PLOS Pathogens now suggests a mechanism by which early infection impairs the heart's ability to tolerate stress at later stages of life.CVB infection is very common and affects mostly children. The symptoms range widely: over half of the infections are thought to be asymptomatic, the majority of children who get sick have only a mild fever, and a very small proportion get inflammation of the heart or brain. On the other hand, 70 – 80% of patients with heart failure show signs of a previous CVB infection but have no history of viral heart disease, raising the possibility that even a mild earlier infection makes them more vulnerable to get heart disease later on.To investigate this, researchers from San Diego State University, USA, led by Roberta Gottlieb and Ralph Feuer, first established a mouse model of mild juvenile CVB infection. Mice infected with a non-lethal dose of the virus shortly after birth did not develop any heart disease symptoms during the infection or into adulthood, but they had a predisposition to heart disease later in life.Read More... Read more »

  • August 4, 2014
  • 07:29 AM
  • 303 views

Interview: Battling HIV-treatment With Computer Simulation

by Pieter Carriere in United Academics

Prof. Mancini computationally models HIV and other viruses’ dynamics and explains its clinical relevance.... Read more »

  • August 4, 2014
  • 04:10 AM
  • 166 views

Stopping gliadin peptides in their tracks?

by Paul Whiteley in Questioning Answers

A micropost if you will, to bring to your attention the paper by Marco Sarno and colleagues [1] and their suggestion of "a novel effect of probiotics in the prevention of undigested gliadin peptides toxic effects".Knitting on't Moors @ Wikipedia The probiotic in question is something called Lactobacillus paracasei CBA L74, which if I'm not mistaken is connected with a certain '57 varieties' company. The authors (which included one Alessio Fasano) indicated that said probiotic appeared to inhibit two gliadin peptides, P31-43 and P57-68, entrance in Caco2 cells, a model of the intestinal barrier [2]. Given that the entrance of such gliadin peptides into the gut mucosa (well the lamina propria) is part of the autoimmune condition known as coeliac (celiac) disease (see here), one might reasonably assume that use of Lactobacillus paracasei CBA L74 (LP CBA L74) might hold some potential as a possible treatment strategy outside of the standard gluten-free diet. At the very least, assuming some further investigations are indicated, it might be added to the list of other compounds being tested with coeliac disease in mind (see here).I note that this is not the first time that LP CBA L74 has come under the peer-reviewed research spotlight as per the paper by Elena Zagato and colleagues [3] (open-access here). On that occasion the authors reported that: "fermented products of Lactobacillus paracasei CBA L74 act via the inhibition of proinflammatory cytokine release" and "could protect against colitis and against an enteric pathogen infection". With those statements in mind, I wonder whether coeliac disease might just be the tip of the iceberg when it comes to the applications for LP CBA L74 as per the work of a distant relation?Speaking of tracks, here's Smokey and the Tracks of My Tears.----------[1] Sarno M. et al. Lactobacillus paracasei CBA L74 interferes with gliadin peptides entrance in Caco-2 cells. Int J Food Sci Nutr. 2014 Jul 17:1-7.[2] Sambuy Y. et al. The Caco-2 cell line as a model of the intestinal barrier: influence of cell and culture-related factors on Caco-2 cell functional characteristics. Cell Biol Toxicol. 2005 Jan;21(1):1-26.----------Sarno M, Lania G, Cuomo M, Nigro F, Passannanti F, Budelli A, Fasano F, Troncone R, Auricchio S, Barone MV, Nigro R, & Nanayakkara M (2014). Lactobacillus paracasei CBA L74 interferes with gliadin peptides entrance in Caco-2 cells. International journal of food sciences and nutrition, 1-7 PMID: 25030417... Read more »

Sarno M, Lania G, Cuomo M, Nigro F, Passannanti F, Budelli A, Fasano F, Troncone R, Auricchio S, Barone MV.... (2014) Lactobacillus paracasei CBA L74 interferes with gliadin peptides entrance in Caco-2 cells. International journal of food sciences and nutrition, 1-7. PMID: 25030417  

  • August 4, 2014
  • 12:05 AM
  • 237 views

Concussion Indicators of a Phenomenon Yet to be Defined

by Jane McDevitt in Sports Medicine Research (SMR): In the Lab & In the Field

Prevalent and consistent indicators of a concussion include observing disorientation or confusion immediately after the injury, and slower reaction time, poor balance, and impaired verbal learning and memory within 2 days after the injury.... Read more »

Carney N, Ghajar J, Jagoda A, Bedrick S, Davis-OʼReilly C, du Coudray H, Hack D, Helfand N, Huddleston A, Nettleton T.... (2014) Concussion guidelines step 1: systematic review of prevalent indicators. Neurosurgery. PMID: 25006974  

  • August 3, 2014
  • 05:00 PM
  • 247 views

Resuscitation characteristics and outcomes in suspected drug overdose-related out-of-hospital cardiac arrest

by Rogue Medic in Rogue Medic

This study is interesting for several reasons.

In a system that claims excellence, the most consistent way to identify the study group is by documentation of a protocol violation - but it is not intended as a study of protocol violations.

This may hint at some benefit from epinephrine (Adrenaline in Commonwealth countries), but that would require some study and we just don't study epinephrine. We only make excuses for not studying epinephrine.

The atropine results suggest that the epinephrine data may be just due to small numbers, or that we may want to consider atropine for drug overdose cardiac arrest patients, or . . . .... Read more »

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