Saturday, March 28, 2015

Psychiatrist Dr Henderson: ME/CFS: in 85% (92% in adolescents) symptoms resolve in 3-5 months on valacyclovir

Theodore Henderson, MD, PhD, March 25, 2015:

A recent consensus review on Chronic Fatigue Syndrome (CFS) and Myalgic Encephalomyelitis (ME)concluded that CFS/ME is significantly underdiagnosed and that the condition is likely caused, in part, by viruses. These findings are in line with my clinical work. Together, these two sources of data point to a pathway which may help the 2.5 million sufferers of this disease in the United States.
In February, the Institute of Medicine (IOM) completed its committee review on CFS/ME. This study was sponsored by the Department of Health and Human Services, the National Institutes of Health, and the Centers for Disease Control, among others.1
A comprehensive literature review and critique was completed by the Agency for Healthcare Research and Quality in December  as part of this process.2 Many important advancements in the medical conceptualization of CFS/ME are included in this 282 page document.
Perhaps the most important evolutionary step was the clear message delivered on page 15 of the introduction: CFS/ME is underdiagnosed and misunderstood. More than 80% of patients go undiagnosed, while 65% of patients spend more than a year seeking the correct diagnosis. A lack of understanding of this disorder has contributed to many patients feeling maligned, blamed, and undertreated.
Some patients told the committee that they felt belittled, dismissed, and ignored by their health care professionals. Patients also have reported that some treatment strategies, including the oft-cited graded exercise regimen, exacerbated their symptoms.3
Equally striking in this report was the clear assertion that CFS/ME likely has an infectious etiology and that viruses, in particular Epstein-Barr virus (EBV), are high on the list of suspected agents.1
My clinical work has focused on the viral and immunological pathogenesis of CFS/ME. In my clinic, I have treated over 200 adults and over 30 adolescents with what the IOM now says should be called Systemic Exertion Intolerance Disease (SEID). While I have not published my adult cases, a case series of adolescents was published last year.4 What has emerged from my work is that over 85% of patients with SEID (diagnosed by Fukuda criteria5) respond to antiviral therapy. Among adolescents, the outcome is better with 92% responding.
A critical second conclusion of my work is that a subset of patients diagnosed with depression — particularly treatment-resistant depression — actually had SEID. The adolescents in the case series were all referred for evaluation of depression or mood disorder. They all presented with marked fatigue, exertion induced malaise, brain fog, and impaired academic performance.
In addition, most reported daily naps and unrefreshing sleep.4 They had not responded to adequate trials of antidepressants and the duration of symptoms ranged from 6-96 months. There was no history of abuse or neglect, although this has been suggested as an etiology of SEID in the past.6,7 Patients completed the Children's Depression Inventory8 and the mean score was 14 (+2.83), below the typical cut-off for depression.
Patients were treated with the antiviral, valacyclovir (Valtrex), at a dose of 1000 mg twice a day. Only one patient experienced nausea and discontinued the antiviral. Improvement occurred over the course of 3-5 months. Eighty-six percent of the patients responded by 3 months, and 92% responded by 5 months. Symptoms of fatigue, exertion induced malaise, excessive sleep, napping, unrefreshing sleep, headaches, cognitive symptoms, and emotional symptoms all resolved.

Thursday, March 26, 2015

The Naked Scientists: Is ME an autoimmune disease? Interview with oncologists Prof Mella and Dr Fluge

Chris Smith,The Naked Scientists, 24TH MAR 2015:

INTERVIEW
TUE, 24TH MAR 2015

Is ME an autoimmune disease?

Øystein Fluge and Olav Mella, Haukeland University Hospital, in Bergen

Chronic Fatigue Syndrome(CFS), also known as ME, affects about 1 person in 500. Sufferers describe symptoms of profound tiredness and lethargy that doesn’t improve with sleep or rest. consensus on what might be causing the condition, there are no tests to confirm the diagnosis, and nor is there a cure. But now we may be closer to understanding what causes at least some of the cases of the condition thanks to research carried out in Norway, as Øystein Fluge and Olav Mella from Haukeland University Hospital, in Bergen, explain to Chris Smith...


Øystein - We are oncologists that work mainly on lymphomas and brain tumours. But in 2004, we observed a patient with longstanding ME who got lymphoma and she experienced a totally unexpected and very marked recovery of ME symptoms after she received lymphoma treatment with cancer chemotherapy. We speculated on this case and when we met new ME patients, it was striking to learn how similar the patients were in symptoms and how they described to be previously completely healthy and often, with an abrupt start of ME after infections. So, we reasoned that B-cells could be important in a subgroup of ME patients.
Chris - When you say, B-cells, these are the white blood cells, the lymphocytes that make say, antibodies and have a memory against infections we’ve seen before, aren't they?
Øystein - Yes, but we did a small pilot case series with a single infusion of the drug rituximab which targets these B-cells to 3 ME patients and they all had a marked but transient clinical response. We published this case series in 2009.
Chris - So, you were giving these people in the course of treating their blood cancer, their lymphoma, the drug rituximab which hits and destroys B-cells in the body which are in these patients, the cancer cells. And as a side effect almost of that treatment, these people who had previously said they had disabling symptoms of ME, chronic fatigue syndrome, they got better.
Øystein - That's correct.
Chris - Olav, I was going to bring you in and say, what actually happened to these people when you did this?
Olav - The 3 pilot patients all had response to treatment and one thing we observed in these 3 patients is that we have a pattern of responses and relapses after the rituximab treatment with a lag time of several months from initial and rapid B-cell depletion until they start getting clinical responses. Such patients are also seen in established autoimmune diseases after rituximab treatment. We believe that this fits with B-cells not being produced for a period after rituximab which allows a natural degradation of autoantibodies – that is antibodies that have adverse effects on bodily functions, with the symptom improving when the antibody level drops. We really think this points at ME at least in a large subportion is an autoimmune disease. It’s also spotted that 70% of the patients with ME, they get it immediately after an infection and there's, like in other autoimmune diseases, 3 to 4 times as many women as men who get the disease. And also, a big study from the US has shown a moderate and highly significant risk of B-cell lymphoma in elderly ME CSF patients, showing that the patients may have chronically activated B-cell system. We see the same lymphoma risk also in established autoimmune diseases like rheumatoid arthritis, lupus and Sjogren’s disease.
Chris - So, putting all of this together, you get these patients who, they happen to have a lymphoma – a cancer of the blood system – but they also have chronic fatigue syndrome. You treat their lymphoma with a drug which takes down their B-cells which are the cause of their cancer. They get this pattern of, their disease recovers when the B-cells go away but with the time lag corresponding to the time it takes the B-cells to go and the antibodies to go. And then when the B-cells come back in these patients, then the symptoms come back which looks like it’s tying the two things together, doesn’t it? So, what do you think that the B-cells are doing in these people to actually make, Olav, the symptoms of chronic fatigue syndrome in those patients?
Olav - Well, we think that it is a kind of an immune response and it obviously affects some very central function in the body. We’re not at all convinced that ME is kind of inflammatory condition in the brain. Probably, more important, I think what is happening in blood vessels, we have indications that the blood vessel do not function as they should, given the dynamic flow to different parts of the body when it is needed.
Øystein - It’s like the patients have a problem in the fine-tuning or regulation of blood flow according to the demands of the tissues for oxygen and nutrients. The patients often describe they feel like running a marathon when they have done a limited exertion and they get brain fog from exertion and so on. So, our hypothesis is that the immune system somehow disturbs the fine-tune regulation of blood flow and tissues including in the brain.
Chris - Øystein, what are you now doing to try to firm this up because your initial results as you published, while very interesting are on very small numbers of patients? Obviously, we’d like to see big numbers of patients in order to make sure that this is not a statistical blip, it’s not happening due to chance, it’s real.
Øystein - To try to convince ourselves, we first did, as you say, a small randomised study which was published in 2011 with 15 patients given two infusions of rituximab and 15 patients given placebo, turn out that the 15 that got rituximab had a clinical response while 2 of the 15 in the placebo group. So, that was some kind of sign of clinical activity to us. So then we did an open label study with no placebo group, further rituximab infusion, prolonging the period with low B-cells. We gave 6 infusions of rituximab up to 15 months and then followed the patient for 3 years. So, this study is now submitted for publication but we can say that again, 2/3 had a clinical response and the response durations were much prolonged when we gave maintenance treatment. But these two studies are not designed to give a definite answer to whether rituximab works in ME. So therefore, we are now performing a larger phase III study in Multicentre in Norway with 152 patients. Half of them will receive 6 rituximab infusions during the first year and half of them will receive placebo. And then we will follow the patients for 2 years. And we hope that this study will either verify or refute if rituximab may give benefit to ME patients in a significant proportion.

Saturday, March 21, 2015

Oncologists squash Mats Reimer's Wesselyan psycho blah blah

By deleder2k, 20.3.2015:

Norwegian Daily Medicine 2015.03.20 

dr. Øystein Fluge and dr. Olav Mella comments on Reimer's concern regarding the upcoming cylophosphamide study



Original article in Norwegian: http://www.dagensmedisin.no/debatt/-kan-mecfse-respondere-pa-immunmodulerende-behandling/
Translated by Google Translate and 

deleder2k


Saturday, March 7, 2015

Reduced CD2, CD4 and CD8 lymphocytes and also reduced immunoglobulin (Ig) in ME / CFS

@ PubMed:

  Med J Aust.  1989 Aug 7;151(3):122-4.Immunological abnormalities in the chronic fatigue syndrome.Lloyd AR 1, Wakefield D , Boughton CR , Dwyer JM .Author information

  Abstract The chronic fatigue syndrome is a disorder of unknown aetiology which is characterized by debilitating fatigue. Recent evidence has suggested that viruses may persist in the tissues of patients with chronic fatigue syndrome. A concurrent immunological disturbance is likely to be associated with the persistence of viral antigens. Therefore, the humoral and cellular immunity of 100 patients who were suffering from chronic fatigue syndrome and that of 100 healthy, age- and sex-matched control subjects were compared.

  This study documents the frequent occurrence of abnormalities within the cellular and humoral immune systems of patients with well-defined chronic fatigue syndrome. Disordered immunity may be central to the pathogenesis of chronic fatigue syndrome.

  In patients with chronic fatigue syndrome, a significant (P less than 0.01) reduction was found in the absolute number of peripheral blood lymphocytes in the total T-cell (CD2), the helper/inducer T-cell (CD4) and the suppressor/cytotoxic T-cell (CD8) subsets. A significant (P less than 0.001) reduction also was found in T-cell function, which was measured: in vivo by delayed-type hypersensitivity skin-testing (reduced responses were recorded in 50 [88%] of 57 patients); and in vitro by phytohaemagglutinin stimulation.

  Reduced immunoglobulin (Ig) levels were common (56% of patients), with the levels of serum IgG3- and IgG1-subclasses particularly (P less than 0.05) affected.

Monday, March 2, 2015

Scientists Successfully Remove HIV From Human Cells

BY Dan Avery:

  "Researchers at Temple University in Philadelphia have been able to destroy HIV in human cells, rather than simply suppress it, a breakthrough in the ongoing fight against HIV/AIDS.

  “It’s an important finding because, for the first time in laboratory setting, we show that the virus can be eradicated from human culture, cell culture, said Dr. Kamel Khalili, who led the research team at Temple’s Center for Neurovirology.

  “Basically [we're] converting infected cells to un-infected cells,” he explains “And that is very important because the current therapy can not eliminate the virus from cells.”

  Dr. Khalili’s team developed molecular tools that can operate on DNA and delete HIV in cells."

  more

Sunday, March 1, 2015

The NewYorker: People with ME/CFS are more “functionally impaired” than those with MS and congestive heart failure

BY MEGHAN O’ROURKE, FEBRUARY 27, 2015:

  "People with ME/CFS, the report noted, are more “functionally impaired” than those with Type 2 diabetes, multiple sclerosis, and congestive heart failure—diseases that we know to be very grave indeed."

  more @ newyorker.com

Saturday, February 28, 2015

Psychiatrists commenting on immunological abnormalities, typical science media Center crap

By Utting Wolff:

  "The Science Media Centre surpassed itself in its coverage of the Columbia University study[6]. Of seven experts chosen to respond to the study, not one gives a positive analysis, no medical adviser from an ME charity or, non-psychosomatic promoting, ME researcher is quoted.

  The featured experts are: Professors Michael Sharpe and Peter White, and Dr Esther Crawley, all notorious proponents of the psychogenic ME model.

  Professor Stephen Lawrie, head of The Division of Psychiatry at the University of Edinburgh: ‘This is a small study’ he states[6]; a study encompassing 20 participants is small professor Lawrie, one involving over 600 participants is not[1]. One has to ask why is a psychiatrist being consulted?"

Thursday, February 26, 2015

IOM: ME/CFS "is a medical—not a psychiatric or psychological—illness"

@ PubMed:

 

Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness.

Editors

Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome; Board on the Health of Select Populations; Institute of Medicine.

Source

Excerpt

Myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) are serious, debilitating conditions that affect millions of people in the United States and around the world. ME/CFS can cause significant impairment and disability. Despite substantial efforts by researchers to better understand ME/CFS, there is no known cause or effective treatment. Diagnosing the disease remains a challenge, and patients often struggle with their illness for years before an identification is made. Some health care providers have been skeptical about the serious physiological—rather than psychological—nature of the illness. Once diagnosed, patients often complain of receiving hostility from their health care provider as well as being subjected to treatment strategies that exacerbate their symptoms. 

Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome proposes new diagnostic clinical criteria for ME/CFS and a new term for the illness - systemic exertion intolerance disease(SEID). According to this report, the term myalgic encephalomyelitis does not accurately describe this illness, and the term chronic fatigue syndrome can result in trivialization and stigmatization for patients afflicted with this illness. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome stresses that SEID is a medical—not a psychiatric or psychological—illness. This report lists the major symptoms of SEID and recommends a diagnostic process. One of the report's most important conclusions is that a thorough history, physical examination, and targeted work-up are necessary and often sufficient for diagnosis. 

The new criteria will allow a large percentage of undiagnosed patients to receive an accurate diagnosis and appropriate care. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome will be a valuable resource to promote the prompt diagnosis of patients with this complex, multisystem, and often devastating disorder; enhance public understanding; and provide a firm foundation for future improvements in diagnosis and treatment.
Copyright © 2015, National Academy of Sciences.

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    Tuesday, February 24, 2015

    The real reason why Prof Edward Shorter is ridiculing and attacking severely ill patients

    So why did professor Edward Shorter write his 2 very aggressive / hostile / vile articles in psychologytoday, attacking patients who are severely ill?

      Even though he is a psychiatrist and a medical historian, he shows a total lack of knowledge about basic facts about this disease and totally ignores all clinical evidence etc that what he says is total rubbish / nonsense.

      The answer to the question can be found in one of his tweets, ie his new book is out on the 7th of march.

      @DrEdwardShorter: "amazon.com/What-Psychiatr… The pub date for this is Mar 7 but Amazon up now. Theme: what should have been in but wasn't and shouldn't but was."

      So all he cares about is selling books, earning money and getting his name in the paper, that he has to ridicule and attack severe ill patients to do so, is obviously no problem to him or to psychologytoday.

      And that's the sad state of affairs of psychiatry and psychology in 2015.

      See also Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence

     

    Monday, February 23, 2015

    Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence

    A phenomenon well familiar to historians of medicine is the psychic epidemic of ignoring clinical evidence by psychiatrists and medical historians, a belief that spreads epidemically, until the evidence become so overwhelming that it becomes clear that these people have been telling porkies for decades, and then their nonsense is forgotten.

      In the 20th century, psychiatry fostered such an epidemic with the belief that ego masturbation caused their bank accounts to inflate. Many medical historians and psychiatrists obsessed for years over the thought that their “self-abuse” had pleased their bank managers.

      Another epidemic focused on the toxic  effects of ignoring clinical evidence on the ovaries. Many male medical historians and male psychiatrists would plead for ovariectomies, on the grounds that their irritated ovaries were blocking clinical evidence which their penis had spotted, to go all the way to their brain. And that this was leading to erectile dysfunction and the inability to have an orgasm.

      Once their ovaries were removed, their penis size increased by more than 5 inches. So all these male medical historians and male psychiatrists were pleading their doctors for ovariectomies.

      In the late 1980s the belief spread epidemically that reading clinical evidence caused irreversible brain damage, and a number of leading medical historians and psychiatrists wrote books full of advice about eating small meals upside down, with your eyes closed and your brain in hibernation mode, to make sure that clinical evidence would not reach your brain to prevent brain damage.

      I realize that these words will fall unreceptively upon some ears, and I regret that some medical historians and psychiatrists, especially from Toronto, may feel slighted by the clinical evidence that is readily available, if only they where willing to turn on their computer and were willing to read biomedical research, for example the fMRI studies from Stanford, or the PET scan study from Japan. 

      Yet there are larger stakes here. In the way that lives were once ruined with such toxic diagnoses as hysteria, which in this day and age is called MS, millions of lives today are ruined by medical historians and pinocchio psychiatrists who have made a fortune out of ignoring clinical evidence.

      Many psychiatrists and medical historians choose their profession so that they didn't have to become productive members of the community.  (The IOM report dwelled upon the dangers of severely ill patients being abused by the medical profession.) 

      Such a waste of human potential is tragic, and if there are lessons that we may draw from the history of medicine, it is that doctors who discover the underlying metabolic problem or cause of such diseases, which medical historians and psychiatrists call psychosomatic, even though they do not have any evidence to back up this claim, will go on to win the Nobel prize for medicine, as the Nobel Prize winner in medicine, Dr Barry Marshall stated a few years ago.

    Friday, February 20, 2015

    Social sciences lecturer Angela Kennedy: Psychogenic explanations for physical illnesses are almost always fatally flawed

    @ amazon.co.uk:

    Since the advent of "medicine" as a discrete practice, beliefs that bodily illness can somehow be caused by psychological, emotional, and behavioural "disorder" have been claimed by many in the discipline. Such beliefs became less creditable as scientific methods of detecting disease developed, with discoveries such as the physiological and anatomical abnormalities in Parkinson's disease and Multiple Sclerosis, for example, and the organisms causing syphilis and duodenal ulcers.

      Nevertheless, psychogenic explanations for illnesses still appear frequently within medical and academic literature, in "common sense" public discourses, and in medical diagnoses of patients. But how plausible are these explanations? Authors of our Own Misfortune? proposes that psychogenic explanations for physical illnesses are subject to a complex mix of confusing concepts, accompanied by certain moralistic and ideological assumptions about people and their illnesses.

      Most crucially, such explanations are also, almost always, fatally flawed, both scientifically and logically.

      Furthermore, the widespread, uncritical acceptance and use of such explanations has had serious and specific adverse effects on the people upon whom they are used.

      This is a timely, groundbreaking book about a critical theme in medicine. It provides rigorous analysis of the claims made about "mental disorder" and bodily illness, using current "medical controversies" (such as, but not limited to, Myalgic Encephalomyelitis and Chronic Fatigue Syndrome) to demonstrate the problems with and adverse effects of such claims. Authors of our Own Misfortune? is essential reading for academics, health professionals, and those directly or indirectly affected by psychogenic explanations for illness.

      Angela Kennedy is a social sciences lecturer and researcher at a number of universities in London, and author of numerous articles, papers and books in lay, professional and academic media over a 30 year career.

      Her academic research interests include: the social stratification, scapegoating and social exclusion of disadvantaged groups, and the effects of these; constructions of moral panics; and the sociology of science and medicine, including manifestations of the 'science wars'.

    Monday, February 16, 2015

    The denial of this illness by doctors means that patients are suffering slow, horrific deaths

    By Kristy Muir, 13th February 2015 :

      "The 37-year-old Bribie Island woman is in the fight of her life against a debilitating disease and consequential infections.

      In February 2013 Amara was diagnosed with Lyme disease (borrelia), bartonella, babesia and multiple other infections.

      Prior to that she suffered chronic fatigue syndrome, diagnosed when she was 23. Amara's condition means she suffers severe seizures daily, as well as photophobia (sensitivity to light), severe cramps and muscle spasms."

      ##########

      ""Amara is desperately unwell with late (stage) neurological Lyme disease," Ms Collingwood said.

      "What makes her illness different is that the medical profession do not recognise Lyme disease in Australia, despite the fact that thousands of Australians have tested positive to Lyme (via testing facilities in overseas labs) and the numbers are only continuing to increase.

      "The denial of this illness in Australia by the health fraternity means that there is very little to no treatment available here.

      "People are suffering slow, horrific deaths and it is completely unnecessary.""

    Saturday, February 14, 2015

    The Guardian: ME/CFS, a serious disease dismissed as laziness says The Institute of Medicine

    The Guardian, 13 February 2015:

      "People often dismiss sufferers of chronic fatigue syndrome as lazy because the seriousness of the disease is not understood."

    ###########


    • "“Having called this serious disease by an inappropriate and frankly insulting name is one of the factors that kept doctors, friends, family members, even employers from affording it the seriousness it deserves,” she said."

    Friday, February 13, 2015

    The causative role of alum adjuvant in vaccines in slow brain translocation and delayed neurotoxicity in ME/CFS

    Front. Neurol., 05 February 2015; FULL article @ journal.frontiersin.org:
    REVIEW ARTICLE Biopersistence and brain translocation of aluminum adjuvants of vaccinesimageRomain Kroum Gherardi* , imageHousam Eidi, imageGuillemette Crépeaux, imageFrançois Jerome Authier  and imageJosette Cadusseau * Faculté de Médecine and Faculté des Sciences et Technologie, INSERM U955 Team 10, Université Paris Est-Créteil, Créteil, France Aluminum oxyhydroxide (alum) is a crystalline compound widely used as an immunological adjuvant of vaccines. Concerns linked to the use of alum particles emerged following recognition of their causative role in the so-called macrophagic myofasciitis (MMF) lesion detected in patients with myalgic encephalomyelitis/chronic fatigue/syndrome. MMF revealed an unexpectedly long-lasting biopersistence of alum within immune cells in presumably susceptible individuals, stressing the previous fundamental misconception of its biodisposition. We previously showed that poorly biodegradable aluminum-coated particles injected into muscle are promptly phagocytosed in muscle and the draining lymph nodes, and can disseminate within phagocytic cells throughout the body and slowly accumulate in brain. This strongly suggests that long-term adjuvant biopersistence within phagocytic cells is a prerequisite for slow brain translocation and delayed neurotoxicity. The understanding of basic mechanisms of particle biopersistence and brain translocation represents a major health challenge, since it could help to define susceptibility factors to develop chronic neurotoxic damage. Biopersistence of alum may be linked to its lysosome-destabilizing effect, which is likely due to direct crystal-induced rupture of phagolysosomal membranes. Macrophages that continuously perceive foreign particles in their cytosol will likely reiterate, with variable interindividual efficiency, a dedicated form of autophagy (xenophagy) until they dispose of alien materials. Successful compartmentalization of particles within double membrane autophagosomes and subsequent fusion with repaired and re-acidified lysosomes will expose alum to lysosomal acidic pH, the sole factor that can solubilize alum particles. Brain translocation of alum particles is linked to a Trojan horse mechanism previously described for infectious particles (HIV, HCV), that obeys to CCL2, signaling the major inflammatory monocyte chemoattractant. Billions of humans have been vaccinated and marked regression or eradication of several severe infectious diseases was observed. Nowadays, the potential applications of vaccines extend far beyond prevention of infectious diseases, and vaccination is considered to be a most promising weapon against a variety of different conditions. Vaccine safety has been regarded as excellent at the level of the population (1 ), but adverse effects have also been reported (2 ). Concerns about the use of aluminum adjuvants have emerged following (i) recognition of their role at the origin of the so-called macrophagic myofasciitis (MMF) lesion in 2001 (3 , 4 ), which revealed fundamental misconception of their adjuvant effect and pointed out their unexpectedly long-lasting biopersistence (4 ); and (ii) demonstration of their apparent capacity to migrate in lymphoid organs and then disseminate throughout the body within monocyte-lineage cells and progressively accumulate in the brain (5 ). The present paper will review these emerging characteristics of alum adjuvant particles that raise concerns about innocuity of this widely used compound.

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