CO-CURE Medical & Research Posts Only Digest - 11 Dec 2006 to 18 Dec 2006 (#2006-57)
There are 18 messages totaling 2563 lines in this issue. Topics of the week:
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Write to mailto:firstname.lastname@example.org --------------------------------------------- ---------------------------------------------------------------------- Date: Tue, 12 Dec 2006 14:02:14 +0100 From: Jan van Roijen <email@example.com> Subject: med: Martin Pall, PhD -a Conversation & more ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 12 December 2006 <<<< Editorship : firstname.lastname@example.org Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ From: "Frank Twisk" <email@example.com> http://www.findarticles.com/p/articles/mi_m0ISW/is_265-266/ai_n15622556/print A conversation with MCS researcher, Martin Pall, PhD ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Linda Powers Dr. Pall is Professor of Biochemistry and Basic Medical Sciences at Washington State University. He is currently writing a book called Explaining "Unexplained Illnesses." * How did you become interested in researching this group of illnesses--MCS, Chronic Fatigue, Fibromyalgia, Post Traumatic Stress Disorder? I came down with a case of chronic fatigue syndrome (CFS) in the summer of 1997. Unlike most CFS sufferers, I had a complete recovery, over a period of about a year and a half. I decided to dedicate the rest of my scientific career to understanding the mechanisms causing this group of illnesses. * Who is at-risk for developing MCS? Is a genetic pre-disposition necessary? Is early exposure to toxic chemicals in pesticides and solvents critical? There is evidence for an important genetic role in determining one's tendency to get each of these related illnesses. For MCS, the evidence so far implicates genes involved in chemical metabolism, as well as a gene that helps determine the activity of the NMDA receptors in the brain, receptors that I believe are central to the mechanism of MCS. I would expect that a number of vitamins, magnesium, selenium and a variety of antioxidants may well have a role in preventing MCS. I think that in some individuals, early life stressors may well make them more susceptible to MCS, but in others this will not be a factor. There are multiple short term stressors that are implicated in this whole group of illnesses, including pesticides and volatile organic solvents, particularly in MCS, infection, particularly in CFS, both infection and physical trauma (particularly head and neck trauma) in fibromyalgia and severe psychological stress in posttraumatic stress disorder. All of these stressors can produce increases in nitric oxide and I have proposed that they may trigger a common biochemical/physiological response that is responsible for these illnesses. * Why is there so much variation of symptoms from one individual to another within this group of illnesses? One can explain many of the symptoms as being produced by impact on different regions of the brain, as well as different parts of the rest of the body. For example, some people with MCS have lower lung, asthma-like sensitivities, sometimes abbreviated RADS and some do not--and those who have this have tissue impact in the lower lungs. So a specific tissue when impacted by this biochemistry produces a specific response. * Describe the focus of your work with these illnesses and the grants/funding sought Most of my work, over the past seven years or so has been trying to master large areas of the scientific literature to develop the best possible theory of the etiologic (causal) mechanism of these illnesses. This does not require any outside funding and fortunately, my university has been satisfied to have me do this and has not "bugged" me to seek more grant funding. This is the type of work that nobody does. The reason for that is two-fold. Firstly, you cannot get research funding to do this type of work. Secondly it is damn hard work and most people do not have either the breadth of background or the interest in pursuing it. This is despite the fact that some very prominent scientists have commented that this is just the type of work that we most need in the biomedical area. We are inundated by experimental results in many areas of biomedical science (not on MCS, however) but have little time to integrate these results into understandable conceptual frameworks. I did have a small grant on CFS, which allowed me to publish two experimental papers providing support for my theory. I also tried to get funding for two similar trials, one for CFS treatment and second for fibromyalgia treatment. The two foundations that I went to for funding both had the same response. They felt that if the trial worked, we would not know why it worked because there were so many components involved in the trial, and so the foundations were not interested in it. I guess I'd like them to try to convince the sufferers that an effective treatment would not be worth supporting even if one cannot determine exactly how it works. * You've developed a treatment protocol that has a nutritional focus. Describe it. First, let me remind you that I am a PhD, not an MD, so nothing I write should be interpreted as a recommendation or as medical advice. I have been interested in therapy issues ever since I got involved with this group of illnesses. I think that any etiologic (causal) theory has got to show its value through its ability to suggest effective therapeutic approaches. Dr. Grace Ziem asked me to come up with a treatment protocol. She had my protocol compounded by a compounding pharmacy and is trying it on her MCS patients. She reports it seems to be substantially more effective than her previous treatment approaches. The approach that I have taken is based on the use of nutritional supplements rather than conventional pharmaceuticals, and this approach was taken for two reasons. One is that there are not a lot of conventional pharmaceuticals that are attractive candidates for therapy. Secondly, Dr. Ziem wanted us to use as natural an approach as possible, one that might give the injured body (including brain, of course) an opportunity to heal itself. Most of the nutritional supplements we are using are already being sold to people with these illnesses, so individually they are of limited effectiveness. If any one of them was a magic bullet, we would know about it. The goal is to come up with a series of over a dozen such compounds expected to act synergistically with each other to lower the biochemistry and physiology that maintains these illnesses. We have used a large number of antioxidants (over a dozen of these alone), several minerals and some odd compounds, such as the amino acid betaine. Among the specific goals is to try to improve energy metabolism and lower the activity of the NMDA receptors in the brain and other parts of the body, as well as to lower the synthesis of and effects of nitric oxide and peroxynitrite. * Describe the human clinical research you'd like to do, and explain why placebo-controlled trials are important. What is known as a double-blind, placebo controlled trial is considered to be the "gold standard" of trials and such an approach is needed to convince people of possible effectiveness. The idea is that if an individual in the trial does not know whether he/she is receiving the active material or a placebo, that comparing a substantial number of individuals in each of the two groups will allow one to determine whether the treatment is effective and to quantify how effective it may be. We may end up with two types of tablets, a gel cap and an inhalant and if this is the final approach, we will need four different placebos, one for each. * How much funding is needed for this research? Dr. Ziem estimates that it will take about $50,000 for the trial. I will be donating my time to it. This is for a trial containing a group of 30 for treatment and 30 for the placebo. * If the funding did come through, how would participants in the trials be chosen? Dr. Ziem has a large backlog of patients. If that is insufficient, we can contact support groups near her (she is located in rural Maryland). She will have to examine potential participants to determine if they fit the appropriate case definition. Each participant will have a small blood sample taken before starting the trial and two times after the initiation of the trial so that I can measure some biochemical parameters that may be a measure of treatment response. Response to the trial will also be measured through the use of a previously validated questionnaire. After the placebo-controlled part of the trial is completed, the placebo group will be offered the opportunity to try the active supplements, so everyone will have the opportunity to see how well the therapy works in their case. * Can interested individuals donate to your research? They can make a tax deductible contribution through the WSU foundation by including a note with a check indicating it is to support the Martin Pall research fund, sent to: Carol Sayles-Rydbom Assistant Director of Development College of Sciences Morrill Hall 144B P.O. Box 643520 Pullman, Washington 99164-3520 USA COPYRIGHT 2005 The Townsend Letter Group COPYRIGHT 2005 Gale Group ```````````````````````````````````````````````` http://www.haworthpress.com/store/PDFFiles/ForReps/Pall-Explaining.pdf Martin L. Pall, PhD, BA Professor, Biochemistry and Basic Medical Sciences, Washington State University, Pullman complete contents for Explaining "Unexplained Illnesses" Start treating the causes of these baffling diseases, instead of the symptoms: • Acknowledgments • Chapter 1. The NO/ONOO- Cycle and the Cause of Chronic Fatigue Syndrome, Multiple Chemical Sensitivity, Fibromyalgia, and Post-traumatic Stress Disorder • Chapter 2. Important Components and Their Properties • Chapter 3. Generation of Symptoms and Signs of Multisystem Illness • Chapter 4. The Local versus Systemic Nature of the NO/ONOO- Cycle Mechanism and Its Implications for Nomenclature and Treatment • Chapter 5. Chronic Fatigue Syndrome • Chapter 6. Agents That Lower Nitric Oxide Levels Are Useful in the Treatment of Multisystem Illnesses • Chapter 7. Multiple Chemical Sensitivity • Chapter 8. Fibromyalgia • Chapter 9. Post-traumatic Stress Disorder • Chapter 10. Gulf War Syndrome: A Combination of All Four • Chapter 11. The Toll of Multisystem Illnesses • Chapter 12. Overall Evidence: What Else Is Needed? • Chapter 13. What About Those Who Say It Is All in Your Head? • Chapter 14. A Major New Paradigm of Human Disease? • Chapter 15. Therapy • Chapter 16. Conclusions • References • Index `````````````````````````````````````````````````` Martin L. Pall, Ph.D. Professor of Biochemistry and Basic Medical Sciences Washington State University Pullman, WA 99164-4234 USA 509-335-1246 firstname.lastname@example.org Multiple Chemical Sensitivity: ~~~~~~~~~~~~~~~~~~~~~~~~~ Towards the End of Controversy see this article in pdf format at: http://www.mcs-america.org/pall.pdf [Return to top] ------------------------------ Date: Tue, 12 Dec 2006 19:04:41 +0000 From: Maggie Wallace <email@example.com> Subject: RES: 'What is it like to have ME?': The discursive construction of ME in computer-mediated communication and face-to-face interaction 'What is it like to have ME?': The discursive construction of ME in computer-mediated communication and face-to-face interaction Jennifer Guise, Sue Widdicombe, and Andy McKinlay Health (London) . 2007; 11(1): p. 87-108 http://hea.sagepub.com/cgi/content/abstract/11/1/87?ct=ct Jennifer Guise University of Abertay, Dundee, UK Sue Widdicombe University of Edinburgh, UK Andy McKinlay University of Edinburgh, UK ME (Myalgic Encephalomyelitis) or CFS (chronic fatigue syndrome) is a debilitating illness for which no cause or medical tests have been identified. Debates over its nature have generated interest from qualitative researchers. However, participants are difficult to recruit because of the nature of their condition. Therefore, this study explores the utility of the internet as a means of eliciting accounts. We analyse data from focus groups and the internet in order to ascertain the extent to which previous research findings apply to the internet domain. Interviews were conducted among 49 members of internet groups (38 chatline, 11 personal) and 7 members of two face-to-face support groups. Discourse analysis of descriptions and accounts of ME or CFS revealed similar devices and interactional concerns in both internet and face-to-face communication. Participants constructed their condition as serious, enigmatic and not psychological. These functioned to deflect problematic assumptions about ME or CFS and to manage their accountability for the illness and its effects. Key Words: computer-mediated communication (CMC) • discursive psychology • illness descriptions • ME/CFS Copyright © 2007 by SAGE Publications [Return to top] ------------------------------ Date: Wed, 13 Dec 2006 16:15:55 -0500 From: Fred Springfield <firstname.lastname@example.org> Subject: RES: Chronic fatigue syndrome is accompanied by an IgM-related immune response directed against neopitopes formed by oxidative or nitrosative damage to lipids and proteins Chronic fatigue syndrome is accompanied by an IgM-related immune response directed against neopitopes formed by oxidative or nitrosative damage to lipids and proteins. Journal: Neuro Endocrinol Lett. 2006 Oct 12;27(5) [Epub ahead of print] Authors: Maes M, Mihaylova I, Leunis JC. Affiliation: MCare4U Outpatient Clinics, Belgium. NLM Citation: PMID: 17159817 There is now some evidence that chronic fatigue syndrome (CFS) is accompanied by signs of oxidative stress and by a decreased antioxidant status. The aim of the present study was to examine whether CFS is accompanied by an immune response to neoepitopes of a variety of modified lipids and proteins indicating damage caused by oxidative and nitrosative stress. Toward this end we examined serum antibodies to fatty acids (oleic, palmitic and myristic acid), by-products of lipid peroxidation, i.e. azelaic acid and malondialdehyde (MDA), acetylcholine, S-farnesyl-L-cysteine, and N-oxide modified amino-acids in 14 patients with CFS, 14 subjects with partial CFS and 11 normal controls. We found that the prevalences and mean values for the serum IgM levels directed against oleic, palmitic and myristic acid, MDA, azelaic acid, S-farnesyl-L-cysteine, and the N-oxide derivates, nitro-tyrosine, nitro-phenylalanine, nitro-arginine, nitro-tryptophan, and nitro-cysteinyl were significantly greater in CFS patients than in normal controls, whereas patients with partial CFS took up an intermediate position. There were significant and positive correlations between the serum IgM levels directed against fatty acids, MDA and azelaic acid and the above N-oxide-derivates and the severity of illness (as measured by the FibroFatigue scale) and symptoms, such as aches and pain, muscular tension and fatigue. The results show that CFS is characterized by an IgM-related immune response directed against disrupted lipid membrane components, by-products of lipid peroxidation, S-farnesyl-L-cysteine, and NO-modified amino-acids, which are normally not detected by the immune system but due to oxidative and nitrosative damage have become immunogenic. [Return to top] ------------------------------ Date: Wed, 13 Dec 2006 20:35:02 +0100 From: Jan van Roijen <email@example.com> Subject: res: Journal of Chronic Fatigue Syndrome ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 13 December 2006 <<<< Editorship : firstname.lastname@example.org Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Journal of Chronic Fatigue Syndrome (ISSN: 1057-3321) Volume: 14 Issue: 1 Cover Date: 2007 Prepublication CONTENTS `````````````````````````````````````` EDITORIAL Elke Van Hoof, Kenny De Meirleir, Neil McGregor ``````````````````````````````````````````````````````````````` ORIGINAL RESEARCH Service Utilization, Barriers to Service Access, and Coping in Adults with Chronic Fatigue Syndrome Rosemary A. Underhill, Ruth O'Gorman Objective: In a sample of 47 adults with CFS, we aimed to describe patterns of service utilization, identify barriers to service access, and explore the relationship between service utilization and coping styles. Method: A questionnaire assessing service utilization frequency and barriers to service access was administered to a sample of 47 individuals with CFS. The Illness Management Questionnaire was used to assess relationships between coping styles and service utilization. Results: A Cochran's Q test of homogeneity revealed that medical and CFS self-help services were most frequently used and rehabilitation services were least frequently used. In terms of service accessibility, 80.9% of participants reported at least one barrier. Lack of financial (including insurance) resources and lack of knowledge about service availability were the two most frequently reported. In terms of coping styles, symptom focusing was positively associated with use of CFS self-help services and with use of in-home services and social service agencies. Information seeking was negatively associated with use of in-home and social service agencies and with use of mental health services. Conclusion: These findings can be used by health-care professionals and advocacy-based organizations to develop programs focused on mass education campaigns for health-care providers, increase knowledge of service availability among individuals with CFS, and to understand relationships between certain types of coping styles and service preferences. Keywords: Chronic fatigue syndrome, service utilization, access, coping ``````````````````````````````````````````````````````````````` The Feasibility of Reviewing Chronic Fatigue Syndrome Clients at a Distance: A Teleconference Pilot Study Gwyneth C. Weatherburn, Amelia Goldsmith Lister, Leslie J. Findley Objective: There continues to be a shortage of clinical staff specialising in the treatment of CFS (ME). In order to access specialist care, many clients have to undertake long or difficult journeys that may exacerbate their symptoms. This exploratory study aimed to reduce these travel problems by the introduction of a Teleconference Review Clinic (TRC). Method: A TRC was booked for six CFS clients who would normally have face-to-face review by specialists 44 miles away. Questionnaires were used to elicit the views of both clients being reviewed and clinicians undertaking the review at a distance. Differences in distances travelled by clients for conventional face to face and telemedicine review were calculated and comments about the teleconference made by clients and therapists were noted. Results: There was general satisfaction with the quality of the pictures and sound during the reviews. Clinicians were able to obtain all the information required to undertake all clinical assessments. For two clients the clinical management was changed after the consultation and for one client an issue was identified that required referral to another clinician. For clients who lived nearer to the teleconference hospital, the journey saved ranged between 1 mile and 85.8 miles, the mean being 64.2 miles. Conclusion: This pilot study does suggest that telemedicine in this area of medicine is logistically viable and effective, and indicates that a larger study is needed. Keywords: Chronic fatigue syndrome, teleconference, review ``````````````````````````````````````````````````````````````` Changes in Functional Status in Chronic Fatigue Syndrome Over a Decade: Do Age and Gender Matter? Rosalind M. Matthews, Anthony L. Komaroff Objective: Patients with chronic fatigue syndrome (CFS) have substantial deficits in functional capacity, but the course of these deficits over time has not often been studied. This study measured functional capacity on three occasions over a decade, in patients with CFS. Methods: The study was a longitudinal cohort study, and employed the Medical Outcomes Study Short-Form 36 (SF-36) instrument to assess physical and mental/ emotional functional status. Results: Physical function, as reflected in several different scales, improved modestly but significantly over time, particularly for patients aged 18-60 years and for women. Mental/emotional function was not substantially impaired at the outset of the study, and did not change over time. Conclusion: This study found that physical function tended to improve for many patients over time, despite the fact that theywere aging. Physical function did not deteriorate with time. Keywords: CFS, functional status, SF-36, subgroups, over time ``````````````````````````````````````````````````````````````` Physiological Responses to Arm and Leg Exercise in Women Patients with Chronic Fatigue Syndrome Casimiro Javierre, José Alegre, José Luis Ventura, Ana García-Quintana, Ramon Segura MD, PhD, Andrea Suarez, Alberto Morales, Agusti Comella, Kenny De Meirleir Patients affected by chronic fatigue syndrome (CFS) characteristically show easy and unexplained fatigue after minimal exertion that does not resolve with rest and is associated with specific symptoms lasting for more than six months. Cardiopulmonary exercise testing is a valid procedure for determining functional capacity in patients with CFS. We compare cardioventilatory adaptation to exercise between a group of eighty-five consecutive women patients affected by CFS and a group of fifteen healthy women extremely sedentary individuals, with the use of maximum incremental exercise testing on a cycle ergometer and arm ergometer, assessing possible differences. The majority of values achieved at peak exhaustive exercise were significantly lower in CFS patients than controls, including the percentage of maximum oxygen uptake in arm physical test (37.4 ± 10.0% in CFS vs. 58.9 ± 15.8% in controls) and leg physical test (53.4 ± 15.0% in CFS patients vs. 76.2 ± 18.0% in controls). In conclusion, the CFS group show a lower work capacity in arm or leg exercise that would not be justified exclusively by their personal characteristics or deconditioning. Keywords: Chronic Fatigue Syndrome, maximal oxygen uptake, lactate ``````````````````````````````````````````````````````````````` Personality Profile of Patients with Chronic Fatigue Syndrome Olivier Le Bon, Bernard Cappeliez, Daniel Neu, Luc Stulens, Guy Hoffmann, Michel Hansenne, Luc Lambrecht, Marc Ansseau, Paul Linkowski Personality may play a role in the predisposition, the precipitation and/or the maintenance of the CFS. Thirty-six consecutively examined female patients hospitalised for a sleep workup, filledout a Temperament and Character Inventory (TCI) questionnaire. A MANOVA compared the patients with a control group of females matched for age. Significant scores were obtained for dimensions such as Harm Avoidance, Reward Dependence, and Self-Directedness. However, the only subdimension of Harm Avoidance that proved significantly higher in CFS than in controls was "Fatigability," which is likely to overlap with the core CFS symptom. All in all, the personality structure does not appear to play a major role in the CFS. Keywords: Lipids, antioxidants, therapy, dietary supplement, fatigue, mitochondria, chronic fatigue syndrome ``````````````````````````````````````````````````````````````` Body Mass Index and Fatigue Severity in Chronic Fatigue Syndrome Ellen A. Schur, Carolyn Noonan, Wayne R. Smith, Jack Goldberg, Dedra Buchwald Background: It is uncertain how much fatigue is related to weight in patients with chronic fatigue syndrome (CFS). Objective: To assess the association of body mass index (BMI) and fatigue in CFS patients. Methods: Consecutive patients seen in a referral-based specialty clinic were eligible if they met CFS criteria and had completed required measures. Fatigue measures were the vitality subscale of the Medical Outcomes Short-Form 36 and the global fatigue index from the Multidimensional Assessment of Fatigue. Results: In women, there was no relationship between BMI and vitality subscale or global fatigue index scores (P = 0.99 and P = 0.44). For men, vitality subscale scores significantly decreased as BMI increased (P = 0.02). Conclusions: In CFS patients, the prevalence of obesity was low despite risk factors for weight gain. Fatigue severity and BMI were unrelated in women with CFS, but this relationship may differ for men. Keywords: Chronic Fatigue Syndrome, fibromyalgia, fatigue, weight ``````````````````````````````````````````````````````````````` Table of Contents/Front Matter DOI: 10.1300 ``````````````````````````````````````````````````````````````` [Return to top] ------------------------------ Date: Wed, 13 Dec 2006 20:21:54 +0000 From: Mary Schweitzer <email@example.com> Subject: RES,MED: Current state of information on HHV-6 viruses A great deal of confusion seems to surround the HHV-6 viruses, Variant A and Variant B. This information from ongoing studies may clear some of it up. 1. HHV-6B causes exanthema subitum and not measles. 2. The distribution of HHV-6 is high in the general population (over 95 percent), but in most cases that is HHV-6B, not HHV-6A. HHV-6B is contracted in childhood, usually between 1-3 years of age. In contrast, HHV-6A is rare in childhood. In the adult population, it is not clear how many cases exist of HHV-6A; studies have ranged from rare to as high as one-third. 3. Active HHV-6A is found more often than HHV-6B in in patients with CFS-Fukuda. It has also been found in the spinal fluid of M.S. patients; Alvarez La Fuente found it most often in M.S. patients who are in relapse. Again, studies as to the actual frequency of HHV-6A in MS and CFS are conflicting because of the difficulties of diagnosing active HHV-6A depending on the method used. Using reverse transcriptase and serum PCR, some researchers have found few cases of HHV-6A, while others have found the rate to be as high as 50 percent. Using the early antigen assay, Dr. Dharam Ablashi found even more cases. More research is needed (and probably a better way to nail down the patient population) to achieve consistent prevalence rates. 4. Researcher Carolyn Hall has demonstrated that HHV-6A can be detected in spinal fluid long after it is no longer detectable in blood samples. 5. One of the problems in diagnosing HHV-6A is that unlike most viruses, it does not go through a stage where it is released into blood serum. HHV-6A apparently releases a substance that causes the cells to clump together, allowing it to spread by moving through the cell walls. Hence the best way to detect HHV-6A is to look at antibodies to the viral proteins, not PCR tests looking for the actual viral copies themselves. Needless to say, this is easier said than done. Researchers are working on more reliable methods of detection for HHV-6A. In sum, HHV-6, Variant A, is very different from HHV-6, Variant B - so different that Dr. Gallo (formerly of NIH) has called for the renaming of HHV-6, Variant B, to resolve confusion caused by clumping the two diseases together. For patients with M.E. or CFS, HHV-6A is the pathogen that has been linked to severity of symptoms, not HHV-6B. General studies of HHV-6 (not distinguishing which type) are not particularly helpful. It is intriguing that HHV-6A in the spinal fluid has also been linked to progressive or relapsing M.S. For more information on HHV-6A or HHV-6B, I would recommend the HHV-6 Foundation's website: <http://www.hhv-6foundation.org>. Mary Schweitzer [Return to top] ------------------------------ Date: Wed, 13 Dec 2006 13:50:06 -0800 From: "Neil Abbot <Neil.Abbot@xxxxx.xx.xx> via Co-Cure Moderators" Subject: RES, MED: Essay on the ME/CFS NICE draft Guideline 2006 ME/CFS NICE Guideline "Poor naked wretches, whereso'er you are, That bide the pelting of this pitiless storm, How shall your houseless heads and unfed sides, Your loop'd and window'd raggedness, defend you >From seasons such as these?...." King Lear Act 3, Scene 4 Read ME Research UK's comments on the NICE guideline: pdf format 163 KB MS Word format 111 KB The publication of the ME/CFS Guideline Draft For Consultation by National Institute for Clinical Excellence (NICE) has energised patient support groups and ME/CFS charities like nothing in recent memory. Their response has been overwhelmingly hostile, and those which are Registered Stakeholders have registered their protest by supplying detailed critiques of the document (we have added our own voice to the clamour). Nothing new in that, you might say: as Polly Toynbee's defence of NICE over its refusal to approve the cancer drug Velcade pointed out, "Patient groups understandably want everything for their sufferers." The role of NICE and the controversies surrounding its decisions are well known - see the article, "Debate - National Institute for Clinical Excellence"; the Institute expects to come under fire, and probably treats its wounds as badges of honour. Yet, there is something unusual - unique, in fact - about the current uproar. Today, almost certainly for the first time since it started work in April 1999, the Institute is faced with a united body of patient-based opinion which does NOT want the guideline it has produced, certainly not in its current form, and if push comes to shove would rather have a non-guideline on ME/CFS (the first Clinical Guidance with a minus number) than the one on offer. Restlessness in the natives is one thing, but a full-scale rebellion by deeply ungrateful wretches - poor mostly, and certainly naked of the kind of randomised clinical trial evidence recognised by the Institute - is quite another. What's it all about? Well, it's simple really. The draft produced by the Guideline Development Group (GDG) is unfit for purpose, i.e., for informing the diagnosis and management of ME/CFS patients, primarily because it flags up as treatments for the illness psychosocial management and coping strategies that at best have an adjunctive role to play. Patient-based charities and self-help groups (and there are around 20,000 members of these in the UK alone) recognise this, and can foresee that the major recommendations of the guideline will not, unfortunately, solve the problem on the ground. Essentially, the Institute has not got to grips with core issues surrounding ME/CFS. These are explored in depth in our submission, but can be briefly stated. The first, and most central, is the problem of diagnosis: whichever definition is used, ME/CFS is widely recognised to be an impossibly wide diagnostic marquis and to contain different patient groups; the formation of clinical guidance inevitable raises the question of guidance for what and for whom. The second problem concerns the randomised controlled trial (RCT) evidence upon which NICE puts a premium, and the devaluation of evidence from scientific studies and surveys. This is a continuing area of controversy for the Institute, but it has a particular poignancy in the case of ME/CFS since the evidence-base is skewed towards a small group of mildly positive RCTs on psychosocial strategies; thus, instead of finding the "best" evidence garnered from the work of a range of biomedical and biopsychosocial scientists working on a level playing field, what is found is quite modest evidence in a forgotten field put there by proponents of psychosocial strategies. Multiple sclerosis with the formal evidence-base that currently exists for ME/CFS would be no less a physical illness, and the non-specific management and coping strategies would be no more specifically effective for the underlying disease, yet these adjunctive strategies have an unduly prominent role in the Institute's draft guideline... This can be nicely illustrated by a Table in which the ME/CFS NICE Guideline Draft is placed side by side with other Clinical Guidelines in the NICE pantheon, representing 19 different clinical conditions. The full Table "NICE Clinical Guidance recommendations on the use of cognitive behavioural therapy (CBT) for 19 different clinical conditions (excludes clinical guidance on interventional procedures, technology appraisals etc.)" can be read here http://www.meresearch.org.uk/information/publications/niceguideline.html The Table shows that cognitive behavioural therapy (CBT) is postulated to be a specific treatment for Anxiety, Bipolar disorder, Depression, Eating disorders, Obsessive-compulsive disorder, and Schizophrenia; this is an unsurprising finding since a psychological therapy surely has some utility for some psychological disorders. It also shows that in none of the remaining 12 conditions, all primarily physical in origin, is CBT proposed as a treatment for the illness or disease; where CBT is mentioned, its role is clearly constrained, for example to co-morbid emotional disorders, for rehabilitation programmes or psychosocial support. Only in the case of the physical illness ME/CFS is CBT proposed as a specific treatment; moreover, only in the case of ME/CFS is the basis of CBT - "relationship between thoughts, feelings, behaviours", "discussion of the patient's attitudes and expectations" etc. - described in the NICE guideline outside of the standard glossary. This is a strange development, even stranger given that the Institute's Full Draft Guideline on ME/CFS, page 203, says: ...The GDG did not regard CBT or other behavioural treatments as curative or directed at the underlying disease process, which remains unknown. Rather, such treatments can help some patients cope with the condition and consequently experience a improved quality of life. Indeed, organisations representing people with the physical illness ME/CFS are marvelling why the Institute has delivered a draft guideline that is unique even in its own pantheon, as well as being inappropriate for their needs. While everyone recognises that psychiatry has been desirous of a greater role in physical illness for over a decade - a thrust nicely expressed by Jeremy Couper (Australian and New Zealand Journal of Psychiatry 2000; 34:762-769), "...chronic fatigue syndrome can be seen as a potential Trojan horse for psychiatry, enabling psychiatry to perform a broader role in medical research and a more truly integrated role in the health system" - it had been assumed that the Institute valued it's independence too much to be fooled by smoke and mirrors. The unfitness of this guideline draft is a terrible blow to people with ME/CFS who already exist in a pelting storm of disbelief and sometimes professional distain. Clinical guidelines are routinely circulated to all NHS primary care trusts, strategic health authorities, GPs and practice nurses in England and Wales, and representative bodies for health services, professional organisations and statutory bodies, so there could be severe consequences for patients - particularly negative effects in the form of the denial of other treatment options - if the draft guideline was published in its present form. Rather than incorporate an inadequate and skewed evidence-base into established guidelines which feed into clinical care and government policy, the Institute should withdraw the draft pending a complete overhaul to reflect the simple truth: that specific, rigorous, evidence-based recommendations for treatment of people falling under the diagnostic marquis ME/CFS probably cannot be made at present, but that (as in other physical illnesses) psychosocial coping and management strategies, such as CBT, may be an option for symptom management or comorbid anxiety or depression. ME Research UK's full comments on the draft NICE guideline can be read here http://www.meresearch.org.uk/information/publications/NICE%20CFS_ME%20Guideline%20-%20MERUK%20comments.doc Dr Neil C. Abbot Director of Operations ME Research UK The Gateway North Methven St Perth PH1 5PP, UK firstname.lastname@example.org ME Research UK (formerly MERGE) is a national UK charity funding biomedical research into Myalgic Encephalomyelitis (also known as ME/CFS) and related illnesses. Our principal aim is to commission and fund high-quality scientific (biomedical) investigation into the causes, consequences and treatment of ME, but we also have a mission to "Energise ME Research" http://www.meresearch.org.uk/ [Return to top] ------------------------------ Date: Wed, 13 Dec 2006 18:04:10 -0500 From: "Bernice A. Melsky" <email@example.com> Subject: RES: Metabolic syndrome in women with chronic pain Metabolic syndrome in women with chronic pain. Metabolism. 2007 Jan;56(1):87-93. Loevinger BL, Muller D, Alonso C, Coe CL. Center for Women's Health Research, University of Wisconsin School of Medicine and Public Health, Madison, WI 53715, USA. PMID: 17161230 Fibromyalgia is a prevalent syndrome characterized by chronic pain, fatigue, and insomnia. Patients with fibromyalgia commonly have an elevated body mass index and are physically inactive, 2 major risk factors for metabolic syndrome. Yet little is known about the relationship between chronic pain conditions and metabolic disturbances. Our study evaluated the risk for, and neuroendocrine correlates of, metabolic syndrome in this patient population. Women with fibromyalgia (n = 109) were compared with control healthy women (n = 46), all recruited from the community. Metabolic syndrome was identified by using criteria from the Adult Treatment Panel III with glycosylated hemoglobin concentrations substituted for serum glucose. Catecholamine and cortisol levels were determined from 12-hour overnight urine collections. Women with fibromyalgia were 5.56 times more likely than healthy controls to have metabolic syndrome (95% confidence interval, 1.25-24.74). Fibromyalgia was associated with larger waist circumference (P = .04), higher glycosylated hemoglobin (P = .01) and serum triglyceride (P < .001) levels, and higher systolic (P = .003) and diastolic (P = .002) blood pressure. Total and low-density lipoprotein cholesterol were also significantly higher in women with fibromyalgia (P = .001 and .02, respectively), although high-density lipoprotein cholesterol was in the reference range. These associations were not accounted for by age or body mass index. Meeting criteria for more metabolic syndrome components was related to higher urinary norepinephrine (NE)/epinephrine and NE/cortisol ratios (P < .001 and P = .009, respectively). Women with chronic pain from fibromyalgia are at an increased risk for metabolic syndrome, which may be associated with relatively elevated NE levels in conjunction with relatively reduced epinephrine and cortisol secretion. [Return to top] ------------------------------ Date: Thu, 14 Dec 2006 13:08:19 -0500 From: "Bernice A. Melsky" <firstname.lastname@example.org> Subject: RES: Pharmacologic treatment of fibromyalgia Pharmacologic treatment of fibromyalgia. Curr Psychiatry Rep. 2006 Dec;8(6):464-9. Baker K, Barkhuizen A. Arthritis & Rheumatic Diseases, Oregon Health & Science University, Portland, OR 97239, USA. email@example.com PMID: 17162828 Fibromyalgia is a syndrome of widespread pain, non-restorative sleep, disturbed mood, and fatigue. Optimal treatment involves a multidisciplinary approach with a team of health care providers using pharmacologic and nonpharmacologic treatment. Because of the heterogeneity of the illness, management should be individualized for the patient. Pharmacologic treatment should address issues of pain control, sleep disturbance, fatigue, and any underlying coexisting mood disorder. Nonpharmacologic treatment should include patient education, a regular exercise and stretching program, and cognitive behavioral therapy. All of these are essential to improving functional capacity and quality of life. This review provides general guidelines in initiating a successful pharmacologic treatment program for patients with fibromyalgia. [Return to top] ------------------------------ Date: Fri, 15 Dec 2006 02:49:32 +0100 From: Jan van Roijen <firstname.lastname@example.org> Subject: not,res: Poster Presentations IACFS 2007 ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 15 December 2006 <<<< Editorship : email@example.com Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ From: "Frank Twisk" <firstname.lastname@example.org> http://www.aacfs.org/p/263.html The 8th International IACFS Professional Conference. Friday, Jan 12- Sunday, Jan 14, 2007- Fort Lauderdale Poster Presentations ~~~~~~~~~~~~~~~~ Behavioral Section ````````````````````````` Computer-Assisted Cognitive Function Assessment in Fibromyalgia, Chronic Fatigue Syndrome and Multiple Chemical Sensitivity Patients Cusco-Segarra AM,Garcia-Fructuoso FJ,Lopez_Crespi F, Poca-Dias, V, Garcia-Blanco S, Santos, C A Qualitative Analysis of the Experience and Influence of Low Intensive Interval Training in Women with Chronic Fatigue Syndrome Lennartsson Claudia , Tyni-Lenné Raija , Lindh Gudrun A Chronic Fatigue Syndrome Health Behavior and Education Train-the-Trainer Program for Primary Care Providers Dana Jones Benet , Ph.D., M.P.H., K. Kimberly McCleary,B.A., Teresa A. Lupton , R.N., B.S.S., Katherine M. Faryna , B.A., Kevin Hynes, Ph.D., and William C. Reeves, M.D. Using Comprehensive Clinical Case Management to Improve Health-Care Utilization and Coping in Patients and Families Affected by CFS/FM Patricia Fennell, MSW, LCSW-R Depression and CFS: Similarities and Differences From Psychological Evaluation Tokuzo Matsui M.D., Ph.D., Nobuo Kiriike M.D., Ph.D., Sanae Fukuda Ph.D. , Hirohiko Kuratsune M.D., Ph.D., Seiki Tajima M.D., Ph.D., Yoshiki Nishizawa M.D., Ph.D., Sasuyoshi Watanabe M.D., Ph.D. Family Experience of Parental Chronic Fatigue Syndrome: A Pilot Study Julie G. Donalek, R.N.,D.N.Sc.,A.P.R.N.,B.C. The Impact of an Early Educational Intervention Program on Future Physicians Perceptions and Attitudes Regarding Chronic Fatigue Syndrome (CFS) Lu, T.V. & Jason, L.A. Stagnation in CFS Publishing? Comparisons with Fibromyalgia and Fatigue: 1995-2004 Fred Friedberg, PhD, Brett Schmeizer, BA & Stephanie Sohl, MA A Standardized Test for Postexertional Malaise in CFS Ruud C.W. Vermeulen MD PhD, Ruud M. Kurk MD and Hans R. Scholte PhD A Proposed Clinical Protocol for Occupational Therapy in the Treatment of CFS/FM Utilizing the Model of Human Occupation and Fennell Four-Phase Treatment Jennifer Burke, OTR/L, Patricia Fennell, MSW, LCSW-R Intravenous Saline Administration Improves Physical Functioning Travis L. Stiles, Staci R. Stevens, Christopher R. Snell, Lucinda Bateman, and J. Mark VanNess. Treating People with CFS/FM Who Have Been Victims of Disaster or Trauma Patricia Fennell, MSW, LCSW-R, Margaret Butkereit, MS, LMSW The Buddy Program: Support for Individuals with Chronic Fatigue Syndrome Till, L.D., Jason, L.A., Porter, N., Andrews, M. F. Evaluating the CDC Criteria for an Empirical CFS Case Definition Najar, N.S., BA., Porter, N. Ph.D., & Jason, L.A., Ph.D. `````````````````````````````````````````````````````````````` Brain Function Section `````````````````````````````` Metabolic and Immune Responses to Exercise Testing J. Mark VanNess, Christopher R Snell, Staci R Stevens, Lucinda Bateman and Travis Stiles Psychomotor Slowing in Chronic Fatigue Syndrome Greta Moorkens, Filip Van Den Eede, Bernard G.C. Sabbe Study of Biological Markers, Ergometric Parameters and Cognitive Function in a Cohort of Patients with Chronic Fatigue Syndrome Alegre-Martin J, Soriano Sanchez T, Javierre C, Garcia Quintana J, Ruiz E, Fernández de Sevilla T, De Meirleir K, Garcia Quintana AM. Associations Between Biological Markers and Ergometric Parameters and Cognitive Function in Patients with Chronic Fatigue Syndrome Alegre-Martin J, Soriano Sanchez T, Javierre C, Garcia Quintana J, Ruiz E, Fernández de Sevilla T, De Meirleir K, Garcia Quintana AM Evidence of Increased Frequency of Patent Foramen Ovale (PFO) in the Chronic Fatigue Syndrome with Enriched Oxygen Modulation of the PFO Cheney, PR and Lucki, NC ``````````````````````````````````````````````````````````````` Clinical Trials Section ````````````````````````````` Effect of Modafinil on Daytime Hypersomnia in Patients with Chronic Fatigue Syndrome Garcia-Fructuoso F, Fernández-Solá J, Poca-Dias V, Fernández-Huerta JM, Fernandez-Sola A Lipid Replacement and Antioxidant Therapy for Restoring Mitochondrial Function in Fatiguing Illnesses and Chronic Fatigue Syndrome Garth L. Nicolson, Ph.D., Rita Ellithorpe, M.D. and Robert Settineri, M.S. A Randomized Double-blind, Placebo-Controlled Cross-Over Study with Methylphenidate in Sixty Patients with Chronic Fatigue Syndrome Daniel Blockmans, Philippe Persoons, Boudewijn Van Houdenhove, Herman Bobbaers Comprehensive Treatments with IVIG For CFS Tae H. Park, M.D. A Proposed Protocol for the Dental Treatment of Patients With CFS Wanda I. SaldaZa, DDS, Patricia Fennell, MSW, LCSW-R Treatment of Elevated C4a in Patients with CFS Using Low Doses of Erythropoietin Safely Reduces Symptoms and Lowers C4a: A Prospective Clinical Trial Ritchie C. Shoemaker, MD, Margaret S. Maizel Treatment of CFS Patients With Low Levels of Vasoactive Intestinal Polypeptide (VIP) and Shortness of Breath with Tadalafil Improves Exercise Tolerance and Pulmonary Artery Responses to Exercise Ritchie C. Shoemaker, MD, Margaret S. Maizel Treatment of CFS Patients With Elevated C4a Using Low Dose Erythropoietin Corrects Abnormalities in Central Nervous System Metabolites and Restores Executive Cognitive Functioning Ritchie C. Shoemaker, MD, Margaret S. Maizel `````````````````````````````````````````````````````````````` Epidemiology Section `````````````````````````````` Self-Reported Chronic Fatigue and Timed Loaded Standing in The Gambia and in Belgium Jan Eyskens, Marie Ielegems, Greta Moorkens Chronic Fatigue Syndrome and Fibromyalgia in Patients Affected of Multiple Chemical Sensitivity Joaquim Fernandez-SolB M.D., Santiago Nogué M.D., Elisabet Rovira M.D., José- Manuel Fernández-Huerta M.D., Esther Gómez M.D., Teresa GodBs Ph.D, Antoni Fernandez-SolB M.D and Ferran Garcia Fructuoso M.D The Development of an Epidemiological Case Definition for Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS/ME) T Osoba, D Pheby, S Gray, L Nacul, J Duffield, Toward an Empirical Case Definition of CFS Leonard A. Jason, Karina Corradi, Susan Torres-Harding Chronic Fatigue Syndromes: To Exclude to Not to Exclude Other Diagnoses James F. Jones, MD, Jin-Mann Lin, Elizabeth M. Maloney, William C. Reeves. Myalgic Encephalomyelitis (M.E.), The Definition: Byron Hyde M.D. Major Findings in 150 Consecutive M.E. and CFS Patients Who Were Subjected to Total Body Physical and Technological Examination of All Organs and Systems Byron Hyde MD A Discussion of the Los Angeles County Hospital 1934 M.E. epidemic and the Akureyri M.E. Epidemics Byron Hyde MD `````````````````````````````````````````````````````````````` Fatigue Section `````````````````````` Comparing Heart Rate Variability in Chronic Fatigue Syndrome and Healthy Controls using Commercially Available Software Eleanor Stein MD FRCP(C) Post-Exertional Malaise Following an Exercise Challenge Staci R. Stevens, Christopher R. Snell, Lucinda Bateman, Travis L. Stiles and J. Mark VanNess Lactose Intolerance and/or Fructose Malabsorption: A Predisposing Factor for the Development of CFS? P. De Becker, K. De Meirleir, J. De Leerssnijder, L. De Meirleir Glutathione Depletion--Methylation Cycle Block Hypothesis for the Pathogenesis of Chronic Fatigue Syndrome Richard A. Van Konynenburg, Ph.D. Effective Treatment of Chronic Fatigue Syndrome and Fibromyalgia with D-Ribose Jacob E. Teitelbaum, MD, J.A. St.Cyr, MD, PhD, Clarence Johnson What Do We Know About Multiple Chemical Sensitivity? An Overview of the Research Pamela Reed Gibson, Ph.D., Amanda Lindberg*, M.A. Candidate Physicians Perceptions and Practices Regarding Patient Reports of Chemical Sensitivity Pamela Reed Gibson, Ph.D., Amanda Lindberg, M.A. Candidate Unexplained Fatigue in Patients With and Without Symptoms of Chronic Rhinosinusitis: Do These Populations Differ? Alexander C. Chester, MD, Georgetown University Medical Center, Washington, DC Decreased Renal Function in CFS Patients Tae Park, M.D. Validation and Usefulness of the Quick Environment Exposure Sensivity Inventory (QEESI©) The Spanish Population Cusco-Segarra AM, Garcia-Fructuoso FJ, Lopez-Crespi F, Poca-Dias, V Thyroid Malignancy Association with Cortical & Subcortical Brain SPECT Changes In Patients Presenting with a Myalgic Encephalomyelitis / Chronic Fatigue Syndrome Hyde, Byron M.D, Green, Tracy, Jean Léveillé M.D Effect of Supplement With Lactic-Acid Producing Bacteria on Fatigue and Physical Activity in Patients with Chronic Fatigue Syndrome Sullivan A, Nord CE, Evengard B `````````````````````````````````````````````````````````````` Gender Section `````````````````````` Why is the Prevalence of Chronic Fatigue Syndrome Higher in Women than in Men?--A Hypothesis Richard A. Van Konynenburg, Ph.D. Specific Cardioventilatory Response in SFC Women During a Very Light Intensity of Exercise Suarez A, Javierre C, Alegre J, Garcia Quintana A, Barbany JR, Morales A, Ventura JL Differences in the Recovery Period Between a Group of CSF Women and a Matched Control Group After a Supramaximal Effort Suarez A, Javierre C, Garcia-Quintana A, Alegre J, Ventura JL, Barbany JR and Segura R `````````````````````````````````````````````````````````````` Genetics / Proteomics Section `````````````````````````````````````````` Genetics of Chronic Fatigue Syndrome and its Subgroups Defined by Latent Class Analysis Mangalathu S. Rajeevan†, Alicia K. Smith, Elizabeth Maloney, Eric Aslakson, Suzanne D. Vernon, William C. Reeves Expression of MicroRNAs (miRNAs) in Chronic Fatigue Syndrome (CFS) Robert Petty, Tim Rutherford, Ken Laing, Jane Montgomery, Selwyn CM Richards, Jonathan R Kerr Transcriptome Analysis of Peripheral Blood Mononuclear Cells from Patients with Chronic Fatigue Syndrome Hanna Gräns, Birgitta EvengDrd and Peter Nilsson Case-Control Study of Genotypes in Multiple Chemical Sensitivity: CYP2D6, NAT1, NAT2, PON1, PON2 and MTHFR Gail McKeown-Eyssen, Cornelia Baines, David EC Cole,Nicole Riley, Rachel F Tyndale, Lynn Marshalland Vartouhi Jazmaji Presented by Alison C. Bested, M.D., FRCPC Investigation of Human Gene Signatures of Past Persistent Microbial Infections in Unstressed Normal Blood donors; Possible Relevance to the Pathogenesis of Chronic Fatigue Syndrome Beverley Burke, Jonathan R Kerr `````````````````````````````````````````````````````````````` Pain Section `````````````````` Chronic Fatigue Syndrome and Fibromyalgia Sufferers: Now There's Hope and Help! Alison C. Bested, M.D., FRCPC `````````````````````````````````````````````````````````````` Pediatrics Section ```````````````````````` Are 'Hypoglycaemic' Symptoms in CFS Associated with Hypoglycaemia? Fergus Cameron and Katherine Rowe Pediatric Chronic Fatigue Syndrome and Munchausen-by-proxy: A Case Study Van Hoof E , De Becker P and De Meirleir K. `````````````````````````````````````````````````````````````` Sleep Section ```````````````````` Defining the Occurrence and Influence of Alpha-Delta Sleep in Chronic Fatigue Syndrome Elke Van Hoof, PhD, Pascale De Becker PhD, Charles Lapp MD, Raymond Cluydts PhD, Kenny De Meirleir PhD Perception versus Polysomnographic Assessment of Sleep in CFS and Non-Fatigued Controls: Results from a Population-Based Study Matthias Majer, Ph.D., James F. Jones, M.D, Elizabeth R. Unger MD, Ph.D, Laura Solomon Youngblood, MPH , Michael J. Decker, R.N., Ph.D., Elizabeth Maloney, M.S., Dr. P.H., Brian Gurbaxani Ph.D. , Christine Heim, Ph.D., William C. Reeves, M.D., M.Sc `````````````````````````````````````````````````````````````` Viral / Immune Section `````````````````````````````` The Establishment of a National ME Observatory for the UK D Pheby, PD Campion, M de L Drachler, E Lacerda, JC de Carvalho Leite, L Nacul, F Poland, Trish Taylor. Incidence of Chromosomally Integrated HHV-6 (CIHHV-6) in a Cohort of CFS Patients with Clonal TCR- and Lymphoid Malignancies David Pomeranz1, Kathryn Hagen, Byron Hsu, Judy A. Mikovits and Daniel L Peterson. In Vivo-Induced Antigen Technology for Detection of Antibodies Against Borrelia Burgdorferi and its Cross-reactive Antigens in Patients with Chronic Fatigue and Fibromyalgia Aristo Vojdani, Ph.D., M.T., Immunosciences Lab., Inc., Bernard Raxlen, M.D. The Life Cycle of Cryptostrongylus pulmoni in Chronic Fatigue Syndrome Lawrence A. Klapow, PhD Immune Effects of an Acute Exercise Challenge in Gulf War Illness Nancy G. Klimas, Martin Rosenthal and Mary A. Fletcher. Visible and Near-Infrared Spectroscopy for Diagnosis of Systemic Lupus Erythematosus, Showing Fatigue Symptoms like Chronic Fatigue Syndrome Yukiko Hakariya1, Akikazu Sakudo, Takanori Kobayashi, Seiki Tajima, Junzo Nojima, Hirohiko Kuratsune, Yasuyoshi Watanabe, and Kazuyoshi Ikuta1 Comparison of the Composition of the Intestinal Microflora of FS Patients When in the Acute Phase of Illness Brigitta Evengard, M.D., Ph.D. Enteroviruses and Chronic Fatigue Syndrome John K. Chia, M.D., Andrew Y. Chia, B.S. Meta-Analysis of Well-Controlled, Randomized, Double-Blinded, Phase II/III Clinical Trials of Poly I : Poly C12U vs. Placebo in Chronic Fatigue Syndrome David R. Strayer, Tom McCarron, Ying Han, William A. Carter, Staci Stevens Absence of TH2 – Biased Mucosal Immunity As Measured by Eosinophil Peroxidase Susana Repka-Ramirez, Kristina Naranch-Petrie, Gerald Gleich, James N. Baraniuk [Return to top] ------------------------------ Date: Fri, 15 Dec 2006 16:21:36 -0500 From: "Bernice A. Melsky" <email@example.com> Subject: MED: Botulinum toxin in primary care medicine Botulinum toxin in primary care medicine. J Am Osteopath Assoc. 2006 Oct;106(10):609-14. Felber ES. 402 Chestnut Ct, Bensalem, PA 19020-4315. firstname.lastname@example.org PMID: 17122031 Clostridium botulinum, a gram-positive anaerobic bacterium, produces a potent neurotoxin that causes muscle paralysis. The therapeutic use of botulinum toxin was discovered in the 1970s and has since been used to treat patients with a broad range of medical complaints. Botulinum toxin (BTX) is used in the primary care setting to treat conditions such as allergic rhinitis, hyperhidrosis, lichen simplex chronicus, migraine, myofascial pain syndrome, and certain task-specific idiopathic focal dystonias (eg, writer's cramp)-in addition to its more publicized use for cosmetic enhancement of the face. The expanding range of therapeutic applications for BTX make it necessary for primary care physicians to understand the biochemistry, preparation, indications, and interactions of BTX. [The full text of this article is available for free at http://www.jaoa.org/cgi/content/full/106/10/609 ] [Return to top] ------------------------------ Date: Sat, 16 Dec 2006 12:42:27 -0500 From: Fred Springfield <email@example.com> Subject: RES: Low-resolution electromagnetic brain tomography (LORETA) of monozygotic twins discordant for chronic fatigue syndrome Low-resolution electromagnetic brain tomography (LORETA) of monozygotic twins discordant for chronic fatigue syndrome. Journal: Neuroimage. 2006 Dec 12; [Epub ahead of print] Authors: Leslie Sherlin [a,*], Thomas Budzynski [c], Helen Kogan Budzynski [c], Marco Congedo [b], Mary E. Fischer [e] and Dedra Buchwald [d] Affiliations: [a] Nova Tech EEG, Inc., 8503 E Keats Ave, Mesa, AZ 85208, USA [b] Nova Tech EEG, Inc., Grenoble, France [c] The Department of Psychosocial and Community Health, University of Washington, Seattle, WA, USA [d] The Department of Medicine, University of Washington, Seattle, WA, USA [e] The Division of Epidemiology and Biostatistics, University of Illinois, Chicago, USA [*] Corresponding Author: LeslieSherlin@aol.com Received 14 September 2005; revised 28 October 2006; accepted 2 November 2006. Available online 13 December 2006. NLM Citation: PMID: 17169580 BACKGROUND: Previous work using quantified EEG has suggested that brain activity in individuals with chronic fatigue syndrome (CFS) and normal persons differs. Our objective was to investigate if specific frequency band-pass regions and spatial locations are associated with CFS using low-resolution electromagnetic brain tomography (LORETA). METHODS: We conducted a co-twin control study of 17 pairs of monozygotic twins where 1 twin met criteria for CFS and the co-twin was healthy. Twins underwent an extensive battery of tests including a structured psychiatric interview and a quantified EEG. Eyes closed EEG frequency-domain analysis was computed and the entire brain volume was compared of the CFS and healthy twins using a multiple comparison procedure. RESULTS: Compared with their healthy co-twins, twins with CFS differed in current source density. The CFS twins had higher delta in the left uncus and parahippocampal gyrus and higher theta in the cingulate gyrus and right superior frontal gyrus. CONCLUSIONS: These findings suggest that neurophysiological activity in specific areas of the brain may differentiate individuals with CFS from those in good health. The study corroborates that slowing of the deeper structures of the limbic system is associated with affect. It also supports the neurobiological model that the right forebrain is associated with sympathetic activity and the left forebrain with the effective management of energy. These preliminary findings await replication. Keywords: Chronic fatigue syndrome; Twins; Electroencephalography; Low resolution electromagnetic tomography; LORETA [This work was partially funded by grant U19Al38429 from the National Institutes of Health (Dr. Buchwald) and Nova Tech EEG, Inc.] [Return to top] ------------------------------ Date: Sat, 16 Dec 2006 20:21:25 -0000 From: Tom Kindlon <firstname.lastname@example.org> Subject: RES: Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature Title Supraphysiological cyclic dosing of sustained release T3 in order to reset low basal body temperature. Author(s) Friedman M, Miranda-Massari JR, Gonzalez MJ Institution Friedman Clinic, Montpelier, VT, USA. Source P R Health Sci J 2006 Mar; 25(1) :23-9. Abstract The use of sustained release tri-iodothyronine (SR-T3) in clinical practice, has gained popularity in the complementary and alternative medical community in the treatment of chronic fatigue with a protocol (WT3) pioneered by Dr. Denis Wilson. The WT3 protocol involves the use of SR-T3 taken orally by the patient every 12 hours according to a cyclic dose schedule determined by patient response. The patient is then weaned once a body temperature of 98.6 degrees F has been maintained for 3 consecutive weeks. The symptoms associated with this protocol have been given the name Wilson's Temperature Syndrome (WTS). There have been clinical studies using T3 in patients who are euthyroid based on normal TSH values. However, this treatment has created a controversy in the conventional medical community, especially with the American Thyroid Association, because it is not based on a measured deficiency of thyroid hormone. However, just as estrogen and progesterone are prescribed to regulate menstrual cycles in patients who have normal serum hormone levels, the WT3 therapy can be used to regulate metabolism despite normal serum thyroid hormone levels. SR-T3 prescription is based exclusively on low body temperature and presentation of symptoms. Decreased T3 function exerts widespread effects throughout the body. It can decrease serotonin and growth hormone levels and increase the number of adrenal hormone receptor sites. These effects may explain some of the symptoms observed in WTS. The dysregulation of neuroendocrine function may begin to explain such symptoms as alpha intrusion into slow wave sleep, decrease in blood flow to the brain, alterations in carbohydrate metabolism, fatigue, myalgia and arthralgia, depression and cognitive dysfunction. Despite all thermoregulatory control mechanisms of the body and the complex metabolic processes involved, WT3 therapy seems a valuable tool to re-establish normal body functions. We report the results of 11 patients who underwent the WT3 protocol for the treatment of CFS. All the patients improved in the five symptoms measured. All patients increased their basal temperature. The recovery time varied from 3 weeks to 12 months. Language eng Pub Type(s) Journal Article PubMed ID 16883675 [For some reason, the abstract has disappeared from PubMed. TK] [Return to top] ------------------------------ Date: Sat, 16 Dec 2006 20:30:02 -0000 From: Tom Kindlon <email@example.com> Subject: RES: The epidemiology of chronic syndromes that are frequently unexplained: do they have common associated factors? [This also showed up on PubMed then disappeared. It does seem to have been published - see http://ije.oxfordjournals.org/cgi/content/abstract/35/2/468. TK] The epidemiology of chronic syndromes that are frequently unexplained: do they have common associated factors? Int J Epidemiol. 2006 Apr;35(2):468-76. Epub 2005 Nov 22. Vishal R Aggarwal1,*, John McBeth2, Joanna M Zakrzewska3, Mark Lunt2 and Gary J Macfarlane1 1 Unit of Chronic Disease Epidemiology, School of Epidemiology and Health Sciences, The University of Manchester, Manchester, UK 2 Arthritis Research Campaign Epidemiology Unit, School of Epidemiology and Health Sciences, The University of Manchester, Manchester, UK 3 Barts and the London, Queen Mary's School of Medicine and Dentistry, London, UK * Corresponding author. Arc Epidemiology Unit, School of Epidemiology and Health Sciences, The Medical School, University of Manchester, Oxford Road, Manchester M13 9PT, UK. E-mail: firstname.lastname@example.org PMID: 16303810 Background Syndromes for which no physical or pathological changes can be found tend to be researched and managed in isolation although hypotheses suggest that they may be one entity. The objectives of our study were to investigate the co-occurrence, in the general population, of syndromes that are frequently unexplained and to evaluate whether they have common associated factors. Methods We conducted a population-based cross-sectional survey that included 2299 subjects who were registered with a General Medical Practice in North-west England and who completed full postal questionnaires (response rate 72%). The study investigated four chronic syndromes that are frequently unexplained: chronic widespread pain, chronic oro-facial pain, irritable bowel syndrome, and chronic fatigue. Validated instruments were used to measure the occurrence of syndromes and to collect information on a variety of associated factors: demographic (age, gender), psychosocial (anxiety, depression, illness behaviour), life stressors, and reporting of somatic symptoms. Results We found that 587 subjects (27%) reported one or more syndromes: 404 (18%) reported one, 134 (6%) reported two, 34 (2%) reported three, and 15 (1%) reported all four syndromes. The occurrence of multiple syndromes was greater than would be expected by chance (P < 0.001). There were factors that were common across syndromes: female gender [odds ratio (OR) = 1.8; 95% confidence interval (95% CI) 1.5-2.2], high levels of aspects of health anxiety like health worry preoccupation (OR = 3.5; 95% CI 2.8-4.4) and reassurance seeking behaviour (OR = 1.4; 95% CI 1.1-1.7), reporting of other somatic symptoms (OR = 3.6; 95% CI 2.9-4.4), and reporting of recent adverse life events (OR = 2.3; 95% CI 1.9-2.8). Conclusion This study has shown that chronic syndromes that are frequently unexplained co-occur in the general population and share common associated factors. Primary care practitioners need to be aware of these characteristics so that management is appropriate at the outset. [Return to top] ------------------------------ Date: Sat, 16 Dec 2006 23:32:03 +0100 From: "Dr. Marc-Alexander Fluks" <email@example.com> Subject: RES,NOT: CFS - The Chocolate Remedy Source: Hull Daily Mail Date: December 16, 2006 URL: http://www.thisishull.co.uk/displayNode.jsp?nodeId=197370&command=displayContent&sourceNode=197368&home=yes&more_nodeId1=136245&contentPK=16204319 Chocolate's Good for You - It's Official ---------------------------------------- It is the news anyone with a sweet tooth has been waiting for - chocolate is officially good for you. Doctors at Hull and East Yorkshire Hospitals NHS Trust have found eating small bars of dark chocolate every day helps stop symptoms of chronic fatigue syndrome (CFS). The illness, also known as myalgic encephalomyelitis (ME), leaves sufferers with debilitating fatigue and neurological problems. People taking part in a study at Hull Royal Infirmary found they felt better after eating specially formulated dark chocolate each day for eight weeks. However, only chocolate made with 85 per cent cocoa was found to have health benefits. Professor Steve Atkin, consultant endocrinologist, conducted the study. He said: "No one has examined the effects of chocolate on CFS before, so this is a very exciting result for us. The participants took 45g of specially formulated chocolate high in polyphenols for eight weeks. They then had a two-week period of rest before taking a placebo chocolate, low in polyphenols, for another eight weeks. After the first period they reported feeling less fatigue and once they moved to the placebo chocolate they began feeling more fatigue again. They didn't experience any significant weight gain either, which is an extra positive." Chocolate contains a complex mixture of chemicals called polyphenols, which are also reported to reduce the risk of death from coronary heart disease, cancer and strokes. Chocolate also increases serotonin, which regulates mood and sleep. Tracy Denholm, 39, of Beckside Close, west Hull, has suffered from CFS for more than 10 years. She said: "I have really bad attacks, where I cannot see and I cannot use my body properly, like a newborn baby. My husband Ian is my carer and, because I cannot guarantee how well I am going to feel, I cannot work. I am quite cynical, but it did work and I felt much more alert. I had more energy and didn't have any attacks." The research was funded by the Diabetes Endowment Fund charity, for which Professor Atkin is asking for donations. The trust is now looking for people with type two diabetes, linked to age or weight, or polycystic ovary syndrome, where many cysts grow on a woman's ovaries, to see if chocolate helps. Professor Atkin said: "I have a large amount of chocolate in the department waiting to be eaten." Anyone who is interested, or wants to donate to the fund, should call Professor Atkin's research team on (01482) 675387. firstname.lastname@example.org Links Hull and East Yorkshire Hospital NHS Trust http://www.hey.nhs.uk White Rabbit chocolatier http://www.white-rabbit-chocolate.co.uk -------- (c) 2006 Hull Daily Mail [Return to top] ------------------------------ Date: Sat, 16 Dec 2006 23:33:13 +0100 From: Jan van Roijen <email@example.com> Subject: res: ME/CFS & Low-resolution electromagnetic brain tomography ~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Send an Email for free membership ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ >>>> Help ME Circle <<<< >>>> 13 December 2006 <<<< Editorship : firstname.lastname@example.org Outgoing mail scanned by Norton AV ~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~:~ Sat, 16 Dec 2006 Fred Springfield posted the abstract of *Low-resolution electromagnetic brain tomography (LORETA) of monozygotic twins discordant for chronic fatigue syndrome* - Sherlin L et al. - Co-Cure: http://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0612c&L=co-cure&T=0&P=285 ----------------------------------------------------------------------------- ~jvr: as fair use I add the discussion section of this article ----------------------------------------------------------------------------- Discussions LORETA is a technique that facilitates a deeper understanding of the neurological findings present in the EEG (Pascual-Marqui et al., 2002). LORETA does not assume a limited number of dipolar point sources or a distribution on a known surface, but directly computes a current distribution throughout the full brain volume. The result is a true 3-dimensional tomography with localization that is preserved with a relatively low spatial resolution. A direct comparison of results obtained from fitting one and 2 dipoles with LORETA shows that the latter provides physiologically meaningful results in many situations where dipolar solutions fail (Pascual-Marqui, 1995). LORETA also offers new hypotheses on the location of higher cognitive functions in the brain (Pascual-Marqui, 1995), an area of great interest to CFS patients and investigators. LORETA results are reference-free, whereas surface EEG results inherently depend upon the chosen reference. Taken together, the advantages of LORETA over surface EEG analysis include the ability to visualize anomalies in the deeper brain structures, and to specify anomalies in frequency band and spatial location. Our study found that the CFS twins had significantly higher levels of current source density in the delta band in the left uncus and parahippocampal gyrus, cingulate gyrus, and right precentral gyrus of the frontal lobe. These findings are consistent with those obtained with quantified surface EEG techniques both in our experience (T. Budzynski, personal communication, 2005) as well as in the literature (Billiot et al., 1997). Previous studies have found that slowing of the deeper structures of the limbic system is associated with effect. Limbic inputs from the amygdala, entorhinal and perirhinal cortex, and subiculum, may serve as a visceromotor system to provide frontal cortical influence over autonomic and endocrine function. This system appears to be involved in guiding behavior and regulation of mood. It has been suggested that the right forebrain is associated with sympathetic activity that includes negative effect, withdrawal, and survival emotions (Craig, 2005). Findings of increased theta in the specific Brodmann areas mentioned may indicate blunted emotional processing, apathy, attention difficulties, and motivation. Although these Brodmann areas are less often correlated with increases in delta frequency, the left forebrain has been implicated in the effective management of energy, both mental and physical (Craig, 2005). Functional imaging studies indicate that many of these areas also show volume changes and decreased glial number and density in mood-disordered subjects (Price, 1999). One aspect of this study that deserves emphasis is the fact that the participants were carefully chosen illness discordant twins. To our knowledge, no previous studies of LORETA involving families or twins have been published. However, previous twin studies have demonstrated that many EEG features are predominantly determined by heredity (Stassen et al., 1988; Christian et al., 1996; Martinovic et al., 1997), including peak alpha frequency (Posthuma et al., 2001). Of additional relevance, in a study of older adults, 11% of "normal" control subjects exhibited an abnormal EEG (Leuchter et al., 1993), underscoring the value of exceedingly well-matched controls such as the ones we used in this study. This co-twin control study has several limitations related to our sample selection and methods. Solicitation by advertisement resulted in a volunteer sample of twin pairs with the potential for ascertainment problems. However, the more desirable strategy of systematically identifying twins from a well-defined populationbased twin registry is not readily accomplished in the United States. Thus, how representative the twins in this study were either of twins in general, or of persons with CFS, is not known. Because our twins were adults, primarily female, drawn from community practices, and the ill twins met strict criteria for CFS, we cannot generalize our findings to other samples and more specialized settings. Nonetheless, the demographic and clinical characteristics of our sample are similar to those previously described in the CFS literature. Fourth, the order of testing of the twins was not formally randomized, so that even though technicians and investigators were blinded, some unrecognized and unaccounted for biases might have resulted. Finally, of concern given the high rates of depression in CFS, we were not able to control for major depression. Due to the constraints of the procedure implemented, no other factors entered into the statistical design. In conclusion, objective measures of delta and theta current source density differed in twins with CFS and their healthy cotwins. Because twin studies are especially well suited to the study of illnesses for which the appropriate comparison groups are not clearly defined (Hrubec and Robinette, 1984), they offer an alternative approach to examine possible patterns of brain activity in CFS. Future research should focus on investigating larger groups of patients and control subjects. Although these results await replication by others, they provide preliminary evidence that objective electrophysiological parameters may help identify persons with CFS. If alterations in LORETA patterns in CFS can be confirmed, this technique could find clinical applications. [Return to top] ------------------------------ Date: Sun, 17 Dec 2006 02:48:23 -0000 From: Tom Kindlon <email@example.com> Subject: RES: High cocoa polyphenol rich chocolate improves the symptoms of chronic fatigue http://www.endocrine-abstracts.org/ea/0012/ea0012p68.htm Endocrine Abstracts (2006) 12 P68 Abstract High cocoa polyphenol rich chocolate improves the symptoms of chronic fatigue T Sathyapalan1, P Campion1, S Beckett2, AS Rigby1 & SL Atkin1 1University of Hull, Hull, United Kingdom; 2Nestlé PTC, York, United Kingdom. ---------------------------------------------------------------------------- Background Chronic fatigue syndrome (CFS) is a debilitating condition with high morbidity and associated reduced quality of life. There are data suggesting neuro-endocrine axis involvement in CFS including disturbance in hypothalamic-pituitary-adrenal axis, growth hormone axis, opioidergic system and interactions with 5-Hydroxy Tryptamine (5-HT) system. Studies with selective 5-HT-releasing agents, using prolactin or cortisol responses to stimulation, found evidence of enhanced serotonergic responses in patients with CFS. Cocoa is known to increase neurotransmitters like phenyl ethylamine, serotonin, and anandamide in the brain. Objective To study the effect of high cocoa polyphenol rich chocolate in patients with Chronic Fatigue Syndrome. Design Double blinded, randomised, placebo controlled fashion using high cocoa polyphenol rich chocolate in comparison to simulated iso-calorific chocolate dyed brown as placebo. Results Ten patients were enrolled in the study of which 5 patients completed both arms. The Chandler Fatigue Scale score improved significantly after 8 weeks of the high cocoa polyphenol rich chocolate phase (32.6 vs. 22.0 p value 0.012) and, interestingly, fell significantly when patients were given simulated iso-calorific chocolate (25.3 vs. 28.6 p value 0.026). The residual function, as assessed by the London Handicap scale, also improved significantly after the active phase (0.485 vs. 0.628 p value 0.018). The mean weight before and after the placebo arm were also unchanged (73.43 kg vs. 73.85 kg, respectively p value 0.345). Anecdotally, two patients were able to return back to work after having had their symptoms for a 2 year period and continued on high cocoa polyphenol rich chocolate. Conclusion High cocoa polyphenols rich chocolate 15 g three times daily improved fatigue and function in patients with chronic fatigue syndrome over a period of 8 weeks compared to simulated iso-calorific chocolate. Whether hormonal modulation by this high cocoa polyphenols rich chocolate also occurred needs clarification. [Return to top] ------------------------------ Date: Sun, 17 Dec 2006 14:01:52 -0500 From: "Bernice A. Melsky" <firstname.lastname@example.org> Subject: RES: Evidence of diffuse noxious inhibitory controls (DNIC) elicited by cold noxious stimulation in patients with provoked vestibulodynia Evidence of diffuse noxious inhibitory controls (DNIC) elicited by cold noxious stimulation in patients with provoked vestibulodynia. Pain. 2006 Dec 12; [Epub ahead of print] Johannesson U, de Boussard CN, Brodda Jansen G, Bohm-Starke N. Karolinska Institutet, Department of Clinical Sciences, Division of Obstetrics and Gynecology, Danderyd Hospital, 182 88, Stockholm, Sweden. PMID: 17169489 Provoked vestibulodynia is a common cause of superficial dyspareunia in young women. Recent evidence has pointed out the importance of studying endogenous pain modulation in these women. An impairment of diffuse noxious inhibitory controls (DNIC) has been suggested in chronic pain conditions with a female predominance such as fibromyalgia and temporomandibular disorder. Our aim was to examine whether patients with provoked vestibulodynia and healthy women with or without combined oral contraceptives (COC) display a DNIC response to cold noxious stimulation. Twenty patients with provoked vestibulodynia not using COC, 20 healthy women on COC and 20 healthy women without COC were included and tested days 7-11 of their menstrual cycle. Pressure pain thresholds (PPTs) and pain ratings using VAS were measured on the arm and leg before and during a cold pressor test. A socio-medical questionnaire, the Hospital and Anxiety Depression Scale and the Short Form-36 were completed. The majority of the subjects in all three study groups significantly increased their PPTs during cold noxious stimulation indicating a DNIC response. The patients displayed lower PPTs compared to the healthy women. Depression, anxiety and bodily pain were more often reported by the patients. No differences related to the intake of COC were observed between the healthy women. In conclusion, women with provoked vestibulodynia as well as healthy women irrespective of COC status display a DNIC response indicating an endogenous pain inhibition. However, the results imply a systemic hypersensitivity in women with vestibulodynia with low general pain thresholds as compared to healthy women. [Return to top] ------------------------------ Date: Mon, 18 Dec 2006 19:34:38 -0800 From: Kimberly Hare <email@example.com> Subject: RES: Evidence Shows Fibromyalgia Pain Is Real: Experts - And yet many patients still face skepticism from doctors Evidence Shows Fibromyalgia Pain Is Real: Experts And yet many patients still face skepticism from doctors MONDAY, Dec. 18 (HealthDay News) -- The pain of fibromyalgia is real, and doctors need to take patients' complaints seriously, concludes a review paper by University of Michigan Health System doctors. "It is time for us to move past the rhetoric about whether these conditions are real, and take these patients seriously as we endeavor to learn more about the causes and most effective treatments for these disorders," Richard E. Harris, research investigator in the division of rheumatology, department of internal medicine at the U-M Medical School and a researcher at the U-M Health System's Chronic Pain and Fatigue Research Center, said in a prepared statement. Fibromyalgia is a debilitating pain syndrome that affects 2 percent to 4 percent of the population. However, the condition is often mistakenly diagnosed as arthritis or even a psychological issue, and many patients face questions about whether their condition is real, according to background information. In their review, the U-M doctors said there is now "overwhelming data" that fibromyalgia is real. They said it's characterized by a lower pain threshold and is associated with genetic factors that can increase the risk of developing the condition. The authors cited recent studies involving pain, genetics and brain activity, and said they hoped their findings would improve understanding and acceptance of fibromyalgia and related conditions. The paper appears in the December issue of Current Pain and Headache Reports. More information The American College of Rheumatology has more about fibromyalgia at http://www.rheumatology.org/public/factsheets/fibromya_new.asp? (SOURCE: University of Michigan Health System, news release, November 2006) Copyright © 2006 ScoutNews LLC. All rights reserved. HealthDayNews articles are derived from various sources and do not reflect federal policy. healthfinder® does not endorse opinions, products, or services that may appear in news stories. For more information on health topics in the news, visit the healthfinder® health library at http://healthfinder.gov/library [Return to top] ------------------------------
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