Discussion in 'Fibromyalgia Main Forum' started by fight4acure, Jul 26, 2006.

  1. tansy

    tansy New Member

    Health-Related Quality of Life in Chronic Fatigue Syndrome versus
    Rheumatoid Arthritis as Control Group

    Journal: J of Chronic Fatigue Syndrome, Vol. 14, No. 2, 2007, pp.31-43

    Authors: Montserrat Núñez PhD, Esther Núñez PhD, Jos Luis del Val MD,
    Jos Manuel Fernández-Huerta, Cayetano Alegre MD, Maria Bonet MD,
    Daniel Roig MD, Esther Gomez MD, Teresa Godas Sieso, Joaquim Fernández-Sol MD

    The objectives of this study were

    (1) evaluate health-related quality of life (HRQL) in patients with
    chronic fatigue syndrome (CFS);

    (2) to compare the HRQL of these patients with that of rheumatoid
    arthritis (RA) patients and healthy Spanish reference population
    values (RPV); and

    (3) to identify the influence of sociodemographic and clinical
    variables on HRQL in CFS patients.

    We included 216 outpatients: 94 females/14 males (age 42.9 ± 9.9
    years) with CFS and 94 females/14 males with RA (age 42.9 ± 9.9
    years). We used a cross-sectional, observational design.
    Sociodemographic data, comorbidities, pain (VAS) and global
    functional status were determined. HRQL was measured by the SF-36 and
    HAQ questionnaires.

    CFS patients had worse scores than RA patients in all SF36 dimensions
    except emotional role (p < 0.01). Both CFS and RA patients had worse
    scores in all SF36 dimensions than RPV. In CFS patients, pain
    negatively influenced HRQL (p < 0.05) except for physical role,
    social function and emotional role. Global functional status
    negatively influenced HRQL (p < 0.05) except for bodily pain, general
    health and mental health. Comorbidities worsened scores for physical
    and social functions and mental health.

    In conclusion, HRQL was worse in patients with CFS than in those with
    RA. Both CFS and RA patients had worse HRQL compared with RPV.
    Comorbidities, pain and global functional status influenced HRQL in
    CFS patients. Standardised HRQL instruments are of value in
    determining the quality of life in these patients.

    Keywords: Chronic fatigue syndrome, quality of life, functional involvement
  2. tansy

    tansy New Member

    A subset of fibromyalgia patients have findings suggestive of chronic
    inflammatory demyelinating polyneuropathy and appear to respond to IVIg.

    Rheumatology (Oxford). 2008 Feb;47(2):208-11.

    Caro XJ, Winter EF, Dumas AJ.

    18350 Roscoe Blvd., Suite 418, CA 91325-4174, USA.

    PMID: 18208823


    The aetiopathogenesis of the fibromyalgia syndrome (FMS)
    remains unknown. Recent reports, however, suggest that a subgroup of
    FMS subjects has an immune-mediated disease. Therefore, our primary
    objective was to study FMS subjects for evidence of an
    immune-mediated demyelinating polyneuropathy. Our secondary objective
    was to determine the effects of treating these FMS subjects with the
    immune modulator, intravenous immunoglobulin (IVIg).


    Fifty-eight FMS subjects, 26 rheumatic non-FMS subjects and
    52 non-rheumatic non-FMS subjects were studied. Subjective measures
    of paraesthesias, weakness, stocking hypaesthesia, pain, fatigue and
    stiffness were made. Objective measures of tenderness, proximal
    muscle strength and electrodiagnostic (EDX) evidence of
    polyneuropathy and demyelination were also made. Eleven other FMS
    subjects underwent sural nerve biopsy.


    Paraesthesias, subjective weakness and stocking hypaesthesia
    were more common in FMS than in rheumatic non-FMS (P </= 0.0001).
    Proximal muscle strength was less in FMS than in rheumatic non-FMS (P
    </= 0.0001). EDX demonstrated a distal demyelinating polyneuropathy,
    suggestive of chronic inflammatory demyelinating polyneuropathy
    (CIDP), in 33% of FMS subjects. No rheumatic non-FMS subject had
    polyneuropathy (P = 0.005), or demyelination (P = 0.05). Fifteen
    FMS/CIDP subjects were subsequently treated with IVIg (400 mg/kg each
    day for 5 days). Pain (P = 0.01), tenderness (P = 0.001) and strength
    (P = 0.04) improved significantly. Fatigue and stiffness trended
    towards improvement.


    A significant subset of FMS subjects have clinical and
    EDX findings suggestive of CIDP. IVIg treatment shows promise in
    treating this subset. These observations have implications for better
    understanding and treating some FMS patients.

    [This Message was Edited on 01/29/2008]
  3. fight4acure

    fight4acure Member

    Thank you for posting more research articles!

    Hugs :)

    [This Message was Edited on 02/04/2008]
  4. tansy

    tansy New Member

    i will endeavour to do this more often.

  5. tansy

    tansy New Member

    Paradoxical Nrems Distribution in "Pure" Chronic Fatigue PAtients A
    Comparison With Sleep Apnea-Hypopnea Patients and Healthy Control Subjects

    Journal: J of Chronic Fatigue Syndrome

    Authors: Olivier Le Bon MD, PhD, Daniel Neu MD, Filomena Valente PhD,
    Paul Linkowski MD, PhD

    Objective: The chronic fatigue syndrome (CFS) is a debated clinical
    entity, not presently associated with specific sleep abnormalities.
    However, higher levels of deep sleep and/or lower levels of light
    sleep have been reported in several all-night polysomnography studies
    in CFS patients. This distribution of Non-Rapid Eye Movement Sleep
    (NREMS) contrasts with what would be expected if sleep was
    interrupted by microawakenings, such as in sleep apneas or periodic
    limb movements, where more light sleep and less deep sleep are
    commonly observed. This "paradoxical" distribution of NREMS could
    represent a characteristic feature of chronic fatigue and deserved to
    be investigated.

    Methods: A retrospective comparison of the NREMS distribution was
    performed between 28 "pure" Chronic Fatigue Syndrome patients
    (without primary sleep or psychiatric disorders), 27 Apneic-Hypopneic
    patients and 27 Healthy Controls.

    Results: Data showed CFS patients to have a higher stage 4/stage 2 or
    stage 4/light sleep ratios than the other two conditions.

    Conclusion: This sleep pattern is closer to what is observed in cases
    of infections than to what is seen after sleep fragmentation by
    primary sleep or in psychiatric disorders. Such a particular sleep
    pattern could provide insights into the pathophysiology of fatigue.
  6. ephemera

    ephemera New Member

    Nine Yr FollowUp, Danish Chronic Fatigue Syndrome

    I saw this elsewhere & thought it of interest to many here. ( I posted it under this title, but now I'm putting it here. Does anyone know more about this?)

    Subject: RES: Nine-Year Follow-Up of Danish Chronic Fatigue Syndrome (CFS) Patients Impact on Health, Social, Vocational, and Personal Lives

    Nine-Year Follow-Up of Danish Chronic Fatigue Syndrome (CFS) Patients Impact on Health, Social, Vocational, and Personal Lives

    Journal: J of Chronic Fatigue Syndrome, Vol. 14, No. 2, 2007, pp. 7-23

    Authors: Mette Marie Andersen, Henrik Permin, Frank Albrecht

    Objective: To determine quality of life (QOL) and health in Danish CFS patients 9 years after diagnosis.

    Methods: Thirty-four adults with CFS responded to questions regarding QOL at diagnosis, and again 5 and 9 years later. At 9-year followup patients also responded to questions regarding health, fatigue, use of Health Care system, alcohol and exercise.

    Results: Two patients (6%) had recovered and 3 patients (10%) had received secondary diagnoses. Overall, there was no improvement, except with depression/anxiety. The order of severity among disabilities remained the same. Work had the highest disability score, followed by post-exertional malaise. Patients slept and rested 13.6 hours a day (mean). Self-reported physical health correlated
    with hours sleeping and resting. Rheumatic symptoms dominated the health symptoms. Alcohol consumption was low, and the use of the Health Care system was modest.

    Conclusion: After 9 years QOL was the same as at diagnosis, only mental health had improved.

    Keywords: Chronic fatigue syndrome, 9-year follow-up, quality of life, work disability, post-exertional malaise, mental health, hours sleeping and resting, physical health

  7. fight4acure

    fight4acure Member

    Thank you Tansy and eph!

    I find it hard to keep up with posting new stuff each day, and I so much appreciate the help!

    Hugs! :)
  8. tansy

    tansy New Member

    by Caroline Cassels

    January 23, 2008

    Genetic variations among patients with remitting-relapsing multiple
    sclerosis (RMSS) may help predict which individuals are likely to respond to
    interferon-beta therapy.

    Using a genomewide pharmacogenomic approach to identify single nucleotide
    polymorphism (SNP) allelic differences among RMSS patients, investigators at
    the University of California, San Francisco identified 18 genetic variations
    significantly associated with interferon-beta response.

    "The identification of pharmacogenetic polymorphisms provides important new
    insights into the mechanism of interferon-beta action, bringing the
    paradigms of rational drug design and personalized medicine 1 step further,
    " the authors write.

    Personalized Medicine

    According to the investigators, while beta interferon is widely used to
    treat MS, as many as 50% of treated patients continue to experience relapses
    and worsening disability.

    They also note that adverse effects from the drug, including flulike
    symptoms and depression, are common and lead many patients to discontinue
    Further, the researchers point out that the mechanism of action of
    interferon beta is incompletely understood, and currently there are no
    reliable clinical or biological markers that accurately predict therapy

    In the face of variable responsiveness and clinical heterogeneity, the
    researchers hypothesized that pharmacogenomic research might help "uncover
    unexpected mechanistic processes and potentially achieve the elusive goal of
    personalized medicine in MS."

    - The study included 206 RMSS patients from 4 centers in southern Europe who
    were followed up for an average of 2 years after interferon-beta therapy was

    - Responders were individuals who had no relapses and no increase in the
    Expanded Disability Status Score (EDSS) during the follow-up period.
    Nonresponders were patients with at least 2 relapses or an increase in
    EDSS of at least 1 point.

    - Patients' disability levels were assessed every 3 months using the EDSS.
    Relapses were defined as a new symptom or worsening of a preexisting
    symptom attributable to MS activity and confirmed by examination within 3
    days of onset.

    - At the end of the follow-up period, there were 99 responders and 107

    The researchers then pooled the DNA of individuals in each group and
    used microarrays to identify, across the genome, genetic markers associated
    with the response to interferon beta. The top 35 SNPs were
    identified as candidates for further analysis.

    ****Eighteen Variants Identified*****

    They then located these SNPs in each study subject to determine whether
    mutations in responders differed from those in nonresponders and found
    significant associations between several SNPs and treatment response.

    After validating these results, the investigators added 81 individuals with
    RRMS - 44 responders and 35 nonresponders - to the analysis to increase
    In the combined screen, a total of 18 SNPs were significantly associated
    with treatment response.

    + According to the study, candidate SNPs that significantly differed between
    responders and nonresponders in the final joint analysis included 7 located
    within the genes.

    + They report the remaining SNPs are located in intergeneic regions.

    "The beneficial outcomes of interferon-beta therapy for patients in the
    relapsing-remitting phase of MS have been clearly shown," the authors write.
    "On the other hand, the effect of this treatment is partial, and a
    substantial amount of patients are not responders.

    "Hence, in the absence of prognostic clinical, neuroradiological, and/or
    immunological markers of response, the question remains who and when to
    treat when adverse effects, inconvenience, and the cost of the drug are
    significant," they write. Further research is needed before DNA analysis can
    be used to predict treatment outcomes.

    The study was funded by the National Institutes of Health (NIH).

    Led by Esther Byun, MD, the study is published online January 14 in Archives
    of Neurology.
    Arch Neurol. Published online January 14, 2008. Abstract
  9. tansy

    tansy New Member

    in Adolescents with Chronic Fatigue

    Journal: Ann Noninvasive Electrocardiol. 2008 Jan;13(1):67-73.

    Authors and Affiliations:
    * Vegard Bruun Wyller, M.D., Ph.D., Department of Pediatrics,
    Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway;
    Department of Physiology, University of Oslo, Oslo, Norway,
    * Riccardo Barbieri, P.h.D., Department of Anesthesia and Critical
    Care, Massachusetts General Hospital/Harvard Medical School, Boston,
    * Erik Thaulow, M.D., Ph.D., Department of Pediatrics,
    Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway, and
    * J. Philip Saul, M.D.§§Department of Pediatrics, Medical University
    of South Carolina, Charleston, South Carolina

    Address for reprints: Vegard Bruun Wyller, M.D., Ph.D., Department of
    Pediatrics, Rikshospitalet-Radiumhospitalet Medical Center, N-0027
    Oslo, Norway. Fax: +47-23-07-45-10

    Financial support: Vegard Bruun Wyller has received a grant from the
    University of Oslo.

    A.N.E. 2008;13(1):6773

    NLM Citation: PMID: 18234008


    Background: Hemodynamic abnormalities have been documented in the
    chronic fatigue syndrome (CFS), indicating functional disturbances of
    the autonomic nervous system responsible for cardiovascular
    regulation. The aim of this study was to investigate autonomic heart
    rate control during mild orthostatic stress in adolescents with CFS.

    Methods: A total of 14 CFS patients and 56 healthy controls having
    equal distribution of age and gender underwent lower body negative
    pressure (LBNP) of mmHg. The RR interval (RRI) was recorded
    continuously, and spectral power densities were computed in the
    low-frequency (LF) band (0.040.15 Hz) and the high-frequency (HF)
    band (0.150.50 Hz) from segments of 120-second length, using an
    autoregressive algorithm. In addition, the time-domain indices SDNN,
    pNN50, and r-MSSD were computed.

    Results: At rest, CFS had lower RRI than controls (P < 0.05), but
    indices of variability were similar in the two groups. During LBNP,
    compared to controls, CFS patients had lower normalized and absolute
    HF power and r-MSSD (P < 0.05), and higher RRI (P < 0.001),
    normalized LF power and LF/HF (P < 0.05).

    Conclusions: During mild orthostatic stress, adolescents with CFS
    appear to have enhanced vagal withdrawal, leading to a sympathetic
    predominance of heart rate control compared to controls. Possible
    underlying mechanisms include hypovolemia and abnormalities of reflex
  10. stschn

    stschn New Member

    I so appreciate the imput of the people here. Thank you from the bottom of my heart.
  11. fight4acure

    fight4acure Member

    Diminished Cardiopulmonary Capacity During Post-Exertional Malaise

    Journal, J of Chronic Fatigue Syndrome, Vol. 14, No. 2, 2007, pp. 77-85

    Authors: J. Mark VanNess PhD, Christopher R. Snell PhD, Staci R. Stevens

    Reduced functional capacity and post-exertional malaise following
    physical activity are hallmark symptoms of Chronic Fatigue Syndrome
    (CFS). That these symptoms are often delayed may explain the
    equivocal results for clinical cardiopulmonary exercise testing with
    CFS patients. The reproducibility of VO2max in healthy subjects is
    well documented. This may not be the case with CFS due to delayed
    recovery symptoms.

    Purpose: To compare results from repeated exercise tests as
    indicators of post-exertional malaise in CFS.

    Methods: Peak oxygen consumption (VO2 peak), percentage of predicted
    peak heart rate (HR%), and VO2 at anaerobic threshold (AT), were
    compared between six CFS patients and six control subjects for two
    maximal exercise tests separated by 24 hours.

    Results: Multivariate analysis showed no significant differences
    between control and CFS, respectively, for test 1: VO2 peak (28.4 ±
    7.2 ml/ kg/min; 26.2 ± 4.9 ml/kg/min), AT (17.5 ± 4.8 ml/kg/min; 15.0
    ± 4.9 ml/ kg/min) or HR% (87.0 ± 25.4%; 94.8 ± 8.8%). However, for
    test 2 the CFS patients achieved significantly lower values for both
    VO2peak (28.9 ± 8.0 ml/kg/min; 20.5 ± 1.8 ml/kg/min, p = 0.031) and
    AT (18.0 ± 5.2 ml/kg/min; 11.0 ± 3.4 ml/kg/min, p = 0.021). HR% was
    not significantly different (97.6 ± 27.2%; 87.8 ± 9.3%, p = 0.07). A
    follow-up classification analysis differentiated between CFS patients
    and controls with an overall accuracy of 92%.

    Conclusion: In the absence of a second exercise test, the lack of any
    significant differences for the first test would appear to suggest no
    functional impairment in CFS patients. However, the results from the
    second test indicate the presence of a CFS related post-exertional
    malaise. It might be concluded then that a single exercise test is
    insufficient to demonstrate functional impairment in CFS patients. A
    second test may be necessary to document the atypical recovery
    response and protracted malaise unique to CFS.

    Keywords: Serial exercise testing, functional impairment,
    differential diagnosis
  12. victoria

    victoria New Member

    This interview/discussion is from a 2005 CFIDS Chronicle, they've been around a long time ago.

    Go to:

  13. tansy

    tansy New Member

    Transcriptome Analysis of Peripheral Blood Mononuclear Cells from
    Patients with Chronic Fatigue Syndrome

    Journal: J of CFS, Vol. 14, No. 3, 2007, pp. 7-25

    Authors: Hanna Gräns PhD, Birgetta Evengård MD, Peter Nilsson PhD

    Objective: Chronic fatigue syndrome (CFS) is an illness defined by
    unexplained disabling fatigue lasting longer than six months,
    together with at least four out of eight specified symptoms. The
    etiology and pathophysiology of CFS are to a large degree unknown.
    Since much remains unclear about CFS we wanted to investigate
    transcript expression levels in peripheral blood mononuclear cells to
    identify genes that are involved in CFS.

    Method: Transcript expression profiles for 20 CFS patients were
    compared with 14 healthy controls using microarray technology.
    Results were verified with real-time PCR.

    Results: We have identified significantly differentially expressed
    genes comparing a female CFS patient subgroup with gradual illness
    onset and no previously documented infection with female healthy
    controls. We have also created a list of genes with indicated, but
    not verified, expression differences from comparisons between other
    subgroups and healthy controls. These genes are candidates for
    further study of potential involvement in CFS.

    Conclusion: Our results stress the necessity of subgrouping the
    heterogeneous CFS patient cohort. The mRNA expression differences
    identified here may be causal factors for the illness or symptoms
    observed in these patients, or a result of altered functions of other
    cellular components involved in the illness. The role of these genes
    in the CFS pathology needs further investigation.
  14. fight4acure

    fight4acure Member

    (Posted previously by ephemera)

    February 5, 2008 NY Times

    A Medical Mystery Unfolds in Minnesota

    AUSTIN, Minn. — If you have to come down with a strange disease, this town of 23,000 on the wide-open prairie in southeastern Minnesota is a pretty good place to be. The Mayo Clinic, famous for diagnosing exotic ailments, owns the local medical center and shares some staff with it. Mayo itself is just 40 miles east in Rochester. And when it comes to investigating mysterious outbreaks, Minnesota has one of the strongest health departments and best-equipped laboratories in the country.

    And the disease that confronted doctors at the Austin Medical Center here last fall was strange indeed. Three patients had the same highly unusual set of symptoms: fatigue, pain, weakness, numbness and tingling in the legs and feet.

    The patients had something else in common, too: all worked at Quality Pork Processors, a local meatpacking plant.

    The disorder seemed to involve nerve damage, but doctors had no idea what was causing it.

    At the plant, nurses in the medical department had also begun to notice the same ominous pattern. The three workers had complained to them of “heavy legs,” and the nurses had urged them to see doctors. The nurses knew of a fourth case, too, and they feared that more workers would get sick, that a serious disease might be spreading through the plant.

    “We put our heads together and said, ‘Something is out of sorts,’ ” said Carole Bower, the department head.

    Austin’s biggest employer is Hormel Foods, maker of Spam, bacon and other processed meats (Austin even has a Spam museum). Quality Pork Processors, which backs onto the Hormel property, kills and butchers 19,000 hogs a day and sends most of them to Hormel. The complex, emitting clouds of steam and a distinctive scent, is easy to find from just about anywhere in town.

    Quality Pork is the second biggest employer, with 1,300 employees. Most work eight-hour shifts along a conveyor belt — a disassembly line, basically — carving up a specific part of each carcass. Pay for these line jobs starts at about $11 to $12 an hour. The work is grueling, but the plant is exceptionally clean and the benefits are good, said Richard Morgan, president of the union local. Many of the workers are Hispanic immigrants. Quality Pork’s owner does not allow reporters to enter the plant.

    A man whom doctors call the “index case” — the first patient they knew about — got sick in December 2006 and was hospitalized at the Mayo Clinic for about two weeks. His job at Quality Pork was to extract the brains from swine heads.

    “He was quite ill and severely affected neurologically, with significant weakness in his legs and loss of function in the lower part of his body,” said Dr. Daniel H. Lachance, a neurologist at Mayo.

    Tests showed that the man’s spinal cord was markedly inflamed. The cause seemed to be an autoimmune reaction: his immune system was mistakenly attacking his own nerves as if they were a foreign body or a germ. Doctors could not figure out why it had happened, but the standard treatment for inflammation — a steroid drug — seemed to help. (The patient was not available for interviews.)

    Neurological illnesses sometimes defy understanding, Dr. Lachance said, and this seemed to be one of them. At the time, it did not occur to anyone that the problem might be related to the patient’s occupation.

    By spring, he went back to his job. But within weeks, he became ill again. Once more, he recovered after a few months and returned to work — only to get sick all over again.

    By then, November 2007, other cases had begun to turn up. Ultimately, there were 12 — 6 men and 6 women, ranging in age from 21 to 51. Doctors and the plant owner, realizing they had an outbreak on their hands, had already called in the Minnesota Department of Health, which, in turn, sought help from the federal Centers for Disease Control and Prevention.

    Though the outbreak seemed small, the investigation took on urgency because the disease was serious, and health officials worried that it might indicate a new risk to other workers in meatpacking.

    “It is important to characterize this because it appears to be a new syndrome, and we don’t truly know how many people may be affected throughout the U.S. or even the world,” said Dr. Jennifer McQuiston, a veterinarian from the disease centers.

    In early November, Dr. Aaron DeVries, a health department epidemiologist, visited the plant and combed through medical records. The disease bore no resemblance to mad cow disease or to trichinosis, the notorious parasite infection that comes from eating raw or undercooked pork. Nor did it spread person to person — the workers’ relatives were unaffected — or pose any threat to people who ate pork.

    A survey of the workers confirmed what the plant’s nurses had suspected: those who got sick were employed at or near the “head table,” where workers cut the meat off severed hog heads.

    On Nov. 28, Dr. DeVries’s boss, Dr. Ruth Lynfield, the state epidemiologist, toured the plant. She and the owner, Kelly Wadding, paid special attention to the head table. Dr. Lynfield became transfixed by one procedure in particular, called “blowing brains.”

    As each head reached the end of the table, a worker would insert a metal hose into the foramen magnum, the opening that the spinal cord passes through. High-pressure blasts of compressed air then turned the brain into a slurry that squirted out through the same hole in the skull, often spraying brain tissue around and splattering the hose operator in the process.

    The brains were pooled, poured into 10-pound containers and shipped to be sold as food — mostly in China and Korea, where cooks stir-fry them, but also in some parts of the American South, where people like them scrambled up with eggs.

    The person blowing brains was separated from the other workers by a plexiglass shield that had enough space under it to allow the heads to ride through on a conveyor belt. There was also enough space for brain tissue to splatter nearby employees.

    “You could see aerosolization of brain tissue,” Dr. Lynfield said.

    The workers wore hard hats, gloves, lab coats and safety glasses, but many had bare arms, and none had masks or face shields to prevent swallowing or inhaling the mist of brain tissue.

    Dr. Lynfield asked Mr. Wadding, “Kelly, what do you think is going on?”

    The plant owner watched for a while and said, “Let’s stop harvesting brains.”

    Quality Pork halted the procedure that day and ordered face shields for workers at the head table.

    Epidemiologists contacted 25 swine slaughterhouses in the United States, and found that only two others used compressed air to extract brains. One, a plant in Nebraska owned by Hormel, has reported no cases. But the other, Indiana Packers in Delphi, Ind., has several possible cases that are being investigated. Both of the other plants, like Quality Pork, have stopped using compressed air.

    But why should exposure to hog brains cause illness? And why now, when the compressed air system had been in use in Minnesota since 1998?

    At first, health officials thought perhaps the pigs had some new infection that was being transmitted to people by the brain tissue. Sometimes, infections can ignite an immune response in humans that flares out of control, like the condition in the workers. But so far, scores of tests for viruses, bacteria and parasites have found no signs of infection.

    As a result, Dr. Lynfield said the investigators had begun leaning toward a seemingly bizarre theory: that exposure to the hog brain itself might have touched off an intense reaction by the immune system, something akin to a giant, out-of-control allergic reaction. Some people might be more susceptible than others, perhaps because of their genetic makeup or their past exposures to animal tissue. The aerosolized brain matter might have been inhaled or swallowed, or might have entered through the eyes, the mucous membranes of the nose or mouth, or breaks in the skin.

    “It’s something no one would have anticipated or thought about,” said Dr. Michael Osterholm, an epidemiologist who is working as a consultant for Hormel and Quality Pork. Dr. Osterholm, a professor of public health at the University of Minnesota and the former state epidemiologist, said that no standard for this kind of workplace exposure had ever been set by the government.

    But that would still not explain why the condition should suddenly develop now. Investigators are trying to find out whether something changed recently — the air pressure level, for instance — and also whether there actually were cases in the past that just went undetected.

    “Clearly, all the answers aren’t in yet,” Dr. Osterholm said. “But it makes biologic sense that what you have here is an inhalation of brain material from these pigs that is eliciting an immunologic reaction.” What may be happening, he said, is “immune mimicry,” meaning that the immune system makes antibodies to fight a foreign substance — something in the hog brains — but the antibodies also attack the person’s nerve tissue because it is so similar to some molecule in hog brains.

    “That’s the beauty and the beast of the immune system,” Dr. Osterholm said. “It’s so efficient at keeping foreign objects away, but anytime there’s a close match it turns against us, too.”

    Anatomically, pigs are a lot like people. But it is not clear how close a biochemical match there is between pig brain and human nerve tissue.

    To find out, the Minnesota health department has asked for help from Dr. Ian Lipkin, an expert at Columbia University on the role of the immune system in neurological diseases. Dr. Lipkin has begun testing blood serum from the Minnesota patients to look for signs of an immune reaction to components of pig brain. And he expects also to study the pig gene for myelin, to see how similar it is to the human one.

    “It’s an interesting problem,” Dr. Lipkin said. “I think we can solve it.”

    Susan Kruse, who lives in Austin, was stunned by news reports about the outbreak in early December. Ms. Kruse, 37, worked at Quality Pork for 15 years. But for the past year, she has been too sick to work. She had no idea that anyone else from the plant was ill. Nor did she know that her illness might be related to her job.

    Her most recent job was “backing heads,” scraping meat from between the vertebrae. Three people per shift did that task, and together would process 9,500 heads in eight or nine hours. Ms. Kruse (pronounced KROO-zee) stood next to the person who used compressed air to blow out the brains. She was often splattered, especially when trainees were learning to operate the air hose.

    “I always had brains on my arms,” she said.

    She never had trouble with her health until November 2006, when she began having pains in her legs. By February 2007, she could not stand up long enough to do her job. She needed a walker to get around and was being treated at the Mayo Clinic.

    “I had no strength to do anything I used to do,” she said. “I just felt like I was being drained out.”

    Her immune system had gone haywire and attacked her nerves, primarily in two places: at the points where the nerves emerge from the spinal cord, and in the extremities. The same thing, to varying degrees, was happening to the other patients. Ms. Kruse and the index case — the man who extracted brains — probably had the most severe symptoms, Dr. Lachance said.

    Steroids did nothing for Ms. Kruse, so doctors began to treat her every two weeks with IVIG, intravenous immunoglobulin, a blood product that contains antibodies. “It’s kind of like hitting the condition over the head with a sledgehammer,” Dr. Lachance said. “It overwhelms the immune system and neutralizes whatever it is that’s causing the injury.”

    The treatments seem to help, Ms. Kruse said. She feels stronger after each one, but the effects wear off. Her doctors expect she will need the therapy at least until September.

    Most of the other workers are recovering and some have returned to their jobs, but others, including the index case, are still unable to work. So far, there have been no new cases.

    “I cannot say that anyone is completely back to normal,” Dr. Lachance said. “I expect it will take several more months to get a true sense of the course of this illness.”

    Dr. Lynfield hopes to find the cause. But she said: “I don’t know that we will have the definitive answer. I suspect we will be able to rule some things out, and will have a sense of whether it seems like it may be due to an autoimmune response. I think we’ll learn a lot, but it may take us a while. It’s a great detective story.”

  15. victoria

    victoria New Member

    sounds a LOT like the basis for Rife machines, they're just using lasers... and if they just use it on the blood, how are they going to get to the viruses that are in tissue?

    BUT still interesting... they have a long way to go I'm sure:

    New Way to Kill Viruses: Shake Them to Death By Michael Schirber, Special to LiveScience

    posted: 05 February 2008 09:27 am ET

    Scientists may one day be able to destroy viruses in the same way that opera singers presumably shatter wine glasses. New research mathematically determined the frequencies at which simple viruses could be shaken to death.

    "The capsid of a virus is something like the shell of a turtle," said physicist Otto Sankey of Arizona State University. "If the shell can be compromised [by mechanical vibrations], the virus can be inactivated."

    Recent experimental evidence has shown that laser pulses tuned to the right frequency can kill certain viruses. However, locating these so-called resonant frequencies is a bit of trial and error.

    "Experiments must just try a wide variety of conditions and hope that conditions are found that can lead to success," Sankey told LiveScience.

    To expedite this search, Sankey and his student Eric Dykeman have developed a way to calculate the vibrational motion of every atom in a virus shell. From this, they can determine the lowest resonant frequencies.

    As an example of their technique, the team modeled the satellite tobacco necrosis virus and found this small virus resonates strongly around 60 Gigahertz (where one Gigahertz is a billion cycles per second), as reported in the Jan. 14 issue of Physical Review Letters.

    A virus' death knell

    All objects have resonant frequencies at which they naturally oscillate. Pluck a guitar string and it will vibrate at a resonant frequency.

    But resonating can get out of control. A famous example is the Tacoma Narrows Bridge, which warped and finally collapsed in 1940 due to a wind that rocked the bridge back and forth at one of its resonant frequencies.

    Viruses are susceptible to the same kind of mechanical excitation. An experimental group led by K. T. Tsen from Arizona State University have recently shown that pulses of laser light can induce destructive vibrations in virus shells.

    "The idea is that the time that the pulse is on is about a quarter of a period of a vibration," Sankey said. "Like pushing a child on a swing from rest, one impulsive push gets the virus shaking."

    It is difficult to calculate what sort of push will kill a virus, since there can be millions of atoms in its shell structure. A direct computation of each atom's movements would take several hundred thousand Gigabytes of computer memory, Sankey explained.

    He and Dykeman have found a method to calculate the resonant frequencies with much less memory.

    In practice

    The team plans to use their technique to study other, more complicated viruses. However, it is still a long way from using this to neutralize the viruses in infected people.

    One challenge is that laser light cannot penetrate the skin very deeply. But Sankey imagines that a patient might be hooked up to a dialysis-like machine that cycles blood through a tube where it can be hit with a laser. Or perhaps, ultrasound can be used instead of lasers.

    These treatments would presumably be safer for patients than many antiviral drugs that can have terrible side-effects. Normal cells should not be affected by the virus-killing lasers or sound waves because they have resonant frequencies much lower than those of viruses, Sankey said.

    Moreover, it is unlikely that viruses will develop resistance to mechanical shaking, as they do to drugs.

    "This is such a new field, and there are so few experiments, that the science has not yet had sufficient time to prove itself," Sankey said. "We remain hopeful but remain skeptical at the same time."

  16. fight4acure

    fight4acure Member

    (Previously posted by Gapsych)

    Global Fibromyalgia Syndrome (FMS) and Chronic Fatigue Syndrome (CFS) News.
    « A FIBROMITE’S ‘WRINKLIES’Chronic pain harms the brain
    CHICAGO — People with unrelenting pain don’t only suffer from the non-stop sensation of throbbing pain. They also have trouble sleeping, are often depressed, anxious and even have difficulty making simple decisions.

    In a new study, investigators at Northwestern University’s Feinberg School of Medicine have identified a clue that may explain how suffering long-term pain could trigger these other pain-related symptoms.

    Researchers found that in a healthy brain all the regions exist in a state of equilibrium. When one region is active, the others quiet down. But in people with chronic pain, a front region of the cortex mostly associated with emotion “never shuts up,” said Dante Chialvo, lead author and associate research professor of physiology at the Feinberg School. “The areas that are affected fail to deactivate when they should.”

    They are stuck on full throttle, wearing out neurons and altering their connections to each other.

    This is the first demonstration of brain disturbances in chronic pain patients not directly related to the sensation of pain. The study will be published Feb. 6 in The Journal of Neuroscience.

    Chialvo and colleagues used functional magnetic resonance imaging (fMRI) to scan the brains of people with chronic low back pain and a group of pain-free volunteers while both groups were tracking a moving bar on a computer screen. The study showed the pain sufferers performed the task well but “at the expense of using their brain differently than the pain-free group,” Chialvo said.

    When certain parts of the cortex were activated in the pain-free group, some others were deactivated, maintaining a cooperative equilibrium between the regions. This equilibrium also is known as the resting state network of the brain. In the chronic pain group, however, one of the nodes of this network did not quiet down as it did in the pain-free subjects.

    This constant firing of neurons in these regions of the brain could cause permanent damage, Chialvo said. “We know when neurons fire too much they may change their connections with other neurons and or even die because they can’t sustain high activity for so long,” he explained.

    ‘If you are a chronic pain patient, you have pain 24 hours a day, seven days a week, every minute of your life,” Chialvo said. “That permanent perception of pain in your brain makes these areas in your brain continuously active. This continuous dysfunction in the equilibrium of the brain can change the wiring forever and could hurt the brain.”

    Chialvo hypothesized the subsequent changes in wiring “may make it harder for you to make a decision or be in a good mood to get up in the morning. It could be that pain produces depression and the other reported abnormalities because it disturbs the balance of the brain as a whole.”

    He said his findings show it is essential to study new approaches to treat patients not just to control their pain but also to evaluate and prevent the dysfunction that may be generated in the brain by the chronic pain.

    Chialvo’s collaborators in this project are Marwan Baliki, a graduate student; Paul Geha, a post-doctoral fellow, and Vania Apkarian, professor of physiology and of anesthesiology, all at the Feinberg School.

    For more information on Dante Chialvo visit:

    Contact: Marla Paul
    Northwestern University


    FMS Global News

    Fibrohugs Support

    Tenderpoints Newsletter

  17. fight4acure

    fight4acure Member

    Thanks Fibro for posting this, now it is added to the list!

    Also, NYTimes article on CFS and XMRV...

    Virus Is Found in Many With Chronic Fatigue Syndrome

    Published: October 8, 2009

    Many people with chronic fatigue syndrome are infected with a little known virus that may cause or at least contribute to their illness, researchers are reporting.

    The syndrome, which causes prolonged and severe fatigue, body aches and other symptoms, has long been a mystery ailment, and patients have sometimes been suspected of malingering or having psychiatric problems rather than genuine physical ones. Worldwide, 17 million people have the syndrome, including at least one million Americans.

    An article published online Thursday in the journal Science reports that 68 of 101 patients with the syndrome, or 67 percent, were infected with an infectious virus, xenotropic murine leukemia virus-related virus, or XMRV. By contrast, only 3.7 percent of 218 healthy people were infected. Continuing work after the paper was published has found the virus in nearly 98 percent of about 300 patients with the syndrome, said Dr. Judy A. Mikovits, the lead author of the paper.

    XMRV is a retrovirus, a member of the same family of viruses as the AIDS virus. These viruses carry their genetic information in RNA rather than DNA, and they insert themselves into their hosts’ genetic material and stay for life.

    Dr. Mikovits and other scientists cautioned that they had not yet proved that the virus causes the syndrome. In theory, people with the syndrome may have some other, underlying health problem that makes them prone to being infected by the virus, which could be just a bystander. More studies are needed to explain the connection.

    But Dr. Mikovits said she thought the virus would turn out to be the cause, not just of chronic fatigue, but of other illnesses as well. Previous studies have found it in cells taken from prostate cancers.

    “I think this establishes what had always been considered a psychiatric disease as an infectious disease,” said Dr. Mikovits, who is research director at the Whittemore Peterson Institute in Reno, a nonprofit center created by the parents of a woman who has a severe case of the syndrome. Her co-authors include scientists from the National Cancer Institute and the Cleveland Clinic.

    Dr. Mikovits said she and her colleagues were drawing up plans to test antiretroviral drugs — some of the same ones used to treat HIV infection — to see whether they could help patients with chronic fatigue. If the drugs work, that will help prove that the virus is causing the illness. She said patients and doctors should wait for the studies to be finished before trying the drugs.

    Dr. William Schaffner, an infectious disease expert at Vanderbilt University, said the discovery was exciting and made sense.

    “My first reaction is, ‘At last,’ ” Dr. Schaffner said. “In interacting with patients with chronic fatigue syndrome, you get the distinct impression that there’s got to be something there.”

    He said the illness is intensely frustrating to doctors because it is not understood, there is no effective treatment and many patients are sick for a long time.

    He added, “This is going to create an avalanche of subsequent studies.”

    (A version of this article appeared in print on October 9, 2009, on page A14 of the New York edition.)
  18. AuntTammie

    AuntTammie New Member

    If this has already been posted, I am sorry - I'm too wiped and too sensitive to the computer lighting (or something) rt now to stay on here long enough to read all this

    anyway, on the Phoenix Rising site, there is a whole section devoted to XMRV research, other sections devoted to other research, and somewhere on there is a recently published article about why exercise is truly harmful for us (it brings up several reasons that have been previously researched and puts them all together in a very good article)

  19. fight4acure

    fight4acure Member

    Thank you for adding info to this! this is the website you're refering too, right?

  20. fight4acure

    fight4acure Member

    bumping for newbies or those who have not yet seen our collection of articles we have here.