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  • he 3 pilot patients all had response to treatment and one thing we observed in these 3 patients is that we have a pattern of responses and relapses after the rituximab treatment with a lag time of several months from initial and rapid B-cell depletion until they start getting clinical responses. Such patients are also seen in established autoimmune diseases after rituximab treatment
  • So, our hypothesis is that the immune system somehow disturbs the fine-tune regulation of blood flow and tissues including in the brain.
  • But these two studies are not designed to give a definite answer to whether rituximab works in ME
Jun 10, 15

"A Vast Graveyard of Undead Theories"

  • Publication bias remains a controversial issue in psychological science. The tendency of psychological science to avoid publishing  null results produces a situation that limits the replicability assumption of science, as replication cannot be meaningful  without the potential acknowledgment of failed replications. We argue that the field often constructs arguments to block the  publication and interpretation of null results and that null results may be further extinguished through questionable researcher  practices. Given that science is dependent on the process of falsification, we argue that these problems reduce psychological  science’s capability to have a proper mechanism for theory falsification, thus resulting in the promulgation of numerous “undead”  theories that are ideologically popular but have little basis in fact.
  • Psychological science will benefit greatly from  increased efforts to improve rigor in meta-analyses and by ending the culture in which null results are aversely treated.  Otherwise psychology risks never rising above being little more than opinions with numbers

  • Abstract

    Background

    In 2010–2011, two large waterborne outbreaks caused by Cryptosporidium hominis affected two cities in Sweden, Östersund and Skellefteå. We investigated potential post-infection health consequences in people who had reported symptoms compatible with cryptosporidiosis during the outbreaks using questionnaires.

    Methods

    We compared cases linked to these outbreaks with non-cases in terms of symptoms present up to eleven months after the initial infection. We examined if cases were more likely to report a list of symptoms at follow-up than non-cases, calculating odds ratios (OR) and 95 % confidence intervals (CI) obtained through logistic regression.

    Results

    A total of 872 (310 cases) and 743 (149 cases) individuals responded to the follow-up questionnaires in Östersund and Skellefteå respectively. Outbreak cases were more likely to report diarrhea (Östersund OR: 3.3, CI: 2.0-5.3. Skellefteå OR: 3.6, CI: 2.0-6.6), watery diarrhea (Östersund OR: 3.4, CI: 1.9-6.3. Skellefteå OR: 2.8, CI: 1.5-5.1) abdominal pain (Östersund OR: 2.1, CI: 1.4-3.3, Skellefteå OR: 2.7, CI: 1.5-4.6) and joint pain (Östersund OR: 2.0, CI: 1.2-3.3, Skellefteå OR: 2.0, CI: 1.1-3.6) at follow-up compared to non-cases.

    Conclusions

    Our findings suggest that gastrointestinal- and joint symptoms can persist several months after the initial infection with Cryptosporidium and should be regarded as a potential cause of unexplained symptoms in people who have suffered from the infection.

  • Microglial Activation in Immunologically Induced Fatigue
  • Abstract:   The clinical symptoms of chronic fatigue syndrome (CFS) have been shown to include disorders in the neuroendocrine, autonomic, and immune systems. On the other hand, it has been demonstrated that cytokines produced in the brain play significant roles in neural-immune interactions through their various central actions, such as activation of the hypothalamo-pituitary axis. We have recently developed an animal for fatigue induced by intraperitoneal (i.p.) injection of synthetic double-stranded RNAs, polyriboinosinic: polyribocytidylic acid (poly I:C, 3 mg/kg), in rats, and shown a decrease in the daily amounts of spontaneous running wheel activity to about 60% of preinjection level for more than 1 week. Simultaneously, mRNA for Interleukin-1β (IL-1β) increased for 1 day following poly I:C injection in the same hypothalamic nuclei. It is thus possible that brain cytokines may play some roles in the central mechanisms of fatigue. In this review article, we showed a role of microglia, one of the major cytokine-producing cells in the central nervous system, in the onset of fatigue using immunologically induced fatigue model rats. Microglia were morphologically activated in the medial preoptic area (MPO) and periventricular hypothalamic nucleus (Pe) 24–48 hrs after the injection of poly I:C. Pretreatment with minocycline for the consecutive 3 days (40 mg/kg/day), the poly I:C-induced decrease in the running wheel activity recovered to the base line levels, and the activation of microglia was suppressed. Following poly I:C injection, the expression of IL-1β was markedly increased in microglia in the MPO and Pe, since the IL-1β-positive cells were double-labeled with an antibody for the microglia marker, Iba-1. Furthermore, the poly I:C-induced increase in the expression of IL-1β was also prevented by pretreatment with minocycline. These findings, taken together, suggest that the activation of microglia, which is accompanied by the enhanced expression of IL-1β, is involved in the onset of the immunologically induced fatigue.

  • The BPND values of 11C-(R)-PK11195 were low. This result is highly dependent on there being no differences in the reference region. 11C-(R)-PK11195 is known to offer a poorer signal-to-noise ratio than the second-generation radioligands for TSPO such as 11C-PBR28 (37). Therefore, we are currently performing the next-phase international collaboration study using 11C-PBR28 with arterial input function to evaluate neuroinflammation of CFS/ME patients in relation to other neurotransmitter  dysfunctions. Furthermore, we hope that more specific radioligands for TSPO or glial cells, such as 11C-(S)-ketoprofen-methyl ester, which is a good radiotracer for cyclooxygenase-1 imaging in brain microglia activation (38), will provide more information on neuroinflammation in CFS patients

  • As Ioannidis concluded more recently, “many published research findings are false or exaggerated, and an estimated 85 percent of research resources are wasted.”2
  • Psychologists have shown that “most of our reasoning is in fact rationalization,” he says. In other words, we have already made the decision about what to do or to think, and our “explanation” of our reasoning is really a justification for doing what we wanted to do—or to believe—anyway. Science is of course meant to be more objective and skeptical than everyday thought—but how much is it, really?
  • Given that science has uncovered a dizzying variety of cognitive biases, the relative neglect of their consequences within science itself is peculiar.

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  • The HLA locus is the strongest risk factor for anti-citrullinated protein antibody (ACPA)+ rheumatoid arthritis (RA)
  • Here we identify (citrullinated) vinculin, present in the joints of ACPA+ RA patients, as an autoantigen targeted by ACPA and CD4+ T cells.
  • These T cells recognize an epitope with the core sequence DERAA, which is also found in many microbes and in protective HLA-DRB1*13 molecules, presented by predisposing HLA-DQ molecules. Moreover, these T cells crossreact with vinculin-derived and microbial-derived DERAA epitopes.

2 more annotations...

  • Most people with rheumatoid arthritis have special antibodies known as anti-citrullinated protein antibodies (ACPA). Citrullination is a normal chemical modification of a protein, but it seems in the case of rheumatoid arthritis this modification singles it out for attack.
  • researchers wanted to find out what the ACPAs were targeting in the joints, to help them understand how to come up with treatments for rheumatoid arthritis.
  • The researchers found that a citrullinated form of the protein vinculin was a target for ACPAs. It was also a target for the immune system cells – called T cells – involved in the self-attack.

    The ACPAs and T cells appeared to recognise part of the vinculin protein that was also present in common bacteria, as well as in another protein that occurs naturally in some people, giving them some protection against rheumatoid arthritis. When this "protective" protein was absent, T cells targeted the part of vinculin found earlier. 

1 more annotation...

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