A possible role for mitochondrial-derived peptides humanin & MOTS-c in patients with Q fever & CFS

Posted on 06/04/2019 by wames

A possible role for mitochondrial-derived peptides humanin and MOTS-c in patients with Q fever fatigue syndrome and chronic fatigue syndrome, by Ruud PH Raijmakers, Anne F M Jansen, Stephan P Keijmel, Rob ter Horst, Megan E Roerink, Boris Novakovic, Leo AB Joosten, Jos W M van der Meer, Mihai G Netea and Chantal P Bleeker-Roversen, in Journal of Translational Medicine 2019 17:157 [https://doi.org/10.1186/s12967-019-1906-3]

 

Research abstract:

Background:

Q fever fatigue syndrome (QFS) is a well-documented state of prolonged fatigue following around 20% of acute Q fever infections.

General schema showing the relationships of the genome, transcriptome, proteome, and metabolome (lipidome).

It has been hypothesized that low grade inflammation plays a role in its aetiology. In this study, we aimed to identify transcriptome profiles that could aid to better understand the pathophysiology of QFS.

Methods:

RNA of monocytes was collected from QFS patients (n = 10), chronic fatigue syndrome patients (CFS, n = 10), Q fever seropositive controls (n = 10), and healthy controls (n = 10) who were age- (± 5 years) and sex-matched. Transcriptome analysis was performed using RNA sequencing.

Results:

Mitochondrial-derived peptide (MDP)-coding genes MT-RNR2 (humanin) and MT-RNR1 (MOTS-c) were differentially expressed when comparing QFS (− 4.8 log2-fold-change P = 2.19 × 10−9 and − 4.9 log2-fold-change P = 4.69 × 10−8), CFS (− 5.2 log2-fold-change, P =3.49 × 10−11 − 4.4 log2-fold-change, P = 2.71 × 10−9), and Q fever seropositive control (− 3.7 log2-fold-change P = 1.78 × 10−6 and − 3.2 log2-fold-change P = 1.12 × 10−5) groups with healthy controls, resulting in a decreased median production of humanin in QFS patients (371 pg/mL; Interquartile range, IQR, 325–384), CFS patients (364 pg/mL; IQR 316–387), and asymptomatic Q fever seropositive controls (354 pg/mL; 292–393).

Conclusions:

Expression of MDP-coding genes MT-RNR1 (MOTS-c) and MT-RNR2 (humanin) is decreased in CFS, QFS, and, to a lesser extent, in Q fever seropositive controls, resulting in a decreased production of humanin. These novel peptides might indeed be important in the pathophysiology of both QFS and CFS.

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Autonomic function in ME & CFS: comparing self-report & objective measures

Posted on 06/03/2019 by wames

Autonomic dysfunction in myalgic encephalomyelitis and chronic fatigue syndrome: comparing self-report and objective measures, by Jane Kemp, Madison Sunnquist, Leonard A Jason, Julia L Newton in Clin Auton Res [Preprint 21 May 2019]

 

Letter extracts:

Myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) have debilitating impacts on affected individuals. Core symptoms include post-exertional malaise, neurocognitive challenges, and sleep dysfunction [1]. Additionally, a significant minority of patients experience autonomic symptoms, including orthostatic intolerance, gastrointestinal disturbances, and circulation issues [2].

Several case definitions for ME and CFS require the presence of autonomic dysfunction for diagnosis [2], while other researchers have proposed an ‘autonomic dysfunction’ subtype of ME and CFS [3]. Identifying the appropriate measures of autonomic symptomatology for individuals with ME and CFS will further contribute to understanding the role of the autonomic system in this illness.

Heart rate variability (HRV), a measure of the variation in time between heart beats, has been utilized as an objective measurement of autonomic functioning in ME and CFS research, and some researchers have suggested that HRV could be utilized as a “potential bedside diagnostic tool” for ME and CFS [4]. HRV can be divided into two major components, the low-frequency (LF) component, indicative of sympathetic dominance, and the high-frequency (HF) component, indicative of parasympathetic dominance. In
addition, the LF to HF ratio is considered to be an indicator of sympatho-vagal balance [5].

As objective measures can be costly and time-intensive, some researchers utilize self-report measures of autonomic symptoms. Previous research has compared results from the self-report Composite Autonomic Symptom Scale (COMPASS) [6] and HRV and found a significant negative correlation between LF-HRV and COMPASS scores [7].

The aim of the study reported here was to extend upon this body of literature by examining the association between HRV and autonomic items from another self-report measure, the DePaul Symptom Questionnaire (DSQ) [8].

The study protocol was approved by the ethical review board (ethical approval number: 12/NE/0146) of the Royal Victoria Infirmary (Newcastle upon Tyne, UK). Informed consent from participants was obtained by staff trained in Good Clinical Practice guidelines. All participants (n = 141) met the Fukuda et al. (1994) criteria for CFS [9]. After completing the DSQ, participants underwent a battery of autonomic tests (described below) using the Task Force® Monitor program version 2.2 (CNSystems Medizintechnik
GmbH, Graz, Austria).

The mean age of the participant cohort was 45.9 (standard deviation 13.6) years; 80.9% were female, and 98.6% were Caucasian. While over half of the participants (51.5%) held Bachelor’s or graduate degrees, only 35.8% were working at the time of the study. Additionally, 35.0% of the sample reported being on disability (the remainder of the sample comprised students, homemakers, and individuals who were unemployed or retired).

The DSQ is a freely-available, reliable diagnostic measure of both core and subtyped symptoms of ME/CFS [3, 8] and includes seven items related to autonomic symptoms:
bladder problems; irritable bowel problems; nausea; feeling unsteady on feet (like you might fall); shortness of breath or trouble catching your breath; dizziness or fainting; and
irregular heartbeats. Participants rated the frequency and severity of each symptom for the preceding 6 months. Frequency ratings ranged from 0 (symptom not present) to 4 (all
of the time). Severity ratings ranged from 0 (symptom not present) to 4 (very severe). A composite score was calculated for each symptom by multiplying the frequency and severity ratings by 25 (to form a 100-point scale) and averaging the symptom’s frequency and severity scores….

… The results of this analysis provide some support for consistency between participants’ reports of autonomic symptoms on the DSQ and objective measures of autonomic symptomatology. As the self-report items in the current study referred to the preceding 6 months of an individual’s symptoms, while the objective tests measured symptoms at the exact moment of the study, high correlation coefficients were not expected. The results further support previous research [7] indicating that individuals are accurate reporters of autonomic symptoms.

This study had several limitations: its sample was small, demographically homogenous, and referral based; therefore, additional research is required to verify the study’s findings.

Despite these limitations, the results provide initial evidence of the construct validity of the DSQ’s autonomic items and indicate that individuals with ME and CFS are accurate reporters of autonomic symptoms.

In addition to providing evidence for the construct validity of DSQ items, this finding of accurate self-reporting of autonomic symptoms by individuals is significant in that previous studies have found that individuals with ME and CFS often face de-legitimization by physicians and loved ones [10]. Validating the individual’s self-reported symptoms using objective data, such as HRV, may help in reducing stigma towards individuals with ME and CFS.

Read full letter

 

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Genetic predisposition for immune system, hormone, & metabolic dysfunction in ME/CFS

Posted on 05/31/2019 by wames

Genetic predisposition for immune system, hormone, and metabolic dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: a pilot study, by Melanie Perez,  Rajeev Jaundoo,  Kelly Hilton,  Ana Del Alamo,  Kristina Gemayel,  Nancy G. Klimas,  Travis J A Craddock and  Lubov Nathanson in Front. Pediatr., 24 May 2019 [https://doi.org/10.3389/fped.2019.00206]

 

Introduction:

SNP model by David Eccles, Wiki commons

Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS) is a multifactorial illness of unknown etiology with considerable social and economic impact. To investigate a putative genetic predisposition to ME/CFS we conducted genome-wide single-nucleotide polymorphism (SNP) analysis to identify possible variants.

Methods:
383 ME/CFS participants underwent DNA testing using the commercial company 23andMe. The deidentified genetic data was then filtered to include only non-synonymous and nonsense SNPs from exons and microRNAs, and SNPs close to splice sites. The frequencies of each SNP were calculated within our cohort and compared to frequencies from the Kaviar reference database. Functional annotation of pathway sets containing SNP genes with high frequency in ME/CFS was performed using over-representation analysis via ConsensusPathDB. Furthermore, these SNPs were also scored using the Combined Annotation Dependent Depletion (CADD) algorithm to gauge their deleteriousness.

Results:
5693 SNPs were found to have at least 10% frequency in at least one cohort (ME/CFS or reference) and at least two-fold absolute difference for ME/CFS. Functional analysis identified the majority of SNPs as related to immune system, hormone, metabolic, and extracellular matrix organization. CADD scoring identified 517 SNPs in these pathways that are among the 10% most deleteriousness substitutions to the human genome.

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Searching for serum antibodies to neuronal proteins in patients with ME/CFS

Posted on 05/29/2019 by wames

Searching for serum antibodies to neuronal proteins in patients with Myalgic Encephalopathy/Chronic Fatigue Syndrome, by Maria Pia Giannoccaro, Judith Cossins, Kari Sorland, Oystein Fluge, Angela Vincent in Clinical Therapeutics Vol 41, Issue 5, May 2019, Pages 836-847

 

Research abstract:

Purpose:
A role for the immune system in causing myalgic encephalopathy/chronic fatigue syndrome (ME/CFS) is long suspected, but few studies have looked for specific autoantibodies that might contribute to the symptoms. Our aim was to look for evidence of antibodies to neuronal proteins in patients with ME/CSF.

Methods:
Sera samples from 50 patients and 50 healthy individuals were sent coded to the Neuroimmunology Laboratory in Oxford. Screening for antibody binding to neuronal tissue was performed on brain tissue and neuronal cultures. Specific serum antibodies were assessed by antigen-specific cell-based assays and radioimmunoassays. After antibody testing, the associations between seropositive status and clinical data were
investigated.

Findings:
Overall, 8 patients and 11 participants were found to have some serum immunoreactivity toward neuronal or neuromuscular junction proteins, but only 1 patient and 2 participants had specific serum antibodies. Nevertheless, seropositive status in patients with ME was associated with shorter duration since onset and a more severe disease.

Implications:
The results indicate no overall increased frequency of antibodies to neuronal proteins in ME/CSF and no evidence of a specific antibody that might be causative or contribute to clinical features in patients. However, the association of seropositive status with shorter duration of disease and more severe symptoms suggests a possible role of antibodies
at onset in some patients and should be the focus of future studies.

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Biotransformation profiles from a cohort of chronic fatigue women in response to a hepatic detoxification challenge

Posted on 05/28/2019 by wames

Biotransformation profiles from a cohort of chronic fatigue women in response to a hepatic detoxification challenge, by Elardus Erasmus, Francois E Steffens, Mari van Reenen, B Chris Vorster, Carolus J Reinecke in  PLoS ONE 14 (5) May 2019 [https://doi.org/10.1371/journal.pone.0216298]

 

Research abstract:

Chronic fatigue, in its various manifestations, frequently co-occur with pain, sleep disturbances and depression and is a non-communicable condition which is rapidly becoming endemic worldwide. However, it is handicapped by a lack of objective definitions and diagnostic measures.

This has prompted the World Health Organization to develop an international instrument whose intended purpose is to improve quality of life (QOL), with energy and fatigue as one domain of focus. To complement this objective, the interface between detoxification, the exposome, and xenobiotic-sensing by nuclear receptors that mediate induction of biotransformation-linked genes, is stimulating renewed attention to a rational development of strategies to identify the metabolic profiles in complex multifactorial conditions like fatigue.

Here we present results from a seven-year study of a cohort of 576 female patients suffering from low to high levels of chronic fatigue, in which phase I and phase II biotransformation was assessed. The biotransformation profiles used were based on hepatic detoxification challenge tests through oral caffeine, acetaminophen and acetylsalicylic acid ingestion coupled with oxidative stress analyses.

The interventions indicated normal phase I but increased phase II glucuronidation and glycination conjugation. Complementarity was indicated between a fatigue scale, medical symptoms and associated energy-related parameters by application of Chi-square Automatic Interaction Detector (CHAID) analysis.

The presented study provides a cluster of data from which we propose that multidisciplinary inputs from the combination of a fatigue scale, medical symptoms and biotransformation profiles provide the rationale for the development of a comprehensive laboratory instrument for improved diagnostics and personalized interventions in patients with chronic fatigue with a view to improving their QOL.

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Health services for ME in Wales – a 20 year WAMES update

Posted on 05/27/2019 by wames

Health services for ME in Wales – a WAMES update

 

WAMES in Wales

It is now 20 years since the Welsh Government (WG) was established. At that time NHS Wales became independent and WAMES began campaigning in Wales for improvements to health services.  Over the years we have talked to numerous Health Ministers, civil servants, AMs, Health Board executives and NHS staff. We have taken part in focus groups, stakeholder groups, working groups and scoping exercises. We have run surveys of patient experience and campaigns to raise awareness in government and the NHS.

That is what WAMES has done, largely behind the scenes, to try to improve healthcare for people with ME. How did the Welsh Government and NHS Wales respond?

Welsh Government & ME

  • Since 1999 many AMs over the years have joined us in asking questions about the lack of awareness and services, leading to one of the largest postbags the government have received on a single medical condition.
  • In 2004 a series of Masterclasses were planned around the country.  The interest shown by GPs was so low, only one took place.
  • In 2009 a Task & Finish Group was set up to explore whether a clinical pathway was needed and decided it was.
  • WAMES joined a pathway working group to produce a Map of Medicine pathway for Wales. This was unfortunately based on the NICE guidelines and shortly afterwards the WG withdrew from the Map of Medicine database (based in England).
  • The Health Minister wrote to Health Boards urging them to implement the pathway and improve services. None appeared to do so.
  • In 2013 a second Task & Finish Group was set up with representation from the WG, NHS and patients. A report was published in 2014 outlining steps each Health Board should take to improve services. Few Health Boards have implemented more than one or two of the steps!
  • In 2014 An All Wales Implementation group (AWiG) was set up with reps from WG, the NHS and patients to oversee the implementation of the report.

Has healthcare for ME improved?

It is clear that there is an increase in the number of GPs who have heard of ME, though many still wish to call it CFS and focus on fatigue. There is still a belief that ME is difficult to diagnose and nothing can be done to help. Some still believe it is a psychological condition or that it simply doesn’t exist at all. Many patients tell us they still cannot find someone within Wales to give them an informed diagnosis or to refer them to support services.

WAMES and local groups in Wales still get too many helpline calls from people who are enduring appalling treatment from untrained and prejudiced health care professionals.

The existing services for pain and fatigue continue to offer rehabilitation services based on GET and CBT, though few people with ME are interested. Reports of relapse caused by this approach continue to reach us from people with ME who have undergone the course in NW Wales. Suicides and attempted suicides have increased in number.

Why is progress so slow?

There are many possible reasons contributing to this:

  • Continuing reorganisation and financial difficulties in Health Boards
  • Constantly changing personnel in HBs and Welsh Government
  • Lack of a clinical champion for Wales
  • No funding from the Welsh Government
  • Insistence that answers should come from within Wales, when no-one has sufficient experience or knowledge of ME
  • No obligation for HBs to implement improvements
  • Overworked doctors, who are waiting for a diagnostic test and treatments to materialise before becoming involved with this patient group
  • An unwillingness to look beyond NICE and listen to patients and explore the biomedical research
  • A feeling that ME is controversial due to the continuing activities of a biopsychosocial community that view ME as perpetuated by muscle deconditioning and faulty illness beliefs – in contradiction to the latest research.

WAMES believes that a key stumbling block is the shortage of informed GPs willing and able to diagnose.   Should diagnosis improve there would be statistics of the numbers and location of patients and it would be harder for HBs to ignore ME. The evidence for the need for services for this patient group would then be clear.

What next?

The All Wales Implementation Group (AWIG) has a new government policy lead.

Current work priorities are:

  • Inclusion of ME/CFS in IMTPs (Health Boards 3 year work plans)
  • Redesigning a clinical pathway
  • Developing patient information sheets
    Discussing the development of GP training resources with Health Education and Improvement Wales (HEIW)

WAMES will:

  • continue to represent people with ME on AWiG
  • continue to explore awareness raising possibilities with the RCGP;
  • work with the NHS in devising an ME self-management programme
  • represent Welsh people with ME on the NICE guideline review
  • take every opportunity to raise awareness of neurological ME in NHS Wales

Get in touch if you would like to support WAMES continue its work to improve services for people with ME in Wales  jan@wames.org.uk

 

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WAMES AGM 15th June 2019

Posted on 05/24/2019 by wames

Annual General Meeting of WAMES

 

The annual business meeting of the Welsh Association of ME & CFS Support will be held by Skype to review past events and plan future activities.

Please contact jan@wames.org.uk if you have anything to report to WAMES, or topics you wish us to discuss or more importantly, if you would like to join the team or volunteer in a any way.  Let Jan know if you wish to attend.

When:

Saturday 15th June 2019   at  10.30am

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ME, CFS & chronic fatigue: three distinct entities requiring complete different approaches

Posted on 05/23/2019 by wames

Myalgic Encephalomyelitis, Chronic Fatigue Syndrome, and Chronic Fatigue: three distinct entities requiring complete different approaches, by Frank NM Twisk in Current Rheumatology Reports June 2019, 21:27 [https://doi.org/10.1007/s11926-019-0823-z]

 

Letter abstract:

Purpose of Review:
A recent review implicates that myalgic encephalomyelitis (ME), chronic fatigue syndrome (CFS), and chronic fatigue are part of the “fatigue spectrum” and recommends “longitudinal studies integrating biopsychosocial approaches to inform early management and targeted rehabilitation strategies.”

Recent Findings:
ME is a neuromuscular disease distinguished by muscle fatigability (prolonged muscle weakness after minor exertion) and specific signs of neurological dysfunction. ME is not equivalent to CFS, as proposed by the authors. CFS is defined as unexplained chronic fatigue accompanied by at least four out of a list of eight specific symptoms. CFS is a distinct clinical entity and not merely a severe variant of CF, as suggested.

Proof that CF, CFS, and ME are part of a “fatigue continuum” and that CF can convert to CFS at a later stage is lacking. Biopsychosocial approaches for early management and rehabilitation of CF, as promoted by the authors, are at odds with the current understandings of ME, CFS, and CF. The (bio)psychosocial explanatory models for ME and CFS have proven to be invalid, and the associated interventions, cognitive behavioral therapy and graded exercise therapy, have shown to be ineffective and even potentially harmful.

Summary:
ME, CFS, and CF are three very distinct clinical entities. Interventions justified by (bio)psychosocial models appear to be unsuccessful and potentially noxious. To develop effective treatments, it is crucial to make a clear distinction between ME, CFS, and CF and to leave the (bio)psychosocial explanations and therapies behind us.

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Increased risk of CFS following psoriasis in Taiwan

Posted on 05/22/2019 by wames

Increased risk of chronic fatigue syndrome following psoriasis: a nationwide population-based cohort study, by Shin-Yi Tsai, Hsuan-Ju Chen, Chi Chen, Chon-Fu Lio, Chien-Feng Kuo, Kam-Hang Leong, Yu-Ting Tina Wang, Tse-Yen Yang, Ching-Hui You and Wei-Sheng Wang in Journal of Translational Medicine 2019 May 17:154
[https://doi.org/10.1186/s12967-019-1888-1]

 

Research abstract:

Background:
The onset of chronic fatigue syndrome (CFS) has been shown to be associated with several immunological conditions such as infections or atopy. The aim of this study was to clarify the risk of chronic fatigue syndrome following the diagnosis of psoriasis, an immune-related dermatological disease, by analyzing the National Health Insurance Research Database of Taiwan.

Method:
2616 patients aged 20 years or older with newly diagnosed psoriasis during 2004–2008 and 10,464 participants without psoriasis were identified. Both groups were followed up until the diagnoses of CFS [Fukuda] were made at the end of 2011.

Results:
The relationship between psoriasis and the subsequent risk of CFS was estimated through Cox proportional hazards regression analysis, with the incidence density rates being 2.27 and 3.58 per 1000 person-years among the non-psoriasis and psoriasis populations, respectively (adjusted hazard ratio [HR] = 1.48, with 95% confidence interval [CI] 1.07–2.06). In the stratified analysis, the psoriasis group were consistently associated with a higher risk of CFS in male sex (HR = 2.05, 95% CI 1.31–3.20) and age group of ≥ 60 years old (HR = 2.32, 95% CI 1.33–4.06). In addition, we discovered that the significantly increased risk of CFS among psoriasis patients is attenuated after they receive phototherapy and/or immunomodulatory drugs.

Conclusions:
The data from this population-based retrospective cohort study revealed that psoriasis is associated with an elevated risk of subsequent CFS, which is differentiated by sex and age.

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Validation of impaired TRPM3 ion channel activity in natural killer cells from CFS/ME

Posted on 05/21/2019 by wames

Validation of impaired Transient Receptor Potential Melastatin 3 ion channel activity in natural killer cells from Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis patients, by H Cabanas, K Muraki, C Balinas, N Eaton-Fitch, D Staines, S Marshall-Gradisnik in Mol Med. 2019 Apr 23;25(1):14. doi: 10.1186/s10020-019-0083-4

 

Research abstract:

BACKGROUND:

Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis (CFS/ME) is a complex multifactorial disorder of unknown cause having multi-system manifestations. Although the aetiology of CFS/ME remains elusive, immunological dysfunction and more particularly reduced cytotoxic activity in natural killer (NK) cells is the most consistent laboratory finding.

The Transient Receptor Potential (TRP) superfamily of cation channels play a pivotal role in the pathophysiology of immune diseases and are therefore potential therapeutic targets. We have previously identified single nucleotide polymorphisms in TRP genes in peripheral NK cells from CFS/ME patients. We have also described biochemical pathway changes and calcium signaling perturbations in NK cells from CFS/ME patients. Notably, we have previously reported a decrease of TRP cation channel subfamily melastatin member 3 (TRPM3) function in NK cells isolated from CFS/ME patients compared with healthy controls after modulation with pregnenolone sulfate and ononetin using a patch-clamp technique.

In the present study, we aim to confirm the previous results describing an impaired TRPM3 activity in a new cohort of CFS/ME patients using a whole cell patch-clamp technique after modulation with reversible TRPM3 agonists, pregnenolone sulfate and nifedipine, and an effective TRPM3 antagonist, ononetin. Indeed, no formal research has commented on using pregnenolone sulfate or nifedipine to treat CFS/ME patients while there is evidence that clinicians prescribe calcium channel blockers to improve different symptoms.

METHODS:

Whole-cell patch-clamp technique was used to measure TRPM3 activity in isolated NK cells from twelve age- and sex-matched healthy controls and CFS/ME patients, after activation with pregnenolone sulfate and nifedipine and inhibition with ononetin.

RESULTS:

We confirmed a significant reduction in amplitude of TRPM3 currents after pregnenolone sulfate stimulation in isolated NK cells from another cohort of CFS/ME patients compared with healthy controls.

The pregnenolone sulfate-evoked ionic currents through TRPM3 channels were again significantly modulated by ononetin in isolated NK cells from healthy controls compared with CFS/ME patients. In addition, we used nifedipine, another reversible TRPM3 agonist to support the previous findings and found similar results confirming a significant loss of the TRPM3 channel activity in CFS/ME patients.

CONCLUSIONS:

Impaired TRPM3 activity was validated in NK cells isolated from CFS/ME patients using different pharmacological tools and whole-cell patch-clamp technique as the gold standard for ion channel research. This investigation further helps to establish TRPM3 channels as a prognostic marker and/ or a potential therapeutic target for CFS/ME.

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