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Invest in ME conference –
London - May 2011
Rosamund Vallings
of the Associated New Zealand ME Society
I was
privileged to attend the Invest in ME
conference on 20th May in
London. The day before there were several
events which helped set the scene leading up
to the conference. In the morning I was
invited to join a delegation to parliament
to meet with several MPs and the Countess of
Mar, from the House of Lords, who has been
very supportive of ME/CFS. The meeting was
ably chaired by Annette Brooke, MP, Mid
Dorset and North Poole, and several MPs
attended to hear our concerns. The
delegation was well represented
internationally, and we all had an
opportunity to speak.
In the
afternoon, top researchers who were
presenting at the conference, and a few
others who were attending, were gathered
together to discuss their current research
and to look at opportunities for ongoing
collaboration. This was a “closed” meeting,
but I was lucky to be able to go along as an
observer. Much of the research discussed
was embargoed for any mention here, as is
still awaiting publication. However we were
fortunate to have a fascinating 30 minute
talk from Professor Burnstock on his
theories and research on purine signalling.
This talk was repeated the following day at
the conference (see below). I was glad to
be able to hear it twice as it was complex
biochemically. This could have much
relevance in ME/CFS. All the researchers
were keen to have ongoing contact with a
view to collaboration.
Later
that day there were evening presentations,
the first by Professor Ian Gibson – a
long-term stalwart of ME/CFS research and it
was good to hear about the development of a
research and clinical centre associated with
the University of Norwich and the hospital
there. The second presentation was by
Hillary Johnson, the author of Osler’s Web,
and she outlined a history of ME/CFS from a
political perspective. Both talks were
peppered with humour and emotion, and
provided us with a good lead-up to the hard
science of the next day.
The main
conference opened on Friday 20th
May, and after an introduction by Professor
Malcolm Hooper, the Key Note speaker was
Annette Whittemore, President of the
Whittemore-Peterson Institute, Nevada, .
Their Institute for Neuro-immune diseases
is now running, and encompasses
administration, research and clinical work.
Physicians and researchers are working
there, and a systems biological approach is
taken for diagnosis and treatment of ME/CFS,
the aim being to translate science into
patient care. She explained how this illness
presents many challenges with serious and
debilitating symptoms. She went on to
compare this illness with MS, from the point
of view of funding and then illness and
biomedical differences. As well as
differences there are many similarities. MS
is usually diagnosed as a result of brain
scanning. She asked the questions “Is ME an
auto-immune condition or an infectious
illness?” many pathogens have been
implicated including viruses, bacteria,
fungi and parasites. She then compared
ME/CFS to HIV infection, and again outlined
many similarities. The main difference here
is that HIV is sexually transmitted and
there is no evidence yet to suggest sexual
transmission in ME/CFS.
When the
WPI first started out in research into
ME/CFS they initially looked at herpes
viruses, and then finally looked at
retroviruses using multiple detection
methods. Issues of contamination have
arisen, but this is unlikely in view of the
fact that XMRV is a distinctly human virus.
It has been implicated in cancers. Lab
protocol to avoid contamination is
stringent.
She
feels there are now many opportunities for
research, and is hopeful that the systems
biological approach will give answers.
Treatment plans are being addressed to
support the immune system, to kill organisms
and to correct biochemical and hormonal
abnormalities. She stressed the importance
of medical education, development of
potential drugs and the setting up of other
centres. She feels strongly that governments
should fund clinical treatment centres, and
encouraged everyone to become an advocate.
The
conference then focussed on clinical and
research papers:
David
Bell (Lyndonville NY,USA)
presented his work on the 25 year follow-up
of the young people from the initial illness
which triggered his research. He described
this initial outbreak in 1985 in a small
rural community just south of Toronto. 210
people remained ill following a flu-like
illness. Many more had the illness, but had
recovered by 6 months. Those remaining ill
were finally diagnosed as suffering from
ME/CFS. 60 were children and adolescents.
The 13 year follow-up was written up in the
Journal of Paediatrics. 80% described
themselves as doing well. Half of these
still had symptoms but leading a reasonably
normal life, the other half seemed OK. 20%
had ongoing illness and were “disabled”. He
then asked “How should recovery be defined?”
– “Is it absence of symptoms or
adaptation?” If the answer is adaptation,
this leads to confusion and a false
perception of health. Factors included here
would be: patient looks OK, tests are
normal, specialists come up with no
diagnosis and there is a lack of evolution
into an illness such as MS. This confusion
is damaging for adolescents.
The
current study included a follow up of 28
people, and a wide range of assessment tools
was used. 3 had developed malignancies
(thyroid cancer, cervical cancer and
leukaemia) and were excluded. The remainder
(25) were represented by 3 groups. 2/25 (8%)
were well. 18/25 (72%) had remitting
illness – they considered themselves
alright, but scores indicated they were not
well. The third group - 5/25 (20%) had
persistent ME/CFS. They considered
themselves disabled with severe symptoms and
reduced activity. These people were on
disability pensions, but ME/CFS was not used
as the diagnosis to be eligible, and the
illness was often called other names to
ensure the benefit.
He
pointed out how people do learn to adapt to
this illness. Many seem to recover but then
slide down again. The worst symptoms seem to
be associated with sleep and pain. He
described his disability scale from 0-100
with 100 being entirely well. Many of these
patients scored around 30. He felt one of
the most important questions for the
clinician to ask was the number of hours of
upright activity attainable each day. In
his current study, controls scored 15 hours,
the persisting severe group 1-5 hours and
the remitting group 13 hours.
In
summary he concluded that at follow up 72%
had mild to moderate illness, although
considered themselves OK. There was health
identity confusion, by remembering self
being much worse, and now considering self
“well”. Time will tell the long term
outcome. He felt strongly that he was
looking at the natural history and course of
the illness rather than any medication or
vitamins promoting recovery.
Andreas Kogelnik
(Stanford University, USA) described himself
as director of the Open Medicine Institute
(OMI), a community-based collaborative
research unit. He has a background in
infectious diseases and has worked in ME/CFS
for 7 years. His unit uses an interactive
approach between biotechnology, informatics,
social networking and bio sampling all
focussing on clinical medicine and research.
He feels we need to redefine diseases such
as ME/CFS using research and network tools.
He gave an excellent overview of medicine
leading up to the whole genome sequencing.
He then described ME/CFS as a syndrome with
many symptoms overlapping with other
diseases, immature definition and scarcity
of biomarkers. Treatments are not
standardised and outcome data is limited. He
feels medicine is at a crossroads with
“guidelines based medicine” not a
particularly good system, but a more
personalised medicine approach would cost
more. He discussed the interaction between
genomics, biotechnology, informatics,
clinical medicine guidelines and
individualised clinical medicine. He showed
how with the use of ROC curves and array
with multiple levels, groups of patients can
be followed over time.
He then
went on to discuss the nosology of disease.
This is a very old classification system and
has not changed much. This system does not
fit with genes, biomarkers etc. We can now
define diseases from a molecular point of
view. A focus on differential diagnoses can
help, but may lead to many tests. Rather
than doing many tests situational genomic
profiling maybe more useful. Unique host
expression signatures can be used to define
disease. Signatures may be predictive of
susceptibility, and may indicate a
predictive response to therapy.
At the
OMI clinicians are provided with the
opportunity to participate, there is an
integrated informatics registry and a
biobank. Collaboration is paramount.
Clinicians and patients can participate at
any level. For the clinician this all means
better knowledge, electronic practice,
involvement in clinical trials and strength
in numbers. For the patients there may be
answers to vexing questions, opportunity to
participate in research and listening ears
for concerns. For the researcher there is
better and more data, access to resources
etc. They want to do large scale trials and
focus on chronic and syndromic diseases. He
emphasised the importance of the
continuation of the work as started by
Jonathan Kerr.
John
Chia (Torrance CA,USA)
discussed his clinical and research
experience of enteroviral involvement in
ME/CFS. He started his talk with a case
presentation – this patient had had ongoing
bowel problems and associated severe
ME/CFS. Enteroviral RNA was detected in the
biopsies from the stomach 2 years later.
The patient was treated with Chinese herbs
and regained 70% normal health.
There
are 7 serotypes and 100 genotypes of human
enteroviruses (HEV), many systems can be
involved leading to many symptoms. In
particular there maybe leucopenia associated
with fevers. Many flu-like illnesses are
implicated in the lead up. In one study 38%
of 131 sick ME/CFS patients tested were
positive twice for HEV compared to only 4%
of controls. The more severe the symptoms,
the greater was the positivity. In one
patient who had died, HEV was found in the
heart, muscles and brain. Positive biopsies
are most likely to be obtained from the
throat or stomach, but throat biopsies are
very painful. Clinically the commonest
symptoms are epigastric pain and pain in
either iliac fossa. Of the patients who were
positive, 84% were seriously disabled.
The
diagnostic approach should start with very
careful history taking, which would include
information about the infection at onset,
past history of previous infections
(particularly URTIs and asthma),
vaccinations, steroid use, contaminated
water exposure, ticks etc. A review of
medical records and lab tests is needed.
There are usually few physical signs,
although throat may be inflamed and there
can be abdominal tenderness. Tests for HEV
should include neutralising antibody and
immunoperoxidase staining on biopsies. The
finding of dsRNA in the stomach tissue
supports the mechanism of viral
persistence. Symptoms should be correlated
with results.
Treatment may include antivirals such as
pleconaril, acyclovir, ganciclovir and
cidofavir; and immune modulation such as use
of ampligen, IV immunoglobulin, interferon
and herbal immune boosters. He presented a
further study relating to the herbal
product, oxymatrine. 52% had a positive
response, and these were those with the
positive biopsies. There were some side
effects with increase of CFS-like symptoms
initially. The dose needs to be increased
very slowly. The herb is now refined and
marketed as Equilibrant, which is better
tolerated, although patients can still
experience an initial increase in symptoms.
Dose should be built up slowly over 2-4
weeks.
Professor Geoffrey Burnstock (University
College, London)
had originally discovered that ATP is a
transmitter in non-adrenergic,
non-cholinergic nerves, and the discovery
and definition of P2 purinergic receptors.
His work has had an enormous impact on the
understanding of pain mechanisms. He
discussed purinergic signalling and CNS
disorders, and is hopeful this could be
translated into some understanding of
mechanisms in ME/CFS. He described the
purine nucleotide ATP as an extracellular
signalling molecule, which is relevant in
pain and CNS inflammatory disorders. He gave
a historical overview of his early work
starting in the 1960s, when the
adenosine/isonine connection was identified.
They looked then at whether some nerve cells
make more than one transmitter, and found
that ATP was a co-transmitter in all nerves,
peripheral and central. It is a signalling
molecule. In 1982 two types of purinergic
receptors were identified : AD and ATP. In
1985, two subtypes of P2 purine receptors
and 4 subtypes of P1 purine receptors were
found to be involved in several diseases. In
1993, initial cloning of P2 receptors
identified P2X and P2Y. And then 7 subtypes
of P2X were shown to affect many systems.
P2X7 led to apoptic cells in the immune
system, pancreas, skin etc and is involved
in inflammation and cancer. P2Y has up to 14
subtypes and again is involved in many
systems.
Nearly
all the cells in the body are involved with
purinergics. It is possible that the P2X7
involved in the immune system may be
important in ME/CFS. It is now known that
many cells release ATP, not just damaged or
dying cells as previously thought. There
are 2 types of purinergic signalling : short
term e.g. neurotransmission and long term
such as associated with development,
proliferation, cell death etc. The brain
development is associated with purinergics,
and in particular the glial cells are
important. There is interest in purinergic
signalling in learning and CNS disorders. He
therefore feels this area is well worth
exploring in ME/CFS.
There is
also involvement in pain. ATP may initiate
the pain. In migraine, ATP pours out in the
hyperaemic stage. It is important therefore
to consider antagonists. A study in Japan
(Xiang et al) showed that antagonists may be
effective. There could also be some
relevance in Alzheimers disease, mood
disorders and epilepsy. Drugs are being
developed such as inhibitors of ATP, control
of expression of P2 receptors and
antagonists of P2Xs.
There is
now a Journal of Purinergic Signalling,
providing an opportunity to follow this
research.
James
Baraniuk (Washington DC, USA)
discussed the proteomics of ME/CFS. His
group had done tests on the spinal fluid.
They were particularly interested in those
with CNS dysfunction, which is a critical
component of ME/CFS and related syndromes.
These patients had symptoms of central
sensitisation including hyperalgesia and
allodynia, autonomic dysfunction, cognitive
dysfunction and severe headaches. Increased
spinal tap pressure had been found in the
CFS patients which correlates with the
intensity of headaches, sleep problems,
memory problems, fatigue and pain.
In the
spinal fluid they looked for diagnostic
biomarkers. Their aim was to. help with
understanding of pathophysiological
mechanisms, provide diagnostic biomarkers
for future testing and work on potential new
treatments. They had looked at as many
proteomes as possible in the cerebro-spinal
fluid (CSF). Methods of analysis were
outlined.
The
first study looked at 3 groups:
fibromyalgia, Gulf war illness (GWI) (most
had ME/CFS) and controls. 10 proteomes
different to controls were found. The sets
of proteomes identified correlated with
function. (e.g. vascular regulation, immune
and structural injury, structure and repair
etc). Baraniuk then discussed the Schutzer
study (psychiatric patients had been
excluded). They had compared CFS patients
with those who had had Lyme disease. 2630
proteins were identified in the CSF. 95-99%
of the proteomes were removed (the most
abundant) and 738 proteins were found in the
CFS patient samples alone. Some were shared
between CFS and Lyme patients. Proteomic
detection is very expensive ($500,000 per
single run). It was concluded that CSF
proteomes can distinguish between subtypes
of fatiguing illnesses.
Once a
single protein has been identified as a
biomarker, it can be compared with other
illnesses and controls to confirm that it is
unique. Further methods then need to be
developed for validation. Combined biomarker
proteins and peptides can form valid
biosignatures. Pathways become targets for
drug development. Unsequenced ion peaks can
be assessed for post-translational
modifications that may infer additional
disease mechanisms such as oxidation.
Future
directions include: defining of illness by
pathophysiological mechanisms,
multidisciplinary outcomes and studies,
randomised placebo controlled trials,
continuing prospective studies of
well-defined phenotypes and a full review of
the GWI cohort. They have hypothesised that
GWI illness may be related to a certain
genotype for an enzyme, carnosine
dipeptidase-1, which degrades an important
anti-oxidant, carnosine. Carnosine has
potential for symptom relief.
Simon
Carding (Norwich, UK)
presented an overview of the work being done
with Tom Wileman at the University of East
Anglia and Norwich Hospital. They are
particularly interested in the gut/brain
link. He gave an overview of the anatomy
and physiology of the gastrointestinal
tract. This 9 m long tube is the largest of
the organs of the immune system. It has the
second largest number of neurones and is the
major route for pathogens to enter the body.
It is exposed daily to many micro-organisms.
The immune system has to mount a response
being constantly vigilant, and has learnt
discrimination. There can be a breakdown in
tolerance, which then leads to disease. The
microbiotica are the normal resident
bacteria in the gut. There is an increase
from top to bottom of the gut, with most
being in the lower bowel. There are 10
times as many bacteria than cells in our
bodies and bacterial genes are 100-fold.
Genomics provides more accurate
identification of bacteria, Sequence
information transmits to the function of the
bacteria, and diet shapes the gut
communities. In humans there are 2 main
sequences in the gut, in animals many more.
In humans, 57 species are common to more
than 90% of individuals. 3 clusters of
organisms dominate worldwide, and 2 phyla
dominate. These are essential for gut
health. Among many functions they have
breakdown effects and produce vitamins and a
mixture of viruses too. The functions on
viromes may provide signatures of health and
disease. Microbiotica are essential for
health and wellbeing. Many actions include:
defence, source of vitamins, provision of
energy, epithelial barrier, promotion of
motility, local immunity and oral
tolerance.
If an
animal is completely germ free, there will
be an immature immune system, a defective
gut barrier, defective lymphoid tissue and
defective IgA, leading to susceptibility to
infection. There is a
microbiotica-gut-brain axis. Infection is
often linked to diagnosis. Both antibiotics
and probiotics can improve symptoms.
Infections can impact on memory and learning
too. If the microbiotica are normal, this
modulates brain development, behaviour and
the gut/brain axis. Stress can induce
changes in the gut. Gut activity releases
neurotransmitters with immune mucosal
responses. Genes, lifestyle, birth and
nurturing and medical practices can all
alter microbiotica. Symbiosis leads to
regulation and homeostasis.
In
relation to diet, an imbalance of bacteria
can lead to alterations in weight. Rat
studies were shown as an example. For
instance an overgrowth of bacteroides leads
to rats becoming very skinny. Alterations in
microbiotica can also impact on ability to
fight infections. Usually opportunistic
infections such as H.pylori, enterococcus
and clostridium are controlled naturally,
but maybe upset by the use of antibiotics.
Auto-immunity is also affected by bacterial
imbalance.
In
ME/CFS irritable bowel syndrome and leaky
gut may occur. There is often a predominance
of lactic acid forming bacteria, with high
levels of enterococci and low levels of E
coli. Manipulation of the bacteria has
potential for health improvement.
The
first probiotics were described by
Metchnikoff, who won a Nobel prize for this
work in 1908. His work used sour milk! There
is no scientific evidence to support the
health claims for probiotics, but clinically
there are indications that this approach can
help, and may be useful in ME/CFS.
The talk
finished with a brief description of the
facilities being developed in Norwich as a
centre for study of virology, genomics and
gastrointestinal microbiology. This will
all be happening alongside the facility
specialising in management of ME/CFS.
Øystein Fluge and Olav Mella (Bergen,
Norway) then
presented their fascinating research and
exciting results covering much detail, but
the paper is embargoed for mention here at
present as is awaiting publication. This
section will be completed then.
Kenny
de Meirleir (Brussels, Belgium)
gave an excellent overview of his work to
date and related this in particular to
clinical management. He outlined the many
tests that he does with his patients in
order to make the diagnosis and proceed to
treatment. The tests and predicted possible
abnormalities are listed below:
Blood
1-Basic tests:
Low ESR,
CRP normal
Normal or elevated haematocrit
Thrombocytosis
Lowered urate (associated with
Th2 shift)
Cu/ceruloplasmin elevated
AST/ALT elevated (increased
Kupffer cell activity)
gammaGT abnormal (liver
steatosis) alcohol intolerance
vitD3(OH)/VitD1,25dOH low
Alkaline phosphatase low
Ferritin maybe low or high –
alert for haemochromatosis
IgG1/IgG3 deficiencies
Abnormal protein electrophoresis
Blood
2-Immunophenotyping:
Low lymphocytes
Altered CD4/CD8 ratio
Variable CD4 and CD8 cells.
Abnormal NK cell ratio
B cells maybe high or low.
Blood 3:
CD14 elevated in 90%
CD57+lymphocytes decreased
Leucocyte elastase activity
elevated in a sub group
C4A increased in 80%
Perforin expression
Blood 4:
IgM and IgG – checking for
borrelia, coxiella, rickettsia – all can be
elevated
IgG for mycoses, moulds,
aspergilla and candida etc
Blood 5:
Cytokines
Interleukins 8,6,10,12
MCP1, MIP-1beta
TGF beta 1
Alpha TNF
Blood 6:
Food intolerance panel
Casein
Gluten
Tissue transaminases and gliadin
antibodies
Lactase gene defect
Blood 7:
XMRV
Envelope
Gag
XMRV serology
Blood 8:
XMRV in relation to blood donation
50 non
CFS donors - 14% +ve XMRV)
84 CFS
patients – 57% +ve XMRV – of these:
If had transfusion – 61%
positive
Those who had donated – 43%
positive
i.e. the
blood was not “clean”
He had
looked at 61 patients in Europe for XMRV,
MLV and XMRVc and all were positive to at
least one. XMRV replicates preferentially
in mucosal sites and there maybe relevance
for transmission.
Faecal
analysis: many abnormalities found. Looked
at;
Fungi,parasites and pathogens
Giardia antigen
Cryptosporidium antigen
Stool IgA (often v low in CFS)
Stool antichymotrypsin (elevated
in colitis)
Stool chymotrypsin (test of
exocrine pancreatic function)
Occult blood
Microbiology: enterococcus,
staphylococcus elevated
Overgrowth
of prevotella
H2S
lactate producing bacteria
Salivary
analysis:
Cortisol
H Pylori
Giardia
Urinalysis:
Th1/Th2 balance – controlled by
redox status.
He has
developed a test to check Th1/Th2 shift –
colour change depends on degree of shift.
80%
samples in CFS were positive. (cf 4% in
controls)
He then
went on to talk about therapy for patients
with CFS. A dietician is needed to deal
with issues such as fructose malabsorption,
intolerances of gluten, lactose and casein,
histamine hypersensitivity. Intestinal
dysbiosis needs treatment, and he uses
pulsed antibiotherapy, probiotics,
prebiotics, digestive enzymes, biofilm
removal, and if elastase elevated,
beta-lactamase antibiotics. For an
anti-inflammatory effect, he does not use
oral NSAIDs, but may use artesunate,
curcumin and hydroxy- or
methyl-cobalamin. He also uses DMSO,
Isoprinosine and kutapressin in some
patients. He has also used GcMAF (vitamin D
binding protein) compassionately for some
patients who are either XMRV or MLV positive
(25-100 nanogram weekly for 5-40 weeks). 68%
showed noticeable improvement particularly
with symptoms of orthostatic intolerance.
Antivirals such as valcyte, valtrex and
acyclovir and zoonoses (according to the
ILADS protocol) were also used in selected
patients.
Judy
Mikovits (Reno, Nevada,USA)
initially stressed that XMRV is not an
endogenous retrovirus in mice or humans. It
is a simple retrovirus and it is unsure how
it got into humans. It is stimulated by
androgens and inflammation, and responds to
cortisol, androgens and inflammation. MLV
(mouse leukaemia virus) is a related virus
gene and was detected by Lo and Alter in
86.5% CFS patients. (6.8% in controls). The
same sequences were found in patients 15
years after the initial investigations using
their stored bloods.
The
reason some studies searching for the virus
fail may be because of variations of XMRV
sequences or low levels of replicating
viruses. The Reno team have looked
therefore at unmanipulated plasma. Assays
have been done to detect anti-XMRV
antibodies. Bands were seen in Western blot
expression. Plasma from XMRV/MLV infected
CFS patients are reactive to multiple XMRV
proteins. Other assays included activated
PBMCs from heparin tubes and infectious cell
assays. In a cohort of UK patients, XMRV
was positive in 65%.
She then
went on to discuss the clinical implications
of XMRV. Retroviruses can induce profound
metabolic activity. This can be induced by
virus or viral particles or viral protein.
There is marked oxidative stress and
glutathione depletion, and there maybe
aberrant DNA methylation. These all increase
viral replication. This means 2 important
lessons can be learnt: leukaemias and
lymphomas can develop, and .and inflammatory
response can be triggered. As viral load in
peripheral blood is low, B cells in tissues
such as the spleen and lymph nodes could be
a reservoir for XMRV. In chronic diseases
viruses seldom come alone, and in ME/CFS
many viruses may be implicated. Also having
XMRV may not necessarily mean disease.
She
talked about HTLV-1 (a retrovirus causing
leukaemias and lymphoma). The majority of
carriers of this virus are asymptomatic, but
there is a 5-8% lifetime risk of getting
leukaemia or an inflammatory syndrome (arthropathy,
myelopathy etc). It occurs mainly in Africa,
Japan and S America.
They
have identified an inflammatory cytokine and
chemokine signature that distinguishes XMRV
infected patients from healthy controls with
94% sensitivity and specificity; an XMRV
patient population with aberrant methylation
profiles consistent with gammaretroviral
infection, and a patient population with
high nagalase activity. Nagalase is an
enzyme that blocks tumour-killing by
macrophages. Patients have responded to
treatment with the immune modulator GcMAF.
Non-steroidal anti-inflammatory drugs and
antivirals may be appropriate. She favours
metabolic and nutritional support. There is
evidence that immunomodulation with a drug
such as ampligen can help some patients too.
Monitoring XMRV viral load, co-infection and
immune dysfunction are all helping to
understand the clinical implications and
lead to better treatment of ME/CFS.
The
final presentation was by Wilfried Bieger
(Munich,Germany). He mentioned their
earlier studies to detect XMRV, which had
been negative. His team had then
collaborated with Judy Mikovits and set up a
highly sensitive, specific and
uncontaminated protocol for virus detection,
sequencing of viral DNA and antibody testing
with western blot. Viral DNA and RNA were
not detected in fresh blood, but after
cultivation of PBMCs for 6 weeks under
stimulation and using partly co-culture with
virus permissive LnCap cells, culture cells
turned positive in some patients. Presence
of XMRV was confirmed by sequencing XMRV
specific DNA. There have been approximately
40% positives so far.
He went
on to say that EBV reactivation seems common
in ME/CFS. Anti-herpes viral therapy has
promise of success.
The
conference concluded with a short question
time to clarify some points and discussion
with a representative from the British
Medical Journal board, who had found the day
extremely interesting.
I wish
to thank ANZMES for their help in enabling
me to attend this extremely worthwhile
rewarding day. And thanks also to Invest in
ME for such splendid organisation.
Rosamund
Vallings, MNZM, MB BS
Auckland
NZ
Burst Our Bubble - ME
Awareness Month 2011
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