Wednesday, July 10, 2013

Mary Schweitzer's husband

 
 
In lieu of flowers, the family suggests contributions may be made to The Robert Schweitzer Scholarship Fund, The University of Delaware, 82 East Main Street, 3rd Floor, Newark, DE 19716.

Sunday, July 7, 2013

IACFS/ME 2014 conference in San Francisco

IACFS/ME

www.iacfsme.org/ - Similar to IACFS/ME

The IACFS/ME announces our 11th Biennial International Research and Clinical Conference to be held in San Francisco, California, USA, March 20-23, 2014.

Facebook link for clinical trial info

From the Dr. Judy interview with Sue Vogan, if you want to sign up for clinical trials:
 

US/UK joint research into immune dysfunction

[Tom: This has more details for the UK study for which (US) NIH
funding of US$1.6m was recently announced. It got its seed money from
Action for ME, the (UK) ME Association, ME Research UK and a private
donor. I have given each sentence its own paragraph to make it a bit
easier to read.]


http://1.usa.gov/14z0EGN i.e.
http://projectreporter.nih.gov/project_info_description.cfm?aid=8574256&icde=0

Project Information

Project Number: 1R01AI103629-01A1

Contact PI / Project Leader: NACUL, LUIS


Title: A LONGITUDINAL IMMUNOLOGICAL AND VIROLOGICAL STUDY FOR ME CFS
BIOMARKER DISCOVERY

Awardee Organization: LONDON SCH/HYGIENE & TROPICAL MEDICINE

Description

Abstract Text:

DESCRIPTION (provided by applicant):

A longitudinal study will be conducted of clinical presentation,
immune phenotype, gene expression and virus infection among ME/CFS
patients and MS and population controls frequency-matched by
geographical area of residence, age-group (within 5 years), and sex.

Clinical samples will be collected for studies of NK cell functi on
virology (herpesvirus infection), and gene expression and for banking
as a resource for future ME/CFS research.

Hypothesis:

ME/CFS is associated with immune dysfunction, which results from - or
predisposes to - herpesvirus infections.


Immune dysfunction will present as alterations in NK cell function
that may lead to, or result from, alterations in cytokine production
and altered expression of diverse immune-associated genes.

Finally, we predict that the ME/CFS immune phenotype may fluctuate
over time and in association with clinical presentation and that the
majority of patients clinically characterized as having ME/CFS will
show a biosignature distinct from that of controls, and that further
alterations will be seen during episodes of clinical exacerbation.

Activities and objectives:

i) Collect clinical and other data and venous blood samples at
baseline and 6 months or at another time during the 6- month follow-up
period when there is a perceived "significant" deterioration in
symptoms;

ii) Analyze blood samples for NK cell phenotype and function;

iii) Screen samples for evidence of herpesvirus infection and viral
load, focusing on Epstein Barr virus (EBV), cytomegalovirus (CMV), and
human herpesvirus-6 (HHV-6);

iv) Describe clinical phenotype and fluctuations over time;

v) Correlate the presence of symptoms and severity with markers of
virus activity and immune function;

vi) Investigate gene expression profiles associated with ME/CFS and
how they vary in relation to changes in disease severity, virus
activity, NK cell function, and other markers of immune function;

and

vii) Securely store blood samples from patients and controls,
anonymously linked to clinical and other data, as an open resource for
researchers to conduct ethically-approved studies of ME/CFS.

Recruitment:

150 ME/ CFS cases (50 severe, 100 non-severe), 75 MS controls, and 75
healthy controls will be recruited.


For immunology and virology, 100 cases, 50 MS controls, and 50 healthy
controls will be sampled at 2 time points.

For gene expression, we will analyze 50 ME/CFS cases, 25 MS and 25
healthy controls, each at recruitment and one follow-up.

Cases will be selected from UK ME/CFS Disease Register and NHS ME/CFS
specialty and primary care services in London and Norfolk, Suffolk,
and Great Yarmouth and Waveney, UK; MS controls via the NHS; and
healthy controls will be identified by ME/CFS patients (excluding
blood relatives) or GPs.

Outcomes:

Identification of putative biomarkers for diagnosis, severity, and
prognosis of ME/CFS, which can be evaluated in larger (ideally
prospective) future studies.

In the long term, identification of robust biomarkers will allow
clinicians to correlate ME/CFS phenotype (including c linical
presentation, genetic, immune, and viral markers) with disease
severity and prognosis and may reveal new options for interventions
research.


PUBLIC HEALTH RELEVANCE:

This is, to our knowledge, the first longitudinal study of ME/CFS to
incorporate both mild and severe cases, age, sex, and
residence-matched Multiple Sclerosis (MS) and healthy controls, and to
incorporate virological, immunological and gene expression data into
the same study.

There is a clear need for research in these areas, and the inclusion
of severe cases using home visits will allow for research on a subset
of patients often neglected in ME/CFS studies.

Because approximately 1-4 million Americans have ME/CFS, this study
has the potential to impact the lives of a large patient population in
the US as well as advance the state of the field in the US, UK, and
globally through the potential identification of evidence related to
disease etiology and pathophysiology as well as disease subtypes and
biomarkers, revealing potential routes for treatment.


Public Health Relevance Statement:

This is, to our knowledge, the first longitudinal study of ME/CFS to
incorporate both mild and severe cases, age, sex, and
residence-matched Multiple Sclerosis (MS) and healthy controls, and to
incorporate virological, immunological and gene expression data into
the same study. There is a clear need for research in these areas, and
the inclusion of severe cases using home visits will allow for
research on a subset of patients often neglected in ME/CFS studies.
Because approximately 1-4 million Americans have ME/CFS, this study
has the potential to impact the lives of a large patient population in
the US as well as advance the state of the field in the US, UK, and
globally through the potential identification of evidence related to
disease etiology and pathophysiology as wel l as disease subtypes and
biomarkers, revealing potential routes for treatment.

Project Terms:

Age; age group; American; Area; biobank; Biological Markers;
biosignature; Blood; Blood specimen; Cell physiology; Clinical;
Clinical Data; clinical phenotype; Controlled Study; cytokine;
Cytomegalovirus; Data; Deterioration; Diagnosis; Disease; disorder
subtype; Etiology; follow-up; Frequencies (time pattern); Functional
disorder; Future; Gene Expression; Genes; Genetic Markers; Goals;
Herpesviridae; Herpesviridae Infections; Home visitation; House Call;
Human Herpesvirus 4; Human Herpesvirus 6; Immune; immune function;
Immune System Diseases; Immunologic Markers; Immunology; improved;
Intervention Studies; Lead; Link; London; Longitudinal Studies;
medical specialties; Molecular; Molecular Profiling; Multiple
Sclerosis; Natural Killer Cells; neglect; Outcome; outcome forecast;
patient population; Patients; Phenotype; Population Control;
Preventive Intervention; Primary Health Care; Production; prospective;
Prospective Studies; Recruitment Activity; Relative (related person);
Research; Research Personnel; residence; Resources; Route; Sampling;
Services; Severities; Severity of illness; sex; Symptoms; Therapeutic
Intervention; Time; Venous blood sampling; Viral; Viral Load result;
Viral Markers; virology; Virus; Virus Diseases