People live in a World of growing interdependency and complexity. The old English word connexity is an appropriate description that helps to define the combination of connectivity and complexity that is our reality.
Tick-borne diseases (TBDs) including Lyme disease are certainly embedded in our world of “connexity.”
This group of diseases defies simple cause and effect explanations and, while science has enabled us to uncover critical information on TBDs, we also realize that much more remains hidden.
The above extract from the Critical Needs and Gaps in Understanding Prevention, Amelioration, and Resolution of Lyme and Other Tick-Borne Diseases: The Short-Term and Long-Term Outcomes - Workshop Report see here
With the recent information finding that some patients with ME/CFS are being found to have XMRV and Lyme Disease this is not only of significance to just patients with Lyme Disease.
Wednesday, 20 April 2011
Thursday, 14 April 2011
LYME DISEASE FIGURES UP IN ENGLAND AND WALES
The Health Protection Agency is advising people to take care when visiting areas where ticks are present, to prevent tick bites and reduce the risk of catching Lyme disease.
Latest provisional figures from the Health Protection Agency (HPA) show there were 953 laboratory-confirmed cases of Lyme disease reported in England and Wales in 2010. The majority of these cases were acquired in the UK rather than overseas, with two-thirds of cases identified among residents in the South of England.
According to Centres for Disease Control in USA and Dr Ho Yen from HPA in Scotland the actual figure of people infected by Lyme Disease is more likely to be in the region of 10x that of serological positive tested cases so nearly 10000 cases in England and Wales last year. I don't have the figures for Scotland yet.
Advising people on the HPA website to take care of being bitten by a tick is just not good enough more publicity needs to be done by our Health Authorities.
Currently it is the patients and the UK charities that are raising awareness of this debilitating and often painfull disease. Thank you to BADA UK for the latest drive for Tick Bite Prevention Week and for getting information into various newspapers recently including
The Independent 'Lyme disease nearly made me come indoors,' says Ray Mears and
The Daily Mail Survival expert Ray Mears reveals how simple tick bite nearly ended his career
Shame on our Health Protection Agency for their failure to raise public awareness.
Latest provisional figures from the Health Protection Agency (HPA) show there were 953 laboratory-confirmed cases of Lyme disease reported in England and Wales in 2010. The majority of these cases were acquired in the UK rather than overseas, with two-thirds of cases identified among residents in the South of England.
According to Centres for Disease Control in USA and Dr Ho Yen from HPA in Scotland the actual figure of people infected by Lyme Disease is more likely to be in the region of 10x that of serological positive tested cases so nearly 10000 cases in England and Wales last year. I don't have the figures for Scotland yet.
Advising people on the HPA website to take care of being bitten by a tick is just not good enough more publicity needs to be done by our Health Authorities.
Currently it is the patients and the UK charities that are raising awareness of this debilitating and often painfull disease. Thank you to BADA UK for the latest drive for Tick Bite Prevention Week and for getting information into various newspapers recently including
The Independent 'Lyme disease nearly made me come indoors,' says Ray Mears and
The Daily Mail Survival expert Ray Mears reveals how simple tick bite nearly ended his career
Shame on our Health Protection Agency for their failure to raise public awareness.
Saturday, 9 April 2011
LETS WORK WITH THE LYME DOCTORS AND LETS START CALLING THIS ILLNESS ANYTHING BUT CFS
Dr Judy Mikovits at the NIH State of Knowledge Workshop in 2011 on ME/CFS. She says XMRV is allowing all the other viruses (entero, herpes etc) to keep going,
i.e it's similar to the way HIV causes AIDS, which is anything up to 25 different infections in the end.
Then she also says let's work with the Lyme doctors and lets start calling this illness anything but CFS
Tuesday, 5 April 2011
SEEK AND YE SHALL FIND
RETROSPECTIVE ANALYSIS OF A COHORT OF INTERNATIONALLY CASE DEFINED CHRONIC FATIGUE SYNDROME PATIENTS IN A LYME ENDEMIC AREA
Samuel Shor1, MD, FACP Principle Investigator:1Samuel Shor, MD, FACPAssociate Clinical ProfessorGeorge Washington University Health Care SciencesInternal Medicine of Northern Virginia1860 Town Center Drive #230Reston, Virginia 20190Phone 703 709-1119 Fax 703 709-7496samshormd@gmail.com ABSTRACT
Background Chronic fatigue syndrome is a diagnosis of exclusion for which there are no markers. Lyme disease is the most common vector borne illness in the United States for which chronic fatigue is a frequent clinical manifestation. Intervention of patients with Lyme disease with appropriately directed antimicrobials has been associated with improved outcomes. Methods
An arbitrary date was chosen such that all patients registered in the database of the practice of the PI, which is located in the Lyme endemic area of Northern Virginia area were reviewed. The diagnosis of clinically significant fatigue > 6 months was chosen. Inclusion criteria required fulfilling the International Case Definition for CFS. Results
Of the total 210 included in the analysis, 209 or 99% were felt to represent a high likelihood of “seronegative Lyme disease.” Initiating various antimicrobial regimen, involved at least a 50% improvement in clinical status in 130 or 62%. Although not achieving the 50% threshold according to the criteria discussed, another 55 patients subjectively identified a beneficial clinical response to antimicrobials, representing a total of 188 or 88% of the total identified as having a high potential for seronegative Lyme disease.
Conclusions
A potentially substantial proportion of patients with what would otherwise be consistent with internationally case defined CFS in a Lyme endemic environment actually have a perpetuation of their symptoms driven by a persistent infection by Borrelia burgdorferi. By treating this cohort with appropriately directed antimicrobials, we have the ability to improve outcomes.
----------------------------------------------
I have been remiss in posting recently ( busy enjoying life ) and also finding lots of interesting info on Lyme Disease and ME/CFS through Facebook but I had to post the above excellent research.
The above study concentrated on a known endemic area but here in the UK there is not so much research done on Lyme Disease areas to see where it is endemic.
My own diagnosis was part of a domino affect.
A nurse training at the Royal Surrey hospital had a patient admitted, on the ward with a tick bite and overheard talk about Lyme Disease.
Never having heard of Lyme Disease she looked it up on the Internet.
Only a fortnight later her new found knowledge proved useful when her husband had a tick attached whilst sitting in his garden. The husband attended the local surgery and Lyme Disease was dismissed as unlikely as the patient had not been infected in a known Lyme endemic area.
However a few days later the typical bulls eye rash appeared (lucky him as 40% of cases often don't get a rash). Still his GP and Dermatologist shook their heads and dismissed Lyme Disease, however the wife had by then pursuaded the GP to prescribe antibiotics and just as well as the NHS blood tests came back positive for Lyme.
That was the first known case at my surgery, later other cases presented in the early stages of tick bite and bulls eye rashes and eventually led to my GP suspecting I had Lyme when a chance course of antibiotics significantly improved my chronic arthritis and muscle weakness (My story is in the right hand column).
Since, there have been several patients present at my surgery and several other surgeries in the Guildford locality- seems once doctors start to look they find.
An area is only endemic when sufficient research has been done to establish that it is endemic - if the research is not done that does not mean there is no Lyme Disease in the area.
Samuel Shor1, MD, FACP Principle Investigator:1Samuel Shor, MD, FACPAssociate Clinical ProfessorGeorge Washington University Health Care SciencesInternal Medicine of Northern Virginia1860 Town Center Drive #230Reston, Virginia 20190Phone 703 709-1119 Fax 703 709-7496samshormd@gmail.com ABSTRACT
Background Chronic fatigue syndrome is a diagnosis of exclusion for which there are no markers. Lyme disease is the most common vector borne illness in the United States for which chronic fatigue is a frequent clinical manifestation. Intervention of patients with Lyme disease with appropriately directed antimicrobials has been associated with improved outcomes. Methods
An arbitrary date was chosen such that all patients registered in the database of the practice of the PI, which is located in the Lyme endemic area of Northern Virginia area were reviewed. The diagnosis of clinically significant fatigue > 6 months was chosen. Inclusion criteria required fulfilling the International Case Definition for CFS. Results
Of the total 210 included in the analysis, 209 or 99% were felt to represent a high likelihood of “seronegative Lyme disease.” Initiating various antimicrobial regimen, involved at least a 50% improvement in clinical status in 130 or 62%. Although not achieving the 50% threshold according to the criteria discussed, another 55 patients subjectively identified a beneficial clinical response to antimicrobials, representing a total of 188 or 88% of the total identified as having a high potential for seronegative Lyme disease.
Conclusions
A potentially substantial proportion of patients with what would otherwise be consistent with internationally case defined CFS in a Lyme endemic environment actually have a perpetuation of their symptoms driven by a persistent infection by Borrelia burgdorferi. By treating this cohort with appropriately directed antimicrobials, we have the ability to improve outcomes.
----------------------------------------------
I have been remiss in posting recently ( busy enjoying life ) and also finding lots of interesting info on Lyme Disease and ME/CFS through Facebook but I had to post the above excellent research.
The above study concentrated on a known endemic area but here in the UK there is not so much research done on Lyme Disease areas to see where it is endemic.
My own diagnosis was part of a domino affect.
A nurse training at the Royal Surrey hospital had a patient admitted, on the ward with a tick bite and overheard talk about Lyme Disease.
Never having heard of Lyme Disease she looked it up on the Internet.
Only a fortnight later her new found knowledge proved useful when her husband had a tick attached whilst sitting in his garden. The husband attended the local surgery and Lyme Disease was dismissed as unlikely as the patient had not been infected in a known Lyme endemic area.
However a few days later the typical bulls eye rash appeared (lucky him as 40% of cases often don't get a rash). Still his GP and Dermatologist shook their heads and dismissed Lyme Disease, however the wife had by then pursuaded the GP to prescribe antibiotics and just as well as the NHS blood tests came back positive for Lyme.
That was the first known case at my surgery, later other cases presented in the early stages of tick bite and bulls eye rashes and eventually led to my GP suspecting I had Lyme when a chance course of antibiotics significantly improved my chronic arthritis and muscle weakness (My story is in the right hand column).
Since, there have been several patients present at my surgery and several other surgeries in the Guildford locality- seems once doctors start to look they find.
An area is only endemic when sufficient research has been done to establish that it is endemic - if the research is not done that does not mean there is no Lyme Disease in the area.
Friday, 18 March 2011
PREVENTION OF ALZHEIMER'S
Prevention of Alzheimer's
Alzheimer's disease is the most frequent cause of dementia.
Accumulation of senile plaques and neurofibrillary tangles are the characteristic lesions, which leads to neuronal damage and brain atrophy.
Alzheimer's disease is slowly progressive. It starts several years or decades before the diagnosis of dementia is made and the patients can survive in an advanced stage of dementia, necessitating continuous care for years or decades.Alzheimer's disease causes the suffering of the patients and those also of caring family members and affects the dignity of the patients.
Senile plaues exhibiting red and neurofibrillary tangles green fluorescence (first panel) Thioflavin S fluorescence of senile plaques and tangles (second panel).
Growing number of epidemiological studies in the U.S. and Europe indicate that dementia will be the most intractable problem to confront by our health system in the next decades. Around 5.3 million Americans are diagnosed with Alzheimer's disease today and the estimated prevalence for 2050 is expected to approach 11 to 16 million. The annual direct and indirect costs related to Alzheimer's disease and other dementias are an estimated 148 billion dollars, without the inclusion of an annual 94 billion dollars of unpaid services provided by 10 million caregiversotre.
In Europe these direct and indirect costs are estimated to correspond to 87 billion Euros. It is also expected to double or even triple by 2050.
Alzheimer's disease represents a public health emergency problem around the world, including Switzerland. Based on demographic data the number of patients with Alzheimer's disease is around 100'000 today and similarly to other countries a two or three fold increase is expected during the next decades. Unless treatments to delay or prevent the disease are developed, the world will face an unsustainable care bill by the middle of this century.
Prompt action is needed! In addition to support health care needs, investing heavily in research on Alzheimer's disease and other chronic disorders (e.g. vascular disorders, diabetes etc…) is critical. The goal of the foundation is to prevent Alzheimer's disease and other devastating chronic disorders in the framework of an international effort.
The realization that pathogens can evade from destruction by the host immune system and produce slowly progressive chronic diseases has resulted in a new concept of infectious diseases and opened a new avenue for the treatment and prevention of these chronic disorders.
This "health revolution" started by the studies of Warren and Marshall who following 25 years of continuous research have finally received the Noble prize for their discovery that stomach ulcer is caused by the slightly curved bacterium, called Helicobacter pylori.
Increasing number of recent observations show the involvement of bacteria and viruses in various chronic inflammatory disorders, including atherosclerosis, cardio- and cerebro-vascular disorders, diabetes, neurodegenerative disorders and Alzheimer's disease. Activated macrophages and microglial cells are the principal players in this pathogen chronic infection, which leads to slowly progressive parenchymal damage and tissue atrophy.
The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past.
During infection, active oxygen and nitrogen species generated by inflammatory cells can cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression. Depending upon the biology of the pathogen and the host defense mechanisms the microorganisms can persist in the infected tissues and cause chronic, persistent inflammation and slowly progressive tissue damage. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent. Environmental factors, including stress and nutrition are critical determinants of disease expression as well.
Further research in this direction is essential as these chronic inflammatory disorders affect a large part of the population up to 50 years and represent an enormous socio-economical charge.
The possibility that microorganisms may play a role in senile plaque formation has been discussed by Fischer, Alzheimer and their colleagues more than a century ago.
It has also been known from more than a century that chronic bacterial infection can cause dementia.
The spirochete Treponema pallidum in syphilis, can cause slowly progressive dementia, cortical atrophy and amyloid deposition, which revealed to be beta-amyloid.
Recently it was shown that other types of spirochetes, including Borrelia burgdorferi, the causative agent of Lyme disease are also able to persist in the brain, and cause dementia, brain atrophy and beta-amyloid deposition.
Bacteria, including spirochetes, are powerful stimulators of inflammation and are amyloidogenic and they can initiate and sustain chronic inflammation and amyloid deposition in Alzheimer’s disease. Recent observations also revealed that beta-amyloid, which is the most important biological marker of Alzheimer's disease belongs to the family of antimicrobial peptides (AMP).
The goal of the foundation is to support and accelerate this new emerging field of research on Alzheimer's disease and related chronic inflammatory disorders. Some pathogens have been already analyzed and serological and diagnostic tests for their detection are commercially available. Others still need to be characterized in order to detect and eradicate them.
Treatments presently used for Alzheimer's disease and other chronic inflammatory disorders are mostly symptomatic.
Antibiotics and antiviral drugs for the treatment of bacterial and viral infections are available, however, to optimize available treatments and develop new therapies is essential.
To develop international collaborations, organize symposiums, congresses, and seminars for discussing and exchanging knowledge worldwide is important.
The medical, social, and economical repercussion of such research in the framework of an international effort will be substantial.
The President of the foundation, Judith Miklossy, MD, PhD, is one of the pioneers who contributed to this emerging field of research and has more than 30 years of clinical and research experience in Switzerland, in the US and in Canada.
More details of research related to the activity of Prevention Alzheimer Foundation and Alzheimer Research Center can be seen on the website: www.miklossy.ch
Alzheimer's disease is the most frequent cause of dementia.
Accumulation of senile plaques and neurofibrillary tangles are the characteristic lesions, which leads to neuronal damage and brain atrophy.
Alzheimer's disease is slowly progressive. It starts several years or decades before the diagnosis of dementia is made and the patients can survive in an advanced stage of dementia, necessitating continuous care for years or decades.Alzheimer's disease causes the suffering of the patients and those also of caring family members and affects the dignity of the patients.
Senile plaues exhibiting red and neurofibrillary tangles green fluorescence (first panel) Thioflavin S fluorescence of senile plaques and tangles (second panel).
Growing number of epidemiological studies in the U.S. and Europe indicate that dementia will be the most intractable problem to confront by our health system in the next decades. Around 5.3 million Americans are diagnosed with Alzheimer's disease today and the estimated prevalence for 2050 is expected to approach 11 to 16 million. The annual direct and indirect costs related to Alzheimer's disease and other dementias are an estimated 148 billion dollars, without the inclusion of an annual 94 billion dollars of unpaid services provided by 10 million caregiversotre.
In Europe these direct and indirect costs are estimated to correspond to 87 billion Euros. It is also expected to double or even triple by 2050.
Alzheimer's disease represents a public health emergency problem around the world, including Switzerland. Based on demographic data the number of patients with Alzheimer's disease is around 100'000 today and similarly to other countries a two or three fold increase is expected during the next decades. Unless treatments to delay or prevent the disease are developed, the world will face an unsustainable care bill by the middle of this century.
Prompt action is needed! In addition to support health care needs, investing heavily in research on Alzheimer's disease and other chronic disorders (e.g. vascular disorders, diabetes etc…) is critical. The goal of the foundation is to prevent Alzheimer's disease and other devastating chronic disorders in the framework of an international effort.
The realization that pathogens can evade from destruction by the host immune system and produce slowly progressive chronic diseases has resulted in a new concept of infectious diseases and opened a new avenue for the treatment and prevention of these chronic disorders.
This "health revolution" started by the studies of Warren and Marshall who following 25 years of continuous research have finally received the Noble prize for their discovery that stomach ulcer is caused by the slightly curved bacterium, called Helicobacter pylori.
Increasing number of recent observations show the involvement of bacteria and viruses in various chronic inflammatory disorders, including atherosclerosis, cardio- and cerebro-vascular disorders, diabetes, neurodegenerative disorders and Alzheimer's disease. Activated macrophages and microglial cells are the principal players in this pathogen chronic infection, which leads to slowly progressive parenchymal damage and tissue atrophy.
The fact that pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection has received little attention in the past.
During infection, active oxygen and nitrogen species generated by inflammatory cells can cause DNA damage, induce apoptosis, and modulate enzyme activities and gene expression. Depending upon the biology of the pathogen and the host defense mechanisms the microorganisms can persist in the infected tissues and cause chronic, persistent inflammation and slowly progressive tissue damage. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent. Environmental factors, including stress and nutrition are critical determinants of disease expression as well.
Further research in this direction is essential as these chronic inflammatory disorders affect a large part of the population up to 50 years and represent an enormous socio-economical charge.
The possibility that microorganisms may play a role in senile plaque formation has been discussed by Fischer, Alzheimer and their colleagues more than a century ago.
It has also been known from more than a century that chronic bacterial infection can cause dementia.
The spirochete Treponema pallidum in syphilis, can cause slowly progressive dementia, cortical atrophy and amyloid deposition, which revealed to be beta-amyloid.
Recently it was shown that other types of spirochetes, including Borrelia burgdorferi, the causative agent of Lyme disease are also able to persist in the brain, and cause dementia, brain atrophy and beta-amyloid deposition.
Bacteria, including spirochetes, are powerful stimulators of inflammation and are amyloidogenic and they can initiate and sustain chronic inflammation and amyloid deposition in Alzheimer’s disease. Recent observations also revealed that beta-amyloid, which is the most important biological marker of Alzheimer's disease belongs to the family of antimicrobial peptides (AMP).
The goal of the foundation is to support and accelerate this new emerging field of research on Alzheimer's disease and related chronic inflammatory disorders. Some pathogens have been already analyzed and serological and diagnostic tests for their detection are commercially available. Others still need to be characterized in order to detect and eradicate them.
Treatments presently used for Alzheimer's disease and other chronic inflammatory disorders are mostly symptomatic.
Antibiotics and antiviral drugs for the treatment of bacterial and viral infections are available, however, to optimize available treatments and develop new therapies is essential.
To develop international collaborations, organize symposiums, congresses, and seminars for discussing and exchanging knowledge worldwide is important.
The medical, social, and economical repercussion of such research in the framework of an international effort will be substantial.
The President of the foundation, Judith Miklossy, MD, PhD, is one of the pioneers who contributed to this emerging field of research and has more than 30 years of clinical and research experience in Switzerland, in the US and in Canada.
More details of research related to the activity of Prevention Alzheimer Foundation and Alzheimer Research Center can be seen on the website: www.miklossy.ch
Monday, 14 March 2011
LYME DISEASE CASES SOAR IN TAYSIDE BUT WHERE ELSE?
Lyme Disease in the news :-
The New Scotsman here
Case study: Diagnosed after two-year illness
Scotland on Sunday here
Warning as ticks carry disease south
The Press and Journal here
Tayside revealed as a Lyme disease hotspot as cases soar
visitors warned to take precautions against tick bites, which can cause condition
No surprises here then to those of us who take an interest in Lyme Disease here in the UK - The words seek and ye shall find come to mind.
The most significant thing in these articles I think was in the Press and Journal
Dr Darrell Ho-Yen, of Scotland’s Lyme disease testing service, warns that the number of cases could be as much as 10 times higher despite being a notifiable disease.
He said: “The figures do not take into account wrongly diagnosed cases, tests giving false results, sufferers who weren’t tested, people who are infected but not showing symptoms, failures to notify and infected individuals who don’t consult a doctor.”
I posted earlier on the statistics of Lyme Disease cases in UK here
The New Scotsman here
Case study: Diagnosed after two-year illness
Scotland on Sunday here
Warning as ticks carry disease south
The Press and Journal here
Tayside revealed as a Lyme disease hotspot as cases soar
visitors warned to take precautions against tick bites, which can cause condition
No surprises here then to those of us who take an interest in Lyme Disease here in the UK - The words seek and ye shall find come to mind.
The most significant thing in these articles I think was in the Press and Journal
Dr Darrell Ho-Yen, of Scotland’s Lyme disease testing service, warns that the number of cases could be as much as 10 times higher despite being a notifiable disease.
He said: “The figures do not take into account wrongly diagnosed cases, tests giving false results, sufferers who weren’t tested, people who are infected but not showing symptoms, failures to notify and infected individuals who don’t consult a doctor.”
I posted earlier on the statistics of Lyme Disease cases in UK here
Thursday, 24 February 2011
NEW ME/CFS AND LYME DISEASE RESEARCH
New research has just been published, highly significant for those with Chronic Lyme disease and ME/CFS.
Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome
Can be accessed through Plos One click here
Abstract Top
Background
Neurologic Post Treatment Lyme disease (nPTLS) and Chronic Fatigue (CFS) are syndromes of unknown etiology. They share features of fatigue and cognitive dysfunction, making it difficult to differentiate them. Unresolved is whether nPTLS is a subset of CFS.
Methods and Principal Findings
Pooled cerebrospinal fluid (CSF) samples from nPTLS patients, CFS patients, and healthy volunteers were comprehensively analyzed using high-resolution mass spectrometry (MS), coupled with immunoaffinity depletion methods to reduce protein-masking by abundant proteins. Individual patient and healthy control CSF samples were analyzed directly employing a MS-based label-free quantitative proteomics approach. We found that both groups, and individuals within the groups, could be distinguished from each other and normals based on their specific CSF proteins (p<0.01). CFS (n = 43) had 2,783 non-redundant proteins, nPTLS (n = 25) contained 2,768 proteins, and healthy normals had 2,630 proteins. Preliminary pathway analysis demonstrated that the data could be useful for hypothesis generation on the pathogenetic mechanisms underlying these two related syndromes.
Conclusions
nPTLS and CFS have distinguishing CSF protein complements. Each condition has a number of CSF proteins that can be useful in providing candidates for future validation studies and insights on the respective mechanisms of pathogenesis. Distinguishing nPTLS and CFS permits more focused study of each condition, and can lead to novel diagnostics and therapeutic interventions.
Distinct Cerebrospinal Fluid Proteomes Differentiate Post-Treatment Lyme Disease from Chronic Fatigue Syndrome
Can be accessed through Plos One click here
Abstract Top
Background
Neurologic Post Treatment Lyme disease (nPTLS) and Chronic Fatigue (CFS) are syndromes of unknown etiology. They share features of fatigue and cognitive dysfunction, making it difficult to differentiate them. Unresolved is whether nPTLS is a subset of CFS.
Methods and Principal Findings
Pooled cerebrospinal fluid (CSF) samples from nPTLS patients, CFS patients, and healthy volunteers were comprehensively analyzed using high-resolution mass spectrometry (MS), coupled with immunoaffinity depletion methods to reduce protein-masking by abundant proteins. Individual patient and healthy control CSF samples were analyzed directly employing a MS-based label-free quantitative proteomics approach. We found that both groups, and individuals within the groups, could be distinguished from each other and normals based on their specific CSF proteins (p<0.01). CFS (n = 43) had 2,783 non-redundant proteins, nPTLS (n = 25) contained 2,768 proteins, and healthy normals had 2,630 proteins. Preliminary pathway analysis demonstrated that the data could be useful for hypothesis generation on the pathogenetic mechanisms underlying these two related syndromes.
Conclusions
nPTLS and CFS have distinguishing CSF protein complements. Each condition has a number of CSF proteins that can be useful in providing candidates for future validation studies and insights on the respective mechanisms of pathogenesis. Distinguishing nPTLS and CFS permits more focused study of each condition, and can lead to novel diagnostics and therapeutic interventions.
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