make sure your dr tests for you that!

you could have gotten lyme from the vaccine, and if you did might be able to put a lawsuit together versus GlaxoKlineSmith, the vaccine maker.

there is a lot of info available on this subject if you are interested i can email you some info. just ask.

best of luck and hope this resolves for you easily....

Could you send me your vaccine info?

BTW, scientists identified the first extracellular Bb neurotoxin secretion in November. It's called Porin, and it's commonly thought to help organisms punch holes in healthy cell walls. Here's the citation:
"Extracellular secretion of the Borrelia burgdorferi Oms28 porin and Bgp, a glycosaminoglycan binding protein."
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abs tract&list_uids=15501754

best bet is to go to entrez pub med and enter "lyme vaccine ospA"

as for the middlebury study above how did you deduce that porin (oms28) is a bb toxin. it states that is an extracellular protein but not that is gram negative.

anyhow can only read the abstract, unfortunately.

it does seem as it is quite possible to deduce that it is a protein toxin. good news, bad news.

Here are some good backgrounder links. The first is testimony supporting recall of Lymerix by Karen Vanderhoof-Forschner, who founded the Lyme Disease Association. She explains the scientific basis for the vaccine, and why she thinks it stinks.
http://www.lyme.org/vaccine/3yrsrteslong.html

Donta says:
The Lyme OspA vaccine has appeared to reactivate Lyme Disease in a number of individuals who knew, but some who did not know, they had prior Lyme Disease (11). The mechanisms responsible for the reactivation of the disease have not been defined, but may include both molecular mimicry and underlying infection. http://www.canlyme.com/donta.html

And there's quite a bit of info at Cheryl's Lyme Info pages at http://www.lymeinfo.net/vaccine.html

I have been told by two well know LLMD that the vaccine triggers a non-symptom case of lyme into full blown lyme. People with the HLA-DR4 are subject to a form of arthritis that does not respond to treatment.

If anyone needs more information on the Lymerix vaccine I can be contacted at
[email protected]

Here is something from the Boston Globe from May 2002.

News
May 18, 2002
The life and death of a vaccine

Boston Globe; www.boston.com; Stephen Smith

As drug discoveries go, it was a spectacular rise - followed by an even more astonishing fall.
LYMErix, the first vaccine against Lyme disease, burst onto the market in the spring of 1999 with the promise of reversing the march of a tick-borne illness that strikes thousands of people every year, mostly in the Northeast. In that first year alone, hundreds of thousands of people took the shot, generating $40 million in sales.
Then, just as quickly as it arrived, LYMErix was gone, yanked voluntarily in February by its manufacturer, GlaxoSmithKline, which cited a precipitous drop in sales, with fewer than 10,000 people expected to get the vaccine this year. Because Lyme disease is rarely fatal, potential customers apparently decided the vaccine wasn't worth the risk.
In its wake, LYMErix has left hundreds of lawsuits alleging that the shot caused painful, even ruinous complications in patients.
The demise of LYMErix - and what caused it to ''crash and burn,'' as one Tufts University researcher put it - provides a vivid answer to the question: Why don't scientists develop vaccines for more diseases?
Researchers familiar with vaccine development speculate that the inoculation was doomed by the calculus that determines the success of any drug: People decided that the perceived risk of complications from the shot outweighed the benefit of preventing a disease that can be treated if caught early enough and avoided altogether by keeping deer ticks off the skin.
''If people are hearing news reports that you can get autoimmune disease from taking this vaccine, they're going to run away screaming,'' said Dr. Janice Reichert, a senior research fellow at the Tufts Center for the Study of Drug Development. ''So your market basically goes down the tubes.''
The failure of LYMErix represents the latest challenge in a segment of the pharmaceutical industry often viewed as a stepchild. Vaccine development does not have the same income potential as blockbuster drugs to treat chronic conditions such as high blood pressure. Vaccines must be priced affordably to reach the broadest market, and they're often a one-shot deal.
Since the 19th century, vaccines have ranked among medicine's greatest successes. But in recent years, a small, albeit vocal, lobby emerged to oppose vaccination, arguing that shots meant to grant protection too often cause harm.
''For somebody like me, it's very straightforward - why would you not want to prevent infectious diseases?'' said Dr. Charles Prober, a Stanford University specialist in infectious diseases. ''But there are some people who do not want foreign proteins in their body.''
The market appeared promising when LYMErix was approved by federal drug regulators in December 1998. Lyme disease had spread fear throughout the 1980s and 1990s, as tiny deer ticks infected people with bacteria that can cause severe joint pain and debilitating fatigue. While antibiotics successfully treated the illness in many patients, others were beset with persistent symptoms. Researchers turned their microscopes toward a vaccine.
LYMErix contains a protein designed to marshal the human body's army of disease fighters to repel the bacteria that cause illness.
In a review of the dozen drug studies that led to the federal approval of LYMErix, Reichert found that almost 22,000 people participated in the trials. For a biopharmaceutical such as LYMErix, Reichert said, that gave great credibility to the conclusion that the vaccine was safe.
The Lyme vaccine required three shots given over a year, and Glaxo reports that 1.5 million doses were supplied during 1999.
By July 1999, however, problems allegedly associated with the vaccine already were being reported. Philadelphia attorney Stephen A. Sheller was beginning to receive calls from patients and doctors reporting that LYMErix had caused severe side effects. Vaccine recipients reported aches and pains that resembled arthritis, while others complained of malaise and memory loss. In December 1999, Sheller sued the drug maker; today, the roster of LYMErix clients at Sheller's firm stretches 400 names long.
Dr. Norman Latov, a neurologist at Cornell University's Weill Medical College in New York, first became aware of the alleged complications caused by the vaccine a few months ago. He started seeing patients with unusual neurological problems. They reported weakness, numbness, and pain in their arms and legs. In some of the 10 patients whose conditions Latov links to LYMErix, their brains had been damaged, leaving the patients unable to retrieve the details needed for the chores of daily life. Those neurological complications had not been predicted in the trials of LYMErix.
A risk of any vaccine is that it will overstimulate the body's immune system or provoke an inappropriate response. Latov and other doctors believe that LYMErix caused some patients' immune systems to turn on their own bodies, becoming a force of destruction rather than an agent of protection.
The Food and Drug Administration and Centers for Disease Control examined 905 reports of adverse events. Their conclusion: Neither the number of complaints nor their severity was beyond what would have been anticipated, based on the clinical studies.
''I think the vaccine was a useful tool for preventing Lyme disease,'' said Dr. Ned Hayes, epidemiology chief in CDC's Lyme disease program.
The decision to withdraw LYMErix, a Glaxo spokeswoman said, was driven exclusively by the lack of sales. After the first year of strong results, sales plummeted to less than $5 million by 2001, Ramona DuBose said.
Although the company would not disclose how much was spent to develop the vaccine, trade groups cite a figure of $800 million as the average cost to bring a drug to the pharmacy shelf.
''Despite our best efforts, the demand for the vaccine just never reached a sustainable level,'' DuBose said. ''We knew that the marketing of this vaccine would be a challenge, because Lyme disease is poorly understood. We worked on trying to overcome that by educating physicians and the public about why it could be beneficial to take the vaccine. But still there was not enough demand.''
This story ran on page A1 of the Boston Globe on 5/18/2002. http://www.boston.com/dailyglobe2/138/nation/The_life_and_death_of_a_vaccine+.shtml
View News Archive >>

I have a bunch of papers my lyme doc gave me but I just dont have it in me to find them and try and figure out how to get them to you over the net. To tell you the truth I really cant decipher most of them.

I suffer from a major case of the "STUPIDS"

If you dont get the info you are looking for from the above posts let me know here and I will try hard to get you what I have.

Im have just decided that I may not get better. Im not giving up the fight but am trying to learn how to live life to the fulles with what I have.

dr.k in ct is very into the work concerning lyme vaccine and hla-dr4. he is orange, ct just outside new haven.

if you want the info for him i can email you his tel number.

"both lyme disease and the anit lyme vaccine (LYMErix) can trigger neurologic autoimmune disease. Since the Lyme vaccine is a pure preparation of OSP A (outer surface protein A coated onto aluminum hydroxide) it is reasonable to assume that this protein is also responsible for the autoimmune disease triggered by Lyme infection.

This autoimmune disease is especially common in indviduals with class II, MHC HLA DR4 (an immune marker). Persisting abundant presence of IgM antibodies reacting to OSP A (Wester Blot of 3+ at band 31) is a good indicator of an autoimmune condition triggered by this protein."

under this category post Lyme vaccination syndrome should be included. read "The Bitter Feud over LYMErix - Big Pharma Takes on the wrong Little Osp" -
http://www.whale.to/m/lymerix8.html

articles :

"The post Lyme autoimmune syndrome"

1."Association of chronic Lyme arthritis with HLA-DR4 and HLA-DR2 alleeles" NEJM. July 26, 1990, Volume 323, Issue 4, page 219-223

Association of chronic Lyme arthritis with HLA-DR4 and HLA-DR2 alleles.

Steere AC, Dwyer E, Winchester R.

Division of Rheumatology/Immunology, New England Medical Center, Tufts University School of Medicine, Boston, MA 02111.

BACKGROUND AND METHODS. A small percentage of patients infected with Borrelia burgdorferi have chronic Lyme arthritis that does not respond to antibiotic therapy.

To learn whether genetically determined variations in the host immune response might account for such outcomes, we determined the immunogenetic profiles of 130 patients with various manifestations of Lyme disease. RESULTS.

Of the 80 patients with arthritis, 57 percent of those with chronic arthritis (12 to 48 months in duration) had the HLA-DR4 specificity; only 23 percent of those with arthritis of moderate duration (6 to 11 months) and only 9 percent of those with arthritis of short duration (1 to 5 months) had this specificity (P = 0.003). After the HLA-DR4-positive patients were excluded from each group, a secondary association was noted with HLA-DR2, which was found in 75 percent of the remaining patients with chronic arthritis and in 50 percent of those with arthritis of moderate duration, but in only 20 percent of those with arthritis of short duration (P = 0.023).

Altogether, 25 of the 28 patients with chronic arthritis (89 percent) had HLA-DR2 or HLA-DR4, or both, as compared with 27 percent of those with arthritis of short duration (relative risk, 22; P = 0.00006). These HLA specificities appeared to act as independent, dominant markers of susceptibility. Nucleotide-sequence typing, performed in five patients with chronic arthritis, identified the HLA-DR2 allele as Dw2 (DR beta 1*1501), and the HLA-DR4 alleles as Dw4, Dw14, and Dw13 (DR beta 1*0401, DR beta 1*0404, and DR beta 1*0403, respectively). The presence of HLA-DR4 in patients with arthritis was associated with a lack of response to antibiotic therapy (P = 0.01).

CONCLUSIONS. Particular Class II major histocompatibility genes determine a host immune response to B. burgdorferi that results in chronic arthritis and lack of response to antibiotic therapy.

2. "Autoimmune mechanisms in antibiotic treatment resistant Lyme arthritis" Journal of Autoimmunity. May 2001, volume 16, issue 3, pages 263-268.

Autoimmune mechanisms in antibiotic treatment-resistant lyme arthritis.

Steere AC, Gross D, Meyer AL, Huber BT.

Division of Rheumatology/Immunology (Medicine) and the Department of Pathology, Tufts University School of Medicine, New England Medical Center, Boston, MA, USA. [email protected]

In about 10% of patients with Lyme arthritis in the United States, joint inflammation persists for months or even several years after the apparent eradication of the spirochete, Borrelia burgdorferi, from the joint with antibiotic treatment.

We propose a model of molecular mimicry affecting genetically susceptible individuals to explain this treatment-resistant course.

The majority of patients with treatment-resistant Lyme arthritis have HLA-DRB1*0401 or related alleles, and the severity and duration of their arthritis correlate with cellular and humoral immune responses to outer-surface protein A OspA) of the spirochete.

Using an algorithm, the immunodominant epitope of OspA presented by the DRB1*0401 molecule was predicted to be located at aa 165-173.

In a search of the Genetics Computer Group gene bank, only one human protein was identified, lymphocyte function associated antigen-1 (hLFA-1), that had sequence homology with OspA(165-173)and predicted binding in the DRB1*0401 molecule. Synovial fluid T cells from most patients with treatment-resistant arthritis responded to both OspA and hLFA-1, whereas those from patients with other forms of chronic inflammatory arthritis did not.

Molecular mimicry between a dominant T cell epitope of OspA and hLFA-1 may be an important factor in the persistence of joint inflammation in genetically susceptible patients with treatment-resistant Lyme arthritis. Copyright 2001 Academic Press.

Im on my 3rd treatment now and no better. Unfortunately, even the most knowledgable doc cant make you respond if your body refuses to.

I still have hope but am trying hard to have a life if this is all I am going to be. He didnt leave me with a lot of hope after last visit.

personally i'm not the hugest fan of dr.k but his ideas are good, he's very smart. i just don't know if he is a very good LLMD.

anyhow have you guys tried IVIG yet? that will definitlely help you. harp him on that. tell him that's what you want and need, since you are not making progress.

tell him to send you for an immunological workup and then see if it you fit the criteria for the IVIG.

if you meant is was your 3rd treatment on IVIG sometimes it can take a few months to begin to have a very good response.

The biggest problem will be getting insurance approval. I will be on medicare by then but he says he knows a doc who accepts medicare who would probable do it in his office if we can get the ok.

He did all that testing when I first went to see him. Everything was just fine except for a low modulation, whatever that means.

He definately says mine is an autoimmune problem.

Im on doxy right now and I beginning to wonder if its not doing something cuz my muscle pain is so much worse. Perhaps that is a herx. Lets hope so.

There are some good reasons to try doxy for me that are too involved to go into right now. Im keepin my fingers crossed.

Anyway here is the abstract and the web site
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Display&DB=pubmed

Neuropathy and cognitive impairment following vaccination with the OspA protein of Borrelia burgdorferi.

Latov N, Wu AT, Chin RL, Sander HW, Alaedini A, Brannagan TH 3rd.

Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY 10022, USA. [email protected]

Neurological syndromes that follow vaccination or infection are often attributed to autoimmune mechanisms. We report six patients who developed neuropathy or cognitive impairment, within several days to 2 months, following vaccination with the OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment, one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense white matter lesions on magnetic resonance imaging. The similarity between the neurological sequelae observed in the OspA-vaccinated patients and those with chronic Lyme disease suggests a possible role for immune mechanisms in some of the manifestations of chronic Lyme disease that are resistant to antibiotic treatment.

Here is the complete research paper that you had the abstract for. Hope it helps people to understand what this vaccine had did to people.

GP

RESEARCHREPORT
Neuropathy and cognitive impairment following
vaccinationwith the OspA protein of Borrelia burgdorferi
Norman Latov, Anita T. Wu, Russell L. Chin, Howard W. Sander, Armin Alaedini, and
Thomas H. Brannagan, III
Department of Neurology and Neurosciences, Weill Medical College of Cornell University, New York, NY, USA
Abstract Neurological syndromes that follow vaccination or infection are often attributed
to autoimmune mechanisms. We report six patients who developed neuropathy or
cognitive impairment, within several days to 2 months, following vaccination with the
OspA antigen of Borrelia burgdorferi. Two of the patients developed cognitive impairment,
one chronic inflammatory demyelinating polyneuropathy (CIDP), one multifocal motor
neuropathy, one both cognitive impairment and CIDP, and one cognitive impairment and
sensory axonal neuropathy. The patients with cognitive impairment had T2 hyperintense
white matter lesions on magnetic resonance imaging. The similarity between the neurological
sequelae observed in the OspA-vaccinated patients and those with chronic Lyme
disease suggests a possible role for immune mechanisms in some of the manifestations
of chronic Lyme disease that are resistant to antibiotic treatment.
Key words: Borrelia burgdorferi, cognitive impairment, Lyme disease, neuropathy, OspA,
vaccination
Introduction
Neurological sequelae of vaccination are often acute
and fulminate as in the Guillain-Barre� syndrome or acute
disseminated encephalomyelitis (Tselis and Lisak, 1998)
but can also be chronic and indolent, or involve both the
central and peripheral nervous systems (Poser, 1982;
Vital et al., 2002).We report the development of chronic
neuropathies or cognitive impairment in six patients,
following vaccination with the LYMErix vaccine, which
contains the OspA protein of Borrelia burgdorferi coated
onto aluminum hydroxide.
Patients
The medical records of six patients seen at our
center over a 2-year period, who reported developing
neurological sequelae after vaccination with the OspA
protein in the form of the LYMErix vaccine, were
reviewed. Patients with clinical evidence for peripheral
neuropathy underwent electromyography and nerve
conduction studies or skin biopsies to assess for intradermal
nerve fiber density, and those that had cognitive
impairment underwent brain magnetic resonance
imaging (MRI), with and without gadolinium. Vaccination
was typically given in three doses, the second
dose 1 month following the first, and the third dose
1 year later. Some of the patients received the full
three doses, but others developed neurological syndromes
after only one or two doses. They were not
tested for Lyme antibodies before vaccination.
Results
Results of neurological evaluation and ancillary
investigations of the six patients are summarized in
Table 1. Two of the patients had cognitive impairment,
Address correspondence to: Norman Latov, MD, PhD, The
Peripheral Neuropathy Center, Weill Medical College of Cornell
University, New York, NY 10022, USA. Tel: �1-212-888-8516;
Fax: �1-212-888-9206; E-mail: [email protected]
Journal of the Peripheral Nervous System 9:165-167 (2004)
_ 2004 Peripheral Nerve Society 165 Blackwell Publishing
two had demyelinating neuropathies, one had both
cognitive impairment and demyelinating neuropathy,
and one had cognitive impairment and sensory axonal
neuropathy. In all cases, onset of symptoms was
hours to 8 weeks after vaccination. One of the patients
(patient 2) with demyelinating neuropathy also had
diabetes mellitus, but it is unlikely that the diabetes
was responsible, as it was controlled with diet, the
neuropathy responded to IVIg, and there were no
symptoms of neuropathy before vaccination in contrast
to the severe neuropathy which followed. No
other causes for cognitive impairment or neuropathy
were found in any of the patients.
All four patients with cognitive impairment had difficulty
with concentration, short- and long-term memory
impairment, and chronic fatigue. All four had evidence
on MRI of subcortical white matter lesions (Table 1).
Patients 2 and 3, with CIDP, and patient 1 with
multifocal motor neuropathy, partly improved following
treatment with IVIg, but relapsed, and required
repeated or maintenance therapy. The cognitive
impairment in patients 3, 4, 5, and 6 persisted but
stabilized, both in those that were treated with IVIg
for their demyelinating neuropathy and those that were
not treated. The cognitive impairment was sufficiently
severe, so that the patients could no longer carry out
their usual work-related functions.
Discussion
Neurological syndromes that follow vaccination or
infection are often considered to be immune-mediated
and result from molecular mimicry or non-specific activation
of pre-existing autoreactive lymphocytes (Wraith
et al., 2003). Neurocognitive dysfunction with musculoskeletal
pain and chronic fatigue was also previously
reported in another 15 patients who received the OspA
vaccine, but the patients were not neurologically evaluated
and the symptoms were attributed to reactivation of
Lyme disease, although some of the patients had no
history of exposure (Donta, 2001). Of interest, the only
two patients (patients 4 and 5) in this study to develop
symptoms following the first vaccine gave a history of
previously treated Lyme disease, which might have
primed their immune system to a subsequent challenge.
The incidence of neurological sequelae following
LYMErix vaccination is unknown. No increase in
neurological disease was noted in the original efficacy
studies of the vaccine (Steere et al., 1998) or by the
Vaccine Adverse Event Reporting System (Lathrop
et al., 2002). However, a subsequent comparison to
the adult tetanus-diphtheria vaccine indicated a higher
incidence of `neuropathy and paralysis' in the LYMErixvaccinated
patients, although the diagnoses were not
verified (Geier and Geier, 2002). The vaccine has since
been withdrawn from the market.
Table1. Neurological sequelae following LYMErix vaccination.
Patient (age/sex) Clinical syndrome Onset of symptoms Ancillary studies
1 (56/F) Multifocalmotor neuropathy,
responsive to IVIg
2 months after second vaccine Electrodiagnostic studies ^ multifocalmotor
neuropathy with conduction block
2 (63/M)z Sensorimotor neuropathy,
improved on IVIg
2 months after second vaccine Electrodiagnostic studies ^ severe
demyelinating sensorimotor neuropathy
3 (60/M) Sensorimotor neuropathy,
slightly improved
and stabilized on IVIg;
cognitive impairment*
Hours following third vaccine,
with systemic symptomsy
EMG �NC ^ sensorimotor neuropathy
Nerve biopsy ^ myelinopathy
MRI ^ multiple scattered foci of white
matterT2 hyperintensities, one with
enhancement. CSF ^ normal protein and
cell count
4 (29/F)� Persistent cognitive
impairment
Several days after first
vaccine, with systemic
symptomsy
MRI ^ multiple hyperintense signal
abnormalities in subcortical white matter
CSF ^ normal protein and cell count and
nagative oligoclonal bands
5 (53/F){ Persistent cognitive
impairment
Several days after first vaccine,
with systemic symptomsy
MRI ^ scattered areas of increased
signal in the periventricular region
6 (52/F) Persistent sensory
neuropathy and
cognitive impairment
Several days after the second
vaccine,with systemic
symptomsy
MRI ^ single moderate size focus ofT2
hyperintensityin subcortical white matter.
EMG �NC ^ normal; Skin biopsy ^ reduced
intradermal nerve fiber density; Sural nerve
biopsy ^ axonal neuropathy
*Symptoms of cognitive impairment included forgetfulness with impairment of short- and long-term memory, difficulty in concentrating, and difficulty
in organizing thoughts.
ySystemic symptoms included muscle aches and pains, fever and chills, and fatigue.
zPatient had diabetes mellitus, well controlled with diet and oral medications for 5 years, with no symptoms of neuropathy.
�Patient had history of Lyme disease, diagnosed 1year before LYMErix vaccination, with resolution of systemic symptoms after treatment with antibiotics.
{Patient had history of Lyme disease, diagnosed 1year before first vaccination, with resolution of symptoms after treatment with antibiotics.
Latov et al. Journal of the Peripheral Nervous System 9:165-167 (2004)
166
OspA is a lipoprotein with immuno-stimulatory properties
that can activate pro-inflammatory toll-like receptors
of the innate immune system (Bulut et al., 2001).
Such receptors are also found on Schwann cells, microglia,
astrocytes, and oligodendroglia (Bsibsi et al., 2002;
Oliveira et al., 2003), possibly contributing to the development
of the autoimmune response. It has also been
reported to induce proliferation and apoptosis of astrocytes
(Ramesh et al., 2003) and implicated in the pathogenesis
of Lyme arthritis, possibly through its immuneactivating
mechanisms (Steere and Glickstein, 2004).
Of interest, neuropathy and cognitive impairment,
as seen in the vaccinated patients, are also common
manifestations of chronic Lyme disease that are resistant
to antibiotic treatment (Duray, 1989; Steiner, 2003).
The cognitive impairment, in particular, that is manifested
by forgetfulness, inability to focus, disorganization
of thought, and chronic fatigue, without focal neurological
signs, is not commonly seen in other conditions (Caudino
et al., 1997; Krupp et al., 1991; Morgen et al., 2001). Brain
white matter lesions, as were seen in some of our
patients, can be non-specific in the elderly but were more
numerous or larger than that which would be expected
in our patients' age group and are commonly seen in
patients with chronic Lyme encephalopathy (Morgen
et al., 2001). Neuropathies in patients with chronic
Lyme disease commonly present as nonvasculiticmononeuritis
multiplex (Logigian, 1997; Kindstrand et al.,
2000; Halperin, 2003), but demyelinating neuropathies,
including those with multifocal conduction block, have
also been reported (Oey et al., 1991; Zifko et al., 1995).
The neurological manifestations of chronic Lyme
disease are often attributed to persistent infection,
although autoimmunity has also been suggested
because of the resistance to antibiotics (Halperin, 2003;
Steiner, 2003). The observed similarities between the
neurological manifestations of chronic Lyme disease
and those following vaccination with the OspA protein
suggest that some of the manifestations may result
from autoimmune mechanisms that can be triggered
by infection or vaccination. Similar mechanisms have
been proposed to explain antibiotic-resistant arthritis in
chronic Lyme disease (Steere and Glickstein, 2004).
These observations warrant further investigation.
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