Birdshot
Retinochoroidopathy
An
informational site about BSRC and Uveitis.
It has many
names: birdshot retinochoroidopathy, birdshot choroidopathy, birdshot retinochoroiditis,
birdshot choroidretinitis.
If it is an eye disorder with birdshot in the name, this is the place for
information.
Usually a patient
is diagnosed with uveitis.
This is the inflammation of the uvea in the eye and
has over 100 causes ranging from AIDS to unknown. Typically
the diagnosis of BSRC is made after seeing white and yellow spots in the eye
and followed up with a battery tests ruling out other causes and testing
positive for the presence of HLA-A29.
My birdshot
group:
http://groups.msn.com/BSRC/_whatsnew.msnw
My other
birdshot site:
http://home.comcast.net/~dagmara56/wsb/html/view.cgi-home.html-.html
This
information is paraphrased from The Eye Book by Gary H. Cassel, MD; Mchael D. Billog, OD, and Harry
G. Randall, MD
The eye is
approximately the size of a ping pong ball. The inside
of the eyeball is a jelly-like substance called the vitreous; in the front of
the its held together with the sclera (white of the
eye), in the back its the retina. I'm going to skip
the details about the front of the eye and skip to just the part we are all
interested it: the retina.
Holding the
vitreous jelly together are different membranes: The layers are:
- vitreous
- internal limiting membrane
- blood vessels
- ganglion cells
- bipolar cells
- rod cells
- cone sells
- pigment epithelial cell
- Bruch's
membrane
- choroid
The retina
starts at the blood vessel layer and includes all the layers down to Bruch's
membrane. The choroid is external to the retina. The uvea is a term for the iris, ciliary
bodies and choroid (like this isn't
confusing enough!). Uveitis is the general term for
anything wrong with the uvea. itis means "inflammation of", -opathy means "disease of". Thus
BSRC has so many names depending upon the MD's view of what has gone wrong, the
retina or the choroid. Symptoms of uveitis may be redness, throbbing pain, difficulty
with bright light or silent. Determining the cause of uveitis
is difficult. There are over 100 causes from AIDS to unknown.
I hope you
are all as throughly confused as I am!
Uveitis
by Dr. S. Foster, MEEI
Uveitis
and Other Eye Conditions (includes a personal story)
Birdshot, Retinochoroidopathy
by Dr. Michael Samson Excellent!
Birdshot Chorioretinopathy: Clinical
Characteristics and Evolution
Choroidal Abnormalities In Birdshot Chorioretinopathy: An Indocycanine Green Angiography Study
Retinal Function in Birdshot Retinochoroidopathy
Mintravenous immunoglobulin (IVIg) for the treatment of birdshot retinochoroidopathy
From The
Casey Eye Institute, Department of Ophthalmology
Excellent
source for a basic explanation of uveitis, the eye,
and various medications to include oral and injected steroids, cyclosporin, and other treatments. This site goes into the how, why, of each
medication as well as the side effects.
I have copied only the sections on oral steroids and cyclosporin.
Oral
Corticosteroids
Many
patients with uveitis may be
treated with a hormone known as corticosteroid. This is
most commonly taken by mouth in the form of a pill known as prednisone. Normally
the body produces the equivalent of about 7.5 mg of prednisone per day.
Inflammation is treated with variable amounts of
prednisone. The side effects of prednisone depend upon the individual, the
dosage of therapy, and the duration of therapy. Some of the side effects
associated with prednisone therapy are listed in the
accompanying table. Prednisone has the advantage of working quickly to reduce
the inflammatory response. It is one of the most potent anti
inflammatory medications known. However, it must be
used cautiously because of the numerous side effects. In addition, the
benefits from prednisone may diminish with long standing
use as the body seems to adjust to chronic dosage.
It is often recommended that prednisone be taken in the morning
since the body tends to produce its own cortisone mostly in the early morning
hour. Prednisone is normally taken with food as it can
increase acid production and lead to heart burn or ulcers at higher dosages.
The body can become dependent upon prednisone. Consequently
patients who have been on prednisone for longer periods of time need to reduce
prednisone dosage gradually. Patients on prednisone therapy should normally
carry a card in one's wallet listing this medication. Patients who have surgery
or who are in an emergency situation such as a serious
motor vehicle accident will need to receive extra amounts of prednisone
temporarily since the body normally responds to stress by producing its own
cortisone and its ability to respond to stress disappears when one is taking
prednisone by mouth.
Examples of
corticosteroid side effects:
Weight gain
Facial
puffiness
Fluid
retention
Mood change
Sleep
disturbance
Acne
Lowered
resistance to infection
Diabetes
Easy
bruising
Osteoporosis
Glaucoma
Cataracts
Adrenal suppression
Ulcers
Cyclosporine
Cyclosporine
is an effective medication for the treatment of uveitis
in many instances. Cyclosporine helps to suppress the function of cells in the
immune system without killing those cells. This distinguishes cyclosporine from
other medications such as imuran, methotrexate,
or cytoxan. Cyclosporine is a very popular medication
in the treatment of medications who have received organ transplants. Patients
who receive a donated organ such as a kidney will experience their immune
system trying to reject this donated tissue. Cyclosporine helps to suppress the
immune system sufficiently such that organ rejection is
prevented. Cyclosporine is generally taken as a
capsule every 12 hours. The dosage is based upon one's
weight. Cyclosporine therapy can be associated with side effects
which include flu-like symptoms, muscle cramps, tingling, sore gums, and
hair growth. The chronic use of cyclosporine can cause kidney damage.
Cyclosporine often elevates the blood pressure and an elevated blood pressure
(hypertension) is a relative contraindication to the use of cyclosporine.
Periodic laboratory tests and blood pressure determinations are important for
patients who are receiving cyclosporine therapy. Patients on cyclosporine
therapy may be more likely to develop infections because the immune system is
impaired. Patients with diabetes may experience a worsening of that disease
because of cyclosporine. Nonsteroid antiinflammatory drugs such as ibuprofen, motrin, advil, aleve, naprosyn, aspirin, voltaren, or orudis should be minimized while taking cyclosporine because these
increase the kidney side effects of cyclosporine. In addition, cyclosporine
interacts with many different medications and one may need to check with a
physician specifically about potential interactions. Other names for
cyclosporine include sandimmune or neoral.
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From: C. Michael Samson, M.D.,
Fellow, Ocular Immunology and Uveitis Service,
Harvard Medical School, Massachusetts Eye and Ear Infirmary and C. Stephen Foster,
Professor, Director of Ocular Immunology & Uveitis
Service, Ocular Immunology & Uveitis Service,
Massachusetts Eye & Ear Infirmary
This
is THE BEST explanation I have found for BSRC. Because the
information is copywrited by eMedicine,
it is not possible to reproduce any of the article
here, but I highly recommend using the link to read it. I was
treated by both, Dr. Sampson and Dr. Foster at MEEI, and found them to both be
unusually empathetic and knowledgable physicians.
From:
Retinal Insider, Edited by Jay S. Duker, MD and Carl Regillo, MD
This
disease usually affects middle-aged individuals. There is no gender
predominance.
This may be an autoimmune disease. Almost 90 percent of patients demonstrate
HLA-A29 antigen, the strongest association of all the HLA-associated immune eye
diseases. Presenting symptoms include blurry vision, photopsias,
floaters, and night blindness. Most patients have bilateral involvement.
Ophthalmoscopy reveals multiple white or yellow,
medium to large lesions scattered like "birdshot" around the
posterior pole (Fig. 3). These lesions appear to be at the level of the choroid and deep retina. Posterior vitreous cellular
reaction is always present. Vascular sheathing, disc edema and CME may also
appear. As the lesions mature, they may enlarge, resulting in RPE atrophy. In
the late stages, RPE hyperpigmentation and retinal
arteriolar narrowing can appear, and the disc may be pale. Some patients
develop disc neovascularization and vitreous
hemorrhage.
Angiography reveals marked disc and cystoid macular
leakage. The lesions stain relatively poorly, or not at all. The ERG is usually
abnormal in both rod and cone function.
Because of the vision-threatening nature of this disease, systemic steroids and
sometimes steroid sparing medications such as
cyclosporine are necessary. The response is usually good. Though the disease is
chronic, most patients retain useful vision in at least one eye.
From Priem HA, Oosterhuis JA, Eye
Clinic,
During the
period 1980-6 102 patients from 14 European eye
clinics were diagnosed as having birdshot chorioretinopathy
(BSCR). All were Caucasian, and the series consisted of 47 men and 55 women,
with a mean age of 52.5 years. The major findings in this rare disorder concern
the ocular fundus. Most marked are the patterned distribution
of depigmented spots without hyperpigmentation,
radiation from the optic disc in association with vitritis,
retinal vasculopathy with frequent cystoid macular oedema, and
involvement of the optic nerve head. The distribution and appearance of the
lesions suggest that they are related to the major choroidal veins. Complications of the disease were epiretinal membranes, retinal neovascularisation,
recurrent vitreous haemorrhage, subretinal
neovascular membranes occurring both
in the juxtapapillary and macular regions, and
optic atrophy. The medical history was not contributary.
HLA testing showed very strong disease association with HLA
A29 (95.8%). The evidence suggests that it is a single disease entity
rather than a group of disorders because of the remarkable similarity in the ophthalmological appearance and the clinical course,
combined with the exceptionally high association with HLA A29.
(c) 1988 by the British Journal of Ophthalmology
From: Eye
1997;11, Howe LJ, Stanford MR, Graham EM, Marshall J (
Pt 4):554-9, Department of Ophthalmology, UMDS, London, UKReview
of Opthamology
Birdshot chorioretinopathy is a rare inflammatory disorder with an
insidious onset that can slowly progress to severe visual loss. The
pathogenesis is unknown. This study used indocyanine
green (ICG) angiography to investigate the degree of choroidal
vascular involvement with progression of disease and to determine the nature of
the birdshot lesions. Seven patients with birdshot chorioretinopathy
had ICG angiography performed with a scanning laser ophthalmoscope at various
stages of clinical disease. Results were compared with
fluorescein fundal
angiography (FFA). All large choroidal vessels
appeared normal. The birdshot lesions were demonstrated
with ICG but not with FFA and were represented by dark areas on ICG
angiography. Typically these areas were bordered by
large or medium-sized choroidal vessels and their
appearance suggested small choroidal vessel hypoperfusion. In disease of recent onset, some lesions
masked fluorescence from large underlying choroidal
vessels possibly due to inflammatory choroidal
infiltrates. In long-standing disease, the choroidal angioarchitecture was relatively normal within the birdshot
lesions. This study of birdshot chorioretinopathy
demonstrates abnormalities in the small choroidal
vessels within the birdshot lesions. ICG angiography detects the birdshot lesions
more readily than FFA and may be of benefit in assessing disease activity.
PMID:
9425423, UI: 98086560
From: Ryan
SJ, Maumenee AE; American Journal of Opthamology, 1980 Jan ; 89(1): 31-45
Thirteen
patients had a new syndrome and entity in intraocular inflammation called
birdshot retinochoroidopathy, which was characterized by a white, painless eye with minimal
anterior segment inflammation but particlate debris
in the anterior and posterior vitreous. There was profuse retinal vascular
leakage with resultant retinal macular, and disk edema, which are the primary
causes of the decreased vision in this syndrome. Long-term follow-up (mean of
ten years) revealed that only two patients seemed to respond to
anti-inflammatory therapy (systemic coricosteroids)
and five patients progressed to 6/60 (20/200) or less visual acuity in at least
one eye.
PMID:
7346785, UI: 80106925
From: Eye
Research Institute,
The electroretinograms (ERGs) of 15
patients with birdshot retinochoroidopathy varied
from super-normal to non-recordable, depending upon the severity and the stage
of the disease. The abnormal ERGs were
characterized by a disproportionate decrease of the b-wave amplitude
compared with the a-wave amplitude demonstrating the negative (-) type
response. This distinct ERG pattern has not been observed
in any other type of uveitis or chorioretinitis,
and appears specific to birdshot retinochoroidopathy.
ERG findings indicate that in birdshot retinochoroidopathy
the neural layers of the retina are more diffusely and severly
involved than the receptor-retinal pigment epithelium-choroid
complex. In the most advanced stage, the patient becomes night blind with a
non-recordable ERG, a situation that is essentially the same as retinitis pigmentosa, except that pigmentation is conspicuously
absent in the fundus.
PMID:
1927315, UI: 92024929
Intravenous
immunoglobulin (IVIg) for the treatment of birdshot retinochoroidopathy Ocular Immunology and
Inflammation
Phuc LeHoang1,
Nathalie Cassoux1, Françoise George2, Nathalie Kullmann1
and Michel Kazatchkine2
1University Pierre et Marie Curie, Hôpital
de la Pitié-Salpêtrière, Department of Ophthalmology,
Paris, France
2University Pierre et Marie Curie, Hôpital
Broussais, Department of Immunology, INSERM U430,
Paris, France
Intravenous
polyclonal immunoglobulin (IVIg) treatment has been successfully used in a number of autoimmune
conditions. Birdshot retinochoroidopathy (BRC) is a
bilateral autoimmune posterior uveitis which, in its progressive form, frequently requires
immunosuppressive therapy. We report a clinical study aimed at determining the
tolerance and efficiency of IVIg treatment in
patients with active BRC. The study was conducted in
an open manner. Eighteen patients were included. The initial visual acuity (VA)
was ≤20/30 in 26 eyes, 20/25 in five eyes, and 20/20 in five eyes. IVIg was given as sole treatment
at 1.6 g/kg every four weeks for six months, followed by injections of 1.2-1.6
g/kg at six to eight-week intervals. The mean follow-up was 39 months, ranging
between 12 and 53 months. The results showed that the final VA of the 26 eyes
with an initial VA of ≤20/30 was increased by two lines or more in 14
eyes (53.8%) and decreased in two (7.7%). Of the five eyes with an initial VA
of 20/25, four had improved to 20/20 and one remained stable. Of the five eyes
with an initial VA of 20/20, four remained stable and one deteriorated to
20/25. When present, macular edema was improved in
half of the eyes on fluorescein angiography. Benign
side effects were observed in 12 patients: moderate
transient arterial hypertension (7), headache (6), eczematous lesions (6), and
hyperthermia (4). The results suggest that IVIg may
represent a safe alternative therapy for patients with BRC.
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In 1991, when I was 34 years old, while driving home from work, I
noticed some floaters in my right eye. Two days later, I noticed the same
floaters were still in my right eye, as well as my left. I knew enough about
biology to realize floaters didn't migrate from eye to
the other, and spent the next day in search of an opthamologist.
The opthamologist I went to told me he thought he
knew what the problem was, and it was not serious, but since he had never seen
an actual case, he referred me to a retinologist for
confirmation. I didn't want to go to the retinologist, but my husband co-erced
me.
I knew I was in trouble when the retinologist
asked me into his office. I sat down, I
was by myself, because I was so sure it was
“nothing”. The retinologist
told me I had uveitis, that I was going to go blind. I asked him, what is the cause of uveitis? He told me:
number 1 cause was AIDS, #2, syphilis, #3 TB, #4/5; kidney/liver failure, 20%
of the time it was idiopathic, no known cause.
Think of uveitis as a rash; something else
causes it, and it is up to your MD to find the source. Based on my experience
with three different MDs at three different times, they tend to start with
testing for AIDS, syphilis, lupus, arthritis, TB, liver and kidney malfunction.
In my case, everything they tested for came back negative. If the cause is unknown it is referred to as ideopathic;
ideopathic uveitis occurs
in about 20% - 30% of uveitis cases. That other 20 – 30% can be nearly 100 other
conditions, so it takes quite a bit of knowledge on the part of the MD to
determine what the cause is; this is why its great to see an expert, such as Dr.Stephen Foster, MERSI.
(http://www.uveitis.org/contact.html)
I remember sitting there, his mouth was opening and closing, and I went
deaf. I couldn’t
hear a word he said, I saw his mouth moving, but no sound was coming out. The next thing I knew, I was standing in my
kitchen. I know that I went to a clinic
and an xray taken, who knows what else happened, but
I have no recollection of this. So, I was standing in the kitchen, with my husband and the
phone, and I said to him, good news is, I’m going blind. Bad news is, there is a
80% chance I have AIDs, syphilis, TB, kidney or liver
failure. I don’t
remember what happened after that, but he came home with a bouquet of
carnations and a box of chocolates and said, you’ll be okay. I told him, I will never be okay, I’ll be freaking blind, and there are no jobs for blind
software engineers. He told me, okay,
you had your cry and your pity party, now get off your butt and make some plans
and some decisions. I told him again,
are you nuts? There are NO FREAKING JOBS
FOR BLIND DATABASE ADMINSTRATORS. He
said to me, (very patiently), you trained to be a software engineer, didn’t you? Well, you
are more than just a software engineer, and you can be retrained. Now, go figure out what you can do if you go
blind, and get some training in that. I
thought, okay, there are blind people out there working every day, if they
could do it, so can I. And so, I calmed down.
I had to quit my consulting practice, because I had to see the MD every
other day. My optic nerves were under a
great deal of pressure, and my retinologist started
me on a course of steroids. After the completion of the course, I was taken off steroids, and the uveitis
came back. This continued for another cycle; after the third cycle the uveitis was quiet and I was declared
"cured". My vision was 20/20, but with little gray dots in both eyes;
this was annoying, but not life-changing. I went back to work, and life was good.
I've always felt there
was a reason for the 1991 episode, and that it would return. In 1999, I had a
hemorrhage in the left eye requiring laser surgery to seal the tear. My opthamologist
assured me it was just a one-time occurrence not related to my previous episode
of uveitis; I was not convinced. My primary care physician, Dr. David Deems,
of
For those of you who have this condition, it may not be as terrible as
it initially seems. For me, there were three distinct phases: the initial
bleeds, the dispersion of the blood clots, and the final "settling".
When the hemorrhages first occur, the blood clots appear to be large
brown amoebas "swimming" about the eye. I refer to them as
"tadpoles" because they are brown in color, and over time the clots developed a tail. It has some odd side
effects. I drove my husband crazy swatting and stomping on imaginary insects;
it turned out the things flying around my head or crawling around on the floor
were merely my "tadpoles". Another problem I encountered was I became
horribly seasick. The tadpoles were swimming from side-to-side, with a slight
up-and-down motion. I was not able to read, do computer work, or drive for more
than a few minutes at a time without feeling as though I was standing on the
deck of a ship in the middle of an Atlantic storm. After a few weeks, I adapted
and nausea was no longer a problem.
In the second phase, the clots thinned, but were
distributed throughout the eye fluid, which appeared as though I was
looking through muddy brown river water. This was more frightening to me than
the initial hemorrhages as I lost more vision. Gravity and physics eventually
play their part, and in the settling phase, the blood particles and small clots
fell to the bottom of my eye. The larger clots have thinned so they appear to
be greasy, opaque blobs that still "swim" around in the center of my
vision. Oddly, we see opposite, so the streamers and debris appear to me to be
at the top of the eye, like little brown lightening bolts. I found wearing dark
tinted glasses help immensely with my increased sensitivity to light and it
reduces the contrast between my eye debris and my visual field.
I've experienced few
effects, none are greatly life changing. One loss is the ability to do
"fine" work; I can not knit or embroider
with itsy bitsy needles. Using tweezers or other such items is difficult, but I've found special supplies for the visually disabled with
magnifiers help (check out http://www.lighthouse.org/). I can't read tiny print, or print with little
contrast (and for some reason, my co-workers enjoy making powerpoint
slides that are dark with lines so I can't read the print). To solve this, my
husband gave me a beautiful gold magnifier that hangs on a chain; so I can wear it around my neck during work to magnify the
print. I no longer drive at night or before daylight, since its
difficult for me to see in the dark (I'm the opposite of a vampire, I can only
come out during daylight hours). I had
difficulty in driving during twilight and storms; this was
alleviated by a brainstorm my husband had, by using driving/shooting
lenses. These are amber/yellow lenses
which intensive the light and sharpen things up. Clip ons can be purchased at sporting goods stores for around $10,
glasses can be purchase for around $20.
I have two pair of Fitovers; Fitover Shooting glasses, and Fitover
Sunglasses; I highly recommend both; an example are
at:
Two areas that did cause me some distress was I
could not read or sit in front of a PC for long periods of time (challenging
for someone who is a systems analyst). My retinologist
told me to limit my computer work and/or reading to 45 - 50 consecutive minutes
and rest my eyes for 10 - 15 minutes; no more than 8 -
9 hours per day. When I tried
to cheat, I experience excruciating pain in both of eyes as well
as recurrence of flashing lights. It hurts enough that I adhered very strictly
to her guidelines. For me, it feels as though someone has rubbed the back of my
eyes with sandpaper, and as though I'm being stabbed
through my eyes. It starts at the back and continues through
the entire eyeball with such a force it literally makes me physically ill.
So if your retinologist tells you to limit your
reading, DO IT!
Additional restrictions may include no physical exertion, sleeping on
three pillows, keeping my head propped up above my torso (don't
forget to tell your dentist so they don't drop your head down too low!), and
resting my eyes as much as possible. When I've tried
to do moderate exercise, I have "flashing lights"; and Dr. Dharma has
put fear in my heart that flashing lights are bad if you have BSRC. Therefore,
if you have uveitis or BSRC, the presence of flashing
lights should warrant a visit to your MD to ensure all is well. I was
restricted from lifting more than 5 lbs, (which in my case required cleaning
out my purse). After work, I go home, sit in my chair, and wear an eye shade. Ask your relatives and friends to buy audio books
for you to keep from going crazy on the weekends.
I was treated originally consists of steroids and cyclosporin
in varying doses. Cyclosporin is the same drug given to transplant patients to prevent organ
rejection, it dampens the immune system. There
are some unpleasant side effects from the cyclosporin:
bleeding gums, tremors, growing hair where it shouldn't, losing hair where it
should be; and damage to the liver and kidneys to name a few.
Taking immunosupprssants can increases one's probability of contracting lymphoma, so you
don't want to stay on this treatment any longer than necessary. However, please remember, that thousands,
(millions?) of transplant patients are out there, walking around, living their
life, and they are on much higher doses of immuno-suppressants
than we take, for many more years than we take, and never get lymphoma.
Taking prednisone over 5 mg/day makes me either ravenously hungry or
horrendously nauseous. I had hirsuitism, growing facial hair, and looked like
monkey woman. A very,
round-faced, monkey woman. If
you are a woman, I recommend waxing the face; it removes the unwanted hair,
leaves your skin a glowing pink, and when you are off the drugs, the hair will
stop growing, and you will never knew there was problem. If you do not know how to wax, I highly
recommend spending the $12 every 2 months to have a professional do it for
you. When I was looking in the mirror
one day, complaining about my fat face, and that I would never see my checkbones again, my husband asked me, would you rather
never see your fat face, or never see? Point taken. Fear
not, if you work at it, the weight can be lost as well.
Staying away from crowds and sick people are
recommended. So far I have been extraordinarily
lucky in staying well. I attribute this to avoidance of stores (my husband does
the grocery shopping these days and I purchase other stuff via catalogs or the
Internet), no traveling. The few times I venture out to eat,
I ensure I wash my hands before I eat; in fact, I wash my hands after I get to
work or touch anything in a public place (at least the length of the time it
takes to sing "Twinkle Twinkle Little Star"
per Discovery Magazine and strict instruction from my good friend
For me, cyclosporin and steriods
made me tire easily. Initially, I could barely make it through the work day, and when I came home I'd eat, lay down, and sleep
for three or four hours before going to bed. I've
found two herbs that work wonders: ashwaghandra,
which is for energy; and shizandra, which flushes
toxins out of the liver; (I found out about these from Prevention magazine).
This is not a medical recommendation, merely a personal anecdote.
I am currently on Cellcept and prednisone, and
to date, have not had any new flares.
BSRC may change your life, but it is not
necessarily the total loss of vision you may believe it is. If you are
living with someone with BSRC, try to be patient, because having
"stuff" swimming around in your eyes and facing possible blindness is
quite frightening and takes some adjustment. When I first had uveitis in 91, I was an emotional wreck because I was
terrified I would lose my sight. Knowing I have BSRC actually had a calming
effect, because I know what I'm up against, and what
the odds are. In my case, I'm on the treatment to save my sight, but there are
days when I wonder if the treatment is not worse than going blind; and then I
look at my husband and I have my answer. I hate to go to sleep at night,
because I always wonder if I'll be able to see in the
morning. Each morning I wake up and I do see, I feel I've
received a precious gift. No one knows what will happen in life, and we just
have to adjust to whatever occurs. For those of you with uveitis
or BSRC, it will take some emotional adjustment, and some counseling is not a
bad idea. For those of you living with someone with this; try to be
understanding; sometimes the patient needs to vent and
be angry.
I have a support group, and recommend interested individuals to read the
posts:
http://groups.msn.com/BSRC/_whatsnew.msnw
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If you
would like to participate in a community of those interested in or have BSRC,
you are invited to join our group at:
http://groups.msn.com/BSRC/_whatsnew.msnw
My second
web site:
http://home.comcast.net/~dagmara56/wsb/html/view.cgi-home.html-.html
If you have
questions, concerns, etc. feel free to email me:
Dagmar Bogan
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updated: