-
New Forum Software Installed (Still a few issues but reopening the forum) More details.
Open Medicine Foundation (OMF)
- Thread starter DokaGirl
- Start date
Samuel
Senior Member (Voting Rights)
Merged thread
===
From the desk of Ronald W. Davis, PhD
Chair of OMF Scientific Advisory Board
ME/CFS Working Group at Stanford Meeting September 8-10, 2021
Summary by Ronald W. Davis, PhD, and Janet L Dafoe, PhD
This was a great meeting and showed a lot of activity and progress in
ME/CFS research in an ever-growing number of groups. Researchers
presented unpublished and often preliminary results. This style of
scientific meeting can greatly accelerate research because scientists
learn new information much earlier. It can often take a year or more
to get a research paper published. Because of the preliminary nature
of the results, it is essential that they remain confidential and not
made public. Therefore, this is a summary without too many details.
The speakers are listed at the end.
There is continued search for a pathogen(s) that can sustain ME/CFS.
Most studies look for DNA or RNA from a pathogen. In addition, EBV and
HHV6 have gained renewed interest for researchers due to evidence of
activation of these viruses in the absence of DNA replication and
amplification.
There were a number of talks about the metabolomics of ME/CFS. This
work is moving from finding lists of metabolites involved in the
disease to investigating various metabolic pathways. A major focus is
on the nitrogen and BH4 pathways. There is a new focus on pathways in
the mitochondria. This is difficult to study because of the small
amount of mitochondrial metabolites in blood samples. However, this
focus may be at the heart of what=E2=80=99s wrong in ME/CFS.
There was new work presented regarding autoantibodies and immune
dysregulation. It is believed this dysregulation is what is causing
autoantibodies to be present. The next question is, =E2=80=9CWhat is causin=
g
the immune dysregulation?=E2=80=9D There was also new work on
neuro-inflammation, which also might result from the immune
dysregulation.
There was a preliminary report of the molecular changes occurring with
PEM. This will be a major endeavor.
A major effort was reported of an extensive genetic analysis from
published and unpublished DNA sequence data looking for single genes
and combinations of genes and any correlations with phenotypes. This
is the first attempt to put together these previously disparate groups
of data, and it was exciting to see. Thus far, the results are
preliminary, but this is a very important investigation.
We heard an update on red cell deformability. In previous work, some
labs have found a difference in red cell deformability between
patients and healthy controls, and one lab found no difference.
However, it was recently discovered that oxygen levels in the blood
have a major impact on deformability. New instruments are being
developed to measure deformability under controlled oxygen levels.
There is a clear difference in deformability between patients and
healthy controls under low blood oxygen levels. Thus, this continues
to provide promise for a fast and inexpensive biomarker and diagnostic
test.
New results on metabolic traps were presented. It is possible that
there are many different metabolic traps and that these traps may be
the cause of a number of chronic diseases. The tryptophan to
kynurenine trap has been the first to be explored as an underlying
cause of ME/CFS. This trap was first demonstrated in a test tube using
purified enzymes, but does it exist in vivo in isolated cells? Yes! It
was demonstrated that yeast with the Human IDO1 gene inserted into it
became trapped when tryptophan was increased in the medium. Work is
now progressing to determine if human cells can be trapped. Using the
yeast system, screening is proceeding for an FDA approved drug that
will reactivate the Human IDO1 enzyme and get the cell out of the
trap. In addition, a new trap or energy bypass in mitochondria was
presented that could explain the low energy in patients and PEM.
In between the presentations, there was a significant amount of time
for questions, discussions, brainstorming and the forming of
collaborations. It felt like the research on ME/CFS has reached a new
level, and it engendered an ever growing spirit of hope for eventual
treatments and a cure.
Participants:
Christopher Armstrong, Rahaf Assil, Lucinda Bateman, Jonas Bergquist,
Joseph Breen, Lily Chu,Jane Collins, Laurel Crosby, Janet Dafoe, Mark
Davis, Ron Davis, Kenny de Meirleir, Mary Dimmock, Donna Felsenstein,
Jennifer Frankovich, Keith Geraghty, Arnaud Germain, Anna Gil, Ludovic
Giloteaux, Eric Gordon, Michael Gresser, Andrew Crimson, Paul Guyre,
Rebecca Hamlin, Maureen Hanson, Ashley Haugen, Craig Heller, Katrina
Hong, Mady Hornig, Li-Yuan Hung, Fereshteh Jahaniani, Michael Jensen,
Sharada Kalanidhi, David Kaufman, Betsy Keller, Ryan Kellog, Vinod
Khosla, Seoyeon Kim, Nancy Klimas, Kevin Kramer, Crystal Lantz, Joshua
Leisk, Susan Levine, Alan Light, Kathleen Light, Ami Mac, Jessica
Maya, Roya Mazrouei, Neil McGregor, Alain Moreau, Karl Morten, Adam
O=E2=80=99Neal, Anna Okumu, Robert Phair, Bhupesh Prusty, Anand
Ramasubramanian, Amit Saha, Carmen Scheibenbogen, Liisa Selin, Jaime
Seltzer, Amrit Shahzad, Peidong Shen, Richard Simpson, Michael Snyder,
Rivka Solomon, Franziska Sotzny, Linda Tannenbaum, Ronald Tompkins,
David Tuller, Marielle van Kooten, Vanessa Velasco, Jiandi Wan, John
Whiting, Vicky Whittemore, Julie Whilhelmy, Wenzhong Xiao, Sitong Zhou
We are all extremely grateful to all the funders of this research,
including NIH, OMF, Vinod Khosla, international funders, and the
awesome generosity of patients and their loved ones. As usual, the
progress of this research is always slower than it potentially could
be due to limited funds. Donations are so deeply appreciated!
And don't forget: Donations received from now until November 30, 2021
will be TRIPLE matched up to $600,000. So if you donate $10, you
really donate $30!
Donate Now
https://www.omf.ngo/?form=3DTripleTuesday2021
More ways to donate
===
from tom kindlon, public
===
From the desk of Ronald W. Davis, PhD
Chair of OMF Scientific Advisory Board
ME/CFS Working Group at Stanford Meeting September 8-10, 2021
Summary by Ronald W. Davis, PhD, and Janet L Dafoe, PhD
This was a great meeting and showed a lot of activity and progress in
ME/CFS research in an ever-growing number of groups. Researchers
presented unpublished and often preliminary results. This style of
scientific meeting can greatly accelerate research because scientists
learn new information much earlier. It can often take a year or more
to get a research paper published. Because of the preliminary nature
of the results, it is essential that they remain confidential and not
made public. Therefore, this is a summary without too many details.
The speakers are listed at the end.
There is continued search for a pathogen(s) that can sustain ME/CFS.
Most studies look for DNA or RNA from a pathogen. In addition, EBV and
HHV6 have gained renewed interest for researchers due to evidence of
activation of these viruses in the absence of DNA replication and
amplification.
There were a number of talks about the metabolomics of ME/CFS. This
work is moving from finding lists of metabolites involved in the
disease to investigating various metabolic pathways. A major focus is
on the nitrogen and BH4 pathways. There is a new focus on pathways in
the mitochondria. This is difficult to study because of the small
amount of mitochondrial metabolites in blood samples. However, this
focus may be at the heart of what=E2=80=99s wrong in ME/CFS.
There was new work presented regarding autoantibodies and immune
dysregulation. It is believed this dysregulation is what is causing
autoantibodies to be present. The next question is, =E2=80=9CWhat is causin=
g
the immune dysregulation?=E2=80=9D There was also new work on
neuro-inflammation, which also might result from the immune
dysregulation.
There was a preliminary report of the molecular changes occurring with
PEM. This will be a major endeavor.
A major effort was reported of an extensive genetic analysis from
published and unpublished DNA sequence data looking for single genes
and combinations of genes and any correlations with phenotypes. This
is the first attempt to put together these previously disparate groups
of data, and it was exciting to see. Thus far, the results are
preliminary, but this is a very important investigation.
We heard an update on red cell deformability. In previous work, some
labs have found a difference in red cell deformability between
patients and healthy controls, and one lab found no difference.
However, it was recently discovered that oxygen levels in the blood
have a major impact on deformability. New instruments are being
developed to measure deformability under controlled oxygen levels.
There is a clear difference in deformability between patients and
healthy controls under low blood oxygen levels. Thus, this continues
to provide promise for a fast and inexpensive biomarker and diagnostic
test.
New results on metabolic traps were presented. It is possible that
there are many different metabolic traps and that these traps may be
the cause of a number of chronic diseases. The tryptophan to
kynurenine trap has been the first to be explored as an underlying
cause of ME/CFS. This trap was first demonstrated in a test tube using
purified enzymes, but does it exist in vivo in isolated cells? Yes! It
was demonstrated that yeast with the Human IDO1 gene inserted into it
became trapped when tryptophan was increased in the medium. Work is
now progressing to determine if human cells can be trapped. Using the
yeast system, screening is proceeding for an FDA approved drug that
will reactivate the Human IDO1 enzyme and get the cell out of the
trap. In addition, a new trap or energy bypass in mitochondria was
presented that could explain the low energy in patients and PEM.
In between the presentations, there was a significant amount of time
for questions, discussions, brainstorming and the forming of
collaborations. It felt like the research on ME/CFS has reached a new
level, and it engendered an ever growing spirit of hope for eventual
treatments and a cure.
Participants:
Christopher Armstrong, Rahaf Assil, Lucinda Bateman, Jonas Bergquist,
Joseph Breen, Lily Chu,Jane Collins, Laurel Crosby, Janet Dafoe, Mark
Davis, Ron Davis, Kenny de Meirleir, Mary Dimmock, Donna Felsenstein,
Jennifer Frankovich, Keith Geraghty, Arnaud Germain, Anna Gil, Ludovic
Giloteaux, Eric Gordon, Michael Gresser, Andrew Crimson, Paul Guyre,
Rebecca Hamlin, Maureen Hanson, Ashley Haugen, Craig Heller, Katrina
Hong, Mady Hornig, Li-Yuan Hung, Fereshteh Jahaniani, Michael Jensen,
Sharada Kalanidhi, David Kaufman, Betsy Keller, Ryan Kellog, Vinod
Khosla, Seoyeon Kim, Nancy Klimas, Kevin Kramer, Crystal Lantz, Joshua
Leisk, Susan Levine, Alan Light, Kathleen Light, Ami Mac, Jessica
Maya, Roya Mazrouei, Neil McGregor, Alain Moreau, Karl Morten, Adam
O=E2=80=99Neal, Anna Okumu, Robert Phair, Bhupesh Prusty, Anand
Ramasubramanian, Amit Saha, Carmen Scheibenbogen, Liisa Selin, Jaime
Seltzer, Amrit Shahzad, Peidong Shen, Richard Simpson, Michael Snyder,
Rivka Solomon, Franziska Sotzny, Linda Tannenbaum, Ronald Tompkins,
David Tuller, Marielle van Kooten, Vanessa Velasco, Jiandi Wan, John
Whiting, Vicky Whittemore, Julie Whilhelmy, Wenzhong Xiao, Sitong Zhou
We are all extremely grateful to all the funders of this research,
including NIH, OMF, Vinod Khosla, international funders, and the
awesome generosity of patients and their loved ones. As usual, the
progress of this research is always slower than it potentially could
be due to limited funds. Donations are so deeply appreciated!
And don't forget: Donations received from now until November 30, 2021
will be TRIPLE matched up to $600,000. So if you donate $10, you
really donate $30!
Donate Now
https://www.omf.ngo/?form=3DTripleTuesday2021
More ways to donate
===
from tom kindlon, public
Last edited by a moderator:
Kiristar
Senior Member (Voting Rights)
Merged thread
3 New OMF Studies on Biomarkers, Phenotyping and ME onset post Covid
I thought that this Article Interviewing Alain Moreau was Interesting and the research studies outlined seem to focus on really key aspects. Ie Onset, Biomarkers for diagnosis (and destigmatization) and the Phenotyping challenge.
To have found 11 potential Biomarkers over 90% accurate sounds great but I have read so many study results in the last 4 years now that claim x or y finding represents a good potential Biomarker and should be developed further but nothing ever happens. It's a shame we can't find all such report authors lock them in a room and do one big master "Biomarker or bust" project until one wins!
Surely by now a combination of 2 or 3them would be sufficient to isolate disease, phenotype and duration variables?? Sigh. It really frustrates me.
But I digress, good focused work by the Canadian Moreau team anyway by the sounds of it.
Link
https://www.omfcanada.ngo/three-new-groundbreaking-research-projects/
Text pasted
(forgive the FR plug it's from their fb page)
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME / CFS) Post Treatment Lyme Disease Syndrome (PTLDS), Fibromyalgia Leading Research. Delivering Hope.Open Medicine Foundation® Canada
3 New OMF Studies on Biomarkers, Phenotyping and ME onset post Covid
I thought that this Article Interviewing Alain Moreau was Interesting and the research studies outlined seem to focus on really key aspects. Ie Onset, Biomarkers for diagnosis (and destigmatization) and the Phenotyping challenge.
To have found 11 potential Biomarkers over 90% accurate sounds great but I have read so many study results in the last 4 years now that claim x or y finding represents a good potential Biomarker and should be developed further but nothing ever happens. It's a shame we can't find all such report authors lock them in a room and do one big master "Biomarker or bust" project until one wins!
Surely by now a combination of 2 or 3them would be sufficient to isolate disease, phenotype and duration variables?? Sigh. It really frustrates me.
But I digress, good focused work by the Canadian Moreau team anyway by the sounds of it.
Link
https://www.omfcanada.ngo/three-new-groundbreaking-research-projects/
Text pasted
(forgive the FR plug it's from their fb page)
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME / CFS) Post Treatment Lyme Disease Syndrome (PTLDS), Fibromyalgia Leading Research. Delivering Hope.Open Medicine Foundation® Canada
More at link
Last edited by a moderator:
Mij
Senior Member (Voting Rights)
From the link above:
"Those results add to our understanding of Brain Fog and, combined with the OMF-funded neuroinflammation study described above, open the door to potential treatment for people with ME/CFS. If microglial activation is identified in the brains of people with ME/CFS, Harvard researchers would have a compelling and unprecedented “compassionate use” argument to launch a drug trial of medications used to treat other types of brain impairment.
Inflammation in the central nervous system (CNS) could significantly contribute to many neurological symptoms in ME/CFS, including non-restorative sleep, cognitive impairment, circadian rhythm disturbances, and sensory sensitivities".
If this is the case then wouldn't a drug alleviate physical impairment and PEM too? I don't have neuroinflammation based on the results/symptoms they describe.
"Those results add to our understanding of Brain Fog and, combined with the OMF-funded neuroinflammation study described above, open the door to potential treatment for people with ME/CFS. If microglial activation is identified in the brains of people with ME/CFS, Harvard researchers would have a compelling and unprecedented “compassionate use” argument to launch a drug trial of medications used to treat other types of brain impairment.
Inflammation in the central nervous system (CNS) could significantly contribute to many neurological symptoms in ME/CFS, including non-restorative sleep, cognitive impairment, circadian rhythm disturbances, and sensory sensitivities".
If this is the case then wouldn't a drug alleviate physical impairment and PEM too? I don't have neuroinflammation based on the results/symptoms they describe.
John Mac
Senior Member (Voting Rights)
An update from Dr. Ron Davis:
Improving diagnostic tools for ME/CFS
#TripleGivingTuesday Research Update
As OMF comes closer to the end of its #TripleGivingTuesday campaign, I’m pleased to share this special Research Update for our supporters.
OMF has recently funded a project, under my direction, at University of California, Davis to improve a microfluidic diagnostic device to measure red blood cell deformability in people with ME/CFS. This effort is led by Jiandi Wan and Sitong Zhou, in collaboration with myself and my colleague, Mohsen Nemat-Gorgan of the ME/CFS Collaborative Research Center at Stanford University.
Several prior studies have implicated a role of “oxidative” stress in ME/CFS. Red blood cells (RBCs) are potent scavengers of oxidative stress and their shape changes noticeably in response to oxidative stress; this has also been observed in certain inflammatory conditions including obesity and diabetes. The shape of RBCs determines how well these cells can move through blood vessels, so it seems pertinent to determine if RBCs in ME/CFS patients are affected. This has led to the development of a microfluidic device that mimics blood flow through microcapillaries.
We are developing a recording device using electrical flow to measure RBC movement and measure differences in cell velocity. It will be inexpensive and easy to operate in different clinical settings, and in a relatively short time.
The project undertaken by the team at UC Davis includes:
Improving diagnostic tools for ME/CFS
#TripleGivingTuesday Research Update
As OMF comes closer to the end of its #TripleGivingTuesday campaign, I’m pleased to share this special Research Update for our supporters.
Several prior studies have implicated a role of “oxidative” stress in ME/CFS. Red blood cells (RBCs) are potent scavengers of oxidative stress and their shape changes noticeably in response to oxidative stress; this has also been observed in certain inflammatory conditions including obesity and diabetes. The shape of RBCs determines how well these cells can move through blood vessels, so it seems pertinent to determine if RBCs in ME/CFS patients are affected. This has led to the development of a microfluidic device that mimics blood flow through microcapillaries.
We are developing a recording device using electrical flow to measure RBC movement and measure differences in cell velocity. It will be inexpensive and easy to operate in different clinical settings, and in a relatively short time.
The project undertaken by the team at UC Davis includes:
- Designing and fabricating new microfluidic devices with implanted microelectrodes inside the channel
- Testing the device using RBCs from healthy controls and ME/CFS patients under hypoxia (low levels of oxygen)
- Testing the behavior of RBCs suspended in their respective plasma, compared with a phosphate-buffered saline solution for sensitivity and reproducibility, and for possible effects on cell speed; and
- Calibrating the device using RBCs from healthy controls with different age groups and gender, and thereby establishing the related “normal ranges”, which can subsequently be used for patient diagnosis.
There is to be a new announcement/interview with Dr. Ron Davis today. I do not know what time. Someone please post. All I have is the you tube account:
https://www.youtube.com/channel/UCFPlxCFpu1L9nI2oJjXhr3w
Thank you.
https://www.youtube.com/channel/UCFPlxCFpu1L9nI2oJjXhr3w
Thank you.
The video and discussion have been moved to this thread:
Dr Ron Davis Gives Updates on ME/CFS research - September 2019 onwards
Sly Saint
Senior Member (Voting Rights)
An Update from Dr. Chris Armstrong,
Director of the Melbourne ME/CFS Collaboration
https://www.omf.ngo/an-update-from-dr-chris-armstrong/
Director of the Melbourne ME/CFS Collaboration
https://www.omf.ngo/an-update-from-dr-chris-armstrong/
Possibly James May
Established Member
Here we go again...
Last edited by a moderator:
TiredSam
Committee Member
Another one for the album. On Jan 1st 2021 Whitney wished us "Happy Cure Year" on facebook, so I was expecting a cure in the next 3 days. We are now in our 6th year of those folks at OMF promising us great things just around the corner. You'd think they'd have realised by now that things don't happen as quickly as they expect, and to modify their PR accordingly to reflect reality and experience. Why do they think it's so important to keep on offering us "hope"?
https://www.s4me.info/threads/open-medicine-foundation-omf.11075/page-6#post-316086
https://www.s4me.info/threads/open-medicine-foundation-omf.11075/page-6#post-316086
Last edited by a moderator:
Possibly James May
Established Member
@TiredSam, they know exactly what they're doing. Every 6 months to a year, there is a vague update saying a cure is right around the corner that conveniently coincides with a fundraiser. The cure year was to get enough patients to buy The Puzzle Solver so it could become a NYT bestseller, before that for a few years it was Ron giving video updates right before or during May Momentum or Triple Tuesday alluding to they were close to solving ME.
They have a captive audience that is blinded by desperation. I've emailed multiple people at the OMF about toning down the claims of cures right around the corner, but it seems to fall on deaf ears. I touched on it in a previous post they might be able to acquire funding at the micro level (patients on fixed incomes or on disability), but not being able to back up their claims, they're just throwing their reputation down the shitter, as well as harming ME's legitimacy. Other ME researchers publicly and privately have expressed Dr. Davis & familys claims are highly unethical and unfounded.
I know this is hard for some people to hear, but it's time for The Puzzle Solver to hang it up. He's solely riding on his past performance. Past performance is no guarantee of future results. We're going on 5 years of nanoneedle R&D and no diseases officially have been tested to compare against ME patients. Not anxiety, depression, PTSD, diabetes, cancer, nothing. The NIH doesn't want to fund it for "ridiculous reasons" (1,3,4), and the private sector is allegedly not interested in it. Who the hell knows what's really going on with the metabolic trap. Every time they talk about it now the research is halted because they need some trivial amount of money to fix or buy something critical to research that could easily be covered by the OMF. The Kynurenine trial you need to pull teeth just to get the answer they postponed it because of Covid. The cure year fell off the face of the earth when Whitney's "I feel like shit" post came out (can't find the post, assuming it got deleted. Happened around the end of June).
I'm sorry if this comes off harsh. I'm just tired of people preying on desperate and cognitively impaired patients to fund their projects. They claim they care about the patients, but all I see is plastic carrots being dangled in front of patients who are dealing with housing instability, physical and/or emotional abuse, lack of care/empathy from medical professionals, and planning suicides. It's just wrong.
They have a captive audience that is blinded by desperation. I've emailed multiple people at the OMF about toning down the claims of cures right around the corner, but it seems to fall on deaf ears. I touched on it in a previous post they might be able to acquire funding at the micro level (patients on fixed incomes or on disability), but not being able to back up their claims, they're just throwing their reputation down the shitter, as well as harming ME's legitimacy. Other ME researchers publicly and privately have expressed Dr. Davis & familys claims are highly unethical and unfounded.
I know this is hard for some people to hear, but it's time for The Puzzle Solver to hang it up. He's solely riding on his past performance. Past performance is no guarantee of future results. We're going on 5 years of nanoneedle R&D and no diseases officially have been tested to compare against ME patients. Not anxiety, depression, PTSD, diabetes, cancer, nothing. The NIH doesn't want to fund it for "ridiculous reasons" (1,3,4), and the private sector is allegedly not interested in it. Who the hell knows what's really going on with the metabolic trap. Every time they talk about it now the research is halted because they need some trivial amount of money to fix or buy something critical to research that could easily be covered by the OMF. The Kynurenine trial you need to pull teeth just to get the answer they postponed it because of Covid. The cure year fell off the face of the earth when Whitney's "I feel like shit" post came out (can't find the post, assuming it got deleted. Happened around the end of June).
I'm sorry if this comes off harsh. I'm just tired of people preying on desperate and cognitively impaired patients to fund their projects. They claim they care about the patients, but all I see is plastic carrots being dangled in front of patients who are dealing with housing instability, physical and/or emotional abuse, lack of care/empathy from medical professionals, and planning suicides. It's just wrong.
Last edited by a moderator:
Charles B.
Senior Member (Voting Rights)
Much of the time I interpret OMF’s musings as an effort to delude themselves, rather than us (not that I disagree with sentiments expressed above). Ron, first and foremost, is a desperate father clamoring to return his son to the realm of the living. Given that reality, there is likely a subjective belief in the feasibility of an imminent miracle cure, even if it seems romantic and quixotic to many of us.
Yes, this comes across as harsh and unhelpful. If you have issues with the messaging of OMF, you should communicate with them (as it looks like you might have done). Criticism here doesn't move the needle forward and change what you regard as unhelpful messaging. It's always easier to criticize then to come up with helpful suggestions. Why don't you reply back here with your suggestion of what their messaging should be, and I'll see if I can forward it to them? I don't think people (you included) understand how long some of these investigations take and how costly they are. They simply have to put *some* hope into their messaging. All disease NGO's do.
Alternatively you could start your own NGO as @paused_me is doing in Germany, and report back to us how your fundraising is going.
Last edited by a moderator:
TiredSam
Committee Member
I think suggesting that OMF's regular publicity and fundraising drives be tailored to reflect the reality and experience of the last 6 years that they have been doing it is a helpful suggestion. It would certainly be helpful to the millions of ME sufferers who are regularly having their hopes artificially raised and being asked for money.
Whether it is easier to criticize or not isn't really relevant - this forum was set up to allow critical views of scientific research and all manner of purported cures and protocols. I don't see why publicity drives and fundraising campaigns should be exempt from criticism, and it isn't our job to come up with a campaign for OMF which doesn't regulary falsely raise the hopes of desperate people.
That's exactly the point. OMF should understand that and stop promising a cure within a year. They've been doing that for six years now and it's getting tiresome.
Sure, criticize away. But the point of most criticism is to affect change so that things become better or less bad. If one wants to accomplish change to make the OMF outreach campaign better, then the way to do that is by contacting them and letting them know that you believe that their outreach is not helpful or is harmful. If you or whomever doesn't do that, then how are they to know that some people feel that their outreach is not good? Sniping on here doesn't affect change. This is my point.
J.G
Established Member (Voting Rights)
If you can't recapture Jerusalem, might as well sack Constantinople instead, right?