Wings for Autism helps autistic kids practice at airports
The "Wings for Autism" program helps kids with autism acclimate to the airport environment through a mock plane boarding.
By: CNN
More here:
Wings for Autism helps autistic kids practice at airports - Video
Autism becomes the new normal for five moms
Five moms bare their souls and spoke openly and candidly about the joys and the heartache of raising a child with autism. Tisha Campbell-Martin, LaDonna Hugh...
By: HLN
See the original post:
Autism becomes the new normal for five moms - Video
Three of the better known efforts to create a drug that modestly slows the rate of aging are centered on the following items:
Of these, ways to manipulate the activity of sirtuins have received the greatest attention over the past decade, but there is little to show for all that money and time beyond a modest gain in the understanding of metabolism. There are no replicated, solid results of life extension in mice via sirtuin-influencing drugs, and I'd go so far as to say that the field is under something of a cloud at present. Metformin is in a similar position: while a large body of work relates to its use as a treatment for type 2 diabetes, the evidence for its ability to extend life in laboratory animals is mixed at best. Rapamycin is the only one of the three that can boast solid, replicated evidence of life extension in mice. It is a drug that has been in use as an immunosuppressant for more than a decade, but its ability to extend life is a more recent finding.
For today I thought I'd point out a couple of open access items containing recent findings on the use of rapamycin and metformin in the context of aging. While I don't believe that this branch of research is particularly relevant to extending human life by any meaningful amount in the near term, it is interesting to watch and may help to shed more light on the relative importance of various aspects of our biology in aging. The metformin paper in particular is an educational attempt to tie in the senescent cell aspect of aging to study results:
Metformin, a widely used antidiabetic drug, has been linked to a reduced cancer incidence in some retrospective, hypothesis-generating studies. What is the mechanism by which aging may increase cancer incidence? Although many molecular changes correlate with aging, the presence of senescent cells capable of secreting inflammatory cytokines may be involved. This senescence associated secretory phenotype (SASP) consists of multiple cytokines, chemokines, growth factors and extracellular matrix degrading enzymes that can potentially affect normal tissue structure.
The SASP probably evolved as a gene expression program to assist the senescent tumor suppression response and tissue repair after damage and should be viewed as an initial adaptive response. However, [chronic] SASP [like chronic inflammation] may cause a microenvironment in old tissues that facilitates tumor initiation and then stimulates cancer cell growth.
This unfortunate interaction between senescent cells and cancer cells has been reproduced in experimental mouse models where senescent fibroblasts stimulated tumor progression. [During] experiments to study the potential cancer prevention activity of metformin, we found serendipitously that the drug prevented the expression of many proteases, cytokines and chemokines in senescent cells. We thus propose that metformin prevents cancer by modulating the SASP in tissues where senescent cells were not naturally cleared.
Prolonged Rapamycin treatment led to beneficial metabolic switch
In the first robust demonstration of pharmacologically-induced life extension in a mammal, rapamycin increased longevity of mice via either feeding or injection. However, rapamycin treatment also showed the detrimental metabolic effects, including hyperinsulinemia, hyperlipidemia, glucose intolerance and insulin resistance. Those observations present a paradox of improved survival despite metabolic impairments. How rapamycin extended lifespan with such paradoxical metabolic effects remains to be elucidated.
In the various studies of rapamycin treatment, length of rapamycin treatment varied from two weeks to two years. With short-term rapamycin treatment, mice showed the detrimental metabolic effects, while a much longer length (up to 1.5 to 2 years) of rapamycin treatment led to increased longevity. Duration of rapamycin treatment may be one of the key factors that determine outcomes of the treatment. Longer-term rapamycin treatment may cause beneficial metabolic "switch" that is associated with enhanced insulin signaling and extended longevity.
We [recently] reported that duration of rapamycin treatment indeed has differential effects on metabolism. In our study, rapamycin was given to mice for two, six or 20 weeks. Consistently with the previous reports, mice with two weeks of rapamycin treatment had characteristics of metabolic syndrome. Mice with six weeks of rapamycin treatment were in the metabolic transition status. When rapamycin treatment continued for 20 weeks, the detrimental metabolic effects were reversed or diminished.
It's worth taking some time to look over the state of research for these front-runners in the old-school drug discovery approach to extending life. I find it serves well as a way to inoculate yourself against unfounded optimism and unreasonable expectations, both now and the next time that both the "anti-aging" marketplace and biotech startups tout something that you can buy to supposedly influence metabolism and aging. If you have an enthusiasm for living longer, better to channel it into exercise, calorie restriction, and fundraising for the SENS Research Foundation.
Source:
http://www.fightaging.org/archives/2013/05/comments-on-rapamycin-and-metformin.php
Retinal implants that can provide a crude substitute for vision in some forms of blindness are a work in progress at this time, but the path ahead seems fairly clear:
Some people with artificial retinas can read large letters, see slow-moving cars, or identify tableware. Other patients experience no benefit. The variation can be ascribed in some cases to the exact placement of the neuron-stimulating array in the tissue-paper-thin retina as well as the state of the remaining neurons and pathways in each individual's eye. How well people can learn to use the device and retrain their brain is also important. At its best, the current level of vision is very pixelated. What's seen are bursts of light called phosphenes. "It's not restoring vision like you and I think of, it's restoring mobility. They provide contrast so that someone can see a difference in light and dark to the point where they can tell how to walk through a doorway. This is very much the beginning. Retina prostheses are at the stage cochlear implants were 30 years ago. That technology went from being an aid for lip reading to the point now where children with a cochlear implant can go through normal school and even use mobile phones. With retinal implants, we now know it has clinical benefit to patients, and I think we are going to see this technology develop very rapidly over the next decade."
Thousands of pixels [in comparison to the present 60 or so] will likely be required for facial recognition and other detailed visual tasks, and many artificial retina technologies will have trouble getting to such large numbers of pixels because they depend on wires. Wires are used to connect a power supply to electrodes, which requires a surgical procedure to lay the connection through the eyeball. To avoid this limitation, [researchers] are developing a wireless system that transmits image data captured by a video camera to a photovoltaic chip in the eye. Instead of transmitting visible light to the chip, his system uses near-infrared light that is beamed to flexible arrays of small pixels in the retina. The team has tested the system in blind rats and is now working with a company to test the device in patients. But even thousands of pixels are a long way from one million, "which is roughly what we have in the natural eye. And even at that, there is a lot of processing that the retina does that we are going to be skipping with an artificial retina."
Link: http://www.technologyreview.com/news/514081/can-artificial-retinas-restore-natural-sight/
Source:
http://www.fightaging.org/archives/2013/05/the-present-state-of-artificial-retinas.php
An article on the development of prosthetic organs, a field that continues to provide competition for regenerative medicine:
Proponents of biological organ replacements have recently been encouraged by the development of 3D tissue printing, which offers the tantalising possibility that we might build organs mechanically, layer by layer - a much faster process than growing them in the lab. But printing complex internal organs like the liver or heart is still some way off, and the technology will face similar issues to traditional tissue engineering when it comes to implanting. In the meantime, some scientists are pursuing a different approach, combining biological tissue with synthetic materials and/or mechanical and electronic components to create what could be called hybrid or even cyborg organs (cyborgans, if you will), which are more easily manufactured, longer lasting and more successful once implanted into the body.
On one level this means incorporating some biological material into a largely man-made device. French firm Carmat [has] begun animal trials on one of the world's most advanced designs for an artificial heart, which includes some biological elements.The two chambers inside the Carmat heart are each divided by a biomembrane that separates blood on side from hydraulic fluid on the other. Tiny motors controlled by an electronic sensor system pump the hydraulic fluid in and out of the chambers, in turn causing the membrane to pump the blood. To increase haemocompatiblity, the membrane is made from animal tissue that helps move the blood without damaging cells. Microporous biological and synthetic biomaterials also cover every other surface that comes in contact with the blood, in order to prevent material from sticking to them.
But scientists are also combining biological and synthetic materials in a more fundamental way, creating permanent artificial structures or scaffolds and then growing living cells around them. [Researchers are] already preparing to clinically trial blood vessels and tracheae (windpipes) made in this way, and [are] also developing urethrae, bladders and cardiac patches for healing hearts.
Parabiosis involves joining the circulatory systems of two animals. This is of interest for a number of studies in which old mice and young mice are linked together, known as heterochronic parabiosis. The young mice acquire a little of the metabolic, cellular, and gene expression changes characteristic of old mice, while in the the old mice some of these measures reverse towards more youthful levels. In stem cell activity in particular, the environment of signals present in the blood seems to dictate age-related decline as much as does any inherent damage to stem cells or their niches. This reinforces the view of stem cell aging as an evolved reaction to the cellular damage of aging that acts to extend life by reducing cancer risk, but at the cost of a slow decline into death due to ever more poorly maintained tissues and organs.
Heterochronic parabiosis studies in mice have been taking place for some years now, and researchers are beginning to link differences in gene expression and protein levels in old tissues versus young tissues to specific age-related conditions. The next logical step is to see if age-related dysfunction can be reversed by changing these protein levels in old animals:
Young blood reverses heart decline in old mice
Pumping young blood around old bodies - at least in mice - can reverse cardiac hypertrophy - the thickening and swelling of the heart muscle that comes with age and is a major cause of heart failure. After just four weeks, the older mouse's heart had reverted to almost the same size as that of its younger counterpart. The hearts of the young mice were unaffected, even though they were pumping some blood from the older mice.
After ruling out the effect of reduced blood pressure on the older mice, the team identified a potential candidate: a protein called GDF11, which was present in much higher quantities in the blood of the young mice. To test the effect of GDF11, the researchers gave old mice with cardiac hypertrophy daily injections of it for 30 days. At the end of the treatment, their hearts were significantly smaller than those in a second group of mice of the same age and with the same condition, but that had been injected with saline.
The most common form of heart failure occurs with normal systolic function and often involves cardiac hypertrophy in the elderly. To clarify the biological mechanisms that drive cardiac hypertrophy in aging, we tested the influence of circulating factors using heterochronic parabiosis, a surgical technique in which joining of animals of different ages leads to a shared circulation.
Using modified aptamer-based proteomics, we identified the TGF-? superfamily member GDF11 as a circulating factor in young mice that declines with age. Treatment of old mice to restore GDF11 to youthful levels recapitulated the effects of parabiosis and reversed age-related hypertrophy, revealing a therapeutic opportunity for cardiac aging.
Overriding declines in stem cell activity and forms of tissue degeneration by changing the levels of protein signals present in aged tissues is clearly going to be an important field of medicine in the near future. It may ultimately even take over from stem cell transplants as the principle mode of treatment for many age-related conditions. Some of those transplant therapies are most likely working through the same mechanisms, after all. Regeneration happens because the introduced stem cells are altering the signaling environment and waking up native stem cells, not because they are building new cells and patching up tissue structures.
However, one caveat is that this sort of work doesn't address any of the cellular and molecular damage that initiated the evolved response to reduce stem cell activity. That damage is still there: mitochondrial DNA mutations, high levels of oxidative damage, harmful build up of various forms of metabolic byproducts in and around cells, and so on. At the very least one would expect a growing risk of cancer to accompany a resurgence in stem call activity in an old person - which may be an entirely acceptable risk as cancer therapies improve past chemotherapy and towards targeted cell killers with no side effects.
Even if short term benefits can be obtained via altered signaling protein levels in old tissue, it is still the case that the underlying damage of aging must be repaired. Boosting stem cell activity so far appears to be a better class of potential treatment for many conditions than the best of what can be found in the clinic today, but it is still a form of patching over the underlying causes rather than fixing them.
In later years the immune system falls into a malfunctioning state of overactivation and ineffectiveness, generating damaging chronic inflammation while at the same time failing to defend against pathogens and destroy damaged cells.
It is recognized that the immune system, comprising both innate (nonspecific) and acquired (specific) components, is an intricate defence system that is highly conserved across vertebrate species, and has, from an evolutionary perspective, undergone strong pressures to maximize survival to allow procreation. The significant improvements in human survival and lifespan to well beyond childbearing ages have been totally "unpredicted" by evolution. As a consequence, human immune systems are exposed to considerable additional antigenic exposure outside the forces of natural selection. It is in this situation that immunity begins to exert negative effects on human ageing (antagonistic pleiotropy), leading to gradual systemic failures.
Research into age-related changes of the immune system is gathering pace as its importance within the context of multiple pathologies in ageing populations is realized. As part of this advance, [researchers] described the phenomenon of "inflammaging" at the turn of the millennium as part of the spectrum of immunosenescence. Inflammaging denotes an upregulation of the inflammatory response that occurs with age, resulting in a low-grade chronic systemic proinflammatory state.
Inflammaging is believed to be a consequence of a cumulative lifetime exposure to antigenic load caused by both clinical and subclinical infections as well as exposure to noninfective antigens. The consequent inflammatory response, tissue damage and production of reactive oxygen species that cause oxidative damage also elicits the release of additional cytokines, principally from cells of the innate immune system but also from the acquired immune response. This results in a vicious cycle, driving immune system remodelling and favouring a chronic proinflammatory state where pathophysiological changes, tissue injury and healing proceed simultaneously. Irreversible cellular and molecular damage that is not clinically evident slowly accumulates over decades.
Link: http://hplusmagazine.com/2013/05/07/understanding-how-we-age-insights-into-inflammaging/
Source:
http://www.fightaging.org/archives/2013/05/insights-into-inflammaging.php
Here is the text of the key comments
from the California stem cell agency in response to questions from
the California Stem Cell Report (CSCR) concerning the $21,630
contribution by Robert Klein. Here is a link to the full story on the matter.
“Is CIRM concerned about the
appearance created by the donation from Bob Klein to enable scientific
staff to attend the ISSCR meeting in Yokohoma, coming one
month after the GWG (the review group) rejected StemCells Inc's Alzheimer's application
and one month before the July Board meeting that led to the approval
of the award?”(Editor's note: It was actually two months before the board meeting.)
“No, the two items are entirely
separate with no connection. Item 1 involved Bob Klein making a
donation to allow science officers to attend a critically important
scientific meeting on stem cell research. The science officers
had originally planned on attending but then were told they
could not because of cuts in our out-of-state travel budget – Bob
Klein’s donation, without using state funds, enabled the science
officers to attend. Item 2 is an ICOC decision to fund a
research project that they felt had promise and was important for the
people of California.”
“Under the Gift Policy, the President
had the authority to accept Mr. Klein’s generous offer as a 'Direct
payment or reimbursement by third parties for the costs of general
operation or grant management administrative activities.' (Gift
Policy, Sec. III(A)(2).) Because CIRM receives gifts only
infrequently, CIRM staff determined that it would be more efficient
to report gifts to the Board on a semi-annual basis. Mr.
Klein’s donation was the first gift CIRM had received in some
years. Due to the lack of additional donations, a transition in
CIRM’s finance office, and an oversight, CIRM staff has not yet
presented a report including Mr. Klein’s gift. Staff plans to
report Mr. Klein’s gift as part of the finance report at the May
Board meeting. Because the President had the authority to
accept the gift pursuant to section III(A)(2) of the Gift Policy, it
did not require a commitment letter. (See Gift Policy, Sec.
III(C)(1) ['A Commitment Letter is not required for gifts described
under III.A.2., 3. and 4.'].) However, consistent with the
policy, Dr. Trounson sent Mr. Klein a letter of appreciation, a copy
of which we have already provided you.”
Here is the text of the key comments
from the California stem cell agency in response to questions from
the California Stem Cell Report (CSCR) concerning the $21,630
contribution by Robert Klein. Here is a link to the full story on the matter.
“Is CIRM concerned about the
appearance created by the donation from Bob Klein to enable scientific
staff to attend the ISSCR meeting in Yokohoma, coming one
month after the GWG (the review group) rejected StemCells Inc's Alzheimer's application
and one month before the July Board meeting that led to the approval
of the award?”(Editor's note: It was actually two months before the board meeting.)
“No, the two items are entirely
separate with no connection. Item 1 involved Bob Klein making a
donation to allow science officers to attend a critically important
scientific meeting on stem cell research. The science officers
had originally planned on attending but then were told they
could not because of cuts in our out-of-state travel budget – Bob
Klein’s donation, without using state funds, enabled the science
officers to attend. Item 2 is an ICOC decision to fund a
research project that they felt had promise and was important for the
people of California.”
“Under the Gift Policy, the President
had the authority to accept Mr. Klein’s generous offer as a 'Direct
payment or reimbursement by third parties for the costs of general
operation or grant management administrative activities.' (Gift
Policy, Sec. III(A)(2).) Because CIRM receives gifts only
infrequently, CIRM staff determined that it would be more efficient
to report gifts to the Board on a semi-annual basis. Mr.
Klein’s donation was the first gift CIRM had received in some
years. Due to the lack of additional donations, a transition in
CIRM’s finance office, and an oversight, CIRM staff has not yet
presented a report including Mr. Klein’s gift. Staff plans to
report Mr. Klein’s gift as part of the finance report at the May
Board meeting. Because the President had the authority to
accept the gift pursuant to section III(A)(2) of the Gift Policy, it
did not require a commitment letter. (See Gift Policy, Sec.
III(C)(1) ['A Commitment Letter is not required for gifts described
under III.A.2., 3. and 4.'].) However, consistent with the
policy, Dr. Trounson sent Mr. Klein a letter of appreciation, a copy
of which we have already provided you.”
Here is the text of the initial
response from Robert Klein, chairman of the California stem
cell agency until July 2011, to questions from the California Stem Cell Report (CSCR)
concerning his $21,630 donation to the agency. The questions posed by
CSCR on precede the response by Klein. Here is a link to a story on
the matter.
“Why did you give the agency the
money?
“Did you place on conditions on its
use?
“Did anyone connected with the agency
indicate in advance that your donation would be desired? If so
who? Who did you deal with primarily on the donation -- Trounson,
Thomas or...?
“The donation came one month after
grant reviewers rejected StemCells Inc.'s Alzheimer's application. Do
you think it was appropriate to make the donation and then ask the
board twice to override its reviewers?
“Do you think the donation and
subsequent action on StemCells, Inc.'s Alzheimer's application will
negatively color the perception of future efforts by CIRM at private
fundraising?”
(Editor's note: The applications in this round were reviewed once in April 2012 by CIRM's full grant review group. StemCells, Inc.'s application was subject to a reevaluation after Klein's appeal in July 2012 and rejected again, but it was not a full review. Klein may be referring also an earlier round that provided grants for planning to apply for the full $20 million.)
Here is the text of the initial
response from Robert Klein, chairman of the California stem
cell agency until July 2011, to questions from the California Stem Cell Report (CSCR)
concerning his $21,630 donation to the agency. The questions posed by
CSCR on precede the response by Klein. Here is a link to a story on
the matter.
“Why did you give the agency the
money?
“Did you place on conditions on its
use?
“Did anyone connected with the agency
indicate in advance that your donation would be desired? If so
who? Who did you deal with primarily on the donation -- Trounson,
Thomas or...?
“The donation came one month after
grant reviewers rejected StemCells Inc.'s Alzheimer's application. Do
you think it was appropriate to make the donation and then ask the
board twice to override its reviewers?
“Do you think the donation and
subsequent action on StemCells, Inc.'s Alzheimer's application will
negatively color the perception of future efforts by CIRM at private
fundraising?”
(Editor's note: The applications in this round were reviewed once in April 2012 by CIRM's full grant review group. StemCells, Inc.'s application was subject to a reevaluation after Klein's appeal in July 2012 and rejected again, but it was not a full review. Klein may be referring also an earlier round that provided grants for planning to apply for the full $20 million.)
Here is the text of comments from
Robert Klein, former chairman of the California stem cell agency,
concerning his $21,630 donation to the agency and subsequent actions
by the agency. Klein's comments May 1 came in response to questions
from the California Stem Cell Report(CSCR) on April 30. The text of
the inquiry from CSCR precedes Klein's response. Here is a link to the story on the matter.
"I have sent the following to CIRM
asking for their response and am offering the same opportunity to
you. Here is what I sent the agency:
'The documents that I have received so
far show that after Klein gave CIRM $21,000 the agency instructed six
of its science officers to give him special access to their
activities and apparently did not object to additional instructions
from another member of the public, Melissa King, to provide Klein and
her with written summaries about their activities at the ISSCR
convention and “details” about their work at CIRM. Email
addresses of the six were also provided to Klein, who may have
additionally received their cell phone numbers although that is not
entirely clear. The CIRM documents show that the six were told to
engage in one-on-one sessions with Klein, which actually included a
third person, a wealthy Canadian mining company executive. One
document indicates that the science officers should assist in
fundraising for CIRM by identifying areas of “special importance”
to Klein and 'other donors.'
"'Additionally, Alan Trounson, at
Klein's request, invited the mining executive to a closed door
session involving the agency's international partners, a session at
which presumably valuable, little known scientific information would
be discussed and future directions charted. Trounson specifically
told the executive that it was Klein who asked that executive be
invited to the session, adding to Klein's clout in any business or
other dealings that Klein might have with the executive.'
My questions to CIRM deal with the
special treatment that was provided in connection with your donation.
I would ask you if you think that state agencies should provide this
sort of extraordinary treatment for individuals who donate to the
agency. At the very least, doesn't this raise questions about the
integrity of the agency and doubts in the public mind about whether
it can be fair and even-handed in its activities?
"In April or May of 2012 I committed
to contribute a charitable donation to CIRM to cover the travel costs
for 5-7 additional science officers to attend the International Stem
Cell Conference in Japan. It is important to CIRM that their
science officers understand the cutting edge research being developed
around the world so that CIRM does not fund redundant research; but,
to the contrary, the science officers understand how to create
networks between California scientists and scientists in other
foreign countries who are doing complementary research that can
potentially accelerate the advancements of therapies for patients. I
do not hold any financial interest in biotech companies. I have
historically been involved in encouraging international collaboration
to advance medical therapies; for patients, every day of delay in the
development of a therapy is a delay they cannot afford. To
conceptually document the value of additional scientists traveling to
these meetings, it was discussed that there should be conceptual,
bullet point summaries about the value for CIRM obtained through the
scientists discussions at the international conference. The
idea was to create bullet points of information about a few of the
most meaningful scientific concepts and contacts the science officers
benefitted from each day of attendance at the conference. I did not
participate in the selection of the science officers who attended and
I did not play any part in determining what activities they
participated in. There were two fundamental goals to the very short
one-on-one sessions that were arranged at "down time" that
would not conflict with their other activities. The first goal was to
conceptually understand if each of the science officers believed that
the benefit to the agency was sufficient to justify the cost of their
attending, when considering the learning and contacts they had gained
which might accelerate research and therapies for patients. The
second goal was to assist universities and non-profits, principally
in Canada - a research partner of CIRM - in advancing their
contributions from an existing donor or donors."The Canadian mining executive had an
important history in contributing to the International Stem Cell
Society and to Canadian non-profit research institutions. This
individual has an expert background in mining and a passionate
personal commitment to medical research; but, he does not engage in
technical discussions of research. On a conceptual basis it was
important for him to understand the spectrum of medical advances
towards therapies. His additional contributions to Canadian
non-profits could assist Canada in collaborating with California on
more international research, with California only funding the
research done in California and the donor helping to fund the
research done in Canada. No specific grant applications were
discussed. Finally, the discussion with the international partners
focuses on the funding process and funding collaboration it does not
discuss any individual grants. The value of international
collaboration and the benefits of collaborating with new
international partners is discussed. Scientific theories and
individual grants are not discussed and new scientific information is
not presented. I attended this session of international partners to
support international collaboration; again, I do not hold any
financial interest in any biotech organizations. Additionally, I do
not have any business or financial relationship with the Canadian
mining executive. The Canadian executive, based upon family and
friends who have had chronic disease, is a significant donor to
non-profit research institutions in Canada. All of my activities, the
donation and the encouragement to develop information to validate the
future benefits of science officers traveling to international stem
cell conferences were focused on benefitting California patients with
chronic illness or injury and the agency formed through Proposition
71."
http://feedproxy.google.com/~r/blogspot/uqpFc/~3/SBGFem2qPWo/the-klein-donation-text-of-robert.html
Here is the text of comments from
Robert Klein, former chairman of the California stem cell agency,
concerning his $21,630 donation to the agency and subsequent actions
by the agency. Klein's comments May 1 came in response to questions
from the California Stem Cell Report(CSCR) on April 30. The text of
the inquiry from CSCR precedes Klein's response. Here is a link to the story on the matter.
"I have sent the following to CIRM
asking for their response and am offering the same opportunity to
you. Here is what I sent the agency:
'The documents that I have received so
far show that after Klein gave CIRM $21,000 the agency instructed six
of its science officers to give him special access to their
activities and apparently did not object to additional instructions
from another member of the public, Melissa King, to provide Klein and
her with written summaries about their activities at the ISSCR
convention and “details” about their work at CIRM. Email
addresses of the six were also provided to Klein, who may have
additionally received their cell phone numbers although that is not
entirely clear. The CIRM documents show that the six were told to
engage in one-on-one sessions with Klein, which actually included a
third person, a wealthy Canadian mining company executive. One
document indicates that the science officers should assist in
fundraising for CIRM by identifying areas of “special importance”
to Klein and 'other donors.'
"'Additionally, Alan Trounson, at
Klein's request, invited the mining executive to a closed door
session involving the agency's international partners, a session at
which presumably valuable, little known scientific information would
be discussed and future directions charted. Trounson specifically
told the executive that it was Klein who asked that executive be
invited to the session, adding to Klein's clout in any business or
other dealings that Klein might have with the executive.'
My questions to CIRM deal with the
special treatment that was provided in connection with your donation.
I would ask you if you think that state agencies should provide this
sort of extraordinary treatment for individuals who donate to the
agency. At the very least, doesn't this raise questions about the
integrity of the agency and doubts in the public mind about whether
it can be fair and even-handed in its activities?
"In April or May of 2012 I committed
to contribute a charitable donation to CIRM to cover the travel costs
for 5-7 additional science officers to attend the International Stem
Cell Conference in Japan. It is important to CIRM that their
science officers understand the cutting edge research being developed
around the world so that CIRM does not fund redundant research; but,
to the contrary, the science officers understand how to create
networks between California scientists and scientists in other
foreign countries who are doing complementary research that can
potentially accelerate the advancements of therapies for patients. I
do not hold any financial interest in biotech companies. I have
historically been involved in encouraging international collaboration
to advance medical therapies; for patients, every day of delay in the
development of a therapy is a delay they cannot afford. To
conceptually document the value of additional scientists traveling to
these meetings, it was discussed that there should be conceptual,
bullet point summaries about the value for CIRM obtained through the
scientists discussions at the international conference. The
idea was to create bullet points of information about a few of the
most meaningful scientific concepts and contacts the science officers
benefitted from each day of attendance at the conference. I did not
participate in the selection of the science officers who attended and
I did not play any part in determining what activities they
participated in. There were two fundamental goals to the very short
one-on-one sessions that were arranged at "down time" that
would not conflict with their other activities. The first goal was to
conceptually understand if each of the science officers believed that
the benefit to the agency was sufficient to justify the cost of their
attending, when considering the learning and contacts they had gained
which might accelerate research and therapies for patients. The
second goal was to assist universities and non-profits, principally
in Canada - a research partner of CIRM - in advancing their
contributions from an existing donor or donors."The Canadian mining executive had an
important history in contributing to the International Stem Cell
Society and to Canadian non-profit research institutions. This
individual has an expert background in mining and a passionate
personal commitment to medical research; but, he does not engage in
technical discussions of research. On a conceptual basis it was
important for him to understand the spectrum of medical advances
towards therapies. His additional contributions to Canadian
non-profits could assist Canada in collaborating with California on
more international research, with California only funding the
research done in California and the donor helping to fund the
research done in Canada. No specific grant applications were
discussed. Finally, the discussion with the international partners
focuses on the funding process and funding collaboration it does not
discuss any individual grants. The value of international
collaboration and the benefits of collaborating with new
international partners is discussed. Scientific theories and
individual grants are not discussed and new scientific information is
not presented. I attended this session of international partners to
support international collaboration; again, I do not hold any
financial interest in any biotech organizations. Additionally, I do
not have any business or financial relationship with the Canadian
mining executive. The Canadian executive, based upon family and
friends who have had chronic disease, is a significant donor to
non-profit research institutions in Canada. All of my activities, the
donation and the encouragement to develop information to validate the
future benefits of science officers traveling to international stem
cell conferences were focused on benefitting California patients with
chronic illness or injury and the agency formed through Proposition
71."
http://feedproxy.google.com/~r/blogspot/uqpFc/~3/SBGFem2qPWo/the-klein-donation-text-of-robert.html
The California stem cell agency today
said that it has awarded $458 million to fund research involving
human embryonic stem cells (hESC) out of a total of $1.8 billion it
has given away during the past eight years.
The California stem cell agency this
month received what some might consider a gesture of approval from a
longtime foe – LifeNews.com.
“CIRM has been steadily moving away
from its original mission to give preferential
treatment to funding for human embryonic stem cell research
(hESCR). Instead, after adopting a renewed
emphasis on translating research into clinical trials, CIRM
has more and more shifted the bulk of its grants towards funding
research utilizing adult stem cells and other alternatives to hESCR,
such as induced
pluripotent stem cells (iPSCs).”
“(T)he lack, once again, of funding
for hESCR only serves to highlight how old and dated that approach to
finding treatments and cures increasingly seems.”
The California stem cell agency this
month received what some might consider a gesture of approval from a
longtime foe – LifeNews.com.
“CIRM has been steadily moving away
from its original mission to give preferential
treatment to funding for human embryonic stem cell research
(hESCR). Instead, after adopting a renewed
emphasis on translating research into clinical trials, CIRM
has more and more shifted the bulk of its grants towards funding
research utilizing adult stem cells and other alternatives to hESCR,
such as induced
pluripotent stem cells (iPSCs).”
“(T)he lack, once again, of funding
for hESCR only serves to highlight how old and dated that approach to
finding treatments and cures increasingly seems.”
Some people are more predisposed to suffer Parkinson's disease than others, a fraction of those due to mutations in genes involved in mitochondrial quality control. The state of mitochondrial function shows up as an important component of many different conditions and indeed in aging itself. In Parkinson's disease it is thought that mitochondrial dysfunction contributes to the conditions in which the population of dopamine-producing neurons in the brain die off, producing the characteristic symptoms of the disease.
It may be that more of Parkinson's disease is genetic than was previously thought, and the odds of that being the case increase as the chain of molecular machinery involved in mitochondrial quality control is followed and new components identified. This sort of work also helps clarify the mechanisms associated with mitochondrial dysfunction in aging:
Mitofusin 2 (Mfn2) is known for its role in fusing mitochondria together, so they might exchange mitochondrial DNA in a primitive form of sexual reproduction. "Mitofusins look like little Velcro loops. They help fuse together the outer membranes of mitochondria. Mitofusins 1 and 2 do pretty much the same thing in terms of mitochondrial fusion. What we have done is describe an entirely new function for Mfn2."
Mitochondria work to import a molecule called PINK. Then they work to destroy it. When mitochondria get sick, they can't destroy PINK and its levels begin to rise. Once PINK levels get high enough, they make a chemical change to Mfn2, which sits on the surface of mitochondria. This chemical change is called phosphorylation. Phosphorylated Mfn2 on the surface of the mitochondria can then bind with a molecule called Parkin that floats around in the surrounding cell.
Once Parkin binds to Mfn2 on sick mitochondria, Parkin labels the mitochondria for destruction. The labels then attract special compartments in the cell that "eat" and destroy the sick mitochondria. As long as all links in the quality-control system work properly, the cells' damaged power plants are removed, clearing the way for healthy ones. "But if you have a mutation in PINK, you get Parkinson's disease. And if you have a mutation in Parkin, you get Parkinson's disease. About 10 percent of Parkinson's disease is attributed to these or other mutations that have been identified." The discovery of Mfn2's relationship to PINK and Parkin opens the doors to a new genetic form of Parkinson's disease.
Link: http://www.sciencedaily.com/releases/2013/04/130425142357.htm
Source:
http://www.fightaging.org/archives/2013/04/joining-the-dots-in-genetic-parkinsons-disease.php
Some people are more predisposed to suffer Parkinson's disease than others, a fraction of those due to mutations in genes involved in mitochondrial quality control. The state of mitochondrial function shows up as an important component of many different conditions and indeed in aging itself. In Parkinson's disease it is thought that mitochondrial dysfunction contributes to the conditions in which the population of dopamine-producing neurons in the brain die off, producing the characteristic symptoms of the disease.
It may be that more of Parkinson's disease is genetic than was previously thought, and the odds of that being the case increase as the chain of molecular machinery involved in mitochondrial quality control is followed and new components identified. This sort of work also helps clarify the mechanisms associated with mitochondrial dysfunction in aging:
Mitofusin 2 (Mfn2) is known for its role in fusing mitochondria together, so they might exchange mitochondrial DNA in a primitive form of sexual reproduction. "Mitofusins look like little Velcro loops. They help fuse together the outer membranes of mitochondria. Mitofusins 1 and 2 do pretty much the same thing in terms of mitochondrial fusion. What we have done is describe an entirely new function for Mfn2."
Mitochondria work to import a molecule called PINK. Then they work to destroy it. When mitochondria get sick, they can't destroy PINK and its levels begin to rise. Once PINK levels get high enough, they make a chemical change to Mfn2, which sits on the surface of mitochondria. This chemical change is called phosphorylation. Phosphorylated Mfn2 on the surface of the mitochondria can then bind with a molecule called Parkin that floats around in the surrounding cell.
Once Parkin binds to Mfn2 on sick mitochondria, Parkin labels the mitochondria for destruction. The labels then attract special compartments in the cell that "eat" and destroy the sick mitochondria. As long as all links in the quality-control system work properly, the cells' damaged power plants are removed, clearing the way for healthy ones. "But if you have a mutation in PINK, you get Parkinson's disease. And if you have a mutation in Parkin, you get Parkinson's disease. About 10 percent of Parkinson's disease is attributed to these or other mutations that have been identified." The discovery of Mfn2's relationship to PINK and Parkin opens the doors to a new genetic form of Parkinson's disease.
Link: http://www.sciencedaily.com/releases/2013/04/130425142357.htm
Source:
http://www.fightaging.org/archives/2013/04/joining-the-dots-in-genetic-parkinsons-disease.php
http://feedproxy.google.com/~r/blogspot/uqpFc/~3/0HfVYv0XVQg/california-stem-cell-agency-seeks.html
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