From Eric Dondero:
Obama major snub of 9/11 Families leader Debra Burlingame at the White House. After expressing concerns to him directly over continued prosecution of CIA interrogators by Eric Holder's Justice Dept.
"He turned and walked away..."
See related LR article - "Rep. Peter King: Definitely Waterboarding that led us to Osama"
Does anyone know a website that could tell me how long it takes #2 home heating oil to evaporate if spilled on concrete (less than a gallon) and how slippery it would be on concrete?
by Clifford F. Thies
The latest proof of President Obama's qualification as a "natural born citizen" reminds us of the sad reality that the issue just kind of touches and yet misses by miles. I am speaking of his coping with his abandonment by his natural father and his rejection of his mother.
Along with the release of a photocopy of his "long form" certificate of live birth, we have the release of his father's immigration file.
In the birth certificate, filed on August 8, 1961, his mother says that her child, who is named Barack Hussein Obama II, was born on August 4th. She also states that the father of her son is Barack Hussein Obama, an African, who is 25 years old, and a student.
In the immigration file, we find out that the Barack Hussein Obama "Sr." variously claims to be married to two women, one back in Keyna and another in Hawaii, or to not be married at all, to have and to not have children, but never to have Barack Hussein Obama II as a child, and to have and to not have worked in the United States.
As Pamela Geller at Atlas Shrugs Atlas Shrugs points out:
Stanley Ann Dunham could not have been so savvy as to know that BHO I was a Muslim polygamist. Yet clearly, Barack Hussein Obama Sr., was never divorced from his first wife in Kenya.
The Immigration and Naturalization Service suspected that the elder Obama’s marriage to Dunham was a sham, arranged strictly to secure immigration status for him. Despite the fact that BHO I had married Dunham, the government wasn’t buying it: An INS official wrote in 1961 that the agency should “make sure an investigation is conducted as to the bona-fide of the marriage.”
Specifically, in a certificate dated June 6, 1963, seeking an extension of his student visa, Obama "Sr." fails to mention his marital status, the name or names of any spouses, and the name or names of any children. He then signs the form certifying to the government of the United States that it is correct and complete.
In a certificate dated August 17, 1962, the Kenyan indicates that he is married, although he does not indicate the name or names of the women to whom he is married, and he lists one child, viz., Roy Obama, the President's half-brother.
In a certificate dated August 31, 1961, the Kenyan indicates that he is married, naming his spouse as Ann S. Dunham of Hawaii, after marking over whatever he first put into the box, and - voila! - not mentioning the names of any children. Going by the certificate of live birth, this was about four weeks after the birth of Barack Hussein Obama II.
Eventually, immigration rejected extension of the Kenyan's student visa. Barack Hussein Obama II would be raised first by his mother, during which time a decent Indonesian man who married his mother acted for a time as a stepfather. Later he was raised by his maternal grandparents.
You might think, based on his the races of his natural parents and on his upbringing, that he might consider himself biracial. But, no, as we all know, he claimed only to be black on his 2010 census form. As we all known, in Chicago, he attended a white-hating, Afro-centric church. As we all know, he reflexively blames the white person in any high profile altercation involving a white person and a black person.
As we here at LR discussed during the election campaign of 2008, this is just so obvious from a reading of his book, Dreams from my Father. Our President is working through some issues. In a country where most children, nowadays, are not raised in homes headed by their father, he is not so unusual. It is really such a sad predicament for our country and for so many of our children.
Obama killing Osama okay cause he's Black
From Politico:
"The first thing I thought was, I felt the same way everyone else did, mixed emotions about the fact that we killed someone. ... We know that killing is not right. In this particular instance, we have such an association with this person for having dealt us such a heinous blow. So, you know, mixed emotions of finally justice has been served and, secondly, we've just killed somebody…"
“It’s just fascinating that we have a black man, who has Muslim ties with his father, even though he’s a Christian, it’s amazing how far our country has come, that that’s the man who took down Osama bin Laden. It makes you feel very patriotic.”
H/t Photo - Breitbart. Weasel Z...
How the ambient temperature compensation depends MCB working.
Cellular differentiation is the process by which stem cells and other progenitor cells divide to form specialized cell populations - of which there are a great many different types in the body. Much of stem cell research to date has been focused on finding out how to first obtain stem cells and then differentiate them to form specific desired types of specialized cell. This has been a challenging process, but advances in biotechnology are making it easier and less costly as the years go by.
Cells are programmable machinery; it seems to be the case that any given type of cell holds the potential to produce any other type of cell, if researchers just understood the right chemical and genetic cues and instructions. Thus in addition to the work of reverting specialized cells into stem cells, and differentiating stem cells into desired specialized cells, there is also the possibility of achieving transdifferentiation - converting one type of cell directly into another without passing through a stem cell stage.
In recently reported research, researchers are making inroads in converting various types of cell in the pancreas - which offers the possibility of a fairly direct path towards providing new beta cells to diabetes patients:
While the current standard of treatment for diabetes - insulin therapy - helps patients maintain sugar levels, it isn't perfect, and many patients remain at high risk of developing a variety of medical complications. Replenishing lost beta cells could serve as a more permanent solution, both for those who have lost such cells due to an immune assault (Type 1 diabetes) and those who acquire diabetes later in life due to insulin resistance (Type 2).
"Our work shows that beta cells and related endocrine cells can easily be converted into each other," said study co-author Dr. Anil Bhushan, an associate professor of medicine in the endocrinology division at the David Geffen School of Medicine at UCLA and in the UCLA Department of Molecular, Cell and Developmental Biology.
It had long been assumed that the identity of cells was "locked" into place and that they could not be switched into other cell types. But recent studies have shown that some types of cells can be coaxed into changing into others - findings that have intensified interest in understanding the mechanisms that maintain beta cell identity.
This is as much the age of controlling cells as it is the age of biotechnology. Researchers are presently building the foundation for complete control over the component machinery of the human body. Along the way to that goal lies the production of ever more effective general repair kits for all forms of damage that originate in missing or damaged cell populations - including one portion of aging itself.
Mitochondria are the cell's roving herd of bacteria-like power plants, and the damage they suffer in the course of their operation is strongly implicated as a contributing cause of aging. Here researchers show that calorie restriction appears to boost the rate at which new mitochondria are spawned: "mice with increased respiratory rates and reduced energetic conversion efficiency due to spontaneously uncoupled mitochondria lived longer than their counterparts. Indeed, different uncoupling strategies were able to extend lifespan in models ranging from yeast to mammals. ... uncoupling could be an approach to promote lifespan extension due to its ability to prevent the formation of reactive oxygen species (ROS). Indeed, mild mitochondrial uncoupling is a highly effective intervention to prevent the formation of ROS ... CR also increases the number of functional respiratory units (mitochondrial biogenesis) [and researchers] demonstrated that mitochondrial biogenesis was essential for many beneficial effects of dietary limitation in mice. ... We recently demonstrated that murine lifespan can be extended by low doses of the mitochondrial uncoupler 2,4-dinitrophenol (DNP) in a manner accompanied by weight loss, lower serological levels of glucose, insulin and triglycerides as well as a strong decrease in biomarkers of oxidative damage and tissue ROS release. Similar effects have been repeatedly reported using CR diets ... Based on the similarities between these two interventions, we hypothesized that DNP treatment could also lead to enhanced mitochondrial biogenesis. In this manuscript, we measured the effects of DNP treatment and CR on mitochondrial biogenesis and associated pathways. We observed that both DNP and CR increase mitochondrial biogenesis, [confirming] that signaling events in both treatments converge."
Link: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0018433
A fairly long open access commentary on metformin and its effects on slowing aging in mice: "A recent study [may] certainly establish that metformin should be defined as geroprotective or gerosuppressant rather than bona fide [calorie restriction mimetic]. Long-living female mice from the outbred SHR strain were fed metformin in drinking water beginning at 3, 9 or 15 months of age and they were then analyzed for reproductive aging, mean and maximal lifespan and incidence of malignant tumors ... In female SHR mice, [researchers] now confirm that metformin treatment, if started early in life, notably increases by 21% the mean lifespan of tumor-free mice. In contrast, if started late in life, metformin treatment appears to significantly reduce (by 13%) the mean lifespan of tumor-free mice. ... It is perhaps relevant to note that, if started early in life, metformin treatment decreased the risk of death compared to the control group whereas similar treatment with metformin at older ages did not affect the relative risk of death in SHR female mice. Metformin's ability to increase the mean lifespan of tumor-free mice while simultaneously decreasing the risk of death in an age-related manner somewhat recapitulate metformin's ability to reduce cancer incidence among type 2 diabetic individuals."
Link: http://www.impactaging.com/papers/v3/n4/full/100316.html
What is the Vegas Group initiative setting out to achieve, in a nutshell? I'm still working on that short explanation, but here is one attempt at it. Thanks to the present regulatory situation in the US - where aging is not recognized as a disease, and therefore no therapy for aging can be legally developed - there are any number of potentially useful biotechnologies presently languishing without further development. These are methods and techniques shown to extend life in mice or repair and reverse specific biochemical aspects of aging, but for which there is no further funding for clinical development. Nothing may be happening for these technologies in the US, but there are active biotechnology and medical development communities in other parts of the world who are not so encumbered by local regulation: many of the developed Asia-Pacific countries, for example. What the Vegas Group initiative ultimately aims to do is build a bridge between these undeveloped technologies and the developers who could bring them into the clinic for human use.
How will that bridge be built? I believe that the growing garage biotechnology and DIYbio communities will play a pivotal role in the US - validating, documenting, and lowering the cost for overseas ventures to pick up and further develop longevity therapies. From my perspective then, the very earliest actions for the first Vegas Group volunteers involve building the foundations for a repository of how-to documentation: guides that clearly explain how the garage biotechnology community could validate and further develop the best and latest techniques in longevity science.
At the outset this is less a matter of writing documents and more a matter of figuring out a sustainable process and organizational structure - the business of freelance writing is much akin to herding cats even when money is involved.
So I can envisage a guiding council of advisors putting together a plan for the hierarchy of topics they would like to see in the Vegas Group codex, from basic methods in biotechnology through to best attempt reverse engineering of things we know to be possible and that have been published: such as Cuervo's work on restoring youthful levels of autophagy, or protofection to replace mitochondrial DNA. The end result of that process might look something like a distillation of Fight Aging! mixed with the very elegant materials produced by the Science for Life Extension Foundation.
Codex project volunteers would then run an ongoing process of hiring post-graduates and interested researchers to write, and passing the results to starving authors who improve the output to a quality suitable for the open biotechnology community. There would of course be some back and forth between the post-graduates and the starving authors in order to reduce the inevitable translation errors, but I see this as a viable way to produce a body of knowledge that is sufficiently good to begin with - not perfect, not even necessarily very good, but sufficient.
I mentioned rejuvenation of autophagy above as one of the possible projects for documentation, and at present, the Vegas Group discussion list is focused on mitochondrial protofection - and we could certainly use another life science volunteer or two to help lay out the skeleton for full documentation, or work on one of the other potential projects. If you're interested, come on over and join in.
Some of the other possible projects that have been mentioned or came to mind include the following:
1) LysoSENS
LysoSENS isn't an established methodology, but it is an ongoing research program that aims to find bacterial enzymes capable of breaking down harmful aggregates that build up with age. This is a matter of synthesizing the chemicals to be broken down, digging up some dirt from likely locations, culturing bacteria, and matching them up against your unwanted chemicals to see if you have a hit. This seems like an excellent project for DIYbio enthusiasts - someone is going to find an existing bacterial strain containing enzymes that can be adapted to safely destroy lipofuscin in human cells, and there's no reason that person has to be working in an institutional establishment.
2) Manufacturing Targeted Mitochondrial Antioxidants
A number of research groups have been publishing in recent years on ingested targeted mitochondrial antioxidants that appear to slow aging in mice. It seems a viable sophisticated garage or shared lab-space chemistry experiment to replicate their published work, and then a biotech experiment to validate your synthesized antioxidants in cell cultures.
3) Upregulation of PEPK-C
This is a manipulation of gene expression show to increase longevity in mice. As gene engineering goes, this is about as straightforward as it is going to get - which is to say still a fair hurdle for the garage biotech community to work towards - a single gene altered, and an impressive result. Managing to document the process sufficiently well to recreate this intervention in cell cultures would be, I think, a real showpiece for a laboratory cooperative.
Now all of these items, when carried out as projects, can be expected to sit atop a pyramid of supporting techniques and documentation, some of which will be common to many different projects. Producing that material sufficiently well will, I think, help in the growth of the garage biotechnology and DIYbio communities. Documentation is key for newcomers and recruitment, and you can never have too much of it.
A study of markers of oxidative stress in centenarians: "Human longevity is a complex phenotype that is determined by environment, genetics, and chance. Understanding the mechanisms by which aging leads to longevity, particularly healthy longevity would be of enormous benefit to our aging population. Unfortunately, most research on human aging has focused on phenomenological description of age-related diseases, and much less is known about the mechanisms of aging itself. Among the most promising theories about how and why we age is the Free Radical Theory, initially proposed by Denham Harman in 1956. Harman proposed that oxygen radicals produced during aerobic respiration induce oxidative damage in DNA, cells, tissues, and organisms that lead to aging and death. ... Harman hypothesized, based on observations of enzymatic redox chemistry, that oxygen radical generation occurs in vivo and that mechanisms exist to protect against such damage. Mitochondria were later found to be a principal source of these oxygen radicals ... Okinawa has among the world's longest-lived populations but oxidative stress in this population has not been well characterized. ... The low plasma level of [oxidized lipids] in Okinawan centenarians, compared to younger controls, argues for protection against oxidative stress in the centenarian population and is consistent with the predictions of the Free Radical Theory of Aging."
An open access paper: "Aging is the single most important risk factor in human disease in developed countries but when it comes to research on prevention or cures, aging is seldom taken into account. Nevertheless if aging is a significant contributor to age-related conditions, we would hope that an understanding of aging mechanisms could prompt the design of rational therapies. Moreover, if aging causes multiple diseases then it is reasonable to think that pharmacological agents that slow aging could be also effective in preventing or slowing a wide spectrum of diseases. ... Protein aggregation is a hallmark of aging and several age-related pathologies, collectively known as conformational diseases (CD). This similarity strongly suggests a crosstalk between aging and disease. Although it is not clear how protein aggregation occurs, dramatic alterations in the balance of protein synthesis, protein folding and protein degradation (together representing 'protein homeostasis') are likely to play important roles in this process. As a consequence, modified proteins tend to accumulate into soluble oligomers and insoluble aggregates that may actively influence cell function. Neurodegenerative diseases are arguably the best studied CD and the aberrant aggregation of several insoluble molecules [has] long been associated with the development of these pathologies. ... The general picture that that has emerged is that conformationally-altered proteins escape the surveillance of repair and degradation systems, form aggregates, and this process contributes to aging; aging could be therefore a manifestation of a loss in protein homeostasis. This then prompts the question: to what extent could chemical modulation of protein aggregation alter the rate of aging? Furthermore, would such an intervention influence disease pathology? In a recent publication, we addressed this issue by identifying small molecules able to slow protein aggregation in the C. elegans model. We were then able to directly assess the degree to which protein aggregation influences normal aging rates."
Link: http://www.impactaging.com/papers/v3/n4/full/100317.html
LysoSENS is the SENS Foundation initiative to build a platform for medical bioremediation capable of breaking down the damaging byproducts of metabolism that build up in old cells and degrade their ability to recycle garbage. The short of is that we know that out there somewhere are bacteria that can eat these compounds, such as the lipofuscin that contributes to many age-related conditions. There is no buildup of prominent components of lipofuscin in graveyards, for example - so something is consuming it. That bacterial something will be armed with enzymes, biological knifes and saws that might be turned into a therapy to destroy lipofuscin if identified and introduced into the human body.
You might recall that the early LysoSENS volunteers ran a contest for soil samples from obscure locations back in 2006, the better to get a good mix of bacterial origins for analysis.
The search for bacterial enzymes that can safely attack lipofuscin in the body presently gets the lion's share of research funding at the SENS Foundation, and, appropriately, they are hiring in the Bay Area, California:
SENS Foundation is hiring for our research center located in Mountain View, CA. We are seeking a team lead for our LysoSENS project, which contains both intra- and extramural components.
Qualified candidates will have an MS, or Ph.D. in the chemical/biological sciences and at least 5 years of work experience that must include prior project management experience. Duties will include the preparation of grant proposals, internal and external progress reports, individual and collaborative publication. The project lead will develop, interpret and implement standards, procedures, and protocols for the LysoSENS research program and may collaborate on determining strategic directions in the research program. Candidates must have a proven ability to lead other professionals.
Seems like the community has come a long way from the turn of the century, doesn't it? Raising enough money for formal hires is always a big organizational milestone, and congratulations are due to the SENS Foundation staff and volunteers who have worked hard to get to this point.
A translated interview with SENS Foundation co-founder Aubrey de Grey: "I have identified seven types of damage [that cause aging]. In five cases we can repair the damage in my opinion, by replacing irreversibly damaged cells by stem cells, or when garbage accumulates, we will remove [it]. In two cases, we need to engage in gene therapy, for example, through new DNA counteract mutations in the mitochondria. ... We should intervene as little as possible in the metabolic pathways themselves. This is too complicated, we do not know enough yet about it. I prefer the regenerative approach, the repair and maintenance. It is [sufficient] to repair the damage after it occurred. In this way, we do not [need to] understand all the molecular details and how they come about. But we have to intervene before the problems get out of control. ... A simple example is the stiffening of the extracellular matrix - this is the fibrous scaffold between cells. The stiffening occurs because certain molecules network with each other. There is a principal [agent], a molecule called [glucosepane], which has the largest share of the networking and reinforcement. We must find a way to break up about two-thirds of them again. If we break these reinforcements, it would eliminate about half of the damage. ... I think the probability is about 50 percent, that all of these therapies in 25 years actually show the desired results. The average life span might then be [increased by] about 30 years."
News from the field of stem cell research: "researchers [report] a game-changing advance in stem cell science: the creation of long-term, self-renewing, primitive neural precursor cells from human embryonic stem cells (hESCs) that can be directed to become many types of neuron without increased risk of tumor formation. ... It means we can generate stable, renewable neural stem cells or downstream products quickly, in great quantities and in a clinical grade - millions in less than a week - that can be used for clinical trials and, eventually, for clinical treatments. Until now, that has not been possible. ... Human embryonic stem cells hold great promise in regenerative medicine due to their ability to become any kind of cell needed to repair and restore damaged tissues. But the potential of hESCs has been constrained by a number of practical problems, not least among them the difficulty of growing sufficient quantities of stable, usable cells and the risk that some of these cells might form tumors. ... [Researchers] added small molecules in a chemically defined culture condition that induces hESCs to become primitive neural precursor cells, but then halts the further differentiation process. ... And because it doesn't use any gene transfer technologies or exogenous cell products, there's minimal risk of introducing mutations or outside contamination."
Link: http://www.sciencedaily.com/releases/2011/04/110425153554.htm
The jellyfish Turritopsis nutricula is one of the few species whose members might be considered immortal, based on what is presently known of its biology. The life course of this jellyfish is very far removed from that of humans; even more so than that of the lobster, another marine species that might be immortal - though there researchers know far too little to make the call one way or another.
Immortality in the sea lasts right up until something larger eats you, of course. The form of agelessness enjoyed by Turritopsis nutricula appears to be an adaptation to periods of starvation: it can retreat to earlier stages of its life cycle, and in the process its cells alter their character in an usual way:
It starts out as a larva that eventually sinks to the bottom of the ocean and attaches to a sturdy substrate and continues development into a polyp that resembles a sea plant. The polyp then matures to become a free-floating medusa, what we commonly recognize as jellyfish resembling an upside down saucer with tentacles. ... However, during times of stress like a shortage of food, Turritopsis responds by beginning to reverse the process before eventually becoming a polyp again. From this point then, it can again develop into a sexually mature medusa when conditions become more favorable. Theoretically, it can repeat this process indefinitely as its cells undergo a process called transdifferentiation, a rare biological process whereby any non-stem cell can become a different cell entirely. It is still unclear whether only specific cells can only become other specific cells or if any cell in Turritopsis has the potential to become any other cell.
Unlike other long-lived or apparently ageless animals, the principle biological process of interest here is transdifferentiation - being able to produce any type of cell from any other type of cell without having to go through intermediary stages such as the generation and differentiation of stem cells. Modern stem cell medicine depends on techniques for controlling and changing the state of cells - to be able to engineer pluripotent cells from ordinary cells, for example, or produce unlimited numbers of a particular type of cell for research, transplantation, and tissue engineering.
When it comes to transdifferentiation, the hope is that we will eventually be able to learn how creatures like Turritopsis skip the stem cell step and go directly from one cell type to another.
Reliable control over that process for human cells would greatly improve the state of the art in the field of regenerative medicine - and in fact research groups in the space are headed in that direction already.
One of the most dreaded consequences of cancer is when the disease metastasizes -- meaning it spreads from the primary site where it started to other parts of the body. But University of California, Riverside (UCR) scientists have announced what could be a major breakthrough in halting metastasis. They've discovered components in pomegranate juice that inhibit the movement of cancer cells and weaken the attraction of malignant cells to a chemical signal that has been shown to promote metastasis.
The UCR findings were just presented at the American Society for Cell Biology's 50th Annual Meeting, which is being held in Philadelphia. Specifically, the research team from the UCR laboratory of Manuela Martins-Green, Ph.D., found that pomegranate juice seems to block the spread of prostate cancer cells to the bone. The group is planning additional tests to determine the effects of various doses of the natural pomegranate compounds and whether there are any side effects. Read more...
Cardiofy Heart Care Supplement
Aids researchers and advocates were devastated in 2007, when a much anticipated vaccine against HIV unexpectedly failed to protect anyone in a clinical trial of 3,000 people. Even worse, the experimental inoculation, developed with money from the Merck pharmaceutical company and the National Institute of Allergy and Infectious Diseases, actually increased the chances that some people would later acquire HIV. Millions of dollars and more than a decade of research had gone into creating the vaccine. Meanwhile, in that same 10-year period, 18 million people died of AIDS, and millions more were infected.
The Merck vaccine failed in large part because investigators do not yet know how to create the perfect vaccine. Yes, a number of vaccines have been spectacularly successful. Think of polio and smallpox. In truth, though, luck played a big role in those successes. Based on limited knowledge of the immune system and of the biology of a pathogen, investigators made educated guesses at vaccine formulations that might work and then, perhaps after some tinkering, had the good fortune to be proved right when the vaccine protected people. But all too often lack of insight into the needed immune response leads to disappointment, with a vaccine candidate recognized as ineffective only after a large human trial has been performed.
Poor sanitation can foster transmission of all sorts of nasty bacterial bugs. But a new study has found that among common bacteria, antibiotic resistance is brewing in the New Delhi water supply--and spreading in at least 20 strains, including some that cause dysentery and cholera. [More]
Data from successful animal study using liver cells derived from human parthenogenetic stem cells to be presented at two upcoming scientific conferences
Company also announces collaboration with Cedars-Sinai Medical Center for liver disease research, and completion of research on cytochrome P450 activity
International Stem Cell Corporation (OTCBB:ISCO) (ISCO) announces successful completion of the first series of preclinical testing of hepatocytes derived in the lab from human parthenogenetic stem cells (hpSC). In the transplantation mouse model, inoculated cells were capable of engrafting and surviving in specific niches within the liver, and were further developing into cells with essential hepatocyte-like features. Moreover, the transplanted cells could be identified in recipient tissue for a prolonged period of time.
The findings of these studies will be presented at the annual meeting of American Society of Gene & Cell Therapy, May 18-21 in Seattle, and at the International Society for Stem Cell Research annual conference, June 15-18 in Toronto.
"These results mark the achievement of a key milestone in our preclinical research," said Andrey Semechkin, Ph.D., ISCO's Chief Executive Officer. "Specifically, we have perfected the technique to transplant hepatocytes, an extremely fragile cell type, into the liver of animals, which is an easily injured organ. This preclinical research helps us develop our collaborations with clinics."
Nikolay Turovets, Ph.D., ISCO's Director of Research and Therapeutic Development commented "The next phase of research is to conduct experiments to demonstrate the ability of the transplanted cells to perform the vital functions of normal hepatocytes and, accordingly, their ability to modify disease by restoring the missing function of a patient's diseased liver."
The Company also announces the signing of a joint collaboration agreement with Cedars-Sinai Medical Center in Los Angeles to conduct research to develop therapies for liver diseases, in particular urea cycle disorders. Jeffrey Fair, MD., a liver transplant surgeon and Director of Translational Research for the Cedars-Sinai Comprehensive Transplant Center and Department of Surgery, will lead the Cedars-Sinai research team.
Dr. Fair said, "Urea cycle disorders are genetic deficiencies of liver function, which mostly affect newborns and oftentimes cause catastrophic neurological injury. It has been shown that transplantation of donor hepatocytes can save patient lives. Therefore, derivation of hepatocytes from hpSCs that can be immune-matched to the patient is a very pressing goal."
The Company also announces the completion of research focused on the investigation of cytochrome P450 activity and corresponding genes in hepatocytes derived from hpSC. According to the results, the differentiation technology developed by ISCO allows the creation of hepatocytes in the fetal stage of development. This research may contribute to the design of a product for future drug testing and discovery.
About International Stem Cell Corporation
International Stem Cell Corporation is focused on the therapeutic applications of human parthenogenetic stem cells and the development and commercialization of cell-based research and cosmetic products. ISCO's core technology, parthenogenesis, results in the creation of pluripotent human stem cells from unfertilized oocytes (eggs). hpSCs avoid ethical issues associated with the use or destruction of viable human embryos. ISCO scientists have created the first parthenogenic, homozygous stem cell line that can be a source of therapeutic cells with minimal immune rejection after transplantation into hundreds of millions of individuals of differing genders, ages and racial background. This offers the potential to create the first true stem cell bank, UniStemCell™. ISCO also produces and markets specialized cells and growth media for therapeutic research worldwide through its subsidiary Lifeline Cell Technology, and cell-based skin care products through its subsidiary Lifeline Skin Care. More information is available at http://www.internationalstemcell.com.
To subscribe to receive ongoing corporate communications, please click on the following link:http://www.b2i.us/irpass.asp?BzID=1468&to=ea&s=0.
Forward-looking Statements
Statements pertaining to anticipated developments, research and development goals and related potential therapeutic treatments, the potential benefits of products, and other opportunities for the company and its subsidiaries, along with other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements. Any statements that are not historical fact (including, but not limited to statements that contain words such as "will," "believes," "plans," "anticipates," "expects," "estimates,") should also be considered to be forward-looking statements. Forward-looking statements involve risks and uncertainties, including, without limitation, risks inherent in the development and/or commercialization of potential products and the management of collaborations, regulatory approvals, need and ability to obtain future capital, application of capital resources among competing uses, and maintenance of intellectual property rights. Actual results may differ materially from the results anticipated in these forward-looking statements and as such should be evaluated together with the many uncertainties that affect the company's business, particularly those mentioned in the cautionary statements found in the company's Securities and Exchange Commission filings. The company disclaims any intent or obligation to update forward-looking statements.
International Stem Cell Corporation
Kenneth C Aldrich, Chairman
760-940-6383
kaldrich@intlstemcell.com
or
Nikolay Turovets, Ph.D.
Director, Research and Therapeutic Development
nturovets@intlstemcell.com
My advice for doctors who are interested in starting using social media for professional purposes is simple:
- Start on Twitter, expand to a blog as natural progression.
I posted this on Twitter yesterday: Doctors, when you don't have time to write a blog post, record a video - the orthopedic surgeon @hjluks shows how it's done: http://goo.gl/jL73J
@Doctor_V (Bryan Vartabedian) said, "My blog is my home. Twitter and Facebook are outposts."
I actually disagree a bit. My use of Twitter goes beyond a simple outpost though. It's my digital notebook and idea feedback system.
The circle of online information for me is as follows: Google Reader -> Share on Twitter -> Get feedback -> Write a blog post -> Share via RSS and Twitter -> Get feedback, go on.
The circle of online information (full version) (click to enlarge).
Going back to the video embedded above, I think that @hjluks is the current leader in creating original, honest, tell-it-like-it-is clinical content among physicians. This is an example to follow. The technical execution does not have to be perfect, as you will see from the discussion started on Twitter and summarized below. However, the content must be factually correct and professional.
@yayayarndiva (P. Mimi Poinsett MD) had a few comments about the technical aspects of the video such as "if you are going to do a video - make your background a tad less busy:)"
I actually liked the background - it's "authentic" and gives you something to look at during the 8-minute video.
@hjluks actually polled 100 patients on that. They like the laid back office view.
@yayayarndiva P. (Mimi Poinsett MD) thought that "authentically messy AND 8 min video with a head in bouncing chair - think I would rather read the transcript... I think docs like everyone else can sharpen their presentation skills with video... still good to continue. Video? A talking head doesn't confer authenticity- just a new toy:)... Or you could use Dragon software and dictate your post..."
@ePatientDave (Dave deBronkart) convinced @hjluks to do the transcripts, primarily for Google. "Otherwise, thy pearls of light are hidden under a YouTube bushel. I emphasize it's not just *marketing* SEO - it's for being findable for those in need", said @ePatientDave.
I agree. You need the transcript for SEO and quick info. SEO doesn't just apply to marketing - it's a way for people (real humans) to find you online.
Nothing beats video for authenticity though. I understand the concept of creating technically flawless presentations but if you wait to do a perfect video and you are a busy doctor, you may never do it. The same applies to blog posts - if you are going to write a blog post for 2 months, write a journal article instead.
I had some final encouragement for @hjluks: "You don't have to be pro with video. You are pro as orthopod - who uses video."
I think he liked that.
Another good discussion point was brought up by an office manager of a pediatric group in Chicago: Do you need a social media policy for your medical practice? http://goo.gl/7APvI - I think you do.
This is a list of the Top Twitter Doctors arranged by specialty in alphabetical order - feel free to add your own suggestions. The list is open to anybody to edit:
Posted at Clinical Cases and Images. Stay updated and subscribe, follow us on Twitter and connect on Facebook.
