Grey #39;s Anatomy 9x22 Promo "Do You Believe in Magic"
The doctors reach out to Bailey but she continues to shut everyone out; after an incident with Ethan #39;s grandmother, Owen fears the child could end up in fost...
By: CalliopeRobbins
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Grey's Anatomy 9x22 Promo "Do You Believe in Magic" - Video
Italian ex votos
An ex-voto is created when an individual's prayers for a miracle are answered. After praying to a saint for a miraculous healing, an individual would commission a local artist to create a small painting that would be hung in the local church as a public testimony of that individual's faith and gratitude for a miracle. Usually done on canvas or tin, ex-votos generally consist of three basic elements: the illustrative depiction of the event, the narrative, and the depiction of the saint or deity. Variations of this standard form can be seen over time, but the central elements remain the same. Ex-votos are not only symbols of faith and devotion, but also serve to document diseases and their treatments including smallpox and tuberculosis. Emphasis is placed on the dramatic aspects of an illness including exaggerated symptoms evoking sympathy for the sufferer and validating the importance of the divine in the sufferer's recovery. Many depictions take place in the home where doctors and family members tend to the sick. Homes are generally modestly decorated and always include religious icons. Settings also include hospitals and operating rooms where doctors and nurses can be seen using surgical instruments and other medical equipment. Patients are seen in bed or on an operating room table. They appear calm and serene as their faith and devotion enables them to transcend their pain and suffering.More info:
http://en.wikipedia.org/wiki/Ex-voto
http://www.nlm.nih.gov/exhibition/exvotos/italian.html
http://www.mariolinasalvatori.com/?p=10
Source:
http://morbidanatomy.blogspot.com/2013/04/italian-ex-votos-20th-century.html
How to provide proper nutrition for your child
A broad mix of nutrients are essential to children #39;s development. Dr. Scott Shannon explains how you can provide proper nutrition to ensure your child #39;s ment...
By: HowdiniGuru
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How to provide proper nutrition for your child - Video
NEW YORK--(BUSINESS WIRE)--
Nutrition Capital Network (NCN) (www.nutritioncapital.com), an organization that connects investors with high-potential growth companies in the nutrition and health & wellness industry, is holding its Spring Investor Meeting on April 29-30 in New York City, where 20-22 selected growth companies will present to 50-70 investment groups representing $6 billion in capital.
With private equity leaders and strategic investors such as Bayer, DSM, Coca-Cola, Kelloggs, Pepsi and Unilever among its distinguished Cornerstone Investors, NCN serves as a gateway for growth companies to obtain both capital and seasoned partners. The NCN XII Spring Investor Meeting in New York will highlight growth companies in a range of segments, including dietary supplements, natural & organic food and beverages, and nutritional ingredients, among others. Presenting companies are selected and coached by NCNs committee of industry veterans.
NCN investment meetings also present the Health & Wellness Investor Forum, where NCN Principals and Partners present industry data and insights into recent transactions.
NCN tracks investment activity in the nutrition and health & wellness industry throughout the year. The industry is on track to equal, if not surpass, the record high of 287 transactions posted in 2012 with recent Q1 transactions showing sustained interest among investors, noted Grant Ferrier, NCN CEO and co-founder. Last year, we saw over 50% growth in financings despite a 12% drop in M&A activity, indicating strong momentum in the nutrition and health & wellness markets served by NCN.
NCN has a successful track record of matching entrepreneurs, growth companies and technology innovators with suitable investors, acquirers and strategic partners. Of the 287 companies that have presented at NCN Investor Meetings from 2007-2012, 43% have completed some form of transaction. Past presenters that have closed significant transactions include Food Should Taste Good, a company acquired by General Mills in February 2012, in addition to Annies, Immaculate Baking, Zico and Zhenas Gypsy Tea.
For more information about Nutrition Capital Network and the upcoming NYC Investor Meeting, please contact Alissa Sears of Christie Communications at (805) 969-3744 or email alissa@christiecomm.com.
See the rest here:
Nutrition Capital Network's NYC Investor Meeting April 29 – 30 Highlights High Growth Companies and Emerging Market ...
NYU School of Medicine Professor Joins World Leaders in Academia, Business, Public Affairs, Humanities and the Arts
Newswise New York, NY, April 25, 2013 NYU School of Medicine is pleased to announce that The American Academy of Arts and Sciences (AMACAD) has elected Martin J. Blaser, MD, the George and Muriel Singer Professor of Medicine, professor of microbiology, and director of the Human Microbiome Program at NYU Langone, to this years class of members. The new class will be inducted at a ceremony on October 12, 2013, at the Academys headquarters in Cambridge, Massachusetts.
Members of the 2013 class include winners of the Nobel Prize; National Medal of Science; the Lasker Award; the Pulitzer and the Shaw prizes; the Fields Medal; MacArthur and Guggenheim fellowships; the Kennedy Center Honors; and Grammy, Emmy, Academy, and Tony awards.
Dr. Blaser is a world renowned researcher in microbiology and infectious disease. His work over the past three decades has helped transform our understanding of the human microbiome, the bacteria that live on and inside us. In particular, his lab has helped untangle the complex molecular behavior of Helicobacter pylori, a widespread species of bacteria linked to gastritis, peptic ulcers and stomach cancer. In addition to developing the first blood test for H. pylori, his team has recast the microbe in a new light, showing how its depletion in the gut through the use of antibiotics increases the risk of childhood asthma. Dr. Blaser holds 24 U.S. patents relating to his research into bacterial diseases and the microbiome, and has authored over 500 original articles.
Martin Blaser has made invaluable contributions not only to the study of the microbiome and disease, but as an educator and mentor to many fellow scientists, said Dafna Bar-Sagi, PhD, senior vice president and vice dean for Science and chief scientific officer at NYU School of Medicine. Through his leadership and intangible interpersonal qualities as well as his research, he stands out as a model for the scientific community and beyond. His election to the AMACAD is richly deserved."
Dr. Blaser is the principal investigator on five peer reviewed grants, including three from the NIH, and serves as chair of the Advisory Board for Clinical Research at the NIH. Dr. Blaser also leads the Human Microbiome Program at NYU Langone.
Dr. Blaser is a member of the American Society for Clinical Investigation, the Association of American Physicians, the American Epidemiologic Society, and the American Clinical and Climatological Association, as well as a Governor of the American Academy of Microbiology and a Master of the American College of Physicians. He currently serves as the Chair of the Advisory Board for Clinical Research of the National Institutes of Health, and the Scientific Advisory Board of the Doris Duke Charitable Foundation. Previously he served as president of the Infectious Diseases Society of America and as Chair of the Board of Scientific Counselors of the National Cancer Institute.
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About NYU School of Medicine: NYU School of Medicine is one of the nations preeminent academic institutions dedicated to achieving world class medical educational excellence. For 170 years, NYU School of Medicine has trained thousands of physicians and scientists who have helped to shape the course of medical history and enrich the lives of countless people. An integral part of NYU Langone Medical Center, the School of Medicine at its core is committed to improving the human condition through medical education, scientific research and direct patient care. The School also maintains academic affiliations with area hospitals, including Bellevue Hospital Center, one of the nations finest municipal hospitals where its students, residents and faculty provide the clinical and emergency care to New York Citys diverse population, which enhances the scope and quality of their medical education and training. Additional information about the NYU School of Medicine is available at http://school.med.nyu.edu/.
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American Academy of Arts and Sciences Elects Martin J. Blaser, MD, Professor of Medicine and Microbiology, to 2013 ...
The secret to strengthening your immune systems ability to fight off illness might be right under your nose-- or rather, in it, according to a University of Saskatchewan researcher. Scott Napper, an associate professor of biochemistry at the University, has suggested that there may be health benefits to that most icky of icky habits: picking our noses and eating it.
Almost all kids have a compulsion to taste the things that come out of their noses, Napper said. He suggested that its possible that nature is pushing humans to adopt the behaviour because it is somehow to our natural advantage. Nasal mucous traps germs and stops them from getting into our lungs, Napper explained, but its possible that if we eat the mucous, exposure to those germs could actually help build immunity. It might teach your immune system about what's it's likely to get exposed to, so it might serve as almost a natural vaccination, if you will, he told CTV Saskatoon.
Its possible, he stated, that by blowing our noses into handkerchiefs or tissues, we might be robbing our bodies of the chance to develop valuable antibodies. Napper said his idea is still very preliminary, but admitted that it's gotten a lot of attention. He now hopes to conduct a study in which some type of molecule could be inserted into peoples noses, with half the participants picking their nose and eating it, and then seeing if the molecule still makes them ill.
Read more:
Picking your nose and eating it 'may be good for your health'
Allen Park - It was suggested to Brandon Hepburn, the linebacker from Florida A&M the Lions took with their final pick Saturday, that he might be wasting his time playing football.
"Yeah," he said, "I get that a lot."
It's not that Hepburn doesn't have a chance to make an NFL roster. He's an overachieving, multi-dimensional athlete who, if nothing else, can make a good living on special teams.
But he can possibly do more for mankind by pursuing his other passion science. Hepburn, who scored 1400 on his SATs, got his degree in biochemistry and during an internship at North Texas University worked on a team that helped find a way to kill certain cancer cells in rats using copper-loaded nano particles.
"We haven't cured cancer, yet," he said, chuckling. "But we were able to do a lot of great work."
He hopes one day to own his own biochemical company and lead research against deadly diseases.
"But football is my No. 1 dream," he said. "I've always wanted to be in the position I am in now, to live out my dream of playing professional football. At the end of the day, you can't play forever. I hope after a long career I can go into that other aspects of my life."
Position: Inside linebacker
School: Florida A&M
Height/weight: 6-2, 240
Go here to see the original:
Lions' select future biochemist Brandon Hepburn in seventh round
Human calorie restriction studies continue onward at the normal sedate pace of all human research, as noted in a recent post on the CALERIE program. It remains the case that the vast majority of work on calorie restriction and its beneficial effects involves mice, flies, worms, and other laboratory animals. Most such species exhibit increased longevity and improved measures of long term health when on a calorie restricted diet, provided that they still receive suitable levels of nutrition. That this is so universal is one of the reasons to suggest calorie restriction with optimal nutrition as a lifestyle choice in humans.
Other reasons include the results from human studies to date; if there was a pill you could take that provided half the benefits that calorie restriction has been shown to produce in humans, then everyone would be falling over themselves to take it. It’s somewhat harder to convince people to eat less in this day and age, however, no matter how beneficial the results might be. The paper quoted below is illustrative of results from human studies, in that the measures taken tend to line up with what is seen in short-lived animals like mice and rats:
Caloric restriction (CR) and down-regulation of the insulin/IGF pathway are the most robust interventions known to increase longevity in lower organisms. However, little is known about the molecular adaptations induced by CR in humans. Here we report that long-term CR in humans inhibits the IGF-1/insulin pathway in skeletal muscle, a key metabolic tissue. We also demonstrate that CR-induced dramatic changes of the skeletal muscle transcriptional profile that resemble those of younger individuals. Finally, in both rats and humans CR evoked similar responses in the transcriptional profiles of skeletal muscle. This common signature consisted of three key pathways typically associated with longevity: IGF-1/insulin signaling, mitochondrial biogenesis and inflammation.
If you wander over to Extreme Longevity you can find a PDF copy of the full paper.
The fact that more easily gathered measures of metabolism like those noted above are similar for rat and human calorie restriction makes CR look like a good option – where these measures match up, the hope is that the long term rewards do so as well. Studies in rats can achieve what studies in humans cannot, which is to follow large numbers of rats for their entire lives and catalog the impressive long term health benefits, as well as the characteristic increase in life expectancy, that accompanies CR in rodent species. This is one of many examples, in which the researchers focus as much on exercise as CR:
Effects of dietary restriction and exercise on the age-related pathology of the rat
The most efficacious and commonly used intervention used to retard the aging processes is dietary restriction (DR). It increases mean and maximum life spans, delays the appearance, frequency, and severity of many age-related diseases, and more importantly, attenuates much of the physiological decline associated with age. Although the subject of intense research, the mechanism by which DR alters the aging processes is still unknown.
Physical exercise is another effective intervention shown to affect aging phenomena, especially when applied in combination with DR. Mild exercise in concert with DR is beneficial, but vigorous exercise coupled with DR could be deleterious. With regard to pathology, exercise generally exerts a salutary influence on age-related diseases, both neoplastic and non-neoplastic, and this effect may contribute to the increase in median life span seen with exercised rats.
Exercise coupled with 40% DR was found to suppress the incidence of fatal neoplastic disease compared to the sedentary DR group. Exercise with mild DR suppressed the incidence of multiple fatal disease and chronic nephropathy, and also delayed the occurrence of many age-related lesions compared to the ad libitum (AL) control group. However, these effects may have little bearing on the aging process per se, as maximum life span is only minimally affected. Although not as intensively studied as DR, results from studies that utilize exercise as a research probe, either alone or in combination with DR, have helped to assess the validity of proposed mechanisms for DR and aging itself.
Neither the retardation of growth rate nor the increase in physical activity, observed with either exercise or DR, appear to contribute to the anti-aging action of DR. Moreover, results from lifelong exercise studies indicate that the effects of DR do not depend upon changes in energy availability or metabolic rate. The mechanisms involving effects on adiposity or immune function are also inadequate explanations for the action of DR on aging. Of the proposed mechanisms, only one, as postulated by the Oxidative Stress Hypothesis of Aging, tenably accounts for the known effects of DR and exercise on aging.
Source:
http://www.fightaging.org/archives/2013/04/recent-calorie-restriction-research.php
Source:
http://www.longevitymedicine.tv/recent-calorie-restriction-research/
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
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
Source:
http://www.longevitymedicine.tv/joining-the-dots-in-genetic-parkinsons-disease/
The electron transport chain is the core piece of biological machinery inside mitochondria, the cell’s power plants. It occupies a central place in the various free radical theories of aging as well. A good number of longevity-related mutations in laboratory animals appear to alter electron transport chain function as their primary mode of operation, and a good case is made for a large portion of degenerative aging to rest atop damage to the mitochondrial genes that encode proteins essential to proper electron transport chain function.
Most biogerontologists agree that oxygen (and nitrogen) free radicals play a major role in the process of aging. The evidence strongly suggests that the electron transport chain, located in the inner mitochondrial membrane, is the major source of reactive oxygen species in animal cells.
It has been reported that there exists an inverse correlation between the rate of superoxide/hydrogen peroxide production by mitochondria and the maximum longevity of mammalian species. However, no correlation or most frequently an inverse correlation exists between the amount of antioxidant enzymes and maximum longevity. Although overexpression of the antioxidant enzymes SOD1 and CAT (as well as SOD1 alone) have been successful at extending maximum lifespan in Drosophila, this has not been the case in mice. Several labs have overexpressed SOD1 and failed to see a positive effect on longevity. [Although overexpression of CAT has been shown to extend life in mice by some groups].
An explanation for this failure is that there is some level of superoxide damage that is not preventable by SOD, such as that initiated by the hydroperoxyl radical inside the lipid bilayer, and that accumulation of this damage is responsible for aging. I therefore suggest an alternative approach to testing the free radical theory of aging in mammals. Instead of trying to increase the amount of antioxidant enzymes, I suggest using molecular biology/transgenics to decrease the rate of superoxide production, which in the context of the free radical theory of aging would be expected to increase longevity.
Personally I think the better approach to testing theory here is to implement mitochondrial repair or replacement, both of which are very feasible, and see what effect that has on older animals. It will both extend life and produce some degree of rejuvenation if the mitochondrial free radical theory of aging is correct.
Link: http://www.ncbi.nlm.nih.gov/pubmed/23604868
Source:
http://www.fightaging.org/archives/2013/04/considering-the-electron-transport-chain-in-aging.php
Source:
http://www.longevitymedicine.tv/considering-the-electron-transport-chain-in-aging/
I mentioned GIFT/LIFT, the immune cell transplant approach to cancer therapy in a short list of research that might lead to cancer cures yesterday. This line of research derives from the fortuitous discovery of a cancer-immune lineage of laboratory mice, followed by the finding that this immunity is transferable via transplant of granulocyte or other forms of leukocyte immune cells.
This discovery raises the possibility that effective cancer treatments can be established by finding donors with appropriately equipped immune cells and then transplanting those cells into patients, even in advance of a complete understanding of how this all works. That complete understanding might enable an effective cure for cancer therapy based on altering a patient’s own immune cells, or a much more reliable way to determine useful donors, but it’ll take much longer to get to that point, possibly decades. Thus there is considerable incentive to take the shortcut if there’s one to be had, in the same way as first generation stem cell transplant therapies continue to be established usefully far in advance of the complete understanding of how they work.
You can look back in the archives for posts that cover this topic, though I should mention that the younger organizations mentioned as being involved in work on this are mostly defunct or going nowhere, it seems. Finding funding is an issue, though the Florida clinical trial partially funded by the Life Extension Foundation is apparently still ongoing. Good for them.
Today a reader pointed me to recently published research on the cancer-immune mice, which is much appreciated. Follow-on research often drifts by me, as it’s harder to pick out papers from the flow once they start to focus on specific concerns and subtopics. This open access paper reinforces the previous work by Zheng Cui and others, demonstrating once more a transfer of cancer immunity between mice, but the authors note that the approach isn’t as general as hoped – meaning that there are other factors at work that will make it much more of a hard slog to either (a) find a donor with immune cells that will work on your cancer, or (b) figure out how what’s going on under the hood here. Why does it work for some cancers and not for others? So it’s the same old story: biology is always considerable more complicated than we’d like it to be.
Immune Cells from SR/CR Mice Induce the Regression of Established Tumors in BALB/c and C57BL/6 Mice
Mouse strains that survive injection of large numbers of cancer cells are rare. Such mice constitute important experimental models for cancer resistance at the cellular and molecular levels. The spontaneous regression/complete resistance (SR/CR) mice were derived from BALB/c mice and described by Cui and colleagues in 1999. The phenotype was characterized by the ability to resist challenges from a number of cancer cell lines. This resistance involved innate immune cells, including polymorphonuclear granulocytes (PMNs), macrophages, and NK cells.
Interestingly, adoptive transfer (AT) of SR/CR leukocytes rendered recipients resistant to the intraperitoneal injection of S180 [sarcoma cancer] cells and also induced the regression of solid tumors. [In] this study we tested whether the cancer resistance of the SR/CR mice could be transferred to cancer susceptible mice by AT of selected immune cells.
In contrast to previous observations, the cancer resistance was limited to S180 sarcoma cancer cells. We were unable to confirm previous observations of resistance to EL-4 lymphoma cells and J774A.1 monocyte-macrophage cancer cells. The cancer resistance against S180 sarcoma cells could be transferred to susceptible non-resistant [mice. In] the responding recipient mice, the cancer disappeared gradually following infiltration of a large number of polymorphonuclear granulocytes and remarkably few lymphocytes in the remaining tumor tissues. This study confirmed that the in vivo growth and spread of cancer cells depend on a complex interplay between the cancer cells and the host organism.
Here, hereditary components of the immune system, most likely the innate part, played a crucial role in this interplay and lead to resistance to a single experimental cancer type. The fact that leukocytes [could] be transferred to inhibit S180 cancer cell growth in susceptible recipient mice support the vision of an efficient and adverse event free immunotherapy in future selected cancer types.
The failure to replicate early work for more than one form of cancer suggests that the underlying mechanisms here are, as mentioned above, not as general or as simple as we’d like them to be. It is very effective when it does work, however, not just causing remission of cancer, but also granting immunity. This means that research will continue, though as usual never as rapidly nor with as much funding as we’d like.
Source:
http://www.fightaging.org/archives/2013/04/more-data-on-granulocyte-transplant-cancer-therapies.php
Source:
http://www.longevitymedicine.tv/more-data-on-granulocyte-transplant-cancer-therapies/
Damage to mitochondrial DNA accumulates as a side-effect of the operation of mitochondria in your cells, and per the mitochondrial free radical theory of aging proceeds to cause some fraction of degenerative aging though a long chain of ever worsening consequences.
Below you’ll find recently published research that shows long-lived mice to have less mitochondrial DNA damage, which is what you’d expect to see under this model. This reinforces the need for ways to repair or replace mitochondrial DNA throughout the body in order to remove this contribution to degenerative aging. A wide range of possible approaches exist, but currently little funding is devoted towards realizing them and there is no path to getting treatments to reverse aging through the regulatory process – the standard lament when it comes to rejuvenation biotechnology.
The single gene mutation of Ames dwarf mice increases their maximum longevity by around 40% but the mechanism(s) responsible for this effect remain to be identified. This animal model thus offers a unique possibility of testing the mitochondrial theory of aging.
In this investigation, oxidative damage to mitochondrial DNA (mtDNA) was measured for the first time in dwarf and wild type mice of both sexes. In the brain, 8-oxo,7,8-dihydro-2′-deoxyguanosine (8-oxodG) in mtDNA [a measure of oxidative stress] was significantly lower in dwarfs than in their controls both in males (by 32%) and in females (by 36%). The heart of male dwarfs also showed significantly lower mtDNA 8-oxodG levels (30% decrease) than the heart of male wild type mice, whereas no differences were found in the heart of females.
The results, taken together, indicate that the single gene mutation of Ames dwarfs lowers oxidative damage to mtDNA especially in the brain, an organ of utmost relevance for aging. Together with the previous evidence for relatively lower level of oxidative damage to mtDNA in both long-lived and caloric restricted animals, these findings suggest that lowering of oxidative damage to mtDNA is a common mechanism of life extension in these three different mammalian models.
Link: http://www.ncbi.nlm.nih.gov/pubmed/23604907
Source:
http://www.longevitymedicine.tv/measures-of-mitochondrial-dna-damage-lower-in-long-lived-mice/
Anna French and David A. Brindley, along with some of my assistance, captured and have now published the main themes of the meeting and the major questions facing the regenerative medicine industry and its rapidly emerging subsets of cellular and gene therapies. Source:
http://feedproxy.google.com/~r/CellTherapyBlog/~3/4Uv2o54_hWQ/commercialization-of-regenerative.html
Source:
http://www.longevitymedicine.tv/commercialization-of-regenerative-medicine-learning-from-spin-outs/
http://feedproxy.google.com/~r/blogspot/uqpFc/~3/0HfVYv0XVQg/california-stem-cell-agency-seeks.html
The California stem cell agency today clarified the size of the assumed "public investment" in its rough outline of its plan for future activities.
"This hypothetical range of public investment ($50 million to $200 million) is thought of as a one-time investment, with hope of private investments in multiples of that with the fund recharging to some extent based on revenue."
"We have not wanted to post the budget range because we want honest estimates of what folks think the budget should be rather than having them penciling estimates that max out the budget."
The $3 billion California stem cell
agency, which is currently scheduled to go out of business in a few
years, hopes to come up with a detailed plan by this fall for a novel
public-private arrangement that would extend its life.
“...an in-depth analysis of various
public-private funding models with potential to attract private
sector investment to, and facilitate further development of the most
promising CIRM-supported research projects; and recommend a single
preferred approach for achieving this goal, complete with details
relating to the recommended structure and an operational plan.”
“The nature of CIRM as a state agency
is perhaps the biggest weak point (and) has to be addressed politically
and cleared up as soon as possible or raising money will be
unnecessarily challenging.”
We were treated to another super fun episode of Doctor Who in "Journey to the Centre of the TARDIS" and got to see, no surprise here, the center of the TARDIS.
It seems like Clara's arrival the TARDIS itself has become much more of a character than a vessel. Yes, I know it's always had a life of its own and been responsible for a great many things, but we've learned an awful lot about it in fairly short period of time.
I had no idea it held a book on board entitled "The History of the Time War" that referenced The Doctor's name. It would seem others would have found it by now. More on that below.
The salvage brothers were kind of a pointless device to give someone for The Doctor to run around with so he didn't have to talk to himself, but other than that, I really enjoyed with the premise. To think of marauders coming on board to steal parts of the TARDIS is almost ludicrous.
It was also pretty cool that the ship was even willing to turn against The Doctor to protect itself if he wasn't able to contain the guys himself. For as much as he does to protect the TARDIS, the TARDIS has to look out for itself first. I can understand and respect that.
I knew the monsters were going to turn out to be someone or something that was known to Clara, had no idea one of them was Clara. Honestly, that was a pretty cool twist.
Was I the only one who expected her to reach out to herself and try to make some sort of connection? Clara is so inquisitive and wants to help everyone and everything - it shocked me The Doctor was able to keep her from helping herself.
The Eye of Harmony, an exploding star in the act of becoming a black hole - just your basic bit of time lord engineering - was just one of the many other groovy things on the TARDIS that I didn't know about. The seemingly never ending swimming pool, the rocket; it made sense that The Doctor thought bringing Clara to the TARDIS would keep her safe.
Even in the face of so many dangers, the TARDIS has everything. When she realized she was the crispy creature chasing herself, and asked what he meant about bringing there to save her but she died again, I thought - oh no - we're getting into the she's going to start dying a lot part. They've just kept it from us until now.
Thankfully, I was wrong! But, it was enough to tip the scales of The Doctor's noggin in the direction of finding out just who the hell Clara was. He asked her flat out, told her about their previous encounters and her deaths. She wasn't overly frightened like a normal girl would have been, but instead kind of intrigued.
That's when she admitted she knew his name from reading the book, and when I knew that his relief at her not knowing anything about what he was saying was a ruse. She will be somebody special and his expectation that she would know, that anyone would know but him, was just crazy. Whoever she is, she's known only to Doctor Who. The reveal will be amazing.
There has been so much in this short second half of Doctor Who Season 7 that I know the finale is going to be killer and full of mind blowing information. I'm excited to see how they incorporate more than one Doctor and companion, whether it will be through a time rift or parallel universes, but I don't care.
Who wouldn't want to be The Doctor's companion? Even if it meant dying and coming back to life every few decades, it just seems worth it for all the fun and adventure.
What did you think about the adventure inside the TARDIS and The Doctor's continued quest to discover who Clara really is? It's your turn - hit the comments!
Source:
http://www.tvfanatic.com/2013/04/doctor-who-review-journey-to-the-centre-of-the-tardis/
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