Studio City Science Tutor

Hello All!

I've passed CBEST (the test teachers take to get licensed in California), CSET General Science subject tests, and also the CSET Biology and Chemistry subtests. I graduated from college summa cum laude with a 3.9 GPA. I received a Bachelor of Science in Biology, with a Psychology minor. I achieved a lot of advanced, in-depth science knowledge from attending medical school. In any case, the strength of a good tutor lies not only in mastering the knowledge, but in also being able to deliver it to the student effectively. I've been told by my students that I am a pro at this! If you let me tutor you, I guarantee that you will truly understand the material better. Also, I have a magnetic personality, so I guarantee that you will have a lot of fun during our tutoring sessions!

One of my strengths as a tutor lies in the fact that I am very versatile, both in terms of the age groups I can work with, and the subjects I can teach. This versatility is actually what I enjoy most about my tutoring experiences. Currently, I am working with students in elementary school, high school, college and also graduate school. Some of the subjects I teach include Algebra, Biology, Chemistry, Physiology, Biochemistry and English. I am also tutoring a number of students in SAT, ACT, ISEE, and SSAT prep.

Source:
http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

Kansas City Math Tutor

My name is Zachary. My interest in tutoring started when I was a middle school student myself, helping a few classmates study for tests or cram for the state-required evaluations. When I was in high school, I started tutoring students in Algebra, Geometry, and Calculus I for cash, and quickly found I could make good money tutoring a wide range of subjects. I obtained my undergraduate degree from Baker University in Psychology, while continuing to tutor in increasing subject areas like English, biology, chemistry and philosophy. My graduate degree is a Master's of Science in Experimental Psychology, which was a statistics-heavy degree path.

When I tutor, I like to first discover how students are most comfortable learning. Psychology has long held that multiple learning styles exist, and while debate continues to rage over which style is best I prefer to think of each style as having its own strengths and drawbacks. However, I have learned to teach to many different styles, and can teach contextually, rote, test-oriented or experience-based lessons. I am also comfortable with group tutoring, having led several classes of students in graduate school.

Source:
http://www.ilcusa.org/modules/mediablog/rss.php?page_id=43

A bold set of claims from this group working on the genetics of natural variation in longevity for humans: "Like most complex phenotypes, exceptional longevity is thought to reflect a combined influence of environmental (e.g., lifestyle choices, where we live) and genetic factors. To explore the genetic contribution, we undertook a genome-wide association study of exceptional longevity in 801 centenarians (median age at death 104 years) and 914 genetically matched healthy controls. Using these data, we built a genetic model that includes 281 single nucleotide polymorphisms (SNPs) ... Consistent with the hypothesis that the genetic contribution is largest with the oldest ages, the sensitivity of the model increased in the independent cohort with older and older ages ... Further [analysis] suggests that 90% of centenarians can be grouped into clusters characterized by different 'genetic signatures' of varying predictive values for exceptional longevity. ... The different signatures may help dissect this complex phenotype into sub-phenotypes of exceptional longevity." The researchers are claiming some moderately common sets of SNPs found in centenarians (but not so common in the general population) can predict exceptional longevity with odds of 70% or higher, with the much more predictive combinations of SNPs - some at 95% odds of exceptional longevity - being correspondingly very rare. The caveat here is that this is heavily statistical work, and we've already seen one paper from this group withdrawn last year for issues with the statistics.

Link: http://dx.doi.org/10.1371/journal.pone.0029848

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Last week I posted on what seems to be the strikingly different nature of aging at very advanced ages. For example, there is what is known as the mortality plateau in very late life, a period in which mortality rates stop increasing. This has been studied in flies, and there is a small amount of evidence that suggests it might also exist in humans. But I thought I'd point you in the opposite direction today. The research partnership of Leonid Gavrilov and Natalia Gavrilova published a study on mortality at advanced ages not so very long ago, and their data suggests that there is no mortality plateau for humans. The link below is a PDF version of the paper:

Mortality measurement at advanced ages: A study of the Social Security Administration Death Master File

Accurate estimates of mortality at advanced ages are essential to improving forecasts of mortality and the population size of the oldest old age group. However, estimation of hazard rates at extremely old ages poses serious challenges to researchers: (1) The observed mortality deceleration may be at least partially an artifact of mixing different birth cohorts with different mortality (heterogeneity effect); (2) standard assumptions of hazard rate estimates may be invalid when risk of death is extremely high at old ages and (3) ages of very old people may be exaggerated.

One way of obtaining estimates of mortality at extreme ages is to pool together international records of persons surviving to extreme ages with subsequent efforts of strict age validation. This approach helps researchers to resolve the third of the above-mentioned problems but does not resolve the first two problems because of inevitable data heterogeneity when data for people belonging to different birth cohorts and countries are pooled together. In this paper we propose an alternative approach, which gives an opportunity to resolve the first two problems by compiling data for more homogeneous single-year birth cohorts with hazard rates measured at narrow (monthly) age intervals.

...

Study of several single-year extinct birth cohorts shows that mortality trajectory at advanced ages follows the Gompertz law up to the ages 102-105 years without a noticeable deceleration. Earlier reports of mortality deceleration (deviation of mortality from the Gompertz law) at ages below 100 appear to be artifacts of mixing together several birth cohorts with different mortality levels and using cross-sectional instead of cohort data. Age exaggeration and crude assumptions applied to mortality estimates at advanced ages may also contribute to mortality underestimation at very advanced ages.

All the more reason to work harder on the development of rejuvenation biotechnology, capable of repairing the damage of aging. Time waits for no one.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

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

There are a lot of genes wherein alterations correlate with longevity - either mutations, removal of the gene, or epigenetic variations. Some of these are similar between many species, some restricted to a few small branches of the evolutionary tree. As the costs of investigating the genome and the proteome fall rapidly, ever more data is accumulated on the detailed relationships between biology and longevity at the level of molecular mechanisms.

There really is too much new work emerging to point out every study - it has become unremarkable to discover new correlations in the genetics of longevity. Also, when it comes down to it, little of this research will be of any real relevance to the most direct and important work on rejuvenation biotechnology. The research community knows more than enough to enable work on repairing the damage that causes aging.

In any case, here is a recent and representative selection from the ongoing flood of new results on genetics and longevity:

Reduction of Mitoferrin Results in Abnormal Development and Extended Lifespan in Caenorhabditis elegans

Iron is essential for organisms. It is mainly utilized in mitochondria for biosynthesis of iron-sulfur clusters, hemes and other cofactors. Mitoferrin 1 and mitoferrin 2, two homologues proteins belonging to the mitochondrial solute carrier family, are required for iron delivery into mitochondria. ... In this study we found that reduced mitoferrin levels in C. elegans by RNAi treatment causes pleiotropic phenotypes such as small body size, reduced fecundity, slow movement and increased sensitivity to paraquat. Despite these abnormities, lifespan was increased by 50% to 80% in N2 wild type strain, and in further studies using the RNAi sensitive strain eri-1, more than doubled lifespan was observed. The pathways or mechanisms responsible for the lifespan extension and other phenotypes of mitoferrin RNAi worms are worth further study, which may contribute to our understanding of aging mechanisms and the pathogenesis of iron disorder related diseases.

Activity of mannose-binding lectin (MBL) in centenarians

We analyzed MBL2 gene variants in two cohorts of centenarians, octo- and nonagenarians and in the general population, one from Sardinia island (Italy), recruited in the frame of the AKea study, and another from Campania (southern Italy), to search for haplotypes related to longevity. ...The frequency of high and null activity haplotypes was significantly lower and the frequency of intermediate activity haplotype significantly higher in centenarians and in subjects between 80 and 99 years from both the cohorts as compared each to the general population from the same geographic area.

MICS-1 interacts with mitochondrial ATAD-3 and modulates lifespan in C. elegans

Here, we provide evidence that MICS-1 is an interacting partner of the mitochondrial protein ATAD-3 (homologue of human ATAD3), which is essential for C. elegans development. We demonstrate that [RNA interference of mics-1 causes] enhanced longevity with an increased mean lifespan of up to 54% compared to control animals. Of note, also [RNA interference of atad-3] promoted longevity, although to a lesser extend (29% compared to controls).

Linkage of Cardiac Gene Expression Profiles and ETS2 with Lifespan Variability in Rats

Longevity variability is a common feature of aging in mammals, but the mechanisms responsible for this remain largely unknown. Using microarray datasets [we] identified a set of 252 cardiac transcripts predictive of relative lifespan in [rats]. ... four transcription factors (Max, Ets2, Erg, and Msx2) present in heart displayed longevity-dependent, strain-independent changes in abundance, but only ETS2 had an expression profile that directly correlated with the relative lifespan gene set. ... We conclude that variations in ETS2 abundance in hearts of adult rodents and the associated loss of CMs, contribute at least partially, to the longevity variability observed during normal aging of rats through activation of programmed necrosis.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

An example of the world moving forward, even though the really flashy biotechnology is still in the laboratory rather than the clinic: "Age-related macular degeneration (AMD) is the most frequent cause of blindness in the Western World. A [report] shows the number of new cases of blindness and severe visual loss in Denmark has been halved during the last ten years. ... [Researchers] examined the records of 11,848 new cases of legal blindness. The rate of blindness from AMD fell from 522 cases per million inhabitants aged 50 years or older in 2000, to 257 cases per million in 2010, a reduction by over 50 per cent. The bulk of the decrease occurred after 2006, following the introduction of new effective treatment for wet AMD, which is characterised by leaking blood vessels having formed under the fovea. The treatment consists of repeated injections into the eye of a medication that inhibits the signalling molecule vascular endothelial growth factor (VEGF). ... The observations from Denmark were published together with a corroborating report from Israel that found comparable changes in the incidence of legal blindness in that country. ... The massive implementation of modern wet AMD therapy has been a challenge. It is therefore very important that we can now show an impact on public health and it is wonderful to see a reduction in severe visual loss."

Link: http://news.ku.dk/all_news/2012/2012.1/danish-report-shows-risk-of-blindness-halved/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Another study to show that transplanting young ovaries into old mice extends life quite significantly: "successful ovarian transplants increased the lifespan of the mice by more than 40% ... All the mice in both experiments that had received transplants resumed the normal reproductive behaviour of young mice. They showed interest in male mice, mated and some had pups. Normally, old mice stay in the corner of the cage and don't move much, but the activity of mice that had had ovarian transplants was transformed into that of younger mice and they resumed quick movements. Furthermore, the lifespan of the mice who received young ovaries was much longer than that of the control mice: the mice that had received two ovaries lived for an average of 915 days, and the mice that had received one ovary, for an average of 877 days. The newest of our data show the life span of mice that received transplants of young ovaries was increased by more than 40%. ... The average normal lifespan for this particular breed of mice [is] 548 days. ... it was not known why the ovarian transplant increased the lifespan of the mice, but it might be because the transplants were prompting the continuation of normal hormonal functions."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-06/esoh-otr062810.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Your cells are constantly creating and destroying the protein components of their machinery. All of the known metabolic alterations that enhance longevity affect these processes in some way: "Cellular homeostasis, which is needed for the cells to survive, requires a well-controlled balance in protein turnover. Both protein synthesis and degradation are influenced by distinct genetic pathways that control aging in divergent eukaryotic species. ... In addition to providing building blocks for generation of new proteins and fuelling the cell with energy under starvation, the protein degradation processes eliminate damaged, nonfunctional proteins, the accumulation of which serves as the primary contributory factor to aging. Interestingly, a complex, intimate regulatory relationship exists between mechanisms promoting protein synthesis and those mediating protein degradation: under certain circumstances the former downregulate the latter. Thus, conditions that favor protein synthesis can enhance the rate at which damaged proteins accumulate. This may explain why genetic interventions and environmental factors (e.g., dietary restriction) that reduce protein synthesis, at least to tolerable levels, extend lifespan and increase resistance to cellular stress in various experimental model organisms of aging."

View the Article Under Discussion: http://www.ncbi.nlm.nih.gov/pubmed/20886758

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Another paper looks at some of the consequences of becoming obese. In a more fair and productive world, medical costs would be an individual responsibility rather than being socialized as they are at present: "The prevalence of adult obesity has increased in recent decades. It is important to predict the long-term effect of body weight, and changes in body weight, in middle age on longevity and Medicare costs in older ages. ... We predicted longevity and lifetime Medicare costs via simulation for 45-year-old persons by body weight in 1973 and changes in body weight between 1973 and 1983. ... Obese 45-year-olds had a smaller chance of surviving to age 65 and, if they did, incurred significantly higher average lifetime Medicare costs than normal-weight 45-year-olds ($163,000 compared with $117,000). Those who remained obese between ages 45 and 55 in 1973 to 1983 incurred significantly higher lifetime Medicare costs than those who maintained normal weight. ... Chronic obesity in middle age increases lifetime Medicare costs relative to those who remained normal weight. As the survival of obese persons improves, it is possible that Medicare costs may rise substantially in the future to meet the health care needs of today's obese middle-aged population."

View the Article Under Discussion: http://pmid.us/20473195

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Following on from a demonstration of decellularized rat lungs, another team has produced similar work: "Researchers have been able to create tiny mouse lungs in the lab that are able to breathe. The lungs were created with stem cells and attached to a ventilator. ... They used a technique called decellularization, similar to the method used to create a beating mouse heart in a different lab at the University of Minnesota in 2008. In the cancer center, they took a mouse lung and stripped away all its cells. Then, injected the natural framework with stem cells. At first they used fetal mouse lung cells, but this year they had another breakthrough using adult stem cells called 'induced pluriopotent stem cells.' ... That's basically a cell that we can take from anybody and re-program to act like an embryonic stem cell ... The hope is one day human lungs could be re-created for transplant with a greater chance of success. Right now, there is no tissue matching for lung transplants. ... The beauty of that is that you can then create a tissue for an organ that's transplantable that is derived from the patient and therefore would not be recognized as foreign by the immune system and not rejected. By adding the ventilator to make the lungs breathe, the stem cells are further trained to act like lung cells. It's a huge success considering lungs are such complicated organs with some 60 different kinds of cells."

View the Article Under Discussion: http://wcco.com/health/lungs.stem.cells.2.1774895.html

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Research is fundamentally broken by regulation in much of the world. One facet of this problem is that the cost of obtaining approval for new drugs and technologies is so astronomical that large swathes of the research community are directed towards finding marginal new uses for drugs that are already approved by regulators. This activity is, despite occasional successes like the one linked here, always going to be far less productive and useful than tailoring new technologies to the problem at hand. This is one of many ways in which regulation slows progress to a grinding crawl. Because people only pay attention to the occasional successes, they don't see or much care about the many other potential successes that never happened and were never worked on because of the perverse financial incentives put upon the research community by the regulators: "Bexarotene has been approved for the treatment of cancer by the U.S. Food and Drug Administration for more than a decade. These experiments explored whether the medication might also be used to help patients with Alzheimer's disease, and the results were more than promising. ... the main cholesterol carrier in the brain, Apolipoprotein E (ApoE), facilitated the clearance of the amyloid beta proteins. [Researchers] chose to explore the effectiveness of bexarotene for increasing ApoE expression. The elevation of brain ApoE levels, in turn, speeds the clearance of amyloid beta from the brain. Bexarotene acts by stimulating retinoid X receptors (RXR), which control how much ApoE is produced. ... The present view of the scientific community is that small soluble forms of amyloid beta cause the memory impairments seen in animal models and humans with the disease. Within six hours of administering bexarotene, however, soluble amyloid levels fell by 25 percent; even more impressive, the effect lasted as long as three days. Finally, this shift was correlated with rapid improvement in a broad range of behaviors in three different mouse models of Alzheimer's."

Link: http://medicalxpress.com/news/2012-02-fda-approved-drug-rapidly-amyloid-brain.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Rapamycin recently showed promise as a potential treatment for Alzheimer's disease, and here more researchers are working on that: "A few weeks after a report that rapamycin, a drug that extends lifespan in mice and that is currently used in transplant patients, curbed the effects of Alzheimer's disease in mice, a second group is announcing similar results in an entirely different mouse model of early Alzheimer's. ... The second report [showed] that administration of rapamycin improved learning and memory in a strain of mice engineered to develop Alzheimer's. The improvements in learning and memory were detected in a water maze activity test that is designed to measure learning and spatial memory. The improvements in learning and memory correlated with lower damage in brain tissue. ... Strikingly, the Alzheimer's mice treated with rapamycin displayed improved performance on the maze, even reaching levels that were indistinguishable from their normal littermates. Levels of amyloid-beta-42 were also reduced in these mice after treatment, and we are seeing preserved numbers of synaptic elements in the brain areas of Alzheimer's disease mice that are ravaged by the disease process."

View the Article Under Discussion: http://www.eurekalert.org/pub_releases/2010-04/uoth-adt040110.php

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

The Seattle Times notes recent research: "A new study finds that calorie restriction may bolster the immune system in adults. Researchers [randomly] placed 46 overweight, but not obese, men and women age 20 to 40 on one of two diets for six months: one in which calories were reduced 10 percent, and another in which they were reduced 30 percent. All food was supplied to the test subjects. The participants were tested to see what effect calorie restriction had on their immune system. They were given a delayed-type hypersensitivity test, which can detect allergens, among other things, and is considered a way to check whole-body immune response. Researchers also checked T-cells, a kind of white blood cell, and another immune system marker. At the end of the six months, [delayed type hypersensitivity] response went up in both the 10 percent and the 30 percent calorie-restricted groups compared with the beginning of the study. Both groups also showed improvement in T-cell function."

View the Article Under Discussion: http://seattletimes.nwsource.com/html/living/2011767490_calories03.html

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

Here is another example of work on creating patient-specific cells to order, one of the necessary building block technologies needed for an industry that constructs organs and other larger masses of tissue in the body: researchers have "discovered a method of generating different types of vascular smooth muscle cells (SMCs) - the cells which make up the walls of blood vessels - using cells from patients' skin. ... Cardiovascular disease is the leading cause of death in the world. These deaths are mainly caused by the hardening and subsequent blockage of blood vessels due to the accumulation of fatty materials, a condition called atherosclerosis. As not all patients are suitable for conventional stenting or bypass treatment, an option in the future may be to grow new blood vessels to bypass their own blocked vessels. The [team] worked with embryonic stem cells and reprogrammed skin cells, collectively known as human pluripotent stem cells (hPSCs), which have the potential to form any cell type in the body. They discovered a method of creating all the major vascular smooth muscle cells in high purity using hPSCs which can also be easily scaled up for production of clinical-grade SMCs. This is the first time that such a system has been developed and will open the door for comparative studies on different subtypes of SMCs to be carried out, which are otherwise extremely difficult to obtain from patients."

Link: http://medicalxpress.com/news/2012-01-cambridge-team-smooth-muscle-cells.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The course of our future lives, our health and longevity, is swayed by a population of timid mice - but malicious mice, ever ready to use state force to punish and hold back anyone they see as being insufficiently timid. These are people who support the ball and chain of centralized regulation of medical research, people who fear all change, people who fear everything they don't understand, and people who rush to prevent anyone else from enjoying the freedom to undertake personal risk in the course of advancing progress. This describes the vocal mainstream of Western culture: risk-averse, ignorant, and enamored of control for its own sake: a dangerous combination for those who pull upon the strings of law and regulation.

As I have often remarked in the past, freedom is absolutely essential to progress in medicine: the freedom for researchers to attempt goals as they see fit; the freedom for anyone to fund the research and clinical development they desire; the freedom for people to take personal risks in the use of medical technology; the freedom for groups to create an unhampered marketplace in medicine, in which technologies are rapidly sifted for those with the greatest benefit. These are all simply parts of economic and personal liberty, something that is in extremely short supply in the medical industry.

So the mice stamp their little feet, and the impersonal engines of government - the unaccountable employees of bureaucratic bodies such as the FDA - move to prevent us all from undertaking rapid development in medicine, on penalty of jail. For our own good, supposedly.

If anti-aging drugs are possible, they will require dangerous - and ethically troubling - clinical trials. ... If anti-aging medicine is to become a reality, then the various theories about how to halt or reverse the aging process will require testing on human subjects. Carrying out such tests will place unprecedented pressure on the rules protecting human participants in clinical trials. I suspect, then, that human guinea pigs for anti-aging trials will come disproportionately from the poor and disempowered. ... The rich and powerful will be looking to do away with rules that they perceive as denying them millennial life spans.

Those would be the rules preventing terminal cancer patients from choosing to up and pay for their own personal trial of a promising therapy-in-development - forcing them to die without any recourse. The rules that make formal clinical trials so lengthy and expensive that many potential therapies are simply never developed or tried by humans, and those that are might be a decade in the slow regulatory grind from readiness to actual availability. The rules that raise the costs of medicine too high for those poor folk that the author seems to be concerned about. Regulation of medicine, which raises costs, disrupts the effective market mechanisms of progress, and prevents people from using potential therapies that are technologically feasible and ready to field-test, is a morally bankrupt affair.

But this is the culture we live in, sad to say: one in which vague and poorly articulated discomfort with potential future inequities are given more consideration than the ongoing massive toll of death and suffering that we should be working day and night, as fast as possible, to prevent. A toll of 100,000 lives every day, and the hundreds of millions who are crippled, diminished, and in pain. Instead we get institutions like the FDA, whose staff toil to prevent new medicine from ever seeing the light of day. The mice would close their eyes and drown the world in blood just to feel a little better in their own vague sense of disquiet: they are the very worst of humanity, not even willing to acknowledge the fearsome costs of their own timidity.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

From the New York Times: "A treatment for eye diseases that is derived from human embryonic stem cells might have improved the vision of two patients. The report, published online in the medical journal The Lancet, is the first to describe the effect on patients of a therapy involving human embryonic stem cells. ... The results [come] from the second clinical trial involving the stem cells, using a therapy developed by Advanced Cell Technology to treat macular degeneration, a leading cause of blindness. ... Both patients, who were legally blind, said in interviews that they had gains in eyesight that were meaningful for them. One said she could see colors better and was able to thread a needle and sew on a button for the first time in years. The other said she was able to navigate a shopping mall by herself. ... esearchers at Advanced Cell Technology turned embryonic stem cells into retinal pigment epithelial cells. Deterioration of these retinal cells can lead to damage to the macula, the central part of the retina, and to loss of the straight-ahead vision necessary to recognize faces, watch television or read. Some 50,000 of the cells were implanted last July under the retinas in one eye of each woman in operations that took about 30 minutes. ... Before the treatment, the woman with Stargardt's was able to see the motion of a hand being waved in front of her but could not read any letters on an eye chart. Twelve weeks after the treatment, she was able to read five of the biggest letters on the eye chart with the treated eye, corresponding to 20/800 vision, according to the paper."

Link: http://www.nytimes.com/2012/01/24/business/stem-cell-study-may-show-advance.html

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

This year's Buck Symposium, an event hosted by the Buck Institute for Research on Aging, will be held on March 1st. The Institute is very much a part of the mainstream of biogerontology, wherein frank talk of extending human life span is rare, and the public relations tends to focus on age-related diseases and length of healthy life within the current human life span:

At the Buck Institute, world-class scientists work in a uniquely collaborative environment to understand how normal aging contributes to the development of conditions specifically associated with getting older such as Alzheimer's and Parkinson's disease, cancer, stroke, heart disease, diabetes, macular degeneration and glaucoma. Our interdisciplinary approach brings scientists from disparate fields together to develop diagnostic tests and treatments to prevent or delay these maladies.

Some of their work has application to more useful research programs, however, those that aim directly to extend human life and reverse aging - such as SENS. That said, the program for the event is attractive, and in the speakers list you'll see a few noted researchers who are in fact public supporters of SENS, such as Irina Conboy.

The 2012 Buck Symposium: Stem Cell Research and Aging provides a stage for key players in the rapidly developing areas of stem cell research and the basic biology of aging to share their research, findings and thoughts. Some of the world's most influential and respected investigators from diverse background, in fields such as development, diseases, stem cell biology and model systems will be sharing their ideas, sparking new dialog, new alliances and promising collaborations.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The principle use of stem cells in the near future is actually research, not therapy - generating diseased cells to order will lower the cost of better understanding the mechanisms of disease and age-related conditions. For example: "scientists have, for the first time, created stem cell-derived, in vitro models of sporadic and hereditary Alzheimer's disease (AD), using induced pluripotent stem cells from patients with the much-dreaded neurodegenerative disorder. ... It's a first step. These aren't perfect models. They're proof of concept. But now we know how to make them. It requires extraordinary care and diligence, really rigorous quality controls to induce consistent behavior, but we can do it. ... We're dealing with the human brain. You can't just do a biopsy on living patients. Instead, researchers have had to work around, mimicking some aspects of the disease in non-neuronal human cells or using limited animal models. Neither approach is really satisfactory. ... With the in vitro Alzheimer's neurons, scientists can more deeply investigate how AD begins and chart the biochemical processes that eventually destroy brain cells associated with elemental cognitive functions like memory. Currently, AD research depends heavily upon studies of post-mortem tissues, long after the damage has been done. ... The differences between a healthy neuron and an Alzheimer's neuron are subtle. It basically comes down to low-level mischief accumulating over a very long time, with catastrophic results. ... The researchers have already produced some surprising findings. ... In this work, we show that one of the early changes in Alzheimer's neurons thought to be an initiating event in the course of the disease turns out not to be that significant."

Link: http://www.sciencedaily.com/releases/2012/01/120125131029.htm

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

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."

Link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3068305/