text:
Position Statement on Human Aging
S. Jay Olshansky, Ph.D.
Leonard Hayflick, Ph.D.
Bruce A. Carnes, Ph.D.
In the past century a combination of successful public health campaigns, changes in living environments and advances in medicine have led to a dramatic increase in human life expectancy. Long lives experienced by unprecedented numbers of people in developed countries are a triumph of human ingenuity. This remarkable achievement has produced economic, political and societal changes that are both positive and negative. Although there is every reason to be optimistic that continuing progress in public health and the biomedical sciences will contribute to even longer and healthier lives in the future, a disturbing and potentially dangerous trend has also emerged in recent years. There has been a resurgence and proliferation of health care providers and entrepreneurs who are promoting antiaging products and lifestyle changes that they claim will slow, stop or reverse the processes of aging. Even though in most cases there is little or no scientific basis for these claims [1], the public is spending vast sums of money on these products and lifestyle changes, some of which may be harmful [2]. Scientists are unwittingly contributing to the proliferation of these pseudoscientific antiaging products by failing to participate in the public dialogue about the genuine science of aging research. The purpose of this document is to warn the public against the use of ineffective and potentially harmful antiaging interventions and to provide a brief but authoritative consensus statement from 51 internationally recognized scientists in the field about what we know and do not know about intervening in human aging. What follows is a list of issues related to aging that are prominent in both the lay and scientific literature, along with the consensus statements about these issues that grew out of debates and discussions among the 51 scientists associated with this paper.
Life span is defined as the observed age at death of an individual; maximum lifespan is the highest documented age at death for a species. From time to time we are told of a new highest documented age at death, as in the celebrated case of Madame Jeanne Calment of France who died at the age of 122 [3]. Although such an extreme age at death is exceedingly rare, the maximum life span of humans has continued to increase because world records for longevity can move in only one direction: higher. Despite this trend, however, it is almost certainly true that, at least since recorded history, people could have lived as long as those alive today if similar technologies, lifestyles and population sizes had been present. It is not people that have changed; it is the protected environments in which we live and the advances made in biomedical sciences and other human institutions that have permitted more people to attain, or more closely approach, their life-span potential [4] Longevity records are entertaining, but they have little relevance to our own lives because genetic, environmental and lifestyle diversity [5] guarantees that an overwhelming majority of the population will die long before attaining the age of the longest-lived individual.
Life Expectancy
Life expectancy in humans is the average number of years of life remaining for people of a given age, assuming that everyone will experience, for the remainder of their lives, the risk of death based on a current life table. For newborns in the U.S. today, life expectancy is about 77 years.6 Rapid declines in infant, child, maternal and late-life mortality during the 20th century led to an unprecedented 30-year increase in human life expectancy at birth from the 47 years that it was in developed countries in 1900. Repeating this feat during the lifetimes of people alive today is unlikely. Most of the prior advances in life expectancy at birth reflect dramatic declines in mortality risks in childhood and early adult life. Because the young can be saved only once and because these risks are now so close to zero, further improvements, even if they occurred, would have little effect on life expectancy [7-9]. Future gains in life expectancy will, therefore, require adding decades of life to people who have already survived seven decades or more. Even with precipitous declines in mortality at middle and older ages from those present today, life expectancy at birth is unlikely to exceed 90 years (males and females combined) in the 21st century without scientific advances that permit the modification of the fundamental processes of aging [10]. In fact, even eliminating all aging-related causes of death currently written on the death certificates of the elderly will not increase human life expectancy by more than 15 years. To exceed this limit, the underlying processes of aging that increase vulnerability to all the common causes of death will have to be modified.
Eliminating all the aging-related [11] causes of death presently written on death certificates would still not make humans immortal [12]. Accidents, homicides, suicide and the biological processes of aging would continue to take their toll. The prospect of humans living forever is as unlikely today as it has always been, and discussions of such an impossible scenario have no place in a scientific discourse.
Geriatric Medicine versus Aging
Geriatric medicine is a critically important specialty in a world in which population aging is already a demographic reality in many countries and a future certainty in others. Past and anticipated advances in geriatric medicine will continue to save lives and help to manage the degenerative diseases associated with growing older [13,14], but these interventions only influence the manifestations of aging--not aging itself. The biomedical knowledge required to modify the processes of aging that lead to age-associated pathologies confronted by geriatricians does not currently exist. Until we better understand the aging processes and discover how to manipulate them, these intrinsic and currently immutable forces will continue to lead to increasing losses in physiological capacity and death even if age-associated diseases could be totally eliminated [15-20].
Antiaging Medicine
Advocates of what has become known as antiaging medicine claim that it is now possible to slow, stop or reverse aging through existing medical and scientific interventions [21-26]. Claims of this kind have been made for thousands of years [27], and they are as false today as they were in the past [28-31]. Preventive measures make up an important part of public health and geriatric medicine, and careful adherence to advice on nutrition, exercise and smoking can increase one's chances of living a long and healthy life, even though lifestyle changes based on these precautions do not affect the processes of aging [32-33]. The more dramatic claims made by those who advocate antiaging medicine in the form of specific drugs, vitamin cocktails or esoteric hormone mixtures are, however, not supported by scientific evidence, and it is difficult to avoid the conclusion that these claims are intentionally false, misleading or exaggerated for commercial reasons [34]. The misleading marketing and the public acceptance of antiaging medicine is not only a waste of health dollars; it has also made it far more difficult to inform the public about legitimate scientific research on aging and disease [35]. Medical interventions for age-related diseases do result in an increase in life expectancy, but none have been proved to modify the underlying processes of aging. The use of cosmetics, cosmetic surgery, hair dyes and similar means for covering up manifestations of aging may be effective in masking age changes, but they do not slow, stop or reverse aging. At present there is no such thing as an antiaging intervention.
The scientifically respected free-radical theory of aging [36] serves as a basis for the prominent role that antioxidants have in the antiaging movement. The claim that ingesting supplements containing antioxidants can influence aging is often used to sell antiaging formulations. The logic used by their proponents reflects a misunderstanding of how cells detect and repair the damage caused by free radicals and the important role that free radicals play in normal physiological processes (such as the immune response and cell communication) [37-39]. Nevertheless, there is little doubt that ingesting fruits and vegetables (which contain antioxidants) can reduce the risk of having various age-associated diseases, such as cancer [40], heart disease [41,42], macular degeneration and cataracts [43,44]. At present there is relatively little evidence from human studies that supplements containing antioxidants lead to a reduction in either the risk of these conditions or the rate of aging, but there are a number of ongoing randomized trials that address the possible role of supplements in a range of age-related conditions [45-49], the results of which will be reported in the coming years. In the meantime, possible adverse effects of single-dose supplements, such as beta-carotene [50], caution against their indiscriminate use. As such, antioxidant supplements may have some health benefits for some people, but so far there is no scientific evidence to justify the claim that they have any effect on human aging [51-52].
Telomeres, the repeated sequence found at the ends of chromosomes, shorten in many normal human cells with increased cell divisions. Statistically, older people have shorter telomeres in their skin and blood cells than do younger people [53,54]. In the animal kingdom, though, long-lived species often have shorter telomeres than do short-lived species, indicating that telomere length probably does not determine life span [55-57]. Solid scientific evidence has shown that telomere length plays a role in determining cellular life span in normal human fibroblasts and some other normal cell types [588]. Increasing the number of times a cell can divide, however, may predispose cells to tumor formation [59-60]. Thus, although telomere shortening may play a role in limiting cellular life span, there is no evidence that telomere shortening plays a role in the determination of human longevity.
A number of hormones, including growth hormone, testosterone, estrogen and progesterone, have been shown in clinical trials to improve some of the physiological changes associated with human aging [61,62]. Under the careful supervision of physicians, some hormone supplements can be beneficial to the health of some people. No hormone, however, has been proved to slow, stop or reverse aging. Instances of negative side effects associated with some of these products have already been observed, and recent animal studies suggest that the use of growth hormone could have a life-shortening effect [63-65]. Hormone supplements now being sold under the guise of antiaging medicine should not be used by anyone unless they are prescribed for approved medical uses.
Caloric Restriction
The widespread observation that caloric restriction will increase longevity must be tempered with the recognition that it has progressively less effect the later in life it is begun [66], as well as with the possibility that the control animals used in these studies feed more than wild animals, predisposing them to an earlier death. Although caloric restriction might extend the longevity of humans, because it does so in many other animal species [67-69], there is no study in humans that has proved that it will work. A few people have subjected themselves to a calorically restricted diet, which, in order to be effective, must approach levels that most people would find intolerable. The fact that so few people have attempted caloric restriction since the phenomenon was discovered more than 60 years ago suggests that for most people, quality of life seems to be preferred over quantity of life. The unknown mechanisms involved in the reduced risk of disease associated with caloric restriction are of great interest [71] and deserve further study because they could lead to treatments with pharmacological mimetics of caloric restriction that might postpone all age-related diseases simultaneously.
Determining Biological Age
Scientists believe that random damage that occurs within cells and among extracellular molecules are responsible for many of the age-related changes that are observed in organisms [72-74]. In addition, for organisms that reproduce sexually, including humans, each individual is genetically unique. As such, the rate of aging also varies from individual to individual [75]. Despite intensive study, scientists have not been able to discover reliable measures of the processes that contribute to aging [76]. For these reasons, any claim that a person's biological or "real age" [77] can currently be measured, let alone modified, by any means must be regarded as entertainment, not science.
Are There Genes That Govern Aging Processes?
No genetic instructions are required to age animals, just as no instructions on how to age inanimate machines are included in their blueprints [79-80]. Molecular disorder occurs and accumulates within cells and their products because the energy required for maintenance and repair processes to maintain functional integrity for an indefinite time is unnecessary after reproductive success. Survival beyond the reproductive years and, in some cases, raising progeny to independence, is not favored by evolution because limited resources are better spent on strategies that enhance reproductive success to sexual maturity rather than longevity [81]. Although genes certainly influence longevity determination, the processes of aging are not genetically programmed. Overengineered systems and redundant physiological capacities are essential for surviving long enough to reproduce in environments that are invariably hostile to life. Because humans have learned how to reduce environmental threats to life, the presence of redundant physiological capacity permits them and the domesticated animals we protect to survive beyond the reproductive ages. Studies in lower animals that have led to the view that genes are involved in aging have demonstrated that significant declines in mortality rates and large increases in average and maximum life span can be achieved experimentally [82-85]. Without exception, however, these genes have never produced a reversal or arrest of the inexorable increase in mortality rate that is one important hallmark of aging. The apparent effects of such genes on aging therefore appear to be inadvertent consequences of changes in other stages of life, such as growth and development, rather than a modification of underlying aging processes. Indeed, the evolutionary arguments presented above suggest that a unitary programmed aging process is unlikely to even exist and that such studies are more accurately interpreted to have an effect on longevity determination, not the various biological processes that contribute to aging. From this perspective, longevity determination is under genetic control only indirectly [86,87]. Thus, aging is a product of evolutionary neglect, not evolutionary intent [88-91].
Can We Grow Younger?
Although it is possible to reduce the risk of aging-related diseases and to mask the signs of aging, it is not possible for individuals to grow younger. This would require reversing the degradation of molecular integrity that is one of the hallmarks of aging in both animate and inanimate objects. Other than performing the impossible feat of replacing all of the cells, tissues or organs in biological material as a means of circumventing aging processes, growing younger is a phenomenon that is currently not possible.
Genetic Engineering
After the publication of the human genome sequences, there have been assertions that this new knowledge will reveal genes whose manipulation may permit us to intervene directly in the processes of aging. Although it is likely that advances in molecular genetics will soon lead to effective treatments for inherited and age-related diseases, it is unlikely that scientists will be able to influence aging directly through genetic engineering [92,93]. because, as stated above, there are no genes directly responsible for the processes of aging. Centuries of selective breeding experience (in agricultural, domesticated and experimental plants and animals) has revealed that genetic manipulations designed to enhance one or only a few biological characteristics of an organism frequently have adverse consequences for health and vigor. As such, there is a very real danger that enhancing biological attributes associated with extended survival late in life might compromise biological properties important to growth and development early in life.
Replacing Body Parts
Suggestions have been made that the complete replacement of all body parts with more youthful components could increase longevity. Though possible in theory, it is highly improbable that this would ever become a practical strategy to extend length of life. Advances in cloning and embryonic stem cell technology may make the replacement of tissues and organs possible [94-99] and will likely have an important positive impact on public health in the future through the treatment of age-related diseases and disorders. But replacing and reprogramming the brain that defines who we are as individuals is, in our view, more the subject of science fiction than science fact.
Lifestyle Modification and Aging
Optimum lifestyles, including exercise and a balanced diet along with other proven methods for maintaining good health, contribute to increases in life expectancy by delaying or preventing the occurrence of age-related diseases. There is no scientific evidence, however, to support the claim that these practices increase longevity by modifying the processes of aging.
Concluding Remarks
Since recorded history individuals have been, and are continuing to be, victimized by promises of extended youth or increased longevity by using unproven methods that allegedly slow, stop or reverse aging. Our language on this matter must be unambiguous: there are no lifestyle changes, surgical procedures, vitamins, antioxidants, hormones or techniques of genetic engineering available today that have been demonstrated to influence the processes of human aging [100,101]. We strongly urge the general public to avoid buying or using products or other interventions from anyone claiming that they will slow, stop or reverse aging. If people, on average, are going to live much longer than is currently possible, then it can only happen by adding decades of life to people who are already likely to live for 70 years or more. This "manufactured survival time" [102] will require modifications to all of the processes that contribute to aging--a technological feat that, though theoretically possible, has not yet been achieved. What medical science can tell us is that because aging and death are not programmed into our genes, health and fitness can be enhanced at any age, primarily through the avoidance of behaviors (such as smoking, excessive alcohol consumption, excessive exposure to sun, and obesity) that accelerate the expression of age-related diseases and by the adoption of behaviors (such as exercise and a healthy diet) that take advantage of a physiology that is inherently modifiable [103].
We enthusiastically support research in genetic engineering, stem cells, geriatric medicine and therapeutic pharmaceuticals, technologies that promise to revolutionize medicine as we know it. Most biogerontologists believe that our rapidly expanding scientific knowledge holds the promise that means may eventually be discovered to slow the rate of aging. If successful, these interventions are likely to postpone age-related diseases and disorders and extend the period of healthy life. Although the degree to which such interventions might extend length of life is uncertain, we believe this is the only way another quantum leap in life expectancy is even possible. Our concern is that when proponents of antiaging medicine claim that the fountain of youth has already been discovered, it negatively affects the credibility of serious scientific research efforts on aging. Because aging is the greatest risk factor for the leading causes of death and other age-related pathologies, more attention must be paid to the study of these universal underlying processes. Successful efforts to slow the rate of aging would have dramatic health benefits for the population by far exceeding the anticipated changes in health and length of life that would result from the complete elimination of heart disease, cancer, stroke and other age-associated diseases and disorders.
Authors and Endorsers
Dr. Olshansky is Senior Research Scientist and Professor at the School of Public Health, University of Illinois at Chicago. Dr. Hayflick is Professor of Anatomy at the University of California at San Francisco. Dr. Carnes is Assistant Professor of Geriatric Medicine at the University of Oklahoma. Drs. Olshansky and Carnes are also coauthors of The Quest for Immortality (Norton, 2001), a book-length antidote to anti-aging hype.
The Position Statement on Human Aging has been endorsed by Robert Arking, Allen Bailey, Andrzej Bartke, Vladislav V. Bezrukov, Jacob Brody, Robert N. Butler, Alvaro Macieira-Coelho, L. Stephen Coles, David Danon, Aubrey D.N.J. de Grey, Lloyd Demetrius, Astrid Fletcher, James F. Fries, David Gershon, Roger Gosden, Carol W. Greider, S. Mitchell Harman, David Harrison, Christopher Heward, Henry R. Hirsch, Robin Holliday, Thomas E. Johnson, Tom Kirkwood, Leo S. Luckinbill, George M. Martin, Alec A. Morley, Charles Nam, Sang Chul Park, Linda Partridge, Graham Pawelec, Thomas T. Perls, Suresh Rattan, Robert Ricklefs, Ladislas (Leslie) Robert, Richard G. Rogers, Henry Rothschild, Douglas L. Schmucker, Jerry W. Shay, Monika Skalicky, Len Smith, Raj Sohal, Richard L. Sprott, Andrus Viidik, Jan Vijg, Eugenia Wang, Andrew Weil, Georg Wick and Woodring Wright. Drs. Olshansky and Carnes received funding for this work from the National Institute on Aging. The position paper was previously published in Scientific American Magazine and the Journal of Gerontology: Biological Sciences.
- Workshop Report, Is There an Antiaging Medicine? International Longevity Center, Canyon Ranch Series; New York, 2001.
- U.S. General Accounting Office. "Antiaging Products Pose Potential for Physical and Economic Harm." Special Committee on Aging, GAO-01-1129. September 2001.GAO-01-1129
- Allard M, Lebre V, Robine JM., Calment J. Jeanne Calment: From Van Gogh's time to ours: 122 extraordinary years. W.H. Freeman & Co.: New York; 1998.
- Carnes BA, Olshansky SJ, Grahn D. Continuing the search for a law of mortality. Popul Dev Rev. 1996;22(2):231-264.
- Finch C, Kirkwood TBL. Chance, Development, and Aging. Oxford University Press; 2000.
- Anderson RN. United States life tables, 1998. National Vital Statistics Reports. 2001;48:1-40.
- Olshansky SJ, Carnes BA, Cassel C. In Search of Methuselah: Estimating the upper limits to human longevity. Science. 1990;250:634-640.
- Demetrius L, Ziehe M. The measurement of Darwinian fitness in human populations. Proc R Soc Lond B Biol Sci. 1984;B222:33-50.
- Demongeot J, Demetrius L. La derivé demographique et la selection naturalle: étude empirique de la France (1850-1965). Population. 1989;2:231-248.
- Olshansky, S.J., Carnes, B.A., Désesquelles, A. 2001. Prospects for Human Longevity. Science 291 (5508):1491-1492.
- Carnes BA, Olshansky SJ. A Biologically Motivated Partitioning of Mortality. Exp Gerontol. 1997;32:615-631.
- Hayflick L. How and why we age. Exp Gerontol. 1998;33:639-653.
- Cassel CK, Cohen HJ, Larson EB, Meier DE, Resnick NM, Rubenstein LZ, Sorensen LB. (Eds.). Geriatric Medicine. New York: Springer; 2001.
- Evans JG, Williams FT. (Eds) Oxford Textbook of Geriatric Medicine. Oxford University Press, Oxford; 2001.
- Hayflick L. How and Why We Age. 1994. Ballantine Books: New York.
- Medina J. The Clock of Ages. Why We Age – How We Age – Winding Back the Clock. 1996. Cambridge University Press.
- Gosden R. Cheating Time: Science, Sex, and Aging. 1996. W.H. Freeman & Co.: New York.
- Bailey AJ. Molecular mechanisms of ageing in connective tissues. Mech Ageing Dev. 2001;122:735-755.
- Bailey AJ, Sims TJ, Ebbesen EN, Mansell JP, Thomsen JS, Moskilde L. Age-related changes in the biochemical and biomechanical properties of human cancellous bone collagen: Relationship to bone strength. Calcif Tis Res. 1999;65:203-210.
- Wick G, Jansen-Durr P, Berger P, Blasko I, Grubeck-Loebenstein B. Diseases of aging. Vaccine. 2000;18:1567-1583.
- Chopra D. Grow younger, live longer: 10 steps to reverse aging. Harmony Books: New York; 2001.
- Klatz R. Grow young with HGH: The amazing medically proven plan to reverse aging. Harper Perennial Library; 1998.
- Brickey MP. Defy aging: Develop the mental and emotional vitality to live longer, healthier, and happier than you ever imagined. New Resources Press; 2000.
- Carper J. Stop aging now!: The ultimate plan for staying young and reversing the aging process. Harper perennial Library; 1996.
- Null G, Campbell A. Gary Null's ultimate anti-aging program. Broadway Books; 1999.
- Pierpaoli W, Regelson W, Colman C. The melatonin miracle. Simon and Schuster: New York; 1995.
- Gerald J. Gruman, A history of ideas about the prolongation of life. Trans Amer Phil Soc. 1966;56(9):1-102.
- Austad S. Why we age: What science is discovering about the body's journey through life. John Wiley & Sons: New York; 1999.
- Holliday R. Understanding ageing. Cambridge University Press; 1995.
- Arking R. Biology of aging: Observations and principles, 2nd edition. Sinauer Associates, Sunderland, MA.; 1998.
- Arking R. The Biology of aging: What is it and when will it become useful? Infertility and Reproductive Medicine Clinics of North America. 2001;12:469-487.
- Fries JF. Aging, natural death, and the compression of morbidity. N Engl J Med. 1980;303:130-135.
- Rogers RG, Hummer RA, and Nam CB. Living and dying in the USA: Behavioral, health, and social differentials of adult mortality. Academic Press; 2000.
- Olshansky SJ, Carnes BA. The quest for immortality: Science at the frontiers of aging. Norton: New York; 2001.
- Miller R. Extending life: Scientific prospects and political obstacles. Milbank Q. 2002;80(1):155-74.
- Harman D. Aging: A theory based on free radical and radiation chemistry. J Gerontol. 1956;11:298-300.
- Robert L, Labat-Robert J. Aging of connective tissues: from genetic to epigenetic mechanisms. Biogerontology. 2000;1:123-131.
- Fülöp Jr T, Douziech N, Jacob MP, Hauck M, Wallach J, Robert L. Age-related alterations in the signal transduction pathways of the elastin-laminin receptor. Pathol Bio. 2001;49:339-348.
- Labat-Robert J. Cell-matrix interactions, alterations with aging and age associated diseases. A review. Pathol Bio. 2001;49:349-352.
- World Cancer Research Fund. American institute for cancer research. Food, nutrition and the prevention of cancer: A global perspective; 1997.
- Tavani A, La Vecchia C. Beta-carotene and risk of coronary heart disease. A review of observational and intervention studies. Biomed Pharmacother. 1999;53(9):409-416.
- Hu FB, Willett WCJ. Diet and coronary heart disease: findings from the Nurses' health study and health professionals' follow-up Study. Nutr Health Aging. 2001;5(3):132-138.
- Van Duyn MA, Pivonka EJ. Overview of the health benefits of fruit and vegetable consumption for the dietetics professional: selected literature. Am Diet Assoc. 2000;100(12):1511-1521.
- Christen WG. Antioxidant vitamins and age-related eye disease. Proc Assoc Am Physicians. 1999;111(1):16-21.
- MRC/BHF Heart Protection Study Collaborative Group. MRC/BHF heart protection Study of cholesterol-lowering therapy and of antioxidant vitamin supplementation in a wide range of patients at increased risk of coronary heart disease death: early safety and efficacy experience. Eur Heart J. 1999;20:725-741.
- Manson JE, Gaziano M, Spelsberg A, et al for the WACS Research Group: A secondary prevention trial of antioxidant vitamins and cardiovascular disease in women. Rationale, design, and methods. Ann Epidemiol. 1995;5:261-269.
- Egan DA, Garg R, Wilt TJ, et al for the ADMIT Investigators: Rationale and design of the arterial disease multiple intervention trial (ADMIT) Pilot Study. Am J Cardiol. 1999;83:569-575.
- The Age-Related eye disease research group: The age-related eye disease study (AREDS): Design implications. AREDS Report No. 1. Control Clin Trials 1999;20:573-600.
- Tikellis G, Robman LD, Harper CA, et al. The VECAT study: methodology and statistical power for measurement of age-related macular features. Ophthalmic epidemiology. 1999;6:181-194.
- Paolini M, Abdel-Rahman SZ, Cantelli-Forti G, Legator LS. Chemoprevention or Antichemo- prevention? A salutary warning from the Beta-Carotene experience. J Natl Cancer Inst. 2001;93(14):1110-1111.
- Morley AA, Trainor KJ. Lack of an effect of vitamin E on lifespan of mice. Biogerontology. 2001;2:109-112.
- de Grey ADN. Noncorrelation between maximum life span and antioxidant enzyme levels among homeotherms: implications for retarding human aging. J Anti-Aging Med. 2000;3:25-36.
- Harley CB, Futcher AB, Greider CW. Telomeres shorten during ageing of human fibroblasts. Nature 1990;345:458-460.
- Vaziri H, Dragowska W, Allsopp RC, Thomas TE, Harley CB, Lansdorp PM. Evidence for a mitotic clock in human hematopoietic stem cells: loss of telomeric DNA with age. Proc Natl Acad Sci USA 1994;91:9857-9860.
- Hemann MT, Greider CW. Wild-derived inbred mouse strains have short telomeres. Nucleic Acids Res 2000;28:4474-4478.
- Kakuo S, Asaoka K, Ide T. Human is a unique species among primates in terms of telomere length. Biochem Biophys Res Commun. 1999;263(2):308-14.
- Holliday R. Endless quest. Bioessays. 1996;18(1):3-5.
- Bodnar AG, Ouellette M, Frolkis M, et al. Extension of life span by introduction of telomerase into normal human cells. Science. 1998;279:349-352.
- Wang J, Hannon GJ, Beach DH. Risky immortalization by telomerase. Nature 2000;405:755-756.
- de Lange T, Jacks T. For better or worse? Telomerase inhibition and cancer. Cell 1999;98:273-275.
- Rudman D, Feller AG, Nagraj HS, et al. Effects of growth hormone in men over 60 years old. N Eng J Med. 1990;323:1-6.
- Gallagher JC. Role of estrogens in the management of postmenopausal bone loss. Rheum Dis Clin North Am. 2001;1:143-
- Wolf E, Kahnt E, Ehrlein J, et al. Effects of long-term elevated serum levels of growth hormone on life expectancy of mice: Lessons from transgenic animals. Mech Ageing Dev. 1993;68:71-87.
- Bartke A, Brown-Borg H, Mattison J, et al. Prolonged longevity of hypopituitary dwarf mice. Exp Gerontol. 2001;36:21-28.
- Coschigano KT, Clemmons D, Bellush LL, and Kopchick JJ. Assessment of growth parameters and life span of GHR/BP gene disrupted mice. Endocrinology. 2000;141:2608-2613.
- Weindruch R, Walford RL. Dietary restriction in mice beginning at 1 year of age: effect on life-span and spontaneous cancer incidence. Science. 1992;215(4538):1415-8.
- Weindruch R, Walford RL. The retardation of aging and disease by dietary restriction. Charles C. Thomas. Springfield, IL.; 1988.
- Harrison DE, Archer JR. Natural selection for extended longevity from food restriction. Growth Dev Aging. 1989;53:3-6.
- Duffy PH, Seng JE, Lewis SM, et al. The effects of different levels of dietary restriction on aging and survival in the Sprague-Dawley rat: implications for chronic studies. Aging Clin Exp Res 2001;13:263-272.
- Journal of Gerontology: Biological Sciences. 2001;56,3: entire issue.
- Masoro EJ. Dietary restriction: current status. Aging Clin Exp Res 2001;13:261.
- Hayflick L. The Future of aging. Nature. 2000;408:267-269.
- Morley AA. The somatic mutation theory of ageing. Mut Res. 1995;338:19-23.
- Odagiri Y, Uchida H, Hosokawa M, Takemoto K, Morley A, Takeda T. Accelerated accumulation of somatic mutations in the senescence-accelerated mouse. Nat Genet. 1998;19:117-118.
- Carnes BA, Olshansky SJ. Heterogeneity and its biodemographic implications for longevity and mortality. Exp Gerontol. 2001;36:419-430.
- Workshop Report, Biomarkers of Aging: From Primitive Organisms to Man. International Longevity Center – Canyon Ranch Series, New York, NY.; 2001.
- Roizen M. RealAge: Are you as young as you can be? Cliff Street Books; 1999.
- Roizen M, La Puma J. The RealAge diet: Make yourself younger with what you eat. Cliff Street Books; 2001.
- Hayflick L. The Future of aging. Nature. 2000;408:267-269.
- Miller RA. Kleemeier award lecture: are there genes for aging? J Gerontol A Biol Sci Med Sci. 1999;54(7):B297-307.
- Kirkwood TBL. Evolution of aging. Nature. 1977;270:301-304.
- Johnson TE. Aging can be genetically dissected into component processes using long-lived lines of Caenorhabditis elegans. Proc Natl Acad Sci. USA. 1987;84:3777-3781.
- Johnson TE. Increased life span of age-1 mutants in Caenorhabditis elegans and lower Gompertz rate of aging. Science. 1990;249:908-912.
- Vaupel JW, Carey JR, Christensen K, et al. Biodemographic trajectories of longevity. Science. 1998;280:855-859.
- Johnson TE, Wu D, Tedesco P, Dames S, Vaupel JW. Age-specific demographic profiles of longevity mutants in Caenorhabditis elegans show segmental effects. J Gerontol Bio Sci. 2001;56:B331-339.
- Hayflick L. How and Why We Age. 1994. Ballantine Books: New York.
- Demetrius L. Mortality plateaus and directionality theory. Proc R Soc Lond B; 2001,268:1-9.
- Olshansky SJ, Carnes BA, Butler RA. If humans were built to last. Sci Am; 2001.
- Carnes BA, Olshansky SJ, Gavrilov L, Gavrilova N, Grahn D. Human longevity: nature vs. nurture—fact or fiction. Perspect Biol Med. 1999;42(3):422-441.
- Robert L. Cellular and molecular mechanisms of aging and age related diseases. Pathol Oncol Res. 2000;6:3-9.
- Robert L. Aging of the vascular wall and atherosclerosis. Exp Gerontol. 1999;34:491-501.
- Rattan SIS. "Gene therapy for aging: mission impossible?" Hum Reprod Gen Ethics. 1997;3:27-29.
- Rattan SIS. "Is gene therapy for aging possible?" Ind J Exp Biol. 1998;36:233-236.
- Stem Cells: Scientific Progress and Future Research Directions. Department of Health and Human Services. June 2001.
- Stem Cells and the Future of Regenerative Medicine. Committee on the Biological and Biomedical Applications of Stem Cell Research, Board on Life Sciences National Research Council, Board on Neuroscience and Behavioral Health, Institute of Medicine. National Academy Press, 2002.
- Cardiomyocytes Induce Endothelial Cells to Trans-Differentiate into Cardiac Muscle: Implications for Myocardium Regeneration. G. Condorelli et al. in Proceedings of the National Academy of Sciences USA, Vol. 98, No. 19, pages 10733-10738; September 11, 2001.
- Heart Regeneration in Adult MRL Mice. J. M. Leferovich et al. in Proceedings of the National Academy of Sciences USA, Vol. 98, No. 17, pages 9830-9835; August 14, 2001.
- Segregation of Human Neural Stem Cells in the Developing Primate Forebrain. V. Ourednik et al. in Science, Vol. 293, pages 1820-1824; September 7, 2001.
- A Genome-Wide Scan for Linkage to Human Exceptional Longevity Identifies a Locus on Chromosome 4. A. A. Puca in Proceedings of the National Academy of Sciences USA, Vol. 98, No. 18, pages 10505-10508; August 28, 2001.
- Living to 100: Lessons in Living to Your Maximum Potential at Any Age. Thomas T. Perls, et al. Basic Books, 1999.
- Time of Our Lives: The Science of Human Aging. Tom Kirkwood. Oxford University Press, 1999.
- Confronting the Boundaries of Human Longevity. S. J. Olshansky, B. A. Carnes and D. Grahn in American Scientist, Vol. 86, No. 1, pages 52-61; 1998.
- Aging, Health Risks, and Cumulative Disability. A. J. Vita, R. B. Terry, H. B. Hubert and J. F. Fries in New England Journal of Medicine, Vol. 338, No. 15, pages 1035-1041; April 9, 1998.
This article was posted on August 27, 2004.


text:
Item Description
Letter, C. K. Holliday, et al, to Charles Robinson
Author: Crane, Franklin L.; Dickey, Milton C.; Farnsworth, Loring ; Giles, Frye W.; Holliday, Cyrus Kurtz, 1826-1900
Date: December 26, 1857
In this brief letter from Topeka, signed by C. K. Holiday, M. C. Dickey, F. L. Crane, Loring Farnsworth, and F. W. Giles, "Governor" Robinson was "respecfully and cordially" invited to participate in a "mass convention" at Topeka (December 28, 1857) convened "to deliberate upon the political questions of the day; and more especially upon the action of the late 'Lawrence Convention.'"
Location of Original: KSHS Call Number: Charles & Sara Robinson Collection, # 488, Box 1, Folder 5
Item Number: 101145 Number of images: 1
Keywords: Crane, Franklin Loomis; Dickey, Milton C.; Farnsworth, Loring; Free State Party; Free state cause; Free state supporters; Giles, Frye W.; Holliday, Cyrus Kurtz, 1826-1900; Lawrence, Kansas Territory; Lecompton Constitution; Robinson, Charles, 1818-1894; Topeka, Kansas
pg. 1

subset: commoncrawl


text:
Sunday, December 14, 2008
Queenie on FAcebook
Posted by kimmie e at 8:21 PM 0 comments
Labels: sh*t to put in ur facebook
queenie, cutie wit tha real phat booty ((the social class))
Posted by kimmie e at 7:29 PM 1 comments
I Know Its Been Awhile
Hello! I know its been awhile...ok a long ass time but I have been through so much in the last 4 months. Hit by a drunk driver, school, men lol, and some more shit. Plus my computer was broke so I really couldn't do much for Queenie and I'm glad my right hand woman was here to continue our legacy of running this shit lol. Luv ya Kim! But I'm back now and got alot to say about everything......o yea and I got my pc fixed. I will always love Queenie, she is like my child and I have been a neglectful mother.
-Doe Chee$e
Posted by Doe Cheese at 1:27 PM 0 comments
Labels: kimmie e and dom


text:
GEOPROCESSING SERVICE Esri ArcGIS Server – Line Of Sight DMR 4G
|Product information
|GEOPROCESSING SERVICE Esri ArcGIS Server – Line Of Sight DMR 4G
|Commercial code
|Commercial code is not defined.
|Export unit
|No export unit defined.
|Unit price
|No export unit defined.
|Product description
|Geoprocessing service Esri ArcGIS Server - Line Of Sight DMR 4G is a public service intended for visibility analysis execution using the dataset Digital Terrain Model of the Czech Republic of the 4th generation (DMR 4G). The geoprocessing service enables to find out, which parts of terrain along given line leading from observation to target point are visible. When using the service it is necessary to choose the observation location, choose the target location and specify offset above the terrain. The result of the analysis is line of sight (line of visibility) with visible and invisible parts leading on the terrain. The geoprocessing service LineOfSight_DMR 4G is distinctly faster in contrast with geoprocessing service Visibility_DMR4G. The service can be used with advantage for visibility analysis for longer distances. The geoprocessing service is published as asynchronous. The result can be downloaded from server and saved to a local disc as shapefile using URL, which is generated and sent by the geoprocessing service. URL for the result downloaded throught a web client is published in running service record, that is sent from server to the client.
|Service characteristics
|Download document service characteristics
|Service location
|Data set provided by the service
Provided data
|Access restriction - licence agreement and other restriction
|Terms of use see Terms of trade
|Service view with the public client
|Run the service
|Czech Office for Surveying, Mapping and Cadastre, Křížek, Milan , phone: +420 284 041 860 , e-mail: firstname.lastname@example.com
Product last update:
Information last update:


text:
Hello everyone! Welcome to our weekly end of week open thread, where you can share hacks, recipes, DIY plans, and what have you. Or talk about life, the universe, that thing you need advice about, and whatever else you're finding interesting at the moment.
We're also soliciting comments on what sorta content you'd like to see on Hackerspace. Happy with our open threads, Android roundups, etc? Want something new and different? Bored with x? Let us know in the comments.
If you'd like to join our happy little commenter-driven community, read this first, then ask for your posting privs in the space below.
[Image via Reddit]


text:
LAKE MARY, Fla. – Florida Fish and Wildlife Conservation Commission said that people feeding bears in the Lake Mary neighborhood where a woman was attacked are "signing their (the bears) death warrant."
Officials said on Wednesday that they've received many calls about having to take action against the bears. FWC responded saying that they are not killing all bears they see in the Carisbrooke neighborhood, only the ones that show no fear to humans, meaning they cannot be safely relocated anywhere in Florida.
"We are having to do and take action against the bears for a specific reason and public safety is number one," said FWC.
On Tuesday, FWC said they had captured and killed a seventh bear near the subdivision, which backs up to the Wekiva Wildlife preserve.
FWC didn't say that they have identified the bear that attacked Terri Frana Saturday night at her home at 1900 Brackenhurst Place. FWC said although they are testing the bears for DNA, the tests may come back inconclusive and they may never find the exact bear that attacked Frana.
Six of the bears were captured and euthanized and one was shot and killed, officials said. The latest bear captured and euthanized was an adult female bear, according to FWC.
Residents are also aiming to take measures if there are bear problems in their neighborhoods. Teri Miller started a Facebook page five years ago called "Bears of Wekiva" when she realized her neighborhood had a bear problem.
Since the Lake Mary attack, Miller says more than 100 people joined. She said she understands officers are targeting bears that have no fear of people, but believes that the state needs to do a better job of educating the public about co-existing with bears/
FWC said if you encounter a bear at close range speak to the bear in a calm, assertive voice while backing up slowly toward a secure area. Be sure you are leaving the bear a clear escape route. Stop and hold your ground if your movement away seems to irritate instead of calm the bear. Do not run or play dead. If a black bear attacks you, fight back aggressively.
The FWC also reminded residents to be aware of their surroundings and always supervise pets and children while outdoors. Residents should contact the FWC Wildlife Alert Hotline at 888-404-FWCC to report any threatening bear activity.
Watch Local 6 News and stay with ClickOrlando.com for more on this story.


text:
Kenya Airways receives its 8th Embraer aircraft
Kenya Airways, the Pride of Africa, is expected to grow its capacity with the arrival of a new Embraer E190 jet to KQ's fleet.
Kenya Airways, the Pride of Africa, is expected to grow its capacity with the arrival of a new Embraer E190 jet to KQ's fleet.
Registered as 5Y-KYR, the E190 touched down at the Jomo Kenyatta International Airport yesterday at 2100hrs from Sao Jose dos Campos, Embraer Headquarters in Brazil. As the KYR made its way to Nairobi another Kenya Airways E190 made its maiden test flight in Brazil and is expected to be delivered to Nairobi by next month.
KYR is expected into service within the next two weeks and will be deployed to operate to the South, Central and North Africa regions.
The new 96seater aircraft will join the growing family of Embraer jets that Kenya Airways uses for its regional operations in Africa. This is in line with the plans to build capacity that is more efficient for its Africa market which is the core focus for the Pride of Africa.
"With our route network expansion firmly on course, the addition of a new aircraft into the fleet is quite timely," said the Group Managing Director and Chief Executive Officer Dr. Titus Naikuni.
He added that the increase in capacity had been necessitated by growing regional passenger and cargo demand and a rapidly expanding route network.
The third Embraer E190 arrival is in fulfillment of an order that the airline placed last year. The first jet was delivered in December 2010 with the second jet joining KQ fleet in June this year. Two more E190 jets are yet to be delivered with one E190 expected in a few weeks.
Recently Embraer and Kenya Airways finalized the contract for the acquisition of 10 EMBRAER 190 jets. The deal also includes purchase rights for 16 aircraft, which could be either the EMBRAER 190 or other models of the E-Jet family.
The Embraer E190 is a Brazilian-built state of the art regional jet. Kenya Airways' E190s will be configured in a dual-class layout with 96 seats: 12 in business class and 84 in economy. Furthermore, all passengers will benefit from a modern in-flight entertainment system with individual touch screens. It brings to Kenya Airways an even higher level of technological advancement, lower maintenance and operational costs.
The airline now has five E170s and three E190s as part of its aggressive network and fleet expansion program to cater for the growing travel market.
Dr. Naikuni said "The combination of the E170 and E190 in our network will offer greater flexibility in right-sizing the aircraft to meet route demand, using the same crew and ensuring consistent, high comfort for our passengers".
This fleet modernization will boost the airline's aggressive network expansion strategy and in particular, boost plans to fly to all African capital cities by the end of 2013.


text: If there's one thing Quincy Jones can't stand, it's people without a sense of history. The music legend is dumbfounded by kids (and adults) who have no knowledge of American music greats. Many of them can be found in his new book, "The Complete Quincy Jones: My Journey & Passions." full story


text:
PR WINNER OF THE WEEK: "A" (PR PERFECT) to former New York City Mayor Michael Bloomberg, for his first act post-office: taking on the formidable US National Rifle Association. Bloomberg has pledged to spend $50 million this year on gun control, a topic that Americans continue to debate though nary a week goes by without a tragic shooting incident. The former mayor's last initiative, curbing large-size sugary drinks, incurred jokes and charges of creating a nanny state. This issue is a far better fit for his bulldog approach and financial muscle.
PR LOSER OF THE WEEK: "F" (Full Fiasco) to the Homeless GoPro project team, whose attempt to create empathy for the plight of the homeless succeeded mostly in creating enmity for themselves. The idea: give homeless people GoPro cameras to record their daily routines and interactions with the often-callous more fortunate. Though surely well-intentioned, the project comes off as exploitative, tone-deaf and not particularly helpful to those it would seek to help. As the Valleywag blog critically noted, the project says more about a tech-savvy "coding class" that needs a high-tech fad to experience empathy. "Poverty, homelessness, and inequality are bigger than any app," they wrote. "Your tech isn't helping."
THE PRV "THERE'S NO 'THERE' THERE" AWARD to North Korea for its bizarre overreaction to a London hair salon that had a bit of fun at the expense of the country's leader Kim Jong-Un. Mo Nebbach, owner of M&M Hair Academy in Ealing, put up a poster of Kim with his characteristically closely shorn sideburns and the question "Bad Hair Day?" The next day Nebbach was visited by two apparent strongmen who demanded that the poster be removed, which Nabbach declined to do. One could be forgiven for thinking the visit a prank, but Nabbach contacted the police, only to find out that they'd already heard from the North Korean Embassy. It seems the diminutive leader's feelings were, indeed, hurt. Where's Dennis Rodman when you need him?


text:
What is a Resistor?
How to read a resistor
The color bands on a resistor allow you to determine the resistance of the resistor. The first band determines the first digit of the resistance. The second resistor specifies the second digit. The third digit is the multiplier. So you take the first and second digit, say 47, and you take the multiplier, and multiply the number by the multiplier.
The forth band is for the tolerance. The tolerance is the range of valid resistances for that resistor. This is included to specify the maximum variations from manufacturing.
Using a Resistor
Unlike some electronics components like LEDs, resistors are not polarized. This means that current can flow through them in either direction.
Just like most electronics, resistors have a limit to how much power they can handle. Most resistors are limited to 0.25 Watts. If you want to know if you are safe to use a specific resistor in a circuit you can use P=V2/R, where P is the power in watts, V is the voltage drop, and R is the resistance of the resistor. Since calculating the voltage drop requires a more in-depth understanding of electronics, you can calculate that for 5V systems like the Arduino, any resistor with a resistance of 100Ω or more is safe. However we do encourage you to learn more about electronics, and learn how to check the power through each resistor.


text:
Results 1 to 1 of 1
#1 "Once Again Slick Willy Screws America !"
- Join Date
- Aug 2005
- Posts
- 22,889
How A Clinton-Era Rule Rewrite Made Subprime Crisis Inevitable
One of the most frequently asked questions about the subprime market meltdown and housing crisis is: How did the government get so deeply involved in the housing market?
The answer is: President Clinton wanted it that way.
Fannie Mae and Freddie Mac, even into the early 1990s, weren't the juggernauts they'd later be.
While President Carter in 1977 signed the Community Reinvestment Act, which pushed Fannie and Freddie to aggressively lend to minority communities, it was Clinton who supercharged the process.
After entering office in 1993, he extensively rewrote Fannie's and Freddie's rules.
In so doing, he turned the two quasi-private, mortgage-funding firms into a semi-nationalized monopoly that dispensed cash to markets, made loans to large Democratic voting blocs and handed favors, jobs and money to political allies. This potent mix led inevitably to corruption and the Fannie-Freddie collapse.
Despite warnings of trouble at Fannie and Freddie, in 1994 Clinton unveiled his National Homeownership Strategy, which broadened the CRA in ways Congress never intended.
Addressing the National Association of Realtors that year, Clinton bluntly told the group that "more Americans should own their own homes." He meant it.
Clinton saw homeownership as a way to open the door for blacks and other minorities to enter the middle class.
Though well-intended, the problem was that Congress was about to change hands, from the Democrats to the Republicans. Rather than submit legislation that the GOP-led Congress was almost sure to reject, Clinton ordered Robert Rubin's Treasury Department to rewrite the rules in 1995.
The rewrite, as City Journal noted back in 2000, "made getting a satisfactory CRA rating harder." Banks were given strict new numerical quotas and measures for the level of "diversity" in their loan portfolios. Getting a good CRA rating was key for a bank that wanted to expand or merge with another.
Loans started being made on the basis of race, and often little else.
"Bank examiners would use federal home-loan data, broken down by neighborhood, income group and race, to rate banks on performance," wrote Howard Husock, a scholar at the Manhattan Institute.
But those rules weren't enough.
Clinton got the Department of Housing and Urban Development to double-team the issue. That would later prove disastrous.
Clinton's HUD secretary, Andrew Cuomo, "made a series of decisions between 1997 and 2001 that gave birth to the country's current crisis," the liberal Village Voice noted. Among those decisions were changes that let Fannie and Freddie get into subprime loan markets in a big way.
Other rule changes gave Fannie and Freddie extraordinary leverage, allowing them to hold just 2.5% of capital to back their investments, vs. 10% for banks.
Since they could borrow at lower rates than banks due to implicit government guarantees for their debt, the government-sponsored enterprises boomed.
With incentives in place, banks poured billions of dollars of loans into poor communities, often "no doc" and "no income" loans that required no money down and no verification of income.
By 2007, Fannie and Freddie owned or guaranteed nearly half of the $12 trillion U.S. mortgage market a staggering exposure.
Worse still was the cronyism.
|« Previous Thread | Next Thread »


text:
Reserve directamente en el Hotel Kooyk
Reservation request
If you don't want to pay through PayPal, you can also send us your CreditCard details by Phone, Fax or E-mail. Please mention your name and booking number when faxing or e-mailing.
Phone: +3120 62 30 295
Fax: +3120 63 88 337
E-mail: email@example.com
Please note: only send your payment details after we have confirmed your reservation.


text:
Jay-Z might have the rap game in New York on lock, but Boca Raton belongs to Hindy Melzer.
The 64-year-old rapping grandmother recently dropped a remix to Jay-Z's anthem "Empire State of Mind" with her own rendition of the town she loves, Boca. The video to the song has become a YouTube.com sensation with over 46,000 viewers coming to get a glimpse of Melzer dropping lyrics like this:
"Eating world famous Veggie Boca Burgers. Shout out to FAU. Owls. Schnellenberger.
Sandy beaches, beware of gators at golf courses. Palm Beach, champagne and polo horses."
Melzer also busts rhymes about all the Jewish people that live in her 'hood and gives shout outs to Einstein Bros Bagels, homeowner association fees, and slow-driving retirees playing shuffleboard.
The idea of the song came from her grandkids, who gave her a crash course in spitting bars and introduced her to a Jay-Z CD. The dance moves might be out of 1970, but Melzer moves pretty well for a senior citizen. She also sings the hook, which is belted by Alicia Keys for Jay-Z on the original.
"I have a new respect for rappers, I'll tell ya," Melzer told WPTV News. "It's so fast you cant even catch your breath."
But don't expect her to drop her day job to go on tour anytime soon. The dental hygienist said she will not be performing at a Bingo parlor near you.
"I've had people tell me to keep my day job," she said.
You go, granny.


text:
Aneurin Bevan (1897-1960)
Is he still relevant? I think so. Especially when in America medicare is still an explosive issue.
The collective principle asserts that… no society can legitimately call itself civilised if a sick person is denied medical aid because of lack of means.
—Aneurin Bevan, In Place of Fear, p100
On the "appointed day", 5 July 1948, having overcome political opposition from both the Conservative Party and from within his own party, and after a dramatic showdown with the British Medical Association, which had threatened to derail the National Health Service scheme before it had even begun, as medical practitioners continued to withhold their support just months before the launch of the service, Bevan's National Health Service Act of 1946 came into force. After 18 months of ongoing dispute between the Ministry of Health and the BMA, Bevan finally managed to win over the support of the vast majority of the medical profession by offering a couple of minor concessions, but without compromising on the fundamental principles of his NHS proposals. Bevan later gave the famous quote that, in order to broker the deal, he had "stuffed their mouths with gold". Some 2,688 voluntary and municipal hospitals in England and Wales were nationalised and came under Bevan's supervisory control as Health Minister.
When he was Britain's minister of Health, he returned home each night with cabinet papers and retreated to a small top bed room with them. Once he called late in the night for his second brief case as bulging with sheaves of papers as before.
At this his wife remonstrated, 'No' said she, 'One you may take. But taking two to bed is positively immoral.'
Archive for September 11th, 2010
Their Great Moments-3
Posted in anecdotes, health, tagged medical profession, National Health Service, NHS Act of 1946, UK, welfare state on September 11, 2010| Leave a Comment »
Aneurin Bevan (1897-1960)


text: I found a gratis forum service provider for foss projects https://blog.discourse.org/2016/03/free ... -projects/ . Maybe you can save money and/or server administration work. There are scripts available for migrating content from phpbb. Discourse also has a nice feature called 'mail mode'. If the user activates it, it can use the forum like a mailing list. Maybe you like it. I just want to mention it.


text:
Does JPMorgan suffer from Dimon discount?May 7, 2013: 12:31 PM ET
The opinions expressed in this commentary are solely those of Paul R. La Monica. Other than Time Warner, the parent of CNNMoney, Abbott Laboratories and AbbVie, La Monica does not own positions in any individual stocks.
JPMorgan Chase has made it painstakingly clear that the bank is better off with Jamie Dimon serving as both chief executive officer and chairman.
But the market seems to disagree ... which is one reason why the company's board might want to listen to the growing cries from some JPMorgan (JPM) investors to separate the two roles. The bank will have its annual shareholder meeting in Tampa in two weeks.
Related: Jamie Dimon is under fire
Shares are trading at a lower price-to-earnings ratio (based on 2013 profit forecasts) than its five biggest rivals: Bank of America (BAC), Citigroup (C), Goldman Sachs (GS), Morgan Stanley (MS) and Wells Fargo (WFC).
JPMorgan is also trading slightly below book value, the price that a company is theoretically worth if you subtract its liabilities from its assets. Book value is a key metric that many financial analysts look at when evaluating banks.
By way of comparison, the Financial Select Sector SPDR exchange traded fund (XLF), a collection of 83 banks, insurers and real estate companies, is trading at 1.2 times book value. Goldman Sachs and Wells Fargo both trade above book value as well.
And while JPMorgan's stock hasn't been a terrible performer per se -- it's up 10% year-to-date after all -- it has trailed the broader market and other bank stocks. That has to be disappointing, given that Wall Street banks operate in a world where you're only doing well if you are outperforming the competition.
The fact that JPMorgan is lagging instead of leading the bank pack is pretty shocking. In the immediate aftermath of the credit crisis, JPMorgan was thought to be the best of the financials. It traded at a premium to most of its peers.
The rationale was that the bank, despite receiving $25 billion in TARP funds, was in a much stronger position than the other financial giants who also got massive bailouts. It also took advantage of the downturn to get even bigger, scooping up investment bank Bear Stearns and savings and loan Washington Mutual on the cheap.
But JPMorgan is no longer being viewed as banking's star performer and the bloom is off of Jamie Dimon's rose as well.
Related: Who could succeed Dimon as chairman?
The London Whale trading debacle, which led to a $6 billion loss, dented the bank's image ... if not its balance sheet. Recent allegations that the bank may have manipulated the power trading markets, which JPMorgan has denied, also have hurt the stock.
Even the Federal Reserve is taking a closer and more skeptical look at the bank. Earlier this year, the Fed merely granted conditional approval to JPMorgan's proposal to buy back stock and raise its dividend. The bank will have to resubmit its capital plan to the Fed later this year. (Goldman Sachs got a similar "yes, but" request from the Fed.) But 15 other banks, including Citi, BofA and Wells, received a green light from the Fed with no strings attached.
Related: If Dimon left, who would be next JPM CEO?
So what should JPMorgan do? Is there anything it can do? Shaking up the board might help. And naming a new chairman might convince some shareholders that JPMorgan is taking corporate governance issues more seriously.
But stripping Dimon of the chairman role (he's not going anywhere as CEO unless a dinosaur-sized skeleton is found lurking in the company's corporate closet) may not be a panacea either.
Of the other large banks, only BofA and Citi have split the chairman and CEO roles. Goldman, Morgan and Wells have all outperformed JPMorgan this year despite the fact that their CEO and chairman are the same person.
Related: JPMorgan Chase earnings fail to impress Wall Street
The problem may not be Dimon, but that JPMorgan has simply proven to be fallible. Investors got too used to the bank outshining its brethren and steering clear of the industry's worst sins.
"JPMorgan Chase is akin to an A student that is now getting B grades. The fallout from last year's London Whale loss seems to increase risk with management, reporting, consistency and brand," wrote CSLA analyst Mike Mayo in a recent report. "In short, we feel that other banks provide greater potential at this time."
Still, one institutional shareholder thinks JPMorgan Chase will get back in investors' good graces as long as the economy continues to improve.
John Snyder, manager of the John Hancock Sovereign Investors Fund (SOVIX), said the recent relative weakness of the stock is more about headline risk than anything truly broken with the company. Snyder noted that some investors may have also been disappointed to see that one of Dimon's top allies, co-chief operating officer Frank Bisignano, is leaving the bank to become the CEO of payment processing company First Data.
Related: Charlie Munger says it's time to break up the big banks
But Snyder, who also owns Wells Fargo, Goldman Sachs and Texas regional bank Cullen/Frost (CFR) in his fund, said it's now a great opportunity to buy JPMorgan given that it's a better bargain than its peers and also pays a dividend that yields 3.2%.
"There may be more uncertainty with JPMorgan Chase now but the stock is still cheap and you have to trust that Dimon will do what's right for shareholders," he said.
And by that, Snyder means he thinks Dimon will continue to boost the company's dividend and repurchase more stock ... assuming the Fed lets it, of course.
Whether or not Dimon falls on his sword and gives up the chairman title in the interest of shareholders remains to be seen ... but that seems like a long shot.


text:
HELENA, Mont. (AP) — A judge has ordered the Fort Harrison VA Medical Center to pay nearly $60,000 to a Winston man who was wrongly diagnosed with brain cancer and told he had just a few months to live.
U.S. District Judge Donald Molloy wrote that the distress Mark Templin and his family suffered was caused by Dr. Patrick Morrow's "negligent failure to meet the standard of care" in delivering the diagnosis in 2009.
Molloy's decision noted that in the months Templin believed he was dying he quit his job, sold his pickup truck, celebrated a "last" birthday, bought a prearranged funeral service and contemplated suicide. His son-in-law built a box for his ashes.
As Templin began to feel better, he underwent additional testing that determined he had instead suffered several small strokes.
"It is difficult to put a price tag on the anguish of a man wrongly convinced of his impending death," Molloy wrote. "Mr. Templin lived for 148 days ... under the mistaken impression that he was dying of metastatic brain cancer."
In his May 6 ruling, Molloy decided to award $500 per day for the initial period of severe mental and emotional distress and $300 per day for the latter period until Templin received his new diagnosis. He also ordered the VA to repay Templin for the cost of the birthday party and funeral. The total award was $59,820.
Templin's said in his 2011 lawsuit that he went to the VA in January 2009 for chest pain and had a stent inserted. Weeks later, he developed problems with his memory, vision and speech and was having headaches.
Morrow, an internist, referred Templin to an ophthalmologist who suspected Templin had suffered a stroke. A CT scan showed brain abnormalities, which Morrow discussed with a neuroradiologist who told Morrow that Templin could be suffering from a brain tumor, stroke or something else. The radiologist said further testing was needed to confirm the diagnosis.
Later that day, Morrow met with the VA's tumor board and presented the case as a strong suspicion of brain cancer, apparently without mentioning it could have been a stroke, according to court records.
Morrow testified during a trial that his "greatest fear" was brain cancer and that further diagnostics were needed and he advised Templin to undergo an MRI. That contradicted Templin's medical records that gave no indication further tests were needed or given.
Templin, who's in his 70s, was prescribed two drugs to treat brain cancer, one of which is not supposed to be given to stroke patients, according to court records. Hospice care also was ordered.
Templin testified that he cried often and considered shooting himself so his family wouldn't have to watch him wither away.
He started feeling better and terminated hospice care in June. In July, he underwent additional testing at Fort Harrison. The doctor told him a CT scan showed multiple small strokes, but no brain cancer. An MRI in December 2009 confirmed that it was a stroke that caused his symptoms earlier that year.


text:
Social Occasions by Mon Cheri 216869
- Brand: Social Occasions by Mon Cheri
- Style #: 216869 - Quick Delivery*Quick Delivery*
- Availability: In Stock
- $218
Two-piece stretch taffeta dress set, sleeveless knee-length sheath features surplus bodice with ruffle trimmed V-neckline and peplum, detachable sash at natural waist, center back slit. Matching shawl included.
Quick Delivery:
- Dark Teal: 10, 12
- Grape: 6, 14
- Royal Blue: 6
*A style on our web site listed as in-stock can usually be shipped today or next day for immediate delivery or quick delivery. An item listed as "Ships Today" can be sent the same business day as long as the order is placed before the cutoff time.


text:
Although Entertainment Weekly promised a look ahead at next year's The Hobbit: The Desolation of Smaug in their upcoming collector's issues, they're going even further ahead with this new image from 2014's The Hobbit: There and Back Again. It features a good look at both Luke Evans (The Raven), who plays Bard the Bowman, and Orlando Bloom, who returns as the Elf, Legolas. Bard was mentioned in J.R.R. Tolkien's The Hobbit but Legolas didn't turn up until The Lord of the Rings series, so what's he doing here other than looking all immortal and pretty? Hit the jump to see the full image along with an explanation from the filmmakers.
[Update: A new image from An Unexpected Journey has been released that features Gandalf squaring off against the Goblin King, which is now included after the jump.]
Check out the first image from The Hobbit: There and Back Again, courtesy of EW:
As for the on-screen presence of Laketown's hero, Bard the Bowman, screenwriter and producer Philippa Boyens had this to say:
"Bard is an interesting character, but [in the book] he's kind of a random character who comes in after the fact. We take more time introducing him. We know from what follows that he was a father, so we [explore] that. I don't think we take liberties, because it's all there in the storytelling."
Regarding the return of fan-favorite Legolas, director Peter Jackson commented as such:
"He's [elven king] Thranduil's son, and Thranduil is one of the characters in The Hobbit, and because elves are immortal it makes sense Legolas would be part of the sequence in the Woodland Realm."
The Hobbit: An Unexpected Journey opens December 14th, with The Hobbit: The Desolation of Smaug opening December 13, 2013 and The Hobbit: There and Back Again debuting on July 18, 2014.
Peruse all of our recent coverage of The Hobbit below:
- Dave's review of the film.
- Steve's set visit round-up and 70 things to know.
- Peter Jackson on-set interview.
- Ian McKellan on-set interview.
- Martin Freeman on-set interview.
- Richard Armitage on-set interview.
- Weta Workshop head Richard Taylor on-set interview.
- 6 clips from the film.
- 20-minutes of behind-the-scenes footage.
Here's the image from An Unexpected Journey via EW.


text:
When C.J. Fowler was murdered in Kamloops last week, the 16-year-old was hours away from returning to Terrace.
Kamloops RCMP Staff Sgt. Grant Learned said investigators have learned Fowler, whose body was found on an embankment in Guerin Creek on Dec. 5, had purchased a bus ticket home for later that day.
She had been in Kamloops since Dec. 1, police believe, spending time couch-surfing with friends in the Tournament Capital.
Learned said investigators have interviewed many of those acquaintances, as well as a male companion with whom Fowler is believed to have travelled to Kamloops.
Eight detectives are working full-time to find out what happened to Fowler.
"It's still very, very active," Learned said.
"The homicide investigators have characterized the investigation as proceeding favourably."
According to Learned, police are working more than 200 leads — the result of public tips and interviews.
Investigators have narrowed their interest to the period between midnight and 8 a.m. on Dec. 5.
Police are asking anyone in the Guerin Creek area who saw or heard anything suspicious during those hours to contact them.
Additionally, Learned said, Mounties are hoping someone in the Grandview Terrace and Dalgleish Drive areas with a home-security surveillance system might have caught useful evidence on tape.
An autopsy was completed last week, but police are still waiting on toxicology results, which aren't expected for a period of weeks.
Describing Fowler as "a troubled youth," Learned said she was known to have used drugs and investigators want to know if drugs played a role in her death.
Mounties are not saying publicly how Fowler was killed.
"There's a lot of information that's not being disclosed," Learned said.
"It's very important to maintain the integrity of the investigation."
Kamloops Mounties have said Fowler was a missing person at the time of her death, but it's not known from where she was missing.
Terrace RCMP have said she was not the subject of a missing-person complaint there.
Learned said Fowler let friends and family in Terrace know she was going to Kamloops.
"It was to come down and see friends," he said.
"That was the reason she had given."
Gitsan First Nation hereditary Chief Simidiiks is Fowler's great-uncle and told CTV her death may be connected to drugs.
"If this is related to drugs, I would like to pass the message on to other drug users to try and find a way to get away from this drug business and become a person who would think safe and no longer get hooked on that stuff."
Police believe Fowler knew her killer.
"In reality, there is someone who is responsible for her death that is still out and about in the community," Learned said.
"But, the investigators don't believe there is a broader threat. If there was, we have a responsibility to communicate that to the community."
Anyone with information, or area residents with video surveillance, is asked to contact police at 250-828-3000 or Crime Stoppers at 1-800-222-8477.


text:
What is hypermetropia (farsightedness)?
Hyperopia, also called hypermetropia, farsightedness, or long-sightedness, is a vision problem that causes blurry vision when focusing on nearby places and objects, but clear vision when focusing at a greater distance. The condition is caused by an eye that is shorter than normal, or a cornea that's not as curved as it should be. Eyes that are slightly misshapen won't be able to focus light accurately onto the retina, which results in blurred vision.
There are several kinds of irregular shapes than an eye can take, each moving the focal point of the light away from the retina, resulting in a different form of vision impairment. When the shape of an eye focuses light in front of the retina, the resulting condition is called myopia, or nearsightedness. A focal point behind the retina is hyperopia. Corrective lenses are available for both conditions, and are designed to move the focal point to the surface of the retina, restoring clear and focused eyesight.
The Causes of Hypermetropia
Farsightedness is largely hereditary, but can develop in anyone. It's possible to experience symptoms even during childhood, but is much more common later in life. In fact, anyone above the age of 40 has a much greater chance of experiencing symptoms of hyperopia, with the likelihood growing every year. Aging doesn't necessarily cause the eyes to change shape any more, but it does diminish the eyes ability to flex enough to accommodate for the refractive error. Additionally, some forms of hyperopia can be causes by injury, drugs, or disease.
It's common for farsightedness to be confused with presbyopia. Both conditions have similar results - difficulty focussing on objects that are near - but they have different causes.
What are the Symptoms of Hypermetropia?
Everything may seem clear and in focus when viewing at a distance more than a few meters away, but any closer than that and things may start to get blurry. The closer they get, the less focused they become. As it becomes more difficult to read and write, squinting will cause eye strain and fatigue, leading to headaches.
If you're experiencing any of these symptoms, it's recommended than you make an appointment with an eye care professional. A comprehensive eye exam will help determine what kind of issue you're having, and what steps can be taken to get it resolved.
Are there Different Types of Hypermetropia?
There are, in fact, several different categorizations of hyperopia, depending on the root causes and how advanced the condition is. Below are the four main forms of hyperopia.
- Latent Hyperopia – When in it's early stages, and not yet fully developed. At this point, symptoms are just beginning to appear, and may not even be noticeable unless actively looking for them. It's at this stage where even a small amount of squinting is enough to correct the blurry vision.
- Low/Moderate/High Hyperopia – Once the condition becomes more developed, it can grow to three different levels of severity. Low hyperopia will have the least drastic change in eye sight, with a prescription measurement of +2.00D or below. Moderate hyperopia, follows next, with prescription measurements between +2.25 and +5.00D. Finally High Hyperopia will have the greatest effect on vision, and have prescription measurements of +5.25 or higher.
- Pathologic Hyperopia – Caused by irregular development of the structure of the eye, injury to the eye, or disease. Some diseases that can possible lead to hyperopia are cataracts, microphthalmia, nanophthalmia, and aniridia.
- Functional Hyperopia – Unlike other forms of hyperopia, caused by an irregularly shaped eye, this form is caused by a failure of the muscles around the eye that would normally allow it to focus.
How is Hypermetropia Detected and Treated?
Farsightedness is not usually diagnosed in basic eye-screenings because those tests only measure the ability to see objects in the distance. If an individual is suspected to be farsighted, a more comprehensive Optometrist examination should be carried out to diagnose the condition.
Corrective eyeglasses, contact lenses, and even surgery can all help to restore clear and focused eyesight. Each has their own advantages and disadvantages, though, and lifestyle, work environment, and personal preference all play a role in deciding which is best. You should discuss with your eye care professional which one is right for you.
- Eyeglasses are inexpensive and effective, but not always convenient. If you have an active lifestyle, or play sports, it may be difficult to keep them firmly in place. They come in many different shapes and sizes, and can be quite fashionable. With so many options available, it may take some time to find a set that's comfortable, but the right ones will feel like they aren't even there. Tinted lenses are also available, allowing you to stay protected from bright sunlight and damaging UV rays.
- Contact Lenses are much more subtle, providing no change in your personal appearance at all (unless you're looking to change you eye color). They're designed to be worn all day long, and removed at night. Different types of lenses can be worn for varying lengths of time. Some last for several weeks before needing to be replaced, while others are worn only for a single day before being disposed of. With proper hygiene and some practice, contact lenses are one of the more versatile options for people looking for corrective eye wear.
- Surgery is also an option. LASIK and PRK are two examples of surgical methods that reshape the surface of the eye, allowing it to refract light accurately without any need for corrective lenses. This is a more expensive method of fixing the problem, but it's also more permanent. The recovery time is usually only a few days, but only one eye is corrected at a time, so multiple visits will be required.
For mild cases of farsightedness, you may only need to wear your corrective lenses when doing tasks at close range - such as reading or using a computer. Those who have more severe farsightedness, or who suffer from other conditions like astigmatism, may need to wear their lenses more often.
It's also important for everyone to get their eyes checked on a regular basis because vision problems tend to slowly change over time. For those diagnosed with farsightedness, this will enable your eye care professional to monitor your condition and make adjustments to your corrective lenses prescription as appropriate.
During your eye examination, you should be advised on how often you should wear your lenses to correct your hypermetropia. You'll probably be asked questions about your lifestyle and the type of work that you do in order to determine the best way of dealing with farsightedness.
Correct hypermetropia with contact lenses
If you have been diagnosed with farsightedness and need corrective lenses, contact lenses could be the perfect choice: they're safe and easy to use and don't have any affect on your appearance.
On our website, we offer a range of contact lenses that will help farsighted individuals see clearly. And with our simple and fast service, you can order your new contact lenses without ever leaving the comfort of home.
In addition, research into new and better ways of treating conditions like hypermetropia is constantly being done around the world.
Author: John Dreyer Optometrist Bsc(Hons), MCOPTOM, DipCLP
Created: 24 Apr 2015, Last modified: 11 Sep 2020


text:
Fortissimo Films has sold Japanese rights to Matthew Miele's documentary feature Scatter My Ashes At Bergdorf's to Showgate Japan.
The film tells the story of New York's famous Fifth Avenue store Bergdorf Goodman and includes appearances by fashion legends Karl Lagerfeld and Christian Louboutin.
Fortissimo hold all rights outside of North America to the film, which Entertainment One will distribute in the US in mid-2013. The deal with Showgate was negotiated by Fortissimo's Winnie Lau and Showgate's Chizu Ogiya.
"It's wonderful to find such an enthusiastic and passionate distributor in Showgate to bring this fun, classy and very entertaining iconic fashion powerhouse to the Japanese audience," said Lau.


text:
Something I don't understand is why people have always got to pay what the banks lend them. I have a friend in hard times I lend money to. He calls it a loan. I know he is not going to pay it back. He says the loan is just to help him "get back on his feet." We both understand that unless he wins the Lottery I won't see that money again.
I understand that banks should pay back loans they lend to one another. Honor is involved. They are the professionals. If you can't trust one another who can you trust etc. etc. But why should that extend to the rest of us? How many of us, when we took out large mortgages in 2006, were relying on the soothing words of the bankers. We put ourselves in their hands.
The lengths that banks go to to get their loans paid back is amazing to me. You thought that countries were the most powerful entities on the planet. Bankers are currently bringing certain countries to their knees. Huge hardships are demanded of the people who live in these countries. They lose their jobs. They are living hand to mouth.
Most of these countries have big armies, or anyway medium sized armies. The bankers have no weapons. What is wrong with this picture? The only country that stood up to these banks during this recent recession was Iceland. They threw all the bankers out, the debts unpaid. Then they started over.
In the current circumstances, the residents of Greece are suffering terribly. Spain is suffering. Cyprus is suffering. Even America, the strongest country in the world, is buckling under. We are cutting service. We suffered a slight downgrade in the rating of U.S. credit from AAA to AA+ and that was it. There is now less childcare, education, health. And we hope the rating will soon be restored. Celebrations will begin everywhere when it is. What an accomplishment! Thank goodness we cut healthcare, education and childcare. Of course they stay cut.
A few years ago, video game people began developing "money" you could win if you beat the monster and got to the upper levels. The "money" had no value, except to people playing the game. You could buy "things" with this money, for example an "AK47 Machine Gun" that, on your screen, would help you get to the upper level faster.
About five years ago, some Silicon Valley people took it a step further. They started using something they called Bitcoins, and these Bitcoins could be used not only for make believe things, but for real things among the geeks in Silicon Valley. Not only did those living in the cyber world trade them, but various merchants in the valley began accepting them. I've seen this phenomenon in certain resort islands I have visited, although not in the Hamptons. The resort issues "scrip." It has the name of the island on it. And you get a bigger bang for the buck when you use the "scrip" than when you use the dollar. Such phenomena come and go.
But this is different. The creators of Bitcoins are smart. They decided that if Bitcoins were to become a viable alternative on a wider scale than just in the immediate area, they'd have to limit it. They could do that. After all, you can't counterfeit Bitcoins. They don't exist.
An easy fix, of course, would be to link Bitcoins to the dollar, but that leads you down the garden path to having Bitcoins just be another currency, like the Shekel or the Pound or the Ruble.
So instead, the Bitcoin people dug deeper. They realized that all modern currencies are linked to one another but also are linked to a physical element: gold. You dug up gold. Currency would be the calling card of gold. And it would be limited to the amount of gold that could be dug up.
What could a currency that did not exist in the physical world be linked to? The Geeks decided to link it to something else that does not exist in the real world, the ability of mathematical geniuses to solve complex formulas. There is a lot we don't know about the world. There is no dearth of formulas. But solving them is another matter. At the present time, there are mathematicians working away solving formulas. When they solve one, from the sweat of their collective brows, it means they can create more Bitcoins. The total number of Bitcoins allowed is 21 million. When we get to that, that's it. Currently, there are 11 million. But there are a lot of mathematical formulas waiting to be solved.
Into this situation have now come the Winklevoss Twins. You recall them. They are the big muscular fellows who rowed crew for Harvard, claimed they started up a social media for fellow students there and elsewhere which they later claimed that Mark Zuckerberg stole and enlarged into Facebook. When he became a billionaire, they sued him. Zuckerberg settled, rather than go to war with them. I think the Winklevosses each got about $30 million, a drop in the bucket as far as Zuckerberg was concerned.
About a year ago, some banker types, without the approval of the original Bitcoin people, began linking its value to the dollar and doing "trading" in Bitcoin. Who could stop them? Nobody. For the first year, the value of a Bitcoin hovered around $15. But then it caught fire. Everybody wanted them. This past Spring, the value of a Bitcoin leaped to $250, then settled back. Currently if you want one it will cost you $75. Hmmm.
Now the Winklevoss Twins have announced that they are opening an exchange for Bitcoin. It will be like the current exchanges you read about for copper or hog bellies or gold. But they will run it. It is to be called Index Universe. And what they will do is put up the daily prices of Bitcoin, track them higher and lower, buy and sell, and take a small cut of each transaction. They are looking for approval from bank regulators for this new product. I have no doubt they will get these approvals because it is quite clear that Bitcoin, unregulated, could mean the death of money. Approving it will tractor beam it all into the system, thereby ending the problem.
When the White Men first came to Long Island, they were met by the original Indian tribes who, among other things, offered to trade some of the unique goods the White Men brought—gunpowder, swords, belt buckles, hats—for what they called Wampum.
The Indian tribes got Wampum from the beaches of Montauk where a particular kind of clamshell was to be found. They'd punch a hole in each clamshell, then string them together on leather strips and worn as necklaces. From a certain perspective, you could say either they had the money or they didn't, and you could see it right there.
The tribe in charge of making the Wampum was the local tribe known as the Montauketts. They'd find the shells, string them, and then either gift them to others, trade them to others, or be robbed of them by others. That way Wampum would circulate through the various tribes on Long Island all the way to the other end of Long Island. It was a primitive system. No trading floor, stock exchange, contracts to be signed—you signed a paper!—the Indians had no idea about that. When the daughter of Wyandanch, chief of the Montauks, made a treaty with the Montauks and the White Men, she signed her name with an "X." She didn't even know what X meant. And she surely didn't know the White Men would now take over the land and kick them off.
There was honor and a person's word of course. But Wampum was not that important and did not rule the world. There is no story from the Indian world about any tribe that couldn't give Wampum back and thus was reduced to an impoverished
That only happened after the White Men arrived.


text:
Egitto: la mano invisibile colpisce ancora
El-Koshary Today, un giornale satirico online, scrive questo sarcastico pezzo su una "mano invisibile" che guida le camionette della polizia militare egiziana contro i manifestanti copti, che arma dozzine di teppisti contro i copti.
"Invisible hands" strike again
Initially held responsible for the January uprising by the former regime, "invisible hands" continue to menace a fragile Egypt.
| Written by makarona
Mon, 10/10/2011 – 13:23
Intelligence reports from the Egyptian National Security Agency have revealed that "invisible hands" were yet again behind another bloody night in Cairo. During a peaceful demonstration of Copts demanding their rights, the hands apparently hijacked a large armoured military vehicle and – while apparently sober – ran over several Coptic protesters.
Information Minister, Kalami Fasya, stated that "the invisible hands have also been found to have armed dozens of thugs during the night after angry Copts used large wooden crosses to destroy several military tanks without being provoked."
Irrefutable evidence implicating the conniving hands has been provided by a fresh SCAF Facebook statement: "While it is impossible to see them with the naked eye, infrared sensors detected the heat signals of two very large hands hovering above Maspiro during the night. Their fingers were being rhythmically tapped together in turn – as though they were concocting an evil plan, like Mr. Burns, the Simpsons character. This is true."
It is unclear why SCAF thought it was appropriate to refer to The Simpsons at this time.
It is also unclear where the mysterious hands themselves actually come from. Most pundits believe that while the left hand is composed of "foreign elements", the right one is made of "felool" — an Arabic term believed to originally refer to the so-called "skid marks" that stain the inside of a toilet after a particularly violent – or at least misdirected – bowel movement.
As to the "foreign elements" composing the left hand, these are believed to be simultaneously Saudi, American, Hamas-ian, Israeli and Iranian, along with other states, and possibly even planets, associated with this well-known allied group.
The deviant duo is believed to have been on the run since late last January, when in one of the biggest heists in the history of Egypt robberies, the hands allegedly stole the country's "wheel of production" – a similarly invisible, but highly valuable large spinning thing that is said to drive the local economy.
The invisible hands are now even thought to be behind the infamously high rate of women having their butt cheeks groped while walking down busy Egyptian streets. "Who else could it be?" said a tense 28 year old Egyptian male virgin who can't afford to get married, and for whom tradition dictates he can only have anal sex with his girlfriend so as not to dishonour her — something he has been unable to convince of at the time of writing.
Currently, the interim government has vowed to renew efforts to hunt down the diabolical invisible hands so as to bring a final end to all the sectarian strife, misinformation, lack of security, economic woes, bad traffic, and sexual harassment that they are directly the cause of. Meanwhile, political activists continue to point out that the hidden hands are most likely cozily residing deep inside the pockets of the head of the SCAF.


text:
In a cutscene for the upcoming downloadable standalone Cole MacGrath adventure, inFamous 2: Festival of Blood, we learn why bloodsuckers from fake New Orleans would go to all the trouble of kidnapping a guy with superpowers.
It's amazing how a being born of new technology can be the key to reviving an ancient evil like that. It's good to know Cole is backwards compatible, even if the older software sucked hard.
inFamous 2: Festival of Blood will be available via the PlayStation Network in October.
inFAMOUS 2: Festival of Blood – Witness the Resurrection [PlayStation Blog]
You can contact Michael Fahey, the author of this post, at email@example.com. You can also find him on Twitter, Facebook, and lurking around our #tips page.