Trường thọ

Advocacy, Vietnamese Tiếng Việt
Trường thọ

Chúng tôi ủng hộ sự tiến bộ của tuổi thọ khỏe mạnh cho toàn bộ dân số thông qua nghiên cứu khoa học, y tế công cộng, vận động và hoạt động xã hội. Chúng tôi nhấn mạnh và thúc đẩy cuộc đấu tranh chống lại kẻ thù chính của tuổi thọ khỏe mạnh – quá trình lão hóa.
Quá trình lão hóa là gốc rễ của hầu hết các bệnh mãn tính đau đớn dân số thế giới. Quá trình này làm cho tỷ trọng lớn nhất của người khuyết tật và tử vong, và cần phải được điều trị phù hợp. Xã hội cần dành nỗ lực hướng tới điều trị và điều chỉnh của nó, như đối với bất cứ căn bệnh vật chất khác.
Các vấn đề của lão hóa là nghiêm trọng và đe dọa. Tuy nhiên, chúng ta thường chứng kiến sự lãng quên gần như hoàn toàn với thực tế và mức độ nghiêm trọng của nó. Có một xu hướng nhẹ nhàng để bỏ qua tương lai, để đánh lạc hướng tâm từ lão hóa và tử vong do lão hóa, và thậm chí để trình bày quá trình lão hóa và chết trong một ánh sáng gây hiểu nhầm, xin lỗi và không tưởng. Đồng thời, có một niềm tin vô căn cứ rằng lão hóa là một quá trình không thể lay chuyển hoàn toàn không thể quản lý. coi thường này của vấn đề và ý nghĩa vô căn cứ này bất lực không góp phần vào việc cải thiện sức khỏe của người già và tuổi thọ khỏe mạnh của họ. Có một nhu cầu để trình bày các vấn đề trong mức độ đầy đủ của nó và tầm quan trọng và hành động để giải quyết hoặc giảm thiểu nó đến hết khả năng của chúng tôi.
Chúng tôi kêu gọi nâng cao nhận thức của công chúng về các vấn đề lão hóa trong phạm vi đầy đủ của nó. Chúng tôi kêu gọi công chúng để nhận ra vấn đề nghiêm trọng này và dành những nỗ lực và nguồn lực – trong đó có nguồn lực kinh tế, xã hội, chính trị, khoa học, công nghệ và truyền thông – để giảm tối đa khả năng của mình vì lợi ích của dân số lão hóa, kéo dài tuổi thọ cho sức khỏe của họ. Chúng tôi thúc đẩy ý tưởng rằng sự trưởng thành về tinh thần và tâm linh và sự gia tăng tuổi thọ khỏe mạnh không đồng nghĩa với sự lão hóa và thoái hóa.
Chúng tôi ủng hộ việc tăng cường và đẩy mạnh nghiên cứu y sinh học cơ bản và ứng dụng, cũng như sự phát triển của công nghệ, công nghiệp, môi trường, y tế công cộng và các biện pháp giáo dục, đặc biệt là đạo diễn cho tuổi thọ khỏe mạnh. Nếu được hỗ trợ đầy đủ, các biện pháp như vậy có thể tăng tuổi khỏe mạnh tuổi thọ của dân số già, thời gian sản xuất của họ, đóng góp của họ cho sự phát triển của xã hội và nền kinh tế, cũng như ý thức của họ về hưởng thụ, mục đích và giá trị của cuộc sống.
Chúng tôi ủng hộ sự phát triển của các biện pháp khoa học để mở rộng cuộc sống khỏe mạnh được sự hỗ trợ công cộng và chính trị có thể tối đa mà nó xứng đáng, không chỉ bởi các cộng đồng nghề nghiệp mà còn bởi sự rộng rãi công chúng.

Gerontological Manifesto

Advocacy

The Gerontological Manifesto

By Alexey Olovnikov, PhD

The necessity to create various remedies for degenerative age-related diseases is beyond any doubts. But this process is somewhat like a Sisyphean task, because the aging of each person only deepens over time, persistently destroying the results of treatment. Pharma is forced to deal with the countless consequences, rather than with their cause. The primary cause of aging is still deeply buried in gerontological terra incognita. Meanwhile, a growing and imminent new threat for humankind is becoming increasingly apparent. This threat is the increasing aging of the human population as a whole. The menace to the society is in the ongoing change in the ratio of the able-bodied and the disabled-bodied populations in the advanced countries. This trend may lead to the numerical superiority of disabled old persons already by the middle of the 21st century. According to the current estimates, the medical expenses on non-communicable diseases for the period 2010-2030 will be $47 trillion by 2030, with two thirds of this sum to be linked to the costs of the elderly healthcare. (http://www.weforum.org/news/non-communicable-diseases-cost-47-trillion-2030-new-study-released-today) A solution to this problem by attracting young migrants only shifts the burden of care to the countries of exodus. If no action is taken to radically enhance the ongoing studies in the field of aging biology, this problem will became a burden unbearable for our civilization: Humanity will not be able to maintain the elderly people! The solution to such a gerodemographic situation, the potentially fatal and vitally important problem, can be achieved only through a radical slowing down of the pace of the aging process, or by stopping it! And this can be done only via the discovery of the primary causes of aging that still remain elusive. The search for medicines against degenerative diseases of aging and the studies of the primary mechanism(s) of aging are two related but clearly independent tasks. The striving to the radical slowing down of aging is as important today as the struggle against infectious pandemics was in the past. Even under the most favorable scenario, several decades will be spent until finding the conditions for the radical slowing down of mammalian aging (and for the subsequent translation of the results to the clinic). But within the next several decades, the number of disabled elderly people in the developed countries can exceed the number of able-bodied adults. The favorable resolution of this unprecedented historic challenge can be found only in case of the unprecedented concentration of intellectual and financial efforts in a new life extension project. The enemy, that has quietly crept up onto our civilization, is quite capable of either destroying the basic moral values (in the way of forced absence of care for the elderly), or undermining the financial foundations of the society (in the way of the back-breaking costs of servicing the elderly). A more likely scenario is that it will do both! The non-biological alternatives to the ongoing efforts in biology and medicine are the robots, but they are not ready to take the frail portion of mankind on their iron shoulders. But even with the robots, the humans would hardly have forgotten their oldest dream – the dream of a significant life extension. Non-aging or delayed aging in essence means the potential for a very long healthy life. A potential critic may argue that a very long healthspan will lead to overpopulation. However the answer to this objection is known. The experience of birth control on the large state scale has already been gained, albeit with other goals. It is of course possible to leave everything as it is, so that life itself will put everything in its place. Life will do it, but at the cost of mass misery and huge losses. Are those necessary or can be avoided by human effort?

And finally we should note one of the most formidable companions of aging – cancer. It is known that, after sexual maturity, cancer incidence increases exponentially with age (de Magalhães JP. How ageing processes influence cancer. Nat Rev Cancer. 2013 May;13(5):357-65.). Why? According to a widespread view, occasional changes in chromosomal DNA accumulate as long as there will appear some fatal mutations. However, there are some facts that do not fit into such a simple scheme, and therefore, a generally accepted theory of cancer origin is still absent. There are reasons to suppose that the genuine cause of this multiform pathology is the non-mutational flaws in the functioning of a special, so called chronographic, mechanism. This hypothetical mechanism directs the timely sequential changes of the body structures (hence, it directs the control over the biological age of an individual organism) in the course of the development, maturation and aging of multicellular organisms (Olovnikov A.M. Chronographic Theory of Development, Aging, and Origin of Cancer: Role of Chronomeres and Printomeres. Current Aging Science, 2015, Vol. 8, No.1, 76-88.). Non-mutational errors, which rarely occur during the functioning of this mechanism changing the age, can lead to a loss of proper genetic control in some cells. Only after that, the progeny of these cells begins to obtain and accumulate mutations which eventually can give rise to a malignant growth. If so, the delaying of aging can bring another nice bonus – the prevention of cancer. The sooner we will get this bonus, the better for all of us.

Alexey M. Olovnikov   

olovnikov@gmail.com

January 19, 2016

https://healthspanpolicy.org/person/alexey-matveyevich-olovnikov/

alexey-olovnikov2 Alexey Matveyevich Olovnikov, PhD, Institute of Biochemical Physics, Russian Academy of Sciences.

In 1971, Olovnikov was the first to recognize the problem of the DNA end underreplication and to suggest the telomere hypothesis of cellular aging and the relationship of telomeres to cancer. In more details: 1) He predicted telomere DNA shortening during normal cell doublings and foretold the correlation between telomere length and the cell doublings potential, or Hayflick’s limit; 2) He predicted also the existence of a compensatory DNA polymerase responsible for maintenance of telomeres (now the compensatory enzyme is known as telomerase); 3) He supposed that cancer cells should have the same compensatory DNA polymerase (telomerase) as the  germline cells, and assumed that this enzyme endows cancer cells, like the  germline cells, with their immortality; 4) In addition, Olovnikov interpreted a circular form of bacteria’s genome as a means of protection of their DNA from shortening.

History has shown the validity of these basic predictions and explanations that were made by Olovnikov at the tip of a pen and essentially began a new area of research. Later, other researchers, for their experimental demonstration of how chromosomes are protected by telomeres and the enzyme telomerase, were awarded the Nobel Prize (2009).

Currently, A.M. Olovnikov is elaborating a new “Chronographic Theory of Development, Aging, and Origin of Cancer”, positing a critical role of new hypothetical organelles – chronomeres and printomeres –  in these processes. According to this theory, aging of a multicellular organism is caused by the stepwise programmed loss of chronomeres, whereas senescence of dividing cells is associated with the shortening and loss of printomeres. Both printomeres and chronomeres are small perichromosomal amplificates of the regulatory segments of chromosomal DNA, and they encode regulatory RNAs. Chronomeres are located in neurons of brain’s chronograph, or a specialized clock, which records the lived time in the form of nonrandom changes of body structures. According to the new theory, in the future, the key techniques to postpone organismal aging and to stop tumor growth could be: 1) a stopping of the pacemaker of the biochronograph mechanism, and 2) a forced regeneration, or re-synthesis, of chronomeres and printomeres.

 

 

Some potential interventions to ameliorate degenerative aging

English, Science

 

balanceSome potential interventions to ameliorate degenerative aging

By Ilia Stambler, PhD

 

The interventions into the degenerative aging process are still in their infancy. A long effortful road will yet need to be traveled from basic research on cell cultures and animal models to effective, safe and widely available human therapies. And many dangers to human health (such as overdose and overstimulation) and many unsubstantiated false claims yet await on this road that need to be guarded against as much as possible. Yet vast promising research is progressing, especially as regards potential pharmaceutical interventions into the aging process.[1] [2] [3] Below are some examples.

1. On November 28, 2015, the FDA approved the testing of Metformin, a decades-old anti-diabetic (blood sugar reducing) medication, as the first drug to treat degenerative aging, rather than particular diseases, due to its capacity to reduce cancers and other morbidities.[4]

2. On November 25, 2015, the FDA approved an adjuvant therapy (developed by Novartis) for a flu vaccine to boost immune response in older persons. This development goes beyond “a drug against a disease” model, but seeks an appropriate regulatory framework to support the underlying health of older persons, using “adjuvant” (i.e. “supportive/additional”) therapy.[5]

3. The immunosuppressant drug Rapamycin, believed to mimic the healthspan extending effects of calorie restriction (CR-mimetic), has produced improvements of energy metabolism, and to extend lifespan and delay aging in mice, and was also effective against particular aging-related diseases, such as Alzheimer’s disease, in human studies. Further research is done on Rapamycin’s analogs – the so called “rapalogs”, potentially with less side effects.[6]

4. By splicing the circulatory systems of animals (mice) together, via the process of “parabiosis”, young blood was shown to have rejuvenating effects on old tissues, including the heart, brain, and muscle tissues, with improved strength and cognitive ability. Some of the implicated rejuvenating substances included: Notch signaling activators, deactivation of the transforming growth factor (TGF)-β that blocks cell division, oxytocin, and Growth Differentiation Factor 11 (GDF11). In September 2014, a clinical trial by Alkahest in Menlo Park, California, became the first to start testing the benefits of young blood and young plasma in older people with Alzheimer’s disease.[7]

5. A new class of drugs – the “senolytics” capable of eliminating senescent cells and the accompanying pathologies – are being developed, in Mayo Clinic, Rochester, Minnesota and elsewhere.[8] Thus the combinations of the “senolytic” drugs Dasatinib and Quercetin proved effective against senescent human cells and in a mouse model. Together these drugs were able to reduce senescent cell burden, extend healthspan and improve physical exercise capacity in old mice, reducing their osteoporosis and other age-related pathologies.[9] Senescent cells can also be eliminated by immunological means, such as vaccines, antibodies and killer T cells.[10]

6. Resveratrol, a natural polyphenolic compound, among other sources found in red wine, has demonstrated the ability to up-regulate Sirtuin 1 (SIRT1) – an acknowledged prolongevity enzyme[11] important for enhanced stress response, cardiovascular protection, improved cognitive function and synaptic plasticity, and suppressing inflammation.[12] SIRT1 expression is generally related to the levels of energy metabolism, as indicated by NAD/NADH levels, which have also become targets for diverse pharmaceutical interventions (NAD replacement therapy).[13]

7. Dichloroacetate and bicarbonate represent a class of compounds and therapies that may have systemic effects on tissue redox and pH state, with broad implications for the aging process and derivative pathologies, such as cancer.[14]

8. Generally, regenerative medicine, using stem cells of various origins to rebuild, “regenerate” or improve the function of worn out and aging organs and tissues, can be promising for combating the degenerative pathologies of aging.[15] Even entire “replacement organs and tissues” can be grown outside of the body – using such methods as growing tissues on biodegradable scaffolds, 3D tissue printing, bioreactors or self-organization — to “replace” the worn out and aging body parts.[16] Yet, very recently a very promising direction in regenerative medicine has emerged – the induction of regeneration within the body by pharmacological means (e.g. using inhibitors of prostaglandin breakdown thus promoting cell proliferation).[17]

9. Of special importance for regenerative medicine against aging-related degeneration is the ability to regenerate the thymus gland (that produces the immune T-cells that play the crucial role for the immune defense). This importance derives from the fact that such an ability could dramatically improve therapy not only for aging-related non-communicable chronic diseases (such as heart disease and neurodegenerative diseases that are strongly related to altered immune response), but also help combat infectious, communicable diseases (like AIDS, Herpes and Influenza) thanks to improved immunity. Such regenerative ability for the thymus was shown by genetic engineering interventions (e.g. using over-expression of the FOXO gene)[18] and even pharmaceutical treatments (e.g.  using the FGF21 hormone).[19]

10. The extension of the telomere end points of the chromosomes, thus increasing the number of cell replications, by such means as genetically engineered overexpression of the telomere-repairing enzyme – telomerase, and even by some pharmacological stimulators of telomerase activity, have been associated with increased lifespan and reduced pathology in animal models.[20] [21] [22]

11. There have been many methods investigated for improving mitochondrial function and cellular respiration. Thus anti-oxidant molecules attached to positively charged ions (cations) have been targeted into mitochondria to eliminate oxidative damage at its origin (the SkQ ions).[23] In another approach, chemical compounds (in particular suppressors of the IIIQsite of the respiratory chain in the mitochondria) have been identified that can block the production of certain free radicals in cells without changing the energy metabolism of these cells.[24] A large additional array of boosters of mitochondrial activity and cellular respiration has been proposed, e.g. methylene blue, the naphthoquinone drug β-lapachone, supplementation with various components of the respiratory oxidative phoshorylation system – such as CoQ10, pyruvate, succinate, vitamins C and K, quercetin, various other anti-acidic, anti-toxic, and anti-oxidant substances.[25]

12. Anti-inflammatory medications have been widely tested to diminish aging-related degenerative pathologies, such as neuro-degenerative pathologies, and to extend healthy lifespan in animal models.[26] But also pro-inflammatory effects have been shown to be important for tissue regeneration.[27]

13. Diverse means are being developed to dissolve macro-molecular (cross-linked) aggregates that “clog” cell machinery. Some approaches include stimulation of cell autophagy that can help remove such aggregates (e.g. by introducing Beclin protein). Various “AGE-breakers” are being developed. These are, as a rule, small molecules capable of breaking “Advanced Glycation Endproducts” (AGE) that are chiefly responsible for the formation of macromolecular aggregates (e.g. glucosepane, one of the most common forms of cross-linked AGE products in collagen). Some of the therapeutic means against cross-linked aggregates include chelators (removing the metal ions that are important for the formation of the cross-links), enzymatic clearance (oxidoreductive depolymerization of the aggregates by enzymes), immunoclearance (using immune mechanisms, e.g. antibodies, to remove the aggregates), etc.[28] Yet, it needs to be noted that macromolecular aggregates, in certain amounts and under certain circumstances, may have a necessary function in the body too.[29] Removing too much of them and in wrong places may do more damage than good.

14. Keeping the body chemistry in balance is hoped to be achieved by supplementing deficient elements in the diet (e.g. vitamins, microelements, other essential nutrients), while eliminating excessive and therefore toxic elements (by such means as chelators, enterosorbents, dietary restriction, enhanced elimination).[30] But what is “the balance”? How much is “too much” or “too little”? The guiding rule is always “The dose makes the poison”.[3] Dietary interventions, that are being tested, include dietary restrictions of various kinds (mainly protein restriction and calorie restriction) that have been associated with extended lifespan in animal models and some health benefits in humans.[31] Also new ways are being sought to enrich the “microbiome” (intestinal bacteria populations) for healthy longevity[32], for example using probiotic diets – the idea that goes back to the origins of scientific aging research, over a century ago.[33]

15. Epigenetics (acquired or heritable changes in gene function without changes in DNA sequence), has been increasingly investigated and manipulated for its effects on aging and aging-related diseases, and their amelioration, at the level of the entire organism as well as particular tissues, for example, using demethylating agents, small interfereing RNAs (siRNAs) and micronutrients as potential therapeutic agents.[34]

16. Interventions into degenerative aging are now beginning to reach the “nano” level. Some of the uses of nanomedicine against degenerative aging include nanoparticles, such as Buckminsterfullerene or “bucky-balls” C60 with assumed antiviral, antioxidant, anti-amyloid, immune stimulating and other therapeutic activities, and some reported lifespan extending results in animal models.[35] Moreover, there even have been announced the first operating medical nanorobots, mainly intended to assist in precise drug delivery, acting as prototypes of artificial immune cells.[36] [37] These nanodevices were mainly intended to eliminate cancer cells, but could also be used to eliminate other types of cells, e.g. senescent cells. In another area of development, oxygenated micro-particles seem to be very promising for life extension, especially in critical conditions, as oxygen deprivation is the main (or even the ultimate) cause of death.[38]

17. Anti-aging and life-extending interventions do not necessarily need to be chemical or biological, but can also be physical, in particular as relates to various resuscitation technologies (hypothermia and suspended animation,[39] oxygenation,[40] electromagnetic stimulation[41]). Such technologies represent probably the most veritable means for life extension, demonstrably saving people from an almost certain death. But similar principles could perhaps be used for more preventive treatments and in less acute cases.

18. It seems to be impossible to speak of “treating” or “curing degenerative aging” without the ability to diagnose this condition and to reliably assess the effectiveness of interventions against it.[42] Hence a wide array of biomarkers and clinical end points are being sought to diagnose degenerative aging and aging-related ill health, and to determine correct “biological age”.[43] Clinically applicable and scientifically grounded diagnostic criteria and definitions for aging may also have profound encouraging implications for the regulation and promotion of research, development, application and distribution of anti-aging and life-extending and healthspan-extending  therapies.[44] [45]

 

Aknowldgedment

I thank Steve Hill and Kevin Perrott for their suggestions regarding the diverse research areas. Any additional suggestions are appreciated.

 

References

[1] Jin K, Simpkins JW, Ji X, Leis M, Stambler I. 2015. The critical need to promote research of aging and aging-related diseases to improve health and longevity of the elderly population. Aging and Disease  6, 1-5 http://www.aginganddisease.org/EN/10.14336/AD.2014.1210

[2] Stambler I. 2015. Stop Aging Disease! ICAD 2014. Aging and Disease 6 (2), 76-94 http://www.aginganddisease.org/EN/10.14336/AD.2015.0115

[3] Stambler I. 2014. A History of Life-Extensionism in the Twentieth Century, Longevity History. http://www.longevityhistory.com/

[4] Macdonald F. December 1, 2015. A common diabetes drug will be trialled as an anti-ageing elixir from next year. Research suggests it could help people live to 120. Science Alert

http://www.sciencealert.com/a-common-diabetes-drug-will-be-trialled-as-an-anti-ageing-elixir-from-next-year

[5] Preidt R. November 25, 2015. FDA Approves Flu Shot to Boost Immune Response.Vaccine can be used in seniors, who are often hit hardest by illness. WebMD News from HealthDay.

http://www.webmd.com/cold-and-flu/news/20151125/fda-approves-first-flu-shot-with-added-ingredient-to-boost-immune-response

[6] Richardson A, Galvan V, Linc AL, Oddo S. 2015. How longevity research can lead to therapies for Alzheimer’s disease: The rapamycin story. Experimental Gerontology. 68, 51–58 http://www.sciencedirect.com/science/article/pii/S0531556514003490

[7] Scudellari M. 21 January 2015. Ageing research: Blood to blood. Nature 517 (7535). http://www.nature.com/news/ageing-research-blood-to-blood-1.16762

[8] Wadenov N. November 2, 2011. Purging Cells in Mice Is Found to Combat Aging Ills. New York Times. Based on Darren J. Baker, …, Jan M. van Deursen. 2011, Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders. Nature 479(7372), 232-236.

http://www.nytimes.com/2011/11/03/science/senescent-cells-hasten-aging-but-can-be-purged-mouse-study-suggests.html?_r=0

[9] Yi Zhu et al. 2015. The Achilles’ heel of senescent cells: from transcriptome to senolytic drugs. Aging Cell 14, 644–658.  http://onlinelibrary.wiley.com/doi/10.1111/acel.12344/abstract

[10] Sagiv A, Krizhanovsky V. 2013. Immunosurveillance of senescent cells: the bright side of the senescence program. Biogerontology 14 (6), 617-628 http://link.springer.com/article/10.1007/s10522-013-9473-0

[11] Ledford H. 22 February 2012. Sirtuin protein linked to longevity in mammals. Male mice overproducing the protein sirtuin 6 have an extended lifespan. Nature News. Based on Yariv Kanfi, …, Haim Y. Cohen. 08 March 2012. The sirtuin SIRT6 regulates lifespan in male mice. Nature 483, 218–221. http://www.nature.com/news/sirtuin-protein-linked-to-longevity-in-mammals-1.10074

[12] Maheedhar Kodali, Vipan K. Parihar, Bharathi Hattiangady, Vikas Mishra, Bing Shuai & Ashok K. Shetty. 2015. Resveratrol Prevents Age-Related Memory and Mood Dysfunction with Increased Hippocampal Neurogenesis and Microvasculature, and Reduced Glial Activation. Scientific Reports 5, 8075http://www.nature.com/articles/srep08075

[13] Weintraub K. February 3, 2015. The Anti-Aging Pill. MIT Technology Review.http://www.technologyreview.com/news/534636/the-anti-aging-pill/

[14] Ian F Robey and Natasha K Martin. 2011. Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer. BMC Cancer 11, 235 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3125283/

[15] Jennifer L. Olson, Anthony Atala, and James J. Yoo. 2011. Tissue Engineering: Current Strategies and Future Directions. Chonnam Med J. 47(1), 1–13 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214857/

[16] Giuseppe Orlando, Shay Soker, Robert J. Stratta, and Anthony Atala. 2013. Will Regenerative Medicine Replace Transplantation? Cold Spring Harb Perspect Med.  3(8), a015693 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214857/

[17] New drug triggers tissue regeneration: Faster regrowth and healing of damaged tissues. Science Daily. June 11, 2015. Based on Yongyou Zhang, et al. 2015 June 12. Inhibition of the prostaglandin-degrading enzyme 15-PGDH potentiates tissue regeneration. Science 348(6240), aaa2340 http://www.sciencedaily.com/releases/2015/06/150611144438.htm

[18] Living organ regenerated for first time: Thymus rebuilt in mice. Science Daily. April 8, 2014. Based on N. Bredenkamp N., Nowell C. S., Blackburn C. C. 2014. Regeneration of the aged thymus by a single transcription factor. Development 141 (8), 1627 http://www.sciencedaily.com/releases/2014/04/140408115610.htm

[19] Life-extending hormone bolsters the body’s immune function. Science Daily. January 12, 2016. Based on Yun-Hee Youm, Tamas L. Horvath, David J. Mangelsdorf, Steven A. Kliewer, Vishwa Deep Dixit. 2016. Prolongevity hormone FGF21 protects against immune senescence by delaying age-related thymic involution. Proceedings of the National Academy of Sciences, 201514511 http://www.sciencedaily.com/releases/2016/01/160112093545.htm

[20] Mariela Jaskelioff, …, Ronald A. DePinho. January 6, 2011, first published online on November 28, 2010. Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice. Nature, 469, 102-106. Reported in Ian Sample, November 28, 2010. Harvard scientists reverse the ageing process in mice – now for humans, Guardian  http://www.guardian.co.uk/science/2010/nov/28/scientists-reverse-ageing-mice-humans

[21] Bär C and Blasco MA. 2016. Telomeres and telomerase as therapeutic targets to prevent and treat age-related diseases. F1000Research 2016, 5 (F1000 Faculty Rev):89 (doi:10.12688/f1000research.7020.1)http://f1000research.com/articles/5-89/v1

[22] Erez Eitan, …, Esther Priel. 2012. Novel telomerase-increasing compound in mouse brain delays the onset of amyotrophic lateral sclerosis. EMBO Mol Med. 4(4), 313-329 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3376858/

[23] Skulachev VP, et al. 2009. An attempt to prevent senescence: a mitochondrial approach. Biochimica et Biophysica Acta, 1787(5), 437-61 http://www.sciencedirect.com/science/article/pii/S0005272808007573

[24] Bender E. September 22, 2015. Stopping free radicals at their source. Novartis Institute for Biomedical Research. Based on Adam L. Orr et al. 2015. Suppressors of superoxide production from mitochondrial complex III. Nature Chemical Biology 11(11), 834-836 https://www.nibr.com/stories/discovery/stopping-free-radicals-their-source

[25] Eric A. Schon and Salvatore DiMauro. 2003. Medicinal and Genetic Approaches to the Treatment of Mitochondrial Disease. Current Medicinal Chemistry, 10, 2523-2533 http://homepages.ihug.co.nz/~Smconnell/Medicinal%20and%20Genetic%20Approaches%20to%20Mitochonrial%20Disease.pdf

[26] Could ibuprofen be an anti-aging medicine? Buck Institute. December 11, 2014. Based on Chong He, et al. 2014. Enhanced Longevity by Ibuprofen, Conserved in Multiple Species, Occurs in Yeast through Inhibition of Tryptophan Import. PLoS Genet 10(12): e1004860 http://www.buckinstitute.org/buck-news/could-ibuprofen-be-an-anti-aging-medicine

[27] Michael Karin and Hans Clevers. 21 January 2016. Reparative inflammation takes charge of tissue regeneration. Nature 529, 307–315 http://www.nature.com/nature/journal/v529/n7586/full/nature17039.html

[28] SENS Research Foundation. A Reimagined Research Strategy for Aging. GlycoSENS: Breaking extracellular crosslinks http://www.sens.org/research/introduction-to-sens-research/extracellular-crosslinks

[29] In defense of pathogenic proteins. January 8, 2016. Science Daily. Based on Juha Saarikangas, Yves Barral. 2015. Protein aggregates are associated with replicative aging without compromising protein quality control. eLife, 2015;4 http://www.sciencedaily.com/releases/2016/01/160108083456.htm

[30] Santos J, Leitão-Correia F, Sousa MJ, Leão C. 2016. Dietary Restriction and Nutrient Balance in Aging. Oxid Med Cell Longev. 2016:4010357 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4670908/

[31] Dryden J. September 2, 2015. Drastically cutting calories lowers some risk factors for age-related diseases​​. Healthchannel. Based on Ravussin E, et al. September 2015. A 2-Year Randomized Controlled Trial of Human Caloric Restriction: Feasibility and Effects on Predictors of Health Span and Longevity. Journal of Gerontology: Medical Sciences http://www.healthcanal.com/geriatrics-aging/66558-drastically-cutting-calories-lowers-some-risk-factors-for-age-related-diseases%E2%80%8B%E2%80%8B.html

[32] O’Toole PW, Jeffery IB. 2015. Gut microbiota and aging. Science. 350(6265), 1214-1215 http://science.sciencemag.org/content/350/6265/1214

[33] Ilia Stambler. 2015. Elie Metchnikoff – the founder of longevity science and a founder of modern medicine: In honor of the 170th anniversary. Advances in Gerontology, 28 (2), 207-217, 2015 (Russian) and 5(4), 201-208 (English). http://www.longevityhistory.com/articles/ab15.php

[34] Brunet A, Berger SL. 2014. Epigenetics of aging and aging-related disease. J Gerontol A Biol Sci Med Sci. 69 Suppl 1:S17-20 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022130/

[35] Tarek Baati, …, Fathi Moussa. 2012. The prolongation of the lifespan of rats by repeated oral administration of [60] fullerene. Biomaterials, 33(19), 4936-4946 http://www.sciencedirect.com/science/article/pii/S0142961212003237

[36] Shawn M. Douglas, Ido Bachelet, George M. Church. 17 February 2012. A Logic-Gated Nanorobot for Targeted Transport of Molecular Payloads. Science, 335 (6070), 831-834 http://science.sciencemag.org/content/335/6070/831

[37] Griffiths S. 18 March 2015. Nanorobots trial to begin in humans: Microscopic DNA devices could be injected into a leukaemia patient in a bid to destroy abnormal cells. Daily Mail http://www.dailymail.co.uk/sciencetech/article-3000904/Nanorobots-trial-begin-humans-Microscopic-DNA-devices-injected-leukaemia-patient-bid-destroy-abnormal-cells.html

[38] Kheir JN, et al. 2012 June 27. Oxygen gas-filled microparticles provide intravenous oxygen delivery. Science Translational Medicine, 4(140):140ra88 https://www.researchgate.net/publication/228089270_Oxygen_Gas-Filled_Microparticles_Provide_Intravenous_Oxygen_Delivery

[39] Bellamy R, et al. 1996. Suspended animation for delayed resuscitation. Critical Care Medicine. 24(2 Suppl):S24-47 http://www.ncbi.nlm.nih.gov/pubmed/8608704

[40] Rogatsky GG, Mayevsky A. 2007. The life-saving effect of hyperbaric oxygenation during early-phase severe blunt chest injuries. Undersea Hyperbaric Medicine 34(2), 75-81 http://archive.rubicon-foundation.org/xmlui/bitstream/handle/123456789/6468/17520858.pdf?sequence=1

[41] NIH/National Institute of Biomedical Imaging and Bioengineering. July 30, 2015. Paralyzed men move legs with new non-invasive spinal cord stimulation. Based on Gerasimenko Yury P., et al. December 2015. Noninvasive Reactivation of Motor Descending Control after Paralysis. Journal of Neurotrauma. 32(24), 1968-1980 http://www.eurekalert.org/pub_releases/2015-07/niob-pmm073015.php

[42] Blokh D and Stambler I. 2015. Information theoretical analysis of aging as a risk factor for heart disease. Aging and Disease, 6 (3), 196-207 http://www.aginganddisease.org/EN/10.14336/AD.2014.0623

[43] Georg Fuellen, et al. December 17, 2015. Living Long and Well: Prospects for a Personalized Approach to the Medicine of Ageing. Gerontology https://www.researchgate.net/publication/287212601_Living_Long_and_Well_Prospects_for_a_Personalized_Approach_to_the_Medicine_of_Ageing

[44] Zhavoronkov A and Bhullar B. 2015. Classifying aging as a disease in the context of ICD-11. Frontiers in Genetics 6, 326. doi: 10.3389/fgene.2015.00326 http://journal.frontiersin.org/article/10.3389/fgene.2015.00326/full

[45] Stambler I. January 1, 2016. Recognizing Degenerative Aging as a Treatable Medical Condition – Policy and Methodology. Longevity for All http://www.longevityforall.org/recognizing-degenerative-aging-as-a-treatable-medical-condition-policy-and-methodology/

 

 

Långt liv

Advocacy, Swedish Svenska

Vi jobbar för ett långt friskt liv för alla invånare genom forskning, folkhälsa, och social aktivism. Vi vill betona vikten av att prioritera den vetenskapliga kampen mot den stora fienden till ett långt friskt liv – åldrandeprocessen. Åldrandeprocessen är roten till de flesta kroniska sjukdomar som drabbar jordens befolkning. Denna process orsakar majoriteten av handikapp, sjukdom och lidande, och måste behandlas därefter. Samhället måste lägga sina resurser för att behandla åldrande precis som övriga sjukdomar. Åldrandeproblemet är allvarligt och hotande. Trots detta ser vi ofta ett total likgiltighet till dess realitet och allvar . Det finns en tendens att ignorera framtiden, att distrahera sig från åldrande och död, och även att presentera åldrande och död på ett missvisande, ursäktande och utopiskt synsätt. Samtidigt, finns det en ogrundad tro att åldrandet är en fullständigt ohanterbar, oundviklig process. Denna ignorans av problemet och den ogrundade känslan av vanmakt hjälper inte till med att förbättra hälsan hos de äldre och deras möjligheter till ett långt friskt liv. Det finns ett stort behov av att presentera problemet med dess fulla allvar och vikt och agera för dess lösning med det bästa av vår förmåga. Vi vill öka allmänhetens medvetande kring problemet med åldrande med de följder som det innebär. Vi vill att allmänheten ska erkänna detta allvarliga problem och lägga våra resurser – ekonomiska, socio-politiska, vetenskapliga, teknologiska och media – till mesta möjliga nytta för att hjälpa den åldrande befolkningen, för möjligheten till ett långt friskt liv. Vi hävdar att mental och själslig mognad och förlängningen av ett långt friskt liv inte nödvändigtvis är samma sak som åldrande och försvagning. Vi kämpar för tillämpningen och ökningen av basal och applicerad biomedicinsk forskning, och även utvecklandet av teknologier, industriella, miljömässiga, kring folkhälsoaspekter och utbildningar, speciellt inriktat på ett långt friskt liv,. Om dessa satsningar ges tillräckligt stöd, så kan de öka den friska livslängden hos den åldrande befolkningen, perioden av produktivitet,de äldres bidrag till utvecklingen av samhället och ekonomin, såväl som deras känsla av mening och livskvalite. Vi förespråkar utvecklandet av vetenskapliga metoder för förlänging av det friska livet, och att detta får mesta möjliga genomslag och det politiska stöd som det förtjänar, inte bara av det grupper av experter utan också av den stora allmänheten.

The 21st Century Cures Act

Advocacy, English

The 21st Century Cures Act

Summary:

The 21st Century Cures Act (House Resolution 6) is a bi-partisan proposal  introduced by US Congressman Fred Upton (R-MI) and introduced May 19 2015 and assigned to the House Energy and Commerce Committee chaired by Rep. Upton. Representative Diana DeGette as cosponsor and 230 cosponsors, received a favorable vote of 344 – 77 in the House and on July 13, 2015 was sent to the Senate Committee on Health, Labor and Pensions. It has been called a “breakthrough” in bi-partisan politics by none other than former House Speaker Newt Gingrich, and is designed to streamline medical interventions for cures.

 

What Can Be Done Generally:

Provide bi-weekly updates tracking progress of bill through Senate and Executive Office

 

Support recognition of degenerative aging processes as a medical condition, and as the major underlying factor of all aging-related diseases and conditions (incl. cancer, cardiovascular disease, neurodegenerative disease, pulmonary obstructive disease, type 2 diabetes, frailty) hence subject to diagnosis, development and application of “cures” and therefore an indispensable part of the Act, entitled to participate in all its programs.

 

Use it as a rallying call to enlist top researches of aging (from Buck Institute, Barshop Institute, Albert Einstein College of Medicine, Rochester University, University of North Texas Health Science Center, etc. etc) to support our coalition.

 

Key Point A

The 21st Century Cures Act would establish in the U.S. Treasury an NIH and Cures Innovation Fund endowed with $1.86 billion in mandatory funds per year for FY2016 through FY2020 to be disbursed across the following initiatives: biomedical research, cures development, an accelerating advancement program, high-risk high-payoff research, and special funding support for early career researchers. The fund offers encouragement to researchers seeking assurance that lack of money will not represent a prominent roadblock to advancement of their lines of inquiry.

 

What Can Be Done Specifically:

Connect researchers and fellows to appropriate contact persons overseeing CI Fund.

 

Support dedication of funds to translational aging research within the Cures Innovation Fund.

 

Key Point B

The 21st Century Cures Act authorizes annual increases in NIH’s overall budget from $3.1 billion in 2016 to $3.4 billion by 2018, while directing the agency to target resources, through a “strategic plan,” which it is directed to develop to broaden its mission beyond its stronghold in crucial biomedical research and identify contributions to improving U.S. public health through biomedical research.

 

What Can Be Done Specifically:

Learn how it may be possible to become a part of strategic plan, or how one of the fellows and allies could.

 

Include fundamental and translational research of aging into the “strategic plan” of the NIH.

 

Key Point C

It accepts alternatives to multiphase clinical trials in certain circumstances, and permits accelerated approval pathways for certain classes of drugs such as novel antibiotics. Under the new criteria the agency may consider not only randomized clinical trial data, but also, observational studies, registries and therapeutic use as evidence of efficacy for drug and device approvals.

 

What Can Be Done Specifically:

Create brief to distribute to fellows, allies and labs, to enlighten on new opportunities for bringing their work to market.

 

Support inclusion of trials specifically directed for diagnosis and treatment of degenerative aging processes, as underlying causes of aging-related diseases.

 

Support increased transparency and reproducibility of studies as additional proofs of efficacy and thus additional indications for accelerated approval.

 

Support complementary modes of evidence (e.g. comprehensive in silico modeling or integrative models relating different levels of biological complexity) as additional proofs of efficacy and thus additional indications for accelerated approval.

 

Support international collaboration in the development and distribution of cures against aging-related ill health.

 

Key Point D

Over 250 organizations sent a letter of support to Congress.

 

What Can Be Done Specifically:

Contact the person who organized the sign-ons to that letter (or coalition/alliance org) and ask to sign on, and to connect to their contacts OR just go about forming strategic, PR-based partnerships with the biggest organizations listed.

 

In negotiations with the partners in the Act support coalition, urge them to recognize the importance of degenerative aging processes as the main underlying risk factor and often direct cause of all aging-related non-communicable diseases, and as a strong aggravating factor in communicable infectious diseases – and therefore in need of urgent inclusion into the Act.

 

References:

http://managedhealthcareexecutive.modernmedicine.com/managed-healthcare-executive/news/21st-century-cures-act-five-things-know?page=0,3

The critical need to promote research of aging and aging-related diseases to improve health and longevity of the elderly population. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4306469/

 

Provided by Global Healthspan Policy Institute

 

დღეგრძელობა

Advocacy, Georgian ქართული

  • დღეგრძელობა

    ჩვენ ვიღწვით სრულიად მოსახლეობის ჯანსაღი დღეგრძელობის განვითარებისთვის მეცნიერული კვლევების, ჯანმრთელობის დაცვის, პროპაგანდის და სოციალური აქთიურობების დახმარებით. ჩვენ მკაფიოთ გამოვხატავთ, რომ ჯანსაღი დღეგრძელობის მთავარ მტერს – დაბერებას- გამოვუცხადეთ ბრძოლა!

    დაბერების პროცესი არის ფუძე და ფუძე უმეტესი ქრონიკული დაავადების, რომელიც ადამიანებს ტანჯავს. ის ავსებს ინვალიდობისა და სიკვდილიანობის უდიდეს წილს და მოითხოვს შესაბამის მკურნალობას. ყველამ უნდა გამოვიჩინოთ ძალისხმევა, რომ სიბერის მკურნალობა შესაძლებელი გახდეს ისევე, როგორც სხვა დაავადებები.

    დაბერების პრობლემა თვალსაჩინო საფრთხეა. ამის მიუხედავად ხშირად ვაწყდებით მის მივიწყებას რეალობის და სერიოზულობის მიუხედავად. საზოგადოებაში დამკვიდრებულია მომავლის იგნორირების ტენდენცია რათა ადამიანების გონებამ ყურადღება არ მიაქციოს სიკვდილს და დაბერებას. მეტიც, დაბერება და სიკვდილი უტოპიურ კონტექსტში განიხილება. გავრცელებულია აზრი, რომ “ბუნებრივი” დაბერება სრულიად უმართავია და გარდუვალი. ეს პრობლემაზე თვალების დახუჭვაა. ასეთი უსაფუძვლო უძლურების პოზიცია ხელს არ უწყობს ხანდაზმული ადამიანების მდგომარეობის გაუმჯობესებას და ჯანსაღი დღეგრძელობის მიღწევას. აუცილებლია დაბერების პრობლემის მნიშვნელობის სრული ხარისხით წარმოჩინება და მისი გადაჭრისთვის მოქმედება.

    მოგიწოდებთ სიბერის პრობლემის გათვითცნობიერების ხარისხი გაზარდოთ საზოგადოებაში.. ვაღიაროთ ამ პრობლების სერიოზულობა, არ დავიშუროთ ძალისხმევა და რესურსები – ეკონომიკური, სოციალური, პოლიტიკური, მეცნიერული, ტექნოლოგიური, მასმედიური – იმისთვის, რომ მაქსიმალურად გაიოლდეს ჯანსაღი დღეგრძელობის მიღწევა. ჩვენ ვნერგავთ იდეას, რომ გონებრივი და სულიერი განვითარება, ჯანსაღი დღეგრძელობა არ არის სიბერის და გაუარესების სინონიმები.

    ჩვენ ვაცხადებთ, რომ მხარს ვუჭერთ ფუნდამენტალური და გამოყენებითი ბიომედიცინური კვლევების წარმოებას და მათ დაჩქარებას. ასევე მხარს ვუჭერთ ტექნოლოგიურ, სამეწარმეო, ეკოლოგიურ, ჯანდაცვით, საგანმანათლებლო ღონისძიებებს, რომლებიც მიმართულია ჯანსაღი დღეგრძელობის მისაღწევად. ვთვლით, რომ საკმარისი მხარდაჭერის პირობებში შესაძლებელია ხანდაზმულთა სიცოცხლის გახანგრძლივება, მათი სიცოცხლის ხარისხის შეცლა, რაც საზოგადოების და ეკონომიკის განვითარებას წაადგება და მათ სიამოვნებას მოუტანს, სიცოცხლეს გაუხალისებს და ახალ მიზნებს გაუჩენს.

    ჩვენ ვაცხადებთ, რომ ჯანსაღი დღეგრძელობისთვის მეცნიერული კვლევების განვითარება საჭიროებს მაქსიმალურ საზოგადოებრივ და პოლიტიკურ მხარდაჭერას. ეს პრობლემა იმსახურებს არა მხოლოდ პროფესიულ, არამედ სრულიად საზოგადებრივ ყურადღებას.

     

    See further materials from Georgia Longevity Alliance http://www.longevity.ge/

South Korea – 2007 – The law proposal for the support of scientific and technological research of aging

Advocacy, Korean 한국어

South Korea – 2007 – The law proposal for the support of scientific and technological research of aging

In Korean:

노화과학기술연구촉진법

(Editor’s note: Please see the The Korean original. Corrections for the English translation below are welcome!)

The law proposal to support scientific and technological research of aging includes establishing a main plan and monitoring program for the proposed law (Articles 2 – 5), the creation and support of a scientific and technological research council in the field of aging, and creation and support of a scientific and technological research committee on aging, their structure and administration (Articles 6 – 12), support and supervision for the manufacturing of  new technological products (Article 14), clinical trials and experimental testing (Articles 14, 15), etc.

The law proposal for the support of scientific and technological research of aging

  1. Purpose

The purpose of this law is to provide the basis for the wide support of scientific and technological research of aging, to ensure the effective prioritizing of this research, facilitating the technological development and commercial utilization of its results, as well as the development of methods to improve the health of the nation and the state of the economy.

  1. Definitions

Research of aging, defined under this law, is scientific and technological biomedical research aimed to elucidate the mechanisms of aging with the purpose to achieve healthy and active longevity, prevent and treat age-related diseases due to the aging process, promote active longevity with good functional abilities, strong physical and mental health of the aged. The research of aging involves a multidisciplinary framework of societal, educational, as well as scientific, technological and methodological areas.

  1. Scope

All research of aging must be performed under this Law, except for cases particularly stipulated under other laws containing specific rules.

  1. Responsibilities of the government

(1).  It is the responsibility of the government to establish and actively pursue a main plan for the development and support of research of aging.

(2). All legal entities, such as universities, research institutes, and companies, and individuals involved in research of aging, must cooperate in developing and pursuing the policy and the main plan to support research of aging, in accordance to paragraph 1.

  1. Developing the main plan to support research of aging

(1). The appointed central Administration Agency (Administration Center) for the research of aging within the Ministry of Science and Technology must prepare a document containing the goals and directions for research of aging, as well as a planned annual schedule of research of aging, and a report on the research of aging in the previous year, and must submit it to the Minister of Science and Technology.

(2) The minister, based on the plans provided by the Administration Center as of paragraph 1, must issue the main plan (hereafter “the plan”) for research of aging, which, after adjustments suggested by the appointed Research Council on Aging (as of Article 7 below), must be submitted to the Administration Center. The procedure of changing the main plan is the same.

(3). The plan referred to in paragraph 2 must include:

  1. The long-term and short-term purpose and content of the research on aging;
  2. Ways to attract investors and plans to use funds for research of aging.

iii. An analytic plan for the development and utilization of aging research in terms of education, science, engineering and technology, agriculture, information, environment, fisheries, etc.

  1. A specification of human resources and specialists needed for research of aging and plans for their training and recruitment.
  2. The plan for preserving and utilizing the results of research of aging.
  3. Other necessities and relevant studies needed to support research of aging.
  4. Implementation of the action plan for the support of research of aging

 

(1). Annually, the Administration Center will supervise and report to the Minister of Science and Technology on the implementation of the plan for research of aging.

(2). Head of the Administration Center must discuss in advance with the Minister of Science and Technology regarding measures intended to implement the plan for research of aging.

(3). When necessary, the Minister of Science and Technology may establish basic guidelines for the implementation of the plan via prior consultation with the head of theAdministrationCenter.

(4). The development and implementation of the plan must be approved by a presidential decree.

  1. Council for the support of scientific and technological research of aging

 

(1). For the deliberation on matters pertaining to the support of research of aging, the special advisory Council for the support of research of aging (hereafter “the Council”) shall be established.

(2) The Council shall deliberate on the following matters:

  1. Developing the main plan for the support of research of aging, and the consequent formulation of relevant policies, coordination and supervision of their implementation.
  2. Increasing the budget and investments for long-term technological and scientific research of aging.

iii. Establishing the requirements and developing plans for attracting professional human resources to the research of aging according to specialty, category, fields and projects, formulating the recruitment policy, supervising and adjusting the implementation of the plans.

  1. Developing plans for the preservation and utilization of the results of research of aging, coordination and supervision of their implementation.
  2. Providing additional information regarding resources needed for research of aging, as considered appropriate by the Council head.

(3). The Council shall consist of the head (Chairman) and not more than 20 members.

(4). The chairman of the Council shall be appointed by the Minister of Science and Technology, and shall coordinate between theAdministrationCenter officials, the scientific community (academics, research institutes), and industry professionals.

(5). The Council must include 6 members of academia, 3 representatives of research institutes, and 2 representatives of industry.

(6). The structure and operational requirements for the Council will be established by a Presidential Decree.

  1. Working Committee for the support of scientific and technological research of aging

(1) The Working Committee (“the Committee”) shall be established to conduct practical tasks assigned by the Council and approved by the Minister of Science and Technology.

(2). The Committee shall consist of governmental officials of the Administration Center, members of academia and research institutes, and industry professionals working in research of aging.

(3). The Committee structure and requirements for its effective operation will be established by a Presidential Decree.

  1. Increasing the investment in research of aging

(1) It is the duty of the government, as stipulated in Article 5, paragraph 2 (ii), to support the expansion of investments into research of aging, according to the main plan and the scope of the budget.

(2). The Minister of Science and Technology is responsible for developing the annual investment plan for research of aging and, after consultation with the Council, it must be submitted to the National Science and Technology Council.

  1. Scientific and technological cooperation

The government must promote international cooperation in aging research and related technological development, and attract foreign experts to work in this area.

  1. Promotion of cooperative research and development

The government will actively promote collaborative research projects involving academic and research institutes and industry in order to jointly develop scientific and technological capabilities for the purposes of research of aging.

  1. Support of industrial production

The government will facilitate the manufacturing of new products, created as a result of research of aging.

  1. Collection and dissemination of technical information

The government will collect and widely spread information on research of aging. At the same time, the various agencies involved in this area will be recruited to assist the government in collecting and spreading information on the subject.

  1. Promotion measures for research of aging

To increase the efficiency of research of aging, the relevant ministries will undertake the following measures:

(1). The Minister of Education will support training in the field of research of aging and provide incentives to educators in this field.

(2). The Minister of Science and Technology will be chiefly responsible for developing the Main Plan for the Support of Research of Aging, will direct its design and implementation, collection of resources, facilitation of information exchange and cooperation in the field, development of new related technologies, preservation and utilization of research results in practice, promotion of public access, support and education in the field, assisting agencies involved in research of aging.

(3). Minister of Agriculture will promote the experimental research of aging  related to the development of agriculture, animal husbandry and forestry, and will advance the translation of this research into related technologies followed by their wide application in production.

(4). Minister of Commerce, Industry and Energy Resources will facilitate the creation of new manufacturing processes, engineering applications and industrial deployment of technologies originating in research of aging.

(5). Minister of Information and Communication will develop information and communication technologies for research of aging, promote the dissemination and practical application of the gathered knowledge.

(6). Minister of Health and Welfare will ensure the application of the results of research of aging in health care practice, will support the development and application of biomedical technologies based on this research.

(7). Minister of the Environment will ensure the application of research of aging in the related fields of environmental protection and public health, will contribute to the wide introduction of improved environmental and public health technologies and utilities originating in research of aging.

(8). Minister of Maritime Affairs and Fisheries will promote studies related to research of aging, and facilitate their translation into advanced fishery, seafood and other derived production technologies.

  1. Testing and safety

(1). The government must supervise the manufacturing, testing and safety of products originating from research of aging.

(2). The criteria for effective testing and safety will be determined by a Presidential Decree.

  1. Procedures for planning and conducting experiments

(1). To promote the scientific research and industrial production in the area of aging research, the government must develop procedures for planning and conducting experiments.

(2). In accordance to paragraph (1), guidelines must be established to ensure biological safety, prevention of adverse effects, and avoidance of ethical problems that may arise as a result of scientific research and industrial production originating from research of aging.

  1. Establishment of research institutes.

(1). In order to support research of aging, as well as utilize its results in scientific, technological and industrial development, special institutes for research of aging will be established that will work in close cooperation with industry. The government will supervise and support the establishment of such research institutes.

(2). The special research institutes established in accordance with paragraph (1) shall operate under the provisions of this Law.

Note: This Law will enter into force from the date of its publication.

 

Degenerative Aging as a Medical Condition

Advocacy, English

whologo Degenerative Aging as a Medical Condition

By Ilia Stambler, PhD

Summary of issue: There has been recently an intensifying discussion among longevity researchers and advocates about the inclusion of the Degenerative Aging Process as a recognized and treatable medical condition, that would include the systemic factors that contribute to diseases and frailty.

The underlying, apparently plausible rationale for this suggestion is that the recognition of degenerative aging as a treatable medical condition would enable the existing legal frameworks to better tackle diseases and conditions that arise from the aging process from a preventative healthcare model. In particular, pharmaceutical, biomedical and wellness industry could then develop for market quickly new and existing preventative medications, biomedical technologies and regimens, that would decrease long-term healthcare costs. Moreover, such a recognition would open up new public funding for new pharmaceutical and biomedical research and development

What can be done generally:

Degenerative aging needs to be recognized as a diagnosable and treatable medical condition, starting with the appropriate WHO frameworks, setting the global standards for disease definitions. Yet, the methods of achieving this recognition with the WHO framework may vary.

This issue must become a subject of massive and pluralistic consultation of scientists and other stakeholders. An initial deliverable could be a collection of papers and expert opinions dedicated to the subject. With this evidential and expert basis and publication, it may be expedient to develop more precise policy recommendations and approaches for further consultation with the relevant WHO departments and affiliates, such as the Global Burden of Disease (GBD) program, the WHO Multi-Country Studies Unit, the WHO Collaborating Centre on International Longitudinal Studies of Gender, Ageing and Health, the developers of the ICD and ICF, WHO Department of Aging and Lifecourse, in particular the GSAP, WHO Program on Non-communicable Diseases and their Risk Factors, UN NGO Committee on Aging, UN Department of Economic and Social Affairs – Division for Social Policy and Development, implementation agencies of the UN Sustained Development Goals (esp. SDG3 on healthcare)  and other relevant authorities.

http://www.who.int/entity/en/

 

 

Local heterogeneity of basal cells of the epidermis

Russian Русский, Science

Alexander Khalyavkin

—

Local heterogeneity of basal cells of the epidermis

 

Izvestia Akademii Nauk SSSR. Seria Biologicheskaya. 5, 778-780, 1982.

 

(Bulletin of the USSR Academy of Sciences. Biology Series. Vol. 5, pp. 778-780, 1982)

 

Alexander Khalyavkin

In Russian: Локалная гетерогенность базальных клеток эпидермиса.

Khalyavkin Local Heterogeneity of Basal Epidermis Cells 82 5

 

 

Abstract:

We have critically analyzed the concept that posits local heterogeneity of basal cells of the epidermis, namely their separation into stem cells and cells that started differentiation. We show that the experimental data on which this concept is based, can be interpreted within the framework of the classical scheme of keratinocyte histogenesis, according to which all basal cells are stem cells and their heterogeneity with reference to several attributes can be related to their different stages within the cell cycle.

 

—

A series of experimental data, obtained within the last years, indicated the presence of two different types of cells within the population of the basal cells of the epidermis, namely basal stem cells and basal cells committed to differentiation, which differ in their ability for proliferation and differentiation (Potten, Hendry, 1973; Krieg et al., 1974; Marks, 1976; Potten et al., 1979; Potten, 1981). The present article analyzes the justification for this concept which is proposed on the basis of experiments studying clonogenic properties of basal cells and their sensitivity to the effect of G1-Chalone (Potten, Hendry, 1973; Marks, 1976).

 

In radio-biological experiments studying clonogenicity of basal cells in the epidermis of irradiated animals, there was registered the number of colonies formed after certain times following different doses of radiation exposure. Under low doses, there were many surviving cells, the colonies merged and their number was impossible to determine. Therefore the initial number of clonogenic cells was estimated indirectly by extrapolating the data obtained to zero radiation dose, while taking into account the possibility of an initial shoulder in the dose-effect relation. The number of clonogenic basal cells, estimated this way, was much less than the general number of basal cells. This led to the hypothesis that only a part of basal cells are clonogenic stem cells, while the rest are their more differentiated progeny (Potten, Hendry, 1973). This concept was developed in the works studying the effects of exposure of basal cells to the endogenous tissue-specific inhibitor of proliferation – the epidermal G1-Chalone (Krieg et al., 1974, Marks, 1976). These experiments showed that the actively proliferating epidermis (neonatal skin, regenerating skin and skin subjected to tumor promoters) demonstrates reduced sensitivity to G1-Chalone as compared to normal adult epidermis. Within the framework of the concept under consideration, this was explained by suggesting that the basal cells of actively proliferating epidermis contain a larger proportion of stem cells presumably insensitive to the effect of G1-Chalone (Krieg, et al., 1974; Marks, 1976).

 

Thus, based on the different sensitivity to the influence of G1-Chalone and based on experiments studying colony formation in epidermis of irradiated animals, a concept was advanced suggesting the attribution of basal cells to two populations: stem cells-progenitors and their progeny committed to differentiation (Potten, Hendry, 1973; Marks, 1976). This means that, instead of the known histogenic series of stages of keratinocyte maturation (the basal cell → spinous cell → granular cell, etc.), the following modification of this scheme is proposed: the basal stem cell → the basal cell that started differentiation → spinous cell → granular cell, etc. This modified scheme is further supported by the data regarding colony formation of epidermal cells in culture. It is known that the number of colonies formed is much less than the number of seeded basal cells (Rheinwald, Green, 1977). This also seems to indicate that not all basal cells are clonogenic stem cells.

 

However, it is possible that the observed differences in the properties of basal cells are the results of other causes, namely the heterogeneity of their positioning within the cell cycle.

 

It is known that a part of basal cells is outside the mitotic cycle (Fukuda et al. 1978). This state is termed “proliferative rest” i.e. Phase G0 (Lajtha, 1963) or Phase R1 (Epifanova, Terskikh, 1968; Terskich, 1973). The rest of the cells undergo different stages of the mitotic cycle. Insofar as the resting cells are more resistant to external influences than the proliferating cells (Terskich, 1973), the dependence of the number of colonies formed on high doses of irradiation can reflect the radio-sensitivity of resting basal cells. Therefore the extrapolation of this dependence to the zero dose, taking into account the initial shoulder, gives the value equal to the number of basal cells that are found outside the mitotic cycle. Clearly, their number should be less than the general number of basal cells. This can also explain the different ability of basal cells for colony formation in culture. It is assumed that the signal for the transition of basal cells to the path of irreversible differentiation is their detachment from the dermo-epidermal boundary (Flaxman 1972). Therefore, when preparing their reseeding into culture, basal cells are detached from dermal substrate, a part of them, found in G0 state, begin irreversible differentiation and are unable to form colonies. The rest of the cells, found in the mitotic cycle, before transition to differentiation, must complete it. However, during the time of the cycle, their majority gets to precipitate in the culture vessel, attach to the appropriate substrate and therefore is able to form colonies. Hence, an increase of the time interval between the detachment of basal cells form dermal substrate and their placement in the culture on the feeder fibroblast layer, leads to a reduction in the number of colonies formed, while an increase of the proportion of proliferating cells of the epidermis raises this number (Rheinwald, Green, 1977).

 

In order to explain the mechanism of cell transition to the state of proliferative rest, it was suggested that the cells are affected by tissue-specific inhibitors of the mitotic cycle (Bullough, 1963, Lajtha, 1969). The cells can reside in the resting state for a prolonged time and enter the mitotic cycle under the influence of an inductive stimulus (Lajtha, 1969; Smith, Martin, 1973). It is assumed that at any time, under constant conditions, the mitotic cycle is entered by the same proportion of the remaining resting cells (Smith, Martin, 1973). Apparently, the proliferation starts in cells in which the stimulating signal prevails over the inhibiting signal. If assuming that the stationary distribution of resting cells according to the inhibiting signal value, created by the chalones, is nearly Gaussian bell-shaped curve, then the proportion of cells entering the mitotic cycle under the inductive stimulus will be determined by the area beneath the distribution curve, limited on the right by the inhibiting signal value, equal to the stimulating signal value (the inductive stimulus). The addition of chalones will shift the distribution to the right, hence the proportion of cells entering the cycle will diminish. The ratio of the proportion of cells entering the mitotic cycle after the addition of chalones to the proportion of cells entering the cycle without the addition of the chalone, reflects its inhibiting action. The lower this ratio, the more expressed is the chalone’s inhibiting action. These considerations explain why the inhibiting activity of the chalones is better expressed in a cell population subjected to the influence of a small inductive stimulus. Therefore there is no need to adduce the hypothesis about the larger proportion of stem cells presumably insensitive to the effect of chalones, in an actively proliferating population of basal cells. Also the very suggestion about the insensitivity of stem cells to chalones is quite vulnerable (Krieg et al. 1974; Marks 1976).

 

Thus the present analysis allows us to conclude that, despite the attraction of the concept that only a part of basal cells are stem cells, it would be premature to accept it as a final conclusion. This is because the experimental facts, lying at the foundation of that concept, can be explained by the heterogeneity of basal cells with reference to their position in the cell cycle.

 

In conclusion, we would like to note that the study of colony formation in a culture of epidermal cells, obtained from irradiated animals, would allow the evaluation of the real character of the dose-effect dependence under low irradiation doses. This could serve as one of the proofs or refutations for the correctness of the concept under consideration.

 

 

References:

 

Епифанова О.И., Терских В.В. Периоды покоя и активной пролиферации в жизненном цикле клетки. – Ж. Общ. Биол. 1968б т. 29. № 4, с. 392. (Epifanova O.I. Terskich V.V. Period of Rest and active proliferation in cell life cycle. Journal of General Biology – in Russian, vol. 29, no. 4, p. 392, 1968).

Терских В.В. Периоды покоя в нормальных и малигнизированных клетках. – В кн. Клеточный цикл. М. Наука 1973, с. 165. (Terskich V.V. Periods of rest in normal and malignant cells, in Cell Cycle, Nauka, Moscow, 1973, p. 165).

Bullough W.S. Analysis of the life cycle in mammalian cells. – Nature, 1963, v. 199, No. 4896, p. 859.

Flaxman B.A. Replication and differentiation in vitro of epidermal cells from normal skin and from benign (psoriasis) and malignant (basal cell cancer) hyperplasia. – In Vitro, 1972, v. 8, No. 3, p. 327.

Furuda M., Okamura K, Fujita S, Bohm M, Rohbach R, Sandritter W. The different stem cell populations in mouse epidermis and lingual epithelium. – Path. Res. Pract., 1978, v. 163, No. 3, p. 205.

Krieg L, Kuhlmann I, Marks F. Effect of tumor-promoting phorbol esters and acetic acid on mechanisms controlling DNA synthesis and mitosis (chalones) and on the biosynthesis of histidine-rich protein in mouse epidermis. – Cancer Res. 1974, v. 34, No. 11, p. 3135.

Lajtha L.G. On the concept of the cell cycle. – J. Cell Compar. Physiol., 1963, v. 60, No. 2, Suppl. 1, p. 143.

Lajtha L.G. Kinetic models of hemopoietic stem cell population. – Hemic cells in vitro, 1969, v. 4, p. 14.

Marks F. Epidermal growth control mechanisms hyperplasia, and tumor promotion in the skin. – Cancer Res. 1976, v. 36, No. 7, part 2, p. 2636.

Potten C. S. Cell replacement in epidermis (keratopoiesis) via discrete units of proliferativation. – Int. Ev. Cyt. 1981, v. 69, p. 271.

Potten C.S., Hendry J.H. Clonogenic cells and stem cells in epidermis. – Intern. J. Radiat. Biol, 1973, v. 24, No. 5, p. 537.

Potten C.S. Schofield R, Lajtha L.G. A comparison of cell replacement in bone marrow, testis and three regions of surface epithelium. – Biochem. Biophys. Acta, 1979, v. 560, No. 2, p. 281.

Rheinwald J.G. Green H. Epidermal growth factor and the multiplication of cultured human epidermal keratinocytes. – Nature, 1977, v. 265, No. 5593, p. 421.

Smith J.A., Martin L. Do cell cycle? – Proc Natl. Acad. Sci. USA, 1973, v. 70, No. 4, p. 1236.

 

Institute of Chemical Physical – The USSR Academy of Sciences, Moscow

 

Arrived to the editorial office

3.XI.1981

 

Khyalyavkin A.V.

The local heterogeneity of the basal cells of epidermis

 

Institute of Chemical Physics, Academy of Sciences of the USSR, Moscow

 

The critical analysis of the concept, postulating the subdivision of the basal cells of the epidermis into the stem cells and the cells at the beginning of the differentiation is given. It was shown that the experimental data, providing the basis of the concept, can be interpreted within the limits of the classical scheme of keratinocyte’s histogenesis, according to which all basal cells are know as stem cells, but their heterogeneity in a number of properties can be related with the different place in the cellular cycle. The experiment, the results of which can be used as the argument in favor of one of the alternative concepts, is suggested.

 

 

In Russian:

Локалная гетерогенность базальных клеток эпидермиса.

Khalyavkin Local Heterogeneity of Basal Epidermis Cells 82 5

 

УДК 576.321.34

Халявкин А.В.

Локальная гетерогенность базальных клеток эпидермиса.

 

Проведен критический анализ концепции, постулирующей локальную гетерогенность базальных клеток эпидермиса, которая заключается в подразделении их на стволовые клетки и клетки, приступившие к дифференцировке. Показано, что экспериментальные данные, лежащие в основе этой концепции, могут быть интерпретированы в рамках классической схемы гистогенеза кератиноцита, согласно которой все базальные клетки являются стволовыми, а их гетерогенность по ряду свойств может быть связаны с различным положением в клеточном цикле.

 

Ряд экспериментальных данных, полученных в последние годы, привел к представлении о наличии в популяции базальных клеток эпидермиса двух различных типов клеток – стволовых базальных клеток и коммтированных к дифференцировке (Potten, Hendry, 1973; Krieg et al. 1974; Makrs, 1976; Potten et al. 1979; Potten 1981). В настоящем сообщении анализируется обоснованность этой концепции, высказанной на основе экспериментов по изучению клоногенных свойств базальных клеток и их чувствительности к действию G1-кейлона (Potten, Hendry, 1973; Marks, 1976).

 

В радиобиологических экспериментах по изучению клоногенности базальных клеток в эпидермисе облученных животных регистрировалось число колоний, образовавшихся спустя определенное время после действия разных доз облучения. При низких дозах выживших клеток было много, колонии сливались, и их количество определить было невозможно. Поэтому начальное число клоногенных клеток оценивалось косвенно экстраполяцией полученных данных к нулевой дозе облучения с учетом возможного начального плеча на зависимости доза – эффект. Оцененное таким образом число клоногенных базальных клеток оказалось гораздо меньше общего числа базальных клеток. Это дало повод предположить, что только часть базальных клеток является стволовыми (Potten, Hendry, 1973). Данная концепция получила развитие в работах по изучению действия на базальные клетки эндогенного тканеспецифического ингибитора пролиферации – эпидермального G1-кейлона (Krieg et al., 1974, Marks, 1976). В этих опытах было показано, что активно пролиферирующий эпидермис (неонатальная кожа, регенерирующая кожа и кожа, находящаяся под воздействием опухолевого промотера) проявляет пониженную чувствительность к действую G1-кейлона в сравнении с нормальным эпидермисом взрослого. В рамках рассматриваемой концепции это объяснялось тем, что базальные клетки активно пролиферирующего эпидермиса содержат большую долю стволовых клеток, предположительно нечувствительных к действию G1-кейлона (Krieg et al., 1974, Marks, 1976).

 

Таким образом, на основании различной чувствительности к действию G1-кейлона и на основании экспериментов по изучению колониеобрзования в эпидермисе облученных животных была выдвинута концепция о принадлежности базальных клеток к двум популяциям: стволовых клеток-предшественников и их потомков, коммитированных к дифференцировке (Potten, Hendry, 1973 Marks, 1976). Это означает, что вместо известного гистогенетического ряда стадий созревания кератиноцита (базальная клетка ->шиповатая->зернистая и т.д) предполагается следующая модификация этой схемы: базальная стволовая клетка –< базальная клетка, приступившая к дифференцировке –> шиповатая –> зернистая и т.д. В пользу такой модифицированной схемы можно привести и данный по колониеобразованию эпидермальных клеток в культуре. Известно, что число образуемых колоний гораздо меньше числа высеваемых базальных клеток (Rheinwald, Green, 1977). Это как будто бы тоже говорит за то, что не все базальные клетки являются стволовыми клоногенными клетками.

Однако возможно, что наблюдаемые различия в свойствах базальных клеток являются следствием других причин, а именно гетерогенность по положению в клеточном цикле.

Известно, что часть базальных клеток находится вне митотического цикла (Fukuda et al, 1978). Это состояние называется пролиферативным покоем, фазой G0 (Lajtha, 1963) или фазой R1 (Епифанова, Терских, 1968; Терских, 1973). Остальные клетки проходят различные стадии митотического цикла. Поскольку покоящиеся клетки более резистентны к внешним воздействиям, чем пролифирирующие (Терских, 1973), зависмость числа образованных колоний от высоких доз облучения может отражать радиочувствительность покоящихся базальных клеток. Поэтому экстраполяция этой зависимости к нулевой дозе с учетом начального плеча даст величину, равную числу базальных клеток, находящихся вне митотического цикла. Ясно, что их число должно быть меньше общего числа базальных клеток. Этим же можно объяснить и различную способность базальных клеток к колониеобразованию в культуре. Считается, что сигналом для перехода базальных клеток на пусть необратимой дифференцировки является их отрыв от дермо-эпидермальной границы (Flaxman, 1972). Поэтому, когда для подготовки к пересеву их в культуру базальные клетки отделяются от дермальной подложки, часть из них, находящаяся в состоянии G0, начинает необратимую дифференцировку и не способна образовывать колонии. Остальные клетки, находящиеся в митотическом цикле, до перехода в дифференцировку должны завершить его. Однако за время прохождения цикла большинство из них успевает осесть в сосуде для культивирования, закрепиться на соответствующем субстрате и поэтому способно образовывать колонии. Таким образом, увеличение интервала времени между отделением базальных клеток от дермальной подложки и помещением их в культуру на фидерный слой фибробластов приводит к уменьшению количества образуемых колоний, а повышение доли пролиферирующих клеток эпидермиса увеличивает это количество (Rheiwald, Green, 1977).

 

Для объяснения механизма перехода клеток в состоянии пролиферативного покоя было предложено, что на клетки действуют тканеспецифические ингибиторы митотического цикла (Bullough, 1963; Lajtha, 1969). Клетки могут находиться в периоде покоя длительное время и вступать в митотический цикл под влиянием индуктивного стимула (Lajtha, 1969; Smith, Martin, 1973). Считается, что каждый момент времени при постоянных условиях в митотический цикл вступает одна и та же доля оставшихся покоящихся клеток (Smith, Martin, 1973). Видимо, начинают пролиферацию те из них, у которых стимулирующий сигнал превалирует над ингибирующим. Если предположить, что стационарное распределение покоящихся клеток по величине ингибирующего сигнала, создаваемого кейлоном, близко к колоколообразной кривой, то доля клеток, вступающих в митотический цикл под воздействием индуктивного стимула, определится площадью под кривой распределения, ограниченной справа величиной ингибирующего сигнала, равной величине стимулирующего сигнала (индуктивного стимула). Добавление кейлона сместит распределение вправо, поэтому доля клеток, входящих в цикл, уменьшится. Отношение доли клеток, входящих в митотический цикл после добавления кейлона к доле клеток, входящих в митотический цикл после добавления кейлона к доле клеток, входящих в цикл без добавления кейлона, отражает его ингибирующее действие. Чем это отношение ниже, тем ингибирующее действие кейлона выражено больше. Из этих рассуждений видно, почему ингибирующая активность кейлона лучше проявляется в популяции клеток, находящихся под воздействием небольшого индуктивного стимула. Поэтому нет никакой необходимости привлекать гипотезу о большей доле стволовых клеток, предположительно не чувствительных к действию кейлона, в активно пролиферирующей популяции базальных клеток. Достаточно уязвимо и само предположение о нечувствительности стволовых клеток к кейлону (Krieg et al., 1974; Marks, 1976).

 

Таким образом, проведенный анализ позволяет заключить, что, несмотря на привлекательность концепции о том, что только часть базальных клеток является стволовыми, окончательность такого вывода была бы преждевременной. То следует из того, что экспериментальные факты, на которых построена данная концепция, могут объясняться гетерогенностью базальных клеток по их положению в клеточном цикле.

 

В заключение отметим, что изучение колониеобразования в культуре эпидермальных клеток, взятых от облученных животных, позволило бы судить об истинном характере зависимости доза – эффект в области низких доз облучения. Это могло послужить одним из доказательств или опровержения справедливости рассматриваемой концепции.

 

Литература

Епифанова О.И., Терских В.В. Периоды покоя и активной пролиферации в жизненном цикле клетки. – Ж. Общ. Биол. 1968б т. 29. № 4, с. 392.

Терских В.В. Периоды покоя в нормальных и малигнизированных клетках. – В кн. Клеточный цикл. М. Наука 1973, с. 165.

Bullough W.S. Analysis of the life cycle in mammalian cells. – Nature, 1963, v. 199, No. 4896, p. 859.

Flaxman B.A. Replication and differentiation in vitro of epidermal cells from normal skin and from benign (psoriasis) and malignant (basal cell cancer) hyperplasia. – In Vitro, 1972, v. 8, No. 3, p. 327.

Furuda M., Okamura K, Fujita S, Bohm M, Rohbach R, Sandritter W. The different stem cell populations in mouse epidermis and lingual epithelium. – Path. Res. Pract., 1978, v. 163, No. 3, p. 205.

Krieg L, Kuhlmann I, Marks F. Effect of tumor-promoting phorbol esters and acetic acid on mechanisms controlling DNA synthesis and mitosis (chalones) and on the biosynthesis of histidine-rich protein in mouse epidermis. – Cancer Res. 1974, v. 34, No. 11, p. 3135.

Lajtha L.G. On the concept of the cell cycle. – J. Cell Compar. Physiol., 1963, v. 60, No. 2, Suppl. 1, p. 143.

Lajtha L.G. Kinetic models of hemopoietic stem cell population. – Hemic cells in vitro, 1969, v. 4, p. 14.

Marks F. Epidermal growth control mechanisms hyperplasia, and tumor promotion in the skin. – Cancer Res. 1976, v. 36, No. 7, part 2, p. 2636.

Potten C. S. Cell replacement in epidermis (keratopoiesis) via discrete units of proliferativation. – Int. Ev. Cyt. 1981, v. 69, p. 271.

Potten C.S., Hendry J.H. Clonogenic cells and stem cells in epidermis. – Intern. J. Radiat. Biol, 1973, v. 24, No. 5, p. 537.

Potten C.S. Schofield R, Lajtha L.G. A comparison of cell replacement in bone marrow, testis and three regions of surface epithelium. – Biochem. Biophys. Acta, 1979, v. 560, No. 2, p. 281.

Rheinwald J.G. Green H. Epidermal growth factor and the multiplication of cultured human epidermal keratinocytes. – Nature, 1977, v. 265, No. 5593, p. 421.

Smith J.A., Martin L. Do cell cycle? – Proc Natl. Acad. Sci. USA, 1973, v. 70, No. 4, p. 1236.

 

Институт химической физики АН СССР

Москва

 

Поступила в редакцию

3.XI.1981

 

Khyalyavkin A.V.

The local heterogeneity of the basal cells of epidermis

 

Institute of Chemical Physics, Academy of Sciences of the USSR, Moscow

 

The critical analysis of the concept, postulating the subdivision of the basal cells of the epidermis into the stem cells and the cells at the beginning of the differentiation is given. It was shown that the experimental data, providing the basis of the concept, can be interpreted within the limits of the classical scheme of keratinocyte’s histogenesis, according to which all basal cells are know as stem cells, but their heterogeneity in a number of properties can be related with the different place in the cellular cycle. The experiment, the results of which can be used as the argument in favor of one of the alternative concepts, is suggested.

 

 

Локалная гетерогенность базальных клеток эпидермиса.

Khalyavkin Local Heterogeneity of Basal Epidermis Cells 82 5

 

—–

Epidermal homeostasis and the problem of psoriasis

 

Izvestia Akademii Nauk SSSR. Seria Biologicheskaya. 1, 156-159, 1982.

 

(Bulletin of the USSR Academy of Sciences. Biology Series. Vol. 1, pp. 156-159, 1982)

 

Alexander Khalyavkin

In Russian: Эпидермальный Гомеостаз и Проблема Псориаза

Khalyavkin Epidermal Homeostasis 82 1

 

 

Abstract

We consider a qualitative model of epidermal homeostasis, based on literature data. It is assumed that heterogeneous mitotic activity of the basal layer is responsible for the wave-like form of the dermo-epidermal boundary and is related to the specifics of the position of sub-epidermal lymphatic capillaries. We consider the conditions under which an increase of mitotic activity leads to an abnormally high transition of cells to differentiation, but only in some zones of the basal layer. We show that such an imbalance of cell streams can lead to the main histological signs of psoriasis, namely acanthosis, papillomatosis and parakeratosis.

 

—

Psoriasis is a widespread chronic disease of the skin with uncertain etiology and pathogenesis (Mordovzev, 1977; Skripkin, 1980; Flaxman et al. 1979 and others). The main signs of the disease are increased squamous appearance of the surface layers of the epidermis and their immaturity (parakeratosis), the anomalously high mitotic activity of the keratinocytes, the elongation of epidermal outgrowths accompanied by in-growth into the epidermis of dermal papillae along with thinning of the above-papillae areas of the epidermis (acanthosis and papillomatosis) and some others. The existing methods of therapy do to produce a lasting effect. The absence of an analogous disease in animals is a serious drawback for the experimental study of this pathology. The matter is further complicated by the fact that the epidermal homeostasis itself, whose impairment is assumed in psoriasis, has not been studied sufficiently (Mikhailv 1979, Skerrow1978). Therefore the current work makes an attempt to consider, based on the exiting data and concepts, a qualitative model of epidermal homeostasis and its impairment, possibly leading to psoriasis.

 

The surface of normal epidermis is the cornea, the end product of the skin epithelium differentiation. During the life course, the cells of the upper layers of the cornea are gradually shed and gradually replaced by mature cells from lower differentiating layers. These, in turn, are replaced by cells of the basal layer making a transition toward differentiation. The replenishment of the population of basal stem cells takes place thanks to their proliferation.

 

The profile of the epidermis at the border with the dermis is a wave-like line. The degree of undulation in different parts of the skin varies greatly, in correlation with the thickness of the epidermis and mitotic activity (Bullough, Deol, 1975). The proliferative activity of the basal layer is maximal at the basis of epidermal outgrowths. At a greater distance from these zones, the activity gradually decreases, reaching the minimal values at the basal cells, found above the dermal papillae (Flaxman, 1972; Fukuda et al. 1978). The reason for this is unknown. Possibly, the proliferative zones concentrate clonogenic cells, whose existence was hypothesized by Potten (Potten, Hendry, 1973), or non-committed stem cells insensitive to the action of G1-Chalone, posited by Marks (Marks 1976). It was also suggested that the localization of proliferative and non-proliferative zones is related to the specific location of blood vessels in the underlying derma (Fukuda et al. 1978). However, apparently, the heterogeneous mitotic activity of the basal layer is not related to the underlying blood vascular net. This follows from the fact that the sub-epidermal plexus of blood capillaries repeats the contours of the dermo-epidermal boundary. In contrast to blood capillaries, the blind outgrowths of lymphatic capillaries reach only to the basis of epidermal outgrowths (Nadezhdin, 1951). Therefore the humoral factors, found in the lymphatic vessels, unlike mitogens carried by the blood stream, can stimulate the proliferation of basal cells located mainly in the immediate proximity of the expanded ends of lymphatic capillaries. Perhaps this is what causes the heterogeneous mitotic activity of the basal layer. The presumed mitogens circulating in the lymphatic system may be the hypothetical “mesenchymal factor” (Bullough, Deol, 1975) or normal anti-tissue antibodies which are dedicated to tissue-specific stimulation of proliferation, according to several authors (Piatnizky, Makhlin, 1969, Babaeva, 1972; Khalyavkin 1975; Burwell, 1963). Healthy persons show the presence of normal anti-epidermal auto-antibodies, while psoriasis patients show their increased amounts (Beutner et al. 1977; Krogh, 1977). Even though in these and other studies, the main focus is on auto-antibodies to the surface layer of the epidermis, Krogh does not exclude the possibility that increased amounts of auto-antibodies to the growth layer can be the cause of its enhanced proliferation as observed in psoriasis (Krogh, 1977). It should be noted that for the first time such a concept was expressed in a theoretical work dedicated to the problem of psoriasis, already in 1965 (Burch, Rowell, 1965). In any case, whatever the actual cause for the heterogeneous mitotic activity of the basal cells, found in different locations of the dermo-epidermal boundary, it can also be the cause for the wave-like appearance of this boundary. Indeed, normally the speed of migration for cells transiting to differentiation from various locations of the basal layer should be balanced in such a way that such cells should reach the skin surface simultaneously. The mechanism of cell migration into the upper layers of the epidermis is little known (Skerrow, 1978). It may be assumed that the probability of transition to differentiation and therefore the starting speed of migration depend on dermo-epidermal adhesion and local inter-cellular pressure, created by mitotic activity (Iversen et al. 1968; Bullough, Deol, 1975). It is assumed that the dermo-epidermal adhesion is maximal for the basal cells found in the mitotic cycle, and minimal for the cells found in late G1 phase (apparently in G0 phase), therefore it is those cells that are most easily pushed toward differentiation (Iversen et al, 1968; Bullough, Deol, 1975). Therefore, for basal cells found in G0 phase, the probability to transit to differentiation and the starting speed of migration is the highest in places of maximal mitotic activity. When distancing from such places, the initial speeds of migration should decrease. Possibly, this is why the profile of the dermo-epidermal boundary is so convoluted that cells migrating upward with different average speed pass different distances, so that during the differentiation time Td they should reach about the same plane, which is the lower boundary of the cornea layer. An increase of average mitotic activity should and normally does lead to a more or less proportional increase of the maximal and minimal speeds of migration, and therefore to the thickening of the epidermis and greater convolution of the dermo-epidermal boundary. A significant increase in the average mitotic activity can result in a situation when the force of inter-cellular pressure, acting on the basal cells located at the basis of epidermal outgrowths, will exceed the maximal force of adhesion of cells with the underlying derma. Then the basal cells, found in the mitotic cycle and located in places of maximal inter-cellular pressure, under its effect will be either completely expelled toward differentiation, or more likely will change their orientation. The change of orientation can lead to the transformation of “horizontal” symmetrical mitoses into asymmetrical “vertical” ones, whose percentage increase under increased proliferation has been noted in the literature (Pinkus, Hunger, 1966; Duffill et al. 1977; Bullough, Mitrani, 1978). The proportional increase of the maximal and minimal speeds of migration implies a coordination of the action of two sub-epidermal humoral systems – the lymphatic and the blood systems. If there is no such coordination for some reason, there may emerge a situation when rapid increase of mitotic activity of basal cells located at the basis of epidermal outgrowths will not be accompanied by a proportional increase of this activity in basal cells located above the dermal papillae. This will lead to a disproportional elongation of epidermal outgrowths (acanthosis and papillomatosis). Such an elongation of outgrowths also means the increase of its basal cells. Since in this case this increase cannot take place at the expense of replication of cells found in the zones of maximal proliferation, where mitoses are asymmetrical, then it proceeds at the expense of cells in other zones. This should lead to a decline of transition to differentiation from these zones, and therefore to a shortening of the thickness of epidermis above the dermal papillae, exacerbating papillomatosis. Acanthosis and papillomatosis are the main histological signs of psoriasis alongside with parakeratosis or the immaturity of the surface layer. It is possible that parakeratosis is also the result of imbalance of cellular streams – a drastic increase of the maximal migration without a proportional increase of the minimal speed. Indeed, despite the significant elongation of epidermal outgrowths, the speed of migration is so large that the lower boundary of the cornea layer, formed above dermal papillae (Flaxman 1972), is reached by cells that transited to differentiation from the bottom of the epidermal outgrowth at a time significantly smaller than Td. During that time, judging form morphological and biochemical data, they do not mature even to the stage of granular cells. The increased amount of auto-antibodies to the surface layer of the epidermis, observed in psoriasis, according to some authors (Beutner et al. 1977; Krogh, 1977) facilitates the stratification of this immature layer, which normally has quite strong inter-cellular adhesion (Skerrow, 1978).

 

In the early stages of ontogenesis, when the biosynthesis of antibodies is still low, and the blind outgrowths of the lymphatic capillaries are not pronounced (Nadezhdin, 1951), the leading role in the control of proliferation may be played by humoral factors carried by the blood stream and equally available for all basal cells. Therefore the mitoses are distributed quite homogeneously, which can explain the smooth profile of epidermis in the new born and the low incidence of psoriasis at this age.

 

Thus, the present literature analysis allows us to conclude that the lack of coordination of sub-epidermal humoral systems accompanied by increased mitotic activity of keratinocytes can lead to an impairment of epidermal homeostasis and the emergence of the main signs of psoriasis.

 

References

 

Бабаева А. Г. Иммунологические механизмы регуляции восстановительных процессов. М. Медицина. 1972. 158 с. Babaeva A.G. Immunological mechanisms of regulation of repair processes. Moscow. Medicine, 1972 (in Russian)

 

Михайлов И. Н. Структура и функция эпидермиса. М. Медицина. 1979. 239 с. Mikhailov I.N. Structure and function of epidermis. Moscow. Medicine. 1979 (in Russian)

 

Мордовцев В. Н. Роль наследственных факторов при псориазе. Автореферат диссертации на соискание ученой степени доктора медицинских наук.. Москва. Центральный научно-исследовательский Кожно-венерологически институт. 1977. 35 с. Mordovzev V. N. The role of hereditary factors in psoriasis. PhD dissertation. Moscow. 1977 (in Russian).

 

Надеждин. В.Н. Архитектура начальных лимфатических сетей кожи нижней конечности человека. В кн – Анатомия лимфатической системы кожи человека. Л. Гос. Изд-во Мед. Лит. 1951. с. 115. Nadezhdin V.N. Architecture of the initial lymphatic nets of skin of human lower extremities. In: Anatomy of the lymphatic system of human skin. Leningrad. 1951.

 

Пятницкий Н.Н., Махлин Н.В. Нормальнее антитела, физиологическая регенерация и трансплантация органов. В кн. Актуальные проблемы пересадки органов. М. Медицина. 1969. с. 41. Piatnizky N.N. Machlin N.V. Normal antibodies, physiological regeneration and transplantaiton of organs. In: Current problems of organ transplantation. Moscow. 1969.

 

Скрипкин Ю.К. Кожные и венерологические болезни. М. Медицина. 1980. 550 с. Skripkin Y. K. Skin and venereal diseases. Moscow. 1980.

 

Халявкин А.В. Цензорно-ростовая модель и иммунитет. Изв. АН ГССР. Сер биол. 1975. т. 1. н. 5. с 490. Khalyavkin A.V. The censorial-growth model and immunity. 1975.

 

Beutner E. H. Chorzelski T.P., Jablonska S. Autoimmunity in psoriasis. Studies on the possible significance of the universal stratum corneum antibodies in the pathogenesis of psoriasis. In: Psoriasis. N.Y. Yorke Medical books, 1977, p. 63.

 

Bullough W.S., Deol J.U.R. Dermo-epidermal adhesion and its effect on epidermal structure in mouse. Brit Dermatol. 1975, v. 93, No. 4, p. 417.

 

Bullough W.S., Mitrani E. The significance of vertical mitosis in epidermis. Brit J. Dermatol. , 1978, v. 99, no. 6, p. 603.

 

Burch P.R.J., Rowell N.R. Psoriasis: aetiological aspects. Acta Derm-venereol. 1965, v. 45, No. 5, p. 366.

 

Burwell R. S. The role of lymphoid tissue in morphostasis. Lancet, 1963. v. 2, No. 7297, p. 69.

 

Duffill M.B., Appleton D.R., Dyson P., Shuster S., Wright N.A. The measurement of the cell cycle time in squamous epithelium using the metaphase arrest technique with vincristine. Brit. J. Dermatol. 1977, v. 96, p. 493.

 

Flaxman B.A. Replication and differentiation in vitro of epidermal cells from normal skin and from benign (psoriasis) and malignant (basal cell caner) hyperplasia. In vitro, 1972, b. 8, No. 3, p. 327.

 

Flaxman B.A., Karasek M., Voorhess J.J. Research needs in 11 major areas in dermatology. 1. Psoriasis. J. Invest. Dermatol. 1979, v. 73, No. 5, part 2, p. 402.

 

Fukuda M. Okamura K, Fujita S., Bohm M, Rohrbach R., Sadritter W. The different stem cell populations in mouse epidermis and lingual epithelium. Path Res. Pract. 1979. v. 1963, No. 3, p. 205.

 

Iversen O.H., Bjerknes R., Devik F. Kinetics of cell renewal, cell migration and cell loss in the hairless mouse dorsal epidermis. Cell Tissue Kinet. 1968, v. 1 No. 4, p. 351.

 

Krogh H. The significance of stratum corneum antibodies: an experimental model in guinea pigs. In: Psoriasis. N.Y. Yorke Medical Books. 1977. p. 55.

 

Marks F. Epidermal growth control mechanisms, hyperplasia, and tumor promotion in the skin. Cancer Res. 1976, v. 36, no. 7, part 2, p. 2636.

 

Pinkus H., Hunter R. The direction of the mitotic axis in human epidermis. Arch Dermatol 1966. v. 94, no. 4, p. 351.

 

Potten C.S., Hendry J.H., Clonogenic cells and stem cells in epidermis. Int J. Radiat. Biol. 1973, v. 24, No. 5, p. 537.

 

Skerrow C. J. Intercellualr adhesion and its role in epidermal differentiation. Invest. Cell Pathol. 1978, v. 1, No. 1, p. 23.

 

 

Institute of Chemical Physics. USSR Academy of Sciences. Msocw.

 

Arrived at the Editorial Office. 10. II. 1981.

 

Original abstract:

 

Khalyavkin A.V. The Epidermal homeostasis and the problem of psoriasis

 

Institute of Chemical Physics, Academy of Sciences of the USSR, Moscow

 

It was stated that the irregular mitotic activity of the basal layer is responsible for the wavy character of the dermo-epidermal borderline and related by the specificity of the subepidermal lymphatic capillaries’ distribution. On the basis of the literature data’s analysis the conclusion is made that the non-co-ordination of the action of the subepidermal human systems, aimed at the increase of the mitotic activity of the keratinocytes can lead to the disturbances in the epidermal homeostasis and appearance of acanthosis, papillomatosis and parakeratosis in the psoriasis development.

In Russian: Эпидермальный Гомеостаз и Проблема Псориаза

Khalyavkin Epidermail Homeostasis 82 1

—

Censor-Growth Model and Immunity

Censor-Growth Model and Immunity ORIGINAL 1975

Halyavkin-Censor Growth Model and Immunity-Thymus

ИЗВЕСТИЯ   АКАДЕМИИ   НАУК   ГССР Серия биологическая, т. 1, № 5, 6, 1975

КРАТКИЕ СООБЩЕНИЯ

 

УДК 577.95

ТЕОРЕТИЧЕСКАЯ БИОЛОГИЯ

 

ЦЕНЗОРНО-РОСТОВАЯ МОДЕЛЬ И ИММУНИТЕТ* А. В. Халявкин

Институт физиологии АН ГССР, Тбилиси Поступила в редакцию 10.10.1975

 

CENSOR-GROWTH MODEL AND IMMUNITY

  1. V. HALYAVKIN

Institute of Physiology, Georgian Academy of Sciences, Tbilisi. USSR Summary

A model is offered according to which the immunological phenomena are соnsidered not as the obligatory defense mechanisms, but as a particular case of the mechanism of specific stimulation of mitosis.

In Russian: Ц Е Н З О Р Н О – Р О С Т О В А Я М О Д Е Л Ь И И М М У Н И Т Е Т

Censor-Growth Model and Immunity

Censor-Growth Model and Immunity ORIGINAL 1975

Halyavkin-Censor Growth Model and Immunity-Thymus

 

 

 

 

Degenerative Aging as a Treatable Condition

Advocacy, English

whologoRecognizing Degenerative Aging as a Treatable Medical Condition

 

Ilia Stambler, PhD

 

There has been recently an intensifying discussion among longevity researchers and advocates about the inclusion of the Degenerative Aging Process as a recognized and treatable medical condition, that would include the systemic factors that contribute to diseases and frailty.

http://journal.frontiersin.org/article/10.3389/fgene.2015.00205/full

http://journal.frontiersin.org/article/10.3389/fgene.2015.00202/full

The underlying, apparently plausible rationale for this suggestion is that the recognition of degenerative aging as a treatable medical condition would enable the existing legal frameworks to better tackle diseases and conditions that arise from the aging process from a preventative healthcare model. In particular, pharmaceutical, biomedical and wellness industry could then develop for market quickly new and existing preventative medications, biomedical technologies and regimens, that would decrease long-term healthcare costs. Moreover, such a recognition would open up new public funding for new pharmaceutical and biomedical research and development. However, how do we achieve this recognition within the existing legal frameworks? And, more importantly, how do we translate this formal recognition into implementation, into establishing new research, development and healthcare programs at the international, national and institutional levels? And even more importantly, how do we translate these programs into actual biomedical treatments and cures, effective, safe and accessible for the widest public possible?

All these issues must become a subject of massive and pluralistic consultation of scientists and other stakeholders. An initial deliverable could be a collection of papers and expert opinions dedicated to the subject. With this evidential and expert basis, it may be expedient to develop more precise policy recommendations and approaches for further consultation with the relevant WHO departments and affiliates, such as the Global Burden of Disease (GBD) program, the WHO Multi-Country Studies Unit, the WHO Collaborating Centre on International Longitudinal Studies of Gender, Ageing and Health, the developers of the ICD and ISF, WHO Department of Aging and Lifecourse, in particular the GSAP, WHO Program on Non-communicable Diseases and their Risk Factors, UN NGO Committee on Aging, UN Department of Economic and Social Affairs – Division for Social Policy and Development, implementation agencies of the UN Sustained Development Goals (esp. SDG3 on healthcare)  and other relevant authorities.

http://www.who.int/entity/en/

 

 

 

Promotion of Longevity and Quality of Life for the Elderly Population in Israel (Hebrew)

Advocacy, Hebrew עברית

הכנסת התשע-עשרה

 

הצעת חוק הקמת ועדה לאומית מייעצת

לאריכות ואיכות החיים לאוכלוסיה המבוגרת

(הערות: פרקי תוכן – “דברי הסבר”, פרק א’ “פרשנות” סעיפים 1-5, סעיף 6 “מועצת הוועדה”, סימן ז’ “תיקונים לחוקים אחרים”,

הסעיפים האדמיניסטרטיביים – 7-27

הגרסה האנגלית

http://www.longevityforall.org/promotion-of-longevity-and-quality-of-life-for-the-elderly-population-in-israel

דברי הסבר

האריכות ואיכות החיים הבריאים של האוכלוסיה המבוגרת הן עדיפויות לאומיות ראשוניות הנחוצות לתפקוד תקין של כלל החברה. בניגוד לכך, תהליך ההזדקנות הניווני הנו השורש וגורם הסיכון העיקרי לרוב המחלות הכרוניות הפוקדות את העולם המפותח בכלל ואת ישראל בפרט.

שיעור התמותה בישראל עומד על כ-0.52%. מתוך שיעור זה למעלה מ-90% מתים עקב מחלות התלויות בגיל כתוצאה מתהליך ההזדקנות. במילים אחרות, בכל שנה מתים כ-40,000 ישראלים ממחלות אלה, פי 2 ממספר כל חללי מערכות ישראל לדורותיהם, פי 2 ממספר כל הרוגי תאונות הדרכים לדורותיהם.

לפי דו”ח בנק ישראל שפורסם במרץ 2012, ההוצאה הלאומית – הציבורית והפרטית – לטיפול באוכלוסיית הקשישים בישראל (כ-10% מכלל האוכלוסיה שהם מעל גיל 65) מגיעה לכ-9.9 מיליארד ש”ח בשנה, שהם כ-1.2% מסך כל התוצר הלאומי.

תהליך ההזדקנות הוא תהליך חומרי בסיסי המתבטא בהצטברות נזקים, הפרת האיזון המטבולי ופגיעה בתפקוד התקין. זהו תהליך אשר גורם לשיעור המוגבלות והתמותה הגבוה ביותר, אשר מהווה גורם הסיכון המכריע לרוב המחלות הכרוניות – כגון סרטן, מחלות לב, סכרת, דמנציה ועוד – ויש להתייחס אליו בהתאם.

עם זאת, המחקר הרפואי בישראל ובשאר המדינות המפותחות מתרכז בסימפטומים של תהליך ההזדקנות ולא במניעתו או טיפולו. למרות חשיבותם המיידית, אמצעים פליאטיביים כמו טיפול סיעודי לא ישפרו את אריכות החיים הבריאים לאוכלוסיה המבוגרת בצורה דרמטית, ולא יפתרו את בעיית הנטל הכלכלי או את הסבל האנושי הכרוכים בהליך ההזדקנות, אלא רק יקלו עליהם וידחו אותם במעט. לעומת זאת, השקעות ומאמצים במחקר ופיתוח למניעה וטיפול של הנזק הנגרם ע”י תהליך ההזדקנות הניווני, בהינתן תמיכה מספקת, עשויים להביא לשיפור משמעותי.

כאמור באם תהליך ההזדקנות, דהיינו הצטברות הנזקים המבניים וההפרה הדרגתית של האיזון המטבולי והתפקוד התקין, הוא תהליך מגביל ומחליא המצריך מניעה וטיפול, העלייה בתוחלת החיים הבריאים היא המזור לו. ובמילים אחרות, ההתבגרות הנפשית עם השנים והעלייה באורך החיים הבריאים אינם ולא צריכים להיות מילים נרדפות להזדקנות ניוונית והידרדרות.

מגמות העלייה בתוחלת החיים הבריאים, בנוסף לממצאי מחקר בסיסי אודות תהליך ההזדקנות, מצביעים על האפשרות המעשית של התערבות בתהליך ההזדקנות ובמחלות הכרוניות הנגזרות ממנו, וכתוצאה מכך על האפשרות של הארכת חיים בריאים לאוכלוסיה המבוגרת.

ניתן להגביר ולזרז תהליך חיובי זה לטווח ארוך על ידי עידוד מבוקר של מחקר בסיסי ויישומי, וכן פיתוח טכנולוגי, תעשייתי וסביבתי המכוונים לעיכוב וטיפול של תהליך ההזדקנות ולמען אריכות ואיכות החיים לאוכלוסיה המבוגרת. אמצעים אלה עשויים לצמצם את נטל תהליך ההזדקנות על המשק הישראלי, את סבל המזדקנים ואת שכול יקיריהם. ולחיוב, בהינתן תמיכה מספקת, הם עשויים להאריך את תוחלת החיים הבריאים לאוכלוסיה המבוגרת, להגביר את תקופת תעסוקתם ותרומתם לפיתוח החברה הישראלית, ולהעצים את תחושת ההנאה, היעוד והערך בחייהם.

אי לכך ובהתאם לחוק יסוד: כבוד האדם וחירותו, וכן על פי העיקרון היהודי “אין דוחים נפש מפני נפש”, יש לתת לפיתוח אמצעים למען אריכות ואיכות החיים לאוכלוסיה המבוגרת את התמיכה הראויה להם, ומכאן להקים ועדה מייעצת ומתאמת לאריכות ואיכות החיים לאוכלוסיה המבוגרת.

פרק א’: פרשנות

1. הגדרות

“השר” – ראש הממשלה

“הועדה” – הועדה הלאומית המייעצת לאריכות ואיכות החיים לאוכלוסיה המבוגרת

פרק ב’: הועדה הלאומית המייעצת

סימן א’: הקמת הועדה ותפקידיה

2. הקמת הועדה

מוקמת בזה הועדה הלאומית המייעצת לאריכות ואיכות החיים לאוכלוסיה המבוגרת.

3. הועדה כתאגיד

הועדה היא תאגיד.

4. הועדה כגוף מבוקר

הועדה תהיה גוף מבוקר כמשמעותו בסעיף 9(6) לחוק מבקר המדינה, התשי”ח-1958 (נוסח משולב.)

5. תפקידי הועדה

(א) הועדה תקבע מדיניות מחקר מדעי, פיתוח טכנולוגי, חינוך אקדמי וציבורי, הסברה ותאום בתחום שיפור אריכות ואיכות החיים לאוכלוסיה המבוגרת כדי שזו תהווה בסיס לפעילותה ולפעילות הממשלה בנושא; גיבשה הועדה מדיניות באחד הנושאים שבתחום תפקידיה, יביאה ראש הועדה לאישור הממשלה אם ביקשה זאת הועדה.

(ב) בלי לפגוע בכלליות האמור בסעיף קטן (א’) יכללו תפקידי הועדה גם את אלה:

(1) לגבש מדיניות ולפעול לקידום שיתוף פעולה בין משרדי הממשלה, מכוני המחקר הארציים והבינלאומיים וגופים אחרים הפועלים בתחום שיפור אריכות ואיכות החיים לאוכלוסיה המבוגרת;

(2) לתכנן תכנון ארוך טווח של השלכות העלייה בתוחלת החיים בישראל;

(3) לפעול להקמתם, לפיתוחם, לניהולם ולהחזקתם של מסגרות מתאימות, שירותים ותכניות פעולה לשיפור אריכות ואיכות החיים לאוכלוסיה המבוגרת בשיתוף עם המשרדים הנוגעים בדבר.

בכלל זה:

להעניק מלגות ומענקי מחקר בתחום טיפול בתהליך ההזדקנות ושיפור אריכות ואיכות החיים לאוכלוסיה המבוגרת, ובפרט בתחומים של רפואה רגנרטיבית, ננו-רפואה, ביו-גרונטולוגיה ואורח חיים אופטימאלי והיגייני לגיל המתקדם;

לעודד השקעות בחברות ביוטכנולוגיה וטכנולוגיה רפואית, ובארגוני מחקר, פיתוח ויישום אקדמיים וציבוריים, שיעסקו בטיפול בתהליך ההזדקנות ובמחלות הכרוניות הנגזרות ממנו;

(4) לפעול להרחבת ההסברה ולהעמקת המודעות הציבורית לנזקי ההזדקנות, לדרכים האפשריות להקטין אותם ולפיתוחים המדעיים בתחום.

בכלל זה:

לעודד איסוף מידע מדעי עדכני ומוסמך מדעית אודות אורח החיים ההיגייני האופטימלי לגיל המבוגר ולספק הסברה בנושא לקהילה הטיפולית ולציבור הרחב;

לפעול ליצירת והרחבת מסגרות ותוכניות לימוד אקדמיות ועיוניות בנושא מחקר בסיסי ויישומי אודות תהליך ההזדקנות ושיפור אריכות ואיכות החיים לאוכלוסיה המבוגרת, על ההיבטים הביולוגיים, הרפואיים והחברתיים;

(5) לסייע לשירותים הממלכתיים ולשירותי הרשויות המקומיות בייעוץ ובהכוונה בנוגע לטיפול בקשישים בישראל.

בכלל זה:

לפעול לשיפור תנאי המחיה של הקשישים, כולל פיתוח אמצעי נגישות ונוחות בחיי היום-יום

לפעול להקמתם והרחבתם של מסגרות חברתיות, חינוכיות ותעסוקתיות המערבות את אוכלוסיית הקשישים ומעודדות את האינטגרציה שלהם עם כלל האוכלוסיה.

סימן ב’: מועצת הועדה

6. מועצת הועדה

(א) לועדה תהיה מועצה ובה עשרים ושנים חברים שימנה השר באישור הממשלה; הודעה על המינוי תפורסם ברשומות.

(ב) המועצה תהיה מורכבת מאלה:

(1) נציג אחד מבין עובדי משרדו של כל אחד מאלה: ראש הממשלה, שר הפנים, שר הבריאות, שר האוצר, שר החינוך, השר לאזרחים ותיקים ושר המדע והטכנולוגיה;

(2) נציג אחד של כל אחד מאלה: המועצה להשכלה גבוהה; ההסתדרות הרפואית בישראל; המוסד לביטוח לאומי; המועצה הלאומית למחקר ופיתוח; המדען הראשי.

(3) מומחה אחד בכל אחד מהתחומים האלה: ביו-גרונטולוגיה; גריאטריה, ביוטכנולוגיה; טכנולוגיה רפואית; עבודה סוציאלית; תכנון פיננסי; ומדע, טכנולוגיה וחברה, שימונו על ידי השר בהמלצת ראשי מוסדות אקדמיים רלוונטיים בישראל.

(4) שלושה נציגי ציבור הפעילים למען שיפור אריכות ואיכות החיים לאוכלוסיה המבוגרת במישור המדעי והחברתי, שיקבע השר ובהמלצת שאר חברי המועצה מבין נציגי המשרדים, המוסדות הציבוריים והאקדמיה.

(ג) לבקשת השר רשאית המועצה להזמין נושא תפקיד נוסף לדיוניה כמשתתף קבע.

(ד) המועצה רשאית להזמין נושא תפקיד נוסף לדיוניה כמשתתף קבע בהמלצת תת-ועדה בהרכב של לפחות שלושה חברי המועצה הכוללים נציגי משרדי הממשלה, המוסדות הציבוריים והאקדמיה.

7. יושב-ראש וסגן יושב-ראש

יושב ראש הועדה יבחר מבין כלל חברי המועצה על ידי כל חברי המועצה ובאישור השר;

ממלא-מקום וסגן יושב-ראש הועדה יבחר על ידי כלל חברי המועצה מבין המומחים חברי המועצה ובאישור השר.

8. תקופת כהונה

תקופת כהונתם של חברי המועצה שמונו בהתאם לסעיף 6 תהיה שלוש שנים; חבר מועצה שתקופת כהונתו תמה ניתן למנותו מחדש. חבר מועצה שכהונתו תמה יוסיף לכהן עד מינוי חבר אחר במקומו, או עד מינויו מחדש, לפי העניין.

9. העברת חבר מכהונתו

השר רשאי להעביר חבר מועצה מכהונתו אם הוא:

(1) הורשע בעבירה שיש עמה קלון;

(2) אינו מסוגל מטעמי בריאות למלא את תפקידיו;

(3) נעדר ללא סיבה מוצדקת מארבע ישיבות רצופות של המועצה.

10. חילופי חברים

חדל חבר מועצה לכהן בתפקיד שבשלו מונה חבר מועצה או שלא נתקיימו בו עוד התנאים שבשלהם מונה וכן אם התפטר מהמועצה, הועבר מכהונתו או נפטר, יתמנה במקומו חבר אחר באותה דרך בה נתמנה אותו חבר מועצה.

11. תפקידי המועצה

תפקידי המועצה יהיו:

(1) להתוות את קווי הפעולה של הועדה;

(2) להנחות את המנהלה במילוי תפקידיה ולפקח על פעולותיה;

(3) לדון בהצעת התקציב השנתי כאמור בסעיף 18, בדין-וחשבון השנתי ובכל עניין אחר הנוגע לפעילותה של הועדה.

12. מינוי תת-ועדה

המועצה רשאית למנות מבין חבריה, לנושא שבתחום תפקידיה, תת-ועדה קבועה או תת-ועדה לעניין מסוים, למנות לה יושב ראש ולאצול לה מסמכויותיה, כפי שתקבע; אולם המועצה לא תאצול לתת-ועדה שמינתה כאמור את הסמכויות הבאות:

(1) הסמכות להתוות את קווי הפעולה של הועדה הראשית לפי סעיף11(1);

(2) הסמכות לדון ולהכניס שינויים בהצעת התקציב לפי סעיף 11(3) רישה.

12א. תוקף

החלטה של המועצה או של תת-ועדה מתת-ועדותיה לא תיפסל מחמת זה בלבד שבזמן קבלתה היה מקומו של חבר המועצה או חבר התת-ועדה פנוי מכל סיבה שהיא.

13. סדרי דיון

(א) השר, בהתייעצות עם המועצה, רשאי לקבוע בתקנות הוראות בדבר מנין חוקי, דרכי כינוס המועצה ותת-ועדותיה וניהול ישיבותיהן, סדרי ההצבעה, סמכויות יושב-ראש המועצה או יושב-ראש תת-ועדה, והחזר הוצאות שנגרמו לחברי המועצה ולחברי המנהלה שאינם עובדי הועדה או עובדי מדינה עקב השתתפותם בישיבות המועצה, תת-הועדות או המנהלה.

(ב) המועצה ותת-ועדותיה יקבעו את סדרי עבודתם אם לא נקבעו בתקנות כאמור בסעיף קטן (א).

(ג) המועצה תתכנס ארבע פעמים בשנה לפחות.

סימן ג’: מנהל הועדה, המנהלה ותפקידיה

14. מנהל הועדה, כהונתו וסמכויותיו

(א) השר, בהתייעצות עם המועצה, ובאישור הממשלה, ימנה מנהל לועדה. השר בהתייעצות עם המועצה רשאי למנות סגן למנהל הועדה.

(א1) תקופת כהונתו של המנהל תהיה חמש שנים; השר, בהתייעצות עם המועצה ובאישור הממשלה, רשאי לשוב ולמנותו בתום כל תקופת כהונה, לתקופת כהונה נוספת.

(א2) כהונת המנהל תפקע באחת מאלה:

(1) התפטר בהודעה בכתב שהגיש לשר באמצעות המועצה;

(2) השר, בהתייעצות עם המועצה ובאישור הממשלה, קבע כי נבצר מהמנהל, דרך קבע, למלא את תפקידו;

(3) השר, בהתייעצות עם המועצה ובאישור הממשלה, החליט להעבירו מכהונתו מטעמים שיפורטו.

(א3) בכפוף להוראות חוק זה ולהחלטות המועצה והמנהלה יהיו למנהל כל הסמכויות הדרושות לניהול הועדה ובכלל זה לייצגה ולחתום על הסכמים בשמה, למעט הסמכות לחתום על הסכמים בינלאומיים.

(א4) המנהל רשאי לאצול מסמכויותיו לפי חוק זה לעובד מעובדי הועדה וליפות את כוחו לחתום על כל מסמך בשם הועדה.

(ב) עניני הועדה ינוהלו בידי המנהלה, שתהא מורכבת ממנהל הועדה, סגנו – אם נתמנה כאמור, ועשרה חברים שימונו מבין עובדי משרדו של כל אחד מאלה: השר, שר האוצר, שר הבריאות, שר החינוך, שר המדע והטכנולוגיה, השר לאזרחים ותיקים, ושר הפנים, וכן נציג ציבור אחד ושני נציגי אקדמיה שימנה השר בהתייעצות עם המועצה מבין חברי המועצה שאינם עובדי מדינה.

(ג) מספר חברי המנהלה לא יעלה על שנים עשר.

15. תפקיד המנהלה

תפקידי המנהלה הם:

(1) לפעול לביצוע תפקידי הועדה בהתאם להנחיות המועצה;

(2) להכין את התקציב השנתי של הועדה ולהגישו למועצה;

(3) להגיש למועצה דין-וחשבון שנתי על פעולות הועדה וכל דין-וחשבון

אחר שתדרוש המועצה על פעולות הועדה;

(4) לפרסם סיכום שנתי על פעולות הועדה;

(5) להעביר לשר לפי דרישתו דין-וחשבון או מידע על עניין שהוא בגדר תפקידיה וסמכויותיה של המנהלה.

(6) למנות את עובדי הועדה ולקבוע את תפקידיהם וסמכויותיהם, כאמור בסעיף 17.

16. סמכויות המנהלה

המנהלה מוסמכת לבצע בשם הועדה כל פעולה הדרושה למילוי תפקידי הועדה על פי חוק זה, למעט פעולות שיוחדו בחוק זה למועצה.

17. עובדי הועדה

(א) השר יקבע בהתייעצות עם שר האוצר את התקן לעובדי הועדה.

(ב) דין קבלתם של עובדים לועדה ומינויים יהיה כדין זה של עובדי המדינה, בשינויים שייקבעו בתקנות.

(ג) שכרם ותנאי עבודתם של עובדי הועדה, לרבות המנהל וסגנו, יהיו כתנאי עבודתם של עובדי המדינה ובתיאומים שתקבע המנהלה באישור השר.

סימן ד’: תקציב וכספים

18. תקציב

(א) המנהלה תכין, לתאריך שקבעה המועצה, תקציב שנתי לועדה ותגיש אותו למועצה. בנסיבות מיוחדות רשאית המנהלה להגיש הצעת תקציב לתקופה קצרה משנה וכן הצעת תקציב נוסף.

(ב) המועצה תדון בהצעת התקציב ותעביר אותה לשר בשינויים שייראו לה.

(ג) תקציב הועדה טעון אישור השר.

19. מימון

תקציב הועדה ימומן מאוצר המדינה וממענקים ותרומות שתקבל הועדה.

סימן ה’: פעילות משרדי הממשלה והפיקוח על הועדה

20. פעילות משרדי הממשלה

משרדי הממשלה יפעלו בשיתוף עם הועדה בעניינים שבתחומה של הועדה. תקנות שיתקין השר בעניינים שמתפקידי הועדה יהיו בהתייעצות עם השר הממונה על ביצוע חוק זה.

21. פיקוח

(א) הועדה תעביר מדי שנה לשר דין-וחשבון על פעולותיה; וכן תפרסם הועדת סיכום שנתי של פעולותיה.

 (ב) הועדה תעביר בכל עת לשר לפי דרישתו, דין וחשבון וכן מידע שוטף או חד-פעמי על כל עניין שהוא בגדר תפקידיה וסמכויותיה.

סימן ו’: הוראות שונות

22. קיום סמכויות

קיומם של המועצה, תת-ועדותיה או המנהלה ותוקף החלטותיהם לא ייפגעו מחמת שנתפנה מקומו של חבר או שהיה פגם במינויו.

23. דין הועדה כדין המדינה

דין הועדה כדין המדינה לעניין:

(1) תשלום מסים, מס בולים, אגרות, ארנונות, היטלים ותשלומי חובה אחרים;

(2) חוק הנזיקים האזרחיים (אחריות המדינה), התשי”ב-1952;

(3) סעד בדרך צו מניעה.

24. דין מנהל הועדה, סגן מנהל הועדה ועובדיה

(א) דין מנהל הועדה, סגן מנהל הועדה ועובדי הועדה (להלן – עובדי הועדה) לעניין חיקוקים אלה כדין עובדי המדינה:

(1) חוק הבחירות לכנסת (נוסח משולב), התשכ”ט-1969;

(2) חוק שירות המדינה (סיוג פעילות מפלגתית ומגבית כספים), התשי”ט-1959;

(3) חוק שירות הציבור (מתקנות), התש”ם-1980;

(4) חוק שירות הציבור (הגבלות לאחר פרישה), התשכ”ט-1969;

(5) פקודת הראיות (נוסח חדש), התשל”א-1971;

(6) פקודת הנזיקין (נוסח חדש).

(ב) חוק שירות המדינה (משמעת), התשכ”ג-1963 (להלן – חוק המשמעת) יחול על עובדי הועדה כאילו היו עובדי המדינה; לעניין זה בחוק המשמעת יבוא ראש הממשלה במקומו של השר בכל מקום שמדובר בחוק האמור בשר ומנהל הועדה יבוא במקום המנהל הכללי בכל מקום שמדובר בו בחוק האמור.

25. שמירת סמכויות

הוראות חוק זה אינן באות לגרוע מסמכות שניתנה על-פי כל דין.

26. ביצוע ותקנות

ראש הממשלה ממונה על ביצוע חוק זה והוא רשאי להתקין באישור ועדת החוקה חוק ומשפט של הכנסת תקנות בכל עניין הנוגע לביצועו.

27. תחילה

תחילתו של חוק זה בתום ששה חדשים מיום פרסומו.

סימן ז’: תיקונים לחוקים אחרים

לפקודת בריאות העם: הוספת חלק ז’

אחרי חלק ה’, “הוראות בענין המלחמה במלריה”, יבוא חלק ז’, “הועדה הלאומית המייעצת לאריכות ואיכות החיים לאוכלוסיה המבוגרת”, ובסעיף זה יכתב:

“1. הועדה הלאומית המייעצת לאריכות ואיכות החיים לאוכלוסיה המבוגרת תספק הוראות שוטפות ועדכניות לקהילה הטיפולית ולציבור הקשישים לגבי האמצעים הזמינים כדי להקטין את נזקי ההזדקנות וכדי להאריך את תוחלת החיים הבריאים והפעילים לאוכלוסייה הקשישה, וזאת בהתאם לחוק הקמת הועדה הלאומית המייעצת לאריכות ואיכות החיים לאוכלוסיה המבוגרת.

2. הועדה הלאומית המייעצת לאריכות ואיכות החיים לאוכלוסיה המבוגרת תפעל לקידום מחקר מדעי, פיתוח טכנולוגי, טיפול רפואי וחינוך אקדמי וציבורי להקטנת נזקים הנגרמים על ידי תהליך ההזדקנות ומחלות כרוניות הנלוות והנגזרות ממנו, כגון מחלות הסרטן, הלב והסוכרת, וכל מחלה מטבולית נוספת התלויה בגיל.”

לחוק שוויון זכויות לאנשים עם מוגבלות, תשנ”ח-1998: תיקון פרק א’: עקרונות יסוד. 2

אחרי המשפט “חוק זה מטרתו להגן על כבודו וחירותו של אדם עם מוגבלות” יבוא “הנגרמת מכל סיבה שהיא, כולל הזדקנות.”

דהיינו, בסעיף זה יכתב:

“חוק זה מטרתו להגן על כבודו וחירותו של אדם עם מוגבלות הנגרמת מכל סיבה שהיא, כולל הזדקנות, ולעגן את זכותו להשתתפות שוויונית ופעילה בחברה בכל תחומי החיים, וכן לתת מענה הולם לצרכיו המיוחדים באופן שיאפשר לו לחיות את חייו בעצמאות מרבית, בפרטיות ובכבוד, תוך מיצוי מלוא יכולתו.”

לחוק ביטוח בריאות ממלכתי, תשנ”ד-1994: תיקון “סעיף 3. הזכות לשירותי בריאות, ד”

אחרי “שירותי הבריאות” יבוא “ושירותים למען הארכת חיים פעילים.”

דהיינו, בסעיף זה יכתב:

“ד. שירותי הבריאות ושירותים למען הארכת חיים פעילים הכלולים בסל שירותי הבריאות ינתנו בישראל, לפי שיקול דעת רפואי, באיכות סבירה, בתוך זמן סביר ובמרחק סביר ממקום מגורי המבוטח, והכל במסגרת מקורות המימון העומדים לרשות קופות החולים לפי סעיף 13.”

לחוק לא תעמוד על דם רעך, התשנ”ח, 1998: תיקון לסעיף 1.א.

אחרי “1.א. חובה על אדם להושיט עזרה לאדם הנמצא לנגד עיניו, עקב אירוע פתאומי” יבוא “מחלה, תשישות או תאונה.”

דהיינו, בסעיף זה ייכתב:

“1.א. חובה על אדם להושיט עזרה לאדם הנמצא לנגד עיניו, עקב אירוע פתאומי, מחלה, תשישות או תאונה, בסכנה חמורה ומיידית לחייו, לשלמות גופו או לבריאותו, כאשר לאל-ידו להושיט את העזרה, מבלי להסתכן או לסכן את זולתו.”

Promotion of Longevity and Quality of Life for the Elderly Population in Israel

Advocacy, Hebrew עברית

Knesset 19

Law Proposal for the Establishment of the National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population – updated version (March 2013).

Note: First written and submitted for consideration in March 2012.

Content parts – “Rationale”, Sections 1-6, Section G – “Amendments to other laws”, Administrative parts – sections – 7-27

Hebrew version – http://www.longevityforall.org/promotion-of-longevity-and-quality-of-life-for-the-elderly-population-in-israel-hebrew/


 

Rationale

The longevity and quality of life of the elderly population are crucial national priorities, necessary for the normal functioning of the entire society. On the contrary, the deteriorative aging process is the root cause and main endangering factor for most chronic diseases afflicting the developed world generally and Israel in particular.

The death rate in Israel is approximately 0.52%, out of which over 90% die as a result of age-related diseases due to the aging process. In other words, each year approximately 40,000 residents of Israel die from aging, twice the number of all the casualties of war throughout the country’s history, and twice the number of all deaths from traffic accidents throughout the country’s history.

According to the report of the Bank of Israel, published in March 2012, both the private and public national expenditures on the senescent population in Israel (persons over 65 years old, comprising about 10% of the country’s population) is NIS 9.9 billion (~$ 2.5 billion) yearly, which comprises 1.2% of the entire Gross Domestic Product.

Aging is a basic material process manifesting in the accumulation of damage, the gradual deregulation of metabolic balance, and impairment of normal functioning. This is a process causing the largest proportion of disability and mortality, and is the major endangering factor for most chronic diseases, such as cancer, heart disease, type 2 diabetes, dementia, and other diseases – and it should be treated accordingly.

Yet, medical research in Israel and other developed countries focuses on the symptoms of the deteriorative aging process and not on its prevention or treatment. Despite their immediate importance, palliative measures, such as increasing nursing care, will not drastically improve the healthy longevity of the elderly, will not resolve the economic burden and human suffering caused by the process of aging, but will only slightly relieve and postpone them. In contrast, investments and efforts in the research and development directed toward prevention and treatment of the deteriorative aging process, if given sufficient support, may be able to bring about a substantial improvement.

While the deteriorative aging process, that is the accumulation of structural damage, impairment of metabolic balance and functioning, is a disabling and debilitating process that requires prevention and treatment; the rise in healthy life-expectancy is its cure. In other words, the spiritual maturation during the years and the increase in healthy life expectancy are not and should not be synonymous with degeneration and deterioration.

The trends of increasing healthy life-expectancy, as well as the results of basic research on aging, indicate the practical possibility of intervention into the aging process and the chronic diseases derived from it, and as a result demonstrate the practical possibility of healthy life extension for the elderly population.

This positive process can be reinforced and accelerated for the long term by regulated support of basic and applied research, as well as technological, industrial and environmental development directed toward delaying and treatment of the deteriorative aging process and for improving the quantity and quality of life for the elderly population.

These measures will reduce the burden of the aging process on Israeli economy and will alleviate the suffering of the aged and the grief of their close ones. On the positive side, if granted sufficient support, these measures can increase the healthy life expectancy for the elderly, extend their period of productivity and their contribution to the society, and enhance their sense of enjoyment, purpose and valuation of life.

In view of this and in accordance to the Basic Law: Human Dignity and Liberty, and in accordance to the Jewish principle: “Do not reject a soul for another soul” – there is a need to give to the Promotion of Longevity and Quality of Life for the Elderly Population the necessary support that they deserves, and hence establish the National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population.

 

 

Part A. Commentary

 

  1. Definitions

“Minister” – Prime Minister.

“Committee” – the National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population.

 

Part B. The National Advisory Committee

Section A. The Establishment of the Committee and it Functions

 

  1. The establishment of the committee

Hereby the National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population is established.

  1. The committee as a corporate entity

The committee is a corporate entity

  1. The community as a regulated body

The committee is a regulated body as defined in paragraph 9(6) of the State Controller Law of 1958 (consolidated version).

  1. The committee functions:
  2. The committee will determine the policy for scientific research, technological development, public and academic education and institutional coordination for the improvement of longevity and quality of life for the elderly population, so it shall become the basis for the committee activity and the government activity in this area. In case the committee determines a policy on a subject within the area of its function, the head of the committee will submit it for the government approval upon a request by the committee.
  3. Without detracting from the general statement in paragraph (a), the committee functions will include the following:
  4. Formulating policy and acting to promote cooperation between governmental departments, national and international research institutes and other organizations active for improving longevity and quality of life for the elderly population;
  5. Providing long-term planning for the implications of an increase in life-expectancy in Israel;
  6. Acting for the establishment, development, management and maintenance of appropriate research and action frameworks, services and programs, for improving longevity and quality of life for the elderly population, in cooperation with relevant governmental departments.

These include:

– Providing grants and scholarships for research aimed to delay and treat the deteriorative aging process and promote longevity and quality of life for the elderly population, particularly in the fields of regenerative medicine, nano-medicine, bio-gerontology and optimal hygienic life-style for aging persons;

– Encouraging investments in biotechnology and medical technology companies, as well as in academic and public organizations for research, development and application – that will be involved in the prevention and treatment of the deterioration caused by the aging process and its derivative chronic diseases.

  1. Acting for the expansion of education and raising public awareness about the damage caused by the aging process, about potential ways to minimize this damage and scientific developments in the field.

These include:

– Encouraging the collection of up-to-date, evidential scientific information regarding the optimal hygienic life-style for aging persons and providing education on the subject to the health care community and the wide public.

– Acting to create academic and communal learning frameworks and programs on basic and applied research of aging and promotion of longevity and quality of life for the elderly population, including its biological, medical and social aspects;

  1. Assisting governmental and local services in providing consultation and direction for the treatment of the aged in Israel.

These include:

– Acting to improve the living conditions of the elderly, including the development of means of access and convenience in their daily life.

– Acting to create and expand social, educational and occupational frameworks involving the aged and encouraging their integration with the entire population.

 

Section B. The committee council

 

  1. The committee council
  2. The committee will have a council including 22 members who will be appointed by the minister, subject to approval by the government. The appointment announcement will be published on record.
  3. The council will include the following members:
  4. A representative worker of each of the following government departments: the office of the prime minister; the ministry of interior; the ministry of health; the ministry of finance; the ministry of education; the ministry for senior citizens; and the ministry of science and technology;
  5. A representative of each of the following organizations: the Council for Higher Education; the Israeli Medical Association; the National Insurance Institute of Israel; the National Council for Research and Development; the Office of the Chief Scientist;
  6. An expert in each of the following fields: bio-gerontology; geriatrics; biotechnology; medical technology; social work; financial planning; science, technology and society – who will be appointed by the minister, on the recommendation of heads of relevant Israeli academic institutions.
  7. Three representatives of the public active in the promotion of longevity and quality of life for the elderly, in the scientific and social fields, who will be appointed by the minister and on the recommendation of the rest of the council consisting of the representatives of the government departments, the public organizations and academic institutions.
  8. Upon request of the minister, the council is entitled to invite to its meetings an additional functionary as a constant participant.
  9. The council is entitled to invite to its meetings an additional functionary as a constant participant on the recommendation of a sub-committee consisting of a least three members of the council, including representatives of government departments, public organizations and academic institutions.

 

  1. Chair and vice-chair

The chair of the committee will be elected out of all the members of the council by all the members of the council and with an approval by the minister.

The vice-chair, acting as chair-deputy, will be elected by all the members of the council out of the experts who are members of the council and with an approval by the minister.

 

  1. Term of service

The term of service of the members of the council who were appointed according to paragraph 6, will be three years. A council member whose term of service ended can be reappointed. A council member whose term of service ended will continue to serve until the appointment of another member instead or until reappointment according to the circumstance.

 

  1. Relief from duty of a council member

The minister can relieve a council member from duty in the following cases:

  1. The committee member has been convicted of a morally reprehensible offence;
  2. The committee member is unable to carry out his/her function due to health reasons;
  3. The committee member has been unjustifiably absent from four consecutive meetings of the committee.

 

  1. Replacement of members

If a council member stopped the service for which she/he was appointed to the council, or did not fulfill the conditions under which he/she was appointed, or else resigned, was relieved from duty or died, a new council member will be appointed in his/her stead in the same way in which the exiting council member was appointed.

 

  1. The council functions

The council functions will be:

  1. Establishing the directions of the committee activity;
  2. Guiding the committee directorate in its duties and supervising its activities;
  3. Discussing the annual budget proposal as stipulated in paragraph 18, as well as the annual report and every other subject related to the committee activity.

 

  1. Appointment of a Sub-Committee

The council is authorized to appoint, out of its members, for a subject within the area of its function, a permanent sub-committee or a sub-committee for a specific topic. It can appoint a chair for the sub-committee and delegate to the sub-committee a part of its powers as it determines. However, the council will not delegate to the appointed sub-committee the following powers:

  1. The power to establish the directions of the main committee activity according to paragraph 11.1.
  2. The power to discuss and introduce changes to the budget proposal according to paragraph 11.3 preface.

 

12a. Validity

A decision of the committee or a sub-committee will not be made invalid only because, at the time of the decision making, a position of a member of the committee or a sub-committee was vacant due to any reason.

 

  1. Order of discussions
  2. The minister, in consultation with the committee, is authorized to determine regulatory instructions regarding the legal quorum, the methods of convening the committee council and its sub-committees and the management of their meetings, the order of voting, the powers of the chair of the committee council or the powers of a chair of a sub-committee, the reimbursement of expenses incurred by the committee council members and directorate members who are not committee workers or state workers, due to their participation in the committee council meetings, its sub-committees or its directorate.
  3. The committee council and its sub-committees will determine their working orders, if those were not determined by regulations as said in sub-paragraph “a.”
  4. The committee council will convene at least four times a year.

 

Section C. The committee director, the committee directorate and its functions

 

  1. The committee director, his/her service and powers
  2. The minister, in consultation with the committee council, and with an approval by the government, will appoint the committee director. The minister, in consultation with the committee council, is authorized to appoint a deputy to the committee director.

a1. The term of service of the director will be five years. The minister, in consultation with the committee council and with an approval by the government, is authorized to re-appoint the director at the end of every term of service for an additional term of service.

a2. The service of the director will terminate in one of the following events:

1) The director resigns with a written announcement that is submitted to the minister via the committee council;

2) The minister, in consultation with the committee council and with an approval by the government, determines that the director is permanently unable to perform his/her function;

3) The minister, in consultation with the committee council and with an approval by the government, decides to relieve the director from duty due to reasons that will be specified.

a3. Subject to the directives of the present law and according to the decisions of the committee council and its directorate, the director will have all the powers necessary to manage the committee, including representing it and signing agreements in its name, excluding the power to sign international agreements.

a4. The director is permitted to delegate his/her powers according to this law to a worker among the workers of the committee and to authorize him/her to sign any document in the name of the committee.

  1. The affairs of the committee will be managed by the directorate which will consist of the committee director, his/her deputy – if appointed as said, and ten members who will be appointed from among workers of each of the following government departments: the office of the prime minister, the ministry of finance, the ministry of health, the ministry of education, the ministry of science and technology, the ministry for senior citizens, and the ministry of interior, one representative of the public and two representatives of academia who will be appointed by the ministers in consultation with the committee council from among the committee council members who are not state employees.
  2. The number of the directorate members will not exceed twelve.
  3. The directorate functions

The directorate functions are:

  1. Acting to implement the functions of the committee according to the instructions of the council;
  2. Preparing the annual budget of the committee and its submission to the committee directorate;
  3. Submitting to the committee directorate the annual report regarding the committee activities and any other report as requested by the committee directorate regarding the committee activities;
  4. Publishing the annual summary regarding the committee activities;
  5. Submitting to the minister, according to his/her request, reports or information regarding any affair within the framework of the functions and powers of the committee directorate;
  6. Appointing the committee workers and determining their functions and powers, according to paragraph 17.

 

  1. Powers of the committee directorate

The committee directorate is empowered to implement, in the name of the committee, any activity required for the execution of the committee functions in accordance with this law, excluding the activities that have been dedicated by this law to the committee council.

  1. Committee workers
  2. The minister will determine, in consultation with the minister of finance, the standards for the committee workers.
  3. The law for accepting workers to the committee and their appointment will be as the law for state employees, with changes that will be determined by regulations.
  4. The salary and working conditions for the committee workers, including the director and director deputy, will be as the working conditions for state employees and will be coordinated as determined by the committee directorate with an approval by the minister.

 

Section D. Budget and Finance

 

  1. Budget
  2. The directorate will prepare, to the date determined by the council, the annual committee budget and will submit it to the council. In special circumstances, the directorate is allowed to submit a budget proposal for a period shorter than a year as well as an additional budget proposal.
  3. The council will discuss the budget proposal and will submit it to the minister with an addition of changes as it sees fit.
  4. The committee budget is subject to an approval by the minister.
  5. Financing

The committee budget will be financed from the state treasury and from grants and donations that the committee will receive.

 

Section E. Activities of the government departments and supervision over the committee

 

  1. Activities of the government departments

The government departments will act in cooperation with the committee on subjects within the area of the committee functions. Regulations determined by the minister as regards the committee functions will be performed in consultation with a minister responsible for implementing the particular law.

  1. Supervision
  2. The committee will submit to the minister a report each year, regarding its activities. Also, the committee will publish the yearly summary of its activities.
  3. The committee will submit to the minister, at any time by the minister’s request, reports as well as current and topical information on any subject within the framework of the committee functions and powers.

 

Section F. Various regulations

 

  1. Exercise of power

The existence of the council, its sub-committees or the directorate and the validity of their decisions will not be impaired if a position was vacated by a member whose appointment was flawed.

  1. The law pertaining to the committee is as the law pertaining to the state

The law pertaining to the committee is as the law pertaining the state, in the following matters:

  1. Payment of taxes, stamp duty, fees, rates, levies and other compulsory payments;
  2. Civil Wrongs (Liability of the State) of 1952;
  3. Relief by way of injunction.
  4. The laws pertaining to the committee director, deputy of the committee director and the committee workers
  5. The laws pertaining to the committee director, deputy of the committee director and the committee workers (hereafter “committee workers”) as regards this legislation are as the laws pertaining to state employees:
  6. The Knesset Elections Law (Consolidated Version), 1969;
  7. The Civil Service Law (Classification of Party Activity and Fundraising), 1959;
  8. The Public Service Law (the Regulations), 1980;
  9. The Public Service Law (Restrictions After Retirement), 1969;
  10. The Evidence Ordinance (New Version), 1971;
  11. The Civil Wrongs Ordinance (New Version).
  12. The Civil Service (Discipline) Law of 1963 (hereinafter – the discipline law) shall apply to the committee employees as if they were state employees. For this purpose, in the discipline law, “the Prime Minister” will replace the “Minister,” in every place in the said law referring to the Minister. And “the committee director” will replace “the general director” in every relevant place in the said law.
  13. Preservation of powers

The directives of this law do not detract from the power of authority granted by any law.

  1. Implementation and Regulations

The prime minister is responsible for the implementation of this law and he is entitled to introduce regulations in any matter pertaining to its implementation, with an approval of the Knesset Committee for the Constitution, Law and Justice.

  1. Commencement

This law will commence at the end of six months after the day of its publication.

 

Section G. Amendments to Other Laws.

 

  1. The Public Health Ordinance. Addition of Part 7.

 

After Part 6 “Directives for the Struggle against the Disease of Malaria,” there will appear Part 7 “National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population.”

In this part, it will be written:

“1. The National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population will supply continuous directives and updates to the health care community and the senior citizens community regarding the currently available means to reduce the damage of aging and prolong the healthy and active life for the aged population. This will be done according to the law for the establishment of the National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population.

  1. The National Advisory Committee for the Promotion of Longevity and Quality of Life for the Elderly Population shall act to advance scientific research, technological development, medical treatment and public and academic education in order to reduce the damage caused by the deteriorative aging process and the chronic diseases which accompany it and derive from it, such as cancer disease, heart disease and diabetes, and any additional age-related metabolic disease.”

 

  1. The Equality for People With Disabilities Law, 1998. Amendment to Chapter A:

Fundamental Principles 2

 

After the sentence “The purpose of this law is to protect the dignity and liberty of a person with a disability,” there will appear “produced by any cause whatsoever, including aging.”

That is to say, in this chapter, it will be written:

“The purpose of this law is to protect the dignity and liberty of a person with a disability, produced by any cause whatsoever, including aging, and uphold his/her right to participate equally and actively in the society in every aspect of life, as well as to provide a worthy solution for his/her special needs in such a way that will allow him/her to live the life with maximal independence, privacy and dignity, while fully fulfilling one’s capabilities.”

 

  1. The National Health Insurance Law, 1994. Amendment to “Section 3. The right to health care services. D”

 

After “health services” there will appear “and services for the extension of active life.”

That is to say, in this section, it will be written:

“D. Health services and services for the extension of active life, included in the basket of health services, will be granted in Israel according to the medical judgment, with a reasonable quality, within a reasonable time, and at a reasonable distance from the residence place of the insured – all within the framework of the financing sources available to the Health Maintenance Organizations according to section 13.”

 

  1. The Good Samaritan Law (“Do not stand idly by the blood of your neighbor”), 1998. Amendment to Section 1a.

 

After “1a. A person must provide help to a person found in front of him, due to a sudden event” it will be written “disease, exhaustion or accident,”

That is to say, in this section, it will be written:

”A person must provide help to a person found in front of him, due to a sudden event, disease, exhaustion or accident, in a situation of grave and immediate danger to his/her life, to the integrity of his/her body or his/her health, when it is within the person’s reach to offer help, without endangering oneself or others.”