Monthly Archives: December 2015

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.

 

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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.”

 

 

Should India Promote Scientific Research on Aging?

Advocacy, Hindi हिन्दी

Should India Promote Scientific Research on Aging?

Prof Kalluri Subba Rao. *

 

Should India promote scientific research on aging? This was the question put to me by a learned friend of mine during our discussion on the ever increasing population of India and in particular that section of the population beyond 60 years of age. I was suggesting, rather emotionally, that it is high time that India had taken the health and other problems of senior citizens seriously and active research be promoted on the phenomenon of getting old and such age associated health and social problems. To this my friend brought out the above question with an equally involved gesture. The summary of his argument was simple and straightforward. In India we have the faith that this life is only a transitory phase of never ending cycle of birth and death. Every one who is born is certain to die. In fact, according the Indian ethos, every one should strive to attain janmarahityam or moksha a state where one becomes free from the cycle of birth and death. Under these circumstance why to worry that we are aging which inevitable? Instead, one should adopt vanaprastha and indulge in such activities that might take one nearer to moksha or even to moksha itself. Therefore, it is silly for any nation to spend a good chunk of its resources on finding out how we become old and die.

For a moment, I thought my esteemed friend might, after all, be right. Having spent good part of my life on aging research, my mood became very gloomy and I even allowed the sense of guilt into my mind. But then why in many other countries, aging research has become, during the last few decades, an important thrust area of research when every one knows the end is inevitable? My thoughts started reeling in all directions.

India is a unique country. It has at least 5000 years of history. It has nurtured many religious groups and faiths yet developed a way of life and a culture which is an intricate blend of many faiths projecting like a laser beam pointing towards what can be described as Indian culture characterized by deep faith in providence which is astonishingly combined with most modern scientific thinking which is claimed to be an Indian trait for thousand of years.

Other wise how else one can explain Indian interest to reach moon some day, if necessary with the help from our foreign friends and their technology without bothering to optimize our food production, lay good roads and worry over the threatening increase in population?
Yes indeed, the ever-increasing population on this planet has crossed the 6.5 billion mark in the month of July 2005. Although the rate of increase of population has decreased from 2 percent in 60s to 1.2 percent to day, the nine billion mark is expected to reach around 2050. That is only one side of the story and the problem there off. Out of this 9 billion people in 2050, a large chunk of them would be from developing countries with India’s share being close to 2 billion. Secondly the “grandparents boom” would become clearly visible and pose a major problem to the countries concerned and to the world at large. This means a significant percentage (according to my rough estimate-10%) of this 9 billion people would be in the age bracket of 60 and above. More than 150 million of this global aging population will be from India. This demography is likely to bring up peculiar challenges including the national budgets for aged, health care problems, retirement policies, and utilization of the elderly and social management of the aged.
Advanced countries have sensed this imminent “grandparents boom” almost 50 years ago and launched measures to alleviate the pressures that this demographic change could bring in. The reasons for the expected changes were looked into. It was obvious that reduction in the infant mortality coupled with improved nutrition and health care, resulting from the fruits of medical and biological research, are the reasons. It would be unwise and even uncivilized to make any effort to reverse these achievements. On the other hand emphasis was turned to see why we become “old” and what is the molecular mechanism(s) of this fascinating yet undesirable process. Would it be possible to modulate/control this process? The Science of getting “old” was born with a bang. Separate Institutes and centers were created both from philanthropic and Governmental initiatives to understand the science of aging and age associated debilities as well as to formulate innovative and humane management of elderly. Above all to examine how to prolong the “health span” of aging populations and convert them into a national asset. Today aging is one the thrust areas of research in almost all the developed nations and many others are following the suit.
For example, USA has created a new Institute for Aging Research, called National Institute on Aging (NIA) almost 40 years ago. Japan, European and many other countries have followed the suit. In fact the European countries have got together and formed a European Research Area in Ageing (ERA-AGE, Gerda Geyer, Experimental Gerontology, 40, 759-762 2005) Apart from the State supported new Institutes, already existing centers, universities have created divisions and centers for gerontological research. These initiatives are yielding rich dividends. Tremendous progress is being made in understanding the biological, clinical and behavioral aspects of the phenomenon of getting ‘old’. To day about 250 genes are identified to be associated with the aging process and therefore the life span. Attempts are also being made to examine whether the process of ‘aging’ can be modulated at genetic, molecular and social levels. Extensive research is also going on to examine the possibility of attenuating the deleterious effects of age dependent disorders including neurodegenerative (Alzheimer, Parkinson, Huntington, Stroke etc.). It is no exaggeration to say that there is no university in USA, which does not have a center or institute for gerontology research.
Independent India is just 60 years old. At the time of independence, the average life expectancy in India was around 40 years. Clearly old age was not a problem to worry about. On the other hand, the average life expectancy of an Indian to day is reported to be around 62 years and this figure is fast improving. Never before have so many people lived for so many years- thanks to the amazing progress made in medical and biological research. As such to day India has nearly 80 million people over sixty and this number is suspected to go up to 117 million in 2010 and further up in the years to come (Registrar General of India and National Commission on population, 1996; http://populationcommission.nic.in). As already mentioned above, it is projected that there will be more than 150 million people above 60 years of age by 2050. This changed demographic profile is likely to exert immense pressure on the Government and the people themselves in many ways that are being experienced by the nation to day as a result of mere increase in the population — not to talk about the bulging portion of the aged population.
Yet India does not seem to show any urgent concern about the fast changing demography. A learned friend of mine attributed this to ancient “Indian Wisdom” mentioned in the beginning of this article. However, this author feels that this premise is unacceptable for more than one reason. Even ancient India has developed medical systems to rejuvenate the health of individuals. Ayurveda is essentially a rejuvenating medicine. Modern India has tried hard to control the rapid growth of its population through scientific methods. Modern India is supporting even subjects like fashion technology in order to be in line with developed nations. Therefore there is no reason why India should not do any thing to achieve “Quality Aging” for its aging population so that this experienced section of the society could be converted into an asset. There is need for launching initiatives to promote research in basic aspects of aging process as well as applied research to innovate scientific methodology to manage elderly people. So far Indian Council of Medical Research is the only organization that has taken at least a minor initiative to promote aging research. A much bigger initiative from different quarters is needed if India has to escape the demographic shocks mentioned above.
I would therefore like answer to the title question of this article as “YES”. India must in its own interest promote research on aging and associated diseases in a big way. There are always some discordant, perverted voices projecting the distorted Indian Wisdom. India’s march towards becoming a global leader should not be allowed to be disturbed by vested and disgruntled arguments.
India has however, as on to day, lagged behind in this aspect for obvious reasons. If the increasing ‘aged’ population of the country is not taken care of and looked after well and maintained at reasonable health levels, then it would eventually become an extraordinary cost burden of no returns to the Government and the society at large. On the other hand, the ‘ageing’ population can also be converted into a national resource and asset with proper planning and imaginary inputs. Thus the older people in any country would pose a challenge as well as an opportunity. It is time that India takes an initiative to make it an opportunity because of the advantage it enjoys in mere numbers. This can be termed as Wisdom Resource (preservation and) Development (WRD) and through this the country can derive the longevity dividend. Thus it pays to keep the people with extended longevity in good health and spirits. It is encouraging that the Govt. of India has indeed started looking seriously at this problem (responsibility) in recent past and announced a policy for senior citizens as below.
The National Policy on Older Persons seeks to assure older persons that their concerns are national concerns and they will not live, unprotected, ignored and marginalized. The National Policy aims to strengthen their legitimate place in the society and to help older people to live the last phase of their life with purpose, dignity and peace. The National Policy on Older Persons inter alia visualizes support for financial security, health care and nutrition, shelter, emphasis upon education, training and information needs, provision of appropriate concessions, rebates and discounts etc. to Senior Citizens and special attention to protect and strengthen their legal rights such as to safeguard their life and property. The National Policy on Older Persons confers the status of senior citizen to a person who has attained the age of 60 years.
This above avowed policy has been capped very recently, in Dec 2007, by a bill passed by parliament. This bill is named “The maintenance and welfare of parents and senior citizens bill-2007”. I would like to describe this bill as an historical one in that the Government of India has perhaps for the first time taken the maintenance and welfare of the senior citizens rather seriously and mooted steps to be taken for dignified living of senior citizens. This bill provides a provision for judicial authority to jail children for three months if the parents complain their negligence by children. This may sound peculiar to Indian society, what is important is that the Govt. has taken cognizance of the plight of some parents and created a deterrent in the form of a law for such social offence. The bill also envisages to establish old age homes in every district and a tribunal to look into the difficulties of senior citizens in that district.
The above bill sounds so good as to raise suspicion about its implementation. Be as it may, this is only one way of tackling the problems of senior citizens and there is yet another and perhaps more important way to empower the aged population in terms of their health and quality living and make use of their expertise in different needs of the country. Concrete steps and inputs are necessary. One such step is to establish one or more (in view of the vastness and diversity of the country) Institutes or Centers for a multidisciplinary scientific study of the phenomenon of aging and the associated diseases/problems. Such Institutes would also prepare a database for the clinical and biological profiles of the populations around particularly of the senior citizens to begin with.

 

In summary the following will be the mission of this proposed Center/Institute. To conduct high quality research on:

1. The process of aging – at genetic, molecular, clinical, biochemical and behavioral levels.

2. Disabilities and diseases, including neurological disorders, associated with age and more prevalent in the aged.

3. Psychosocial aspects of the aged with a special emphasis on the special and peculiar needs of the aged.

4. Connectivity between the laboratory findings and the community to promote health among the aged and to make use of the healthy aged to the societal needs.

Science Academies have a responsibility to alert the Government authorities for initiating ventures that would stabilize a social climate in terms of health and economics. Aging research in the lines cited above, in my opinion, would be one to contribute such a climate.

Prof. Kalluri Subba Rao
Hon. Coordinator for Center for Research and Education in Aging (CREA)
University of Hyderabad
Hyderabad- 500046. India
ksrbrain@gmail.com

See also:

Ilia Stambler. Longevity and the Indian Tradition. 2014 http://www.longevityhistory.com/longevity-and-the-indian-tradition/

Ilia Stambler. The Past, the Present and the Future of Longevity Research. DNA India. 13 October 2014. http://www.dnaindia.com/lifestyle/report-the-present-the-past-and-the-future-of-longevity-research-2025654

Support Aging and Longevity Research in India! http://indiafuturesociety.org/support-ageing-longevity-research-india/

Kalluri Subba Rao 1Prof. Kalluri Subba Rao, Ph.D., D.Sc (IISc), FAS-AP, FAMS, FNASc, FNA., is an Indian National Science Academy Honorary Scientist, working at the School of Medical Sciences, University of Hyderabad, India. He has worked as a Professor of Biochemistry/Neurobiology at the University of Hyderabad, and as an INSA-Senior Scientist/Honorary Scientist & Professor at the Centers for Biotechnology and Innovative Research, Institute of Science and Technology, Jawaharlal Nehru Technological University, Kukatpally, Hyderabad. His research interests include Biochemistry and Molecular Biology of the developing and aging brain with special reference to DNA-damage and its repair. He has more than 120 research publications in national and international journals and books. His contributions include establishing the link between aging and decreased DNA repair, particularly the base excision repair, in the brain. He is presently working on a monograph containing the latest scientific information about the process of aging in higher organisms and also examining the available related traditional Indian (Vedic) concepts. He has advocated for the establishment of Institutes or Centers for multidisciplinary scientific study of the phenomenon of aging and the associated diseases in India.

See: https://ifa.ngo/wp-content/uploads/2014/01/Symposium-Participants-Aging-Process-and-NCDs.pdf

http://www.ifa-fiv.org/ifa-12th-global-conference-on-ageing-symposium/

https://uohyd.academia.edu/SubbaRaoKalluri/CurriculumVitae

https://www.insaindia.res.in/detail.php?id=P03-1348