Practical Class N 10: Postembryonic Development PDF

Summary

This document details the stages of human postnatal ontogenesis from birth to adulthood, exploring the different periods, including the newborn period, infancy, primary and secondary childhood, puberty, and elderly periods. Also touching on the processes of aging, the theories on aging, and other related topics such as regeneration and transplantation.

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1 PRACTICAL CLASS N 10 THEME: POSTEMBRYONIC DEVELOPMENT. POSTNATAL ONTOGENESIS OF A HUMAN BEING. THE TOPIC RELEVANCE: Postembryonic period is from the hatching out or birth to the biological death. This p...

1 PRACTICAL CLASS N 10 THEME: POSTEMBRYONIC DEVELOPMENT. POSTNATAL ONTOGENESIS OF A HUMAN BEING. THE TOPIC RELEVANCE: Postembryonic period is from the hatching out or birth to the biological death. This period in the ontogenesis of multicellular animals that follows the period of embryonic development and usually ends with the onset of sexual maturity and, in most animals, the cessation of growth. Postembryonic development begins after the emergence of the embryo from the egg and embryonic membranes, when the organism becomes capable of active feeding and locomotion. This knowledge is very important for medical professionals. They contribute to the formation of a holistic picture of the development of the body, which is an integral part of the competencies being formed. THE AIM: 1. To study the natural laws of postembryonic development. 2. To study the peculiarities of human postnatal ontogenesis. THE PLAN FOR THEME STUDY: 1. Postembryonic development. 2. Human postnatal ontogenesis. 3. Aging Process in Humans. 4. Theories on the Causes of Aging. 5. Regeneration. 6. Transplantation. THE NOTES: 1. Postembryonic development. Postembryonic period is from the hatching out or birth to the biological death. This period in the ontogenesis of multicellular animals that follows the period of embryonic development and usually ends with the onset of sexual maturity and, in most animals, the cessation of growth. Postembryonic development begins after the emergence of the embryo from the egg and embryonic membranes, when the organism becomes capable of active feeding and locomotion. Types of postembryonic ontogenesis. Upon transition to the postembryonic state the organism either immediately possesses the principal pubertal morphological characteristics (direct development) or essentially differs from the pubertal form, in which case the larva that hatches out of the egg must undergo a metamorphosis before it reaches its adult state (indirect development). Growth continues during the period of postembryonic development and further organogenesis and histogenesis occur. The functions of 2 the developing organism become more complex; establishment of the final proportions of the body is especially characteristic. Two types of postembryonic ontogenesis: direct and development with metamorphosis. The first of them is typical for the organisms with the unlarval and intrauterine type of development, the second one is for the organisms of larval type. In most of non-vertebrate groups, especially amongst insects, and some fish and amphibian species, there is the development with metamorphosis. Metamorphosis means the rapid changes which occur during the transition from larva to adult form. Ontogenesis which includes the following stages: egg-larva-imago is called with incomplete metamorphosis (amphibians). In some arthropods, larva is transformed to another metamorphic stage – pupa, and ontogenesis includes four stages: egg-larva-pupa-imago and is called development with complete metamorphosis. Larva and pupa are the metamorphic stages which need as dispersal phases for the distribution of species and prepare an organism for the adult life in a new habitat or environment. There is direct development in human and most of vertebrates. A new organism has the typical systems of organs as adult, but some of them are not mature. The unvarval direct development is typical for the organisms with rich yolk granules contented eggs (birds, reptiles); and intrauterine type – for the pure yolk granules contented eggs (mammalian and human). Periods of postembryonic development. 1. Growth and morphogenesis. 2. Maturation period. 3. Aging period, ending by biological death. 2. Human postnatal ontogenesis. Table. 3 Age periods of human postnatal ontogenesis 1- 10 day Newborn 16-20 Juvenile period 17 -21 11 day - 1 year Period of lactation 21 -35 Maturity I 22 -35 1 – 3 years Infancy 36 -55 Maturity II 36 - 60 4 – 7 years Primary childhood 56 -74 Elderly period 61 -74 8 – 11 years Secondary childhood 75 -90 Senescence 8 – 12 years 12 – 15 years Puberty period 90 и > Long liver 13 - 16 years The characteristics of the periods of the human postnatal ontogenesis. Newborn period 1) birth to end of 4th week 2) newborn begins to carry on respiration, obtain nutrients, digest nutrients, excrete wastes, regulate body temperature, and make cardiovascular adjustments Infancy 1) end of 4th week to one year 2) growth rate is high 3) teeth begin to erupt 4) muscular and nervous systems mature 5) communication begins Childhood 1) one year to puberty 2) growth rate is high 3) permanent teeth appear 4) muscular control is achieved 5) bladder and bowel controls are established 6) intellectual abilities mature Adolescence 1) puberty to adulthood 2) person becomes reproductively functional and emotionally more mature 3) growth spurts occur 4) motor skills continue to develop 5) intellectual abilities continue to mature 4 Adulthood 1) adolescence to old age 2) person remains relatively unchanged anatomically and physiologically 3) degenerative changes begin Senescence 1) old age to death 2) degenerative changes continue 3) body becomes less able to cope with demands placed on it 4) death results from various conditions and diseases 3. Aging Process in Humans. The aging process in humans is a complex biochemical process which includes all the changes taking place socially, psychologically and physically. The process of aging in the human body is inevitable and there are many signs of aging occurring both within and outside the human body. Aging, also known as senescence, is a process that every human being goes through, but the aging process in women slightly differs from the aging process in men. As we age, there are a number of changes taking place in the various systems of the human body, which may, at times cause age-related problems and disorders. Normal Aging Process in Humans. Normally, the process of aging in the human body starts at middle age around 45. The process and its effects depend on both, the genetic as well as environmental factors and hence, some of the aspects of the aging process mat differ from person to person. To understand the human aging process better understand the different levels of aging process. Molecular changes: - DNA transcription is low; - Translation and intensively of protein synthesis is low; - DNA repair process is low; - Energy metabolism is low, anaerobic processes are prevalent in metabolism. Sub-cellular changes: - storage of lipofutcin pigment in a cytoplasm; - reduction of rough ER; - reduction of cytoplasmic membranous structures; - increasing of cytoplasmic microfibers; - accumulation of free radicals in a cytoplasm; Cellular changes: - reduction of cell mitotic activity; - intensification of the chromosomal mutations formation; Organs changes: - decrease of vital lung capacity; 5 - increase of arterial pressure; - atherosclerosis; - decrease of activity of thyroid glands; - reduction of basal metabolism; - involution of reproductive glands and decreasing of the sex hormone production. Aging Process in Women. Women undergoing a normal aging process tend to go through some major physical as well as psychological changes. Most women tend to put on some weight with the onset of menopause and also acquire some wrinkles and fine lines as signs of aging. Their skin tends to loose all the natural moisture, becomes dry and starts loosening out. There is also a substantial decrease in bone mass, body mass and muscle strength which makes them prone to a number of illnesses especially osteoporosis and arthritis. The process of aging in women also causes them to shrink or loose height due to loss of bone tissue from the vertebrae. Hormonal changes in aging women can bring about a lot of psychological and behavioral changes in them. Aging Process in Men. Men too, go through a number of changes due to the process of aging, hormonal changes being the most important of all changes. This process of hormonal changes taking place in men is known as 'andropause' and can be identified by a marked change in the plasma levels of testosterone, melatonin and dehydroepiandrosterone. These changes lead to a decrease in the levels of libido, muscle and body mass, bone strength and also impotency in some males. Other changes that may be noticed in aging males include increased forgetfulness, insomnia and irritability. However, the aging process in men is far more easier than that in women and most men tend to age without facing any major physical aging problems. Aging men tend to face mental problems like Alzheimer’s disease and dementia and may also face prostrate related disorders and cardiovascular disorders. 4. Theories on the Causes of Aging. Current theories can, in general, be separated into two groups: 1. DNA Damage Theories Aging is caused by accumulated damage to DNA, which in turn inhibits cells' ability to function and express the appropriate genes. This leads to cell death and overall aging of the organism. a) DNA Damage/Repair Theory b) Free Radical/Oxidation Theory c) Mitochondrial DNA Theory d) Radiation Theory 2. Built-In Breakdown Theories 6 Aging is a direct consequence of genetic programming. The causes for aging are directly built into the genome and cellular structure, as a sort of molecular clock. a) Disposable Soma Theory b) Genetic Theory c) Immunological Theory d) Telomere Theory DNA Damage/Repair Theory DNA damages occur continuously in cells of living organisms. While most of these damages are repaired, some accumulate, as the DNA Polymerases and other repair mechanisms cannot correct defects as fast as they are apparently produced. In particular, there is evidence for DNA damage accumulation in non-dividing cells of mammals. These accumulated DNA damages probably interfere with RNA transcription. It has been suggested that the decline in the ability of DNA to serve as a template for gene expression is the primary cause of aging. Most damage comes in the form of oxidative damage, and hence is likely to be a prominent cause of aging. Free Radicals & Anti-Oxidants Free Radicals In general, a free radical is any molecule with one or more unpaired electrons in its valence shell. In the discussion of aging, the free radicals of importance are oxygen-based molecules such as superoxide (O2-), hydroxy radical (OH), singlet oxygen (O), hydrogen peroxide (H2O2), and hypochlorous acid (HOCl). Free radicals, though attractive and charming, are damaging to the body because they are extremely reactive; they tend to rip electrons off of other molecules in order to pair off their lone electrons. In other words, free radicals are strong oxidizing agents. Unfortunately, free radicals cannot be avoided since they are byproducts of essential reactions in the body, such as the process of metabolizing oxygen. Free radicals can also be found in abundance in the environment: air pollution, tobacco smoke, radiation, toxic waste, and certain chemicals. Free radicals wreak havoc at a cellular level since they are able to: - break off cell membrane proteins, thereby destroying cellular identity. - fuse membrane lipid & proteins, hardening the cell membrane and leading to brittle and nonfunctional cells. - disrupt the nuclear membrane. Free radicals may expose genetic material in the nucleus, leaving the DNA open for mutation or destruction. - burden the immune system by damaging immune cells. - cause chronic diseases. These effects are known as oxidative stress, and may lead to DNA mutations, cell death, and disease, all of which contribute to the overall effects of aging. To prevent oxidative stress, one should reduce environmental burdens in the body 7 (chemicals/heavy metals), reduce stress, improve the quality of one's food supply, and (if possible) increase one's antioxidant mechanisms. Antioxidants Antioxidants are the body's solution to oxidative stress. These molecules neutralize free radicals by supplying them with extra electrons. This exchange results in lowering the reactivity of the free radical and leaving the antioxidant itself with an unpaired electron. The structure of an antioxidant, however, is not damaging to the body since it is stabilized through chain reactions with other antioxidants. Known antioxidants include: - enzymes such as glutathione peroxidase, catalase, superoxide dismutase. - nutrients including vitamins C and E, beta carotene, selenium, cystene, uric acid. - synthetic molecules such as DSMO, BHT, and BHA. The Free Radical / Oxidation Theory This, perhaps one of the most respected and well-studied theories, rests on the fact that oxidants induce a variety of distinct biochemical changes in target cells. Hydrogen peroxide is considered one of the more troublesome oxidants, as it diffuses into target cells where site-directed hydroxyl radical formation injures specific targets. DNA is particularly sensitive to hydroxyl radical-induced damage: both DNA strand breakage and base hydroxylations can be detected. The breakage of the DNA strand activates a DNA binding protein (poly(ADP- ribose)polymerase), which forms polymers of ADP-ribose bound to various nuclear proteins using NAD as its substrate. NAD turnover under these circumstances increases so dramatically that it affects ATP synthesis, to the point where high enough concentrations inactivates mitochondrial ATP synthesis. If the concentration of hydrogen peroxide is high enough, these pathways will lead to cell death, and, therefore, hydrogen peroxide-induced alterations will not be passed on to future generations. If, however, cells are exposed to sub-lethal concentrations of hydrogen peroxide, the ensuing injury could cause permanent and transmissible cellular alterations which could be biologically detrimental. For instance, if hydroxyl anion-induced DNA damage fails to be repaired or is improperly repaired, this DNA damage could lead to genetic alterations such as mutations, deletions, and rearrangements. Moreover, if these genetic alterations occur in critical genes that are involved in cell growth and differentiation, they could lead to deregulated cell growth and differentiation and ultimately contribute to the malignant transformation of cells. Hence, the growing number of free radical diseases includes the two major causes of death, cancer and arteriosclerosis. Since hydrogen peroxide easily defuses through cell membranes, hydroxyl anion formation may occur extra- or intracellularly, depending on the availability of transition metals. Because of its high reactivity, the hydroxyl radical will always cause site- directed damage at the site of its formation. However, the body does possess some natural antioxidants in the form of enzymes which help to curb the 8 dangerous build-up of these free radicals, without which cellular death rates would be greatly increased, and subsequent life expectancies would decrease. Mitochondrial DNA Theory This theory suggests that the loss of effectiveness of one of the cell's key organelles paves the way for age-related degenerative diseases. The mitochondria, which are the energy-producing bodies within a cell, have their own genome (mtDNA). This mtDNA is synthesized at the inner mitochondrial membrane near the sites of formation of highly reactive oxygen species. Mitochondrial DNA seems unable to counteract the damage inflicted by these by-products of respiration because, unlike the nuclear genome, it lacks advanced repair mechanisms. Thus, the cell loses its ability to produce energy, and gradually dies. This theory is supported by observations confirming the genomic instability of mitochondria, as well as widespread mtDNA deletions and other types of injury to the mitochondrial genome. Radiation Theory This theory is focused primarily on the aging of skin cells, as they are most directly affected by external sources of radiation. Radiation can create free radicals in cells, as the radiation strikes surrounding water molecules and other proximal targets. Thus the aging process goes back to the free radical theory on aging mentioned above, with radiation serving to increase its rate. Experimental studies have recently shown that the shorter, more energetic spectrum of the ultraviolet range (UVB) is responsible for the dermal connective tissue destruction observed in photoaged skin. Also, it has been shown that UVA and infrared radiation contribute significantly to photoaging, producing, among other changes, severe elastosis. Thus, even small amounts of radiation is enough to accelerate the aging process, although this theory is, as they say, only skin-deep. Disposable Soma Theory Soma, or somatic cells, are all the cells in the body except gametes and cells involved in gamete formation. This theory suggests that because of the requirement for reproduction, natural selection favors a strategy that invests fewer resources in maintenance of somatic cells than are necessary for indefinite survival. Therefore, energy will be spent to ensure minimum damage to molecular structures such as DNA, and to ensure that the animal remains in sound condition through its natural life expectancy in the wild, where accidents are the predominant cause of death. Since longevity is costly energy- wise, and since with age there is no longer any ability to reproduce and hence pass genetic material onto subsequent generations, there is simply no reason to keep an organism alive past its time of procreation. Genetic Theory Experiments have shown that human cells will divide less than 100 times outside the body. Also, there is an inverse correlation between the number of cell divisions and the age of the person from which the cells were taken. This theory 9 suggests that cell senescence is an active process, as even though they are unable to divide, senescent cells are actively metabolizing. It has been suggested that senescence is genetically programmed, and that its phenotype is dominant, illustrated by the fact that when normal and immortal human cells were fused, they showed limited division potential. Senescent cells express highly abundant DNA synthesis inhibitory mRNA's and produce a surface membrane associated protein inhibitor of DNA synthesis not expressed in young cells. Thus, this theory suggests that aging is predetermined in the genome, and that it is a dominant condition, although the onset of the phenomenon is still unknown. Immunological Theory It is well documented that the effectiveness of the immune system peaks at puberty and gradually declines thereafter with advance in age. This seems to be based primarily on T-cells, and it is generally associated with an increase in susceptibility to infections as well as in incidence of autoimmune phenomena in the elderly. T-cells lose effectiveness in early life due to the decay of the thymus gland. In other words, the quality and quantity of T-cells begins to decline after puberty. Therefore, as one grows older, certain antibodies lose their effectiveness, and fewer new diseases can be combated effectively by the body, which causes cellular stress and eventual death. Telomere Theory This theory suggests that cell death is caused by the shortening of telomeres, which are "caps" on the ends of chromosomes. It has been observed that with each cell division the telomeres are shortened by approximately 65 base-pairs. Telomeres function by permitting complete replication of eukaryotic chromosomes, and by protecting chromosome ends from recombination. It has been shown experimentally that cell strains with shorter telomeres undergo significantly fewer doublings than those with longer telomeres. These observations suggest that telomere length is a biomarker of somatic cell aging in humans and is consistent with a causal role for telomere loss in this process. When the telomeres get too short, the cell stops replicating at an appreciable rate, and so it dies off, which eventually leads to the death of the entire organism. Diseases Involving Accelerated Aging. Several diseases have the effect of rapidly increasing the rate at which the carrier ages. For example, patients afflicted by progeria suffer from arteriosclerosis, coronary artery disease, congestive heart failure and non-healing fractures by the age of seven. Degeneration of hair follicles leads to balding. Most progeria sufferers die by the age of 30. Several other diseases are known to have similar effects, including Cockayne syndrome and Werner's syndrome. Possibilities of Increased Lifespan. As things stand, the maximum human lifespan is about 120 years. As a whole, human knowledge is increasing at an exponential rate. By this logic, some 10 scientists believe the human lifespan could be increased to between 400 and 1,000 years within the next 20 years. (Of course, we wouldn't really know for 400 more years...) The following are some theories on increasing the human lifespan: By increasing the amount of antioxidants in one's system, one will have less damaging free radicals in the body. The necessary antioxidants can be found in several sources: Multivitamin pills, especially Vitamins C and E. Beta carotene, Zinc, Selenium, Calcium, Magnesium, Chromium Picolinate, Coenzyme Q-10. Telomerase has been discovered in some germs and cancer cells, but not in most normal organisms. This enzyme replaces/repairs shortened telomeres such that the cells are able to replicate (theoretically) forever. If the telomerase gene could be activated or spliced into regular human cells (assuming telomere theory is correct), human longevity would be greatly increased. A mutant form of the gene age-1 in the worm C. elegans caused the worm's lifespan to double. The gene apparently codes for an enzyme important in the mediation of cellular communication and signal transmission. Increased lifespan was observed when the age-1 gene was nonfunctional. Injection of growth hormone into men seemed to reverse some signs of aging. Experiments with other hormones, such as estrogen and testosterone, are ongoing. 5. Regeneration. Regeneration - is a property of living matter to repair its structures. Physiological - to repair the organs, tissues and cells throughout life (epidermis of skin, blood cells). Repairative – to repair the organs, tissues and cells after trauma or other destructions. 1. Epimorphosis - regeneration in which cell proliferation precedes differentiation and formation of new organs. 2. Morphollaxis – regeneration in which regenerative region is restored. a) hypormorphosis – with incomplete restoration of organ; b) heteromorphosis – with appearance of new structure. 3. Compensatory hypertrophy - increase in size of an organ or tissue when called upon to do additional work or to perform the work of destroyed tissue or of a paired organ (lymph system and spleen). 4. Physiological hypertrophy – increasing of organ size without restoration of initial organ form. (mammalian liver). 6. Transplantation. Transplantation – a property of living matter tom transplanting of an organ or tissue. Types of transplantation: 1. Autotransplantation – tissues or organs are grafted from one area to another on the same individual. 2. Isotransplantation – tissues or organs are grafted between two genetically identical individuals such as identical twins. 11 3. Aullotransplantation – tissues or organs are grafted from one individual to another of the same species but of the different genetic constitution. 4. Xenotransplantation – tissues or organs are grafted between individuals of different species such as from pig to human. PRACTICAL WORKS: Work №1. Plot a graph of age-specific variability of a human being inweight and height of a body. 1). Using the table with parametres of human weight and hight, draw thegraphs. Analize and make the conclusion. Weight of body (kg) Height of body (cm) 0 in birth - 3.37 0 in birth - 51.45 3 months - 6.07 3 months - 61.53 6 months - 8.00 6 months - 66.77 9 months - 9.30 9 months - 71.85 12 months - 10.40 12 months - 76.47 2 years - 12.75 2 years - 86 3 years - 14.60 3 years - 96 4 years - 15.76 4 years - 101 5 years - 17.90 5 years - 108 6 years - 19.63 6 years - 120 7 years - 23.60 7 years - 122 8 years - 27.30 8 years - 131 9 years - 30.00 9 years - 136 10 years - 33.50 10 years - 141 11 years - 36.80 11 years - 146 12 years - 41.80 12 years - 152 13 years - 46.40 13 years - 157 GRAPH OF AGE-SPECIFIC VARIABILITY. Y (weight&height) X (age) HOMEWORK: To study theme № 11: «MAJOR CONTROL IN CYTOLOGY.».

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