Gene Physiology

Gene is the basic hereditary unit of the cell. It is a portion of DNA molecule that contains the message or code for the synthesis of a specific protein from amino acids. It is like a book that contains the information necessary for protein synthesis.

 In the nucleotide of DNA, three of the successive base pairs are together called a triplet or a codon. Each codon codes or forms code word (information) for one amino acid. There are 20 amino acids and there is separate code for each amino acid. For example, the triplet CCA is the code for glycine and GGC is the code for proline. Thus, each gene forms the code word for a particular protein to be synthesized in ribosome (outside the nucleus) from amino acids.

 GENETIC DISORDERS

 Genetic disorder is a disease or condition that occurs due to absence of a gene or a defective gene or by a chromosomal abnormality.

Causes of Genetic Disorders

 Genetic disorders occur due to two causes.

1. Genetic variation

Genetic variation means the presence of a gene that dif- fers from normal gene.

2. Genetic mutation

Generally, mutation means an alteration or a change in nature, form, or quality. Genetic mutation refers to change of the DNA sequence within a gene or chromosome of an organism, which results in the creation of a new character,

 Classification of Genetic Disorders

Genetic disorders are classified into four types:

1. Single gene disorders.

2. Multifactorial genetic disorders.

3. Chromosomal disorders.

4. Mitochondrial DNA disorders.

1. Single gene disorders

 Single gene disorders or mendelian, or monogenic disorders occur because of variation or mutation in one single gene. Examples include sickle cell anemia and Mitochondrial Huntington's disease.

2. Multifactorial genetic disorders

Multifactorial genetic disorders or polygenic disorders are caused by combination of environmental factors and mutations in multiple genes. Examples are coronary heart disease, Alzheimer's disease, arthritis and diabetes,

3. Chromosomal disorders

Chromosomal disorder is a genetic disorder caused by abnormalities in chromosome. It may be due to any change in structure (structural abnormality) or number (numerical abnormality) of chromosomes. It is also called chromosomal abnormality, anomaly or aberration. It often results in genetic disorders, which involve physical or mental abnormalities. Chromosomal disorder is caused by numerical abnormality or structural abnormality.

Chromosomal disorder is classified into two types:

 i. Structural abnormality (alteration) of chromosomes which leads to disorders like chromosome instabil- ity syndromes.

 ii. Numerical abnormality of chromosomes, which is of two types:

a. Monosomy due to absence of one chromosome from normal diploid number. Example is Turner syndrome.

b. Trisomy due to the presence of one extra chro- mosome along with normal pair of chromosomes in the cells. Example is Down syndrome.

 4. Mitochondrial DNA disorders

 Mitochondrial DNA disorders are the genetic disorders caused by the mutations in the DNA of mitochondria (non-chromosomal DNA). Examples are Kearns-Sayre syndrome (neuromuscular disorder characterized by myopathy, cardiomyopathy and paralysis of ocular muscles) and Leber's hereditary optic neuropathy (disease characterized by degeneration of retina and loss of vision).

 RIBONUCLEIC ACID

 Ribonucleic acid (RNA) is a nucleic acid that contains a long chain of nucleotide units. It is similar to DNA, but contains ribose instead of deoxyribose. Various functions coded in the genes are carried out in the cytoplasm of the cell by RNA. RNAS is formed from DNA.

STRUCTURE OF RNA

Each RNA molecule consists of a single strand of poly- nucleotide unlike the double-stranded DNA.

Each nucleotide in RNA is formed by:

 1. Ribose: Sugar.

 2. Phosphate.

3. One of the following organic bases:

Purines:

 i. Adenine (A)

ii. Guanine (G).

Pyrimidines:

 i. Uracil (U)

ii. Cytosine (C).

 Uracil replaces the thymine of DNA and it has similar structure of thymine. 

TYPES OF RNA

RNA is of three types. Each type of RNA plays a specific role in protein synthesis. The three types of RNA are given below.

1. Messenger RNA (mRNA)

Messenger RNA carries the genetic code of the amino acid sequence for synthesis of protein from the DNA to the cytoplasm.

2. Transfer RNA (tRNA)

Transfer RNA is responsible for decoding the genetic message present in mRNA.

3. Ribosomal RNA (rRNA)

 Ribosomal RNA is present within the ribosome and forms a part of the structure of ribosome. It is responsible for the assembly of protein from amino acids in the ribosome.

GENE EXPRESSION

 Gene expression is the process by which the informa- tion (code word) encoded in the gene is converted into functional gene product or document of instruction (RNA) that is used for protein synthesis.

Gene expression involves two steps:

1. Transcription.

 2. Translation.

TRANSCRIPTION OF GENETIC CODE

Transcription means copying. It indicates the copying of genetic code from DNA to RNA. The proteins synthesized in the ribosomes which are present in cytoplasm. However, the synthesis of different proteins depends upon the information (sequence of codon) encoded in the genes of the DNA which is present in the nucleus. Since DNA is a macromolecule, it cannot pass through the pores of the nuclear membrane and enter the cytoplasm. But, the information from DNA must be sent to ribosome. So, the gene has to be transcribed (copied) into MRNA which is developed from DNA.

 Thus, the first stage in the protein synthesis is tran- scription of genetic code, which occurs within the nucleus. It involves the formation of mRNA and simultaneous copying or transfer of information from DNA to MRNA. The MRNA enters the cytoplasm from the nucleus and activates the ribosome resulting in protein synthesis. The formation of mRNA from DNA is facilitated by the enzyme RNA polymerase. 

TRANSLATION OF GENETIC CODE

 Translation is the process by which protein synthesis Occurs in the ribosome of the cell under the direction of genetic instruction carried by MRNA from DNA. Or, it is the process by which the MRNA is read by ribosome to produce a protein. This involves the role of other two types of RNA, namely tRNA and rRNA.

The MRNA moves out of nucleus into the cytoplasm. Now, a group of ribosomes called polysome gets at- tached to MRNA. The sequence of codons in MRNA are exposed and recognized by the complementary sequence of base in tRNA The complementary sequence of base Is called anticodon. According to the sequence of bases in anticodon, different amino acids are transported from the cytoplasm into the ribosome by tRNA that acts as a carrier. With the help of rRNA, the protein molecules are assembled from amino acids. The protein synthesis occurs in the ribosomes which are attached to rough endoplasmic reticulum.

GROWTH FACTORS

 Growth factors are proteins which act as cell signaling molecules like cytokines and hormones. These factors bind with specific surface receptors of the target cell and stimulate proliferation, differentiation and/or maturation of these cells. Often, the term growth factor is interchangeably used with the term cytokine. But growth factors are distinct from cytokines. Growth factors act on the cells of the growing tissues. But cytokines are concerned with the cells of immune system and hematopoietic cells. Many growth factors are identified.

CELL DEATH

 Cell death occurs by three distinct processes:

1. Autophagy.

2. Apoptosis.

3. Necrosis.

AUTOPHAGY

Autophagy is a normal physiological process in the body by which cells are destroyed. The word AUTOPHAGY is derived from Greek (auto = self, phagy = eating). It is also by which cells are destroyed. The word autophagy is de- called autophagocytosis. Autophagy involves formation autophagosome which contains worn-out cytoplasmic organelles. Autophago- some fuses with lysosome. Refer 'Functions of Lysosome in this chapter. Then the enzymes of the lysosome cause destruction of the organelles by protein degradation. The constituents of the organelles are reused for formation of new cells. Thus, it maintains a balance between break down of damaged organelles and formation new cellular organelles. Autophagy is always considered as a nonapoptotic programmed cell death.

 APOPTOSIS

 Apoptosis is defined as the natural or programmed death of the cell under genetic control. Originally, apoptosis refers to the process by which the leaves fall from trees in autumn (In Greek, apoptosis means 'falling leaves'). Apoptosis is referred as 'cell suicide' because the cells activate an intracellular death program and kill themselves in a controlled way. This type of programmed cell death is a normal phe- nomenon and it is essential for normal development of the body. In contrast to necrosis, apoptosis usually does not produce inflammatory reactions in the neighboring tissues. 

Functional Significance of Apoptosis

The purpose of apoptosis is to remove unwanted cells without causing any stress or damage to the neighbor- ing cells.

Functional significance of apoptosis:

1. Plays a vital role in cellular homeostasis. About 10 million cells are produced every day in human body by mitosis. An equal number of cells die by apopto- sis. This helps in cellular homeostasis.

2. Useful for removal of a cell that is damaged beyond repair by a virus or a toxin.

3. An essential event during the development and in adult stage.

 Examples of apoptosis

 i. A large number of neurons are produced during the development of central nervous system. But up to 50% of the neurons are removed by apop- tosis during the formation of synapses between neurons.

 ii. Apoptosis is responsible for the removal of tissues of webs between fingers and toes during developmental stage in fetus. 

iii. It is necessary for regression and disappearance of duct systems during sex differentiation in fetus.

iv. The cell that loses the contact with neighboring cells or basal lamina in the epithelial tissue dies by apop- tosis. This is essential for the death of old enterocytes. v. It plays an important role in the cyclic sloughing of the inner layer of endometrium, resulting in menstru ation.

vi. Apoptosis removes the autoaggressive T cells and prevents autoimmune diseases. 

Activation of Apoptosis

 Apoptosis is activated by either withdrawal of posi tive signals (survival factors) or arrival of hegative signals.

Withdrawal of positive signals

Positive signals are the signals which are necessary for the Jong-time survival of most of the cells. The positive signals are continuously produced by other cells or some chemi- cal stimulants. Best examples of chemical stimulants are:

i. Nerve growth factors (for neurons).

ii. Interleukin-2 (for cells like lymphocytes).

Absence or withdrawal of the positive signals acti- vates apoptosis.

Arrival of negative signals

Negative signals are the external or internal stimuli which initiate apoptosis. External stimuli are applied by stimulus molecules, death-receptor ligands. Internal stimuli are arising from inside the cell (see below).

Death-receptor ligands

 Death-receptor ligands are the substances which bind with specific cell membrane receptors and initiate process of apoptosis. Common death-receptor ligands are of three types.

1. Tumor necrosis factor alpha (TNF-a) TNF-a is a cytokine secreted by may cells including activated T-lymphocytes and natural killer cells.

2. Fas ligand (FASL) Fas ligand (first apoptosis signal ligand) is a trans- membrane protein belonging to tumor necrosis factor superfamily. It is found on activated T-lymphocytes and natural killer cells. It is also called Apo-1L.

 3. Trail ligand Trail ligand (TNF - related apoptosis including ligand) belongs tumor necrosis factor ligand family secreted by many types of normal tissue cells, It is also called Apo-2L.

Death-receptors

death receptors are: Death-receptors are the cell membrane receptors which receive the death-receptor ligands. Well characterized

1. TNF receptor-1 (TNFR1)

2. Fas receptors

3. TNF-related apoptosis inducing ligand (TRAIL) re- ceptors called DR4 and DR5.

Initiation of Apoptosis

Apoptosis is initiated by two pathways, the extrinsic pathway and intrinsic pathway. In extrinsic pathway, the signal (stimulus) for apoptosis is received from outside the cell. In intrinsic pathway, the signal arises from within the cell itself. Both extrinsic and intrinsic pathways lead to an ex- ecution process during with the cell death occurs.

Extrinsic Pathway of Apoptosis

 Extrinsic pathway of apoptosis is initiated stimulation of death receptors of target cells by signal molecules, death ligands. Generally, the death receptors have an extracel- lular domain and an intracellular (cytoplasmic) domain. Extracellular domain is responsible for binding of ligands and interaction with those ligands. The intracellular do- main is called death domain. When the ligand binds with receptor, the death do- main allows recruitment of many proteins to the receptor and formation of a protein complex called death inducing signaling complex (DISC). Now caspase (see below) is recruited to DISC and gets activated resulting in execu- tion process.

Intrinsic Pathway of Apoptosis

Intrinsic pathway is also called of apoptosis is initiated by internal stimuli arising from following conditions:

 1. Cellular stress.

2. Increase in the concentration of intracellular oxi- dants.

3. Viral infection.

 4. Damage of DNA.

                Internal stimuli activate the proapoptotic BCL-2 fam- ily proteins which in turn inactivate antiapoptotic BCL-2 proteins. The interaction between proapoptotic and antia- poptotic proteins causes destabilization of mitochondrial membrane and release of apoptotic factors which induces execution process. BCL-2 (B-cell lymphoma 2) family proteins are the cell death regulators located near mitochondria.

 Execution Process of Apoptosis

 Both extrinsic and intrinsic pathways end in the common execution process. Mitochondria plays and important role during this process.

 Role of mitochondria in apoptosis

 External or internal stimuli initiate apoptosis by activat- ing the proteases called caspases (cysteine-dependent aspartate-specific proteases). Normally, caspases are suppressed by the inhibitor protein called apoptosis inhibiting factor (AIF). When the cells receive apoptotic stimulus, mito- chondria release two protein materials. First one is Cytochrome C and the second protein is called second mitochondria-derived activator of caspases (SMAC) or its homologue diablo.

                         SMAC/diablo inactivates AIF so that the inhibitor is inhibited. During this process SMAC/diablo and AIF ag- gregate to form apoptosome. This activates caspases. Cytochrome C also facilitates caspase activation. Cell shows sequence of characteristic morphological changes during apoptosis, viz.:

 i. Activated caspases digest the proteins of cytoskel- eton and the cell shrinks and becomes round.

ii. Because of shrinkage, the cell losses the contact with neighboring cells or surrounding matrix.

iii. Chromatin in the nucleus undergoes degradation and condensation.

 iv. Nuclear membrane becomes discontinuous and the DNA inside nucleus is cleaved into small fragments.

v. Following the degradation of DNA, the nucleus breaks into many discrete nucleosomal units, which are also called chromatin bodies.

vi. Cell membrane breaks and shows bubbled appear- ance.

vii. Finally, the cell breaks into several fragments con- taining intracellular materials including chromatin bodies and organelles of the cell. Such cellular frag- ments are called vesicles or apoptotic bodies,

viii. Apoptotic bodies are engulfed by phagocytes and dendritic cells.

Abnormal Apoptosis

 Apoptosis within normal limits is beneficial for the body. However, too much or too little apoptosis leads to abnormal conditions. 

Common abnormalities due to too much apoptosis

 a. Ischemic-related injuries.

 b. Autoimmune diseases like:

i. Hemolytic anemia.

ii. Thrombocytopenia.

iii. Acquired immunodeficiency syndrome (AIDS).

c. Neurodegenerative diseases like Alzheimer's disease.

Common abnormalities due to too little apoptosis 

1. Cancer.

 2. Autoimmune lymphoproliferative syndrome (ALPS).

 CANCER

 Cancer is defined as a disease caused by uncontrolled division of abnormal cells in the body.

Apoptosis and Cancer

 Generally, when something goes abnormal in a cell, that cell is immediately destroyed by apoptosis. This also prevents development of cancer. However, some of the cells particularly tumor cells evade apoptosis. The cells escaped from apoptosis become cancer cells and con- tinuously proliferate despite their abnormalities.

 Free Radicals and Cancer

Free radicals or oxidants are the bactericidal agents se- creted by many cells in the body. Free radicals are also called Reactive oxygen species (ROS). Free radicals are the most potent bactericidal agents. So. even the bacteria which cannot be digested by lyso- somal enzymes are degraded by these radicals. At the same time free radicals are able to cause cancer and other diseases such as heart diseases, neu- rological diseases and autoimmune diseases. Free radicals cause oxidative injury in the cells leading to damage of proteins and DNA resulting in develop- ment of cancer.

 Role of Antioxidants

Antioxidants are the substances which protect the cells from damage caused by free radicals. These substances interact with free radicals and stop cellular damage. Hence, the antioxidants are called "free radical scavengers".

Examples of antioxidants

1. Beta-carotene.

2. Vitamin A. 

3. Vitamin C.

4. Vitamin E.

 NECROSIS

 Necrosis (means 'dead' in Greek) is the uncontrolled and unprogrammed death of cells due to unexpected and accidental damage. It is also called 'cell murder' because the cell is killed by extracellular or external events. After necrosis, the harmful chemical substances released from the dead cells cause damage and inflammation of neighboring tissues.

Causes for Necrosis

Common causes of necrosis are injury, infection, inflam- mation, infarction and cancer, Necrosis is induced by both physical and chemical events such as heat, radiation, trauma, hypoxia due to lack of blood flow and exposure toxins.

Necrotic Process

Necrosis results in lethal disruption of cell structure and activity. The cell undergoes a series of characteristic changes during necrotic process, viz.:

1. Cell swells causing damage of the cell membrane and appearance of many holes in the membrane.

2. Intracellular contents leak out into the surrounding environment.

3. Intracellular environment is altered.

4. Simultaneously, a large amount of calcium ions is released by the damaged mitochondria and other organelles.

 5. Presence of calcium ions drastically affects the orga- nization and activities of proteins in the intracellular components.

6. Calcium ions also induce release of toxic materials that activate the lysosomal enzymes.

7. Lysosomal enzymes cause degradation of cellular components and the cell is totally disassembled re- sulting in death.

8. Products broken down from the disassembled cell are ingested by neighboring cells.

Reaction of Neighboring Tissues after Necrosis

 Tissues surrounding the necrotic cells react to the breakdown products of the dead cells, particularly the derivatives of membrane phospholipids like the arachi- donic acid. Along with other materials, arachidonic acid causes the following inflammatory reactions in the sur- rounding tissues:

 1. Dilatation of capillaries in the region and thereby in- creasing local blood flow. 

2. Increase in the temperature leading to reddening of the tissues.

3. Release of histamine from these tissues which in. duces pain in the affected area.

4. Migration of leukocytes and macrophages from blood to the affected area because of increased capillary permeability.

5. Movement of water from blood into the tissues caus- ing local edema,

6. Engulfing and digestion of cellular debris and foreign materials like bacteria by the leukocytes and macro- phages.

 7. Activation of immune system resulting in the removal of foreign materials.

8. Formation of pus by the dead leukocytes during this process.

9. Finally, tissue growth in the area and wound healing.

CELL ADAPTATION

 Cell adaptation refers to the changes taking place in a cell in response to environmental changes.

 Normal functioning of the cell is always threatened by various factors such as stress, chemical agents, dis- eases and environmental hazards. Yet, the cell survives and continues the function by means of adaptation. Only during extreme conditions, the cell fails to withstand the hazardous factors which results in destruction and death of the cell.

Cellular adaptation occurs by any of the following mechanisms:

 1. Atrophy.

2. Hypertrophy.

3. Hyperplasia.

4. Dysplasia.

5. Metaplasia.

 6. Neoplasm.

 ATROPHY

 Atrophy means decrease in size of a cell. Atrophy of a greater number of cells results in decreased size or wast- ing of the concermed tissue, organ or part of the body.

Causes of Atrophy

Atrophy is due to one or more number of causes such

I. Poor nourishment.

 ii. Decreased blood supply.

iii. Lack of workload or exercise.

iv. Loss of control by nerves or homones.

v. Intrinsic disease of the tissue or organ.

Types of Atrophy

 Atrophy is of two types, physiological atrophy and patho- logical atrophy. Examples of physiological atrophy are the atrophy of thymus in childhood and tonsils in adoles- cence. The pathological atrophy is common in skeletal muscle, cardiac muscle, sex organs and brain.

HYPERTROPHY

 Hypertrophy is the increase in the size of a cell. Hypertro- phy of many cells results in enlargement or overgrowth of an organ or a part of the body. Hypertrophy is of three types.

1. Physiological Hypertrophy

 Physiological hypertrophy is the increase in size due to increased workload or exercise. The common physiologi. cal hypertrophy includes.

i. Muscular hypertrophy

 Muscular hypertrophy refers to increase in bulk of skel- etal muscles that occurs in response to strength training exercise.

 ii. Ventricular hypertrophy

 Ventricular hypertrophy means increase in size of ven- tricular muscles of the heart which is advantageous only if it occurs in response to exercise.

 2. Pathological Hypertrophy

 Increase in cell size in response to pathological changes is called pathological hypertrophy. Example is the ven- tricular hypertrophy that occurs due to pathological condi- tions such as high blood pressure, where the workload of ventricles increases.

3. Compensatory Hypertrophy

 Compensatory hypertrophy is the increase in size of the cells of an organ that occurs in order to compensate the loss or dysfunction of another organ of same type. Ex. amples are the hypertrophy of one kidney when the other kidney stops functioning and the increase in muscular strength of an arm when the other arm is dysfunctional or lost.

HYPERPLASIA

Hyperplasia is the increase in number of cells due to increased cell division (mitosis). It is also defined as abnormal or unusual proliferation (multiplication) of cells due to constant cell division. Hyperplasia results in gross enlargement of the organ. Hyperplasia involves constant cell division of the normal cells only. Hyperplasia is of three types.

1. Physiological Hyperplasia

Physiological hyperplasia is the momentary adaptive response to routine physiological changes in the body. For example, during the proliferative phase of each menstrual cycle, the endometrial cels in uterus increase in number.

 2. Compensatory Hyperplasia

Compensatory hyperplasia is the increase in number of cells in order to replace the damaged cells of an organ or the cells removed from the organ. Compensatory hyperplasia helps the tissues and organs in regeneration. It is common in liver. After the surgical removal of the damaged part of liver, there is increase in the number of liver cells resulting in regeneration.

 Compensatory hyperplasia is also common in epithelial cells of intestine and epidermis.

3. Pathological Hyperplasia

 Pathological hyperplasia is the increase in number of cells due to abnormal increase in hormone secretion. It is also called hormonal hyperplasia. For example, in gigantism, hypersecretion of growth hormone induces hyperplasia that results in overgrowth of the body.

DYSPLASIA

 Dysplasia is the condition characterized by the abnor- mal change in size, shape and organization of the cell. Dysplasia is not considered as true adaptation and it is suggested as related to hyperplasia. It is common in epithelial cells of cervix and respiratory tract.

 METAPLASIA

Metaplasia is the condition that involves replacement of one type of cell with another type of cell. It is of two types.

1. Physiological Metaplasia

Replacement of cells in normal conditions is called physiological metaplasia. Examples are transformation of cartilage into bone and transformation of monocytes into macrophages.

2. Pathological Metaplasia

 Pathological metaplasia is the irreversible replacement example, chronic smoking results in transformation of normal mucus secreting ciliated columnar epithelial cells into non-ciliated squamous epithelial cells, which are of cells due to constant exposure to harmful stimuli. For ncapable of secreting mucus. These transformed cells may become cancerous cells if the stimulus (smoking) is prolonged.

INEOPLASM OR TUMOR

Neoplams or tumor is the abnormal growth of any tissue or organ in the body. Neoplasm may be benign (non- cancerous) or malignant (cancerous)

 CELL DEGENERATION

Cell degeneration is a process characterized by damage of the cells at cytoplasmic level, without affecting the nu- cleus. Degeneration may result in functional impairment or deterioration of a tissue or an organ. It is common in metabolically active organs like liver, heart and kidney. Degenerative changes are reversible in most of the cells.

Common Causes for Cell Degeneration

1. Atrophy, hypertrophy, hyperplasia and/or dysplasia of cell.

2. Fluid accumulation in the cell.

 3. Fat infiltration into the cell.

4. Calcification of cellular organelles.

CELL AGING

Cell aging is the gradual structural and functional changes in the cells that occur Over the passage of time. It is now suggested that cell aging is due to damage of cellular substances like DNA, RNA, proteins and lipids, etc. when the cell becomes old. When more cellular substances are damaged, the cellular function decreases. This causes deterioration of tissues, organs or parts of the body. Finally, the health of the body starts declining and this leads to death. So, the cell aging determines the health and life span of the body.

STEM CELLS

Stem cells are the primary cells capable of reforming themselves through mitotic division and differentiating into specialized cells. These cells serve as repair system of the body and are present in all multicellular organisms.

 SOURCE OF STEM CELLS

 Stem cells are derived from, embryo, umbilical cord blood and adult.

1. Embryonic Stem Cells

Embryonic stem cells are derived from the inner cell mass of a blastocyst which is an early stage of embryo. It takes about 4 to 5 days after fertilization to reach the blastocyst stage and it has about 30 to 50 cells.

Embryonic stem cells have two important qualities:

 i. Self-renewal capacity.

 ii. Pluripotent nature, i.e. these cells are capable of differentiating into all types of cells in ectodermal. endodermal and mesodermal layers.

 Because of these two qualities, the embryonic stem cells can be used therapeutically for regeneration or replacement of diseased or destroyed tissues. In fact, embryonic pluripotent stem cells are now cultured and Jot of research is going on to explore the possibility of using these cells in curing the disorders like diabetes mellitus by cell replacement technique. But ethical issues arise because the embryo has to be destroyed to collect the stem cells.

 2. Stem Cells from Umbilical Cord Blood

 Stem cells in umbilical cord blood are collected from the placenta or umbilical cord. Use of these stem cells for research and therapeutic purposes does not create any ethical issue because it does not endanger the life of the fetus or newborn. Because of vitality and easy availability. the umbilical cord blood stem cells are becoming a potent resource for transplant therapies. Nowadays, these stem cells are used to treat about 70 diseases and are used in many transplants worldwide.

 3. Adult Stem Cells

 Embryonic stem cells do not disappear after birth. But remain in the body as adult stem cells and play a role in repair of damaged tissues. However, their number becomes less. Adult stem cells are the undifferentiated multipotent progenitor cells found in growing children and adults. These are also known as somatic stem cells and are found everywhere in the body. These cells are capable of dividing and reforming the dying cells and regenerating the damaged tissues. So, these stem cells can also be used for research and therapeutic purposes. Adult stem cells are collected from bone marrow.

Two types of stem cells are present in bone marrow.

i. Hematopoietic stem cells, which give rise to blood cells.

ii. Bone marrow stromal cells, which can differentiate into cardiac and skeletal muscle cells.

ADVANTAGES OF STEM CELLS

Aduit stem cells from bone marrow are used in bone mai row transplant to treat leukemia and other blood disorders for 30 years. Recently, it is known that these stem cells can develop into nerve cells, liver cells, skeletal muscle cells and cardiac muscle cells. Recent discoveries also reveal that the stem cells are present in several tissues which include blood, blood vessels, skeletal muscle, liver, skin and brain. It is also found that these cells are capable of differentiating into multiple cell types. So, the cell-based therapy using stem cells may be possible to treat many diseases such as heart diseases, diabetes, Parkinson's disease, Alzheimer's disease, spi- nal cord injury, stroke and rheumatoid arthritis

Source K Sembulingam's physiology