Cell Membrane

The maximum effect can take place within five to fifteen minutes. The other routes are orally (via tablets) and intravenously. Salomon has a number of medical uses, but It is mainly used to treat asthma and exercise Induced bronchus’s. Treatment of chronic obstructive pulmonary disease Is another key use of this drug (diseases In this category Include chronic bronchitis and emphysema). Other less widely applied uses is in treatment of premature labor in obstetrics since the drug can also relax uterine smooth muscles intravenous administration) and in the treatment of cystic fibrosis in combination with other drugs (3).

Despite ten Tact Tanat tens Aragua NAS Eden Invaluable In ten treatment AT serious medical conditions like asthma, there is still a serious pitfall in the long-term use of the drug since most people who have been on it for a long duration tend to the develop some form of drug resistance/tolerance to the drug. This results in a slower and less dynamic effect of the drug on patients who have been using it chronically. Therefore, directly translating to the need to adjust dose and frequency of the drug administration, this can become quite a burden to everyone involved.

Down regulation of the ;2-receptors and a reduction of their sensitivity (desensitizing) causes this resistance (4). The drug has an intricate mode of action that involves a number of pathways at microscopic cell level. Initially, it acts by binding on beta adrenaline receptors (4). The receptor is coupled to a stimulatory guanine nucleotide-binding protein (as – protein) and usually fluctuates between different conformations in the inactive state (5). Once the agonies (Salomon) binds to the receptor, it stabilizes one of the information leading to the activation of the G-protein.

The G-protein is a transmigrate signal transducer that has alpha and beta-gamma subunits (6). After activation of the protein the alpha subunit dissociates, resulting in a form that stimulates activity of the enzyme densely cycles (7). This enzyme now increases the production of cyclic adenosine Mephistopheles (CAMP) in the cell. It does this by transforming adenosine troposphere (TAP) into CAMP through depopulation’s and structure shifting (8). Increased levels of CAMP results in activation of CAMP- dependent protein kinas A.

Protein kingies are enzymes that modify proteins by adding to them a phosphate group(usually derived from TAP). This phosphorescently leads to a functional change in the targeted protein either by altering the enzyme activity, its intracellular location or its interaction with other proteins (9). Protein kinas A is a CAMP dependent kinas and in the activated form, it works in two ways (all of which leads to relaxation of a smooth muscle); first, it decreases the acting- myosin interactions by phosphorescently the myosin light chain (10). Secondly, it lowers intracellular calcium concentration in the smooth muscle cells.

This reduction comes about via two well researched and understood mechanisms. The first mechanism involves the regulation of influx and efflux of calcium through the calcium channels in the sarcoma (which is the cell wall). Protein kinas A causes the channels to increase the efflux of calcium from the cell and decreases influx (11). The second mechanism involves the ceroplastic reticulum which is the chief store of calcium in the cell. The kinas stimulates uptake of calcium into the store, therefore, reducing its overall concentration in the cytoplasm (12).

The effect of these woo mechanisms (low calcium) leads to smooth muscle relaxation. Lastly, research shows that raised levels of CAMP causes a cessation of the release of mediators of inflammation from mast cells in the respiratory tract (13). All of these elaborate actions give Salomon its potency in dilating constricted airways and reducing obstruction secondary to inflammatory processes. But prolonged use and exposure to this drug leads to development of a resistance to it. Many schools of thought have come up with possible explanations as to now tens napes rater years AT Intense research.

However, ten most accepted explanation is down regulation of the ;2-receptors and desensitizing of the same (14). It is now universally accepted that a cell’s surface expression of this receptor and its coupling to signaling pathways inside the cell shows a negative feedback loop that works to reduce the cell responsiveness to prolonged occupation of the receptor by agonies lagan’s. When an agonies attaches to the receptor, the stabilization involves phosphorescently (15). This usually interferes with how the receptor couples with the Gas-protein; therefore, limiting its function in what is commonly referred to as desensitizing.

Desensitizing thus leads to reduction in the activation of intracellular signaling pathways secondary to prolonged receptor stimulation (16). This mechanism of uncoupling is rapid and reversible in nature, usually seen after short-term exposure. Phosphorescently of the receptor usually happens due to protein kinas A dependent pathways or by activation of G-protein receptor kingies named beta -ARKS (17). Tissues of different types show different degrees of this uncoupling when exposed to stimulatory lagan’s, and this can be due to the differences in activity of the above mentioned phosphorescently mechanism.

Apart from desensitizing another key process leading to Salomon resistance is the receptor down regulation. When ;2-receptors stimulation occurs for prolonged duration, they show a negative feedback mechanism that reduces their quantity of expression on the cell surface (18). The mechanism behind this is not particularly clear, but it is strongly believed to be due to receptor trafficking to lissome for destruction. Research has shown that chronic exposure to Salomon does not only lead to uncoupling but also receptor initialization from the cell surface.

Initialization occurs through the process indications, which happens via Claritin coated pit endoscope pathway that works by forming buds from the cell membrane (19). When this process begins, Claritin (which is a small intracellular protein) begins to arrange on the inner surface of the cell’s plasma membrane below the soon to be internalized receptor. The linear ends then start coming together to form a circular Claritin coated pit that has now engulfed a part of the plasma membrane, the receptor and some extracurricular fluid (20).

The pit buds off into the cell and the ends of the plasma membrane come together to correct the deficit left on the surface. This pit is now referred to as a vesicle, and it traffics contents to a cell organelle known as a lissome (21). This organelle has an acidic environment and a number of enzymes that breakdown fats, proteins and carbohydrates. The vesicle fusses with the organelle’s membrane and regurgitates its contents leaving the Claritin molecules on the surface (22). The receptor and other contents are consequently degraded. This is not the only aspect of down regulation that plays a part in reducing receptor expression.

Research has shown that ;2-receptor Mrs. levels significantly reduce in the nucleus when levels of protein kinas A become elevated for long durations (days to months). Clinical features Clinical features of Salomon resistance occur when patients are intolerant to the drug therapy. Recovery, after therapy, is prolonged or absent even after maximum amelioration AT receive dose. I en most gallants clinical Torture appears in the deterioration of asthma and the subsequent exacerbation of the symptoms. Drug resistant asthma presents with (23); Worsening dyspepsia. Continuous wheezing and breathlessness. Chest tightness.

These patients have developed tolerance to Salomon, therefore, are resistant to the therapy. With subsequent increase in the dose therapy which is not effective, patients with theoretically hyper-responsiveness with or without exposure to allergens and with the resulting inflammatory changes and bronchi-constriction, asthma worsens. The most severe clinical feature can present like status asthmatics or acute severe asthma. This present as episodes of severe asthma, failing to respond to usual effective doses of Salomon (24). There is progressive respiratory failure even within the course of therapy.

This episode can progress to fatal asthma. Patients present with; Significant wheezing and dyspepsia. Severe respiratory distress. Hyperventilation and subsequent respiratory leukemia. Features of metabolic acidosis due to anaerobic respiration and elevated levels of lactate from the respiratory muscles (25). Severe asthma will occur with increasing degree of hyper-reactivity due to intolerance to drug therapy: ineffective relief and loss of bronchitis tone. Clinical feature can also occur as a result of high drug dosage. Resistance causes a patient who is in respiratory distress to use increasing and more frequent doses of albums.

High doses produce toxicities which can present with systemic features (26). In the respiratory system; there can be hyperemia. Salomon is a psychosomatic agent (beta 2 agonies) the vacillators effect of beta 2 Zionists increases perfusion of poorly ventilated lung units, transiently decreasing arterial oxygen tension (27). Significance of this effect depends on initial partial pressure of oxygen of the patient. Hyperemia will present clinically as occasions, respiratory distress, and tachyons. There can be paradoxical bronchus’s due to the Atonally antagonism to Transcendentalist erect AT Salomon

I en spasms, AT the smooth muscles lining the bronchi, are due to psychosomatic action of Salomon and adrenaline stimulation. In the cardiovascular system, the psychosomatic action of Salomon can cause toxicity which might result in cardiac arrhythmias, arterial fibrillation, supercritical tachycardia and extra systole (29). There can be an occurrence of coronary insufficiency due to hyperemia, atheistically and resulting tachycardia, peripheral bastardization with a compensatory small increase in heart rate, hypertension and palpitation. In the endocrine and metabolic system, there can be hypoglycemia.

Salomon may stimulate sodium and potassium Tapes which causes redistribution of electrolytes (30). Hyperglycemia in a diabetic patient; Salomon stimulates the beta 2 transporters which stimulate hepatic glycogen breakdown for pancreatic release of clangor which increase plasma glucose. In the central nervous system, overdose of Salomon therapy intolerance can produce CONS symptoms such as insomnia, weakness, dizziness, nervousness, tremors, transient muscle cramps and headache. Rarely reported effects include drowsiness, irritability, chest discomfort and difficulty in instruction (31).

Diagnosis Diagnosis of Salomon resistance follows the clinical guidelines of a full comprehensive history of the patient, physical exam, and investigation to confirm the patient’s tolerance to drugs. In taking the history certain question might lead to the discovery that a patient previously on Salomon therapy is unresponsive to the drug. When doing a physical exam, clinician should check out for general observation such as respiratory distress and occasions. In doing a systemic exam, focusing on the respiratory system may bring out worsening respiratory function.

Clinician may find wheezing with other signs indicative of exacerbated asthma. Investigation Investigative studies are confirmatory and supportive to the diagnosis. The base lines include; Full blood count. Urea electrolyte count. Liver function tests. Random blood sugar if suspecting diabetes. I en consoler long toner tests In prospector s o mol toxicity al u TA Pulmonary function tests Serum blood gas analysis with pH profile Cardiograms to check arrhythmias Gene typing; the cornerstone of Salomon resistance detection is gene typing. Experimental studies have shown that tolerance in asthma is in the polymorphism of he DRAB gene.

Analysis show that tolerance is in the glycogen allele at position 16 and 21 at the beta receptor gene. Gene typing for polymorphism can aid in identifying patients with drug resistant asthma (32). Management Management can be categorized as supportive, specific, preventive and rehabilitative. Supportive management include; Outpatient monitoring if not severe Admission to a hospital if severe. Severe asthma necessitates immediate admission as it can be fatal. Oxygen therapy. Intubations and mechanical ventilation if severe. Use of parental corticosteroids which are anti-inflammatory.

Fluid and electrolyte resuscitation in the case of hypoglycemia. Frequent monitoring of patients to the drug. Specific management is both surgical and medical. Surgical management, research is still underway and ongoing. Medical management includes the use of a second-line therapy like monopolies, astatine and antihistamines. There is also use of cardiac-selective beta adrenaline blocking agents and corticosteroids in Salomon toxicity. Other drugs can be used depending on symptom’s of resistance, for example; interventions, insulin and any other depending on the symptoms of the patient.

Surgical intervention for example attempting bronchial thermoplastic. This is a bronchitis procedure in which delivered thermal energy to airways; it reduces airway smooth muscle hyper responsiveness. It has been also shown to be beneficial in treatment of severe asthma where continuous therapy has failed. Preventive management Includes gene typing early enough to Isolate patients wilt Salomon resistance by checking the beta AR gene. The other way is to prevent high-drug toxicity. Rehabilitative management of any complication that might occur is essential.

The structural compartmentation of mammalian cells and the differing functions of these compartments. All mammals are eukaryotes and therefore have eukaryotic cells. These cells contain several organelles suited to a specific function they carry out within the cell. These eukaryotic cells contain a Nucleus, Mitochondria, Ribosomes, Rough and Smooth endoplasmic reticulum, Golgi apparatus and various other organelles. Most of the organelles are separated from each other by a membrane, these membranes are based on lipid bilayers that are similar to each other.

The organelles membrane is there to keep the contents of each organelle separate from the rest of this cell. The membrane consists of a lipid bilayer that may have channels in order to allow the transport of specific molecules which are needed somewhere else in the cell. An example of this is proteins produced by the ribosomes are then moved to the Golgi apparatus in which they are processed and then sent to the correct part of the cell. | Fig 1 – Diagram of a nucleusSource: http://cdn. nursingcrib. om| The nucleus is a large organelle surrounded by a double membrane nuclear envelope; the nuclear envelope contains many pores to allow substances such as tRNA and mRNA to move between the nucleus and the cytoplasm. The nucleus contains most of the cells genetic material in the form of DNA. The DNA and proteins that make up the contents of the nucleus is known as the chromatin. DNA stored in the nucleus codes for different amino acids and proteins to be produced, depending on which genes are being expressed decides what proteins are produced and ultimately the function of the cell.

At the centre of the nucleus is a nucleolus which is where ribosomes are manufactured. A diagram of a nucleus can be seen in figure 1. The double membrane keeps the nucleus separate from all the other organelles and serves as a barrier to prevent molecules diffusing freely into and out of the nucleus. The outer membrane has a structure similar to the rough endoplasmic reticulum with ribosomes scattered across it which are used to make proteins in a process known as translation. The mitochondria are the site in a cell that generates most of the cells energy in the form of ATP.

Oxygen is used in a process called aerobic respiration to produce lots of ATP. The mitochondrion consists of an outer and inner membrane composed of phospholipid bilayers. The inner membrane contains several folding’s forming a structure known as cristae. The cristae increase the surface area of the mitochondria allowing more ATP to be produced. The part enclosed by the inner membrane is the matrix. This matrix contains most of the mitochondria’s proteins. The matrix contains several enzymes needed to synthesise ATP. The ATP produced in the mitochondria is transported to other parts of the cell that require energy.

The ribosome is an important organelle for protein synthesis, it is the site at which the genetic code is converted into protein molecules. It is responsible for a process called translation which converts mRNA into an amino acid chain. The mRNA determine the order of the tRNA molecules that bind to the codons. The order of these tRNA molecule ultimately decide the amino acid chain that will be produced and hence the protein being produced. The proteins produced detatch themselves from the ribosome and move to other parts of the cell where they are needed.

The ribosome is very large composed of many molecules including RNA and proteins. The ribosome is composed of two sub-units, a larger one and a smaller one, each of which have distinct shapes. As protein synthesis is very important to cells there are usually large numbers of ribosomes found throughout a cell. Ribosomes are usually found floating freely around the cell however they are sometimes found bound to the endoplasmic reticulum. The endoplasmic reticulum is the transport network for molecules. It is made up of several tubes and sacs.

The space inside of the endoplasmic reticulum is the lumen. The function of the endoplasmic reticulum depends on the cell type. It is comprised of a rough endoplasmic reticulum and a smooth endoplasmic reticulum. The Rough endoplasmic reticulum has ribosomes attached to its surface which is what causes it to be rough. “The membrane of the rough endoplasmic reticulum forms large double membrane sheets that are located near, and continuous with the outer layer of the nuclear envelope”[1]. Proteins are synthesized in the rough endoplasmic reticulum.

The smooth endoplasmic reticulum is responsible for synthesizing lipids, metabolizing carbohydrates and regulating calcium levels. Lysosomes are also found in most eukaryotic cells. They contain several used to break down worn out cellular components and bacteria. Lysosomes are highly packed spherical vacuoles but have a large variation in size depending on the materials they have taken up for digestion. The lysosome removes any unwanted material inside the cell by secreting these digestive enzymes onto them. Lysosomes protect the cell from foreign bacteria which could be harmful.

They operate in a low PH which is maintained by a membrane around the lysosome, this reduces the risk of the enzymes digesting their own cell. The Golgi apparatus packages proteins inside the cell and are then sent to their destination. The Golgi apparatus is found within the cytoplasm of eukaryotic cells. It is composed of stacks known as cisternae. “The Golgi apparatus is integral in modifying, sorting and packaging these macromolecules for cell secretion”[2]. Proteins synthesized by the rough endoplasmic reticulum are modified in the Golgi apparatus.

The Golgi apparatus is also responsible for transporting lipids around the cells and also producing lysosomes. All of these organelles have different functions and structures but work together to determine the overall function of the cell. The amount of each organelle greatly depends on its function, for example muscle cells will contain lots of mitochondria to produce more ATP as muscles require large amounts of energy. Bibliography [1] Shibata, Yoko; Voeltz, Gia K. ; Rapoport, Tom A. (2006). “Rough Sheets and Smooth Tubules”. Cell 126(3): 435–439. [2] “Regulated Secretion (Golgi): The Movie”. North Dakota State University.

You recorded the data in Chart 1 on page 35. E the data to produce a Graph that will clearly show how the effects Ion the resting membrane potential when the KEF concentration of Is high and when the KEF concentration of An+ is low. Hint: take in consideration that independent variable is not a numeric but a category. (4 points) The following questions will require you to do some Web search. 2. Loading Is a commonly used anesthetic. What is the molecular composition of Loading. (type of macromolecule and formula) (2 points). 3. List three specific usages of loading (1 points each = 3 points) 1. 3. 4.

Provide the name of two vendors of loading and four (4) brand names for this anesthetic (1 points each) Vendors Brand Names 1 OFF 5. Explain the precise mechanism behind Loading effect on action potential in nerves. Indicate to what type of integral proteins Loading binds to, the effect on such proteins and what will be the effect on the generation of an action potential and on the transmission of the action potential. (4 points) 6. Loading is commonly administrated topically to anesthetize the nerve endings in the dermis that are activated by noxious stimulus resulting in the nerve conduction f impulses that are perceived as “pain”.

Draw a figure of the transverse section of the Shinto show the layers of the epidermis and structures of the dermis (do not forget to include the nerve endings). Use the Diagram to indicate all the layers of cells the Loading has to go through to reach the nerve endings. (Figures copied and pasted form the internet will not be accepted, you have to draw your own version of a figure) (5 points). 7. What cell membrane transport do you suspect moves Loading from the surface of the epidermis all the way down the nerve endings. (1 point)

The plasma membrane is a bilipid layered membrane that allows lipid soluble substances to pass through. It is important that other substance pass through although they are not lipid soluble. In line with this, the membrane has specialized transport proteins in the membrane to facilitate the transfer of these non lipid soluble substances across the membrane. It is also useful for the movement of such molecules and ions like glucose, important intracellular and extra cellular ions involved in the maintenance of electrochemical balance. This is reason proteins carry out facilitated diffusion. It is not a waste of energy in any way.

It is one of the ways by which the cell maintains the sanity of the cell. Cells even maximize energy by the use of facilitate diffusion when compared to active transport. Simple diffusion usually applies when the movements of molecules is along concentration gradient, just as in this is the case in facilitated diffusion. The use of proteins as carrier molecules is part of mechanism to maintain the homeostasis of the cell, to speed up the process of transportation and enable the cell survive in its habitat. When we compare this type of transport with active transport against concentration gradient, really minimal energy is used in the process.

Table of Contents Abstract Introduction Aim Hypothesis Material Method Results Discussion Conclusion? Abstract The aim of this experiment was to see whether different temperatures will affect the cell membrane, thus would then releases the purple pigments out of the vacuole which causes the leakage of the purplish liquid.? Background Information The outermost layer is the cell wall, which is present only in plant cells and is made up of a carbohydrate called cellulose and also has other protein substances embedded within it.

The cell wall is a rigid layer and gives structural stability to the cell and also limits the permeability of large substances into and out of the cell. Within the cell wall, surrounding the cytoplasm is the cell membrane which is a semi-permeable membrane consisting of a phospholipid bilayer. The bilayer consists of phospholipids which arrange themselves so that the hydrophobic (‘water hating’) tails are shielded from the surrounding water. The heads of the molecules are hydrophilic (‘water loving’) and face the water.

Overall, the cell membrane acts to selectively allow substances to move into and out of the cell and maintains the cell potential. Proteins within the membrane act as molecular signals allowing the cells to communicate with each other and other substances outside the cell. About 70% of the cell membrane is actually protein. The cytoplasm of the cell has a number of organelles, although there is one in particular that the vacuole. Vacuoles act to store food for the plant and also assist in structural stability of the plant along with the cell wall.

The vacuoles in plant cells are normally larger than those found in animal cells and contain a fluid called, cell sap. This fluid is rich in nutrients and other substances and is surrounded by a membrane called the tonoplast, separating it from the cytoplasm. The tonoplast is similar in composition to the cell membrane. Biological pigments, also known as pigments or biochromes are substances produced by living organisms that have a colour resulting from the selective colour absorption. The pigments in beetroot are betalain pigments; they are located in the vacuole of the cell.

They are named after the Beet family of plants, but are also found in fungi. In the petals they are thought to attract pollinating insects and may be present in seeds/fruits to encourage birds to eat them and so spreading around the seeds. When a beetroot in heated, it tampers with the cell membranes. A membrane is made of a phospholipid bilayer. These are formed because the phospholipids that make it up have a hydrophilic (‘water loving’) head and a hydrophobic (‘water hating’) tail. The tails pack together, exposing only the heads to the water.

This is the phospholipid bilayer. The beetroot pigment is used commercially as food dye. It changes colour when heated so can only be used in ice-cream, sweets and other confectionary, but it is both cheap and has no known allergic side-effects. Aim To investigate whether different temperatures can damage and denature the plasma cell surface membrane of beetroot cells. This would then release the beetroot pigments out of the vacuole which causes the leakage of the purplish liquid. Hypothesis Beetroot in hotter water will release its pigments more than beetroot in cooler water.

The hotter water should break more vacuoles containing the pigments which will make the water appear to be more purple. Meanwhile the colder water will still have pigments throughout the water, and therefore will be scarcer. Materials -x6 Test Tube -x1 Chopping Board -x1 Serrated Knife -x1 Corer -x6 Skewers -x2 Beetroot -x3 Test Tube Rack -x1 Wooden Test Tube Holders -x1 Bunsen Burner -x1 Match Box -x1 Cork Mat Method 1. Use the corer to get equal cylindrical pieces of beetroot 2. Cut pieces to same size if they are unequal 3. Skewer the beetroot through the middle . Rinse the skewers of beetroot 5. Fill the test tubes to half way with water 6. Place beetroot skewers into test tube and test tubes into test tube holder. Cold 1. Put in fridge and freezer 2. Remove after chosen time, and record your observations. Hot 1. Put over a hot flame and a purple flame 2. Remove after chosen time, and record your observations Results TemperatureColour of WaterColour of Beetroot Room Temperature: 23°C Rich and Dense PurpleDeep Red Not visible through water Fridge: 10°C Partially reddish purpleHot Pink Freezer:-9°C

Very light pink barely any change in the colourVery deep red Blue Flame: 100°C A deep, rich redNormal purple colour Discussion Beetroot in hotter water will release its pigments more than beetroot in cooler water. The hotter water should break more vacuoles containing the pigments which will make the water appear to be more purple. Meanwhile the colder water will still have pigments throughout the water, and therefore will be scarcer. The hypothesis was supported by the results as the beetroot in the hotter water did release more pigments than the beetroot in the colder water.

Some problems that came to attention were the exact sizes of the beetroot pieces could not be made the exact same size. Even though cutting them side by side of each other did make them look similar, the sizes were off still. The experiment as brought sight to what can happen when a fruit or vegetable or flower is heated in water will do. The water colouring process will accelerate more than twice as fast and that could provide big opportunities in some companies. A flaw in the experimental design was that attention wasn’t given to the material of test tubes that were used.

A glass test tube was used for the beetroot that was frozen in the freezer; while in fact a plastic test tube should have been used because the glass test tube could not flex to the expansion of the water in the test tube and so resulting it to crack. Conclusion In conclusion, the hypothesis was supported as the beetroot’s pigments were release more in the hot water more than the cold water did. The hotter water made the beetroot cell vacuoles to burst, releasing the pigments, thus colouring the water.

B. Assuming that Joseph’s heart stopped, all of the cellular processes and membrane functions are going to be affected. The loss of oxygen is going to affect everything, ultimately killing off all of the cells. Loss of oxygen and glucose will affect the mitochondria, making it unable to make ATP, the energy the body requires to function. Without any oxygen, the membrane will no longer be able to control its diffusion processes/pumps, allowing anything in and out of the cell and not properly getting rid of wastes.

Leaving all of the waste behind, unable to regulate itself, all of the cells will eventually die off. C. In a human cell, the golgi complex, nucleus(nuclear envelope), and entire cell(plasma membrane) have membranes. During his heart attack the lysosomal enzymes, formed from the golgi complex, began to digest the membranes and all of their organelles, thus affecting the heart because all of the cells are being destroyed and can no longer function homeostatically.

D. Inside the nucleus, the chromosomes house the instructions Joseph’s body needs to repair itself and his predisposition for vascular disease. E. Integral and peripheral proteins are involved in the homeostatic imbalances of Joseph’s heart because now, due to lack of oxygen and glucose, they are not performing their jobs correctly. Both proteins are now allowing anything in and out of the cell at its own will with no system to it. F. Reestablishing oxygen flow to Joseph’s body was so important because it got oxygen to the cells and the carbon dioxide out of the body. All of the process in the body would have ultimately stopped if oxygen flow has not been reestablished. H. Joseph’s heart failed because without oxygen or glucose the cells cannot make ATP. Without ATP the cells do not have the necessary energy to undergo any of their cellular processes. Eventually the cells will actually start digesting themselves, thus making the heart and all the other organs in the body fail.