Modern Birth Control And Gender Roles Essay - 2209 Words

Before the introduction of modern birth control, gender roles emphasized the responsibility of women to conceive and raise children. Although this began to change in the in the mid-twentieth century, with the introduction of the first hormonal birth control pill, Enovid, taking place in 1960, it was not readily accessible during that time period (Buttar and Seward, 2009, p. 1-3). This did not change during the time period immediately following the introduction either; five years after the introduction of Enovid, there was still controversy surrounding the use of contraceptives. In the Supreme Court case of Griswold v. Connecticut, the legality of birth control on the market was debated, and the case concluded with the allowance of hormonal contraceptives, but it was limited to married couples only under the right of marital privacy (George and Lewis, 2016, p. 1). The controversy and secrecy that surrounded the use of birth control shortly after its introduction indicates that althoug h it was certainly present and used in society during this time period, it still carried the negative social connotations of the past, which prevented it from being socially normalized. In contrast, the standardization of birth control in society took place decades later, from approximately the 1990 to 2010s. In contemporary American society, birth control has become more readily accessible to women, which is indicated by the increased usage of contraception in society. The number of birthShow MoreRelatedGender Is A Now A Large Topic For Modern Society938 Words   |  4 PagesGender is a now a huge topic for modern days. How can you classify a gender in modern society? The answer to this question cannot be answered in modern society but in the past countries were the ones to label genders. 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To begin, suffrage for women in America began in the mid 1800s and ended in 1920, when women in America were finally granted with this well-deserved right to vote. In America, suffrage began in the western state of Wyoming in 1869, where women had a slightly more equal role in the economy and were generally more accepted in politics andRead MoreThe Political Economy Of Gender933 Words   |  4 Pagesthe home and workplace. Responses to gender gap problems don’t have the same solutions around the world however. Through the â€Å"The Political Economy of Gender† by Iversen and Rosenbluth the effect modern movements have on women’s beliefs can be examined through Albert Hirschman’s ideas of â€Å"voice and exit† and further applied to situations such as those examined in â€Å"Exit, voice, and family policy in Japan† by Leonard Schoppa. In â€Å"The Political Economy of Gender† background is provided on the economicRead MoreThe Political Economy Of Gender1211 Words   |  5 Pagesthe home and workplace. Responses to gender gap problems don’t have the same solutions around the world however. Through the â€Å"The Political Economy of Gender† by Iversen and Rosenbluth the effect modern movements have on women’s beliefs can be examined through Albert Hirschman’s ideas of â€Å"voice and exit† and further applied to situations such as those examined in â€Å"Exit, voice, and family policy in Japan† by Leonard Schoppa. In â€Å"The Political Economy of Gender† Iversen and Rosenbluth provide backgroundRead MoreThe Yellow Wallpaper And Gender1409 Words   |  6 PagesFajardo December 8, 2015 ENG 180-03 Final Paper The Yellow Wallpaper and Gender Charlotte Perkins Gilman is a feminist American poet, writer and lecturer for social reform (Purvis 2009). 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Fayols “Principles” in a University Library - 2030 Words

In reading through Management Basics for Information Professionals by Evans and Ward, one of the theories of management that stood out to me was the â€Å"administrative approach† (2007). Henry Fayol was one of the main proponents of this approach, though there were many others as well. Fayol â€Å"divided organizational activities into five major groups† and also identified 14 principles of management and believed that â€Å"management is a skill one can learn, rather than a talent received at birth† (Evans Ward, 2007). In the context of my personal experience I found that it might be interesting to compare my experiences as a student employee in the UC Berkeley library to some of the more applicable aspects of Fayols principles of management. I†¦show more content†¦Another of Fayols principles had to do with authority and responsibility. In the department of the main stacks, there was a staff librarian who acted as our manager, as well as a group of s tudents that performed supervisory tasks. In my last year or so in the library I joined this group, and was given the task of doing some of the day-to-day tasks that kept our department running. These included opening and closing procedures, keeping statistics of the work done by students, assigning hourly jobs, training, and so on. The important idea in this principle is that â€Å"giving orders and being responsible must go together† (Evans Ward, 2007). I would argue that in our department, while we were responsible for making sure the work was done as well as assigning jobs, if there was a difficult situation the supervisors were able to refer to the staff librarian for support. For example, if one student was chronically underperforming or late, we would notify the librarian. 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Acute Inflammation Essay Example For Students

Acute Inflammation Essay Acute Inflammation The survival of all organisms requires that they eliminate foreign invaders, such as infectious pathogens, and damaged tissues. These functions are mediated by a complex host response called inflammation. Definition of inflammation Inflammation is fundamentally a protective response, the ultimate goal of which is to rid the organism of both the initial cause of cell injury (e. g. , microbes, toxins) and the consequences of such injury (e. g. , necrotic cells and tissues) The process of inflammation is usually described by the suffix â€Å"itis† The components of the inflammatory reaction that destroy and eliminate microbes and dead tissues are capable of also injuring normal tissues. Therefore, injury may accompany entirely normal, beneficial inflammatory reactions, and the pathology may even become the dominant feature if the reaction is very strong (e. g. , when the infection is severe), prolonged (e. g. , when the eliciting agent resists eradication), or inappropriate (e. g. , when it is directed against self-antigens in autoimmune diseases. r against usually harmless environmental antigens in allergic disorders). Some of the most vexing diseases of humans are disorders in which the pathophysiologic basis is inappropriate, often chronic, inflammation. This is why the process of inflammation is fundamental to virtually all of clinical medicine. ] ACUTE INFLAMMATION Acute inflammatory reactions are triggered by a variety of stimuli: †¢ Infections (bacterial, viral, parasitic) and microbial toxins †¢ Trauma (blunt and penetrating) †¢ Physical and chemical agents (thermal injury, e. . , burns or frostbite; irradiation; some environmental chemicals) †¢ Tissue necrosis (from any cause) †¢ Foreign bodies (splinters, dirt, sutures) †¢ Immune reactions (also called hypersensitivity reactions Cardinal signs of inflammation Celsus, a Roman writer of the first century AD, first listed the four cardinal signs of in flammation Rubor, Calor, Dolor, Tumour Functio laesa Rubor- redness Calor – heat (Increased blood flow can be visualized as redness (rubor) and felt as heat (calor) Tumor – swelling (due to edema) Dolor pain The fourth cardinal sign of inflammation is pain (dolor). This is the result of increased pressure in the interstitium due to edema. Pain fibers are stimulated through pressure receptors but also may be stimulated by the direct effects of bradykinin, a plasma protease end product of the kinin system A fifth clinical sign, Functio laesa- loss of function was later added by Virchow. Acute inflammation has two major components: Vascular events The 2 major vascular changes are: 1) Alterations in vascular caliber that lead to an increase in blood flow (vasodilatation) (2) Structural changes in the microvasculature that permits plasma proteins and leukocytes to leave the circulation (Increased Vascular Permeability) Cellular events 1. Leukocyte extravasation 2. Chemotaxis 3. Phagocytosis Vascular events Vascular changes play an important role in acute inflammation. Normally, plasma proteins and circulating cells are sequestered inside the vessels and move in the direction of fl ow. laminar flow) In inflammation, the blood vessels undergo a series of changes to maximize the movement of plasma proteins and circulating cells, out of the circulation and into the site of injury. The 2 major vascular changes are: 1. Changes in vascular flow and caliber (vasodilatation) †¢ Vasodilation is one of the earliest manifestations of acute inflammation. Sometimes, it follows a transient constriction of arterioles, lasting a few seconds. †¢ Vasodilation first involves the arterioles and then results in opening of new capillary beds in the area. Thus comes about increased blood flow, which is the cause of the heat and the redness. †¢ Vasodilation is induced by the action of several mediators, notably histamine and nitric oxide, on vascular smooth muscle. Histamine causes dilation of arterioles and contraction of endothelial cells in the venule 2. Increased Vascular Permeability (Vascular Leakage) Hallmark of acute inflammation is increased vascular permeability leading to the escape of a protein-rich fluid (exudate) into the extravascular tissue. Alterations in the anatomy and function of the microcirculation are among the earliest responses to tissue injury and may promote fluid accumulation in tissues- â€Å"OEDEMA† Formation of transudates and exudates. | |A, Normal hydrostatic pressure (blue arrows) is about 32 mm Hg at the arterial end of a capillary bed and 12 mm Hg at the venous | |end; the mean colloid osmotic pressure of tissues is approximately 25 mm Hg (green arrows), which is equal to the mean capil lary | |pressure. Therefore, the net flow of fluid across the vascular bed is almost nil. | |B, A transudate is formed when fluid leaks out because of increased hydrostatic pressure or decreased osmotic pressure. |C, An exudate is formed in inflammation | The loss of fluid results in concentration of red cells in small vessels and increased viscosity of the blood, reflected by the presence of dilated small vessels packed with red cells and slower blood flow; a condition termed as stasis. As stasis develops, leukocytes, primarily neutrophils, accumulate along the vascular endothelium, stick to the endothelium and eventually escape into the interstitial tissue via the vascular wall. Normal fluid exchange and microvascular permeability are critically dependent on an intact endothelium. How then does the endothelium become leaky in acute inflammation? Following mechanisms have been proposed: 1. Gaps due to endothelial contraction Endothelial cell contraction leads to intercellular gaps in venules. It is the most common form of increased vascular permeability and is elicited by histamine, bradykinin, leukotrienes and many other classes of chemical mediators. Its action is fast and short lived. 2. Direct Injury Direct endothelial injury results in vascular leakage by causing endothelial cell necrosis and detachment. This effect is usually seen after severe injuries like burns, toxins and chemicals. Venules, arterioles, and capillaries can all be affected depending on site of injury. Its action is fast and may be long lived (hours to days). 3. Leukocyte-dependent injury Leukocyte dependant endothelial injury usually happens in venules and pulmonary capillaries, the vascular sites where leukocytes can adhere to the endothelium. This is a late response and is long lived. 4. Increased transcytosis Increased transcytosis also augments venular permeability, especially after exposure to vascular endothelium derived growth factor. This occurs in venules. 5. New blood vessel formation New blood vessel formation at sites of angiogenesis also increases vascular permeability. This persists till intercellular junctions form. Cellular Events The next requirement for the inflammatory response is to get the inflammatory cells (leukocytes) to the site of injury. Vascular dilatation increases the volume of blood to the tissue site but also changes the flow characteristics within the vessel. The cells are normally contained in the central or axial part of the blood column. Dilatation increases cross sectional area of the vessel and decreases the net flow rate per unit area. This causes cells to fall out of the central region of the vessel; they begin to tumble along the epithelial surface. Sequence of cellular events in journey of leukocytes from vessel lumen to interstitial tissue is divided to 3 phases, in the lumen, diapedesis, and migration in interstitial tissue towards chemotactic stimulus. A: In the lumen: B: Diapedesis The next step is migration of cells through the endothelium, called diapedesis . Therefore the process of transmigration across the endothelium, also known as diapedesis which happens after adhesion Diapedesis occurs predominantly in the venules. PECAM-1 (platelet endothelial cell adhesion molecule-1, CD31) in intercellular junctions of endothelium is involved in the migration of leukocyte towards site of infection. Leukocytes pierce the basement membrane by secreting collagenases, insert pseudopods into the junction between endothelial cells and then squeeze through interendothelial junction. In extravascular connective tissue, leukocytes adhere to extracellular matrix by ? 1 and CD44. Eventually they traverse the basement membrane and escape into extravascular space. Leukocyte adhesion and transmigration is regulated by chemical mediators and binding of complementary adhesion molecules on leukocytes and endothelial surfaces. The adhesion receptors involved belongs to 4 families: ) selectins b) immunoglobulin super family c) integrins d) mucin like glycoprotein a) Selectins are proteins which function in the adhesion of leukocytes to endothelial cells. P-selectin (CD62P) present in platelets and endothelium (Wiebel-Palade bodies) mediates binding of neutrophil, lymphocyte, and monocytes. L-selectin (CD62L) -which are expressed on most leukocyte types, serve as homing receptors for lymphocytes to enter lymph nodes. It also serves to bind neutrophil to endothelial cells t sites of inflammation. E-selectin (CD62E) expressed on endothelium mediates homing of effector and memory T-cells to peripheral sites of inflammation, particularly the skin. b) Immunoglobulin superfamily includes 2 endothelial adhesion molecules: a) ICAM-1 (intracellular adhesion molecules 1) b) VCAM-1 (vascular cell adhesion molecule 1) They both serve as ligands for integrins found on leukocyte c) Integrins are transmembrane heterodimeric glycoproteins that promote cell-cell, or cell-matrix interactions. Integrins are expressed on many cell types. 2 integrins, LFA-1 and Mac-1 bind to ICAM-1. ?1 integrins, VLA-4 binds to VCAM-4 d) Mucin like glycoproteins is found in extracellular matrix and on cell surface. For example heparan sulphate serves for ligand for leukocyte adhesion molecule CD44. Chemotaxis After extravasation, leukocytes emigrate in tissue towards site of injury in a process called chemotaxis. It’s defined as locomotion along a chemical gradient. Both exogenous and endogenous substanc es can act as chemo attractants a) Exogenous – components of bacterial products. ) Endogenous – components of complement system, C5a – products of lipoxygenase pathway, leukotriens B4 – Cytokines like IL-8 All the chemotactic agents bind to 7-transmembrane G-protein coupled receptors on leukocyte surface. v Signals initiated from these receptors result on recruitment of G-protein and activation of several effector molecules, phospholipase C, phophonositol-3-kinase, and protein tyrosine kinase. v PLC? and phophonositol-3-kinase act on membrane inositol phospholipids to generate lipid 2nd messenger that increases cytosolic calcium and activates small GTPases. GTPases cause polymerization of actin, leading to increased amount of polymerized actin at leading edges of the cell. Leukocyte moves by extending filopodia that pull the back of the cell to the direction of extension. (3)Phagocytosis Leukocytes ingest offending agents, kill bacteria and other microb es, and get rid of necrotic tissue and foreign substances. Phagocytosis involves three distinct but interrelated steps †¢ (1) recognition and attachment of the particle to be ingested by the leukocyte (2) its engulfment, with subsequent formation of a phagocytic vacuole †¢ (3) killing or degradation of the ingested material (a) Recognition and attachment of the particle to be ingested by the leukocyte. Phagocytosis of microbes and dead cells is initiated by recognition of the particles by receptors expressed on the leukocyte surface. (1)Mannose receptors (2) Scavenger receptors are two important receptors that function to bind and ingest microbes. The mannose receptor is a macrophage lectin that binds terminal mannose and fucose residues of glycoproteins and glycolipids. These sugars are typically part of molecules found on microbial cell walls, whereas mammalian glycoproteins and glycolipids contain terminal sialic acid or N-acetylgalactosamine. Therefore, the macrophage mannose receptors recognize microbes and not host cells †¢ The process of coating a particle, such as a microbe, to target it for phagocytosis is called opsonization †¢ The efficiency of phagocytosis is greatly enhanced when microbes are opsonized by specific proteins (opsonins) for which the phagocytes express high-affinity receptors Major opsonins are IgG antibodies †¢ C3b breakdown product of complement, †¢ Certain plasma lectins, notably MBL (mannose binding lectin ) (b)Engulfment with subsequent formation of a phagocytic vacuole †¢ During engulfment, extensions of the cytoplasm (pseudopods) flow around the particle to be engulfed, †¢ Eventually resulting in complete enclosure of the particle within a phagosome created by the plasma membrane of the cell. The limiting membrane of this phagocytic vacuole then fuses with the limiting membrane of a lysosomal granule, resulting in discharge of the granules contents into the phagolysosome. †¢ (c) Ki lling or degradation of the ingested material The ultimate step in the elimination of infectious agents and necrotic cells is their killing and degradation within neutrophils and macrophages, which occur most efficiently after activation of the phagocytes Veteran interview EssayLaboratory evaluation †¢ Changes in peripheral white blood cell count Leukocytosis: Normally climbs to 15000 – 20000 Neutrophilia – bacterial infections Lymphocytosis – viral infections ( Infectious Mononucleosis , Mumps) Eosinophilia – allergic or parasitic infestation Leucopenia – Typhoid, virus, rickettsia Lymphocytosis and neutropenia in acute viral infections †¢ Examination of inflammatory infiltrate Changes in plasma proteins Characteristic high protein levels and high specific gravity Presence of acute inflammatory cells Elevated levels of acute phase reactants (C-reactive protein, 1 antitrypsin, Fibrinogen, Serum amyloid protein (SAA) and haptoglobin) †¢ CRP and SAA bind to microbial cell walls , act as opsonins and fix complement †¢ Fibrinogen causes erythrocytes to form rouleaux †¢ Prolonged production of these proteins results in secondary amyloidosis in chronic inflammation †¢ Elevated levels of CRP is a marker of increased risk of myocardial infarction in patients with coronary artery disease †¢ Increased erythrocyte sedimentation rate Biopsy and microscopic examination of tissue; Hyperemia, edema, neutrophil infiltration and fibrin Lymphatics in inflammation †¢ Much of the emphasis in the discussion of inflammation is on the reactions of blood vessels, but lymphatics also participate in the response. †¢ As is well known, the small amount of interstitial fluid formed normally is removed by lymphatic drainage. †¢ In inflammation, lymph flow is increased an d helps drain edema fluid from the extravascular space. †¢ Because the junctions of lymphatics are loose, lymphatic fluid eventually equilibrates with extravascular fluid. In addition to fluid, leukocytes and cell debris may also find their way into lymph. †¢ In severe inflammatory reactions, especially to microbes, the lymphatics may transport the offending agent. †¢ The lymphatics may become secondarily inflamed (lymphangitis), as may the draining lymph nodes (lymphadenitis). †¢ Inflamed lymph nodes are often enlarged, because of hyperplasia of the lymphoid follicles and increased numbers of lymphocytes and phagocytic cells lining the sinuses of the lymph nodes. This constellation of pathologic changes is termed reactive, or inflammatory, lymphadenitis †¢ For clinicians, the presence of red streaks near a skin wound is a telltale sign of an infection in the wound. †¢ This streaking follows the course of the lymphatic channels and is diagnostic of lymp hangitis; it may be accompanied by painful enlargement of the draining lymph nodes, indicating lymphadenitis. Sequelae of inflammation – The possible outcomes of acute inflammation are Resolution When the injury is limited or short-lived and when there has been no or minimal tissue damage, the usual outcome is restoration to histologic and functional normalcy. This involves the clearance of injurious stimuli, removal of chemical mediators and acute inflammatory cells, replacement of the injured cells, and eventually, the restoration of normal function of cells. Events in the resolution of inflammation. Phagocytes clear the fluid, leukocytes and dead tissue, and fluid and proteins are removed by lymphatic drainage. Organization Scarring or fibrosis Scarring or fibrosis results after substantial tissue destruction or when inflammation occurs in tissues that do not regenerate. Extensive fibrinous exudates may not be completely absorbed and are organized by ingrowth of connective tissue with resultant fibrosis. Abscess formation may occur in the setting of extensive neutrophilic infiltrates or in certain bacterial or fungal infections. Due to the extensive underlying tissue destruction, the nly outcome of abscess formation is scarring. Abscesses may form in some bacterial infections Progression to chronic inflammation- Progression to chronic inflammation may follow acute inflammation, although signs of chronic inflammation may be present at the onset of injury. Depending on the extent of the initial and ongoing tissue injury as well as the capacity of the affected tissues to regrow, chronic inflammation may be followed by regeneration of normal structure and function or may lead to scarring. Defects in Leukocyte Function Since leukocytes play a central role in host defense, it is not surprising that defects in leukocyte function, both acquired and inherited, lead to increased susceptibility to infections, which may be recurrent and life-threatening †¢ The most common causes of defective inflammation are bone marrow suppression caused by tumors and chemotherapy or radiation (resulting in decreased leukocyte numbers), and metabolic diseases such as diabetes (causing abnormal leukocyte functions). The genetic disorders, although individually rare, illustrate the importance of particular molecular pathways in the complex inflammatory response. Some of the better understood inherited diseases are the following: a. Defects in leukocyte adhesion. In leukocyte adhesion deficiency type 1 (LAD-1), defective synthesis of the CD18 ? subunit of the leukocyte integrins LFA-1 and Mac-1 leads to impaired leukocyte adhesion to and migration through endothelium, and defective phagocy tosis and generation of an oxidative burst. Leukocyte adhesion deficiency type 2 (LAD-2) is caused by a defect in fucose metabolism resulting in the absence of sialyl-Lewis X, the oligosaccharide on leukocytes that binds to selectins on activated endothelium. Its clinical manifestations are similar to but milder than those of LAD-1. b. Defects in microbicidal activity. An example is chronic granulomatous disease, a genetic deficiency in one of the several components of the phagocyte oxidase responsible for generating ROS. In these patients, engulfment of bacteria does not result in activation of oxygen-dependent killing mechanisms. . Defects in phagolysosome formation. One such disorder, Chediak-Higashi syndrome, is an autosomal recessive disease that results from disordered intracellular trafficking of organelles, ultimately impairing the fusion of lysosomes with phagosomes. ] d. Rare patients with defective host defenses have been shown to carry mutations in Toll-like receptor signaling pathways. |Clinical Examples of Leukoc yte-Induced Injury: Inflammatory Disorders | Disorders |Cells and Molecules Involved in Injury | |Acute | |Acute respiratory distress syndrome |Neutrophils | |Acute transplant rejection |Lymphocytes; antibodies and complement | |Asthma |Eosinophils; IgE antibodies | |Glomerulonephritis |Antibodies and complement; neutrophils, monocytes | |Septic shock |Cytokines | |Vasculitis |Antibodies and complement; neutrophils | |Chronic | |Arthritis |Lymphocytes, macrophages; antibodies | |Asthma |Eosinophils, other leukocytes; IgE antibodies | |Atherosclerosis |Macrophages; lymphocytes? | |Chronic transplant rejection |Lymphocytes; cytokines | |Pulmonary fibrosis |Macrophages; fibroblasts | |Defects in Leukocyte Function | |Disease |Defect | |Acquired |Bone marrow suppression: tumors, radiation, and |Production of leukocytes | |chemotherapy | | |Thermal injury, diabetes, malignancy, sepsis, |Chemotaxis | |immunodeficiencies | | |Hemodialysis, diabetes mellitus |Adhesion | |Leukemia, a nemia, sepsis, diabetes, neonates, |Phagocytosis and microbicidal activity | |malnutrition | | |Genetic | |Leukocyte adhesion deficiency 1 |? hain of CD11/CD18 integrins | |Leukocyte adhesion deficiency 2 |Fucosyl transferase required for synthesis of sialylated | | |oligosaccharide (receptor for selectins) | |Chronic granulomatous disease |Decreased oxidative burst | |  Ã‚  X-linked |NADPH oxidase (membrane component) | |  Ã‚  Autosomal recessive |NADPH oxidase (cytoplasmic components) | |Myeloperoxidase (MPO) deficiency |Absent MPO-H2O2 system | |Chediak-Higashi syndrome |Protein involved in organelle membrane docking and fusion | At the end of reading – try to answering these questions – if you can then you are thro if not go back and read 1. Define inflammation and discuss the causes of inflammation 2. List and explain the cardinal signs of inflammation 3. List and explain the stimuli for inflammation 4. Explain the vascular changes that occur during inflammation 5. Explain the cellular events during inflammation 6. Explain phagocytosis in detail 7. Describe with illustrations how the endothelium becomes leaky in acute inflammation? 8. Discuss the cells that are involved in inflammation 9. Explain in detail the adhesion receptors involved in adhesion and transmigration 10. Explain Diapedesis and chemotaxis 11. Explain the clinical genetic deficiencies due to phagocytosis 12. Explain the regulation of endothelial and leukocyte adhesion molecules 13. Briefly explain the outcomes of acute inflammation 14. Explain the various special macroscopic appearance of acute inflammation 15. Explain the harmful, beneficial and systemic effects of inflammation 16. Define Exudate, Transudate, Edema , Pus 17. Tabulate the differences between exudate and transudate 18. Write briefly on chemoattractants involved in chemotaxis during inflammation 19. Write briefly on inflammatory oedema 20. Explain the various Defects in Leukocyte Function 21. Tabulate and list the Clinical Examples of Leukocyte-Induced Injury: Inflammatory Disorders 22. Tabulate and list Defects in Leukocyte Function 23. Explain the role of lymphatics in inflammation 24. Explain the Clinical and Laboratory Evaluation of Acute Inflammation CAUTION ? If your incredible short-term memory got you through Organic Chemistry, it probably wont get you through Pathology, which is a quantum leap with more material. ? Find some way to organize the material to suit your learning style. ? Adopt active learning (read text books) ? Passive learning (others notes) is not recommended in the medical curriculum ? Don’t memorize without understanding ? MY NOTES ARE THERE TO GUIDE YOU BUT CERTAINLY NOT A SUBSTITUTE TO READING TEXTBOOK

St. John the Evangelist Essay Example For Students

St. John the Evangelist Essay Throughout the human history there have been many saints who have lived among us. They followed Jesus principles and they did Gods will. One of the earliest saints was St. John, and he lived during the times of Jesus. His childhood and his date of birth are unknown, but it is well known that he was one of the best followers and students of Jesus. St. John was the son of Zebedee, and the brother of St. James the Great with whom he was brought up to the trade of fishing. While Jesus was spreading his teachings and his miracles St. John entered public ministry. Then in his first year of public ministry our Lord called him to be an Apostle. He was called to be an Apostle with his brother, as they were mending their nets on the sea of Galilee. St. John was the youngest of all the apostles, and outlived the others. It is hard to list in details, all the challenges that St. John faced. His challenges were truly followed by Gods will and helped many people. St. John was one of the first ones who understood and studied how a person should live, how should he behave, and how moral his life should be. He was one of the first to follow those holy principles, and show them to others. One of his greatest challenges was writing a gospel. St. John the Evangelist is mostly known for writing a fourth Gospel. If you would ask any person to l ist his challenges almost everybody would tell you that he wrote a gospel. It is believed that he wrote a Gospel at the year of 96, after the death of Domitian. His object in writing it he tells us himself: These things are written that you may believe that Jesus is the Christ, the Son of God; and that, believing, you may have life in His name. In order to write a Gospel you have to be truly involved in holy life by yourself. St. John went threw Jesus teachings and he opened himself to Jesus. All of his life he spent by expressing love to others and by implementing Jesus principles. Thus before writing a Gospel, St. John experienced it all on himself. He also wrote three epistles. The first is called catholic, as addressed to all Christians, especially his converts. The other two are short, and directed to particular persons, to Gaius and to local church. The Book of Revelation is also attributed to him. We will write a custom essay on St. John the Evangelist specifically for you for only $16.38 $13.9/page Order now Writing a Gospel was not the only great challenge that St. John performed in his life. He became the beloved disciple and the only one of the Twelve who did not forsake the Savior in the hour of Jesus Passion. He proved it himself by referring to himself in a Gospel with a proud humility as the disciple whom Jesus loved. Jesus would have him present with Peter and James at His transfiguration and His agony in the garden. Also John was chosen to go with Peter into the city to prepare the Last Supper. St. John stood faithfully at the cross when the Savior made him the guardian of his mother. Together with his brother James and with Simon Peter, he formed a kind of inner circle of Three among the Twelve. In that those three were privileged to behold the miracle of the Great Catch of Fish, the healing of Peters mother-in-law, the raising of the daughter of Jairus, the Transfiguration, and the Agony in Gethsemane. So St. John was surrounded with challenges and he applied Jesus principle in every challenge that he faced. Those people who required help and second baptism heard the following word from St. John, I will answer for you to Jesus Chris. I am ready to lay down my life for you. I am sent by Christ. When St. John heard that Christs sepulchre was open, he was the first one to see that Christ was indeed risen. He also assisted at the council, which the apostles held at Jerusalem. Later his life was passed chiefly in Jerusalem and at Ephesus. He founded many churches in Asia Minor. Brought to Rome, tradition relates that he was by order of Emperor Dometian cast into a cauldron of boiling oil but came forth unhurt and was banished to the island of Pathmos for a year. When age and weakness grew upon him at Ephesus so that he wasnt able to preach to the people, he used to be carried to the assembly of the faithful, and every time said to his flock only these words, My little children, love one another. When he was asked why he said it he replied, Because it is the word of the Lord, and if you keep it you do enough. He lived to an extreme old age, surviving all his fellow apostles, and died about the year 100. St. John is called the Apostle of Charity, a virtue he had learned from his Divine Master. He used that virtue in his words and actions. The beloved disciple died at Ephesus, where a stately church was erected over his tomb. It was afterwards converted into a Mohammedan mosque. .u678fb2906aa34572ac5009a3b729b4af , .u678fb2906aa34572ac5009a3b729b4af .postImageUrl , .u678fb2906aa34572ac5009a3b729b4af .centered-text-area { min-height: 80px; position: relative; } .u678fb2906aa34572ac5009a3b729b4af , .u678fb2906aa34572ac5009a3b729b4af:hover , .u678fb2906aa34572ac5009a3b729b4af:visited , .u678fb2906aa34572ac5009a3b729b4af:active { border:0!important; } .u678fb2906aa34572ac5009a3b729b4af .clearfix:after { content: ""; display: table; clear: both; } .u678fb2906aa34572ac5009a3b729b4af { display: block; transition: background-color 250ms; webkit-transition: background-color 250ms; width: 100%; opacity: 1; transition: opacity 250ms; webkit-transition: opacity 250ms; background-color: #95A5A6; } .u678fb2906aa34572ac5009a3b729b4af:active , .u678fb2906aa34572ac5009a3b729b4af:hover { opacity: 1; transition: opacity 250ms; webkit-transition: opacity 250ms; background-color: #2C3E50; } .u678fb2906aa34572ac5009a3b729b4af .centered-text-area { width: 100%; position: relative ; } .u678fb2906aa34572ac5009a3b729b4af .ctaText { border-bottom: 0 solid #fff; color: #2980B9; font-size: 16px; font-weight: bold; margin: 0; padding: 0; text-decoration: underline; } .u678fb2906aa34572ac5009a3b729b4af .postTitle { color: #FFFFFF; font-size: 16px; font-weight: 600; margin: 0; padding: 0; width: 100%; } .u678fb2906aa34572ac5009a3b729b4af .ctaButton { background-color: #7F8C8D!important; color: #2980B9; border: none; border-radius: 3px; box-shadow: none; font-size: 14px; font-weight: bold; line-height: 26px; moz-border-radius: 3px; text-align: center; text-decoration: none; text-shadow: none; width: 80px; min-height: 80px; background: url(https://artscolumbia.org/wp-content/plugins/intelly-related-posts/assets/images/simple-arrow.png)no-repeat; position: absolute; right: 0; top: 0; } .u678fb2906aa34572ac5009a3b729b4af:hover .ctaButton { background-color: #34495E!important; } .u678fb2906aa34572ac5009a3b729b4af .centered-text { display: table; height: 80px; padding-left : 18px; top: 0; } .u678fb2906aa34572ac5009a3b729b4af .u678fb2906aa34572ac5009a3b729b4af-content { display: table-cell; margin: 0; padding: 0; padding-right: 108px; position: relative; vertical-align: middle; width: 100%; } .u678fb2906aa34572ac5009a3b729b4af:after { content: ""; display: block; clear: both; } READ: Essay About Schizophrenia The contribution that St. John made to the Christian community and the world is extremely important. He is the one who will be known forever for his writings and his challenges. He will be never forgotten, as he was the one who passed Jesus teaching to the whole world. He gave his life for the future, so that today we would know how should we live as Christians, and how morally should we behave. There are a lot of things that I learned from St. Johns life. His writings were very important for Christian history, therefore for millions of people who taught from his writings, and that includes me as well. I learned that loving all people is important but not just loving the once who only give you love. Giving love to God important. I should not worry about my clothes or possessions or what worries I should overcome the next day. God takes care of that. I am a lot different right now. I worry about what I will ware the next day, if I lost something I can panic, when I do not realize that the more I panic the less I have a chance of finding the thing that I have lost. St. john was a great hero and he was willing to give up his life for God and for everyone and for the future. From this I learned that this person really was a hero and he was teaching us how to live the right way in life. Today there are a lot of Churches and schools build under his name. Today everybody has a lot to learn from St. John. His life is a perfect example for us. He is the one who can change many lives of different people, and influence their behavior. St. John the Evangelist, the disciple whom Jesus loved will be known forever, as Jesus said, he shall not die.