Oral PE History Essay Example | Topics and Well Written Essays - 1250 words

Oral PE History - Essay Example Stereotypical ideas of True Womanhood constrained girls like Wendy into a tightly defined entity in which physical activity was considered too robust a pursuit for a delicate female and negative connotations of the New Woman who was then threatening this Victorian concept further functioned to reduce her available options. To understand how this could be so, Wendy Strain’s life experiences as a child growing up in 1960s suburban Detroit will be related to these social and cultural concepts. Wendy Strain is a 50 year old woman who spent her childhood in a suburb of Detroit in a middle class household with aspirations for greatness. Clinging to the ideals of the gentry of a century earlier, her parents strongly adhered to the concepts of the True Woman. â€Å"The attributes of True Womanhood, by which a woman judged herself and was judged by her husband, her neighbors and society, could be divided into four cardinal virtues – piety, purity, submissiveness and domesticity. Put them all together and they spelled mother, daughter, sister, wife – woman. Without them, no matter whether there was fame, achievement or wealth, all was ashes. With them, she was promised happiness and power† (Welter, 1966: 152). According to Poovey (1988), it was by â€Å"linking morality to a figure (rhetorically) immune to the self-interest and competition integral to economic success, [the cult] preserved virtue without inhibiting productivity† thus creating a perfec t world in which men were free to pursue every material pursuit they wished while women were constrained to remain at home and protect the moral and ethical values of the family unit. A woman could not participate in competitive sport under this ideology not only because it was against the nature of the True Woman to participate in any activity that could not be conducted inside the home, but also because it would have introduced this element of competition that was restricted to the male world. Strain indicates

Humanity and climate change Essay Example | Topics and Well Written Essays - 1000 words

Humanity and climate change - Essay Example This paper provides evidence that human activities caused climate change. The Human Face behind Climate Change Numerous scholars and scientists agree that human activities have been the predominant root of global warming. Pollution has particularly raised global temperature levels which, in turn, affect numerous life forms. Kluger synthesizes reports that argue that global warming and climate change are real phenomena and that they are mainly the effects of prodigious human emissions. Extraordinary amounts of CO2 released into the air from people’s industries and automobiles have created the problem of global warming, which produce climate changes (Kluger). Glaciologist Rignot examines data from Canadian and European satellites and stipulates that Greenland ice is melting twice as fast than before, with 53 cu. mi. of water melting to the sea in 2005, compared with 22 cu. mi. in 1996 (Kluger). A cubic mile of water is around five times the amount that Los Angeles consumers ever y year (Kluger). In addition, the ocean water level is also rapidly rising and caused flooding in low-coastal areas, such as Bangladesh (Kluger). Schnoor provides additional proof that that increases in greenhouse gases or GHGs, such as carbon dioxide, methane, nitrous oxide, and others, in the atmosphere have produced global warming. NASA also concurs that these gases blankets the atmosphere and trap heat from escaping the Earth’s atmosphere. Schnoor emphasizes that burning fossil fuels, flooded agriculture, animal husbandry, and coal mining principally released higher carbon dioxide emissions (CO2) levels, leaked methane (CH4), and resulted to the denitrification of nitrogen fertilizers, which raised nitrous oxide (N2O) levels in the atmosphere. He stresses that CO2 is accountable for more than half of the greenhouse effect, and it is rising exponentially at ?0.4% per year (1106). He states that each time a person uses 10 gallons for their car; he/she releases 190 lbs of CO 2 into the atmosphere (1106). Schnoor depicts that each person in the United States releases â€Å"6 metric tons of carbon (22 metric tons of CO2) into the atmosphere each year† (1106). The total emissions from global anthropogenic activities are â€Å"more than 6–7 billion metric tons of carbon per year, and approximately half of that are accumulating in the atmosphere† (Schnoor 1106). Studies showed that the rising global atmospheric CO2 concentrations mostly came from humans because of three kinds of evidence. First, the increase in CO2 concentrations only began at the end of the 18th century, the time of the industrial revolution (Schnoor 1106). The Intergovernmental Panel on Climate Change (IPCC) report on the climate change in 2001 asserts that the atmospheric concentration of carbon dioxide has increased from 280 ppm (parts per million) in 1750 to 367 ppm in 1999 (31% increase)† (Khandekar, Murty, and Chittibabu 1563). The IPCC describes also the hu ge increase in other greenhouse gases (GHG) such as, methane and nitrous oxide, which heightened by 145% and 15%, respectively, in the last 250 years, where the Industrial Age coincided with these extraordinary high levels of greenhouse gases

Active Intellect in Aristotle Essay Example for Free

Active Intellect in Aristotle Essay All men by nature desire to know. An indication of this is the delight we take in our senses; for even apart from their usefulness they are loved for themselves; and above all others the sense of sight. This is the foundation of human knowledge Aristotle presents us with in Book Alpha of the Metaphysics. The next question which we must naturally ask ourselves is, How? How is it that we can have any knowledge at all? We by our very nature desire to know and we love the senses in themselves but what is the relationship between the two and by what faculty are we able to call anything knowledge once sense perception has occurred? Aristotle sets up as his faculty for knowledge both the active and the passive intellects. We begin to have knowledge through sense experience. We cannot know without sense experienceand it is from sense experience that all knowledge is therefore generated. Knowledge for Aristotle is a knowledge of universals, that is, a knowledge of Essences. Thought is thus the faculty by which we come to comprehend universals. And since material objects are a composite unity of essence and existence, it naturally follows that we grasp the universal through our encounter with the particular. What follows is a series of events which leads to knowledge. The passive intellect receives the image from the sense data and it is stamped upon the passive intellect from the material impression. From this stamp the active intellect is to draw out of it and somehow make a universal concept from this particular experience. But there is something more at work here. There is something in the mind ( more specifically in the soul) that somehow comprehends and makes universals intelligible. Various theories have been postulated concerning this but we shall concentrate on Aristotle and leave the other philosophies for now. What is at work in man is a divine reason immanent in mans soul. Somehow man is connected to and shares in divine reason. A distinction must be made here. We are not saying that the human souls capacity to grasp universals is in some way a maker or shares in the pure act of God, but that without this divine reason at work in the souls of men no understanding of universals could take place at all. The mind works on the material given to it, that is its potential, and from this material it moves to actuality. An example of this is the man who is without music becoming musical. His potential to be musical always existed in him but it wasnt until he studied the particulars of music that he became a musical  man. Aristotle refers in his Meteorology (1072, b14) that we can live a life like that of a God, a time of reason being broken down where we become aware of the oneness with the principles, whose knowledge is always actual and always complete. The active intellect does not in any way act strictly on material that was already there but undisclosed, it does act on material given to it in sense experience and illuminated by mans reason and divine reason as well. We share in the reason of God Aristotle believed. The philosopher God is a God of pure act, in other words Thought thinking Thought. This is the goal of man, to achieve a similar state of being in contemplation and reflection. And it is only through the active intellect that man is able to come to universals. The active intellect acts on the passive intellect the way an artist acts on stone to create an image. The artist impresses the form of a knowable object into the stone and the active intellect impresses a knowable object onto the passive intellect. We must not make the mistake here of understanding the active intellect as a medium between the passive intellect and the object to be known. Knowledge for Aristotle is a direct and not mediated relationship. The relationship of active to passive intellect is that of illumination shared in divine reason whereby man is able to see the universal in the particular and understand or grasp the idea of universal. This I liken to the statue made by the artist. By sharing in divine reason and the reason in his own soul (which I understand to be an imperfect representation of Gods) the artist is able to take a universal image in his soul and craft a particular. This particular statue thus becomes a representation of the universals we can synthesize through sense experience. Aquinas furthered this theory of the active intellect not as a maker but as an abstraction. This abstraction is taking the impressed species and expressing it through the faculty of the active or agent intellect. The material image is given in sense experience and then expressed as a universal to the mind by the very nature of the active intellect which is abstraction. This abstraction is how for Aquinas that we come to know universals. Gods pure act is translated here to fallen man by which he can begin his ascent to a higher existence. The active intellect in Aristotle is not a reason which creates out of nothing. It works on a material given to it, which it promotes from potentiality into actuality. The one reason is analogous to matter because it becomes all things; the other is analogous to the efficient cause because it makes all things. The first statement points to the act of apprehending, the second to that of art. Art makes its objects by making the material become them. And if the analogy is meant to be an exact one the role of the active intellect must therefore be to make the passive intellect its object so this apprehension can occur. What is potentially comes to be actually. This implies that there is something similar to Platos world of Forms insofar as man is cut off to a pre-existing knowledge and with which we are not in communication. Where Plato called it the re-collection of forgotten forms I believe Aristotle to call it divine reason actuating itself in human reason. Because all men by nature to desire to know, and by knowing we share in the being of God.

Structural and Functional Properties of Tendons

Structural and Functional Properties of Tendons Chapter One Literature Review 1.0 Introduction Tendons are dynamic structures; their extracellular matrices are continuously being synthesised and broken down over the course of an individual’s lifetime. The macromolecules, namely collagen, proteoglycans, hyaluronan and the non-collagenous proteins form the extracellular matrix of tendons. In normal tendon exists a fine balance between the synthesis and degradation of these macromolecules resulting in a strong healthy tendon. It is evident that damage to tendons, such as in overuse tendinopathy results in changes to the levels and types of macromolecules present in tendon with decreased levels of collagen and increased levels of proteoglycans, hyaluronan and non-collagenous proteins, causing a weakened tendon that is prone to rupture. These degenerative features have thus far been partially characterised. By identifying the levels and various types of macromolecules present in normal tendons and tendons exhibiting overuse tendinopathy an understanding of the basis of the condition can be determined and possible ways of preventing or ameliorating tendon degeneration can be considered. The terms overuse tendinopathy and pathological tendon will be used interchangeably throughout this study. This literature review will attempt to define and characterise the structural and functional properties of tendon and will discuss the current literature regarding the levels, types, synthesis and catabolism of macromolecules present in the extracellular matrix of tendons and also attempt to define and characterise the pathological aspects of overuse tendinopathies. Chapter Two of this thesis will dictate the materials and methodology used in these studies. Chapters Three, Four and Five will present the results of this thesis. Finally, chapter Six will include the discussion and discuss any limitations and future considerations. 1.1 Synovial Joint Joints are articulations found between adjacent parts of bone that allow controlled frictionless movement (for review see; Mankin Radin, 1997). In the human body there are three different types of joints and these are grouped according to the type of movement they make. They include the freely movable joints (synovial joints; i.e., most joints of the extremities such as the knee joint), slightly movable (cartilaginous joints; i.e., the vertebrae and ribs) and those that are immovable (fibrous joints; i.e., the skull). The majority of the joints found in the human body are synovial joints (for review see; Mankin Radin, 1997). There are six different types of synovial joints including the ball-and-socket joints, hinge joints, saddle joint, pivot joint, gliding joints and condyloid joints. A synovial joint contains a joint cavity that is enclosed by a fibrous capsule linking the adjoining bones. This joint capsule is lined by a synovial membrane that secretes a lubricating and nutritious fluid called synovial fluid that is rich in albumin and hyaluronan. The surface of each bone is typically covered with articular hyaline cartilage or in some circumstances fibrocartilage. In addition, the joint capsule is supported by accessory structures such as tendons and ligaments, which provide stability to the synovial joint (Sledge et al., 2001). 1.1.1 Articular Cartilage Articular cartilage covers the adjoining ends of bones in joints and has a white colour (for review see; Mankin Radin, 1997). It is a tissue that is devoid of blood and nerves and provides a wear resistant surface with low frictional properties for the joint and attains its nutrients via diffusion from the synovium into the synovial fluid (for review see; Mankin Radin, 1997). Furthermore, articular cartilage is resilient and flexible. This allows articular cartilage to withstand large compressive and tensile forces as well as allowing it to distribute load on subchondral bone during joint loading (Kempson, 1980) even though it is only a few millimetres thick (Hardingham, 1998). Its biomechanical properties are dependent on the structural composition of the extracellular matrix, which is comprised of water (70-80%), collagens (predominantly Type II collagen), proteoglycans (predominantly aggrecan) and non-collagenous proteins (Kuettner et al., 1991; Poole, 1997). The predominant cell type present in articular cartilage is called the chondrocyte. These cells are responsible for the maintenance, synthesis and degradation of all the extracellular matrix components (Kuettner et al., 1991; Buckwalter Mankin, 1998). Mature articular cartilage can be divided up into four zones including the superficial (tangential) zone, the middle (transitional) zone, the deep (radial) zone and the zone of calcified cartilage (Huber et al., 2000). The organisation and composition as well as mechanical properties of the extracellular matrix varies within these zones. The deeper zones have high proteoglycan levels and low cellularity whereas the more superficial zones contain low proteoglycan levels and increased cellularity (Aydelotte et al., 1988; Buckwalter Mankin, 1998). 1.1.2 Joint Capsule and Ligament The joint capsule is a fibrous connective tissue that is attached to the skeletal parts of a joint beyond their articular surfaces. The principal function of the joint capsule is to seal the joint space and to supply stability by limiting movement (for review see; Mankin Radin, 1997). Most joint capsules are strengthened by ligaments. Ligaments act together with the joint capsule and the peri-articular muscles to provide stability to the joint preventing excessive movements. They permit free movements when lax, but can stop unwanted movements when tight by virtue of their high tensile strength. Occasionally joint capsules are strengthened by tendons, such as the extensor tendon in the finger joint. The joint capsule and ligaments proceed to hold the bones together and to guide and limit joint movements. Ligaments attach one bone with another bone and have a limited vascular and neural supply which enable them to repair relatively well after damage (Bray et al., 1990). The knee joint is a good example of different types of ligaments. The medial collateral ligament fuses with the joint capsule, and the cruciate ligaments and the lateral collateral ligament, which are both completely independent of the joint capsule. 1.1.3 Synovial Membrane The synovial membrane (synovium) lines the non-articular surfaces of a joint such as the joint capsule and ligaments, and is responsible for secreting and absorbing synovial fluid, which contains hyaluronan (Mason et al., 1999). Synovial fluid lubricates the joint and provides at least partly for the nutrition of articular cartilage, invertebral discs and menisci. The synovial extracellular matrix acts as a scaffolding to support synoviocytes and plays an important role in cell migration and differentiation. It is mostly composed of collagen particularly Type III collagen, with smaller amounts of proteoglycans such as decorin and biglycan (Mason et al., 1999), non-collagenous proteins such as fibronectin, elastin and lamina, hyaluronic acid as well as lipids, serum proteins and electrolytes (Hirohata Kobayashi, 1964). The synovial membrane has only been detected in vertebrate animals (Henderson Edwards, 1987). Furthermore, synovial tissue is not arranged into discrete layers, but rather represents a continuum from surface to deep zones. The extracellular matrix of the synovial membrane varies in composition from its surface to its deep zones (Hirohata Kobayashi, 1964). 1.1.4 Tendon Tendons are dense fibrous connective tissues found between muscles and bones (for review see; Benjamin Ralphs, 1997). The primary role of tendon is to absorb and transmit force generated by muscle to the bone to provide movement at a joint. In addition tendons operate as a buffer by absorbing forces to limit muscle damage. Each individual muscle has two tendons, one that is proximal and the other distal. The attachment of the proximal tendon of a muscle to bone is called a muscle origin and that of the distal tendon an insertion. A normal tendon has a bright white colour and a fibroelastic texture and enables resistance to mechanical forces. Tendons come in many shapes and this is most likely due to their function, they can be round or oval in cross section or they can come in the form of flattened sheets, fan shaped, ribbon shaped or cylindrical in shape (for review see; Benjamin Ralphs, 1997). In a muscle like the quadriceps which creates strong forces the tendons are short and broad, while those that are involved in more delicate movements like the finger flexors, long and thin tendons are present (Kannus, 2000). Tendons are arranged in a hierarchical fashion (see Figure 1.1). A group of collagen fibres form a primary fibre bundle or subfascicle; this is the basic unit of tendon. A group of subfascicles form secondary bundles or fascicles, which form tertiary bundles constituting the tendon as a whole. The primary, secondary and tertiary bundles are encased in a thin connective tissue reticulum called the endotenon (Elliott, 1965; Kastelic et al., 1978; Rowe, 1985). The endotenon carries blood vessels, nerves and lymphatics to deeper areas of the tendon (Elliott, 1965; Hess et al., 1989). The whole tendon is surrounded by an epitenon, which is a dense fibrillar network of collagen (Jozsa et al., 1991). The epitenon is contiguous with the endotenon and like the endotenon is rich in blood vessels, nerves and lymphatics (Hess et al., 1989). Many tendons are surrounded by a connective tissue called the paratenon. Paratenon allows free movement of the tendon against the surrounding tissues (Schatzker Branemark, 1969; Hess et al., 1989). The myotendinous junction is the site of union with a muscle, and the osteotendinous junction is the site of union with a bone (Kannus, 2000). In tendon, blood vessels represent between 1-2% of the entire extracellular matrix (Lang, 1960; Lang, 1963). Some blood vessels may originate from the perimysium at the musculotendinous junction and blood vessels from the osteotendinous junction (Schatzker Branemark, 1969; Carr Norris, 1989; Clark et al., 2000). At rest, rabbit tendons have been shown to have blood flow of around one-third that of muscle, and it is known that blood flow in tendon increases with exercise and during healing in animals (Backman et al., 1991). The oxygen consumption of tendons is 7.5 times lower than that of skeletal muscles (Vailas et al., 1978). 1.1.5 Tendon Extracellular Matrix The major cell type present in tendon is the fibroblast (also known as tenocytes; Ross et al., 1989; Schweitzer et al., 2001; Salingcarnboriboon et al., 2003), which are embedded within an extracellular matrix (see Figure 1.2). These cells are sparsely distributed, comprising only 5% of the dry weight of adult tendon (Ross et al., 1989; Schweitzer et al., 2001; Salingcarnboriboon et al., 2003). These cells lie in longitudinal rows and have many cell extensions that extend into the extracellular matrix (McNeilly et al., 1996). Fibroblasts are responsible for the synthesis and degradation of all the macromolecular components that make up the extracellular matrix of tendon, including the most abundant macromolecule present in tendon, collagen, as well as proteoglycans, hyaluronan and non-collagenous proteins (Vogel Heinegard, 1985; Curwin, 1997; O’Brien, 1997). The extracellular matrix is made up of parallel bundles of collagen aligned longitudinally (60-85% of tendon dry weight) associated with elastin fibres which constitutes approximately 1-2% of the dry weight of tendon (Tipton et al., 1975; Hess et al., 1989; Jozsa et al., 1989; Curwin, 1997; Kirkendall Garrett, 1997; O’Brien, 1997). Tendon consists of 55-70% water, most of which is associated with proteoglycans in the extracellular matrix (Elliott, 1965; Vogel, 1977; Merrilees Flint, 1980; Riley et al., 1994b; Vogel Meyers, 1999). The proteoglycan content of tendons is approximately 1% of dry weight of tendons (O’Brien, 1997).Water and proteoglycans have important lubricating and spacing roles in tendons that allow collagen fibres to glide over one another (Amiel et al., 1984). The structure, composition and the organisation of the tendon matrix is crucial for the physical properties that tendons posses (Riley, 2004). The collagen component gives tendon its great tensile strength (Scott, 2003) whereas it is the proteoglycan component of the tendon matrix that enables tendons to withstand compressive load (Schonherr et al., 1995), while elastin fibres increase tendon extensibility (Scott, 2003). 1.1.6 Tendon cells The cell population of tendon has so far been poorly characterised (for review see; Riley, 2000), the majority of tendon cells have the appearance of fibroblasts (also known as tenocytes) and constitute about 90-95% of the cells present in tendon (Ross et al., 1989; Schweitzer et al., 2001; Salingcarnboriboon et al., 2003). The remaining 5% to 10% of cells present in tendon are chondrocyte-like cells (fibrochondrocytes), which are mostly present in the fibrocartilaginous regions of tendon where tendon attaches to bone. Also present in tendon are some mast cells, capillary endothelial cells, smooth muscle cells and nerve cells (Hess et al., 1989; Jozsa Kannus, 1997). Fibrocartilage cells are large and have an oval shape and they are often packed with intermediate filaments (Merrilees Flint, 1980; Ralphs et al., 1991). Tendon cells are linked to one another via gap junctions (McNeilly et al., 1996; Ralphs et al., 1998), allowing cell-to-cell interactions (McNeilly et al., 1996). Fibroblasts have a branched cytoplasm surrounding an elliptical, speckled nucleus. The rough endoplasmic reticulum and the Golgi apparatus are well developed with few mitochondria in the cytoplasm (Ippolito et al., 1980; Moore De Beaux, 1987). Like other connective tissue cells, fibroblasts are derived from mesenchyme. It is believed that in tendon there are a small number of mesenchymal stem cells that have the ability to differentiate into chondrogenic, osteogenic and adipogenic cells if the conditions allow (Salingcarnboriboon et al., 2003). Tendons have been shown to respond to mechanical load by modifying their extracellular matrix (Banes et al., 1988; Ehlers Vogel, 1998; Buchanan Marsh, 2002; Lavagnino Arnoczky, 2005). Tendon cells receive their vascular supply from the surrounding paratenon. Tendons were once considered almost static and unable to participate in repair. However, the activity of tendon cells has been shown to be active throughout an individual’s life as they express various matrix components (Chard et al., 1987; Ireland et al., 2001; Riley et al., 2002). Regional differences in cell morphology and activity exists in tendons, synovial-like cells that are found in the endotenon and epitenon surround the main fibre bundles (Banes et al., 1988). A greater proliferative capacity and a different matrix synthetic activity is characteristic of these synovial-like cells compared to the fibroblasts within the fibres, and are the first cells to respond following acute tendon injury (Gelberman et al., 1986; Banes et al., 1988; Garner et al., 1989; Gelberman et al., 1991; Khan et al., 1996b). Tendon Extracellular Matrix Macromolecules The following section will discuss the major extracellular matrix proteins and their roles in tendon. This will include the major constituent of tendon, collagen, the small and large proteoglycans and the non-collagenous proteins as well as hyaluronan. This section will also discuss the synthesis of collagens, proteoglycans and hyaluronan. 1.2.1 Collagens Collagen is the most copious protein present in the extracellular matrix of connective tissues and accounts for approximately 90% of the total protein of tendons, or 65% to 75% of the dry weight of tendons (von der Mark, 1981; O’Brien, 1992). There are currently 28 different collagen types (numbered I-XXVIII) present in vertebrates with at least 42 different alpha chains (Veit et al., 2006) with this number continuing to mount (Brown Timpl, 1995; Aumailley Gayraud, 1998). Collagen molecules can be defined as an extracellular protein that contains at least one triple helical domain (van der Rest Bruckner, 1993). Collagen provides the tendon with its structural integrity as well as assisting in various physiological functions. Collagen consists of three polypeptide alpha chains, which combine to form a homotrimer (three identical alpha chains) or a heterotrimer (two or three different alpha chains). Covalent bonds known as collagen cross-links develop between individual collagen molecules in a collagen fibre (Eyre et al., 1984; Bailey et al., 1998; Bailey, 2001; Brady Robins, 2001). The collagen arrangement gives tendon its great tensile strength. Cross-links are formed from a pathway of different chemical reactions that result in divalent cross-links that join two polypeptide chains, to multivalent, i.e. tri- or even tetravalent, cross-links (Bailey Lapiere, 1973; Eyre et al., 1984). These cross-links come about from enzymatic modification of lysine or hydroxylysine residues by the copper-dependent enzyme lysine oxidase (Robins, 1988). Collagens are divided into two subgroups, the fibrillar and non-fibrillar collagens. Non-fibrillar collagens can be further divided into seven subfamilies including microfibril collagens, fibril-associated collagens with interrupted helices (FACIT) collagens, network collagens, MULTIPLEXIN collagens (proteins with multiple triple helix domains and interruptions), basement membrane-associated collagens, transmembrane-associated collagens and epithelium-associated collagens (von der Mark, 1999). The non-fibrillar collagens present in tendon include Types IV, VI, IX, X, XII and XIV (von der Mark, 1999). The fibrillar collagens present in tendon include, Types I, II, III, V and XI (Kielty et al., 1993; Kadler et al., 1996; Fukuta et al., 1998; von der Mark, 1999). The fibrillar collagens contain a continuous triple helix domain, 300 nm in length, capable of undergoing the staggered, lateral associations required to form fibrils (Mayne, 1997). The resulting fibrils provide the structural support for tissues. All the fibril-forming collagens have a similar structure and size, being composed of a large, continuous central triple-helical domain (COL1) of approximately 1000 amino-acid residues Collagen Type Structure type Distribution Function I Fibril forming Occurs in most tissues, tendon, bone, skin etc Main component of tendon, skin, bone, dentin, cartilage, ligament etc II Fibril forming Hyaline cartilage, invertebral disc Restricted to fibrocartilage; forms less-organised meshwork III Fibril forming Vessels, kidney, liver, skin, tendon Normally restricted to endotenon; forms smaller less organised fibrils IV Forms meshwork Basement membranes, tendon Basement membrane of tendon blood vessels V Fibril forming Skin, bone Core of Type I collagen fibril forms template for fibrillogenesis VI Beaded filaments Vessels, skin, intervertebral disc Cell associated found in seams between fibrils VII Epithelial-associated Dermoepidermal junction Forms anchoring fibrils in the skin VIII Microfibril Descements membrane in the cornea Forms a lattice IX FACIT Hyaline cartilage, vitreous humour, tendon Cell and matrix interactions with Type II collagen fibril surface X Forms meshwork Growth plate, tendon Restricted to insertion fibrocartilage XI Fibril forming Hyaline cartilage Core of Type II collagen fibril forms template for fibrillogenesis XII FACIT Embryonic tendon and skin, periodontal ligament Mediates cell/matrix interactions with Type I collagen fibril surface XIII Transmembrane Endothelial cells Adhesion of cells to basement membranes XIV FACIT Foetal skin, tendon Mediates cell/matrix interactions with Type I collagen fibril surface XV Multiplexin Blood vessels Stabilizes skeletal muscle cells and microvessels XVI FACIT Skin, Cartilage XVII Transmembrane Skin, cornea, lung Connects epithelial cells to the matrix XVIII Multiplexin Endothelial cells, liver, eye Needed for normal development of the eye XIX FACIT Basement membranes Forms radially distributed aggregates XX FACIT Corneal epithelium, skin, cartilage and tendon Binds to collagen fibrils XXI FACIT Many tissues Matrix assembly of vascular networks in blood vessel formation XXII Fibril forming Tissue junctions Interacts with components of microfibrils XXIII Transmembrane Metastatic tumour cells, heart retina Cell adhesion, Binds to heparin XXIV Fibril forming Expressed in tissues containing Type I collagen Developing bone and cornea Regulating Type I collagen fibrillogenesis XXV Transmembrane Neurons May play a role in adherens junctions between neurons XVI Testis and ovary of adult tissues Development of the reproductive tissues XVII Fibril forming Cartilage, ear, eye and lung Unknown XVIII Basement membranes around Schwann cells in the peripheral nervous system. Unknown flanked by a variable amino-terminal domain of about 50-520 amino acid residues and a highly conserved non-triple-helical carboxyl-terminal domain of about 250 amino acid residues (for reviews see; Kielty et al., 1993; Fichard et al., 1995; Pihlajaniemi Rehn, 1995; Prockop Kivirikko, 1995; Bateman et al., 1996). The amino- and carboxyl-terminal extensions are commonly referred to as amino- and carboxyl- propeptides, respectively. The C-propeptide is called the NC1 domain, whereas the amino-propeptide is divided into sub-domains. The first is a short sequence (NC2) that links the major triple helix to the minor one (COL2) and a globular amino-terminal end (NC3) that shows structural and splicing variations. Collagen Types II, IX, X and XI (Fukuta et al., 1998) are present at specific sites within the fibrocartilage region of tendon, found at the bone insertion and where the tendon is subjected to shear forces or compression (Fukuta et al., 1998; Waggett et al., 1998). Collagen Types II, IX, X and XI were once thought to occur only in cartilage (Visconti et al., 1996; Fukuta et al., 1998; Riley, 2000). It has now been shown that these collagens are found in the fibrocartilaginous regions of tendon, which wraps under bone. Their presumed function is to help resist compression and shear forces at these sites (Visconti et al., 1996; Fukuta et al., 1998; Waggett et al., 1998). Collagen also plays an important role in attaching tendons to bone. Where the tendon attaches to bone, tendons commonly widen and give way to fibrocartilage, a transformation where the aligned fibres originating from the tendon are separated by other collagen fibres arranged in a three dimensional network surrounding rounded cells (Liu et al., 1995). This arrangement helps to transmit tensile forces onto a broad area and reduces the chance of failure under excessive loading. The following review will focus on the collagens that are known to exist in tendon; this includes collagen Types I-VI, IX-XII and XIV. 1.2.1.1 Type I Collagen Type I collagen is the predominant and most studied collagen type present in the extracellular matrix of tendon, ligament and bone representing approximately 95% of the total collagen content or 60% of the tendon dry weight (Evans Barbenel, 1975; von der Mark, 1981; Riley et al., 1994b; Rufai et al., 1995). It is synthesized by a number of cell types such as fibroblasts, osteocytes and odontoblasts. Type I collagen consists of two ÃŽ ±1(I) chains and a shorter ÃŽ ±2(I) chain (Kielty et al., 1993), these two chains are products of separate genes and are not a posttranslational modification of a single molecule (for review see; Kivirikko Prockop, 1995). The two ÃŽ ±1(I) and one ÃŽ ±2(I) chains of a monomer of Type I collagen are primarily comprised of approximately 338  repeating tripeptide sequences of Gly-X-Y in which X is frequently proline and Y is frequently hydroxyproline (OHPr). The ends of the ÃŽ ±1(I) and one ÃŽ ±2(I) chains consist of short telopeptides of between 11-26 amino acids per chain. In longitudinal sections, the monomers are arranged in fibrils in a head-to-head-to-tail orientation. Each Type I collagen molecule consists of a long central helical region with a short non-helical domain on both the amino- and carboxyl-terminal ends. In tendon, the Type I collagen-containing fibril, organized into fibres (fibril bundles), is the major element responsible for structure stabilization and the mechanical attributes of this tissue. The fibril contains collagen molecules assembled into a quarter-staggered array, and this striated fibril has a 67 nm periodicity (for review see; Kadler et al., 1996; Orgel et al., 2006). Each alpha chain consists of a repeating triplet of glycine and two other amino acids marked as (Gly-X-Y)n. It is the glycine residues located in every third position that makes it possible for the three alpha chains to coil around the other. It has a molecular weight of 290 kDa. When viewing collagen fibrils under the light microscope they have a crimped appearance, during tendon loading the crimp stretches and the fibrils become aligned, and after loading the crimp will reappear, this is an important elastic component that tendon possesses (O’Brien, 1992). The Type I collagen ÃŽ ± chains contain approximately 290 residues of OHPr per molecule. Proline and OHPr constitute 20% to 25% of all amino acid residues of Type I collagen. The parallel arranged bundles formed by the Type I collagen fibrils gives tissues a high tensile strength with limited elasticity, and therefore is suitable for force transmission. The Type I collagen molecule has the ability to form microfibrils (filaments) as well as larger units of the fibrils or fibres (for review see; Kivirikko Prockop, 1995). The diameter of the collagen fibril is usually between 20 nm and 150 nm but can range up to 300 nm, this depends on the stage of development (Dyer Enna, 1976; Jozsa et al., 1984; Fleischmajer et al., 1988). 1.2.1.2 Type II Collagen The homotrimeric Type II collagen molecule was first discovered in cartilage by Miller and Matukas in 1969 who extracted collagen from cartilage in an experiment that involved pepsin digestion. Type II collagen, although most commonly found in articular and hyaline cartilage is also expressed in tendon particularly around the fibrocartilaginous region and consists of three identical ÃŽ ±1(II) chains (Eyre et al., 1992) which forms a meshwork structure that gives Type II collagen the ability to entrap the negatively charged proteoglycan molecules, thereby resisting the swelling pressure of proteoglycans. Each Type II collagen chain has a molecular weight of approximately 95 kDa. The entire collagen Type II molecule is shaped like a thin rod and is 300 nm long and 1.5 nm wide and has a total combined molecular weight of 295 kDa. This molecule is essential in connective tissues that are subjected to compression such as tendon and articular cartilage. Type II collagen molecules consists of a long central helical region flanked at its amino- and carboxyl-terminus by short non-helical regions termed amino and carboxyl telopeptides (Eyre et al., 1992). As with all fibrillar collagens, Type II collagen molecules are arranged in a quarter-staggered array to form collagen fibrils. Lateral associations of these collagen fibrils forms collagen fibres (Mayne, 1997). In tendon, collagen Types IX and XI as well as the proteoglycans decorin, fibromodulin and lumican inhibit collagen Type II fibril formation reducing fibril thickness (Vogel et al., 1984; Hedbom Heinegard, 1989; Hedbom Heinegard, 1993). 1.2.1.3 Type III Collagen Type III collagen is the second most abundant collagen present in tendon, representing up to 10% of the total collagen content in various tendons (Hanson Bentley, 1983; Riley et al., 1994b). Type III collagen is a thin collagen fibre consisting of three ÃŽ ±1(III) chains with a molecular weight of 290 kDa. In tendon most Type III collagen is found in the endotenon and epitenon (Duance et al., 1977), and is also found in between Type I collagen fibril bundles in aging tendons and at the insertion (Kumagai et al., 1994). It can also be found in skin, blood vessels, ligament and internal organs such as the gastro-intestinal tract but is not found in bone (Epstein Munderloh, 1978; McCullagh et al., 1980; Amiel et al., 1984). It strengthens the walls of hollow structures like the intestines and uterus. The fibrils of Type III collagen have a generally thinner diameter compared with Type I collagen fibrils (Lapiere et al., 1977; for review see; Kadler et al., 1996), however the triple helical domain is longer in length being composed of 340 amino acid repeats compared to 338 amino acid repeats in Type I collagen. In the early repair of the injured tendon, Type III collagen fibrils are quickly synthesized to restore strength and elasticity (Williams et al., 1984; Dahlgren et al., 2005). However, the fibrils do not have the same tensile strength quality as Type I collagen and so lack the functional properties needed in a tendon experiencing maximal load. The repair processes continues with Type III fibrils slowly being replaced by Type I collagen fibrils in an attempt to normalize the properties of the tendon (Duance et al., 1977; Williams et al., 1984; Dahlgren et al., 2005). Type III collagen contains high levels of OHPr and glycine. It has been reported that these high levels of glycine may cause localised helix instability resulting in increased susceptibility to proteolytic cleavage and rapid turnover of the extracellular matrices containing this collagen (Linsenmayer, 1991). The frequency of Type III collagen is considered to be an indicator of tissue age, and is common in the early stages of healing and scar tissue formation where it provides mechanical strength to the matrix (Burgeson Nimni, 1992). 1.2.1.4 Type IV Collagen The non-fibrillar collagen, Type IV (Bailey et  al., 1979), is a basement membrane-associated collagen (Light Champion, 1984) composed of triple helical isoforms consisting of six genetically distinct chains [ÃŽ ±1(IV) to ÃŽ ±6(IV)]. Each chain is characterised by a long collagenous domain of approximately 1400 amino acid residues of Gly-X-Y repeats, that are interrupted at several sites by a short non-collagenous sequence and approximately 15 amino acid residue non-collagenous amino-terminus, and an approximately 230 amino acid residue non-collagenous domain at the carboxyl-terminus (Mayne, 1997). Type IV collagen has been reported to represent approximately 2% of the total collagen content of tendon (Ahtikoski et al., 2003). Unlike the fibrillar collagens discussed so far this collagen does not form fibrillar aggregates but are directly incorporated into the basement membrane without any prior excision of the pro-peptide extensions. Type IV collagen is found uniquely in the basement membrane of tendon blood vessels (von der Mark, 1981) where it forms a key structural compo

Evil Reaps Darkness in Shakespeares Macbeth Essay examples -- Macbeth

Evil Reaps Darkness in Macbeth       "By their deeds you shall know them" is a Biblical passage which seems to state a lesson reiterated in Shakespeare's Macbeth. We intend to examine closely the dark future which the Macbeths deserved because of their sinful conduct.    A.C. Bradley in Shakespearean Tragedy comments on the darkness within the play:    The vision of the dagger, the murder of Duncan, the murder of Banquo, the sleep-walking of Lady Macbeth, all come in night scenes. The Witches dance in the thick air of a storm or, 'black and midnight hags', receive Macbeth in a cavern. The blackness of night is to the hero a thing of fear, even of horror; and that which he feels becomes the spirit of the play. The faint glimmerings of the western sky at twilight are here menacing: it is the hour when the traveller hastens to reach safety in his inn, and when Banquo rides homeward t meet his assassins; the hour when 'light thickens', when 'night's black agents to their prey do rouse', when the wolf begins to howl, and the owl to scream, and withered murder steals forth to his work. (307)    In his book, On the Design of Shakespearean Tragedy, H. S. Wilson identifies the darkness in the play with evil, hell, devils:    Mr. Kenneth Muir, in his introduction to the play - which does not, by the way, interpret it simply from this point of view - aptly describes the cumulative effect of the imagery: "The contrast between light and darkness [suggested by the imagery] is part of a general antithesis between good and evil, devils and angels, evil and grace, hell and heaven . . . (67-68)    In "Macbeth as the Imitation of an Action" Francis Fergusson states the place of darkness in the action of the pla... ...are: The Tragedies. A Collectiion of Critical Essays. Alfred Harbage, ed. Englewwod Cliffs, NJ: Prentice-Hall, Inc., 1964.    Knights, L.C. "Macbeth." Shakespeare: The Tragedies. A Collectiion of Critical Essays. Alfred Harbage, ed. Englewwod Cliffs, NJ: Prentice-Hall, Inc., 1964.    Lamb, Charles. On the Tragedies of Shakespeare. N.p.: n.p.. 1811. Rpt in Shakespearean Tragedy. Bratchell, D. F. New York, NY: Routledge, 1990.    Shakespeare, William. The Tragedy of Macbeth. http://chemicool.com/Shakespeare/macbeth/full.html, no lin.    Warren, Roger. Shakespeare Survey 30.   N.p.: n.p., 1977. Pp. 177-78. Rpt. in Shakespeare in the Theatre: An Anthology of Criticism. Stanley Wells, ed. England: Oxford University Press, 2000.    Wilson, H. S. On the Design of Shakespearean Tragedy. Toronto, Canada: University of Toronto Press, 1957.

Julius Caesar :: essays research papers

Based on his thoughts and actions, how would you describe Caesar? In Act II Julius Caesar is barraged with warnings to stay home and not go to the Senate, but he ignores them. Calpurnia, his spouse, tells of a dream she had and fears for Caesar's safety. The priests also warn Caesar. However, Decius is able to persuade Caesar to go to the Senate that morning. Considering his actions and thoughts in Act II, Caesar is a ruler who rejects superstitions and is concerned about how he is perceived by others. As scene 2 opens, there is a thunder storm that sets an eerie tone. Calpurnia reveals her dream to Caesar and expresses concern for his safety. She then warns Caesar to stay home. Julius replies that the work of the mighty gods can not be avoided. He also contends that death is inescapable and therefore he will go to the Senate. His servant thereupon returns with the news that the priests likewise warn Caesar not to go out that morning. Caesar also discards the advice of the priests and asserts his bravery and superiority over others. Eventually, Calpurnia persuades him to stay at home. This shows Caesar as a man who is willing to set aside his priorities to please his wife. Once Decius enters Julius is content to stay home. However, Decius manipulates Calpurnia's dream into a positive one and starts to question Caesar's manhood and power because he is afraid of the hallucinations of his wife. Caesar is now afraid and concerned of what the senators will think of him and fears that will see him as weak. This convinces Caesar to dismiss the warnings of his wife and the priests and go to the Senate. From his statements Caesar first concedes to his wife but once his considers the thoughts of others about him he decides to 'save face' and attend the senate. Compare and contrast the motives that Brutus and Cassius have for wanting to kill Caesar. Brutus and Cassius, both conspirators against Caesar both have dramatically different views on the reasons why Caesar should be assassinated. Brutus is a main of morals, reason and honor while Cassius is deceitful and manipulative. Brutus seeks to glorify Rome and avoid tyranny by assassinating Caesar. Cassius wants to destroy his enemy and severely dislikes being under the control of a tyrant. As leaders in the Senate, Brutus and Cassius confederate to assassinate

My Theory of Human Nature Essay

It is human nature to treat other people, animals, and yourself in different ways depending on how you feel, experiences you have had, and your upbringing in life. From the way that people act you can group people into different categories. These categories are based off people’s culture, economic situation, and values and faith. Throughout my life and especially this semester of college I have witnessed people treat other people, animals, and themselves considerately, inconsiderately, fair, unfair mean, kind, destructive, and prudent. I am not sure what made these people treat these things in that way, but each person has their own reason on why they did it. In this essay I am going to talk about examples of how people treated animals, people, and themselves in different ways, different ways you can group people, and if people are born the way they are, or molded into the person they are through their upbringing. A very common thing in today’s society is inconsiderate people and a more rare thing are people that are considerate. It used to be common manners to do simple things that made you be considerate, but as time has passed many people have become more inconsiderate. During this semester I have witnessed many people act inconsiderately and considerately towards others and themselves. I see examples of inconsiderate people and considerate people everyday, whether I am walking to class, trying to sleep, or just sitting in my room. On example of this is the most common and easiest way to be inconsiderate. I see this when I am walking to class and someone goes into a door ahead of me and they do not hold the door open for me and instead just let it slam in my face. Another example is when I was in Chicago my friend Josh Rainer was sitting in a seat on the train and an elderly lady got on the bus and instead of asking her if she wanted his seat he stayed seated and the elderly lady had to stand up. Along with the inconsiderate people in society there are considerate people. Simple tasks like my friend introducing their friends to me is an example of a considerate thing that I have witnessed this semester. Finally this week Dr. Monaco asked my class is we would rather have a take home final or an in class final. A little considerate task like this changed the whole week for many of us students and took stress off of us. So even if you are having a bad day going out of your way to do something considerate for someone else could change your day and that person’s day for the best. Unfair people and fair people have been around forever and always will be. People are unfair for many different reason, whether it is because they feel like they need to have an advantage, or they dislike the person they are being unfair to, or many other reasons, but we see these types of people in our everyday lives. Along with this people are fair because they feel like it is the right thing to do, they like the person, or for other reasons, but we also see these people in our everyday lives. During this year of football I saw coached treat players unfair everyday. Eddie Pope is a player on my football team and just because he was out of shape the coached would not let me participate in team sessions. He was only allowed to participate in individual sessions because they did not want him taking up time. Another example of people being unfair is seen in the work place. At my moms work my mom, Debbie Graves, and one of her co-workers, David Brookfield, have the exact same job and credentials, but he gets paid more than she does and more opportunities than she does. This is seen all the time in the work place whether is because of sex or race. While we see many unfair things everyday we also see things that are fair. Everyday in my dorm room I witness people being fair. I see it when people take turns playing the Xbox and sharing food and drinks with each other. Finally many people believe that life is not fair and they are always getting cheated, when in reality life is fair it is all about the effort you put into it. People know that they should be kind and that being mean can hurt people, but they still decide to act that way. In our lives we have been mean and kind and have also witnessed other people being mean and kind. During this semester this has been the easiest thing to notice. In the locker room during football I witnessed people being mean to each other everyday. Whether it was name-calling, fighting, or just taking things from each other. An example of this is Quentin taking different freshmen’s game pants until he finds the pair that he thinks fits the best. Many players on the teams call my roommate, Dominic, names about because he is over weight. People do kind things everyday whether they want to make somebody’s day better or are just kind person. My parents send me cards in the mail for no reason, but to tell me they love me and hope I am having a good semester. Kate complements different people everyday just to put a smile on their face and make their day better. Finally these are examples of people that I have witnessed being kind and mean throughout the semester. When people are self-destructive and prudent they usually harm themselves and can sometimes harm others. These are things that I have not witnessed as much as the others things that I have talked about. My roommate Zach is self-destructive by his money spending habits and studying habits. He is self-destructive in these ways because in the long run these will hurt him because he will become poor and could fail classes if he does not change them. Examples of people being prudent that I have witnessed is my roommate Scott. He plans ahead and when shopping looks for discounts to save money. These things are acts of being prudent because he is looking out for the well being of him and these things will help him out in the long run. Finally people think that being self-destructive and prudent have to be things that will hurt you right then and there, but really they are things down the road that will help or hurt you. Philosophers question is every human is alike or not. I believe that every human is not alike, but quite different. Humans act in different ways because of things that they have experienced, the way that they were brought up, how they feel, what they know, and may other reasons. Not all humans have experienced the same thing, were brought up the same way, feel the same way about things, have the same knowledge, or are the same in other ways. How can humans be all be alike of this is the case? Finally humans may have the same features or look the same, but their nature is not all alike. Human nature is different from person to person, but it is similar enough between certain people that you are able to group humans in to different groups by how they act. I came up with three different groups that I can group people into. These groups are by culture, economic status, and values and faith. I chose these groups because these groups are distinct things that make their human nature different. I chose culture because where you grow up and how you grow up shape you into what you will be and how you will act. People that all grew up under the same culture will have similar human characteristics in nature. Economic situation is the same way. People that grew up in a wealthy family are going to act the same and have the same tendencies, while people that grew up poor are going to have different tendencies because of how they grew up. An example of this is that wealthy people will take more things for granted and be more inconsiderate about what they get, while poor people are going to be more considerate about what they get. I also picked values and faith as groups for humans because when you grow up your parents teach you their values and faith. If a kid grows up learning about God and learns to always be kind, fair considerate, and prudent they are going to act differently than someone that grew up in a family that did not teach about God and taught their kid that it did not matter if you were inconsiderate or considerate, unfair or fair, mean or kind, and self-destructive or prudent. Some people believe that humans act the way they do because of their upbringing while other believe that humans act the way they do because of genetics, but I believe that humans act the way they do because of only their upbringing. Every human is born with different traits from their parents, but these traits are not what will make them who they are when they are adults. The things that their parents teach them, where they grow up, and how they grow up is going to be the final molding process for how they will act when they are adults. The environment that they grow up in, the things that they experience when they are growing up, and the values that they learn are what is going to make them act the way they will when they are adults. Finally even though they are born with traits of their parents these traits are not what will make them act in different ways. The way they will act is learnt through their lives. Finally as the semester passed and I learnt more about ethics and philosophy I decided that Aristotle came closest to the truth as I saw it. He agrees that humans are born with traits, but these traits are not what make us who we are as adults. â€Å"Virtue, then, being of two kinds, intellectual and moral, intellectual virtues in the main owes both its birth and its growth to teaching (for which reason it requires experience and time)†(Denise Nicholas Sheldon 28). This supports how we are born with some traits, but these traits are not we act how we do. It is the experience and time that make us the way we are. Aristotle also agrees how nature is what molds us into who we are as adults. â€Å"Neither by nature, then, nor contrary to nature do the virtues arise in us; rather we are adapted by nature to receive them, and are made perfect by habit† (Denise Nicholas Sheldon 28). This also supports how nature is not what makes us who we are. It is the morals our family teaches us and nature is only what molds those teachings. Finally traits like intelligence is not what makes a human act the way he does when he grows up, but it is the things he learns that does. â€Å"For in speaking about a man’s character we do not say that he is wise or has understanding but that he is good tempered or temperate† (Denise Nicholas Sheldon 28). In conclusion I believe that humans do not act the way they do because they are born with these traits, but they are molded from different experiences in their lives, the environment they grew up in, and the family values they are taught. Humans are not all alike, but they can be grouped together into three different categories, culture, economic situation, and values and religion. Work Cited Denise, Theodore Cullom, Nicholas P. White, and Sheldon Paul Peterfreund. Great Traditions in Ethics. Australia: Thomson/Wadsworth, 2008. Print.