Intercultural communication Essay Example | Topics and Well Written Essays - 500 words

Intercultural communication - Essay Example This happens when cultural differences interfere in the interpretation of the message, wherein difficulties may arise, as well as misunderstandings and hatred. Surface-structure cultural transfer comes in either the language form or the speech act. The language form involves understanding of the different lexical culture, such a vacant words, words with strong cultural connotation, idioms, proverbs and polite formulas. Since native speakers acquire them unconsciously, second language learners learn them according to their own cultural background. On the other hand, speech act may only be avoided if the people involved in the communication process should take time in analyzing first the culture of the speaker in which the speech is delivered. The negative transfer of deep-structure culture, on the other hand, occurs in situations where individuals have varying cultural values, thought patterns, religious beliefs and ethics. In Wei’s study of Chinese and the American intercultural communication, culture plays a big factor in the negative transfer of ideas. China, as a country driven by collectivism, puts emphasis on the views, needs and goals of the in-group (relatives, clans, organizations) rather than oneself; social norms and duty defined by the in-group rather than behavior to get pleasure; beliefs shared with the in-group rather than beliefs that distinguish self from in-group; great readiness to cooperate with in-group members. In contrast, American culture is deeply rooted in individualism, thus the interpretation of these two cultures vary. In addition, Chinese associate and depend their decision according to their past experiences. They give emphasis on their past such that they believe that the past guide s them for their actions in the present. However, Americans believe the other way. They give more emphasis on the future such that they give much attention to what would happen next rather than look at the

Physical development observation of a special need child in a group of diverse children Essay Example for Free

Physical development observation of a special need child in a group of diverse children Essay ASSIGNMENT # 2: PARENT INFORMATION/EDUCATION SHEET In Chapter six, Stress is the bodys reaction to a physical or emotional situation that causes discrepancy in a persons life. On the other hand, all children will experience stress, sometimes significant amounts of it, in their lives. The author depict the stress that young children may experience and it may well be resulting from disrupted homes, blended families, both parents working outside the home; increased exposure to violence, Parents working all the time, death, poverty Experts agree that for some children, growing up in today’s world may be tougher. As many as 25% of all children are at risk of academic failure because of physical, emotional, or social problems and are less able to function well in the classroom because they are hungry, sick, troubled, or depressed. Children seem to have fewer sources of adult support than in the past, and many are being pressured to grow up faster (Honig, 2009; Marks, 2002).We need to be concerned about accumulated childhood stress and to be watchful about the types of stress-coping responses children are developing. Children experience stress from time to time in growing up. We have good evidence that children in poor families are less able to function well academically, socially, and physically. Despite this, almost 12 million children in the United States (16%) live in poverty, and another 5 million (7%) live in extreme poverty (Luthar Sexton, 2007. Many children live in families that are typically overwhelmed with high levels of substance abuse, domestic abuse, and mental health problems. Poor children are more inclined to have developmental delays and behavioral and disciplinary problems than other children. They experience malnutrition, health problems, and below average school performance. Five suggested techniques for reducing childhood stress and supporting young children at home are: For parents that are working all the times, quality time is important as kids get older. Allow time for fun activities, Its really hard to come home after a long day of work to get down on the floor, and p lay with your kids or just talk to them about their day especially if theyve had a stressful one themselves. Whether they need to talk or just be in the same room with you, make yourself available because expressing interest shows that theyre important. Complicating factors, like a divorce or separation, when these are added to the everyday  pressures that kids are facing, the stress is overstated. Divorce has been embattled as the single largest cause of childhood depression. Almost all children in that situation manifest some signs of psychological imbalance or feelings of insecurity. Even the most amicable divorce can be a difficult experience for kids because of uncertainty, it is a tough change. Parents should never put kids in a position of having to choose sides or expose them to negative comments about the other spouse. Parents need to sit down and explain to children the changes in an age appropriate way about what to expect, reassure them that the love both parents have for them will never change and that both of you will always be there to support them in any way. Another Suggested technique is Life event like death of a love one, Parents feel uncertain about how to comfort their children who have experienced the loss of a love one. Children understand very little about death, it is the parent’s responsibility to help their children develop a healthy understanding about the subject matter. Different families have different views when talking to children about death, it is a day to day event that even adult cannot comprehend but in that circumstance parents have no choice but to help their children cope with their loss by allowing them to talk and express their feelings and emotions. Additional suggested technique is natural disaster, as we seen in many countries where a hurricane or an earthquaque cause a family to lose their home and all their belongings. In time of hardship and confusion such as this, Children are thrown out of balance, they feel disoriented and will develop stress and anxiety caused by fear. Parents need to shield their children and help them get back into control. Talk to the children, reassure them that this situation is temporary and promise them that things will get better or seek professional help. Conclusion Our complex modern society has greatly increased the amount of stress adults and children are exposed to. Children are experiencing more stress at younger and younger ages Children react in different ways to stress. Some children become ill. Some may become withdrawn and nervous while others show anger and demand attention. It is not easy to recognize when kids are stressed out, but listen and watch for behavioral changes, mood swings, acting out, changes in sleep patterns, or bedwetting can be indications. Some kids have trouble concentrating or completing schoolwork. Still others become withdrawn or spend a lot of time alone even very young children have worries and feel stress to some degree. Adults ordinarily fail to recognize the incidence and magnitude of stress in the lives of children the author went on to explain how to help kids cope with stress, it is to provide proper rest and good nutrition, to create time for your kids each day. No technique will work all of the time. But Pay a little extra attention to her Some children experience more stress than others, some are more sensitive to stress and some are better at handling it than others. We cannot eliminate all stress from children’s lives, nor can we always succeed in making stressed children feel better immediately. Stress is a part of life, and children learn how to handle child-sized stress by dealing with it, with appropriate help and support. By practicing stress-reduction and relaxation strategies with your children, you’re helping them build skills they will use throughout their lives. Create an information sheet that can be sent home to help families support their children in times

Advanced Glycation End Products (AGE) for Diabetes

Advanced Glycation End Products (AGE) for Diabetes Diabetes mellitus is a syndrome which defined as a group of metabolic diseases characterized by hyperglycemia, that result from insufficient production of insulin, or body cells poorly respond to the insulin that is produced, or both. Insulin is a hormone produced in the pancreas and secreted in the blood to maintain blood glucose in the body through enables body cells to absorb glucose, to turn into energy. If the body cells enable to absorb the glucose, the glucose will accumulates in the blood (hyperglycemia), leading to many and different potential medical complications (Harmel Mathur, 2004). Diabetes have several categories but the majority of cases fall into two categories which are type 1 diabetes mellitus and type 2 diabetes mellitus. These two types are powerful and highly independent risk factors causing coronary artery disease, stroke, peripheral arterial disease and organ damage and dysfunction including eyes and nerves (Harmel Mathur, 2004). Type 1 Diabetes Mellitus: Type 1 diabetes mellitus resulting from pancreas failure to produce insulin hormone. Person at risk of developing type 1 can be identified by doing serologic test markers that showing evidence of autoimmune destruction of beta cells (islet cells) of the pancreas which is responsible for insulin production. Type 1 diabetes is manifested in childhood and early adulthood, but can patient present at any age (Goroll Mulley, 2009). Type 2 diabetes mellitus: Patients with type 2 diabetes mellitus are prone with wide range of series complications. Type 2 is characterized by high blood glucose due to insulin resistance and relative insulin deficiency. There are 20.8 million people in United State with type 2 diabetes mellitus. Type 2 diabetes traditionally is seen in elderly people. However it is diagnosed in obese children. Many studies shows that type 2 diabetes mellitus are associated with high calorie diet, physical inactivity and life style (Feinglos Bethel, 2008). Other Types of Diabetes: There are other types of diabetes but they are less common but patients who are underlying defect or disease process can be identified in a relatively specific manner. These types are Genetic defects of beta-cell function, Diseases of the exocrine pancreas e.g Fibrocalculous pancreatopathy, Endocrinopathies and cystic fibrosis and Uncommon forms of immune-mediated diabetes. Diabetes mellitus complications: Diabetic complications can be grouped into macrovascular and microvascular disease. Macrovascular diseases are result from atherosclerosis which develops in earlier age in patient with diabetes. There are several factors contribute to atherosclerosis such as lipidemia, hypertension, increased platelets adhesion and aggregation, elevated factor V, factor VII and fibrinogen concentration. Macrovascular diseases are seen in both type one and two of diabetes mellitus and they include coronary heart disease, Ischemic stroke and peripheral vascular disease (which can lead to ulcers, gangrene and amputation) (Winter Signorino, 2002). Whereas, Microvascular complications is seen in type one diabetes mellitus. Hyperglycemia damages the basement membrane of capillaries in the retina and glomerulars which leads to retinopathy and neuropathy. Microvascular diseases include neuropathy (nerve damage), nephropathy (kidney disease) and vision disorders (eg retinopathy, glaucoma, cataract and corneal disease). Furthermore there are other complications of diabetes include infections, metabolic difficulties, dental disease, autonomic neuropathy and pregnancy problems (Winter Signorino, 2002). Several clinical research show a strong relationship between hyperglacemia and diabetic microvascular complications in both type 1 and type 2 diabetes. High glucose and insulin resistance play important roles in the pathogenesis of macrovascular complications due to atherosclerosis. Diabetes-specific microvascular disease in the retina, glomerulus and vasa nervorum has same pathophysiological features. Intracellular hyperglycaemia causes abnormalities in blood flow and increased vascular permeability which leads to decreased activity of vasodilators such as nitric oxide, increased activity of vasoconstrictors such as angiotensin II and endothelin-1, and elaboration of permeability factors such as vascular endothelial growth factor (VEGF) (Brownlee, 2001). There are several factors which contribute the formation of inflammation, atherosclerosis and diabetes mellitus complication. These factors are hyperglycemia, accumulation of advanced glycation endproducts, dyslipidemia and oxidative stress which lead to endothelial dysfunction resulting in thrombotic complications and cardiovascular (Altman, 2003). In type 1 diabetes mellitus, high blood glucose is usually as result of low level of insulin secretion whereas in type2 hyperglycemia is caused by resistance of insulin at the cellular level. Low insulin levels or insulin resistance enable the body to convert glucose into glycogen (a starch-as source of energy which stored in the liver). In type 1 diabetes, pancreatic beta cells are attacked by auto-immune which cause infiltration of inflammatory cells and increased expression and secretion of S100-calcium binding protein and high-mobility group protein 1 (HMGP1) through inflammatory cells which consequently lead to islet damage and increased blood glucose level, subsequent accumulation of AGE (Bierhaus Nawroth, 2009). Comparing to T1D, in type 2 diabetes mellitus, different metabolic disturbances stimulates inflammatory cells to secretes RAGE ligands, which cause low-grade inflammation and increased oxidative and carbonly stress, all these play roles in promoting AGE formation and RAGE expression in respective organs (Bierhaus Nawroth, 2009). Insulin resistance and Inflammation: In diabetic patients with hyperglycemia, cause by 1) impaired insulin secretion by the pancreatic ß-cells, 2) muscle insulin resistance, and 3) hepatic insulin resistance all play central roles in the development and progression of glucose intolerance. As I mention before, type 2 diabetes mellitus (T2DM) is characterized by insulin resistance in liver and muscle and impaired insulin secretion. Also include deranged adipocyte metabolism and modified fat topography in the pathogenesis of glucose intolerance in T2DM. Fat cells are resistant to insulins antilipolytic effect, which result in increased plasma free fat acid levels. Long period of increasing plasma fat fee acid stimulates gluconeogenesis, promote hepatic and muscle insulin resistance, and impairs insulin secretion in genetically predisposed patients. These pathways of FFA-induced are known as lipotoxicity. Fat cells Dysfunction makes excessive amounts of insulin resistance-inducing, inflammatory, and atherosclerotic-provoking cytokines and fails to secrete normal level of insulin-sensitizing adipocytokines. Enlarged fat cells are insulin resistant and have minimized capacity to store fat. When storage capacity of adipocyte is exceeded, lipid overflows into muscle, liver, a nd perhaps ß-cells, resulting in muscle, hepatic insulin resistance and impaired insulin secretion. In type 2 diabetics, the ability of insulin to stop lipolysis and to decrease the plasma FFA levels is markedly impaired. It is clearly that chronic elevated levels of plasma free fat acid leads to insulin resistance in muscle and liver, and impair insulin secretion. In addition to FFA in plasma, increase stores of triglycerides in muscle and liver which correlate closely with the presence of insulin resistance in tissues. The triglycerides in liver and muscle are in a state of constant turnover, and the metabolites of intracellular triglyceride lipolysis impair action of insulin in liver and muscle (Bays et al, 2004). This pathway of events has been referred to as lipotoxicity . The accumulation of lipid in dipocytes leads to activate NADPH oxidase which increases the production of reactive oxygen species (ROS). The mechanisms increased production of cytokines including TNF-ÃŽ ±, IL-6 and monocyte chemoattractant protein-1 and reduce the production of adiponectin (Shoelson et al, 2006). Furthermore accumulation of lipid activates the protein response to increased ER stess in fat and liver. All these have accumulated to induce lipotoxicity as an important cause of ß-cell dysfunction (Bays et al, 2004). Receptor for advanced glycation end products (RAGE): RAGE is type I transmembrane receptor of the immunogloblin superfamily. It is a receptor for advanced glycation endproducts (AGE). It is about 45-KD a protein and it is consist of 403 amino acids in human, rate and mouse. Its extracellular region consists of one V-type (variable) immunoglobulin domina, which followed by two C-type (constant) immunoglobulin dominas (Basta, 2004). Its name drive from its ability to bind AGE and also it is known as AGER. It is located within the major histocompatibility complex (MHC) class III region on chromosome 6, which contains numbers of genes involved predominantly in inflammatory and immune responses and several components of complements. Beside AGE, RAGE is able to bind several ligands therefore is called a pattern-recognition receptor. These ligands are high-mobility group protein 1 (HMGP1), S100-calicum binding protein (S100b) which is family of pro-inflammatory cytokines and it can be found in any inflammatory lesion and vascular walls of diabetics patients, amyloid-ß-protein and macrophage-1 glycoprotein (CD11B/CD18). RAGE plays role in diabetes and other metabolic disease. The interaction of RAGE and its ligands cause pro-inflammatory activation. It is involved in several diseases such as innate immune response, mediating immune and inflammatory response, cancer promoting and progressing and microvascular and mi crovascular diseases (Bierhaus Nawroth, 2009). Moreover, RAGE expression is increased in the cells of the vascular walls, at the site where AGEs and S100/calgranulins are accumulated, including endothelium vascular smooth muscle cells, glomerular mesangial cells and mononuclear phagocytes. This destrbution of RAGE and its ligands leads to increased cellular activation, causing further raised expression of the receptor (Basta et al, 2004). Recently the studies have been proved that RAGE and its ligands accumulate in diabetes and contribute to its pathology. Serum levels of S100A8/9 and S100A12 increased in type 2 diabetic patients. Also, evidence was provided by raised serum levels HMGB1 were linked to coronary artery disease in type 2 diabetes. In addition the studies which have been done in streptozotocin-induced diabetic rats proved that diabetes increased amyloid-beta-peptide (1-40) levels in the brain. Furthermore, CML-modification of S100A8 and S100A9 are seen in inflammatory bowel disease and promote RAGE-mediated sustained inflammatory. Moreover, Carboxylated N-glycans on RAGE eases binding of HMGB and mediates ligation of S100A8/A9 to subpopulation of RAGE on colon cancer cells (Bierhaus Nawroth, 2009). Advanced Glycation End products (AGE) and its biochemical mechanism production: There are various pathways involved in stimulation of atherosclerosis in diabetes mellitus. However the most important one is formation and deposition of AGEs through nonenzymetic reaction between extracellular protein and glucose and it accumulates within cells of the vascular walls, in the extracellular space, kidney, nerves and retina (Basta et al, 2004). Possible mechanism of AGEs formation arise from intracellular auto-oxidation of glucose to glyoxal, decompounding of the Amadori product (glucose-derived 1-amino 1-deoxyfructose lysine adducts) to 3-deoxyglucosone and fragmentation of glyceraldehyde-3-phosphate and dihydroxyacetone phosphate to methylglyoxal. These reactive intracellular dicarbonyls (glyoxal, methylglyoxal and 3-deoxyglucosone) which can react with amino groups of intracellular and extracellular proteins to form AGEs (pyrraline, pentosidine, CML, crossline) (Balasubramanyam et al, 2002). Several experimental studies evidenced that advanced glycation end products can alter vascular wall homeostasis in atherogenic through different ways which are: AGEs and mononuclear phagocytes Interaction: The binding of AGEs with mononuclear phagocytes MPs induces the activation of platelet-derived growth factor, insulin-like growth factor-1, and pro-inflammatory cytokines, such as IL-1ß and TNF-ÃŽ ±. Furthermore the interaction of AGEs with its receptor (RAGE) in the mononuclear phagocytes promotes cell migration (chemotaxis) (Basta et al, 2004). AGEs and vascular smooth muscle cells Interaction: Interaction of AGE with smooth muscle cells (SMCs) exhibits the proliferative activity and production of fibronectin. SMC growth are indirectly mediate by cytokines or growth factors which induced by AGEs in the MPs. Transforming growth factor-ß (TGF-ß) act as an intermediate factor in AGE-induced fibronectin formation by SMC(Basta et al, 2004). AGEs with vascular endothelium Interactions: alterations of vascular permeability and of adhesive properties As result its unique position and numerous properties, the vascular endothelium has important role in the regulation of extracellular permeability, the maintenance of blood fluidity, metabolism of hormones and vasoactive mediators and the regulation of vascular growth and tone. The endothelium is exposed to AGEs located on circulating proteins and cells (such as, diabetic RBCs), also those found in the underlying subendothelial matrix. Receptors for AGEs present on the endothelial cell surface, and mediate both the uptake and AGEs transcytosis, and the internal signal transduction. AGE-RAGE interaction leads to alteration of barrier function and an increased permeability of endothelial cells interact with AGEs and increased migrate of macromolecules through the endothelial monolayer. The increase in permeability is associated by alterations of the physical integrity of the endothelium, as shown by the destruction of structures and alterations of cellular morphology (Basta et al, 2004 ). Also, it has been proved that AGEs cause alterations of endothelial anti-hemostatic functions in vitro, through a reduction of thrombomodulin expression and accompanied with induction of tissue factor expression. The promoting of tissue factor and the decreasing in thrombomodulin activity change the dynamic endothelial features with regard to hemostasis from those of an anticoagulant to those of a procoagulant surface (Basta et al, 2004). Intraction of AGEs with endothelial RAGE also causes the depletion of cellular antioxidant defense mechanisms (such as glutathione, vitamin C) and the generation of reactive oxygen species. As a result of the increased cellular oxidative stress, NF-ÃŽ ºB activation occurs, thus inducing the expression of NF-ÃŽ ºB-regulated genes including, in addition to the procoagulant tissue factor, adhesion molecules, such as E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1); this past may prime diabetic vasculature towards enhanced interaction with circulating monocytes. Furthermore, the incubation of endothelial cells with EN-RAGE or S100B results in VCAM-1 induction, in a RAGE-dependent manner, as sustained by the inhibitory effect of anti-RAGE IgG or soluble RAGE (Basta et al, 2004). Alterations of endothelium-dependent vasodilatation AGEs linked to the vascular matrix may quench bioavailability of nitric oxide (NO), which is an important regulator of vascular tone inducing smooth muscle cell relaxation. Studies provided that, AGE inhibits NO activity, when it added to NO in vitro. Studies on animal exterminate induced diabetes show that an alteration of endothelium-dependent dilatation occurs in short period, within 2 months, from diabetes induction. A direct reaction between NO radical and other free radicals which are formed during the reactions of AGEs assumable leads to inactivation of NO. In parallel, advanced glyaction end products promote the expression of the potent vasoconstrictor endothelin-1 changing endothelial function towards vasoconstriction (Basta et al, 2004).   Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  Ã‚  These four mechanisms promote and alter vascular wall homeostasis. When mononuclear phagocytes migrate to the site of immobilized AGEs in the tissue, their migrations allow them to interact with AGE -modified surface and become activated. This mechanism cause attracting and retaining MPs in tissue where AGEs deposit. Migration and activation of MPs and T cells (inflammatory cells) promote and cause chronic vascular inflammation through alter vessel wall (Basta et al, 2004). Promotion of atherogenesis pathways by AGEs: AGEs are most important factors in endothelial dysfunction in diabetic patients through binding its receptor (RAGE). Advanced Glycation Endproducts stimulate the expression of proinflammatory cells and molecules (Altman, 2003). AGEs can be seriously deleterious to the function of blood vessel walls in various ways. First it causes blood vessel dysfunction through cross bridges among vessel macromolecules. Secondly of damage is that accumulation of AGEs lead circulating blood cells to adhere to the vascular walls which promote atherosclerosis. Third way is through binding different receptors which have been recognized on various cell types such as macrophages, endothelial cells, and smooth muscle cells, renal and neuronal cells (Basta et al, 2004). Hyperglycaemia Mechanisms-caused damage: Hyperglycemia diverse microvascular and macrovascular complications in diabetic patients through several mechanisms such as increased formation and accumlation of advanced glycation end-product (AGE); activation of protein kinase C (PKC) isoforms; and increased generation of reactive oxygen species (Bonke et al,2008) Increased production advanced glycation end-products AGE promote atherogenesis pathway through accumulation of AGEs and AGEs ligation to RAGE on endothelial cells and macrophages induce inflammation through activating pro-inflammatory cytokines including TNF-ÃŽ ±, 1L-6 a L-1ß, induction of reactive oxygen species (ROS) and through increased oxidative stress which lead to degradation of IKBs (IKBs is normally bound to NF-KB to prevent translocation of NF-KB to nucleus). ROS activates NF-KB which results in translocation of NF-KB to nucleus. Activation of NF-KB cause pathological change of gene expression which is highly related to inflammation, immunity and atherosclerosis, increased expression of inflammatory mediators which lead to insulin resistance and increased RAGE expression as well (Basta et al, 2004). Mechanisms by which intracellular production of advanced glycation end-product (AGE) precursors damages vascular cells. Cellular functions are altered by dicarbonyl advanced glycation end products. Alteration of extracellular matrix proteins results in abnormal interactions with other matrix proteins and with integrins. Alteration of plasma proteins by AGE precursors generate ligands that bind to AGE receptors, inducing conversion of gene expression in endothelial cells, mesangial cells and macrophages. Activation of protein kinase C: The protein kinace C (PKC) family compromises at least eleven isoforms, nine are induced by the lipid second messenger diacylglycerol (DAG). Altered DAG-PKC pathway play an important role in diabetic complications. Intracellular hyperglycaemia raises the amount of DAG which activate PKC in cultured vascular cells and in the retina and renal glomeruli of diabetic animals. Hyperglycaemia may also activate PKC isoforms indirectly by AGEs bind receptors and increased activity of the polyol pathway, possibly through increased reactive oxygen species (ROS). AGE stimulated diacylglycerol (DAG) and activate protein kinase C (PKC) in VSMC. PKC is one of important signal transduction elements involved with multiple cell response. In early studies of diabetes, retinal and renal blood flow abnormalities are due to activation of PKC-ß isoforms perhaps through depressing nitric oxide production or increasing endothelin-1 activity. Abnormal activation of protein kinase C has several pathogenic c onsequences: It leads to decreased production of nitric oxide in smooth muscle cells and glomerular mesangial cells that is induced by hyperglycemia (Brownlee, 2001). Activation of PKC causes inhibition of insulin-stimulated expression of mRNA for endothelial nitric oxide synthase (eNOS) in cultured endothelial cells. Hyperglycaemia activates PKC to increased endothelin-1, permeability of endothelia cells and increased expression of the vascular permeability angiogenesis factor (VEGF) in smooth muscle cells (Brownlee, 2001). Increased generation of reactive oxygen species: Increased generation of reactive oxygen species (ROS) is another possible pathways of diabetes complications especially nephropathy complication. Production of Reactive oxygen species can be result from the activation of various enzymes, including NADPH oxidase, nitric oxide (NO) synthase, and myeloperoxidase, with arising evidence that NADPH oxidase is the major cytosolic source of ROS generation in diabetes. NADPH has homologues that are present within the kidney, namely nox-3, seen in fetal kidney, and nox-4, which is predominately expressed in the renal cortex. AGE bind RAGE induces signal transduction and activate NADPH oxidase in endothelial cells. The interaction between AGE-RAGE enhances production of the cytokine vascular endothelial growth factor (VEGF), which is directly induced by NADPH oxidase and is associated with the pathogenesis of albuminuria in diabetes (Bonke et al, 2008). Diabetes mellitus control and treatment: Both type 1 and 2 diabetes mellitus are characterized by elevated blood glucose level due to insufficiency of insulin level. Therefore, diabetes patients need to reduce blood glucose level through healthy diet, drugs such as (hypoglycemic tablets and anti-atherosclerosis drugs), insulin injection and regular physical exercise. Healthy Diet: In general, healthy diet for diabetes patients should include: limit fats (especially saturated fats and trans-fat acid), proteins and cholesterol. Also, patient should consume a lot of fiber and vegetables. Patients with insulin-producing or insulin synthesis treatment should monitor their blood glucose level to avoid hyperglycemia. For example, adults and teenager patients should maintain their blood glucose level between 80-120 mg/dl, and 100-200 mg/dl for children under 12 year old. Type 1 diabetes patients should test their blood glucose level four to more per day. However, in type 2 diabetes, patients recommend to measure blood glucose level 1 to 2 times daily, because glucose level in type 2 diabetes is more stable than in type 1. Such important tests are important during diet plans and treatment. For example, glycosylated hemoglobin test (HbA1 c) is an indicator for carbohydrate level. Micro and macroalbuminuria indicates of the proteinuria and renal function, for instance if the teat showed high level of proteinuria then the patient need to lowering protein intake (Flaws et al, 2002). Exercise: Physical exercise is important to manage diabetes complications. Regular exercise improves the status of both type 1 and 2 diabetes through transporting sugar to muscles, improving blood circulation, and increasing insulin receptors. Exercise has specific effects on diabetes patients include: reducing blood glucose level during and after exercise, increased insulin sensitivity, reduced triglyceride level and increased good cholesterol (HDL) (Flaws et al, 2002). However, diabetes patients may have several risks associated with exercise which include: hypoglycemia if patient under treatment with hyperglycemia agents, hyperglycemia and ketosis in insulin-deficient patients, and exacerbation of cardiovascular disease. Therefore, patients who are over 30 year old should be examined before doing physical exercise. These examinations include: cardiovascular exams such as blood pressure, blood lipid and ECG, and neurological evaluation such as eye exam (Flaws et al, 2002). Anti-inflammatory drugs Various drugs in recent clinical practice have been used as anti-inflammatory agents such as thiazolidinedione (TZD) class of PPARÃŽ ³ agonists and members of statin class of HMG CoA reductase inhibitors. Both of them have importane anti-inflammatory properities and both have action on glucose homeostasis and cholesterol redusing (Shoelson et al, 2006). TZDs are used to induced insulin sensivity and decresed hyperglicemia in patient with type 2 diabetes mellitus. TZDs drugs inculde pioglitazone, rosiglitazone and troglitazone. The role of TZDs is through binding and activiting PPARÃŽ ³ to induce a number of gene expression products in a dipocyte. TZDs action are attributed to fatty acid in the a dipose tissue. TZD decreases circulating free faty acid and keep faty acid out of musle and liver because accumalte of fatty acide in these tissue lead to insulin resistance. In addition, PPARÃŽ ³ is not only present in dipocyte but also in it is expressed in macrophages and other immune cells response, hepatocyte, endothelial cells and vascular smooth mucsle cells (VSMC). TZD play role in reduce the expression of targets gene for cytokines, growth factors, proliferation and migration of cells, and cell cycle progression (Shoelson et al, 2006). Rosigliatozone: Rosigliatozone decreses the inflammatory markers such as serum C-reactive protein, metalloproteinase-9, white blood cell, tumer necrosis factor-ÃŽ ± and serum amyloid-A in type two diabetes mellitus (Altman, 2003). Group of studies done on Diabetes Rodents: The recent research has demonstrated that rosiglitizone, a PPARÃŽ ³ agonist, attenuates diabetes associated atherosclorosis. The reaserch has studied the direct antiathersclosis effects of PPARÃŽ ³ afer long beriod of therapy in an experiment of insulin deficiency. This study show that rosiglitezone has no effect on glucose level in both control or diabetes mice. However, rosiglitizone , PPARÃŽ ³ (acting as insulin sinstiser) significally decresed plasma insulin level in control mice (Calkin et al, 2005). In addition to Calkin study and his collegous, another study shows that rosiglitazone increase the insulin content and iselt cells number and total mass of pancreas in diabetes rats. However, it is unknown if this is adirect effect of rsiglitazone by activation of PPARÃŽ ³ mediated pathway in islets or indirect effect of normalizing the hyperglicemia (Sanchez et al, 2002). Increaesd secration rate of proinsulin relative to insulin is one oa acommon feature in type 2 diabetes mellitus. The normal range of proinsulin in normal subjects is about 2 to 4% of the total amount of insulin and in type 2 diabetes proinsulin rate is about 15%. Curently the studies has been demonstrated that rosiglitazone in type 2 diabetes decrease proinsulin secretion. Proinsulin has been associated with activity of carboxypeptidase E. Fricker and collegous have evidenced that carboxypeptidase are present in secretory pathway and participate in peptide processing. CarboxypeptidaseB has similler feature as carboxypeptidaseE but the precursor sequence of carboxypeptidaseB has been seen in an adult mouse islet cells. Thus suggest that rosiglitazone may has primery effect on increasing the expression of carboxypeptidaseB precursor protein resulting in increse proinsulin to insulin conversion (Sanchez et al, 2002). Further more, rosiglitizone did not affect fasting insluin level in diabetic mice due to streptozotocin which induce insulin insufficency. Also, another group of study has curently demonstrated that short period of treatment with rosiglitizone decreased plaque area in diabetic mice but had no determination if effects seen were linked to insulin sensitization (Calkin et al, 2005). More current sutdies have evedanced that rosiglitezone treatment in diabetes mice reduce gene expression of the NF-KB subunit p65. Further study has shown that rosiglitizone has no direct effect o glucose-induce upregulation of oxidative stress. Same study had investigated RAGE expression acording to preveious finding that first of all, RAGE expression increse oxidative stress and secondly rosiglitezone which used in culture media alter RAGE expression. The study had shown, the expression of RAGE gene wasnt altered by rosiglitizone (Calkin et al, 2005). Some study showed no significant alteretion in gene expression after TZDs treatment. This is because of almost studies were not preformed in human adipose tissue in vivo but they used adipose tissue of rodents and adipocyte cell line. Actually under such study we should consider about some facts that, for example rosiglitazone dose which used in rodents study (10 mg/kg) is higher than human dose about 100-fold. furthermore, TZD may has an action on gene expressed in rodents but it is not necessarily to has same action on human gene. For example carbonic anhydrase 3 protein raised 2-fold after treated the mice with rosiglitazone, however there was no increasing in carbonic anhydrase 3 mRNA in human adipocyte. Although there were similarities in the action of TZD-induced insulin sensitivity, there may be TZD action has different mechanisms on experimental models and human (Kolak et al,2007). Therfore, Im going to discuss about the studies which have been done on human adipose tissue and there findings. Group of studies done in human patient with type 2 diabetes: Overactivity of ubiquitin-proteasome system is associated with the inflammation and atherosclerotic plaques in type 2 diabetes. Study by Marfella and his colegous on human diabetes patients has been shown that the PPAR-ÃŽ ³ agonist rosiglitazone reduce ubiquitin-proteasome activity and thuss prevent plaque progression to unstable phenotype in diabetes individulas (Marfella et al, 2006). Also, same study shows, the production of O2- by monocytes is reduced after rosiglitazone treatment. Thus proteasome reduction is induced by inhibition of oxidative stress and polyubiquitination. As oxidative stress induce insulin resistence through NF-kB activation, rosiglitazone enhance insulin sensivity and plaque stability in diabetes patien through reducing oxidative stress and ubiquitin-proteasome activity. Further possibility that, NF-KB activation is inhibited by rosiglitazone through a PPAR-ÃŽ ³ independent pathway. PPAR-ÃŽ ³ agonist inhibits NF-KB translocation and subsequent DNA binding through inhibits immune response which induce degradation of IKBs (Marfella et al, 2006). Rosiglitazone have significant effects on metabolism of faty acid and lowering circuliting non-esterified fatty acid. Therfore rosiglitazone prevent islet cells through reducing fatty acid exposure (Sanchez et al, 2002) Kolak and his colleagues investigated the gene of expression in human adipose tissue in vivo in type two diabetes mellitus, befor and after tratment with rosigliatozone and metformin. Reosigliatozone modulates expression of gene which involved in free faty acid synthesis and storage, protein strcture, inflammatory cells inculde macrophage and gene associated in glucose transport and insulin sensivity. Whereas metformin has no effect on these gene (Kolak et al, 2007). TZD decrease the expression of RAGE endothelial protien. From preveious finding, TNF-ÃŽ ± increase the expression of RAGE on endothelial cells, so

Weapons of the American Civil War Essays -- History Weapons Historical

Weapons of the American Civil War Amongst the most lasting of factors stemming from the Civil War are the weapons that were developed. Before the Civil War, the weapons used were highly unreliable, and were not advanced enough to provide the needed defense for a young nation such as our own. Innovative minds created many interesting ways to demolish their enemies without ever having to fire a shot or go into full combat through different types of bombs that were in disguise. Among the advancements in the Civil War were the torpedo, the carbine rifle, the minie` ball, several models of rifle-muskets, rocket launchers, rocket bombs, "Greek Fire," and a wide array of other secret weapons. Torpedoes were quite possibly the most destructive weapons created in the Civil War times. There is a great number of models of torpedoes that come from the Civil War; ranging all the way from models that were anchored to the ocean floor to drifting torpedoes that hung beneath driftwood and moved with the current. The first torpedoes from the south were simple powder filled tin cans with trigger attachments. The torpedoes were later developed to have a thin brass cap with a beeswax solution. If pressure was placed on the cap, then the torpedo would explode. The same structure was used in the development of landmines, the "sub-terra booby traps" as they were so affectionately named by the Union officers. Though in the early stages of development, these primitive looking war machines could destroy a fleet. The Carbine Rifle was a small, easy breechloading rifle. This abnormality made this rifle capable of firing much faster than its predecessors were able to. The Carbine was most effective when using the tactic of riding up, dismounting, and concentrating rapid carbine fire on the enemy. The Carbine rifles developed from single-shot "Burnside" models, named after Ambrose E. Burnside, into repeating rifles dubbed "Henry's". Three French army officers would share the credit for the bullet that caused nearly ninety percent of the soldier casualties in the Civil War. Captain Henri-Gustave Delvigne, Colonel Louis-Etienne de Thouvenin, and Captain Claude-Etienne Minie` were the men which developed this masterpiece. This bullet was designed after discovering that when a standard bullet was put down the barrel of a rifle and was pounded with the ramrod,... ... firing again. Since the gun could fire six hundred rounds of ammunition per minute, each barrel fired one hundred rounds per minute. Coehorn Mortars and Armstrong Rifles were used as projectile attack alternatives when a garrison needed a powerful blow to be delivered. The projectiles used in the Coehorn Mortars ranged form a weight of seventeen pounds, all the way up to 24 pounds. Named after Dutch engineer Baron van Coehorn, this mortar was a light seige weapon used mostly in trench warfare, and was carried by four men. The Armstrong Rifle, on the other hand was quite a large piece of equipment weighing over seven tons. The Civil War did very much for our nation, one key aspect of which was the development and advancement of our nation's defense mechanisms. The United States advanced leaps and bounds in the development of new weapons, and improvements on weapons that previously existed. This is merely a small display of all of the improvements the United States made during the Civil War; a war of bloody conflict and spite. Without these weapons, the war may not have ended just as it did, and we would also not have the advanced weapons systems that we have today.

Tsmg5340 Huawei

TSMG 5340 Wenzhao Li HUAWEI: CISCO’S CHINESE CHALLENGER The explosive growth of mobile Internet, fueled by the technological innovations, has affected every aspect of our lives. Mobile devices such as smart phones and PDA and even smart pets are now being interwoven into the fabric of our lives. The ultimate goal of all these devices is to bring all people into a networked society. Behind all these amazing devices, however, are the efforts of the telecom equipment companies, such as Alcatel, Lucent, 3Com and Cisco.Among all of these companies, there is a Chinese company, named Huawei, gradually being attention by the global telecom industry. For Huawei, its ambition is to catch up with Cisco as a world leader other than a domestic giant, which we know that none Chinese company has ever achieved in an industry as important as telecommunication. In my reading of this issue, trying to comprehensively understand Huawei's situation in venturing into international market, four obser vations stand out: strength of Huawei, weakness of Huawei, Huawei's opportunities and threats faced by Huawei. Strength:Firstly, China’s telecom equipment market is the background of Huawei. China’s telecom industry achieved substantial double-digit growth in 1980s, and surpassed US to become the largest telecom market by the end of 2002. The glooming growth in Chinese market is an initial power of Huawei’s growth. Table 2 in the case shows that as early as 2005, Huawei had achieved the market leader with the share of 13. 5%. And since China was the largest market, Huawei had become the largest domestic telecom equipment company. Secondly, the special company culture and foresight shown by the company make Huawei an extraordinary different company.The military-styled â€Å"Wolf-Pack† corporate culture and relationship with Chinese government are the â€Å"trump cards† of Huawei. The chairman, Zhengfei, admitted that: â€Å"If there had been no gov ernment policy to protect, Huawei would no longer exist†. But this is not the only reason of Huawei’s success. Different from other companies, who following the country’s policy of â€Å"exchanging market for technology†, Huawei put more efforts on research and development, and investing huge punch of money in the future technology (example of investment in 3G).In this way, Huawei becomes more competitive, holding large amounts of cash and patents. As Huawei becoming more and more powerful, they start to build a national recruitment system with exceptionally high pay by Chinese standards, making them an ideal employer of college graduates. R&D investment, patents, high salaries†¦all of these characteristics belonging to western technology powerhouse are replicated by Huawei to its model of corporate management. Thirdly, Huawei was undoubted the largest Chinese telecom equipment manufacturer, with integrated and Omni form products.Weakness: The culture gap between Huawei and other companies may be a headache to the Huawei’s managers. The military-styled wolf-pack corporate culture looks not attractive to the employees overseas, who prefer a workplace with more relax and less stress. Besides this, the closed relationship between Huawei and Chinese government, especially the military, should be considered by the other countries of security issues when they planning to cooperate with Huawei. Opportunities: Huawei’s move in the markets of developing countries has been proved to be successful.Huawei has printed its steps in Russia, South Africa, South America and Europe. The market of USA is an opportunity for Huawei to make their next global expansion. Threats: â€Å"Incumbent Western firms should be very scared of Huawei. Its reputation as a low-cost vendor is only the visible part of the iceberg†, As J. Doineau said, Huawei’s threat to the international telecom equipment suppliers was not to be overlooke d. But in Huawei’s viewpoint, if all the competitors and potential partner regarding them as an intruder from â€Å"Chinese Military†, they would face serious threats due to the culture misunderstanding.On the other hand, the world leaders, like Cisco, could not freely give up their market shares to Huawei. The threat of face to face competition with them is another challenge to Huawei. Huawei began considering international expansion in 1996 when it was looking for diverse sources of growth beyond the Chinese market. The company made its initial overseas moves in the markets of developing countries, to avoid â€Å"head to head competition with its international rivals such as 3Com and Cisco†.Huawei made its first significant international sale to a Russian telecom service provider in 2000, which was quickly followed by Advanced Info Service, Thailand’s largest mobile service provider, and Tele Norte Leste Participacoes, Brazil’s fixed line carrier . What’s more, major contracts won in United Arab Emirates, making UAE the first Arab country with 3G wireless communications. They set up CDMA network in Europe and expanded business in Portugal, Netherlands and GB.Huawei’s success in global expansion cannot live without its competitive advantages comparing to the other companies: low-cost engineering, wolf-pack culture, and government support. As concluded by an industry analyst, Huawei’s threat came not from low-cost manufacturing, but from low-lost engineering. With an inexpensive and highly qualified research and development (R&D) workforce, the company was able to deliver customized, innovative solutions to global enterprises looking to reduce their capital expenditures. The support from the Chinese government is another good news to Huawei.As cited in the case, the company received financial support from the state-owned Chinese Development Bank in the form of a US$10 billion credit facility for Huaweiâ₠¬â„¢s international expansions over five year. We never expect that happening in an US company. Last but not least, the management philosophy â€Å"Wolf-Pack† is regarded as a precious to Huawei. We can imagine that a company believing themselves as a pack of wolves-very confident and aggressive. That is why many incumbents feel scared of Huawei like sheep scaring of wolves. However, the competitive advantages cannot sustain forever.The highly qualified employees cannot satisfy the contemporary salary standards, which are high in China, but comparably low in developed countries. The pressure of the salary expenditure increasing makes a threat to Huawei in global expansion. The news shows that Huawei has recently come under attacks by the US government. The reason why US government did that mostly considers the national security issues, because Huawei has a close guanxi with Chinese military. As stated by Cisco’s CEO John Chambers, â€Å"Network would have to be capabl e of responding to intrusions and viruses before human operators become aware of them.And security will be the most effective and efficient if a common strategy extends through all of a corporation’s wired and mobile networks†. US government is alert to anything related to security. And what looks ironic here is that the words coming from CEO of Cisco, who is mainly competitor of Huawei in US market. With its bountiful political resources, Cisco is considered to be director of attacks. Whether the issue could be resolved is determined by the communications between Huawei and US government, and of course, the local incumbents.

Matriarchy In Cuckoos Nest essays

Matriarchy In Cuckoo's Nest essays Until modern times, society advocated that a man's role was at work, while a woman was required to stay home and assume the role of the main caregiver. Men were given power and authority, and women, conversely, were expected to be meek and subservient. These roles extended beyond the family and out into society, and materialized in areas such as education, politics, and occupations. In One Flew Over the Cuckoo's Nest, Ken Kesey uses the reversal of these stereotypical gender roles to demonstrate the chaotic and sometimes tragically comic world of a mental institution. In the novel One Flew Over the Cuckoo's Nest by Ken Kesey, the women are the power figures and are able to significantly manipulate the patients on the ward, as shown by the characters of Nurse Ratched, Mrs. Bibbit, and Vera Harding. Nurse Ratched, whose power is expressed in bluntly sexual terms despite her attempts to deny her sexuality, maintains her position as the sloe voice of authority on the ward by suppressing the patients' laughter. The men under her jurisdiction use sexual references when talking about her, and after the first group therapy session the new admission R.P. McMurphy calls her a "ball-cutter." The nurse attempts to hide her sexuality, and the schizophrenic Chief Bromden first brings the reader's attention to this denial in saying, "A mistake was made somehow in manufacturing, putting those big, womanly breasts on what otherwise would have been a perfect work, and you can see how bitter she is about it." (Kesey 11) Nurse Ratched's ultimate authority on the ward stems from the fact that she controls people who would normally be her superiors, namely Dr. Spivey, who Dale Harding says is, "'exactly like the rest of us. . .completely conscious of his inadequacy. He's a frightened, desperate, ineffectual little rabbit, totally incapable of running this ward without our Miss Ratched's help and he knows it. And, worse, she knows he knows it and reminds...