The global recession and workplace malfeasance Essay

The global recession and workplace malfeasance - Essay Example nnot influence those with the opportunities to malfeasance in workplace as they are trying to maintain their jobs to reduce the impact of the global recession. Though there are media reports that there has been malfeasance in workplace, it has no clear evidence that the malfeasance is because of the economic downturns and company layoffs. The Times of London for example reports that job losses in the United States is directly linked to 58 fatalities of which 13 people were killed by a Vietnamese man who was later fired from his factory job; this does not prove it was because of the recession just because the crime was committed during that recession (35). The case proves that we can learn nothing from the business press; this is because the press does not present accurate information to the public but reports opposite of the real situations. A poll conducted among 400 employers asking whether recession has brought a recent rise in monetary theft among employees such as missing cash or fraudulent transaction showed that 18% said yes, 41% were unsure, and 41% said they had not. The poll results indicates that a small percentage of employers thought the employee theft is caused by the recession, but the business press reports that â€Å"Business Say Theft by Their Workers Is Up,† which is a complete opposite of the poll result thus we cannot learn from the business press. Regarding on how to be an informed consumer on business news, difficulty illustrations by OB help in the investigation by asking questions, analyzing situations, and considering the information source. This helps the consumers in critically thinking about problems and careful analysis of the same. Therefore, the chapter provides clues on OB issues that can inform the consumer (35). Individual privacy is violated when measurers, such as fingerprint scanner are put in all cash register to monitor what the employees do. Employees feel that their privacy is violated when every move he or she makes in

Micro and Macro Economics Assignment Example | Topics and Well Written Essays - 500 words

Micro and Macro Economics - Assignment Example So the jobless workers used to join the companies where there is no existence of the union. As the number of employees increased in those nonunion companies, salary/wages used to get reduce. In this case the spillover effect is [($20-$10)/10]*100= 100%Estimated Union Advantage with the Spill-Over Effect:The revised salary of the nonunion company is $10 where as new salary in the Union based company is $20. Although the spillover growth is showing a value of 100% growth in actual term, growth in the wages in the union based company is 33.33%.Increase at wages in Firm B: The increase in the wages of firm B is known as threat effect. Generally, companies where no union is present used to take this way to minimize the possibility of development of concept of union controlled labour system. Generally, the increase in wages is lesser in this companies compared to that of the unionized firms. As an example, in this example, the rate of increase in the wage for firm A is 50% ($20 to $30) whi ch is unionized whereas for B it is 25%. ($20 to $ 25)Union Advantage: In firm A, the growth in wages are [($30-$20)/$20]*100=50%; whereas for firm b, which is a non-union firm growth in wages are: [($25-$20)/$25]*100= 20%. There is a clear difference of 5% in increase of wages between union and nonunion firm.Prevailing Wage can be defined as hourly wage system, usually added benefit and structured overtime compensation paid to the majority of the people belonging to working group within a particular area.

Business Economics Essay Example | Topics and Well Written Essays - 1500 words - 2

Business Economics - Essay Example In fact the choice problem of the monopolist is to choose the per-unit price and quantity of output to maximise profits. This is achieved by producing that level of output (Qm) for which the MC = MR (with the MR being intersected by the MC from below as a second order condition). The price charged will be Pm as it can be seen from the demand curve that it is what the consumers shall be willing to pay for each unit if Qm is the available output in the market. Here the profit level shall be supernormal (represented as the shaded area in the diagram) i.e, over and above the normal profits. The absence of close substitutes allows the monopolist to charge a price high enough that ensures supernormal profits. However one should note that the monopolist can actually be bearing losses as well in the short run. This occurs simply if the AC corresponding to the profit maximising output lies above the corresponding price. In this case however the short run problem for the monopolist becomes one of minimising the loss. However, a firm will go on operating in a monopoly market through the long run if only he earns positive profits. Such profits can be sustained in the long run since in spite of the supernormal profits that may act as incentives to new firms, the barriers to entry are assumed to be strong enough to prevent new entry in a monopoly market structure. In the long run, the equilibrium condition is LMC = MR with the MR curve being intersected from below by the LMC curve. However the monopolist is limited in hiking the pricing over a certain extent as the negative income effect it generates may cause consumers to move on to substitute goods and thus causing a loss in revenue. However as long as the monopolist produces the profit maximising output and charges the corresponding optimal price, he/she shall be earning supernormal profits in the long run as well. Oligopoly is a type of

Economy versus the Environment Essay Example for Free

Economy versus the Environment Essay Down to Earth by Ted Steinberg highlights the role of nature in US history. Steinberg provides historical events, from minute detail of migrating birds to monumental breaking up of Pangeae, to support his analysis and for readers to fully grasp the course of American history. He maintains that the continuous interaction between human and nature drives them to evolve. But the truth, of course, is that human has tendencies to disregard nature to achieve their ideal standard of living. Moreover, human’s present consumption puts the life of future generation at risk. Long before the European settlement in the region, America’s natural resources were already being threatened. Native American hunters utilized the world around them according to their needs. These early hunters drove mammoths to extinction, as well as the giant ground sloths and other prehistoric species. Many of them used fire to clear landscape which did served their purpose but harmed other plants and animals. Eventually, however, they became gifted stewards of their environment. Their activities, hunting, gathering and farming, were influenced by the cycles of nature. The early exploration dictated by personal consumption quickly followed by exploitation. Migrants poured in pursuit of gold and silver in the English colonies which was abandoned for intensive harvesting of lucrative crops or the trapping of animals. The slang â€Å"buck† for money in America refers to deer hides called buckskins, being exported for glove making and other forms of leather manufacturing. This economic system persists until the end of the colonial period. By mid-1800s, regions were identified by the kind of cash crops they produced. Tobacco, â€Å"King Cotton,† rice from South Carolina lowlands, timber from the virgin forests of the Great Lakes, Texas cattle and wheat from the Great Plains. The system made the nation wealthy but at a devastating cost to biodiversity. Steinberg pointed out that the major factor that brought the ecological change in America is â€Å"putting a price tag on the natural world. † Cities were expanding, farmers were becoming more specialized in their cash crops and companies were pushing for more profits. Nature was transformed to articles of trade. Lumber companies, for instance, led to much deforestation which led to loss of other plants and habitat of animals. The citizens of the US seemed to have a sense of â€Å"ecological amnesia,† oblivious to the effect on nature of ruthless exploitation despite the mounting evidence. Aside from lumber companies, other businesses and industries abused the natural resources for profit to further degrade the environment. A common man specializing in one type of cash crop had to rely on other farmers to provide for the needs not met by his own produce. Rivers where fish used to spawn were dammed and converted to companies’ energy source. Nature was completely ignored in the interest of commerce and industry. As trade and commercialization intensifies so as reliance of everyone on someone else. Economic activity, both production and consumption, relates to the environment in two ways: the environment provides the raw materials for production, and through the process of production and consumption, we emit wastes into the environment (Worster, 1994). However, human wants are limited while resources are finite. Demand always exceeds supply. So what happens now if we continue to strive to obtain more goods and services from our limited supply of non-renewable resources? Our present and future generations are in peril. Economic theories of trade argue that a country should concentrate on trading and producing goods and services where they have the comparative advantage (Krugman Obstfeld, 2008). The comparative advantage in production is achieved if the input that was used is abundant in the country. For instance, labor intensive goods should be traded by countries with large population, while countries should concentrate in producing capital intensive goods if they are abundant in capital. This exactly what the early traders did. They traded according to their comparative advantage, maximized their profit and yes, abused the environment to further their gains. The economic thinking that competitiveness as a function of efficiency of labor and capital is outmoded (Epping, 2001). In other parts of the world, industries are starting to factor in the efficient way of using their natural resources. These efficiencies benefit countries, companies and local communities. Japan and Germany use half the energy input of American industry in their products. Energy represents about 10 percent of the cost of production and so they achieve with their efficiency about a five percent comparative advantage in world markets relative to US goods. The idea is to have a sustainable supply of both non-renewable and renewable resources relative to demand, to use the natural resources in a more efficient way to make the goods and services of a country, a company or a community more competitive in the market. We do not want to be the generation that kills everything. References Epping, Randy Charles (2001). A Beginner’s Guide To World Economy. New York: Random House, Inc. Krugman, P. Obstfeld, M. (2008). International Economics: Theory and Policy. Boston: Pearson Education, Inc. Steinberg, Ted (2002). Down To Earth (pp. 1-115). New York: Oxford UP. Worster, Donald (1994). Nature’s Economy: The History of Ecological Ideas. United Kingdom: Cambridge UP.

What Is Sugar Sweetened Beverages Health And Social Care Essay

What Is Sugar Sweetened Beverages Health And Social Care Essay Sugar sweetened beverage means any nonalcoholic beverage Carbonated or noncarbonated, which is intended for human consumption and contains any added caloric sweetener. [1] In addition, it contains more than 10 calories per 8 ounce. These beverages include: sweetened water, non diet soda, fruit or vegetable drinks containing less than 70 % natural fruit or vegetable juice, sports drinks, energy drinks and sweetened bottled coffee or tea. Sugar sweetened beverages provide little or no nutritional value, but contain huge amount of sugar. [2] Ø ªÃƒËœÃ‚ ¹ÃƒËœÃ‚ ¯Ãƒâ„¢Ã…  Ãƒâ„¢Ã¢â‚¬Å¾.. One 12-ounce can of sugar-sweetened soda contains 150 calories and 40 to 50 grams of sugar. If these calories are added to a typical US diet with no offsetting reduction in other caloric sources, one can of soda per day can lead to a 15-pound weight gain in a year. A better mechanism for weight gain could not have been developed than introducing a liquid carbohydrate with calories that are not fully compensated for by increasing satiety. Liquid calories are a relatively new addition to the human diet-perhaps the human satiety circuit has not yet adapted to register these calories for what they are. Dr. Caroline Apovian, Sugar-Sweetened Soft Drinks, Obesity, and Type 2 Diabetes, American Medical Association,2004; Emerging_ evidence_ also_ suggests_ that_ higher_ consumption_of_ sugar_sweetened_ soft_ drinks_ may_ raise_ the_risk_of_developing_type_2_diabetes_and_the_metabolic_syndrome._Soft_drinks_contain_large_amounts_ of_ simple_ sugars,_ which_ can_ induce_ higher_ glycemic_ and_ insulinemic_ responses._ Soft_ drinks_ are_ an_ important_source_of_glycemic_load_in_the_diet,_which_has_been_associated_with_the_risk_of_developing_ type_2_diabetes_and_cardiovascular_disease. Frank B. Hu MD, PhD, SUGAR_SWEETENED_SOFTDRINK__ CONSUMPTION_AND_RISK_OF_TYPE_2__ DIABETES_AND_CARDIOVASCULAR_RISK,CMR,2009;2,2,13-18 Health consequences of (SSB): In fact, sugar sweetened beverages cause health risks both because of what they include (mainly sugars, extra calories, and various additives) and what they replace in the diet (foods and beverages that provide minerals, vitamins, and other nutrients). SSB and Obesity: Obesity becomes the most prevalence public health problem that increases dramatically. The prevalence of overweight is tripled in children and adult. There are many environmental factors that associated with development of obesity due to change in food and beverage consumption. These factors that may influence children to consume soft drinks are different such as taste, preference, soft drink availability and television viewing. From the survey which was done for 560 American children, the researchers found that over 80% of respondent consume soda at least weekly, and 30% consume soda daily [3]. Also they found that these children who consume soft drinks, their parents and peers share them and they watched TV 3.5hday and have easily access to soft drinks in both home and school. Researchers also found that there is association between increased sweetened beverage and increase in BMI. Some studies show a clear relationship between consumption of sugar sweetened beverage, particularly soft drinks, and increase in the prevalence of overweight and obesity. Knowing the factors that contribute to the consumption of soft drinks will aid in prevention and treatment of overweight in children and adolescent. Dietitian must increase parents awareness of unhealthy life style, behavior, help them to control familys eating habits, limit watching TV. For children who are at risk of overweight, limit access to soft drinks and decrease TV viewing [4]. In some point, families and their children may resist making life style changes, so addressing these factors may encourage them to make decision in their eating habits. Family can also develop a strategy to modify their life style and improve their health, so the results will be healthier children, families who can battle the epidemic of obesity [5]. Indeed a number of large scale epidemiological studies have found consistent positive associations between SSB consumption and long-term weight gain and risk of chronic diseases including metabolic syndrome (MetSyn), T2DM and CHD. SSB consumption is thought to lead to weight gain because of the high added sugars content and low satiety of these beverages and incomplete compensation for total energy at subsequent meals following intake of liquid calories. In addition, because of their high amounts of rapidly absorbable carbohydrates such as sucrose or high-fructose corn syrup (HFCS), coupled with the large quantities often consumed, SSBs may increase risk of T2DM independent of obesity as a potential contributor to a high dietary glycemic load (GL) which lead to inflammation , insulin resistance, and impaired beta-cell function. Hu FB, Malik VS, Sugar-sweetened beverages and risk of obesity and type 2 diabetes: Epidemiologic evidence, Physiol Behav (2010), doi:10.1016/j.physbeh.2010.0 1.036 Several recent studies suggest that increased abdominal adiposity and waist circumference (W_ C) is a strong predictor of all cause mortality [7]. The consumption of nonalcoholic carbonated beverages or soft drinks and sweetened juices by children has rapidly increased during short period displacing water and nutrient dense beverage such as dairy products. [8] As it stated before that obesity among children becomes a big health concern around the world. The prevalence of overweight and obesity amongst children in Qatar state has previously been reported between 37.5% and 41.6 % [9] males and females children respectively. In general, obesity presents an entirely new set of public health problem reported in Qatar, considering a major risk factor for non- communicable diseases. Obesity is a risk factor for cardiovascular disease [10], Diabetes [11] and certain types of cancer [12]. It can also be associated with non- fatal but debilitating illnesses such as respiratory difficulties, infertility and musculoskeletal disorders [13]. According to data available in previous studies, overweight and obesity among Qatari adolescents from both sexes are 23.6% and 36.5% [14] females and males respectively. Childhood corpulence is a predictor for adult disease [15]. In particular recent studies have shown that increased BMI in childhood may predict the occurrence of obesity in adulthood [16, 17]. In children as apposed to adults, the BMI values vary with both age and gender, thus the proffered assessment is BMI- for- age, in which children with body mass index (BMI) for age between 85th and 95th percentile are classified as being overweight and those in the à ¢Ã¢â‚¬ °Ã‚ ¥ 95th percentile are considered obese [18]. Excessive calorie intake in the form of a number of macronutrients has been associated with weight gain. energy intake from sugar- sweetened beverage (SSB) now accounts for a significant fraction of the total caloric intake of young people[19], and consumption has been implicated in promoting obesity in several ,but not all studies[20]. The World Health Organization has implicated the consumption of sugar sweetened beverages (SSBs) as probable contributor to the obesity epidemic. The National Food Survey in the United Kingdom documented a five fold increase in household consumption of SSBs between 1974 and 1999, from 180 to 976 g/wk. A similar trend was observed in the United States, where the average daily consumption of SSBs by children (6 to 17 y of age) more than doubled between 1977 and 1998, from 150 to 350 g/d (5 to 12 oz/d) [21]. Sucrose, fructose and glucose -sweetened beverage intake has been associated with poor diet quality and fast food consumption [22]. In a study published in United State, they include desire to drink DD scale which measure difference in the quality and frequency with which children want to drink. Behavioral correlate of DD: High scoreÆ’Â   more frequent desire to have drink but indication of type of drink. DD relates to thirstÆ’Â   scores should be associated to or with all consumption of all drinks. DD relates to liking for sweet things in mouthÆ’Â   high score would be expected to consume higher quantities of sweetened beverage [23]. Consumption of SSB and obesity in childhood Studies reviewed Several studies have been published examining the potential contribution of sugar-sweetened beverages (SSB) to weight gain in children. There are many cross-sectional studies identified, some of these reported a positive association between the frequencies of intake sugar sweetened drinks and obesity while some found no association. Overall, there is extensive evidence that sugary drinks contribute to weight gain in children. Both baseline intake and changes in the intakes of these drinks are associated with an increase risk of weight gain in both children and adolescents Ludwig DS, Peterson KE, Gortmaker SL. Relation between consumption of sugar-sweetened drinks and childhood obesity: a prospective observational analysis. Lancet 2001; 357:505-508. A study conducted in United State on sample of 10,371 boys and girls aged 2-19 years from representative US sample. The results were positive linked that overweight children BMI > 95th consume a grater % of energy from soft drinks and total beverages than non-overweight children. Troiano RP, Briefel RR, Carroll MD, Bialostosky K. Energy and fat intakes of children and adolescents in the United States: data from the National Health and Examination Surveys. Am J Clin Nutr 2000; 72:1343S-1353S. Another study conducted on 185 Canadian children aged 4-16 years also indicated appositive association between high consumption of SSB and increase BMI and overweight. Gillis LJ, Bar-Or O. Food away from home, sugar-sweetened drink consumption and juvenile obesity. J Am Coll Nutr 2003; 22:539-545. The results of a study on 3048 multi- ethnic New Zealand children from both gender aged 5-14 years stated that children dinking soft drinks > 1 per day had higher mean BMI than those with intake Scragg R, Wilson N, Schaaf D, Fitzgerald E, Utter J. Risk factor for obesity in New Zealand children aged 5-14 years: results from the 2002 national Children.s Nutrition Survey. Australasian Epidemiologist 2004;11:23-24. Findings from small food consumption studies from various countries including South Africa, the Philippines and New Zealand are also indicative of high consumption levels of sugar sweetened beverages. A recent study was conducted in Saudi Arabia, a total study sample consisted of 9433 males and females aged 10- 19 years old participated in a designed Food Frequency Questionnaire. BMI and W_C measurements were obtained and correlated with dietary Intake. The results show that the overall prevalence of overweight and obesity was 12.2% and 27.0% respectively, with boys having higher obesity rates than girls. W_C and BMI was positively correlated with sugar sweetened carbonated beverages (SSCB) intake in boys only. Kate S Collison, Marya Z Zaidi, Shazia N Subhani.al, Sugar- sweetened carbonated beverage consumption correlated with BMI, waist circumference, and poor dietary choices in school children, BMC Public Health, 2010;10: 234,2-12. Bones and osteoporosis People who prefer to drink soft drinks and or any type of sweetened beverages instead of milk or other daily products probable their intake of calcium will be low and this will lead to osteoporosis, which is a disease that cause bone fragile and broken . The risk factor of osteoporosis depends on how much bones mass is built up early in life. Girls build 92 percent of their bone mass by age 18, but if they dont consume sufficient calcium in their teenage years, they can not catch up later. Thats why experts recommend higher calcium intakes for youths aged 9 to 18 than for adults aged 19 to 50 [24]. Although osteoporosis takes decades to develop, preliminary research suggests that the lower calcium intake that may result for example from drinking soda pop instead of milk can contribute to broken bones in children [25]. Heart Disease Heart disease is the nations number- one killer. Some of the most important causes are diets high in saturated and trans fats and cholesterol. In many adults, a diet or beverage that is high in sugar may also be a modest contributor to heart disease [ 26]. A study of young adults (19 to 38 years old) in Louisiana found a strong association between consumption of sweetened beverages and risk factors for syndrome X [27]. Diabetes In fact, soft drinks are harmful for people with diabetes since one pack of them contain 33 grams of table sugars (sucrose) and this type of sugar is absorbed rapidly which will raise blood sugars quickly. This action impacts negatively on controlling diabetes [28]. Kidney stones Kidney stones consider as one of the most painful disorders to distress humans and one of the most common disorders of the urinary tract. Researchers had subjects consume large volume of cola drinks for one or several days. The next day, the subjects urine contained higher levels of oxalate and lower levels of magnesium and citrate, changes that could contribute to kidney stone formation [29 ]. SSB and Tooth Decay Scientists have noticed a connection between soft drink consumption and dental health. Like obesity (or any issue involving human health), tooth decay is a complex subject. It is the result of many factors, including the types of foods that are consumed and frequency of eating occasions. Foods that are sticky and cling to the teeth are more likely to cause tooth decay. The amount of time that sugar remains in contact with teeth is another important variable. Soft drinks and other sugar-containing liquids pass over the teeth very quickly. A recent study examined dental caries and beverage consumption among 1- to 5-year-old children and found an association between soft drinks and increased caries. Marr Barr,Longmont, Colorado, Soft Drinks, Childhood Overweight, and the Role of Nutrition Educators, Nutrition Education and Behavior, 2004; 36:258-265. In addition, drinking soft drinks between meals was found to increase the number of dental decay and caries in a twenty-year longitudinal study. As a result of an increasing consumption of soft drinks and commercial fruit juices, over the past years, the prevalence of dental erosion and decay has increased dramatically. Acids from the soft drinks have been known to induce the dissolution or erosion of dental enamel as well as caries lesion due to the combined effect of bacteria and degradation of carbohydrates present in the drinks [30]. Nationally, there is great concern about the effects of carbonated- beverages consumption on obesity, osteoporosis, heart diseases, tooth decay, and other health problems. Sites in blue is Okay  Ã…  

Cardiovascular Effects of Necrostatin-1 (Nec-1)

Cardiovascular Effects of Necrostatin-1 (Nec-1) Abstract Necrostatins have been identified as cardioprotective agents to reduce reperfusion injury after ischemia, preventing necroptosis due to their RIPK1 inhibitory effect. In this study basal cardiovascular effects of Nec-1 and its inactive analog Nec-1i was investigated in healthy rats under anesthesia. Relatively low doses of Nec-1 and Nec-1i were administered (0.8mg/kg and 0.846 mg/kg, respectively) in line with the in vivo dose response model described by Takahashi et al (2012). Basal heart functions were recorded namely, systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), P interval, PR interval and QTc interval. The results of this study indicated that administration of Nec-1 but not Nec-1i raised systolic and diastolic blood pressure, heart rate, while PR interval was depressed. No statistically significant effect on P interval, and QTc was observed by administration of both necrostatins. The effectiveness of Nec-1 reveals a dual cardiovascular effects, exerting both vasodilator and vasoconstrictor actions as well as a positive inotropic effect on cardiomyocytes. Since no conditions of ischemia or any other oxidative stress are present, which means that no type of programmed cell death is triggered (apoptosis, necrosis, or necroptosis), it can be assumed that Nec-1 acts in a RIPK1-independent manner. Thus, this action of Nec-1 under normal heart conditions remains to be clarified at a cellular level investigating its involvement in signaling pathways (e.g. NO pathway, ÃŽ ²-AR pathway) of all cell types involved cardiovascular function (endothelial cells and smooth muscle cells of blood vessels), and cardiomyocytes as well. In general, after the elucidation of the exact mechanisms of action of Nec-1 at a molecular basis, Nec-1 could be applied as a positive inotrope that enhances basal cardiac function in pathological conditions. Discussion Degterev et al (2005) initially introduced necrostatins as therapeutic agents for ischemic brain injury through chemical inhibition of non apoptotic cell death. Three years later the same research group identified RIPK1 as a specific cellular target of necrostatins (Degterev et al, 2008). In parallel necrostatins were also reported as potential cardioprotective agents by Smith et al (2007) as they reduced ischemia reperfusion injury in their experimental trials. Although, current research has used necrostatins as potential inhibitors of necroptosis in ischemic heart experimental designs in vitro and in vivo (Smith et al 2007, Takahashi et al 2012), basal effects of these substances on heart function and haemodynamics have not yet been investigated. In this study administration of necrostatins (Nec-1 and its inactive analog Nec-1i) in healthy rats under anesthesia was performed. The results of this study indicated that administration of Nec-1 but not Nec-1i raised systolic and diastol ic blood pressure, heart rate, while PR interval was depressed. No statistically significant effect on P interval, and QTc was observed by administration of both necrostatins. Interpreting the results of this study is a complicated issue as the availability of comparable data is restricted and sometimes contradictory. The effectiveness of Nec-1 on increasing mean systolic and diastolic blood pressure and heart rate, reveals a dual cardiovascular effects, exerting both vasodilator and vasoconstrictor actions. When evaluating the effectiveness of Nec-1 using in vivo murine disease models, Nec-1 was suggested to reduce ischemia reperfusion injury as an RIPK1 inhibitor in the TNF signalling pathway, thus preventing necroptosis (Smith et al 2007). But when no conditions of ischemia or any other oxidative stress are present, which means that no type of programmed cell death is triggered (apoptosis, necrosis, or necroptosis), it can be assumed that Nec-1 acts in a RIPK1-independent manner. Thus, this action of Nec-1 under normal heart conditions remains to be clarified at a cellular level investigating its involvement in signaling pathways of all cell types involved cardiovascular function (endothelial cells and smooth muscle cells of blood vessels), and cardiomyocytes as well. Interestingly, Eefting et al (2004) reviewed the role of apoptosis in reperfusion injury discussing both pharmacological as well as genetic interventions in animal models. Nitric oxide (NO) appeared to increase myocardial contractility, myocardial function and endothelial function in many reports of this review. NO is a well known regulator of excitation-contraction coupling in myocardial function (Ziolo et al, 2001a) and ÃŽ ²-adrenergic receptor (ÃŽ ²-AR) signalling (Ziolo et al, 2001b). In line with this notion, a recent study in rats demonstrated that renal vasodilatation was induced through the NO pathway with a pharmacological agent (Garcia-Pedraza et al, 2015). Thus, further research could aim in identifying potential interplay of Nec-1 through other signaling pathways starting from the NO pathway. Another approach could be the potential relation of Nec-1 with vascular ATP levels, as the vasodilatory action of intravascular ATP in the coronary circulation was reported to be attributed to the dual and e qual activities of adenosine and ADP acting at purinergic P1 and P2Y1 receptors, respectively (Korchazhkina et al, 1999). Nevertheless, the results of this study indicate that Nec-1 exerts a positive effect on basal cardiac function, by raising heart rate, blood pressure and by depressing PR interval. Since, stimulation of ÃŽ ²-adrenergic receptor (ÃŽ ²-AR) pathway has been reported as the most important regulator of cardiac contractility (Bers and Ziolo, 2001), it could be assumed that Nec-1 affects electrical signal transduction in some way of this pathway. In general, activation of ÃŽ ²-AR activates the cAMP-dependent protein kinase A (PKA) leading to the phosphorylation of several target proteins within the cardiomyocyte, such as Ica (L-type membrane Ca+2 channels), RyR (ryanodine receptors of the sarcoplasmic reticulum), TnI (troponin I), and PLB (phospholamban). Interstingly, it has been suggested that PLB phosphorylation at Ser 16 by PKA is one the major factors affecting positively cardiomyocyte contraction after ÃŽ ²-AR stimulation (Kohr et al, 2012). In line with these observations, Nec-1 coul d somehow affect the phosphorylation status of proteins responsible for cardiac function. The observed depression of PR interval, in this study, after administration of Nec-1, which represents not only atrial depolarization but also the beginning of ventricular depolarization, reflects that the signal conductance through AV node/His bundle was increased possibly through increased phosphorylation of intracellular proteins involved in cardiac contractility. Noteworthy, Nec-1s has been shown to stimulate directly cardiac contractility through myosine binding protein C (MYBP-C) phosphorylation (Szobi et al. 2015, unpublished data) in animal experiments. Regulation of cardiac contractility by MYBP-C through phosphorylation has been reviewed by Saul Winegrad (1999), along with its role in the formation of the sarcomeric myofibril as a result of binding to myosin and titin. Although, not statistically significant in this study, QTc interval tended to be shortened under the effect of Nec-1. Preliminary data from animal experiments with Nec-1s after ischemia reperfusion indicated decreased QTc intervals, suggesting that Nec-1s might be protective on ventricular arrhythmias (Szobi et al. 2015, unpublished data). The comparison of Nec-1 and its inactive demethylated derivative Nec-1i as factors effecting basal haemodynamics and heart function appears confusing, as previous experimental approaches were applied on disease models using in vivo and/or in vitro ischemic conditions (Degterev et al 2005, Degterev et al 2008, Smith et al 2007, Takahashi et al 2012), and not healthy animals under anesthesia. Additionally, the effectiveness of these substances in previous reports varied not only in a time and dose dependent manner, but also regarding species specificity (Takahashi et al 2012). Nonetheless, in this study Nec-1 but not Nec-1i influenced positively systolic and diastolic blood pressure and heart rate, while PR interval was depressed. These results could be compared with the ones obtained from the in vivo murine model of ischemia-reperfusion injury reported by Smith et al (2007), where Nec-1 (1.65 mg/kg) reduced infarct size whilst Nec-1i (1.74 mg/kg) was ineffective. On the other hand, in vivo Nec-1i was as protective as Nec-1 against lethality associated with TNF-induced necroptosis in high doses (6mg/kg) (Takahashi et al 2012). As both necrostatins were proven to inhibit human IDO as predicted by molecular modeling by Takahashi et al (2012), it can be assumed that Nec-1i cannot be used us a reliable ineffective control for Nec-1. Alternatively, Nec-1s which is a more specific RIPK1 inhibitor lacking the IDO-targeting effect, was suggested by Takahashi et al (2012) as a control substance in experiments investigating the potent effect of necrosatins (Vandenabeele et al 2013). Interestingly, in vitro Nec-1i exhibited paradoxically higher cardioprotection that Nec-1 at high doses (100ÃŽ ¼ÃŽÅ") (Smith et al 2007). In the present in vivo study, relatively low doses of Nec-1 and Nec-1i were used (0.8mg/kg and 0.846 mg/kg, respectively) in line with the in vivo dose response model described by Takahashi et al (2012). Although, low doses (0.6mg/kg) of both Nec-1 and Nec-1i had a toxic effect increasing lethality during TNF-induced necroptosis, suggesting that RIPK1/RIPK3- dependent pathway drives TNF-induced mortality (Takahashi et al 2012), this toxicity effect was not observed in the present study. Of course, in their experiments necrostatins were administered during TNF-induced mortality, demonstrating that low doses were toxic in terms that they were not sufficient enough to protect form induced mortality. In contrast, in this in vivo study, evaluating the comparative effect of low doses of both necrostatins, it could be assumed that these substances maintain their profile of active (Nec-1) and inactive (Nec-1i) factors when administered under normal-non stressful condition. But which signaling pathway is triggered, under the effect of Nec-1 but not Nec-1i, leading to this elevated systolic and diastolic blood pressure, heart rate) remains to be clarified. In general, as demonstrated in this study, enhancement of basal cardiac performance by Nec-1, evidenced by increased systolic and diastolic blood pressure heart rate, and depressed PR interval could be a double-edged sword. Although Nec-1 has been introduced as an agent reducing injury after reperfusion in brain and heart (Degeterev et al 2005, Smith et al 2007, Takahashi et al 2012), the effect of this substance under normal conditions must be further investigated before its administration in other pathological conditions. Thus, examining the response of all cell types (cardiomyocytes, smooth muscle and endothelial cells of blood vessels) under the effect of Nec-1 could be a first step under this point of view. Each cell type, and eventually the overall response to any pharmacological administration, will depend on several distinct or sometimes overlapping factors, such as changes in metabolic conditions (pH, calcium levels, ATP levels), or even active (under phosphorylation or not) signaling molecules and transcription factors. Additionally, in order to clarify the molecular mechanism of action of Nec-1 on basal cardiac function, the comparative effect of other necrostatins apart from Nec-1i, e.g. Nec-1s which lacks the IDO inhibitor effect, would provide meaningful insights. Conclusions Although Nec-1 was introduced to prevent necroptosis as a RIPK1 inhibitor reducing ischemia reperfusion injury, the enhancement of basal cardiac activity by Nec-1 in healthy anesthetized rats, as demonstrated by this study, indicates that this molecule may also act in an RIPK1-independent manner. Thus, further research is needed in order to clarify the molecular mechanism underlying this effect. For example, future directions could aim at identifying the potential interplay of Nec-1 in signaling pathways, such as the NO pathway and the ÃŽ ²-AR pathway, of all cell types involved cardiovascular function. The biochemistry of this involvement could be comparatively analyzed by administration of other necorstatinsm, such as Nec-1s. Finally, Nec-1 after evaluating all these parameters, Nec-1 could be used a positive inotropic agent in cases of cardiomyopathy, congestive heart failure, heart attack or cardiogenic shock. References Bers DM, Ziolo MT. (2001). When is cAMP not cAMP? Effects of compartmentalization. Circ.Res. 89, 373–375. Degterev A, Huang Z, Boyce M, Li Y, Jagtap P, Mizushima N et al. Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury. Nat Chem Biol 2005; 1: 112–119. Degterev A, Hitomi J, Germscheid M, Ch’en IL, Korkina O, Teng X et al. Identification of RIP1 kinase as a specific cellular target of necrostatins. Nat Chem Biol 2008; 4: 313–321. Eefting F, Rensing B, Wigman J, Pannekoek WJ , Liu WM, Cramer MJ, Lips DJ, Doevendans PA. Role of apoptosis in reperfusion injury. Cardiovascular Research 61 (2004) 414– 426. Garcia-Pedraza JA, Garcia M, Martin ML, Moran A, Pharmacological evidence that 5-HT1D activation induces renal vasodilation by NO pathway in rats. Clin Exp Pharmacol Physiol. 2015 doi: 10.1111/1440-1681.12397. Korchazhkina O, Wright G, Exley C. Intravascular ATP and coronary vasodilation in the isolated working rat heart. British Journal of Pharmacology (1999) 127, 701  ± 708 Kohr MJ, Roof SR, Zweier JL, Ziolo MT. Modulation of myocardial contraction by peroxynitrite. Frontiers in Physiology (2012);3:468(1-10). Smith CCT, Davidson SM, Lim SY, Simpkin JC, . Hothersall JS, Yellon DM. Necrostatin: A Potentially Novel Cardioprotective Agent? Cardiovasc Drugs Ther (2007) 21:227–233. Takahashi N, Duprez L, Grootjans S, Cauwels A, Nerinckx W, DuHadaway JB, Goossens V, Roelandt R, Van HauwermeirenF, Libert C, Declercq W, Callewaert N, Prendergast GC, Degterev A, Yuan J and Vandenabeele P. Necrostatin-1 analogues: critical issues on the specificity, activity and in vivo use in experimental disease models. Cell Death and Disease (2012) 3, e437; doi:10.1038/cddis.2012.176. Vandenabeele P, Grootjans S, Callewaert N , Takahashi N. Necrostatin-1 blocks both RIPK1 and IDO: consequences for the study of cell death in experimental disease models. Cell Death and Differentiation (2013) 20, 185–187. Winegrad S. Cardiac Myosin Binding Protein C Circ Res. 1999;84:1117-1126.) Ziolo MT, Katoh H, and Bers DM. (2001a). Expression of inducible nitric oxide synthase depresses beta-adrenergic-stimulated calcium release from the sarcoplasmic reticulum in intact ventricular myocytes. Circulation 104, 2961–2966. Ziolo MT, Katoh H, and Bers DM. (2001b). Positive and negative effects of nitric oxide on Ca(2+) sparks: influence of beta-adrenergic stimulation. Am.J. Physiol.HeartCirc.Physiol. 281, H2295–H2303.

The Civil Reserve Air Fleet :: essays research papers

Abstract The Civil Reserve Air Fleet is a partnership between the Department of Defense and commercial airlines where the airlines contractually commit a portion of their aircraft and crews to be used by the Department in the event of any level of military conflict. These aircraft can be â€Å"called up† and required to respond quickly to provide airlift support to the Department of Defense. There are minimum required levels of participation in order for the airlines to be eligible, and in turn they receive peace time business including passenger and cargo movement approximately in proportion to their commitment level. The program is divided into three segments which include varying amounts and sizes of aircraft that serve specific purposes. There are also three levels of activation depending on the severity of the conflict, which also require different amounts and sizes of aircraft. This program has been in place for nearly 53 years, and has become an essential partnership required fo r an effective United States military. The following pages are an investigation various aspects of the Civil Reserve Air Fleet such as its purpose, history, and effectiveness. The Civil Reserve Air Fleet   Ã‚  Ã‚  Ã‚  Ã‚  The Civil Reserve Air Fleet (CRAF) is a network of select aircraft from several commercial airlines that are all committed in various amounts to the Department of Defense (DoD) to provide airlift resources when the capability of U.S. military aircraft is exceeded. This system is designed so that these carriers can provide military cargo movement and troop transportation to anywhere in the world on short notice in the event of a military conflict. In order for airlines to join the CRAF, they must commit at least 30 percent of their long-range passenger fleet and 15 percent of their long-range cargo planes (Fact Sheet, 2004). These aircraft must also be U.S. registered, capable of over water operations, and have at least four complete crews assigned for each aircraft (Fact Sheet, 2004). Airlines that participate in CRAF have provided vital support to our military since the Korean War (Graham, David, 2003). The Persian Gulf War was the first official activation of th e CRAF, where two thirds of the troops and one quarter of the air cargo was moved by commercial airplanes (Graham, 2003). Though not officially activated, the CRAF is currently supporting Operation Iraqi Freedom, providing nearly double the amount of aircraft that the DoD has estimated for its most demanding war strategies. This paper will provide a brief explanation of the purpose of the CRAF, its history, the effectiveness of the program, and a quick look towards the future of the CRAF.