Market Strategy of Blue Cross Blue Shield Assignment

Market Strategy of Blue Cross Blue Shield - Assignment Example Conducive research indicates that even during the financial crisis of 2008, the organization has been stellar because of their high customer equity and premiums. Healthcare is one the elements that were always solid. Looking at the financial statements, the company made annual sales of $75.7 million. This allowed the company to leverage itself in the industry.   One of the major strengths of the organization is its ability to have a strong customer base supported by its technological infrastructure. The infrastructure is heavily supported by its business model and understanding how technology can serve its needs. However, the key benefit that the Blue Cross achieved was the fact that it allowed its customers to the accessibility of information without much delay. In an industry where information is vital, this organization was able to accommodate the needs of their growing customers as well as provide information that was compliant with HIPAA and ACA.   One of the major strengths, as mentioned before, was the fact that it had a strong customer and revenue base. The premiums that were being derived from the organization truly harnessed growth and allowed the company to get a strong threshold as a company.   One of the major challenges of the company was to expand its private and public cloud with compliance. It was evident that the risk management involved in the insurance business is a huge focal point.   Blue Cross had a huge dilemma of expanding their IT infrastructure boundaries by maintaining old records and creating space for new customers. Furthermore, the company’s auditing team was able to ensure the legitimacy of network passwords within their own IT infrastructure. When it comes to cloud computing, many flavors are present.

The CIA Research Paper Example | Topics and Well Written Essays - 1750 words

The CIA - Research Paper Example The agency was established in the year 1947 through an act accented to by the then President. The National Security Act was signed by President Truman. Apart from creating the agency, this act also established the office of the Director of Central Intelligence (DCI) who was supposed to be the President’s chief advisor on matters of national security as he was also the head of the United States intelligence community. The DCI was also supposed to head the Central Intelligence Agency. However, in the year 2004, the National Security Act was amended through the Intelligence Reform and Terrorism Prevention Act. This amendment created the office of Director of National Intelligence to take up a number of roles previously carried out by the DCI. It also ensured that the Central Intelligence Agency was under a separate Director. Such agencies as the CIA are employed in performing intelligence gathering services and not the US military as these can easily lead to the declaration of wars. During World War II, the Office of Strategic Services (OSS) was created with the purpose of coordinating espionage activities against the Axis Powers. The CIA was thus created as a successor of this office. Basically, the CIA is charged with the responsibility of collecting information about corporations, foreign governments and individuals in addition to advising policymakers. The agency is headquartered in McLean, Virginia. In some quarters, the CIA is referred to as Other Government Agencies (OGA), The Agency, Langley and The Company. In trying to accomplish its mission, the CIA requires the deployment of high leverage technology, carrying out of research and development for purposes of intelligence. To ensure that the intelligence consumer acquires the best possible intelligence, the CIA engages closely with other agencies and organizations within the Intelligence Community and also carries out independent analyses of topics that are of concern2. The agency

E-Business and e-Marketing Essay Example | Topics and Well Written Essays - 4250 words

E-Business and e-Marketing - Essay Example The whole world has become a small place because of internet. Everyone can have all the information pertaining to any field or subject using internet. There have been significant advancements in technology over the years and it had a significant impact and changes on the people's way of leaving. It has brought about changes in the way people access different kinds of information online and the ways in which they communicate with each other. World Wide Web is also having its significant impact on the ways through which businesses are now being conducted in different organisations all over the world. The term e-business can be referred to as the utilisation of internet technology for the improvement in efficiency of business processes conducted by various organisations. It has also resulted in the establishments of different new kinds of business models. E-Business is believed to have emerged during the mid 1990s (Maruyama). It was mostly concerned about bringing enterprise systems tha t existed then to the internet audience in general through internet or World Wide Web. E-Business now can be found at the mainstream of most of the organisations. E-Business helps in the improvement of business performances through the use of information technology and thereby facilitates connection between customers and suppliers at every step in the value chain. Hence it could result in significant shift or changes in the field of technology, business and the society as a whole along with the changes in interactions between them. As regards technology, information technology has been revolutionised over the past years. It has its impact in almost all the economic sectors and in every sphere of our lives. The processing power relative to the digital technologies is expected to have a rapid increase because of decline in the cost associated with the advancements of technology in future (The Levin Institute). As a result of new technological advancements, most of the business transac tions are expected to be done over internet which would lead to the reduction in the transaction costs as well. The job structure is also expected to change and more people can use internet sitting back at home and performing their business tasks. More and more people would shift towards jobs offered online which could be done at their convenient place and flexible work timings for the employees as well. With the growing expansion of World Wide Web, different new technologies like location-based technologies and radio frequency identification (RFID) are expected to lead to the development of innovative applications resulting in the evolution of networks which can be termed as "Internet of Things" (OECD). In the longer run, small sized wireless sensor devices which are embedded in different objects, facilities and equipments are most likely to get integrated with internet with the help of wireless networks. This would enable interconnectivity anytime and anywhere. The future capaciti es and uses of technologies which bridge the virtual worlds with the physical world are supposed to result in significant societal changes as well as bring about increased economic benefits. Economic activity is becoming faster, cheaper and efficient as a result of World Wide Web.

Economic development Essay Example for Free

Economic development Essay Population growth Ââ€" some Filipinos believe that it is natural for every married woman to bear a child in their wombs because they are with their husbands. And this are very wrong beliefs since if you will be reasonable enough, you will realize that having a child is always together with great responsibility that has no end. And that you will realize that having more and more children will cause great scarcity in your family such as you would not be able to send your children to school and you would not be able to provide enough foods so that you children will be healthy and do good in school. Population growth is also the reason for a number of malnourish children in the Philippines. 2. Unemployment Ââ€" this is a very common cause of poverty in the Philippines since there are several Filipinos who are unemployed plus the fact that there are many companies that are affected of the global economic crisis. And the least thing that you can do about unemployment is to find a best way on generating money like you can accept laundry services, plumbing services, or electrical repair services if you are skilled enough to do the job. Then, you could start a certain profitable business like food house or a small store that does not require you much capital so that you will not find it hard to save enough money from the services that you are offering. 3. Governance concern Ââ€" one of the main reasons of poverty in the Philippines is the activities of the corrupt government officials. They are using the money of the people to achieve the power and authority that they wanted to have and once they have it they will automatically take advantage of their power to the point that they will neglect the yoke of the people and set aside their promises when they are just campaigning and try to convince the people to vote for them. 4. Agricultural problems Ââ€" this is the natural cause of the poverty in the Philippines that is because of the wrong activities of people. They ruin the treasure of the nature for their own sake without any idea that the nature they are destroying is the main source of almost all the products that exist in this world. Some of the examples of destroying the nature are the irresponsible disposal of wastes and trash, dynamite fishing, illegal logging and more. 5. Disability Ââ€" this is also one of the possible causes of poverty in the Philippines since more and more people nowadays become disabled because of several illnesses and diseases that arise like AH1N1 virus, SARS, dengue, and more. Disability may be also caused by uncontrolled population growth, for instance, you have ten kids in the house, and can you imagine attending to their needs everyday? Well, definitely not so the tendency is that they are prone to accidents that will cause them to be disabled since they are at very young age that are typically playful. RECOMMENDATION The World Bank suggests several solutions to combat poverty in the Philippines. 1. There is a need to have a strong focus on continued economic growth, driven by openness and macroeconomic stability. 2. Increased market access to the poor could be achieved by promoting tenancy, market-based land reform, and investing in essential rural infrastructure and agriculture extension services. 3. The scarcity of housing and threats to environmental health in urban areas could be reduced by promoting urban land reform and extending water and sanitation services. 4. Quality improvements in primary education and access to primary health services such as immunization and the prevention of water-borne and respiratory diseases are needed. 5. Social safety net programs can be rationalized and the targeting improved by strengthening institutional capacity building and eliminating food price subsidies in favor of targeted income subsidies or food stamps. Some of widely accepted principles in the mainstream development community, at the three descending levels of the world as a whole, Asia as a region, and the Philippines specifically. All three share in common placing poverty reduction at the core of development work. Philippines Level: The Arroyo administrations official development agenda focuses specifically on issues of poverty and unemployment. The key document here is the Medium-Term Philippine Development Plan (MTPDP), 2001-2004, which stresses poverty reduction through equitable growth, rural development, and social sector investment. The four primary strategies are: †¢ Macroeconomic stability and equitable growth, using sound fiscal and monetary policies to keep inflation low and avoid surges in unemployment; modernize all sectors through HR development and technology; †¢ Comprehensive HR development, basic education, health, shelter, water, electricity; safety nets for most vulnerable sectors; encouraging poor to participate There are many causes of economic difficulties leading to mass poverty and hunger. One cause could be foreign debts servicing. This means that the Philippines must owe money to the World Bank. More than 60% of the Philippines budget goes to the World Bank. Unequal distribution of land and other resources is another cause that leads to poverty. Out of the whole population, only 20% own and control agricultural lands. Another cause could be under cultivation of agricultural lands. Only 13 million hectares are cultivated. There are about 17 million hectares of land that are not being used. There is a lot of poverty in the Philippines. Some people, called squatters, live near trash mounds and scavenge through the rubble to find materials that they can re-sell. Many are living in extreme poverty and unsanitary conditions. One of the effects this impoverished lifestyle has on them is an extremely short life expectancy. But there are some rays of hope. For one, slow but steady economic improvements are providing jobs in places like call centers. Secondly, charitable organizations like the Philippine Aid Society are growing and working hard to fight poverty. For those who want to do their part to help, consider a financial donation to one of these charities.

Activation of the G Protein-coupled Estrogen Receptor

Activation of the G Protein-coupled Estrogen Receptor Activation of the G protein-coupled estrogen receptor ameliorates salt-induced vascular remodeling Abstract The mRen2.Lewis (mRen2) female rat is an estrogen- and salt-sensitive model of hypertension which may reflect the higher pressure and salt sensitivity associated with menopause. We previously showed in salt-loaded mRen2 female rats that activation of the G protein-coupled estrogen receptor (GPER) does not lower blood pressure but attenuates renal damage. The current study hypothesized that GPER protects against vascular injury in this model. Intact mRen2.Lewis female rats were fed a normal (0.5% Na+) or high salt diet (HS; 4% Na+) for 10 weeks and treated with vehicle or the selective GPER agonist G-1 for the last two weeks of the study. Systolic blood pressure was measured by tail cuff plethysmography, and aortic sections were mounted on a wire myograph or formalin-fixed for histological analysis. Systolic blood pressure increased with HS (137  ± 2 mmHg, n=7 to 224  ± 8, n=9; P0.05). While aortic reactivity to phenylephrine and acetylcholine were not different between groups (P> 0.05), chronic G-1 treatment reduced vasoconstriction to angiotensin II (Pex vivo G-1 vasorelaxation (P Introduction Sodium balance plays an integral role in cardiovascular homeostasis. A high salt diet is considered a major risk for cardiovascular morbidity and mortality independent of other cardiovascular risk factors (Beil et al. Blood Pressure, 1995). Excessive salt intake has been associated with vascular remodeling, including the reorganization of the extracellular matrix and hypertrophy and/or hyperplasia of vascular smooth muscle cells. Although vascular remodeling is considered a protective adaptation to a higher wall stress, it contributes to the development of hypertension by creating a thicker, less compliant wall. Aortic stiffness, which contributes to isolated systolic hypertension in human subjects, is an excellent example of the complications presented by vascular remodeling (Lemarie et al. Journal of Molecular and Cellular Cardiology, 2009). The ability of estrogen to attenuate vascular remodeling in injured arteries may at least partly occur via activation of the classic steroid receptors ERÃŽ ± and ERÃŽ ² in VSMC and endothelial cells (Xing et al. Arteriosclerosis, Thrombosis, and Vascular Biology, 2009). Brouchet et al. showed that estrogen’s protective effects on vascular remodeling were abolished in female ERÃŽ ± knockout mice (Brouchet et al, Circulation, 2001). Moreover, in porcine aortic smooth muscle cells, the downregulation of ERÃŽ ² protein levels by mRNA antisense oligomers abrogated the inhibitory effects of estrogen on mitogen-activated protein kinase (MAPK) phosphorylation, migration, and proliferation (Geraldes et al. Circ Res, 2003; Xing et al. Am J Physiol., 2007). However, the protective effects of estrogen on vascular injury are evident in both ERÃŽ ± and ERÃŽ ² knockout mice, suggesting that another receptor may be necessary (Iafrati et al. Nat Med. 1997; Karas et al. Proc Natl Acad Sci USA. 1999). The novel G protein-coupled estrogen receptor (GPER) is a membrane-bound receptor linked to acute signaling pathways (Revankar et al. Science, 2005; Thomas et al. Endocrinology, 2005). Our previous studies showed that GPER activation lowers blood pressure in ovariectomized mRen2.Lewis rats and attenuates salt-induced renal and cardiac remodeling in intact mRen2.Lewis rats (Lindsey et al Endocrinology, Jessup et al, PLOS one, 2010 and Lindsey et al Hypertension). Therefore, this novel receptor may play an important role in mediating estrogenic effects in the vasculature. In the current study, we hypothesized that chronic GPER activation is protective against aortic remodeling due to salt-sensitive hypertension. To test this hypothesis, we utilized mRen2.Lewis (mRen2) rats, a unique congenic model of hypertension in which HS profoundly elevates blood pressure in females (Chappell et al, Am J Physiol Regul Integr Comp Physiol., 2006). We compared aortic remodeling in high salt-fed rats with or without treatment with the selective GPER agonist G-1. Because estrogen modulates oxidative stress to attenuate vascular remodeling in injured arteries (Hayashi et al, Biochem Biophys Bes Commun, 1995; Xing et al. Arteriosclerosis, Thrombosis, and Vascular Biology, 2009) and GPER reduces oxidative stress in the kidneys of female mRen2 rats (Lindsey et al. Hypertension, 2011), we further determined whether the effects of HS and G-1 were mediated by modulating oxidative stress. To further elucidate the cellular mechanisms responsible for vascular remodeling, we uti lized primary cultured female rat aortic smooth muscle cells to determine the effects of salt on cellular hypertrophy. Methods Animals All procedures were approved by the institutional Animal Care and Use Committee. Hemizygous mRen2.Lewis congenic female rats were obtained from the Wake Forest Hypertension Center breeding colony. Rats had free access to food and water in a temperature-controlled room (22  ± 2 °C) with a 12 hour light to dark cycle. At five weeks of age, the normal salt diet (NS, 0.5% Na) was switched to high salt (HS; 4% Na), as previously described (1, 2). The selective GPER agonist G-1 (400  µg/kg/day; EMD Chemicals, Gibbstown, NJ) or vehicle was administered for two weeks beginning at 13 weeks of age via subcutaneous osmotic minipump (Model 2ML2; Alza Corporation, Palo Alto, CA). Blood pressure was measured via tail cuff plethysmography (Narco Bio-systems, Houston, TX). Animals were randomly assigned to three experimental groups: intact NS (n=7), intact HS+vehicle (veh; n=9), and intact HS+G-1 (n = 9). Vascular Reactivity. After sacrifice, the upper thoracic aorta was submerged in formalin for histology and the lower portion used for vascular reactivity as previously described (Lindsey et al Endocrinology). Aortas were equilibrated with 2 g tension and the responses to 1 uM phenylephrine, 1 uM acetylcholine, 10 nM angiotensin II (Ang II), and 3 uM G-1 were measured. Histology. Formalin-fixed aortas were embedded in paraffin, cut into 5 um sections, and mounted on slides. To evaluate aortic wall thickness, slides were stained with hematoxylin and images analyzed using ImagePro software (XXX company, XXX city,XX state). Aortic medial area was calculated by the subtraction of the area of the inner border of the lumen (inner area) from the area of the outer border of the tunica media (outer area). Collagen staining was performed using picrosirius red and images were taken using a Texas Red fluorescent filter. The medial area was selected and the mean luminosity was recorded for each section. The NovaUltra Orcein Elastin Stain Kit (IHC World, XXX) was used for elastin staining. For analysis of oxidative stress, sections were immunostained with an antibody against 4-hydroxynonenal as previously described (Lindsey et al Hypertension). For analysis of brightfield images, positive staining was identified and the percent of positive pixels in the medial a rea recorded. For all analyses, the average of four cross-sectional measurements was calculated for each animal. Cell Studies. Aortic smooth muscle cells were isolated from adult f emale Lewis rats by explant method. Aortas were excised, cleaned of fat, cut longitudinally, scraped of endothelial cells, laid luminal side down in a cell culture dish containing Medium 199 (Invitrogen, XXX) and 5% fetal bovine serum (Gibco, XXX), and cut into small strips. Cells were subcultured up to four passages. When cells reached 80% confluence, the medium was switched to Medium 199 without phenol red or fetal bovine serum and sodium chloride (Sigma) was added to the increase the concentration to 152 mM, 160 mM, and 182 mM. Add NaCl to make high salt CS medium (152, 160, and 182 mM), Normal medium 142 mM NO, I find 117 mM Add 0.02 g NaCl to 50 ml of normal medium, that makes 152 mM Add 0.045 g NaCl to 50 ml of normal medium, that makes 160 mM Add 0.11 g NaCl to 50 ml of normal medium, that makes 182 mM After 5 days of exposure to high sodium medium, cells were harvested for further experiments. Cells were harvested using trypsin to obtain single cell suspensions. A sample was taken for determination of cell number and diameter using XXX cellometer (XXX company, XXX city, XXX state). Mean cell diameter was determined on 200 randomly chosen cells in each sample. The remaining cells were lysed in XXX with protease inhibitor cocktail (XXX company). Cellular protein content was determined in duplicate using bovine serum albumin as a standard (Bio-Rad Protein Assay Kit). Results As previously reported, a high salt diet (HS) significantly increased systolic blood pressure in intact mRen2 female rats (Figure 1A). Chronic treatment with the selective GPER agonist G-1 for two weeks did not influence blood pressure. G-1 did not influence the aortic response to acetylcholine (Figure 1B) or phenylephrine (Figure 1D). However, G-1 treatment in vivo amplified the vasorelaxant response to ex vivo application of G-1 (Figure 1C) and decreased the vasoconstrictor response to Ang II (Figure 1E). Salt-sensitive hypertension in female mRen2 rats significantly increased aortic thickness, as determined by the media/lumen ratio (Figure 2A-B). This remodeling was associated with a significant decrease in lumen area but no change in the external diameter of the aorta (Figures 2C-D). Chronic G-1 significantly attenuated remodeling, as evidenced by a decreased media/lumen ratio and an increased lumen area, with no change in external diameter. The average measurements for all groups are graphically represented in Figure 2E. In order to determine whether extracellular fibrosis was altered by HS and G-1, aortic sections were analyzed for collagen and elastin content. Figure 3 shows that picrosirius red staining was similar in all groups (Figure 3). Elastin staining was significantly decreased by HS but this effect was not reversed by G-1 (Figure 4). Elastin Breaks Space between elastin fibers Sections were assessed for proliferation using antibodies against proliferating cell nuclear antigen and Ki-67. No evidence of immunostaining was found in the medial sections of aorta for these two nuclear proteins necessary for cellular proliferation (data not shown). However, in comparison to aortas from normal salt-fed rats, HS aortas showed a significant increase in oxidative stress as measured by staining for the lipid peroxidation product 4-HNE (Figure 5). In addition, chronic G-1 treatment significantly attenuated 4-HNE staining. Aortic smooth muscle cells were isolated and cultured in order to determine the Effects of HS and G-1 on cellular hypertrophy. Discussion The present study demonstrated that estrogen receptor GPER activation attenuated salt-induced increase of aortic wall thickness in mRen2 rats. The mechanism for the G-1 effect most likely involves counteracting oxidative stress and reducing vascular smooth muscle cell hypertrophy. This study demonstrating GPER-induced vascular protection nicely complements our previous work showing similar results in the kidney and heart (ADD REF). Interestingly, GPER’s renoprotective effects were also associated with a reduction in oxidative stress. Moreover, the beneficial effects in the heart were similarly independent of alterations in the extracellular matrix but directly associated with a reduction in cardiomyocyte size. Vascular GPER protein is clearly expressed in both endothelial and smooth muscle cells of the aorta (Lindsey et al, Endocrinology, 2009; Ding et al, Am J Physiol Cell Physiol, 2009; Gros et al, Hypertension, 2011). In native vessels, the extracellular matrix (ECM) is composed mostly of collagen, elastin and proteoglycans. These proteins inà ¯Ã‚ ¬Ã¢â‚¬Å¡uence cell functions and play an important role in maintaining vessel structure by providing tensile strength (collagens) and elasticity (elastin) (Lemarie et al. Journal of Molecular and Cellular Cardiology, 2009). One of the earliest steps of vascular remodeling is the reorganization of the ECM. In the current study, we have shown that HS increased collagen levels and suppressed elastin content in the aorta, indicating increased stiffness and less elasticity. Most importantly, the finding that G-1 ameliorates salt-induced collagen increase, without altering salt-induced decreases in elastin content, suggests that GPER activation protects against the remodeling process via suppressing collagen levels, instead of elastin. The amount and composition of collagen depends on a balance between synthesis / deposition and degradation. The exact effects of GPER on collagen protein expression, degradation, or both remain to be investigated. Another important step during vascular remodeling is the hypertrophy and / or hyperplasia of the VSMCs (Lemarie et al. Journal of Molecular and Cellular Cardiology, 2009). To address this possibility, we used primary cultured ASMCs isolated from female mRen2 rats. We found that both cellular protein content and cell size increased in high salt media (160 mM and 182 mM), indicating that high salt induces cellular hypertrophy. The cellular protein content of 152 mM media-treated cells is significantly higher than that of normal media (142 mM)-treated group. However, the cell size has no significant difference. One possible explanation is that the protein started to accumulate inside cells, but cells had not begun to enlarge yet. More importantly, we found G-1 abolished the hypertrophy of cells. The hypertrophy appears to result from an increase in the rate of protein synthesis and / or a decrease in the rate of protein degradation (Berk et al, Hypertension, 1989; Gu et al, Hypertension , 1998). Future studies are required to determine the effects of GPER activation on protein expression, degradation, or both. We further looked into the possibility of salt-induced proliferation in ASMCs. Although it has been shown that GPER induced the activation of MAPK signaling and cellular hyperplasia in VSMCs, other studies have demonstrated that G-1 inhibited serum-stimulated growth in VSMCs lacking ERÃŽ ± and ERÃŽ ² (Haas et al, Circ Res, 2009,; Ding, Am J Physiol Cell Physiol, 2009; Gros et al, Hypertension, 2011). In our study, we did not observe any evidence of Ki67 or PCNA staining in the medial layer of aortas from any group, although significant staining was found in the adventitia. These results are supported by our in vitro studies which show no change in cell number in response to HS. The finding that G-1 attenuates aortic thickening and cellular hypertrophy, without altering blood pressure, suggests that GPER has protective effects in the cardiovascular system that are independent of blood pressure. One possible mechanism is acute increases in oxidative stress. Oxidative stress is linked to damage within the vasculature and may contribute to vascular remodeling (Hayashi et al, Biochem Biophys Bes Commun, 1995; Xing et al. Arteriosclerosis, Thrombosis, and Vascular Biology, 2009). To address this possibility, we first stained 4-HNE, a marker for oxidative stress, in the aorta. We found significantly stronger staining of 4-HNE in HS-fed rats. However, this was attenuated by G-1 treatment, suggesting that GPER activation attenuates salt-induced oxidative stress. To further confirm this finding, we used tempol, an antioxidant, or G1 to treat ASMCs and measured several hypertrophy parameters. Tempol or G-1 treatments abolished the increase of both cellular protein con tent and cell size. Broughton et al demonstrated that G1 reduces NADPH-dependent oxidase activity in isolated carotid and intracranial arteries of normotensive Sprague-Dawley rats (Broughton et al, Am J Physiol Heart Circ Physiol, 2010). Elucidation of the underlying mechanisms of GPR 30 to attenuate reactive oxygen species within aorta awaits future studies. Another possibility is that HS stimulates renin-angiotensin system (RAS) in mRen2 rats. Ang II increased medial thickening of aorta due to VSMC hypertrophy without increase in cell number (Owens et al, Circ Res, 1982 1983). However, GPER activation may reduce expression of the angiotensin II (Ang II) AT1 receptor (AT1R) and angiotensin-converting enzyme (ACE) but increase the expression of ACE2. Alterations in ACE and ACE2 may increase the ratio of Ang-(1-7) to Ang II in tissues (Lindsey et al, Gender Medicine, 2011). Ang-(1-7) inhibited vascular remodeling in rat jugular vein grafts (Wu et al, J Int Med Res, 2011). In the present study, the HS medium (152, 160, 182 mM) was made by simply adding sodium chloride to normal medium (142 mM). This increases both sodium concentration and osmolarity in the medium. It is likely that increased osmolarity plays a significant role in salt-induced hypertrophy. Future studies using mannitol are needed to rule out this possibility. In summary, this study showed a beneficial effect of the GPER agonist G-1 in salt- and pressure-induced vascular remodeling. These protective effects of G-1 may be due to suppression of oxidative stress and associated cellular hypertrophy. What about aldosterone? 1.Chappell MC, Westwood BM, and Yamaleyeva LM. Differential effects of sex steroids in young and aged female mRen2.Lewis rats: a model of estrogen and salt-sensitive hypertension. Gender medicine 5 Suppl A: S65-75, 2008. 2.Lindsey SH, Yamaleyeva LM, Brosnihan KB, Gallagher PE, and Chappell MC. Estrogen receptor GPR30 reduces oxidative stress and proteinuria in the salt-sensitive female mRen2.Lewis rat. Hypertension 58: 665-671, 2011.

Analysis of Google :: Internet Search Engines Technology Essays

Analysis of Google Google is a play on the word googol, which was coined by Milton Sirotta, nephew of American mathematician Edward Kasner, and was popularized in the book, "Mathematics and the Imagination" by Kasner and James Newman. It refers to the number represented by the numeral 1 followed by 100 zeros. Google's use of the term reflects the company's mission to organize the immense, seemingly infinite amount of information available on the web. Back before Google? Aye, there's the Rub. According to Google lore, company founders Larry Page and Sergey Brin were not terribly fond of each other when they first met as Stanford University graduate students in computer science in 1995. Larry was a 24-year-old University of Michigan alumnus on a weekend visit; Sergey, 23, was among a group of students assigned to show him around. They argued about every topic they discussed. Their strong opinions and divergent viewpoints would eventually find common ground in a unique approach to solving one of computing's biggest challenges: retrieving relevant information from a massive set of data. By January of 1996, Larry and Sergey had begun collaboration on a search engine called BackRub, named for its unique ability to analyze the "back links" pointing to a given website. Larry, who had always enjoyed tinkering with machinery and had gained some notoriety for building a working printer out of Legoâ„ ¢, took on the task of creating a new kind of server environment that used low-end PCs instead of big expensive machines. Afflicted by the perennial shortage of cash common to graduate students everywhere, the pair took to haunting the department's loading docks in hopes of tracking down newly arrived computers that they could borrow for their network. A year later, their unique approach to link analysis was earning BackRub a growing reputation among those who had seen it. Buzz about the new search technology began to build as word spread around campus. The search for a buyer Larry and Sergey continued working to perfect their technology through the first half of 1998. Following a path that would become a key tenet of the Google way, they bought a terabyte of disks at bargain prices and built their own computer housings in Larry's dorm room, which became Google's first data center. Meanwhile Sergey set up a business office, and the two began calling on potential partners who might want to license a search technology better than any then available.

Radio Waves :: essays research papers

Before beginning our research on radio waves, to us, radio waves were just waves going through the atmosphere, carrying sound from one place to another. Those were our ignorant days! We did not realize the complicated terms and theories involved. In the following report you will see how we advanced in our knowledge of radio waves, and we hope it will do the same for you. Radio waves are a combination of two kinds of electric vibrations. Audio frequency waves, which represent voice and other sounds and radio frequency waves, which carry audio waves after being combined with them. Two examples of broadcast waves are AM waves and FM waves. AM which stands for amplitude modulation, is a broadcasting method in which the carrier waves (carry the sounds of a program) are changed to match changes in the audio frequency waves. These are electric waves that represent the sounds of a radio broadcast. FM stands for frequency modulation and these waves, that go skyward, are not reflected. Instead, they pass through the atmosphere and go into space. AM signals, however, reflect off the atmosphere and travel back down to earth, causing broadcasts to be received at a much greater distance than FM signals. Since FM travels all the way to space and it does not bounce off the ground it does not create as much static as AM does. Radio waves, which travel at the speed of light, cannot be seen, heard, or felt in any way. When you listen to the radio, contrary to what some think, you are hearing the receivers pick up the waves and turn them into sound. Three more types of radio waves are; ground waves, ionospheric waves and tropospheric waves. Ground waves travel from the antenna along the surface of the earth. Ionospheric waves, otherwise known as sky waves, are made up of radio waves that come from a transmitting antenna and go into the sky. The ionosphere is the region of the rare field and ionized atmosphere around the earth, from 50 to 200 miles. Last but not least are the tropospheric waves. These waves are parts of the original wave which is reflected into the troposphere, an area of clouds and storms from 3 to 7 miles high. Radios change sound into electrical patterns with transmitters. In a radio transmitter, the circuit that generates the high frequency AC current that produces radio waves from an antenna, is called an oscillator. Electrical patterns are then changed into broadcast waves of electromagnetic energy. The Kenelly-Heairside layer, found in a transmission of a radio is now well known. This keeps the energy spent by a shortwave transmitter from escaping into space. This is why we are able