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World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
10-12-2008, 04:41 PM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
you manner if which you evade simple questions suggests a career in politricks
10-13-2008, 12:51 PM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
Im just happy drew isnt talking about his pineal glands anymore. Thankyou drew. keep it up, if you pardon the pun:)
10-16-2008, 12:27 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
Has CERN fucked up the melatonin-pineal gland testes cycles of the scientists, if not the one-humped camels?

Seasonality and the melatonin signal in relation to age as correlated to the sexual cycle of the one-humped male camel (Camelus dromedatius)

Author(s): Al Qarawi AA (Al Qarawi, Ali Abdulla), Elmougy SA (Elmougy, Samy Ahmed)
Source: BIOLOGICAL RHYTHM RESEARCH Volume: 39 Issue: 2 Pages: 131-142 Published: APR 2008
Times Cited: 0 References: 97 Citation MapCitation

Abstract: Heparinized blood samples were taken from male immature and mature camels of the Sha'alah breed, housed at the University Animal farm, during the rutting and non-rutting period. Other blood samples were also collected from camels slaughtered at defined seasons (summer, autumn, winter and spring) and from the Buraydah slaughter-house. In addition, specimens from the testes were also taken to confirm the difference between the immature and the mature animals during the non-rutting and rutting seasons. The plasma obtained from the collected blood samples was used for estimation of the following hormones, Melatonin (MLT), Follicle Stimulating Hormone (FSH), Leutinizing Hormone (LH), Testosterone and Prolactin (PRL) using the radioimmunoassay technique. Specimens of testes tissue were fixed in calcium formol, processed for histological examination using standard procedures and stained with H&E. The results clearly differentiated the samples as immature and mature during the non-rutting and rutting seasons. Commercially available human radioimmunoassay (RIA) kits for MLT, FSH, LH, testosterone and PRL were adapted for quantitation of these hormones in serum from the one-humped camel (Camelus dromedarius). Serum samples from 40 camels were assayed in order to determine possible differences between various groups in the concentrations of MLT, FSH, LH, testosterone and PRL in these animals. Among the camels, serum concentrations of melatonin, FSH, LH, testosterone and prolactin reflected age and seasonal differences. Immature camels had overall significantly lower levels in MLT, FSH, LH, testosterone and PRL. Mean FSH and LH levels from confirmed non-rutting (sexually inactive) camels were 0.22 +/- 0.08 and 0.37 +/- 0.18 ng/mL, respectively. Although rutting (sexually active) camels had higher FSH and LH levels, the differences were not statistically significant (P less than 0.07). Our observations indicate that these RIAs can reliably detect serum MLT, FSH, LH, testosterone and PLT from camels and represent the first quantitation of melatonin in Camilidae in correlation with FSH, LE, testosterone and prolactin.
Document Type: Article
Language: English
Author Keywords: camelus dromedarius; melatonin; FSH; LH; testosterone; prolactin; rutting
10-16-2008, 12:40 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
not that it is a problem but it is not my problem that you have a complex about your genitalia - muffled giggling in the corner whilst cranking out obscure academic abstracts is not the way foward - you have a bitch problem with me because I told you to stop gumming up threads with your repetitive 'OataD' accounts - get it off your chest in a different dedicated thread for all to see, if you need - but posting your personal grievances like this in a manner that you presume will elude, is convoluting threads and bullshit ja?
10-16-2008, 12:45 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
The persistent problem of malaria: Addressing the fundamental causes of a global killer

Leeanne Strattona, E-mail The Corresponding Author, Marie S. O'Neillb, Corresponding Author Contact Information, E-mail The Corresponding Author, Margaret E. Krukb, E-mail The Corresponding Author and Michelle L. Bellc, E-mail The Corresponding Author
aWeill Cornell Medical College, New York, NY, USA bUniversity of Michigan School of Public Health, Ann Arbor, MI, USA cYale University School of Forestry and Environmental Studies, New Haven, CT, USA

Available online 26 June 2008.


Despite decades of global eradication and control efforts and explosive global economic development, malaria is the most important vector-borne disease of our day, killing more people today than 40 years ago and affecting millions worldwide, particularly poor residents of tropical regions. Global eradication efforts from the 1950s through the 1980s largely failed, leaving vector and parasite resistance in their wake. The persistence of malaria and the magnitude of its effects call for an action paradigm that links the traditional proximal arenas of intervention with malaria's fundamental causes by addressing the environmental, economic, and political dimensions of risk. We explore the more distal determinants of malaria burden that create underlying vulnerabilities, evaluating malaria risk as a function of socioeconomic context, environmental conditions, global inequality, systems of health care provision, and research. We recommend that future action to combat malaria be directed by a broad-spectrum approach that meaningfully addresses both the proximal and fundamental causes of this disease.

Keywords: Malaria; Poverty; Developing countries; Environment; Political economy
Article Outline

Framework: fundamental and proximal causes of malaria
Environment, behavior, and malaria risk

Climate change

Economic inequality and malaria risk

Global inequalities

Sub-national inequalities

Political economy, health systems, and malaria risk
Health care research and malaria risk
Antimalarial drugs

Malaria is a parasitic infection, caused by the Plasmodium parasite and mainly transmitted by female Anopheles mosquitoes, prevalent throughout Africa, Latin America, and Asia. The disease is particularly severe in Africa with over 900,000 deaths annually, mostly in children (WHO, 2006c). In holoendemic1 areas, where transmission is stable and perennial, malaria accounts for approximately 25% of deaths in children under five ([Root, 1999] and [Snow et al., 1999]). Malaria epidemics often affect vulnerable sub-populations with existing compromised health status and limited access to health care services (Kiszewski & Teklehaimanot, 2004). Worldwide, malaria affects 300 million people annually, and approximately 2 billion more people are susceptible to malaria today than before the major global malaria eradication campaigns of the mid-20th century (Hay, Guerra, Tatem, Noor, & Snow, 2004). Malaria cases may be increasing due to changes in population, demographics, and land-use, as well as malaria reemergence in areas where control efforts were once effective ([Kublin et al., 2003], [Martens and Hall, 2000] and [Nchinda, 1998]). Rising mortality is linked to the growing incidence of chloroquine-resistant Plasmodium falciparum infections ([Hay et al., 2004] and [Kublin et al., 2003]), the most lethal malaria strain.

Malaria is one of the most persistent and pressing global public health problems of our time, and much has been written about its determinants and control strategies. This paper aims to evaluate the social, political, economic, and environmental factors representing upstream, underlying causes of malaria and to discuss how long-term efforts aimed at reducing malaria's toll may benefit from a perspective that integrates these fundamental causes. We investigate the distribution of malaria risk as a function of environmental change, economic inequality, political economy, health care systems, and global health care research. This focus on the fundamental causes of malaria is not intended to minimize or downplay the relevance of proximal determinants and focal interventions but, rather, to advocate a balance between strategies addressing biological and behavioral determinants and the more distal determinants of the global malaria burden.
Framework: fundamental and proximal causes of malaria

Socioeconomic development is a fundamental determinant of the global distribution of morbidity and mortality for many health outcomes. The epidemiologic transition model introduced in the 1970s describes shifts in the disease profile of developing countries, characterized by non-uniformly decreasing birth and mortality rates (Omran, 1971). Initial analyses of health responses to development described a decreasing burden of infectious disease and an increase in chronic diseases, as early public health measures (e.g., sanitation, potable water) were implemented and greater longevity increased the relevance of chronic health conditions to population health. However, Smith and Ezzati (2005) illustrated that low-income countries bear a disproportionately high burden of both infectious and chronic diseases, which decreases only with socioeconomic development.

Global patterns of malaria morbidity and mortality are neither randomly occurring nor predominantly due to biological susceptibility (Kaplan, 1998), but are broadly symptomatic of underlying disparities in the allocation of local and global resources. In fact, the World Health Organization (WHO) concluded in 1998 that poverty is the greatest risk factor for malaria (Lucas & McMichael, 2005). Over two-thirds of malaria cases occur in the poorest fifth of the world's population (Guerin et al., 2002). The linkages between poverty and poor health outcomes are widely acknowledged ([Carrin and Politi, 1997], [Farmer, 2005] and [Sen, 1998]).

(Link and Phelan, 1995) and (Link and Phelan, 1996) posit that social conditions are the fundamental causes of observed health disparities and that likely mechanisms include restricted access to social and material resources. They argue that although an exclusive focus on the more proximal variables in the causal pathway from exposure to disease may remediate specific mechanisms that generate inequity, the underlying social–ecological conditions will manifest through different mechanisms, perpetuating health inequities. An exclusive focus on controlling malaria either through lessening exposure (e.g., use of mosquito nets) or treating the disease (e.g., administering medicine) may provide a more realistic and immediate solution than more integrated approaches, partly due to the infeasibility of radical systems reform in the short-term. However, while such strategies may provide tangible health benefits, given the vast scale of poverty in the most malaria endemic regions, the efforts will be less effective in the long run at reducing total health burden than approaches aimed at underlying causes of differential vulnerability.

The public health community remains divided over whether research and other efforts should address malaria directly through exposure prevention and treatment or through the fundamental causes of underlying vulnerabilities. Some have called for focusing on individual biomedical or behavioral risk factors and molecular mechanisms in research, challenging the proposition that epidemiology is bound to an agenda of poverty eradication. They argue that focusing on the fundamental causes and socio-historical context of disease is a “superficial” treatment of the exposure-disease pathway (Rothman, Adami, & Trichopoulos, 1998). However, others contend that if poverty limits the effectiveness or distribution of available technologies, a commitment to reducing malaria requires research and action in development and poverty eradication ([Kaplan, 1998] and [McMichael, 1998]).

The literature addressing which indicators of development are most relevant to health outcomes is strongly influenced by the methodology and ideology of the disciplines involved. As economist Angus Deaton wrote in 2003, “Much of the health-economics literature does not accept the existence of any causal effect running from income to health, except possibly through the purchase of health care.” Because much neoclassical economic research focuses on narrowly defined health outcomes such as health care consumption, the conclusions from this field reflect these preferences and do not necessarily capture the true nature of interplay between multiple measures of development, the social environment, individual socioeconomic status and health (Deaton, 2003). Economics, social epidemiology and other disciplines continue to address these issues, but much remains to be clarified about the relationship between various indicators of development and health. For example, it is unclear from a theoretical perspective whether absolute or relative income disparity or even education, alone, is most closely linked to individual health outcomes (Deaton, 2003). Such distinctions are not merely academic, since each indicator implies a different set of policy-based interventions. No consensus exists on any single indicator that, if acted upon, would yield the most benefit for health. The WHO commissioned a special panel on the social determinants of health in 2006 to evaluate the social determinants literature, clarify mechanisms, and identify appropriate policy interventions (Kelly, Bonnefoy, Morgan, & Florenzano, 2006). This discussion provides context in which we discuss the social determinants of malaria, and is relevant also to other infectious diseases that are more prevalent among the poor.

A dynamic interplay of biological, social, and environmental susceptibilities define malaria risk. Land-use patterns and agricultural practices, along with the climate and economics-driven migration of workers into regions of differing malaria endemicity, are part of “a wider historical narrative in which human actions have encouraged the breeding of malaria vectors, exposed populations to infection, and facilitated the movement of malaria parasites” (Packard, 2007).

Although the development process is essential to addressing the fundamental determinants of malaria risk, development projects, and their unintended consequences have often undermined malaria control by increasing parasite exposures, undermining local immunities and preventing populations from “growing out of malaria” (Packard, 2007). The current focus on the basic science of malaria prevention, to the neglect of traditional environmental modification and other social-behavioral interventions, ignores this context in which particular trajectories of the development process may conflict with health priorities, including reduction of malaria risk.

The contextual determinants of malaria risk (Casman et al., 2002) are an important component for understanding and reducing the burden of this disease. Our assessment of malaria control and prevention actions incorporates interventions at both the proximal and distal levels. Thus, efforts that address socioeconomic development or even efforts to mitigate climate change may have profound implications for the malaria burden, even if they are not directed specifically to malaria.
Environment, behavior, and malaria risk

Smith and Ezzati, 2005 K.R. Smith and M. Ezzati, How environmental health risks change with development: the epidemiologic and environmental risk transitions revisited, Annual Review of Environment and Resources 30 (2005), pp. 291–333. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (13)Smith and Ezzati (2005) use the term “super distal risk factor” to refer to any underlying determinant, from environmental risk to social inequality, that affects disease distributions. In addition to socioeconomic factors affecting vulnerabilities, malaria risk is strongly linked to environmental context, including climatic factors and patterns of land-use ([Lindblade et al., 2000], [Prothero, 1995] and [Vittor et al., 2006]) that impact malaria transmission. Mitigation strategies, such as use of the pesticide DDT, in turn, impact the environment (see Box 1). The WHO recently concluded that 42% of the global malaria incidence is attributable to modifiable environmental factors such as land and water resource management (Pruss-Ustun & Corvalan, 2006). Meanwhile, population movement, fueled in part by environmental degradation, famine and drought, is reshaping the distribution of resistance as people move between malarious and nonmalarious regions and the borders between susceptible and infected populations disappear ([Casman et al., 2002] and [Martens and Hall, 2000]). Even non-endemic countries such as the United States are vulnerable through the confluence of travel and immigration and even minor modifications to the environment ([Maroushek et al., 2005], [Packard, 2007] and [Vicas et al., 2005]). The spatial distribution of vectors and human populations throughout malarious regions, and modifying socioeconomic factors like education and nutrition (Root, 1999), shape both disease susceptibility and outcomes.
Climate change

Malaria risk is circumscribed by geography and the presence of climatic conditions favorable to the anopheline mosquito vectors. Tropical zones like sub-Saharan Africa are amenable to high endemic stability, and strongly anthropophilic mosquitoes in many of these areas makes malaria transmission very effective (National Center for Infectious Diseases, 2004). Because temperatures suitable for timely vector development and survival are necessary for stable transmission of the malaria pathogen (Craig, Snow, & le Sueur, 1999), global warming could affect the global distribution of malaria ([Casman et al., 2002], [Hales and Woodward, 2005], [Reiter, 2004], [Tanser and Sharp, 2005] and [Thomas and Hay, 2005]). Climatic change is likely to increase the risk of malaria through reduced time to infection (Pascual, Ahumada, Chaves, Rodó, & Bouma, 2006) and increased suitability of mosquito habitats in African highlands (Ebi et al., 2005). The impact of climatic change on malaria is likely to be complex and involve large spatial heterogeneity ([Martens et al., 1995] and [Thomas, 2004]), and will also be affected by changing populations and economies.

Indeed, some have questioned the hypothesis that global warming on its own can exacerbate patterns of malaria transmission ([Casman et al., 2002], [Dye and Reiter, 2000], [Hay et al., 2002], [Hay et al., 2002], [Reiter, 2000] and [Rogers and Randolph, 2000]). A downward trend in malaria transmission, despite warming, occurred throughout Europe and the United States during the previous century, while transmission appears to have continued throughout England during a sustained drop in temperatures in the latter half of the 16th century (Reiter, 2000). Small, Goetz, and Hay (2003) analyzed climate-driven models of malaria transmission throughout Africa during the 20th century and found that rising temperatures did not result in increased malaria suitability anywhere on the continent. Instead, the observed trends and fluctuations in suitability were more strongly related to patterns of precipitation, with low mean monthly rainfalls limiting the rate of transmission. Similarly, Rogers and Randolph (2000) argue that temperature is but a single feature of climate change and poorly predictive of malaria transmission patterns. They used a multivariate model derived from the current distribution of P. falciparum malaria to predict a future distribution for the year 2050. Along with temperature, Rogers and Randolph included mean, maximum and minimum values for precipitation and saturation vapor pressure and found that the predicted covarying temperature, rainfall, and moisture variables resulted in a P. falciparum distribution remarkably similar to the current distribution.

Efforts to characterize the effect of climate and land-use variables on malaria are complicated by potential confounding from changing drug resistance and malaria control activities, which can play a larger role than climate itself, as well as by data limitations ([Hay et al., 2002] and [Woolhouse, 2002]). The debate over climate-change driven patterns of malaria transmission also reflects gaps in knowledge about the epidemiology of transmission and the biology of malaria parasites and vectors and host susceptibility ([Guerin et al., 2002], [Hay et al., 2004] and [Rogers and Randolph, 2000]). Distribution maps of malaria risk may help guide global allocation of anti-malaria efforts by highlighting the regions of greatest need, but they lack methodological consistency and are of limited use for research and control purposes ([Craig et al., 1999], [Hay et al., 2004] and [Rogers and Randolph, 2000]). While understanding the potential implications of climate change for future malaria risk is critical, and efforts to develop adaptive capacities may reduce the burden of malaria and other climate-sensitive diseases (Ebi, Kovats, & Menne, 2006), such efforts must be balanced with the current need to address the known determinants of malaria risk.

The effects of environmental conditions and climate change on malaria are not easily parsed from the effects of social and economic conditions (Packard, 2007). The world's poorest countries are typically those most vulnerable to environmental risk, and within these areas, the poorest persons may be at greater risk. For example, lower socioeconomic status was associated with less access to vector-control tools such as nets in Sudan (Onwujekwe, Malik, Mustafa, & Mnzavaa, 2006), poor housing and crowding (affecting malaria rates) in Indonesia (Roosihermiatie, Nishiyama, & Nakae, 2000), and increased transmission in Brazil (Castilla & Sawyer, 1993). On a broader scale, the poor in these regions contribute the least to greenhouse gas emissions but have less capacity to adapt to altered climates. Proximally, behavior and education mediate the relationship between socioeconomic status and malaria risk, as demonstrated in Gambia (Dike et al., 2006). Although the current social science literature on malaria control and behavior faces limitations with respect to methodology and knowledge gaps (Williams & Jones, 2004), the WHO's recent findings on modifiable environmental risk underscore the importance of education and individual behavior change to malaria control efforts.

A necessary component of malaria-related needs assessments is ethnographic narratives of people's lived experiences with the disease. These narratives are crucial to understanding how the disease fits into people's interpretive frameworks and the ways in which competing needs are prioritized and met. Few ethnographic data on malaria illness experiences and risk perception exist. Past anthropological research into malaria has been largely restricted to biological and ecological analyses (Inhorn & Brown, 1990). While some literature addresses ethnomedical beliefs surrounding the etiology and treatment of malaria, the coping mechanisms and illness experiences of people in malaria endemic areas are not well studied. Specific research needs include comparison of epidemiologic and perceived risks, and what that comparison implies for the sustainability or appropriateness of particular local health interventions and large-scale programmatic efforts (Panter-Brick, Clarke, Lomas, Pinder, & Lindsay, 2006). Opportunities to document the experiences and shifting perspectives of local communities will arise with newly formed antimalaria global partnerships.

Box 1. DDT: a panacea?

The discovery of DDT's residual insecticidal properties in 1939 led to its widespread application in the United States south from 1947 to 1952. However, the impact of spraying in the United States is uncertain, since it began when domestic malaria rates were already at an all-time low and had been steadily declining after an earlier, Depression-era surge in transmission (Humphreys, 1996). Nevertheless, the Communicable Disease Center (later to become the Centers for Disease Control and Prevention), which grew out of wartime malaria control efforts, launched a 5-year intradomiciliary spraying campaign amidst a popular fear that soldiers returning from abroad would re-introduce malaria to the United States. By the 1960s, however, it became clear that DDT spraying, even when coupled with follow-up drug treatment, could not eradicate malaria in the most highly endemic regions like rural sub-Saharan Africa due to the high cost, logistic complexity, and only moderate effectiveness of established interventions against prevalent mosquito species (Klausner & Alonso, 2004). The necessary technical capability and infrastructure were not in place for global eradication (Rogan & Chen, 2005).

Recurring debate over DDT application centers on the largely uncharacterized risk trade-off between malaria and DDT's human health effects at environmentally relevant levels, as well as the absence of superior alternatives ([Attaran et al., 2000], [Chanon et al., 2003], [Rogan and Chen, 2005] and [Yanez et al., 2004]). Given DDT's persistence and mobility in the environment, concern regarding long-term ecological effects led to a ban on most uses of DDT in the United States and other industrialized countries in the early 1970s, spurred by mounting conservationist concerns in the wake of Rachel Carson's Silent Spring (Walker, Ricciardone, & Jensen, 2003). Eventually, calls for the gradual phasing out of DDT spraying by environmental organizations like the World Wildlife Fund were seconded by groups like Physicians for Social Responsibility, who were concerned primarily with DDT's potential human health effects ([Attaran et al., 2000] and [Walker et al., 2003]).

Many governments and agencies have now concluded that the balance of known health risks supports the continued use of DDT (WHO, 2006b). In 2001, the United Nations-led Stockholm Convention on Persistent Organic Pollutants recommended the provisional use of DDT for WHO-approved disease control efforts, while calling upon developed nations to invest in the development of less toxic methods (Walker et al., 2003). In September 2006, the WHO reiterated support for DDT use and urged that indoor residual spraying be extended to stable, high-transmission areas (WHO, 2006b). Technical and infrastructural barriers to widespread DDT application in most of sub-Saharan Africa, together with inadequate deployment of insecticide-treated nets (ITNs) ([Breman et al., 2004] and [Klausner and Alonso, 2004]) and growing drug resistance, perpetuate the burden of malaria in these regions, while gaps in the scientific understanding of the true consequences of DDT hinder informed decision making.

Economic inequality and malaria risk
Global inequalities

While poverty is an important determinant of malaria, the disease also contributes to poverty, with malaria slowing economic growth and poverty limiting the health sector response. Long-term, economists estimate that holoendemic malaria is correlated with at least a 1% decline in annual economic growth (Sachs, 2003). The bidirectional relationship between disease burden and growth underscores the uneven nature of global patterns of malaria susceptibility, and the implications of a high malaria burden for development and social well-being ([McCarthy et al., 2000], [Sachs and Malaney, 2002] and [Sachs et al., 2004]).

In 1995, the gross domestic product (GDP) of malaria-endemic countries was only one-third that of non-endemic countries, without controlling for geographic latitude (Guerin et al., 2002). The United Nations Development Programme reports human development indices (HDI) for most countries in its annual Human Development Report. A composite measure of life expectancy, adult literacy, and school enrollment and standard of living, the HDI is a richer, more rigorous measure of human well-being than any single measure of income ([UNDP, 2003] and [UNDP, 2004]). A steep downward trend in malaria burden, as measured in disability-adjusted life years (DALYs), is visible when plotted against rising HDI (Fig. 1) (Smith & Ezzati, 2005). The same trend holds when malaria burden is plotted against rising purchasing power parity, which indicates greater wealth (Smith & Ezzati, 2005). Similarly, per capita GDP, along with access to rural health care and income equality, surpass geography and climate as the most powerful discriminants between high and low endemicity countries (McCarthy et al., 2000).

Full-size image (26K) - Opens new window Full-size image (26K)

Fig. 1. Malaria burden in DALYs per 1000 by Human Development Index (HDI). The UNDP's Human Development Index (HDI) is a more rigorous measure of human well-being than any single measure of income. When malaria burden, as measured in disability-adjusted life years (DALYs), is plotted against HDI, a steep downward trend in malaria burden occurs with rising HDI. In least developed countries, malaria is responsible for a greater portion of the disease burden than the otherwise significant environmental health risks of indoor air pollution and unsafe water and sanitation. Malaria risk is more sensitive to incremental improvements in standard of living and education. The risk associated with indoor air pollution, unsafe water, and sanitation is more resistant to incremental improvements in HDI. As HDI rises, the disease burden attributable to malaria sharply declines. Reprinted, with permission, from Annual Review of Environment and Resources, 30, 291–333 (2005).

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Another example of the impact of global economic inequity on malaria risk is the variable success in fighting malaria in rich and poor countries. Over the past century, malaria mortality rates in sub-Saharan Africa have remained consistently higher and have fallen much more slowly than in the rest of the world. In 1900, an estimated 223 malaria deaths per 100,000 people occurred in sub-Saharan Africa, compared with 192 deaths per 100,000 throughout the rest of the world; by 1997, 165 per 100,000 people were still dying in sub-Saharan Africa from malaria, compared with 1 per 100,000 in the rest of the world (McCarthy et al., 2000). The success of malaria reduction efforts has been inversely proportional to the initial prevalence of malaria in affected areas. The greatest reductions in malaria over the past century occurred in lower endemicity regions, with the highest reductions in epidemic (100% reduction), hypoendemic (68%), and mesoendemic (45%) areas (Hay et al., 2004). In contrast, success was minimal in areas of hyperendemic and holoendemic malaria, with 16% and 0% reductions in incidence over the past century, respectively (Hay et al., 2004).

The highest endemicity regions of the world, those most insensitive to eradication efforts, were among the poorest nations to start, with overly centralized and underdeveloped health infrastructures (Packard, 2007). Resistance in these countries quickly resulted as pesticides and chloroquine were ineffectively administered through these poorly developed systems. Successful eradication in tropical and sub-tropical regions was predicted by the degree of investment in public sanitation and public services, “regardless of the level and frequency of insecticide saturation and drug treatment” (Packard, 2007). Thus, malaria susceptibility is not simply a function of poverty and latitude, but of specific local biological, economic, political, and social conditions.
Sub-national inequalities

Poverty also contributes to inequities in malaria burden within countries. All-cause children's mortality is higher in the poorest quintile of the population than in richer groups across a range of countries ([Victora et al., 2003] and [Wagstaff, 2000]). Children in the poorest quintile in Tanzania had a 39% higher rate of death following fever (most of which would be expected to be due to malaria) than the richest quintile (WHO/UNICEF, 2003). The poorest quintile also had a three-fold higher incidence of malaria prevalence measured by blood parasitemia in Zambia, compared to the richest quintile (WHO/UNICEF, 2003). These results are consistent with data showing that the poorest children in sub-Saharan Africa are typically half as likely to sleep under a bednet and less likely overall to use antimalarials (WHO/UNICEF, 2003).
Political economy, health systems, and malaria risk

Malaria risk is as much determined by prevailing systems of political economy as by environmental or social (including behavioral) factors. The structural adjustment program (SAP) conditionalities of the International Monetary Fund (IMF) and World Bank sought to reduce macroeconomic inefficiencies and thereby stimulate long-term economic growth in developing countries through a series of austerity policy measures. The SAP reforms, first implemented in the 1980s, often brought widespread cuts in public spending on health and education (Peabody, 1996). Such measures were designed to free national resources for servicing debt and reflected the IMF's primary interest in ensuring loan recovery for major creditors like the World Bank (Homedes & Ugalde, 2005). Within the first decade of implementation, household and community resource constraints, engendered or exacerbated by austerity programs, led to rising infant mortality rates and worsening health, overall, in sub-Saharan African countries under adjustment ([Manfredi, 1999] and [Packard, 2007]).

Manfredi (1999) suggested mechanisms by which rising malaria rates in sub-Saharan Africa throughout the late 20th century could be attributed to structural adjustment reforms: the devolution of the health sector led to a greater individual responsibility for malaria treatment and follow-up; rising income disparity and greater absolute poverty reinforced the tendency to self-medicate, while rising health care costs delayed treatment-seeking for serious cases of malaria; economic deprivation led to environmental degradation and diverted the resources necessary to address environmental risk factors for malaria; and worsening women's health, resulting from the uneven allocation of household resources in scarce times, worsened child and infant health. While the relative significance of each pathway to malaria's rise in sub-Saharan Africa under structural adjustment is unknown, socioeconomic impoverishment probably undermined anti-malaria efforts. Ultimately, the adverse population health consequences of structural adjustment reforms can be attributed to the failure of the international financing institutions to appreciate the links between development and health.

SAPs also reduced the ability of national health systems to respond to malaria. Governments were forced to lay off doctors and nurses to meet new civil service ceilings and reduce their spending on health in favor of “productive” sectors of the economy ([Jowett, 1999] and [Peabody, 1996]). During the 1990s, World Bank conditionalities capped wages in Zambia, prompting many health care workers to leave the health care sector or take better-paying jobs abroad (Packard, 2007). The shortage of health care professionals forced many rural health clinics to close, reducing delivery of antimalarials to these areas. Decentralization of health systems and devolution of decision-making to districts was thought to promote greater community participation but often diffused responsibility for service delivery. Due to weak economic growth in much of sub-Saharan Africa and the ravages of AIDS, health systems today are massively underfunded and understaffed. Thus, while the WHO recommends a minimum per capita expenditure of $35 for basic health services (Commission on Macroeconomics and Health, 2001), in 2003 over half the countries in sub-Saharan Africa spent $20 or less (WHO, 2006c). As a result, health systems cannot afford to maintain functioning rural clinics with health workers who can diagnose malaria and oversee its treatment. With such minimal public funding, purchase of antimalaria bednets falls to individual households who frequently cannot afford them. As a result, only 15% of children across 28 African countries sleep under a bednet and only 2% under the more expensive ITNs, which are similar in efficacy to indoor residual spraying ([Schapira, 2006], [WHO, 2006b] and [WHO/UNICEF, 2003]).

Treatment for malaria also has suffered from neglect due to weak health systems in holoendemic areas. Since 2001, the WHO has recommended artemisinin-based combination therapies (ACTs), which have a cure rate of nearly 95% and low likelihood of engendering parasite resistance (WHO, 2006a). Field trials with ACTs have led to significant long-term reductions in malaria incidence on the Thai–Burma border and a drastically reduced malaria incidence and 87% higher cure rate in South Africa's KwaZulu-Natal province ([Frankish, 2003] and [Yeung et al., 2004]). However, despite the promise of ACTs, of the 34 African countries that have updated their national drug formularies to reflect WHO recommendations, only 10 are actually distributing ACTs through the public sector (WHO, 2006c). The high cost of ACTs, the rise in the availability of artemisinin-derived monotherapies through the informal sector, a lack of knowledge and public awareness about combination therapies ([Mutabingwa, 2005] and [Yeung et al., 2004]), and the collapse of primary health care systems throughout Africa (Alilio, Bygbjerg, & Breman, 2004), have limited large-scale use of ACTs in sub-Saharan Africa. Additionally, the cost of treating presumptive cases of malaria with ACTs further deters the poor from seeking treatment (Mutabingwa, 2005). The inability to provide ACTs at scale is especially tragic given that a potentially life-saving course of treatment costs $2–$3. By comparison, the average Organization for Economic Cooperation and Development member country and the United States spend an annual average of $239 and $690 per capita, respectively, for drugs ([Smith et al., 2006] and [Trouiller et al., 2002]).

In sum, the failure of current malaria control efforts highlights the urgent need for adequately funded, functioning health systems ([Alilio et al., 2004], [Barat et al., 2003] and [Pruss-Ustun and Corvalan, 2006]). Care provision remains poor in the most malarious regions, while “[t]he quality of care for people with malaria today is simply unacceptable” (Guerin et al., 2002). See Box2 for more on this issue.

Box 2. User fees and the medical poverty trap

SAP reforms, while designed to stimulate growth in the long-term, often proved disastrous for human security in the short-term (Manfredi, 1999). Currency devaluations were a fundamental feature of SAPs, and they had the effect of lowering domestic purchasing power and raising the price of food and health care. Simultaneously, user fees for both health care and education were often introduced, sometimes in an effort to subsidize poorly funded health systems or to reign in “consumer demand” for care, and occasionally as a crude measure of local commitment to development efforts. In fact, there is little evidence that user fees generate a significant source of revenue for the poorest of health care systems (Creese, 1997). Critically, user fees ignored the resource-scarce reality for many people in developing countries, with devastating implications for health and human security.

User fees can threaten human security because they ignore the elastic nature of preventive care utilization and the relatively inelastic nature of emergent care utilization: user fees and rising health care costs delay treatment-seeking behavior until the need for care is urgent and the associated costs are catastrophic (Whitehead, Dahlgren, & Evans, 2001). Following the introduction of user fees in Zambia in 1993, outpatient visits in the capital of Lusaka fell 60 percent, while visits to maternal delivery services fell 20 percent (Packard, 2007). The medical poverty trap refers to the long-term impoverishment that both brings about and is sustained through household medical debt. In servicing this debt, the global poor liquidate their limited assets, take out high interest rate loans from private lenders, increase their work burden and pull their children out of schools and into the workforce to eliminate the burden of school fees and raise the household's earning potential. Clearly, in this last instance, the medical poverty trap has direct multigenerational repercussions, with serious implications for long-term economic growth as well as household and community well-being (Sachs & Malaney, 2002).

Health care research and malaria risk

New antimalarial medicines and tools are urgently needed. While ensuring broader access to existing diagnostic (e.g., microscopy), preventive (e.g., ITN, spraying) and treatment tools (Klausner & Alonso, 2004) is an immediate priority, widespread P. falciparum resistance to traditional medicines like chloroquine and sulfadoxine-pyrimethamine, which is over 90% in parts of Africa (MSF, 2006), highlights the need for new therapies. Malaria drug resistance is developing faster than new drugs are being created (Hay et al., 2004).
Antimalarial drugs

In a ground-breaking 1990 report, the Global Forum for Health Research estimated that of the approximately $30 billion spent globally on health research and development (R&D) each year, only 10% was being spent on 90% of the world's health problems (the “10/90 gap”), which account largely for diseases of the developing world (Global Forum for Health Research, 2005). For example, as few as 0.1 new chemical entities per one million DALYs attributable to malaria were developed for the disease, from 1975 to 1999, and nearly all antimalarial drugs currently in use were developed over 30 years ago (Trouiller et al., 2002). While health research spending rose to $105.9 billion in 2001, the gap between spending and need stayed roughly the same (Global Forum for Health Research, 2004). About half of global R&D spending comes from private industry, and nearly half of this came from the United States (Global Forum for Health Research, 2004). The market orientation of much of the pharmaceutical industry lowers incentive to invest in new drugs for diseases of poor countries. Infectious and parasitic diseases account for one-third of the global burden of disease, with 95% of that burden in developing countries, but they accounted for only 10% of pharmaceutical industry investments in research development in 1999 (Trouiller et al., 2002). Governments, public–private partnerships, and foundations like the Bill and Melinda Gates Foundation are trying to close this gap (Hemingway, Beaty, Rowland, Scott, & Sharp, 2006), but market-based pharmaceutical production may need to be transformed to better respond to the health needs of the poor.

The emergence of multiple anti-malaria multilateral initiatives in the 1980s and 1990s, including the large-scale Medicines for Malaria Venture, marked a new phase in the history of malaria control efforts and signaled a renewal of a global commitment to disease control efforts in the developing world (Alilio et al., 2004). Today, this commitment is confined largely to malaria and tuberculosis, at least in part due to the perceived public health threat to developed nations (Trouiller et al., 2002). Little support remains for efforts to respond to other, less mobile parasitic diseases that afflict only the poorest countries (Trouiller et al., 2002).

In the 21st century, malaria risk is inextricably linked to the related factors of environmental degradation, economic power, the availability of functioning health care systems, and access to essential medicines. Each of these factors is intertwined with the prevailing political system. Access to health care resources, including new drugs, is increasingly determined in the global arena by the skewed distribution of funding and attention to needs of developed countries. The role of anthropogenic climate change, largely caused by industrialized countries, in exacerbating the burden of malaria is still controversial, but a growing body of research provides evidence that environmental conditions in the developing world contribute significantly to the higher burden of malaria (Pruss-Ustun & Corvalan, 2006). The emergence of malaria in previously non-malarious areas, and its spread into new regions of India and Latin America, demonstrates the inability of modern science or structural reforms, alone, to solve the global problem of malaria. For example, migration of workers between malarious and non-malarious areas and the unwitting creation of new vector breeding sites through development projects have raised malaria susceptibility throughout Latin America (Prothero, 1995). If the Millennium Development Goal to reduce malaria incidence by 2015 is to be met, a long-view and comprehensive approach is necessary. There is an urgent need for a sustained multilateral and multisectoral commitment to addressing malaria as a disease of poverty and structural global inequality. A focus on poverty reduction along with investments in the environment, health care systems, and malaria research will lay the foundation for sustainable change. Failure to recognize the toll of malaria as persistent evidence of inequitable global systems and patterns of resource allocation undermines our ability to reduce the global burden of malaria and sustain those improvements over time.

Robert Wood Johnson Health & Society Scholars Program for financial support of Dr. O'Neill and Ms. Stratton.

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Corresponding Author Contact In
10-16-2008, 01:00 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
Pollutants contaminating aquatic ecosystems may affect the health of fish either indirectly through their diet or directly by uptake from the water. Fish populations and health are a growing concern as they provide an increasingly important source of protein for humans and are part of the natural diet of both aquatic mammals and birds (Kime et al., 1996). It has been suggested that the cause of declining male reproductive health is related to synthetic substances that bioaccumulate and act as hormonally active substances, such as organochlorines (Skakkebaek and Keiding, 1994; Dalvie et al., 2004a). It is not surprising that even chemicals with a low affinity for a hormone receptor can still manage to compete with endogenous hormones for binding sites, given the increased levels of chemicals present in certain aquatic ecosystems and the relatively low levels of circulating hormones within a living organism (Alavi et al., 2008). It is often not clear if this is due to interference with the pituitary–hypothalamic system or to direct action on the testes themselves.
10-16-2008, 01:11 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
Drew, what does malaria have to do with CERN?
“Today’s scientists have substituted mathematics for experiments, and they wander off through equation after
equation, and eventually build a structure which has no relation to reality. ” -Nikola Tesla

"When the power of love overcomes the love of power the world will know peace." -Jimi Hendrix
10-16-2008, 01:27 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
les mal aryens en Geneve?
10-16-2008, 01:32 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
Quote:les mal aryens en Geneve?

10-16-2008, 01:55 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
no, too many tabs cause havoc, like the shoutbox turns into the searchfunction and then all the forcefully fashionable quoting. moderation please!

since 1+2=5 is so popular, wonder if there is a deeper meaning to it?

1521 = INRI, btw for some extra solarworship spice
bahai seem to be on the same enneadic trip of bondage and sacrifice.

back to particle torture for false intelligence.
10-16-2008, 02:08 AM,
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
Quote:no, too many tabs cause havoc

yup - we are trying to moderate everything into dedicated threads - without stemming th flow of things - the nature of causative thought makes it difficult..

hold onto your witch hat it's an ever ongoing process.

10-16-2008, 02:28 AM, (This post was last modified: 10-16-2008, 02:34 AM by drew hempel.)
World's biggest experiment to unlock secrets of Big Bang could cause the end of the world
I'm convinced that CERN is a huge Pavlovian Fear Learning System and Salvia is the defense against it:

Exposure to the selective kappa-opioid receptor agonist salvinorin A modulates the behavioral and molecular effects of cocaine in rats

Author(s): Chartoff EH (Chartoff, Elena H.), Potter D (Potter, David), Damez-Werno D (Damez-Werno, Diane), Cohen BM (Cohen, Bruce M.), Carlezon WA (Carlezon, William A., Jr.)
Source: NEUROPSYCHOPHARMACOLOGY Volume: 33 Issue: 11 Pages: 2676-2687 Published: OCT 2008
Times Cited: 0 References: 69 Citation MapCitation Map beta

Abstract: Stress and chronic exposure to drugs of abuse can trigger addictive and depressive disorders. Both stimuli increase activity of dynorphin, a neuropeptide that acts at kappa-opioid receptors (KORs). In humans, KOR agonists cause dysphoria, raising the possibility that dynorphin modulates the depressive-like effects of stress and chronic drug use. We examined if KOR activation alters sensitivity to stimulant drugs by assessing the effects of the selective KOR agonist, salvinorin A (SalvA), on cocaine-induced locomotor activity and c-Fos expression. Acute administration of SalvA blocked the locomotor-stimulant effects of cocaine, whereas repeated SalvA together with concomitant exposure to activity testing chambers potentiated the locomotor response to a cocaine challenge. In contrast, repeated SalvA administered in home cages rather than the activity chambers failed to potentiate the locomotor response to a cocaine challenge. One potential explanation for these findings is that activation of KORs disrupts context conditioning: acute locomotor responses to SalvA alone did not fully habituate with repeated testing in the activity chambers. The effects of SalvA on locomotor activity paralleled its effects on cocaine-induced c-Fos expression in the dorsal striatum: acute SalvA attenuated cocaine-induced c-Fos, whereas repeated SalvA potentiated it when administered in the activity chambers but not the home cage. Acute SalvA also blocked the locomotor stimulant effects of the D1 receptor agonist SKF 82958, whereas repeated SalvA potentiated these effects when administered in the activity chambers. These findings suggest that SalvA regulates the stimulant effects of cocaine through interactions with D1 receptor-mediated signaling in the dorsal striatum.
Document Type: Article
Language: English
Author Keywords: locomotor activity; c-Fos; dynorphin; striatum; dopamine; D1 receptor
Reprint Address: Chartoff, EH (reprint author), Harvard Univ, Sch Med, McLean Hosp, Dept Psychiat, MRC 218,115 Mill St, Belmont, MA 02478 USA
1. Harvard Univ, Sch Med, McLean Hosp, Dept Psychiat, Belmont, MA 02478 USA
2. Harvard Univ, Sch Med, McLean Hosp, Behav Genet Lab, Belmont, MA 02478 USA
3. Harvard Univ, Sch Med, McLean Hosp, Mol Pharmacol Lab, Belmont, MA 02478 USA

Opioid receptors in the midbrain periaqueductal gray regulate prediction errors during Pavlovian fear conditioning

Author(s): McNally GP, Cole S
Source: BEHAVIORAL NEUROSCIENCE Volume: 120 Issue: 2 Pages: 313-323 Published: APR 2006
Times Cited: 8 References: 53

Abstract: The authors used a within-subject blocking design to study the role of ventrolateral periaqueductal gray (vIPAG) opioid receptors in regulating prediction errors during Pavlovian fear conditioning. In Stage I, the authors trained rats to fear conditioned stimulus (CS) A by pairing it with shock. In Stage II, CSA and CSB were copresented and followed with shock. Two novel stimuli, CSC and CSD, were also copresented and followed with shock in Stage II. CSA blocked fear from accruing to CSB. Blocking was prevented by systemic pretreatment with naloxone. Blocking was also prevented in a dose-dependent and neuroanatomically specific fashion by vIPAG infusions of the mu-opioid receptor antagonist CTAP. These experiments show that vIPAG mu-opioid receptors contribute to Pavlovian fear learning by regulating predictive error.

Author Keywords: blocking; surprise; predictive learning; PAG; opiod
Reprint Address: McNally, GP (reprint author), Univ New S Wales, Sch Psychol, Sydney, NSW 2052 Australia
1. Univ New S Wales, Sch Psychol, Sydney, NSW 2052 Australia

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