9 research outputs found

    Quo vadis \u3ci\u3eEquus hemionus hemionus\u3c/i\u3e in Mongolia?

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    Caused in studies on biodiversity in the South Gobi we were confronted with the human impact on animal communities and endangered animal species, especially the Asiatic wild ass. So was born the idea to organize an international conference with the aim to actualize the status of Equus hemionus in Central Asia and to find ways for better conservation of this species and its habitats. A short review is given on historical exploration, decreasing area and population number of the Dschiggetai. Today the range of the nominate form of Equus hemionus is located in the Gobi region of southern Mongolia/northern China only. Therefore international engagement is necessary to save this indicator species of the arid zone of Central Asia

    Decay-Accelerating Factor Suppresses Complement C3 Activation and Retards Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient Mice

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    Decay-accelerating factor (DAF; CD55) is a membrane protein that regulates complement pathway activity at the level of C3. To test the hypothesis that DAF plays an essential role in limiting complement activation in the arterial wall and protecting from atherosclerosis, we crossed DAF gene targeted mice (daf-1−/−) with low-density lipoprotein-receptor deficient mice (Ldlr−/−). Daf-1−/−Ldlr−/− mice had more extensive en face Sudan IV staining of the thoracoabdominal aorta than Ldlr−/− mice, both following a 12-week period of low-fat diet or a high-fat diet. Aortic root lesions in daf-1−/−Ldlr−/− mice on a low-fat diet showed increased size and complexity. DAF deficiency increased deposition of C3d and C5b-9, indicating the importance of DAF for downstream complement regulation in the arterial wall. The acceleration of lesion development in the absence of DAF provides confirmation of the proinflammatory and proatherosclerotic potential of complement activation in the Ldlr−/− mouse model. Because upstream complement activation is potentially protective, this study underlines the importance of DAF in shielding the arterial wall from the atherogenic effects of complement

    Atherosclerosis

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    In this chapter, we discuss the manner through which the immune system regulates the cardiovascular system in health and disease. We define the cardiovascular system and elements of atherosclerotic disease, the main focus in this chapter. Herein we elaborate on the disease process that can result in myocardial infarction (heart attack), ischaemic stroke and peripheral arterial disease. We have discussed broadly the homeostatic mechanisms in place that help autoregulate the cardiovascular system including the vital role of cholesterol and lipid clearance as well as the role lipid homeostasis plays in cardiovascular disease in the context of atherosclerosis. We then elaborate on the role played by the immune system in this setting, namely, major players from the innate and adaptive immune system, as well as discussing in greater detail specifically the role played by monocytes and macrophages.This chapter should represent an overview of the role played by the immune system in cardiovascular homeostasis; however further reading of the references cited can expand the reader's knowledge of the detail, and we point readers to many excellent reviews which summarise individual immune systems and their role in cardiovascular disease

    Bibliography

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    Immunological aspects of atherosclerosis

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    Platelet–neutrophil interactions under thromboinflammatory conditions

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