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This book revisits the long contested negotiation between the Thatcher administration and Nissan for the latter's first green-field plant in Europe. From the very beginning, the plant took Britain’s EC/EU membership and tariff-free access to the single market as a token. A considerable amount of aid including component supplies was provided to attract Japanese investment and to prevent its transfer to the continent. The successful launch of Sunderland highlighted improved Anglo-Japanese relations and put an end to the Japan-EC/EU trade conflict. But the price was paid by Nissan’s slump and fall, and by trade unions in both countries failing to keep counterchecks on management. Brexit and the fall of Carlos Ghosn were a double blow to Anglo-Japanese relations which are in a state of drift and need redefinition.

History, Modern. --- International relations. --- European Economic Community literature. --- Trade. --- Business. --- Commerce. --- Modern History. --- International Relations. --- European Integration. --- Trade --- Economics --- Business --- Transportation --- Management --- Commerce --- Industrial management --- Coexistence --- Foreign affairs --- Foreign policy --- Foreign relations --- Global governance --- Interdependence of nations --- International affairs --- Peaceful coexistence --- World order --- National security --- Sovereignty --- World politics --- Modern history --- World history, Modern --- World history --- Investments, Japanese --- Labor unions --- History --- Industrial unions --- Labor, Organized --- Labor organizations --- Organized labor --- Trade-unions --- Unions, Labor --- Unions, Trade --- Working-men's associations --- Labor movement --- Societies --- Central labor councils --- Guilds --- Syndicalism --- Japanese investments

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Muziekanalyses --- Travail de fin d'études (TFE)

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Kurds --- Kurds

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IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and a frequent cause of kidney failure. Better understanding of the pathogenesis of IgAN and the related genetic, immunological, and cellular susceptibility factors are needed to enable the development of effective disease-specific therapy. This book brings together international experts to provide clinical and experimental studies and reviews with an emphasis on early diagnosis, prognosis, disease pathogenesis, determination of disease activity, and new strategies for treatment for IgAN.

Medicine --- obesity --- mesangial matrix expansion --- body mass index --- IgA nephropathy --- IgA Vasculitis --- IgA Nephropathy --- adults --- children --- presentation --- physiopathology --- genetics --- prognosis --- treatment --- IgA --- clinical trials --- kidney mesangium --- mouse model --- aberrantly glycosylated IgA1 --- galactose-deficient IgA1 --- glycosylation of IgA1 --- biomarker --- complement C3 --- O-glycosylation --- IgA1 --- autoantibody --- immune complex --- complement --- kidney --- nephrology --- IgA vasculitis --- nephritis --- kidney biopsy --- plasma cells --- CD38 --- renal pathology --- urinary galactose-deficient IgA1 --- KM55 --- crescents --- proteinuria --- glomerular filtration rate --- Oxford score --- n/a

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IgA nephropathy (IgAN) is the most common form of primary glomerulonephritis worldwide and a frequent cause of kidney failure. Better understanding of the pathogenesis of IgAN and the related genetic, immunological, and cellular susceptibility factors are needed to enable the development of effective disease-specific therapy. This book brings together international experts to provide clinical and experimental studies and reviews with an emphasis on early diagnosis, prognosis, disease pathogenesis, determination of disease activity, and new strategies for treatment for IgAN.

Medicine --- obesity --- mesangial matrix expansion --- body mass index --- IgA nephropathy --- IgA Vasculitis --- IgA Nephropathy --- adults --- children --- presentation --- physiopathology --- genetics --- prognosis --- treatment --- IgA --- clinical trials --- kidney mesangium --- mouse model --- aberrantly glycosylated IgA1 --- galactose-deficient IgA1 --- glycosylation of IgA1 --- biomarker --- complement C3 --- O-glycosylation --- IgA1 --- autoantibody --- immune complex --- complement --- kidney --- nephrology --- IgA vasculitis --- nephritis --- kidney biopsy --- plasma cells --- CD38 --- renal pathology --- urinary galactose-deficient IgA1 --- KM55 --- crescents --- proteinuria --- glomerular filtration rate --- Oxford score --- obesity --- mesangial matrix expansion --- body mass index --- IgA nephropathy --- IgA Vasculitis --- IgA Nephropathy --- adults --- children --- presentation --- physiopathology --- genetics --- prognosis --- treatment --- IgA --- clinical trials --- kidney mesangium --- mouse model --- aberrantly glycosylated IgA1 --- galactose-deficient IgA1 --- glycosylation of IgA1 --- biomarker --- complement C3 --- O-glycosylation --- IgA1 --- autoantibody --- immune complex --- complement --- kidney --- nephrology --- IgA vasculitis --- nephritis --- kidney biopsy --- plasma cells --- CD38 --- renal pathology --- urinary galactose-deficient IgA1 --- KM55 --- crescents --- proteinuria --- glomerular filtration rate --- Oxford score