The thesis seeks to examine practices of British economic warfare towards Germany during the First World War. In particular it focuses on the development of methods to weaken the German will for war by convincing Germany that winning, a military victory would be pointless if it destroyed her commercial position. In doing so it brings together two separate elements of British economic warfare -trade war and control of raw materials - into a single strategy with a unified aim. It explores British attempts to destroy Germany's foreign trade organisation in order to induce German commercial interests to end to the war through fear of losing post-war markets. However, in attempting this Britain was hampered by wartime conditions which interrupted the provision of shipping, capital and goods needed to make the policy a permanent success. Many Germans believed their production and marketing methods would enable them to reclaim their share of world trade after the war. This was providing there was no punitive post-war penalisation of German trade. In June 1916 the Allies met in Pans to outline such a plan which involved the creation of an economic bloc to isolate Germany from the world trading system. At this point supplies rather than markets became the focus of economic warfare against Germany. With control of the world's raw materials, the Allies hoped to create an economic weapon capable of threatening German post-war recovery and thus have an important psychological impact on the German commercial mind-set. However such a scheme had to contend with the differing variables of Allied, American and Imperial interests. It is hoped the thesis will not only illuminate British economic policies during the First World War, but also contribute to the debate amongst historians on the relationship between international economic relations and foreign and security policies in the twentieth century.

Thesis (doctoral)--Georg-August-Universität zu Göttingen.

Thèse--Université de Zurich. / Vita. "Sources": p. [5]-9.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1937. / Typescript. Includes abstract and vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 214-222).

University, Diss., 2004--Freiburg (Breisgau).

No description available.

No description available.

Mechanical unloading and food restriction (FR) are leading causes of bone loss, which increase the risk of fracture later in life. Leptin, a 16kDa cytokine like hormone principally produced by white adipocytes, may be involved in bone metabolism with physiological or mechanical changes causing bone loss. The hypotheses of the first study were aimed at determining if serum leptin is reduced by unloading or FR. The serum leptin level reduced by unloading or by global FR, is associated with the decline in bone formation rate. It was conjectured that decreased serum leptin may be due to reduced adipocyte number/size and/or sympathetic nervous system (SNS) activation of betaadrenoreceptors with unloading or FR, inhibiting the release of leptin from adipocytes. In the second experiment, we tested whether leptin or beta-adrenoreceptor blockade attenuates bone loss during unloading and whether such an effect due to beta blockade is associated with changes in serum leptin level. Beta-blockade mitigated unloading induced reduction in serum leptin and also beta blockade was as effective as leptin administration in mitigating a reduction in cancellous bone mineral density with unloading through both stimulation of bone formation and suppression of resorption. It was previously demonstrated that energy restriction (ER) is a major contributor to the bone loss during global FR. In the third study, we tested whether beta- blockade attenuates bone loss during ER and whether such an effect is associated with changes in serum leptin level and leptin localization in bone tissues. Beta blockade attenuated the ER induced reduction in serum leptin level, cancellous bone mineral density and bone formation rate, and also abolished the ER induced increase in bone resorption. Reduction in leptin expression in bone marrow adipocytes observed with ER was attenuated by beta-blockade. Reduction in the number of cells (bone lining cells, osteocytes and chondrocytes in cartilage) which are stained positive for leptin was also attenuated by beta-blockade. Collectively, these data identify circulating leptin effects on preventing bone loss during mechanical unloading or energy restriction. Also beta blockade is associated with mitigating reduction in serum leptin and subsequently with mitigating reduction in bone mass with unloading or ER.

Thesis--University of Pennsylvania. / Reprint of the 1919 ed. Bibliography: p. 378-413.

Inaug.-diss.--Bonn. / Lebenslauf. "Literatur": p. [98]-100.