Sugar also led to some industrialization of areas where sugar cane was grown. For example, Lieutenant J. Paterson, of the Bengal establishment, persuaded the British Government that sugar cane could be cultivated in British India with many advantages and at less expense than in the West Indies; as a result, sugar factories were established in Bihar in eastern India.  During the Napoleonic Wars , sugar beet production increased in continental Europe because of the difficulty of importing sugar when shipping was subject to blockade . By 1880, the sugar beet was the main source of sugar in Europe. It was cultivated in Lincolnshire and other parts of England, although the United Kingdom continued to import the main part of its sugar from its colonies. 
In July 2011, FDA began a pilot program to notify people of drug recalls before they are classified in an effort to expedite notifications of human drug product recalls to the public. FDA is now able to accomplish the goal of expedited notification within the Enforcement Report. These recalls are identified within the Enforcement Report by the label of “Not Yet Classified” in the “Classification” column. It is also possible to search the Enforcement Report for these “Not Yet Classified” recalls using the filter drop down menu. Therefore, as of September 15, 2017 FDA will discontinue the pilot program, and will no longer post drug recalls that are pending classification on this webpage. To see posted recalls that are pending classification go to the weekly Enforcement Report.
Known or suspected deficiency in protein C mediated anticoagulant response: Hereditary or acquired deficiencies of protein C or its cofactor, protein S, have been associated with tissue necrosis following warfarin administration. Not all patients with these conditions develop necrosis, and tissue necrosis occurs in patients without these deficiencies. Inherited resistance to activated protein C has been described in many patients with venous thromboembolic disorders but has not yet been evaluated as a risk factor for tissue necrosis. The risk associated with these conditions, both for recurrent thrombosis and for adverse reactions, is difficult to evaluate since it does not appear to be the same for everyone. Decisions about testing and therapy must be made on an individual basis. It has been reported that concomitant anticoagulation therapy with heparin for 5 to 7 days during initiation of therapy with warfarin sodium may minimize the incidence of tissue necrosis. Warfarin therapy should be discontinued when warfarin is suspected to be the cause of developing necrosis and heparin therapy may be considered for anticoagulation.