Managerial case study, In 2012, the Copenhagen City administration released the 2012 CPH2025 Climate Plan, thereby becoming the first capital city in the world to commit itself to achieving carbon dioxide (CO2) neutrality by 2025. The plan envisaged collaborative efforts by various stakeholders including city authorities, the private sector, utilities, universities, and citizens. The climate plan was an important element of the city's green growth strategy. The strategy also aimed at the city becoming an important player in the growing global market for green technology. The deployment of the technology and implementation of measures was expected to generate jobs and income to the city as well.

The climate plan envisaged implementation of initiatives in four important areas viz., energy consumption, energy production, mobility, and city administration. Earlier, in 2009, the Copenhagen City Council had set itself the target of reducing carbon emissions by 20 per cent by 2015 compared to the levels in 2005 and also announced its vision of achieving carbon neutrality by 2025. The target was achieved in 2011 itself, well ahead of schedule.

An interesting aspect of the initiative was the involvement of the city's residents. Half of the investment in the wind generators planned as part of the initiative came from individual Copenhagen shareholders.

In recognition of its consistent record of achieving high environmental standards and its commitment to ambitious goals, Copenhagen city received the 2014 European Green Capital Award from the European Commission. The award also recognized the unique characteristic of Copenhagen as a Cyclist's Dream and the good buy-in that the city obtained from all its stakeholders for the initiative to promote cycling.

Question 63 Last week, in a neurology viva, I was asked about the indications for heparinization in patients with a stroke. I want to know when I can stop heparin and what test I should use for assessing its therapeutic range. Question 64 Has heparin a role in the management of acute ischaemic stroke not accompanied by atrial fibrillation? Question 65 1. In the treatment of a stroke, does low-molecular-weight heparin (LMWH) have an advantage over heparin? 2. In an ischaemic stroke in evolution, for how long should heparin be administered? Question 66 Can streptokinase be used in acute cerebral infarction and, if so, what is the dose? Question 67 There seems now to be a consensus about starting aspirin therapy in acute ischaemic strokes as early as possible. Why has this changed from past recommendations to avoid aspirin early (during the first 48 hours) during the ischaemic stroke on the pretext that it could convert an ischaemic infarct into a haemorrhagic one, thus increasing the dangers of complications like cerebral oedema and raised intracranial pressure? If both opinions are based on clinical trials, what is the significance of the much hyped 'evidence-based medicine'? Question 68 I understand that a loading dose of clopidogrel 600-900 mg can be given to ischaemic stroke in evolution and can stop the evolving deficit. Would you agree? Question 69 Is there any rationale for giving patients with recurrent strokes a combination of aspirin and anticoagulant? Question 70 1. Does a dipyridamol-aspirin combination have any superiority over aspirin alone in the secondary prevention of a stroke? 2. Is an aspirin plus anticoagulant combination superior to a dipyridamol aspirin combination in the treatment of recurrent ischaemic stroke not controlled by aspirin alone? Question 71 1. Is it safe to give piracetam to patients with primary intracerebral haemorrhage? Does it have a neuroprotective effect? 2. Is it safe to give a patient with excessively high blood pressure (as a sequela to recent primary intracerebral haemorrhage) angiotensin-converting enzyme inhibitors to lower the blood pressure? 3. Is it indicated to give piracetam or vincamine to a patient with middle cerebral artery territorial infarction? Do these have any neuroprotective effect? Question 72 What is the mechanism by which subarachnoid haemorrhage is associated with subhyaloid haemorrhages on fundus examination, and how can cerebrospinal fluid (CSF) gain access to the subhyaloid space inside the eye? Question 73 What is the recommended dosage for nimodipine given intravenously in cases of subarachnoid haemorrhage, and when should the treatment start? For how long should the dose be continued?