Bronchiectasis is defined as the irreversible dilatation of the bronchi and is characterized by chronic cough, sputum, and recurrent exacerbation due to airway infection. The mechanisms underlying the dilatation of the bronchi have been explained as follows: chronic infection causes airway inflammation and epithelial injury with mucociliary dysfunction, resulting in persistent airway infection and inflammation that lead to airway wall destruction and ectasia of the bronchi in a vicious cycle. Intriguingly, the pathogenesis of bronchiectasis with rheumatoid arthritis (RA) or inflammatory bowel disease (IBD) has been interpreted in terms of its autoimmune mechanisms in recent years. Bronchiectasis shows an abnormal increase in the size of the bronchi and is easily identified by computed tomography. However, the diagnosis requires further investigation, as the etiology of bronchiectasis is diverse, e.g. post-infectious, immunodeficiency, mucociliary dysfunction, bronchial obstruction, allergic bronchopulmonary aspergillosis, and inflammatory conditions, such as RA and IBD. Careful investigation of these etiologies may aid in a precise diagnosis and the patient' s management. The care of patients with bronchiectasis involves physical therapies, pharmacological therapies, and, in some instances, surgical therapy. In the past quarter-century, significant achievements have been made in this field in the establishment of macrolide therapy for diffuse panbronchiolitis and its application to the other conditions with bronchiectasis; however, the treatment methods available for bronchiectasis are not yet satisfactory. Further clarification of the pathogenesis and development of effective therapeutic procedures are needed.

The ischemic penumbra is the region of the brain surrounding the ischemic core that receives limited blood supply via collateral circulation. When the occluded artery is not recanalized, the penumbra and the consequent neurological deficit worsen with time. Early recanalization after intravenous thrombolysis with tissue-type plasminogen activator (tPA; alteplase) improves dependence-free survival in patients with ischemic stroke. However, tPA is effective primarily in patients presenting without major arterial occlusion. Arterial recanalization and subsequent reperfusion with a stent retriever concomitant with the use of tPA greatly improve clinical outcomes even in those with large artery occlusion. Several randomized controlled trials have established the advantages of intra-arterial treatment in patients with acute ischemic stroke showing anterior large vessel occlusion, and these principles have been incorporated into clinical practice. However, some patients continue to show poor outcomes even after successful recanalization, which may be secondary to reperfusion injury. Inducing selective brain hypothermia by transarterial cooling may offer effective neuroprotection and could serve as a prospective/potential treatment strategy worth exploring for the management of reperfusion injury.