Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma.As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling.Anti-inflammatory therapy, however, does not ''cure'' asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM.In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.

Asthma is a chronic inflammatory disease of the airways in which the majority of patients respond to treatment with corticosteroids and b 2 -adrenoceptor agonists. Acute exacerbations of asthma substantially contribute to disease morbidity, mortality and healthcare costs, and are not restricted to patients who are not compliant with their treatment regimens. Given that respiratory viral infections are the principal cause of asthma exacerbations, this review article will explore the relationship between viral infections and asthma, and will put forward hypotheses as to why virus-induced exacerbations occur. Potential mechanisms that may explain why current therapeutics do not fully inhibit virus-induced exacerbations, for example, b 2 -adrenergic desensitisation and corticosteroid insensitivity, are explored, as well as which aspects of virus-induced inflammation are likely to be attenuated by current therapy. @ERSpublications Why do virus-induced asthma exacerbations occur? Mechanisms and interventions

Gametogenesis and ovarian development were examined by means of histologic, cytologic and radioisotopic techniques in porcine ovaries of ages ranging from 13 days post coitum (PC) to birth (114 days PC). Limited observations were made i n postnatal ovaries (birth to 130 days post parturn).Primordial germ cells were noted at 18 days PC in the region of the germinal ridge (border of mesonephros) seven days prior to its formation (24-25 days). Meiosis began as early as day 40 in some cases and was a characteristic of most ovaries by day 50.Diplotene, the resting stage of porcine oocytes, first appeared at 50 days PC and 99% of all germ cells were at diplotene by 20 days p o s t partum. Both the paucity of oogonia and absence of oogonial mitoses at day 100 PC signaled the end of oogenesis.