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(1975). Early African leadership: the Copperbelt disturbances of 1935 and 1940. Journal of Southern African Studies: Vol. 2, No. 1, pp. 83-97.

This article draws attention to the comparative lack of material on the origins of African nationalism in Zambia, and suggests a framework of analysis and possible future areas of research on the subject. In contrast with some other East and Central African territories, Zambia offered little or no primary resistance to the imposition of colonial rule, but in other respects the country resembled neighbouring territories in the first three decades of colonial rule. There is a need for further study of Watch Tower and the Welfare Associations, the former in the inter-war years, the latter in the 1940s. The Copperbelt from 1930 to 1950, with its problems of urbanization and the colour bar, is a vital factor setting Zambia apart from other tropical dependencies. Here, Africans were confronted with the determination of Europeans to retain political and economic power, whatever the policy declarations of the government. The politicization of the territory can be traced from here, and the role of the Bemba-speaking peoples as the spearhead of protest had its origin in their powerful position on the Copperbelt.

The question of populism in Uganda was investigated by Professor D. A. Low in this journal in 1964.1 He argued that the concept of populism was appropriate to describe the political agitation by the independent small landholders and poor peasants against the breakdown of the traditional hierarchical structure of Buganda under the impact of colonial rule. The populists were particularly concerned to reduce their economic disabilities through control of the marketing system for cotton, but at the same time were concerned to articulate ‘the kingdom's corporate solidarity’. To that extent Buganda populism was socially conservative, though it may have seemed radical to the colonial rulers.

Proteolytic processing of the amiloride-sensitive epithelial sodium channel (ENaC) by serine proteases is known to be important for channel activation. Inappropriate ENaC activation by proteases may contribute to the pathophysiology of cystic fibrosis and could be involved in sodium retention and the pathogenesis of arterial hypertension in the context of renal disease. We hypothesized that in addition to serine proteases, cathepsin proteases may activate ENaC. Cathepsin proteases belong to the group of cysteine proteases and play a pathophysiological role in inflammatory diseases. Under pathophysiological conditions, cathepsin-S (Cat-S) may reach ENaC in the apical membrane of epithelial cells. The aim of this study was to investigate the effect of purified Cat-S on human ENaC heterologously expressed in Xenopus laevis oocytes and on ENaC-mediated sodium transport in cultured M-1 mouse renal collecting duct cells. We demonstrated that Cat-S activates amiloride-sensitive whole-cell currents in ENaC-expressing oocytes. The stimulatory effect of Cat-S was preserved at pH 5. ENaC stimulation by Cat-S was associated with the appearance of a γENaC cleavage fragment at the plasma membrane indicating proteolytic channel activation. Mutating two valine residues (V182 and V193) in the critical region of γENaC prevented proteolytic activation of ENaC by Cat-S. Pre-incubation of the oocytes with the Cat-S inhibitor morpholinurea-leucine-homophenylalanine-vinylsulfone-phenyl (LHVS) prevented the stimulatory effect of Cat-S on ENaC. In contrast, LHVS had no effect on ENaC activation by the prototypical serine proteases trypsin and chymotrypsin. Cat-S also stimulated ENaC in differentiated renal epithelial cells. These findings demonstrate that the cysteine protease Cat-S can activate ENaC which may be relevant under pathophysiological conditions.