Chinese Nationalism and the Fate of Tibet: Implications for India and Future Scenarios
Abstract Chinese nationalism primarily represents Han nationalism and ignores ethnic minority sub-nationalisms and identities in the larger cause of the state's unity and integrity. The Chinese state calls for submerging of all minority identities within the predominant Han identity, for promoting national cohesion and nationalism, effectively precluding the possibility of the assertion of Tibetan nationalism and autonomy. Because of the suppression of Tibetans in China, a large number of them have fled and settled in India and elsewhere. The Tibetan movement for safeguarding their identity, culture and political space has grievously suffered as a result of Chinese nationalism and China's Tibet policy. The fate of Tibetan nationalism is, to a large extent, tied to the dynamics of the Sino-Indian relations and the course of the internal Tibetan politics and that of its relationship with the community in exile in the post-Dalai Lama era.
Chinese Nationalism: The State of the Nation
It is not difficult to understand the worldwide upsurge of interest during the last decade in questions relating to the state, the nation and nationalism. The collapse of the Soviet Union and the emergence of new national states in its place; the fragmentation of Yugoslavia and the ensuing nationalist conflicts in the Balkans; evidence of ultra-nationalist sentiment in Russia, France and Germany; the systemic crisis affecting the national state in Africa; and unpredictable nationalist trends in China ? all these have aroused intense speculation about the capacity of national loyalties to survive peacefully, and about the meanings of concepts like nationalism in a world where so many political ideas are in doubt.
The bradykinin B1 receptor and the central regulation of blood pressure in spontaneously hypertensive rats
We evaluated if the brain bradykinin (BK) B1 receptor is involved in the regulation of blood pressure (BP) in conscious rats. Basal mean BP and HR were 115±2 and 165±3 mmHg and 345±10 and 410±14 beats min−1 in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR), respectively. Intracerebroventricular (i.c.v.) injection of 1 nmol B1 receptor agonist Lys‐desArg9‐BK significantly increased the BP of WKY and SHR by 7±1 and 19±2 mmHg, respectively. One nmol Sar[D‐Phe8]‐desArg9‐BK, a kininase‐resistant B1 agonist, increased the BP of WKY and SHR by 19±2 and 17±2 mmHg, respectively and reduced HR in both strains. I.c.v. injection of 0.01 nmol B1 antagonists, LysLeu8‐desArg9‐BK or AcLys[D‐βNal7,Ile8]‐desArg9‐BK (R715), significantly decreased mean BP in SHR (by 9±2 mmHg the former and 14±3 mmHg the latter compound), but not in WKY. In SHR, the BP response to R715 was associated to tachycardia. I.c.v. Captopril, a kininase inhibitor, increased the BP of SHR, this response being partially prevented by i.c.v. R715 and reversed into a vasodepressor effect by R715 in combination with the B2 antagonist Icatibant. I.c.v. antisense oligodeoxynucleotides (ODNs) targeted to the B1 receptor mRNA decreased BP in SHR, but not in WKY. HR was not altered in either strain. Distribution of fluorescein‐conjugated ODNs was detected in brain areas surrounding cerebral ventricles. Our results indicate that the brain B1 receptor participates in the regulation of BP. Activation of the B1 receptor by kinin metabolites could participate in the pathogenesis of hypertension in SHR.