"Feed from the Service": Corruption and Coercion in the State-University Relations in Central Eurasia

Education in Central Eurasia has become one of the industries, most affected by corruption. Corruption in academia, including bribery, extortions, embezzlement, nepotism, fraud, cheating, and plagiarism, is reflected in the region’s media and addressed in few scholarly works. This paper considers corruption in higher education as a product of interrelations between the government and academia. A substantial block of literature considers excessive corruption as an indicator of a weak state. In contrast to standard interpretations, this paper argues that in non-democratic societies corruption is used on a systematic basis as a mechanism of direct and indirect administrative control over higher education institutions. Informal approval of corrupt activities in exchange for loyalty and compliance with the regime may be used in the countries of Central Eurasia for the purposes of political indoctrination. This paper presents the concept of corruption and coercion in the state-university relations in Central Eurasia and outlines the model which incorporates this concept and the “feed from the service” approach. It presents implications of this model for the state-university relations and the national educational systems in Central Eurasia in general and offers some suggestions on curbing corruption

Losartan Decreases p42/44 MAPK Signaling and Preserves LZ+ MYPT1 Expression

Heart failure is associated with impairment in nitric oxide (NO) mediated vasodilatation, which has been demonstrated to result from a reduction in the relative expression of the leucine zipper positive (LZ+) isoform of the myosin targeting subunit (MYPT1) of myosin light chain phosphatase. Further, captopril preserves normal LZ+ MYPT1 expression, the sensitivity to cGMP-mediated vasodilatation and modulates the expression of genes in the p42/44 MAPK and p38 MAPK signaling cascades. This study tests whether angiotensin receptor blockade (ARB) with losartan decreases p42/44 MAPK or p38 MAPK signaling and preserves LZ+ MYPT1 expression in a rat infarct model of heart failure. In aortic smooth muscle, p42/44 MAPK activation increases and LZ+ MYPT1 expression falls after LAD ligation. Losartan treatment decreases the activation of p42/44 MAPK to the uninfarcted control level and preserves normal LZ+ MYPT1 expression. The expression and activation of p38 MAPK, however, is low and does not change following LAD ligation or with losartan therapy. These data suggest that either reducing or blocking the effects of circulating angiotensin II, both decreases the activation of the p42/44 MAPK signaling cascade and preserves LZ+ MYPT1 expression. Thus, the ability of ACE-inhibitors and ARBs to modulate the vascular phenotype, to preserve normal flow mediated vasodilatation may explain the beneficial effects of these drugs compared to other forms of afterload reduction in the treatment of heart failure