Nephrotoxic effects of tetanus toxin: An ultrastructural study

Generalized nephrotoxicity was observed in the rat as early as 6 hr after intramuscular injection of 1000 of tetanus toxin. The most striking morphological changes, including swelling and rupture of the mitochondria, sloughing of the microvilli, and dissolution of cells, were found exclusively in the renal proximal tubule. Acute tubular necrosis with degeneration of the organelles and disruption of the cell membrane were also encountered throughout the entire nephron.Since these observations parallel those reported in patients with complicated acute tubular necrosis secondary to nephrotic syndrome and chemical toxicity, perhaps the kidney is one of the major targets in tetanus intoxication. It is possible that injury to the nephron results in electrolyte imbalance that can contribute to the neuromuscular manifestation accompanying tetanus toxicity.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/21937/1/0000344.pd

The cultural and geopolitical dimensions of nation-building in the Ukraine

Ukraine belongs among those young countries where the beginnings of democratisation and nation-building approximately coincided. While the development of nation states in Central Europe was usually preceded by the development of nations, the biggest dilemma in the Ukraine is whether a nation-state programme — parallel to the aim of state-building — is able to bring unfinished nation-building to completion. Ukraine sways between the EU and Russia with enormous amplitude. The alternating orientation between the West and the East can be ascribed to superpower ambitions reaching beyond Ukraine. Eventually, internal and external determinants are intertwined and mutually interact with one another. The aim of the paper is to explain the dilemmas arising from identity problems behind the Ukraine’s internal and external orientation

Epileptic seizures cause extended postictal cerebral vascular dysfunction that is prevented by HO-1 overexpression

The extended postictal state is characterized by neurological problems in patients. Inadequate blood supply to the brain and impaired cerebral autoregulation may contribute to seizure-induced neuronal damage. Recent evidence in newborn pigs indicates that activation of the antioxidative enzyme heme oxygenase (HO) at the onset of seizures is necessary for increased cerebral blood flow during the ictal episode and for normal cerebral vascular functioning during the immediate postictal period. We hypothesized that seizures cause prolonged postictal cerebral vascular dysfunction that can be accentuated by HO inhibition and rescued by HO overexpression. Cerebral vascular responses to endothelium-dependent ( hypercapnia, bradykinin) and - independent ( isoproterenol, sodium nitroprusside) stimuli were assessed 48 h after bicuculline-induced seizures in: 1) saline-control newborn piglets, 2) HO-inhibited animals ( HO was inhibited by tin protoporphyrin, SnPP, 3 mg/kg iv), and 3) HO-overexpressing piglets (HO-1 was upregulated by cobalt protoporphyrin, CoPP, 50 mg/kg ip). Extended alterations of HO expression in cerebral microvessels were confirmed by measuring CO production and inducible HO (HO-1) and constitutive HO (HO-2) proteins. Our data provide evidence that seizures cause a severe, sustained, postictal cerebral vascular dysfunction as reflected by impaired vascular reactivity to physiologically relevant dilators. During the delayed postictal state, vascular reactivity to all dilator stimuli was reduced in saline control and, to a greater extent, in HO-inhibited animals. In CoPP-treated piglets, no reduction in postictal cerebral vascular reactivity was observed. These findings may indicate that CoPP prevents postictal cerebral vascular dysfunction by upregulating HO-1, a finding that might have implications for preventing postictal neurological complications