Concomitant rotavirus serotypes 1 and 4 infections in a diarrhoeic child from Belém, Brazil

With the discussion of the quality of medical education in Germany the importance of evaluating the curriculum has grown. A working group of representatives of the German scientific societies for general medicine and the so-called "psychosocial" disciplines in medical education had adapted a questionnaire from Harvard Medical School and tested this version for the first time in summer 1995. 56 teachers and 1250 students took part in this pilot study. The instrument proved to be sufficiently valid to evaluate the quality of different types of teaching lessons. The disciplines (Medical Sociology, Medical Psychology, Social Medicine, General Medicine, Psychotherapy/Psychosomatics) were valued equally with concern to their relevance for medical education. They got significantly better values for quality of teaching and teaching engagement of the professors. It is recommended to notice these results in the actual debate on the reform of the medical curriculum and to include other disciplines in further evaluative investigations.     

Sequential Dynamic Logic

We introduce a substructural propositional calculus of Sequential Dynamic Logic that subsumes a propositional part of dynamic predicate logic, and is shown to be expressively equivalent to propositional dynamic logic. Completeness of the calculus with respect to the intended relational semantics is established.     

Reactive automata

A reactive automaton has extra links whose role is to change the behaviour of the automaton. We show that these links do not increase the expressiveness of finite automata but that they can be used to reduce dramatically their state number both in the deterministic case and the non-deterministic case.Typical examples of regular expressions associated with deterministic automata of exponential size according to the length of the expression show that reactive links provide an alternative representation of total linear size for the language.     

Capture-avoiding substitution as a nominal algebra

Substitution is fundamental to the theory of logic and computation. Is substitution something that we define on syntax on a case-by-case basis, or can we turn the idea of substitution into a mathematical object? We give axioms for substitution and prove them sound and complete with respect to a canonical model. As corollaries we obtain a useful conservativity result, and prove that equality-up-to-substitution is a decidable relation on terms. These results involve subtle use of techniques both from rewriting and algebra. A special feature of our method is the use of nominal techniques. These give us access to a stronger assertion language, which includes so-called ‘freshness’ or ‘capture-avoidance’ conditions. This means that the sense in which we axiomatise substitution (and prove soundness and completeness) is particularly strong, while remaining quite general.     

Embedding and automating conditional logics in classical higher-order logic

A sound and complete embedding of conditional logics into classical higher-order logic is presented. This embedding enables the application of off-the-shelf higher-order automated theorem provers and model finders for reasoning within and about conditional logics.     

A redox-based mechanism for the neuroprotective and neurodestructive effects of nitric oxide and related nitroso-compounds

Congeners of nitrogen monoxide (NO) are neuroprotective and neurodestructive. To address this apparent paradox, we considered the effects on neurons of compounds characterized by alternative redox states of NO: nitric oxide (NO.) and nitrosonium ion (NO+). Nitric oxide, generated from NO. donors or synthesized endogenously after NMDA (N-methyl-D-aspartate) receptor activation, can lead to neurotoxicity. Here, we report that NO.- mediated neurotoxicity is engendered, at least in part, by reaction with superoxide anion (O2.-), apparently leading to formation of peroxynitrite (ONOO-), and not by NO. alone. In contrast, the neuroprotective effects of NO result from downregulation of NMDA-receptor activity by reaction with thiol group(s) of the receptor's redox modulatory site. This reaction is not mediated by NO. itself, but occurs under conditions supporting S-nitrosylation of NMDA receptor thiol (reaction or transfer of NO+). Moreover, the redox versatility of NO allows for its interconversion from neuroprotective to neurotoxic species by a change in the ambient redox milieu. The details of this complex redox chemistry of NO may provide a mechanism for harnessing neuroprotective effects and avoiding neurotoxicity in the central nervous system.     

The modulatory role of nitric oxide in the regulation of proenkephalin and prodynorphin gene expressions induced by kainic acid in rat hippocampus

The effect of L-arginine (L-ARG), a nitric oxide donor, or Nomega-nitro-L-arginine (L-NAME), a nitric oxide synthase inhibitor, on the regulation of kainic acid (KA)-induced proenkephalin (proENK) and prodynorphin (proDYN) mRNA expressions in rat hippocampus was studied. The proENK and proDYN mRNA levels were markedly increased 6 h after KA (10 mg/kg, i.p.) administration. The elevations of both proENK and proDYN mRNA levels induced by KA was effectively inhibited by pre-administration of L-ARG (400 mg/kg, i.p.), but was not affected by pre-treatment with L-NAME (200 mg/kg, i.p.). The blockade of KA-induced proENK and proDYN mRNA levels by the pre-treatment with L-ARG was well correlated with proto-oncoprotein levels, such as c-Fos, Fra-2, FosB, JunD, JunB, and c-Jun, as well as AP-1 and ENKCRE-2 DNA binding activities. The pre-administration with L-NAME further increased KA-induced c-jun and c-fos mRNA levels in addition to their protein product levels, although the pre-treatment with L-NAME did not affect KA-induced FosB, Fra-2, JunB, and JunD protein levels at 6 h after treatment. In addition, the pre-administration with L-NAME further increased the KA-induced AP-1 and ENKCRE-2 DNA binding activities. Our results suggest that L-ARG plays an important role in inhibiting KA-induced proENK or proDYN mRNA expression, and its inhibitory action may be mediated through reducing the proto-oncoprotein levels, such as c-Fos, Fra-2, FosB, c-Jun, JunD, and JunB. In addition, L-NAME potentiated the c-Fos or c-Jun gene expression, as well as AP-1 or ENKCRE-2 DNA binding activity. However, these increases did not show the potentiative effect on KA-induced increases of proENK and proDYN mRNA level.