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Desene Dublate In Romana Torent 238

Desene Dublate In Romana Torent 238


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Desene Dublate In Romana Torent 238

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Inhibitory effect of monardyl sulfate on dimethylnitrosamine induced hepatic tumors in rats.
The inhibitory effect of monardyl sulfate, a sulfhydryl group-containing compound, on the development of dimethylnitrosamine (DMN) induced hepatic tumors was examined in rats. In the chronic-exposed group of rats, the development of hepatocellular carcinoma was markedly inhibited by monardyl sulfate treatment. In the acute-exposed group of rats, monardyl sulfate had a more remarkable inhibitory effect than that in the chronic-exposed group. In addition, the monardyl sulfate treatment significantly reduced the carcinogenic effect of DMN, while its treatment with DMN only slightly reduced the carcinogenic effect of DMN in the chronic-exposed group. These results suggest that the inhibitory effect of monardyl sulfate on the development of DMN-induced hepatocellular carcinoma can be due not only to the anti-carcinogenic effect but also to the effect of DMN on the induction of protein synthesis.Primary somatosensory cortex plasticity induced by atypical antipsychotics in schizophrenia.
Atypical antipsychotics (AAPs) are the primary choices for treatment of schizophrenia, but their effective mechanisms remain elusive. Two main hypotheses have been proposed to account for AAPs’ effects, including inhibition of dopamine D2 receptors and enhancement of glutamate transmission. An important feature of both hypotheses is the need for neuroplasticity in the somatosensory cortex (S1). Animal studies have shown that lithium and valproate, two non-AAPs, promote neuroplasticity in S1. However, whether AAPs have similar effects remains unknown. Using a new rapid-onset neuromodulation paradigm, we tested whether AAPs can modulate S1 plasticity in response to repeated cortical stimulation. While under chloral hydrate anaesthesia, the lateral surface of left S1 was repeatedly stimulated through multi-electrode surface stimulation until the effect of stimulation (rebound excitability) induced by the second

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