Surface tension as a function of concentration and temperature was measured for solutions of N-acyl sarcosinates, RCON(CH 3 )CH 2 COONa. From the intersection points in the (γ-log c) curves, the critical micelle concentration (CMC) was determined at 20, 35, 50, and 65°C. Structural effects on the CMC, maximum surface excess, and the minimum area per molecule at the aqueous solution/air interface are discussed. The free energy, enthalpy, and entropy of micellization and adsorption of surfactant solutions also were investigated. JAOCS 74, 43-47 (1997).
Summary:Purpose: Amygdala kindling is an epilepsy model involving long-term network plasticity in the nervous system. In this model, repeated weak stimulation of the amygdala eventually leads to severe motor seizures. The mechanisms for worsening behavioral seizures, and the possible role of enhanced connectivity between the amygdala and other structures have not been thoroughly investigated.Methods: We performed simultaneous field potential recordings from the amygdala, frontal cortex, and medial thalamus during kindling in rats. Seizures were analyzed for signal power compared with baseline and for correlation between recording sites. Interictal signals were analyzed for changes in coherence between electrode contacts in kindled animals compared with sham kindled controls.Results: We found that increased behavioral severity of seizures was related to increased seizure duration and to increased signal power in the frontal cortex and medial thalamus. Kindling was associated with increased connectivity between the amygdala and frontal cortex, based on increased amygdalafrontal signal correlation during seizures. In addition, during the interictal period, increased coherence was noted between amygdala and frontal contacts in kindled animals compared with controls.Conclusions: We found evidence for increased connectivity between the amygdala and frontal cortex both during seizures and in the interictal period, as a result of kindling. Enhanced connections between limbic and neocortical circuits may be important for the development of epilepsy, as well as for normal long-range network plasticity in the nervous system.
This study was conducted to evaluate the potency of the newly prepared germanium L-cysteine a-tocopherol complex [germanium dichloro tetrakis (L-cysteinyl-a-tocopherol amide) dichloride] as a protective agent against g-irradiation-induced free radicals production and liver toxicity. Male Swiss albino rats were injected intraperitoneally with the germanium complex in a concentration of 75 mg kg -1 body mass per dose, for 6 successive doses, last dose administered twenty minutes pre-exposure to a single dose of whole body g-irradiation of 6.5 Gy. Lipid peroxidation (LPx), nitric oxide (NO), glutathione (GSH) levels, and activity of the antioxidant enzymes glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) were estimated in blood and liver. Blood total protein, cholesterol, triglyceride and a-tocopherol content were estimated as well. The results revealed that administration of germanium complex pre-irradiation resulted in significant (p < 0.001) improvement compared to the irradiated group in the level of hepatic and blood LPx. Hepatic GSH revealed a significant increase (p < 0.001), while its level showed no significant variation in blood. Also, the level of NO in blood and liver increased significantly (p < 0.001). On the other hand, pretreatment with the germanium complex normalized the activities of SOD, GPx and CAT in blood and liver when compared to the irradiated group. The study also documents a marked decrease in a blood triglyceride and cholesterol (p < 0.001) and a significant increase (p < 0.001) of a-tocopherol and total protein contents in blood. These biochemical changes were associated with marked improvement of histological status. Therefore, the germanium L-cysteine a-tocopherol complex may be a good candidate for ameliorating the changes induced by irradiation, which indicates the beneficial radio-protective role of this antioxidant agent.
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