[Comments concerning a series of 25 cases of omphalocele].
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Biomedical subjects
Publications and source records attributed to D Richard.
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Latency distribution of responses to optic nerve stimulation has been compared between the Lateral Geniculate Nucleus (L.G.N.) and Superior Colliculus (S.C.), in rabbits. Histograms revealed that in both structures the latency distributions are very similar. Results suggest that all groups of retinofugal fibers project to both sites, although longer latencies are more frequently met at the collicular level. In addition evidence is presented that in rabbit's optic nerve there are at least three populations of axons with different conduction velocities.
The objective of the present study was to determine the combined effects of dietary protein and carbohydrate sources on total body energy and protein and fat gains as well as on plasma insulin and glucose and tissue lipoprotein lipase activity in male Sprague-Dawley rats fed semipurified diets for 28 days. The diets varied in both protein and carbohydrate sources, namely, casein-cornstarch, casein-sucrose, soy protein isolate (SPI)-cornstarch, SPI-sucrose, cod protein-cornstarch, and cod protein-sucrose. When SPI was combined with cornstarch, lower total body energy and fat gains were observed compared with the combination of either casein and sucrose, casein and cornstarch, or SPI and sucrose. Plasma glucose and insulin concentrations in addition to total and metabolizable energy intake and body weight gain were lower in rats fed the SPI-cornstarch diet than in those fed the casein-sucrose diet. Feeding the SPI-cornstarch diet compared with feeding either the casein-cornstarch or the SPI-sucrose diet also caused lower plasma glucose concentrations and a concomitant trend (p = 0.06) to reduced energy intake and body weight gain. Therefore, the reducing effects of the SPI-cornstarch diet compared with the casein-cornstarch, the casein-sucrose, and the SPI-sucrose diets on body energy and fat gains may result from reductions in energy intake and in plasma glucose concentrations.
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Toxoplasma gondii (Me49 strain) infection into Swiss Webster mice is followed by hypermetabolism and weight loss in the acute phase lasting 14 days. In the subsequent chronic phase of infection, mice showed either a resolution of hypermetabolism and partial weight recovery (Gainers) or persistent hypermetabolism, with stable weight loss (Non-Gainers). The hypermetabolic response was not associated with an augmentation in the thermogenic uncoupling protein 1 (UCP1) mRNA expression in interscapular brown adipose tissue (BAT), but rather UCP1 expression was reduced. Hypermetabolism is associated with high lipid oxidation as attested by a low respiratory quotient (RQ). Neither BAT nor sympathetic nervous system appear to be involved in the increased lipid utilization, since propranolol did not increase the lower RQ in infected mice. The mitochondrial lipid oxidation blocker mercaptoacetate did not reestablish the respiratory quotient RQ in acute infection (on day 4) and in chronically infected Non-Gainer mice. This suggests an important extra-mitochondrial mechanism of lipid oxidation. Increased lipid peroxidation was detected especially in serum, lung, spleen and liver, which are rich in macrophage-type cells. Following infection peritoneal macrophages exhibited an enhanced capacity to produce reactive oxygen species (ROS). Using IFN-gamma knockout mice we observed that not only the hypermetabolic response was ablated in these mice but there was not a marked increase in ROS production or preferential oxidation/peroxidation of lipids in the acute phase of infection prior to the cachectic phase. The present study described a novel hypermetabolic mechanism involving enhanced lipid peroxidation dependent on IFN-gamma, especially associated with tissues rich in macrophages.
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Intraperitoneal (IP) or intraportal epinephrine (E) administration produces strong hypophagia in rats whereas intravenous or intramuscular (IM) injection does not. These results suggest that E acts on liver to control food intake through vagal afferents to the brain. In the present work, immediate-early gene c-fos expression was used as an index of neuronal activity, comparing the respective effects of IP and IM E on food intake and on activation of brain areas that receive vagal information. Male Wistar rats were IP or IM injected with saline or E (100 micrograms/kg). In a first experiment, food intake was measured. In a second experiment, c-fos expression in different brain areas was assessed immunohistochemically. IP E administration reduced food intake by 75% (p < 0.01) whereas IM E had no effect. C-fos expression results showed that those solitary tract nucleus/area postrema regions receiving gastrointestinal and hepatic vagal afferents were specifically activated by IP E administration. These results support the possibility that E decreases food intake through a hepatic action involving vagal sensory neurons. However, higher integration levels of vagal information, such as lateral parabrachial nucleus or paraventricular nucleus, do not seem to be implicated in IP E effect on food intake.
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