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Phosphorylation of glial fibrillary acidic protein (GFAP) in slices from immature rats is stimulated by glutamate via a group II metabotropic glutamate receptor (mGluR II) and by absence of external Ca2+ in reactions that are not additive (Wofchuk and Rodnight, Neurochem. Int. 24:517-523, 1994). These observations suggested that glutamate, via an mGluR, inhibits Ca(2+)-entry through L-type Ca2+ channels and down-regulates a Ca(2+)-dependent dephosphorylation event coupled to GFAP. Because ryanodine receptors are present on internal Ca2+ stores and are associated with L-type Ca(2+)-channels, we investigated the possibility that the glutamatergic modulation of GFAP phosphorylation involves internal Ca2+ stores regulated by ryanodine receptors and whether the Ca2+ originating from these stores acts in a similar manner to external Ca2+. The results showed that the ryanodine receptor-agonists, caffeine and ryanodine and thapsigargin, all of which in appropriate doses increase cytoplasmic Ca2+, reversed the stimulation of GFAP phosphorylation given by 1S,3R-ACPD, an mGluR II agonist.

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Retrograde tracing in fixed tissue with the fluorescent carbocyanine dye, DiI, was used to identify neurons that project to paravertebral sympathetic ganglia 9 and 10 in bullfrog tadpoles. Applying DiI to ganglion 9 at stage II labelled spinal preganglionic neurons and sensory neurons in dorsal root ganglia. When examined in a stage V tadpole, the segmental boundaries of the preganglionic cell column which supply the lumbar chain ganglia were identical to that in the adult. Using immunocytochemistry, luteinizing hormone releasing hormone-like immunoreactivity, calcitonin gene-related peptide-like immunoreactivity, and substance P-like immunoreactivity were localized at stage III in axons within sympathetic ganglia 9 and 10. During subsequent stages, the density of fibers containing these peptides increased and it became easier to identify synaptic boutons in contact with postganglionic neurons. These observations demonstrate that projections to the lumbar sympathetic ganglia are already formed by the earliest tadpole stages, they are consistent with the previous physiological observation of nicotinic synapses in stage III ganglia, and they suggest that neuropeptide function may also begin during early stages.

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Because growth failure is a frequent complication of chronic liver disease in childhood, we examined the growth hormone/insulin-like growth factor type I axis and its relationship to growth disturbances, nutritional status, and carbohydrate metabolism in nine children (2.1 to 18.6 years of age) with chronic cholestatic liver disease. Seven had cholestasis associated with splenomegaly and histologic findings of cirrhosis; two patients had Alagille syndrome. Stature was less than or equal to 15th percentile in all except the youngest subject and less than 5th percentile in five subjects. Ten-hour, nocturnal, integrated serum concentrations of growth hormone were considerably higher in patients with cholestasis than in control subjects (mean +/- SD) 9.7 +/- 3.8 vs 4.7 +/- 1.9 ng/ml; p less than 0.02). Serum concentrations of insulin-like growth hormone type I were less than 95th percentile confidence intervals for age- and sex-matched norms in five patients and at the lower limits of normal in the remaining four patients. Insulin sensitivity, determined with the minimal model intravenous glucose tolerance test, was not decreased in five patients despite elevated levels of circulating growth hormone. The estimated mean caloric and protein intake exceeded the recommended dietary allowance and the weight-for-height index was greater than 90% for six of nine patients. Triceps and subscapular skin-fold thicknesses, indicators of body fat stores, were greater than 25th percentile for five of nine and eight of nine patients, respectively, suggesting deficient lipolytic action of GH. We conclude that children with cholestatic liver disease have a resistance to the growth-promoting, diabetogenic, and lipolytic properties of growth hormone.

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The response to aluminum loading from parenteral nutrition (PN) solutions was determined in 20 infants with gestational ages 29 to 41 weeks and birth weights 880 to 3630 gm. Mean duration of PN was 43 days (range 5 to 175 days). Ten infants received a high Al load (from an experimental high calcium- and phosphorus-containing PN solution, with a measured Al content of 306 +/- 26 micrograms/L (mean +/- SE), n = 11), for up to 6 weeks. Ten infants received a lower Al load (from standard Ca-P solutions, measured Al content 144 +/- 16 micrograms/L, n = 11). Five infants received PN with a low Al load for longer than 6 weeks. The mean urine Al/creatinine (Cr) ratio (micrograms/mg) increased threefold, from 0.3 +/- 0.09 to 0.97 +/- 0.17 during PN in the entire group (P less than 0.001), and was significantly higher in infants who received greater Al loading (P less than 0.001). There was no significant difference between preterm and term infants in the rate of change in urine Al/Cr during the study. Urine Al was calculated to account for less than 50% of Al load. During the study, serum Al concentrations ranged from 6 to 318 micrograms/L (median 37 micrograms/L, compared with the median 18 micrograms/L for normal infants and children). Serum Al concentrations were not significantly changed during the study, or between infants in high or lower Al loading groups. Vertebrae from autopsy of two infants who received the lower Al containing PN for 71 and 152 days, respectively, stained positive for Al at the bone mineralization front. Thus, currently used PN solutions are contaminated with Al, urine Al concentration is higher with higher Al loading, and is not different in term and preterm infants. We suggest that renal elimination of Al in infants is incomplete, as assessed by lower urine Al excretion versus load, elevated serum Al concentration, and bone deposition of Al.

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Despite a victorious social revolution, a self-proclaimed "revolutionary" government, and a significant post-war economic growth, Mexico has not achieved a just or equitable social system. The Mexican Revolution led to the emergence of a new bureaucratic class whose "trickle-down" development strategy sacrificed social welfare to capital accumulation. Mexican morbidity and mortality patterns resemble those of more impoverished developing nations without revolutionary experience. The patterns of health care in Mexico reflect inequities and contradictions in the society and economy at large and flow from the erosion of the egalitarian aims of the revolution concomitant with the expansion of capitalism and the concentration of the benefits of "modernization" in the hands of privileged elites. Mexico's health problems are symptomatic of a general socio-economic malaise which questions the legitimacy of the Revolution.

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Post-1964 political changes in Brazil had dire implications for the health sector as successive governments pursued economic and social policies which aggravated inequities and benefitted narrow elites. The "military modernizers" embraced a concept of development inimical to basic human needs, an economic model favoring growth over distribution and development over social welfare, and budget priorities favoring vocal, urban middle sectors at the expense of marginal populations. The result was deteriorating health and social conditions among the majority of the population that did not share in the benefits of the "economic miracle."

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