[A fatal case of miliary tuberculosis of the liver].
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Biomedical subjects
H Kojima
Publications and source records attributed to H Kojima.
Effects of nefiracetam (DM-9384), a pyrrolidone derivative, on brain monoamine systems.
The pyrrolidone cyclic gamma-aminobutyric acid (GABA) derivative nefiracetam [DM-9384; N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl)acetamide] has been shown to enhance acquisition and ameliorate amnesia in different learning tasks in rodents. In the present study, the effects of nefiracetam on the brain monoamine systems were studied. Male, adult Sprague-Dawley rats were treated with nefiracetam in single doses (0, 1, 3, 10, 30 or 100 mg/kg, p.o.) and analyzed after 1 and 4 hr, or treated by daily doses (0, 1, 3, 10 or 30 mg/kg, p.o.) for 2 weeks. In general, no or only weak effects were observed on tissue monoamine levels, either following acute or 14 days treatment with nefiracetam. Acute administration of intermediate doses of nefiracetam induced minor increases in dopamine (DA) and homovanillic acid (HVA) tissue levels in the striatum, while hypothalamic 3,4-dihydroxyphenylacetic acid (DOPAC) decreased at 1 hr. Noradrenaline (NA) and serotonin (5-HT) levels increased in some regions after higher doses of nefiracetam. Increases in 5-hydroxyindoleacetic acid (5-HIAA) were also seen at 4 hr, but only after the 3 mg/kg dose. Minor decreases of HVA and DOPAC levels were seen in some regions after treatment with various doses of nefiracetam for 14 days, while an increase in 5-HT levels was observed occasionally. Using in vivo microdialysis in freely moving animals, no significant effects on extracellular levels of HVA, DOPAC and 5-HIAA in the striatum or of HVA, DOPAC and NA levels in the dorsal hippocampus were seen after acute administration of nefiracetam. On the other hand, extracellular hippocampal 5-HIAA levels decreased by 20% after the 1 and 3 mg/kg doses. Nefiracetam, in a concentration range of 1 nM to 10 microM, did not affect the in vitro synaptosomal uptake of [3H]NA and [3H]5-HT in the cortex or of [3H]DA in the striatum. Taken together, nefiracetam appears to exert minor, regionally restricted and not dose-dependent effects on the monoamine systems following either acute or repeated administrations in normal rats. A direct or indirect, possible GABA-mediated, influence of nefiracetam may underlie the modest changes seen on monoamines. The cognitive-enhancing action of nefiracetam does not seem to be related to effects on presynaptic monoamine functions.
3,4-Dihydroxyphenylacetic Acid↗
Triple-X syndrome accompanied by single maxillary central incisor: case report.
Facial, oral, and dental findings of an 11-year-old girl with XXX syndrome are reported. Clinical examination reveals midfacial hypoplasia, congenital absence of teeth, and solitary maxillary central incisors both in primary and permanent dentitions.
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Concerted regulation of early enterocyte differentiation by insulin-like growth factor I, insulin, and transforming growth factor-beta1.
To clarify the roles of insulin on the proliferation and differentiation of intestinal epithelial cells (IECs), we examined the effect of insulin-like growth factor-I (IGF-I) and insulin for the growth and differentiation of IEC-6 cells, a crypt cell line derived from rat small intestine. IGF-I (100 nM) stimulated the proliferation of IEC-6 cells, and insulin (1-100 nM) antagonized the IGF-I effect and caused the cells' G1-arrest, resulting in differentiated characteristics of IECs, such as increased general protein synthesis and the formation of microvilli. To clarify the mechanisms of these phenomena, cell surface [125I]insulin binding and the content of immunoreactive insulin receptors were analyzed by Western blotting. Insulin receptors transiently appeared on the cell surface during the early G1 phase after the IGF-I stimulation. Under those conditions, the concomitant presence of insulin stimulated the appearance of active transforming growth factor-beta1 (TGF-beta1) in the media, and then TGF-beta1 antagonized the IGF-I-induced cell proliferation. Such a TGF-beta1 effect was blunted by a neutralizing antibody against TGF-beta1, indicating that the insulin effect was in part mediated through the autocrine-paracrine secretion of TGF-beta1. These results suggest that the regulation of the proliferation of IECs are an early step in those cells' differentiation that may accompany hormonal changes during nutrient intake and may be caused by the sequential effects of IGF-I, insulin, and TGF-beta1.
Animals↗