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M Niimi

Publications and source records attributed to M Niimi.

188 records · Page 11Linked to original sources

Sites of origin of growth hormone-releasing factor-containing neurons projecting to the stalk-median eminence of the rat.

The topographical location of neurons containing GRF which project to the median eminence were studied with immunofluorescence for GRF in combination with the retrograde transport of True blue. After the injection of True blue into the median eminence, retrogradely-labeled GRF neurons were identified in the arcuate nucleus and the lateral basal hypothalamus. GRF neurons in the perifornical area contained no positive dye. We concluded that the location of neurons containing hypophysiotrophic GRF are confined within the arcuate nucleus and the lateral basal hypothalamus.

Afferent Pathways↗

Effect of central and continuous intravenous injection of interleukin-1 beta on brain c-fos expression in the rat: involvement of prostaglandins.

Utilizing immunohistochemistry for the c-fos protein to detect neuronal activity, we examined the effects of continuous intravenous and intracerebroventricular infusion of interleukin (IL)-1 beta in the rat brain, and the involvement of prostaglandins (PGs) in IL-1 beta-induced c-fos expression. Continuous intravenous infusion of IL-1 beta (10 ng/min) markedly augmented c-fos expression in the paraventricular (PVN) and the supraoptic (SON) nuclei of the hypothalamus as well as in the central amygdaloid nucleus (CeA). The number of IL-1 beta-induced c-fos-positive cells in the PVN and SON was significantly lower in rats pretreated with indomethacin than in vehicle-treated rats. However, the number of IL-1 beta-induced c-fos-positive cells in the CeA remained unchanged. c-fos protein was induced after intracerebroventricular infusion of IL-1 beta (200 ng) in the PVN, SON, and arcuate nuclei of the hypothalamus, and in the CeA. The induction of c-fos immunoreactivity by central administration of IL-1 beta was blocked by indomethacin (500 micrograms/rat), except in the CeA. These findings suggest that PGs are involved in the complex transmission of signals from circulating or central IL-1 beta to hypothalamic neurons.

Amygdala↗

Levels of soluble adhesion molecules and cytokines in patients with septic multiple organ failure.

Multiple organ failure (MOF) is a common complication of sepsis or septic shock. In this condition, it is believed that activated neutrophils adhere to the vascular endothelium and induce various mediators and tissue damage, leading to organ damage. We investigated the plasma levels of inflammatory cytokine activating neutrophils, soluble adhesive molecules, and endotoxin in 8 patients with septic MOF, 15 patients with sepsis but without MOF, and in 5 patients with MOF unrelated infection. The soluble intercellular adhesion molecule-1 (sICAM-1) concentration in sepsis-complicated groups was significantly higher than that in the multiple organ failure (MOF) group without infection. Of sepsis-complicated groups, the sICAM-1 value in the MOF group was significantly higher than that in the sepsis group without MOF. In sepsis-complicated groups, both soluble endothelial-leukocyte adhesion molecule-1 (sELAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) concentrations were significantly higher than those in the MOF group without infection. However, there was no significant difference between the septic MOF group and the sepsis group without MOF. In patients showing high levels of soluble adhesion molecule, prognosis was poor, and the concentration of soluble adhesion molecules rapidly decreased during recovery from MOF. It is speculated that endotoxin and inflammatory cytokines damage vascular endothelium as well as various other cells and produce, a large number of adhesion molecule, especially in patients with septic MOF, causing leakage of adhesion molecules into blood.

Adult↗