We investigated the effects of the odor of jasmine tea on autonomic nerve activity and mood states in a total of 24 healthy volunteers. We used the odor of jasmine tea at the lowest concentration that could be detected by each subject but that did not elicit any psychological effects. R-R intervals and the POMS test were measured before and after inhalation of the odors for 5 min. Both jasmine tea and lavender odors at perceived similar intensity caused significant decreases in heart rate and significant increases in spectral integrated values at high-frequency component in comparison with the control (P < 0.05). In the POMS tests, these odors produced calm and vigorous mood states. We also examined the effects of (R)-(-)-linalool, one of its major odor components, at the same concentration as in the tea, and (S)-(+)-linalool. Only (R)-(-)-linalool elicited a significant decrease in heart rate (P < 0.05) and an increase in high-frequency component in comparison with the controls, and produced calm and vigorous mood states. Thus, the low intensity of jasmine tea odor has sedative effects on both autonomic nerve activity and mood states, and (R)-(-)-linalool, one of its components, can mimic these effects.
The effect of jasmine tea odor on the autonomic nervous system was investigated by a power spectral analysis of the heart rate variability. We assigned eight volunteers to two groups with either a predilection for or antipathy toward the jasmine tea odor. We tested both high- and low-intensity jasmine tea odors. The low-intensity odor was produced by diluting 20-fold the jasmine tea used for the high-intensity odor test. The low-intensity odor produced an increase in parasympathetic nervous activity in both the predilection and antipathy groups. The high-intensity odor produced an increase in parasympathetic nervous activity in the predilection group, but an increase in sympathetic nervous activity in the antipathy group. The odor of Chinese green tea, a basic ingredient of jasmine tea, produced no effects similar to those of the jasmine tea odor. These results suggest that the jasmine tea odor activated the parasympathetic nerve, whereas the higher-intensity odor activated the sympathetic nerve in those subjects who disliked the odor.
Cerebrospinal fluid (CSF) taken from rats after stimulation by an aversive quinine taste (hereafter called quinine CSF) administered into the fourth ventricle of mice suppressed their intake of 5% sucrose solution. We examined the effects of CSF on glutathione-induced tentacle ball formation (TBF) of hydra to determine the change in CSF components associated with aversive taste stimuli. The suppressive activity of quinine CSF on TBF in the presence of 3 microM S:-methyl-glutathione (GSM) was markedly lower than that of CSF obtained from control rats (control CSF). Pronase-treated quinine CSF had suppressive activity similar to that of control CSF. The active principle passed through an ultrafiltration membrane, with a molecular weight cut-off of 30 kDa, but not through one with a cut-off of 3 kDa. A peptide fragment of diazepam-binding inhibitor (DBI) nullified the suppression of TBF at 3 microM GSM by control CSF. The nullifying activity of quinine CSF was not observed after treatment with a benzodiazepine receptor preparation that was able to bind DBI. When flumazenil, a benzodiazepine receptor antagonist, was given to mice, the suppression of the intake of 5% sucrose solution by quinine CSF was partially reversed. It is suggested that quinine CSF contains a DBI-like substance.
A fatal case of Yersinia enterocolitica septicemia which was complicated by unique hemosiderosis is reported. On admission, the patient had diabetes and showed unusual hyperferritinemia. Postmortem examination revealed that the liver was studded with abscesses, and Yersinia antigen was expressed in foamy macrophages within these abscesses. Moreover, the cadaver showed generalized hemosiderin deposition, which was mainly observed in the liver and, to lesser degrees, in the pancreas, spleen, lymph nodes, brain, thyroid and kidneys. Since there was no apparent cause of the hyperferritinemia and generalized hemosiderosis, consideration was given to possible primary hemo‐chromatosis. However, no liver or pancreatic fibrosis was demonstrated. Kupffer cells were also loaded with hemosiderin, and therefore it was considered that these cells had lost their ability to phagocytize the microorganism adequately, leading to major liver involvement. Interestingly, hemosiderin deposits in the kidneys were mostly present in glomerular epithelial cells. To our knowledge, this unique presentation has not been previously described in humans. ACTA PATHOL JPN 38: 1461–1472. 1988.
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