The present study was investigated the effect of Houttuynia cordata THUNB water extract (HCWE) on mast cell-mediated anaphylactic reactions. The mast cell-mediated anaphylactic reaction is involved in many allergic diseases such as asthma and allergic rhinitis. HCWE has been used as a traditional medicine in Korea and is known to have an antioxidant and anti-cancer activities. However, its specific effect of mast cell-mediated anaphylactic reactions is still unknown. We examined whether HCWE could inhibit compound 48/80-induced systemic anaphylaxis, IgE-mediated passive cutaneous anaphylaxis (PCA), and mast cell activation. The oral administration of HCWE inhibited compound 48/80-induced systemic anaphylaxis in mice. HCWE also inhibited the local allergic reaction, PCA, activated by anti-dinitrophenyl (DNP) IgE antibody in rats. HCWE reduced the compound 48/80-induced mast cell degranulation and colchicine-induced deformation of rat peritoneal mast cells (RPMC). Moreover, HCWE dose-dependently inhibited histamine release and calcium uptake of RPMC induced by compound 48/80 or anti-DNP IgE. HCWE increased the level of intracellular cAMP and inhibited significantly the compound 48/80-induced cAMP reduction in RPMC. These results suggest that HCWE may be beneficial in the treatment of mast cell-mediated anaphylactic responses.

Background:The changes in the functional magnetic resonance imaging signal during anticipation, pain stimulation, and the poststimulation periods were investigated to determine whether changes in sex hormones affect brain activity.Methods: Eighteen participants were examined twice, once in the follicular phase and once in the luteal phase. Half the participants were tested first during the follicular phase, and the other half were tested first in the luteal phase.Results: The pain and unpleasantness ratings were significantly higher in the luteal phase than in the follicular. During the anticipation of pain, the prefrontal cortices were activated during the follicular phase, whereas the parahippocampal gyrus and amygdala were activated during the luteal phase. During the pain stimulation, putamen and cerebellum and precentral gyrus involving motor preparation and defense mechanism related to antinociceptive behavior were activated during the follicular phase, whereas the thalamus was activated during the luteal phase. During the poststimulation periods, the prefrontal cortices were activated during the follicular phase, whereas parahippocampal gyrus was activated during the luteal phase. The temporal pole was activated during the anticipation, pain stimulation, and poststimulation periods of the luteal phase.Conclusions: During surgical and medical procedures, requirements of anesthetic and analgesic and anxiolytic drugs may be reduced during the follicular phase and increased during the luteal phase. These results highlight the need to consider the effects of the sex hormones in women when designing clinical or neuroimaging studies or when treating patients for pain and pain-related unpleasantness.

SummaryMast cells have long been believed to be the central effector cells in the development of immunoglobulin (Ig)E-dependent anaphylaxis. In this study, we investigated the role of mast cells in IgE-dependent hapten-induced active fatal anaphylaxis using mast cell-deficient WBB6F1-W/W v ( W/W v ) and congenic normal ( ϩ / ϩ ) mice. Although a 5-min delay in shock signs and death were observed in W/W v mice, 100% fatal reactions to penicillin V (Pen V) occurred in both ϩ / ϩ and W/W v mice. Administration of monoclonal anti-IL-4 antibody completely prevented the fatal reactions, and the effect of anti-IL-4 was associated with its suppressive activity on Pen V-specific serum levels of IgE, but not IgG. The platelet-activating factor (PAF) antagonist, BN 50739, completely prevented the fatal reactions in both strains of mice. Our kinetic study revealed, in contrast to no elevation of plasma histamine level in W/W v mice, high levels of PAF in the circulation after challenge in both ϩ / ϩ and W/W v mice, albeit to a lesser degree in the latter case. These data indicate that cells other than mast cells are sufficient to induce an IgE-dependent active fatal anaphylaxis by elaborating PAF, which is the critical mediator for fatal murine anaphylaxis. Thus, mast cells may not contribute importantly to protein-induced anaphylaxis. Some evidence indicates that protein-induced anaphylaxis can be elicited by IgG Abs (9, 10) even in the absence of IgE Abs (11), suggesting that cells other than mast cells that bind IgG Abs elaborate sufficient mediators leading to fatal reactions. Nevertheless, mast cells have long been believed to be the central effector cells in the development of IgE-dependent anaphylaxis. However, the in vivo extent to which the reactions are mast cell-dependent remains to be elucidated due to the lack of a suitable animal model of IgE-dependent anaphylaxis.We have recently developed a murine model of IgEdependent, penicillin V (Pen V)-induced active fatal anaphylaxis (12). The reaction was 100% fatal in C57BL/6 mice and was exclusively IgE dependent, since ( a ) IgE, but not IgG, Abs against Pen V passively sensitized normal mice to develop severe anaphylactic reactions; ( b ) anti-IL-4 mAb completely prevented the fatal reaction; and ( c ) the effect of anti-IL-4 was associated with its suppressive activity on Pen V-specific serum IgE, but not IgG, levels. This model allowed us to investigate the role of mast cells in IgE-dependent anaphylaxis. In this study, the role of mast cells in IgE-dependent Pen V-induced anaphylaxis using genetically mast cell-deficient WBB6F1-W/W v ( W/W v ) and congenic normal ( ϩ / ϩ ) mice was investigated. It was 1 Abbreviations used in this paper: CGG, chicken gammaglobulin; NP, nitrophenol; PAF, platelet-activating factor; PCA, passive cutaneous anaphylaxis; Pen V, penicillin V.

We studied the variations in the ventral rami of 152 brachial plexuses in 77 Korean adults. Brachial plexus were composed mostly of the fifth, sixth, seventh and eighth cervical nerves and the first thoracic nerve (77.0%). In 21.7% of the cases examined, the fourth, fifth, sixth, seventh and eighth cervical and the first thoracic nerves contributed to the plexus. A plexus composed of the fourth, fifth, sixth, seventh and eighth cervical and the first and second thoracic nerves, and a plexus composed of the fifth, sixth, seventh eighth cervical nerves were also observed. The plexuses were classified into three groups according to cephalic limitation, and the plexus of group 2 in which the whole fifth cervical nerve enters the plexus, were observed the most frequent. The average diameter of the sixth and the seventh cervical ventral rami of the plexus was greatest and that of the fifth cervical was smallest. The largest nerve entering the plexus was the sixth or the seventh cervical nerve in about 79% of cases. The dorsal scapular nerve originated from the fifth cervical ventral ramus in 110 cases (75.8%). The long thoracic nerve was formed by joining of roots from the fifth, sixth, and seventh cervical nerves in 76.0% of cases. Also, a branch to the phrenic nerve, the suprascapular nerve, a nerve to the pectoralis major muscle and a nerve to the subscapular muscle arising from the ventral rami of the plexus were observed.