Bronchial asthma is characterized by increased airway responsiveness and reversible bronchial constriction. The bronchial hyperreactivity is associated with localized inflammation and related to chemical mediators in the airway. Platelet-activating factor (PAF) is one of these mediators. Previous reports showed that inhaled PAF caused a bronchoconstriction in man. They suggested that PAF may contribute to the pathogenesis of bronchial hyperresponsiveness, which is the most characteristic abnormality in asthma. In the present study, PAF was detected in sputa from asthmatics and patients of various pulmonary diseases. The amounts of PAF in sputa which were quantified by bioassay using washed rabbit platelets aggregation were, respectively,0.73 ± 0.32,1.27 ± 0.98,17.82 ± 11.42 and 0.15 ± 0.08 pmol/ml (mean ± standard error) for the patients with bronchial asthma (n = 22), pulmonary emphysema (n = 5), chronic bronchitis (n = 4) and pneumonia (n = 4). Additionally, some of the patients were tested for bronchial responsiveness by a methacholine bronchial provocation test by an Astograph at the same time of sputum collection (n = 19). The data of bronchial responsiveness were not correlated with the amounts of PAF. A close correlation was found between PAF amounts and leukocytes counts in sputa from asthmatics (p< 0.01, r=0.90, n=22), especially neutrophils counts (p< 0.01, r=0.91, n=18). Adding other diseases, there was also a significant correlation between PAF amounts and leukocytes counts (p< 0.01, r =0.89, n=35) or neutrophils counts (p< 0.01, r =0.88, n=28). However, no relationship between the amounts of PAF and the number of eosinophils or lymphocytes was shown. These findings do not support a conclusion that PAF is a specific chemical mediator in asthmatic response. PAF is considered to be commonly present in the airway inflammatory lesion related to neutrophils.

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Although functional disorder of gall bladder and duct associated with upper abdominal pain is known as biliary dyskinesia (BD), the pathophysiology of this disease remains to be elucidated and clinical daiagnostic criteria are not well established. In order to make a diagnosis of BD, I employed an ultrasonographical measurement of the size of gall bladder before and after oral administration of two egg yolks in patients who complained of right hypochondralgia without organic abnormality. Serum levels of cholecystokinin (CCK) were also examined in the same subjects. A definite diagnosis of BD was made when the size of gall bladder showed abnormal changes with reappearance of right hypochondralgia. According to patterns of gall bladder contraction, BD was classified into three groups: hypocontraction, hypercontraction, and biphagic types. Serum CCK levels did not show any difference between normal control and each types of BD before administration of yolks but significantly (P < 0.05) increased after 90 minutes in hypercontraction and biphagic types compared to the normal control. The contraction rate of gall bladder was related to the pattern of reappearance of abdominal pain. It was high in those who had the reappearance of hypochondralgia longer than an hour. In conclusion, the ultrasonographical measurement of gall bladder might be useful in diagnosing BD.

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In the hepatocytes of adult female rats injected i. p. daily with 0.5 mg/kg of phalloidin for a week, some minute, flocculent and osmiophilic structures were observed sporadically in the cytoplasms adjoining to accumulating foci of markedly hyperplastic microfilaments surrounding an abnormal bile canaliculus. The particular structures were examined ultracytochemically with both so-called “enzymic digestive methods for lipids” proposed by the authors and a double fixation method using tannic acid, and they were indicated to contain much more phospholipids and cholesterol esters. These minute osmiophilic structures, therefore, might be resulted from the deposition of biliary lipids, which was induced by microfilament dysfunction within the livers. A moderate accumulation of hyperplastic microfilaments around the bile canaliculi 3days after the daily injection of phalloidin did not modify an initial stage of ethionine-induced triglyceride fatty liver. Lipid traffic in the hepatocytes was discussed from a standpoint of cytoskeletal pathology.

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Electronmicroscopic immunohistochemical examination using monoclonal anti-serotonin(5-HT) antibody was performed to determine the localization of 5-HT in human and rabbit platelets. The immunological specificity of the platelet membrane, namely, nonspecific adsorption and its impermeability, to antibodies, was resolved by enzymatic treatment of glutaraldehyde-fixed platelets with trypsin. Immunological reactions of anti-5-HT antibody were clearly detected on many α-granules -4. as well as on dense granules. From the manner of these reactions, serial development from α-granules to dence granules was suspected.

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Using rabbits, changes in uterine movement induced by electric stimulation of the amygdaloid nucleus which belongs to the limbic system were investigated in relation to electrical activities of the central nervous system expressed by these stimuli.
1) When 3Hz stimuli were applied to the amygdaloid nucleus, spike and wave complexes appeared on the cerebral cortex EEG. When the stimulus frequency was increased to 8Hz, the EEG showed a recruiting response. With 100Hz, an arousal pattern appeared on the EEG.
2) Stimulation of the corticomedial division of the amygdaloid nucleus induced an acceleration of uterine movement, suggesting a close association between the corticomedial division and uterine movement-accelerating system.
3) Stimulation of the basolatera l division induced an inhibition of uterine movement, suggesting a close association between the basolateral division and uterine movement-inhibiting system.
4) Administration of anticholinergic drugs led to complete disappearance of the accelerating effect of the corticomedial division, while the inhibiting effect of the basolateral division persisted. In contrast, with the administration of β-adrenergic blocking agents the entire accelerating effect of the corticomedial division persisted, while the inhibiting effect of the basolateral division disappeared. With the administration of α- adrenergic blocking agents the inhibiting effect of the basolateral division persisted. These findings suggest that the changes in uterine movement induced by stimulation of the corticomedial division are mediated by cholinergic receptors while the changes in uterine movement induced by stimulation of the basolateral division are mediated by β-adrenergic receptors.
5) When changes in uterine movement induced by stimulation of the amygdaloid nucleus were similarly followed in rabbits subjected to adrenalectomy or destruction of the infundibulum, the results were similar to those obtained prior to these procedures. These findings suggest that the influence exerted by stimulation of the amygdaloid nucleus on uterine movement is not mediated by humoral factors.
6) No changes in amygd aloid nucleus stimulation-induced uterine movement were found in rabbits subjected to transection of the spinal cord at the C6-C7 level.
7) In rabbits subjected to transection of the spinal cord at the L5-L6 level the accelerating effect on uterine movement induced by stimulation of the corticomedial division disappeared. This finding suggests that the effect of stimulation of the corticomedial division is mediated by the sacral parasympathetic nerves.

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Light transmission (LT) through platelet rich plasma (PRP) is sometimes increased by unfractionate heparin. The mechanisms of this increase are classified into two types, one in the presence and the other in the absence of involvement of immune processes. We investigated the direct effects of heparin on platelets in the absence of involvement of immune processes. In this case in which an increase in LT in PRP was induced by heparin alone, the addition of 10 units/ml of heparin gradually increased percent transmission to a maximum of 8 % after about 7minutes. Maximum percent transmission depended upon the concentration of heparin, and was highest at a concentration of 10 units/ml. The platelet count was decreased at heparin concentrations of 1-100 units/ml. This increase in LT disappeared following complete chelation of Ca²⁺ in the extracellular fluid by EGTA. In addition, this increase was not inhibited by pre treatment with monoclonal antibody against GP I b, but was completely inhibited by monoclonal antibody against GP II b-III a complex. LT was not increased by heparin addition to washed platelet suspensions (WPS). However, an increase in LT by heparin similar to that through PRP was also observed following the addition of fibrinogen (Fbg) and CaCl₂ in WPS. None of fibronectin, vitronectin and laminin had effects similar to those of Fbg. In this reaction, there was no release of platelet factor-4, β-thromboglobulin or serotonin. In addition, there was no production of inositol 1,4,5-trisphosphate, and no increase of intracellular Ca²⁺ concentration. Thus, it seems possible that heparin itself dose not directly activate platelets. The concentration of bound Fbg on the surface of platelet membranes was increased by the addition of heparin in the presence of Fbg. These findings suggest that the increase in LT in PRP induced by heparin was not due to contact by heparin itself with platelets but required at least the presence of Fbg to crosslink platelets. Heparin induces structual changes at the Fbg binding site on platelet membranes. For this reaction, the presence of Ca²⁺ in the extracellular fluid is required.

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Electrical silence in the shoulder adductor muscles observed before ball impact in the tennis ground stroke was investigated in terms of the neurophysiolosical and dynamical features. Subjects employed in the experiments were 10 healthy adults including skilled tennis players of top level. Electrom yograms were recorded from the pectralis major, clavicular [Pc] and sternal [Ps] portions, and the deltoid, anterior [Da] and posterior [Dp] portions utilizing an electromagnetic oscillograph and datarecorder with surface electrodes. An electrogoniogram of the shoulder angle between the upper arm and the frontal plane, utilizing a specially constracted electrogoniometer, was simultaneously recorded with the EMGs.
The discharges of Pc, Ps and Da ceased before the ball impact in the forehand ground stroke. It did not make any significant difference whether the subjects had their eyes open or closed, and with or without ball. Horizontal adduction of the upper arm produced electrical silence in the adductors only when the swing speed exceeded a certain value (about 200 degree/s) and the shoulder position was firmly fixed.
No d istinguishable discharge in the Dp suggesting the existence of antagonistic inhibition was observed while the spike cessations occurred in the adductor muscles. During the horizontal arm swing on the fixed shoulder side, the passive backward movement at the contralateral shoulder produced clearer and faster spike cessations in the adductors-the Da, Pc and Ps- than in the control situation. On the contrary, the passive forward movement induced the partial spike inhibitions in the adductors, particularly in the Ps, and small spikes continued through the swing motion.
Backward or forward push at the contralateral shoulder during the arm swing at the fixed shoulder side produced passive lengthening or shortening of the adductors, respectively. In the case of the shortened muscular length, the latency of 34.3 ms (mean) suggested that it was caused by a spindle silence. The shortened muscular length might also release a I-B inhibition.
Therefore, in this case, the small remaining spike may be the command impulses in the central nervous system. On the contrary, it can be argued that the muscular elongation cause facilitation on spindle and I-B afferents. The clearer and faster spike cessations than in the control situation might be caused by predominantly facilitated I-B inhibitory activity which swept away all electrical activities. In the nomal tenn is ground stroke, the increased muscular activity inducing a fast swing might raise the level of the I-B inhibition enough to cancel out all electorical activities.

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