Interleukin 1 (IL-1) is a macrophage derived cytokine that is identified as a thymocyte comitogenic activity. It is now recognized that IL-1 is produced by many cell types and has multiple biological activities on immune and inflammatory reactions. Various cytokines are reported to influence inflammatory reactions either directly or indirectly. However, IL-1 is recognized to be a major inflammatory cytokines with broad spectrum. IL-1 exhibits a number of biological activities on connective tissue cells. IL-1 stimulates rheumatoid synovial cells to produce PGE₂, collagenase, type I collagen and a number of cytokines such as interleukin 6, interleukin 8 and colony stimulating factors. IL-1 also stimulates proliferation of synovial fibroblasts, cartilage degradation and bone resorption. Increased production of IL-1 was reported at the sites of synovitis in patients with rheumatoid arthritis and animal models for arthritis. These findings indicate that IL-1 play an important role in destruction and remodeling of connective tissue in joints.

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Bronchial asthma is characterized by eosinophilic inflammation, desquamation of airway epithelium and bronchial hyperresponsiveness. Eosinophil causes desquamations of epithelium and damages to epithelial cells, following the reduction of the mediators which relaxes bronchial muscle.
Human epithelial cells can produce PGE₂, 15-HETE, 8, 15-diHETE, 8, 15-LT. PGE₂ causes the relaxation of airway smooth muscle. 15-HETE inhibits LT B₄ release from rabbit neutrophil and LT C₄ release from human eosinophil, respectively. Furthermore, epithelial cells may release epithelium-derived relaxing factor (s) (EpDRF) which cause airway muscle relaxation. Neutral endopeptidase (NEP, enkephalinase) in the epithelium destroys substance P and neurokinin A which induce bronchoconstriction.
Desquamations and damages of airway epithelium reduce these relaxing factors and cause bronchial hyperresponsiveness to bronchoconstractive effects.

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Far infrared ray (4-14 μm) emitting materials or products including platinum electro-magnetic wave fiber have recently been widely used for improving various disorders, promoting health and beauty, and preserving food freshness etc. This mechanisms is to decrease the size of water structure (cluster) by cleaving the bonds of H₂O in polymer, which leads to the better penetration of water into the cell mem-brane with resultant increase in intracellular calcium concentration [Ca²⁺] i and potentiation of cell activa-tion. In this connection, we examined the effect of this platinum colloid fiber on [Ca²⁺] i, chemotaxis, phagocytosis and O^-₂ generation of normal human neutrophils, and blastogenesis of lymphocytes. Its effect on lipid peroxidation from unsaturated fatty acids was also tested. The test tubes containing neutro-phils and lymphocytes, and docosahexaenoic acid were surrounded and contacted with platinum colloid fiber.
The result revealed that platinum fiber significantly enhanced [Ca²⁺] i, chemotaxis, phagocytosis and O^-₂ generation by normal neutrophils, and the blastogenesis of the lymphocytes. Lipid peroxidation was also markedly inhibited. Our study suggests that platinum colloid fiber promotes our health by potentiating the cell function.

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Platelet-activating factor (PAF) has been implicated as an important mediator of the lethal effect of endotoxin. To establish the acute toxicity of PAF, we infused 2.5 μg/kg of PAF into endotoxin-sensitive mice (C3H/HeN) via the tail vein over 5 minutes.
At necropsy, the heart revealed none of the changes in four out of five mice. Multiple hyaline thrombi in the lungs were observed in all animals. This histopathologic finding was the most characteristics in endotoxin sensitive mice treated with PAF.
It was almost the same findings as endotoxin shock. The liver was observed congestion, focal necrosis, central vein dilatation, hyaline thrombi and fatty metamorphosis. The renal medulla showed congestion but the renal cortex and renal glomeruli were intact. The small intestine was also intact.

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In an in vitro study to examine whether corneocytes stimulate neutrophils to cause a respiratory burst, we found that stratum corneum (SC) homogenates obtained from the sole of healthy individuals induced a substantial respiratory burst in human neutrophils when assessed by lucigenin-dependent chemiluminescence (CL) in the presence of the nontreated fresh human serum (NTS) . Electronmicroscopically the interaction between corneocyte and neutrophils was shown as distinctive deformation of the neutrophils adhering to the surface of the corneo-cytes that suggested a specific binding between them. In contrast, in the heat-inactivated serum (HIS) -supplemented system the peak inensity of SC-induced CL was significantly decreased, being only slightly higher than that noted in the SC-free background. To circumvent the time-consuming preparation of the SC homogenates we measured CL with a sheet of SC obtained by stripping with adhesive cellophane tape. In this case we used plasma because complement in the serum was easily activated by cellophane tape itself. To evaluate the influence of the location of horny tissue in the SC on the induction of CL responses, we used SC sheets stripped with cellophane tape from various levels of the SC. Howeve, there was no significant difference in CL response between SC sheets obtained 1, 2, 3, 5, 10 or 15 strippings.
Our findings suggest that, when the SC comes in contact with serum, it is opsonized by C 3 b and that such SC causes a respiratory burst of neutrophils following their physical contact. Extracellular release of the resultant active oxygen species probably causes damaging effects on the surrounding SC and epider_ mal tissue and such an interaction between SC and neutrophils seems to be involved in the formation of subcorneal sterile pustules noted in pustular dermatoses.

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To study the growth mechanism of jaw cyst, the authors investigated the arachidonic acid (AA) metabolites in cyst fluids. AA metabolites were separated and quantitated by high performance liquid chromatography (HPLC) .
The amount of leukotriene C₄ (LTC₄) and leukotriene B₄ (LTB₄) in the cyst fluid with inflammation was more than that without inflammation. On the contrary, the amount of prostaglandin D₂ (PGD₂) in the cyst fluid with inflammation was less than that wihtout inflammation.
To confirm the origin of leukotriens (LTs) in the cyst fluid, the authors measured the LTs produced by polymorphonuclear leukocytes (PMNs) obtained from peripheral blood and studied the effects of AA 861 and α-tocopherol. As a result, LTs could be detected in the PMNs suspension stimulated with Ca ionophore A 23187. Furthermore, the generation of LTs was completely inhibited by AA 861 and α-tocopherol.
These findings suggested that AA metabolites are important in the enlargement of jaw cysts.

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Rat mast cell granules and the plasma membrane fractions were obtained by the homogenization of highly purified rat mast cells and their isolation in a Percoll or sucrose gradient respectively. Immuno-stainings of non-stimulated rat mast cells, compound 48/80 or calcium ionophore A 23187-stimulated rat mast cells, the granules and the plasma membrane fractions were performed with a monoclonal antibody, M 6764, which recognizes HNK-1 epitope. HNK-1 epitope was present in rat mast cells and the granules, but not in the plasma membrane fractions. The granules fixed with glutaraldehyde showed ring-like figures by immunostaining with M 6764. Rat mast cells and the granules treated with chloroform-methanol after fixation were also densely stained with M 6764. Western blot analysis of rat mas tcells and the granule homogenates with M 6764 antibody showed broad protein bands ranging from 100 to 250 KDa.
These results showed the presence of HNK-1 epitope in rat mast cell granules. This HNK-1 epitope could be a glycoprotein.

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The effects of Ca-antagonists on the release of IL-1β by LPS stimulated human blood monocytes (HBMs) were examined by radioimmunoassay. Caantagonists used were nicardipine, nifedipine, nimodipine, flunarizine, verapamil and diltiazem. Flunarizine strongly inhibited the IL-1β release from HBMs by LPS with an IC₅₀ of 25.9 μM. Diltiazem and verapamile inhibited at the higher concentration (IC₅₀> 160 μM), but the other Ca-antagonists, dihydropyridine type, such as nicardipine, nifedipine and nimodipine did not affect the IL-1β release from HBMs. In order to investigate the mechanism of IL-1β inhibition of flunarizine, forskolin was used. Forskolin was 2 fold potentiated the IL-1β release from HBMs stimulated by LPS. Flunarizine pretreatment with dose of IC₅₀ completely inhibited IL-1β release from HBMs increased by forskolin.
Taken together, these results suggest that the mechanism of the inhibition of IL-1β release from HBMs by flunarizine may be closely related to cyclic AMP.

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The changes of the synovial fluid properties of patients with rheumatoid arthritis who were treated with intraarticular steroid injections combined with hyaluronate solution were investigated. Concentra-tions of hyaluronate and total protein, viscosity, molecular weight of hyaluronate, grade of stringing, and grade of formation of mucin clot of the synovial fluid were examined before and after the intraarticular administration of hyaluronate. 2.5 ml of 1% solution of hyaluronate, molecular weight 80 × 10⁴, were admini-strated into the knee joints combined with steroid, the average times of injection in each patients were 3.3 times during 9.2 weeks. And the joint fluid was examined 2.9 weeks later in average. However no significant changes were observed in hyaluronate and protein concentration, viscosity and mucin clot formation, molecular weight increased from pre-treatment value of 198 × 10⁴ to post-treatment value of 223 × 10⁴ (P<0.2) and length of stringing also increased from 17.7 mm to 22.7 mm (P<0.2) .
Because it has been reported that high molecular weight hyaluronate could inhibit the synovial cell proliferation, synovial angiogenesis and lymphocyte stimulation, the results obtained in this study might be beneficial for the local treatment of joint inflammation.

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In 178 RA patients, I studied the continued use rate and clinical results of bucillamine over a 2-year period. The results indicate that the continued use rate was 69.1% which was more favorable than in the groups treated using GST or auranofin. Most probably the reason for this is that in the long term administration cases there were few ineffective drop-out cases.
Clinical results included a slight or moderate improvement on the final Lansbury improvement rate in more than 68.9% of the cases. On various evaluation items, periodic changes showed improvement up to the 6 th month of administration and these improvements were maintained for up to 2 years.
The continuity of these effects supports the fact that the number of cases who discontinued due to decrease of efficacy was small.

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