Inhibitory mechanisms of kinetin, a plant growth-promoting hormone, in platelet aggregation.

Kinetin has been shown to have anti-aging effects on several different systems including plants and human cells. The aim of this study was to examine the detailed inhibitory mechanisms of kinetin in platelet aggregation. In this study, kinetin concentration-dependently (50-150 microM) inhibited platelet aggregation in human platelets stimulated by agonists. Kinetin (70 and 150 microM) also concentration-dependently inhibited intracellular Ca2+ mobilization and phosphoinositide breakdown in platelets stimulated by collagen (1 microg/ml). Kinetin (70 and 150 microM) significantly inhibited thromboxane A2 formation stimulated by collagen (1 microg/ml) and arachidonic acid (60 microM) in human platelets. In addition, kinetin (70 and 150 microM) significantly increased the formation of cyclic AMP. Intracellular pH values were measured spectrofluorometrically using the fluorescent probe BCECF-AM in platelets. The thrombin-evoked increase in pHi was markedly inhibited in the presence of kinetin (70 and 150 microM). Rapid phosphorylation of a platelet protein of molecular weight (Mr) 47000 (P47), a marker of protein kinase C activation, was triggered by collagen (1 microg/ml). This phosphorylation was inhibited by kinetin (70 and 150 microM). In conclusion, these results indicate that the anti-platelet activity of kinetin may be involved in the following pathways: kinetin's effects may initially be due to inhibition of the activation of phospholipase C and the Na+/H+ exchanger. This leads to lower intracellular Ca2+ mobilization, followed by inhibition of TxA2 formation and then increased cyclic AMP formation, followed by a further inhibition of the Na+/H+ exchanger, ultimately resulting in markedly decreased intracellular Ca2+ mobilization and phosphorylation of P47. These results suggest that kinetin has an effective anti-platelet effect and that it may be a potential therapeutic agent for arterial thrombosis.

The protective effects of PMC against chronic carbon tetrachloride-induced hepatotoxicity in vivo.

In this study, PMC (2,2,5,7,8-pentamethyl-6-hydroxychromane), a derivative of alpha-tocopherol, dose-dependently (1-10 mg/kg) ameliorated the increase in plasma aspartate aminotransferase (GOT) and alanine aminotransferase (GPT) levels caused by chronic repeated carbon tetrachloride (CCl4) intoxication in mice. Moreover, PMC significantly improved the CCl4-induced increase of hepatic glutathione peroxidase, reductase, and superoxide dismutase activities. PMC also restored the decrement in the glutathione content of hepatic tissues in CCl4-intoxicated mice. Furthermore, it also dose-dependently inhibited the formation of lipid peroxidative products during carbon tetrachloride treatment. Histopathological changes of hepatic lesions induced by carbon tetrachloride were significantly improved by treatment with PMC in a dose-dependent manner. These results suggest that PMC exerts effective protection in chronic chemical-induced hepatic injury in vivo.

Optimization for solidification of low-level-radioactive resin using Taguchi analysis.

Solidification of low-level-radioactive (LLW) resin was optimized using Taguchi analytical methodology. The ingredients in LLW mortar which caused the solidification of cement were evaluated through consecutive measurements of the effects of various concentrations of ingredients. Samples selected according to Taguchi's method were separated into 18 different categories and measured at the 7th, 21st, and 28th day after fabrication on developing effects. Evaluations of the various samples focused on whether the compressive and bending strength fulfilled the special criteria of the Taiwan Power Company (TPC). Similar results indicated that both furnace slag and fly ash were the dominant material resulting from the solidification of LLW mortar. The superior combination was obtained as furnace slag 24 wt.%, fly ash 24 wt.%, and cement 8 wt.% to mix 24 wt.% of resin with 20 wt.% of water, to fulfill the contemporary requirements of TPC.

Bicipitoradial bursitis: MR imaging findings in eight patients and anatomic data from contrast material opacification of bursae followed by routine radiography and MR imaging in cadavers.

PURPOSE: To use radiography and magnetic resonance (MR) imaging after contrast material opacification of the bursae in cadaveric specimens to demonstrate the anatomy of the bicipitoradial bursa and to report MR imaging findings in patients with bicipitoradial bursitis. MATERIALS AND METHODS: Bicipitoradial bursa in eight cadaveric elbows were injected with a solution containing gadodiamide, iodinated contrast agent, and gelatin. Radiographs and MR images were obtained in each specimen, with both supination and pronation of the forearm. The morphology and relationships of the bursa were studied. Anatomic sections subsequently were obtained. MR imaging studies in eight patients with bicipitoradial bursitis were also evaluated. RESULTS: The bicipitoradial bursa revealed a smooth outline and a wide base along the superficial aspect of the radius. The mean volume of contrast material that could be injected before extravasation was 4 mL. The mean size of the bursa was 1.8 x 2.5 cm. The bicipitoradial bursa enveloped the biceps tendon, with internal septation seen in two cases. Displacement of the superficial branch of the radial nerve by the bursa was found in two specimens. Communication between the bicipitoradial bursa and elbow joint was not observed. In patients, MR imaging demonstrated fluid collections in the bicipitoradial bursa in all cases, with compression of branches of the radial nerve in two cases. CONCLUSION: The anatomy of the bicipitoradial bursa is demonstrated with radiography and MR imaging of bursae. MR imaging allows accurate diagnosis of bicipitoradial bursitis and its effects on adjacent structures.

Evaluation of articular cartilage thickness of the humeral head and the glenoid fossa by MR arthrography: anatomic correlation in cadavers.

OBJECTIVE: To evaluate the accuracy of MR arthrography in determining the thickness of articular cartilage of the humeral head and glenoid fossa. DESIGN AND PATIENTS: MR arthrography of the glenohumeral joint was performed in 17 cadaveric shoulders. Articular cartilage thickness was measured on the MR arthrographic images and corresponding anatomic sections. RESULTS: The correlation coefficients for MR arthrographic measurement versus anatomic measurement of the cartilage thickness were 0.7324 and 0.8757 for humeral head and glenoid fossa, respectively. With regard to the humeral head, there was a tendency to overestimate regions of thin cartilage and underestimate regions of thick cartilage. This tendency was not found in the assessment of glenoid cartilage. The mean of the absolute value of MR-anatomic differences was similar on the glenoid side (0.27 mm) and the humeral side (0.29 mm). The accuracy of measurement was significantly better on the glenoid side (Fisher's r-to-Z transformation: Z=5.21, P=0.000001). CONCLUSION: MR arthrography causes a moderate degree of error in the naked-eye measurement of the cartilage of the glenohumeral joint. The accuracy is higher on the glenoid side than on the humeral side.

Mechanism of cooling-induced relaxation in the isolated guinea-pig trachea.

In this study, we explored the possible mechanism of cooling-induced relaxation of the isolated guinea-pig trachea. A rapid cooling (-4 degrees C/min) from 37 +/- 0.5 degree C to 25 +/- 0.5 degree C induced a transient and small contraction followed by a sustained cooling-relaxation. This relaxation was not blocked by propranolol or tetrodotoxin. Various concentrations of four contractile agonists (histamine, carbachol, 5-HT and ryanodine) all enhanced cooling-relaxation in a concentration-dependent manner which correlated well with their increase in the developed muscular tension, suggesting an inherent counterbalance between cooling-relaxation and the bronchoconstriction. Treating with either indomethacin or nordihydroguaiaretic acid (NDGA) did not affect the contractile properties of histamine, carbachol and 5-HT except ryanodine, but reversed cooling-relaxation into sustained cooling-contraction. Indomethacin partially inhibited but NDGA abolished cooling-relaxation induced by ryanodine. Moreover, ryanodine, but not the other three contractile agonists, could antagonize indomethacin in inducing cooling-contractions by various agonists. From above findings, we can conclude that eicosanoids including prostaglandins particularly leukotrienes, which would be produced by the elevated Ca(2+)-release from the ryanodine sensitive Ca(2+)-store, play prominent roles in inducing cooling-relaxation.