Motoharu Kondo

Significant prolongation of disease-free period gained by oral polysaccharide K (PSK) administration after curative surgical operation of colorectal cancer

SummaryTo examine the clinical efficacy and the mechanism of action of polysaccharide K (PSK), a proteinbound polysaccharide extracted from a Basidiomycetes fungus, a randomized double-blind trial was performed by administering PSK to 56 patients and a placebo to another group of 55 patients after surgical operations on their colorectal cancers. The rate of patients in remission (or disease-free) was significantly higher in the PSK group than in the placebo group; the difference between both groups was statistically significant atP <0.05 by the logrank test. The survival rate of patients was also significantly (P <0.05) higher in the PSK group than in the control group. The most significant laboratory finding was that polymorphonuclear leukocytes from PSK-treated patients showed remarkable enhancement in their activities, such as random and/or chemotactic locomotion, and phagocytic activity, when compared with those in the control group. In conclusion, PSK was useful as a maintenance therapy for patients after their curative surgical operations for colorectal cancer. The beneficial effects were probably due to the activation of leukocyte functions as one of the many biological-response-modifying (activities induced by PSK).

Vitamin E in gastric mucosal injury induced by ischemia-reperfusion

To clarify the relationship among vitamin E, oxygen radicals, and lipid peroxidation in ischemia-reperfusion, we produced an experimental model of gastric mucosal injury in rats by ischemia-reperfusion with clamping of the celiac artery and measurements of the area of gastric erosion, thiobarbituric acid (TBA)-reactive substances, and alpha-tocopherol in serum and gastric mucosa during ischemia-reperfusion. The area of gastric erosions and TBA-reactive substances in gastric mucosa were significantly increased after 30 and 60 min of reperfusion. The serum alpha-tocopherol-cholesterol ratio and gastric mucosal alpha-tocopherol were significantly decreased after 30 and 60 min of reperfusion. On the other hand, in vitamin E-deficient rats, gastric mucosal injury induced by ischemia-reperfusion was more severe than that in vitamin E-nondeficient rats. These results indicate that vitamin E is consumed in the process of lipid peroxidation induced by oxygen radicals in ischemia-reperfusion to prevent the development of tissue damage.

Glucose intolerance in chronic renal failure

慢性腎不全に耐糖能異常が存在することはよく知られているが, その成因については不明な点が少なくない. インスリン抵抗性もその一因と考えられているが, この点をさらに明らかにするためにインスリン受容体の面から検討した. 未透析腎不全患者10名, 透析患者12名および正常者6名を対象に赤血球のインスリン受容体を検討し, 0.5g/kgのIVGTTを行い, K値 (血糖消失率) およびΣIRI (IRIの総和) を求めた. K値は未透析群 (1.32±0.30) では正常群 (1.92±0.25), 透析群 (1.82±0.34) と比べて低値を示したが, 正常群と透析群との間には差がなかった. ΣIRIは未透析群 (445±78μU/ml), 透析群 (420±80μU/ml) は正常群 (260±38μU/ml) と比べて高値を示したが, 未透析群と透析群との間には差がなかった. インスリン特異結合率 (赤血球2.4×109個/mlへの0.2ng/mlの125I-インスリン) は未透析群 (3.99±0.76%) は低値を示したが, 正常群 (5.50±0.69%) と透析群 (5.11±0.80%) との間には有意差がなかった. Scatchard解析より, 未透析群におけるインスリン特異結合率の低下はインスリン受容体数の減少によるものと思われた (正常群64個/cell; 透析群58個/cell; 未透析群45個/cell).さらに, 耐糖能異常とインスリン受容体との関係を明らかにするために, インスリン特異結合率とK値および空腹時IRI, ΣIRIとの関係をみたが, 透析群において特異結合率とK値との間に正の相関を認めた. このことより, 未透析腎不全患者の耐糖能異常はインスリン受容体数の低下によるものと思われ, 透析療法はインスリン受容体レベルでの改善により耐糖能障害を正常化させるものと思われた.