Various pathologic findings provided important foundations for discussing the pathogenesis of lesions in ligamentum flavum. Calcification was frequently observed in elderly patients and those with cauda equina symptoms, and these patients tended to have severer preoperative symptoms. Chondroid cells were frequently observed in patients with spondylolisthesis, and patients with ossification had a greater % slip, suggesting involvement of mechanical load in ossification of ligaments. The pathologic findings were significantly related to the clinical features, and these findings will be profitable for understanding the pathogenesis of degenerative lumbar disease.

Our results demonstrate that the pre-operative high blood pressure value was the most essential risk factor for PSEH, although there was no difference in the preoperative hypertension treatment. Consequently, management of pre-operative blood pressure and post-operative drainage will be crucial for preventing PSEH.

No abstract

These results suggest that M (an active metabolite of erdosteine) may exert an antiinflammatory effect by scavenging inflammatory cells-derived reactive oxygen species.

The effects of (Z)-11-[(3-dimethylamino)propylidene]-6,11-dihydrodibenz[b.e.] oxepin-2-acetic acid monohydrochloride (KW-4679), an orally active antiallergic drug, on the production of platelet-activating factor (PAF), leukotriene (LT) and thromboxane (TX) induced by Ca²⁺ ionophore A23187 were examined. KW-4679 at 10 μM reduced the amount of cell-associated PAF by 52.8% in human polymorphonuclear leukocytes (PMNs). KW-4679 (1–100 μM) also inhibited the release of both LTB₄ and TXB₂, a stable metabolite of TXA₂, by human PMNs in a concentration-dependent manner, but did not influence the release of β-glucuronidase. The 50% inhibitory concentration (IC₅₀) values for LTB₄ and TXB₂ release were 5.9 and 6.0 μM, respectively. In guinea pig eosinophils, KW-4679 inhibited the release of peptide LTs at a concentration higher than 10 μM (IC₅₀ = 66.9 μM). KW-4679 failed to inhibit PAF acetyltransferase, 5-lipoxygenase and TX synthase, but inhibited the arachidonic acid rlease by human PMNs in a concentration-dependent manner at a similar concentration as that inhibiting production or release of lipid mediators (IC₅₀ =19.5 μM). These results indicate that KW-4679 suppresses LTs and TX release and PAF formation by reducing arachidonic acid release from phospholipids, probably through interference with phospholipase A₂. The inhibitory action of KW-4679 on PAF, LT and TX production is a beneficial effect of an antiallergic drug.