To elucidate the relationship between activation of neutrophils and their subsequent death, the effect of phorbol 12-myristate 13-acetate (PMA), a potent activator of neutrophils, was examined. PMA-treated neutrophils showed morphological changes quite different from those of typical apoptosis or necrosis. After fusion of the lobate nucleus, nuclear contents of chromatin uniformly decreased in compactness and soon after the nuclear envelope was broken. Even at this stage, cytoplasmic organelles did not undergo degeneration. Membrane permeability began increasing at 3 h of incubation with PMA, subsequent to nuclear change. Conventional agarose gel electrophoresis and pulsed field gel electrophoresis of DNA from PMA-treated neutrophils revealed no DNA degradation products smaller than 300 kbp. PKC inhibitors, staurosporine and H-7, prevented cytotoxicity by PMA. Furthermore, antioxidants, thiourea, dimethylthiourea, pyrrolidinethiocarbamate, and N-acetyl-L-cysteine, but not superoxide dismutase, were also active in preventing PMA cytotoxicity, suggesting that cell suicide resulting from PMA treatment is due to oxygen radicals, especially the hydroxyl radical. A certain population of neutrophils phagocytosing opsonized zymosan also showed changes similar to those observed in PMA-treated cells.

The cytotoxic effect of different concentrations of titanium particles on osteoblasts was studied in vitro. It was found that the viability of the osteoblasts was inversely proportional to the particle concentration. Phagocytosis of particles by the osteoblasts was evident and was demonstrated to be responsible for cell necrosis. Moreover, during and after phagocytosis, the osteoblasts released products that were cytotoxic for other osteoblasts, as established with a conditioned medium assay. The titanium particles thus had both a direct and an indirect effect on osteoblast viability. It also was observed that the titanium particles induced a process of programmed cell death (apoptosis) when co-cultured with osteoblasts. The results of this study suggest that not only is the amount of wear debris generated important, but the local accumulation of the debris also may have a significant impact on bone cell function.

In a review of the vertebral angiograms of 300 patients free from disease at the craniovertebral junction, we found atlantoaxial arterial anomalies in 2,3%. These were: 2 cases in which the vertebral artery ran in the spinal canal below C1, 3 cases of duplication of the vertebral artery above and below C1, and 2 cases of origin of the posterior inferior cerebellar artery at C2. Although these arteries ran in the spinal canal between C1 and C2, they never encroached upon the posterior third of the canal. From the survey of another 21 patients having bony abnormalities at the craniovertebral junction, the first type of arterial anomaly described above was seen in 4 patients and associated with failure of segmentation of the embryonic sclerotome such as occipitalization of the atlas or Klippel-Feil syndrome. It is possible to relate the development of these anomalous vessels to malarrangement of the embryonic segmental arteries. Our results indicate that one must be cautious with lateral C1/2 puncture or surgical exposure of the region.

Background: There is no validated gold-standard diagnostic support tool for LSS, and therefore an accurate diagnosis depends on clinical assessment. Assessment of the diagnostic value of the history of the patient requires an evaluation of the differences and overlap of symptoms of the radicular and cauda equina types; however, no tool is available for evaluation of the LSS category. We attempted to develop a self-administered, self-reported history questionnaire as a diagnostic support tool for LSS using a clinical epidemiological approach. The aim of the present study was to use this tool to assess the diagnostic value of the history of the patient for categorization of LSS.

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