PubMed · 8753551
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T Akatsu. 1995. [Calcium].. https://pubmed.ncbi.nlm.nih.gov/8753551/
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A greenhouse experiment was conducted evaluating the effects of water stress on uptake and accumulation of selenium (Se) as well as on uptake of calcium (Ca), potassium (K), and magnesium (Mg) in tall fescue (Festuca arundinacea Schreb). Also, this study has documented changes in soil Se inventory of Se-contaminated field soil. The findings of this experiment suggest that low soil moisture and plant water stress had a positive effect on plant tissue Se concentration. However, the negative effect of water stress on plant growth superimposed the increase of plant tissue Se concentration. Therefore, Se accumulation and soil Se removal by tall fescue became largely dependent on plant dry weight production. Strategies utilizing for remediation of Se-contaminated soils should maximizing the growth rates of tall fescue by maintaining soil moisture levels above water-stress conditions (greater than -1.0 MPa). The results of this study also suggest that the relative sensitivity of net uptake of Se and the three macronutrients to reduced soil moisture is: Ca uptake < Se uptake < Mg uptake < K uptake.
This paper presents a design for randomized clinical trials in which incomplete data are collected on the occurrence of potentially recurrent events through periodic monitoring. In particular, events are assumed to arise according to a point process, but information is available at the times of monitoring only if one or more events has occurred since the preceding monitoring point. The event process is modelled via a piecewise Poisson process, and a proportional rates model is introduced to represent the difference in event rates between treatment groups. The design was developed on the basis of a Wald-type test derived from the generalized estimating equations of Liang and Zeger (Biometrika 73, 13-22 (1986)). Robustification of the variance of the estimator of the treatment effect was considered under a random effects model with a semi-parametric mixture distribution. The design was adopted to address issues which arose in an osteoporosis trial conducted in Japan.
We have investigated the role of mitochondrial Ca(2+) (Ca(m)) homeostasis in cell survival. Disruption of Ca(m) homeostasis via depletion of the mitochondrial Ca(2+) store was the earliest event that occurred during staurosporine-induced apoptosis in neuroblastoma cells (SH-SY5Y). The decrease of Ca(m) preceded activation of the caspase cascade and DNA fragmentation. Overexpression of the anti-apoptosis protein Bcl-2 led to increased Ca(m) load, increased mitochondrial membrane potential (DeltaPsi(m)), and inhibition of staurosporine-induced apoptosis. On the other hand, ectopic expression of the pro-apoptotic protein Bik led to decreased Ca(m) load and decreased DeltaPsi(m). Inhibition of calcium uptake into mitochondria by ruthenium red induced a dose-dependent apoptosis as determined by nuclear staining and DNA ladder assay. Similarly, reducing the Ca(m) load by lowering the extracellular calcium concentration also led to apoptosis. We suggest that the anti-apoptotic effect of Bcl-2 is related to its ability to maintain a threshold level of Ca(m) and DeltaPsi(m) while the pro-apoptotic protein Bik has the opposite effect. Furthermore, both ER and mitochondrial Ca(2+) stores are important, and the depletion of either one will result in apoptosis. Thus, our results, for the first time, provide evidence that the maintenance of Ca(m) homeostasis is essential for cell survival.