Synthesis and characterization of the GeO(4)Al(12)(OH)(24)(OH2)(12)(8+) polyoxocation.
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Biomedical subjects
Publications and source records attributed to A P Lee.
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Raman spectroscopy has been used to demonstrate, for the first time, that calcium mineralization in the core of the major lateral teeth of the chiton Acanthopleura echinata takes place as an ordered process, with crystalline carbonated apatite being the first mineral deposited. Deposition begins at the top of the tooth core, under the so-called tab region, progresses down the interior surface of the tab and lepidocrocite layer, and then extends outwards to the anterior surface. Mineralization is not initiated until the lepidocrocite layer has isolated the core of the tooth from the magnetite cap. The last region to be infiltrated is the anterior basal region of the tooth cusp, immediately above the junction zone. The junction zone is also a region of high ion density, as determined by energy dispersive spectroscopy (EDS) analysis, but we show here for the first time that it is free of mineral deposits, acting instead as a transfer and storage region.
The authors of this paper chose several target compounds that have been found in average US homes, applied the current United States Environmental Protection Agency (USEPA) Superfund risk assessment methodologies to indoor air quality, and produced risk numbers for hazard quotients and predicted increases in incidence of cancer which would be unacceptable at US hazardous waste sites. The calculations were made for the average child and adult with USEPA default exposure values. Calculations were also made for a worst case scenario using maximum concentrations and exposure estimates defined by the USEPA as describing the reasonable exposure (RME). Significant cancer risks and non-cancer hazard quotients were predicted.
A tumor model involving stereotactically implanted culture-reared tumor cells is presented. Stainless steel cannulas were stereotactically and permanently implanted into the caudate nucleus of 30 rats. The animals were separated into two groups. In Group I, 15 animals received a 10-microliters injection containing 10(6) C6 glioblastoma cells (five rats), 10(6) Walker 256 breast carcinoma cells (five rats), or cell medium (five rats). The coordinates were A(+1.5), L(+3.0), and DV(-5.0). In Group II, the coordinates were changed to A(+1.0), L(+3.0), and DV(-5.0) and the same number of rats received a 1-microliter injection containing 10(5) cells of each tumor in an attempt to produce more focal tumors. Two weeks after implantation, brain sections were stained with cresyl violet and a subset was stained for glial fibrillary acid protein (GFAP). A computerized morphometric analysis system was used to quantify tumor size. In Group I, the mean C6 tumor areas (+/- standard error of the mean) at specific coordinates were (in sq mm): A(+4.7) 0.4 +/- 0.2; A(+3.7) 3.5 +/- 1.1; A(+2.7) 5.7 +/- 1.7; A(+1.7) 9.5 +/- 2.3; A(+0.7) 7.5 +/- 3.2; A(-0.3) 3.7 +/- 2.9; and A(-1.3) 0.3 +/- 0.3. A nearly identical tumor mass and extension into the brain was produced in rats injected with Walker 256 cells. Similar C6 tumor areas were indicated in adjacent sections stained with cresyl violet and GFAP. Tumor was found in the caudate nucleus in all 10 rats, but not in the nucleus accumbens, fornix, or hippocampus. In Group II animals, tumor magnitude and extension into the brain were greatly reduced. The 10(6) cells in the 10-microliters volume was the most reliable tumor load for obtaining uniform tumors in different animals. The similarity of tumor distribution across different animals was indicated by the low variance of tumor area at specific anteroposterior coordinates. Reproducible and well-circumscribed caudate nucleus tumors were produced using this stereotactic procedure.
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Eighteen patients with coronary heart disease and an ejection fraction of 0.40 or less were entered into an individualized exercise training program. Maximal symptom-limited exercise stress test and cardiac catheterization studies were performed initially and 12--42 months (average 18.5 months) after exercise training. At the time of the follow-up study, the mean functional aerobic impairment (FAI) improved from 32.1 to 23.4% (p less than or equal to 0.01); resting and submaximal heart rates were significantly lower (p less than 0.01 and 0.05, respectively). There was no significant change in the pulmonary artery or left ventricular end-diastolic pressure, cardiac index, stroke index, left ventricular end-diastolic volume or ejection fraction. Exercise training, therefore, can be beneficial even for patients with impaired ventricular function. Increase in physical work capacity was not correlated with improvement of ventricular function; on the other hand, exercise training did not cause deterioration of ventricular function.