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J Hatfield

Publications and source records attributed to J Hatfield.

5 recordsLinked to original sources

Airborne asbestos in public buildings.

The U.S. Environmental Protection Agency sampled air in 49 government-owned buildings (six buildings with no asbestos-containing material, six buildings with asbestos-containing material in generally good condition, and 37 buildings with damaged asbestos-containing material). This is the most comprehensive study to date of airborne asbestos levels in U.S. public buildings during normal building activities. The air outside each building was also sampled. Air samples were analyzed by transmission electron microscopy using a direct transfer preparation technique. The results show an increasing trend in average airborne asbestos levels; outdoor levels are lowest and levels in buildings with damaged asbestos-containing material are highest. However, the measured levels and the differences between indoors and outdoors and between building categories are small in absolute magnitude. Comparable studies from Canada and the UK, although differing in their estimated concentrations, also conclude that while airborne asbestos levels may be elevated in buildings that contain asbestos, levels are generally low. This conclusion does not eliminate the possibility of higher airborne asbestos levels during maintenance or renovation that disturbs the asbestos-containing material.

Air Pollutants

Arrest and extravasation of B16 amelanotic melanoma in murine lungs. A light and electron microscopic study.

The arrest and extravasation of tail vein-injected B16 amelanotic melanoma (B16a) cells, disaggregated from subcutaneous tumors, were studied at intervals from 10 minutes to 5 days in lungs of C57BL6J mice. Tumor cells were found in the pulmonary vasculature at 10 minutes postinjection and were commonly associated with platelets and fibrin. Tumor cells with associated thrombi increased, reaching a peak at 4 hours. Arrest of the B16a melanoma tumor cells appears to involve contact with endothelial plasma membrane, often with adjacent but not interposed platelet and fibrin thrombus formation. The tumor cell-associated thrombi subsequently decreased in frequency and were rarely found after 48 hours. The arrested tumor cells were initially in contact with the endothelial cells, which were gradually displaced by tumor cells achieving contact with the vascular basal lamina (BL). Initial contact with the vascular BL was observed at 4 hours, with a progressive increase in contact over the subsequent 2 days. Blood flow was commonly reestablished past the BL-attached tumor cells after dissolution of the thrombi. Mitotic figures in the tumor cells attached to the BL were frequent after 24 hours and the tumor appeared to proliferate intravascularly along the basal lamina. Penetration of the BL by tumor cell cytoplasmic processes was first observed at 3 days with continued dissolution of the vascular BL developing through day 5. Extravasation occurred through a combination of intravascular tumor cell proliferation and destruction of vascular BL by the B16a cells. Migration or diapedesis of the tumor cells was not observed in any of the time periods studied.

Animals

Nuclear activity.

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Cell Nucleolus