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J Hatfield

Publications and source records attributed to J Hatfield.

7 recordsLinked to original sources
PubMed1994

Aging diminishes gastric mucosal regeneration: relationship to tyrosine kinases.

BACKGROUND: Increased incidence of gastric ulcer observed in the aged could be partly attributed to increased susceptibility of the mucosa to various damaging agents together with impediment of the repair process. The present investigation was undertaken to compare the rate of mucosal regeneration and the role of tyrosine kinases in regulation of this process between young (4-month-old) and aged (24-month-old) rats during the first 24 hours after injury. EXPERIMENTAL DESIGN: Groups of young and aged rats were given intragastrically with either 2 M NaCl (1.5 ml/130 gm body weight), or an equivalent volume of water and killed 1, 6, and 24 hours later. Each animal was injected intraperitoneally with 5-bromo-2'-deoxyuridine (BrdU; 50 mg/kg) 1 hour before killing to assess proliferative activity by immunocytochemistry. The stomach (oxyntic gland area) was also evaluated by light microscopy for the extent of injury and subsequent regeneration, and mucosa assayed for ornithine decarboxylase and tyrosine kinase (Tyr-k) activity and tyrosine phosphorylation of membrane proteins. RESULTS: Although 2 M NaCl caused extensive damage to the gastric mucosa in both young and aged rats, as evidenced by the total loss of the surface epithelium at 1 hour postinjury, the degree of regeneration was faster in young animals. In young rats, gastric epithelium showed signs of regeneration at 6 hours postinjury and was essentially complete by 24 hours. In contrast, in aged rats, only intermittent surface cells were seen 24 hours after injury. In both age groups, injury resulted in stimulation of mucosal proliferative activity. However, whereas ornithine decarboxylase activity in both age groups was maximally stimulated (350% in young versus 80% in aged) at 6 hours after injury, the number of BrdU-positive cells in young rats increased steadily with time after injury. In contrast, aged rats showed a biphasic pattern in that the number of BrdU-positive cells/gland remained decreased for up to 6 hours, whereafter a steep rise occurred. At 24 hours after injury, the number of BrdU-positive cells/gastric gland in aged rats were found to be higher than in young rats (6 +/- 1.5 cells/gland in young rats versus 9 +/- 2.1 cells/gland in aged rats). The pattern of Tyr-k activity in young and aged rats after injury was found to be quite different from that observed for proliferative activity. In young rats, mucosal Tyr-k activity increased by about 60% at 1 hour after injury, then decreased slightly over the next 5 hours and increased again revealing a 120% rise at 24 hours postinjury. This was associated with a concomitant change in tyrosine phosphorylation of six membrane proteins with molecular weight (in kilodalton) of 30, 35, 50, 55, 60 and 70. In contrast, in aged rats, Tyr-k activity was increased only marginally (about 20%) during the first 6 hours, but at 24 hours postinjury it was found to be 70% above the control. In aged rats, injury produced no significant stimulation in tyrosine phosphorylation of gastric mucosal membrane proteins. CONCLUSIONS: We conclude that aging is associated with the diminished regenerative capacity of the gastric mucosa. This could partly be attributed to diminished activation of mucosal Tyr-k and decreased tyrosine phosphorylation of certain membrane proteins.

Aged↗
PubMed1993

The difficulties with low-level asbestos exposure assessments in public, commercial, and industrial buildings.

A method by which the airborne concentration of asbestos, low enough to substantiate that a significant health risk does not exist, is presented. The method is different from that used for the determination of occupational exposure, which is shown to be inadequate in this concentration range and a justification of how this alternative procedure might be used to achieve compliance is put forward. The difficulties associated with both the physical measurement and the significance of the concentrations that are determined are discussed.

Air↗
PubMed1990

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↗
PubMed1985

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↗
PubMed1970

Nuclear activity.

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Cell Nucleolus↗