Modification of the 1979 "Denver wire code" for different wire or plumbing types.

This article examines "wire configuration coding" as used to estimate relative residential AC magnetic field exposure in epidemiological studies--and the need to alter such coding for time or locations other than those in which the code was developed. Effects of different secondary wire practices are particularly examined.     

Cell cycle age dependence for radiation-induced G2 arrest: evidence for time-dependent repair

Exponentially growing eucaryotic cells, irradiated in interphase, are delayed in progression to mitosis chiefly by arrest in G2. The sensitivity of Chinese hamster ovary cells to G2-arrest induction by X rays increases through the cell cycle, up to the X-ray transition point (TP) in G2. This age response can be explained by cell cycle age-dependent changes in susceptibility of the target(s) for G2 arrest and/or by changes in capability for postirradiation recovery from G2-arrest damage. Discrimination between sensitivity changes and repair phenomena is possible only if the level of G2-arrest-causing damage sustained by a cell at the time of irradiation and the level ultimately expressed as arrest can be determined. The ability of caffeine to ameliorate radiation-induced G2 arrest, while inhibiting repair of G2-arrest-causing damage makes such an analysis possible. CHO cell monolayers were irradiated (1.5 Gy), then exposed to 5 mM caffeine for periods of 0-10 hr. Cell progression was monitored by the mitotic cell selection procedure. In the presence of caffeine, progression of irradiated cells was relatively unperturbed, but on caffeine removal, G2 arrest was expressed. The duration of G2 arrest was independent of the length of the prior caffeine exposure and, since cells of all ages were ultimately examined, the duration of arrest was also independent of cell cycle age at the time of irradiation. This finding indicates that the target for G2-arrest induction is present throughout the cell cycle and that the level of G2-arrest damage incurred is initially constant for all cell cycle phases. The data are consistent with the existence of a time-dependent recovery mechanism to explain the age dependence for radiation induction of G2 arrest.     

Repair Kinetics of Radiation-Induced Mitotic Delay

The recovery from radiation-induced mitotic delay in asynchronous sarcoma-180 (S-180) ascites tumor cells has been analyzed in a manner analogous to the repair of sublethal damage. 200-R increments were separated by various fraction intervals (not exceeding the time necessary for mitosis to return to control levels) for total exposures up to 1600 R. The accumulated mitotic delay after the last exposure increment, in percent of an equivalent single exposure, decreased exponentially with overall treatment time in a bimodal fashion. An initial repair process displayed a half time of 2.3 h of overall elapsed time and was followed by a slower process with a half time of 15.1 h. Such a bimodal recovery provides an explanation of why fractionation intervals long with respect to the amitotic period resulting from a single 200 R exposure enhance mitotic delay over that of equivalent single exposures, while shorter fractionation intervals diminish it. It also predicts that mitotic delay vs. dose curves should bend toward the abscissa as the exposure time is increased with large single exposures and large fractionated exposures given over short fraction intervals.     

Fine structure of polysaccharide microcrystals

Summary Negative staining showed the presence of microcrystals in various polysaccharides. Cellulose microcrystals from Valoniopsis, Vaucheria, and an unidentified tunicate had widths of 20, 27, and 30 Å, respectively. Mannan microcrystals from Acetabularia were 10x25 Å and were oriented in linear arrays with their long axis perpendicular to the array axis. dichotomosiphon and Caulerpa xylans had respective microcrystal widths of 22 and 24 Å. All microcrystals appeared as component part of microfibrils.     

Response of murine bone marrow granulocyte-macrophage colony-forming units to hyperthermia in situ

A detailed understanding of how bone marrow stem cell progenitors are affected by heat is prerequisite to predicting how whole-body or regional hyperthermia protocols may affect bone marrow function. This investigation reports the reproductive integrity of murine tibial bone marrow granulocyte-macrophage colony-forming units (CFU-GM) after in situ hyperthermia. Heat was applied by water bath immersion of the leg of male BALB/c mice anesthetized with 90 mg/kg pentobarbital given subcutaneously. Tibial and rectal temperatures were monitored in representative animals by microthermocouples (tip diameter approximately 100 microns). By approximately 3 min after immersion of the limb, marrow temperature was within 0.3 degree C of water bath temperature (O'Hara et al., Int. J. Hyperthermia 5, 589-601, 1989) and was within 0.1 degree C by 5 min after immersion. The CFU-GM were cultured in "lung-conditioned" McCoy's 5A medium supplemented with 15% fetal calf serum and 0.3% Bacto agar. In situ heating of tibial marrow to exposure temperatures of 42, 42.5, 43, 44, and 45 degrees C gave D0's (+/- 95% CI) of 91 +/- 44, 44 +/- 27, 27 +/- 2.2, 16 +/- 6, and 7 +/- 4 min, respectively. Heating to 41.5 degrees C for up to 180 min did not result in cytotoxicity. Development of thermotolerance after approximately 100 min of heating was apparent by the presence of a "resistant tail" of the 42 degrees C survival curve. A plot of D0 vs water bath temperature was bimodal with an inflection point at approximately 42.5 degrees C. The inactivation enthalpy for temperatures above 42.5 degrees C was 586 kJ/mol (140 kcal/mol) and for temperatures below 42.5 degrees C was estimated to be 1205 kJ/mol (288 kcal/mol). These results show that CFU-GM can be heated predictably in situ, can be inactivated with thermal exposures as low as 42 degrees C, and are capable of developing thermotolerance. These findings underscore the necessity to understand stem cell inactivation by hyperthermia in situ prior to widespread implementation of clinical hyperthermia protocols where bone marrow may be included in the treatment field.     

Plankton composition, abundance and dynamics in a severely stressed cooling reservoir

The effects of severe thermal stress imposed by the intermittentoperation of a nuclear reactor on plankton abundance and dynamicswere investigated in Pond C, a cooling reservoir on the SavannahRiver Site in South Carolina, USA. Temperatures in Pond C rangedup to 58°C during reactor operation. The thermal effluenteliminated zooplankton from regions where the temperature exceeded45°C, reduced zooplankton abundance by 1–3 ordersof magnitude and typically halved the number of taxa. Reactoroperation also reduced phytoplankton biovolume, often by >70%.During intermittent reactor operation, the rotifer Filinia longisetadominated the zooplankton and two cladocerans of the genus Moinawere abundant. These species were not abundant during extendedreactor shutdowns. The success of Filinia and Moina was dueprimarily to their tolerance of high temperatures. Sparse phytoplanktonprobably limited some zooplankton taxa, although other taxa,such as Filinia may have utilized bacterial resources. Reactoroperation may have intensified predation on crustacean zooplanktonwhen fish were concentrated in refuge areas with zooplankton.Processes by which zooplankton repopulated the reservoir afterreactor shutdown were inferred from zooplankton distributionpatterns, and population growth and birth rates. Repopulationtypically occurred within a few days due to rapid growth ofpopulations from refuge areas within the reservoir and colonistsbrought in through a tributary canal. Mechanisms of zooplanktonrepopulation in Pond C suggest that refuges or colonizationcorridors should be maintained when the re-establishment ofcommunities following cessation of stresses is desired.     

Plasminogen activator and collagenase production by cultured capillary endothelial cells

Cultured bovine capillary endothelial (BCE) cells produce low levels of collagenolytic activity and significant amounts of the serine protease plasminogen activator (PA). When grown in the presence of nanomolar quantities of the tumor promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA), BCE cells produced 5-15 times more collagenolytic activity and 2-10 times more PA than untreated cells. The enhanced production of these enzymes was dependent on the dose of TPA used, with maximal response at 10(-7) to 10(-8) M. Phorbol didecanoate (PDD), an analog of TPA which is an active tumor promoter, also increased protease production. 4-O-methyl-TPA and 4α-PDD, two analogs of TPA which are inactive as tumor promoters, had no effect on protease production. Increased PA and collagenase activities were detected within 7.5 and 19 h, respectively, after the addition of TPA. The TPA-stimulated BCE cells synthesized a urokinase-type PA and a typical vertebrate collagenase. BCE cells were compared with bovine aortic endothelial (BAE) cells and bovine embryonic skin (BES) fibroblasts with respect to their production of protease in response to TPA. Under normal growth conditions, low levels of collagenolyic activity were detected in the culture fluids from BCE, BAE, and BES cells. BCE cells produced 5-13 times the basal levels of collagenolytic activity in response to TPA, whereas BAE cells and BES fibroblasts showed a minimal response to TPA. Both BCE and BAE cells exhibited relatively high basal levels of PA, the production of which was stimulated approximately threefold by the addition of TPA. The observation that BCE cells and not BAE cells produced high levels of both PA and collagenase activities in response to TPA demonstrates a significant difference between these two types of endothelial cells and suggests that the enhanced detectable activities are a property unique to bovine capillary and microvessel and endothelial cells.     

The influence of scald water pH on the death rates of Salmonella typhimurium and other bacteria attached to chicken skin

Factory trials where scald tank water was maintained at pH 9.0 +/- 0.2 showed that compared with the usual system of scalding when the water is at pH 6.0 for much of the working day the bacterial counts on carcases post scalding and plucking were significantly lower. In laboratory experiments, attached Salmonella typhimurium and the naturally occurring skin flora were found to be killed significantly more quickly in water at pH 9.0 +/- 0.2.