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PubMedDate not supplied

Calculation of three-dimensional photon primary absorbed dose using forward and backward spread dose-distribution functions.

This paper describes a method of calculating three-dimensional (3-D) photon primary absorbed dose in a homogeneous or heterogeneous medium. The method is based on a technique of convolving a pair of forward and backward spread dose-distribution functions with the primary water collision kerma distribution. Both spread dose-distribution functions can be constructed by analyzing the zero-area tissue-maximum ratio, the primary absorbed dose near the beam exit surface, and the laterally spread dose distribution. Primary absorbed dose calculations are performed along the beam axis for 10-MV x rays. The characteristic patterns of primary dose in heterogeneous phantoms containing an aluminum or lunglike material slab can be obtained.

Models, Structural↗

PubMed1999

A comparison of Monte Carlo and analytic first scatter dose spread arrays.

We compare first scattered point dose spread arrays generated by Monte Carlo and an analytic method. The analytic method models energy deposition using Klein-Nishina cross sections for Compton scatter and approximations for electron transport. Assumptions in the analytic method are shown to be valid within a region of the point dose spread kernel in which meaningful comparisons can be made. Differences between the models are less than 10% for the forward scatter directions for radii greater than the electron range associated with the first scattered Compton photon. Differences in the backscatter region are discussed and indicate that the analytic model is useful for identifying large errors that might be present in numerically generated first scatter point dose spread arrays. The analytic method is simple and useful for validating first scatter kernels.

Monte Carlo Method↗

PubMed1966

Severe impairment of heat-induced saliva-spreading in rats recovered from lateral hypothalamic lesions.

A method has been devised to record saliva-spreading on fur and skin by rats in the heat. Normal males and females increase saliva-spreading with increasing ambient temperatures. Rats recovered from lateral hypothalamic lesions do not spread saliva in the heat, confirming the inference drawn from studies of their drinking behavior that their saliva production is severely impaired. Recovered lateral rats do produce saliva when injected with pilocarpine. The failure to salivate is, therefore, a result of the lateral hypothalamic lesions and is not due to an incompetence of the glands.

Animals↗

PubMed1971

Amnesia produced by spreading depression and ECS: evidence for time-dependent memory trace localization.

Rats were given electroconvulsive shock and bilateral cortical spreading depression, either alone or in combination, at various times after a single passive avoidance training trial. Assessment of retention deficits, 24 hours after training, revealed a U-shaped amnesic function for cortical spreading depression as compared with the short linear function consistently obtained with electroconvulsive shock in this situation. Induction of cortical spreading depression immediately after training resulted in an extension of the amnesic gradient produced by electroconvulsive shock, presumably by disruption of the subcortically confined memory trace. In addition to indicating a stibcortical locus of action for the amnesic effects of electroconvulsive shock, these results are interpreted as favoring a hypothesis of time-dependent memory trace localization in short-term memory processing, which involves an initial subcortical localization of the trace followed by a phase involving either direct or indlirect cortical participation in a mulltistage memory fixation process.

Amnesia↗

PubMed1996

Spread of synaptic depression mediated by presynaptic cytoplasmic signaling.

Postsynaptic activity may modulate presynaptic functions by transsynaptic retrograde signals. At developing neuromuscular synapses in Xenopus nerve-muscle cultures, a brief increase in the cytosolic calcium ion (Ca2+) concentration in postsynaptic myocytes induced persistent depression of presynaptic transmitter secretion. This depression spread to distant synapses formed by the same neuron. Clearance of extracellular fluid did not prevent the spread of depression, and depression could not be induced by increasing the Ca2+ concentration in a nearby myocyte not in contact with the presynaptic neuron. Thus, the spread of depression is mediated by signaling in the presynaptic cytoplasm, rather than by a retrograde factor in the extracellular space.

Animals↗

PubMed1993

Dynamics, spread, and persistence of a single genotype of Pseudomonas syringae relative to those of its conspecifics on populations of snap bean leaflets.

A rifampin-resistant strain of Pseudomonas syringae (R10) was introduced onto bean plants grown in field plots to examine the processes of growth, spread, and survival of a single genotype relative to the dynamics of its conspecifics on populations of individual leaflets. R10 was applied to four plots (400, 200, 100, and 50 m2), each of which was centered in a quadrant of a bean field (90 by 90 m). Population sizes of the species P. syringae and of R10 were determined on each of 25 individual leaflets collected from the largest plot (A) at approximately weekly intervals during a 10-week period following application. The spread of R10 from all plots was monitored by leaf imprinting of individual leaflets collected at sites along four transects, each of which bisected two of the plots. The introduced strain was a dominant component of the species for about 5 weeks postinoculation on leaflets from plot A. Although the population sizes of R10 remained at about 5.0 to 5.5 log10 CFU per leaflet, the strain became a progressively minor component of the species as the population sizes of its conspecifics continued to increase during the latter part of the growing season. In general, a positive correlation was found for the population sizes of R10 and its conspecifics on individual leaflets collected throughout the growing season. This result suggests that large numbers of R10 early in the growing season did not exclude the colonization of bean leaflets by its conspecifics. It is apparent that the species pool comprised genotypes that were more fit than R10 under the conditions that prevailed during the latter part of the growing season. By 6 weeks postinoculation, R10 was detected at all sites sampled within the unsprayed areas of the field. However, it was present as a minor component of the species. The persistence of R10 throughout the winter and into the following growing season was monitored in plot A, which was plowed and replanted with wheat in the fall. R10 was detected on some of the samples (wheat seedlings or soil) taken at approximately monthly intervals from November to June of the following year. In June, the field was plowed and replanted with beans. We could not detect R10 on emerging bean seedlings in plot A. The results demonstrate that the successful spread and persistence of an introduced bacterium do not necessarily lead to the establishment of large populations of the bacterium in adjacent untreated areas or on its host plant in subsequent growing seasons.

Ecology↗

PubMed1997

Molecular genetic evidence for the involvement of a specific polygalacturonase, P2c, in the invasion and spread of Aspergillus flavus in cotton bolls.

Isolates of Aspergillus flavus can be differentiated based on production of the polygalacturonase P2c. One group of isolates produces P2c, whereas the other group does not. In general, the group that produces P2c causes more damage and spreads to a greater extent in cotton bolls than those isolates that do not produce P2c. To determine whether P2c contributes to disease, the expression of pecA, the gene previously determined to encode P2c, was genetically altered. Adding the pecA gene to a strain previously lacking the gene resulted in the ability to cause significantly more damage to the intercarpellary membrane and the ability spread to a greater extent within the adjacent locule compared to the abilities of a control transformant. Conversely, eliminating the expression of pecA by targeted disruption caused a significant reduction in aggressiveness compared to that of a nondisrupted control transformant. These results provide direct evidence that P2c contributes to the invasion and spread of A. flavus during infection of cotton bolls. However, other factors not evaluated in this study also contribute to aggressiveness.

Aspergillus flavus↗

PubMed2003

Spread of recombinant DNA by roots and pollen of transgenic potato plants, identified by highly specific biomonitoring using natural transformation of an Acinetobacter sp.

Transgenic potato plants with the nptII gene coding for neomycin phosphotransferase (kanamycin resistance) as a selection marker were examined for the spread of recombinant DNA into the environment. We used the recombinant fusion of nptII with the tg4 terminator for a novel biomonitoring technique. This depended on natural transformation of Acinetobacter sp. strain BD413 cells having in their genomes a terminally truncated nptII gene (nptII'; kanamycin sensitivity) followed by the tg4 terminator. Integration of the recombinant fusion DNA by homologous recombination in nptII' and tg4 restored nptII, leading to kanamycin-resistant transformants. DNA of the transgenic potato was detectable with high sensitivity, while no transformants were obtained with the DNA of other transgenic plants harboring nptII in different genetic contexts. The recombinant DNA was frequently found in rhizosphere extracts of transgenic potato plants from field plots. In a series of field plot and greenhouse experiments we identified two sources of this DNA: spread by roots during plant growth and by pollen during flowering. Both sources also contributed to the spread of the transgene into the rhizospheres of nontransgenic plants in the vicinity. The longest persistence of transforming DNA in field soil was observed with soil from a potato field in 1997 sampled in the following year in April and then stored moist at 4 degrees C in the dark for 4 years prior to extract preparation and transformation. In this study natural transformation is used as a reliable laboratory technique to detect recombinant DNA but is not used for monitoring horizontal gene transfer in the environment.

Acinetobacter↗

PubMed1981

Persistence and spread of Candida albicans after intragastric inoculation of infant mice.

Infant mice have been shown previously to be a useful model for the study of gastrointestinal (GI) and systemic candidosis. In this study, the virulence of four strains of Candida albicans was compared in intragastrically inoculated infants and in adult mice inoculated intravenously. The four strains differed in their ability to kill both infant and adult mice. A smaller inoculum was required to kill adult mice inoculated intravenously. Neonates could not be inoculated intravenously. The ability of the strains to spread systemically from and to persist for long periods of time in the digestive tract was also examined in intragastrically inoculated infants. The yeast cells spread to liver, lungs, kidneys, and spleen within 30 min postinoculation. Yeast were not detectable in the lungs or in blood from the pleural cavity up to 15 min post-inoculation, thus making it unlikely that systemic spread resulted from faulty inoculation or from aspiration. The region where C. albicans crossed the GI tract of infant mice was visualized histologically in the upper third of the small intestine. The four strains varied in their ability to persist for long periods in the GI tract, in the rate at which they appeared systemically, and in ability to kill infant mice. Three of the four strains colonized the gut for up to 10 weeks postinoculation without use of any compromising agents.

Animals↗

PubMed1983

Legionella pneumophila-induced suppression of macrophage spreading in vitro.

Incubation of normal mouse resident peritoneal cell suspensions rich in macrophages with Legionella pneumophila whole cell vaccine or soluble preparations thereof resulted in marked inhibition of the ability of the cells to spread on glass surfaces during a 24-h period. This inhibition, however, was transient in that by day 2 to 3 after culture initiation only partial inhibition was evident, and by day 4 to 5 thereafter most of the treated macrophage cultures showed normal spreading activity. Suppression of macrophage spreading was evident not only with intact Legionella preparations and the sonic extract but also with a lipopolysaccharide-rich somatic antigen preparation and flagella. The suppressive effects of Legionella preparations on a functional activity of normal macrophages in vitro indicate that these bacteria may have a detrimental effect on an important activity of cells involved in the immune defense system.

Animals↗

PubMed1990

Intracellular and cell-to-cell spread of Listeria monocytogenes involves interaction with F-actin in the enterocytelike cell line Caco-2.

Listeria monocytogenes penetrates and multiplies within professional phagocytes and other cells such as the Caco-2 human enterocytelike cell line. Listeriolysin O, a membrane-damaging cytotoxin accounts for intracellular multiplication through lysis of the membrane-bound phagocytic vacuole. This work demonstrates that once released within the cytosol, L. monocytogenes acquires the capacity to spread intracellularly and infect adjacent cells by interacting with host cell microfilaments. Such evidence was obtained by using drugs which disrupt the cell cytoskeleton. Nocodazole, which blocks polymerization of microtubules, did not affect intracellular spread, whereas cytochalasin D, which blocks polymerization of G-actin, inhibited the intracellular motility of the bacteria. By using fluorescence staining with 7-nitrobenz-2-oxa-1,3-diazole-phallacidin (NBD-phallacidin), transmission electron microscopy, and immunogold labeling, direct evidence was obtained that intracellular bacteria were enveloped with a thick layer of F-actin. Within 2 h after entry, it was demonstrated by confocal microscopy that bacteria were following highly organized routes corresponding to stress fibers. Four hours after entry, some bacteria presented random movements which could be seen by the presence of a large trail of F-actin. Such movements also caused protrusions which deeply penetrated adjacent cells and resulted in the formation of vacuoles limited by a double membrane. After subsequent lysis of these membranes, bacteria released within the cytoplasm were able to multiply and invade new cells. In contrast, an hly::Tn1545 mutant of the wild-type microorganism demonstrated almost no intracellular spread. Only a few bacteria displaying delayed lysis of the phagocytic vacuole behaved like the wild-type strain. Hemolysin-mediated lysis of the phagocytic vacuole and subsequent interaction with host cell microfilaments may represent a major virulence factor allowing tissue colonization during listeriosis.

Actin Cytoskeleton↗

PubMed1999

Microtubules are associated with intracellular movement and spread of the periodontopathogen Actinobacillus actinomycetemcomitans.

Actinobacillus actinomycetemcomitans SUNY 465, the invasion prototype strain, enters epithelial cells by an actin-dependent mechanism, escapes from the host cell vacuole, and spreads intracellularly and to adjacent epithelial cells via intercellular protrusions. Internalized organisms also egress from host cells into the assay medium via protrusions that are associated with just a single epithelial cell. Here we demonstrate that agents which inhibit microtubule polymerization (e.g., colchicine) and those which stabilize polymerized microtubules (e.g., taxol) both increase markedly the number of intracellular A. actinomycetemcomitans organisms. Furthermore, both colchicine and taxol prevented the egression of A. actinomycetemcomitans from host cells into the assay medium. Immunofluorescence microscopy revealed that protrusions that mediate the bacterial spread contain microtubules. A. actinomycetemcomitans SUNY 465 and 652, strains that are both invasive and egressive, interacted specifically with the plus ends (growing ends) of the filaments of microtubule asters in a KB cell extract. By contrast, neither A. actinomycetemcomitans 523, a strain that is invasive but not egressive, nor Haemophilus aphrophilus, a noninvasive oral bacterium with characteristics similar to those of A. actinomycetemcomitans, bound to microtubules. Together these data suggest that microtubules function in the spread and movement of A. actinomycetemcomitans and provide the first evidence that host cell dispersion of an invasive bacterium may involve the usurption of host cell microtubules.

Aggregatibacter actinomycetemcomitans↗

PubMed2006

Colony spreading in Staphylococcus aureus.

Wild-type Staphylococcus aureus rapidly expands on the surface of soft agar plates. The rates of expansion and the shapes of the resultant giant colonies were distinct for different strains of laboratory stocks and clinical isolates. The colony spreading abilities did not correlate with the biofilm-forming abilities in these strains. Insertional disruption of the dltABCD operon, which functions at the step of D-alanine addition to teichoic acids, and of the tagO gene, which is responsible for the synthesis of wall teichoic acids, decreased the colony spreading ability. The results indicate that wall teichoic acids and D-alanylation of teichoic acids are required for colony spreading.

Agar↗

PubMed1985

Quantification of medically important Candida species and Torulopsis glabrata by a spiral inoculation system: correlation with pour plate and spread plate methods.

A new method of quantifying Candida spp. and Torulopsis glabrata suspensions, the spiral inoculation system, was studied to compare its accuracy, efficiency, and cost with the standard pour plating and spread plating methods. Concentrations of yeast suspensions ranging from 10(2) to 10(5) CFU were quantified simultaneously by the three methods. Linear regression analysis was used to determine the correlation between the spiral inoculation system and pour plating and between the spiral system and spread plating for Candida albicans, C. tropicalis, C. krusei, and T. glabrata. Spiral system and pour plating techniques correlated very well for all species, as did the spiral system and spread plating techniques (r greater than 0.95; P greater than 0.001).

Candida↗

PubMed1991

Potential role of hands in the spread of respiratory viral infections: studies with human parainfluenza virus 3 and rhinovirus 14.

Hands often become contaminated with respiratory viruses, either directly or through contact with contaminated surfaces. Spread of such viruses could then occur by touching the nasal mucosa or the conjunctivae. In this quantitative study, we compared the survival of mucin-suspended human parainfluenza virus 3 (HPIV-3) and rhinovirus 14 (RV-14) and the transfer of the viruses to and from the fingers of adult volunteers. When each finger pad was contaminated with 10 microliters of either HPIV-3 (1.3 x 10(5) to 5.5 x 10(5) PFU) or RV-14 (2.1 x 10(4) to 1.1 x 10(5) PFU), less than 1.0% of HPIV-3 and 37.8% of RV-14 remained viable after 1 h; after 3 h, nearly 16% of RV-14 could still be detected, whereas HPIV-3 became undetectable. Tests on the potential spread of viruses from contaminated hands or surfaces were conducted 20 min after contamination of the donor surface by pressing together donor and recipient surfaces for 5 s. Transfer of HPIV-3 from finger to finger or finger to metal disk could not be detected, but 1.5% of infectious HPIV-3 was transferred from disk to finger. Irrespective of the type of donor or recipient surface, 0.7 to 0.9% of RV-14 was transferred. The relatively rapid loss of HPIV-3 infectivity on hands suggests that their role in the direct spread of parainfluenza viruses is limited. However, the findings of this study further reinforce the view that hands can be vehicles for rhinovirus colds. These results also suggest a role for nonporous environmental surfaces in the contamination of hands with respiratory viruses.

Adult↗

PubMed1996

Use of in-house studies of molecular epidemiology and full species identification for controlling spread of vancomycin-resistant Enterococcus faecalis isolates.

Infection with multidrug-resistant (MDR) organisms is a major clinical challenge, and few, if any, therapeutic options remain available. Increasingly, infection control measures have taken on greater importance in preventing the nosocomial transmission of MDR organisms. During December 1994 and January 1995, we identified a cluster of vancomycin-resistant Enterococcus faecalis isolates involving 16 patients situated in different areas of our university-affiliated teaching hospital. Initial review of laboratory requisition forms for the patients' locations revealed no common association, suggesting that the occurrence was not due to horizontal spread. However, using genomic DNA extraction, restriction enzyme analysis, and gel electrophoresis, we found that 12 patients were infected with isolates originating from a single clone, 2 other patients were infected with isolates from a different clone, and the remaining 2 patients were infected with unique strains. Because the typing data suggested nosocomial spread, chart review was undertaken to determine a possible common exposure source. With three exceptions, clonal isolates were linked to patient movement between surgical floors, intensive care units, and a rehabilitation unit. A detailed review of patient records revealing the association would not have been performed without realization of clonality. Thus, the data demonstrate the utility of genomic typing for epidemiological purposes. In turn, targeted infection control measures that halted the spread of the potentially lethal MDR pathogen were instituted.

Anti-Bacterial Agents↗

PubMed2006

Extensive hospital-wide spread of a multidrug-resistant enterobacter cloacae clone, with late detection due to a variable antibiogram and frequent patient transfer.

A hospital-wide increase in the number of patients with aminoglycoside-resistant Enterobacter cloacae (AREC) isolated from clinical cultures was detected in December 2002 using a classical surveillance system (CSS). CSS refers to a strategy based on the recognition of an increased incidence of a species with a particular antibiogram at certain wards in a limited period. Since clonal spread was suspected, hospital records were reviewed for E. cloacae culture-positive patients. Based upon genotyping of 139 clinical E. cloacae isolates from 80 patients, it was concluded that 53 patients had had clinical cultures with a single AREC clone since April 2001. Determinants for unnoticed spread were investigated retrospectively, as was the possibility that a computer-assisted surveillance method would have detected this outbreak at an earlier stage. Determinants associated with late detection of clonal spread were the following: (i) the absence of a hospital-wide increase in incidence of E. cloacae cases for 1.5 years, (ii) the long time interval between cases, (iii) the hospital-wide occurrence of new cases, due to a high number of patient transfers between wards, (iv) the large variety of clinical sites, and (v) the high variability of antibiograms (n = 33). Retrospective application of a recently described computer-assisted surveillance method as well as an "in-house"-developed algorithm resulted in earlier detection of the outbreak of 6 and 12 months, respectively. These findings suggest that computerized tools for surveillance may recognize resistance trends that are too complex to be detected by manual review and indicate the need for prospective evaluation of such algorithms.

Algorithms↗

PubMed2006

Extraintestinal spread and replication of a homologous EC rotavirus strain and a heterologous rhesus rotavirus in BALB/c mice.

Although rotavirus infection has generally been felt to be restricted to the gastrointestinal tract, over the last two decades there have been sporadic reports of children with acute or fatal cases of rotavirus gastroenteritis testing positive for rotavirus antigen and/or nucleic acid in various extraintestinal locations such as serum, liver, kidney, bladder, testes, nasal secretions, cerebrospinal fluid, and the central nervous system. Recently, studies in animals and people have demonstrated that rotavirus antigenemia is a common event during natural infection. In this study, we extend these observations and compare the intestinal and extraintestinal spread of wild-type homologous murine rotavirus EC and a heterologous strain, rhesus rotavirus (RRV), in newborn mice. A strand-specific quantitative reverse transcription-PCR (ssQRT-PCR) assay was used to quantify the ability of different rotavirus strains to spread and replicate extraintestinally. Both strain EC and RRV were detected extraintestinally in the mesenteric lymph nodes (MLN), livers, lungs, blood, and kidneys. Extraintestinal replication, as measured by ssQRT-PCR, was most prominent in the MLN and occurred to a lesser degree in the livers, kidneys, and lungs. In the MLN, strain EC and RRV had similar (P < 0.05) RNA copy numbers, although EC was present at a 10,000-fold excess over RRV in the small intestine. Rotavirus nonstructural protein 4 (NSP4) and/or assembled triple-layered particles, indicated by immunostaining with the VP7 conformation-dependent monoclonal antibody 159, were detected in the MLN, lungs, and livers of EC- and RRV-inoculated mice, confirming the ssQRT-PCR findings. Infectious RRV was detected in the MLN in quantities exceeding the amount present in the small intestines or blood. The cells in the MLN that supported rotavirus replication included dendritic cells and potentially B cells and macrophages. These data indicate that extraintestinal spread and replication occurs commonly during homologous and some heterologous rotaviral infections; that the substantial host range restrictions for rhesus rotavirus, a heterologous strain present in the intestine, are not necessarily apparent at systemic sites; that the level and location of extraintestinal replication varies between strains; that replication can occur in several leukocytes subsets; and that extraintestinal replication is likely a part of the normal pathogenic sequence of homologous rotavirus infection.

Animals↗