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At least 163 records · Page 9Linked to original sources

In vivo verification of electron beam energy by patient exit dose and optical density of portal films.

BACKGROUND AND PURPOSE: The depth-dose curve of electron beams is mainly determined by their energy. For accelerators with scatter foils, the electron energy can, in principle, be verified by measuring the amount of the contaminating photons. This paper investigates whether exit dose measurements and evaluations of the optical density of portal films can be used to verify the energy of the electron beam in a clinically relevant setting. MATERIAL AND METHODS: During irradiation of the head and neck region of an Alderson-Rando phantom with 6- to 21-MeV electron beams, the exit dose rates behind the phantom and the dose rates at the position of a film cassette were measured. The optical density of films (EC film/EC-L Regular and EC-L Fast cassettes, Eastman Kodak Comp., Rochester, NY, USA) exposed to beams of different energies was evaluated. RESULTS: The exit and the cassette dose rates showed a steep increase with increasing electron energy. Due to its density behavior, the film with both types of cassettes failed to generate images for lower electron energies (6 and 9 MeV) but presented a strong ascent of the optical density-until reaching the saturation-with increasing electron energy. CONCLUSION: Measurements of the exit dose and evaluations of the optical density of portal films can be used to verify and document the energy of electron beams during radiotherapy.

Artifacts↗

Gunshot-related displacement of skin particles and bacteria from the exit region back into the bullet path.

In previous studies, it was shown that there is a gunshot-related transport of skin particles and microorganisms from the entrance region into the depth of the bullet path. The present study deals with the question of whether gunshots may also cause a retrograde transport of skin particles and microorganisms from the bullet exit region back into the bullet path. For this purpose, we used a composite model consisting of rectangular gelatin blocks and pig skin. The skin pieces were firmly attached to the gelatin blocks on the side where the bullet was to exit. Prior to the test shots, the outer surface of the pig skin was contaminated with a thin layer of a defined bacterial suspension. After drying the skin, test shots were fired from a distance of 10 m using cartridges calibre .38 spec. with different bullet types. Subsequent analyses showed that in all shots with full penetration of the composite model, the bullet path contained displaced skin particles and microorganisms from the skin surface at the exit site. These could be regularly detected in the distal 6-8 cm of the track, occasionally up to a distance of 18 cm from the exit hole. The distribution of skin particles and microorganisms is presented and the possible mechanism of this retrograde transport is discussed.

Animals↗

Nontuberculous mycobacterial exit-site infection and abscess in a peritoneal dialysis patient. A case report and review of the literature.

Nontuberculous mycobacterial infections of peritoneal dialysis catheter exit sites have rarely been reported in patients on peritoneal dialysis. We report here a case of Mycobacterium abscessus exit site infection with abdominal wall abscess formation in an adolescent on peritoneal dialysis, which required long-term antibiotic therapy, peritoneal dialysis catheter removal, and surgical debridement of the abscess. Nontuberculous mycobacteria should be considered as a possible causative organism for an exit site infection that fails to respond to usual antibiotic therapy. Nontuberculous mycobacterial exit site infections may require peritoneal dialysis catheter removal and surgical debridement.

Abdominal Abscess↗

Evidence for non-uniform distribution of D-glucose within human red cells during net exit and counterflow.

The kinetic parameters of net exit of D-glucose from human red blood cells have been measured after the cells were loaded to 18 mM, 75 mM and 120 mM at 2 degrees C and 75 mM and 120 mM at 20 degrees C. Reducing the temperature, or raising the loading concentration raises the apparent Km for net exit. Deoxygenation also reduces the Km for D-glucose exit from red blood cells loaded initially to 120 mM at 20 degrees C from 32.9 +/- 2.3 mM (13) with oxygenated blood to 20.5 +/- 1.3 mM (17) (P less than 0.01). Deoxygenation increases the ratio Vmax/Km from 5.29 +/- 0.26 min-1 (13) for oxygenated blood to 7.13 +/- 0.29 min-1 (17) for deoxygenated blood (P less than 0.001). The counterflow of D-glucose from solutions containing 1 mM 14C-labelled D-glucose was measured at 2 degrees C and 20 degrees C. Reduction in temperature, reduced the maximal level to which labelled D-glucose was accumulated and altered the course of equilibration of the specific activity of intracellular D-glucose from a single exponential to a more complex form. Raising the internal concentration from 18 mM to 90 mM at 2 degrees C also alters the course of equilibration of labelled D-glucose within the cell to a complex form. The apparent asymmetry of the transport system may be estimated from the intracellular concentrations of labelled and unlabelled sugar at the turning point of the counterflow transient. The estimates of asymmetry obtained from this approach indicate that there is no significant asymmetry at 20 degrees C and at 2 degrees C asymmetry is between 3 and 6. This is at least 20-fold less than predicted from the kinetic parameter asymmetries for net exit and entry. None of the above results fit a kinetic scheme in which the asymmetry of the transport system is controlled by intrinsic differences in the kinetic parameters at the inner and outer membrane surface. These results are consistent with a model for sugar transport in which movement between sugar within bound and free intracellular compartments can become the rate-limiting step in controlling net movement into, or out of the cell.

Blood Glucose↗

Lifetime exit events and recent social and family adversities in anxious and depressed school-age children and adolescents--I.

The number of lifetime exit events occurring over the lives of 7-16-year-old children was compared between cases with new onset episodes of anxiety and depression (n = 100) and community controls (n = 100). The reporting of events by adult responders appears reliable and not subject to distortions of recall. Overall the likelihood of experiencing exit events increases with age. A significant association was found between current disorder and two or more previous lifetime exit events. There is, however, a non-significant trend for those cases who experience multiple lifetime exits to be younger than the controls and to be female rather than male. These findings are uninfluenced by pubertal stage at time of onset of disorder or by diagnosis.

Adolescent↗

Mitotic-exit control as an evolved complex system.

The exit from mitosis is the last critical decision during a cell-division cycle. A complex regulatory system has evolved to evaluate the success of mitotic events and control this decision. Whereas outstanding genetic work in yeast has led to rapid discovery of a large number of interacting genes involved in the control of mitotic exit, it has also become increasingly difficult to comprehend the logic and mechanistic features embedded in the complex molecular network. Our view is that this difficulty stems in part from the attempt to explain mitotic-exit control using concepts from traditional top-down engineering design, and that exciting new results from evolutionary engineering design applied to networks and electronic circuits may lend better insights. We focus on four particularly intriguing features of the mitotic-exit control system and attempt to examine these features from the perspective of evolutionary design and complex system engineering.

Biological Evolution↗

Reduction of exit-site infections of tunnelled intravascular catheters among neutropenic patients by sustained-release chlorhexidine dressings: results from a prospective randomized controlled trial.

Exit-site and tunnel infections of tunnelled central intravascular catheters are a frequent source of morbidity among neutropenic patients and may necessitate catheter removal. They require antimicrobial therapy that increases healthcare costs and is associated with adverse drug reactions. A prospective randomized clinical trial was conducted among adult patients undergoing chemotherapy in a haematology unit. Tunnelled intravascular catheters were randomized to receive the control of a standard dressing regimen as recommended by the British Committee for Standards in Haematology, or to receive the intervention of a sustained-release chlorhexidine dressing. Follow-up data were available in 112 of 114 tunnelled intravascular catheters which were randomized. Exit-site or combined exit-site/tunnel infections occurred in 23 (43%) of 54 catheters in the control group, and five (9%) of 58 catheters in the intervention group [odds ratio (OR) for intervention group compared with control group =0.13, 95% confidence intervals (CI) 0.04-0.37, P<0.001]. More tunnelled intravascular catheters were prematurely removed from the control group than the intervention group for documented infections [20/54 (37%) vs 6/58 (10%), OR=0.20, 95%CI 0.53-0.07]. However, there was no difference in the numbers of tunnelled intravascular catheters removed for all proven and suspected intravascular catheter-related infections [21/54 (39%) vs 19/58 (33%)], or in the time to removal of catheters for any reason other than death or end of treatment for underlying disease. Thus chlorhexidine dressings reduced the incidence of exit-site/tunnel infections of indwelling tunnelled intravascular catheters without prolonging catheter survival in neutropenic patients, and could be considered as part of the routine management of indwelling tunnelled intravascular catheters among neutropenic patients.

Administration, Topical↗

Kin4 kinase delays mitotic exit in response to spindle alignment defects.

For many polarized cells, it is critical that the mitotic spindle becomes positioned relative to the polarity axis. This is especially important in yeast, where the site of cytokinesis is predetermined. The spindle position checkpoint (SPOC) therefore delays mitotic exit of cells with a mispositioned spindle. One component of the SPOC is the Bub2-Bfa1 complex, an inhibitor of the mitotic exit network (MEN). Here, we show that the Kin4 kinase is a component of the SPOC and as such is essential to delay cell cycle progression of cells with a misaligned spindle. When spindles are correctly oriented, Kin4 and Bub2-Bfa1 are asymmetrically localized to opposite spindle pole bodies (SPBs). Bub2-Bfa1 then becomes inhibited by Cdc5 polo kinase with anaphase onset, a prerequisite for mitotic exit. In response to spindle misalignment, Kin4 and Bub2-Bfa1 are brought together at both SPBs. Kin4 now maintains Bub2-Bfa1 activity by counteracting Cdc5, thereby inhibiting mitotic exit.

Cell Cycle↗

The protein kinase Kin4 inhibits exit from mitosis in response to spindle position defects.

Accurate nuclear position is essential for each daughter cell to receive one DNA complement. In budding yeast, a surveillance mechanism known as the spindle position checkpoint ensures that exit from mitosis only occurs when the anaphase nucleus is positioned along the mother-bud axis. We identified the protein kinase Kin4 as a component of the spindle position checkpoint. KIN4 prevents exit from mitosis in cells with mispositioned nuclei by inhibiting the mitotic exit network (MEN), a GTPase signaling cascade that promotes exit from mitosis. Kin4 is active in cells with mispositioned nuclei and predominantly localizes to mother cells, where it is ideally situated to inhibit MEN signaling at spindle pole bodies (SPBs) when anaphase spindle elongation occurs within the mother cell.

Anaphase↗

Resolution extension and exit wave reconstruction in complex HREM.

Direct methods in real and reciprocal space are developed for structural reversion. The direct method in real space involves the use of a novel method to retrieve the phase in the image plane using transport of intensity equation/maximum entropy method (TIE/MEM) and exit wave reconstruction by self-consistent propagation. Since the exit wave is restored from the complex signal in the image planes, no image model between the exit wave and image is assumed. The structural information in the reconstructed exit wave is then further extended by a "complex" maximum entropy method as a direct method in reciprocal space to extrapolate the phase to higher frequencies.

Journal Article↗

Effective phase correction function for high-resolution exit wave reconstruction by a three-dimensional Fourier filtering method.

The phase correction function used in the three-dimensional Fourier filtering method (3D-FFM) for compensating lens aberrations was investigated to reconstruct a high-resolution exit wave of a sample. An appropriate function, which hardly suffered from imperfect illumination conditions, was determined by comparing two types of phase correction functions with numerical calculations and experiments using through-focus images of an amorphous thin film and a [110]-oriented Si single crystal taken under tilted illumination or partially coherent illumination. Theoretical calculations indicated that a function in terms of w (an axial Fourier component), available uniquely in the 3D Fourier space, compensated for the phase shift due to the spherical aberration more precisely than did a conventional function in terms of g (the two-dimensional (2D) planar Fourier components). Experimentally, exit waves reconstructed using the w-function showed sample structures at approximately 20% higher resolution than those reconstructed using the g-function. Image contrast simulations proved that the w-function had a significant advantage over the g-function: the former canceled out the effect of illumination divergence, resulting in a high-resolution exit wave. These results demonstrated that exit waves, which are uniquely realized in the 3D-FFM, should be reconstructed using the w-type phase correction function.

Fourier Analysis↗

A cell-autonomous requirement for Cip/Kip cyclin-kinase inhibitors in regulating neuronal cell cycle exit but not differentiation in the developing spinal cord.

Control over cell cycle exit is fundamental to the normal generation of the wide array of distinct cell types that comprise the mature vertebrate CNS. Here, we demonstrate a critical role for Cip/Kip class cyclin-kinase inhibitory (CKI) proteins in regulating this process during neurogenesis in the embryonic spinal cord. Using immunohistochemistry, we show that all three identified Cip/Kip CKI proteins are expressed in both distinct and overlapping populations of nascent and post-mitotic neurons during early neurogenesis, with p27(Kip1) having the broadest expression, and both p57(Kip2) and p21(Cip1) showing transient expression in restricted populations. Loss- and gain-of-function approaches were used to establish the unique and redundant functions of these proteins in spinal cord neurogenesis. Using genetic lineage tracing, we provide evidence that, in the absence of p57, nascent neurons re-enter the cell cycle inappropriately but later exit to begin differentiation. Analysis of p57(Kip2);p27(Kip1) double mutants, where p21 expression is confined to only a small population of interneurons, demonstrates that Cip/Kip CKI-independent factors initiate progenitor cell cycle exit for the majority of interneurons generated in the developing spinal cord. Our studies indicate that p57 plays a critical cell-autonomous role in timing cell cycle exit at G1/S by opposing the activity of Cyclin D1, which promotes cell cycle progression. These studies support a multi-step model for neuronal progenitor cell cycle withdrawal that involves p57(Kip2) in a central role opposing latent Cyclin D1 and other residual cell cycle promoting activities in progenitors targeted for differentiation.

Animals↗

Maximum forces sustained during various methods of exiting commercial tractors, trailers and trucks.

Many commercial vehicles have steps and grab-rails to assist the driver in safely entering/exiting the vehicle. However, many drivers do not use these aids. The purpose of this study was to compare impact forces experienced during various exit methods from commercial equipment. The study investigated impact forces of ten male subjects while exiting two tractors, a step-van, a box-trailer, and a cube-van. The results showed that exiting from cab-level or trailer-level resulted in impact forces as high as 12 times the subject's body weight; whereas, fully utilizing the steps and grab-rails resulted in impact forces less than two times body weight. An approach that emphasizes optimal design of entry/exit aids coupled with driver training and education is expected to minimize exit-related injuries.

Adult↗

The effect of ATP-depletion on the inhibition of glucose exits from human red cells.

The effect of ATP-depletion or its consequence, by metabolic inhibition, on the inhibition of glucose transport by various inhibitors was studied in human red cells. In cells depleted of ATP, glucose exit times were longer than in normal cells and the times increased with the duration of depletion. The Km for external glucose was higher in ATP-depleted cells than in normal undepleted cells (3.0 mM c.f. 2.5 mM at 30 degrees C). In contrast, the apparent Ki for cytochalasin B decreased from 0.85 microM in the normal cells to 0.5 microM after ATP-depletion. Half-maximal rates of glucose exit in the absence, and in the presence of 2 microM cytochalasin B were found at ATP concentrations of 0.43 and 0.68 microM, respectively. Although glucose exits from ATP-depleted cells exposed to the irreversible inhibitor of glucose transport, 1-fluoro-2,4-dinitrobenzene (FDNB) were slower than in normal cells, the relative degrees of inhibition were not significantly different. However, normal and ATP-depleted cells responded differently to treatment with 1,2-cyclohexanedione, a modifier of arginine residues which inhibits glucose exit. While normal cells were markedly inhibited, depleted cells were much less affected and the inhibitory effect of cytochalasin B seen in normal cells was reduced. These findings demonstrate that the glucose transport system of human red cells is affected by intracellular ATP and that ATP alters the affinity of the transporter for certain inhibitors. The implications of these findings are discussed.

Adenosine Triphosphate↗

A mechanism for coupling exit from mitosis to partitioning of the nucleus.

Exit from mitosis must not occur prior to partitioning of chromosomes between daughter cells. We find that the GTP binding protein Tem1, a regulator of mitotic exit, is present on the spindle pole body that migrates into the bud during S phase and mitosis. Tem1's exchange factor, Lte1, localizes to the bud. Thus, Tem1 and Lte1 are present in the same cellular compartment (the bud) only after the nucleus enters the bud during nuclear division. We also find that the presence of Tem1 and Lte1 in the bud is required for mitotic exit. Our results suggest that the spatial segregation of Tem1 and Lte1 ensures that exit from mitosis only occurs after the genetic material is partitioned between mother and daughter cell.

Cell Cycle↗

Entrance and exit dose measurements with semiconductors and thermoluminescent dosemeters: a comparison of methods and in vivo results.

BACKGROUND AND PURPOSE: In order to compare diodes and TLD for in vivo dosimetry, systematic measurements of entrance and exit doses were performed with semiconductor detectors and thermoluminescent dosemeters for brain and head and neck patients treated isocentrically with external photon beam therapy. MATERIAL AND METHODS: Scanditronix EDP-20 diodes and 7LiF thermoluminescent chips, irradiated in a 8 MV linac, were studied with similar build-up cap geometries and materials in order to assure an equivalent electronic equilibrium. Identical calibration methodology was applied to both detectors for the dose determination in clinical conditions. RESULTS: For the entrance dose evaluation over 249 field measurements, the ratio of the measured dose to the expected dose, calculated from tabulated tissue maximum ratios, was equal to 1.010 +/- 0.028 (1 s.d.) from diodes and 1.013 +/- 0.041 from thermoluminescent crystals. For the exit dose measurements, these ratios were equal to 0.998 +/- 0.049 and 1.016 +/- 0.070 for diodes and TLDs, respectively, after application of a simple inhomogeneity correction to the calculation of the expected exit dose. CONCLUSIONS: Thermoluminescence and semiconductors led to identical results for entrance and exit dose evaluation but TLDs were characterised by a lower reproducibility inherent to the TL process itself and to the acquisition and annihilation procedures.

Brain Neoplasms↗

First order release rate from porous PLA microspheres with limited exit holes on the exterior surface.

We applied the finite element method (FEM) to calculate release profiles from computer simulated slabs, one with a limited number of exit holes on the exterior surface, and the other with uniform structure. The former slab showed a first order release rate, and a nearly uniform drug concentration distribution within the device during the release process. It was concluded that circulation of the drug molecules within the slab resulted in the uniform concentration and consequently first order release rate. This theoretical work was used to explain the first order release rate of an active ingredient (flourescin-4-isothiocyanate-dextran, M(W)=71000 Da) from porous PLA (poly(D,L)-lactic acid) microspheres, which by canning electron microscopy (SEM) examination showed only a few exit holes on their exterior surface. Calculations indicated that the internal surface adsorption of the active ingredient, or the pore size distribution of the microspheres, could not influence the mechanism for the first order release rate, and the small number of exit holes on the exterior surface was likely to be the rate-determining factor. The exit holes could be observed by SEM and their size and number is consistent with our interpretations.

Computer Simulation↗

The use of povidone iodine in exit site care for patients undergoing continuous peritoneal dialysis (CAPD).

Exit site infection is a major risk factor for the development of peritonitis in continuous ambulatory peritoneal dialysis. The frequency of infection can be reduced by scrupulous exit site care with or without topical antiseptics. A randomized trial was performed of 149 catheters in 130 patients to assess any additional benefits conferred by the use of povidine iodine dry powder spray at dressing changes over an existing strict protocol of exit care. Exit infections occurred in 14 (18%) of 77 patients using spray and in 15 (21%) of 72 patients not using spray. The risk of peritonitis was also similar in each group. The proportion of infections caused by Staphylococcus aureus was reduced in the spray group, but those caused by Pseudomonas aeruginosa were increased. Rash occurred in 6% of those using the spray. The use of the spray did not therefore seem justified.

Aged↗