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F Q Ngo

Publications and source records attributed to F Q Ngo.

32 records · Page 2Linked to original sources
PubMed1986

Evidence for differences among the sectors of potentially lethal damage expressed by hypertonic treatment in plateau-phase V79 cells after exposure to neutrons or gamma rays: the importance of distinction between alpha and beta-PLD forms.

Expotentially growing and plateau-phase V79 cells were exposed to various doses of neutrons and plated either immediately or after treatment in hypertonic medium (250-500 mM NaCl) to express radiation-induced potentially lethal damage (PLD). Postirradiation treatment of exponentially growing cells in hypertonic medium (500 mM) resulted in a decrease in both Dq and D0, whereas postirradiation treatment of plateau-phase cells in hypertonic medium (in the range between 200 to 1,500 mM) resulted mainly in a reduction of Dq. This difference in response between exponentially growing and plateau-phase cells may reflect differences in the chromatin structure in cells at various stages of the cell cycle, affecting fixation of radiation-induced damage. Exposure of plateau-phase cells to gamma rays, on the other hand, resulted in a treatment time and salt concentration-dependent decrease in Dq along with a decrease in D0. Repair of neutron-induced, hypertonic treatment-sensitive PLD, measured by delaying treatment for various periods after irradiation, was found to proceed with a t1/2 of about 1 h. This is similar to the repair kinetics obtained by delaying treatment of plateau-phase cells with 150 microM beta-D-arabinofuranosyladenine (araA) after exposure to gamma rays or neutrons and contrasts the repair kinetics observed after exposure of cells to gamma rays. In this case, hypertonic treatment was found to affect a form of PLD repaired with a t1/2 of 10-15 min (beta-PLD) and araA, a different form of PLD, repaired with a t1/2 of about 1 h (alpha-PLD). Based on these results it is hypothesized that the sector of lesions affected by hypertonic treatment and araA coincides after exposure to neutrons (effect on alpha-PLD) but only partly overlaps after exposure to gamma rays (due to the effect on beta-PLD of hypertonic treatment). The results presented, together with previously published observations, suggest a differential induction and/or fixation by hypertonic medium of the alpha- and beta-PLD forms as the LET of the radiation increases. Furthermore, they indicate that direct comparison of the effects of a postirradiation treatment, as well as of the repair kinetics obtained by its delayed application after exposure to radiations of various LET, should be made with caution.

Animals↗
PubMed1985

Effects of adenosine deaminase inhibitor 2'-deoxycoformycin on the repair and expression of potentially lethal damage sensitive to beta-araA.

The effects of 2'deoxycoformycin, a specific inhibitor of adenosine deaminase, on the repair and fixation of potentially lethal damage (PLD) sensitive to treatment with beta-araA, an adenosine analogue acting via inhibition of DNA polymerases alpha and beta, have been studied. Given after irradiation deoxycoformycin alone had little effect on cell survival. More damage was nevertheless fixed by a given concentration of beta-araA in the presence of deoxycoformycin to a degree that 35 microM beta-araA given simultaneously with 1 microgram/ml deoxycoformycin produced the same effect (survival decrease to 20% of the controls) as 90 microM beta-araA given alone. Maximum potentiation of the beta-araA effect was observed at 1 microgram/ml deoxycoformycin with a slight decrease at higher concentrations. Combined treatment with beta-araA and deoxycoformycin reduced or eliminated the shoulder from the survival curve without affecting the slope, an effect similar to that observed after treatment of cells with beta-araA alone. The results indicate the importance of adenosine deaminase in the inactivation of nucleoside analogues and are discussed vis-a-vis the possible practical application of this inhibitor in both experimental and therapeutic applications.

Adenosine Deaminase Inhibitors↗
PubMed1985

Effects of aphidicolin on the repair and fixation of potentially lethal damage sensitive to beta-araA.

The effects of aphidicolin, a specific inhibitor of DNA polymerase alpha, on the repair and fixation of potentially lethal damage (PLD) sensitive to treatment with beta-araA--a drug acting via inhibition of DNA polymerases alpha and beta-have been studied. Three micrograms/ml of aphidicolin given after irradiation did not produce any significant modification in cell survival. More damage was nevertheless fixed by a given concentration of beta-araA in the presence of aphidicolin to a degree that 10 microM beta-araA given together with 3 micrograms/ml aphidicolin produced an effect similar to that of 70 microM beta-araA given alone. Although aphidicolin significantly enhanced the effectiveness of beta-araA in fixing PLD, it did not significantly increase the sector of lesions affected. Combined treatment with beta-araA and aphidicolin reduced or eliminated the shoulder from the survival curve without affecting the slope, an effect similar to that observed after treatment of cells with beta-araA alone. The presence of aphidicolin during the time interval trep allowed for repair of the beta-araA sensitive PLD resulted in a significant reduction in the repair rate. Based on these results, the necessity of distinction between inhibition of a repair process and fixation of the damage undergoing repair is discussed, as well as the possible involvement of DNA polymerase alpha and beta in the repair and fixation of the DNA damage that underlies repair of PLD.

Animals↗
PubMed1985

Magnetic resonance of brain tumors: considerations of imaging contrast on the basis of relaxation measurements.

Proton spin-lattice and spin-spin relaxation times have been measured in surgically-removed normal CNS tissues and a variety of tumors of the brain. All measurements were made at 20 MHz and 37 degrees C. Between grey and white matter from autopsy human or canine specimens significant differences in T1 or T2 were observed, with greater differences seen in T1. Such discrimination was reduced in samples obtained from live brain-tumor patients due to lengthening in T1 and T2 of white matter near tumorous lesions. Edematous white matter showed T1 and T2 values higher than those of autopsy disease-free white matter. Compared to normal CNS tissues, most brain tumors examined in this study demonstrated elevated T1 and T2 values. Exceptions, however, did exist. No definitive correlation was indicated on a T1 or T2 basis which allowed a distinction to be made between benign and malignant states. Furthermore, considerable variation in relaxation times occurred from tumor to tumor of the same type, suggesting that within a tumor type there are important differences in physiology, biology, and/or pathologic state. Such variation caused partial overlap in relaxation times among certain tumor types and hence may limit the capability of magnetic resonance imaging (MR) alone for the diagnosis of specific disease. Nonetheless, this study predicts that on the basis of T1 or T2 differences most brain tumors are readily detectable by MR via saturation recovery or inversion recovery with appropriate selections of pulse-spacing parameters. In general, tumors can be discriminated against white matter better than grey matter and contrast between glioma and grey matter is usually superior to that between meningioma and grey matter. This work did not consider tissue-associated proton density which should be addressed together with T1 and T2 for a complete treatment of MR contrast.

Adenoma↗
PubMed1985

Evidence for similarities between radiation damage expressed by beta-araA and damage involved in the interaction effect observed after exposure of V79 cells to mixed neutrons and gamma radiation.

Plateau-phase V79 cells were exposed sequentially to fast neutrons and gamma rays. A dose-dependent reduction in the shoulder width of the gamma-ray survival curve was observed after preexposure of cells to neutrons. A similar effect was demonstrated on the neutron survival curve when cells were preirradiated with gamma rays. Treatment of cells with 150 microM beta-araA after either gamma or neutron irradiation reduced primarily the shoulder of the survival curve. When beta-araA was given to the cells after exposure to mixed radiation modalities, survival curves similar to those observed after exposure to a single radiation modality and treatment with beta-araA were obtained. The kinetics of loss of the interaction observed after exposure of cells to gamma rays following neutron irradiation was similar to the kinetics of loss of sensitivity to beta-araA (T1/2 = 1 h) measured by delaying drug administration after exposure to gamma rays. The results suggest that the PLD expressed by beta-araA is at least partly involved in the interactive effect observed after combined exposure of plateau-phase V79 cells to neutrons and gamma rays.

Animals↗
PubMed1985

Independent forms of potentially lethal damage fixed in plateau-phase Chinese hamster cells by postirradiation treatment in hypertonic salt solution or araA.

Plateau-phase Chinese V79 hamster cells were sequentially treated after exposure to gamma rays in medium made hypertonic by the addition of sodium chloride (370 mM) and with various concentrations of 9-beta-D-arabinofuranosyladenine (araA) to study their combined effect on fixation of potentially lethal damage (PLD). A 10-min treatment in hypertonic medium fixed an extensive amount of PLD and caused a decrease in D0 from 1.8 to 1.2 Gy without significantly affecting Dq. Subsequent treatment with araA caused further fixation of PLD but resulted in a specific, concentration-dependent reduction in Dq from 4.9 to 1.6 Gy after a 4-h exposure to 150 microM araA. A 30-min treatment in hypertonic medium reduced not only Do (from 1.8 to 1.0 Gy) but also Dq (from 4.9 to 2.7 Gy). Subsequent treatment with araA in this case affected only the residual shoulder, reducing it to 1.6 Gy after a 4-h treatment with 100 microM araA, a value similar to that obtained after treatment with araA of cells exposed to salt for only 10 min. When the repair of PLD fixed by a 10-min treatment with salt was measured by delaying its postirradiation application in the presence of various amounts of araA, a small decrease in the repair rate was observed but no significant effect on the relative increase in survival. Qualitatively similar results were obtained for repair of PLD sensitive to araA after a 10-min treatment in hypertonic medium. These results suggest the radiation induction of forms of PLD with different sensitivity to fixation by postirradiation treatments. araA is proposed to fix a form of PLD termed alpha-PLD, the repair of which takes place within 4-6 h and which causes the formation of the shoulder in the survival curve of cells plated immediately after irradiation. Short treatments in hypertonic medium (less than 10 min) are proposed to fix a form of PLD termed beta-PLD, the repair of which takes place within 1 h and leads to restoration of the slope to values equal to those obtained in the survival curve of cells plated immediately after irradiation. However, longer treatments in hypertonic medium also affect Dq and thus also alpha-PLD. Repair of beta-PLD was not significantly affected by araA and repair of alpha-PLD was not significantly affected by short hypertonic treatment, thus indicating the independence of the two forms of PLD.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1985

Biological considerations for treating alternate fields versus all fields daily with high and low LET radiation.

The rationale for treating all fields every day with photons was reviewed. Since the effects of neutron radiation are much less dependent on alterations of fractionation schedules, and since preferential sparing for late effects is not obtained by fractionation of neutron dose, less convincing reasons exist for treating all fields every day with neutrons. Treating one field/day would not alter the physical dose distribution or overall treatment time, yet still maintain biological homogeneity. Preliminary in vitro experiments support this conclusion.

Animals↗
PubMed1982

Molecular and cellular radiobiology of heavy ions.

Quantitative studies at the BEVALAC have demonstrated some of the physical and radiobiological factors that promise to make accelerated heavy ions important for the therapy of cancer. The measured physical dose-biological effect relationships allow the safe and effective delivery of therapeutic schedules of heavy ions. Among the charged particle beams available, carbon, neon and helium ions in the "extended Bragg peak mode" have optimal physical and biological effectiveness for delivery of therapy to deep seated tumors. The depth-dose profiles of these beams protect intervening and adjacent tissues as well as tissues beyond the range of the particles. For the treatment of hypoxic tumors, silicon and argon beams are being considered because they significantly depress the radiobiological oxygen effect in the region of the extended Bragg ionization peak. The depth-effectiveness of the argon beam is somewhat limited, however, because of primary particle fragmentation. Silicon beams have a depth-dose profile which is intermediate between that of neon and argon, and are candidates to become the particle of choice for maximizing high LET particle effects. Heavy accelerated ions depress enzymatic repair mechanisms, decrease variations of radiosensitivity during the cell division cycle, cause greater than expected delays in cell division, and decrease the protective effects of neighboring cells in organized systems. Near the Bragg peak, enhancement of heavy particle effects are observed in split dose schedules. Late and carcinogenic effects are being studied. With the newly developed Repair-Misrepair theory we can quantitatively model most observations.

Animals↗
PubMed1980

Survival and kinetic response of V79-spheroids after exposure to heavy ion beams.

Multicellular V79-spheroids and V79-monolayer cultures were irradiated with charged particle beams. The beams studied and their initial extraction energies were carbon (400 MeV/amu), neon (425 MeV/amu) and argon (570 MeV/amu). Survival was measured at a position in the plateau, and at a position in the middle of a 4 cm extended Bragg peak. Relative biological efficiency (r.b.e.) values for survival of spheroid cells at peak positions were high (4.1--4.2) in comparison to those obtained with monolayer cultures (1.8--2.4) of the same cell line. This finding is explained by the fact that three dimensional cell contact, which benefits survival after low LET radiation, does not influence survival after heavy ion irradiations in the Bragg peak. The peak-plateau r.b.e.-ratio was most advantageous for the carbon-ion beam (= 4.2). Whereas non-cycling inner spheroid cells showed hardly any kinetic changes up to 24 hours after heavy ion irradiation, outer cycling spheroid cells were arrested in G2 + M within a few hours after exposure.

Animals↗