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Biomedical subjects

R Dickerson

Publications and source records attributed to R Dickerson.

At least 19 recordsLinked to original sources
PubMed2003

Effect of zero- to one-dimensional transformation on multiparticle Auger recombination in semiconductor quantum rods.

We study the effect of the zero- to one-dimensional (1D) transformation on multiparticle Auger recombination using a series of elongated semiconductor nanocrystals (quantum rods). We observe a transition from the three- to two-particle recombination process as the nanocrystal aspect ratio is increased. This transition indicates that in the 1D confinement limit, Auger decay is dominated by Coulomb interactions between 1D excitons that recombine in a bimolecular fashion. One consequence of this effect is strongly reduced decay rates of higher multiparticle states that lead to increased optical-gain lifetimes and efficient light amplification due to involvement of excited electronic states.

Journal Article↗
PubMed1998

Exaggerated precocious centromere separation in cells of a human breast cancer line treated with a green tea extract.

In a breast cancer cell line, MDA-MB-468, established in our laboratory, an average of 3% of the mitotic cells exhibited a phenomenon known as centromere splaying, which is a characteristic feature of cells of patients with Roberts syndrome. However, centromere splaying in cells of Roberts syndrome patients is limited to i) the centromere region and ii) chromosomes with large amounts of heterochromatin. When the breast cancer cells were treated with an extract of green tea GTE-TP91, up to 45% of the metaphases were observed to exhibit this behavior; and the precocious centromere separation was highly exaggerated, affecting all chromosomes in such metaphases. Apparently, as the sister centromeres continued to pull apart, they carried the chromatids with them, except for the telomere regions, giving a ring-like configuration. Eventually, the sister chromatids became completely separated. Whether this bizarre phenomenon was induced by the polyphenols contained in this green tea extract GTE-TP91 is not known, but this phenomenon, upon further investigation, may throw some light on chromosomal proteins, centromere behavior, telomere behavior and related questions.

Breast Neoplasms↗
PubMed1996

High temporal resolution diffusion MRI of global cerebral ischemia and reperfusion.

Although brain ischemia has been extensively studied using diffusion-weighted magnetic resonance imaging, most studies performed so far have not had adequate time resolution to follow the temporal changes in the water apparent diffusion coefficient (ADC) in hyperacute ischemia. Using diffusion echo planar imaging, we obtained ADC maps (calculated from measurements made with 8 b-values) with a time resolution of 43 s in a feline model of global brain ischemia and reperfusion. Different protocols were performed: 10-min hypoperfusion, 10- and 22-min ischemia followed by reperfusion, and cardiac arrest. ADC values were obtained from white matter of the internal capsule and from the thalamus. Cortical gray matter measurements were not deemed reliable due to the close proximity of CSF in the cortical sulci. Following occlusion, the ADC declined in the thalamus to < 2 SD of its normal baseline value within 1.5-2.5 min. This decay was exponential with a time constant (tau +/- SD) of 6.0 +/- 2.6 min; no further decrease in the ADC was observed 10 min following ischemia. Following reperfusion, in animals that showed ADC recovery, the ADC began increasing immediately, returning to its preischemic value in approximately 15 min. No significant ADC changes were observed during hypoperfusion. Following cardiac arrest, the decay of ADC was more rapid in the thalamus (tau = 2.6 +/- 0.6 min) than in white matter (tau = 6.6 +/- 1.8 min). We observed that the ADC at 40 min after cardiac arrest was similar to the ADC at 10 min after ischemia. Given that all animals subjected to 10-min ischemic episodes showed ADC recovery with reperfusion, doubt is cast on whether it is possible to define a threshold value of the ADC below which brain tissue is irreversibly damaged. Finally, despite variability in the time constants of the ADC decay induced by ischemia, the ADC values at 10 min were very similar in all the animals. This suggests that when blood flow is diminished sufficiently to induce an ADC reduction, differences in perfusion affect the rapidity of the decrease but not the final asymptotic value reached.

Animals↗
PubMed1995

Alkyl polychlorinated dibenzofurans and related compounds as antiestrogens in the female rat uterus: structure-activity studies.

The antiestrogenic activity of a series of alkyl-substituted polychlorinated dibenzofurans (PCDFs) were determined in the immature female Sprague-Dawley rat uterus. The compounds utilized in this study contain two, three, or four lateral substitutents and include: 6-methyl-1,3,8-triCDF, 6-ethyl-1,3,8-triCDF, 6-n-propyl-1,3,8-triCDF, 6-i-propyl-1,3,8-triCDF, 6-t-butyl-1,3,8-triCDF, 8-methyl-1,3,6-triCDF (two lateral substituents); 6-methyl-2,3,8-triCDF, 6-methyl-2,3,4,8-tetraCDF, 8-methyl-1,3,7-triCDF, and 8-methyl-1,2,4,7-tetraCDF (three lateral substituents); 8-methyl-2,3,7-triCDF, 8-methyl-2,3,4,7-tetraCDF (four lateral substituents). Two additional compounds, 8-methyl-2,3,7-trichlorodibenzo-p-dioxin and 8-methyl-2,3,7-tribromodibenzo-p- dioxin (four lateral substituents), were also utilized. All of the alkyl-substituted compounds inhibited estrogen-induced uterine wet weight increase and cytosolic and nuclear progesterone and estrogen receptor binding. The effects of structure on the antiestrogenic potencies were determined using 6-i-propyl-1,3,8-triCDF, 6-methyl-2,3,4,8-tetraCDF, and 8-methyl-2,3,4,7-tetraCDF as representative congeners containing two, three, and four lateral substituents, respectively. The ED50 values for antiestrogenicity were similar for the three compounds; however, the ED50 values for induction of hepatic CYP1A1-dependent activity were 73,600 (estimated), 8.52, and 5.31 mumol/kg for 6-i-propyl-1,3,8-triCDF, 6-methyl-2,3,4,8-tetraCDF, and 8-methyl-2,3,4,7-tetraCDF, respectively. Since CYP1A1 can be used as a surrogate for toxic potency in the rat then high ED50 (induction)/ED50 (antiestrogenicity) ratios would be indicative of low toxicity and high antiestrogenic potency. The ratio was 13,990 to 17,100 for 6-i-propyl-1,3,8-triCDF, whereas the corresponding value for the compounds with three or four lateral substituents varied from 0.64 to 3.34. The results suggests that the 1,3,6,8-substituted alkyl PCDFs are useful structural models for developing new aryl hydrocarbon receptor-mediated antiestrogens for future clinical use as antiestrogens.

Animals↗
PubMed1994

Objective performance characteristics of a new asymmetric screen-film system.

A study of the objective imaging characteristics of a new asymmetric screen-film system is presented herein. The system is characterized by high x-ray absorption asymmetric screens, and a low-noise, high-contrast asymmetric film having near-zero crossover. Comparisons are made with the imaging characteristics of two widely used conventional screen-film systems. Sensitometry, modulation transfer function, and noise power spectra were measured using standard methods. Granularity, noise equivalent quanta, and detective quantum efficiency were computed from these. The new screen-film system has an average gradient at lung-field densities between the two conventional systems studied, while the mediastinum contrast exceeds both conventional systems. The lung-field modulation transfer function half bandwidth of the new asymmetric system exceeds that of both conventional systems by 60%. At mid exposures the detective quantum efficiency of the new asymmetric system is comparable to those of the conventional systems studied. However, the exposure range over which detective quantum efficiency remains high is substantially wider.

Humans↗
PubMed1993

Immunosuppressive effects of highly chlorinated biphenyls and diphenyl ethers on T-cell dependent and independent antigens in mice.

The dose-dependent effects of 2,2',3,3',4,4',5,5',6-nonachlorobiphenyl (nonaCB), 2,2',3,3',4,4',5,6,6'-nonaCB, 2,2',3,3',4,5,5',6,6'-nonaCB and decaCB on the suppression of the splenic plaque-forming cell (PFC) response to the T-cell-dependent antigen, sheep red blood cells (SRBCs) and the T-cell-independent antigen, trinitrophenyl-lipopolysaccharide (TNP-LPS), were determined in genetically inbred mice. In addition, the induction of hepatic microsomal ethoxyresorufin O-deethylase (EROD) activity was also measured. The highly chlorinated biphenyls suppressed the splenic PFC response to SRBCs in C57BL/6 and DBA/2 mice and were relatively more active in the former strain. The C57BL/6 mice are more responsive to aryl hydrocarbon (Ah) receptor agonists than DBA/2 mice and these data support a possible role for the Ah receptor in mediating this response. However, previous studies with polychlorinated biphenyls (PCBs) indicate that congeners with 3 or 4 ortho-chloro substituents are inactive as Ah receptor agonists and this was consistent with the minimal induction of hepatic microsomal EROD activity by the highly chlorinated biphenyls in both strains of mice. Thus, the results suggest that the inhibition of the splenic PFC response to SRBCs observed in this study was primarily an Ah receptor-independent response. Some of the highly chlorinated diphyenyl ethers namely decachlorodiphenyl ether and 2,2',3,3',4,4',5,6,6'-nonachlorodiphenyl ether, inhibited the antigenic response to TNP-LPS in C57 BL/6 mice. The results indicate that the suppression of the TNP-LPS-mediated immune response may be a more reliable indicator of the Ah receptor-dependent immunotoxicity of halogenated hydrocarbons.

Animals↗
PubMed1993

Immunosuppressive and monooxygenase induction activities of highly chlorinated diphenyl ether congeners in C57BL/6 and DBA/2 mice.

The dose-response effects of 2,2',3,3',4,5,5',6,6'-2,2',3,3',4,4',5,6,6'- and 2,2',3,3',4,4',5,5',6- nonachlorodiphenyl ether (non-aCDE) and decachlorodiphenyl ether (decaCDE) on the splenic plaque-forming cell (PFC) response to sheep red blood cells (SRBCs) and the induction of hepatic microsomal ethoxyresorufin O-deethylase (EROD) activity was determined in aryl hydrocarbon (Ah)-responsive C57BL/6 and less Ah-responsive DBA/2 mice. All the congeners exhibited immunotoxicity at doses between 2.5 and 10 mumol/kg in C57BL/6 mice whereas in DBA/2 mice doses > or = 25 mumol/kg were required to cause inhibition of the PFC response to SRBCs. The results also showed that the nonaCDE isomers and decaCDE were more active as inducers of hepatic EROD activity in C57BL/6 than DBA/2 mice; however, there was not a correlation between the induced EROD activity and the CYP1A1 and CYP1A2 mRNA levels in the C57BL/6 mice. These data suggested that the immunotoxicity of these compounds was mediated through the Ah receptor. However, the results showed that the immunotoxicity of the nonaCDE isomers and decaCDE was unexpectedly high compared to that of lower chlorinated diphenyl ethers and there were no apparent structure-activity relationships among the higher chlorinated congeners. This suggests that some of the immunosuppressive effects observed for the nonaCDE isomers and decaCDE may be Ah receptor-independent.

Animals↗
PubMed1993

Resistance to flow through the valves of mouth-to-mask ventilation devices.

UNLABELLED: We conducted this study to determine the inspiratory and expiratory flow resistance of the valves of eight commercially available mouth-to-mask ventilation devices. METHODS & MATERIALS: We evaluated the valves of Intertech, Laerdal, Life Design Systems (LDS), Res-Q, Respironics, Rondex, Vital Signs, and White. The devices were supplied by the manufacturers and included the valve and any filter or extension tube supplied with the valve. Expiratory resistance was evaluated by directing air through the valve in the direction of flow when the patient exhales. Inspiratory resistance was evaluated by directing air through the valve in the direction of flow when a breath is delivered to the patient. Flow was controlled by a Timeter 0-75 flowmeter and measured using a calibrated Timeter RT-200. Flows of 10, 20, 30, 40, 50, 60, 70, 80, and 90 L/min were used. 'Back' pressure due to the resistance of the valves was measured using a calibrated Timeter RT-200. Resistance was calculated by dividing back pressure by flow. Five measurements were made at each flow setting for each valve. RESULTS: We observed significant differences in back pressures and resistances between the flows evaluated (p < 0.001 for both inspiratory and expiratory flows), and between the commercially available devices (p < 0.001 for both inspiratory and expiratory flows). At a flow of 50 L/min, the inspiratory back pressures produced by the devices were [mean (SD) in cm H2O] Intertech 5.2 (0.06), Laerdal 4.6 (0.09), LDS 4.7 (0.03), Res-Q 3.1 (0.04), Respironics 3.3 (0.04), Rondex 1.1 (0.02), Vital Signs 4.0 (0.06), and White 4.3 (0.10). At this same flow, the expiratory back pressures were Intertech 4.8 (0.30), Laerdal 9.1 (0.10), LDS 3.3 (0.02), Res-Q 3.7 (0.35), Respironics 0.5 (0.01), Rondex 1.4 (0.01), Vital Signs 3.6 (0.05), and White 13.7 (0.48). CONCLUSIONS: In some cases, the resistance through these devices might be considered excessive; however, most of the devices meet the International Standards Organization (ISO) standard (back pressure < 5 cm H2O at 50 L/min).

Data Collection↗
PubMed1992

Reduced Leydig cell volume and function in adult rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin without a significant effect on spermatogenesis.

Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to alter testicular function. However, its effect on the efficiency of spermatogenesis or on Leydig cell volume has not been determined in adult rats. In two replicas, adult male rats received a single intraperitoneal injection of TCDD at a rate of 0, 12.5, 25.0, or 50.0 micrograms/kg body weight. Rats were sacrificed 4 weeks after treatment. The cytosolic Ah receptor in the testis was estimated at 10.3 +/- 1.2 fmol/mg protein in these adult rats. The presence of the Ah receptor at this concentration in the testis reveals that the testis is a possible target organ for TCDD-induced responses. Left testes were homogenized and testicular spermatids were counted by phase contrast cytometry to determine daily sperm production. Right testes were vascularly perfused with glutaraldehyde, embedded in Epon 812, sectioned at 0.5 micron, stained with toluidine blue and evaluated by stereology for germ cells or Leydig cells. Body weight was reduced (P < 0.01) in a dose-dependent fashion. Testicular weight and daily sperm production per testis were not significantly reduced by TCDD. Androgen receptor concentrations in the testis and prostate were not affected. Weights of two androgen-sensitive organs (seminal vesicles and epididymis) were reduced (P < 0.01) in a dose-dependent fashion and serum concentrations of testosterone were reduced in a dose-dependent fashion in Replica 2. Due to low numbers of animals in Replica 1, the reduced Leydig cell volume was not significant after TCDD treatment; however, in Replica 2 there was a dose-dependent reduction (P < 0.01) in volume per testis of Leydig cell cytoplasm, nuclei, or total Leydig cell volume. Production of testosterone was sufficient to maintain spermatogenesis quantitatively; however, TCDD caused a dose-dependent reduction in Leydig cell function and Leydig cell volume per testis. This study showed for the first time that TCDD-induced androgen deficiency of male rats may be explained by the loss of total volume of Leydig cell cytoplasm. This study also further illustrates the reserve capacity of Leydig cell function to maintain spermatogenesis when the volume of these cells is significantly reduced.

Animals↗
PubMed1992

The effect of 6-nitro-1,3,8-trichlorodibenzofuran as a partial estrogen in the female rat uterus.

Administration of 6-nitro-1,3,8-trichlorodibenzofuran (6-NCDF) caused a dose- and time-dependent increase in uterine wet weight and cytosolic and nuclear estrogen receptor (ER) and progesterone receptor (PR) levels in immature female Sprague-Dawley rats. These estrogenic effects persisted for up to 96 or 144 hr after initial administration of 6-NCDF and could be observed at a dose as low as 2 mumol/kg. In contrast, 6-NCDF (25 mumol/kg) did not increase rat uterine peroxidase activity or epidermal growth factor (EGF) receptor binding activity. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), which exhibits a broad spectrum of antiestrogenic effects in the female rat uterus, inhibited the 17 beta-estradiol-induced increase in uterine wet weights, cytosolic and nuclear ER and PR levels, peroxidase activity, and EGF receptor binding activity. In contrast, 2,3,7,8-TCDD inhibited the uterotropic effects caused by 6-NCDF but did not affect the 6-NCDF-induced uterine ER and PR levels. 6-NCDF is a weak inducer of hepatic microsomal ethoxyresorufin O-deethylase activity and competitively binds to the aryl hydrocarbon (Ah) receptor but not the PR or ER. Thus both 6-NCDF and 2,3,7,8-TCDD, two ligands which bind to the Ah receptor, exhibit both partial estrogenic and antiestrogenic properties and serve as useful models for delineating the complex biochemical interactions between the ER and Ah receptor signal transduction pathways.

Animals↗
PubMed1991

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related compounds as antioestrogens: characterization and mechanism of action.

In the female Sprague-Dawley rat uterus 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds exhibited a broad spectrum of antioestrogenic responses. For example 2,3,7,8-TCDD inhibited the 17 beta-oestradiol-induced uterine wet weight increase, peroxidase activity, oestrogen and progesterone receptor levels, epidermal growth factor (EGF) receptor binding, and EGF receptor and c-fos protooncogene mRNA levels. The aryl hydrocarbon (Ah) receptor was identified in the rat uterus and the antioestrogenic activities of TCDD and related compounds were structure-dependent. In parallel studies, the effects of TCDD as an antioestrogen in MCF-7 human breast cancer cells was also investigated. TCDD inhibited the 17 beta-oestradiol-induced proliferation of these cells and the secretion of the 34-, 52- and 160-kDa proteins. Treatment of MCF-7 cells with 1 nM [3H]-17 beta-oestradiol resulted in a rapid accumulation of nuclear oestrogen receptor (ER) complexes. Pretreatment of the cells with TCDD caused a rapid decrease in nuclear ER binding activity and immunoreactive protein; moreover, the structure-dependent potencies of TCDD and related compounds as antioestrogens were similar to their Ah receptor binding affinities. TCDD also caused a decrease in nuclear ER levels in wild-type Ah-responsive Hepa 1c1c7 cells but was inactive in Ah non-responsive mutant Hepa 1c1c7 cells. Moreover, in the wild-type cells, both actinomycin D and cycloheximide blocked the effects of TCDD. 6-Methyl-1,3,8-trichlorodibenzofuran (MCDF) has previously been characterized as a TCDD antagonist in rodents and in transformed rodent cell lines. However, like TCDD, MCDF also exhibited a broad spectrum of antioestrogenic activities in both the female Sprague-Dawley rat uterus and MCF-7 cells. MCDF is relatively non-toxic compared to TCDD and is being investigated as a compound which may be clinically useful for the treatment of mammary cancer.

Animals↗
PubMed1990

2,3,7,8-Tetrachlorodibenzo-p-dioxin inhibition of 17 beta-estradiol-induced increases in rat uterine epidermal growth factor receptor binding activity and gene expression.

Treatment of immature female Sprague-Dawley rats with 17 beta-estradiol (5 micrograms/animal) resulted in an increase in uterine epidermal growth factor (EGF) receptor binding activity. Moreover, in a separate study it was also shown that 17 beta-estradiol increased steady-state levels of rat uterine EGF receptor mRNA as determined by Northern analysis. In contrast, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) caused a dose-response decrease in constitutive rat uterine EGF receptor binding activity and this was paralleled by a decrease in steady-state levels of uterine EGF receptor mRNA. Cotreatment of the animals with both TCDD (16 nmol/kg) and 17 beta-estradiol (5 micrograms/rat) gave results which showed that TCDD significantly inhibited the estrogen-induced increases in rat uterine EGF receptor binding activity and EGF receptor mRNA levels. These results further extend the range of antiestrogenic properties of TCDD and suggest that the inhibition of growth factor expression may play a role in the growth-inhibiting properties of TCDD in estrogen-responsive tissues or cells.

Animals↗
PubMed1990

Immunosuppressive and monooxygenase induction activities of polychlorinated diphenyl ether congeners in C57BL/6N mice: quantitative structure-activity relationships.

The dose-response effects of several polychlorinated diphenyl ether (polyCDE) congeners on the inhibition of the splenic plaque-forming cell (PFC) response to sheep red blood cell antigen and the induction of hepatic microsomal aryl hydrocarbon hydroxylase (AHH) and ethoxyresorufin O-deethylase (EROD) activities were determined in male C57BL/6 mice. The immunotoxic potencies for the polyCDE congeners (ED50 values for the suppression of PFCs/spleen and PFCs/10(6) cells) followed the order 2,3,3',4,4',5-hexaCDE (0.5 and 2.2 mumols/kg) greater than 3,3',4,4',5-pentaCDE (8.8 and 5.1 mumols/kg) greater than 2,3',4,4',5-pentaCDE (21.8 and 14.2 mumols/kg) greater than 3,3',4,4'-tetraCDE (50.6 and 28.7 mumols/kg) greater than 2,2',4,4',5,5'-hexaCDE (81.2 and 56.5 mumols/kg) greater than 2,2',4,5,5'-pentaCDE (258 and 228 mumols/kg) greater than 2,2',4,4',5,6'-hexaCDE (greater than 400 mumols/kg for both responses). The potencies of the polyCDE congeners as inducers of hepatic microsomal AHH and EROD activities were similar to their immunotoxicities and only one compound, namely, 2,3',4,4',5,5'-hexaCDE, did not cause dose-response immunosuppressive effects in the mice. The structure-activity relationships for the polyCDEs exhibited both differences and similarities. For example, the coplanar 3,3',4,4'-tetraCDE and 3,3',4,4',5-pentaCDE congeners were less immunotoxic than their monoortho 2,3',4,4',5-pentaCDE and 2,3,3',4,4',5-hexaCDE analogs, respectively, and similar results were also observed for their enzyme induction potencies. For the corresponding polychlorinated biphenyls (PCB) congeners the coplanar compounds were significantly more active than their monoortho analogs. In addition, two diortho-substituted compounds, namely, 2,2',4,5,5'-pentaCDE and 2,2',4,4',5,5'-hexaCDE, were also immunotoxic at a dose of 400 mumols/kg whereas, their PCB analogs were inactive. These studies clearly demonstrate that for the polyCDE congeners, increasing ortho-chloro substitution is less effective in reducing the activity of these congeners compared to the well-recognized ortho effects reported for the PCBs. The differences in the structure-activity relationships between polyCDEs and PCBs are related to the ether bridge in the polyCDEs in which the resultant increased bond length between the two phenyl rings thereby diminishes the effects of ortho substituents on the biochemical and toxic potencies of these compounds.

Animals↗
PubMed1990

The structure-dependent effects of heptachlorodibenzofuran isomers in male C57BL/6 mice: immunotoxicity and monooxygenase enzyme induction.

The dose-response effects of the 1,2,3,4,6,7,8-, 1,2,3,4,7,8,9-, 1,2,3,4,6,8,9-, and 1,2,3,4,6,7,9-heptachlorodibenzofurans (HpCDFs) on the splenic plaque-forming cell (PFC) response to sheep erythrocytes and on the induction of hepatic microsomal aryl hydrocarbon hydroxylase (AHH) and ethoxyresorufin-O-deethylase (EROD) activities were determined in male C57BL/6 mice. The ED50 values for the decrease in the PFCs/spleen, the number of PFCs/10(6) viable cells, and the induction of AHH and EROD activities were 1,2,3,4,6,7,8-HpCDF, 0.011, 0.018, 0.11, and 0.315 mumol/kg, respectively; 1,2,3,4,7,8,9-HpCDF, 0.012, 0.054, 0.70, and 0.20 mumol/kg, respectively; 1,2,3,4,6,7,9-HpCDF, 1.2, 1.3, greater than 43, and greater than 43 mumol/kg, respectively; 1,2,3,4,6,8,9-HpCDF, 1.5, 3.4, 22, and 22 mumol/kg, respectively. It was apparent from these studies that the 2,3,7,8-substituted HpCDF isomers (1,2,3,4,6,7,8- and 1,2,3,4,7,8,9-) were significantly more potent than the compounds which contained only three lateral C1 groups. These results were obtained using a multiple dosing regimen in which 10 separate doses of the HpCDF isomers were administered to the mice by intraperitoneal injection over a period of 12 days. However, when the mice were treated with a single dose of an HpCDF congener, which was equivalent to the total dose used in the multiple dose study, the responses were comparable. A comparison of the relative immunotoxic potencies of the 2,3,7,8-substituted HpCDFs and 2,3,7,8-tetrachlorodibenzo-p-dioxin showed that the latter compound was approximately 10 times more active than the HpCDFs.

Animals↗
PubMed1988

Differential silver staining in lymphocytes and lymphoblastoid cell cultures.

An analysis of the patterns of silver-stained nucleolar organizer regions (AgNORs), an indication of rDNA transcriptional activity, was carried out in metaphases from peripheral lymphocytes and young lymphoblastoid cell cultures (LCL) transformed by Epstein-Barr virus. Four individuals previously shown to carry a double NOR (dNOR) were studied. The dNOR varied in staining frequency and showed intra-individual variation in appearance in both cell types. For each individual a significantly greater mean number of AgNORs was observed in LCL (7.0-8.04) when compared with lymphocytes (5.8-6.4). To control for possible serum stimulation effects, lymphocytes from one individual were cultured in 20% serum as was the LCL of all subjects. The mean number of AgNORs in these lymphocytes remained significantly lower than in the LCL, as did the mean size of the dNOR, based on a relative score. Our results suggest that LCL have increased expression of rDNA, as evidenced by silver staining.

Cells, Cultured↗