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Biomedical subjects

W Zhao

Publications and source records attributed to W Zhao.

At least 325 records · Page 18Linked to original sources
PubMed1995

Pleckstrin inhibits phosphoinositide hydrolysis initiated by G-protein-coupled and growth factor receptors. A role for pleckstrin's PH domains.

Pleckstrin is a 40-kDa protein present in platelets and leukocytes that contains two PH domains separated by a 150-residue intervening sequence. Pleckstrin is a major substrate for protein kinase C, but its function is unknown. The present studies examine the effects of pleckstrin on second messenger generation. When expressed in cos-1 or HEK-293 cells, pleckstrin inhibited 1) the G alpha-mediated activation of phospholipase C beta initiated by thrombin, M1-muscarinic acetylcholine, and angiotensin II receptors, 2) the stimulation of phospholipase C beta by constitutively active Gq alpha, 3) the G beta gamma-mediated activation of phospholipase C beta caused by alpha 2A-adrenergic receptors, and 4) the tyrosine phosphorylation-mediated activation of phospholipase C gamma caused by Trk A. However, pleckstrin had no effect on either the stimulation or inhibition of adenylyl cyclase. The inhibition of phosphoinositide hydrolysis caused by pleckstrin was similar in magnitude to that caused by activating protein kinase C with phorbol 12-myristate 13-acetate (PMA). When combined, pleckstrin and PMA had an additive effect, inhibiting phosphoinositide hydrolysis by as much as 90%. Structure-function analysis highlighted the role of pleckstrin's N-terminal PH domain in these events. Although deleting the C-terminal PH domain had no effect, deleting the N-terminal PH domain abolished activity (but not expression) and mutating a highly conserved tryptophan residue within the N-terminal PH domain decreased activity by one-third. Notably, however, a pleckstrin variant in which the N-terminal PH domain was replaced with a second copy of the C-terminal PH domain was nearly as active as native pleckstrin. These results show that: 1) pleckstrin can inhibit pathways leading to both phospholipase C beta- and phospholipase C gamma-mediated phosphoinositide hydrolysis, 2) this inhibition affects activation of phospholipase C beta mediated by either G alpha or G beta gamma, but does not affect the regulation of adenylyl cyclase activity by G alpha or G beta gamma, 3) although pleckstrin is a substrate for protein kinase C, the effects of pleckstrin and PMA are at least partially independent, 4) the inhibition caused by pleckstrin appears to be mediated by the PH domain at the N terminus, rather than the C terminus of the molecule, and 5) location of the two PH domains within the molecule clearly contributes to their individual activity.2+1

Animals↗
PubMed1995

Inhibition of DNA synthesis in primary cultures of adult rat hepatocytes by benzo[a]pyrene and related aromatic hydrocarbons: role of Ah receptor-dependent events.

Studies were conducted to examine the effects of benzo[a]pyrene (BaP) and related-aromatic hydrocarbons (AHs) on the DNA synthetic profiles of adult rat hepatocytes in primary culture. Scheduled DNA synthesis in control cultures peaked at 64 h and was negligible by 72 h after initial seeding of freshly isolated hepatocytes. A concentration-dependent inhibition of DNA synthesis was observed in 1-day old hepatocyte cultures treated with BaP (0.3-30 microM) for up to 28 h. Comparable inhibitory responses were observed in cultures treated for 24 h with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 0.01-1 nM) or 2,3,7,8-tetrachlorodibenzofuran (TCDF, 0.01-1 nM), but not in cultures treated with perylene (0.01-100 nM) or benzo[e])pyrene (1-1000 nM). Ethoxyresorufin-O-deethylase (EROD) activity was highly inducible in hepatocytes challenged for 24 h with BaP (0.3-3 microM) or TCDD (0.1-100 nM) with peak induction observed at 12 or 36 h after chemical challenge, respectively. To determine if DNA synthesis inhibition by these agents involved aryl hydrocarbon receptor (AhR)-related events, subsequent experiments were conducted to examine the interactions of alpha-naphthoflavone (alpha-NF) and ellipticine (ET) with BaP and TCDD in this cell system. Pretreatment with alpha-NF (10 nM) for 24 h prevented the inhibitory effects of both BaP (3 microM) and TCDD (1 nM), while ET (0.01 nM) pretreatment selectively antagonized the effects of BaP (3 microM). Pretreatment of hepatocytes with TCDD or TCDF (1 nM) for 24 h before the onset of DNA synthesis followed by challenge with BaP (3 microM) partially antagonized the inhibitory response to BaP. These data implicate AhR-related signal transduction in the inhibition of hepatocyte DNA synthesis by BaP and related AHs and suggest that in the case of BaP, metabolism by cytochrome P450 to toxic intermediates contributes to the inhibitory response.

Analysis of Variance↗
PubMed1995

Bone regrowth in young mice stimulated by nail organ.

Recent studies of postamputational repair following digit-tip amputation revealed an unexpected correlation between nail regrowth and bone regrowth in mice. To examine putative effects of nail on bone regrowth, phalangeal tips were amputated such that nail was artificially removed from distal levels or retained following proximal level amputations. In the absence of nail, bone did not regrow at distal levels. Conversely, when nail was surgically retained bone regrew from proximal levels. The nail organ profoundly influences bone regrowth.

Amputation, Surgical↗
PubMed1995

SH3 domains specifically regulate kinase activity of expressed Src family proteins.

The Src homology 2 (SH2) and Src homology 3 (SH3) domain are approximately 50% conserved in various Src family kinase members. Several lines of evidence suggest that in Src these domains are sequence motifs that direct substrate recognition, regulate kinase activity, or control subcellular localization. We sought to investigate the function of the homology domains in human Lyn, and to determine whether the differences between various SH3 domains affect function. To do this, we generated variant forms of Lyn lacking SH2 and SH3 domains, and created chimeras in which the SH3 domains in human c-Src and Lyn were replaced with SH3 domains from other family members. In contrast to similar deletions in Src, forms of Lyn lacking SH2 or SH3 had decreased kinase activity. The SH3 chimeras all had individual characteristics. Insertion of the Blk SH3 domain into Lyn restored kinase activity, while insertion of the Fyn or Src SH3 into Lyn enhanced the kinase activity 2-3-fold. Insertion of the Lyn SH3 into Src also doubled kinase activity. Expression of the Lyn-Src SH3 chimera in mammalian cells induced cell transformation. This study 1) demonstrates that the regulation of Lyn is different than Src, and 2) provides new evidence that despite their homology, there are important functional differences between the SH3 domains of the various Src family members.

3T3 Cells↗
PubMed1995

The role of macrophages, perivascular cells, and microglial cells in the pathogenesis of experimental autoimmune encephalomyelitis.

Clinical signs of experimental autoimmune encephalomyelitis (EAE) in rats can be suppressed by treatment with liposomes containing dichloromethylene diphosphonate (Cl2MDP liposomes). Here we investigated whether besides the blood-borne macrophages also ED2+ perivascular cells and microglia are affected by this treatment. For this purpose we examined the central nervous system of bone marrow chimeras in which EAE was induced with encephalitogenic T cells. Quantification of cell numbers of various cell types in inflammatory lesions in the spinal cord showed that after treatment with Cl2MDP liposomes more than 95% of the bone marrow derived (I1-69+) macrophages were eliminated. In addition the number of ED2+ perivascular cells were seen to be decreased by 68% as compared to ED2+ cells in control liposome treated animals. However the number of these perivascular cells in Cl2MDP liposome treated animals did not differ from the number of perivascular cells in naive animals, indicating that only newly recruited, inflammation associated, ED2+ macrophages were eliminated. Moreover, detection of degenerating nuclei by in situ nick translation (ISNT) in combination with staining for ED1 or ED2 showed that in the perivascular space no degenerating cells were present. Cl2MDP liposome treatment furthermore decreased the numbers of T cells infiltrating the parenchyma by more than 50%. Instead T cells were found in large numbers in the perivascular space. Microglia did not seem to be eliminated by Cl2MDP liposome treatment as shown by the absence of ED1+/ISNT+ cells in the CNS parenchyma. However the number of ED1+ (I1-69-) microglial cells decreased by more than 80%, indicating that the activation of this cell type was impaired. It is concluded that bone marrow derived macrophages play an important role in the pathogenesis of EAE via interactions with lymphocytes and the activation of resident microglia.

Animals↗
PubMed1995

DNA binding by C/EBP proteins correlates with hepatocyte proliferation.

The leucine zipper transcription factors C/EBP alpha and C/EBP beta exhibit growth-related variations of expression and DNA binding during liver regeneration. We examined the expression of C/EBP proteins in relation to hepatocyte proliferation by studying their DNA-binding activity in primary mouse hepatocytes in vitro. Mouse hepatocytes were dissociated by collagenase perfusion and cultured in a serum-free, defined medium containing a variety of growth factors and hormones. Cell protein extracts were collected every 24 h for up to 10 d and examined for DNA-binding activity by gel retardation analysis using a C/EBP consensus sequence oligomer (bZIP). C/EBP alpha is the major bZIP-binding protein present in the dissociated cells prior to plating. With the culture conditions we employed, little or no binding of C/EBP proteins was observed in the first 24 to 48 h of cultivation. After 48 h, C/EBP beta binding activity was elevated relative to the level seen in freshly dissociated cells. In contrast, C/EBP alpha binding continued to be greatly reduced and no C/EBP delta binding was observed. C/EBP beta binding remained elevated for the duration of the experiment. Additional growth factor treatment (EGF, FGF, TGF alpha, and HGF) of the hepatocytes did not appreciably alter the pattern of C/EBP binding. However, TGF beta treatment, known to decrease hepatocyte proliferation, increased C/EBP beta binding activity earlier and more actively than in control cells. This study confirms a negative correlation between DNA binding by the C/EBP transactivator proteins and the proliferation of primary mouse hepatocytes in vitro.

Animals↗
PubMed1995

Bibenzyls from Stemona tuberosa.

Three new bibenzyls were isolated from the roots of Stemona tuberosa. Their structures were identified by spectroscopic methods as 3,5-dihydroxy-4-methylbibenzyl, 3,5-dihydroxy-2'-methoxy-4-methylbibenzyl and 3-hydroxy-2',5-dimethoxy-2-methylbibenzyl.

Animals↗
PubMed1995

Calorie restriction modulates lymphocyte subset phenotype and increases apoptosis in MRL/lpr mice.

Defective expression of the Fas apoptotic gene may account for overproduction of CD4- CD8- B220+ cells (double-negative) in MRL/MpJ-lpr/lpr (lpr) mice. Previous studies have shown that calorie restriction (CR) inhibits the development of autoimmune disease and extends life span in these animals. The present studies describe the effects of CR on the distribution of lymphocyte phenotypes, lymphocyte proliferative response, and cytokine release. The effects of CR on dexamethasone (DEX)-induced apoptosis were also studied using propidium iodide (PI) uptake and DNA fragmentation in splenocytes and lymph node (LN) cells. Weanling female mice were fed a nutritionally adequate semipurified diet either ad libitum (AL) or with 40% fewer calories than AL (CR), and killed at 5 months of age. CR mice had fewer palpable lymph nodes, and decreased serum anti-dsDNA antibodies. Mitogen (ConA, anti-CD3, and LPS) and superantigen (SEB)-induced proliferative response was significantly lower in lymphoid cells from AL fed animals. FACS analysis of cells from CR animals showed decreased CD4- CD8- cells in spleen (1.7-fold, P < 0.025) and LN (1.6-fold P < 0.01) and significantly higher CD4+ (spleen, 1.7-fold, P < 0.0001; LN, 2.6-fold, P < 0.025) and CD8+ (spleen, 1.6-fold, P < 0.001; LN, 5.2-fold, P < 0.005) cells. ConA-stimulated IL-2 release was increased in CR animals (splenocytes, 7.5-fold, P < 0.001; LN cells, 6.1-fold, P < 0.01). Finally, apoptosis in response to Dex was increased in CR animals as indicated by the presence of more PI-positive cells (spleen, 15.8%; LN, 10.7%; P < 0.01) and increased DNA fragmentation. In summary, the amelioration of autoimmune disease in MRL/lpr mice by CR is accompanied by prevention of the rise in 'double-negative' T cells and by maintenance of lymphocyte responsiveness to mitogens and DEX-induced apoptosis at higher levels.

Animals↗
PubMed1995

Passive avoidance learning induced change in GAP43 phosphorylation in day-old chicks.

Day-old chicks trained on a single trial passive discriminated avoidance task demonstrated a significant increase in in vitro phosphorylation of a 50 kDa protein in P2M fractions of total forebrain. The increase occurred 30 min posttraining, at a time when previous reports suggest that mechanisms for triggering protein synthesis-dependent long-term memory consolidation are activated. These changes in phosphorylation rates were accompanied by a substantial enhancement of total kinase activity. Immunoblotting studies with monoclonal anti-GAP43 antibody indicate that this protein is GAP43. These results contradict previous reports of a decrease in in vitro GAP43 phosphorylation following the same learning paradigm. A number of procedural differences may account for this discrepancy. The results suggest that changes in the phosphorylation state may be associated with mechanisms triggering long-term memory consolidation.

Animals↗
PubMed1995

Phosphorylation changes following weakly reinforced learning and ACTH-induced memory consolidation for a weak learning experience.

The formation of a protein synthesis-dependent long-term memory stage in day-old chicks trained on a passive discriminated avoidance task has been shown to occur only with an adequate level of reinforcement, and is preceded by a significant change in the phosphorylation state of the forebrain synaptosomal membrane protein GAP43 protein. In the present study, it is shown that weakly reinforced training did not lead to formation of a long-term memory stage or to any change in phosphate incorporation into forebrain P2M protein bands. However, administration of ACTH immediately posttraining led to both the formation of the long-term memory stage and a preceding significant increase in the phosphorylation of GAP43. These findings are consistent with the view that a reinforcement-dependent neurohormone-mediated change to the phosphorylation of this synaptosomal membrane protein may be implicated in the triggering of long-term memory consolidation.

Animals↗
PubMed1995

The impairment of long-term memory formation by the phosphatase inhibitor okadaic acid.

While there is considerable evidence that protein kinase activity is involved in memory formation, there has been, as yet, no direct investigation of a role for protein phosphatases. However, phosphatases have been implicated in the effects of the activation of glutamate receptors of the NMDA type, in long-term depression, and in the regulation of transmitter release and membrane ion channel activities, phenomena which have been shown to be possibly involved in cellular memorial processes. In the present paper, inhibition of protein phosphatase by 0.5 nM okadaic acid, a selective inhibitor of phosphatases 1 and 2A, is demonstrated to prevent memory consolidation in day-old chicks trained on a single trial passive avoidance task. Retention losses first occurred after 30 min post-learning, at an intermediate stage of memory formation preceding a protein synthesis-dependent long-term stage. It is suggested that protein phosphatase activity is involved in precursor processes to long-term memory consolidation.

Animals↗
PubMed1995

An in vitro EPR study of the free-radical scavenging actions of the lazaroid antioxidants U-74500A and U-78517F.

Oxygen-based free radicals have been shown to play a major role in the acute destruction of neurons following cerebral ischemia and may be involved in the chronic neurodegeneration seen in Parkinson's disease, Alzheimer's disease, and other conditions characterized by the progressive death of neurons in the central nervous system. Drugs belonging to a group of antioxidant compounds, collectively known as the lazaroids, have strong neuroprotective effects in experimental models of acute ischemia. However, the specific mechanisms by which these drugs reduce the harmful actions of free radicals have not been established. Using electron paramagnetic resonance (EPR) spectroscopy with spin trapping, we investigated the interaction of U-74500A, a first-generation lazaroid, and U-78517F, a second-generation lazaroid, with two species of oxygen-based free radicals in aqueous solution and with the stable nitrogen-based free radical diphenylpicrylhydrazyl in dimethyl sulfoxide. Superoxide radicals were generated by the action of xanthine oxidase on hypoxanthine. Hydroxyl radicals were generated by the Fenton reaction involving aqueous ferrous iron and hydrogen peroxide. Both lazaroids reduce the EPR signal of all three radicals, but the drugs differ in potency and relative radical selectivity. These observations are consistent with the lazaroids being scavengers of oxygen-based and nitrogen-based free radicals and suggest that the neuroprotective actions of the lazaroids in cerebral ischemia may involve direct interactions of the lazaroids with several different species of free radicals.

Antioxidants↗
PubMed1995

A dual role for nitric oxide in NMDA-mediated toxicity in vivo.

Nitric oxide has been implicated in N-methyl-D-aspartate (NMDA)-mediated damage in vitro; however, its role in excitotoxic damage in vivo is not clear. In the present study we evaluated the histopathological and hemodynamic consequences of intrastriatal injections of various doses of NMDA and determined the effects of nitric oxide synthase inhibition on these changes. NMDA was injected into the striatum at doses of 50, 150, and 300 nmol with or without N omega-nitro-L-arginine methyl ester (L-NAME; 100 micrograms, locally). Three days following injections histopathological assessment was performed by morphometric analysis of the lesion area in multiple sections taken from the anterior to the posterior borders of the lesion. In animals injected with 150 and 300 nmol of NMDA (+/- L-NAME), local CBF (lCBF) was determined 30 min following injections using 14C-iodoantipyrine autoradiography. All NMDA-treated animals showed a well-demarcated lesion extending beyond the injection site. The volume of the lesion correlated significantly with the NMDA dose injected. The effects of L-NAME on lesion size were dependent on the dose of the NMDA. The lesion induced by 50 nmol of NMDA was not affected by L-NAME. With a dose of 150 nmol of NMDA, L-NAME induced a 43% increase in lesion volume. In contrast, a 38% decrease in lesion size was observed in animals treated with 300 nmol of NMDA combined with L-NAME. At a dose of 150 nmol, NMDA induced a significant elevation in lCBF, which was restricted to regions close to the injection site including the center areas of the anterior and middle striatum. The increase in lCBF observed with 150 nmol of NMDA was significantly attenuated in the NMDA + L-NAME-treated group. The lCBF changes induced by 300 nmol of NMDA were not significantly different from those in the 150-nmol group; however, the extent of the regions involved was larger. The increases in lCBF were observed in all striatal regions including the central and peripheral areas. L-NAME did not have a significant effect on the lCBF changes induced by NMDA at a dose of 300 nmol. These data suggest that in vivo the involvement of nitric oxide in NMDA toxicity depends on the NMDA dose and on the participation of hemodynamic mechanisms secondary to NMDA exposure.

Animals↗
PubMed1995

Three-dimensional quantitative autoradiography by disparity analysis: theory and application to image averaging of local cerebral glucose utilization.

Traditional autoradiographic image analysis has been restricted to the two-dimensional assessment of local cerebral glucose utilization (LCMRglc) or blood flow in individual brains. It is advantageous, however, to generate an entire three-dimensional (3D) data set and to develop the ability to map replicate images derived from multiple studies into the same 3D space, so as to generate average and standard deviation images for the entire series. We have developed a novel method, termed "disparity analysis," for the alignment and mapping of autoradiographic images. We present the theory of this method, which is based upon a linear affine model, to analyze point-to-point disparities in two images. The method is a direct one that estimates scaling, translation, and rotation parameters simultaneously. Disparity analysis is general and flexible and deals well with damaged or asymmetric sections. We applied this method to study LCMRglc in nine awake male Wistar rats by the [14C]2-deoxyglucose method. Brains were physically aligned in the anteroposterior axis and were sectioned subserially at 100-microns intervals. For each brain, coronal sections were aligned by disparity analysis. The nine brains were then registered in the z-axis with respect to a common coronal reference level (bregma + 0.7 mm). Eight of the nine brains were mapped into the remaining brain, which was designated the "template," and aggregate 3D data sets were generated of the mean and standard deviation for the entire series. The averaged images retained the major anatomic features apparent in individual brains but with some defocusing. Internal anatomic features of the averaged brain were smooth, continuous, and readily identifiable on sections through the 3D stack. The fidelity of the internal architecture of the averaged brain was compared with that of individual brains by analysis of line scans at four representative levels. Line scan comparisons between corresponding sections and their template showed a high degree of correlation, as did similar comparisons performed on entire sections. Fourier analysis of line scan data showed retention of low-frequency information with the expected attenuation of high-frequency components produced by averaging. Region-of-interest (ROI) analysis of the averaged brain yielded LCMRglc values virtually identical to those derived from measurements and subsequent averaging of data from individual brains.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1995

Three-dimensional image analysis of brain glucose metabolism-blood flow uncoupling and its electrophysiological correlates in the acute ischemic penumbra following middle cerebral artery occlusion.

The relationship between local cerebral glucose utilization (LCMRglc) and local CBF (LCBF) is known to be disturbed in regions surrounding an acute focal ischemic lesion--areas that undergo repeated transient depolarizations. In this study, we evaluated the relationship between LCMRglc and LCBF in the acute focal ischemic penumbra to quantify metabolism-flow uncoupling, and we related these findings to local electrophysiological measurements. A novel strategy utilizing three-dimensional (3D) autoradiographic image averaging yielded group 3D reconstructions of LCBF, LCMRglc, and the CMR/CBF ratio. The distal right middle cerebral artery of Sprague-Dawley rats was occluded by laser-driven photothrombosis following administration of the photosensitizing dye rose bengal; this was coupled with permanent ipsilateral and 1-h contralateral common carotid artery occlusions. LCBF (n = 7) and LCMRglc (n = 7) were measured autoradiographically at 1.25 and 1.5-2 h postocclusion, respectively, in matched animal groups. Within the ischemic penumbra (defined as having LCBF of 20-40% of control or 0.23-0.47 ml g-1 min-1), LCMRglc showed a heterogeneous pattern with values ranging from near normal to markedly increased. The resulting CMRglc/CBF ratio in this zone was 234 +/- 100 mumol/100 ml (mean +/- SD), representing a severe degree of metabolism-flow dissociation when compared with the CMRglc/CBF ratio of 51.0 +/- 28.7 mumol/100 ml of the contralateral (normal) hemisphere. Metabolism-flow uncoupling was confined to the ipsilateral cortex and was most prominent at the anterior and posterior coronal poles of the ischemic lesion. In the frontoparietal penumbra, where marked uncoupling was observed, sustained deflections of the DC potential were recorded, which increased significantly in duration over the initial 65 min postocclusion. Both the heterogeneous pattern of LCMRglc and the widespread distribution of increased CMRglc/CBF ratio in the ischemic penumbra are thought to reflect the metabolic consequences of periinfarct depolarizations. Analysis of averaged 3D autoradiographic data sets provides a powerful means for assessing metabolism-flow uncoupling surrounding an ischemic focus.

Animals↗
PubMed1995

Changes in primary and secondary lymphoid organ T-cell subpopulations resulting from acute in vivo exposure to propanil.

Acute exposure to the herbicide propanil is immunotoxic for selected immune functions, as well as causing changes in the weights of the thymus and spleen. Although spleen cellularity and weight increase with propanil exposure, the thymus: body weight ratio decreases with increasing doses of propanil. The present study analyzes the thymocyte subpopulations in the thymus, spleen, and mesenteric lymph nodes. C57Bl/6 mice were treated with either 0, 100, 150, or 200 mg/kg propanil, and 7 d later thymocyte populations were analyzed by flow cytometry. In the thymus, propanil exposure resulted in a dose-dependent decrease in total numbers of T cells, as would be expected with its reduced weight. Determination of the thymocyte subpopulation distribution in the thymus showed a significant reduction in the number of CD3+CD4+CD8- (CD3+4+8-), CD3+CD4-CD8+ (CD3+4-8+), and CD3+CD4+CD8+ (CD3+4+8+) cells. Percent distribution of these thymic cell subpopulations showed similar decreases only with the highest dose. Apparent dose-related decreases in the numbers of CD3-CD4+CD8+ (CD3-4+8+) cells were also noted and were attributed to the general decrease in total thymus cells. The percentage of CD3- subpopulations showed an increasing trend with dose, which suggests that at 7 d postpropanil exposure there may be a specific effect on this most immature population. Although the size and cellularity of the spleen were increased, no change in CD4+ or CD8+ cell distribution was observed. Similarly, mesenteric lymph nodes showed no changes in the cell subpopulation distribution between propanil-treated and control animals.

Analysis of Variance↗
PubMed1995

X-ray imaging using amorphous selenium: feasibility of a flat panel self-scanned detector for digital radiology.

We investigate a concept for making a large area, flat-panel detector for digital radiology. It employs an x-ray sensitive photoconductor to convert incident x-radiation to a charge image which is then electronically read out with a large area integrated circuit. The large area integrated circuit, also called an active matrix, consists of a two-dimensional array of thin film transistors (TFTs). The potential advantages of the flat-panel detector for digital radiography include: instantaneous digital radiographs without operator intervention; compact size approaching that of a screen-film cassette and thus compatibility with existing x-ray equipment; high quantum efficiency combined with high resolution. Its potential advantages over the x-ray image intensifier (XRII)/video systems for fluoroscopy include: compactness; geometric accuracy; high resolution, and absence of veiling glare. The feasibility of the detector for digital radiology was investigated using the properties of a particular photoconductor (amorphous selenium) and active matrix array (with cadmium selenide TFTs). The results showed that it can potentially satisfy the detector design requirements for radiography (e.g., chest radiography and mammography). For fluoroscopy, the images can be obtained in real-time but the detector is not quantum noise limited below the mean exposure rate typically used in fluoroscopy. Possible improvements in x-ray sensitivity and noise performance for the application in fluoroscopy are discussed.

Cobalt Radioisotopes↗