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Biomedical subjects

D Feldman

Publications and source records attributed to D Feldman.

At least 181 records · Page 10Linked to original sources
PubMed1986

Tubuloreticular inclusions in placental chorionic villi of rhesus monkeys after maternal treatment with interferon.

Tubuloreticular inclusions were observed in placental chorionic villi of rhesus monkeys after pregnant female monkeys were injected intramuscularly with recombinant leukocyte A interferon (25 X 10(6) units/kg). They were identified in endothelial cells, fibroblasts, and Hofbauer cells of the chorionic villi, providing evidence that interferon crossed at least part of the maternal-fetal partition. Induction of tubuloreticular inclusions in these cells by exogenous interferon has not been previously reported. Tightly packed regular tubular arrangements appeared in endothelial and Hofbauer cells and loosely organized tubular arrays in fibroblasts. The maximum dimension of the tubuloreticular inclusions measured 3 micron and the diameter of the tubules was 20 nm. The tubuloreticular inclusions were continuous with, and surrounded by, smooth endoplasmic reticulum that was often connected to rough endoplasmic reticulum. The tubuloreticular inclusions were not detected in placental chorionic villi from monkeys not treated with interferon or from interferon-treated monkeys 30 days after cessation of treatment. These results indicate that the formation of tubuloreticular inclusions in rhesus monkey placentas was a transient response associated with elevated serum levels of interferon.

Animals↗
PubMed1986

Cleavage of the rat intestinal 1,25-dihydroxyvitamin D3 receptor by an endogenous protease to a form with defective DNA binding.

In this report we describe a form of the 1,25(OH)2D3 receptor which no longer binds to DNA. The defective form of the receptor was produced by the action of an endogenous protease. Rat intestinal receptors, obtained by a two-step procedure of a low salt homogenization followed by extraction of the chromatin pellet with high salt, fail to bind to DNA-cellulose. Inclusion of various serine protease inhibitors during the preparation protects against the loss of DNA binding. Sedimentation analysis in sucrose gradients indicates that the defective receptor is measurably smaller than the native receptor and is unable to aggregate normally under low salt conditions. The size difference, as determined by gel chromatography, is approximately 9,000 Da (56,000 for the protected receptor, 47,000 for the cleaved form). The elution from DEAE-cellulose indicates that the overall charge of both intact and cleaved receptor forms is very similar. Cell fractionation and mixing experiments suggest the enzyme may be located in the lysosomal compartment, organelles which are susceptible to breakage during the extraction procedure. The results demonstrate that an endogenous enzyme preferentially cleaves the 1,25(OH)2D3 DNA binding site resulting in a receptor with altered characteristics. Such an enzymatic activity has not been previously described for the 1,25(OH)2D3 receptor from other tissues or species. Since rat intestine is a classically studied target organ, these findings have additional relevance in receptor purification or other studies to characterize the receptor.

Animals↗
PubMed1986

New method of hepatocyte transplantation and extracorporeal liver support.

A technique has been developed by the authors that allows hepatocyte attachment on collagen-coated microcarriers resulting in prolonged hepatocyte viability and function both in vivo and in vitro. Rat hepatocytes were obtained by portal vein collagenase perfusion. Intraperitoneally transplanted microcarrier-attached normal hepatocytes into congeneic Gunn rats were functioning 3-4 weeks later, as shown by the presence and persistence of conjugated bilirubin in recipient bile, sustained decrease in serum bilirubin, uptake of Tc99m-DESIDA, and morphologic criteria. Intraperitoneal transplantation of normal microcarrier-attached hepatocytes into genetically albumin deficient rats (NAR) resulted in marked increase in plasma albumin levels (6 days without and 21 days with Cyclosporin A immunosuppression). Microcarrier-attached hepatocytes transplanted after 2 weeks of storage at -80 C into congeneic Gunn rats were viable and functional as assessed by criteria outlined above. An extracorporeal liver perfusion system was developed using the microcarrier-attached hepatocytes that was capable of synthesizing and conjugating bilirubin and synthesizing liver-specific proteins.

Animals↗
PubMed1986

Estradiol-binding proteins from mycelial and yeast-form cultures of Paracoccidioides brasiliensis.

Paracoccidioides brasiliensis, the etiologic agent of paracoccidioidomycosis, causes disease much more frequently in men than it does in women, suggesting that the hormonal milieu of the host might influence P. brasiliensis pathogenicity. We recently demonstrated that cytosol from yeast cultures of P. brasiliensis contains a high-affinity, low-capacity, tritiated 17 beta-estradiol [( 3H]estradiol)-binding protein. Estradiol and, to a lesser degree, diethylstilbestrol (DES), inhibited the transformation of P. brasiliensis cultures from the mycelial to the yeast form, an event critical to the establishment of infection. Our current studies demonstrated a somewhat higher affinity (apparent dissociation constant [Kd], approximately equal to 6 to 12 nM) of the estrogen-binding protein for [3H]estradiol than was previously described for yeast cytosol. The presence of both high- and low-affinity estrogen-binding sites in yeast-form P. brasiliensis cytosol was detected after warming the cytosol to 37 degrees C. The high-affinity protein was labile to further heating (56 degrees C), although the low-affinity protein was stable. Additional experiments demonstrated the presence of an estrogen-binding protein in cytosol prepared from mycelial-form P. brasiliensis. This estrogen-binding protein had a slightly lower affinity for [3H]estradiol (Kd approximately equal to 13 nM), and its cytosol contained somewhat fewer binding sites (approximately equal to 78 fmol/mg of protein) than did yeast-form P. brasiliensis cytosol. Of particular interest was the finding that DES, a weak competitor for [3H]estradiol binding in yeast cytosol, displaced [3H]estradiol from the mycelial-form binding moiety. DES had a 50- to 100-fold-lower affinity for the [3H]estradiol-binding protein than did estradiol, consistent with its lower bioactivity in the mycelial-to-yeast-form transformation studies. The current results lend further support to our hypothesis that endogenous estrogens in the host, acting through the cytosol binding protein in the fungus, inhibit mycelial-to-yeast-form transformation, thus explaining the resistance of women to paracoccidioidomycosis.

Binding, Competitive↗
PubMed1986

Progesterone binding and inhibition of growth in Trichophyton mentagrophytes.

Specific binding of [3H]progesterone to cytosol of Trichophyton mentagrophytes was demonstrated. Scatchard analysis of [3H]progesterone binding showed a single class of binding sites with a dissociation constant of 9.5 X 10(-8) [corrected] +/- 2.4 X 10(-8) M (standard deviation) and a maximal binding capacity of 4,979 +/- 3,489 fmol/mg of cytosol protein. Deoxycorticosterone and dihydrotestosterone competitively inhibited binding by 50% at molar ratios of 10:1 and 20:1, respectively. Other steroid hormones that were tested had minimal activity, indicating binding specificity. Steroid hormone actions in T. mentagrophytes were examined in growth studies. Growth was assessed by determination of cellular ATP content. Progesterone inhibited growth in a dose-responsive manner, with a 50% inhibition concentration of 5.5 X 10(-6) M. Partial recovery from inhibition occurred after 24 to 48 h; inhibition could be enhanced by dividing the amount of added progesterone every 24 h. In the same rank order as was their relationship to each other and progesterone in binding studies, deoxycorticosterone and dihydrotestosterone were less effective inhibitors; other steroid hormones that were tested showed no consistent effect. We hypothesize that the binder described, acting as a hormone receptor, is the molecular site of action for the functional effect of the hormone. The functional effect may be related to the observed resistance of females to dermatophytosis.

Binding, Competitive↗
PubMed1986

The effects of 1,25-dihydroxyvitamin D3 and dexamethasone on rat osteoblast-like primary cell cultures: receptor occupancy and functional expression patterns for three different bioresponses.

The effects of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] and dexamethasone to regulate collagen and osteocalcin synthesis and induction of 25-hydroxyvitamin D3-24-hydroxylase (24-hydroxylase) activity were studied in rat osteoblast-like cell primary cultures. In this culture system, the basal levels of collagen and osteocalcin synthesis increased with rising cell density in culture. At maximal doses, both 1,25-(OH)2D3 (8.1 nM) and dexamethasone (130 nM) reduced collagen synthesis to about 50% of the control levels, 1,25-(OH)2D3 affected osteocalcin synthesis in a biphasic manner: stimulatory at low doses, which peaked near 0.33 nM to reach 3- to 5-fold the basal level, followed by a gradual return to the basal level at higher concentrations. Dexamethasone had only a slight stimulatory effect on osteocalcin. 1,25-(OH)2D3 also induced 24-hydroxylase activity in rat osteoblast-like cells, while dexamethasone had no effect on the enzyme. Induction of enzyme activity achieved a 4- to 6-fold rise, but required higher concentrations of 1,25-(OH)2D3 to achieve maximal levels (16 nM). The half-maximal doses (ED50) of 1,25-(OH)2D3 required for each bioresponse were different. The approximate ED50 for the inhibition of collagen synthesis was near the Kin (0.4 nM; apparent dissociation constant of receptor nuclear internalization), while the ED50 for osteocalcin synthesis (0.08 nM) was below the Kin, and the ED50 for 24-hydroxylase induction (20 nM) was greater than the Kin. The ED50 for dexamethasone on collagen synthesis (20 nM) was about 5-fold higher than the Kin (4 nM) of dexamethasone receptor binding. The potencies of various vitamin D3 metabolites in all three functional responses followed their abilities to compete for the 1,25-(OH)2D3 receptor, indicating that these actions were 1,25-(OH)2D3 receptor mediated. In summary, these studies explored bone cell bioresponses to 1,25-(OH)2D3 and dexamethasone and examined the relationship between receptor occupancy and functional expression. Each action exhibited a different dose-response pattern, implying that different levels of control are required for each individual response.

Animals↗
PubMed1986

Dexamethasone increases 1,25-dihydroxyvitamin D3 receptor levels and augments bioresponses in rat osteoblast-like cells.

Glucocorticoids increase the level of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] receptors in primary cultures of rat calvarial osteoblast-like (OB) cells. The present study investigated how this dexamethasone (DEX) up-regulation of 1,25-(OH)2D3 receptors modulates three 1,25-(OH)2D3 bioresponses: inhibition of collagen synthesis, stimulation of osteocalcin synthesis, and induction of 25-hydroxyvitamin D3-24-hydroxylase activity. Pretreatment of OB cells with 13 nM DEX for 24 h doubled the 1,25-(OH)2D3 receptor level without changing receptor affinity for 1,25-(OH)2D3 to study bioresponses. After DEX treatment to increase the 1,25-(OH)2D3 receptor level, the magnitude and sensitivity of all three 1,25-(OH)2D3 bioresponses were enhanced. The maximal 1,25-(OH)2D3 inhibition of collagen synthesis was increased by DEX pretreatment compound to control values: 30 to 50% (1 day treatment) and 50 to 70% (2 day treatment). The sensitivity to 1,25-(OH)2D3, as measured by reduction of the half-maximal inhibitory dose (ED50), was increased 50%. This potentiation of 1,25-(OH)2D3 inhibitory action on collagen synthesis was still evident after correction for the inhibitory effect on collagen synthesis by DEX alone. The maximal stimulation of osteocalcin by 1,25-(OH)2D3 was also enhanced from 2- to 3-fold in controls to over 4- to 5-fold by DEX pretreatment. Similarly, the ED50 of the response was reduced 50%. For the induction of 25-hydroxyvitamin D3-24-hydroxylase activity, DEX doubled the enzyme activity over that seen with 1,25-(OH)2D3 alone, but only slightly affected the sensitivity of the enzyme induction. In conclusion, after DEX up-regulation of 1,25-(OH)2D3 receptor levels, there was a general potentiation of 1,25-(OH)2D3 bioresponses in rat OB cells. However, the detailed patterns of the augmented responses were different for each of the three biological functions we studied.

Animals↗
PubMed1986

Unexpected presence of estrogens in culture medium supplements: subsequent metabolism by the yeast Sacchromyces cerevisiae.

We have previously shown the presence of 17 beta-estradiol in extracts of commercially prepared Saccharomyces cerevisiae ss well as the production of estradiol by yeast grown in the laboratory. In our current study, yeast grown in a chemically defined medium synthesized estradiol in only small amounts, (less than 500 pg/liter). We have analyzed a variety of media commonly used for growing yeast and found that substantial estradiol production (greater than 5 ng/liter) was obtained when yeast were grown in medium supplemented with Bacto-peptone. The peptone was shown to contain significant amounts of estrone, and the results of the experiments establish a precursor-product relationship where estrone from the medium is metabolized to estradiol by S. cerevisiae. Studies with added [3H]estrone demonstrated rapid conversion into [3H]estradiol and a 3H-labeled nonpolar estrogen derivative. The commercially obtained yeast used previously had been grown in a molasses medium. We demonstrate here that the molasses medium contains substantial amounts of estrone and estradiol. We conclude that the conversion of estrone in a culture medium to estradiol in laboratory grown yeast and estrone and estradiol present in the commercially grown yeast medium account for the majority of estradiol found in yeast.

Chromatography, High Pressure Liquid↗
PubMed1986

1,25-dihydroxyvitamin D3 receptors and hormonal responses in cloned human skeletal muscle cells.

Although skeletal muscle is a major calcium-regulated organ, there remains uncertainty about whether muscle is a target organ for the action of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3]. In this study we examine pure populations of clonally derived human muscle cells for the presence of 1,25-(OH)2D3 receptors and direct responses to the hormone. All of the clones tested exhibited specific [3H]1,25-(OH)2D3 binding, with values ranging from 5-70 fmol/mg protein. Scatchard analysis of binding data revealed a dissociation constant (approximately 100 pM) comparable to that of classical receptors in other target organs. The 1,25-(OH)2D3 receptors sedimented at 3.3S on hypertonic sucrose gradients. Specificity for [3H]1,25-(OH)2D3 was demonstrated on gradients by substantially better competition by 1,25-(OH)2D3 than 25-hydroxyvitamin D3 for the 3.3S receptor binding peak. The 1,25-(OH)2D3 receptor complex bound to DNA-cellulose and eluted as a single peak at 0.2 M KCl. Myoblasts and myotubes did not show significant differences in either the amount or characteristics of the 1,25-(OH)2D3 receptor. In addition to the presence of receptors, cells were tested for functional responsiveness to 1,25-(OH)2D3. Both cell types exhibited a dose-dependent induction of 25-hydroxyvitamin D3-24-hydroxylase enzyme activity after treatment of monolayers with 1,25-(OH)2D3. Incorporation of both leucine and thymidine into growing myoblasts and fused myotubes was inhibited in a dose-dependent fashion after treatment with 1,25-(OH)2D3. In summary, cloned human skeletal muscle cells contain a binding protein compatible with classical 1,25-(OH)2D3 receptors as well as functional responsiveness to 1,25-(OH)2D3 at physiological concentrations of hormone.

Calcitriol↗
PubMed1986

Different types of calcium channels.

Ca2+ channels allow passage of Ca2+ ions into the cytoplasm through a selective pore which is opened in response to depolarization of the cell membrane (for reviews see Hagiwara & Byerly, 1981, 1983; Tsien, 1983; Reuter, 1983). The Ca2+ flux creates a net inward, depolarizing current and the resulting accumulation of Ca2+ in the cytoplasm can act as a chemical trigger for secretion of hormones and neurotransmitters, contraction of muscle and a variety of other Ca2+-sensitive events. Thus, upon sensing membrane potential changes, Ca2+ channels simultaneously generate an electrical signal while directly creating an intracellular chemical messenger. This dual ability is unique among the family of ion channels and allows the Ca2+ channel to play a variety of roles in excitation-secretion and excitation-contraction coupling. It has now become clear that versatility of function is reflected by diversity of the types of Ca2+ channels on the membrane of individual cells. This article describes the nature of data which have demonstrated multiple channel types, reviews the literature suggesting that many cells have several kinds of Ca2+ channels, and discusses newer data regarding a neurotoxin that distinguishes among different Ca2+ channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

C-type virus particles in spontaneous and virus-induced leukemia and malignant lymphomas in mice and rats.

The presence and numbers of C-type virus particles in an animal model consisting of mice and rats with either spontaneous or virus-induced leukemia and lymphomas were studied, in order to determine the relation of the appearance of virus particles to viral etiology of such neoplasms. The numbers and distribution of C-type virus particles in organs from 13 mice with spontaneous leukemia and lymphomas were compared with the presence of virus particles in organs of 13 mice with leukemia and lymphomas induced by passage A (Gross) virus inoculation. C-type virus particles were present in organs of all mice with either spontaneous leukemia or leukemia and lymphomas induced by virus inoculation. However, the number of particles observed was significantly higher in those mice in which leukemia was induced by virus inoculation. Virus particles were also observed, but in substantially smaller numbers, in organs of 13 of 25 untreated, healthy mice of the nonleukemic C3H(f) inbred line. In contrast to mice, C-type, or any other virus particles, were not found in organs of 10 Sprague-Dawley, Long-Evans or Sprague-Dawley X Long-Evans F1 hybrid rats with spontaneous leukemia. However, C-type virus particles were consistently present in organs of 11 Sprague-Dawley rats with leukemia induced by rat-adapted passage A (Gross) mouse leukemia inoculation. The virus particles appeared in the organs of the inoculated rats 5 days after i.p., and 11 days after s.c. inoculation. Virus particles were not found in organs of 10 healthy untreated Sprague-Dawley rats. The implications of these observations are discussed.

Animals↗
PubMed1985

Retinoic acid modulation of 1,25(OH)2 vitamin D3 receptors and bioresponse in bone cells: species differences between rat and mouse.

Retinoic acid (RA) caused a reduction in the level of 1,25(OH)2D3 receptors to 1/3 of control in rat osteoblast-like cells (ROB) while increasing the receptor level to 3-fold the control in mouse osteoblast-like cells (MOB). Scatchard analysis of receptor binding indicated that there was no change in affinity for 1,25(OH)2D3. The changes in receptor levels required time to develop and were dose-dependent. RA also modulated the ability of cells to respond to 1,25(OH)2D3 as measured by the induction of the enzyme 25(OH)D3-24 hydroxylase. Induction of enzyme activity by 1,25(OH)2D3 closely paralleled receptor level established by RA pretreatment. In MOB, the up-regulation of the receptor occurred despite the action of RA to inhibit DNA, RNA and protein synthesis. However, RA stimulation of 1,25(OH)2D3 receptor levels was blocked by the addition of cycloheximide or actinomycin D, indicating that the up-regulation required protein and RNA synthesis. The opposite effect of RA on mouse and rat cells suggests that important species-dependent factors modulate the action of retinoids on mammalian cells.

Animals↗
PubMed1985

Inhibition of steroidogenic cytochrome P-450 enzymes in rat testis by ketoconazole and related imidazole anti-fungal drugs.

Ketoconazole, an imidazole antifungal drug, has previously been shown to diminish testosterone and cortisol production in patients as well as rat and mouse cells in vitro. Inhibition of adrenal mitochondrial cytochrome P-450 enzymes was demonstrated. In this study we tested several imidazole antifungal drugs and examined the individual steps in testicular steroidogenesis to determine which enzymes in the androgen pathway were blocked. In addition, we studied 25-hydroxyvitamin D 24-hydroxylase activity in cultured pig kidney cells (LLC-PK1) to assess a mitochondrial P-450 enzyme in another organ. All imidazoles tested inhibited both total testosterone production and 24-hydroxylase activity but the relative potencies differed. We next studied the individual testicular enzymatic steps between cholesterol and testosterone. Ketoconazole inhibited cholesterol-side-chain-cleavage enzyme (mitochondrial) and C-17,20 lyase (microsomal). The three inhibited enzymes (two testicular and one renal) are all P-450 cytochromes. Testicular 17-hydroxylase, also a P-450 cytochrome, was not inhibited even at high doses of ketoconazole. This is an interesting finding because the testicular hydroxylase and lyase have been shown to be a single protein. Non-cytochrome P-450 enzymes in the androgen pathway were not inhibited. The results demonstrate that several imidazole antifungal drugs all inhibit both microsomal and mitochondrial cytochrome P-450 enzymes in multiple organs.

Aldehyde-Lyases↗
PubMed1985

Regulation of 1,25-dihydroxyvitamin D3 receptors by vitamin D analogs in cultured mammalian cells.

The pig kidney cell line (LLC-PK1) has been shown to possess 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] receptors and to exhibit functional responses to vitamin D metabolites. Here we report that these receptors appear to undergo homologous up-regulation by 1,25-(OH)2D3 and other vitamin D analogs. This phenomenon was also observed in other cell lines, including human skin fibroblasts and human mammary cancer cells (MCF-7). Treatment with active hormone or vitamin D analogs results in a substantial increase (200-400%) in the number of 1,25-(OH)2D3 receptors without altering the affinity of receptor for hormone. The up-regulated receptor, like the basal receptor, has an apparent Kd of about 0.04 nM and sediments at 3.3S on hypertonic sucrose gradients. In addition, approximately 50% of the total receptors from both control and treated cells bind to DNA-cellulose and elute at 0.18 m KCl. These results indicate that the up-regulated receptor is similar to the classical 1,25-(OH)2D3 receptor. While the time necessary to achieve the maximal receptor increment is 16-20 h, there is a rapid component in the rise observed within 5 min. The maximal effect persists for 4-6 h after hormone removal. The increased binding is not a result of differential receptor localization or extractability. 1,25-(OH)2D3, 1,24,25-trihydroxyvitamin D3, 24,25-(OH)2D3, and 25-hydroxyvitamin D3 all increase receptor binding to similar levels, and the dose required closely reflects the affinities of the various metabolites for the receptor. Treatment of cells with the RNA synthesis inhibitor actinomycin D indicates that the increase in receptors is partially dependent on RNA synthesis. Mutant skin fibroblasts from patients with vitamin D-dependent rickets type II, containing nonresponsive 1,25-(OH)2D3 receptors, failed to exhibit the characteristic up-regulation observed in normal cells. Taken together, these results indicate that vitamin D metabolites regulate the number of 1,25-(OH)2D3 receptors in part by receptor occupancy and, more importantly, by a receptor-mediated induction mechanism.

Animals↗
PubMed1985

Vitamin D resistance and alopecia: a kindred with normal 1,25-dihydroxyvitamin D binding, but decreased receptor affinity for deoxyribonucleic acid.

A new kindred exhibiting vitamin D resistance and alopecia is described. Clinically, three of seven sisters demonstrated rickets, hypocalcemia, elevated serum 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] levels, and alopecia. Biochemical analysis of cultured fibroblasts from skin biopsy explants in two affected and one normal sister revealed normal [3H]1,25-(OH)2D3 binding to receptors (Kd = 0.05 nM; Nmax = 30-50 fmol/mg protein). Despite normal steroid binding, cells from the two affected sisters failed to respond to 1,25-(OH)2D3 in vitro, as measured by induction of the enzyme 25-hydroxyvitamin D-24-hydroxylase. The cells from the normal sister showed a response within the range of five normal cell lines. Sucrose gradient analysis yielded a typical 3.2S protein under high salt conditions in extracts from the three siblings, but with reduced capacity to aggregate to a 6S moiety in low salt gradients in the two affected cells. Whole cell [3H]1,25-(OH)2D3 binding studies revealed nearly normal localization of bound receptor to the nuclear compartment. Elution of bound receptors by KCl gradients from both DNA-cellulose or fibroblast nuclei demonstrated that the receptors from the affected sisters exhibited decreased affinity for DNA compared to those from normal subjects. We conclude that 1,25-(OH)2D3 receptors from these resistant fibroblasts have a normal steroid-binding domain, but a defective nuclear binding domain. We believe that this abnormality may be responsible for the vitamin D resistance observed both in vivo and in vitro.

Adolescent↗
PubMed1985

Conceptual systems and teacher attitudes toward regular classroom placement of mildly mentally retarded students.

The effects of a teacher personality construct (abstract vs. concrete conceptual system) and two pupil variables (race, school behavior) on 454 regular classroom teachers' attitudes toward mainstreaming were determined. Following administration of the Conceptual Systems Test, teachers were randomly assigned a profile of a mildly mentally retarded student that held pupil IQ and school achievement constant while varying pupil's race and school behavior. Subjects responded on an integration inventory comprised of three subscales: social-psychological classroom environment, self-actualization, and classroom cohesiveness. Results revealed a significant main effect on the behavior variable and a significant Personality X Race interaction on all inventory dimensions, suggesting that these teachers perceived maladaptive behavior of mainstreamed retarded students as a significant threat to a conducive instructional atmosphere and the capability of nonretarded students to achieve to their potential. These results have implications for inservice training for teachers based on the pupil race and teacher conceptual system findings.

Black or African American↗