Line D1 Research Articles

EPR observation of first point defects in cubic boron nitride crystalline powders

An X-band electron paramagnetic resonance (EPR) study of nominally pure, diamond-like cubic boron nitride (c-BN) crystalline powders, has led to the first identification of a spectrum attributed to two related paramagnetic species. The composite EPR spectrum can be observed only in dark brown colored powders known to contain excess of boron. It consists of two superimposed lorentzian components, called D1 and D2, centered at g1=2.0063 and g2=2.0084, with peak-to-peak linewidths of 3.3 and 17.9 mT, respectively. The temperature dependence of the integrated intensities, their linewidths and intensity ratio D2/D1 allows one to conclude that the narrow line D1 originates from EPR transitions inside a S=1/2 ground doublet and the broad line D2 from transitions inside the excited levels of another center. Evidence suggests that both centers are boron related paramagnetic species.

Cross-presentation of glycoprotein 96-associated antigens on major histocompatibility complex class I molecules requires receptor-mediated endocytosis.

Heat shock proteins (HSPs) like glycoprotein (gp)96 (glucose-regulated protein 94 [grp94]) are able to induce specific cytotoxic T lymphocyte (CTL) responses against cells from which they originate. Here, we demonstrate that for CTL activation by gp96-chaperoned peptides, specific receptor-mediated uptake of gp96 by antigen-presenting cells (APCs) is required. Moreover, we show that in both humans and mice, only professional APCs like dendritic cells (DCs), macrophages, and B cells, but not T cells, are able to bind gp96. The binding is saturable and can be inhibited using unlabeled gp96 molecules. Receptor binding by APCs leads to a rapid internalization of gp96, which colocalizes with endocytosed major histocompatibility complex (MHC) class I and class II molecules in endosomal compartments. Incubation of gp96 molecules isolated from cells expressing an adenovirus type 5 E1B epitope with the DC line D1 results in the activation of E1B-specific CTLs. This CTL activation can be specifically inhibited by the addition of irrelevant gp96 molecules not associated with E1B peptides. Our results demonstrate that only receptor-mediated endocytosis of gp96 molecules leads to MHC class I-restricted re-presentation of gp96-associated peptides and CTL activation; non-receptor-mediated, nonspecific endocytosis is not able to do so. Thus, we provide evidence on the mechanisms by which gp96 is participating in the cross-presentation of antigens from cellular origin.

Multiresolution wavelet analysis of SUMER/SOHO observations in a solar prominence

We have studied through a multiresolution wavelet analysis the oscillations in a limb prominence. Intensity fluctuations in time and height corresponding to different lines of Si iv and O iv observed with SUMER on board SOHO have been analyzed in the wavelet bands of J3= 1 min 36 s to 3 min 12 s and J4=3 min 12 s to 6 min 24 s. For all species, oscillations in the J4 band were dominant. We found relevant differences between the behavior of line D1 (1393.76 A) corresponding to Si iv and the set D2 (1401.16 A), D3 (1404.81 A), D4 (1402.77 A) corresponding to O iv, O iv and Si iv respectively. We also report the identification of a pulse in the intensity of the line D1 that appears in the range of 15–20 min. This disturbance seems to travel with a speed of about 170 km s−1.

On the Influence of Dislocation on the Luminescence of Si:Er

We have studied by electrical and optical methods the properties of the defects to possibly identify which ones affect the luminescence of the material. We have characterized Er-doped Si samples grown by the Liquid Phase Epitaxy (LPE) method, a relatively simple and inexpensive technique, by means of photoluminescence (PL), cathodoluminescence, EXAFS and deep level transient spectroscopy. The optical methods reveal the presence of two emission bands which coincide with the lines labelled D1 and D2, attributed to dislocations. Since line D1 fortuitously coincides within a few meV with the energy of the transition 4I15/2 → 4I13/2 of Er3+, it could at least partially cover the Er-related emission. Furthermore, as Er and O could both interact with dislocations, the dislocation optical activity might be influenced by their presence and play a significant role in the material overall luminescence.

Radiation-induced tumorigenesis in preneoplastic mouse mammary glands in vivo: significance of p53 status and apoptosis.

In mouse mammary tumorigenesis, p53 mutations facilitate tumorigenesis in concert with other oncogenic alterations. Ionizing radiation enhances tumorigenesis in preneoplastic mammary outgrowth lines and induces p53-dependent apoptosis. We asked if normal p53 function modulates radiation-induced tumorigenesis in preneoplastic mammary lesions by affecting the apoptotic pathway of cell deletion. Three different hyperplastic outgrowth lines were compared. Outgrowth line D1 overexpressed wild-type p53 and responded to irradiation with enhanced tumorigenicity but no induction of apoptosis. Outgrowth line TM12 exhibited normal wild-type p53 expression and responded to irradiation with no alteration in tumorigenicity but with a marked increase in apoptosis. Outgrowth line TM2L also exhibited normal wild-type p53 expression and responded to irradiation with a marked enhancement in both tumorigenicity and apoptosis. These results indicate that the two radiation-induced responses, apoptosis and tumorigenesis, are dissociable events in the mammary gland. Furthermore, radiation-induced tumorigenicity was not abrogated by either enhanced wild-type p53 expression or a robust apoptotic response. The radiation dose of 5 Gy most likely induces multiple genetic alterations in surviving cells, including genomic instability, and this may account for the tumorigenicity. Future experiments will examine lower doses of irradiation that still induce a significant apoptotic response but significantly less genomic instability.

Pituitary corticotrope tumor (AtT20) cells as a model system for the study of early inhibition by glucocorticoids.

The utility of the established ACTH secreting mouse pituitary tumor cell line AtT20 for investigating early glucocorticoid inhibition was examined. Three different strains of the cell line D1, D16v, and D16:16, respectively, were analyzed. In initial studies CRF and phorbol esters were used as secretagogues to examine the properties of hormone secretion. In a perifusion system (cells in suspension) D1 cells failed to respond to the secretagogues, whereas both D16v and D16:16 cells were responsive. However, hormone release declined upon repeated exposure to secretagogue in both D16v and D16:16 cells and similar data were obtained when cells adhering to cover slips were perifused. In static incubation D16:16 cells gave more consistent results especially with respect to inhibition by glucocorticoids and were used in all subsequent studies. Synthetic glucocorticoids acting through the type II receptor inhibited CRF-induced ACTH release within 45 min; at 120 min, stimulated release was strongly (80-90%) suppressed. In contrast, no consistent inhibition by corticosterone could be found. In the presence of glycyrrhetinic acid, an inhibitor of 11 beta-hydroxysteroid dehydrogenase, a high concentration of corticosterone (10 microM) did produce a slight inhibition of ACTH release. Dexamethasone also inhibited ACTH release induced by the calcium channel activator compound (+)202-791. The accumulation of cAMP in response to CRF was not altered by dexamethasone. The inhibitory effect of synthetic glucocorticoids on ACTH release was prevented by blockers of messenger RNA (actinomycin D, dichlorobenzimidazole ribofuranoside) or protein (puromycin) biosynthesis, indicating the induction of new proteins. Immunoblotting for lipocortin I (annexin I) and chromogranin A revealed no induction by dexamethasone of any of these proteins in D16:16 cells. Messenger RNA encoding lipocortin I was not detectable and was not induced by treatment with dexamethasone in D16:16 cells. These data show that the AtT20 D16:16 strain is a useful model for early glucocorticoid action, which is mediated by type II receptors and involves the induction of new protein(s). Notably, induction of lipocortin I messenger RNA or protein could not be detected at a time when the inhibitory effect of glucocorticoids on stimulated hormone secretion was maximal.

Pituitary corticotrope tumor (AtT20) cells as a model system for the study of early inhibition by glucocorticoids

The utility of the established ACTH secreting mouse pituitary tumor cell line AtT20 for investigating early glucocorticoid inhibition was examined. Three different strains of the cell line D1, D16v, and D16:16, respectively, were analyzed. In initial studies CRF and phorbol esters were used as secretagogues to examine the properties of hormone secretion. In a perifusion system (cells in suspension) D1 cells failed to respond to the secretagogues, whereas both D16v and D16:16 cells were responsive. However, hormone release declined upon repeated exposure to secretagogue in both D16v and D16:16 cells and similar data were obtained when cells adhering to cover slips were perifused. In static incubation D16:16 cells gave more consistent results especially with respect to inhibition by glucocorticoids and were used in all subsequent studies. Synthetic glucocorticoids acting through the type II receptor inhibited CRF-induced ACTH release within 45 min; at 120 min, stimulated release was strongly (80-90%) suppressed. In contrast, no consistent inhibition by corticosterone could be found. In the presence of glycyrrhetinic acid, an inhibitor of 11 beta-hydroxysteroid dehydrogenase, a high concentration of corticosterone (10 microM) did produce a slight inhibition of ACTH release. Dexamethasone also inhibited ACTH release induced by the calcium channel activator compound (+)202-791. The accumulation of cAMP in response to CRF was not altered by dexamethasone. The inhibitory effect of synthetic glucocorticoids on ACTH release was prevented by blockers of messenger RNA (actinomycin D, dichlorobenzimidazole ribofuranoside) or protein (puromycin) biosynthesis, indicating the induction of new proteins. Immunoblotting for lipocortin I (annexin I) and chromogranin A revealed no induction by dexamethasone of any of these proteins in D16:16 cells. Messenger RNA encoding lipocortin I was not detectable and was not induced by treatment with dexamethasone in D16:16 cells. These data show that the AtT20 D16:16 strain is a useful model for early glucocorticoid action, which is mediated by type II receptors and involves the induction of new protein(s). Notably, induction of lipocortin I messenger RNA or protein could not be detected at a time when the inhibitory effect of glucocorticoids on stimulated hormone secretion was maximal.

Effect of Dietary Fat on Tumorigenesis in the Mouse Mammary Gland<xref ref-type="fn" rid="FN2">2</xref><xref ref-type="fn" rid="FN3">3</xref>

The effects of dietary polyunsaturated fat in BALB/c mice were determined for several stages of mammary tumorigenesis: a) growth of intact and transplanted normal mammary tissue, b) growth of hyperplastic alveolar nodule (HAN) lines D1/ UCD and Z5C1 , c) incidence of tumors occurring in D1/ UCD , and d) growth rate of the tumors. Growth of transplanted normal mammary epithelium as well as intact glands was faster in mice fed a 10% corn oil (CO) diet, which contains linoleate, than in those fed 10% hydrogenated cottonseed oil ( HCTO ), a diet free of the polyunsaturated fatty acid. We concluded that transplantation itself does not alter the response of mammary tissue to dietary fat. The growth of both HAN lines was unchanged by the presence of CO in the diet. For ascertainment as to whether the difference in response was specific to the tissue, ducts and HAN line D1/ UCD were transplanted into left and right gland-free fat pads of the same mice. The duct tissue grew faster when the hosts were fed the 10% CO diet than in the hosts fed the 10% HCTO diet; however, no effect of dietary fat was noted with the HAN. Although indomethacin retarded the growth of normal tissue in the mice fed CO diet, this prostaglandin inhibitor had no effect on the growth of the HAN transplants. Both incidence and growth rate of tumors arising from transplants of HAN line D1/ UCD were greater in mice fed diets containing either 0.3, 1, or 10% CO than in those fed 10% HCTO . The smaller number of tumors arising in mice fed with 10% HCTO diet may be the result of the slower growth rate of the neoplasms in mice fed diets devoid of linoleate.

Survival of Mouse Mammary Gland Transplants of Normal, Hyperplastic, and Tumor Tissues Exposed to X-Rays<xref ref-type="fn" rid="fn2">2</xref><xref ref-type="fn" rid="fn3">3</xref>

Mouse mammary tissues, including ducts, prelactating lobules, hyperplastic outgrowth lines, and tumors, were exposed to varying doses of X-rays and then transplanted to fat pads of nonirradiated BALB/c mice for study. Estimates of the dose of radiation that would allow survival of 50% of the transplants (SD50) were made with the use of probit analysis. Nearly all duct and lobule transplants survived doses of X-rays from 0 to 800 rad. The survival rate declined rapidly following doses above 800 rad, and the calculated SD50 was 1,020 and 1,260 rad for mammary ducts and lobules, respectively. The three hyperplastic outgrowth lines tested gave very different results. Hyperplastic line Z5C1 transplants had better than 90% survival at doses up to 1,200 rad and an SD50 between 1,200 and 1,600 rad. Hyperplastic line Z5D transplants had an SD50 of between 800 and 1,200 rad. Hyperplastic line D1 transplants had a better than 90% survival following doses of 0-600 rad and an SD50 between 600 and 800 rad. The survival of tumor transplants was 100% following doses of X-rays up to 1,200 rad; the SD50 was in excess of 1,600 rad. The mouse mammary transplantation system can be used to study the direct effect of X-rays on normal, premalignant, and malignant mammary tissues and provides a basis for the study of the radiobiology of mammary tissues.

A Hanawalt Type Phase Identification Procedure for a Minicomputer

The use of computers to aid in the identification of phases from their powder diffraction patterns was pioneered in the mid 1960's by Frevel, Nichols and Johnson (1-3). Today's most widely used Johnson algorithm conducts a reverse sequential search by comparing each reference pattern in the JCPDS powder diffraction file (PDF) to the unknown pattern. A figure of merit is computed for each match and the patterns with the best figures of merit are listed at the end of the search. The Nichols approach is a reverse search of a singly inverted reference file. An inverted file is one which stores the reference patterns according to the d value of the lowest angle 100% intensity line (d1) . This type of file is analogous to the Hanawalt search books distributed by the JCPDS for manual searching. When an inverted file is stored in a random format, along with suitable disk directory files, only reference patterns containing d1 values of interest need be read in the search.

The development of a medium supplemented with egg extract for the maintenance ofDrosophila cell lines

A saline extract was prepared from Drosophila eggs. When diluted to a concentration of 1% with Drosophila tissue culture medium, it did not support growth of cells from the Drosophila line D1 during the first few days of subculture as well as medium containing serum. When cells reached a stationary phase, however, the cell density in medium containing extract was greater than in medium containing serum. By altering the concentrations of the extract, and by adding bovine albumin, a medium was obtained in which D1 cells survived initial culturing, and which supported cell growth by day 4 as well as medium plus serum. The initial retardation of growth in medium containing egg extract might be due to the need of the cells to adapt to the new medium. At the present time four Drosophila cell lines have been maintained in this medium for more than 16 passages. Preliminary experiments with primary embryonic Drosophila cells indicate that medium containing 2% extract and bovine albumin retards the differentiation of these cells.

Combined Effects of 3-Methylcholanthrene, Mammary Tumor Virus, Nodule-Inducing Virus, and Prolonged Hormonal Stimulation on the Tumor-Producing Capabilities of the Nodule Outgrowth Line D12

The scheme for mouse mammary tumorigenesis has been extended to include 3-mefhylcholanthrene (MCA) as an effective tumorigenic agent. Methylcholanthrene is a very poor noduligenic agent in intact virgin BALB/c mice, and the hyperplastic alveolar nodules induced have low tumor-producing capabilities. However, D1 mammary-nodule outgrowths responded to MCA with a relatively high rate of tumor production (50%). Prolonged hormone stimulation by pituitary isografts increased the tumor incidence in MCA-treated D1 nodule outgrowths in a similar fashion, as was shown previously for mammary tumor virus (MTV)-positive and nodule-inducing virus (NIV)-positive D1 nodule outgrowths exposed to prolonged hormone stimulation. When MCA was given to MTV-positive mice bearing D1 nodule outgrowths, the effect appeared to be additive, rather than synergistic. There was no evidence that MCA acted hormonally in the neoplastic transformation. Rather, the results suggested that MCA acted on the D1 nodule cell population to increase the production of tumors from this population, whereas hormone stimulation acted synergistically with MTV and NIV to increase tumor formation from D1 nodule outgrowths.

New Measures of the Sodium Line D1 in the Solar Spectrum

New Measures of the Sodium Line D1 in the Solar Spectrum