Right-hand Panel Research Articles

Volume 39, Issue 9, Pages 2068–2085

Volume 39, issue 9, pages 2068–2085 Due to the vigilance of one of our readers, an error was found in a paper recently published in this journal by Robert Cervero: “Transit-oriented development's ridership bonus” ( Environment and Planning A 2007 39 2068 – 2085). Only one inclusive term and its associated θ coefficient was presented and reported for the upper-nest model in table 3 . Two inclusive terms should have been presented, for ‘living near’ and ‘living away’ transit, respectively, as notated in equation (3) on page 2077 of the paper. It is noted that a circulated working paper by the same author (R Cervero and M Duncan, “Residential self selection and rail commuting: a nested logit analysis”, 2002, working paper, University of California Transportation Center, Berkeley) presented two inclusive terms (and their associated coefficients). However, further investigation revealed these were miscalculated and were in error. This working paper has also been corrected to be consistent with the corrected table 3 below. The corrected upper-nest model has a slightly different specification than originally shown in table 3 of the paper in order to satisfy the condition that the θ values lie between 0 and 1. None of the text about the upper-nest model that appears in the first paragraph of page 2078 and on page 2080 of the paper changes nor do any of the substantive findings or conclusions of the research. The additional variables added to the upper-nest model reveal that low automobile ownership levels tended to be associated with transit-oriented living. Cervero acknowledges that automobile ownership likely both influences and is influenced by transit-oriented living; thus the coefficient on the automobile ownership variables could be subject to endogeneity bias. The revised equation also shows that, controlling for other variables in the equation, having individuals 55 years of age and above in a household reduced the likelihood of living near transit. Lastly, discussions in the last paragraph of section 6.3 regarding the θ values should now be in the plural, indicating that both θnear and θaway are within the 0–1 interval. It is also noted that the estimated coefficients in the lower-nest binomial logit models for predicting rail commuting (shown in the right-hand panel of table 3 ) are unchanged from the original table 3 . The t-statistics presented in the original lower-nest models, however, were actually Wald statistics ( t-statistics squared); in the corrected model, the square roots of the Wald statistics (ie, t-statistics) are presented. None of the significance levels changes. Because a sequential approach was used to estimate the nested logit model, the coefficient estimates of the upper-level model are consistent but not asymptotically efficient, thereby underestimating standard errors and assigning more significance than is likely the case. It is also noted that coefficients in the lower-level models were not transformed using the estimated θs from the upper-level model. Because these coefficients are unchanged, none of the discussions in sections 6.4 and 6.5 (pages 2080 – 2083) of the paper is affected by the corrections made to table 3 . The editors of Environment and Planning A are immensely grateful to the reader who pointed out this important error, and urge our readers to help maintain the quality of the journal by calling our attention to any other significant errors. Robert Cervero also acknowledges the helpful comments and suggestions of two anonymous referees and Kenneth Train in making corrections to the original model. We reproduce below the corrected table (to replace table 3 on page 2079). [Table: see text]

Repetitive Firing Triggers Clustering of Kv2.1 Potassium Channels in Aplysia Neurons

The Kv2.1 gene encodes a highly conserved delayed rectifier potassium channel that is widely expressed in neurons of the central nervous system. In the bag cell neurons of Aplysia, Kv2.1 channels contribute to the repolarization of action potentials during a prolonged afterdischarge that triggers a series of reproductive behaviors. Partial inactivation of Aplysia Kv2.1 during repetitive firing produces frequency-dependent broadening of action potentials during the afterdischarge. We have now found that, as in mammalian neurons, Kv2.1 channels in bag cell neurons are localized to ring-like clusters in the plasma membrane of the soma and proximal dendrites. Either elevation of cyclic AMP levels or direct electrical stimulation of afterdischarge rapidly enhanced formation of these clusters on the somata of these neurons. In contrast, injection of a 13-amino acid peptide corresponding to a region in the C terminus that is required for clustering of Kv2.1 channels produced disassociation of the clusters, resulting in a more uniform distribution over the somata. Voltage clamp recordings demonstrated that peptide-induced dissociation of the Kv2.1 clusters is associated with an increase in the amplitude of delayed rectifier current and a shift of activation toward more negative potentials. In current clamp recording, injection of the unclustering peptide reduced the width of action potentials and reduced frequency-dependent broadening of action potentials. Our results suggest that rapid redistribution of Kv2.1 channels occurs during physiological changes in neuronal excitability.

P166, a link between the trypanosome mitochondrial DNA and flagellum, mediates genome segregation

Kinetoplast DNA (kDNA), the trypanosome mitochondrial genome, is a giant network containing several thousand interlocked DNA rings. Within the mitochondrion, kDNA is condensed into a disk-shaped structure positioned near the flagellar basal body. The disk is linked to the basal body by a remarkable transmembrane filament system named the tripartite attachment complex (TAC). Following kDNA replication, the TAC mediates network segregation, pulling the progeny networks into the daughter cells by their linkage to the basal bodies. So far TAC has been characterized only morphologically with no known protein components. By screening an RNAi library, we discovered p166, a protein localizing between the kDNA and basal body in intact cells and in isolated flagellum-kDNA complexes. RNAi of p166 has only small effects on kDNA replication, but it causes profound defects in network segregation. For example, kDNA replication without segregation causes the networks to grow to enormous size. Thus, p166 is the first reported molecular component of the TAC, and its discovery will facilitate study of kDNA segregation machinery at the molecular level.

Cex1p is a novel cytoplasmic component of the Saccharomyces cerevisiae nuclear tRNA export machinery

The Saccharomyces cerevisiae Yor112wp, which we named Cex1p, was identified using a yeast tRNA three-hybrid interaction approach and an in vivo nuclear tRNA export assay as a cytoplasmic component of the nuclear tRNA export machinery. Cex1p binds tRNA saturably, and associates with the nuclear pore complex by interacting directly with Nup116p. Cex1p co-purifies with the nuclear tRNA export receptors Los1p and Msn5p, the eukaryotic elongation factor eEF-1A, which delivers aminoacylated tRNAs to the ribosome, and the RanGTPase Gsp1p, but not with Cca1p, a tRNA maturation enzyme that facilitates translocation of non-aminoacylated tRNAs across the nuclear pore complex. Depletion of Cex1p and eEF-1A or Los1p significantly reduced the efficiency of nuclear tRNA export. Cex1p interacts with Los1p but not with eEF-1A in vitro. These findings suggest that Cex1p is a component of the nuclear aminoacylation-dependent tRNA export pathway in S. cerevisiae. They also suggest that Cex1p collects aminoacyl-tRNAs from the nuclear export receptors at the cytoplasmic side of the nuclear pore complex, and transfers them to eEF-1A using a channelling mechanism.

Visualizing Inside the Cell

Visualizing Inside the Cell

Recognition and Blocking of HIV-1 gp41 Pre-transmembrane Sequence by Monoclonal 4E10 Antibody in a Raft-like Membrane Environment

The conserved (664)DKWASLWNWFNITNWLWYIK(683) (preTM) sequence preceding the transmembrane anchor of human immunodeficiency virus (HIV-1) gp41 glycoprotein subunit is accessible to the broadly neutralizing 4E10 antibody and, therefore, constitutes a potential target for vaccine design. Recently reported structural data are compatible with preTM insertion into the viral external membrane monolayer in the gp41 pre-fusion state (Zhu, P., Liu, J., Bess, J., Chertova, E., Lifson, J. D., Grisé, H., Ofek, G. A., Taylor, K. A., and Roux, K. H. (2006) Nature 441, 847-852). Here we demonstrate that the broadly neutralizing 4E10 antibody is able to specifically block the membrane-restructuring activity of a peptide mimic inserted into membranes. Recognition and restructuring blocking occurred in the presence of cholesterol, whereas transmembrane versions as those promoted in 1-palmitoyl-2-oleoylphosphatidylcholine:sphingomyelin mixtures could not be effectively arrested. Spectrofluorimetric assays using rhodamine-labeled peptides revealed that recognition correlated better with pore-formation blocking than with membrane-fusion inhibition. The capacity of the antibody to recognize preTM peptides in a raft-like environment was further corroborated employing planar-supported lipid layers and fluorescence microscopy. These data support that membrane-bound epitope recognition by 4E10 results in clustering reorganization of preTM at the membrane interface. We propose that this process might interfere with the formation of fusion-competent complexes at the low spike densities existing in the HIV-1 membrane. This work comprises the first experimental report on a lipid-modulated antibody capacity to bind a membrane-bound epitope sequence and arrest its restructuring activity.

Erratum: Tuning the magnetic coupling across ultrathin antiferromagnetic films by controlling atomic-scale roughness

Nature Materials, 5, 128–133; (2006). In this article, a printing problem caused the top section of the left-hand panel in Fig. 5a to appear partly black, whereas it should have been all blue, as in the right-hand panel.

Postscript: Plaut and Booth's (2006) New Simulations--What Have We Learned?

Plaut and Booth’s (2006) first simulation shows that there is essentially perfect discrimination between word and nonwords sharing the same orthographic structure when the simulation is carried out in the way we suggested. We are therefore satisfied that their model can (now) be characterized as a parallel distributed processing (PDP) model of lexical processing (with the caveat that although it is beyond the scope of the present work, it is important to show at some point that the model “scales up” when it has a more realistically sized vocabulary of 40,000 words or so). We voiced concern that their model makes lexical decisions at the semantic level but there are patients with severe damage to semantics who are nonetheless as accurate at lexical decision as control patients without such damage (Coltheart, 2004). Can a model that makes lexical decisions at the semantic level simulate these data? In reply, Plaut and Booth (2006) reported new simulations showing that increasingly severe “lesioning” of their model at the semantic level impairs lexical decision accuracy in a monotonic way, but it is a remarkably small effect (see their Figure 1). They argue that “distinguishing the semantic activation of one word from that of another requires far more detailed information— and, thus, is less robust to damage—than distinguishing either from the much weaker activation produced by a nonword” (Plaut & Booth, 2006, p. 198). The results of these simulations not withstanding, a substantive difficulty for their account of lexical decision remains. Blazely, Coltheart, and Casey (in press) reported a detailed analysis of two patients (EM and PC) with semantic dementia, both of whom had significant impairments of semantic memory. EM performs slightly worse than PC on semantic tasks, but her visual lexical decision performance (two-alternative forced choice) was virtually perfect (97% correct), whereas PC’s visual lexical decision performance was significantly impaired (75% correct). It is difficult to see how this pattern can be simulated by Plaut and Booth’s (2000) model if lexical decision is carried out at the semantic level, but it is easy to understand if the decisions are carried out at the lexical level and PC’s lexical processing abilities are impaired. Blazely et al. provide converging evidence in support of this conclusion. Our third major concern was that Plaut and Booth’s (2000) PDP model’s use of the sigmoid function relating activation to reaction time (RT) would not permit the joint effect of two factors on RT to be additive when one of these factors and a third factor produce an interaction that lies within the same range of RTs. They responded to this by reporting a new simulation that purports to accomplish this. These data are reported in their Table 1. Some of these data are reproduced in Figure 1 for illustrative purposes. One point here is that this simulation is an unusual way of looking at the joint effects of word frequency and stimulus quality because it entails collapsing across the significant Context Stimulus Quality interaction in the right-hand panel. The joint effects of stimulus quality and word frequency should be examined when there is a neutral prime rather than a related or unrelated word, as argued by Neely (1991; see also Borowsky & Besner, 1993, who used nonword primes, and see Plaut & Booth, 2000, who also used a nonword baseline in their experiments and simulations but have now dropped it in their 2006 simulation). The more important question is whether the model has produced additive effects of stimulus quality and word frequency (as claimed for the data in the left hand panel). The size of the nonsignificant (underadditive) interaction in the left panel (.011 units) is almost double the size of the significant interaction in the right-hand panel (.006 units). Plaut and Booth (2006) do not comment on this. Even if Plaut and Booth were able to provide a more convincing simulation of both additive and interactive effects within the same range of RTs, we would like to know what principled reason makes it possible for the simulation to produce these results given that they now agree that the sigmoid-based explanation “only approximates the actual behavior of the model” (Plaut & Booth, 2006, p. 199). We take the view that Plaut and Booth’s (2006) new simulation work settles little beyond the fact that their model can discriminate 450 500 550 600 650 700

Yield Curve Inversions and Cyclical Peaks

All National Bureau of Economic Research (NBER) business cycle peaks since 1960 have been preceded by a flattening or inversion of the Treasury yield curve, leading some observers to express concern that the recent flattening of the yield curve might presage a near-term business cycle peak. However, the historical record, shown in the table, suggests that the relationship between yield curve inversions (negative slope) and subsequent economic downturns is tenuous. In the table, the yield curve’s slope is measured by the spread between Treasury constant-maturity yields at 10-year and 3-month maturities, a measure that past studies have labeled as the most reliable for predicting changes in economic activity. In the left panel, each row corresponds to a yield curve inversion, the slope having been positive during the previous month; in the right panel, each row corresponds to an NBER business cycle peak. Yield curve inversions tend to predict approximately twice as many recessions as actually occur. The durations and maximum yield spreads also vary sharply. Half of the inversions lasted 3 months or less; only three lasted 1 year or more. Half of the inversions also had maximum spreads of less than 28 basis points, with only three greater than 150 basis points. Finally, the number of elapsed months from the onset of inversion to the cycle peak also is varied. Six episodes lasted 9 months or less; six lasted 1 year or more. Clearly, although a business cycle peak eventually followed each inversion, the timing has been imprecise. In the right-hand panel, the first three NBER cycle peaks were not preceded by inversions (these may be unreliable because the long-term Treasury bond market was thin); only six peaks remain. The next two peaks, 1969 and 1973, are the “classic” cases in which the inversion began approximately 6 months prior to the peak and continued until after the peak. The next cycle peaks, in 1980 and 1981, occurred during the Federal Reserve’s aggressive disinflationary policy and perhaps are difficult to generalize. Finally, although an inversion occurred prior to the past two peaks, in 1990 and 2001, the yield curve regained its positive slope prior to the cycle peak as the Federal Open Market Committee aggressively lowered short-term rates. In short, the variability of inversion episodes suggests caution when interpreting changes in the yield curve as leading indicators of business cycle peaks.

Le triptyque de la Sainte Famille au travail de Pedralbes, une oeuvre flamande 'hispanisée'

AbstractThis article focuses on a Flemish triptych dating from 1530-1540; it is kept in the convent of Clares Santa Maria de Pedralbes (Barcelona), and can be attributed to the workshop of Pieter Coeck of Aelst. On the central panel is a representation of the Holy Family at work. In order to depict this less well-known theme the artist resorted to several models: Durer's woodcut from the Marienleben, another woodcut which was printed in the convent of Onze-Lieve-Vrouw ten Troost in Vilvoorde (Brussels) and a composition known to us from a version of the Master of the Antwerp Adoration belonging to the Stedelijk Museum in Delft. Due to its unusual iconographical programme we may assume that the triptych was commissioned by a Spanish Clare. The presence of Saints Clare and Agnes on the left-hand panel and of Saint Francis on the right-hand panel strongly suggests that the work was meant for a convent. Normally, female saints would have been on the right-hand side and Saint Francis on the left, in keeping with the heraldic conventions for males and females on Flemish triptychs. However, the Spanish Clare, who surely had contacts with the painter, wanted a more privileged place for women on 'her' triptych, ad dexteram Christi. In 1540-1560 the triptych, together with three other paintings, was converted into the form of an Iberian retable, which bears the arms of Mother Teresa de Cardona, who had probably commissioned the Flemish triptych. It looks less exotic in its new configuration of a more Spanish character. One might speak of a certain normalization that is not just aesthetic but iconographic too. When the triptych was inserted into the retabló, its wings were exchanged, so that the female saints now stand on the right side of the central panel, a position that is surely more in keeping with the prevailing conventions.

Bile Acid Synthesis in Humans Has a Rapid Diurnal Variation That Is Asynchronous With Cholesterol Synthesis

The conversion of cholesterol to bile acids by the liver is an important regulator of body cholesterol homeostasis. In rodents, both cholesterol and bile acid synthesis have marked diurnal rhythms that peak synchronously at midnight. The aim of this study was to establish whether such diurnal rhythms are also present in healthy humans. Serum levels of the markers 7alpha-hydroxy-4-cholesten-3-one (C4) monitoring bile acid biosynthesis and lathosterol reflecting cholesterol synthesis were determined at 90-minute intervals in 8 human volunteers during standardized dietary conditions. Serum C4 showed 2 distinct peaks (2- to 4-fold above baseline) during a 24-hour period, the first at 1:00 pm and the second at 9:00 pm. During the night, C4 levels declined, and they returned to baseline levels the next morning. In contrast, serum lathosterol levels peaked at night, between midnight and 4:00 am. The diurnal changes of C4 were not synchronous with serum lipid changes or with the postprandial increase in serum bile acids and were maintained in cholecystectomized subjects. Bile acid synthesis in humans has a diurnal rhythm, with 2 peaks during the daytime, that is opposite from the circadian rhythm of cholesterol synthesis. This is completely different from the pattern in rodents and indicates the presence of an important species variation in the regulation of cholesterol homeostasis.

Schlafen-1 Causes a Cell Cycle Arrest by Inhibiting Induction of Cyclin D1

Schlafen-1 (Slfn-1), the prototypic member of the Schlafen family of proteins, was described as an inducer of growth arrest in T-lymphocytes and causes a cell cycle arrest in NIH3T3 fibroblasts prior to the G1/S transition. How Slfn-1 exerts its effects on the cell cycle is not currently known. We report that synchronized murine fibroblasts expressing Slfn-1 do not exit G1 when stimulated with fetal calf serum, platelet-derived growth factor BB (PDGF-BB) or epidermal growth factor (EGF). The induction of cyclin D1 by these stimuli was blocked in the presence of Slfn-1 as were all downstream cell cycle processes. Overexpression of cyclin D1 in growth-arrested, Slfn-1-expressing cells induced an increase in cell growth consistent with this protein being the biological target of Slfn-1. Activation of the mitogen-activated protein kinase pathway by EGF or phorbol 12-myristate 13-acetate was unaffected by Slfn-1 expression. PDGF signaling was, however, almost completely blocked. This was due to a lack of PDGF receptor expression in Slfn-1-expressing cells consistent with Slfn-1 blocking the cell cycle in G1 where PDGF receptor expression is normally down-regulated. Finally, overexpression of Slfn-1 inhibited the activation of the cyclin D1 promoter. Slfn-1 therefore causes a cell cycle arrest during G1 by inhibiting induction of cyclin D1 by mitogens.

Bruton's Tyrosine Kinase Is Involved in p65-mediated Transactivation and Phosphorylation of p65 on Serine 536 during NFκB Activation by Lipopolysaccharide

Bruton's tyrosine kinase (Btk) has recently been shown to participate in the induction of nuclear factor kappaB (NFkappaB)-dependent gene expression by the lipopolysaccharide (LPS) receptor Toll-like receptor-4 (TLR4). In this study we have examined the mechanism whereby Btk participates in this response. Treatment of the murine monocytic cell line Raw264.7 with LFM-A13, a specific Btk inhibitor, blocked LPS-induced NFkappaB-dependent reporter gene expression but not IkappaB alpha degradation. Transient transfection of HEK293 cells with Btk had no effect on NFkappaB-dependent reporter gene expression but strongly promoted transactivation of a reporter gene by a p65-Gal4 fusion protein. IkappaB alpha degradation activated by LPS was intact in macrophages from X-linked immunodeficiency (Xid) mice, which contain inactive Btk. Transfection of cells with a dominant negative form of Btk (BtkK430R) inhibited LPS-driven p65 mediated transactivation. Additionally LFM-A13 impaired phosphorylation of serine 536 on p65 induced by LPS in HEK293-TLR4 cells, and in Xid macrophages this response was impaired. This study therefore reveals a novel function for Btk. It is required for the signaling pathway activated by TLR4, which culminates in phosphorylation of p65 on serine 536 promoting transactivation by NFkappaB.

Structure of a High Fidelity DNA Polymerase Bound to a Benzo[a]pyrene Adduct That Blocks Replication

Of the carcinogens to which humans are most frequently exposed, the polycyclic aromatic hydrocarbon benzo[a]pyrene (BP) is one of the most ubiquitous. BP is a byproduct of grilled foods and tobacco and fuel combustion and has long been linked to various human cancers, particularly lung and skin. BP is metabolized to diol epoxides that covalently modify DNA bases to form bulky adducts that block DNA synthesis by replicative or high fidelity DNA polymerases. Here we present the structure of a high fidelity polymerase from a thermostable strain of Bacillus stearothermophilus (Bacillus fragment) bound to the most common BP-derived N2-guanine adduct base-paired with cytosine. The BP adduct adopts a conformation that places the polycyclic BP moiety in the nascent DNA minor groove and is the first structure of a minor groove adduct bound to a polymerase. Orientation of the BP moiety into the nascent DNA minor groove results in extensive disruption to the interactions between the adducted DNA duplex and the polymerase. The disruptions revealed by the structure of Bacillus fragment bound to a BP adduct provide a molecular basis for rationalizing the potent blocking effect on replication exerted by BP adducts.

Elf5 is essential for early embryogenesis and mammary gland development during pregnancy and lactation

Elf5 is an epithelial-specific ETS factor. Embryos with a null mutation in the Elf5 gene died before embryonic day 7.5, indicating that Elf5 is essential during mouse embryogenesis. Elf5 is also required for proliferation and differentiation of mouse mammary alveolar epithelial cells during pregnancy and lactation. The loss of one functional allele led to complete developmental arrest of the mammary gland in pregnant Elf5 heterozygous mice. A quantitative mRNA expression study and Western blot analysis revealed that decreased expression of Elf5 correlated with the downregulation of milk proteins in Elf5(+/-) mammary glands. Mammary gland transplants into Rag(-/-) mice demonstrated that Elf5(+/-) mammary alveolar buds failed to develop in an Elf5(+/+) mammary fat pad during pregnancy, demonstrating an epithelial cell autonomous defect. Elf5 expression was reduced in Prolactin receptor (Prlr) heterozygous mammary glands, which phenocopy Elf5(+/-) glands, suggesting that Elf5 and Prlr are in the same pathway. Our data demonstrate that Elf5 is essential for developmental processes in the embryo and in the mammary gland during pregnancy.

Tumor suppression by a proapoptotic calcium-activated chloride channel in mammary epithelium.

Little is known of the roles played by ion channels in cancer. Here we describe a pair of closely related calcium-activated chloride channels whose differential regulation in normal, apoptotic, and transformed mouse cells suggests that channel function is proapoptotic and antineoplastic. While mCLCA1 predominates over mCLCA2 under normal physiological conditions, this relationship is reversed by apoptotic stress both in developing mammary gland and in cultured HC11 mammary epithelial cells. Consistent with an apoptosis-promoting role, splicing of mCLCA2 is disrupted in apoptosis-resistant tumor cell lines and in HC11 cells selected for resistance to detachment-induced apoptosis (anoikis). Unexpectedly, mCLCA1 message is also down-regulated in these cells by at least 30-fold. These results suggest that both genes antagonize survival of mammary tumor cells by sensitizing them to anoikis. When MCF7 or HEK293 tumor cells were transfected with plasmids encoding either mCLCA1 or mCLCA2, colony formation was greatly reduced relative to a vector-transfected control, demonstrating that calcium-sensitive chloride channel (CLCA) expression is deleterious to tumor cell survival. Furthermore, mammary epithelial cells overexpressing mCLCA2 had twice the rate of apoptosis of normal cells when subjected to serum starvation and formed multinuclear giants at a high frequency in normal culture, suggesting that mCLCA2 can promote either apoptosis or senescence.

Cohesion, but not too close.

After DNA replication in eukaryotes, the daughter chromatids remain connected throughout G2 and mitosis until they separate in anaphase. In budding yeast, the chromosomal cohesin complex has been shown to bind the chromatids together tightly at multiple points approximately every 10 kb along their entire length. What happens in human cells? Are sister chromatids also bound along their entire length from S-phase to the onset of anaphase?The two homologues of human chromosome 6 were visualised together with the major histocompatibility complex (MHC) class II region at band 6p21 by fluorescence in situ hybridisation in the human fibroblast cell line MRC5 (see Volpi et al., J Cell Sci 2000, 113:1565-1576). As expected, a single signal is seen at this locus in G0 and G1, which duplicates to form a doublet in S-phase. Surprisingly, however, in many cells the daughter signals are observed some distance apart. In metaphase, signals join again on adjacent sister chromatids (from top to bottom in the left-hand panel; chromosome 6 in green, MHC class II in red).The unexpectedly distant configuration in G2 was also found for the MHC class I and III regions, and for a gene-poor region from band 6p24 (from top to bottom in the right-hand panel). These observations indicate that sister chromatids, at least in human cells, are not always closely aligned in the period between DNA replicationDNA replication and mitosis, thus challenging currently held views on sister chromatid cohesion.Fig. 1Chromosome dynamics during DNA replication in human cells. The left-hand panel shows chromosome 6 (green) and the MHC class II locus at 6p21 (red) at G0/G1, S-phase, G2 and metaphase, from top to bottom. The right-hand panel shows chromosome 6 together with MHC class I and MHC class II regions, and a region at chromosome band 6p24 (from top to bottom) at G2.View Large Image | View Hi-Res Image | Download PowerPoint Slide

The impact of the new fish technologies on the cytogenetics of haematological malignancies.

The impact of the new fish technologies on the cytogenetics of haematological malignancies.

De Meester van de Magdalena-legende en de diptiek van Willem van Bibaut

AbstractWithin the range of works attributed to the Master of the Magdalen Legend are a number of Madonnas generally considered to date back to the last decade of the 15th century. All of these pictures are comparatively small and show a rather chubby type of Madonna with the Child slightly out of proportion. The golden backgrounds are punctuated. All these pictures are by the same hand, and are considered to date from the earliest period of the artist's activity. One of these paintings, now in the Mayer-Van den Bergh Museum in Antwerp, shows the Madonna holding the Child at her left breast. There is a second version of this painting on the left-hand panel of a diptych formerly in the Wetzlar collection in Amsterdam. The right-hand panel bears the portrait of a Carthusian monk, and is inscribed Guilelmus bibaucis primas tot [ius] Ordinis Carthusiemum. 1523.. The sitter has been identified as Willem of Bibaut (1484 1535), who became abbot of the Grand Chartreuse monastery in Grenoble in 1521. The portrait was probably painted to commemorate that event. Given that the stylistically very different paintings belonging to the Magdalen altarpiece which gave the artist his name date from the same period, the Madonnas can no longer be regarded as early paintings by the Master of the Magdalen Legend. Apparently they are the work of another artist.

Le Triptyque du "Buisson ardent" de Nicolas Froment et son programme iconographique

The Burning Bush triptych by the fifteenth-century French painter Nicolas Froment allows a triple thematic reading involving, in addition to the Burning Bush, allusions to the revelations to St. Joachim and St. Joseph. These three themes are closely linked to typological interpretations regarding Christ's genealogy and, by extension, the Immaculate Conception of the Virgin which appeared frequently in the illustrations of the Biblia Pauperum and the Speculum humanae salvationis from the fourteenth century on. The interpretation of the genealogy of Christ is found in the Breviare Romanum, the possible source for the inscription taken from Exodus 111:2 at the bottomof the central panel, which is in accordance with the text of the Book of Hours in front of the donor in the right-hand panel Ecclesiastes 24:11); and in the Missale Romanum, in which the text of Proverbs 8:22-35, part of which is shown at the top of the panel, is followed by the account given by St. Joseph, husband of Mary, of Messianic genealogy in Matthew 1:1-16. The blessing bestowed by Moses on Joseph, son of Israel, in Deuteronomy 33:13-16, corresponds closely to Jacob's blessing in Genesis IXL:22-26 in its reference to the twelve tribes of Israel - which are represented by the figures framing the central panel -and thus could be the primary source for the thematic coupling of Moses and St. Joseph.