Denoising Your Monte Carlo Renders: Recent Advances in Image Space-Adaptive Sampling and Reconstruction

With the ongoing shift in the computer graphics industry toward Monte Carlo rendering, there is a need for effective, practical noise-reduction techniques that are applicable to a wide range of rendering effects and easily integrated into existing production pipelines. This course surveys recent advances in image-space adaptive sampling and reconstruction algorithms for noise reduction, which have proven very effective at reducing the computational cost of Monte Carlo techniques in practice. These approaches leverage advanced image-filtering techniques with statistical methods for error estimation. They are attractive because they can be integrated easily into conventional Monte Carlo rendering frameworks, they are applicable to most rendering effects, and their computational overhead is modest.

Frequency modulation of ERK activation dynamics rewires cell fate.

Transient versus sustained ERK MAP kinase (MAPK) activation dynamics induce proliferation versus differentiation in response to epidermal (EGF) or nerve (NGF) growth factors in PC-12 cells. Duration of ERK activation has therefore been proposed to specify cell fate decisions. Using a biosensor to measure ERK activation dynamics in single living cells reveals that sustained EGF/NGF application leads to a heterogeneous mix of transient and sustained ERK activation dynamics in distinct cells of the population, different than the population average. EGF biases toward transient, while NGF biases toward sustained ERK activation responses. In contrast, pulsed growth factor application can repeatedly and homogeneously trigger ERK activity transients across the cell population. These datasets enable mathematical modeling to reveal salient features inherent to the MAPK network. Ultimately, this predicts pulsed growth factor stimulation regimes that can bypass the typical feedback activation to rewire the system toward cell differentiation irrespective of growth factor identity.

Two distinct filopodia populations at the growth cone allow to sense nanotopographical extracellular matrix cues to guide neurite outgrowth

BACKGROUND The process of neurite outgrowth is the initial step in producing the neuronal processes that wire the brain. Current models about neurite outgrowth have been derived from classic two-dimensional (2D) cell culture systems, which do not recapitulate the topographical cues that are present in the extracellular matrix (ECM) in vivo. Here, we explore how ECM nanotopography influences neurite outgrowth. METHODOLOGY/PRINCIPAL FINDINGS We show that, when the ECM protein laminin is presented on a line pattern with nanometric size features, it leads to orientation of neurite outgrowth along the line pattern. This is also coupled with a robust increase in neurite length. The sensing mechanism that allows neurite orientation occurs through a highly stereotypical growth cone behavior involving two filopodia populations. Non-aligned filopodia on the distal part of the growth cone scan the pattern in a lateral back and forth motion and are highly unstable. Filopodia at the growth cone tip align with the line substrate, are stabilized by an F-actin rich cytoskeleton and enable steady neurite extension. This stabilization event most likely occurs by integration of signals emanating from non-aligned and aligned filopodia which sense different extent of adhesion surface on the line pattern. In contrast, on the 2D substrate only unstable filopodia are observed at the growth cone, leading to frequent neurite collapse events and less efficient outgrowth. CONCLUSIONS/SIGNIFICANCE We propose that a constant crosstalk between both filopodia populations allows stochastic sensing of nanotopographical ECM cues, leading to oriented and steady neurite outgrowth. Our work provides insight in how neuronal growth cones can sense geometric ECM cues. This has not been accessible previously using routine 2D culture systems.

The Differential Requirement of Albumin and Sodium Citrate on the Development of In Vitro Produced Bovine Embryos

In vitro culture for bovine embryos is largely not optimal. Our study was to determine the components necessary for early embryo development. In experiment 1, IVF embryos were cultured for two days in CR1aa medium containing sodium citrate and BSA from two sources (Sigma vs. ICPbio), subsequently for additional five days with cumulus monolayer in 10% FBS CR1aa. We found that supplementation with both Sigma-BSA and sodium citrate significantly increased total blastocyst (BL) development compared with the ICPbio-BSA groups (37% vs. 19-21%), and enhanced the total number of high quality (C1 BL, IETS standard) blastocysts (26% vs. 11-17%) (P < 0.05). In experiment 2 with serum free and/or somatic free culture, we found that CR1aa culture can support a comparable embryo development with a supplement of Sigma BSA. The addition of sodium citrate did not increase blastocyst development in either the Sigma-BSA or the ICPbio-BSA groups. An inferior blastocyst development occurring in ICPbio-BSA culture (1-3%) could be rescued by culture in CRlaa supplemented with 10% FBS (29%), more importantly, by culture in CR1aa with a replacement of Sigma BSA (24%) (P <0.05). C1 blastocysts rescued by FBS and Sigma BSA in ICPbio-BSA culture possessed indistinguishable morphology to embryos developed in a Sigma-BSA, FBS and somatic co-culture system, showing similar cell number/blastocyst (129-180, P > 0.05). Our study found a beneficial effect of sodium citrate and BSA on the in vitro development of bovine IVF embryos during co-culture. We also determined that differential embryotrophic factor(s) contained in BSA and serum, probably not sodium citrate, is necessary for promoting competent morula and blastocyst development in cattle.

The Cell Agglutination Agent, Phytohemagglutinin-L, Improves the Efficiency of Somatic Nuclear Transfer Cloning in Cattle (Bos taurus)

One of the several factors that contribute to the low efficiency of mammalian somatic cloning is poor fusion between the small somatic donor cell and the large recipient oocyte. This study was designed to test phytohemagglutinin (PHA) agglutination activity on fusion rate, and subsequent developmental potential of cloned bovine embryos. The toxicity of PHA was established by examining its effects on the development of parthenogenetic bovine oocytes treated with different doses (Experiment 1), and for different durations (Experiment 2). The effective dose and duration of PHA treatment (150 microg/mL, 20 min incubation) was selected and used to compare membrane fusion efficiency and embryo development following somatic cell nuclear transfer (Experiment 3). Cloning with somatic donor fibroblasts versus cumulus cells was also compared, both with and without PHA treatment (150 microg/mL, 20 min). Fusion rate of nuclear donor fibroblasts, after phytohemagglutinin treatment, was increased from 33 to 61% (P < 0.05), and from 59 to 88% (P < 0.05) with cumulus cell nuclear donors. The nuclear transfer (NT) efficiency per oocyte used was improved following PHA treatment, for both fibroblast (13% versus 22%) as well as cumulus cells (17% versus 34%; P < 0.05). The cloned embryos, both with and without PHA treatment, were subjected to vitrification and embryo transfer testing, and resulted in similar survival (approximately 90% hatching) and pregnancy rates (17-25%). Three calves were born following vitrification and embryo transfer of these embryos; two from the PHA-treated group, and one from non-PHA control group. We concluded that PHA treatment significantly improved the fusion efficiency of somatic NT in cattle, and therefore, increased the development of cloned blastocysts. Furthermore, within a determined range of dose and duration, PHA had no detrimental effect on embryo survival post-vitrification, nor on pregnancy or calving rates following embryo transfer.

Differential Cytoplast Requirement for Embryonic and Somatic Cell Nuclear Transfer in Cattle

Effective activation of a recipient oocyte and its compatibility with the nuclear donor are critical to the successful nuclear reprogramming during nuclear transfer. We designed a series of experiments using various activation methods to determine the optimum activation efficiency of bovine oocytes. We then performed nuclear transfer (NT) of embryonic and somatic cells into cytoplasts presumably at G1/S phase (with prior activation) or at metaphase II (MII, without prior activation). Oocytes at 24 hr of maturation in vitro were activated with various combinations of calcium ionophore A23187 (A187) (5 microM, 5 min), electric pulse (EP), ethanol (7%, 7 min), cycloheximide (CHX) (10 micro g/ml, 6 hr), and then cultured in cytochalasin D (CD) for a total of 18 hr. Through a series of experiments (Exp. 1-4), an improved activation protocol (A187/EP/CHX/CD) was identified and used for comparison of NT efficiency of embryonic versus somatic donor cells (Exp. 5). When embryonic cells from morula and blastocysts (BL) were used as nuclear donors, a significantly higher rate of blastocyst development from cloned embryos was obtained with G1/S phase cytoplasts than with MII-phase cytoplasts (36 vs. 11%, P < 0.05). In contrast, when skin fibroblasts were used as donor cells, the use of an MII cytoplast (vs. G1/S phase) was imperative for blastocyst development (30 vs. 6%, P < 0.05). Differential staining showed that parthenogenetic, embryonic, and somatic cloned BL contained 26, 29, and 33% presumptive inner cell mass (ICM) cells, respectively, which is similar to that of frozen-thawed in vivo embryos at a comparable developmental stage (23%). These data indicate that embryonic and somatic nuclei require different recipient cytoplast environment for remodeling/ reprogramming, and this is likely due to the different cell cycle stage and profiles of molecular differentiation of the transferred donor nuclei.

Der Handel mit abgeschnittenen frischen Blumen von und nach Berlin

von Otto Choné

Der Handel mit abgeschnittenen frischen Blumen von und nach Berlin

von Otto Choné

Na 1 Nachlass Max Horkheimer, 44 - Korrespondenzen u.a. mit Marthe Roth (p. I 21, 313-463)

2 Briefe und 1 Lebenslauf von Max Horkheimer an Arthur Rosenberg, 1939, 1941; 2 Briefe zwischen Kurt Rosenfeld und Karl Brandt, 22.04.1937, 27.04.1937; 5 Briefe von Kurt Rosenfeld an Max Horkheimer, 1937-19378; 4 Brief und Beilage an Kurt Rosenfeld, 1937-1943; 11 Briefe zwischen Hans W. Rosenhaupt und Max Horkheimer, 1935, 1941, 1942, 1947; 4 Briefe zwischen Samuel I. Roseman und Max Horkheimer, 1939, 03.01.1940; 2 Briefe zwischen J. Rosenstock und Max Horkheimer, 15.07.1946; 2 Briefe zwischen Joseph Adolphe Rosenthal und Max Horkheimer, 09.04.1941, 08.05.1941, sowie Briefwechsel mit Sophie Ries; 2 Briefe zwischen Sophie Ries und Max Horkheimer, 08.05.1941, 11.05.1941; 1 Brief von Max Horkheimer an Lore Woedthke, 08.05.1941; 2 Briefe zwischen Morris Rosenthal und Max Horkheimer, 01.10.1935, 04.10.1935; 1 Brief von Max Horkheimer an das Rosenwald Capital Outlay Fund New York, 30.01.1940; 1 Brief B. Lifschitz an Marthe Roth, 21.04.1937; 1 Brief von Chamorel et Simond an Marthe Roth, 11.06.1937; 1 Brief von F.K. Sung an Marthe Roth, 24.06.1937; 12 Briefe zwischen Marthe Roth und Max Horkheimer, Juli 1937-1938, sowie Briefwechsel mit Louis Vogt; 4 Briefe zwischen Louis Vogt und Max Horkheimer, 10.08.1937, 1937; 1 Brief von Max Horkheimer an Dr. Rothen, 31.01.1935; 1 Umzugsmitteilung von Hans Rothmann; 2 Briefe zwischen Richard C. Rothschild und Max Horkheimer, 11.05.1940, 13.05.1940; 4 Briefe zwischen Ludwig Rothschild, Hilde Rothschild und Max Horkheimer, 1936-15.09.1939; 2 Briefe zwischen S. Rothschildt und Max Horkheimer, 23.11.1940, 29.11.1940; 4 Brief zwischen J. S. Roucek und Max Horkheimer, 1941; 1 Brief von Joseph Rovan an Max Horkheimer, 11.05.1948; 2 Brief zwischen Wilmina Rowland und Max Horkheimer, 13.03.1949, 11.04.1949; 2 Briefe zwischen dem Royal Automobile Club und Max Horkheimer, 26.08.1937, 22.09.1937; 2 Briefe zwischen Royal Motors Inc. und Max Horkheimer, 05.02.1940, 06.03.1940; 1 Beitrag von Nina Rubinstein zur Soziologie des Fremden; 1 Brief von Theodor W. Adorno an Rudd, 09.09.1940; 1 Brief von Jay Rumney an Goldstein, 18.06.1936; 20 Briefe und Beilage zwischen Jay Rumney und Max Horkheimer, 1934- 1937, 1949 sowie Briefwechsel mit D. Mitrany; 3 Briefe zwischen D. Mitrany und Max Horkheimer, 01.12.1937, 1937; 3 Briefe von Theodor W. Adorno an Dagobert D. Runes, 1941; 1 Brief und 1 Beilage von N. Waterman an Georg Rusche, 03.05.1939; 12 Briefe und Beilage zwischen Georg Rusche und Max Horkheimer, 1939-1942 sowie Briefwechsel mit N. Waterman; 1 Brief von N. Waterman an Georg Rusche, 03.04.1939; 2 Briefe zwischen N. Waterman und Max Horkheimer, 21.04.1939, 05.05.1939; 1 Brief von Ruth an Max Horkheimer;

The connection between E2F and ATM in p53-dependent apoptosis

Programmed cell death is an anticancer mechanism utilized by p53 that when disrupted can accelerate tumor development in response to oncogenic stress. Defects in the RB tumor suppressor cause aberrant cell proliferation as well as apoptosis. The combinatorial loss of the p53 and RB pathways is observed in a large percentage of human tumors. The E2F family of transcription factors primarily mediates the phenotype of Rb loss, since RB is a negative regulator of E2F. Contrary to early expectations, it has now been shown that the ARF (alternative reading frame) tumor suppressor is not required for p53-dependent apoptosis in response to deregulation of the RB/E2F pathway. In this study, we demonstrate that ATM, known as a DNA double-strand break (DSB) sensor, is responsible for ARF-independent apoptosis and p53 activation induced by deregulated E2F1. Moreover, NBS1, a component of the MRN DNA repair complex, is also required for E2F1-induced apoptosis and apparently works in the same pathway as ATM. We further found that endogenous E2F1 and E2F3 both play a role in apoptosis and ATM activation in response to inhibition of RB by the adenoviral E1A oncoprotein. We demonstrate that, unlike deregulated E2F3 and Myc, ATM activation by deregulated E2F1 does not involve the induction of DNA damage, autophosphorylation of ATM on Ser 1981, a marker of ATM activation by DSB, but does depend on the presence of NBS1, suggesting that E2F1 activates ATM in a different manner from E2F3 and Myc. Results from domain mapping studies show that the DNA binding, dimerization, and marked box domains of E2F1 are required to activate ATM and stimulate apoptosis but the transactivation domain is not. This implies that E2F1's DNA binding and interaction with other proteins through the marked box domain are necessary to induce ATM activation leading to apoptosis but transcriptional activation by E2F1 is dispensable. Together these data suggest a model in which E2F1 activates ATM to phosphorylate p53 through a novel mechanism that is independent of DNA damage and transcriptional activation by E2F1.^

A novel DNA damage inducible inhibitor of p53

p53 is required for the maintenance of the genomic stability of cells. Mutations in the p53 tumor-suppressor gene occur in more than 50% of human cancers of diverse types. In addition, 70% of families with Li-Fraumeni syndrome have a germline mutation in p53, predisposing these individuals to multiple forms of cancer. In response to DNA damage, p53 becomes stabilized and activated. However the exact mechanism by which DNA damage signals the stabilization and activation of p53 still remains elusive. The biochemical activity of p53 that is required for tumor suppression, and presumably the cellular response to DNA damage, involves the ability of the protein to bind to specific DNA sequences and to function as a transcription factor. For the downstream targets, p53 transactivates many genes involved in growth arrest, apoptosis and DNA repair such as p21, Bax and GADD45, respectively. An open question in the field is how cells can determine the downstream effects of p53. ^ We hypothesize that, through its associated proteins, p53 can differentially transactivate its target genes, which determine its downstream effect. Additionally, p53 interacting proteins may be involved in signaling for the stabilization and activation of p53. Therefore, a key aspect to understanding p53 function is the identification and analysis of proteins that interact with it. We have employed the Sos recruitment system (SRS), a cytoplasmic yeast two-hybrid screen to identify p53 interacting proteins. The SRS is based on the ability of Sos to activate Ras when it becomes localized to the plasma membrane. The system takes advantage of an S. cerevisiae strain, cdc25-2 temperature sensitive mutant, harboring a mutation in Sos. In this strain, fusion proteins containing a truncated Sos will only localize to the membrane by protein-protein interaction, which allows growth at non-permissive temperature. This system allows the use of intact transcriptional activators such as p53. ^ To date, using a modified SRS library screen to identify p53 interacting proteins, I have identified p53 (known to interact with itself) and a novel p53-interacting protein (PIP). PIP is a specific p53 interacting protein in the SRS. The interaction of p53 and PIP was further confirmed by performing in vitro and in vivo binding assays. In the in vivo binding study, the interaction can only be detected in the presence of ionizing radiation suggesting that this interaction might be involved in DNA-damage induced p53-signalling pathway. After screening cDNA and genomic libraries, a full-length PIP-cDNA clone ( ∼ 3kb) was obtained which encodes a protein of 429 amino acids with calculated molecular weight of 46 kDa. The results of genebank search indicated that the PIP is an unidentified gene and contains a conserved ring-finger domain, which is present in a diverse family of regulatory proteins involved in different aspects of cellular function. Northern blot analysis revealed that the size of its messenge is approximately 3 kb preferentially expressed in brain, heart, liver and kidney. The PIP protein is mainly located in the cytoplasm as determined by the cellular localization of a green fluorescence fusion protein. Preliminary functional analysis revealed that PIP downregulated the transactivation activity of p53 on both p21 and mdm2 promoters. Thus, PIP may be a novel negative regulator of p53 subsequent to DNA damage. ^

Las formas no finitas en las proposiciones subordinadas de las lenguas patagónicas

En la región patagónica existieron varias lenguas, algunas de las cuales sobreviven en la actualidad. Ellas son: (1) el mapudungun, la lengua más extendida de la Patagonia, que va del centro al sur de Chile y Argentina, y aparentemente relacionada con la familia Arawak de Sudamérica; (2) la familia Chon con las siguientes lenguas: teushen, ubicada entre el río Chubut y el río Santa Cruz; el tehuelche o aonek'o 'a'jen, localizada entre el río Santa Cruz y el Estrecho de Magallanes; el selknam u ona y el haush o manekenk, ambas en la Isla Grande de Tierra del Fuego; (3) el gününa küne, en el centro-norte de la Patagonia, relacionada genéticamente por algunos investigadores con las lenguas Chon, aunque no hay evidencias claras sobre esta filiación; (4) la lengua chono, desconocida hasta el momento. De todas ellas solo se mantiene el mapudungun, aunque ya se halla en un proceso de retracción avanzado. De las restantes solo el tehuelche o aonek'o 'a'jen presenta actualmente dos o tres hablantes y el pueblo se halla preocupado por su revitalización. Las demás ya se extinguieron y cuentan con escasa o nula documentación. A partir de los datos existentes, intentaremos determinar para las lenguas mejor documentadas - mapudungun, tehuelche, selknam y gününa küne- el empleo de las formas no finitas (fnf) en las proposiciones subordinadas, con la intención de definir si existió alguna influencia del mapudungun sobre las otras lenguas continentales para que se desarrollara este tipo de subordinadas en la región, de modo de contribuir al establecimiento de un área lingüística en Patagonia

En los albores de la celestinesca : Sobre el "Romance nuevamente hecho de Calisto y Melibea" en el pliego suelto de 1513

El Romance nueuamente hecho de Calisto y Melibea, pliego suelto impreso en 1513 (Jacobo Cromberger, Sevilla), un "romance-cuento" (según Menéndez Pidal) de 680 versos octosilábicos, atestigua una pronta transformación genérica: de la prosa dramática de Celestina a un poema narrativo con narrador extradiegético. La trama concisa incluye los típicos motivos narrativos del romancero hispánico (por ejemplo, el protagonista como un cazador) y acentúa el tema del pecado y el castigo (tomado de los paratextos de Celestina), también presente en los primeros pliegos sueltos cantados por ciegos. Existen evidencias de que el texto base ha sido la Comedia, no la Tragicomedia. Este texto temprano debería ser considerado un hito en la historia de la celestinesca

La lírica popular-tradicional argentina : Límites difusos

La sociedad argentina puede caracterizarse como "nueva", producto de proyectos poblacionales y migraciones internas y externas. Esta condición determinó que la cultura popular, y la poesía en particular, se manifestaran en distintas tradiciones superpuestas. Una tradición hispánica procedente del período colonial se asentó en el noroeste del país, área de población más antigua en la que fueron documentados romances y coplas tradicionales. Paralelamente, una tradición criolla heredera de la hispánica tuvo expresiones autóctonas en relación con los movimientos independentistas (romancero criollo, pero también décimas y coplas). Por último, una tradición europea se incorporó entre fines del siglo xix y principios del xx con el denominado aluvión inmigratorio. Esta última corriente impregnó todo lo anterior con nuevos temas procedentes especialmente de España, pero en contacto con diversas formas populares de otros países como Italia, Francia y Portugal. El propósito de este artículo es ofrecer un panorama de la superposición de estos distintos estratos culturales tal como se manifiesta en las coplas que se cantaron y se imprimieron en la primera mitad del Siglo xx