Статті в журналах: "Differentiation implicite"

1

Hughes, David. "Differentiating the Corporation: Accountability and International Humanitarian Law." Michigan Journal of International Law, no. 42.1 (2021): 47. http://dx.doi.org/10.36642/mjil.42.1.differentiating.

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Corporations are significant global actors that are continuing to gain international legal status. Regulatory efforts have closely followed persistent claims that various forms of corporate activity are adversely affecting individual welfare and societal objectives. Such observations are perhaps most acute during instances of armed conflict. The history of corporate misdeeds occurring within or contributing to the perpetuation of warfare is now well-documented. However, the relationship between international humanitarian law—the legal field governing the conduct of war—and corporations receives less attention than other areas of international law where the treatment of business entities have made important advancements. This article considers the particularities that affect how accountability is imposed for corporate behavior that implicates IHL. Accordingly, the article has three purposes. First, it describes the (indirect) doctrinal methods through which accountability for corporate conduct implicating IHL may be pursued. Second, it identifies structural challenges and features of the corporate form that compromise the efficacy of these methods and result in accountability gaps. Third, through a series of case studies—addressing the conduct of Blackwater in Iraq, Facebook in Myanmar, and Airbnb in the West Bank—the article categorizes disparate forms of corporate conduct that implicate IHL in previously unforeseen ways and present unidentified regulatory challenges. Collectively, the article suggests that if international law is to contribute to the process of narrowing accountability gaps, if it is to provide an agreeable and accurate vocabulary for determining standards and adjudging conduct, regulatory efforts must begin by embracing those features that differentiate the corporation from those other entities that have traditionally held international law’s attention.

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2

Sarkar, Sukumar, Bijan K. Dey, and Anindya Dutta. "MiR-322/424 and -503 Are Induced during Muscle Differentiation and Promote Cell Cycle Quiescence and Differentiation by Down-Regulation of Cdc25A." Molecular Biology of the Cell 21, no. 13 (July 2010): 2138–49. http://dx.doi.org/10.1091/mbc.e10-01-0062.

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Induction of a G1 phase cell cycle arrest, caused primarily by the inhibition of cyclin-dependent-kinase 2 (cdk2), is a critical step in the differentiation of myoblasts into myotubes. Here, we report that two microRNAs, miR-322/424 and miR-503, are induced and promote cdk2 inhibition during myogenesis. These microRNAs down-regulate Cdc25A, the phosphatase responsible for removing inhibitory phosphorylation of cdk2, both in myoblasts differentiating into myotubes and in nonmuscle cells. Cdc25A is down-regulated during muscle differentiation by multiple pathways: action of these two microRNAs, proteasomal degradation of Cdc25A protein and transcriptional repression. Overexpression of Cdc25A or of cdk2 with mutations on T14 and Y15 (cdk2-AF), so that it cannot be inhibited by phosphorylation, decreases differentiation and differentiation-induced cell cycle quiescence. Introduction of miR-322/424 and miR-503 in heterologous cancer cells induces G1 arrest, which is also attenuated by overexpression of the cdk2-AF mutant. Until now Cdc25A and the inhibitory phosphorylation on T14 and Y15 of cdk2 have only been implicated in the intra-S phase checkpoint pathway after DNA damage. Our results reveal an unexpected role of Cdc25A down-regulation and the inhibitory phosphorylation of cdk2 T14 and Y15 in cell cycle quiescence during muscle differentiation and implicate two muscle differentiation-induced microRNAs in the process.

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3

Bair, Jacques, and Valérie Henry. "Implicit Differentiation with Microscopes." Mathematical Intelligencer 32, no. 1 (November 4, 2009): 53–55. http://dx.doi.org/10.1007/s00283-009-9088-0.

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4

Vachon, Pierre H. "Integrin Signaling, Cell Survival, and Anoikis: Distinctions, Differences, and Differentiation." Journal of Signal Transduction 2011 (July 13, 2011): 1–18. http://dx.doi.org/10.1155/2011/738137.

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Cell survival and apoptosis implicate an increasing complexity of players and signaling pathways which regulate not only the decision-making process of surviving (or dying), but as well the execution of cell death proper. The same complex nature applies to anoikis, a form of caspase-dependent apoptosis that is largely regulated by integrin-mediated, cell-extracellular matrix interactions. Not surprisingly, the regulation of cell survival, apoptosis, and anoikis furthermore implicates additional mechanistic distinctions according to the specific tissue, cell type, and species. Incidentally, studies in recent years have unearthed yet another layer of complexity in the regulation of these cell processes, namely, the implication of cell differentiation state-specific mechanisms. Further analyses of such differentiation state-distinct mechanisms, either under normal or physiopathological contexts, should increase our understanding of diseases which implicate a deregulation of integrin function, cell survival, and anoikis.

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5

Stratton, Damji Heo. "Negative transfer in implicit differentiation." International Journal of Educational Research Open 2-2 (2021): 100051. http://dx.doi.org/10.1016/j.ijedro.2021.100051.

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6

Young, Gary W. De. "Constrained Optimization with Implicit Differentiation." College Mathematics Journal 34, no. 2 (March 2003): 148. http://dx.doi.org/10.2307/3595792.

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7

Matthews, K. R., and K. Gull. "Evidence for an interplay between cell cycle progression and the initiation of differentiation between life cycle forms of African trypanosomes." Journal of Cell Biology 125, no. 5 (June 1, 1994): 1147–56. http://dx.doi.org/10.1083/jcb.125.5.1147.

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Successful transmission of the African trypanosome between the mammalian host blood-stream and the tsetse fly vector involves dramatic alterations in the parasite's morphology and biochemistry. This differentiation through to the tsetse midgut procyclic form is accompanied by re-entry into a proliferative cell cycle. Using a synchronous differentiation model and a variety of markers diagnostic for progress through both differentiation and the cell cycle, we have investigated the interplay between these two processes. Our results implicate a relationship between the trypanosome cell cycle position and the perception of the differentiation signal and demonstrate that irreversible commitment to the differentiation occurs rapidly after induction. Furthermore, we show that re-entry into the cell cycle in the differentiating population is synchronous, and that once initiated, progress through the differentiation pathway can be uncoupled from progress through the cell cycle.

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8

Park, Ji Hye, Na Kyoung Lee, Hye Ji Lim, Seung taek Ji, Yeon-Ju Kim, Woong Bi Jang, Da Yeon Kim, et al. "Pharmacological inhibition of mTOR attenuates replicative cell senescence and improves cellular function via regulating the STAT3-PIM1 axis in human cardiac progenitor cells." Experimental & Molecular Medicine 52, no. 4 (April 2020): 615–28. http://dx.doi.org/10.1038/s12276-020-0374-4.

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Abstract The mammalian target of rapamycin (mTOR) signaling pathway efficiently regulates the energy state of cells and maintains tissue homeostasis. Dysregulation of the mTOR pathway has been implicated in several human diseases. Rapamycin is a specific inhibitor of mTOR and pharmacological inhibition of mTOR with rapamycin promote cardiac cell generation from the differentiation of mouse and human embryonic stem cells. These studies strongly implicate a role of sustained mTOR activity in the differentiating functions of embryonic stem cells; however, they do not directly address the required effect for sustained mTOR activity in human cardiac progenitor cells. In the present study, we evaluated the effect of mTOR inhibition by rapamycin on the cellular function of human cardiac progenitor cells and discovered that treatment with rapamycin markedly attenuated replicative cell senescence in human cardiac progenitor cells (hCPCs) and promoted their cellular functions. Furthermore, rapamycin not only inhibited mTOR signaling but also influenced signaling pathways, including STAT3 and PIM1, in hCPCs. Therefore, these data reveal a crucial function for rapamycin in senescent hCPCs and provide clinical strategies based on chronic mTOR activity.

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9

Yu, Chieh, Ian W. Peall, Son H. Pham, Rachel K. Okolicsanyi, Lyn R. Griffiths, and Larisa M. Haupt. "Syndecan-1 Facilitates the Human Mesenchymal Stem Cell Osteo-Adipogenic Balance." International Journal of Molecular Sciences 21, no. 11 (May 29, 2020): 3884. http://dx.doi.org/10.3390/ijms21113884.

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Bone marrow-derived human mesenchymal stems cells (hMSCs) are precursors to adipocyte and osteoblast lineage cells. Dysregulation of the osteo-adipogenic balance has been implicated in pathological conditions involving bone loss. Heparan sulfate proteoglycans (HSPGs) such as cell membrane-bound syndecans (SDCs) and glypicans (GPCs) mediate hMSC lineage differentiation and with syndecan-1 (SDC-1) reported in both adipogenesis and osteogenesis, these macromolecules are potential regulators of the osteo-adipogenic balance. Here, we disrupted the HSPG profile in primary hMSC cultures via temporal knockdown (KD) of SDC-1 using RNA interference (RNAi) in undifferentiated, osteogenic and adipogenic differentiated hMSCs. SDC-1 KD cultures were examined for osteogenic and adipogenic lineage markers along with changes in HSPG profile and common signalling pathways implicated in hMSC lineage fate. Undifferentiated hMSC SDC-1 KD cultures exhibited a pro-adipogenic phenotype with subsequent osteogenic differentiation demonstrating enhanced maturation of osteoblasts. In cultures where SDC-1 KD was performed following initiation of differentiation, increased adipogenic gene and protein marker expression along with increased Oil Red O staining identified enhanced adipogenesis, with impaired osteogenesis also observed in these cultures. These findings implicate SDC-1 as a facilitator of the hMSC osteo-adipogenic balance during early induction of lineage differentiation.

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10

Clark, Allison J., Kathryn M. Doyle, and Patrick O. Humbert. "Cell-intrinsic requirement for pRb in erythropoiesis." Blood 104, no. 5 (September 1, 2004): 1324–26. http://dx.doi.org/10.1182/blood-2004-02-0618.

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Abstract Retinoblastoma (Rb) and family members have been implicated as key regulators of cell proliferation and differentiation. In particular, accumulated data have suggested that the Rb gene product pRb is an important controller of erythroid differentiation. However, current published data are conflicting as to whether the role of pRb in erythroid cells is cell intrinsic or non–cell intrinsic. Here, we have made use of an in vitro erythroid differentiation culture system to determine the cell-intrinsic requirement for pRb in erythroid differentiation. We demonstrate that the loss of pRb function in primary differentiating erythroid cells results in impaired cell cycle exit and terminal differentiation. Furthermore, we have used coculture experiments to establish that this requirement is cell intrinsic. Together, these data unequivocally demonstrate that pRb is required in a cell-intrinsic manner for erythroid differentiation and provide clarification as to its role in erythropoiesis.

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11

Cai, Jun, Yingchuan Qi, Rui Wu, Geoffrey Modderman, Hui Fu, Rugao Liu, and Mengsheng Qiu. "Mice Lacking the Nkx6.2 (Gtx) Homeodomain Transcription Factor Develop and Reproduce Normally." Molecular and Cellular Biology 21, no. 13 (July 1, 2001): 4399–403. http://dx.doi.org/10.1128/mcb.21.13.4399-4403.2001.

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ABSTRACT The Nkx homeobox genes are expressed in a variety of developing tissues and have been implicated in controlling tissue patterning and cell differentiation. Expression of Nkx6.2(Gtx) was previously observed in the embryonic neural tube, testis, and differentiating oligodendrocytes. To investigate the role of Nkx6.2 in the control of cell specification and differentiation, we generated mice with null mutations inNkx6.2 using the standard gene targeting approach. Null mutant mice were viable and fertile without apparent histological and immunohistochemical changes in the central nervous systems and testis. The absence of detectable phenotypes suggests a redundant function ofNkx6.2 in mouse development.

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12

Fan, Xiaomeng, Yuwei Wu, Zhi Gao, Yunde Jia, and Mehrtash Harandi. "Efficient Riemannian Meta-Optimization by Implicit Differentiation." Proceedings of the AAAI Conference on Artificial Intelligence 36, no. 4 (June 28, 2022): 3733–40. http://dx.doi.org/10.1609/aaai.v36i4.20287.

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To solve optimization problems with nonlinear constrains, the recently developed Riemannian meta-optimization methods show promise, which train neural networks as an optimizer to perform optimization on Riemannian manifolds. A key challenge is the heavy computational and memory burdens, because computing the meta-gradient with respect to the optimizer involves a series of time-consuming derivatives, and stores large computation graphs in memory. In this paper, we propose an efficient Riemannian meta-optimization method that decouples the complex computation scheme from the meta-gradient. We derive Riemannian implicit differentiation to compute the meta-gradient by establishing a link between Riemannian optimization and the implicit function theorem. As a result, the updating our optimizer is only related to the final two iterations, which in turn speeds up our method and reduces the memory footprint significantly. We theoretically study the computational load and memory footprint of our method for long optimization trajectories, and conduct an empirical study to demonstrate the benefits of the proposed method. Evaluations of three optimization problems on different Riemannian manifolds show that our method achieves state-of-the-art performance in terms of the convergence speed and the quality of optima.

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13

Bishop, G. A. "Requirements of class II-mediated B cell differentiation for class II cross-linking and cyclic AMP." Journal of Immunology 147, no. 4 (August 15, 1991): 1107–14. http://dx.doi.org/10.4049/jimmunol.147.4.1107.

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Abstract Cells of the mouse B cell clone, CH12.LX, receive Ag-dependent differentiative signals through their surface membrane class II molecules. The present study was performed to determine the role of class II cross-linking and cAMP in the successful delivery of these signals. Delivery of differentiative signals by anti-Ek mAb was increased by further cross-linking with a secondary anti-isotype antibody. Intact or (Fab')2, but not Fab forms of anti-Ek successfully delivered the Ag-dependent differentiative signal. Inability of monovalent Fab fragments to deliver the signal could not be attributed to an inability to adequately bind Ek molecules. The requirement for cAMP for class II-mediated signaling was also examined, because previous studies have implicated elevated cAMP levels as necessary for class II signaling. Both Ag-dependent, Ek-mediated differentiation and the Ek-mediated inhibition of Ag-independent LPS-induced differentiation were inhibited by the adenyl cyclase inhibitor 2'5'ddA, although elevation of cAMP was not in itself sufficient to deliver the differentiative signal. Inhibition of LPS-induced differentiation could be mediated by mAb binding to either Ek, Abk, or Abb on CH12.LX or an Ab-bearing transfectant, CH12.ABB1. This inhibition was abrogated by 2'5'ddA in the case of Ek or Abb, both of which deliver Ag-dependent differentiative signals to CH12.LX cells. In the case of Abk, which does not deliver such signals to CH12.LX, 2'5'ddA did not abrogate anti-Abk-mediated inhibition of the LPS response. The effects of 2'5'ddA were reversed by the cAMP analog, dibutyryl cAMP, and Ag-dependent-induced differentiation of CH12.LX or CH12.ABB1 was accompanied by an increase in cAMP levels.

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14

Iyer, Ashvin, Adam J. Koch, and James M. Holaska. "Expression Profiling of Differentiating Emerin-Null Myogenic Progenitor Identifies Molecular Pathways Implicated in Their Impaired Differentiation." Cells 6, no. 4 (October 22, 2017): 38. http://dx.doi.org/10.3390/cells6040038.

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15

Calautti, Enzo, Maddalena Grossi, Cristina Mammucari, Yumi Aoyama, Maria Pirro, Yoshitaka Ono, Jie Li, and G. Paolo Dotto. "Fyn tyrosine kinase is a downstream mediator of Rho/PRK2 function in keratinocyte cell–cell adhesion." Journal of Cell Biology 156, no. 1 (January 3, 2002): 137–48. http://dx.doi.org/10.1083/jcb.200105140.

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The Rho GTPase and Fyn tyrosine kinase have been implicated previously in positive control of keratinocyte cell–cell adhesion. Here, we show that Rho and Fyn operate along the same signaling pathway. Endogenous Rho activity increases in differentiating keratinocytes and is required for both Fyn kinase activation and increased tyrosine phosphorylation of β- and γ-catenin, which is associated with the establishment of keratinocyte cell–cell adhesion. Conversely, expression of constitutive active Rho is sufficient to promote cell–cell adhesion through a tyrosine kinase- and Fyn-dependent mechanism, trigger Fyn kinase activation, and induce tyrosine phosphorylation of β- and γ-catenin and p120ctn. The positive effects of activated Rho on cell–cell adhesion are not induced by an activated Rho mutant with defective binding to the serine/threonine PRK2/PKN kinases. Endogenous PRK2 kinase activity increases with keratinocyte differentiation, and, like activated Rho, increased PRK2 activity promotes keratinocyte cell–cell adhesion and induces tyrosine phosphorylation of β- and γ-catenin and Fyn kinase activation. Thus, these findings reveal a novel role of Fyn as a downstream mediator of Rho in control of keratinocyte cell–cell adhesion and implicate the PRK2 kinase, a direct Rho effector, as a link between Rho and Fyn activation.

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16

Syam, Muhammed I., and Hani I. Siyyam. "Numerical differentiation of implicitly defined curves." Journal of Computational and Applied Mathematics 108, no. 1-2 (August 1999): 131–44. http://dx.doi.org/10.1016/s0377-0427(99)00106-5.

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17

Fan, Jianguo, Li Jia, Yan Li, Seham Ebrahim, Helen May-Simera, Alynda Wood, Robert J. Morell, et al. "Maturation arrest in early postnatal sensory receptors by deletion of the miR-183/96/182 cluster in mouse." Proceedings of the National Academy of Sciences 114, no. 21 (May 8, 2017): E4271—E4280. http://dx.doi.org/10.1073/pnas.1619442114.

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The polycistronic miR-183/96/182 cluster is preferentially and abundantly expressed in terminally differentiating sensory epithelia. To clarify its roles in the terminal differentiation of sensory receptors in vivo, we deleted the entire gene cluster in mouse germline through homologous recombination. The miR-183/96/182 null mice display impairment of the visual, auditory, vestibular, and olfactory systems, attributable to profound defects in sensory receptor terminal differentiation. Maturation of sensory receptor precursors is delayed, and they never attain a fully differentiated state. In the retina, delay in up-regulation of key photoreceptor genes underlies delayed outer segment elongation and possibly mispositioning of cone nuclei in the retina. Incomplete maturation of photoreceptors is followed shortly afterward by early-onset degeneration. Cell biologic and transcriptome analyses implicate dysregulation of ciliogenesis, nuclear translocation, and an epigenetic mechanism that may control timing of terminal differentiation in developing photoreceptors. In both the organ of Corti and the vestibular organ, impaired terminal differentiation manifests as immature stereocilia and kinocilia on the apical surface of hair cells. Our study thus establishes a dedicated role of the miR-183/96/182 cluster in driving the terminal differentiation of multiple sensory receptor cells.

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18

Stergiou, Ioanna E., and Efstathia K. Kapsogeorgou. "Autophagy and Metabolism in Normal and Malignant Hematopoiesis." International Journal of Molecular Sciences 22, no. 16 (August 9, 2021): 8540. http://dx.doi.org/10.3390/ijms22168540.

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The hematopoietic system relies on regulation of both metabolism and autophagy to maintain its homeostasis, ensuring the self-renewal and multipotent differentiation potential of hematopoietic stem cells (HSCs). HSCs display a distinct metabolic profile from that of their differentiated progeny, while metabolic rewiring from glycolysis to oxidative phosphorylation (OXPHOS) has been shown to be crucial for effective hematopoietic differentiation. Autophagy-mediated regulation of metabolism modulates the distinct characteristics of quiescent and differentiating hematopoietic cells. In particular, mitophagy determines the cellular mitochondrial content, thus modifying the level of OXPHOS at the different differentiation stages of hematopoietic cells, while, at the same time, it ensures the building blocks and energy for differentiation. Aberrations in both the metabolic status and regulation of the autophagic machinery are implicated in the development of hematologic malignancies, especially in leukemogenesis. In this review, we aim to investigate the role of metabolism and autophagy, as well as their interconnections, in normal and malignant hematopoiesis.

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19

Henrard, Marc. "Adjoint algorithmic differentiation: calibration and implicit function theorem." Journal of Computational Finance 17, no. 4 (June 2014): 37–47. http://dx.doi.org/10.21314/jcf.2014.284.

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20

Baeza-Raja, Bernat, та Pura Muñoz-Cánoves. "p38 MAPK-induced Nuclear Factor-κB Activity Is Required for Skeletal Muscle Differentiation: Role of Interleukin-6". Molecular Biology of the Cell 15, № 4 (квітень 2004): 2013–26. http://dx.doi.org/10.1091/mbc.e03-08-0585.

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p38 MAPK and nuclear factor-κB (NF-κB) signaling pathways have been implicated in the control of skeletal myogenesis. However, although p38 is recognized as a potent activator of myoblast differentiation, the role of NF-κB remains controversial. Here, we show that p38 is activated only in differentiating myocytes, whereas NF-κB activity is present both in proliferation and differentiation stages. NF-κB activation was found to be dependent on p38 activity during differentiation, being NF-κB an effector of p38, thus providing a novel mechanism for the promyogenic effect of p38. Activation of p38 in C2C12 cells induced the activity of NF-κB, in a dual way: first, by reducing IκBα levels and inducing NF-κB-DNA binding activity and, second, by potentiating the transactivating activity of p65-NF-κB. Finally, we show that interleukin (IL)-6 expression is induced in C2C12 differentiating myoblasts, in a p38- and NF-κB-dependent manner. Interference of IL-6 mRNA reduced, whereas its overexpression increased, the extent of myogenic differentiation; moreover, addition of IL-6 was able to rescue significantly the negative effect of NF-κB inhibition on this process. This study provides the first evidence of a crosstalk between p38 MAPK and NF-κB signaling pathways during myogenesis, with IL-6 being one of the effectors of this promyogenic mechanism.

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21

Lemercier, Claudie, Kym Duncliffe, Isabelle Boibessot, Hui Zhang, André Verdel, Dimitar Angelov, and Saadi Khochbin. "Involvement of Retinoblastoma Protein and HBP1 in Histone H10 Gene Expression." Molecular and Cellular Biology 20, no. 18 (September 15, 2000): 6627–37. http://dx.doi.org/10.1128/mcb.20.18.6627-6637.2000.

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ABSTRACT The histone H10-encoding gene is expressed in vertebrates in differentiating cells during the arrest of proliferation. In the H10 promoter, a specific regulatory element, which we named the H4 box, exhibits features which implicate a role in mediating H10 gene expression in response to both differentiation and cell cycle control signals. For instance, within the linker histone gene family, the H4 box is found only in the promoters of differentiation-associated subtypes, suggesting that it is specifically involved in differentiation-dependent expression of these genes. In addition, an element nearly identical to the H4 box is conserved in the promoters of histone H4-encoding genes and is known to be involved in their cell cycle-dependent expression. The transcription factors interacting with the H10 H4 box were therefore expected to link differentiation-dependent expression of H10 to the cell cycle control machinery. The aim of this work was to identify such transcription factors and to obtain information concerning the regulatory pathway involved. Interestingly, our cloning strategy led to the isolation of a retinoblastoma protein (RB) partner known as HBP1. HBP1, a high-mobility group box transcription factor, interacted specifically with the H10H4 box and moreover was expressed in a differentiation-dependent manner. We also showed that the HBP1-encoding gene is able to produce different forms of HBP1. Finally, we demonstrated that both HBP1 and RB were involved in the activation of H10 gene expression. We therefore propose that HBP1 mediates a link between the cell cycle control machinery and cell differentiation signals. Through modulating the expression of specific chromatin-associated proteins such as histone H10, HBP1 plays a vital role in chromatin remodeling events during the arrest of cell proliferation in differentiating cells.

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22

Sarkar, Sanjukta, Anita Petiot, Andrew Copp, Patrizia Ferretti, and Peter Thorogood. "FGF2 promotes skeletogenic differentiation of cranial neural crest cells." Development 128, no. 11 (June 1, 2001): 2143–52. http://dx.doi.org/10.1242/dev.128.11.2143.

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The cranial neural crest gives rise to most of the skeletal tissues of the skull. Matrix-mediated tissue interactions have been implicated in the skeletogenic differentiation of crest cells, but little is known of the role that growth factors might play in this process. The discovery that mutations in fibroblast growth factor receptors (FGFRs) cause the major craniosynostosis syndromes implicates FGF-mediated signalling in the skeletogenic differentiation of the cranial neural crest. We now show that, in vitro, mesencephalic neural crest cells respond to exogenous FGF2 in a dose-dependent manner, with 0.1 and 1 ng/ml causing enhanced proliferation, and 10 ng/ml inducing cartilage differentiation. In longer-term cultures, both endochondral and membrane bone are formed. FGFR1, FGFR2 and FGFR3 are all detectable by immunohistochemistry in the mesencephalic region, with particularly intense expression at the apices of the neural folds from which the neural crest arises. FGFRs are also expressed by subpopulations of neural crest cells in culture. Collectively, these findings suggest that FGFs are involved in the skeletogenic differentiation of the cranial neural crest.

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23

Imakawa, Kazuhiko, Pramod Dhakal, Kaiyu Kubota, Kazuya Kusama, Damayanti Chakraborty, M. A. Karim Rumi, and Michael J Soares. "CITED2 modulation of trophoblast cell differentiation: insights from global transcriptome analysis." Reproduction 151, no. 5 (May 2016): 509–16. http://dx.doi.org/10.1530/rep-15-0555.

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Trophoblast stem (TS) cells possess the capacity to differentiate along a multi-lineage pathway yielding several specialized cell types. The regulatory network controlling trophoblast cell differentiation is poorly understood. Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain, 2 (CITED2) has been implicated in the regulation of placentation; however, we know little about how CITED2 acts to influence trophoblast cells. Rat Rcho-1 TS cells can be manipulated to proliferate or differentiate into specialized trophoblast lineages and are an excellent model for investigating trophoblast differentiation. CITED2 transcript and protein showed a robust induction during Rcho-1 TS cell differentiation. We used an shRNA knockdown approach to disrupt CITED2 expression in order to investigate its involvement in trophoblast cell differentiation. RNA-sequencing was used to examine the impact of CITED2 on trophoblast cell differentiation. CITED2 disruption affected the differentiating trophoblast cell transcriptome. CITED2 possessed a prominent role in the regulation of cell differentiation with links to several signal transduction pathways and to hypoxia-regulated and coagulation processes. In summary, our findings indicate that CITED2 contributes to the regulation of trophoblast cell differentiation.Reproduction (2016) 151 1–8

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24

Kandeel, Refat. "Learners' common errors in implicit differentiation: An analytical study." Journal of Educational Research and Reviews 9, no. 7 (July 22, 2021): 198–207. http://dx.doi.org/10.33495/jerr_v9i7.21.125.

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The purpose of this study is to analyze learners' errors in implicit differentiation and identify common errors committed by 20% or more of Common First Year learners (117 Male) at King Saud University. The researcher prepared a test in implicit differentiation consisting of seven various questions covering almost all ideas of implicit differentiation contained in the textbook (Differential Calculus Math101). By analyzing the learners’ answers, the researcher concluded two types of learners’ common errors, namely Algebra Errors (AE) and Calculus Errors (CE). Algebra Errors appeared when learners isolated the common factor, collected similar terms, simplified Algebra fractions, multiplied Algebra terms, dealt with exponentials and roots functions, and found , and Calculus Errors that appeared when learners applied the Chain rule, applied a multiplication rule, found the derivative of any constant, and differentiated functions. Keywords: Implicit differentiation, functions, common errors.

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25

Kim, Ji-Sun, Chang-Hoon Choi, Sun-Young Jeong, and Sa-Ouk Kang. "1P461 The homeobox-containing protein, Hbx3 is implicated in tip formation and prespore differentiation in Dictyostelium discoideum(21. Development and differentiation,Poster Session,Abstract,Meeting Program of EABS &BSJ 2006)." Seibutsu Butsuri 46, supplement2 (2006): S262. http://dx.doi.org/10.2142/biophys.46.s262_1.

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26

Đorđević, Miroslav. "CONSTITUTIONAL DETERMINATION OF THE ELECTORAL SYSTEM AND THE COUNTRIES OF FORMER YUGOSLAVIA." Strani pravni život 61, no. 4 (December 31, 2017): 181–97. http://dx.doi.org/10.56461/spz17412d.

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The author analyses the constitutional determination of the electoral system, its different manifestations and consequences, hence questions if they should find their place within material constitutions. Comparative constitutional examples show both theoretical and practical ﬂaws of such determination, as both explicit and implicit prediction has more drawbacks than advantages. After explanation and differentiation of related key concepts with comparative examples, the author focuses on former Yugoslav countries that display a variety of possible solutions. Inter alia, he finds that the Serbian constitution implicitly determines the proportional electoral system and advocates future revision of the norms in question, since the present solution can be considered as the least favourable.

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Mohd Zawawi, Iskandar Shah, Zarina Bibi Ibrahim, and Khairil Iskandar Othman. "Derivation of Diagonally Implicit Block Backward Differentiation Formulas for Solving Stiff Initial Value Problems." Mathematical Problems in Engineering 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/179231.

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The diagonally implicit 2-point block backward differentiation formulas (DI2BBDF) of order two, order three, and order four are derived for solving stiff initial value problems (IVPs). The stability properties of the derived methods are investigated. The implementation of the method using Newton iteration is also discussed. The performance of the proposed methods in terms of maximum error and computational time is compared with the fully implicit block backward differentiation formulas (FIBBDF) and fully implicit block extended backward differentiation formulas (FIBEBDF). The numerical results show that the proposed method outperformed both existing methods.

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28

Mackens, W. "Numerical differentiation of implicitly defined space curves." Computing 41, no. 3 (September 1989): 237–60. http://dx.doi.org/10.1007/bf02259095.

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29

Ezratty, Ellen J., H. Amalia Pasolli, and Elaine Fuchs. "A Presenilin-2–ARF4 trafficking axis modulates Notch signaling during epidermal differentiation." Journal of Cell Biology 214, no. 1 (June 27, 2016): 89–101. http://dx.doi.org/10.1083/jcb.201508082.

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How primary cilia impact epidermal growth and differentiation during embryogenesis is poorly understood. Here, we show that during skin development, Notch signaling occurs within the ciliated, differentiating cells of the first few suprabasal epidermal layers. Moreover, both Notch signaling and cilia disappear in the upper layers, where key ciliary proteins distribute to cell–cell borders. Extending this correlation, we find that Presenilin-2 localizes to basal bodies/cilia through a conserved VxPx motif. When this motif is mutated, a GFP-tagged Presenilin-2 still localizes to intercellular borders, but basal body localization is lost. Notably, in contrast to wild type, this mutant fails to rescue epidermal differentiation defects seen upon Psen1 and 2 knockdown. Screening components implicated in ciliary targeting and polarized exocytosis, we provide evidence that the small GTPase ARF4 is required for Presenilin basal body localization, Notch signaling, and subsequent epidermal differentiation. Collectively, our findings raise the possibility that ARF4-dependent polarized exocytosis acts through the basal body–ciliary complex to spatially regulate Notch signaling during epidermal differentiation.

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30

Mulligan, Neil W. "Differentiating Between Conceptual Implicit and Explicit Memory." Psychological Science 23, no. 4 (March 14, 2012): 404–6. http://dx.doi.org/10.1177/0956797611433335.

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31

Johansen, Simone, Sofie Traynor, Malene Laage Ebstrup, Mikkel Green Terp, Christina Bøg Pedersen, Henrik Jørn Ditzel, and Morten Frier Gjerstorff. "ZBED1 Regulates Genes Important for Multiple Biological Processes of the Placenta." Genes 13, no. 1 (January 12, 2022): 133. http://dx.doi.org/10.3390/genes13010133.

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The transcription factor ZBED1 is highly expressed in trophoblast cells, but its functions in the processes of trophoblast and placental biology remain elusive. Here, we characterized the role of ZBED1 in trophoblast cell differentiation using an in vitro BeWo cell model. We demonstrate that ZBED1 is enhanced in its expression early after forskolin-induced differentiation of BeWo cells and regulates many of the genes that are differentially expressed as an effect of forskolin treatment. Specifically, genes encoding markers for the differentiation of cytotrophoblast into syncytiotrophoblast and factors essential for trophoblast cell fusion and invasion were negatively regulated by ZBED1, indicating that ZBED1 might be important for maintaining a steady pool of cytotrophoblast cells. In addition, ZBED1 affected genes involved in the regulation of trophoblast cell survival and apoptosis, in agreement with the observed increase in apoptosis upon knockdown of ZBED1 in forskolin-treated BeWo cells. In addition, genes implicated in the differentiation, recruitment, and function of innate immune cells by the placenta were affected by ZBED1, further suggesting a role for this protein in the regulation of maternal immune tolerance. In conclusion, our study implicates ZBED1 in major biological processes of placental biology.

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32

Rezende-Melo, C. A., A. L. Caldeira-Brant, A. L. Drumond-Bock, G. M. Buchold, G. Shetty, F. R. C. L. Almeida, M. M. Matzuk, et al. "Spermatogonial asynchrony in Tex14 mutant mice lacking intercellular bridges." Reproduction 160, no. 2 (August 2020): 205–15. http://dx.doi.org/10.1530/rep-20-0118.

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The existence of cytoplasmic passages between germ cells and their potential function in the control of the spermatogenic process has long been an intriguing question. Evidence of the important role of such structures, known as intercellular bridges (ICB), in spermatogenesis has been implicated by the failure of spermatogenesis in testis-expressed gene 14 (Tex14) mutant mice, which lack the ICBs, to progress past the pachytene spermatocyte stage. Using these Tex14 mutants, the present study evaluated, for the first time, the behavior and synchrony of the spermatogonial lineage in the absence of ICBs. Our data suggest that the absence of these cytoplasmic connections between cells affects the expansion of the undifferentiated type A (Aundiff) spermatogonia compartment and their transition to A1, resulting in a significant numerical reduction of differentiating A1 spermatogonia, but did not interfere with cell amplification during subsequent mitotic steps of differentiating spermatogonia from A1 through intermediate (In). However, beginning at the type B spermatogonia, the synchrony of differentiation was impaired as some cells showed delayed differentiation compared to their behavior in a normal seminiferous epithelium cycle. Thus although spermatogonial development is able to proceed, in the absence of ICBs in Tex14−/− mutants, the yield of cells, specific steps of differentiation, the synchrony of the cell kinetics, and the subsequent progression in meiosis are quantitatively lower than normal.

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33

Nikishin, Evgenii, Romina Abachi, Rishabh Agarwal, and Pierre-Luc Bacon. "Control-Oriented Model-Based Reinforcement Learning with Implicit Differentiation." Proceedings of the AAAI Conference on Artificial Intelligence 36, no. 7 (June 28, 2022): 7886–94. http://dx.doi.org/10.1609/aaai.v36i7.20758.

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The shortcomings of maximum likelihood estimation in the context of model-based reinforcement learning have been highlighted by an increasing number of papers. When the model class is misspecified or has a limited representational capacity, model parameters with high likelihood might not necessarily result in high performance of the agent on a downstream control task. To alleviate this problem, we propose an end-to-end approach for model learning which directly optimizes the expected returns using implicit differentiation. We treat a value function that satisfies the Bellman optimality operator induced by the model as an implicit function of model parameters and show how to differentiate the function. We provide theoretical and empirical evidence highlighting the benefits of our approach in the model misspecification regime compared to likelihood-based methods.

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34

Weber, MC, and ML Tykocinski. "Bone marrow stromal cell blockade of human leukemic cell differentiation." Blood 83, no. 8 (April 15, 1994): 2221–29. http://dx.doi.org/10.1182/blood.v83.8.2221.bloodjournal8382221.

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Bone marrow (BM) stromal cell inhibition of leukemic cell differentiation was studied in cellular coculture experiments. In coculture, a significant percentage of cells from the human myeloid leukemic cell lines HL-60, PLB-985, and K562 adhere to fibroblastic KM- 102 BM stromal cells. A sensitive two-color immunofluorescence assay was developed to monitor stromal cellular effects upon leukemic cell differentiation. After chemical induction with 1 alpha,25- dihydroxyvitamin D3, strongly adherent HL-60 and PLB-985 cells were inhibited from differentiating into more mature monocytic cells, as measured by the monocytic surface marker CD14. In contrast, loosely adherent and nonadherent HL-60 and PLB-985 leukemic cells in the same cocultures, as well as both adherent and nonadherent K562 cells induced with phorbol ester, were not blocked in their capacity to differentiate. Scanning electron microscopy and intercellular dye transfer experiments correlated intimate stromal cell/leukemic cell interaction and intercellular communication with the blockade of leukemic cell differentiation. These studies indicate that there is significant variability among leukemic lines with respect to the nature of their adhesion to stromal cells. Moreover, the data implicate gap- junction formation as a potentially significant event in stromal cell- mediated leukemic cell regulation.

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35

SMITH, Conrad, Kuichun ZHU, Anita MERRITT, Rhian PICTON, Denise YOUNGS, David GARROD, and Martyn CHIDGEY. "Regulation of desmocollin gene expression in the epidermis: CCAAT/enhancer-binding proteins modulate early and late events in keratinocyte differentiation." Biochemical Journal 380, no. 3 (June 15, 2004): 757–65. http://dx.doi.org/10.1042/bj20040077.

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Desmocollins (Dscs) are desmosomal cadherins that exhibit differentiation-specific patterns of expression in the epidermis. Dsc3 expression is strongest in basal cell layers, whereas Dsc1 is largely confined to upper, terminally differentiating strata. To understand better the processes by which Dsc expression is regulated in the epidermis, we have isolated Dsc3 and Dsc1 5´-flanking DNAs and analysed their activity in primary keratinocytes. In the present study, we found that transcription factors of the CCAAT/enhancer-binding protein family play a role in the regulation of expression of both Dscs and, in so doing, implicate this class of transcription factors in both early and late events in keratinocyte differentiation. We show that Dscs are differentially regulated by C/EBP (CCAAT/enhancer-binding protein) family members, with Dsc3 expression being activated by C/EBPβ but not C/EBPα, and the reverse being the case for Dsc1. Expression of both Dscs is activated by another family member, C/EBPδ. These results show for the first time how desmosomal cadherin gene expression is regulated and provide a mechanism for the control of other differentiation-specific genes in the epidermis.

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36

Jane, Derek T., Leslie C. Morvay, Francis Allen, Bonnie F. Sloane, and Michael J. Dufresne. "Selective inhibition of cathepsin B with cell-permeable CA074Me negatively affects L6 rat myoblast differentiation." Biochemistry and Cell Biology 80, no. 4 (August 1, 2002): 457–65. http://dx.doi.org/10.1139/o02-134.

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Active cathepsin B, in concert with other cellular proteases, has been implicated in the catabolic restructuring associated with myotube formation during skeletal myoblast cell differentiation (i.e., myogenesis). We have examined this role in differentiating myoblasts using the cell-permeable, cathepsin B selective inhibitor CA074Me. Cathepsin B activity levels in differentiating L6 rat myoblasts treated with CA074Me were significantly lower than levels in control myoblasts. Inhibition of cathepsin B activity by CA074Me occurred at each stage of differentiation and was dose related. Myotube size and number and induced levels of fusion-related creatine phosphokinase activity and myosin heavy-chain protein were reduced from 30 to 50% in CA074Me-treated myoblasts. These reductions were also dose related. In contrast, CA074Me did not affect levels of myogenin, an early marker of myogenesis, or levels of cathepsin L type and myokinase activities, two nonspecific enzymes. The negative effects associated with CA074Me were reversed when the drug was removed. Collectively, these data suggest that active cathepsin B plays a role in myoblastmyoblast fusion and consequently may be necessary for the complete expression of those genes associated with the fusion process.Key words: cathepsin B, CA074Me, myogenesis.

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37

Norton, J. D. "ID helix-loop-helix proteins in cell growth, differentiation and tumorigenesis." Journal of Cell Science 113, no. 22 (November 15, 2000): 3897–905. http://dx.doi.org/10.1242/jcs.113.22.3897.

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The ubiquitously expressed family of ID helix-loop-helix (HLH) proteins function as dominant negative regulators of basic HLH (bHLH) transcriptional regulators that drive cell lineage commitment and differentiation in metazoa. Recent data from cell line and in vivo studies have implicated the functions of ID proteins in other cellular processes besides negative regulation of cell differentiation. ID proteins play key roles in the regulation of lineage commitment, cell fate decisions and in the timing of differentiation during neurogenesis, lymphopoiesis and neovascularisation (angiogenesis). They are essential for embryogenesis and for cell cycle progression, and they function as positive regulators of cell proliferation. ID proteins also possess pro-apoptotic properties in a variety of cell types and function as cooperating or dominant oncoproteins in immortalisation of rodent and human cells and in tumour induction in Id-transgenic mice. In several human tumour types, the expression of ID proteins is deregulated, and loss- and gain-of-function studies implicate ID functions in the regulation of tumour growth, vascularisation, invasiveness and metastasis. More recent biochemical studies have also revealed an emerging ‘molecular promiscuity’ of mammalian ID proteins: they directly interact with and modulate the activities of several other families of transcriptional regulator, besides bHLH proteins.

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38

Olguin, Hugo C., Zhihong Yang, Stephen J. Tapscott, and Bradley B. Olwin. "Reciprocal inhibition between Pax7 and muscle regulatory factors modulates myogenic cell fate determination." Journal of Cell Biology 177, no. 5 (June 4, 2007): 769–79. http://dx.doi.org/10.1083/jcb.200608122.

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Postnatal growth and regeneration of skeletal muscle requires a population of resident myogenic precursors named satellite cells. The transcription factor Pax7 is critical for satellite cell biogenesis and survival and has been also implicated in satellite cell self-renewal; however, the underlying molecular mechanisms remain unclear. Previously, we showed that Pax7 overexpression in adult primary myoblasts down-regulates MyoD and prevents myogenin induction, inhibiting myogenesis. We show that Pax7 prevents muscle differentiation independently of its transcriptional activity, affecting MyoD function. Conversely, myogenin directly affects Pax7 expression and may be critical for Pax7 down-regulation in differentiating cells. Our results provide evidence for a cross-inhibitory interaction between Pax7 and members of the muscle regulatory factor family. This could represent an additional mechanism for the control of satellite cell fate decisions resulting in proliferation, differentiation, and self-renewal, necessary for skeletal muscle maintenance and repair.

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39

Alesiani, Francesco. "Implicit Bilevel Optimization: Differentiating through Bilevel Optimization Programming." Proceedings of the AAAI Conference on Artificial Intelligence 37, no. 12 (June 26, 2023): 14683–91. http://dx.doi.org/10.1609/aaai.v37i12.26716.

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Bilevel Optimization Programming is used to model complex and conflicting interactions between agents, for example in Robust AI or Privacy preserving AI. Integrating bilevel mathematical programming within deep learning is thus an essential objective for the Machine Learning community. Previously proposed approaches only consider single-level programming. In this paper, we extend existing single-level optimization programming approaches and thus propose Differentiating through Bilevel Optimization Programming (BiGrad) for end-to-end learning of models that use Bilevel Programming as a layer. BiGrad has wide applicability and can be used in modern machine learning frameworks. BiGrad is applicable to both continuous and combinatorial Bilevel optimization problems. We describe a class of gradient estimators for the combinatorial case which reduces the requirements in terms of computation complexity; for the case of the continuous variable, the gradient computation takes advantage of the push-back approach (i.e. vector-jacobian product) for an efficient implementation. Experiments show that the BiGrad successfully extends existing single-level approaches to Bilevel Programming.

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40

Thiemann, Renee F., Scott Varney, Nicholas Moskwa, John Lamar, Melinda Larsen, and Susan E. LaFlamme. "Regulation of myoepithelial differentiation." PLOS ONE 17, no. 5 (May 26, 2022): e0268668. http://dx.doi.org/10.1371/journal.pone.0268668.

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The salivary gland can be permanently impaired by radiation treatment for head and neck cancers. Efforts at tissue regeneration have focused on saliva-producing acinar cells. However, myoepithelial cells are also critical to gland function, but mechanisms that regulate their differentiation are poorly defined. To study myoepithelial differentiation, we employed mSG-PAC1 murine salivary gland epithelial cells. We demonstrate that mSG-PAC1 spheroids exhibit phenotypic plasticity between pro-acinar and myoepithelial cell fates. Increased expression of pro-acinar/acinar or myoepithelial RNAs was identified from spheroids cultured under different media conditions by microarray followed by gene-set enrichment analysis. Spheroids cultured with different medium components expressed proteins typical of either acinar or myoepithelial cells, as detected by immunocytochemistry. We demonstrate that the pattern of TAZ expression in the epithelial compartment of the differentiating murine salivary gland correlates with the expression of the myoepithelial marker alpha-SMA, as is the case for TAZ expression in mSG-PAC1 spheroids. Our analysis also indicates that YAP/TAZ target genes are upregulated together with myoepithelial markers. Importantly, siRNA targeting of TAZ expression in mSG-PAC1 spheroids diminished the expression of myoepithelial markers. Our results in this in vitro cell model implicate TAZ signaling in myoepithelial differentiation.

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41

Weber, MC, and ML Tykocinski. "Bone marrow stromal cell blockade of human leukemic cell differentiation." Blood 83, no. 8 (April 15, 1994): 2221–29. http://dx.doi.org/10.1182/blood.v83.8.2221.2221.

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Abstract Bone marrow (BM) stromal cell inhibition of leukemic cell differentiation was studied in cellular coculture experiments. In coculture, a significant percentage of cells from the human myeloid leukemic cell lines HL-60, PLB-985, and K562 adhere to fibroblastic KM- 102 BM stromal cells. A sensitive two-color immunofluorescence assay was developed to monitor stromal cellular effects upon leukemic cell differentiation. After chemical induction with 1 alpha,25- dihydroxyvitamin D3, strongly adherent HL-60 and PLB-985 cells were inhibited from differentiating into more mature monocytic cells, as measured by the monocytic surface marker CD14. In contrast, loosely adherent and nonadherent HL-60 and PLB-985 leukemic cells in the same cocultures, as well as both adherent and nonadherent K562 cells induced with phorbol ester, were not blocked in their capacity to differentiate. Scanning electron microscopy and intercellular dye transfer experiments correlated intimate stromal cell/leukemic cell interaction and intercellular communication with the blockade of leukemic cell differentiation. These studies indicate that there is significant variability among leukemic lines with respect to the nature of their adhesion to stromal cells. Moreover, the data implicate gap- junction formation as a potentially significant event in stromal cell- mediated leukemic cell regulation.

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42

Berkowska, Klaudia, Aoife Corcoran, Małgorzata Grudzień, Agnieszka Jakuszak, Michał Chodyński, Andrzej Kutner, and Ewa Marcinkowska. "Investigating the Role of VDR and Megalin in Semi-Selectivity of Side-Chain Modified 19-nor Analogs of Vitamin D." International Journal of Molecular Sciences 20, no. 17 (August 26, 2019): 4183. http://dx.doi.org/10.3390/ijms20174183.

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1,25-dihydroxyvitamin D3 (1,25D3) is implicated in many cellular functions, including cell proliferation and differentiation, thus exerting potential antitumor effects. A major limitation for therapeutic use of 1,25D3 are potent calcemic activities. Therefore, synthetic analogs of 1,25D3 for use in anticancer therapy should retain cell differentiating potential, with calcemic activity being reduced. To obtain this goal, the analogs should effectively activate transcription of genes responsible for cell differentiation, leaving the genes responsible for calcium homeostasis less active. In order to better understand this phenomenon, we selected a series of structurally related 19-nor analogs of 1,25D (PRI-5100, PRI-5101, PRI-5105, and PRI-5106) and tested their activities in blood cells and in cells connected to calcium homeostasis. Affinities of analogs to recombinant vitamin D receptor (VDR) protein were not correlated to their pro-differentiating activities. Moreover, the pattern of transcriptional activities of the analogs was different in cell lines originating from various vitamin D-responsive tissues. We thus hypothesized that receptors which participate in transport of the analogs to the cells might contribute to the observed differences. In order to study this hypothesis, we produced renal cells with knock-out of the megalin gene. Our results indicate that megalin has a minor effect on semi-selective activities of vitamin D analogs.

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43

Dacwag, Caroline S., Yasuyuki Ohkawa, Sharmistha Pal, Saïd Sif, and Anthony N. Imbalzano. "The Protein Arginine Methyltransferase Prmt5 Is Required for Myogenesis because It Facilitates ATP-Dependent Chromatin Remodeling." Molecular and Cellular Biology 27, no. 1 (October 16, 2006): 384–94. http://dx.doi.org/10.1128/mcb.01528-06.

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ABSTRACT Skeletal muscle differentiation requires the coordinated activity of transcription factors, histone modifying enzymes, and ATP-dependent chromatin remodeling enzymes. The type II protein arginine methyltransferase Prmt5 symmetrically dimethylates histones H3 and H4 and numerous nonchromatin proteins, and prior work has implicated Prmt5 in transcriptional repression. Here we demonstrate that MyoD-induced muscle differentiation requires Prmt5. One of the first genes activated during differentiation encodes the myogenic regulator myogenin. Prmt5 and dimethylated H3R8 (histone 3 arginine 8) are localized at the myogenin promoter in differentiating cells. Modification of H3R8 required Prmt5, and reduction of Prmt5 resulted in the abrogation of promoter binding by the Brg1 ATPase-associated with the SWI/SNF chromatin remodeling enzymes and all subsequent events associated with gene activation, including increases in chromatin accessibility and stable binding by MyoD. Prmt5 and dimethylated H3R8 were also associated with the myogenin promoter in activated satellite cells isolated from muscle tissue, further demonstrating the physiological relevance of these observations. The data indicate that Prmt5 facilitates myogenesis because it is required for Brg1-dependent chromatin remodeling and gene activation at a locus essential for differentiation. We therefore conclude that a histone modifying enzyme is necessary to permit an ATP-dependent chromatin remodeling enzyme to function.

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44

Fox, Shaul, and George C. Thornton. "Implicit Distribution Theory: The Influence of Cognitive Representation of Differentiation on Actual Ratings." Perceptual and Motor Skills 76, no. 1 (February 1993): 259–76. http://dx.doi.org/10.2466/pms.1993.76.1.259.

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The article presents the idea that individuals possess three main mental representations of distributions regarding group categories: trait differentiation, person differentiation, and the interaction between trait and person variabilities. These representations are called Implicit Distribution Theory. The study examined the stability of these distributional notions, their interrelationships, and their relation to subsequent judgments. The implicit distribution theories of 89 students regarding university professors were captured twice by asking them to distribute 100 imaginary professors on 5-point scales for each of 13 attributes commonly used in professors' evaluations. Several weeks afterwards 50 of these subjects rated four known professors on the same attributes. Test-retest reliability was quite high for trait and person differentiation, and these constructs were independent. Person differentiation significantly predicted parallel features in raters' judgments of actual performance, while trait differentiation yielded significant correlations with most distribution measures of actual ratings. The findings are related to the concepts of mental representation, cognitive complexity, and cognitive biases in person perception as well as to their potential applications in organizational settings.

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45

Zumwalt, K. W., and M. E. M. El-Sayed. "Design Sensitivity Derivatives for Isoparametric Elements as an Integrated Part of Finite Element Analysis." Journal of Mechanical Design 115, no. 3 (September 1, 1993): 671–74. http://dx.doi.org/10.1115/1.2919243.

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This work presents an approach for incorporating design sensitivity calculations into the finite element analysis. The formulation depends on the implicit differentiation approach and requires few additional calculations to obtain the design sensitivity derivatives. The implicit differentiation approach is developed and implemented to calculate the design sensitivities for continuum and structural isoparametric elements. To demonstrate the developed approach test cases using different structural and continuum element types are presented.

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46

Bègue, Laurent, and Thémistoklis Apostolidis. "Implicit Theories of Reality and Social Differentiation From Gay People." Journal of Social Psychology 141, no. 1 (February 2001): 132–34. http://dx.doi.org/10.1080/00224540109600533.

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47

Belyaev, Alexander. "Implicit Image Differentiation and Filtering with Applications to Image Sharpening." SIAM Journal on Imaging Sciences 6, no. 1 (January 2013): 660–79. http://dx.doi.org/10.1137/12087092x.

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48

Yatheendhar, M., and A. D. Belegundu. "Analytical shape sensitivity by implicit differentiation for general velocity fields." Computers & Structures 46, no. 4 (February 1993): 617–23. http://dx.doi.org/10.1016/0045-7949(93)90390-y.

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49

Borji, Vahid, and Rafael Martínez-Planell. "On students’ understanding of implicit differentiation based on APOS theory." Educational Studies in Mathematics 105, no. 2 (October 2020): 163–79. http://dx.doi.org/10.1007/s10649-020-09991-y.

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50

Wang, Xuan, Diana Bolotin, David H. Chu, Lisa Polak, Trevor Williams та Elaine Fuchs. "AP-2α: a regulator of EGF receptor signaling and proliferation in skin epidermis". Journal of Cell Biology 172, № 3 (30 січня 2006): 409–21. http://dx.doi.org/10.1083/jcb.200510002.

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AP-2 transcription factors have been implicated in epidermal biology, but their functional significance has remained elusive. Using conditional knockout technology, we show that AP-2α is essential for governing the balance between growth and differentiation in epidermis. In vivo, epidermis lacking AP-2α exhibits elevated expression of the epidermal growth factor receptor (EGFR) in the differentiating layers, resulting in hyperproliferation when the receptors are activated. Chromatin immunoprecipitation and promoter activity assays identify EGFR as a direct target gene for AP-2α repression, and, in the absence of AP-2α, this is manifested primarily in excessive EGF-dependent phosphoinositol-3 kinase/Akt activity. Together, our findings unveil a hitherto unrecognized repressive role for AP-2α in governing EGFR gene transcription as cells exit the basal layer and withdraw from the cell cycle. These results provide insights into why elevated AP-2α levels are often associated with terminal differentiation and why tumor cells often display reduced AP-2α and elevated EGFR proteins.

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