Academic literature on the topic 'Intra-side dispersion'

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Journal articles on the topic "Intra-side dispersion"

1

Gavrikov, Vladimir L., Alexey I. Fertikov, Ruslan A. Sharafutdinov, and Eugene A. Vaganov. "Early- and Latewood vs. Stem Asymmetry: Which Is More Important for Dendrochemistry in Scots Pine?" Forests 16, no. 3 (2025): 493. https://doi.org/10.3390/f16030493.

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For dendrochemical research, it may be important to be aware of the effects of stem asymmetry and the intra-ring structure because these may introduce unwanted dispersion in the results. In dendrochemical studies, separate analysis of the elemental content of early- and latewood is rare. Also, explanations of how the elemental content may relate to stem asymmetry originating from conditions at the edges of contrasting environments are largely lacking in these studies. The purpose of the current study was to estimate the impact of the seasonal tree ring structure and stem asymmetry on the distribution of elements in tree stems. The study population was a plantation of Scots pine (Pinus sylvestris L.) at an afforestation experiment area, with the sample trees being at the edge of the stand, causing strong crown asymmetry. Six pine trees were cored through the thickness from the maximal crown side (max-side) to the minimal crown side (min-side), and the cores were subsequently scanned through an Itrax Multiscanner unit. The count rates of aluminum (Al), silicon (Si), phosphorus (P), sulfur (S), chlorine (Cl), calcium (Ca), iron (Fe), copper (Cu), zinc (Zn), and strontium (Sr) in the tree rings from 1990 to 2022 were analyzed. A group of elements (Al, Si, P, S, and Cl) tended to consistently concentrate on the min-side, both in early- and latewood, the difference being most significant for S and Cl. Regarding early- vs. latewood, Al, Si, P, S, Cl, Cu, and Zn always had lower concentration in earlywood than in latewood, while others (Ca, Fe, and Sr) had lower concentrations in latewood, the relations being consistently significant. Overall, the role of the min- or max-side of the stem in allocation of elements appears to have been weaker that the intra-ring structure (early- and latewood). Some elements such as Al, Si, P, S, Cl, and Ca (in latewood) were often more abundant on the min-side; other elements such as Fe and Sr (in latewood) were often more abundant on the max-side, but these relations were significant only on rare occasions. Intra-ring heterogeneity (in early- and latewood) appears to be more decisive than the asymmetry of the tree stem in regard to the distribution of elements in Scots pine xylem. Nevertheless, tree stems with high and obvious asymmetry should be more extensively explored because a possibility remains that extreme asymmetry does impact the allocation of elements.
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2

Raczyński, Kamil, Andrzej Pihut, Jarosław J. Panek, and Aneta Jezierska. "Competition of Intra- and Intermolecular Forces in Anthraquinone and Its Selected Derivatives." Molecules 26, no. 11 (2021): 3448. http://dx.doi.org/10.3390/molecules26113448.

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Intra- and intermolecular forces competition was investigated in the 9,10-anthraquinone (1) and its derivatives both in vacuo and in the crystalline phase. The 1,8-dihydroxy-9,10-anthraquinone (2) and 1,8-dinitro-4,5-dihydroxy-anthraquinone (3) contain Resonance-Assisted Hydrogen Bonds (RAHBs). The intramolecular hydrogen bonds properties were studied in the electronic ground and excited states employing Møller-Plesset second-order perturbation theory (MP2), Density Functional Theory (DFT) method in its classical formulation as well as its time-dependent extension (TD-DFT). The proton potential functions were obtained via scanning the OH distance and the dihedral angle related to the OH group rotation. The topological analysis was carried out on the basis of theories of Atoms in Molecules (AIM—molecular topology, properties of critical points, AIM charges) and Electron Localization Function (ELF—2D maps showing bonding patterns, calculation of electron populations in the hydrogen bonds). The Symmetry-Adapted Perturbation Theory (SAPT) was applied for the energy decomposition in the dimers. Finally, Car–Parrinello molecular dynamics (CPMD) simulations were performed to shed light onto bridge protons dynamics upon environmental influence. The vibrational features of the OH stretching were revealed using Fourier transformation of the autocorrelation function of atomic velocity. It was found that the presence of OH and NO2 substituents influenced the geometric and electronic structure of the anthraquinone moiety. The AIM and ELF analyses showed that the quantitative differences between hydrogen bonds properties could be neglected. The bridged protons are localized on the donor side in the electronic ground state, but the Excited-State Intramolecular Proton Transfer (ESIPT) was noticed as a result of the TD-DFT calculations. The hierarchy of interactions determined by SAPT method indicated that weak hydrogen bonds play modifying role in the organization of these crystal structures, but primary ordering factor is dispersion. The CPMD crystalline phase results indicated bridged proton-sharing in the compound 2.
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3

Mallye, Jean-Baptiste, and Maxime Pelletier. "Les léporidés et les petits carnivores de l'Igue du Gral." Revue de Paléobiologie 43, no. 2 (2024): 353–415. https://doi.org/10.5281/zenodo.13861331.

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Leporids and small carnivores at the Igue du Gral.- This work provides the outcome of the analysis of the remains of Leporidae and small carnivores that were identified at the Igue du Gral. We were able to identify the remains of the mountain hare and brown hare, wild rabbit, red fox and isatis, wolverine, badger, polecat, weasel and ermine. Once the integrity of the bone assemblage had been assessed in relation to the different excavation methods used, we characterised all these taxa from the biological point of view (size, age and sex), the relative conservation of the skeletons and their dislocation, and their distribution in the excavated volume both horizontally and vertically. In the light of these results and the radiocarbon dating carried out, it was possible to propose a biostratigraphy of the deposit and to discuss the palaeoenvironments of this region of Quercy. It was also possible to test the  availability of small game to hunter-gatherers who frequented the region during the Late Palaeolithic.
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4

Suchita, Soham Sarbadhikari, and R. Vijaya. "Spectral broadening due to intra-cavity four-wave mixing at low pump powers in erbium-doped fiber ring laser." International Journal of Modern Physics B 28, no. 12 (2014): 1442008. http://dx.doi.org/10.1142/s0217979214420089.

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In this paper, we present the experimental results of multi-pump-induced four-wave mixing (FWM) in erbium-doped fiber ring laser (EDFRL) in the wavelength range of 1560–1600 nm. The required multiple pumps are generated within the ring cavity by an appropriate choice of the wavelength range of operation with a suitable length of erbium-doped fiber. By introducing the optical nonlinearity with specialty fibers such as the highly nonlinear fiber (HNLF) and dispersion shifted fiber (DSF), FWM processes occurring in the laser are studied at low powers of the pump laser at 980 nm. The prevalent FWM theory is improved to interpret the two-pump and four-pump-induced side band generation in the first- and second-orders, after including the effect of phase mismatch at the wavelengths used in the experiments.
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5

Wesseling, Jelle. "Abstract F1-2: Clonal evolution of DCIS to invasion." Cancer Research 83, no. 5_Supplement (2023): F1–2—F1–2. http://dx.doi.org/10.1158/1538-7445.sabcs22-f1-2.

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Abstract Clonal evolution of DCIS to invasion Ductal carcinoma in situ (DCIS) is the most common form of preinvasive breast cancer and, despite treatment, a small fraction (5-10%) of DCIS patients develop subsequent invasive breast cancer (IBC). If not treated, at least 3 out of 4 women with DCIS will not develop IBC1-3. This implies many women with non-progressive, low-risk DCIS are likely to carry the burden of overtreatment. To solve this DCIS dilemma, two fundamental questions need to be answered. The first question is, how the subsequent IBC is related to the initial DCIS lesion. The second question is how to distinguish high- from low-risk DCIS at the time of diagnosis. This is essential to take well-informed DCIS management decisions, i.e., surgery, followed by radiotherapy in case of breast conserving treatment with or without subsequent endocrine treatment, or test whether active surveillance for low-risk DCIS is safe. How is the subsequent IBC related to the initial DCIS? The high genomic concordance in DNA aberrations between DCIS and IBC suggest that most driver mutations and CNA events are acquired at the earliest stages of DCIS initiation. It has therefore been assumed that most solid tumours arise from a single cell and that the probability of two independent tumours arising from the same tissue is low4-6. However, lineage tracing and genomic studies strongly suggest both direct and independent clonal lineages during the initiation of DCIS and evolution to IBC. In these processes, mammary stem cells have been implicated in DCIS initiation. Role of mammary stem cells in DCIS initiation Lineage tracing mouse model experiments have shown the fate of individual cells and lineages that acquire mutations before a tumour is established7-9. This is also relevant for DCIS initiation10,11, as different pools of MaSCs drive the growth and development of the ductal network and are considered the cell of origin for breast cancers9,10. The ductal trees remain quiescent until puberty, during which extension, branching and termination of terminal end buds (TEBs) leads to its expansion throughout the fat pad7,12,13. Any oncogenic mutation that occurs in a fetal MaSC will spread throughout the ductal network to a large part of the ductal tree, leading to sick lobes9. By contrast, oncogenic mutations acquired by a single MaSC during puberty spread to a smaller number of offspring located in small clusters in a part of the ductal network8,14. Direct lineage models for DCIS progression Direct lineage models postulate that DCIS has a single cell of origin that acquires mutations and progresses to IBC15-18. This is also supported by the high genomic concordance of CNAs and mutations in synchronous DCIS–IBC regions6,15,17,19-21 and the results of a recent large longitudinal study that profiled pure DCIS and recurrent IBC using multiple sequencing techniques, which estimated direct clonal lineages in approximately ~80% of patients18. Two distinct direct lineage models have been proposed: the evolutionary bottleneck model and the multiclonal invasion model. In the evolutionary bottleneckmodel, a single clone (or a limited number of clones) with an invasive genotype is selected and breaks through the basement membrane to migrate into surrounding tissues15,16,22, while other clones are unable to escape the ducts21-28. The multiclonal invasion model posits that most or all subclones can escape the basement membrane, establishing invasive disease6,16,17,20. The multiclonal model has not been studied widely in pure DCIS and recurrent IBC samples. Independent lineage model for DCIS progression DCIS lesions and IBCs can arise from different initiating cells in the same breast independently5,20,29-32. An analysis of sequential DCIS–IBC pairs in a unique, large-scale, in-depth study of 95 matched pure DCIS and recurrent IBC showed that ~20% of the IBC recurrences were indeed clonally unrelated to the primary DCIS18, as is also supported by some mathematical model studies33. The potential role of a field effect IBC can develop in the same breast as an initial DCIS even after treatment, which could be explained by the presence of a field effect34-37. Alternatively, the sick lobe hypothesis proposes that a single lobe harbours first-hit mutations, acquired in utero or during early mammary development37-42. This could also explain the restriction of IBC to the ipsilateral side of the breast39,43,44. Germline mutations may also explain the emergence of independent lineages in DCIS and IBC patients, lowering the threshold for cancer development32,43-46. Convergent evolution model of DCIS progression A third model for the emergence of IBC from DCIS is convergent evolution, in which the same mutations and CNA are selected and expanded during tumour growth such that environmental factors fuel competition between distinct clones and push them towards a similar genotype. Ultimately, two independent clonal lineages from different ancestral cells then happen to share multiple genomic aberrations or driver mutations across regions47-49. Although independent lineages are considered uncommon (~20%) in ipsilateral recurrences, they occur at much higher frequencies in contralateral recurrences (>80%), in which single-nucleotide polymorphism and comparative genomic hybridization microarrays show few (or no) genomic alterations shared in tumours from the contralateral breast cancer18,50,51. How to distinguish high- from low-risk DCIS at the time of diagnosis? The genomic and transcriptomic profile present at the time of DCIS diagnosis may contain crucial information on the risk of progression of DCIS to IBC. Thus far, it has been unclear whether prognostic gene expression markers can be used to separate indolent DCIS from potentially progressive DCIS. To this end, microarrays and RNA-seq have been applied for the comparison of bulk RNA from microdissected DCIS and IBC tissue. In synchronous DCIS–IBC, a limited number of transcriptional differences have been found and the few events discovered often varied extensively across different tumours52-56. Although these differences were strong, the added value of these studies is uncertain as they are often confounded by small sample size, lack of matched receptor status data, and low sample purity. Despite these limitations, these studies have implicated the epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) remodelling pathways as potentially relevant for the progression of DCIS to IBC55-62. We studied two large DCIS cohorts: the Sloane cohort, a prospective breast screening cohort from the UK (median follow-up of 12.5 years), and a Dutch population-based cohort (NKI, median follow-up of 13 years). FFPE tissue specimens from patients with pure primary DCIS after breast-conserving surgery (BCS) +/- RT that did develop a subsequent ipsilateral event (DCIS or invasive) were considered as cases, whereas patients that did not develop any form of recurrence up to the last follow-up or death were considered as controls. We performed copy number analysis (CNA) and RNAseq analysis on 229 cases (149 IBC recurrences and 80 DCIS recurrences) and 344 controls. We classified DCIS into the PAM50 subtypes using RNAseq data which revealed an enrichment of luminal A phenotype in DCIS that did not recur (P = 0.01, Fisher Exact test). No single copy number aberration was more common in cases compared to controls. RNAseq data did not reveal any genes significantly over/under expressed in cases versus controls after false discovery rate (FDR) correction. However, by limiting the analysis to samples that had not had RT and excluding pure DCIS recurrences we developed a penalized Cox model from RNAseq data. The model was trained on weighted samples (to correct for the biased sampling of the case control dataset) from the NKI series with double loop cross validation. Using this predicted hazard ratio, the samples were split into high, medium and low risk quantiles, with a recurrence risk of 20%, 9% and 2.5%, respectively at 5 years (p<0.001, Wald test). The NKI-trained predictor was independently validated in the Sloane No RT cohort (p = 0.02, Wald test). GSEA analysis revealed proliferation hallmarks enriched in the recurrence predictor (FDR = 0.058). The NKI-RNAseq predictor was more predictive of invasive recurrence than PAM50, clinical features (Grade, Her2 and ER) and the 12-gene Oncotype DCIS score (p < 0.001, permutation test using the Wald statistic) in both the NKI and Sloane series. In the methylation analysis, 50 controls were compared with 35 cases. We could identify Variably Methylation Regions (VMRs) and Differentially Methylated Regions (DMRs) between cases and controls. Interestingly, VMRs were enriched in cell adhesion pathways Conclusion The recently acquired knowledge described above on how often the subsequent IBC is directly related to the initial DCIS and on molecular markers predicting the risk of DCIS progression is essential for accurate DCIS risk assessment. This is essential to aid accurate clinical decision making to personalize DCIS management in the near future. References 1. Falk, R. S., Hofvind, S., Skaane, P. & Haldorsen, T. Second events following ductal carcinoma in situ of the breast: a register-based cohort study. Breast Cancer Res Treat 129, 929-938, doi:10.1007/s10549-011-1531-1 (2011). 2. Ryser, M. D. et al. Cancer Outcomes in DCIS Patients Without Locoregional Treatment. Jnci J National Cancer Inst 111, 952-960, doi:10.1093/jnci/djy220 (2019). 3. Maxwell, A. J. et al. Unresected screen detected Ductal Carcinoma in Situ: outcomes of 311 women in the Forget-me–not 2 study. Breast 61, 145-155, doi:10.1016/j.breast.2022.01.001 (2022). 4. Hanahan, D. & Weinberg, R. A. Hallmarks of cancer: the next generation. Cell 144, 646-674, doi:10.1016/j.cell.2011.02.013 (2011). 5. Kim, H., Kim, C. Y., Park, K. H. & Kim, A. Clonality analysis of multifocal ipsilateral breast carcinomas using X-chromosome inactivation patterns. Hum Pathol 78, 106-114, doi:10.1016/j.humpath.2018.04.016 (2018). 6. Bergholtz, H. et al. Comparable cancer-relevant mutation profiles in synchronous ductal carcinoma in situ and invasive breast cancer. Cancer Rep (Hoboken) 3, e1248, doi:10.1002/cnr2.1248 (2020). 7. Giraddi, R. R. et al. Stem and progenitor cell division kinetics during postnatal mouse mammary gland development. Nat Commun 6, 8487, doi:10.1038/ncomms9487 (2015). 8. Scheele, C. L. et al. Identity and dynamics of mammary stem cells during branching morphogenesis. Nature 542, 313-317, doi:10.1038/nature21046 (2017). 9. Ying, Z. & Beronja, S. Embryonic Barcoding of Equipotent Mammary Progenitors Functionally Identifies Breast Cancer Drivers. Cell Stem Cell 26, 403-419.e404, doi:10.1016/j.stem.2020.01.009 (2020). 10. Zhou, J. et al. Stem Cells and Cellular Origins of Breast Cancer: Updates in the Rationale, Controversies, and Therapeutic Implications. Front Oncol 9, 820, doi:10.3389/fonc.2019.00820 (2019). 11. Watson, C. 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J Pathol 227, 42-52, doi:10.1002/path.3990 (2012). 16. Casasent, A. K., Edgerton, M. & Navin, N. E. Genome evolution in ductal carcinoma in situ: invasion of the clones. J Pathol 241, 208-218, doi:10.1002/path.4840 (2017). 17. Casasent, A. K. et al. Multiclonal Invasion in Breast Tumors Identified by Topographic Single Cell Sequencing. Cell 172, 205-217 e212, doi:10.1016/j.cell.2017.12.007 (2018). 18. Lips, E. H. et al. Genomic analysis defines clonal relationships of ductal carcinoma in situ and recurrent invasive breast cancer. Nat Genet 54, 850–860, doi:10.1038/s41588-022-01082-3 (2022). 19. Miron, A. et al. PIK3CA mutations in in situ and invasive breast carcinomas. Cancer Res 70, 5674-5678, doi:10.1158/0008-5472.CAN-08-2660 (2010). 20. Yates, L. R. et al. Subclonal diversification of primary breast cancer revealed by multiregion sequencing. Nat Med 21, 751-759, doi:10.1038/nm.3886 (2015). 21. Pareja, F. et al. Whole-Exome Sequencing Analysis of the Progression from Non-Low-Grade Ductal Carcinoma In Situ to Invasive Ductal Carcinoma. Clin Cancer Res 26, 3682-3693, doi:10.1158/1078-0432.CCR-19-2563 (2020). 22. Trinh, A. et al. Genomic Alterations during the In Situ to Invasive Ductal Breast Carcinoma Transition Shaped by the Immune System. Mol Cancer Res 19, 623-635, doi:10.1158/1541-7786.MCR-20-0949 (2021). 23. Poste, G. & Fidler, I. J. The pathogenesis of cancer metastasis. Nature 283, 139-146, doi:10.1038/283139a0 (1980). 24. Greaves, M. & Maley, C. C. Clonal evolution in cancer. Nature 481, 306-313, doi:10.1038/nature10762 (2012). 25. Kroigard, A. B. et al. Clonal expansion and linear genome evolution through breast cancer progression from pre-invasive stages to asynchronous metastasis. Oncotarget 6, 5634-5649, doi:10.18632/oncotarget.3111 (2015). 26. Martelotto, L. G. et al. Whole-genome single-cell copy number profiling from formalin-fixed paraffin-embedded samples. Nat Med 23, 376-385, doi:10.1038/nm.4279 (2017). 27. Walens, A. et al. Adaptation and selection shape clonal evolution of tumors during residual disease and recurrence. Nat Commun 11, 5017, doi:10.1038/s41467-020-18730-z (2020). 28. Welter, L. et al. Treatment response and tumor evolution: lessons from an extended series of multianalyte liquid biopsies in a metastatic breast cancer patient. Cold Spring Harb Mol Case Stud 6, doi:10.1101/mcs.a005819 (2020). 29. Maggrah, A. et al. Paired ductal carcinoma in situ and invasive breast cancer lesions in the D-loop of the mitochondrial genome indicate a cancerization field effect. Biomed Res Int 2013, 379438, doi:10.1155/2013/379438 (2013). 30. Desmedt, C. et al. Uncovering the genomic heterogeneity of multifocal breast cancer. J Pathol 236, 457-466, doi:10.1002/path.4540 (2015). 31. Visser, L. L. et al. Discordant Marker Expression Between Invasive Breast Carcinoma and Corresponding Synchronous and Preceding DCIS. Am J Surg Pathol 43, 1574-1582, doi:10.1097/PAS.0000000000001306 (2019). 32. McCrorie, A. D. et al. Multifocal breast cancers are more prevalent in BRCA2 versus BRCA1 mutation carriers. J Pathol Clin Res 6, 146-153, doi:10.1002/cjp2.155 (2020). 33. Sontag, L. & Axelrod, D. E. Evaluation of pathways for progression of heterogeneous breast tumors. J Theor Biol 232, 179-189, doi:10.1016/j.jtbi.2004.08.002 (2005). 34. Mai, K. T. Morphological evidence for field effect as a mechanism for tumour spread in mammary Paget’s disease. Histopathology 35, 567-576, doi:10.1046/j.1365-2559.1999.00788.x (1999). 35. Foschini, M. P. et al. Genetic clonal mapping of in situ and invasive ductal carcinoma indicates the field cancerization phenomenon in the breast. Hum Pathol 44, 1310-1319, doi:10.1016/j.humpath.2012.09.022 (2013). 36. Asioli, S., Morandi, L., Cavatorta, C., Cucchi, M. C. & Foschini, M. P. The impact of field cancerization on the extent of duct carcinoma in situ (DCIS) in breast tissue after conservative excision. Eur J Surg Oncol 42, 1806-1813, doi:10.1016/j.ejso.2016.07.005 (2016). 37. Tan, M. P. Integration of ’sick lobe hypothesis’ with concept of field cancerisation for a personalised surgical margin for breast conserving surgery. J Surg Oncol 116, 954-955, doi:10.1002/jso.24728 (2017). 38. Going, J. J. & Mohun, T. J. Human breast duct anatomy, the ’sick lobe’ hypothesis and intraductal approaches to breast cancer. Breast Cancer Res Treat 97, 285-291, doi:10.1007/s10549-005-9122-7 (2006). 39. Tot, T. The theory of the sick breast lobe and the possible consequences. Int J Surg Pathol 15, 369-375, doi:10.1177/1066896907302225 (2007). 40. Dooley, W., Bong, J. & Parker, J. Redefining lumpectomy using a modification of the "sick lobe" hypothesis and ductal anatomy. Int J Breast Cancer 2011, 726384, doi:10.4061/2011/726384 (2011). 41. Tan, M. P. & Tot, T. The sick lobe hypothesis, field cancerisation and the new era of precision breast surgery. Gland Surg 7, 611-618, doi:10.21037/gs.2018.09.08 (2018). 42. Petrova, S. C. et al. Regulation of breast cancer oncogenesis by the cell of origin’s differentiation state. Oncotarget 11, 3832-3848, doi:10.18632/oncotarget.27783 (2020). 43. Knudson, A. G., Jr. Heredity and human cancer. Am J Pathol 77, 77-84 (1974). 44. Park, S., Supek, F. & Lehner, B. Systematic discovery of germline cancer predisposition genes through the identification of somatic second hits. Nat Commun 9, 2601, doi:10.1038/s41467-018-04900-7 (2018). 45. Konishi, H. et al. Mutation of a single allele of the cancer susceptibility gene BRCA1 leads to genomic instability in human breast epithelial cells. Proc Natl Acad Sci U S A 108, 17773-17778, doi:10.1073/pnas.1110969108 (2011). 46. Mazzola, E., Cheng, S. C. & Parmigiani, G. The penetrance of ductal carcinoma in situ among BRCA1 and BRCA2 mutation carriers. Breast Cancer Res Treat 137, 315-318, doi:10.1007/s10549-012-2345-5 (2013). 47. Tegze, B. et al. Parallel evolution under chemotherapy pressure in 29 breast cancer cell lines results in dissimilar mechanisms of resistance. PLoS One 7, e30804, doi:10.1371/journal.pone.0030804 (2012). 48. Gao, Y. et al. Single-cell sequencing deciphers a convergent evolution of copy number alterations from primary to circulating tumor cells. Genome Res 27, 1312-1322, doi:10.1101/gr.216788.116 (2017). 49. Wang, F. et al. MEDALT: single-cell copy number lineage tracing enabling gene discovery. Genome Biol 22, 70, doi:10.1186/s13059-021-02291-5 (2021). 50. Brommesson, S. et al. Tiling array-CGH for the assessment of genomic similarities among synchronous unilateral and bilateral invasive breast cancer tumor pairs. BMC Clin Pathol 8, 6, doi:10.1186/1472-6890-8-6 (2008). 51. Regitnig, P., Ploner, F., Maderbacher, M. & Lax, S. F. Bilateral carcinomas of the breast with local recurrence: analysis of genetic relationship of the tumors. Mod Pathol 17, 597-602, doi:10.1038/modpathol.3800089 (2004). 52. Ma, X. J. et al. Gene expression profiles of human breast cancer progression. Proc Natl Acad Sci U S A 100, 5974-5979, doi:10.1073/pnas.0931261100 (2003). 53. Porter, D. et al. Molecular markers in ductal carcinoma in situ of the breast. Mol Cancer Res 1, 362-375 (2003). 54. Castro, N. P. et al. Evidence that molecular changes in cells occur before morphological alterations during the progression of breast ductal carcinoma. Breast Cancer Research 10, doi:ARTN R87 10.1186/bcr2157 (2008). 55. Dettogni, R. S. et al. Potential biomarkers of ductal carcinoma in situ progression. BMC Cancer 20, 119, doi:10.1186/s12885-020-6608-y (2020). 56. Song, G. et al. Identification of aberrant gene expression during breast ductal carcinoma in situ progression to invasive ductal carcinoma. J Int Med Res 48, 300060518815364, doi:10.1177/0300060518815364 (2020). 57. Abba, M. C. et al. Transcriptomic changes in human breast cancer progression as determined by serial analysis of gene expression. Breast Cancer Res 6, R499-513, doi:10.1186/bcr899 (2004). 58. Schuetz, C. S. et al. Progression-specific genes identified by expression profiling of matched ductal carcinomas in situ and invasive breast tumors, combining laser capture microdissection and oligonucleotide microarray analysis. Cancer Res 66, 5278-5286, doi:10.1158/0008-5472.CAN-05-4610 (2006). 59. Lee, S. et al. Differentially expressed genes regulating the progression of ductal carcinoma in situ to invasive breast cancer. Cancer Res 72, 4574-4586, doi:10.1158/0008-5472.CAN-12-0636 (2012). 60. Coradini, D., Boracchi, P., Ambrogi, F., Biganzoli, E. & Oriana, S. Cell polarity, epithelial-mesenchymal transition, and cell-fate decision gene expression in ductal carcinoma in situ. Int J Surg Oncol 2012, 984346, doi:10.1155/2012/984346 (2012). 61. Knudsen, E. S. et al. Progression of ductal carcinoma in situ to invasive breast cancer is associated with gene expression programs of EMT and myoepithelia. Breast Cancer Res Treat 133, 1009-1024, doi:10.1007/s10549-011-1894-3 (2012). 62. Krstic, M. et al. TBX3 promotes progression of pre-invasive breast cancer cells by inducing EMT and directly up-regulating SLUG. Journal of Pathology 248, 191-203, doi:10.1002/path.5245 (2019). Citation Format: Jelle Wesseling. Clonal evolution of DCIS to invasion [abstract]. In: Proceedings of the 2022 San Antonio Breast Cancer Symposium; 2022 Dec 6-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2023;83(5 Suppl):Abstract nr F1-2.
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6

Li, Cong, and Chunquan Yu. "Seismic Evidence for Crustal Magmatic Intrusion Beneath the Southern Part of the Eastern North American Margin." Journal of Geophysical Research: Solid Earth 129, no. 5 (2024). http://dx.doi.org/10.1029/2023jb028143.

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AbstractThe southern portion of the eastern North American margin (SENAM) is an archetypical volcanic passive margin formed during Mesozoic rifting. How past magmatic events affect the evolution of the SENAM remains an open question of fundamental importance. To better understand this question, here we construct a high‐resolution 3‐D crustal velocity model from the oceanic side to the continental interior with a combination of multimodal dispersion inversion and full‐waveform ambient noise tomography. Our new model reveals an oceanic‐continental transitional crust over a short horizonal distance of 100–150 km across the SENAM, with a local‐scale lower‐than‐surrounding velocity anomaly directly beneath the transitional crust. Furthermore, the new model shows three intra‐crustal higher‐than‐average velocity anomalies beneath the SENAM continent. We suggest that the magmatism assisted the Mesozoic rifting process to form the narrow ocean‐continent transitional crust along the coastline. The underplating of magma beneath the transitional crust led to a reduction of seismic velocity of the uppermost mantle. In addition, it is probable that the emplacement of the Central Atlantic Magmatic Province caused widespread magmatic intrusions within the continental crust of the SENAM, which were later solidified into intra‐crustal high‐velocity plutons. Our findings provide new insights into crustal modification history at the passive margin.
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Singh, Prathvi, Venkatnarayanan Ramanathan, and Ramasubbu Sankararamakrishnan. "Self‐contacting Cys, Ser, and Thr residues in high‐resolution protein crystal structures: Tertiary constraints or hydrogen bonds?" Protein Science 33, no. 12 (2024). http://dx.doi.org/10.1002/pro.5218.

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AbstractFunctional groups in the side‐chains of at least 10 amino acids are mainly involved in tertiary interactions. However, structural and functional significance of intra‐residue interactions has not been fully recognized. In this study, we have analyzed ~5800 non‐redundant high‐resolution protein structures and identified 1166 self‐contacts between the side‐chain S‐H/O‐H and backbone C=O groups in Cys, Ser, and Thr residues that satisfied the geometric criteria to form hydrogen bonds. Quantum chemical calculations using model compounds were used to evaluate single point energy for 45 representative examples from different allowed regions of Ramachandran map. Relative energy profiles obtained by varying the side‐chain dihedral angle χ1 revealed that the energy difference between the crystal structure and the minimum energy conformations is between 0 and 3 kcal/mol. Natural bond orbital analysis (NBO) of self‐contacting Cys residues revealed no charge transfer between Cys side‐chain S‐H and the backbone C=O groups. However, side‐chain hydroxyl and the backbone C=O groups of 90%–95% of all self‐contacting Ser and Thr residues are involved in charge transfer and the second order perturbation energy of majority of them is above 1 kcal/mol. Interaction energies calculated for model compounds along with NBO and NCIPLOT analyses demonstrate that the self‐contacts observed in Ser and Thr residues can be described as hydrogen bonds. These interactions may provide stability to the loop/coil conformations. Self‐contacting Cys residues are buried and the self‐contacts appear to be mostly due to tertiary constraints. Dispersion between the self‐contacting groups is one way to explain the close approach in Cys residues. Mutation studies will further validate and reveal the structural and functional significance of these self‐contacting residues.
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Lapka, Marek, and Zbyněk Straňák. "Therapy for Vitreous Seeding Caused by Retinoblastoma. A Review." Czech and Slovak Ophthalmology, AoP (July 30, 2023). http://dx.doi.org/10.31348/2023/35.

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Retinoblastoma is the most common primary malignant intraocular tumor in children. Seeding, specifically the dispersion of the tumor into the adjacent compartments, represents a major parameter determining the degree of retinoblastoma according to the International Classification of Retinoblastoma. In this article we focused on vitreous seeding, one of the main limiting factors in the successful “eye preservation treatment” of retinoblastoma. This article presents an overview of the history of vitreous seeding of retinoblastoma, established treatment procedures and new-research modalities. The introduction of systemic chemotherapy in the treatment of retinoblastoma at the end of the 1990s represented a significant breakthrough, which enabled the progressive abandonment of radiotherapy with its attendant side effects. However, the attained concentrations of chemotherapeutics in the vitreous space during systemic chemotherapy are not sufficient for the treatment of vitreous seeding, and the toxic effects of systemic chemotherapy are not negligible. A significant change came with the advent of chemotherapy in situ, with the targeted administration of chemotherapeutic drugs, namely intra-arterial and intravitreal injections, contributing to the definitive eradication of external radiotherapy and a reduction of systemic chemotherapy. Although vitreous seeding remains the most common reason for the failure of intra-arterial chemotherapy, this technique has significantly influenced the original treatment regimen of children with retinoblastoma. However, intravitreal chemotherapy has made the greatest contribution to increasing the probability of preservation of the eyeball and visual functions in patients with advanced findings. Novel local drug delivery modalities, gene therapy, oncolytic viruses and immunotherapy from several ongoing preclinical and clinical trials may represent promising approaches in the treatment of vitreous retinoblastoma seeding, though no clinical trials have yet been completed for routine use.
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Arabia, Martina, Eleonora Maretti, Armita Sedighidarijani, Cecilia Rustichelli, and Eliana Leo. "Optimizing Formulation Conditions of PLGA Microparticles to Enhance Indomethacin Encapsulation." Particle & Particle Systems Characterization, August 26, 2024. http://dx.doi.org/10.1002/ppsc.202400135.

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AbstractDrug delivery systems can avoid the drawbacks of Indomethacin (IND), a non‐steroidal anti‐inflammatory drug used to treat osteoarthritis and arthritis, which requires high doses to reach therapeutic plasma levels leading to significant systemic side effects. This study aims to optimize poly(lactic‐co‐glycolic acid) (PLGA) microparticles (MPs) for intra‐articular IND administration. MPs are prepared by solvent evaporation and freeze‐dried for stability. Initial formulations with Tween 80 yield rubbery samples with low drug loading (1%); replacement of Tween 80 with Gelatin produces a stable powder with syringable MPs (particles size: 7 µm), although, DL (3%) and EE (30%) remain suboptimal, due to IND polymorphic transformation. Differential Scanning Calorimetry and Fourier‐Transform Infrared spectroscopy demonstrate a molecular dispersion of IND in PLGA. Adjusting the aqueous phase to pH 3 in the formulation process, i.e below IND pKa, significantly enhances EE (90%) due to the reduction of drug solubility in the external aqueous phase. In vitro release study shows prolonged IND release over several days, confirming an effective drug encapsulation. This study provides a foundational framework toward the optimization of the successful encapsulation of IND in PLGA MPs, potentially advancing future clinical applications of such drug delivery systems.
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Conference papers on the topic "Intra-side dispersion"

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Regalla, Srinivasa Prakash, P. V. Shyam, Sampath Mylavarapu, Sai Harshini Irigineni, and Prakash Narayan Shrivastava. "Study of Flexural Strength and Fracture of Additive Manufactured Parts With Stiffeners." In ASME 2021 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2021. http://dx.doi.org/10.1115/imece2021-71519.

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Abstract The authors have developed trans-tibial prosthetic sockets using additive manufacturing. These sockets made with mono-material thermoplastics such as Acrylonitrile Butadiene Styrene (ABS) and Polylactic Acid (PLA) at lower thicknesses were found to fracture within a few days of use by the amputees. The fracture was repeatedly found to occur at specific locations such as the lobe corners and the socket’s lower one-third zone. The most probable causes of crack initiation are lack of fusion (LOF) sites and voids. The causes of crack propagation are the lower interlayer bond strength compared to intra-layer bond strength. However, no scientific work exists that clearly explains these phenomena and methods to prevent such potential crack initiation sites and arrest the propagation of such fracture in additively manufactured polymeric structures. Therefore, in the present work, the investigation was carried out into possible enhancement in the resistance to fracture by different strength-enhancing post-processing techniques. In the first technique, the placement of stiffener features at selected locations on the socket was investigated. Three-point bending tests were carried out on D790 standard ABS specimens with different stiffeners introduced on the bottom face. The study focused on fracture characteristics in the stiffener-based topologically optimized geometric design of plate structures made by Fused Deposition Modeling (FDM) under flexural loading. The D790 three-point bending specimens were provided with differently shaped stiffeners, namely, triangular, prismatic, cuboidal, and pyramidal, extending all along the specimen’s length and spread with differential gaps in the width direction. In the second method, thermosetting epoxy resin coatings were applied on the three-point bending specimens of ABS, and the effect of the coating on the flexural strength was investigated. Bending tests were done on three specimens, the first specimen without any coating, the second specimen with only the epoxy resin coating, and the third specimen with two different coating layers. The first of the two coating layers on the third specimen was with primer and the second layer was with epoxy resin. Scanning electron microscope (SEM) and energy dispersion spectroscopy (EDS) scanning analyses were conducted on the fractured specimens. The scanning images indicated that both the primer and resin materials showed a tendency to diffuse into the substrate of ABS, thereby weakening the extreme fibers of material on the specimen’s tension side, resulting in premature crack initiation and propagation. Significant gain in the flexural strength was observed in both the strength enhancement techniques compared to plain specimens.
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