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Table of contents
- Mosaic Disorders of the PI3K/PTEN/AKT/TSC/mTORC1 signaling pathway
- Adding new tiles to the omnichannel mosaic
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- Adding new tiles to the omnichannel mosaic – Strategy – CSCMP's Supply Chain Quarterly
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Cuts, shapes, and sets blocks of colored glass, enamel, marble, or ceramic tile for installation on walls, ceilings, or panels or for use as table tops or decorative screens, according to specifications: Selects color and type of tile specified for section according to tile charts.
Mosaic Disorders of the PI3K/PTEN/AKT/TSC/mTORC1 signaling pathway
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Adding new tiles to the omnichannel mosaic
There are many ways to decorate a surface. In this lesson, we'll check out mosaic art, see what exactly it is, and explore the various ways it's been used throughout history. Hard to believe this ceiling in the San Giovanni baptistery of Florence is not a painting, right? Building a Mosaic The creation of a mosaic begins with the surface. History of Mosaics This is a cool art form, but where did it come from?
Roman mosaic from Herculaneum From there, we can see Roman influence diverge in two directions. Try it risk-free No obligation, cancel anytime. Want to learn more? Select a subject to preview related courses: Byzantine mosaic in San Vitale During the Italian Renaissance, an interest in mosaics was rekindled to some degree resulting in incredible works like the Byzantine-inspired Baptistery of San Giovanni in Florence , but never challenged painting's role as the dominant art.
Lesson Summary Mosaics are decorated surfaces created by setting individual components called tesserae into aesthetic patterns.
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Adding new tiles to the omnichannel mosaic – Strategy – CSCMP's Supply Chain Quarterly
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You are viewing lesson Lesson 3 in chapter 9 of the course:.
Elements of Art Lesson What is Mosaic Art? In TSC and PHTS, individuals with an early postzygotic mutation often have similar disease features and distribution of disease as those with a germline mutation. For example, a TSC2 mutation occurring during neuroectodermal development may explain the presence of tubers in TSC, but the absence of subependymal nodules 64 , while a mutation in neural crest cells after migration from the neural tube may account for complete absence of neuroanatomical brain involvement in these patients.
In addition to timing of mutation, tissue type in which the mosaic mutation resides appears to influence the clinical presentation; for instance, an activating AKT1 mutation in keratinocytes is responsible for epidermal nevus formation, yet the same mutation in fibroblasts produces an entirely different clinical entity i.
Indeed, fibroblast-like cells in TSC-related hamartomas have been shown to release paracrine factors that affect the overlying epidermis. Clinical diagnosis alone is often difficult for these conditions, given substantial overlap of characteristic features. While traditional genetic analysis of mosaic patients can be equally difficult, sampling the affected tissue, rather than blood, using deep sequencing methods appears to have greater diagnostic accuracy. While genetic testing may be helpful to guide patient management, caution should be taken when interpreting results.
Thus far, the frequency of mutant cells in affected or normal tissue does not accurately correlate with disease burden in disorders of this pathway. The presence of seemingly benign skin findings or highly limited disease involvement may have greater clinical importance than is apparent. This example has been recently demonstrated in TSC, where patients with mild clinically apparent disease in fact harbored serious internal manifestations that caused morbidity and sometimes, mortality.
Thus, patients with mosaic and germline PTEN mutations should be routinely monitored for breast, endometrial and thyroid cancers according to current guidelines, as even patients with a low frequency of mutant cells may have increased cancer risk. There have been reports of nephroblastomatosis a premalignant lesion and Wilms tumor in several patients with PROS and hemihyperplasia. This appears to be most threatening when patients undergo surgery and surgeons need to be aware of this risk.
Patient education regarding symptoms suggestive of a thromboembolism is also important. In addition to disease surveillance, reproductive counseling for patients with mosaic disorders warrants special mention. Thus, a patient with limited mosaic disease involvement could give birth to a severely affected non-mosaic child. These clinical presentations should be genetically confirmed because each condition has unique implications for disease management. This common pathway may provide insight into treatment. Understanding how mutations in these genes intersect with one signaling pathway explains the similarity among their clinical presentations and provides rationale for practical therapeutic approaches.
Further, recognizing how mosaic involvement leads to variations in patterning explains the patchy and often asymmetric distribution of cutaneous and systemic involvement.
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Author manuscript; available in PMC Jan 1. Darling , MD, PhD 1. Author information Copyright and License information Disclaimer. The publisher's final edited version of this article is available at Dermatol Clin. See other articles in PMC that cite the published article. Abstract Mosaicism is the presence of two or more genetically distinct cell lineages originating from a single zygote. Introduction Mosaicism may occur as a somatic mutation occurring during embryogenesis, resulting in an organism is composed of two or more genetically distinct cell lineages. Open in a separate window. Proposed mechanisms of phenotype divergence Timing of mutations Variation in the timing of post-zygotic mutations may cause phenotypic variability, conferring a spectrum of disease burden.
Tissue specificity In addition to timing of mutation, tissue type in which the mosaic mutation resides appears to influence the clinical presentation; for instance, an activating AKT1 mutation in keratinocytes is responsible for epidermal nevus formation, yet the same mutation in fibroblasts produces an entirely different clinical entity i.
Diagnosis of mosaicism Clinical diagnosis alone is often difficult for these conditions, given substantial overlap of characteristic features. Counseling for prognosis and management The presence of seemingly benign skin findings or highly limited disease involvement may have greater clinical importance than is apparent. Mosaicism may be considered in sporadic cases; there should be a negative history in ancestral generations or siblings, but offspring may be affected through gonadal mosaicism.
A patchy distribution of cutaneous features and tissue overgrowth or disseminated disease that is mild should raise suspicion for mosaicism. Next-generation sequencing, or other methods for detecting low frequency alleles, of affected tissue is frequently necessary to identify the genetic basis of mosaic conditions. Conflicts of interest disclosures: A genomic view of mosaicism and human disease.
The categories of cutaneous mosaicism: Am J Med Genet A. Laplante M, Sabatini DM. Dazert E, Hall MN. Curr Opin Cell Biol. Huang J, Manning BD. Cutaneous manifestations of proteus syndrome: