DOM

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Dom

(dōm), peak, 14,942 ft (4,554 m) high, Valais canton, S Switzerland, in the Mischabelhörner group. It is the highest peak entirely in Switzerland.
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DOM

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DOM

(1) See disk on module.

(2) (Document Object Model) A programming interface (API) from the W3C that lets applications and scripts render the data in XML, XHTML and HTML files as a hierarchical tree structure.

DOM Creates a Database Record (Row/Tuple)
Introduced in 1998, the DOM implementation converts XML documents into a hierarchical node tree in RAM that looks like a database record, a.k.a. a row or tuple. The node tree allows updating in a similar manner to traditional database updating, making data exchange between XML documents and databases more straightforward. Without DOM, the text and tags in an XML document have to be scanned sequentially and rearranged by the program.

Event Processing
In 2000, DOM Level 2 (DOM2) gave the programmer a way to handle events such as mouse down, mouse click and mouse over. Events may be preprocessed at any tag from the top of the tree to the target tag at the bottom ("capture" phase) and then back up ("bubbling" phase). These phases were implemented for backward compatibility with earlier Netscape and IE browsers. See DOM implementation, DOM application, SAX and object model.


Nodes in an XML Record
DOM converts (parses) an XML document into a hierarchical node tree. Writing an XML update program is then similar to writing a database update program, using the same kinds of functions available in a database management system (see DBMS).
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References in periodicals archive ?
A newly developed mouse monoclonal SOX10 antibody is a highly sensitive and specific marker for malignant melanoma, including spindle cell and desmoplastic melanomas.
Primers for the glyceraldehyde 3-phosphate dehydrogenase (GAPDH), HES5, LRP6, SOX10, and MBP genes were designed using the AlleleID software.
The new work documenting Sox10's role in this process represents a major milestone in researchers' understanding of cancer and could open new avenues for diagnosing and treating aggressive breast cancer as well as other types of intractable cancers.
Immunohistochemical staining showed the lesional cells were positive for CK 8/18, CK7, S100, GATA3 (diffusely weak), SOX10 (Fig 2c, 2d), CK 5/6, p40 (patchy) and were negative for GCDFP-15, CD117, SMA, AR, ER, PR, Her2 and DOG1.
Caption: Figure 4: High magnification immunohistochemistry of selected cutaneous basaloid tumor markers: (a) focal membranous and cytoplasmic positivity in center of tumor cell nests with sparing of outer cells, CKAE1/3, 400x; (b) diffuse and strong cytoplasmic positivity in center of tumor cell nests with comparative sparing of myoepithelial-like edges, CK5/6, 400x; (c) patchy cytoplasmic and membranous positivity in center of tumor cell nests with sparing of outer cells, CK7, 400x; (d) diffuse and strong nuclear positivity throughout tumor cell nests, p63, 400x; (e) diffuse nuclear positivity of moderate to strong intensity throughout tumor cell nests, SOX10, 400x.
The underlying cell death mechanism involves activation of Bax and caspase-3/-9, cleavage of PARP, and downregulation of cyclin D1 and Mcl-1 along with inhibition of Sry-related HMg-Box Gene 10 (SOX10) signaling cascade [151, 152].
A set of transcription factors, including Sox10 [30, 31] and Mash1 [32], is induced by BMPs, which in its turn regulates the differentiation of migrating neural crest cells into sympathoadrenal cells.
According to the presence of certain associated clinical features, genetic screening for particular gene(s) may be prioritized: synkinesia (KAL1), dental agenesis (FGF8/FGFR1), digital bony abnormalities (FGF8/FGFR1) and hearing loss (CHD7, SOX10) (19).
Young, "Reversal of congenital hypogonadotropic hypogonadism in a man with Kallmann syndrome due to SOX10 mutation," Clinical Endocrinology, vol.
Germ cell tumour markers (Oct3/4, PLAP, SALL4, Glypican 3, and CD30), pancytokeratin (AE1/AE3), and neurofilament muscle specific markers (Desmin) as well as CD34, CD117, SOX10, MDM2, and EMA were all negative.
Although certain genes such as SOX10, RET, EDNRB, ECE1, and GDNE play important roles during the time required for maturation of ENS [11,13-15], the pathogenesis of the development of ENS still remains unclear especially in terms of formation and function of synapses.
Ambos estados y el proceso de cambio entre ambos es regulado por factores reguladores intrinsecos celulares: unos positivos, como Krox20, Sox10 y Oct6, los cuales aseguran la mielinizacion de nervios el tiempo adecuado durante el desarrollo y restablecen la funcion de las celulas de Schwann despues de la lesion, y otros negativos, como c-Jun, Sox2, Notch, Krox24 y Pax3, los cuales conducen al proceso de dediferenciacion y desmielinizacion, al bloquear la normal induccion de mielinizacion por parte de la adenosina monofostato ciclico.