marianna13/litarch

Textbooks from PubChem Literature Archive.

Image-Text Pairs

[
  ['litarch_figures/ca/84/gene_NBK1116/angelmanF1.jpg', '\nIndividuals depicted have a genetically confirmed diagnosis of Angelman syndrome. Happy expression and an unstable gait accompanied by uplifted arms are commonly observed. At times, the facial appearance can suggest the diagnosis, but usually facial features are not distinctive.\n', ''],
  ['litarch_figures/ca/84/gene_NBK1116/angelmanF2.jpg', '\nSchematic drawing of chromosome region 15q11.2-q13 indicating the breakpoint regions BP1-BP6. Low copy repeat elements are located within these breakpoint regions (see text for details). Approximately 90% of chromosome deletions resulting in Angelman syndrome initiate at BP1 or BP2 and terminate in region BP3 (class I and class II). Approximately 10% of deletions are larger, typically spanning from BP1 to BP5, rarely beyond BP5. Genes that are not imprinted and thus biparentally expressed are noted by the open circles. The two critical imprinting center (IC) elements, the AS-SRO and the PWS-SRO, are drawn as open boxes. The gene SNRUF-SNRPN, drawn as a shaded box, has some overlap with the PWS-SRO. The SNURF-SNRPN sense/UBE3A antisense transcript is labeled UBE3A-AS.\n', ''],
  ['litarch_figures/ca/84/gene_NBK1116/angelmanF3.jpg', '\nThe pedigree illustrates imprinting inheritance in Angelman syndrome (AS). Inheritance of a deleterious UBE3A pathogenic variant from the male (top left, I-1) has no effect on the two children (II-2, II-4) who inherit his pathogenic variant because the mutated UBE3A has already been inactivated in his germ cells (i.e., by imprinting) and because each of these children also inherited a normally activated UBE3A from their mother (I-2). (Note: Only one active UBE3A allele is required for normal brain functioning.) If his carrier daughter (II-2) transmits the UBE3A pathogenic variant to the grandson and granddaughter (III-1, III-2), they both will have AS since each will have also inherited an inactivated UBE3A from their father; thus, neither child will express a UBE3A allele. The same explanation pertains for AS occurring in the great grand-niece (bottom right, IV-2).\n', '']
]

Interleaved:

[
["Getting by with the bare minimum seems to be the modus operandi of Mycobacterium leprae \u2014 the causal agent of leprosy. Its genome sequence reveals that it has undergone massive genome 'downsizing' over time, discarding more than half its genes and rendering it the most striking example of genome reduction in a microbial pathogen."],
["The leprosy bacillus is famed for being the first microorganism definitively shown to be associated with human disease. It evades the host's immune response by invading and propagating inside the vacuoles of macrophages called phagosomes. From there, it infects the Schwann cells of the peripheral nervous system, where it disrupts myelin production, thus leading to the characteristic features of leprosy, which include skin lesions and sensory loss."],
["litarch_figures/df/45/coffeebrk_NBK2345/A559.jpg",
"\nProtein coding genes distribution map for Mycobacterium leprae.\nThe leprosy bacillus genome contains numerous examples of gene deletion and decay. The relative locations of various genes in the genome are depicted in the map above. Protein coding genes are color coded in the map according to their classification within clusters of orthologous groups (COGs) functional categories. COGs represent proteins or groups of paralogs that are found in at least 3 phylogenetically-distant genomes. For more information about COGs, see Science 1997 Oct 24:278(5338):631-7.\n\n",
""],
["Protein coding genes distribution map for Mycobacterium leprae."]
]

Text

"Getting by with the bare minimum seems to be the modus operandi of Mycobacterium leprae \u2014 the causal agent of leprosy. Its genome sequence reveals that it has undergone massive genome 'downsizing' over time, discarding more than half its genes and rendering it the most striking example of genome reduction in a microbial pathogen.\nThe leprosy bacillus is famed for being the first microorganism definitively shown to be associated with human disease. It evades the host's immune response by invading and propagating inside the vacuoles of macrophages called phagosomes. From there, it infects the Schwann cells of the peripheral nervous system, where it disrupts myelin production, thus leading to the characteristic features of leprosy, which include skin lesions and sensory loss... "