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61.
Spacing of cytochrome oxidase blobs in visual cortex of normal and strabismic monkeys 总被引:3,自引:3,他引:0
Murphy KM; Jones DG; Fenstemaker SB; Pegado VD; Kiorpes L; Movshon JA 《Cerebral cortex (New York, N.Y. : 1991)》1998,8(3):237-244
Some models of visual cortical development are based on the assumption that
the tangential organization of V1 is not determined prior to visual
experience. In these models, correlated binocular activity is a key element
in the formation of visual cortical columns, and when the degree of
interocular correlation is reduced the models predict an increase in column
spacing. To examine this prediction we measured the spacing of columns, as
defined by cytochrome oxidase (CO) blobs, in the visual cortex of monkeys
whose binocular vision was either normal or disrupted by a strabismus. The
spatial distribution of blobs was examined in seven normal and five
strabismic macaques. Tangential sections through the upper layers of the
visual cortex were stained to reveal the two-dimensional (2D) pattern of CO
blobs. Each blob was localized and their center-to-center spacing, packing
arrangement and density were calculated using 2D nearest-neighbor spatial
analyses. The mean center-to-center spacing of blobs (590 microm for
normally reared and 598 microm for strabismic macaques) and the mean
density of blobs (3.67 blobs/mm2 for normally reared and 3.45 blobs/mm2 for
strabismic macaques) were not significantly different. In addition, the 2D
packing arrangement of the blobs was not affected by strabismus. While it
is clear that neural activity plays a key role in the elaboration and
refinement of ocular dominance cortical modules, we conclude that it does
not determine the spatial period of the pattern of CO blobs. This suggests
that aspects of the neural circuitry underlying the columnar architecture
of the visual cortex are established prenatally and its fundamental
periodicity is not modifiable by experience.
相似文献
62.
Pancreas divisum: thin-section CT 总被引:1,自引:0,他引:1
Zeman RK; McVay LV; Silverman PM; Cattau EL; Benjamin SB; Fleischer DF; Garra BS; Jaffe MH 《Radiology》1988,169(2):395-398
Twelve patients with known pancreas divisum underwent thin-section computed tomography (CT) to determine the capability of CT to depict this pancreatic anomaly. Focal pancreatic enlargement was present in five patients. Two distinct pancreatic moieties separated by a fat cleft were noted in three patients; a fourth patient had focal atrophy in the distribution of the dorsal pancreas. The two pancreatic moieties were identified at the same craniocaudal level in all four of these patients. The dorsal duct was depicted in all 12 patients, while the short ventral duct was seen in only five of the 12 patients. Failure of the ventral and dorsal pancreatic ducts to fuse was identified in all five patients in whom both ducts were seen. CT may not enable specific diagnosis of pancreas divisum in the majority of patients. If, however, distinct pancreatic moieties or unfused ductal systems are evident, the diagnosis may be confidently suggested. 相似文献
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The pathogenesis of diphenylhydantoin-induced pure red cell aplasia was investigated in the case of a 32-year-old man who developed pure red cell aplasia while he was under treatment with diphenylhydantoin. The patient's serum IgG purified from serum drawn at the time of diagnosis suppressed normal allogeneic marrow colony-forming (CFU-E) and burst- forming (BFU-E) and autologous blood BFU-E growth in vitro only in the presence of diphenylhydantoin. This IgG-diphenylhydantoin complex had no effect on CFU-GM growth in vitro. Normal IgG or patient's IgG purified from serum drawn after the remission of red cell aplasia had no effect on erythroid colony formation in vitro in the presence of diphenylhydantoin. The IgG-diphenylhydantoin complex exerted no direct cytotoxic effect on normal marrow erythroblasts, CFU-E, and BFU-E, nor did it interfere with the action of erythropoietin on marrow erythroblasts. These studies suggest that diphenylhydantoin-induced red cell aplasia is immunologically mediated through an IgG inhibitor, which requires the presence of the drug to suppress erythroid colony formation in vitro. This inhibitor seems to exert its effect on erythroid progenitors at or beyond the stage of differentiation of CFU- E, but not on erythroblasts. 相似文献
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