Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies (Cynader and Mitchell, '80; Mower et al., '81) have shown that total dark rearing prolongs susceptibility to the physiological effects of monocular deprivation (MD) in visual cortex beyond the normal age limits. The present study addressed whether this delayed physiological plasticity is accompanied by delayed anatomical plasticity in the geniculocortical pathway. Ocular dominance (OD) columns as defined by transsynaptic autoradiography following injection of 3H proline into one eye were studied both qualitatively and quantitatively in 17 cats. Compared to normal rearing (N-3), both binocular eyelid suture (N-2) and total dark rearing (N-3) resulted in incomplete segregation of OD columns in area 17. This apparent immaturity after binocular deprivation, however, did not reflect a delayed capacity for development and plasticity. Visual experience after dark rearing produced no marked changes. In cats who experienced MD after dark rearing, injection of either the nondeprived (N-2) or deprived eye (N-3) resulted in a nearly uniform distribution of label throughout layer IV of area 17. The same result occurred with binocular vision after dark rearing (N-1). MD from birth, however, produced expansion of columns from the nondeprived eye (N-1) and contraction of columns from the deprived eye (N-1). MD imposed after 4 months of normal vision resulted in normal OD columns (N-1). Electrophysiological studies revealed a high proportion of binocular cells within layer IV in cats who experienced monocular or binocular vision after dark rearing. Outside of layer IV there were clear environmental effects on OD of single cells in these cats. Measurements of cell sizes in the clateral geniculate nucleus showed shrinkage of cells innervated by the deprived eye when MD was initiated at birth (N-3). MD after dark rearing (N-4) produced no differences in cell sizes. It is concluded that visual input is necessary for the formation of normal OD columns, the critical period for formation and environmental modification of OD columns is limited to early life, and the physiological effects of visual experience after dark rearing reflect changes occurring beyond the geniculocortical pathway.
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PMID:Dark rearing prolongs physiological but not anatomical plasticity of the cat visual cortex. 399 19

DNA and protein synthesis have been studied in placental villi from normal and pathological cases by in vitro incorporation of tritiated thymidine or tritiated proline and subsequent counting or autoradiography. It appeared that cytotrophoblastic DNA synthesis continued until term and that it was particularly important in preeclampsia cases and in cases of villous immaturity (rhesus sensitization). Protein synthesis was also increased in preeclampsia and seemed to be due to a very active cytotrophoblastic metabolism. The most interesting finding was that in preeclampsia cases, especially when intrauterine growth retardation was superimposed, villous capillary endothelial cell proliferation was as prominent as in cases where villous maturation was not achieved. Such results are highly suggestive of an important compensatory proliferative mechanism in the placentae of preeclamptic women.
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PMID:Cellular proliferation in villi of normal and pathological pregnancies. 670 38

The development of the pyramidal tract and other projections from the sensorimotor cortex was studied in the postnatal hamster with both (3H) proline and horseradish peroxidase (HRP) as anterograde tracers. In the 1-day-old animal labeled axons extend as far as the pons. Other corticofugal fibers have penetrated into the corpus striatum and the thalamus. By 2 days postnatally, the pyramidal tract has grown to midmedullary levels and there is substantial retrograde (HRP) and anterograde labeling in the thalamus. The pyramidal decussation is formed at 3 days of age and by 4 days the pyramidal tract has descended in the dorsal funiculus as far as midcervical spinal cord. Corticofugal fibers invade the pontine nuclei at 4 days and both the dorsal column nuclei and the superior colliculus at 6 days of age. At 6 days the pyramidal tract can be traced to mid-thoracic levels of the spinal cord, by 8 days the tract reaches lumbar levels, and by 14 days it has completed its caudal growth to the coccygeal spinal cord. Fibers first penetrate the gray matter of a given spinal cord level approximately 2 days after the tract has grown past that level in the dorsal funiculus. Pyramidal fibers continue their lateral growth into the dorsal horn at all levels of the cord throughout the third postnatal week such that by 21 days of age the pyramidal tract appears similar to that of the adult. The projections from sensorimotor cortex to the pontine nuclei, the superior colliculus, and the dorsal column nuclei appear to have a pattern similar to that of the adult soon after the fibers grown into these structures. There is a consistent delay of 2 to 3 days between the arrival of the pyramidal tract axons in the white matter adjacent to target structures and their innervation of a given terminal field. The pyramidal tract grows more quickly through the dorsal funiculus of the spinal cord than it does along the ventral surface of the medulla. Extensive elongation of pyramidal tract axons is achieved long before the growth and differentiation of the sensorimotor cortical neurons from which they originate. Finally, the pyramidal tract appears to grow as a compact bundle and not by the addition of temporally staggered groups of fibers. The relatively protracted period of innervation of the spinal cord by the pyramidal tract coupled with the immaturity of the cortical neurons at birth may be factors contributing to the significant regrowth of pyramidal tract axons severed early in development.
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PMID:Development of the pyramidal tract in the hamster. I. A light microscopic study. 725 45

Mutations of androgen receptor (AR) are the most frequent cause of 46, XY disorders of sex development and associated with a variety of phenotypes, ranging from phenotypic women (complete androgen insensitivity syndrome (CAIS)) to milder degrees of undervirilization (partial form or PAIS) or men with only infertility (mild form or MAIS). From 2009 to 2012, two young Chinese female individuals with CAIS from two families were referred to our hospital due to primary amenorrhea. Defects in testosterone (T) and dihydrotestosterone (DHT) synthesis were excluded. Physical examination revealed that the patients have normal female external genitalia, normal breast development, vellus hair in the axilla and on the arms and legs, but absence of pubic hair, and a blind-ending vagina. Two different types of AR mutations have been detected by sequencing of genomic DNA: Family A showed deletion of exon 2 in AR gene; Family B showed a single nucleotide C-to-T transition in exon 8 of AR gene resulting in a proline 893-to-leucine substitution (Pro893Leu). Testicular histology showed developmental immaturity of seminiferous tubules with the absence of spermatogenic cells or spermatozoa. No AR immunoreactivity was observed in either case. Three adult patients recovered well from bilateral orchiectomy. The juvenile patient of family B was followed up. Our present study on these two families revealed two different types of AR mutation. The definitive diagnosis of AIS was based on clinical examination and genetic investigations. Our findings verified the mechanism of CAIS and also enriched AR Gene Mutation Database.
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PMID:Different types of androgen receptor mutations in patients with complete androgen insensitivity syndrome. 2567 89