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

The presence of mucosal hyperplasia and sialomucin goblet cell secretion (transitional mucosa) was assessed in various benign, premalignant and malignant colorectal tissues. Transitional mucosa was seen in diverticular disease, solitary ulcer syndrome of the rectum, ischaemic and irradiation colitis and other diseases including pneumatosis coli, endometriosis, haemorrhoids and a colostomy margin. Adenocarcinomas had a sulphomucin or mixed secretion pattern with transitional features in the adjacent mucosa mucosa (18/27). Premalignant adenomatous polyps showed mixed secretion with transitional glands incorporated in the stalk and sometimes in the adjacent mucosa. Epithelium showing dysplasia secreted sulphomucins and in amounts related to its degree of differentiation. Transitional mucosa may not be a primary premalignant phenomemon. The conclusion and unifying concept is that it is a secondary event related to goblet cell immaturity. This can occur, secondary to proliferation in mucosal inflammation, ischaemia and prolapse or as a phenotypic expression of growth derived from underlying dysplastic epithelium.
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PMID:High iron diamine-alcian blue mucin profiles in benign, premalignant and malignant colorectal disease. 322 Apr 65

The fetal endometrium becomes responsive to steroid hormones around the fourth month of pregnancy starting with an oestrogenic phase, which is followed late in pregnancy by a secretory phase. Based on post-mortem studies, the endometrium at birth is secretory in only one-third of neonates and proliferative in the remaining cases. Decidual or menstrual changes are rare in fetal endometrium despite high circulating steroid hormone levels, which drop rapidly after birth. Hence, acquisition of progesterone responsiveness appears to be dependent on endometrial maturation and relative immaturity may persist in a majority of girls until the menarche and early adolescence. Two major reproductive disorders have been linked with either advanced or delayed endometrial maturation. First, early-onset endometriosis may be caused by menstruation-like bleeding in the neonate, leading to tubal reflux and ectopic implantation of endometrial stem/progenitor cells. Second, persistence of partial progesterone resistance in adolescent girls may compromise deep placentation and account for the increased risk of major obstetrical syndromes, including preeclampsia, fetal growth retardation and preterm birth. The concept of neonatal origins of common reproductive disorders poses important research challenges but also subsumes potential new preventative strategies.
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PMID:The perinatal origins of major reproductive disorders in the adolescent: Research avenues. 2563 11