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)

The authors compared the degrees of cell maturity, antigenicity and secretory function of parathyroid (PTG) tissues from cadavers (C-PTG), 20-28 wk fetus (F-PTG) and PTG adenoma (A-PTG). In A-PTG tissues, clustered or scattered immature cells were observed, but there were none in F-PTG and C-PTG. C-PTG and A-PTG tissues revealed better secretory function than F-PTG. No clear difference was found in HLA class I (ABC) antigen quantity among the three donor PTG tissues, but the amount of HLA class II (DR) antigen in A-PTG and F-PTG were significantly lower than that in C-PTG. The results demonstrate that C-PTG, with better function, and F-PTG, with lower antigenicity, can be used in clinical transplantation. A-PTG is not suitable for clinical transplantation due to their immaturity and possibility of carcinomatous change.
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PMID:[Human parathyroid allotransplantation: comparison of donor grafts]. 772 Jan 29

We compared the degrees of cell maturity, antigenicity and secretory function of parathyroid tissues (PTG) from cadavers (C-PTG), 20-28 week fetuses (F-PTG) and PTG adenomas (A-PTG). In A-PTG, scattered or clustered immature cells were observed, but there were none in F-PTG and C-PTG tissues. A-PTG and C-PTG exhibited better secretory function than did F-PTG. No clear differences were found in HLA class I (ABC) antigen quantity among the three donor PTG tissues, but the amounts of HLA class II (DR) antigen in A-PTG and F-PTG were significantly lower than that in C-PTG. The results demonstrate that C-PTG, with its functional advantages, and F-PTG, with its relatively low antigenicity, can be used in clinical transplantation, while A-PTG tissues are not suitable for clinical transplantation on account of their immaturity and the possibility of carcinomatous change.
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PMID:Comparison of parathyroid donor grafts. 829 6

Monocytes as antigen-presenting cells play an important role in host defence. There are several cytokines affecting monocyte function. We demonstrate that both adult and cord blood monocytes constitutively express hepatocyte growth factor (HGF) receptor, MET. HGF significantly down-regulated MET expression of adult blood monocytes, compared with cord blood monocytes, when cultured either in RPMI-1640 containing 10% FBS or serum-free medium. Surface levels of MET correlated with c-met mRNA levels both in adult and cord blood when cultured. MET expression was down-regulated by treating with actinomycin D or cycloheximide. HGF stimulated DNA synthesis of adult monocytes, but not cord blood. HGF enhanced antigen-presenting capacity of adult blood monocytes but not cord blood monocytes. HGF up-regulated HLA class I expression in adult monocytes but not in cord blood monocytes. The current results suggest that the failure of cord blood monocytes to respond to HGF may be responsible, in large part, for their functional immaturity.
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PMID:Differential responsiveness of cord and adult blood monocytes to hepatocyte growth factor. 1152 13

Globally, HIV-1 is most often transmitted heterosexually so that nearly half of all infected adults are women of child-bearing age. Infants may acquire infection from vertical transmission. Without treatment most HIV-1 infected children in Africa die before their third birthday; as a result child mortality has increased overall by 35-50%, and by greater than 100% in areas of high seroprevalence. HIV-1 infection has a heterogeneous spectrum of clinical course. Compared to HIV-1-infected adults, survival times are considerably shorter for children who acquire the virus perinatally or during infancy. Factors contributing to accelerated disease progression in infants and children are poorly understood but may include relative immunological immaturity, thymic HIV-1-mediated destruction at a time of active thymopoiesis, and HLA class I sharing between mother and infant. This review will initially discuss clinical and biological determinants of mother-to-child transmission and disease progression in HIV-infected infants and children. Our current knowledge of the mechanisms of T cell depletion is summarised and the host immune response to HIV-1 (innate and adaptive) described in the context of Pediatric HIV-1 infection.
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PMID:HIV-1 infection in children: a clinical and immunologic overview. 1563 21