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)

Maternal infections during pregnancy are of special relevance because of the risk of transmission to the fetus. Besides serological methods of diagnosing acute maternal infection, new approaches to assess fetal involvement have been made by invasive procedures, such as ultrasound-guided fetal blood sampling or amniocentesis. The most relevant infections in pregnancy are briefly reviewed with their incidence, consequences of fetal infection, and standard diagnostic procedures. Immunological methods are handicapped by the immaturity of the fetal immune system; direct culture is complicated and time-consuming. The application of molecular biological methods to directly identify the RNA- or DNA-sequences of the infectious agent may be an alternative. Two methods, polymerase-chain-reaction (PCR) and in-situ hybridization (ISH) are explained. Broad clinical use is still hindered by problems in specificity and quantitative accuracy. Nevertheless, successful diagnosis of most of the relevant infections in pregnancy by these molecular biological methods, is published, and discussed in a review of the recent literature.
 ...
PMID:[New methods for diagnosing infection in pregnancy]. 132 3

We have developed an animal model for congenital syphilis. Treponema pallidum is injected intravenously into pregnant rabbits and fetuses are infected in utero. As a prelude to characterizing the immunologic consequences of fetal infection, it was necessary to expand on the baseline information about newborn rabbit immune capabilities. Studies were undertaken to determine splenic macrophage and T lymphocyte functions with emphasis on newer immunologic parameters. Newborns aged 2 weeks were compared to adults. Macrophage capabilities in newborn rabbits differed from those of their adult counterparts. These cells produced similar basal levels of interleukin 1 (IL-1) but failed to respond to the IL-1 stimulants of lipopolysaccharide (LPS) or T. pallidum. Macrophages also exhibited diminished levels of la expression and increased levels of prostaglandin E2 (PGE2) secretion. T lymphocyte functions were altered in newborn spleen preparations. Following concanavalin A (Con A) stimulation, interferon gamma production was half that of adults; in direct contrast, IL-2 production was twice that of adults. Con A-induced lymphocyte proliferation was markedly decreased in newborn preparations. This diminished response resulted from down-regulation rather than immaturity. When newborn splenic cells were stimulated with Con A in the presence of indomethacin, anti-transforming growth factor (anti-TGF), or exogenous IL-1/IL-2, better proliferation resulted. PGE2, which is well established as a down-regulator of newborn immune functions in human and mouse systems, also appears to play a role in suppressing newborn rabbit functions. TGF is a potent suppressor of a number of adult immunologic reactions. This is the first documentation of the potential role of this factor in down-regulating newborn immune capabilities. These findings provide a framework for future investigations of our congenital syphilis model.
 ...
PMID:Macrophage and lymphocyte functions are down-regulated in newborn rabbits. 143 51

The authors examined 273 newborns weighing less than 1500 g. Their birth weight was very low (1001-1500 g) in 179 but extremely low (< 1000 g) in 94 newborns. Neurological damage was proved in 101 cases (36.99%). The probable reasons for intra- (peri-) ventricular and cerebral hemorrhages in these newborns were the following: respiratory distress syndrome (in 11 cases or 10.89%), mother-fetal infection (in 16 cases or 15.84%), and combination of asphyxia and infection (in 10 cases or 9.9%). The severe degree of prematurity (and immaturity) remained the only causative factor in the rest 64 premature newborns (63.37% of the cases). The results from the distribution of the neurological lesions according to the gestational age were also considered. Usage of monofactorial regression models detected statistically significant differences between asphyxia, infection and brain damage in the newborns of different gestational age.
 ...
PMID:[Intranatal asphyxia, prematurity and congenital infection--their role for brain damage in very low birth weight newborns]. 1551 66

Perinatal brain injury in survivors of premature birth has a unique and unexplained predilection for periventricular cerebral white matter. Periventricular white-matter injury (PWMI) is now the most common cause of brain injury in preterm infants and the leading cause of chronic neurological morbidity. The spectrum of chronic PWMI includes focal cystic necrotic lesions (periventricular leukomalacia; PVL) and diffuses myelination disturbances. Recent neuroimaging studies support that the incidence of PVL is declining, whereas focal or diffuse noncystic injury is emerging as the predominant lesion. Factors that predispose to PVL during prematurity include hypoxia, ischemia, and maternal-fetal infection. In a significant number of infants, PWMI appears to be initiated by perturbations in cerebral blood flow that reflect anatomic and physiological immaturity of the vasculature. Ischemic cerebral white matter is susceptible to pronounced free radical-mediated injury that particularly targets immature stages of the oligodendrocyte lineage. Emerging experimental data supports that pronounced ischemia in the periventricular white matter is necessary, but not sufficient to generate PWMI. The developmental predilection for PWMI to occur during prematurity appears to be related to both the timing of appearance and regional distribution of susceptible oligodendrocyte progenitors. Injury to oligodendrocyte progenitors may contribute to the pathogenesis of PWMI by disrupting the maturation of myelin-forming oligodendrocytes. Chemical mediators that may contribute to white-matter injury include reactive oxygen species glutamate, cytokines, and adenosine. As our understanding of the pathogenesis of PWMI improves, it is anticipated that new strategies for directly preventing brain injury in premature infants will develop.
 ...
PMID:Perinatal white matter injury: the changing spectrum of pathology and emerging insights into pathogenetic mechanisms. 1680 10