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Query: UMLS:C0029713 (immaturity)
 4,335 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The minimal acute inflammatory response to tissue injury is one of the most dramatic differences between fetal and adult wound healing. Considering the prominent role of inflammation in adult tissue repair, this study tested the hypothesis that the minimal fetal inflammatory response to tissue injury plays a central role in the "scarless" fetal repair process. Sponge implants were treated with lethally irradiated or live bacteria and placed subcutaneously in fetal rabbits to test the ability of the fetus to mount an acute inflammatory response to bacterial antigens present at the wound site and to analyze the effects of this inflammatory response on fetal fibroplasia and neovascularization. After harvest, these implants were examined histologically for inflammation, fibroblast infiltration, collagen deposition, and neovascularization, and collagen deposition was measured using hydroxyproline quantitation by high-performance liquid chromatography. Bacteria-treated implants showed dose-dependent acute inflammatory responses and significant increases in collagen deposition compared with control sponges. Implants containing live bacteria demonstrated maximal fibroplasia and neovascularization. These findings suggest that, despite neutropenia and immaturity of the fetal immune system, the fetus is capable of mounting an acute inflammatory response to avirulent bacteria present at the wound site. Fetal inflammatory cells which respond to this bacterial stimulus appear capable of initiating an adult-like healing response. Thus, by failing to provide a bacterial stimulus for leukocyte recruitment at the site of tissue injury, the sterile fetal environment appears to play a role in effecting "scarless" fetal wound healing.
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PMID:Biology of fetal repair: the presence of bacteria in fetal wounds induces an adult-like healing response. 846 58

To investigate the pathogenesis of osteoarthrosis, we have performed biochemical and morphological studies, other than roentgenological examination, on the soft tissues. Biochemical analyses of collagen were performed on muscles (gluteus medius) in normal and in pathological cases. In the terminal stage of osteoarthrosis, we observed more immature collagen fibers in muscles, than in normal cases. In the preosteoarthrosis stage, immature collagen formation was inconsistent with various degrees of immaturity observed. Morphologically, irregularity in the muscle fibers and interfascicular-fibrosis was observed in the gluteus medius only at the terminal stage but not at the preosteoarthrosis stage. In some cases, we observed a predominance and/or grouping of type 1 fibers. Among the 20 cases with preosteoarthrosis, 3 cases (15%) showed marked biochemical changes in both quantity and quality of collagen fibers in the gluteus medius, as compared with cases at the terminal stage. These findings may be valuable in studying the onset and development of the pathophysiology of osteoarthrosis.
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PMID:[Biochemical and morphological studies on soft tissues in hip osteoarthrosis]. 858 10

One hundred two (102) cases of pre-labour rupture of membrane (PROM) were studied and special attention was given to the histological study of the amniotic membrane as well as to the bacteriological study of high vaginal flora, cervical flora and flora of amniotic fluid, in search of probable causes or factors leading to PROM. The incidence was found to be 3.16% in the age group of 20-25 years without any relation to parity; and the duration of gestation was 38 to 40 weeks in most of the cases. The histological study revealed: (a) Focally denuded amniotic epithelium, focally separated amniotic epithelium from chorion layer, lesser density of focal squamoid change of the epithelium and thicker chorion layer probably indicating focal immaturity of the chorio-amnion, (b) lesser thickness of collagen layer, focal hydropic degeneration and mild cellular infiltrate, (c) presence of focal hyaline degeneration and focal calcification of chorio-amnion. Microbial culture revealed: (a) Higher rate of positive culture in high vaginal swab, cervical swab and amniotic fluid showing presence predominantly of Esch coli, Strept haemolyticus, klebseilla species, Staph aureus, Strept non-haemolyticus, proteus species and pseudomonas species against that of positive cultures in the control cases, (b) no anaerobic bacteria from high vaginal swab, cervical swab or from amniotic fluid. It was presumed that focal immaturity of chorio-amnion or focal irregularity in the chorio-amnion at the microscopical level, focal degeneration of collagen superadded with bacterial infection, however mild, could be the factors leading to weakness in the tensile strength of chorio-amnion, again leading to PROM, in the face of stress factors of foetal origin.
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PMID:Pre-labour rupture of membrane: the histological study of membrane and bacteriological profile. 952 83

It was found that intracerebral blood vessels in human embryo telencephalon first appear on the 7th week of prenatal development as capillaries with poorly differentiated walls and signs of functional immaturity. The formation of the basal capillary membrane consisting of laminin and type IV collagen starts immediately after the formation of primary capillary network.
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PMID:Initial stage of vascular bed development in telencephalon of human embryo. 1097 66

In premature human neonates, immaturity of cerebral vessels can contribute to clinical problems such as germinal matrix hemorrhage and white matter damage. Afferent cerebral vessels in the brain of term babies express alkaline phosphatase (AP), an ectoenzyme located on the surface of endothelial cells. Using AP enzyme histochemistry we have examined the cerebrovasculature of premature live-born human neonates to determine when cerebral afferent vessels begin to express AP. Brains were collected at autopsy and processed for histological examination. AP-stained vessel density in the periventricular white matter was quantified using digital imaging and automated morphometry. Babies born prior to 28 wk gestation display few AP-positive vessels in the periventricular white matter, whereas, babies born after 28 wk gestation exhibit an AP-positive vascular pattern that resembles the adult pattern. In contrast, immunostaining for collagen revealed an extensive vascular network in both early and late gestation infants. Our measurements indicate that neonates born prior to 28 wk gestation are characterized by immature cerebral white matter afferent vessels and raise the possibility that the immaturity compromises vascular function.
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PMID:Temporal expression pattern of cerebrovascular endothelial cell alkaline phosphatase during human gestation. 1182 46

Cell differentiation markers on placental villi from the first trimester of human pregnancy have been studied by indirect immunofluorescence. Fluorescence labelling with antibodies against CD34 and CD31 was conspicuous in the vascular cells. The vascular paracellular clefts were labelled by anti-cadherin-5. A few vascular cells exhibited a positive reaction for von Willebrand factor, high-molecular-weight melanoma-associated-antibody and alpha-sm-actin compared to term pregnancy, indicating changes in protein expression during vascular differentiation. The poor anti-collagen IV reaction and the absence of a sm-myosin fluorescent signal observed around the vessels confirned the immaturity of the vessels. In contrast, strong reactions have previously been obtained with the latter antibodies in similar locations using term placental villi. A labelling was observed for antibodies against alpha3 and alpha5 integrins in these immature placental vessels suggesting cell-matrix interactions with specific domains of laminin or fibronectin. The vascular cells were also stained by anti-CD26. Surprisingly, the fetal vascular cells exhibited immunostainings in common with the villous cytotrophoblast (CD26) or the syncytiotrophoblast (cadherin-5) and cell islands cytotrophoblast (CD31, cadherin-5, alpha3 and alpha5 integrin subunits). These observations suggested a two step process for fetal vasculogenesis in the villi: i/ the formation of peripheral vessels induced by growth factors or cytokines derived from the nearby trophoblast, ii/ the development of muscular vessels due to growth factors or cytokines production induced by circulatory changes.
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PMID:Characterization of first trimester human fetal placental vessels using immunocytochemical markers. 1193 78

Germinal matrix haemorrhage in premature neonates is commonly attributed to vascular immaturity, possibly related to an abbreviated process of angiogenesis. Terminal steps in the progression of angiogenesis are the formation of a subendothelial basal lamina containing collagen IV and an extracellular matrix containing collagens I and III. Immature vessels would predictably be deficient in these collagen subtypes. We analysed germinal matrix (GM), cortical, and white matter (WM) vessels with antibodies specific for collagens I, III and IV to test the hypothesis that GM vessels are immature. Brains were collected during post-mortem from prematurely born human neonates ranging in age from 17 weeks to 36 weeks postconception. All GM vessels were immunoreactive for collagen subtypes I, III and IV. Using digital image analysis, collagen IV immunoperoxidase-labelling was measured in vessels in GM, cortex and WM. Intensity values in GM and WM were normalized relative to cortical intensity within the same subject. At week 17 of gestation, GM vessels exhibited a higher concentration of collagen IV than did WM or cortical vessels. Regression analysis demonstrated that collagen intensity in GM was greater than that in cortex and WM at all stages. We conclude that GM vessels in even the youngest, prematurely born, viable neonates do not exhibit evidence of structural immaturity. The high incidence of GM haemorrhage in premature neonates may be related to factors other than a deficiency in accumulated collagen.
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PMID:Morphometric assessment of collagen accumulation in germinal matrix vessels of premature human neonates. 1577 11

The human intrahepatic biliary epithelium is composed of a morphologically heterogeneous population of epithelial cells. During liver cirrhosis, new biliary ductular structures develop at the portal margins that express markers of immaturity such as CD56 and Bcl-2. These markers are also expressed transiently on immature biliary duct precursors during embryological development; thus their reappearance during cirrhosis suggests a recapitulation of ontogenesis during some liver conditions. Here we describe methods, based on the differential expression of membrane markers, for separating immature biliary epithelial cells from those associated with mature ducts. We also describe two- and three-dimensional culture models for the maintenance of mature and immature populations in vitro. Both populations readily establish colonies in monolayer culture but only cells from mature ducts can be maintained in medium-term culture as serially proliferating, passageable cultures; immature cells deteriorate and detach within 2-3 weeks of isolation. In three-dimensional collagen gel culture, both mature and immature populations form duct-like structures with clearly definable lumena that persist for up to 6 weeks.
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PMID:Human intrahepatic biliary epithelial cell lineages: studies in vitro. 1909

Several factors are associated with bronchopulmonary dysplasia. Among them, hyperoxia and lung immaturity are considered to be fundamental; however, the effect of malnutrition is unknown. Our objective was to evaluate the effects of 7 days of postnatal malnutrition and hyperoxia on lung weight, volume, water content, and pulmonary morphometry of premature rabbits. After c-section, 28-day-old New Zealand white rabbits were randomized into four groups: control diet and room air (CA, N = 17), control diet and > or = 95% O2 (CH, N = 17), malnutrition and room air (MA, N = 18), and malnutrition and > or = 95% O2 (MH, N = 18). Malnutrition was defined as a 30% reduction of all the nutrients provided in the control diet. Treatments were maintained for 7 days, after which histological and morphometric analyses were conducted. Lung slices were stained with hematoxylin-eosin, modified orcein-resorcin or picrosirius. The results of morphometric analysis indicated that postnatal malnutrition decreased lung weight (CA: 0.83 +/- 0.19; CH: 0.96 +/- 0.28; MA: 0.65 +/- 0.17; MH: 0.79 +/- 0.22 g) and water content, as well as the number of alveoli (CA: 12.43 +/- 3.07; CH: 8.85 +/- 1.46; MA: 7.33 +/- 0.88; MH: 6.36 +/- 1.53 x 10-3/mm) and elastic and collagen fibers. Hyperoxia reduced the number of alveoli and increased septal thickening and the mean linear intercept. The reduction of alveolar number, collagen and elastic fibers was intensified when malnutrition and hyperoxia were associated. These data suggest that dietary restriction enhances the magnitude of hyperoxia-induced alveolar growth arrest and lung parenchymal remodeling. It is interesting to consider the important influence of postnatal nutrition upon lung development and bronchopulmonary dysplasia.
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PMID:Effect of postnatal malnutrition on hyperoxia-induced newborn lung development. 1957 40

CXC chemokine receptor 3 (CXCR3) signaling promotes keratinocyte migration while terminating fibroblast and endothelial cell immigration into wounds; this signaling also directs epidermal and matrix maturation. Herein, we investigated the long-term effects of failure to activate the "stop-healing" CXCR3 axis. Full-thickness excisional wounds were created on CXCR3 knockout((-/-)) or wild-type mice and examined at up to 180 days after wounding. Grossly, the CXCR3(-/-) mice presented a thick keratinized scar compared with the wild-type mice in which the scar was scarcely noticeable; histological examination revealed thickening of both the epidermis and dermis. The dermis was disorganized with thick and long collagen fibrils and contained excessive collagen content in comparison with the wild-type mice. Interestingly, the CXCR3(-/-) wounds presented lower tensile/burst strength, which correlates with decreased alignment of collagen fibers, similar to published findings of human scars. Persistent Extracellular matrix turnover and immaturity was shown by the elevated expression of proteins of the immature matrix as well as expression of matrix metallopeptidase-9 MMP-9. Interestingly, the scars in the CXCR3(-/-) mice presented evidence of de novo development of a sterile inflammatory response only months after wounding; earlier periods showed resolution of the initial inflammatory stage. These in vivo studies establish that the absence of CXCR3(-/-) signaling network results in hypertrophic and hypercellular scarring characterized by on-going wound regeneration, cellular proliferation, and scars in which immature matrix components are undergoing increased turnover resulting in a chronic inflammatory process.
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PMID:Lack of CXC chemokine receptor 3 signaling leads to hypertrophic and hypercellular scarring. 2018 79


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