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

Epidermal DNA synthesis, the epidermal mitotic rate, and the responsiveness to the epidermal G1 and G2 inhibitors were examined in newborn mice at different times after birth. The rate of epidermal cell renewal was in general low during the first two weeks of life. Later the two growth parameters increased and reached very high values at 32-33 days after birth. The rate of epidermal cell proliferation then decreased to a level comparable with that found in adult hairless mouse epidermis at 40-45 days. A single i.p. injection of skin extract containing the two epidermal growth inhibitors induced varying types of responses. The epidermal G2 inhibitor stimulated the mitotic rate on day 2 and day 10, but inhibited it on all other days. The epidermal G1 inhibitor brought about an increase in epidermal DNA synthesis on day 6 and possibly on the following days. No response at all seen at 2, 4, 17, and 32 days after birth. At the other examined times the inhibition was similar to that found in adult mice. These findings differed from those made in vitro on separated newborn mouse epidermal cells (our own unpublished data), and we suggest that the variability of newborn mouse epidermis could be an expression of the immaturity of the skin as a whole, and that dermis in some way modifies the response of epidermis to exogenous epidermal chalone. Our study did not support the theory that the nonresponsiveness of newborn mouse epidermal at certain times could be due to the presence of nonresponsive stem cells in epidermis.
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PMID:Growth kinetics in newborn mouse epidermis: response to epidermal chalone. 14 57

In ovaries of immature rats the following parameters were estimated from autoradiographs prepared after pulse labelling with tritiated thymidine: 1) The time it takes follicles to grow from one stage of development to another. This could be derived from the total number of granulosa cells in these stages and from their doubling times. The doubling time of granulosa cells was determined from their labelling index and the duration of their DNA-synthesis phase. 2) The number of follicles present in the ovary at different ages. 3) The number of follicles, which start on their development at different ages. It was found, that more follicles start to grow in 8 and 16 days old rats (2.0/h) than in 28 days old ones (1.0/h). Moreover, the follicles grow somewhat faster earlier in life than later. The development from a follicle with one layer of granulosa cells to one with several layers and antrum formation takes about 15 days in the first half of the period of immaturity while it takes about 17 days as the animal approaches maturity.
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PMID:Follicle growth in the immature rat ovary. 58 Aug 36

33 tissue sections of cases of primary skin-reticulosis showing different degrees of maturity were analysed by means of Feulgen-cytophotometric methods in regard to their DNA-content. The measurements performed disclosed cytophotometric differences of DNA distribution patterns between mature and less mature/immature forms: Mature forms of reticulosis were characterized by predominantly diploid DNA distribution patterns, whereas less mature/immature forms showed a main distribution in the hyperdiploid-hypotetraploid range respectively atypically dispersed aneuploid values with increase of variation and mean DNA-content. Moreover in several cases distribution patterns were seen, which may be regarded as cytophotometric transition forms showing a diploid peak and a higher rate of cells with enhanced DNA-content. Those cases appeared histomorphologically mature with a slight tendency to immaturity.
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PMID:[Feulgencytophotometric DNA distribution patterns of well-differentiated (mature) and undifferentiated (less mature/immature) forms of primary skin-reticulosis]. 79 Nov 55

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.
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PMID:[New methods for diagnosing infection in pregnancy]. 132 3

The effects of the cytokines tumor necrosis factor-alpha and interferon-gamma on the adult beta-cell have been well described: a reduction of insulin secretion and content and death of the cell. For this reason and because these cytokines may be released from activated lymphocytes and macrophages that infiltrate islets in insulin-dependent diabetes, they have been implicated in the pathophysiology of this form of diabetes. As to whether the human fetal beta-cell, which differs from the adult beta-cell in not releasing insulin in response to the nutrient glucose and not being adversely affected by the toxin streptozotocin, is similarly affected is unknown. To examine this question we cultured monolayers of a single cell suspension of human fetal pancreas in the presence or absence of 1000 U/mL of these cytokines for 7 days. Chronic insulin release was enhanced for the first 2 days of culture, but unchanged thereafter. Acute insulin release in response to the secretagogue theophylline (10 mM) was enhanced on day 7, but not earlier. There was an increase in the insulin content of the cells by the fourth day, probably due to an increase in the number of beta-cells present (45 +/- 5% vs. 22 +/- 3%). Microscopically, non-beta-cells also seemed to increase in number; there was an increase in both DNA and cell number by the seventh day. In contrast to these beneficial effects on the human fetal beta-cell, treatment of adult rat insulinoma cells, represented by RIN-m5F cells, resulted in inhibition of insulin secretion during the first day of culture and subsequent death of 86% of the cells by the sixth day of culture. It is hypothesized that the functional immaturity and lack of normal (adult) metabolic activity of the human fetal beta-cell somehow confers protection on these cells from the cytotoxic effects of tumor necrosis factor-alpha and interferon-gamma. Indeed, our findings suggest that these cytokines may be trophic for the developing beta-cell.
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PMID:Role of tumor necrosis factor-alpha and interferon-gamma as growth factors to the human fetal beta-cell. 193 17

Recombinant human erythropoietin (r-HuEPO) is of interest to pediatric hematologists and neonatologists because it may prove to be an effective alternative to blood transfusions in preventing and treating anemia in premature infants. The anemia of prematurity is the most promising setting for initial clinical trials. However, it is conceivable that recombinant erythropoietin will be given at birth to low-birth-weight infants in an effort to stimulate endogenous erythropoiesis and thereby prevent some of the erythrocyte transfusions required to replace blood sampled for laboratory tests. Beyond its appeal as a therapeutic alternative to red blood cell transfusions, recombinant human erythropoietin is likely to be the first member of an entirely new class of drugs to be used widely in neonatal medicine. These are drugs produced by cloning normal human genes and expressing them in the laboratory. Because many of the problems of premature birth are caused by developmental immaturity, transiently replacing crucial proteins with exact copies produced by the techniques of recombinant DNA technology is an approach that may have a major impact on morbidity and mortality of neonates. Carefully designed, controlled clinical trials will be essential to determine the role of new agents like r-HuEPO in the treatment of medical problems of premature infants.
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PMID:Anemia of prematurity: progress and prospects. 217 57

We present the autopsy report of a liveborn triploid female, born after 36 weeks of gestation, who died at the age of 20 hours. External features were diagnostic: fetal hypoplasia, hypertelorism, microstomia, micro-and retrognathia, preauricular skin tag, low-set ears, and 3-4 syndactylia. All internal organs were hypoplastic. There were atrial and ventricular septal defects. Adrenals and kidneys were fused, the gallbladder was absent, and ovarian hilum cell were found to be hyperplastic. Triploidy, 69xxx, was confirmed cytogenetically. The placenta was hypoplastic and, microscopically, revealed a peculiar type of immaturity, so-called hydatidiform villous hypoplasia, findings which have not been previously reported. We suggest that the generalized fetal and placental hypoplasia and the severe hypoplasia of all internal organs are caused by a proliferative deficiency of the triploid cells. In addition, the nuclear DNA content was determined by cytophotometrically from placental stromal cells and was found to be about 50% above the normal diploid DNA value; i.e., a triploid DNA value was confirmed.
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PMID:Triploidy syndrome in a liveborn female. 227 97

Ejaculated human spermatozoa were studied to assess their nuclear maturity. After SDS or SDS-EDTA treatment, asthenozoospermic semen had a lower resistance to decondensation than normozoospermic semen and contained more stained immature nuclei after aniline blue staining. It showed a higher uptake of ethidium bromide, specific for DNA. There was no difference in the binding of 14C iodoacetamide in the two groups. Therefore, asthenozoospermic semen could be characterized by its relative nuclear immaturity.
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PMID:Human spermatozoal nuclear maturity in normozoospermia and asthenozoospermia. 246 2

Deficient responses by NK cells may contribute to the susceptibility of human newborns to severe HSV infections. Furthermore, HSV disseminates widely during neonatal infection and may also infect and interfere with the function of blood mononuclear cells (MNC). To determine whether the function of newborn NK cells would be affected by contact with HSV, and whether newborn NK cells might be permissive for HSV replication, newborn MNC were cultured with HSV in vitro for 3 days. Before culture, the intracellular calcium mobilization in newborn NK cells induced by mAb to CD2 and CD16 did not differ from that of adult NK cells. This result argues against immaturity of an early NK cell activation event in human newborns. After culture with HSV the Ca2+ flux response was unaffected by lysis of K562 targets by newborn NK cells and NK-dependent suppression of HSV replication in fibroblasts were preserved or increased. Incorporation of thymidine by NKH-1 cells following stimulation with PHA and IL-2 was not suppressed. NK cells recovered from these cultures did not contain infectious HSV and synthesis of HSV-specific proteins was not detected by immunoprecipitation although HSV genome was detected by DNA hybridization. Our results extend the in vitro model stimulation systems in which newborn NK cells respond positively to include triggering through the CD2 Ag, cross-linking of cell surface CD 16 Ag and response to a pathogen, HSV.
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PMID:Human newborn natural killer cell responses to activation by monoclonal antibodies. Effect of culture with herpes simplex virus. 253 66

A new retrovirus consisting of the v-myc oncogene sequences of avian MC29 virus inserted into the genome of Moloney murine leukemia virus (M-MuLV) was generated. This was accomplished by constructing a recombinant DNA clone containing the desired organization, introducing the recombinant DNA into mouse NIH 3T3 cells, and superinfecting the cells with replication-competent M-MuLV. The construction was designed so that an M-MuLV gag-myc fusion protein would be produced. The resulting virus, M-MuLV(myc), morphologically transformed uninfected NIH 3T3 cells. Stocks of M-MuLV(myc)-M-MuLV were infected into secondary mouse embryo cultures. M-MuLV(myc) induced striking growth and proliferation of hematopoietic cells. These cells were of the myeloid lineage by morphology, phagocytic properties, and surface staining with Mac-1 and Mac-2 monoclonal antibodies. They resembled mature macrophages, although they displayed minor properties of immaturity. The myeloid cells were transformed in comparison with uninfected myeloid cells since they were less adherent and had unlimited proliferative capacity and reduced growth factor requirements. The transformed myeloid cells with proliferative potential were actually myeloid progenitors which apparently underwent terminal differentiation to macrophages. It was possible to derive a permanent line of factor-independent macrophages from M-MuLV(myc)-transformed myeloid cells. M-MuLV(myc) also immortalized and morphologically transformed mouse embryo fibroblasts. These in vitro properties closely resembled the biological activity of MC29 virus in avian cells and suggested that the nature of the v-myc oncogene was an important determinant in transformation specificity. Neonatal NIH Swiss mice inoculated intraperitoneally with M-MuLV(myc)-M-MuLV only developed lymphoblastic lymphoma characteristic of the M-MuLV helper alone, and no acute fibrosarcomas or myeloid tumors resulted. In light of the strong myeloid transformation observed in vitro, the absence of acute in vivo myeloid disease was noteworthy. Interestingly, when a derivative of M-MuLV(myc) carried by a nonpathogenic amphotropic MuLV helper was inoculated, T lymphomas developed with long latency. Molecular hybridization confirmed that these tumors contained M-MuLV(myc).
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PMID:Generation and characterization of a recombinant Moloney murine leukemia virus containing the v-myc oncogene of avian MC29 virus: in vitro transformation and in vivo pathogenesis. 301 1


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