Academic literature on the topic 'Normal adult human astrocyte'
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Journal articles on the topic "Normal adult human astrocyte"
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Rutka, James T., Masaji Murakami, Peter B. Dirks, Sherri Lynn Hubbard, Laurence E. Becker, Kozo Fukuyama, Shin Jung, and Kazuhito Matsuzawa. "Role of glial filaments in cells and tumors of glial origin: a review." Neurosurgical Focus 3, no. 1 (July 1997): E2. http://dx.doi.org/10.3171/foc.1997.3.1.2.
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In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). This GFAP is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.
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Rutka, James T., Masaji Murakami, Peter B. Dirks, Sherri Lynn Hubbard, Laurence E. Becker, Kozo Fukuyama, Shin Jung, Atsushi Tsugu, and Kazuhito Matsuzawa. "Role of glial filaments in cells and tumors of glial origin: a review." Journal of Neurosurgery 87, no. 3 (September 1997): 420–30. http://dx.doi.org/10.3171/jns.1997.87.3.0420.
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✓ In the adult human brain, normal astrocytes constitute nearly 40% of the total central nervous system (CNS) cell population and may assume a star-shaped configuration resembling epithelial cells insofar as the astrocytes remain intimately associated, through their cytoplasmic extensions, with the basement membrane of the capillary endothelial cells and the basal lamina of the glial limitans externa. Although their exact function remains unknown, in the past, astrocytes were thought to subserve an important supportive role for neurons, providing a favorable ionic environment, modulating extracellular levels of neurotransmitters, and serving as spacers that organize neurons. In immunohistochemical preparations, normal, reactive, and neoplastic astrocytes may be positively identified and distinguished from other CNS cell types by the expression of the astrocyte-specific intermediate filament glial fibrillary acidic protein (GFAP). Glial fibrillary acidic protein is a 50-kD intracytoplasmic filamentous protein that constitutes a portion of, and is specific for, the cytoskeleton of the astrocyte. This protein has proved to be the most specific marker for cells of astrocytic origin under normal and pathological conditions. Interestingly, with increasing astrocytic malignancy, there is progressive loss of GFAP production. As the human gene for GFAP has now been cloned and sequenced, this review begins with a summary of the molecular biology of GFAP including the proven utility of the GFAP promoter in targeting genes of interest to the CNS in transgenic animals. Based on the data provided the authors argue cogently for an expanded role of GFAP in complex cellular events such as cytoskeletal reorganization, maintenance of myelination, cell adhesion, and signaling pathways. As such, GFAP may not represent a mere mechanical integrator of cellular space, as has been previously thought. Rather, GFAP may provide docking sites for important kinases that recognize key cellular substrates that enable GFAP to form a dynamic continuum with microfilaments, integrin receptors, and the extracellular matrix.
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Gasque, Philippe, Jane Jones, Sim K. Singhrao, and B. Morgan. "Identification of an Astrocyte Cell Population from Human Brain that Expresses Perforin, a Cytotoxic Protein Implicated in Immune Defense." Journal of Experimental Medicine 187, no. 4 (February 16, 1998): 451–60. http://dx.doi.org/10.1084/jem.187.4.451.
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The brain is an immunoprivileged organ isolated from the peripheral immune system. However, it has been shown that resident cells, notably astrocytes and microglia, can express numerous innate immune molecules, providing the capacity to generate a local antipathogen system. Perforin is a cytolytic protein present in the granules of cytotoxic T lymphocytes and natural killer cells. Expression in cells other than those of the hemopoetic lineage has not been described. We report here that fetal astrocytes in culture (passages 2 to 15), astrocytoma, and adult astrocytes expressed perforin. Reverse transcriptase polymerase chain reaction followed by Southern blot was carried out using multiple specific primers and all cDNAs were cloned and sequenced. Human fetal astrocyte perforin cDNA sequence was ∼100% identical to the reported perforin cDNA cloned from T cells. Western blot analysis using monoclonal and polyclonal antiperforin peptide antibodies revealed a protein of 65 kD in both human fetal astrocyte and rat natural killer cell lysates (n = 4). Immunostaining followed by FACS® and confocal and electron microscopy analysis revealed that perforin was expressed by 40–50% of glial fibrillary acidic protein positive cells present in the fetal brain culture (n = 11). Perforin was not localized to granules in astrocytes but was present throughout the cytoplasm, probably in association with the endoplasmic reticulum. Perforin was not detected in normal adult brain tissue but was present in and around areas of inflammation (white and grey matter) in multiple sclerosis and neurodegenerative brains. Perforin-positive cells were identified as reactive astrocytes. These findings demonstrate that perforin expression is not unique to lymphoid cells and suggest that perforin produced by a subpopulation of astrocytes plays a role in inflammation in the brain.
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Gasque, Philippe, Sim K. Singhrao, Jim W. Neal, Piao Wang, Sakina Sayah, Marc Fontaine, and B. Paul Morgan. "The Receptor for Complement Anaphylatoxin C3a Is Expressed by Myeloid Cells and Nonmyeloid Cells in Inflamed Human Central Nervous System: Analysis in Multiple Sclerosis and Bacterial Meningitis." Journal of Immunology 160, no. 7 (April 1, 1998): 3543–54. http://dx.doi.org/10.4049/jimmunol.160.7.3543.
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Abstract The complement anaphylatoxins C5a and C3a are released at the inflammatory site, where they contribute to the recruitment and activation of leukocytes and the activation of resident cells. The distribution of the receptor for C5a (C5aR) has been well studied; however, the receptor for C3a (C3aR) has only recently been cloned, and its distribution is uncharacterized. Using a specific affinity-purified anti-C3aR peptide Ab and oligonucleotides for reverse transcriptase-PCR analysis, C3aR expression was characterized in vitro on myeloid and nonmyeloid cells and in vivo in the brain. C3aR was expressed by adult astrocytes, astrocyte cell lines, monocyte lines THP1 and U937, neutrophils, and monocytes, but not by K562 or Ramos. C3aR staining was confirmed by flow cytometry, confocal imaging, and electron microscopy analysis. A 65-kDa protein was immunoprecipitated by the anti-C3aR from astrocyte and monocyte cell lysates. Our results at the protein level were confirmed at the mRNA level. Using reverse transcriptase-PCR, Southern blot, and sequencing we found that C3aR mRNA was expressed by fetal astrocytes, astrocyte cell lines, and THP1, but not by K562 or Ramos. The astrocyte C3aR cDNA was identical with the reported C3aR cDNA. C3aR expression was not detected in normal brain sections. However, a strong C3aR staining was evident in areas of inflammation in multiple sclerosis and bacterial meningitis. In meningitis, C3aR was abundantly expressed by reactive astrocytes, microglia, and infiltrating cells (macrophages and neutrophils). In multiple sclerosis, infiltrating lymphocytes did not express C3aR, but a strong staining was detected on smooth muscle cells (pericytes) surrounding blood vessels.
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Kurihara, Toshihide, Peter D. Westenskow, Tim U. Krohne, Edith Aguilar, Randall S. Johnson, and Martin Friedlander. "Astrocyte pVHL and HIF-α isoforms are required for embryonic-to-adult vascular transition in the eye." Journal of Cell Biology 195, no. 4 (November 14, 2011): 689–701. http://dx.doi.org/10.1083/jcb.201107029.
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Successful transition from embryonic to adult circulation is critical for survival of mammalian organisms. This shift occurs in the central cardiovascular circulation and in the eye as oxygen tension increases. However, its regulation is not well understood. We have used combinatorial gene deletion and overexpression assays to assess the effect of astrocyte-targeted deletion of von Hippel–Lindau tumor suppressor (Vhl), hypoxia-inducible factor-αs (Hif-αs), and Vegf on the normal regression of the hyaloidal vessels, the fetal ocular circulation system. Astrocytic Vhl deletion induced accelerated hyaloidal regression and subsequent massive secondary outgrowth. Combinatorial gene deletion involving Vhl, Hif-αs, and Vegf genes revealed that HIF-2α/vascular endothelial growth factor signaling induces secondary outgrowth in Vhl mutants. Conversely, HIF-1α regulated macrophage migration inhibitory factor and promoted macrophage infiltration that accelerates hyaloidal vessel regression. The phenotype observed in Vhl mutants strongly resembles human persistent hyperplastic primary vitreous cases and may provide insights into vascular remodeling mechanisms in other systems.
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Juul, Sandra E., Anthony T. Yachnis, Amyn M. Rojiani, and Robert D. Christensen. "Immunohistochemical Localization of Erythropoietin and Its Receptor in the Developing Human Brain." Pediatric and Developmental Pathology 2, no. 2 (March 1999): 148–58. http://dx.doi.org/10.1007/s100249900103.
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We have previously shown erythropoietin (Epo) and its receptor (Epo-R) to be present in the fetal human central nervous system (CNS), and Epo to be present in the spinal fluid of normal preterm and term infants. To investigate the cellular specificities and developmental patterns of expression of these polypeptides in the human brain—areas that have not been well researched—we designed the following study. Human brains ranging in maturity from 5 weeks post-conception to adult were preserved at the time of elective abortion, surgical removal (tubal pregnancy, or removal for temporal lobe epilepsy), or autopsy. Immunohistochemistry was used to localize Epo and Epo-R reactivity in brains of different stages of development. Astrocytes, neurons, and microglia were identified in sequential tissue sections by specific antibodies. At 5 to 6 weeks post-conception, both Epo and Epo-R localized to cells in the periventricular germinal zone. At 10 weeks post-conception, Epo immunoreactivity was present throughout the cortical wall, with the most intense immunoreactivity present in the ventricular and subventricular zones. Epo-R, in contrast, was localized primarily to the subventricular zone, with little staining evident in the ventricular zone. In late fetal brains, Epo-R reactivity was most prominent in astrocytic cells, although modest reactivity was observed in certain neuron populations. In contrast, Epo staining localized primarily to neurons in fetal brains, although a subpopulation of astrocytes was also immunoreactive. In postnatal brains, both astrocyte and neuron populations were immunoreactive with antibodies to Epo-R and Epo. From these results it is clear that Epo and its receptor are present in the developing human brain as early as 5 weeks post-conception, and each protein shows a specific distribution that changes with development. We speculate that Epo is important in neurodevelopment, and that it also plays a role in brain homeostasis later in life, functioning in an autocrine or paracrine manner.
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Nagai, Shoichi, Kazuo Washiyama, Masanori Kurimoto, Akira Takaku, Shunro Endo, and Toshiro Kumanishi. "Aberrant nuclear factor-κB activity and its participation in the growth of human malignant astrocytoma." Journal of Neurosurgery 96, no. 5 (May 2002): 909–17. http://dx.doi.org/10.3171/jns.2002.96.5.0909.
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Object. It has been suggested that nuclear factor (NF)-κB, a pleiotropic transcription factor, controls cell proliferation. The authors examined NF-κB activity and its participation in the growth of human malignant astrocytoma. Methods. The authors examined NF-κB activity in human malignant astrocytoma cell lines and high-grade astrocytoma tissues by using electrophoretic mobility shift assays and immunohistochemical studies, respectively. In addition, messenger (m)RNA expression of p50 and RelA, which are representative subunits of NF-κB, and IκBα, which is a representative inhibitory protein of NF-κB, were analyzed using Northern blot hybridization in the astrocytoma cell lines. Furthermore, alterations in DNA synthesis and cell growth in the astrocytoma cell lines were examined after inhibition of NF-κB activity by RelA antisense oligodeoxynucleotide. The authors found NF-κB activity in all astrocytoma cell lines and high-grade astrocytoma tissues that were examined, but not in the fetal astrocyte strain or in normal cerebral tissue. Expression of p50, RelA, and IκBα mRNA was found in the fetal astrocyte strain and normal adult brain tissue, in addition to the astrocytoma cell lines. The relative levels of expression of these mRNAs were similar among these cell lines, the cell strain, and normal tissue. The RelA antisense oligodeoxynucleotide specifically reduced the levels of RelA mRNA expression and NF-κB activity in the astrocytoma cell lines, thus significantly inhibiting their DNA synthesis and cell growth. Conclusions. Human malignant astrocytoma cells have aberrant NF-κB activity, which promotes their growth. This activity is not associated with aberrant expression of p50 and RelA.
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Couldwell, William T., Garnet Fraser, Genvieve De Vellis, Jack P. Antel, Jean-Guy Villemure, and Voon Wee Yong. "Malignant Glioma-Derived Soluble Factors Regulate Proliferation of Normal Adult Human Astrocytes." Journal of Neuropathology and Experimental Neurology 51, no. 5 (September 1992): 506–13. http://dx.doi.org/10.1097/00005072-199209000-00005.
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Tada, Mitsuhiro, Annie-Claire Diserens, Isabelle Desbaillets, and Nicolas de Tribolet. "Analysis of cytokine receptor messenger RNA expression in human glioblastoma cells and normal astrocytes by reverse-transcription polymerase chain reaction." Journal of Neurosurgery 80, no. 6 (June 1994): 1063–73. http://dx.doi.org/10.3171/jns.1994.80.6.1063.
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✓ To elucidate which cytokine receptors may be expressed by human glioblastoma and normal astrocytic cells, the presence of messenger ribonucleic acid (RNA) for a number of cytokine receptors was examined in 16 glioblastoma cell lines and adult and fetal astrocytes. A complementary deoxyribonucleic acid copy of total RNA was synthesized and amplified with specific primers using the polymerase chain reaction method. The receptors studied were interleukin (IL)-1 receptor type I (IL-1RI) and type II (IL-1RII), p75 and p55 tumor necrosis factor (TNF) receptors (p75TNFR and p55TNFR), interferon (IFN)-α/β and -γ receptors (IFN-α/βR and IFN-γR), granulocyte-macrophage (GM) colony-stimulating factors receptor α subunit (GM-CSFR), G-CSF receptor (G-CSFR), M-CSF receptor (c-fms, M-CSFR), stem cell factor receptor (c-kit, SCFR), IL-6 receptor (IL-6R), and IL-8 receptor (IL-8R). Transcripts for IL-1RI, p55TNFR, IFN-α/βR, and IFN-γR were present in all cell lines. The presence of IL-1RII, p75TNFR, GM-CSFR, M-CSFR, SCFR, IL-6R, and IL-8R was identified in 13, eight, seven, eight, 14, three, and one cell lines, respectively. Normal astrocytes were positive for IL-1RI, p75TNFR, p55TNFR, IFN-α/βR, IFN-γR, M-CSFR, and SCFR, showing a similarity to glioblastoma cells. Expression of IL-1RII was observed in adult astrocytes but not in fetal astrocytes. Furthermore, gene expression was assessed in normal brain tissue and 11 glioblastoma tissue specimens. The normal brain tissue expressed IL-lRI, IL-1RII, IFN-α/βR, M-CSFR, and SCFR. Of the 11 glioblastoma tissue specimens, IL-1RI was positive in 11, IL-1RII in 10, p75TNFR in nine, p55TNFR in nine, IFN-α/βR in 10, IFN-γR in 10, GM-CSFR in two, G-CSFR in three, IL-8R in eight, and M-CSFR and SCFR in 11. These expressions were consistent with those in the cell lines, except for IL-8R. It is concluded that glioblastoma cells and normal astrocytes express a similar set of cytokine receptor genes in vitro and in vivo. Possible autocrine loops are suggested for IL-1α/IL-1RI, TNF-α/p55TNFR, IFN-β/IFN-α/βR, M-CSF/M-CSFR, and SCF/SCFR in glioblastomas.
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González-Martínez, Jorge A., William E. Bingaman, Steven A. Toms, and Imad M. Najm. "Neurogenesis in the postnatal human epileptic brain." Journal of Neurosurgery 107, no. 3 (September 2007): 628–35. http://dx.doi.org/10.3171/jns-07/09/0628.
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Object The normal adult human telencephalon does not reveal evidence of spontaneous neuronal migration and differentiation despite the robust germinal capacity of the subventricular zone (SVZ) astrocyte ribbon that contains neural stem cells. This might be because it is averse to accepting new neurons into an established neuronal network, probably representing an evolutionary acquisition to prevent the formation of anomalous neuronal circuits. Some forms of epilepsy, such as malformations of cortical development, are thought to be due to abnormal corticogenesis during the embryonic and early postnatal periods. The role of postnatal architectural reorganization and possibly postnatal neurogenesis in some forms of epilepsy in humans remains unknown. In this study the authors used resected specimens of epileptic brain to determine whether neurogenesis could occur in the diseased tissue. Methods The authors studied freshly resected brain tissue obtained in 47 patients who underwent neurosurgical procedures and four autopsies. Forty-four samples were harvested in patients who underwent resection for the treatment of pharmacoresistant epilepsy. Results Using organotypic brain slice preparations cultured with 5-bromodeoxyuridine (a marker for cell proliferation), immunohistochemistry, and cell trackers, the authors demonstrate the presence of spontaneous cell proliferation, migration, and neuronal differentiation in the adult human telencephalon that starts in the SVZ and progresses to the adjacent white matter and neocortex in human neocortical pathological structures associated with epilepsy. No cell migration or neuronal differentiation was found in the control group. Conclusions The presence of spontaneous neurogenesis associated with some forms of human neocortical epilepsy may represent an erroneous and maladaptive mechanism for neuronal circuitry repair, or it may be an intrinsic part of the pathogenic process.
Dissertations / Theses on the topic "Normal adult human astrocyte"
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Padovani-Claudio, Dolly Ann. "FUNCTIONAL ANALYSES OF THE CHEMOKINE RECEPTOR CXCR2 IN THE NORMAL AND DEMYELINATED ADULT CENTRAL NERVOUS SYSTEM." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1152193193.
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Zhai, Xiao Qun. "Biology of adult human normal and leukaemia CD133+ stem cells." Thesis, University of Central Lancashire, 2010. http://clok.uclan.ac.uk/21488/.
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Recently, CD133 has been used extensively as a marker for identification of stem cells from human normal and malignant tissues. Human normal CD 133+ stem cells are capable of multilineage in vitro and in vivo differentiation providing a novel source of stem cells for regenerative therapy, whereas, malignant CD133+ stem cells are a potential therapeutic target for anti-cancer treatment. This PhD thesis investigated the neural differentiation of human adult bone marrow and foetal liver CD133+ stem cells; explored the presence of CD133 and embryonic stem cell marker Oct-4 positive stem cells in adult human normal and malignant tissues, including normal brain tissues, normal and malignant bone marrow stem cells; and evaluated the anti-acute myeloid leukaemia (AML) effect of 5 novel synthetic ajoene compounds using drug-resistant AML cell line for overcoming drug resistance in elderly AML patients. A novel serum-free culture system for inducing neural differentiation of human adult bone marrow and foetal liver CD 133+ stem cells in vitro was demonstrated. Following only two weeks' culture of selected bone marrow CD 133+ cells in serum-free medium supplemented by 50% human astrocyte conditioned medium and other cytokines, 25.5% of bone marrow CD 133+ stem cells differentiated into neural (17.8%) and glial (7.7%) cells. After three weeks' culture of selected foetal liver CD133+ cells in serum-free medium supplemented by several cytokines without astrocyte conditioned medium, only 10.8% of these stem cells differentiated into neural and glial cells. These neural differentiated cells expressed mature neural and glial markers including NF-h, NF-m, NSF and GFAP, and exhibited mature neural morphologies. The astrocyte conditioned medium was the essential ingredient in all effective serum-free culture conditions suggesting it may contain other more potent neural/glial inducing factors. The serumfree culture system is clinically relevant and provides a vehicle for generating neural cells from adult human bone marrow CD 133+ stem cells for the treatment of patients with neurodegenerative diseases. CD 1 33-isoform 2 (CD 133-2) and embryonic stem cell marker Oct-4 expression was revealed in three adult human normal and malignant tissues and cells, including normal brain (substantia nigra and striatum), normal and malignant CD34+ marrow stem cells. There was no expression of CD133-isoform I (CD133-1) in these tissues. The very small population of CD133-2 and Oct-4 positive stem cells in adult human normal substantia nigra and striatum may represent the embryonic remnants and provide a potential source of adult neural stem cells that may be induced to undergo neural diffeentiation for the treatment of neurodegenerative conditions, such as Parkinson's disease. The substantial expression of Oct-4 in adult human normal and drug-resistant myeloid leukaemia KG1a marrow stem cells demonstrates that, alongside CD133, Oct-4 is a novel cancer stem cell marker suggesting the CD 133-2 and Oct-4 positive KGIa cells are the most likely targets in disease development and are novel therapeutic targets for effective treatment of AML. Novel synthetic ajoene compounds were shown to significantly inhibit growth, induce apoptosis plus necrosis, and reduce Bcl-2 expression in human drug-resistant CD34+ AML KG 1 a cells, both alone and in combination with low dose (1 jxM) cytarabine. E/Zbenzyl was the most potent growth inhibition compound,. whereas, Z-ajoene was the most cytotoxic compound. Low dose cytarabine-induced cytotoxicity was significantly enhanced by the five novel compounds in the following order: Z-ajoene > E-ajoene > Ephthalimide> E/Z-benzyl > Z-pthalimide. The combination of Z-ajoene and low dose cytarabine provides a promising combination therapy for elderly AML patients to overcome drug resistance. This PhD thesis provides the basis for appropriate identification and clinical application of stem cells from adult human normal tissues (brain and bone marrow) and foetal liver for autologous transplantation for the treatment of neurodegenerative diseases, such as Parkinson's disease, and also the identification of cancer stem cells in human AML marrow stem cells indicating novel therapeutic targets for anti-cancer treatment. Moreover, it demonstrates significant anti-cancer effect of 5 novel synthetic ajoene compounds in drug-resistant AML cells highlighting their potential for overcoming drug resistance in elderly patients with AML.
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Hamdalla, Hisham Hamdalla Mohamed. "Transcranial magnetic stimulation in normal human adult subjects and patients with motor neurone disease." Thesis, University of Newcastle upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407642.
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Anwar, Mohammad Akhtar. "A haemorheological study of the human fetus, neonate and adult in normal and pathological states." Thesis, Imperial College London, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295471.
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Stingl, John Patrick. "In vitro phenotypic and functional characterization of epithelial progenitors present in the normal adult human breast." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0018/NQ48722.pdf.
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Al, Abdlseaed Abdlsaed. "Pupil dilation, light source, gender and pigmentation effects on normal adult human ERGs, and an exploration of short latency VEPs." Thesis, Glasgow Caledonian University, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.688309.
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Rutkowski, Paul, and Christian Albrecht May. "Nutrition and Vascular Supply of Retinal Ganglion Cells during Human Development." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-215952.
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Purpose: To review the roles of the different vascular beds nourishing the inner retina [retinal ganglion cells (RGCs)] during normal development of the human eye, using our own tissue specimens to support our conclusions.
Methods: An extensive search of the appropriate literature included PubMed, Google scholar, and numerous available textbooks. In addition, choroidal and retinal NADPH-diaphorase stained whole mount preparations were investigated.
Results: The first critical interaction between vascular bed and RGC formation occurs in the sixth to eighth month of gestation leading to a massive reduction of RGCs mainly in the peripheral retina. The first 3 years of age are characterized by an intense growth of the eyeball to near adult size. In the adult eye, the influence of the choroid on inner retinal nutrition was determined by examining the peripheral retinal watershed zones in more detail.
Conclusion: This delicately balanced situation of RGC nutrition is described in the different regions of the eye, and a new graphic presentation is introduced to combine morphological measurements and clinical visual field data.
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Carrère, Jacqueline. "Etude de trois enzymes pancreatiques : trypsine, chymotrypsine et lipase dans differents liquides biologiques chez le sujet normal et chez le sujet atteint de mucoviscidose." Toulouse 3, 1988. http://www.theses.fr/1988TOU30102.
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BONAFINI, Clara. "Investigations into Alzheimer's disease pathogenetic mechanisms using normal adult human astrocytes in culture." Doctoral thesis, 2011. http://hdl.handle.net/11562/350599.
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La malattia di Alzheimer è una delle principali patologie neurodegenerative legate alla terza età: i casi infatti che si sviluppano in età precoce rappresentano meno dell’1% e sono dovuti ad alterazioni geniche specifiche. L’eziologia di questa malattia resta ancora sconosciuta, sebbene la presenza di placche senili, composte principalmente di Aβ1-40 e Aβ1-42, o aggregati fibrillari intraneuronali della proteina tau, siano caratteristiche ormai note del suo stadio avanzato. Diversi processi patologici sono stati messi in relazione con il danno neuronale e il declino cognitivo tipici della malattia. Tra questi uno dei più studiati è il processo infiammatorio indotto da aggregati di amiloide negli spazi perineuronali e mediato principalmente da astrociti e cellule della microglia. Recentemente anche alterazioni dei meccanismi neurovascolari e della struttura della barriera emato-encefalica sono stati correlati con la progressione del processo patologico e con l’induzione locale di angiogenesi: la presenza di VEGF, una delle principali citochine ad azione angiogenica, è stata dimostrata infatti in corrispondenza di cluster di astrociti reattivi in pazienti AD. Per chiarire il possibile legame tra la neoangiogenesi, la presenza di aggregati di amiloide e la secrezione di mediatori infiammatori, si è deciso di analizzare la modulazione dell’espressione del complesso trascrizionale HIF-1α•HIF-1β in astrociti umani normali adulti (NAHA) a seguito del trattamento con la triade di citochine proinfiammatorie (CM-trio, IL-1β + IFN-γ + TNF-α) e con Aβ25-35, il frammento attivo dell’Aβ1-42. Il legame di HIF-1α•HIF-1β alla sequenza HRE presente nella regione promotoriale di geni correlati alla malattia, quali VEGF e BACE-1, è responsabile della loro induzione in risposta a stimoli quali stress ipossico. Entrambi i trattamenti, pur non alterando in nessun modo la trascrizione delle subunità HIF-1α e HIF-1β, inducono sia una maggiore stabilità della frazione proteica di entrambi i fattori, sia un’aumentata traslocazione del complesso a livello nucleare con conseguente legame alla sequenza HRE. Il trattamento invece con CM-trio determina una significativa riduzione dell’espressione di un altro fattore implicato nell’induzione della trascrizione del VEGF-A, PGC-1α, dimostrando che HIF-1α•HIF-1β è il solo complesso coinvolto nella modulazione del fattore angiogenico. La traslocazione nucleare dell’eterodimero HIF-1α•HIF-1β e il suo legame alla sequenza promotoriale HRE corrisponde ad un aumento dell’espressione di tre varianti di splicing del VEGF-A (121, 165 e 189), ma non all’ accumulo della corrispondente frazione proteica a livello intracellulare. Analisi mediante ELISA hanno dimostrato un aumento del rilascio del VEGF-A nel medium di coltura di cellule trattate con Aβ25-35, con la coppia IFN-γ + TNF-α, ma soprattutto con CM-trio. L’insieme di Aβ25-35 + CM-trio non è in grado di esercitare un’azione sinergica sul rilascio, dimostrando che la triade di citochine proinfiammatorie è il principale induttore della secrezione. Il complesso HIF-1α•HIF-1β si è rivelato inoltre implicato nella regolazione della trascrizione di BACE-1, una delle secretasi coinvolte nella produzione di Aβ. Il trattamento con Aβ25-35 stimola infatti la maggiore espressione dell’mRNA e della proteina BACE-1, inducendo inoltre un aumento della sua attività e di quella della γ-secretasi, altro enzima responsabile del processamento dell’APP. La produzione di peptidi Aβ in NAHA trattati con Aβ25-35 è stata dimostrata tramite immunoblotting e immunofluorescenza; quest’ultima tecnica, in particolare, ha permesso di evidenziare la presenza di aggregati di Aβ25-35 nel citoplasma di astrociti trattati, delineando un loro possibile ruolo nella rimozione di aggregati di amiloide potenzialmente patologici.Alterations in neurovascular mechanisms and blood-brain barrier (BBB) disorders have been related to late-onset Alzheimer’s disease (AD). An increased expression of vascular endhotelial growth factor (VEGF) has seen in cluster of reactive astrocytes in AD brains and into rat hippocampus Aβ1-42 injected. We found that the Aβ25-35, an amyloid β1-42 active fragment, and proinflammatory cytokines (CM-trio, IL-1β + IFN-γ + TNF-α) treatments has induced an increased protein steady state levels of the hypoxia-inducible factor transcriptional complex (HIF-1α•HIF-1β) in normal adult human astrocytes (NAHAs). This transcription factor is the main regulator of the VEGF expression, but also the PGC-1α cofactor seems to be related to its upregulation in AD. We analyzed the mRNA expression of both these factors, but only the complex HIF-1α•HIF-1β was implicated in the VEGF-A expression. Indeed, the enhanced HIF-1α•HIF-1β nuclear translocation and its binding at the hypoxia response element (HRE) sequence in the VEGF-A promoter, found after both treatments, were correlated with the increased VEGF-A mRNA splice variants (121, 165, and 189) expression. The CM-trio was the most powerful stimulus inducing the VEGF-A secretion in NAHAs culture medium, also induced, less than CM-trio, by the paired cytokines IFN-γ + TNF-α, Aβ25-35 and CM-trio + Aβ25-35 treatments. Hence the astrocytes in an AD brain can produce a raised amount of VEGF-A in response to Aβ peptide and the proinflammatory cytokines promoting the neoangiogenic process. We found that the HIF-1α•HIF-1β complex was furthermore responsible for the β-secretase (BACE-1) mRNA and protein up-regulation in our experimental model treated with Aβ25-35. After the same treatment we found moreover an enhancement of the β and γ-secretase activities, the two secretases involved in the amyloid precursor protein (APP) processing. The immunofluorescence and immunoblotting assays confirmed the Aβ production in NAHAs, suggesting the existence of a positive feed-back loop for the Aβ synthesis in astrocytes. This findings support the theory that astrocytes, as well as neurones, are involved in the AD decline of cognitive functions. Moreover, the immunofluorescence assay shows the Aβ25-35 uptake, defining a possible role of astocytes as Aβ peptides scavengers.
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Stingl, John. "In vitro phenotypic and functional characterization of epithelial progenitors present in the normal adult human breast." Thesis, 2000. http://hdl.handle.net/2429/10910.
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The developmental relationships between the different epithelial cell lineages in the normal
human mammary gland are not well defined. To characterize the progenitor activity of freshly
isolated human breast epithelial cells (HBEC), 2- and 3-dimensional culture systems were
developed that optimized their clonal growth, and fluorescence-activated cell sorting was used
to characterize the progenitors of the different types of colonies obtained. These studies
identified one type of progenitor cell that generates colonies of varying sizes with an alveolar-like
morphology and generally contains cells expressing markers of luminal cells; i.e.: the
apical glycoprotein MUC1 and epithelial cell adhesion molecule. They also express relatively
high levels of erbB-2, retain rhodamine 123, express variable levels of the epidermal growth
factor receptor and CD44v6 and express low levels of the ct6 integrin, the histo-blood group
antigen type 2 and the common acute lymphoblastic leukemia antigen. A second type of
progenitor identified is one that generates colonies composed of cells that express
myoepithelial lineage markers and variable numbers of cells that express luminal cell markers.
These progenitors generate colonies in collagen gels that have a branching duct-like
morphology. These bipotent progenitors express the epidermal growth factor receptor, erbB-2,
epithelial cell adhesion molecule, the α6 integrin, the common acute lymphoblastic leukemia
antigen, variable levels of MUC1, and retain low levels of rhodamine 123. Single cell cultures
verified the clonal origin of both types of colonies. Epidermal growth factor at 10 ng/ml within
the breast epithelial colony assay promoted the survival of cells enriched for luminal cell
progenitors, as well as the migration of keratin 14 expressing cells in a manner that could be
interpreted as ductal elongation. Serial passaging of highly enriched populations of bipotent
progenitors indicated that some cells produced in the mixed and pure myoepithelial marker+
colonies can generate colonies composed only of cells expressing myoepithelial characteristics,
but not luminal characteristics. These latter results suggest that the culture conditions used
compromise both the self-renewal of human breast epithelial stem cells and their differentiation
into the luminal lineage.
Books on the topic "Normal adult human astrocyte"
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Stricht, Omer Van Der, and Thomas Wingate Todd. Structure of Normal Fibers of Purkinje in the Adult Human Heart and Their Pathological Alteration in Syphilitic Myocarditis. Creative Media Partners, LLC, 2015.
Find full textBook chapters on the topic "Normal adult human astrocyte"
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Thonar, E. J. M. A., K. Masuda, D. H. Manicourt, and K. E. Kuettner. "Structure and Function of Normal Human Adult Articular Cartilage." In Osteoarthritis, 1–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-60026-5_1.
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Levin, R. J. "SEXUAL OFFENSES, ADULT | Human Normal Sexual Response." In Encyclopedia of Forensic and Legal Medicine, 81–87. Elsevier, 2005. http://dx.doi.org/10.1016/b0-12-369399-3/00325-6.
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Levin, R. J. "Sexual Offenses, Adult: Human Normal Sexual Response." In Encyclopedia of Forensic and Legal Medicine, 272–79. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-800034-2.00340-2.
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Aragon-Alonso, Aurora, Mark Sherlock, and Andrew A. Toogood. "Adult growth hormone deficiency." In Oxford Textbook of Endocrinology and Diabetes, 152–65. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.2086.
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It has been known for many years that growth hormone is essential for normal linear growth, but over the past few years, with the advent of recombinant human growth hormone therapy, the importance of growth hormone during adult life has been described in detail. The growth hormone peptide was first isolated from bovine pituitaries in the 1940s (1), but was found to be species specific and inactive in humans. In 1956, growth hormone was extracted from human cadaveric pituitary tissue (2) and a year later was administered to a 13-year-old boy with hypopituitarism, resulting in an increased growth velocity (3). The first report suggesting growth hormone could have beneficial actions in adulthood was published in 1962 in which a 35-year-old woman with hypopituitarism reported increased vigour, ambition, and wellbeing after 2 months treatment with cadaveric growth hormone (4). However, the limited supply of pituitary-derived growth hormone confined its use to the treatment of children with severe growth failure caused by proven growth hormone deficiency (GHD). In 1985, the association of cadaveric growth hormone treatment with Creutzfeldt–Jakob disease led to its withdrawal from use worldwide (5). Since then, all growth hormone in clinical use has been produced using recombinant DNA technology. The first placebo-controlled trials of growth hormone replacement therapy in adults with GHD were published in 1989 (6, 7). These and subsequent studies have led to the recognition of adult GHD as a specific clinical syndrome and the impact of GHD and replacement therapy in adults with GHD has been studied in detail.
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Morgan, Konrad, and Madeleine Morgan. "Gender-Based Attitudes Toward Technology." In Human Computer Interaction, 2274–77. IGI Global, 2009. http://dx.doi.org/10.4018/978-1-87828-991-9.ch149.
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During the past 30 years of investigation into the ratios of males and females using technology (Harrison, Rainer, & Hochwarter, 1997), there have been consistent reports of males being more positive toward technology and being more likely to adopt the use of new technology on a voluntary basis (Volman, & Van-Eck, 2001). This trend has been reported from early school through adult life, and from diverse geographical sources (Broos, 2005; Heemskerk, Brink, Volman, & Ten-Dam, 2005). Although some scientists have argued that this pattern is changing (Colley & Comber, 2003; Durndell & Thomson, 1997), surveys continue to show an imbalance between the sexes favoring males over females (Colley & Comber; Heemskerk et al., 2005). The authors consider the consequences of this gender bias to be significant not only in terms of maximizing the whole potential workforce, but also because there is some evidence that males design information- and knowledge-based systems in ways that are different from females, and often these differences favor male users in communication and searching methods. The gender imbalance may become of increasing importance as high-technology industries, such as knowledge engineering and Web commerce, become the normal methods of conducting business throughout the global economy.
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Egonsson, Dan. "The Importance of Being Human." In The Paideia Archive: Twentieth World Congress of Philosophy, 24–28. Philosophy Documentation Center, 1998. http://dx.doi.org/10.5840/wcp20-paideia199814287.
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In this paper I will defend a kind of human-centered perspective regarding ethical questions wherein the interests of humans and nonhumans alike are involved. Compared to other species, however, the idea that there is something special about being human is commonly vague. For example, it is unclear whether the thought is (1) being a human being is important in itself, or (2) it is important to be like a human being — that is, to have the capacities which a normal adult human being enjoys. I build my defense of human dignity on the claim that we regard a biological human being as a being of intrinsic importance, which is what (1) is about. However, I also consider the ethical implications of (2), which concerns the moral significance of personhood. I argue that the idea of a special intrinsic value of being a human is applicable only to cases where we deal with nonpersons. I claim that in spite of this qualification, we might defend a substantial principle of human dignity founded upon this generalization.
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Lucchesi, John C. "Aging, cellular senescence and cancer: the role of genomic instability, cellular homeostasis and telomeres." In Epigenetics, Nuclear Organization & Gene Function, 227–37. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198831204.003.0020.
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Aging hallmarks are causative factors of oncogenesis. Genomic instability results from the accumulation of errors that occur during DNA replication or from exposure to endogenous or environmental insults. The genome contains genes responsible for normal cell division and differentiation (oncogenes), and genes that regulate cell division and limit cell growth and proliferation (tumor suppressor genes). Over-expression of oncogenes or inactivation of tumor suppressors results in cancer. During aging, alterations in proteostasis result in the disruption of metabolic pathways that connect with environmental factors. Telomeres are terminal regions of chromosomes that protect the DNA from attack by exonucleases, prevent end-to-end fusions and prevent the shortening of the DNA molecules at each replication cycle. Using RNA as a template, telomerase synthesizes telomeric DNA. Telomerase is absent in most adult human tissues, resulting in a progressive shortening of all telomeres and causing cells to senesce. Cancer cells must activate telomerase to gain “immortality.”
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Bradford, John M., and Fabian M. Saleh. "Pharmacological Treatment of Paraphilic Sex Offenders." In Sex Offenders, edited by Fabian M. Saleh, John M. Bradford, and Daniel J. Brodsky, 292–319. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190884369.003.0014.
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This chapter explores the pharmacological treatment of paraphilic sex offenders. The World Federation of Societies of Biological Psychiatry (WFSBP) established a task force to evaluate the evidence-based treatment of the paraphilic disorders for both adults and adolescents. The primary aim of WFSBP guidelines for the biological treatment of the paraphilias was to evaluate the role of pharmacological agents in the treatment and management of paraphilias with a focus on the treatment of adult males. These guidelines were intended for use in clinical practice by clinicians who diagnose and treat paraphilia, now known as paraphilic disorders. The term paraphilia denotes any intense and persistent sexual interest other than sexual interest in genital stimulation or preparatory fondling with phenotypically normal, physically mature, consenting human partners. A paraphilic disorder is a paraphilia that is currently causing distress or impairment to the individual or a paraphilia whose satisfaction has entailed personal harm, or risk of harm, to others. A paraphilia is a necessary but not a sufficient condition for having a paraphilic disorder, and a paraphilia by itself does not necessarily justify or require clinical intervention.
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Lingvay, Ildiko, and Shelby A. Holt. "The Thyroid." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0015.
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The thyroid gland, which is the largest endocrine organ, secretes primarily thyroid hormones that play a critical role in the normal growth and development of the maturing human. In the adult, thyroid hormones maintain metabolic stability by regulating oxygen requirements, body weight, and intermediary metabolism. Thyroid function is under hypothalamic-pituitary control, and thus, like the gonads and adrenal cortex, it serves as a classical model of endocrine physiology. In addition, the physiological effects of thyroid hormones are regulated by complex extrathyroidal mechanisms resulting from the peripheral metabolism of the hormones, mechanisms that are not under hypothalamic-pituitary regulation. Thyroid function abnormalities are very prevalent, especially in females and in certain geographic areas, and are often a result of autoimmunity or iodine deficiency. The thyroid originates from two distinct parts of the embryonic endoderm: • The follicular structures arise from a midline thickening of the anterior pharyngeal floor (the base of the tongue), adjacent to the differentiating heart. This thyroid diverticulum first expands ventrally while still attached to the pharyngeal floor by its stalk (thyroglossal duct), and then expands laterally, leading to the characteristic bilobed structure. As the developing heart descends, the thyroid gets pulled into its final position, a process that leads to the rapid stretch and degeneration of the thyroglossal duct. • The parafollicular cells are derived from the ultimobranchial bodies (originating from the neural crest) but ultimately are surrounded by the medial thyroid. The parafollicular cells represents <10 % of the adult thyroid gland. The thyroid completes its structural development by 9 weeks of gestation, the first endocrine organ to assume its definitive form during organogenesis; yet full functional maturation and integration with the hypothalamic-pituitary axis continues throughout gestation. Abnormal thyroid development can lead to persistence of the thyroglossal duct, presence of ectopic thyroid tissue (lingual thyroid, lateral aberrant thyroid), and malposition (thoracic goiter), all of which can remain clinically silent or present later in life as diagnostic challenges. The shape of the human thyroid resembles that of a butterfly.
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Parrington, John. "Regenerating Life." In Redesigning Life, 185–208. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198766834.003.0009.
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Stem cells, which are ‘immortal’ cells that divide indefinitely and produce many different cell types, are central to how our body develops and maintains itself. Embryonic stem cells can give rise to all cell types in the body, and there has been lots of interest since their discovery in the 1980s in using such cells to generate new tissues or organs to replace diseased or faulty ones. More recently has come the discovery of induced pluripotent stem cells, which are normal skin cells taken from a person and genetically modified or tweaked chemically to give them stem cell properties. There is now hope that both of these types of stem cells might be used in ‘regenerative’ medicine, for instance in producing pancreatic cells that secrete insulin which could be used to treat diabetes. Perhaps the most remarkable breakthrough in recent years has been the discovery that stem cells introduced into a 3D matrix that is infused with chemicals that stimulate the development of particular cell types, can spontaneously form ‘organoids’, which have many of the cell types and even structural features of human organs such as hearts, kidneys, intestines, and even eyes and brains. Organoids make it possible to study how human organs develop but also this area of science raises many ethical issues. For instance, currently human brain organoids can only grow to the size of an embryonic brain, but if in the future they could be induced to grow to adult brain size, could they develop feelings and thoughts?
Conference papers on the topic "Normal adult human astrocyte"
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Bam, Rakesh, Sathisha Upparahalli Venkateshaiah, Xin Li, Sharmin Khan, Wen Ling, Bart Barlogie, Joshua Epstein, and Shmuel Yaccoby. "Abstract 1648: Primary myeloma plasma cells are capable of growth in adult, normal whole human bone marrow environment ." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1648.
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Hassan, H. J., A. Leonardi, C. Chelucci, R. Guerriero, P. M. Mannucci, and C. Peschle. "EXPRESSION IN ONTOGENESIS OF HUMAN BLOOD COAGULATION FACTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644610.
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We have analyzed the expression of several blood coagulation factors (IX, VIII, X, fibrinogen chains) and inhibitors (antithrombin III, protein C) in human embryonic and fetal livers, obtained from legal abortions at 6-11 week post-conception. The age was established by morphologic staging and particularly crown-rump lenght measurement.Total cellular RNA was isolated from partially purified hepatocytes or total liver homogenate using the guanidine isothiocyanate method. Poly(A)+ RNA was selected by oligodT cellulose chromatography. The size and the number of the embryonic and fetal transcripts are equivalent to those observed in adult liver, as evaluated by Northern blot analysis of total or poly(A)+ RNA hybridized to human cDNA probes.The level of coagulation factor transcripts in embryonic and fetal liver was evaluated by dot hybridization of total RNA (0.5-10 ug), as compared to RNA extracted from normal adult liver biopsies. The expression of blood coagulation factors in embryos is generally reduced for all factors, but at a different degree. In 5-11 wk liver, the level of factor IX is 5-10% of that observed in adults, while fibrinogen, protein C, antithrombin III RNA level rises from 25 to 50% and factor X is expressed at a level comparable to that observed in adult liver.We conclude that during these stages of development blood coagulation factors are expressed according to three different time, curves, possibly due to the effect of different types of regulatory mechanisms.
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SHIRAHATA, A., A. ASAKURA, T. NAKAMURA, and K. YAMADA. "CONTENTS OF PHYLLOQUINONE AND MENAQUINONE FAMILY IN SERUM AND FECES FROM HUMAN NEWBORN INFANTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643605.
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A sensitive and specific method for the determination of phylloquinone (PK) and menaquinone families (MK-n), between MK-4 and MK-10, was developed. Vitamin K (VK) was extracted from serum and feces with n-hexane-ether, and purified with silica gel column and short alumina column. Eluted VK was separated by high performance liquid chromatography using Cosmosil 5 Cie column with ethanol-water as a mobile phase. The separated VK was detected by a fluorometry after its reaction with ethanolic sodium boro-hydride in a reaction coil connected by one-line to a chromatographic column. Minimum detectable quantities of PK, MK-4 and MK-7 were 0.1, 0.1 and 0.15 ng/ml, respectively.In normal adult serum, PK, MK-4, MK-5, MK-6, MK-7 and MK-8 were detected. The meaniSD values of PK and MK-n from normal adult serum were 3.0±1.4 (PK), 0.3±0.2 (MK-4), 0.9±0.4 (MK-5), 0.3 ±0.3 (MK-6), 3.8±1.4 (MK-7) and 0.3±0.2 (MK-8)ng/ml, respectively. On the other hand, VK was not detected in 19 umbilical blood samples, excluding 3 samples in which 0.7, 1.0 and 2.5 ng/ml of PK were detected. In 7 healthy newborn infants under 8 days of age, VK was not detected excluding 3 cases. Of these 3 cases, in one case, 3.16 ng/ml of PK was detected, and in the other two cases, 1.1 and 1.5 ng/ml of MK-7 were detected. In 11 infants at one month of age, PK ( 10 cases ) and MK-7 ( 5 cases ) were detected, and mean+SD values of PK and MK-7 in the detected group were 0.55±0.44 and 0.62±0.18 ng/ml, respectively. VK was not detected in plasma of infants with primary hemorrhagic disease of the newborn ( 4 cases ) and infantile vitamin K deficiency ( 2 cases ). With a wide variation of VK content in each samlpe, PK and all MK families were detected in feces from normal adults. On the other hand, only PK and MK-7 were detected in meconium collected from 6 normal newborn infants before initial feeding. The contents of VK in meconium were less than one percent of those in adult feces. These results indicate that VK supply from maternal side in utero and from intestinal flora after birth is very poor in newborn infants.
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Lin, Tai-Yuan David, Woraphong Manuskiatti, Christine Dierickx, William A. Farinelli, Marney Fisher, Thomas Flotte, Howard Baden, and R. Rox Anderson. "Influence of Hair Growth Cycle on Hair Follicle Destruction by Pulsed Ruby Laser Treatment in Newborn Mice." In Lasers in Dermatology: Bio-Optics and Treatment of Human Skin. Washington, D.C.: Optica Publishing Group, 1997. http://dx.doi.org/10.1364/lid.1997.sac5.
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It has been shown that using normal mode ruby laser pulses (694 nm) is an effective method of selectively destroying brown or black pigmented hair follicles in adult Caucasians (Grossman et al, 1996). The pigment, melanin, contained within the dark hair follicles acts as a target for light absorption when exposed to a well characterized range of wavelengths (Anderson and Parrish, 1981). Based on principles of selective photothermolysis, exposure to carefully chosen wavelength and pulse duration characteristics result in preferential absorption by the target pigment and sufficient heating to cause localized cellular destruction (Anderson and Parrish, 1983).
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Das, Biman. "Advances in Human Strength Measurement and Modeling in Workspace." In Applied Human Factors and Ergonomics Conference. AHFE International, 2018. http://dx.doi.org/10.54941/10034.
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Advances made in human strength measurement and modeling in three dimensional workspace are reported. A comprehensive experimental research was conducted to determine isometric and isokinetic push, pull, push-up and pull-down strengths in the workspace and the corresponding muscle activity during exertions. Data were obtained from able-bodied adult male and female participants in the normal, maximum and extreme reach envelopes at various horizontal and vertical angles/heights in both seated and standing positions. A three dimensional isometric strength measurement system was designed and constructed. The Kin-Com dynamometer was used to measure isokinetic strength. The Flex-Com system recorded electromyography (EMG) of four muscles: biceps, triceps, anterior deltoid and erector spiane. Strength profiles or data for isometric and isokinetic strengths were highlighted. Spatial factors affecting isometric and isokinetic strengths were analyzed. Muscle activity of the selected muscles during force exertions were investigated. Predictive models or equations were developed for isometric pull strengths in maximum reach of standing men by applying multiple regression analysis.
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Chan, D. D., and C. P. Neu. "Human Tibiofemoral Joint Displacements Determined by Displacement-Encoded MRI." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53498.
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Articular cartilage and surrounding soft tissues in the knee are important to normal joint function. Osteoarthritis (OA) is highly prevalent in the United States [1] and features precocious degeneration of articular cartilage. Effective OA treatments require the ability to detect early degeneration, including mechanical and biochemical changes. Magnetic resonance imaging has shown promise for the detection of early degenerative changes, including various quantitative MRI techniques [2]. Displacement-encoded MRI has the ability to detect changes in mechanical behavior, and such techniques have previously been used in cartilage explants [3] and intact juvenile animal joints [4]. However, the authors are aware of no studies with displacement-encoded MRI of human articular cartilage. Tissue-level displacement patterns could be key to revealing early degeneration in articular cartilage. This study demonstrates for the first time displacement encoding with stimulated echoes (DENSE) in an adult human tibiofemoral joint.
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Abdelmessih, Amanie N. "Steady State Temperature Gradients in a Non-Blinking Human Eye Prepared for Surgery." In ASME 2013 Heat Transfer Summer Conference collocated with the ASME 2013 7th International Conference on Energy Sustainability and the ASME 2013 11th International Conference on Fuel Cell Science, Engineering and Technology. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/ht2013-17482.
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LASER surgery on the human eye is intended to reduce a person’s dependency on glasses or contact lenses. Any type of Laser surgery has heat effects on the eye. In laser surgery specific parts of the eye are exposed to concentrated high heat doses, too high heat at a certain spot results in permanent medical damage to the specific exposed eye cells. Precise temperature monitoring of the live interior of the human eye is not possible with the current technology. Published modeling assumes that the human eyeball is at a constant temperature, mostly at 37 °C. Understanding the exact temperature gradients in the prepared open human eyeball in room temperature before surgery is a first step in better understanding the heat effects of either laser surgery on specific treated spots of the cornea, or the effects of insertion of synthetic lenses in the human eye, or treating the retina with laser. In this article the anatomy of the human eyeball, dimensions, and properties are considered in constructing a finite element steady state thermal model of the normal open human eye for an adult, in preparation for surgery under normal room conditions. Also, room boundary conditions are used. Based on the model, the temperature gradients in the open eye are reported.
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MOALIC, P., Y. GRUEL, P. FOLOPPE, B. DELAHOUSSE, G. BODY, and J. LEROY. "LEVELS AND DISTRIBUTION OF FREE AND C4b-BP-B0UND-PR0TEIN S IN HUMAN FETUSES AND FULL-TERM NEWBORNS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644266.
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Levels and plasmatic distribution of protein S were studied on umbilical cordplasmas from 25 normal full-term newborns (N) and 15 normal fetuses (F) between20 and 30 weeks of gestation. Samples from fetuses were collected for antenatal diagnosis by direct puncture of the umbilical vein under high resolution real-time ultrasound. Total protein S(PS) level was determined using Laurell rocket immuno-electrophoresis (Diagnostica Stago, Asnifcres-France). Free PS wasmeasured using this latter method, afterprecipitation of C4b-BP-bound-PS by polyethylene glycol (PEG). Normal pool plasma, treated as well, was considered as the reference curve. C4b-binding protein (C4b-BP) determinations were conducted by Laurell rocket immunoelectrophoresis. The qualitative distribution of free PS and C4b-BP-bound-PS in plasma was also assessed by crossed-immunoelectrophoresis(CIE). Results (mean - SD) were expressed in percentage, in relation to healthy adults values (n = 15). Low levels of total PS were obtained in all fetuses (16.4 ±4.2) and newborns (36.4 ±9.5) as compared to adults (91.6 ± 12.2). Free protein S level was also decreased both in fetuses (22.2 ±6.0) and newborns (48.5 ± 12.1 versus 89.4 ± 26.3 in adults). At these stages of development, the ratio Free PS / Total PS (both values were obtained according to a reference curve performed with a normal adult pool plasma untreated by PEG) was significantly higher as compared to normal adults (0.82 ±0.07 in F, 0.64 ±0.17 in N and 0.39 ±0.11 in A, p‹0.001, Student t test). The predominance of free PS was also visualized in the CIE patterns. These data may be explained by undetectable C4b-BP in 21-week old fetuses (‹2% in 10 cases). After the 26th week of gestation C4b-BP level was 7.8 ±7.4 ‹n=5) and reached a value of 19.2 ±15.6 in newborns (adults = 95.7 ±14.7). In human fetus and newborn, PS essentially circulates under free form and this might compensate the decrease of the total PS level.
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Brown, Angela M. "Development of photoreceptor sensitivity and color vision in early infancy." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1986. http://dx.doi.org/10.1364/oam.1986.ff1.
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Over the course of infancy and early childhood, major changes in visual function occur. A clear understanding of these changes could lead to a more complete understanding of adult vision, because a good theory of vision must parsimoniously account for infant and adult vision and for the smooth transition between them that occurs during normal maturation. This paper summarizes what is known of rod and cone vision in human infants. We include morphology of the rods and cones, psychophysically measured absolute and increment thresholds, photosensitivities and spectral sensitivities of the receptor mechanisms, and the overall luminous efficiency function. The ability to discriminate between lights on the basis of differences in spectral composition emerges over the first three months of life. Four hypotheses are discussed concerning what critical immaturities are responsible for the poor color vision of very young infants: (1) a color vision deficiency of a recognized adult type, (2) extrafoveal detection of stimuli, (3) inadequate spatial resolution for chromatic stimuli, and (4) immaturity of chromatically opponent channels.
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Vorontcova, Olga, Larisa Udochkina, Igor Mazin, and Elena Fedyulina. "Detailed kinematic evaluation of shoulder motion during normal gait in healthy young males." In Innovations in Medical Science and Education. Dela Press Publishing House, 2022. http://dx.doi.org/10.56199/dpcsms.lejq3299.
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Complex kinematic analysis of human motion has become achievable through new technological developments. Several new studies have already taken advantage of the new kinematic approach for documentation and analysis of pathological motion, including palsy, paralyses, Parkinson’s disease and others. However, physiological motion of gait and corresponding upper limb motion has seldom been studied. The aim of this study was to collect and analyse data of shoulder motion of 45 healthy young males during the gait cycle. Detailed dynamic kinematic measurements revealed that the arm remained constantly in an internal rotation position with changing and adapting angle along the gait cycle with maximal internal rotation at mid-stance and at mid-swing, and minimal internal rotation in the beginning and at the end of the cycle, as well as at mid-cycle. At the same time, the arm remained constantly in an adduction position, with maximal adduction by mid-cycle and minimal adduction in the beginning and at the end of the cycle. In parallel, the arm reached maximal extension around the beginning and the end of the cycle, with maximal flexion just before mid-cycle. During the gait cycle, there was regular and repetitive movements of the shoulder joint and the arm with constant range of movements, i.e. for the shoulder: 24.6°±3.4° for the flexion-extension movement, 6.44°±0.2° for the adduction-abduction movement and 4.57°±0.1° for the rotational movement. These data provide a first valuable base of the normal, physiological role of the arm for a stable and balanced gait in young adult males. From there, pathologies of the arm and shoulder may be dissected and their influence on the gait cycle investigated in the future. In addition, these data may also be used for the design and control of robotic arm prosthesis.
Reports on the topic "Normal adult human astrocyte"
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Kahler, David W., and Carmen M. Arroyo. Normal Human Astrocyte Instructions for Initiation of Cultures from Cryopreserved Cells and Subculture. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada442897.
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