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D Heumann

Publications and source records attributed to D Heumann.

77 records · Page 5Linked to original sources
PubMed1977

Postnatal development of the mouse cerebral neocortex. I. Quantitative cytoarchitectonics of some motor and sensory areas.

Quantitative data have been obtained (numbers of neurons and glial cells in a cube of 0.000 25 mm3, thicknesses of cortical layers, nuclear diameters of neurons) on Cresyl Violet stained sections from the six cortical layers of the Swiss Albinos mouse brain through the postnatal development at 5, 10, 30, 60 and 180 days. 1) Normative data of the cortical cell population are now available from motor areas 4 and 10 and sensory areas 3 and 2 according to KRIEG (1946). The evolution of the neuronal densities through time was obtained and was taken as a criterion of maturation for the different layers in the studied cortical areas. 2) Areas 4, 10, 3 and 2 have been described histologically at all the mentioned ages. 3) The nuclear diameter of the neurons increases in all the layers between 5 and 10 days and less between 10 and 30 days. It remains stable from 30 days on. 4) At adult age the sensory areas 3 and 2 show a greater thickness of the group of supragranular layers II, III and IV than of the infragranular layers V and VI together. Layer V shows the same thickness in areas 2, 3 and 4. The same is true for layer VI in the same areas. In area 10 layers V and VI are thicker than in areas 2, 3 and 4. At younger ages (5 and 10 days) the relative thicknesses of the different layers are of the same order but each layer is thinner. 5) The neuronal density shows the same type of development in the four studied areas. Maturation in terms of decrease of neuronal densities is very rapid between 5 and 10 days and slows down till 30 days with speeds depending on the layers. Layers I, V and VI show faster and earlier maturation than layers II, III and IV. 6) The glial density is mostly stable through the development. This does not mean that there is no glial proliferation. 7) The delineation between the different areas according to KRIEG's (1946) atals and/or CAVINESS's (1975) publication are discussed taking into account our quantitative data.

Animals↗
PubMedDate not supplied

Neuronal death in the development and aging of the cerebral cortex of the mouse.

The numbers of neurons and glial cells in the cerebral cortex of the mouse have been estimated during its whole life-span (5 to 720 days), taking into account both the cellular densities of several areas and the cortical volumes. The results clearly demonstrate that there is a massive neuronal loss in the cerebral cortex during early postnatal development, greater in layers II-IV than in layers V-VI. In contrast, aging is characterized by a discrete neuronal loss in the cerebral cortex, purely restricted to layers II-IV. The number of glial cells increases continuously from 5 to 720 days. We emphasize here the need to obtain volumetric measure together with cellular densities in order to get interpretable quantitative data on cellular death and proliferation.

Aging↗
PubMedDate not supplied

Reactivity of murine and human recombinant LPS-binding protein (LBP) within LPS and gram negative bacteria.

The serum lipopolysaccharide (LPS) binding protein, LBP, has been shown to greatly enhance cellular responses to low concentrations of LPS. Purified LBP facilitates the transfer of LPS to membrane-bound or soluble CD14; the CD14/LPS complex then triggers a signal in responsive cells. We have cloned and sequenced a cDNA encoding murine LBP, and produced recombinant murine LBP using a baculovirus expression system. Using either a solid-phase or a cytofluorometric assay, recombinant murine and human LBP were found to bind avidly to free LPS, but only weakly to live bacteria from most LPS-containing Gram negative strains. Binding correlated loosely with the length and composition of the polysaccharide O chains. However, recombinant LBP did bind well to all heat-killed bacterial preparations. These findings suggest that LBP could be implicated in the response to killed but not live Gram negative bacteria.

Acute-Phase Proteins↗
PubMedDate not supplied

Contribution of TNF/TNF receptor and of Fas ligand to toxicity in murine models of endotoxemia and bacterial peritonitis.

Fas/Fas ligand and TNF/TNF receptors are involved in apoptosis. Whether both systems are involved in septic shock has not been determined so far. We investigated the role of TNF/TNFR and Fas/Fas ligand in models of endotoxemia and of speticemia in mice. Upon LPS challenge, TNF and TNFR p55 were involved in the process inducing lethality. FasL did not contribute to enhance lethality, as evidenced in gld mice, lacing FasL. Following an intraperitoneal injection of live E. coli, TNF and TNFR p55 were necessary to combat infection. Disruption of either gene was associated with enhanced lethality and failure to clear the bacteria. No effect observed in gld mice in this peritonitis model. Thus, these observations confirmed the pathogenic role of TNF/TNFR in endotoxemia and its beneficial role in local bacterial infections. In addition the data ruled out a major role for Fas/FasL in septic shock in mice.

Animals↗