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Biomedical subjects

D B Wilson

Publications and source records attributed to D B Wilson.

At least 271 records · Page 15Linked to original sources
PubMed1983

Identification and quantitation of T lymphocyte subsets found in the spinal cord of the Lewis rat during acute experimental allergic encephalomyelitis.

Monoclonal antibodies specific for different rat T cell subsets and Ia-positive cells were used in a quantitative morphologic study of the cellular infiltrates in the spinal cords of Lewis rats during acute, actively induced experimental allergic encephalomyelitis (EAE). The predominant cell types in the inflammatory spinal cord lesions are W3/25-positive and Ia-positive cells. The relative percentages represented by each cell type remain quite constant regardless of the degree of clinical illness exhibited by the rat. These data demonstrate a quantitative profile of the infiltrating cells in acute, active EAE, and suggest that the principal inflammatory cells in these lesions are T helper cells and Ia-bearing cells (macrophages, B cells, or activated T helper cells).

Acute Disease↗
PubMed1983

Tissue interactions in basal regions of the cranial neuroepithelium in the C57BL mouse.

Developmental interactions of neuroepithelial cells with mesenchymal cells and with notochordal cells were analyzed in the presumptive hindbrain of C57BL mouse embryos at stages 13 and 14 (8 and 9 days). Basal regions of the neuroepithelium and its basal lamina were also analyzed ultrastructurally by means of lanthanum tracer studies and with tannic acid treatment, and correlations were made with comparable features at the middle spinal cord level. At stage 13 the presumptive hindbrain showed less intercellular space in the basal one-third of the neuroepithelium than in its intermediate one-third, whereas at stage 14 the basal intercellular space increased to an amount roughly equal to that in the intermediate region. Lanthanum tracer penetrated readily from the basal aspect of the cells into the intercellular spaces. Microfilaments were observed in the basal cytoplasm immediately subjacent to the cell membrane. However, in contrast to apical regions, the microfilaments do not span or constrict the basal portion of the cytoplasm, suggesting a different functional role basally than apically. Projections from mesenchymal cells and from notochordal cells were in contact with the neural basal lamina. The notochordal cells, however, showed a closer relationship, including more processes and broader areas of contact, with strands of basal laminar material spanning the gap between notochord and neural tube.

Animals↗
PubMed1983

Effects of exogenous thyroxine and growth hormone on satellite cell and myonuclei populations in rapidly growing rat skeletal muscle.

We have examined the independent and combined effects of thyroxine (T4) and bovine growth hormone (bGH) on postweaning growth, satellite cell proliferation and accumulation of myonuclei in extensor digitorum longus (EDL) muscles in rats. Daily subcutaneous injections of T4 (1.5 micrograms/100 g BW), but not bGH (.25 IU/100 g BW) or T4 + bGH, resulted in elevated incidence of satellite cell nuclei and satellite cells per muscle fiber in transverse thin section, and a significantly (p less than .05) higher percentage of satellite cell nuclei and percentage satellite cells as a percentage of all muscle nuclei in transverse thin sections after one week of injections. The higher incidence of myonuclei per muscle fiber in transverse section in T4 injected rats at the end of the injection period (p less than .05) was interpreted to be the result of a higher concentration of satellite cells exhibiting normal or elevated mitotic activity during the early part of the injection period. The higher incidence of myonuclei per fiber was not caused by an increased mean fiber cross-sectional area in T4 injected rats. These histological observations relative to T4 injections were not accompanied by significantly greater weight, DNA content or estimates of total satellite cells per EDL muscle after either one or three weeks of hormone injections. These studies support the premise that T4 may be directly involved in the regulation of satellite cell proliferation and myonuclei accumulation, however, they do not support the premise that growth hormone exerts a similar influence during early muscle growth and development.

Animals↗
PubMed1982

Discovery of an arachidonoyl coenzyme A synthetase in human platelets.

Platelets contain small amounts of a variety of free fatty acids but essentially no free arachidonate. When free fatty acids are incubated with platelets, there is preferential incorporation of arachidonic acid and 8,-11,14-eicosatrienoic acid compared to other fatty acids. We now explain these findings by the discovery that platelets contain two long chain acyl-CoA synthetases. One shows activity with a range of different fatty acids, similar to long chain acyl-CoA synthetases studied previously. A crude platelet membrane preparation contains this enzyme that catalyzes the formation of 0.75 nmol of oleoyl-CoA/min/10(9) platelets. The other enzyme is specific for the prostaglandin precursors arachidonic acid and 8,11,14-eicosatrienoic acid. Based on the ability of fatty acids to inhibit arachidonate and 8,11,14-eicosatrienoate activation, we conclude that other fatty acids including linoleic, 5,8,11-eicosatrienoic, and oleic acids are not substrates for the enzyme. Platelet membranes catalyze formation of 2.9 nmol of arachidonoyl-CoA/min/10(9) platelets and 2.5 nmol of 8,11,14-eicosatrienoyl-CoA/min/10(9) platelets. Arachidonoyl-CoA synthetase has optimal activity at pH 8 and requires ATP (Km = 0.5 mM), Mg2+ (Km = 2.5 mM), CoA (Km = 0.13 mM), and arachidonic acid (Km = 0.03 mM). We propose that the arachidonate-specific acyl-CoA synthetase may control the level of free arachidonic acid in platelets, limiting prostaglandin synthesis by the unstimulated cell and capturing free arachidonate from extracellular sources.

Animals↗
PubMed1982

A comparative analysis of [3H]thymidine labeling in the embryonic tectum of the rhesus monkey (Macaca mulatta) and C57BL mouse.

The pattern of [3H]thymidine incorporation in the dorsolateral wall of the embryonic tectum was studied and compared one hour after injection of the label in the rhesus monkey (Macaca mulatta) at stages 11-20 (25-37 days of gestation) and in the C57BL mouse at stages 14-22 (9-14 days of gestation). During the early stages of development, the labeled nuclei were located peripherally in the ventricular zone in both the rhesus monkey and mouse embryo, although a number of labeled nuclei tended to occur closer to the ventricular border in the mouse, whereas there was little or no encroachment at the ventricular border in the rhesus monkey. The ventricular zone of the rhesus monkey and mouse embryos initially showed a high labeling index (LI) of about 59% which subsequently declined with increasing age. However, the decline occurred earlier and more precipitously in the rhesus monkey. At stage 17 of the rhesus monkey the LI had dropped to about 42%, whereas it still remained at 59% in the 12-day mouse, and by stage 20 of the monkey the LI was approximately 26%, in contrast to 41% in the stage 22 (14-day) mouse. At stage 20 of the mouse (12 days of gestation) the intermediate zone became much thicker than in the comparable stage (17) of the rhesus monkey, and this discrepancy continued at each successive stage observed in the current study. Also, whereas lamination became apparent in the intermediate zone of the mouse at stage 22, the monkey tectum at a comparable stage (20) was poorly differentiated.

Animals↗
PubMed1982

Cerebrovascular pathogenesis in the telencephalon of the loop-tail mouse: a transmission electron-microscopic study.

Cerebral capillaries in the telencephalon of normal (+/+; Lp/+) and abnormal (Lp/Lp) loop-tail mutant mice were studied chronologically by means of electron microscopy at stages ranging from 15 through 18 days of gestation. In the abnormal tissue, neural rosettes were common, and cellular material and red blood cells were often contained within the lumen of the rosettes. The endothelial cells of telencephalic blood vessels in the abnormal brains showed a persistence of cellular projections, subluminal vacuoles, and swollen mitochondria beyond the stage when these features ordinarily disappear in normal embryonic cerebral vessels. The endothelial cells in the abnormal brains also failed to become fully invested with pericytes, and red blood cells gradually infiltrated the neural tissue, particularly in subependymal regions, at 16-18 days of gestation.

Animals↗
PubMed1982

An electron microscopic analysis of notochordal and mesenchymal cell abnormalities in embryos of Danforth's short-tail (Sd) mice.

Abnormalities of notochordal cells and of mesenchymal cells in embryos of Danforth's short-tail (Sd) and C57BL mice were examined by means of electron microscopy and cytochemical staining at 11.0 and 11.5 days of gestation. In abnormal (Sd/+; Sd/Sd) embryos, the notochordal cells were markedly deficient in bundles of filaments and lacked surface protrusions, and the notochordal basal lamina was continuous; in contrast, notochordal cells of normal (+/+) littermates and of C57BL embryos contained numerous bundles of filaments and showed fingerlike surface protrusions and discontinuous basal laminae. The pathologic notochordal cells also lacked the accumulations of glycogen revealed in the normals by means of thiocarbohydrazide cytochemical staining at the electron microscopic level. The mesenchymal cells of abnormals also were deficient in filaments but did stain for glycogen, though less prominently than did normal mesenchymal cells.

Animals↗
PubMed1982

Effect of the lambda S gene product on properties of the Escherichia coli inner membrane.

The S gene of bacteriophage lambda is a late gene required for cell lysis, but unlike the other two lysis genes, R and Rz, it does not code for an endolysin. Earlier studies have shown that the S gene product inhibits respiration and macromolecular synthesis and makes the inner membrane permeable to sucrose. In this study, the effect of the S gene product on a number of Escherichia coli membrane functions (active transport, permeability, respiration, and transhydrogenase and ATPase activity) were measured, and a product of the lambda S gene was identified in the inner membrane fraction by two-dimensional polyacrylamide gel electrophoresis. The results of these experiments indicate that the lambda S product is present in the inner membrane, that it increased the permeability of the membrane for all of the small molecules that were tested, and that its action is reversible. The simplest explanation of these results is that the S gene product forms a hydrophilic pore through the inner membrane, allowing small molecules and lambda lysozyme to pass through.

Adenosine Triphosphatases↗
PubMed1982

A second function of the S gene of bacteriophage lambda.

Infection of Escherichia coli by bacteriophage lambda caused an immediate inhibition of uptake by members of all three classes of E. coli active transport systems and made the inner membrane permeable to sucrose and glycine; however, infection stimulated alpha-methyl glucoside uptake. Phage infection caused a dramatic drop in the ATP pool of the cell, but the membrane did not become permeable to nucleotides. Infection by only one phage per cell was sufficient to cause transport inhibition. However, adsorption of phage to the lambda receptor did not cause transport inhibition; DNA injection was required. The inhibition of transport caused by lambda phage infection was transient, and by 20 min after infection, transport had returned to its initial level. The recovery of transport activity appeared to require a lambda structural protein with a molecular weight of 5,500. This protein was present in wild-type phage and at a reduced level in S7 mutant phage but was missing in S2 and S4 mutant phage. Cells infected with S7 phage had a partial recovery of active transport, whereas cells infected with S2 or S4 phage did not recover active transport. Neither the inhibition of transport caused by phage infection nor its recovery were affected by the protein synthesis inhibitors chloramphenicol and rifampin.

Bacteriophage lambda↗
PubMed1982

Prenatal cytodifferentiation in the pars distalis of the dwarf mutant mouse.

The pars distalis of the pituitary gland was studied by means of electron microscopy in 14- to 18-day dwarf embryos (dw/dw) obtained from matings of dwarf homozygotes in which reproductivity was induced by hormone supplementation and pituitary transplants to the renal capsule. At 14 days of gestation the dwarf pars distalis shows fewer granulated cells than in the normal. Although somatotroph-like and mammotroph-like cells are identifiable in the normal pars distalis as early as 15 days, comparable cells are not present in the dwarf. By 17 and 18 days, the dwarf exhibits an ambiguous cell-type with a combination of somatotroph and mammotroph characteristics. At 18 days the dwarf also continues to show numerous nongranulated cells with large aggregates of glycogen, whereas in the normal pars distalis comparable glycogen-containing cells are relatively scarce.

Animals↗
PubMed1981

T lymphocytes specific for immunoglobulin allotype. I. Igh-1b-specific T cells demonstrated by suppression in vivo and cytotoxicity in vitro.

We show that determinants of IgG(2a) of C57BL/6 mice (Igh-1(b)) stimulate allotypespecific T cells in BALB/c mice. Such cells are detected in two different functional assays; chronic allotype suppression and T cell-mediated cytotoxicity. A population of suppressor T cells capable of inducing chronic Igh-1(b) suppression was demonstrated by rosetting procedures to possess Igh-1(b)-specific receptors, a result interpreted as indicating that suppressor T cells may act directly upon allotype-bearing B cells. From similar populations we were also able to demonstrate Igh-1(b)-specific cytotoxic T cells. Such cells were lytic for target myeloma cells expressing the Igh-1(b) allotype of IgG28, and were ineffective against a variant cell line failing to express Igh-1(b), and other target cell lines expressing different allotypes or isotypes. The similar specificity of suppressor T cells and cytotoxic T lymphocytes for Igh-1(b) allotype raises the possibility that the target in allotype suppression is a B cell, and that allotype-specific cytotoxic T cells may play some role in regulation of allotype expression in the suppressed state.

Animals↗
PubMed1981

T lymphocytes specific for immunoglobulin allotype. II. Cloned Igh-1b-specific cytotoxic T cells.

This study describes long-term-cultured lines and clones of cytotoxic T cells (Tc) with specificity for determinants of the Igh-1(b) immunoglobulin allotype. These Tc clones were initiated by repeated stimulation of immune spleen cells from BALB/c mice with an Igh-1(b)-producing myeloma, and then they were maintained in medium supplemented with mitogen-induced growth factors in the absence offurther antigenic stimulation . The lytic potency of these clones was 30-100-fold greater than the primary cultures from which they were derived, and specificity studies showed them to be lytic for Igh-1(b) targets and not for targets expressing Igh-1(a) or Igh-4(b), nor the lipopolysaccharide blasts . Finally, soluble preparations of Ig were tested for their ability to block lysis of labeled Igh-1(b)-expressing targets. The results showed that Igh-1(b) and not other immunoglobulin allotypes or isotypes could block lysis, and that the mechanism of lytic inhibition is due to Igh-1(b)-induced autolysis of the killer cells.

Antibody Specificity↗
PubMed1981

Induced tolerance in F1 rats to anti-major histocompatibility complex receptors on parental T cells. Implications for self tolerance.

The immunogenicity of cell surface markers associated with specific anti-major histocompatibility complex (MHC) alloreactivity of rat peripheral T lymphocyte subpopulations has been demonstrated in the past by the ability of such cell populations to induce a profound and specific resistance to systemic graft-vs.-host (GVH) disease in adult rats. Our studies demonstrate that these specificity-associated anti-MHC parental strain T cell markers are also tolerogenic; if small numbers of parental strain T cells are administered to newborn F1 rats, they result in the specific inability to induce GVH resistance later on in adult life. Moreover, unlike normal animals, these F1 rats are extremely sensitive to systemic GVH disease caused by T cells from the original donor parental strain.

Animals↗