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G C Winkler

Publications and source records attributed to G C Winkler.

15 recordsLinked to original sources
PubMed1989

Review of the significance of pulmonary intravascular macrophages with respect to animal species and age.

Pulmonary intravascular macrophages (PIMs) have been recognized as the site of substantial uptake of blood-borne particles in the lungs of a number of domestic animal species. Concomitantly, there is a pronounced lung susceptibility to endotoxin in calves, goats, sheep, pigs, and cats. Hemodynamic changes and initial lung injury after endotoxin administration are mediated by arachidonic acid metabolites from a pulmonary source. A significant role of PIMs in regulating pulmonary hemodynamics is implicated.

Age Factors↗
PubMed1988

Pulmonary intravascular macrophages in domestic animal species: review of structural and functional properties.

In dogs, laboratory animals, and man, the clearance of bacteria and particulates from blood occurs predominantly in hepatic Kupffer cells and splenic macrophages. In contrast, removal of blood-borne particulates in calves, sheep, goats, cats, and pigs occurs predominantly in pulmonary intravascular macrophages (PIMs). Review of recent studies indicates that PIMs are a resident cell population, junctionally adherent to the capillary endothelium of lungs and morphologically similar to hepatic Kupffer cells. PIMs are a pulmonary constituent of the mononuclear phagocyte system with respect to secretory, endocytic, and functional properties. Differentiated PIMs are rare in newborn pigs, and the majority of cells closely apposed to capillary endothelium consists of monocytes, which are occasionally in mitosis. In 7-day-old and older pigs, most cells apposed to capillary endothelium have characteristics of differentiated PIMs. This suggests a monocytic origin of PIMs in pigs. Perinatal colonization of lung capillaries by monocytes and their subsequent differentiation into PIMs represent a component of postnatal lung development. Estimates of relative PIM numbers in ovine and porcine lung parenchyma suggest cell densities similar to that of rat hepatic Kupffer cells. Apart from phagocytic properties, PIMs participate in the removal and disintegration of aged and impaired blood cells. After phagocytic stimulation, isolated PIMs secrete oxygen radicals, which are essential for microbicidal function. Similarly, by secreting bioactive lipids, stimulated PIMs may contribute to regulation of pulmonary hemodynamics. After receiving minute amounts of bacterial endotoxin, pulmonary injury is pronounced in sheep, calves, pigs, and cats, but not in laboratory animals and dogs. This presumably is related to the secretion of bioactive lipids by PIMs.

Animals↗
PubMed1987

Postnatal colonization of porcine lung capillaries by intravascular macrophages: an ultrastructural, morphometric analysis.

Lungs of newborn and of 7- and 30-day-old pigs were fixed at total capacity by a standardized procedure. Stereologic morphometry was applied to random ultrathin sections of parenchyma. Relative volume density, absolute volume, and capillary surface coverage of intravascular macrophages as well as parameters of relative morphometric diffusion capacity of lungs were assessed. Intravascular macrophages occupied up to 25% of capillary volume in 30-day-old pigs compared with 6% in newborn pigs; this was a 14-fold increase of absolute volume. In 30-day-old pigs, 16% of capillary surface was covered with closely adherent intravascular macrophages in contrast to only 2% in newborn pigs. Determinators of morphometric diffusion capacity were similar in all pigs. Greater thickness of the arithmetic and harmonic mean air-blood tissue barrier in 30-day-old pigs (with included thickness of intravascular macrophages) compared with air-blood tissue barriers (without intravascular macrophages) was not statistically significant. The relative difference of arithmetic mean was larger than the difference of harmonic mean, and reflected preferential adherence of intravascular macrophages to the thick portion of the air-blood tissue barrier. Our findings confirm morphologic observations of perinatal colonization of the porcine lung by monocytes that replicate and differentiate into large, highly phagocytic, resident, intravascular macrophages. Preferential adherence to sites where basal laminae of capillary endothelium and alveolar epithelium were separated by interstitium may explain the minimal morphometric impact of intravascular macrophages on the air-blood tissue barrier thickness. This location would be expected to have less effect on gas diffusion than location of intravascular macrophages on the thin side of the air-blood barrier.

Animals↗
PubMed1987

Detection of antibodies to Anaplasma marginale by an improved enzyme-linked immunosorbent assay with sodium dodecyl sulfate-disrupted antigen.

Sensitivities of two enzyme-linked immunosorbent assays (ELISAs) with particulate and sodium dodecyl sulfate (SDS)-disrupted Anaplasma marginale antigen were compared. The quotient of positive reference sera divided by the absorbance quotient of a negative reference serum at identical dilution was termed the signal-to-noise ratio. Optimal signal-to-noise ratios were dependent on both pretreatment of antigen and antigen concentration. SDS disruption of anaplasmal antigen resulted in a markedly improved signal-to-noise ratio of ELISA compared with ELISA with untreated antigen at identical antigen and serum dilutions. This represented higher sensitivity and lower background absorbance of the ELISA with disrupted antigen. SDS-disrupted A. marginale antigen was standardized by protein determination, and antigen, as well as precoated microtiter wells, was stored frozen without apparent loss of antigenic properties. ELISA results were in agreement with results of positive and negative control sera tested by the complement fixation test or by light microscopy Anaplasma diagnosis in Giemsa-stained blood films.

Anaplasma↗
PubMed1986

Glyceraldehyde-3-phosphate dehydrogenase is a nonhistone protein and a possible activator of transcription in neurons.

A single-stranded DNA-binding protein of Mr 35,000 (35K protein) was isolated from calf cerebral cortex by affinity chromatography on immobilized double-stranded and single-stranded DNA. Its localization in the nuclear compartment was demonstrated by immunohistochemistry. Previous studies had uncovered a homologous nonhistone chromosomal protein in the nuclei of rat cerebral cortex neurons, cerebellar neurons, oligodendrocytes, and liver cells. The rat protein accumulated in the nuclear compartment of neurons in exact temporal coincidence with the arrest of cell division and the initiation of terminal differentiation. Therefore, in the present work, the 35K protein was tested for an activating role in RNA transcription. During the course of this study we became aware that the 35K protein was identical to a glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase (GAPDH, EC 1.2.1.12). When authentic GAPDH from rabbit skeletal muscle was injected into Xenopus laevis oocytes, it greatly stimulated RNA polymerase II transcription, whereas the 35K protein from calf brain did not. This apparent discrepancy was partially resolved by the finding that rabbit muscle GAPDH could be fractionated into two components by affinity chromatography on single-stranded DNA cellulose. Only 5% of the applied protein was retained on the column and could be eluted with a shallow salt gradient identical to the one used for the isolation of the 35K protein. This single-stranded DNA-binding component of rabbit muscle GAPDH did not stimulate transcription. Apparently, the 35K protein from calf brain corresponded to this single-stranded DNA-binding subfraction, which explained its failure to activate transcription.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Ultrastructural morphometric investigation of early lesions in the pulmonary alveolar region of pigs during experimental swine influenza infection.

Experimental infection of specific-pathogen-free pigs with swine influenza virus by the intratracheal route resulted in a severe respiratory disease that closely resembled natural swine influenza in clinical course and pathologic lesions. Alveolar epithelial necrosis with sloughing of necrotic cells occurred from 24 to 96 hours after inoculation (p.i.) and was associated with alveolar edema and diffuse interstitial pneumonitis. The latter, initially of neutrophilic character, became histiocytic 48 hours p.i. Ultrastructural analysis of alveolar parenchyma disclosed viral replication in epithelial cells beginning at 5 hours p.i. and lasting to 96 hours. Budding of pleomorphic virus particles from the surface of alveolar epithelial cells and accumulation of viral proteins within the nucleus and cytoplasm of epithelial cells were seen. The extent of parenchymal lesions as quantified by stereologic morphometry within the whole lung was characterized by a marked relative and absolute volume increase of interalveolar septa and increased air-blood tissue barrier thickness. The volume increase of interalveolar septa was due to an increase of interstitial tissue volume by 85% in pigs at 96 hours p.i., compared with control pigs with similar lung volumes.

Animals↗
PubMed1985

Morphometry of postnatal development in the porcine lung.

Alveolar regions of normal pig lungs (newborn to 60-day-old) were characterized morphometrically to provide a basis for comparison in future investigations of porcine respiratory diseases. Endotracheal installation of fixative was done to expand the lungs uniformly at total capacity. Differential effects of lobar variations were determined by stratified random sampling of lung lobes. A stereologic study was done by point and intersection counts on electron micrographs. At birth, the lungs were remarkably well developed. Relative alveolar and capillary surface densities and air-blood tissue barrier thicknesses were at adult levels. In allometric regressions, volumes and surfaces of lung components regressed directly to lung volume, but monoexponentially (to the 3/4 power) with body weight. In the first postnatal week, however, relative volume densities of cellular interstitium in septal tissue and of capillary lumina in parenchyma increased at statistically significant levels. Composition of lung parenchyma and septa was changed, although without statistically significant direct impact on parameters related to gas exchange. Type II pneumocytes had increased nuclear to cytoplasmic volume ratios in 7- to 14-day-old pigs, probably reflecting cell activation and increased surfactant production. Age (postnatal lung growth) created the most substantial variance of results; interanimal variation in pigs of the same age was less important and no consistent lobar variations were seen.

Animals↗
PubMed1985

Monocytic origin and postnatal mitosis of intravascular macrophages in the porcine lung.

Ultrastructural studies of near-term to 2-month-old pigs were done to document characteristics and developmental changes of intravascular macrophages in pulmonary capillaries. Evidence is presented that blood monocytes colonize the porcine lung perinatally, replicate within capillaries postnatally, and attach to endothelium by intercellular junctions during differentiation. Major ultrastructural features of differentiated intravascular macrophages are adhesion to capillary endothelium, pseudopods, phagosomes, and tubular structures of micropinocytosis vermiformis. Ultrastructure indicates that intravascular macrophages are cells of the mononuclear phagocyte system involved in several functions (eg, blood cell sequestration) that are usually attributed to hepatolineal macrophages. In newborn and 3-day-old pigs, the majority of cells closely apposed to endothelium consisted of few differentiated monocytes, but in 7-day-old and older animals, most cells that were joined to endothelium had characteristics of differentiated intravascular macrophages.

Animals↗
PubMed1984

The neonatal porcine lung: ultrastructural morphology and postnatal development of the terminal airways and alveolar region.

Morphology and postnatal development of the porcine lung are described in animals ranging in age from newborn through 60 days. Standardized fixation was accomplished by intratracheal instillation of glutaraldehyde under constant pressure. Light microscopic, scanning, and transmission electron microscopic investigations revealed that the porcine lung follows the common architecture of mammalian lungs, but has certain peculiarities as well: intravascular macrophages, ultrastructurally similar to Kupffer cells, are attached to endothelial cells in pulmonary capillaries and are involved in erythrophagocytosis during the first postnatal weeks. Type II pneumocytes of newborn pigs exhibit signs of cell activation, mainly complex nuclear bodies in the cell nuclei. At the same time high levels of 17-hydroxycorticosteroids are observed in the newborn blood plasma. Terminal airways of the porcine lung are nonalveolarized and are, therefore, of purely conductive function. At birth the porcine lung exhibits a high degree of maturity, and thick-walled primary saccules, as described in newborn rodents, are not seen. Septa appear straight and smooth, owing to rare ramification. Septal buds are discernible, and two capillary networks visible on both sides of septal cross sections are seen. Further subdivision of the airspaces occurs in the first two postnatal weeks. Precociousness and fast postnatal growth of the porcine species are assumed to be the reason of this advanced degree of lung maturity at birth and the following rapid pulmonary development.

Animals↗
PubMed1983

Early fibrogenicity of asbestos fibers in visceral peritoneum.

Different asbestos types and milled asbestos cement were inoculated intraperitoneally into mice. Mesenteric tissue (appendices epiploicae) was examined by transmission electron microscopy at different intervals between 2 h and 3 weeks after exposure to asbestos. As early as 2 h after asbestos administration, the investigated tissues exhibited focal mesothelial cell loss barring the basement membrane, which at some points was even disrupted. Severe cell damage, obviously caused by the mineral fibers, was discernible in the remaining mesothelial cells. At a later stage, the whole peritoneal sheet underwent inflammatory and diffuse fibrotic processes. The early surface irritation is due to the mechanical influence of the penetrating asbestos fibers. The results confirm our previously published findings with the scanning electron microscope that asbestos has distinct fibrogenic properties.

Animals↗
PubMed1982

Penetration of asbestos fibers in the visceral peritoneum of mice. A scanning electron microscopic study.

Mice were injected intraperitoneally with either amosite, crocidolite or chrysotile. Tissue specimens of the mesentery (appendices epiploicae) were taken after 2 h, 24 h and 7 days and prepared for scanning electron microscopy. Subsequent examination revealed numerous fibers penetrating the mesothelium. The penetration is regarded as the earliest interaction between fibers and mesothelium and is due to the asbestos' inherent needle-like structure and to visceral motility.

Animals↗