Investigations into the origin of mouse liver sinusoidal cellsFreudenberg, N.; Freudenberg, M.; Hoess, C.; Schrecker, H.; Galanos, C.
doi: 10.1007/BF00710899pmid: 3097947
The possibility that liver sinusoidal cells are derived from the bone-marrow was investigated in chimeric mice. H2k-positive bone-marrow cells from F1 (B10.BR × B10.D2) hybrid mice were transplanted into irradiated H2k-negative parental mice (B10.D2), and the liver examined immunohistochemically for the presence of H2k-positive cells, with the help of an anti-H2k monoclonal antibody. With the passage of time (from the fifth week onwards), increasing numbers of transplanted bone-marrow cells enter the liver sinusoids, undergo alteration in their shape, and remain there, probably replacing sinusoidal lining cells. DNA-synthesising cells in the sinusoids were observed, suggesting, in addition, local cell proliferation. The replacement of sinusoidal cells from bone-marrow was greatly accelerated after liver damage had been induced by sublethal doses of endotoxin (LPS), and proliferation was also enhanced after treatment with LPS. These results strongly suggest that the bone-marrow participates in the replacement of liver sinusoidal cells.
Alloxan-induced diabetes in the mouse: Time course of pancreatie B-cell destruction as reflected in an increased islet vascular permeabilityJansson, L.; Sandler, S.
doi: 10.1007/BF00710901pmid: 3097948
The extent to which injections of the pancreatic B-cytotoxin alloxan in C57BL/Ks mice induced an increase in islet vascular permeability, and the time course of this increase, were studied. The vascular permeability was monitored by administration of the dye Monastral blue B, which is entrapped in leaky blood vessels with intact basement membranes. The islets were visualized by a freeze-thawing technique which allows identification of stained islets. Not until four hours after the alloxan injections was there an increase in islet uptake of Monastral blue B when compared with saline-treated control animals. Thereafter the islet staining increased further. The process was accompanied by gradual development of hyperglycaemia and a reduction of number of the islets identified in the pancreatic preparations. It is concluded that alloxan causes an increase in islet vascular permeability, which appears to become manifest at a later stage than the cytotoxic B-cell degeneration.
Reactivity of a monoclonal antibody recognicing an estrogen receptor regulated glycoprotein in relation to lectin histochemistry in breast cancerHelle, Markku; Krohn, Kai
doi: 10.1007/BF00710902pmid: 3097949
We have raised monoclonal antibodies against human milk fat globule membrane antigens and previously shown that one of them, called III D 5, recognises a glycoprotein associated with estrogen receptor activity of breast cancer. In immunoblotting it was shown that the molecule in human milk exclusively stained with III D 5 also binds peanut agglutinin (PNA) and Ricinus communis. In this study we correlate the staining of III D 5 and binding of lectins to tissue sections fixed in formalin and embedded in paraffin. Similar rections were seen only with III D 5 and PNA. Our results suggest that III D 5 and PNA detect overlapping antigenic epitopes in mammary carcinoma. This is in keeping with previous results that PNA or III D 5 reactivity is correlated with estrogen receptor status of breast cancer.
Ultrastructure, renin status, contractile and electrophysiological properties of the afferent glomerular arteriole in the rat hydronephrotic kidneyNobiling, Rainer; Bührle, Christian; Hackenthal, Eberhard; Helmchen, Udo; Steinhausen, Michael; Whailey, Andrea; Taugner, Roland
doi: 10.1007/BF00710903pmid: 3097950
Histological, ultrastructural, immunohistochemical, intravital microscopic and electrophysiological techniques have been applied to study experimental hydronephrosis in rats in order to assess its value as a preparation for the investigation of renal microcirculation and of the electrophysiological properties of the renin-containing juxtaglomerular (JG) cells of the afferent glomerular arteriole.
Experimental staphylococcal endocarditis and aortitisFerguson, D.; McColm, A.; Ryan, D.; Acred, P.
doi: 10.1007/BF00710904pmid: 3097951
The initial colonization, byStaphylococcus aureus, of the catheter damaged aortic valve and aorta of the rabbit, was examined by light and electron microscopy at 15 min, 3 h and 24 h post inoculation (PI). At 15 min PI, the majority of bacteria (80%) were located on the lateral surfaces of the thrombic vegetations while 20% were attached directly to the connective tissue of the aortic valve and aorta in areas where the endothelial lining was disrupted. By 3 h the bacteria on the thrombic vegetations were covered by fibrin. At this time, the bacteria both within the vegetations and on the surface of the vasculature were undergoing multiplication to form small groups. The precipitation of thrombus around the bacteria attached to the surface of the aorta to form microscopic infected vegetations had occurred by 24 h PI. The colonizing bacteria did not elicit any phagocytic response. The colonization of the cardiovasculature byStaph. aureus did not necessarily require pre-existing vegetations.
Lung deformation and macrophage displacement in smoke-exposed and normal mice (Mus musculus) following different fixation proceduresMatulionis, Daniel
doi: 10.1007/BF00710905pmid: 3097952
Lung deformation (shrinkage or inflation) and displacement of pulmonary parenchymal macrophages were evaluated after immersion fixation, intratracheal instillation of fixative and lung lavage followed by intratracheal fixative instillation in cigarette smoke-exposed, sham-treated and control pallid male mice. Lung volume displacement and lung section and alveolar area analysis revealed that degree of deformation was uniform in lungs from all treatment groups fixed by immersion but not by instillation of fixative and fixative instillation following lavage. In situ pulmonary parenchymal macrophage number per lung section area of fixative-instilled lungs and lavaged lungs followed by fixative instillation was significantly greater than in those following immersion fixation in all corresponding treatment groups. A paucity of macrophages was noted in airways of fixative-instilled and lavaged followed by instillation of fixative lungs. Pulmonary macrophages were uniformly distributed throughout lung parenchyma following immersion fixation, while in fixative-instilled and lavaged prior to instillation of fixative lungs these cells tended to be concentrated in alveoli near terminal bronchioles. Lavage procedures removed an unknown portion of lung macrophages and appeared to ineffectively sample the pulmonary parenchymal macrophage population. Intratracheal instillation of fixative with or without prior lavage apparently alters the distribution of pulmonary macrophages by displacing airway phagocytes into the alveoli. Data reported suggest that fractional estimates of in situ lung parenchymal macrophage population can be obtained by counting the number of these cells per area of tissue from lungs fixed by immersion.