M A Bosch, R García, R Pagani, M T Portolés, I Díaz-Laviada, S Abarca, M J Ainaga, C Risco, A M Municio
{"title":"Induction of reversible shock by Escherichia coli lipopolysaccharide in rats. Changes in serum and cell membrane parameters.","authors":"M A Bosch, R García, R Pagani, M T Portolés, I Díaz-Laviada, S Abarca, M J Ainaga, C Risco, A M Municio","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Reversible endotoxic shock was induced in adult rats by i.v. injection of Escherichia coli O111:B4 lipopolysaccharide (1.6 mg/100 g). The shock progression was evaluated by measuring serum glucose levels as well as activities of aspartate aminotransferase (GOT) and alkaline phosphatase in serum. A rapid increase of serum glucose levels occurs, after LPS injection, followed by hypoglycaemia (minimum values at 6 h) with progressive reversion to control values. Serum GOT activity increased (twofold) 6 h after endotoxin administration and returned to control values at 72 h. No appreciable changes occurred in serum alkaline phosphatase activity. Endotoxaemia produced a decrease in the cytochrome P-450 levels in all target organs considered: lung, adrenal glands and liver. The progressive decrease in the serum albumin concentration as well as changes of the physical properties of the plasma membranes observed in vivo, can not be explained only by direct interaction of endotoxin with the target organs, underlining the importance of serum mediators in the induction of the shock response.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 6","pages":"805-12"},"PeriodicalIF":0.0,"publicationDate":"1988-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013297/pdf/brjexppathol00006-0051.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14197055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
W M Bagchus, P J Hoedemaeker, J F Slegers, W W Bakker
{"title":"The specificity of nephritogenic antibodies. V. Glomerular localization of anti-GP 330 and anti-GP 90 antibodies present in passive Heymann serum.","authors":"W M Bagchus, P J Hoedemaeker, J F Slegers, W W Bakker","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Administration in the rat of rabbit antibodies directed against rat tubular brushborder antigens (FXIA) leads to membranous glomerulopathy (HICN) associated with glomerular immune complexes (ICXS). These anti-FXIA antibodies (Abs) contain two major specificities, anti-GP 330 and anti-GP 90. The contribution of each specificity to the localization of anti-FXIA Abs was studied by direct immunofluorescence. Perfusion studies, under conditions which avoid ischaemia, confirmed that in this system glomerular localization of anti-FXIA Abs depends only on anti-GP 90 Abs, and the failure of anti-GP 330 Abs to localize after perfusion could not be attributed to ischaemia. In contrast, intravenous (i.v.) injection of anti-GP 330 Abs results in granular deposits of rabbit IgG, similar to those observed using anti-FXIA Abs. Injection i.v. of anti-GP 90 Abs results only in (faint) linear deposits. Using alternating and combined perfusion studies with these Abs, it is shown that anti-GP 90 Abs do not influence localization of anti-GP 330 Abs. In addition, systemic administration of anti-GP 90 Abs combined with perfusion of anti-GP 330 Abs does not facilitate localization of anti-GP 330 Abs. Although directly after i.v. injection of anti-FXIA Abs some anti-GP 90 Abs probably localize in the glomerular capillary wall, our results exclude a dominant or ancillary role for anti-GP 90 Abs in the formation of glomerular Icxs in HICN.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 6","pages":"855-64"},"PeriodicalIF":0.0,"publicationDate":"1988-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013298/pdf/brjexppathol00006-0099.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14197057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J Cornish, J P Lecamwasam, G Harrison, M A Vanderwee, T E Miller
{"title":"Host defence mechanisms in the bladder. II. Disruption of the layer of mucus.","authors":"J Cornish, J P Lecamwasam, G Harrison, M A Vanderwee, T E Miller","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The urinary bladder wall is lined by a layer of mucus which is believed to provide an important barrier to bacterial invasion of the urinary tract. Abnormal function of this protective layer could therefore be a factor predisposing the host to urinary tract infection (UTI). This study investigated the contribution of the bladder mucus to host defence in both acute and chronic lower UTI, using a non-obstructive animal model of infection which reproduces many features of the disease in man. The ultrastructural appearance of the infected bladder mucosa was assessed in tissue in which both the layer of mucus and bacterial glycocalyces were stabilized prior to examination by scanning and transmission electron microscopy. The protective role of the mucus layer was determined by disrupting the layer immediately prior to bacterial challenge. Both ultrastructural and bacteriological analyses have shown that infection was increased in those animals where the mucus barrier was disrupted.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 6","pages":"759-70"},"PeriodicalIF":0.0,"publicationDate":"1988-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013295/pdf/brjexppathol00006-0005.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14197053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Baskerville, R B Fitzgeorge, M I Gilmour, A B Dowsett, A Williams, A S Featherstone
{"title":"Effects of inhaled titanium dioxide dust on the lung and on the course of experimental Legionnaires' disease.","authors":"A Baskerville, R B Fitzgeorge, M I Gilmour, A B Dowsett, A Williams, A S Featherstone","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Guinea-pigs were exposed for 14 days to an aerosol of titanium dioxide (TiO2) dust to produce macrophage blockade. Groups of the animals were later infected by aerosol with Legionella pneumophila. Histological and ultrastructural studies showed that TiO2 dust alone was inert and non-fibrogenic and even at 6 weeks induced no pathological lesions in the lungs, apart from accumulation of macrophages in interalveolar septa. The macrophage blockade by TiO2 did not alter the animals' susceptibility to Legionnaires' disease nor increase mortality. The blockade was effective in the early stages of the infection and limited multiplication of L. pneumophila in the lungs. Later blood monocytes were recruited into the lungs, where they phagocytosed Legionellae, resulting in lung counts comparable to those of TiO2-free control animals.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 6","pages":"781-92"},"PeriodicalIF":0.0,"publicationDate":"1988-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013290/pdf/brjexppathol00006-0027.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14347687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
J S Beck, S M Morley, J G Lowe, R A Brown, J M Grange, J H Gibbs, R C Potts, T Kardjito
{"title":"Diversity in migration of CD4 and CD8 lymphocytes in different microanatomical compartments of the skin in the tuberculin reaction in man.","authors":"J S Beck, S M Morley, J G Lowe, R A Brown, J M Grange, J H Gibbs, R C Potts, T Kardjito","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The lymphocytes in the perivascular foci of tuberculin skin tests have a similar CD4:CD8 ratio to those in the peripheral blood, suggesting that these subsets do not show bias in their initial emigration. By contrast, the diffusely infiltrating lymphocytes show a relative preponderance of CD4 cells which is progressively greater in successive 250 micron layers into the dermis. A generally similar pattern is seen in healthy controls and in patients with untreated pulmonary tuberculosis, treated leprosy, haemophilia A and chronic obstructive lung disease (COLD) patients treated with prednisolone, but the gradient of increasing CD4:CD8 ratio with depth into the dermis is significantly less steep in patients with tuberculosis, haemophilia and prednisolone-treated COLD than in the healthy controls. Selective migration results in a relative preponderance of CD4 cells in the diffuse infiltrate and it is suggested that this is a mechanism likely to potentiate defensive reaction to Mycobacterium tuberculosis: any deficiency in selective migration may make immunological defences less effective and so contribute to the chronicity of the lesions of tuberculosis.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 6","pages":"771-80"},"PeriodicalIF":0.0,"publicationDate":"1988-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013285/pdf/brjexppathol00006-0017.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14392623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The ultrastructural features of aflatoxin B1-induced lesions in the rat liver.","authors":"D J Pritchard, W H Butler","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Hepatocellular carcinoma was induced in rats by administering aflatoxin B1 (AFB1) for 6 weeks. Malignant tumours were preceded by foci and nodules of altered hepatocytes. The ultrastructural characteristics of the nodular lesions have been studied and compared with those of the hepatocellular carcinoma cells. Alterations in the endoplasmic reticulum, junctional complexes and nuclei were common to both the basophilic and eosinophilic nodular cells and the carcinoma cells. These most likely represent hyperplastic changes rather than malignant alterations. The eosinophilic nodules were distinguished from other lesions by the abundance of concentric, membranous whorls in the cytoplasm of nodular cells. These cytoplasmic structures were also present in some hepatocellular carcinoma cells. The observations provided further evidence suggesting that the eosinophilic nodule, rather than the basophilic nodule, may play a role in the development of malignancy in the rat liver.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 6","pages":"793-804"},"PeriodicalIF":0.0,"publicationDate":"1988-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013296/pdf/brjexppathol00006-0039.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14275626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
G Marquis, S Montplaisir, M Pelletier, P Auger, W S Lapp
{"title":"Genetics of resistance to infection with Candida albicans in mice.","authors":"G Marquis, S Montplaisir, M Pelletier, P Auger, W S Lapp","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>To determine differences in susceptibility, 234 naive mice including xid and beige mutants were infected intravenously with Candida albicans and monitored with survival analysis and quantitative culture of the kidneys. By using survival time as the criterion, animals of seven inbred strains were separated into three groups. C3H/HeJ and Dw/+ were most susceptible; C57BR/cdJ, BRVR and CBA/N (xid) were intermediate in susceptibility; C57BL/KsJ and C57BL/6J were least susceptible. Mean survival times (MST) were markedly influenced by the number of Candida cells injected while the ranking of mouse strains by survival alone was unchanged. There was a dissimilar behaviour of the strains to produce organ weight changes in response to infection when compared with uninfected mice which were matched for age and genetic lineage. Black mice had lower colony forming units (CFU) per mg of tissue at the time of death than animals of other genetic lineage. Nevertheless, the finding that MST and CFU studies were loosely correlated in a few strains of mice indicated that the proliferation of the fungus in the kidneys was not always the major cause of death. The beige mutation was found to determine an increased susceptibility to systemic Candida infection. The differences in survival for beige and nonbeige mice were influenced by the genetic lineage of the host, being much greater in the C57BL/6 strain (36.7 days) than in the C3H/He strain (5 days). C57BL/6 beige-J had significantly higher CFU per organ and per unit of weight than C57BL/6 +/+ mice. These data evinced an important contribution of host genetic factors to resistance to systemic candidiasis. It is suggested that innate resistance genes regulate the differentiation in the bone marrow and the function of cells of granulocyte-macrophage lineage.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 5","pages":"651-60"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013273/pdf/brjexppathol00005-0050.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14190242","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The lipid composition of highly differentiated human hepatomas, with special reference to fatty acids.","authors":"I Eggens, L Bäckman, A Jakobsson, C Valtersson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The lipid compositions of homogenates and microsomal fractions derived from surgical samples of highly differentiated human hepatoma, morphologically normal regions outside the tumours and from normal livers were analysed. A few enzyme activities were also assayed. Hepatoma microsomes demonstrated considerably lowered levels of cytochromes P-450 and b5. Hepatoma homogenates exhibited increased levels of cholesterol, normal amounts of dolichyl-P and slightly lowered levels of total phospholipid. The levels of dolichol, dolichol ester and ubiquinone in hepatoma homogenates were prominently decreased. In tumour microsomes the levels of cholesterol and dolichyl phosphate were increased considerably while the levels of phospholipid and dolichol were lowered. The phospholipid composition of tumour homogenates was roughly similar to that of control tissue. In tumour microsomes the relative amounts of phosphatidylserine and phosphatidylinositol were about 30% decreased, whereas the major phospholipids showed minor increases in amount. The rate and pattern of incorporation of [3H]glycerol into individual phospholipids in liver slices from control and hepatoma tissue did not differ to any larger extent. The fatty acid composition of tumour homogenates exhibited minor differences in comparison to the control with the greatest changes in the sphingomyelin fraction. In hepatoma microsomes the fatty acid compositions of the major phospholipids were altered moderately, with evident decreases in the relative amounts of the long-chain polyunsaturated fatty acids. In hepatoma homogenates the fatty acid composition of dolichol esters differed only slightly from the control pattern. These results indicate that the major disturbance in the lipid metabolism of highly differentiated hepatomas is localized to the mevalonate pathway, thus affecting mainly the levels of cholesterol, dolichol and ubiquinone.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 5","pages":"671-83"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013280/pdf/brjexppathol00005-0070.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13986268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cellular and extracellular plasminogen activator and inhibitor in an experimental tumour.","authors":"Q Dong, M H Zhou, V Subbarao, C H Ts'ao","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We determined plasminogen activator (PA) and PA inhibitor (PAI) activities in the intra- and extracellular compartments of an experimental pancreatic ascites tumour with indirect and direct functional assays, and partially characterized these activities on SDS-polyacrylamide gels coupled with fibrin and reverse fibrin autography. Intact tumour cells caused lysis of plasminogen-rich but not plasminogen-free fibrin clots, and the extent of lysis of the former was related to tumour cell count. Direct assay of PA with a synthetic substrate yielded an equivalent of 109 urokinase units per 10(9) tumour cells. No PAI activity was demonstrated in tumour cells with functional assays. Contrary to tumour cells, cell-free ascitic fluids caused no lysis of fibrin clots. Instead, it inhibited tumour cell- and urokinase-induced, but not plasmin-induced, clot lysis in a dose-dependent fashion. Although functional assays failed to demonstrate PA in ascitic fluid and PAI in tumour cells, both activities were detected in electrophoresed samples of cell lysates and fluids by fibrin and reverse fibrin autography. In tumour cells, a mixture of tissue-type PA (tPA) and urokinase-type PA (uPA) were present. In the fluid, uPA together with two other PAs with greater molecular weights than tPA were detected.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 5","pages":"685-95"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013274/pdf/brjexppathol00005-0083.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14273721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Comparisons of the pathogenicity of long and short fibres of chrysotile asbestos in rats.","authors":"J M Davis, A D Jones","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Long-term inhalation and intraperitoneal injection studies were undertaken with laboratory rats treated with a specially prepared short-fibre sample of Canadian chrysotile asbestos. This was compared, at an equal mass dose, to dust generated from the same chrysotile batch so as to contain the highest possible number of long fibres. The long-fibre cloud contained roughly five times more fibres greater than 5 micron in length as seen by phase contrast optical microscopy (PCOM). For increasing lengths, the ratio between the dust clouds increased progressively, reaching over 80: 1 for fibres greater than 30 microns in length. Rats treated with long-fibre chrysotile developed six times more advanced interstitial fibrosis (asbestosis) than animals treated with short-fibre chrysotile and three times more pulmonary tumours. At the end of the 12-month dusting period, three times more short chrysotile than long had been retained in the rat lung tissues. During the following 6 months, however, the short-fibre chrysotile was removed from the lungs much more rapidly than the long. Following intraperitoneal injection at a mass dose of 25mg of dust, both long and short chrysotile produced mesotheliomas in more than 90% of rats. At a dose level of 2.5mg of dust, the short-fibre chrysotile produced mesotheliomas in only one-third as many rats as the long-fibre dust which still produced mesotheliomas in more than 90% of animals injected. At a dose level of 0.25mg of dust, the short-fibre chrysotile produced no mesotheliomas while the long-fibre chrysotile still produced these tumours in 66% of rats. In the two highest doses, where short-fibre chrysotile produced mesotheliomas, the mean tumour induction period was significantly longer than for tumours produced by long chrysotile.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"69 5","pages":"717-37"},"PeriodicalIF":0.0,"publicationDate":"1988-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2013275/pdf/brjexppathol00005-0114.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13986199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}