{"title":"Echinococcus multilocularis: characterization of an alveolar hydatid cyst-induced amyloid enhancing factor.","authors":"T Alkarmi, Z Alshakarchi, K Behbehani, Z Ali-Khan","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Alveolar hydatid cysts, the larvae of Echinococcus multilocularis, were shown to induce the formation of an amyloid enhancing-like factor (AEF) called alveolar hydatid cyst-AEF (AHC-AEF) in the spleens of infected animals, 5 to 6 weeks post-infection. The adoptive transfer of AHC-AEF results in rapid induction and deposition of amyloid fibrils in the spleens following AgNO3 injection within 24 h. When injected concomitantly with alveolar hydatid cysts, it shortens the induction phase from 5 or 12 weeks to 1 week in C57BL/6J and A/JAX mice respectively. Preliminary characterization of this factor indicates that its bioactivity may be detected in the non-lipid moiety of spleen cell extracts and the sediment of ultracentrifugation. The factor is resistant to trypsin, pepsin, DNA-ase and RNA-ase treatments. It is sensitive to low or high pH (pH 3.0 and 9.5) and boiling. It resists freeze drying, dialysis, and storage at 4 degrees C for 2 weeks or -70 degrees C for more than a year. It may be fractionated using borate buffered saline, pH 7.4, on Sephacryl S-300 gel column. The active moiety eluted mainly in the first peak.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"579-88"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040589/pdf/brjexppathol00149-0083.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13957462","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 mechanisms of toxicity and tolerance in the copper-loaded rat. III. Ultrastructural changes and copper localization in the kidney.","authors":"I C Fuentealba, S Haywood, J Foster","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The distribution of copper and related changes have been studied in copper-loaded rat kidneys at the ultrastructural level by X-ray electron probe microanalysis, in order to clarify the pathogenesis of copper-induced damage and subsequent recovery in this organ. Male rats fed a high copper diet (1500 ppm) for 16 weeks were killed at intervals; their kidneys were removed and portions of kidney cortex fixed in 4% paraformaldehyde and 2% glutaraldehyde for electron microscopy: other samples were analysed for copper by AA spectrophotometry. Increasing copper accumulation was associated with progressive PCT cell disarray and characterized by irreversible nuclear damage coincident with the intranuclear accumulation of Cu, S, P, and Ca. Copper was also identified within structurally intact lysosomes associated with Zn and Fe (Type I lysosomes) or P and S (Type II lysosomes, putative Cu-MT). Subsequent copper decline and tubular recovery was associated with the facilitated lysosomal sequestration of copper and excretion of copper-containing cell products into the tubule lumina, Cu-MT and alpha-2 urinary protein-copper. The cytotoxicity of copper in the kidney, as well as the liver, is associated primarily with irreversible nuclear damage, whereas lysosomal copper sequestration protects the cell from injury.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"543-56"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040601/pdf/brjexppathol00149-0049.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13957460","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 pathology of halothane hepatotoxicity in a guinea-pig model: a comparison with human halothane hepatitis.","authors":"C A Lunam, P M Hall, M J Cousins","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The pathology of halothane hepatotoxicity is described in detail in a guinea-pig model. Twenty-two of 40 guinea-pigs developed liver damage after exposure to 1% halothane in 21% O2 for 4 h. The other 18 animals showed no evidence of hepatic injury. Two distinct patterns of damage were identified: mild damage, in which livers had focal areas of necrosis, and severe damage, where necrosis was confluent around the terminal hepatic venules, often extending to the portal tracts. Serum alanine aminotransferase activity was significantly elevated in guinea-pigs with severe liver damage. Hepatocytes in the damaged areas showed degenerative changes ranging from vacuolization to ballooning degeneration and necrosis. Inflammatory cells, predominantly lymphocytes, were often present in the areas of necrosis. The pathology of mild and severe liver injury in the guinea-pig closely resembles the spectrum of injury observed in non-fatal halothane hepatitis in man.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"533-41"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040590/pdf/brjexppathol00149-0040.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13957459","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":"A comparison of secretory epithelioid cells and phagocytosing macrophages in experimental mycobacterial granulomas.","authors":"J L Turk","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"589-96"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040598/pdf/brjexppathol00149-0093.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13824913","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":"Leucocyte-induced endothelium-dependent vasodilatation and post-ischaemic vasospasm in the isolated rat superior mesenteric artery.","authors":"H J Grossman, M Zambetis","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The purpose of this study was to investigate the possible role of leucocytes in the pathogenesis of reperfusion-induced vasospasm of ischaemic mesenteric arteries. Scanning electron microscopy of the rat superior mesenteric artery (SMA) after 30 min of ischaemia in vivo revealed adherence of leucocytes to the vessel wall. Isolated SMA preparations were perfused with Krebs-Henseleit buffer containing noradrenaline. Infusion of homologous leucocytes resuspended in perfusate (3 x 10(6) cells/ml) into these preconstricted preparations caused a fall in resistance of 29 +/- 2%. Removal of the endothelium by collagenase treatment abolished this response. Indeed, leucocyte infusion caused an increase in resistance of 39 +/- 8% under these circumstances. Following 30 min of normothermic ischaemia, leucocyte infusion caused a transient vasodilatation of 31 +/- 4% followed by an increase of 38 +/- 11% in the perfusion resistance of isolated SMA preparations. In each case, a similar response was obtained to infusion of the cell-free supernatant. These results suggest that leucocyte activation occurs in vivo during reperfusion of the SMA after as little as 30 min of ischaemia, and that activated leucocytes can release humoral vasoactive factors which evoke an endothelium-dependent vasodilator response in normal vessels but a predominantly vasoconstrictor response following brief intervals of ischaemia.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 5","pages":"515-23"},"PeriodicalIF":0.0,"publicationDate":"1989-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040595/pdf/brjexppathol00149-0024.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13956228","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}
K J Thomson, N J Saunders, J G Simpson, P H Whiting
{"title":"Renal structure and function in streptozotocin-diabetic rats treated with cyclosporin A.","authors":"K J Thomson, N J Saunders, J G Simpson, P H Whiting","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The effect of cyclosporin A (CsA), administered daily by gavage at 20 mg/kg body weight, on renal structure and function was investigated in normal and streptozotocin-diabetic male adult Sprague-Dawley rats over 12 weeks. In the non-diabetic animals CsA caused a progressive decrease in glomerular filtration rate and increased enzymuria. In contrast, the diabetic state was associated with massive increases in both enzymuria and urine flow rates, but a trend towards increased urea and creatinine clearance rates. CsA treatment of diabetic animals did not significantly alter the above parameters, nor affect circulating glucose levels, and trough serum CsA concentrations were similar in both diabetic and non-diabetic animals. The kidneys from CsA-treated non-diabetic animals showed chronic tubular damage. In the streptozotocin groups, the only morphological abnormality which could be related to diabetes was excess glycogen deposition in distal renal tubules. CsA-treatment of these groups was not associated with structural enhancement of either the drug's nephrotoxicity or the diabetes-related changes. Indeed the results indicate that the diabetic state affords some protection against the functional aspects of CsA-nephrotoxicity.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 4","pages":"405-14"},"PeriodicalIF":0.0,"publicationDate":"1989-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040564/pdf/brjexppathol00148-0014.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13904054","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":"Alpha-fetoprotein (AFP) in granulomatous inflammation of the mouse.","authors":"J Trojan, J Naval, H Jusforgues, J Uriel","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Inflammatory granulomas constituted of various proportions of macrophages, polynuclear (PMNs) and mononuclear cells were induced in adult pathogen-free mice by injecting polyacrylamide beads into subcutaneous pouches. Using specific anti-mouse alpha-fetoprotein (AFP) antibodies, the presence of AFP was immunocytochemically demonstrated in the cytoplasm of macrophages and of immature PMNs (mature PMNs and mononuclear cells were AFP negative). AFP-labelling started as soon as 36 h after granuloma induction and reached a maximum 60-72 h later, to disappear on day 5. The examination of different organs in these mice also showed a transitory labelling for AFP of liver hepatocytes and of elements of kidney and of exocrine pancreas. Parallel to these findings, the selective concentration inside the granulomatous pouches of radiolabelled AFP injected in the course of inflammation was observed. These results suggest that (a) shortly after the inflammatory reaction the synthesis of AFP is resumed by the liver; (b) the newly synthesized AFP is secreted in the serum and preferentially taken up by the granulomas; and (c) consequently, in adult mice, AFP behaves as a positive acute phase reactant. The physiopathological implications of these facts are discussed in relation with the biological properties of AFP.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 4","pages":"469-78"},"PeriodicalIF":0.0,"publicationDate":"1989-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040556/pdf/brjexppathol00148-0076.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13620629","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":"Coxsackievirus B3-induced acute pancreatitis: analysis of histopathological and viral parameters in a mouse model.","authors":"T Vuorinen, M Kallajoki, T Hyypiä, R Vainionpää","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Coxsackievirus B3 infection in mice was studied histopathologically, by virus isolation and by nucleic acid hybridization after intraperitoneal inoculation of the virus. Extensive viraemia was detected for 1-3 days post-infection. All mice developed necrotizing acute pancreatitis and focal myocarditis. Pancreatitis eventually lead to complete atrophy of the exocrine pancreas. However, the islets of Langerhans and pancreatic ducts remained morphologically intact. Virus could be demonstrated in pancreatic tissue for 1-5 days post-infection by in-situ and spot hybridization as well as by virus isolation. Virus was not detectable on days 7-22 post-infection suggesting an autodigestive aetiology in further destruction of the exocrine pancreas. The mouse model described here permits detailed analysis of viral and host factors in the pathogenesis of enterovirus infections. Since coxsackie B viruses have been proposed to be aetiological agents in human acute pancreatitis, the application of in-situ hybridization allows analysis of enteroviruses directly from pancreatic tissue of clinical routine specimens.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 4","pages":"395-403"},"PeriodicalIF":0.0,"publicationDate":"1989-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040566/pdf/brjexppathol00148-0005.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13691818","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 A Limb, K A Brown, R A Wolstencroft, B A Ellis, D C Dumonde
{"title":"The production of arthritis in the guinea-pig by intra-articular reaction between lymphokines and inflammatory leucocytes.","authors":"G A Limb, K A Brown, R A Wolstencroft, B A Ellis, D C Dumonde","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A single intra-articular injection of lymphokine into the guinea-pig knee joint resulted in a sequence of changes in joint architecture whose histopathological features resembled that of an acute inflammatory reaction progressing to a chronic state. At 24 h there was a mild hyperplasia and hypertrophy of the synovium with intense polymorphonuclear leucocyte infiltration. At 72 h, the synovium was heavily infiltrated with diffuse and focal aggregations of mononuclear cells; erosion of cartilage and bone by synovial pannus was accompanied by a subsynovial fibrosis. By 1 week, leucocytic infiltration of the synovium had decreased markedly although the erosion and fibrosis persisted. However, when lymphokine was injected together with oil-elicited peritoneal exudate cells a more intense arthritis ensued: at 72 h synovial pannus was prominently eroding bone and this was accompanied by the appearance of multinucleate cells resembling osteoclasts in the zone of erosion. These features were shown to resemble closely the histopathology of experimental allergic arthritis in the guinea-pig, in contrast to the lesser severity of synovitis resulting from the adoptive cellular transfer of delayed hypersensitivity into the joint. The results indicate that lymphokines may play a role in the induction of experimental allergic arthritis by recruiting and activating cells involved in chronic inflammation.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 4","pages":"443-56"},"PeriodicalIF":0.0,"publicationDate":"1989-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040561/pdf/brjexppathol00148-0050.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13905226","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":"Muscle fibre necrosis induced by intramuscular injection of drugs.","authors":"D Manor, M Sadeh","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A number of amphiphilic and lipid-soluble drugs of heterogeneous pharmacological properties, when injected into rat anterior tibial muscles, induced acute muscle fibre necrosis. The myotoxic agents were: penicillin, cloxacillin, phenobarbital, haloperidol, diazepam, hydantoin, metoclopramide, pentazocine and chlorpromazine. The regenerative process, studied using the latter three medications, showed rapid regeneration, complete within 3 weeks. Injection of the water-soluble drugs aminophylline, tranexamic acid and vitamins B6 and B12 produced no tissue damage. The pathogenesis of muscle fibre necrosis is suggested to involve direct damage to cell membranes by lipid soluble drugs.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 4","pages":"457-62"},"PeriodicalIF":0.0,"publicationDate":"1989-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040563/pdf/brjexppathol00148-0064.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13905227","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}