{"title":"Murine mercury-induced immune-complex disease: effect of cyclophosphamide treatment and importance of T-cells.","authors":"P Hultman, S Eneström","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The renal immune-complex (IC) disease induced in BALB/c mice by subcutaneous injection of mercuric chloride (1.6 mg/kg b.w.) every third day for 8 weeks was prevented by the intraperitoneal injection of cyclophosphamide (20 mg/kg b.w.) 24 h prior to mercury injection. The importance of T-cells in the induction of immune-complex disease was studied. BALB/c mice given drinking water containing 20 mg/l of HgCl2 for 10 weeks showed an increased titre of granular, mesangial IgG deposits and vessel wall IgG deposits. Identically treated, congenic nude BALB/c mice with a similar body burden of mercury developed no IC-disease. Cytophotometric analysis of the T-cell subsets in subcutaneously mercury-treated mice revealed a decrease in the fraction of T-helper (L3T4+) splenic cells in the SJL and C57BL/6J strains; no significant change in the T-cell subsets was found in BALB/c mice. C57BL/6J mice, resistant to induction of IC-disease by mercury, showed no increase in the fraction of T-suppressor/cytotoxic (Lyt-2+) cells and no change in the T-helper/T-suppressor cell ratio. C57BL/6J mice could not be rendered susceptible to mercury-induced IC-disease by treatment with different doses of cyclophosphamide.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"227-36"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040569/pdf/brjexppathol00147-0005.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13671702","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":"Antioxidants can prevent cerebral malaria in Plasmodium berghei-infected mice.","authors":"C M Thumwood, N H Hunt, W B Cowden, I A Clark","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A/J and CBA/H mice infected with Plasmodium berghei ANKA, a murine model of cerebral malaria, were used to see whether antioxidants influenced the outcome of this disease. Untreated, infected mice died 7 to 9 days after infection, often with cerebral symptoms. Haemorrhages, mononuclear infiltration and oedema were present in the central nervous system (CNS). Feeding a diet containing 0.75% (w/w) butylated hydroxyanisole (BHA) greatly altered the course of this disease. Death was delayed by up to 2 weeks and mice appeared healthy at parasitaemias that would have caused cerebral symptoms and death had they been on a conventional diet. BHA-fed mice showed few or no cerebral symptoms at a time at which control mice were clearly affected, and greatly reduced haemorrhages, mononuclear infiltration and oedema when the CNS was examined. Similar, but more consistent, protective effects were seen after administration of BHA by repeated injections or in osmotic pumps. The combination of superoxide dismutase and catalase, coupled to polyethylene glycol, when administered intravenously also protected mice against death from cerebral complications. Permeability of the blood-brain barrier was monitored by the use of 125I-labelled bovine serum albumin, 51Cr-labelled erythrocytes and the dye Evans blue, all of which are normally excluded from the CNS. Infected mice on control diet showed an increase in Evans blue staining and 125I and 51Cr retention in the CNS tissue itself. Feeding the diet containing BHA reduced these indices of increased blood-brain barrier permeability. In view of the potent radical scavenging activity of BHA in many other systems it is likely, but unproven, that this is its main role here. The protective effect of superoxide dismutase and catalase lends support to the idea that reactive oxygen species are involved in the pathology of experimental cerebral malaria.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"293-303"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040571/pdf/brjexppathol00147-0068.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13810253","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}
P D Winocour, R L Kinlough-Rathbone, M Richardson, J F Mustard
{"title":"Platelet accumulation and turnover on de-endothelialized aortae in rats.","authors":"P D Winocour, R L Kinlough-Rathbone, M Richardson, J F Mustard","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Previous studies indicate that the subendothelium of rabbit aortae de-endothelialized with a balloon catheter rapidly becomes covered with a monolayer of platelets; after 60 min few additional platelets accumulate and although most platelets are lost from the injured surface by 4 days, there is a substantial delay before re-endothelialization. We examined the dynamics of platelet accumulation on rat aortae de-endothelialized with a balloon catheter to determine if the response to this type of injury is similar to rabbit aortae. When 51Cr-platelets were injected prior to aortic de-endothelialization, 25,500 +/- 2,750 platelets/mm2 accumulated on rat subendothelium in the first 15 min. After 60 and 92 h, fewer platelets remained on the surface (13,740 +/- 2,400 and 5,020 +/- 1,330 platelets/mm2, respectively). When 51Cr-platelets were injected into rats 30 min after injury, platelet accumulation in a 30-min period was 8,610 +/- 1,230 platelets/mm2. By 4 days rat aortae did not accumulate newly injected platelets significantly in a 30-min period, but in a 24-h period 20,600 +/- 3,490 platelets/mm2 accumulated. Morphologically, the non-endothelialized areas of rat aortae were almost completely covered with platelets 4 days after injury. Fourteen days after injury, rat aortae did not accumulate newly injected platelets and, morphologically, no platelets were present on the surface which was almost re-endothelialized. Thus, in rats, as with rabbits, platelets rapidly accumulate on de-endothelialized aortae and the ability to attract newly introduced platelets is considerably reduced shortly after injury. In contrast to rabbits, however, de-endothelialized aortae in rats remain attractive to new platelets up to 4 days following injury, but less so than at the time of injury. Also, in contrast to rabbits, 14 days after injury to rat aortae the surface is almost completely re-endothelialized. Thus, there are species differences in platelet interactions with de-endothelialized vessels.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"337-48"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040584/pdf/brjexppathol00147-0108.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13904051","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":"Quantitative electron microscopy of carcinogen-induced alterations in hepatocyte rough endoplasmic reticulum. II. Modulation of the effects of 3'MeDAB by adrenalectomy and adrenal corticosteroids.","authors":"D J Winton, B Flaks","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A quantitative electron microscope study was made of the effects of bilateral adrenalectomy (ADX) and deoxycorticosterone acetate (DOCA) on the state of aggregation of hepatocyte rough ER cisternae in both untreated and 3'MeDAB-fed Leeds strain rats. Disaggregation of hepatocellular rough ER appears to be a common response of the rat liver to hepatocarcinogenic insult, while ADX and DOCA treatment are known to inhibit the chemical induction of neoplasia in this species. In untreated animals both ADX and DOCA significantly increased the mean number of cisternae per array or stack, while an even more pronounced effect was obtained from a combination of the two. The carcinogen 3'MeDAB induced a highly significant loss of aggregation, which was prevented by the combination of ADX and DOCA. In a separate experiment, a single dose of cortisone acetate was also found to partially reverse 3'MeDAB-induced rough ER disaggregation. In the rat hepatocyte, rough ER stacking or aggregation appears to be at least partially under hormonal control.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"369-84"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040579/pdf/brjexppathol00147-0139.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13648962","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":"An electron microscope and immunohistochemical study of the intracellular location of Toxoplasma tissue cysts within the brains of mice with congenital toxoplasmosis.","authors":"T A Sims, J Hay, I C Talbot","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The wall of intact Toxoplasma tissue cysts within the brains of mice with congenital toxoplasmosis was investigated. Smaller cysts were identified within the soma of neurones. With larger cysts, the contained cystozoites were shown by ultrastructural examination to be surrounded by a layer of microtubules; immunohistochemical staining revealed that this layer contained neurofilament protein. Interior to this layer was a much convoluted parasitophorus vacuole membrane; exterior was the host cell membrane. In most cases, synaptic plates were noted on the outer plasma membrane. In no instance were tissue cysts observed either within neuroglial cells or in the absence of host cells. These observations are discussed in relation to the pathogenesis of congenital toxoplasmosis in the brain.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"317-25"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040570/pdf/brjexppathol00147-0090.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13650543","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}
O Hudlicka, D West, S Kumar, F el Khelly, A J Wright
{"title":"Can growth of capillaries in the heart and skeletal muscle be explained by the presence of an angiogenic factor?","authors":"O Hudlicka, D West, S Kumar, F el Khelly, A J Wright","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Capillary growth was induced in rabbit hearts by long-term bradycardial pacing, and in skeletal muscles by long-term electrical stimulation. In order to find out what factors may be responsible for it, samples of all tissues were analysed for angiogenic activity (AA). To estimate the possible role of mechanical factors, blood flow was measured at rest and during maximal dilatation. Rabbit hearts were paced at half the normal frequency for 24 h/day for 1-2 months by electrodes implanted in the right atrium. Gastrocnemius-plantaris muscles were stimulated at 10 Hz via implanted electrodes, 8 h/day for 14 days. Unpaced hearts and non-stimulated muscles served as controls. Capillary density (estimated in frozen cross-sections stained for alkaline phosphatase) was higher in paced than in control hearts (2235 +/- 86, s.e.m. cap/mm2, 1815 +/- 83, P less than 0.005); capillary/fibre ratio was 2.84 +/- 0.21 in stimulated and 1.243 +/- 0.06 in control gastrocnemius (P less than 0.001). The presence of AA was assayed on chicken chorioallantoic membrane (CAM). All paced and 50% of control hearts showed positive CAM results. Control gastrocnemii gave positive results in 25%, plantaris in 30%: stimulated muscles showed 30% and 37.5% positive responses. Coronary blood flow at rest was significantly lower in chronically paced than control hearts (2.172 g/ml/min, 3.025 +/- 0.187, P less than 0.05) and not significantly different during maximal dilatation (9.217 +/- 1.722 and 11.166 +/- 1.158 respectively). Blood flow per heart beat was significantly higher during acute bradycardia as well as in bradycardially paced hearts at rest. Blood flow in stimulated muscles was significantly higher than in controls both at rest (26.2 +/- 3.36 ml/100 g/min as compared to 8.5 +/- 2.15, P less than 0.001) and during muscle contractions (56.1 +/- 4.5 and 20.7 +/- 2.6). It can thus be concluded that growth of capillaries in skeletal muscles may be due to mechanical factors connected with the increased blood flow while in the heart AA may act in concert with blood flow changes.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"237-46"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040577/pdf/brjexppathol00147-0015.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13904047","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":"Serum amyloid A gene expression and AA amyloid formation in A/J and SJL/J mice.","authors":"H Rokita, T Shirahama, A S Cohen, J D Sipe","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Serum amyloid A (SAA) gene expression and AA amyloid fibril formation were studied in A/J and SJL/J mice, two strains which have been reported to possess defects in AA fibril formation. Four types of inflammatory stimulation were employed: acute inflammation stimulated with lipopolysaccharide (LPS), chronic inflammation with casein in complete Freund's adjuvant, amyloidosis with injection of amyloid enhancing factor (AEF) together with casein in complete Freund's adjuvant, and non-amyloidogenic inflammation in the presence of AEF with injection of AEF together with LPS. Both A/J and SJL/J mice developed splenic amyloidosis 1 day after initiation of chronic inflammation in the presence of AEF. No amyloid deposits were detected during any of the other types of inflammation. Amyloidotic mice exhibited decreased amounts of SAA mRNA in liver and spleen concomitant with decreased amounts of SAA in serum. Alpha-I-acid glycoprotein mRNA was present in liver throughout the course of AEF accelerated amyloidosis, indicating that decreased SAA gene expression and AA fibril formation is not part of a general inhibitory effect of AEF on protein synthesis.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"327-35"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040574/pdf/brjexppathol00147-0099.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13904050","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":"Identification of immunoglobulin-containing cells in the central nervous system of the mouse following infection with the demyelinating strain of Semliki Forest virus.","authors":"L M Parsons, H E Webb","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cells within the central nervous system were identified as containing immunoglobulin G, A and M using immunocytochemistry in mice previously infected with Semliki Forest virus, a togavirus causing primary immune-mediated demyelination. Cells positive for these immunoglobulins were counted in cerebellar white matter, parenchyma, meninges and choroid plexus/ventricles. No positively staining cells were seen on day 6 after infection although other inflammatory cells were present at this time and virus-specific immunoglobulin was found in serum. Cells positive for IgG appeared in all areas by day 9 and remained dominant in numbers throughout. IgM-secreting cells appeared in small numbers in the parenchyma first on day 9 and subsequently in other areas, their numbers rising to a maximum on day 12 in all areas and falling thereafter. The number of IgA-secreting cells was small. They appeared by PID 12 and continued to rise on successive sampling days. Initially IgG-positive cells were seen in the perivascular cuffs but by day 12 a few had moved away from the cuffs into the adjacent parenchyma. IgG-positive cells were seen both in and away from cuffs within areas of demyelination. IgM and IgA-positive cells tended to follow the distribution of IgG-positive cells, but in fewer numbers.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"247-55"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040587/pdf/brjexppathol00147-0025.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13692474","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":"Testicular dysfunction in experimental chronic renal insufficiency: a deficiency of nocturnal pineal N-acetyltransferase activity.","authors":"E W Holmes, S A Hojvat, S E Kahn, E W Bermes","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Biochemical correlates of neuroendocrine/gonadal function and nocturnal levels of serotonin N-acetyltransferase (NAT) activity were determined in partially nephrectomized (PNx), male, Long Evans rats following a 5-week period of chronic renal insufficiency (CRI). PNx animals demonstrated two to four-fold elevations in urea nitrogen and three to four-fold reductions (P less than 0.02) in plasma total testosterone concentrations as compared to sham-operated controls. The pituitary LH contents of PNx rats were decreased to approximately 60% of the control value (P less than 0.05). There were no differences in plasma prolactin levels between the control and PNx groups either at mid-day or in the middle of the night. Nocturnal pineal NAT activity in PNx rats was markedly reduced to approximately 20% of the control value (P less than 0.001). Similar evidence of gonadal dysfunction (reduced plasma total testosterone and testes testosterone content) and a significant decrease in night-time levels of pineal NAT activity were also observed after 13 weeks of CRI in PNx rats of the Sprague-Dawley strain that were housed under a different photoperiod. These results suggest that pineal gland dysfunction is a feature of CRI in the PNx model. Such an abnormality might contribute to the pathogenesis of gonadal dysfunction in CRI.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"349-56"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040581/pdf/brjexppathol00147-0120.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13904052","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":"Chlamydia trachomatis oculogenital infection in the subcutaneous autotransplant model of conjunctiva, salpinx and endometrium.","authors":"D L Patton, C C Kuo, R M Brenner","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The subcutaneous pocket model of salpingeal, endometrial, and conjunctival autografts for studying Chlamydia trachomatis infection in monkeys is described. Portions of the salpinx that were transplanted included fimbria, ampulla, and isthmus. The model is an extension of the original model which consists of either salpingeal fimbria or conjunctive autografts. Transplantation of the ampulla portion of the Fallopian tube enabled us to increase the number of pockets or test sites. Salpingeal and conjunctival autografts could be established during a single surgery. In addition, it is possible to autotransplant endometrium and provoke endometritis. The autografts were shown to be susceptible to C. trachomatis infection. Preliminary rechallenge experiments showed infection of the subcutaneous transplants may induce immunity, indicating the model may be used for immunity and vaccine studies. Simultaneous transplantation of different parts of the oviduct, endometrium, and conjunctive should expand the usefulness of the subcutaneous model in other studies on mixed infections or immune responses to infection.</p>","PeriodicalId":9248,"journal":{"name":"British journal of experimental pathology","volume":"70 3","pages":"357-67"},"PeriodicalIF":0.0,"publicationDate":"1989-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2040580/pdf/brjexppathol00147-0128.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13904053","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}