bluuebunny/crossref_metadata_2025_split huggingface dataset:
Acute arterial fibrinoid deposition and ischaemic parenchymal damage of the kidney. Pathogenic factors in the development of malignant hypertension
Authors: Chatelain R. E. , Dardik Beatriz N. , Shainoff J. R. 
Published: June 2005

AbstractThe development and evolution of hypertensive vascular lesions affecting the arterial supply of (a) the kidney and (b) organs other than the kidney were studied in rats developing either malignant (MHY) or benign (BHY) hypertension 3, 6, 9 and 12 days after aortic ligation between the renal arteries. Vascular disease evolved into two distinct patterns which suggested acute renal damage to be the determinant for the development of either the malignant or benign form of hypertension. Three days after aortic ligation MHY and BHY animals showed widespread fibrinoid deposition in vascular territories above the aortic ligature. However, in MHYs these lesions were much more severe and, in the kidney, they were accompanied by the development of focal parenchymal atrophy, microinfarcts and hyalin droplet degeneration of cells of the Bowman capsule. The degree of renal damage correlated with elevations in blood urea nitrogen (BUN) and plasma creatinine; however, there was no correlation with rises in blood pressure, plasma renin activity (PRA), aldosterone or corticosterone which were similarly elevated in 3‐day MHY and 3‐day BHY animals.Between 6 and 12 days a marked clearance of fibrinoid took place in all organ beds of BHYs, but in the non‐renal vasculature of MHY animals fibrinoid remained prominent and served as the central core for necrotising arterial lesions. In the kidney of MHYs some reduction in the fibrinoid content was observed, but the parenchymal damage perpetuating from the earlier stages had exacerbated leading to collagen deposition and a marked increase in the collagen concentration of the renal cortex. These features were accompanied by further elevations in PRA and corticosteroids and a progressive deterioration of renal function. By contrast, in 12‐day BHY animals, despite sustained hypertension, PRA and corticosteroids were falling from their previously higher levels and normal renal function was maintained. These studies warrant inference that extensive parenchymal damage of the kidney due in part to severe arterial fibrinoid deposition is one of the initial events in the development of malignant hypertension.
Acute haematogenous osteomyelitis: An experimental model
Authors: Emslie Kerry R. , Ozanne N. R. , Nade S. M. L. 
Published: June 2005

AbstractA simple and reproducible model of acute haematogenous staphylococcal osteomyelitis is described. Twenty‐nine day‐old chickens were inoculated intravenously with 104–108 viable organisms Staphylococcus aureus per kg body weight and were killed 1–8 days after inoculation. Macroscopic septic foci could be detected within 24 hr of inoculation and were most commonly situated in the metaphyseal region of the proximal tibia and distal femur. Lesions in other organs were not observed. The production of osteomyelitis was dependent on the bacterial inoculum size. It was estimated that 5.5 × 105 viable organisms per kg body weight of chicken were required to produce osteomyelitis in 50 per cent of injected chickens. Chicken weights were monitored throughout the experiment. A close negative correlation existed between the logarithm of the bacterial inoculum size and the chicken growth rate in the first 24 hr following inoculation (r = −0.968, P< 0.01). The chicken growth rate was therefore used as an accurate predictor of osteomyelitis in individual chickens.
Mucosal alkaline phosphatase and bile lipids in the gallbladder in cholecystitis
Authors: Kouroumalis E. , Hopwood D. , Ross P. E. , Bouchier I. A. D. 
Published: June 2005

AbstractHistochemically, alkaline phosphatase was localised in epithelial brush‐border and capillary endothelium of the lamina propria in 41 gallbladders studied. Three distinct patterns of the brush‐border enzyme distribution were observed, namely, complete delineation, patchy localisation and a brush‐border totally devoid of enzyme activity.Where no histochemical activity was found, biliary chenodeoxycholate was 50 per cent. higher than in cases of patchy distribution and twice as high as in cases with complete staining of the brush‐border. Conversely, biliary cholate levels were significantly higher in completely stained cases. Biliary cholesterol was higher in the cases with no histochemical activity and this was reflected in a significantly higher lithogenic index. Significant quantities of cholesterol esters were found in bile from the focal activity group only.Total alkaline phosphatase activity assayed in gallbladders from 112 patients with cholecystitis and/or lithiasis showed that activity was significantly lower in patients with pigment stones than patients with cholecystitis and/or cholesterol stones. This activity was not related to biliary lipid composition in the 77 bile samples analysed.This evidence indicates that biliary lipid composition is associated with the histochemical distribution of alkaline phosphatase in gallbladder mucosa.
Microgibbosities in hydatidiform mole
Authors: Ockleford C. D. , Clode A. 
Published: June 2005

AbstractUltrastructural analysis of the surface of the syncytial absorptive epithelium of the aberrant form of human placenta known as hydatidiform mole reveals modifications of the micro‐villous apical surface. We have described these features as microgibbosities. They are apparently groups or rings of microvilli greater than the usual length in the surrounding cytoplasm. The existence of such microvilli and the probable consequences for the control of the dynamics of microvillar cytoskeletal elements should be accommodated by future theories of microvillar biogenesis.
Methods to analyse the human genome
Authors: Williamson Robert , Darling Susan M. 
Published: June 2005

AbstractThere is much interest in the use of gene‐specific probes for the study of dysfunction in human pathology. For the haemoglobinopathies, globin gene recombinants (either prepared from DNA sequences complementary to messenger RNA, or from genomic DNA) are used to determine whether globin genes are present, whether they are expressed in the nucleus, and whether they are correctly processed to give functional mRNAs. This has not only allowed a fuller understanding of the molecular aetiology of the thalassaemias, but also permitted antenatal diagnosis both by direct analysis of the gene lesion, and by linkage analysis using adjacent genes. Similar approaches are being applied to many other single gene defects.There are, however, other possible ways to study human hereditary disease using recombinants. It is now feasible to use random human chromosome‐specific sequences to establish a linkage map for the entire human genome. Such a map may then be used either to determine the chromosomal localisation of any “single gene” phenotype by linkage analysis, or to study the contribution of different genes to a complex phenotype determined by several genes, as in multifactorial disease.
Growth factors and their action in vivo and in vitro
Authors: Gospodarowicz D. 
Published: June 2005

AbstractThe molecular nature and mechanism of action of several of the growth factors including epidermal growth factor, fibroblast growth factor and platelet‐derived growth factor is reviewed. The ectopic production of growth factors may be important in the growth development of certain tumours. In addition, attention is directed to the importance of the extracellular matrix in controlling cell proliferation and differentiation.
The cell surface and its metabolism
Authors: Crumpton Michael J. , Owens Raymond J. , Gallagher Christopher J. , Davies Adelina A. 
Published: June 2005

AbstractThe cell surface structure is highly dynamic. In particular, binding of ligand induces the redistribution of receptors on the cell surface as well as the internalisation of ligand‐receptor complexes. Internalisation in turn leads to a recycling of the receptor or to a decrease in the cell'S responsiveness to the ligand. Modulation of the cell surface structure is apparently regulated intracellularly by components of the cell'S cytoskeleton. A crucial component in this respect is likely to be a sub‐membranous filamentous network that is linked directly to the cytoplasmic face of the surface membrane. In erythrocytes this network can be separated from purified preparations of the plasma membrane by virtue of its insolubility in nonionic detergents. Application of this procedure to the plasma membrane fraction of human B lymphoblastoid cells has yielded a detergent‐insoluble residue comprising actin and a 68,000‐Mr polypeptide as major components, together with polypeptides of 28,000‐, 33,000‐ and 120,000‐Mr as prominent but more minor components. The association of the 68,000‐Mr protein with the detergent‐insoluble residue and the original plasma membrane is Ca2+‐dependent. Burkitt lymphoma cells differ noticeably from lymphoblastoid cells in that the 68,000‐Mr protein is not associated with the inner face of the surface membrane. This difference may reflect the malignant phenotype of Burkitt lymphomas or the hypothetical sub‐population of normal B lymphocytes from which the lymphomas are derived.
Differentiation and neoplasia. Invasion and metastasis; experimental systems
Authors: Eccles Suzanne A. 
Published: June 2005

AbstractIn a series of six transplantable mammary carcinomas and 11 squamous cell carcinomas of mice, evidence of tumour “progression” was obtained in the majority.Progression was evidenced by increased growth rates, transplantability and metastatic capacity, and decreased differentiation and immunogenicity (when present initially).The degree of differentiation was inversely related to the metastatic capacity of a particular tumour, and the rate of change in both parameters during serial transplantation was comparable.Treatment with retinoids in vivo and in vitro failed to stimulate differentiation of anaplastic cell lines, or to influence their growth and metastasis in the absence of host anti‐tumour immune reactivity.
Decreased numbers of pulmonary blood vessels: Reality or artifact?
Authors: Mooi Wolter , Wagenvoort C. A. 
Published: June 2005

AbstractA decrease in numbers of pulmonary arteries has been implicated in various forms of both human and experimental pulmonary hypertension. However, data in support of this hypothesis have not been conclusive. Especially, intravascular fixation under pressure and the size of the areas of lung tissue subjected to quantitation, may have influenced the results. In order to investigate these factors, we fixed lungs of ten normal rats in three different ways, i. e. by perfusion of the pulmonary vasculature, by immersing collapsed lungs and by instilling the fixative through the trachea with intact thoracic cavity. Subsequently, blood vessels were counted in histological sections. Our study illustrates that perfusion of vessels under pressure decreases the number of recognizable arteries. Also the small areas, used in previous studies for counting vessels, produce unreliable results. Our conclusion is that a decreased number of lung vessels as a factor in pulmonary resistance has not been conclusively demonstrated.
An enzyme histochemical study of the sinuses of reactive lymph nodes
Authors: Crocker J. , Williams Mary 
Published: June 2005

AbstractThe enzyme histochemistry of the cells lining and within the marginal and medullary sinuses of twenty human reactive lymph nodes has been studied. The sinuses contain luminal (‘reticular’) cells which are strongly positive for certain hydrolytic enzymes, including acid‐α‐naphthyl acetate esterase, acid phosphatase and β‐glucuronidase. In addition, the lining (‘littoral’) cells on both sides of the medullary sinuses are positive for these enzymes. In contrast, enzyme‐containing lining (‘littoral’) cells of the marginal (subcapsular) sinuses are observed only on the inner aspect of the sinuses, the outer aspect being negative. Alkaline phosphatase is not present in the sinusoidal cells but 5′‐nucleotidase is seen in varying amounts. These findings are supported by an ultrastructural study of three of the nodes, using a staining method for esterase activity. The different enzyme histochemical properties of the littoral cells in the marginal and medullary sinuses closely mirrors that observed when, for example, these structures are stained immunohistochemically for IgA or J chain.
The effect of prostacyclin on the adhesion of leucocytes to injured vascular endothelium
Authors: Jones Gayle , Hurley J. V. 
Published: June 2005

AbstractThe effect of local application of various solutions on leucocyte adherence to the wall of small blood vessels in the microcirculation of the rat mesentery was examined. Leucocyte adhesion was produced by local application of zymosan‐activated complement. Solutions of EDTA, lignocaine and prostacyclin when applied locally cause the release of a high proportion of leucocytes previously firmly adherent to the endothelium of venules and small veins without producing any significant change in the rate of blood flow through the affected vessels. Acetylcholine injected intravenously increases the rate of blood flow through the mesenteric microcirculation several fold but has no apparent effect on pre‐existing leucocyte sticking. The findings suggest that in normal small blood vessels production of prostacyclin by vascular endothelium may inhibit adhesion of leucocytes to the vascular wall. When endothelium is injured local production of prostacyclin may be inhibited sufficiently to permit adhesion of leucocytes to the injured endothelium and so induce the earliest stage in the emigration of leucocytes into the area of injury. Lignocaine may possibly inhibit leucocyte sticking by increasing local production of prostacyclin, but the mode of action of EDTA and many other aspects of the mechanism responsible for leucocyte sticking remain obscure.
Chromatin cleavage in apoptosis: Association with condensed chromatin morphology and dependence on macromolecular synthesis
Authors: Wyllie A. H. , Morris R. G. , Smith A. L. , Dunlop D. 
Published: June 2005

AbstractIn glucocorticoid‐treated rat thymocytes and the murine lymphoid cell lines L5178 and S49 the morphology of apoptosis is associated with chromatin cleavage. The cleavage is at internucleosomal sites, apparently through activation of an endogenous endonuclease. In variants of the cell lines selected for resistance to glucocorticoid, neither apoptosis nor chromatin cleavage were observed after steroid treatment, and steroid receptors were undetectable. In thymocytes, both the morphological changes of apoptosis and chromatin cleavage were inhibited by cycloheximide and actinomycin D. The calcium–magnesium ionophore A23187 induced apoptosis and chromatin cleavage in thymocytes, and these effects were also inhibited by cycloheximide. The data confirm that the condensed chromatin which characterizes apoptosis morphologically consists of endogenously digested chromatin fragments. They also provide support for the view that at least some cells enter apoptosis by a process dependent upon macromolecular synthesis.
Histopathological characterization of the naturally occurring hepatotropic virus infections of nude mice
Authors: Carthew P. 
Published: June 2005

AbstractIn the last ten years the mutant athymic nude mouse has been used by many researchers as a model for studying pathological conditions in an immunodeficient host. A major problem with such mice is their susceptibility to viral infections indigenous to murine stocks, such as the hepatotropic mouse coronaviruses. In an effort to define the hepatotropic virus diseases indigenous to nude mice this paper details the pathogenesis and associated comparative histopathology of three common strains of mouse hepatitis virus, reovirus 3 and murine cytomegalovirus in the nude mouse.
Immunohistochemical demonstration of cathepsin B in the macrophages of benign and malignant lymphoid tissues
Authors: Crocker J. , Burnett D. , Jones E. L. 
Published: June 2005

AbstractCathepsin B has been demonstrated by immunohistochemical means in the macrophages of palatine tonsils, reactive lymph nodes and in specimens of Hodgkin's disease (HD) and non‐Hodgkin's lymphomas (NHL). Two cases of genuine histiocytic lymphoma showed strong staining for the enzyme in most cells. In Hodgkin's disease, many Reed–Sternberg cells and Hodgkin cells were positive. Branching and ‘tingible body’ macrophages (histiocytic reticulum cells. HRCs) were strongly positive in all of the specimens. In reactive lymph nodes, the sinus‐lining cells and intrasinusoidal macrophages were positive for cathepsin B. True dendritic reticulum cells (DRCs) appeared to be negative. Unlike muramidase (lysozyme), cathepsin B is not seen in neutrophil polymorph leucocytes.
Human gallbladder epithelium: Non‐specific esterases in cholecystitis
Authors: Kouroumais E. , Hopwood D. , Ross P. E. , Bouchier I. A. D. 
Published: June 2005

AbstractEsterases active at neutral and acid pH have been demonstrated in human gallbladder epithelium. Reaction to a wide variety of inhibitors and activators suggests that they probably represent the same enzyme with two active sites while a close correlation with acid phosphatase, a known lysosomal enzyme, suggests a lysosomal localization. Esterase activity in the gallbladder mucosa in significantly decreased in chronic cholecystitis. Polyacrylamide gel electrophoresis suggests that cholesterol stones may be associated with a specific type of isoenzyme pattern. Esterase positive cells are present in the inflammatory infiltrate in the lamina propria of the gallbladder in most cases of chronic cholecystitis. Naphthol AS‐D chloracetate esterase staining indicates that mast cells form a large part of the infiltrate. Bile acids modulate the enzyme activity in vitro. Although the exact substrate specificity is not known, several possibilities are discussed, implicating esterases in the pathogenesis of chronic cholecystitis.
The effects of high dose sporadic (binge) alcohol intake in mice
Authors: Sltuckey E. , Blerry C. L. 
Published: June 2005

AbstractBALB/c and CBA/h mice were used to investigate the teratogenic effects of sporadic high doses of ethanol. Two consecutive days between days 8 and 11 of organogenesis were chosen on which to administer 0·5 ml of 20 per cent ethanol by gavage. An additional group was similarly dosed for four consecutive days starting on the eighth day. All the mice were killed on day 18 of gestation and evidence of growth retardation and malformation in the offspring was sought by skeletal and soft tissue screening. The basic pharmacokinetics of ethanol intake were also investigated. The most marked effects of ethanol were an increase in resorptions, skeletal growth retardation and skeletal variants, however all appeared to be strain specific. The results confirm that ethanol is embryotoxic and suggest that animal models are appropriate for studying aspects of growth retardation.
The endoendothelial layer of normal and injured vascular endothelium—an electron microscope study
Authors: Sztynda Tlamara , Hurley J. V. 
Published: June 2005

AbstractThe ultrastructural appearance of the endoendothelial lining of normal and injured small blood vessels has been examined after staining with alcian blue, ruthenium red or colloidal iron hydroxide. An endoendothelial layer is constantly present in all types of small blood vessel but its appearance and staining reactions are variable and unpredictable. Although normally visible only on the luminal aspect of endothelial cells, study of inflamed vessels suggests that it also covers the deep aspect of endothelium. The endoendothelial layer persists apparently unchanged after mild or severe injury to endothelium. It appears to be to some degree moveable and can be displaced by emigrating leucocytes, but rapidly regains its original position and appearance after the escaping cell has passed. No change in the appearance of the endoendothelial layer could be detected which might account for either the adhesion of leucocytes to vascular endothelium in areas of acute inflammation or of lymphocytes to the surface of high endothelial venules in lymphoid tissues.
Hexachloro‐1:3‐butadiene‐induced renal tubular necrosis in the mouse
Authors: Ishmael J. , Pratt Iona , Lock E. A. 
Published: June 2005

AbstractAdministration of hexachloro‐1:3‐butadiene (HCBD) intraperitoneally at a dose of 50 mg/kg body weight caused necrosis of the proximal tubule of the mouse kidney. The earliest morphological changes detectable by light microscopy were observed after 4 h, and by 16 h extensive proximal tubular necrosis was seen throughout the cortex. Active tubular regeneration was apparent by day 5 and by day 14 substantial recovery of morphology had occurred. In the electron microscope mitochondrial swelling was seen 1 and 2 h after dosing in the S1 and S2 segments of the proximal tubule, whereas by 4 and 8 h the major pathological changes were confined to the lower S2 and S3 segments and consisted of mitochondrial swelling and cellular necrosis. The extent of renal injury and regeneration correlated well with measurement of renal function. In conclusion, HCBD produces necrosis of the S2 and S3 segments of the proximal tubule in the mouse, this pattern of injury is different from that seen in the rat where HCBD produces selective necrosis of the S3 segment.
The glomerular tip lesion: A previously undescribed type of segmental glomerular abnormality
Authors: Howie Alexander J. , Brewer Douglas B. 
Published: June 2005

AbstractWe describe a distinctive and previously undescribed abnormality of the kidney. It consists of a combination of changes in the glomerulus and in the proximal convoluted tubule. The glomerular abnormality consists of a well‐localized collection of intracapillary foam cells and marked vacuolation of the adjacent glomerular epithelial cells. The abnormality is always situated in the same position in the glomerular tuft namely adjacent to the origin of the proximal convoluted tubule, with adhesion to Bowman's capsule. The rest of the tuft appears normal by light microscopy but shows foot‐process fusion by electron microscopy. The abnormality of the proximal convoluted tubular cells invariably affects the first part of the tubule adjacent to the glomerulus but in some cases involves the tubules more extensively in the cortex. Study of a series of 100 2‐μm serial sections from one case indicated that probably every glomerulus had a lesion at the origin of the tubule. A study of 185 renal biopsies nearly all with segmental lesions revealed biopsies from 20 patients with this distinctive abnormality. There were 14 males, age 20‐57, median 44 years, and six females age 19‐65, median 22 years, all presenting with proteinuria. nearly all with the nephrotic syndrome. All except four were treated with steroids and in all those treated the proteinuria improved. Only one patient not treated with steroids had progressive renal impairment. Four patients died, none from renal failure. This lesion, the glomerular tip lesion, as we have called it. seems to be a well‐defined and specific pathological entity. It has some similarities to minimal change nephropathy but there are clear and important differences. Previously it may have been included in series of cases of 'focal glomerulosclerosis' but that term is imprecise and is generally taken to have an unfavourable clinical course. For these reasons it is inappropriate to use ‘focal glomerulosclerosis’ as a name for the glomerular tip lesion.