Search

Evidence from bay floor channelling, seismic surveys and core dating has been used to suggest that Port Phillip Bay dried out for a period between about 2800 and 1000 cal. yr BP as sandbars blocked it off from the sea. This model is now supported by the examination of radiocarbon ages from archaeological excavations of Aboriginal shell middens on the shoreline of the Mornington Peninsula on Bunurong Country. This shows a near-continuous use of marine resources by Bunurong people over the last 6000 years for areas south of Rosebud, while those to the north are only of more recent date, following the refilling of the bay in the last millennium. This study provides an example of the integration of traditional, archaeological and geoscience evidence and the way in which local environmental changes impact on society. Radiocarbon dates from Aboriginal places support the argument that a sandbar blocked much of Port Phillip Bay from the sea between about 2800 and 1000 cal. yr BP. Dates from Aboriginal places south of the sand bar show continuity since the bay formed following the post-Pleistocene rise in sea-levels. Dates north of the sandbar indicate that Aboriginal people began exploiting marine resources in this area once the bay refilled about 1000 years ago. [ABSTRACT FROM AUTHOR]

Rigid endoscopes are complex, expensive, and fragile devices that routinely are subjected to harsh conditions. An endoscope used during only one procedure typically will be handled by a minimum of six people. Understanding what can go wrong with endoscopes and how to test them can help staff members detect problems before rather than during surgery. This article reviews some simple tests that can be used to ensure endoscope quality and provides information about how to demand excellence in endoscope repair. [ABSTRACT FROM AUTHOR]

Blood eosinophils from some patients with an eosinophilia have a higher capacity to bind to IgG antibody-coated red cells (EA) than blood eosinophils from normal people. Twenty per cent of eosinophils from normal blood bound EA, whereas eight of nine patients with hypereosinophilic syndromes and all nine patients with filariasis who were studied had blood eosinophils with EA rosette-forming capacities of between 42 and 89%. High EA binding capacity was reduced in culture, and prednisolone and cytochalasins A and B inhibited normal blood eosinophil EA binding. Normal blood eosinophils developed small increases in EA binding capacity in culture, but marked increases occurred after stimulation with soluble immune complexes, endotoxins and lipid A. Supernatants from granulocytes cultured with zymosan-C3b caused rapid increases in eosinophils EA binding capacity which also occurred with neuraminidase, pronase and trypsin. In vitro alterations in EA rosetting did not require protein synthesis and did not affect eosinophil phagocytic capacity for EA. Substances in culture which did not affect eosinophil EA rosetting capacity included sera from patients with eosinophils with high EA binding capacity and chemotactic substances. Cultured eosinophils also developed an increased capacity to form rosettes with EAC3b, and soluble immune complexes stimulated this further. Conversely, blood eosinophils formed less C3b rosettes when separated from heparinized blood in which C3 activation had occurred. Cytochalasin A (but not B) irreversibly inhibited eosinophils EAC3b rosette formation. Trypsin also inhibited, but this effect was reversed within 30 min after washing. It was concluded that eosinophils from normal blood have an intrinsically low capacity to bind EA, but that in vivo and in response to stimulation in vitro their ability to bind complexed IgG can approach that seen with blood neutrophils. It is suggested that enzymes in granulocyte secretion products may cause the membrane changes which lead to high eosinophils EA binding capacity. This increase, which can occur separately from alterations in EAC binding or phagocytic capacity, may enable eosinophils to take part more effectively in inflammatory reactions in tissues. [ABSTRACT FROM AUTHOR]

Studies were done to see whether large mononuclear cells in human afferent lymph possess cytoplasmic veils or Ia-like antigens on their surface. Small numbers of veiled cells were seen in lymph from five subjects: one with post-phlebitis oedema, one with trophic ulcers of the legs, one with common variable immunoglobulin deficiency, and two control subjects. They were not seen in afferent lymph from two other patients with oedema of the legs, and one control subject. Only occasional large mononuclear (veiled) cells formed rosettes with IgG-coated erythrocytes, and they did not attach to glass after overnight culture. They had a distinctive nuclear structure and fluorescent antisera showed that their membranes and veils possessed large amounts of `Ia-like' antigens. They did not have surface immunoglobulin or a monocyte membrane antigen. It was concluded that the membrane and nuclear structure of human large mononuclear (veiled) cells is in keeping with the possibility that they are derived from Langerhans' cells in the skin, and that they can become interdigitating cells in lymphoid tissues. It is suggested that these cells have an important role in the transport of antigens from the skin and the stimulation of T lymphocytes in lymphoid tissues. [ABSTRACT FROM AUTHOR]

A method has been developed for separating edsinuphils from other types of leucocyte in normal individuals. Erythrocytes are sedimented with dextran, and mononuclcar cells arc removed on an isotonic density gradient of ficoll and sodium diatrizoate. The eosinophils and neutrophils are then washed and sedimented onto plastic petri dishes coated with human IgCi and rabbit antihuman IgG antibody. As neutrophils and monocytes have Fc-binding sites for complexed rabbit IgG they attach to the dishes, and the unabsorbed normal eosinophils which lack this binding site are eluted in a purified suspension. The mean purity of the eosinophils obtained in this way was 70%, range 50-90%, and the mean yield was 40%, range 21-81%. This method provides purified eosinophils from normal people without subjecting them to osmotic or plasma membrane stimulation. Normal eosinophils which are prepared in this way are particularly suitable for studying the ways in which eosinophils become altered in disease states. [ABSTRACT FROM AUTHOR]

Studies were done on blood eosinophils from four patients with raised blood cosinophil counts and heart failure. In three of the patients cardiological studies demonstrated the distinctive endocardial lesions and restrictive cardiomyopathy of Löfller's endocarditis and endomvocardial fibrosis. The fourth patient died with similar symptoms and signs. In blood films it was fimud that all lour had more than 1×109 eosinophils per litre which were vacuolated and contained reduced numbers of crystalloid granules winch were also shown to have ultrastructural changes. Unlike cosinophils from normal individuals the patients' cosinophils possessed receptors for rabbit lgG-coated erythrocytes and actively phagocytosed erythrocytes coated with rabbit IgG or human C3b. It is concluded that in these patients, a large proportion of the circulating cosinophils had developed characteristics of mature or stimulated cosinophils. This enabled them to respond to soluble substances in the bliwdstrearn by forming endocytic vacuoles which led to degranulation of the crystalloid granules. These studies, taken in conjunction with other recent work in this field, support the concept that the restrictive cardiomyopathy of hypereosinophilic states, including Löffler's endocarditis and endomyocardial fibrosis, is a result of prolonged release of products from degranulated cosinophils while they are in the circulation. [ABSTRACT FROM AUTHOR]

Studies were done on blood eosinophils from six patients with a transient eosinophilia, to see whether blood cosinophils were structurally or functionally different front blood eosinophils in eleven normal individuals. It was found that many of the patients' eosinophils were vacuolated, and some contained less specific granules than normal. These cosinophils also possessed Fe receptors kr rabbit lgG. When the eosinophil counts returned to normal these abnormalities were longer found. The nature of these alterations are discussed in relation to the properties of cosinophils in tissues and other n pes of phagocyrtc cells responding to stimulae. Suggestions arc made about the mechanisms by which they could have come about. It was concluded that blood cosinophils in patients with an eosinophilia may be functionally mature or altered in response to unknown stimulae while they are in the blood. [ABSTRACT FROM AUTHOR]

Three patients are described with anorexia nervosa in whom malnutrition was present with neutropenia and a granulocyte bactericidal defect. Their peripheral blood granulocytes were found to have a reduced rate of killing of Staphylococcus aureus and E. coli in vitro. The opsonic activity of the patients' sera towards Staphylococcus aureus was normal. One of these patients had recurrent episodes of infection which stopped after she had gained 13 kg in weight. Clinical recovery was associated with a return of granulocyte function to normal. It is concluded that granulocyte bactericidal capacity towards a activity of bacteria may be reduced in patients with anorexia nervosa who have malnutrition. This type of acquired granulocyte bacterial deficiency appears to be reversible. [ABSTRACT FROM AUTHOR]

During the past decade, clinical and experimental studies have enabled the earliest forms of eosinophilic endomyocardial disease to be diagnosed by endomyocardial biopsy. Experimental studies have confirmed the suggestion that eosinophil granule constituents may be toxic to the heart, and eosinophil granule secretion products have been localized within the areas of acute necrosis. Biochemical and sequencing studies on the cationic proteins within eosinophils have confirmed their potential for causing tissue injury. In addition, the association of microvascular lesions, thrombo-embolic episodes and fibrotic lesions have all been linked to the capacity of eosinophils to produce a range of products of inflammation, including leukotriene C4, platelet activating factor and fibroblast proliferating factors. It is now suggested that these may contribute to the development of endomyocardial damage in patients with hypereosinophilia, irrespective of its cause. However, the proclivity of the endocardium for this type of lesion, and the ‘silent’ preclinical phase of the disease in many patients are important issues which remain unresolved. [ABSTRACT FROM PUBLISHER]

Fifteen patients with tropical endomyocardial disease which had been proved angiographically were studied using M-mode and cross-sectional echocardiography to determine the extent to which specific features of this disease could be recognised by these non-invasive methods. Tethering of the posterior mitral valve leaflet to the ventricular wall in combination with areas of echo-dense material in the posterior left ventricular wall and associated papillary muscle appeared to be a constant diagnostic feature of this disease. Colour coding of regional echo amplitude showed high intensity echoes in a distribution corresponding closely to that of the fibrosis known to occur in this condition. Though M-mode echocardiography did not contribute diagnostic information, it was useful in defining the functional consequences of myocardial or mitral valve disease. Digitisation of records allowed a restrictive pattern of left ventricular filling to be observed. It was concluded that cross-sectional echocardiography, particularly when supplemented by colour coded amplitude processing, can make a confident non-invasive diagnosis of tropical endomyocardial disease and so could be useful in assessing its progression or response to treatment. [ABSTRACT FROM PUBLISHER]

Nine patients with eosinophilic endomyocardial disease who had undergone angiocardiography with histological staging of their disease, were studied by M-mode and two dimensional echocardiography to determine the extent to which specific features of the disease could be evaluated by these non-invasive methods. In seven patients, amplitude processed two dimensional echocardiography showed regions where the relative intensity of endomyocardial echoes was greater than normal, and their distribution corresponded to known areas of fibrosis. Standard two dimensional echocardiography was normal in all but three patients. In eight patients M-mode echocardiography showed only non-specific abnormalities, but appeared to be useful in assessing the functional consequences of myocardial or mitral valve disease. After digitisation a reduction in the duration and an increase in the peak rate of dimension increase during filling was prolonged. It was concluded that amplitude processed two dimensional echocardiography might be useful in diagnosing the extent and severity of endomyocardial disease in patients with hyperosinophilia. These noninvasive techniques may thus provide a means for the early diagnosis of endomyocardial fibrosis and could be useful in assessing in progression or response to treatment. [ABSTRACT FROM PUBLISHER]

Cardiac surgery to treat severe heart failure was of benefit to two patients with endomyocardial disease and hypereosinophilia-eosinophilic endomyocardial disease. Both patients had severe biventricular fibrosis with mitral and tricuspid regurgitation. One had predominant right ventricular disease and was treated by right ventricular endocardectomy with tricuspid and mitral xenograft valve replacement. The second patient's main haemodynamic problem was considered to be mitral regurgitation. His mitral valve was replaced by a Starr-Edwards prosthesis; endocardectomy was not performed. Though both patients had toxic confusional states for several weeks postoperatively there was distinct symptomatic and objective evidence of improvement which has been maintained for over 16 months. Previous reports of surgical treatment of 22 patients without eosinophilia (all of whom had endomyocardial resection) and three other patients with eosinophilia have shown equally encouraging results. There has been no evidence of recurrence or progression of heart damage in follow-up periods of up to seven years. It is concluded that cardiac surgery is an important advance in the treatment of endomyocardial disease in patients with or without an eosinophilia. [ABSTRACT FROM PUBLISHER]

This study was designed to compare the clinical and cardiological features of endomyocardial disease in temperate and tropical regions. Eleven patients were studied in the U.K., 47 in India and 8 in Brazil. The patients in the U.K. were older, with a male predominance, and they had a systemic illness: the hypereosinophilic syndrome. Half of these patients presented in the early necrotic stage of the disease, and all had biventricular involvement. On the other hand, patients in the tropical countries were younger, with an equal sex incidence, and were from poor, malnourished communities with heavy parasite loads, especially filariasis in India. None presented in the early necrotic stage of the disease and a quarter had isolated right or left ventricular disease. In order to account for these differences between patients in temperate and tropical regions with endomyocardial disease, it was proposed that the nature of the underlying disease and the rate at which endomyocardial lesions develop, determine the clinical features of this disorder. In temperate climates eosinophil granule toxins may produce a rapidly progressive form of the disease in patients with the hypereosinophilic syndrome, whereas the disease may take longer to develop in patients in tropical climates, who have a less marked eosinophilia due to parasitic infections. [ABSTRACT FROM AUTHOR]

Although an association between high blood eosinophil counts and endomyocardial disease has been known for nearly a hundred years, the reasons for this were not understood. Brockington, Luzzatto and Osunkoya (1970) suggested that eosinophil leucocytes, in susceptible persons, by some unknown mechanisms, cause endomyocardial damage. Evidence to support this possibility has come from three sources: (1) Clinical studies have shown that very high blood eosinophil counts, from any cause, can be associated with endomyocardial disease, and in some patients it has been possible to show that eosinophilia preceded the onset of heart disease. (2) The development of heart disease has been associated with the presence of degranulated eosinophils in the blood and tissues, including damaged endomyocardium, and raised serum levels of eosinophil granule basic proteins have been found in many of these patients. (3) Low concentrations of eosinophil secretion products (which contain these eosinophil granule basic proteins) have been found to injure isolated heart cells in vitro. Studies with purified eosinophil granule basic proteins have shown that cardiac cell damage is the result of a specific toxic effect of eosinophil cationic protein on the plasma membrane and two enzyme complexes (pyruvate dehydrogenase and 2-oxoglutarate dehydrogenase) involved in mitochondrial respiration. These results support the suggestion that under certain conditions, eosinophils may damage the heart, leading to endomyocardial disease, and they offer new approaches for the early diagnosis and treatment of endomyocardial disease both in temperate and tropical countries. [ABSTRACT FROM PUBLISHER]

About one third of patients with Löffler's endomyocardial disease have abnormal electrocardiograms and some develop arrhythmias and die suddenly. To assess the significance of these findings, continuous ambulatory ECG monitoring was performed for 48 hr on 6 patients with acute or chronic forms of Löffler's endomyocardial disease, and the types and frequencies of arrhythmias were compared with recordings from 6 other patients with equally high blood eosinophil counts who did not have clinically evident cardiac disease. It was hoped that this would show whether arrhythmias were related to high blood eosinophil counts, cardiac injury or other factors. Three of the patients with endomyocardial disease had multiple ventricular extrasystoles with episodes of ventricular arrhythmias and occasional supraventricular arrhythmias which had not been detected with conventional ECGs. These abnormalities did not occur in 2 of the patients with acute endomyocardial lesions who died, nor were they found in patients who did not have congestive cardiac failure or in the control patients. Rhythm disturbances appeared to be most closely related to the development of cardiac failure and they resolved after successful cardiac surgery. Multiple ventricular extrasystoles and arrhythmias occurring in these patients with Löffler's endomyocardial disease are probably due to metabolic changes in the heart associated with cardiac failure and mechanical changes related to valvular dysfunction rather than a direct effect of the eosinophils themselves on the heart. [ABSTRACT FROM PUBLISHER]

Immunohistochemical studies were performed in thirty skin biopsies from patients with Kaposi's sarcoma, who did and did not have the acquired immune deficiency syndrome (AIDS). Tumour histogenesis was rigorously tested using a battery of endothelial cell markers, which included two new monoclonal antibodies, EN4 and PAL E. These are both specific for endothelial cells and can be visualised in appropriately fixed paraffin embedded tissue. Whereas EN4 labels all endothelial cells, PAL E is negative in endothelium of lymphatic derivation. Lectin binding with Ulex europaeus agglutinin 1 (UEA-1) and the presence of factor VIII related antigen (FVIIIRA) and laminin were also examined. In nodular lesions of Kaposi's sarcoma the spindle cell areas were positive with EN4 and UEA-1, negative with PAL E, and showed focal staining for FVIIIRA and laminin. These results confirm that the tumour is of endothelial cell origin. Six patch stage lesions showed a network of angulated spaces, lined by cells that were positive with EN4 and UEA-1, negative with PAL E and anti-FVIIIRA, and showed only weak staining for laminin. This pattern was observed in both AIDS and non-AIDS related cases and strongly favours a lymphatic derivation for the tumour. This has important implications as it suggests that lymphatic endothelium may have special characteristics that lead to neoplastic transformation in patients with retrovirus infection. [ABSTRACT FROM PUBLISHER]

This study was done to examine the nature of the membrane constituents involved in the secretion of eosinophil cationic protein (ECP) from human blood eosinophils. Three mouse monoclonal antibodies were used, which showed greater binding to membrane antigens on activated, and light density eosinophils from patients with an eosinophilia, than on nonactivated or normal density eosinophils. All three antibodies (EoN4, EoN5 & EoN6) stimulated normal density human eosinophils to secrete ECP, either alone or in association with sepharose-C3b. The antibodies bound to at least two separate sites on the membrane, which were distinct from the receptors for immunoglobulins, C3b, and eosinophil activating factor. One combination of antibodies increased the amount of ECP which was secreted. The membrane antigen recognized by antibody EoN4 was a glycoprotein, molecular weight 75 kD. These findings showed that ECP secretion may be induced by a wider range of stimuli than has been previously recognized, and that the antigens recognized by these monoclonal antibodies may play an important role in the induction of eosinophil degranulation. [ABSTRACT FROM AUTHOR]

In order to study the membrane events which lead to human blood eosinophil activation and degranulation, six clone of mouse monoclonal antibodies were made to isolated blood eosinophils from a patient with the hypereosinophilic syndrome (HES). The antibodies were specific for the plasma membranes of blood eosinophils and neutrophils, eosinophil myelocytes and haemopoietic cell lines. A higher proportion of blood eosinophils from eight patients with the HES bound these antibodies compared to normal individuals. Five antibodies stained intermediate density eosinophils preferentially, and one stained the light density eosinophils most strongly. Normal blood eosinophils were induced to express more of these antigens either by culture alone (two antibodies) or culture with monocyte culture supernatant which activates eosinophils for increased cylotoxic capacity (four antibodies). It was concluded that several of the principal antigens on the eosinophil plasma membrane are also present on neutrophils and immature haemopoietic cells, and that their expression in mature blood eosinophils is related to the extent of eosinophil activation and degranulalion. It is suggested that these antigens may be useful in studying the ways in which eosinophils alter their plasma membrane during activation and degranulation in vitro, and in the blood of patients with an eosinophilia. [ABSTRACT FROM AUTHOR]

High blood eosinophil counts in humans are usually due to parasitic infections, allergic processes or malignant diseases, lnterleukin-5 (IL-5) is thought to be the principal eosinopoietic stimulus in most of these patients. As the causes of persistent eosinophilia in patients with the idiopathic hypereosinophilic syndrome (HES) are (by definition) unknown, a semi-quantitative assay for IL-5 mRNA in eosinophils and mononuclear cells was carried out using samples from 11 patients with HES. In three patients, unstimulated peripheral blood mononuclear cells (PBMC) and bone marrow mononuclear cells (BMMC) had markedly raised levels of IL-5 mRNA. In four of five patients studied, phorbol myristate acetate (PMA) stimulation of PBMC induced them to produce more IL-5 mRNA than four healthy subjects. In five patients, bone marrow IL-5 mRNA levels were related to blood eosinophil counts. Blood eosinophils from all six patients tested, and bone marrow granulocytes from four patients had undetectable levels of IL-5 mRNA. It was concluded that HES can be separated into two groups. One has high levels of IL-5 mRNA and/or an enhanced IL-5 mRNA response to stimulation. They may well respond to treatments which inhibit the effects of this cytokine on eosinophil progenitor cells. The second group appears to have a disease which is IL-5 independent. [ABSTRACT FROM AUTHOR]