The majority of women interviewed reported paying out-of-pocket costs for facility-based deliveries. Out-of-pocket costs were highest in Kenya (a mean of US$18.4 for normal and complicated deliveries), where 98% of women who delivered in a health facility had to pay some fees. In Burkina Faso, 92% of women reported paying some fees (mean of US$7.9). Costs were lowest in Tanzania, where 91% of women reported paying some fees (mean of US$5.1). In all three countries, women in the poorest wealth quintile did not pay significantly less for maternity costs than the wealthiest women. Costs for complicated delivery were double those for normal delivery in Burkina Faso and Kenya, and represented more than 16% of mean monthly household income in Burkina Faso, and 35% in Kenya. In Tanzania and Burkina Faso most institutional births were at mid-level government health facilities (health centres or dispensaries). In contrast, in Kenya, 42% of births were at government hospitals, and 28% were at private or mission facilities, contributing to the overall higher costs in this country compared with Burkina Faso and Tanzania. However, among women delivering in government health facilities in Kenya, reported out-of-pocket costs were significantly lower in 2006 than in 2003, indicating that a 2004 national policy eliminating user fees at mid- and lower-level government health facilities was having some impact.
syNopsIs A new test for the detection and measurement of toxoplasma antibody is described. Test sera are reacted with antigen-sensitized wells in micro-haemagglutination plates. Any attached antibody is shown by the addition of an enzyme-labelled antiglobulin followed by assay of the enzyme reaction with its substrate. The test is easy to carry out on a large scale, and there is a positive correlation between the results and dye test and haemagglutination test titres.The diagnosis of toxoplasmosis is not easy and is usually based on the critical assessment of one or more serological tests. The dye test (Sabin and Feldman, 1948), indirect immunofluorescence (Kelen et al, 1962), and passive haemagglutination (Jacobs and Lunde, 1975) are the tests most frequently employed. Karim and Ludlam (1975) London were tested by the dye test (Sabin and Feldman, 1948), by passive haemagglutination (Jacobs and Lunde, 1975), and by the microenzyme linked immunosorbent assay (MICRO-ELISA) described below. These sera came from clinically suspected cases of toxoplasmosis and 16 of them, with dye test titres over > 1/1024, were from typical lymphadenopathy cases. MICRO-ENZYME-LINKED IMMUNOSORBENT ASSAYThe enzyme-linked immunosorbent assay (ELISA) of Engvall and Perlmann (1972) with the modification (MICRO-ELISA) of Voller et al (1975a) was used. The principle of the assay is described in figure 1. For toxoplasmosis the test was carried out as follows: 1 The wells in microhaemagglutination plates (COOKE MICROTITER M29 AR') were sensitized with the toxoplasma antigen, diluted in 0-05M carbonate buffer, pH 9-6, overnight at + 4°C. The plates were then given three washes each of 3 minutes in phosphate buffered saline (PBS) containing 0-05 % Tween 20 and were shaken dry. 2 0 3 ml of the diluted serum was added to each well and incubated for 2 hours at room temperature.The plates were washed as before in PBS/Tween and were shaken dry. 3 0 3 ml of the diluted antiglobulin conjugate was added to each well and incubated for 3 hours
Abstract. The rhoptry is an organelle of the malarial merozoite which has been suggested to play a role in parasite invasion of its host cell, the erythrocyte. A monoclonal antibody selected for reactivity with this organelle identifies a parasite synthesized protein Of 110 kD. From biosynthetic labeling experiments it was demonstrated that the protein is synthesized midway through the erythrocytic cycle (the trophozoite stage) but immunofluorescence indicates the protein is not localized in the organelle until the final stage (segmenter stage) of intraerythrocytic development. Immunoelectron microscopy shows that the protein is localized in the matrix of the rhoptry organelle and on membranous whorls secreted from the merozoite, mAb recognition of the protein is dithiothreitol (DTT) labile, indicating that the conformation of the epitope is dependent on a disulfide linkage. During erythrocyte reinvasion by the extraceUular merozoite, immunofluorescence shows the rhoptry protein discharging from the merozoite and spreading around the surface of the erythrocyte. The protein is located in the plasma membrane of the newly invaded erythrocyte. These studies suggest that the ll0-kD rhoptry protein is inserted into the membrane of the host erythrocyte during merozoite invasion.RYTHROCYTE invasion by the malarial merozoite is a multi-step process, initiated by receptor-mediated binding of the parasite to its host cell (9). Electron microscopic studies show that penetration of the erythrocyte by merozoites involves invagination of the erythrocyte membrane where the apical end of the merozoite contacts the host cell (1). A moving membrane junction is formed and the contact maintained while the merozoite is internalized into a vacuole, which eventually forms the parasitophorous vacuole. Intracellular development of the parasite occurs inside this vacuole. Although it is well documented that invasion occurs by erythrocyte membrane invagination, the biochemical mechanisms whereby the parasite induces such a profound alteration in the rigid membrane-cytoskeletal organization of the erythrocyte are not understood.Endocytosis is not observed in erythrocytes except in druginduced instances (25). It has been proposed that the malarial parasite must initiate the membrane changes by some heretofore unknown process. Implicated in this unusual process are the rhoptries, a pair of electron dense organelles found in plasmodia and in other closely related members of the apicomplexa which are obligate intracellular parasites.Rhoptries of Toxoplasma, Sarcocystis and Besnoitia species have all been implicated in the invasion process. In Toxoplasma, a penetration enhancement factor possessing lytic activity has been identified, and is believed to be secreted by the rhoptries during invasion (15). In plasmodia the rhoptries are club-shaped organelles located randomly in the cytoplasm in the preinvasive stages of the parasite, that appear to subtend ducts to the exterior of the apical portion of the merozoite at the time of invasion. Electro...
The intracellular development of the erythrocytic stage of the malarial parasite (merozoite) is initiated by the attachment of the parasite to the erythrocyte surface. This paper describes an assay system to investigate Plasmodium falciparum merozoite entry into the host cell and reports on three observations regarding this interaction . (a) Merozoites do not invade human erythrocytes treated with either trypsin or neuraminidase, and both enzymes partially cleave glycophorin A, the major erythrocyte surface sialoglycoprotein . (b) A membrane protein fraction containing glycophorin A will, at low concentrations, inhibit the invasion of isolated merozoites into erythrocytes ; no other fractions of membrane proteins have appreciable effects on the reinvasion . (c) Merozoites do not reinvade erythrocytes preincubated with F ab' fragments of antibody prepared against glycophorin A. Together, these three observations imply a role for glycophorin A in the attachment of the malarial parasite to the erythrocyte surface .The development of the human malarial parasite Plasmodium falciparum occurs inside the erythrocyte, where it undergoes a process known as schizogony . The mature shizont ruptures, releasing into the serum individual merozoites which are then free to reinvade other erythrocytes . The attachment of the merozoite to the erythrocyte initiates reinvasion and a second cycle of intraerythrocytic growth. Entry has been observed by interference (1) and electron microscopy (2) and is a rapid event, being complete in 1 min . Biochemical characterization of the attachment phase has proved difficult due to the inherent problems in isolating viable merozoites free from host material. Miller and colleagues (3, 4) have studied the invasion of both P. falciparum and the simian parasite Plasmodium knowlesi.They concluded from a number of investigations that both parasites recognize specific receptors on the surface of the erythrocyte, but that the receptors are different for each parasite ; only P. knowlesi parasites interact with Duffy blood groups (3), whereas P. falciparum appears to interact with a glycoprotein on the erythrocyte surface (4) . Miller et al. (4) and Butcher et al . (5) have proposed that the existence of specific receptors on the different erythrocytes and parasites could explain hostparasite restriction of invasion. Biochemical determinants of the specificity of interaction of erythrocytes with different species of parasites has been reviewed recently by Sherman (6). In this work, the attachment of merozoites to the erythrocytes was studied by investigation of the entry of isolated merozoites.
In recent years, there has been significant concern, and policy activity, in relation to the problem of delayed discharges from hospital. Key elements of policy to tackle delays include new investment, the establishment of the Health and Social Care Change Agent Team, and the implementation of the Community Care (Delayed Discharge) Act 2003. Whilst the problem of delays has been widespread, some authorities have managed to tackle delays successfully. The aim of the qualitative study reported here was to investigate discharge practice and the organisation of services at sites with consistently low rates of delay, in order to identify factors supporting such good performance. Six 'high performing' English sites (each including a hospital trust, a local authority, and a primary care trust) were identified using a statistical model, and 42 interviews were undertaken with health and social services staff involved in discharge arrangements. Additionally, the authors set out to investigate the experiences of patients in the sites to examine whether there was a cost to patient care and outcomes of discharge arrangements in these sites, but unfortunately, it was not possible to secure sufficient patient participation. Whilst acknowledging the lack of patient experience and outcome data, a range of service elements was identified at the sites that contribute to the avoidance of delays, either through supporting efficiency within individual agencies or enabling more efficient joint working. Sites still struggling with delays should benefit from knowledge of this range. The government's reimbursement scheme appears to have been largely helpful in the study sites, prompting efficiency-driven changes to the organisation of services and discharge systems, but further focused research is required to provide clear evidence of its impact nationally, and in particular, how it impacts on staff, and patients and their families.
This paper examines how care home managers in England conceptualised the approach to delivering personalised care in the homes they managed. We conducted interviews with care home managers and mapped the approaches they described on two distinct characterisations of personalised care prominent in the research and practitioner literature: the importance of close care relationships and the degree of resident choice and decision-making promoted by the care home. We derived three ‘types’ of personalised care in care homes. These conceptualise the care home as an ‘institution’, a ‘family’ and a ‘hotel’. We have added a fourth type, the ‘co-operative’, to propose a type that merges proximate care relationships with an emphasis on resident choice and decision-making. We conclude that each approach involves trade-offs and that the ‘family’ model may be more suitable for people with advanced dementia, given its emphasis on relationships. While the presence of a range of diverse approaches to personalising care in a care home market may be desirable as a matter of choice, access to care homes in England is likely to be constrained by availability and cost.
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